Cardiac Surgery Essentials for Critical Care Nursing (Hardin, Cardiac

Hardin

Kaplow SurgeryCardiac

Cardiac Surgery r o f

f o r Nursing Care Critical Essentials Critical Care Nursing Sonya R. Hardin Roberta Kaplow Cardiac Surgery Cardiac Surgery Essentials for Critical Care Nursing is an evidence-based foundation for care of the patient during the vulnerable period immediately following cardiac surgery. A comprehensive resource, this text serves as a building block for nurses f o r beginning to care for cardiac surgery patients, as well as a source of advanced knowledge for nurses who have mastered the essential basic skills. It addresses Essentials significant changes in cardiac surgery and the nursing responsibilities to meet the needs of these acutely ill patients, as well as advances and strategies to optimize Essentials patient outcomes in this dynamic field. Critical Care Nursing The perfect study aid for those readers preparing for the AACN’s Cardiac Surgery Certification, this book features critical thinking questions, multiple-choice self- assessment questions, Web resources, clinical inquiry boxes, and case studies.

www.jbpub.com/nursing For a complete listing of Nursing titles visit: Sonya R. Hardin

ISBN: 978-0-7637-5762-5 Roberta Kaplow 57625_CH00_FM_i_x.pdf 4/10/09 11:09 AM Page i

Cardiac Surgery

Essentials FOR Critical Care Nursing

&EJUPST Sonya R. Hardin, PhD, RN, CCRN, ACNS-BC, NP-C "TTPDJBUF1SPGFTTPS 4DIPPMPG/VSTJOH $PMMFHFPG)FBMUIBOE)VNBO4FSWJDFT 6OJWFSTJUZPG/PSUI$BSPMJOBBU$IBSMPUUF $IBSMPUUF /PSUI$BSPMJOB 4UBGG/VSTF %BWJT3FHJPOBM.FEJDBM$FOUFS 4UBUFTWJMMF /PSUI$BSPMJOB

Roberta Kaplow, PhD, RN, AOCNS, CCNS, CCRN $MJOJDBM/VSTF4QFDJBMJTU &NPSZ6OJWFSTJUZ)PTQJUBM "UMBOUB (FPSHJB 57625_CH00_FM_i_x.qxp:57625_CH00_FM_i_x 3/22/10 11:06 AM Page ii

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Copyright © 2010 by Jones and Bartlett Publishers, LLC All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission from the copyright owner. The authors, editor, and publisher have made every effort to provide accurate information. However, they are not responsible for errors, omissions, or for any outcomes related to the use of the contents of this book and take no responsibility for the use of the products and procedures described. Treatments and side effects described in this book may not be applicable to all people; likewise, some people may require a dose or experience a side effect that is not described herein. Drugs and medical devices are discussed that may have limited availability controlled by the Food and Drug Administration (FDA) for use only in a research study or clinical trial. Research, clinical practice, and government regulations often change the accepted standard in this field. When consideration is being given to use of any drug in the clinical setting, the health care provider or reader is responsible for determining FDA status of the drug, reading the package insert, and reviewing prescribing information for the most up-to-date recommendations on dose, precautions, and contraindications, and determining the appropriate usage for the product. This is especially important in the case of drugs that are new or seldom used. Production Credits Publisher: Kevin Sullivan V.P., Manufacturing and Inventory Control: Acquisitions Editor: Emily Ekle Therese Connell Acquisitions Editor: Amy Sibley Composition: Shepherd, Inc. Associate Editor: Patricia Donnelly Cover Design: Scott Moden Editorial Assistant: Rachel Shuster Cover Image: © Vividfour/Shutterstock, Inc. Associate Production Editor: Sarah Bayle Printing and Binding: Malloy, Inc. Senior Marketing Manager: Barb Bartoszek Cover Printing: Malloy, Inc. Library of Congress Cataloging-in-Publication Data Cardiac surgery essentials for critical care nursing / [edited by] Sonya R. Hardin, Roberta Kaplow—1st ed. p. ; cm. Includes bibliographical references and index. ISBN-13: 978-0-7637-5762-5 ISBN-10: 0-7637-5762-4 1. Heart—Surgery—Nursing. I. Hardin, Sonya R. II. Kaplow, Roberta. [DNLM: 1. Heart Diseases—nursing. 2. Cardiac Surgical Procedures—nursing. 3. Critical Care—methods. WY 152.5 C26737 2009] RD598.C3455 2009 617.4’120231—dc22 2009001294

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Dedication

This book is dedicated to Jack, Eleanor, Susan, Ray, Grace, Princess, Pauline, James, and Bria. We are grateful for your love, support, patience, and encouragement as we worked the production of this book. A special thanks to James R. Perron, PE, our medical illustrator, who was responsive to all of our late-hour requests and showed great patience with our attention to detail. He was a true asset to the development of this book. 57625_CH00_FM_i_x.pdf 4/10/09 11:09 AM Page iv 57625_CH00_FM_i_x.pdf 4/10/09 11:09 AM Page v

Contents

Contributors...... vii Preface ...... ix Chapter 1 Clinical Judgment in Critical Care ...... 1 Susan K. Chase Chapter 2 Cardiovascular Anatomy and Physiology...... 13 Susan K. Chase Chapter 3 Indications for Cardiac Surgery ...... 27 Kristine J. Peterson Chapter 4 Preoperative Cardiac Surgery Nursing Evaluation ...... 53 Roberta Kaplow, Sonya R. Hardin, Brenda Hardin-Wike, and Timothy E. McMurry Chapter 5 Heart Valve Surgery ...... 73 Catherine Drumm and Kristine J. Peterson Chapter 6 Minimally Invasive Cardiac Surgery ...... 93 Jenniffer Hughes and Kirsten Platt Chapter 7 Cardiopulmonary Bypass and Off-Pump Coronary Artery Bypass ...... 115 Julie Miller Chapter 8 Recovery from Anesthesia...... 127 Toni Patrice Johnson Chapter 9 Hemodynamic Monitoring ...... 145 Mary Zellinger Chapter 10 Intra-aortic Balloon Pump...... 165 Barbara Hutton-Borghardt Chapter 11 Mechanical Ventilation After Cardiac Surgery ...... 185 Mary Jane Bowles Chapter 12 Pharmacologic Support Following Cardiac Surgery ...... 205 Timothy E. McMurry, Roberta Kaplow, and Sonya R. Hardin

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vi Contents

Chapter 13 Postoperative Complications of Cardiac Surgery and Nursing Interventions .... 257 Beverly Jones Chapter 14 Pain Management...... 287 Susan Lynch Chapter 15 Postoperative Dysrhythmias ...... 309 Roberta Kaplow and Dawn B. Adams Chapter 16 Neurologic Complications...... 323 Myra F. Ellis Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery ...... 345 Carol Isaac MacKusick Chapter 18 Wound Care ...... 371 Mary Zellinger and Vicki Morelock Chapter 19 Bridge to Transplant and Cardiac Transplantation ...... 393 Rachel S. Ball, Kathy Halabicky, Laurie Hartman, Erin Lindstrom, and Tracey Romans Glossary ...... 433 Index ...... 445 57625_CH00_FM_i_x.qxp:57625_CH00_FM_i_x 3/22/10 11:06 AM Page vii

Contributors

Dawn B. Adams, RN, MSN, CCRN Kathy Halabicky, RN, MSN, ACNP Clinical Nurse Specialist Nurse Practitioner Project Coordinator Cardiac Surgery Critical Care DeKalb Medical University of Michigan Medical Center Decatur, GA Ann Arbor, MI

Rachel S. Ball, RN, MSN, ACNP Brenda Hardin-Wike, RN, MSN, CCRN, CCNS Nurse Practitioner Unit Director CTICU 7 ICU Cardiac Surgery Critical Care University of California at Los Angeles University of Michigan Medical Center Ronald Reagan Medical Center Ann Arbor, MI Los Angeles, CA

Mary Jane Bowles, RN, MSN, CCRN Laurie Hartman, RN, MSN, ACNP Clinical Specialist, CC Dept. Coordinator Advanced Practice Team Mary Washington Hospital Cardiac Surgery Critical Care Fredericksburg, VA University of Michigan Medical Center Ann Arbor, MI Susan K. Chase, EdD, APRN, BC Professor Jenniffer Hughes, RN, CCRN-CSC College of Nursing Clinical Nurse III University of Central Florida Cardiothoracic ICU Orlando, FL University of North Carolina Hospital Chapel Hill, NC Catherine Drumm, RN-BC, MA Nurse Manager Barbara Hutton-Borghardt, RN, MSN, CCRN Private Ambulatory Practices Nursing Supervisor Hospital for Special Surgery Memorial Sloan-Kettering Cancer Center New York, NY New York, NY

Myra F. Ellis, RN, MSN, CCRN-CSC CTICU, Clinical Nurse IV Duke University Hospital Durham, NC

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viii Contributors

Toni Patrice Johnson, RN, MSN, CNS, Julie Miller, RN, BSN, CCRN CPAN Staff Development Educator, Critical Care Clinical Nurse Specialist Trinity Mother Frances Hospitals and Clinics Perioperative and Endoscopic Services Tyler, TX Emory University Hospital, Midtown Atlanta, GA Vicki Morelock, RN, MN, CCRN Clinical Nurse Specialist for Cardiovascular Beverly Jones, RN, MSN, ACNP Surgical Services University of Michigan Medical Center Emory University Hospital, Midtown Cardiac Surgery Critical Care Atlanta, GA Ann Arbor, MI Kristine J. Peterson, RN, MSN, CCRN, Erin Lindstrom, RN, MSN, FNP CCNS Nurse Practitioner Clinical Nurse Specialist, CV and Critical Care Cardiac Surgery Critical Care Park Nicollet Methodist Hospital University of Michigan Medical Center St Louis Park, MN Ann Arbor, MI Kirsten Platt, RN, BSN, CCRN Susan Lynch, RN, MSN Clinical Nurse II RN-BSN Coordinator Cardiothoracic ICU School of Nursing University of North Carolina Hospital University of North Carolina at Charlotte Chapel Hill, NC Charlotte, NC Tracey Romans, RN, MSN, FNP Carol Isaac MacKusick, RN, MSN, PhD(c), Nurse Practitioner CNN Cardiac Surgery Critical Care Assistant Professor of Nursing University of Michigan Medical Center Clayton State University Ann Arbor, MI Morrow, GA Mary Zellinger, RN, MN, ANP, CCRN-CSC Timothy E. McMurry, RN, BSN, CCRN-CSC Clinical Nurse Specialist Clinical Coordinator, CVRU Cardiovascular Surgical Services Presbyterian Hospital Emory University Hospital Charlotte, NC Atlanta, GA 57625_CH00_FM_i_x.pdf 4/10/09 11:09 AM Page ix

Preface

ostoperative care of the cardiac surgery patient is both challenging and dynamic. Changes in technology, new research findings, the advent of minimally invasive procedures, and Pthe development of off-pump procedures now afford patients of advanced age and with higher levels of acuity the opportunity to undergo procedures for which they were deemed unsuitable candidates not so long ago. Hence, patients with more—and more significant— comorbidities are receiving care in the immediate postoperative period in the intensive care unit. Patients who undergo cardiac surgery are at risk for several adverse events not only related to their preoperative condition, but also as a result of effects of the surgical procedure and anesthesia. This requires ICU nurses to demonstrate high levels of clinical judgment, clinical inquiry, and caring practices to effectively manage patients and help optimize outcomes. High-level competency as a facilitator of learning is also required as nurses prepare their patients to undergo cardiac surgery. Clearly, ICU nurses, as members of a multidisciplinary team, play a pivotal role in promoting 10-year survival and high quality of life for patients who undergo cardiac surgery. This book is designed to address the needs of both new and experienced nurses who care for patients in the ICU immediately following cardiac surgery. The purpose of this book is twofold. First, it is designed to prepare the nurse who is first learning to care for patients undergoing cardiac surgery. It addresses significant changes in cardiac surgery and the nursing responsibilities required to meet the needs of these acutely ill patients. Second, the book provides advanced knowledge and a scientific basis for care for nurses who have mastered the essential knowledge and skills necessary to care for this patient population, but who now seek to develop a more in- depth knowledge base about advances in this dynamic field and strategies to optimize patient outcomes. The emphasis throughout the book is providing an evidence-based foundation for care of patients during the vulnerable period immediately following cardiac surgery. A number of chapters in the book will also prove useful to nurses who work in other areas in which there are acute and critically ill patients, as many of the concepts discussed here can be translated into care of patients other than those who have undergone cardiac surgery.

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x Preface

Because this book uses a comprehensive approach to address the needs of patients in the immediate postoperative period following cardiac surgery, it can also be used to help prepare nurses who plan to take the Cardiac Surgery Certification (CSC) subspecialty exam offered by the American Association of Critical-Care Nurses. Throughout the book, Clinical Inquiry Boxes highlight research findings that have implications for nursing practice. Other features that promote critical thinking and provide application of content are the Case Studies and Critical Thinking Questions that follow the respective chapter content. To further enhance critical thinking and for nurses preparing for the CSC exam, the Self-Assessment Questions found at the end of each chapter can be used as practice questions. 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 1

Chapter 1 Clinical Judgment in Critical Care

Susan K. Chase

■ INTRODUCTION The critical care unit provides a location for critical care nurses as they make these deci- continuous monitoring of unstable patients sions. It will be useful to new critical care as well as a context for the use of invasive nurses as they learn to provide safe care. At technology that supports basic life processes the same time, it will also be useful to experi- for acute and critically ill patients. Learning enced critical care nurses who wish to about technology and mastering its safe use improve their processes of thinking and are often the foci of basic critical care educa- communicating. tion and orientation. Aside from its technol- The thinking processes used by critical care ogy, the more basic value of a critical care unit nurses (CCNs) differ quite dramatically from is the level of clinical judgment that occurs the schoolbook description of the “nursing there. The thinking processes of clinicians process.” The linear process of collecting from a variety of disciplines are essential to information, forming a decision, choosing an safe and effective care. The potential for opti- action, and evaluating that action is rarely mal outcomes is enhanced when clinical judg- used in real-world practice. In critical care, ments occur with the nurse synthesizing and multiple conditions are assessed simultane- interpreting multiple, often conflicting ously, a variety of actions and interventions sources of data (Hardin & Kaplow, 2005). are carried out concurrently, and the condi- Working in a critical care area is both excit- tion of the patient changes constantly. There ing and rewarding—but it is also demanding is not a single diagnosis or condition that is and challenging. Nurses in critical care are “resolved.” Because the thinking work of central for rapid response to potentially life- CCNs is not a linear process, this chapter is threatening conditions and key in humaniz- likewise not linear. It deals in general terms ing technological care. Since critical care units with phases of the “thinking work” of nurs- were first developed, the monitoring of, and ing, but acknowledges that thinking and act- early response to changes in, patients’ condi- ing often overlap in real life. tions by nurses have revolutionized care. Clinical judgment is one of the eight nurse Nurses in critical care areas must make rapid competencies of the AACN Synergy Model for and accurate decisions about diagnostic and Patient Care adopted by the American Associ- treatment approaches in an independent way ation of Critical-Care Nurses (AACN) (Reed, or based on protocols or standard orders. Cline, & Kerfoot, 2007). Clinical judgment is This chapter describes the processes used by defined as the use of clinical reasoning

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including decision making, critical thinking, another explanation. In the example just and achieving a global grasp of a situation, given, if the nurse notes cloudiness in urine coupled with nursing skills acquired through and an elevation of body temperature, then a process of integrating education, experi- the probability that the hypothesis of infec- mental knowledge, and evidence-based guide- tion is correct is increased. This, in turn, lines (AACN, 2002). directs further action by the nurse. More data can be collected, such as a urinalysis and ■ CLINICAL JUDGMENT PROCESSES urine culture, to rule in (confirm) a urinary tract infection. Research has provided a window into how The information processing model focuses humans think and make decisions. Several on reevaluating competing hypotheses based models can help clinicians understand their on new data (Thompson & Dowding, 2002). decision-making processes and help them to In critical care areas, nurses frequently work become more efficient and to reduce errors in independently in choosing further data to be judgment. The three models that are useful in collected to support a hypothesis. Units may critical care are information processing, intu- have protocols that authorize the nurse ition, and decision analysis (Chase, 2004). to proceed with further data collection with- Each model contributes a unique perspective out obtaining orders from a physician. This to decision making, and clinicians can choose relative autonomy increases the necessity for which model to apply based on matters of critical care nurses to exercise appropriate individual style. The nature of specific prob- judgment. It would not be appropriate judg- lems may also determine which model is use- ment for the nurse to run expensive tests if ful in a particular situation. the data do not warrant it. Judgment includes the decision to do things or not to do them. Information Processing An economy of practice occurs when all The information processing model uses the appropriate actions—but only appropriate analogy of the human brain working like a actions—are taken. To make the choice of fur- computer as it processes new information ther diagnostic testing, all information pres- that becomes available. It also relies on the ent must be considered. assumption that an “optimal” diagnosis can In real life, nurses frequently need to act be made by taking into account the data that before all information necessary to confirm a are available in the problem situation. The diagnosis is available. If a condition that is possible diagnoses or problems that might be suspected is particularly critical, such as present for a patient are called “hypotheses” impending respiratory failure, actions to sup- before they are confirmed. There are usually port the patient must be taken even before a multiple competing hypotheses to explain a full understanding of the reason for such fail- particular pattern of data. For example, a ure is obtained. To wait to offer support until nurse may notice that a diabetic patient has a the patient is in full respiratory failure is to serum glucose level above baseline. This find- miss the opportunity to offer timely intervening might be a result of several causes—a tions that support the patient’s function. At faster than expected glucose infusion, a new times, by taking the most appropriate actions infection, or a missed insulin dose, among for the most likely problem and then noting other possibilities. Each of these possibilities the patient’s response to those measures, the is a hypothesis. Further data collection can diagnosis is either confirmed or refuted. If the help to narrow the options by ruling out cer- treatment approach does not work, addi- tain problems or increasing the likelihood of tional reasons for the patient’s problems 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 3

Clinical Judgment Processes 3

must be investigated. New data must be con- that the patient is not in impending respira- sidered to help develop a picture that answers tory failure or experiencing anxiety. Standard the question, “What’s going on with this support and monitoring will likely be suffi- patient?” cient to detect any changes in patient status. In any clinical situation, certain diagnoses A rapid respiratory rate or restlessness in the or problems are possible, and some are more patient should cause the nurse to set up dif- likely than others. Critical care units are ferent levels of support and to collect addi- places where monitoring equipment allows tional data. for the collection of a wider range of data than in less acute settings. Critical care nurses Managing Data are the constant collectors and evaluators of In real life, multiple conditions may occur clinical data. Early in their careers, nurses new concurrently, and one finding (e.g., vital sign, to critical care may focus on the compilation hemodynamic parameter, lab value, assess- of data through the use of new or unfamiliar ment finding) may provide evidence for a equipment such as electrocardiography, mon- variety of conditions. Because so much infor- itoring systems that reflect and record hemo- mation is collected and used to form judg- dynamic parameters through the use of a ments in acute and critical care settings, pulmonary artery catheter or continuous flowsheets—either written on paper or assem- blood pressure through intra-arterial lines. It bled electronically—are used to organize and is appropriate that new nurses focus on per- present the many pieces of information. fecting their skills in managing and interpret- Recognition of any condition depends on ing data from these systems. The assembly of seeing patterns in the wide range of data information is just one small aspect of critical available. Additionally, flowsheets enable care nursing, however. The data obtained healthcare providers to see how data points from monitoring systems represent key com- change over time. Individual values in isola- ponents to be utilized in understanding the tion are not reflective of the whole person, full clinical picture presented by the patient. nor are they reflective of the direction that a Nurses collect and evaluate data to arrive at particular patient’s condition is taking. Is the a diagnosis. Even after an initial medical diag- patient becoming more stable or less stable? nosis of acute myocardial infarction (AMI) is Is mechanical ventilation providing adequate made, for example, the critical care nurse has support of physiologic function, or is the many diagnostic options to consider. AMI patient so agitated or distressed by being patients may develop dysrhythmias, cardio- unable to speak that expenditure of unneces- genic shock, pulmonary edema, or anxiety. sary energy is occurring? Is the patient failing Early detection of these conditions can lead to respond to any treatment approach such to early and more effective treatment and bet- that multiple organ dysfunction syndrome is ter outcomes. As more data are collected, they occurring? Seeing the whole of a situation change the likelihood of each of the possible comes with experience. It can lead to intu- complications that might occur. A normal ition, the topic of the next subsection. respiratory rate and arterial blood gas values within normal limits for the patient’s age, for instance, indicate that respiratory failure is Intuition not imminent. Even simple data, such as vital Once the nurse is oriented to critical care, the signs, offer a view of the wholeness of the patterns of human response to challenges patient and change the diagnostic possibili- faced in critical situations become more evi- ties. A normal respiratory rate might indicate dent and easily recognizable. Eventually, the 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 4

4 Chapter 1 Clinical Judgment in Critical Care

nurse is able to see the wholeness of a situa- physiologic support during response from tion. The pieces of data are not seen dis- trauma or surgery? On a larger scale, if a new cretely, but rather as patterns indicative of the closed system suction device is used, what whole. The nurse may simply look at the will be the reduced cost of care if the rate of patient and recognize impending loss of sta- ventilator-associated pneumonia is reduced? bility or the loss of the will to live. At times, Decision analysis uses frequency and cost experienced nurses will see a pattern or feel a data to weigh options in care. It can be used “gut” response to a clinical situation that for either individuals or groups of patients. allows them to “know” the situation of the Many current guidelines for practice are patient without spending time processing based on this kind of mathematical analysis. individual pieces of data. Of course, to provide the data that an interdisciplinary team ■ needs to set up a treatment plan, nurses must RELATIONSHIP-CENTERED generate data and check on those “gut” feel- CARING IN CRITICAL CARE ings they have about the patient. What is All nursing is carried out in the setting of rela- interesting is that the intuition precedes the tionships. Despite the fact that many criti- action. Nurses can develop their intuitive cally ill patients are intubated and unable to skills by discussing their “hunches” about speak, nurses form relationships with their patients, by analyzing which indicators led patients and their families. Such relationships them to their intuitive sense, and by checking are not just “being nice”; rather, they are cen- their own accuracy. Experienced nurses can tral to coming to know patients and how they do this in unit nursing rounds or in clinical respond to the challenges of illness. Critical case discussions. care nurses learn to recognize the patterns of The AACN Synergy Model for Patient Care patient responses. How one patient responds recognizes that as nurses gain expertise, they to the physical challenge of weaning from move from Level 1, which focuses on data col- mechanical ventilation is different from how lection, following decision trees, and using another patient does. For example, one standard protocols, to Level 3, where nurses patient may become tachypneic in response to are able to see the wholeness of situations the increased work of breathing during wean- quickly. A sense of understanding of the direc- ing, whereas another patient may experience an tion of processes is part of the competency of increased heart rate. Recognizing and commu- these nurses. At Level 5, nurses synthesize nicating patient response patterns is important large amounts of data and help the entire to excellence in critical care nursing. Recogniz- team to recognize the “big picture” of what is ing the patterns of how patients respond to happening with the patient (Reed et al., 2007). challenges can help the nurse decide when in the day is best to provide physical care or to attempt a weaning trial. If a patient did not Decision Analysis sleep the previous night, for example, then rest Decision analysis is an approach to decision before weaning may result in a better response. making based on mathematical models that The relationships formed by nurses also take into consideration the likelihood of spe- extend to patients’ families. Family members cific responses given action options. What is can provide needed comfort and a quiet pres- the likelihood that a patient who is intubated ence, or they can spread their own anxiety to will develop pneumonia? What is the likeli- the patient. Supporting the family and man- hood that the same intubation will allow for aging their responses and connection to the 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 5

Day-to-Day Practice 5

patient are important interventions for opti- Establishing and verifying the data collec- mal outcomes. Family members can assist tion and monitoring system are important CCNs in coming to know their patients, first steps in critical care judgment. The next thereby helping ensure that the nurses can step is establishing regular monitoring rou- understand what matters most to the patients. tines. Most critical care units have unit- Now that we have explored the various specific routines for data collection, and some ways of thinking that can be used in clinical establish routines for monitoring particular judgment situations, we will see how CCNs types of clinical problems. These routines are can use these models in day-to-day practice. important because a patient’s status may change frequently in critical care, and regular monitoring allows the nurse to detect ■ DAY-TO-DAY PRACTICE changes early, when intervention can prevent Critical care units are areas where specialized clinical deterioration. The nurse should con- equipment allows for the continuous collec- sider, however, that each decision about data tion of data related to a patient’s status. The collection also has its own cost. For example, quality of the data being collected and frequent blood draws over time can result in recorded is a central issue. If an intra-arterial noticeable blood loss, particularly in pediatric line is improperly zeroed, the readings will be settings. Awakening a patient hourly for days consistent—but they will be consistently inac- and nights in a row can result in sleep depri- curate, which can lead to improper treatment vation, which prevents healing and can lead plans being established. Critical care nurses to delirium. Sending samples for lab analysis learn during orientation how to set up moni- costs the patient and the entire system finan- toring systems in anticipation of patient cially as well. admission to the unit, and they learn routines The timing of data collection is one of the of validating systems as they assume responsi- judgments that nurses should make by con- bility. In many units, technicians are available sidering the entire situation of the patient. to set up lines and equipment, but verifying Additionally, unit protocols for assessment the accuracy of readings is the responsibility should be periodically reviewed after consid- of the nurse. In addition, over time, readings ering published reports and patient data. At can drift for various reasons such as lines which phase of recovery from major surgery is moving, patient position changes, or mechan- the patient most likely to have specific com- ical equipment problems. Experienced nurses plications? When would data collection be learn to constantly assess the reliability of the appropriately timed to detect a specific com- data they collect. If a data pattern does not plication? Unit-level practice committees can match the apparent condition of the patient, address questions such as these. the nurse rechecks the source of the data for Too often, data collection becomes a mind- accuracy. The adage, “Treat the patient, not less routine. The numbers are generated and the numbers,” is good to remember regardless the flowsheet is filled in, but no one really of whether the numbers are accurate. Other considers what the data mean. This situation data that might not be reliable include arte- represents a failure of the nurse to exert clini- rial blood gas values if the sample is not read cal judgment. It results in wasted energy and immediately or if the patient has leukocytosis. resources, and it does not protect the patient. Serum chemistry values may also be inaccu- Several ways that the CCN can be thoughtful rate depending on the quality of the sample about the data that are routinely collected are and the precision of the analysis. discussed next. 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 6

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Trending and Knowing the Patient making and care (Reed et al., 2007). Clearly, Flowsheets are developed for specific critical coming to know the patient involves more care units to help organize data for process- than just gathering physiologic data. ing purposes. By seeing how individual data bits change over time, “trends” can be Common Trajectories detected. These trends are more important in Making sense of data requires knowing the determining the status of the patient than individual patient, but it also requires know- any individual piece of data would be. Is the ing pathophysiology and understanding the blood pressure making a slow decline over the workings of the body’s compensatory mecha- past two hours? Is this patient’s heart rate nisms for a variety of critical care conditions. generally slower than baseline? Identifying Nurses know for their own particular spe- such patterns helps to determine the clinical cialty unit—be it cardiovascular surgical, significance of a change in any data reading. trauma, coronary care, neurosurgical, med- For a patient with a normally slow heart rate, ical, transplant, or some other unit—the par- a new rate of 80 might be worrisome; for ticular problems typically faced by patients in another patient, a rate of 80 would not be a that unit. Critical care judgments are formed reason for clinical concern. Flowsheets also through a blend of knowing individual allow the nurse to see how readings of one patients and knowing the trajectories that parameter change along with other parame- patients are likely to experience in a particular ters. Blood pressure readings that are gradu- setting. In individual orientation programs or ally decreasing but remain in the acceptable staff meetings, the particularities of units can range might not be of concern. However, if be discussed and a common understanding the urine output is dropping during the same developed by nurses or, even more powerfully, period, a condition of low cardiac output in an interdisciplinary perspective. must be considered. Additional data about A trajectory is a predictable path or recent fluid loss, rates of fluid replacement, sequence of events that is commonly seen in a and an assessment for crackles in lungs would particular setting. For example, following be needed. Critical care nurses spend much of open heart surgery for coronary revasculariza- their time collecting data. This is not the end tion with cardiopulmonary bypass, patients of task, however, but just the beginning. Tak- commonly require vasopressor administra- ing time to reflect on the “movement” or tion to maintain blood pressure to support trend of the data is essential for critical care patency of newly implanted vessels. In addi- clinical judgment. tion, patients may experience tachycardia that Even in critical care, contextual patient- can decrease cardiac output. Patients may be related factors are important in coming to mechanically ventilated and have multiple know the patient. The AACN Synergy Model chest tubes and pacing wires implanted for Patient Care points out patient character- directly in the myocardium. They will have istics that are part of each encounter. Central central vascular access to facilitate fluid and to critical care are consideration of patient medication administration. A common trajec- stability and the predictability of the course tory includes weaning the patient from vaso- of recovery. Other key characteristics include pressors on the first night following surgery, patient resiliency, vulnerability, complexity, weaning from mechanical ventilation by the and resource availability. The Synergy Model morning after surgery (if not extubated also incorporates a consideration of the before), and a gradual reduction in chest tube patient’s ability to participate in decision drainage. Deviation from this expected trajec- 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 7

Day-to-Day Practice 7

tory, such as decreased oxygenation when are going as predicted, nurses can alter their weaning from mechanical ventilation is vigilance. Conversely, if the patient is not fol- attempted or continued blood loss from chest lowing the predicted trajectory, then the tubes, indicates that this particular patient nurse considers appropriately other data will require an individualized approach to sources, and discusses possible meanings of support. Experienced CCNs recognize this divergent pattern. The nurse does not patients’ progress along specific trajectories. A “rest” until the picture becomes clearer. Even sense of how the patient is progressing down “hunches” about what is going on can be the predictable path of recovery is one way explored and discussed until the patient’s pic- that the CCN sees patterns and senses the ture becomes clearer and data indicate an wholeness of the situation. appropriate direction for decision. Surveillance One practice that critical care nurses use is that of “running possibilities.” This process is In critical care areas, nurses use a type of a form of hypothesis generation, referred to thinking that assesses for problems that do earlier in this chapter. What could be a possi- not yet exist. This is a different style of think- ble explanation for this finding? Could this ing than problem identification. It is a contin- person have an unusual presentation of a ual scanning for signs that a problem is treatable problem? What if we try a treatment developing. This method of thinking requires option for a while and see how the patient several kinds of knowledge, data collection, responds? This sort of thinking frequently and processing. CCNs who wait until a prob- happens in conversation with other nurses or lem becomes obvious before they intervene with physicians (Chase, 1995). have missed a chance to prevent a cascade of events. Communicating Findings Knowledge that supports effective surveillance includes a deep understanding of the Nurses in critical care have more autonomy physiologic responses to the critical care set- than nurses in many other practice settings ting and to the particular patient problems regarding data collection and treatment deci- being addressed. Knowing that tracheal intu- sions such as weaning from various types of bation exposes a patient to risk of ventilator support. CCNs do not work in isolation, how- associated pneumonia, the CCN with a high ever, and they contribute to excellence in level of clinical judgment monitors arterial patient care by working collaboratively with a blood gas results, breath sounds, airway pres- team of other healthcare providers. One of sures, and vital signs. Waiting until pneumo- the skills that CCNs develop is effective com- nia is fully evident would result in risk of munication of their impressions of the status hemodynamic instability and sepsis, both of of the patient to other members of the team. which can lead to longer ICU stays or death. Many nurses have had the frustrating experi- Regular data collection for evidence of stabil- ence of believing that the patient needs to be ity or signs of problems is essential to the process managed in a certain way, but other members of surveillance. Most important, though, is the of the team do not agree. When the direction nurse’s ability to recognize patterns that indicate of the care and support differs, nurses are deviation from the normal trajectory. obligated to clarify, verify, and question the appropriateness of the treatment plan (if they Investigating Problems believe that harm will come to the patient). Experienced CCNs read their “gut” reactions. Learning to communicate data and impres- When patient responses indicate that things sions in ways that allow others to understand 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 8

8 Chapter 1 Clinical Judgment in Critical Care

the basis for the CCN’s judgment can mini- likelihood of left ventricular failure and mize this source of frustration. increase the likelihood that the patient is vol- Assembly of data into patterns that have ume depleted. The breath sounds and arterial meaning will assist CCNs in communicating blood gas results should be reported even their overall impressions. Calling a physician though they are normal because they assist and offering random bits of data will often the other clinicians to understand the whole not result in a positive response. The nurse picture: They are “pertinent” even though can better organize this process by coming to they are normal. know the types of data that individual clinicians value. For example, even if the findings Mobilizing the Team are not abnormal, the amount of chest tube Sometimes a CCN may detect that the drainage will be important to a cardiac sur- patient’s condition is changing rapidly and geon. When working with new teams of must assemble the necessary team members physicians, an anticipatory question can help to respond appropriately. To do so, the nurse to establish communication, such as, “Is there may need to page respiratory therapy, anes- any particular parameter that you want us to thesia, or other airway management teams, as pay special attention to this evening?” or “I’ve well as the primary physician or designee. noticed a downward trend in blood pressure. Making the decision to mobilize the team can Is there a level at which you want us to notify be a daunting one for new CCNs. Experienced you?” Then, should a call be necessary, it has a nurses and leaders can assist the new CCN in context. This kind of communication making this decision in a timely fashion. On requires “thinking forward.” the one hand, waiting until the situation One method that has been established in becomes obvious would be dangerous for the healthcare settings to assist with the assembly patient. On the other hand, if the nurse calls of data into meaningful patterns is the SBAR the team in unnecessarily, that decision has (Situation–Background–Assessment–Recom- costs, both financial and personal. It is possi- mendation) technique. This framework facili- ble that the CCN’s clinical judgment was at a tates communication among healthcare lower level in the AACN Synergy Model and providers by providing a focused approach for that the call came prematurely or in error. communicating essential patient information To deal with such issues, CCNs can discuss in a usable context so that accurate care deci- the process of mobilizing the team on indi- sions can be made (Institute for Healthcare vidual units and reflect on how the process Improvement, 2008). went: Did the nurse assemble sufficient data By understanding the competing hypothe- to generate the calls? Was the potential ses for the patient’s condition, the CCN will patient problem severe enough to warrant the be better able to present data in a way that call? Was the presentation of findings suffi- assists the entire team in making good deci- ciently clear? Did other members of the team sions. One kind of data that must be consid- respond appropriately? In hindsight, would ered is “pertinent negative” data—that is, any aspect of the patient’s care be managed showing that certain data are normal to differently? reduce the likelihood of one of the diagnostic options. For example, if the blood pressure is Team Decision Making trending down, but breath sounds and arte- Ultimately, the critical care process is a team rial blood gas results are normal, that combi- process. Data support the idea that good nation of findings would decrease the communication on a unit results in better 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 9

Day-to-Day Practice 9

patient outcomes (Baggs et al., 1999; Knaus, appropriate. The AACN Synergy Model pro- Draper, Wagner, & Zimmerman, 1986; Kohn, vides for a way of matching the CCN’s compe- Corrigan, & Donaldson, 2000; Larson, 1999; tencies to the patient’s needs. “Synergy results Page, 2004; Tammelleo, 2001). Units vary widely when the needs and characteristics of a in how effectively communication occurs. Sev- patient, clinical unit, or system are matched eral possible problems can occur that the CCN with a nurse’s competencies” (Hardin & should be aware of and try to correct. Kaplow, 2005, p. 4). Even given the same med- The first consideration is nurse-to-nurse ical condition, the CCN’s response to the communication. Are experienced nurses help- patient should reflect numerous factors, ful to new orientees, or do they require the including those described in the Synergy new nurse to “pay their dues”? This kind of Model. For example, a patient who has high hazing should be recognized as such and levels of resiliency, as evidenced by return to should be dealt with by unit leadership. Other baseline data after treatments, can be expected nurse-to-nurse difficulties can come at to recover more quickly and need less aggres- change of shift report, where one shift does sive support than a patient who, because of not help establish the new shift nurses’ longstanding concurrent conditions, might understanding of patient baselines due to not be capable of rallying. A patient with few emotionally charged communication. external resources might require aggressive Other issues that arise may relate to advocacy on the part of the CCN. whether the patient unit is orderly, with supplies on hand, and with essential data already Goal-Oriented Decisions assembled. Small things like this can lead to In line with the concept of trajectory, CCNs difficult communication and ultimately can should always have a goal in mind when plan- result in poor nursing care. ning specific nursing actions. If the goal is Additional nurse-to-nurse difficulties can stability, then support of basic physiologic happen at the time of patient transfer. It is functioning will support that goal. If the goal essential to the clinical judgment process that is to increase participation in care so as to open and clear communication be established support the patient–family unit, then adjust- between patient care areas. By sharing with ing visiting times to allow for prolonged con- healthcare providers in the new unit what the tact might be chosen, provided that patient patient’s clinical course or trajectory has been, stability is not compromised. The CCN can how this patient is unique, and which then reflect on the effectiveness of those inter- approaches have worked best, better clinical ventions in accomplishing the goal. judgment is promoted on the new unit. CCNs can actively support the unit in developing documentation systems that Choosing Interventional Approaches include goals and nursing actions. If a patient Much of our consideration thus far has is anxious about how the family is responding focused on clinical judgment as it relates to to critical illness, for example, being able to the status of the patient, patient stability, see and be with a family member can reduce patient movement along a recovery trajectory, stress and the related catecholamine release or the identification of problems. Judgment is that can have negative effects on the cardio- also required regarding how best to respond vascular system. Nursing actions can have real to the issues that are identified in the assess- effects on overall patient status. Promoting ment process. All management choices comfort and dignity for patients is a require- should be goal oriented and contextually ment for humanistic care and healing. 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 10

10 Chapter 1 Clinical Judgment in Critical Care

Supporting the Dying can make a real difference in patient out- As discussed earlier, the experienced CCN comes. Ultimately, the clinical judgments develops a sense of the big picture of the made by CCNs are pivotal to providing care patient’s condition and the direction of the to acute and critically ill patients. Nurses are trajectory. Often, critically ill patients have essential to the process of providing care by life-threatening conditions that can result in virtue of their perspective on meeting the death. Death sometimes happens during needs of the whole patient. These needs can aggressive resuscitative efforts. Frequently, be based on the eight patient characteristics however, an impending death is recognized by outlined in the Synergy Model. Nurses’ con- at least one member of the team. The goals of stant presence provides for a way of seeing care may then shift to allow for patient com- and knowing the person who is experiencing fort and family communication. The transi- critical illness. Growing in ability to form tion to caring for the dying patient can be one exquisitely appropriate clinical judgments is a that provides the ultimate meaningful contri- lifetime challenge—but it is one that is bution on the part of the staff. Too often, rewarding to both patient and nurse. however, an impending death is a time of competing goals, shifting direction of care, ■ REFERENCES and difficult communication. American Association of Critical-Care Nurses The CCN can assist in the dying process by (AACN). (2002). Competency level description for maintaining a consideration of “Where are we nurse characteristics. Aliso Viejo, CA: AACN Cer- going?” Asking that question during team tification Corporation. meetings can assist the entire team in Baggs, J. G., Schmitt, M. H., Mushlin, A. I., addressing the futility of care. The patient’s Mitchell, P. H., Eldredge, D. H., Oakes, D. et al. and family members’ goals will also need to (1999). Association between nurse–physician collaboration and patient outcomes in three be determined as part of this process, and it is intensive care units. Critical Care Medicine, often the nurse who assists in clarifying these 27(9), 1991–1998. values (Hiltunen, Medich, Chase, Peterson, & Chase, S. K. (1995). The social context of critical Forrow, 1999). care clinical judgment. Heart & Lung, 24(2), 154–162. ■ SUMMARY Chase, S. K. (2004). Clinical judgment and communication in nurse practitioner practice. Philadelphia: A critical care nurse is not a technician. As a F.A. Davis. professional nurse, the CCN’s focus of care is Hardin, S. R., & Kaplow, R. (Eds.). (2005). Synergy on the whole person and family at a vulnera- for clinical excellence: The AACN Synergy Model for ble time. The focus of care on the physical Patient Care. Sudbury, MA: Jones and Bartlett. problems patients face in critical care is obvi- Hiltunen, E., Medich, C., Chase, S., Peterson, L., & ous. More is known by clinicians about the Forrow, L. (1999). Family decision making for functioning of the human body of patients in end of life treatment: The SUPPORT nurse a critical care unit than by providers in almost narratives. Journal of Clinical Ethics, 10(2), any other environment of the healthcare sys- 126–134. tem. Critical care nurses learn over time, how- Institute for Healthcare Improvement. (2008). SBAR techniques for communication: A situational ever, that more is going on in a critical care briefing model. Retrieved May 31, 2008, unit than simply the care of physical bodies. from www.ihi.org/IHI/Topics/PatientSafety/ Critically ill patients are whole human beings. SafetyGeneral/Tools/SBARTechniquefor Their fear or trust, their will to live, their abil- CommunicationASituationalBriefingModel ity to participate in care, and family support .htm 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 11

References 11

Knaus, W. A., Draper, E. A., Wagner, D. P., & Zim- tee on the Work Environment for Nurses and merman, J. E. (1986). An evaluation of out- Patient Safety, Institute of Medicine. Washing- comes from intensive care in major medical ton, DC: National Academy Press. centers. Annals of Internal Medicine, 104(3), Reed, K. D., Cline, M., & Kerfoot, K. M. (2007). 410–418. Implementation of the Synergy Model in criti- Kohn, L. T., Corrigan, J. M., & Donaldson, M. S. cal care. In R. Kaplow & S. R. Hardin (Eds.), (Eds.). (2000). To err is human: Building a safer Critical care nursing: Synergy for optimal outcomes health system. Committee on the Work Environ- (pp. 3–12). Sudbury, MA: Jones and Bartlett. ment for Nurses and Patient Safety, Institute Tammelleo, A. D. (2001). Failure to keep physi- of Medicine. Washington, DC: National Acad- cians informed: Death results. Nursing Law’s emy Press. Regan Report, 41(2), 2. Larson, E. (1999). The impact of physician–nurse Thompson, C., & Dowding, D. (2002). Clinical deci- interaction on patient care. Holistic Nursing sion making and judgment in nursing. Philadel- Practice, 13(2), 38–46. phia: Churchill Livingstone. Page, A. (Ed.). (2004). Keeping patients safe: Trans- forming the work environment of nurses. Commit- 57625_CH01_001_012.pdf 4/10/09 11:06 AM Page 12 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 13

Chapter 2 Cardiovascular Anatomy and Physiology

Susan K. Chase

■ INTRODUCTION The heart is a muscular organ located of the cardiac muscle within the pericardium. beneath the sternum, between and slightly If fluid or blood fills the pericardium, it puts anterior to the lungs, in a section of the tho- pressure on the heart from the outside and rax known as the mediastinum. The medi- prevents normal filling of heart chambers. astinum also contains the great blood The main function of the heart is to pump vessels—the vena cavae, the pulmonary artery, blood throughout the body, thereby allowing and the aorta—as well as the esophagus and for the delivery of oxygen and nutrients to the (in children) the thymus gland. Figure 2–1 body cells and for the transport of waste prod- illustrates the location of the heart. ucts to processing or removal organs. Other The heart is surrounded by the peri- functions of the cardiovascular system flow cardium, a dual-layer sac that is minimally from the blood itself: The blood consists of elastic. This sac allows for smooth movement cells that support the body’s ability to fight off infection as well as chemicals such as hormones that control processes of bodily systems. In addition, the heart releases hormones that assist in controlling blood flow and pressures.

■ CHAMBERS AND VALVES OF THE HEART The structure of the heart supports its functions. The heart consists of four chambers, each with muscular walls (Figure 2–2). It also has four valves that control the direction of the blood flow through these chambers. The two upper chambers of the heart are the atria; the two lower chambers are the ventricles. Actually, the terminology of “upper” and “lower” refers to a conceptual picture of the heart, with the Figure 2–1 The heart and its location most anterior chambers of the heart being the in the thoracic cavity. right and left ventricles. The muscle walls of the Source: Illustrated by James R. Perron four chambers vary widely in thickness. Because 13 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 14

14 Chapter 2 Cardiovascular Anatomy and Physiology

Aorta Superior Vena Cava Pulmonary Artery Pulmonary Left Vein Atrium Right Atrium Pulmonic Valve (Semilunar Aortic Valve Valve) Left Atrioventricular Mitral (Semilunar (Bicuspid) Valve Valve) Right Left Ventricle Ventricle

Right Atrioventricular Tricuspid Valve Figure 2–2 Chambers of the heart and valves. Source: Illustrated by James R. Perron

the left ventricle must pump blood into the sys- position of the heart (Woods, Froelicher, temic circulation, which has relatively higher Motzer, & Bridges, 2004). pressure than the pulmonary system, the wall Although most of the heart tissue is muscle, of the left ventricle is the thickest (13–15 mm). this organ also has a fibrous band that sepa- The right ventricle is only 3–5 mm thick. The rates the atria from the ventricles and contains atria have the thinnest walls (2–5 mm). the four cardiac valves, which are themselves made up of connective tissue. The cardiac valves consist of fibrous rings to which valve ■ POINT OF MAXIMAL IMPULSE leaflets are attached. The tricuspid valve con- The tip of the left ventricle is positioned ante- tains three flat valve leaflets. The pulmonic rior and to the left in the mediastinum. When and aortic valves each have three leaflets that the left ventricle contracts, its tip is forced are termed “semilunar” because of their cres- even more anteriorly toward the chest wall. cent-like shape. The mitral valve has two flat This movement can be palpated as the “point leaflets that resemble the pointed shape of a of maximal impulse” (PMI). The PMI is nor- bishop’s miter. The valves themselves are cov- mally located in the midclavicular line at the ered with epithelial tissue. The tricuspid and fifth intercostal space, but can sometimes mitral valves (collectively termed the atrioven- vary. Abnormalities in the shape and size of tricular [AV] valves because of their location) the heart, for example, can alter the position are attached to chordae tendinae, which are and location of the heart itself. A distended connected on their opposite ends to papillary abdomen can flatten and elevate the level of muscles in the ventricles. The muscles prevent the heart. Hyperextended lungs can depress the valve leaflets from being pushed backward the level of the heart. Enlargement of the into the atria when pressure rises in the ven- heart can cause the PMI to shift to the left in tricular chambers during ventricular contrac- the chest. Noting the position of the PMI can, tion. Proper functioning of the valves depends therefore, give some indication of the size or on all these features being intact. 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 15

Blood Flow Through the Heart and Major Blood Vessels 15

The right and left sides of the heart are Oxygenated blood returning from the pul- divided by the septa. The interatrial septum monary vein enters the resting left atrium. consists of the fossa ovalis (the sealed fora- When the left atrium pressure rises higher men ovale that normally closes in the post- than the pressure in the resting left ventricle, partum period) and the muscular walls of the the mitral valve opens. Blood then passes to right and left atria. The interventricular sep- the left ventricle across the mitral valve. The tum is formed by the ventricular muscle in contraction of the left atrium forces addi- the lower portions and by the upper membra- tional blood into the left ventricle. Finally, as nous section (Woods et al., 2004). the left ventricle contracts, the pressure there increases and forces the mitral valve closed and the aortic valve open. Blood passes from ■ BLOOD FLOW THROUGH the left ventricle to the systemic circulation THE HEART AND MAJOR across the aortic valve. It flows to the cardiac BLOOD VESSELS muscle itself through the right and left coro- The right atrium receives blood from the body nary arteries, which arise from the lower through the superior and inferior vena cavae as aorta, just above the aortic valves. well as from the coronary sinus, which returns Each of the cardiac chambers has its own the blood that has circulated through the heart range of normal fluid pressures, which muscle itself. Blood enters the right atrium depend on the force of contraction of the during atrial relaxation (and ventricular sys- muscle walls and the position of the cardiac tole). When the pressure in the right ventricle valves in that chamber. Each chamber has a decreases during its resting phase (ventricular phase when its walls are contracting (systole) diastole), the tricuspid valve opens, allowing and a phase when the muscle is resting (dias- the blood flow from the right atrium to the tole). Most of the time, the words “systole” right ventricle. After the right ventricle fills and “diastole” are used to refer to the phases with blood, the muscle wall contracts, increas- of the ventricles. Under normal circum- ing the pressure in its chamber, which in turn stances, due to the electrical control system of forces the tricuspid valve to close. As pressures the heart, the atria contract together and the continue to increase, blood is forced out of the ventricles contract together. right ventricle across the pulmonic valve and It is useful to be able to picture the heart dur- into the pulmonary artery. The pulmonary ing systole and diastole when interpreting heart artery transports the still unoxygenated blood sounds (see Box 2–1). During ventricular sys- into the pulmonary vascular system. tole, the AV valves are closed and the semilunar In the pulmonary system, the blood circu- valves are open; blood flows through the latter lates through a series of arteries, capillaries, valves into the pulmonary and systemic circula- and veins. In the thin-walled capillaries of the tion. During ventricular diastole, the semilunar pulmonary circuit, red blood cells exchange valves close and the AV valves open, with blood carbon dioxide for oxygen. The oxygenated flowing through the latter valves. Unexpected blood then returns to the left ventricle, driven Box 2–1 Murmur Differentiation by the pressure differential: Pressures in the left ventricle are lower than in the pulmonary Valve Stenosis Insufficiency vascular system. When the right ventricle relaxes during diastole, the pressure in the Tricuspid Diastolic Systolic right ventricle decreases, which causes the and Mitral Pulmonic Systolic Diastolic pulmonic valve to close. Blood from the right and Aortic atrium then refills the right ventricle. 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 16

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sounds heard during ventricular systole could arteries are perfused during ventricular dias- result from tight or “stenotic” semilunar valves tole. The left main coronary artery divides fairly (aortic or pulmonic) or from incompetent or quickly into the left anterior descending (LAD) regurgitant AV valves (mitral or tricuspid). artery and the circumflex artery (CA) (Fig-

These sounds are best heard between S1 and S2. ure 2–4). The right coronary artery (RCA) sup- Unexpected sounds heard during ventricular plies most of the right atrium and ventricle

diastole are heard between S2 and S1. These and the SA node (in 60% of people), the AV sounds can be related to mitral/tricuspid steno- node (in 80–90% of people), and part of the sis or aortic/pulmonic insufficiency (regurgita- bundle branches. The left anterior descending tion). Obstruction to forward flow is stenotic, artery supplies the left atrium and ventricle, and backward flow of blood is due to an incom- including the ventricular septum. The circum- petent valve. flex artery supplies the posterior portion of the Being able to think spatially will assist the left ventricle and the left atrium. The blood nurse in making sense of cardiovascular supply to the sinoatrial (SA) node of 40% of the assessment data. The diagram of the cardiac population is received through the left circum- cycle in Figure 2–3 shows the simultaneous flex artery. The venous return of the heart leads events of cardiac function, including pressure to the great coronary vein, which parallels the changes in individual vessels and chambers circumflex artery and eventually returns to the and electrical activity. right atrium.

■ CORONARY ARTERIES ■ CARDIAC LYMPHATIC SYSTEM Because the pressure in the muscle tissue dur- The heart produces a certain amount of lym- ing ventricular systole is so high, the coronary phatic drainage that flows through the pre-

Figure 2–3 The cardiac cycle. Source: Illustrated by James R. Perron 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 17

Pressure of Blood in Major Blood Vessels 17

CA Left Main

RCA LAD PDA RCA

(a) Anterior View (b) Posterior View

LAD ϭ left anterior descending RCA ϭ right coronary artery CA ϭ circumflex artery PDA ϭ posterior descending artery Figure 2–4 Diagram of coronary circulation.

tracheal lymph node and eventually empties ■ PRESSURE OF BLOOD into the superior vena cava. Blockage of IN MAJOR BLOOD VESSELS lymph flow can affect pressures in the heart Major blood vessels experience variations in itself related to venous congestion. The return their pressures related to cardiac events. Pres- of lymph to the systemic circulation is critical sure waves in the great veins and the right to prevent interstitial edema. Also of impor- atrium are given codes (letters) to assist in the tance is that cardiac lymph fluid contains interpretation of waveforms (Figure 2–5). For hormones (atrial natriuretic peptide) and example, the “v” wave represents filling of the adrenergic neurons (norepinephrine) that can atrium from systemic veins. The “x” descent be used as markers for myocardial edema, follows the “v” wave and represents change in reperfusion injury, and myocardial damage shape of the atrium as a result of ventricular (Konuralp, Idiz, & Unal, 2001). emptying. The “a” wave represents increased People can vary somewhat in terms of the right atrial pressure caused by atrial contrac- arrangement and area that the coronary arter- tion and is followed by the “y” descent, which ies supply. Coronary angiography can reveal represents a decrease in pressure as the tricus- the individual’s unique configuration. pid valve opens. The slight rise in right atrial With age, vessels may become narrowed (RA) pressure, called the “c” wave, represents due to plaque and thickening of the arterial the increase in pressure coming from the ven- walls. Collateral circulation may then develop, tricle that causes the tricuspid valve to close. as blood is drawn from nearby arterioles to Arterial pressure increases rapidly with ven- supply areas that might otherwise not be per- tricular systole and attains the pressure repre- fused adequately because of blockages to pri- sented by the systolic blood pressure. The mary blood sources. If collateral circulation is dichrotic notch of the arterial waveform rep- well developed, blockage of a major artery resents the closure of the aortic valve. This may not cause as much damage as it would closure maintains the pressure of the system for a person with no collateral circulation circuit at the level represented by the diastolic (Woods et al., 2004). blood pressure. 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 18

18 Chapter 2 Cardiovascular Anatomy and Physiology

Figure 2–5 Pressure waveforms. Source: Illustrated by James R. Perron

■ ELECTRICAL CONTROL potentials from being transmitted between the OF CARDIAC MUSCLE atria and ventricles. The exception to this Cardiac muscle cells are unique in the body barrier occurs in the AV junction, or the AV for a number of reasons. First, unlike skeletal node. Electrical impulses pass from atria to ven- muscle cells, they are capable of automaticity. tricles across this specialized set of tissues (Fig- That is, cardiac muscle cells do not require ure 2–6). To support simultaneous contraction stimulation from an outside force such as a of the thick ventricular muscle walls, special- nerve to initiate an action potential, which ized conduction tissue transmits electrical causes contraction. Second, cardiac muscle impulses through the bundle branches and the cells are interconnected in web-like fashion Purkinje fibers; the atria have similar transmis- with separation only by intercalated discs, sion fibers. The electrical impulse is slowed at which allows for impulses to pass through the the AV node, a delay that allows for the atria to entire section of the heart like a wave. contract and empty blood into the ventricles. Action potentials occur when the polarity Each cell of the heart is capable of initiat- (i.e., electrical charges) across the cell mem- ing an action potential, but different areas of brane changes rapidly. In the resting state, there the heart have different basic rates of dis- are more positive ions (sodium ions, which are charging. Under normal conditions, the SA present in the largest number, but also calcium node, which is located in the right atrium, has and magnesium ions) outside the cell mem- the fastest rate; depolarization occurs there brane as compared with the positive charges approximately 60 to 100 times per minute. inside the cell. Potassium is the chief intracellu- Cells of the AV node can depolarize 40 to 60 lar cation (positive ion), and there exist rela- times per minute unless a more frequent tively more anions (negative ions) inside the cell impulse, such as from the SA node, is trans- from proteins and other sources. The cell mem- mitted through them. Ventricular cells can brane is therefore “polar”—similar to the initiate an action potential 20 to 40 times per scheme used to power a flashlight battery, minute. This activity is protective to the heart: which has more positive ions on one side than If something happens to prevent normal on the other. An action potential spreads to action potentials from reaching the ventricle, neighboring cardiac cells like a wave. the heart will still beat. Thus the SA node is The atria and ventricles are separated by normally in control of the heart rate because thick fibrous tissue that supports the four it has the fastest intrinsic rate. heart valves. This fibrous tissue prevents action Box 2–2 provides a closer look at the various phases of action potentials to help 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 19

Electrical Control of Cardiac Muscle 19

Bundle Atrioventricular of His Node

Sinoatrial Node Left Bundle Branch

Left Internodal Posterior Pathways Fascicle

Right Bundle Branch

Left Anterior Purkinje Fascicle Fibers Figure 2–6 Electrical conduction system of heart. Source: Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD

explain these events and explain how certain 1 medications can affect them. Action poten- 2 tials for the SA and AV node are somewhat different from the pattern depicted in Figure 2–7, 3 which allows the SA node to operate more 0 independently. These impulses are more tightly controlled by the slow calcium channels than the sodium channels. Calcium- 4 channel blockers can slow heart rate by slowing the transport of calcium across the cell membrane (McCance & Huether, 2006). A refractory period occurs after the action potential before the resting concentrations have fully returned to normal. New impulses that reach the tissue during this period will not be transmitted, or potentially can estab- Figure 2–7 Action potential diagram. lish abnormal rhythm patterns. Because these Source: Illustrated by James R. Perron activities work against the concentration gradient, they require the expenditure of 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 20

20 Chapter 2 Cardiovascular Anatomy and Physiology

Box 2–2 Action Potential Phases

Phase 0: Depolarization. Sodium ions cross the cell membrane rapidly through sodium channels, causing the polarity of the cell membrane to change rapidly. Phase 1: Rapid Repolarization. Potassium ions “leak” outside the cell. Phase 2: Plateau. Opening of slower calcium channels allows cations to enter the cell, balancing the loss of potassium ions. Phase 3: Rapid Repolarization. At the end of the action potential, the channels close and the cell returns to its resting state by pumping sodium ions out of the cell and bringing potassium ions back inside. Phase 4. Resting State. This phase is diastole where cells remain resting until an electrical impulse occurs.

energy. As much as two-thirds of the cardiac from the systemic circulation. Some concepts cell’s energy is spent in supporting the have been developed that assist clinicians in sodium–potassium pump. Any loss in energy understanding overall cardiac function. Car- for the cardiac cell results in interruption of diac output (CO) is a measure of the amount this essential pump fairly quickly. Such a dis- of blood that is ejected by the heart each ruption affects the cell’s ability to return to minute. Stroke volume (SV) represents the normal polarity. Because sodium ions build up amount of blood that is ejected from the left in the cell, water (a polar molecule) is attracted ventricle with one contraction. Cardiac out- to the sodium ion. As a result, internal struc- put, then, is the product of the stroke volume tures of the cardiac cell swell, resulting in the and the heart rate (HR): release of internal cell enzymes. Electrolyte abnormalities can make cardiac cells more CO ϭ SV ϫ HR prone to develop an action potential and more likely to initiate a transmittable impulse, which causes an abnormal cardiac rhythm. Stroke volume is influenced by the amount Electrical events precede mechanical events. of blood in the ventricle and by the force of When a cardiac cell experiences an action contraction of the ventricle. It can also be potential, it contracts. As the wave of electrical affected if the aortic valve restricts flow out activity passes through the cardiac muscle wall, of the left ventricle. The ejection fraction (EF) the muscle contracts in a wave-like fashion. is the percentage of the volume of the left For this reason, cardiac function is often moni- ventricle that is ejected with each contrac- tored by electrocardiography. The nurse must tion. A normal ejection fraction is in the be aware that damaged cardiac muscle may not range of approximately 65% to 70%, where respond with full-force contraction even if the this value reflects the efficiency of the left electrocardiogram tracings appear normal. ventricle in pumping blood forward into the systemic circulation. Preload (sometimes referred to as left ventric- ■ CARDIAC OUTPUT, PRELOAD, ular end-diastolic pressure) is the pressure AND AFTERLOAD found in the left ventricle at the end of diastole. As mentioned earlier, the heart functions to The Frank-Starling law states that stretched pump oxygenated blood to cells, organs, mus- muscle fibers produce a more powerful con- cles, and tissues and deoxygenated blood back traction; thus, when the left ventricle is fully 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 21

Systemic Circulation 21

filled, a more powerful contraction becomes the heart. Sympathetic nerve fibers release possible. Conditions that prevent filling of the norepinephrine, which has profound effect ventricle with blood—such as hypovolemia, on cardiac contractility and vascular resist- dehydration, or external pressure on the heart ance. Additionally, the medulla of the adre- from fluid in the pericardium—will reduce both nal glands is part of the sympathetic nervous the pressure in the ventricle and its ability to system and can stimulate the release of epi- pump blood forward. Nevertheless, the Frank- nephrine into the systemic circulation—a Starling law reaches its limit when cardiac function sometimes termed “adrenergic.” chambers are overstretched: The resulting con- Receptors for adrenergic neurotransmitters traction is not as effective as it would have been can be classified as either alpha (α) or beta with slightly less stretch. The overstretching (β) receptors. Receptors can be further sub- α α β β can eventually result in a lower cardiac output. classified as 1 and 2, or as 1 and 2. Afterload is the resistance against which Dopamine is another neurotransmitter that the left ventricle must pump to move blood affects the cardiovascular system. Table 2–1 forward. The pressure of the arterial systemic summarizes the locations and actions of the circulation produces afterload. Smooth mus- various receptors. cle tone in arterioles can increase the resist- The activity of the sympathetic neurotrans- ance to blood flow and increase afterload. mitters is determined by the location and type Medications can also alter the amount of of receptors in various tissues. In this way, the resistance that arteriolar smooth muscle gen- same chemical can have different effects in erates. For example, arterial vasodilators different locations. The heart is rich in β decrease afterload, whereas vasoconstrictor receptors, so that effect is most prevalent for agents increase preload, afterload, or both. the heart. The systemic circulation has relatively more α receptors, so that effect is more ■ EXTERNAL CONTROL predominant there. Epinephrine stimulates OF THE HEART all types of adrenergic receptors, but norepi- β Nervous system control of the heart comes nephrine has little effect on 2 receptors. Dila- α through the autonomic nervous system and can tion of 2 coronary blood vessels is promoted cause rapid changes in heart activity. The auto- by epinephrine, but not norepinephrine nomic nervous system consists of sympathetic (McCance & Huether, 2006). and parasympathetic nerve fibers. The sympathetic nervous system controls the body’s “fight ■ or flight” mechanisms, quickly preparing the SYSTEMIC CIRCULATION total organism to resist an attack. Blood is pumped from the left ventricle into The parasympathetic system governs the the aorta, the largest artery in the body. The “rest and refresh” responses to stress and has aorta rises from the aortic valve and heads nerves that function more individually. The superiorly and to the right, which explains vagus nerve has the chief parasympathetic why one listens for aortic valve heart sounds influence on the heart by affecting primarily at the first intercostal space on the right ster- the SA and AV nodes and increasing the con- nal border. Arteries branch from the aorta duction block at the AV node. Parasympa- beginning at the aortic arch and continue thetic nerve fibers release acetylcholine, which until the aorta itself branches into the two slows the heart—a function sometimes termed iliac arteries. Multiple systemic arteries “cholinergic.” branch off from the aorta as it passes through Sympathetic stimulation increases heart the body. Arteries then branch into a series of rate and contractility, affecting all parts of increasingly smaller units until they become 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 22

22 Chapter 2 Cardiovascular Anatomy and Physiology

Table 2–1 Autonomic Receptors and Cardiovascular Function

Adrenergic Vagus Nerve Location Receptor Type Adrenergic Effect Cholinergic Effect β Sinoatrial 1 Increased rate Decreased rate, arrest (SA) node β Atrial tissue 1 Increased contractility Decreased contractility, and conduction velocity shorter action potential β Atrioventricular 1 Increased automaticity Decreased conduction (AV) node and conduction velocity velocity and automaticity β Purkinje fibers 1 Increased automaticity No receptors and conduction velocity β Ventricles 1 Increased contractility No receptors α β Coronary 1, 1 Constriction, dilation Dilation α β Skin 1, 2 Constriction Dilation α β Skeletal muscle 1, 2 Constriction, dilation No receptors α Cerebral 1 Constriction (slight) No receptors α β Pulmonary 1, 2 Constriction, dilation α β β Renal 1, 1, 2 Constriction, dilation

the smallest of all blood vessels, the capillar- The endothelial layer of cells constitutes the ies. The capillaries eventually collect into capillary wall. Capillaries have incredibly thin venules, which combine to form veins, which walls; the varying spaces between the cells that return blood to the heart through the inferior line them allow for fluid and blood cells to pass and superior vena cavae. through the capillary cell membranes or The entire circulatory system is lined with through the spaces between the cells. In the endothelial cells that are active in controlling brain, the extremely tight junctions between the local conditions through the release of chemi- endothelial cells force all fluid to go through cals. The types of blood vessels have unique these cells. In contrast, capillaries found in other characteristics that affect their function. parts of the body have relatively more open Arteries have thicker walls containing three spaces between endothelial cells that allow for layers, including a smooth muscle layer. The easier exchange of fluid and dissolved chemi- constriction of the smooth muscle surround- cals; this kind of openness is found in the liver, ing the arteries is controlled by the action of for example. Certain conditions, such as inflam- chemicals such as epinephrine or norepineph- mation or sepsis, can result in widened spaces, rine. The outer layer of the artery consists of leading to a condition euphemistically called connective tissue. Veins have narrower walls “leaky” capillaries. Precapillary sphincters— with a thinner muscle layer. Venous blood is smooth muscle cells that control the smallest squeezed up from the legs through skeletal arterioles—control blood flow to capillary net- muscle contraction; the large veins of the leg works. Under normal circumstances, local aci- have internal valves that prevent blood from dosis causes opening of a precapillary sphincter flowing down by gravity. to an area, thereby increasing its blood supply. 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 23

Disorders of Major Blood Vessels 23

Pressures in the arterial system can be afterload and water retention. Angiotensin- measured by use of a sphygmomanometer or converting enzyme (ACE) inhibitors block by direct arterial cannulation. Pressures in the this pathway, and guidelines now recommend capillary network are lower than arteriolar their use both for heart failure and following pressures; venous pressures are even lower, myocardial infarction. supporting venous return. Blood flow is The body’s water levels are regulated by determined by control of pressures and resist- antidiuretic hormone (ADH), a chemical ance to flow. Pressure inside the circulatory released from the posterior pituitary gland. system (indeed, in any system) favors flow to When diuresis slows, the amount of free body an area of lower pressure. Resistance to blood water increases. This effect then reduces the flow comes in the form of pressure in vessels, concentration (osmolality) of dissolved sub- which is partly determined by smooth muscle stances in the body. tone and length of the blood vessels. In gen- Natriuretic peptides are released by parts of eral, the key principle governing blood flow the body in response to plasma volume can be summarized as “the greater the resist- changes. Atrial natriuretic protein (ANP) is ance, the lower the flow.” Resistance to flow released by atrial monocytes if they detect can also be increased if the blood is more vis- increased pressure in the right atrium. ANP cous, such as occurs with polycythemia. inhibits ADH, thereby causing a loss of body Blood flow can also be affected by the shape water, and ultimately reducing the pressure in and internal smoothness of the blood vessels. the right atrium. Brain natriuretic protein (BNP) was first discovered in the brain, but is also released from the heart cells; the level of ■ SYSTEMIC CONTROL this protein can reflect overall ventricular OF BLOOD PRESSURE function (McCance & Huether, 2006). In addition to acting through the sympathetic nervous system, which can increase the ■ blood pressure by increasing vascular resist- DISORDERS OF MAJOR ance, the body can control blood pressure BLOOD VESSELS through other chemical pathways. The kid- Sometimes, as a result of longstanding pres- neys autoregulate their blood flow so that sure inside arteries or because of turbulent pressures at the glomerulus are sufficiently flow caused by irregularities in the internal high to maintain filtration. If the kidneys shape of the artery, weaknesses may develop detect decreased blood flow, they also release in the arterial wall. An aneurysm is a widening renin. Renin leads to a production of in an artery that can completely surround the angiotensin I, which is later converted to artery or that can consist of an outpouching angiotensin II. Angiotensin II increases sys- at one part of the circumference of the artery. temic vascular resistance by causing vasocon- When aneurysms rupture, they cause rapid striction. It also stimulates the release of blood loss from the artery into surrounding aldosterone from the adrenal glands. Aldos- tissues and a reduction in blood flow to areas terone, a mineralocorticoid, causes sodium— normally supplied by the artery. and therefore water—retention. If the cause of The aorta is prone to aneurysm development renal blood flow decrease is blood loss, these because it sustains the highest pressures in the compensatory mechanisms are helpful. Con- vascular system. When an aneurysm involves all versely, if low cardiac output is caused by three levels of the arterial wall, it is termed a pump failure, then these mechanisms actually “true aneurysm.” This type of aneurysm typi- work against cardiac function by increasing cally involves the entire circumference of the 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 24

24 Chapter 2 Cardiovascular Anatomy and Physiology

vessel. Other aneurysms form between the lay- ■ SUMMARY ers of the artery, particularly following vascu- By understanding the anatomy and physiol- lar surgery. In this case, blood leaks through ogy of the cardiovascular system, the nurse is the endothelial and tunica media layers and able to make reasoned responses to patient collects under the adventitia. problems. Concepts such as cardiac output Aneurysms are usually undetectable until and electrophysiology will be daily concerns of they threaten to rupture or actually do rup- the critical care nurse. Accurate assessment of ture. Symptoms depend on the location of the cardiovascular function and early detection of aneurysm. A widening aneurysm can result in problems are essential to providing high- decreased blood flow to small arteries in the quality care. Cardiovascular conditions remain area. A ruptured aneurysm causes pain, which the leading cause of death in the United States. can often be referred, meaning the pain is per- Nurses caring for acute and critically ill ceived in an area of the body different from patients will be needed who are expert in the where the actual injury is located. Thoracic care of patients with these conditions. aneurysms can cause dyspnea or dysphagia due to pressure on the esophagus and lung tis- ■ sue. An abdominal aortic aneurysm can result SELF-ASSESSMENT QUESTIONS in ischemia to tissues normally supplied by 1. You have a patient who is scheduled to blood from the area below the aneurysm. have a coronary artery bypass graft. On Diagnosis of aneurysms may be made physical exam, you note that the PMI is through ultrasonography and by using imag- located at the left axilla. This assessment ing technologies such as computed tomogra- finding more than likely indicates phy (CT) or magnetic resonance imaging a. cardiac tamponade. (MRI). The goals of treatment are to reduce b. axis deviation. blood loss by reducing blood pressure until c. tension pneumothorax. surgical repair can be accomplished. Asymp- d. hypertrophy. tomatic aneurysms are sometimes detected 2. Blood flowing through the pulmonic on chest radiograph or by abdominal palpa- valve is leaving the tion of an aortic aneurysm. a. right ventricle. The decision to make a surgical repair b. left ventricle. depends on the relative risk of the repair itself c. right atrium. compared with the risk of the aneurysm’s d. left atrium. rupture. If, for example, the renal arteries are 3. The Frank-Starling law illustrates the compromised by the location of the relationship between aneurysm, then the intravascular repair may a. vasoactive agent administration and not be possible. The age of the patient and the hemodynamic response. size of the aneurysm are factored into this b. sympathetic response and decision. Intravascular approaches to sup- parasympathetic response. porting the integrity of the artery have been c. fluid status and cardiac function. developed that allow for much quicker recov- d. acetylcholine and degree of ery by patients. The location of the aneurysm bradycardia. is key to understanding the symptoms produced by the arterial defect. 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 25

Web Resources 25

4. In the presence of increased afterload, 10. Administration of a beta blocker which agents are useful in lowering will result in which of the following resistance to cardiac ejection? outcomes? a. Vasodilator agents a. Increased cardiac output b. Anticholinergic agents b. Vasoconstriction c. Vasoconstrictor agents c. Decreased contractility d. Beta blockers d. Compensation by dopaminergic 5. Decreased left ventricular preload can receptors occur in the setting of Answers to Self-Assessment Questions a. cardiac tamponade. b. hypovolemia. 1. d 6. a c. cardiogenic shock. 2. a 7. b d. hypoxemia. 3. c 8. c 6. Angiotensin II increases systemic vascu- 4. a 9. c lar resistance by causing 5. b 10. c a. vasoconstriction. b. parasympathetic stimulation. c. aldosterone release. ■ REFERENCES d. production of renin. Konuralp, C., Idiz, M., & Unal, M. (2001). Impor- 7. Common signs of thoracic aneurysms tance of the cardiac lymphatic system in open include heart surgery. European Journal of Cardiothoracic a. hypertension and cough. Surgery, 19(3), 372–373. b. dyspnea and dysphagia. McCance, K. L., & Huether, S. E. (2006). Pathophysi- ology: The biologic basis for disease in adults and chil- c. pleuritic chest pain and shortness of dren (5th ed.). St. Louis, MO: Elsevier Mosby. breath. Woods, S. L., Froelicher, E. S., Motzer, S. A., & d. bradycardia and jugular venous Bridges, E. (Eds.). (2004). Cardiac nursing (5th distention. ed.). Philadelphia: Lippincott Williams & 8. Atrial natriuretic protein is released Wilkins. when pressure is detected in the a. left atrium. ■ WEB RESOURCES b. left ventricle. c. right atrium. St. Jude Medical presents an informational video about the anatomy of the human heart and d. right ventricle. how it pumps blood throughout your body: 9. Which neurotransmitter is released by www.heartlibrary.com/heart-library-heart- the sympathetic nerve fibers, resulting in anatomy.aspx?flashmov=heart-anatomy& a profound effect on cardiac contractil- currPage=HD ity and on vascular resistance? Heart Anatomy, Interior View, is an interactive a. Angiotensin photograph that allows the learner to point to b. Acetylcholine any structure for highlighted identification on the picture. GateWay Community College, c. Norepinephrine Phoenix, AZ: www.gwc.maricopa.edu/class/ d. Dobutamine bio202/cyberheart/hartint0.htm 57625_CH02_013_026.pdf 4/10/09 11:09 AM Page 26

26 Chapter 2 Cardiovascular Anatomy and Physiology

Heart Anatomy, Posterior View, is an interactive The Auscultation Assistant provides heart sounds, photograph that allows the learner to point to heart murmurs, and breath sounds to help any structure for highlighted identification on medical students and others improve their the picture. GateWay Community College, physical diagnosis skills: www.med.ucla.edu/ Phoenix, AZ: www.gwc.maricopa.edu/class/ wilkes/intro.html bio202/cyberheart/hartbak.htm Basic cardiac assessment: www.youtube.com/ Assessment with a diaphragm of the stethoscope: watch?v=dp5m2tXHDmA www.youtube.com/watch?v=T2Hs5fqcflg Second Life heart murmur simulator: www Assessment with a bell of the stethoscope: .youtube.com/watch?v=xJY2Iwbzop4 www.youtube.com/watch?v=vSg-AU1EUaM 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 27

Chapter 3 Indications for Cardiac Surgery

Kristine J. Peterson

■ INTRODUCTION The heart has fascinated human beings for are medical therapy, percutaneous revascular- centuries as the seat of life and emotions. ization, and surgical revascularization. Revas- Although the idea of operating on the heart is cularization is the process of restoring blood not new, it was only in the mid-twentieth cen- flow and oxygen delivery to the myocardium. tury that such surgery became practical. With Its dual purposes are to alleviate angina symp- the development of cardiopulmonary bypass toms and to prolong life. Percutaneous trans- came the ability to create a bloodless surgical luminal coronary angioplasty (PTCA) uses an field and a motionless target for surgical ther- arterial catheter and various mechanical means apies. Since that time, multiple advances in to increase the diameter of diseased coronary surgical techniques, patient management, arteries, thereby improving blood flow. Surgi- technology, and pharmacotherapy have cal revascularization, also known as coronary resulted in the emergence of cardiac surgery artery bypass grafting (CABG), uses arterial or as a dynamic and very successful medical and venous vessels to create a new pathway for nursing specialty. blood to reach the coronary arteries, thus The ability to operate on the heart saves “bypassing” the stenosis. In 2004, 427,000 thousands of lives each year. These surgeries coronary artery bypass graft procedures were present exciting and varied challenges for the performed on 249,000 patients in the United critical care nurse and interdisciplinary team. States (AHA, 2007). With advances in percuta- The purpose of this chapter is to review the neous strategies such as drug-eluting stents types of cardiac surgery and their indications. (DES), the number of percutaneous revascularizations has increased while the number of sur- ■ SURGERY FOR ISCHEMIC HEART gical revascularizations has declined (AHA, 2007). Decisions regarding whether coronary DISEASE revascularization is indicated for an individual An estimated 79.4 million adult Americans patient now include which type of revascular- have some form of cardiovascular disease, ization is indicated. with approximately 15,800,000 having coronary heart disease (CHD), according to the Medical Therapy versus Surgical American Heart Association (AHA, 2007). Revascularization Once significant coronary artery stenosis is Several trials comparing medical therapy with established, the three major treatment strate- CABG were conducted between 1972 and gies used to prevent further ischemic damage 1984 (Hueb et al., 1995; Kloster et al, 1979; 27 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 28

28 Chapter 3 Indications for Cardiac Surgery

Varnauskas, 1988; Yusuf et al., 1994). High- It should be noted that these studies were all risk patients were defined based on the sever- conducted prior to 2003, when DES were first ity of their angina or ischemia, the number of introduced. diseased vessels, and the presence of left ven- The ARTS II registry compared outcomes tricular (LV) dysfunction (Brown, Sundt, & with a sirolimus-eluting stent and PCI to those Gersh, 2008). The studies consistently indi- in the PCI and CABG arms of the ARTS I study cated the greatest benefits of CABG over med- (Gruberg, 2005). ARTS II registry patients had ical therapy in those patients at highest risk. a higher incidence of diabetes, hypertension, CABG has not been shown to be of more ben- and hypercholesterolemia than did members efit than medical therapy for patients with of the ARTS I group, but included fewer single-vessel disease (Brown et al., 2008). smokers than in the original study. Rates of Yusuf et al. (1994), in a meta-analysis, demon- stable versus unstable angina were similar in strated significantly higher survival at 5, 7, the two groups, although the patients and 10 years after CABG for patients at high enrolled in ARTS II had more complex lesions and moderate risk, but not for low-risk than those in the first registry. MACCE-free patients. survival at one year was not significantly different between the two groups, probably due Percutaneous versus Surgical to the higher revascularization rate in ARTS II Revascularization patients. In a meta-analysis comparing DES with A large number of clinical trials have com- bare metal stents, Babapulle, Joseph, Belisle, pared short- and long-term outcomes from Brophy, and Eisenberg (2004) found no dif- percutaneous coronary intervention (PCI) ferences in survival or MI. DES placement and surgical revascularization (Goy et al., resulted in fewer restenoses and major cardiac 1999; Goy et al., 2000; Hannan et al., 2005; events. DES technology continues to evolve, Hoffman et al., 2003; Hueb et al., 1995; Ser- and DES are implanted frequently. The ruys et al., 2001). In the Arterial Revascular- impact of these stents on long-term outcomes ization Therapy Study (ARTS—the largest of compared with CABG procedures remains to these trials), 1- and 5-year follow-up data indi- be seen (Brown et al., 2008). cated no differences in major adverse cardiac and cerebrovascular events (MACCE) between ■ CABG and stent placement (Serruys et al., INDICATIONS FOR CORONARY 2001). CABG resulted in fewer revasculariza- ARTERY BYPASS GRAFTING tions, but PCI provided substantial cost sav- The American College of Cardiology (ACC)/ ings (Gruberg, 2005). Other studies have American Heart Association (AHA) Task found that CABG resulted in reduced 5-year Force on Practice Guidelines has established mortality, less angina, and fewer revascular- recommendations for CABG in certain sub- ization procedures than PCI (Hoffman et al., sets of patients. These recommendations 2003). Adding stents to PCI reduced revascu- reflect the severity of angina, the presence of larizations, but the need for such follow-up ST-segment elevation MI (STEMI), the pres- procedures remained significantly lower in ence of unstable angina or non-ST-segment CABG patients (Hannon et al., 2005; Hoff- elevation MI (NSTEMI), left ventricular func- man et al., 2003). Mercado et al. (2005) tion, presence or absence of life-threatening demonstrated that PCI and CABG resulted in ventricular arrhythmias, previous PCI, or pre- no differences in 1-year death, myocardial vious CABG (Eagle et al., 2004). Table 3–1 infarction (MI), and stroke rates, but higher lists the level of recommendations for each revascularization rates than found with PCI. patient population. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 29

Indications for Coronary Artery Bypass Grafting 29

Table 3–1 ACC/AHA Indications for CABG

Asymptomatic or Mild Angina Class I: Evidence and/or general agreement that the intervention is effective. 1. Left main coronary artery stenosis 2. Proximal LAD and proximal left circumflex stenosis 3. Triple-vessel disease 4. Proximal LAD and one- or two-vessel disease with LVEF less than 50% or a large amount of myocardium at risk on noninvasive studies 5. One- or two-vessel disease not involving proximal LAD with LVEF less than 50% or a large amount of myocardium at risk on noninvasive studies Class IIa: Evidence/opinion is in favor of efficacy. 1. Proximal LAD stenosis and one- or two-vessel disease Class IIb: Efficacy is less well established by evidence/opinion. 1. One- or two-vessel disease not involving proximal LAD Stable Angina Class I: Evidence and/or general agreement that the intervention is effective. 1. Left main stenosis 2. Proximal LAD and proximal left circumflex 3. Triple-vessel disease 4. Two-vessel disease with proximal LAD stenosis and LVEF less than 50% or demonstrable ischemia 5. One- or two-vessel disease without proximal LAD stenosis but with a large amount of myocardium at risk and high-risk criteria on noninvasive testing 6. Disabling angina refractory to medical therapy 7. Proximal LAD stenosis with one-vessel disease and meets high-risk criteria or large amount of myocardium at risk 8. One- or two-vessel disease without proximal LAD stenosis but meets high-risk criteria or large amount of myocardium at risk Class IIa: Evidence/opinion is in favor of efficacy. 1. Proximal LAD stenosis with one-vessel disease 2. One- or two-vessel disease without proximal LAD stenosis, but with a moderate amount of myocardium at risk and demonstrable ischemia Unstable Angina/NSTEMI Class I: Evidence and/or general agreement that the intervention is effective. 1. Left main stenosis 2. Proximal LAD and proximal left circumflex stenosis 3. Ongoing ischemia not responsive to maximal nonsurgical therapy 4. One- or two-vessel disease without proximal LAD stenosis when PCI not possible and meets high-risk criteria on noninvasive testing Class IIa: Evidence/opinion is in favor of efficacy. 1. Proximal LAD stenosis with one- or two-vessel disease Class IIb: Efficacy is less well established by evidence/opinion. 1. One- or two-vessel disease without proximal LAD stenosis when PCI not possible STEMI Class I: Evidence and/or general agreement that the intervention is effective. 1. Failed PCI with persistent pain or hemodynamic instability and anatomically feasible 2. Persistent or recurrent ischemia refractory to medical treatment with acceptable anatomy who have a significant amount of myocardium at risk and not a candidate for PCI continues 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 30

30 Chapter 3 Indications for Cardiac Surgery

Table 3–1 ACC/AHA Indications for CABG (continued)

3. Requires surgical repair of post-infarction ventricular septal rupture or mitral valve insufficiency 4. Cardiogenic shock in patients younger than 75 years of age who have ST-segment elevation, left bundle branch block (LBBB), or a posterior MI within 18 hours of onset 5. Life-threatening ventricular arrhythmias in the presence of 50% or more left main stenosis or triple-vessel disease Class IIa: Evidence/opinion is in favor of efficacy. 1. Primary reperfusion in patients who have failed fibrinolytics or PCI and are in the early stages (6–12 hours) of an evolving STEMI 2. Mortality for CABG is elevated in the first 3–7 days after STEMI/NSTEMI; after 7 days, the criteria for revascularization in previous sections apply Presence of Poor LV Function Class I: Evidence and/or general agreement that the intervention is effective. 1. Left main stenosis 2. Proximal LAD and proximal left circumflex stenosis 3. Proximal LAD stenosis and two- to three-vessel disease Class IIa: Evidence/opinion is in favor of efficacy. 1. Significant amount of viable myocardium and noncontractile myocardium Presence of Life-Threatening Ventricular Arrhythmias Class I: Evidence and/or general agreement that the intervention is effective. 1. Left main disease 2. Three-vessel disease 3. Bypassable one- or two-vessel disease if resuscitated cardiac arrest or sustained ventricular tachycardia 4. Proximal LAD disease and one- or two-vessel disease if resuscitated cardiac arrest or sustained ventricular tachycardia Class IIa: Evidence/opinion is in favor of efficacy. 1. Bypassable one- or two-vessel disease 2. Proximal LAD disease and one- or two-vessel disease Failed PCI Class I: Evidence and/or general agreement that the intervention is effective. 1. Ongoing ischemia with a significant amount of myocardium at risk 2. Hemodynamic instability Class IIa: Evidence/opinion is in favor of efficacy. 1. Foreign body in critical position 2. Hemodynamic instability with coagulopathy and no previous sternotomy Class IIb: Efficacy is less well established by evidence/opinion. 1. Hemodynamic instability with coagulopathy and previous sternotomy Previous CABG Class I: Evidence and/or general agreement that the intervention is effective. 1. Disabling angina refractory to medical therapy 2. Nonpatent previous bypass grafts, but with Class I indications for native CABG Class IIa: Evidence/opinion is in favor of efficacy. 1. Large amount of myocardium at risk 2. Vein grafts supplying LAD or large amount of myocardium are greater than 50% stenosed LAD ϭ left anterior descending coronary artery; LV ϭ left ventricle; LVEF ϭ left ventricular ejection fraction; LBBB ϭ left bundle branch block; STEMI ϭ ST-segment elevation myocardial infarction; PCI ϭ percutaneous coronary intervention; NSTEMI ϭ non-ST-segment elevation myocardial infarction. Source: Brown, Sundt, & Gersh, 2008. Used with permission. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 31

Transmyocardial Laser Revascularization 31

The recommendations are categorized into outcomes from CABG in patients with dia- three classes: I, II, and III. Class I indicates betes. Currently, these patients should be that evidence and/or general agreement exists evaluated with revascularization standard cri- that the intervention is effective. Class II indi- teria (Brown et al., 2008). cates that conflicting evidence and/or a divergence of opinion exists about the efficacy of CABG in Patients with Concomitant the intervention. Class II is further divided Carotid Disease into Class IIa and Class IIb: Class IIa indicates that evidence/opinion is in favor of the inter- Perioperative stroke risk ranges from 2% to vention’s efficacy, whereas Class IIb interven- 12% in patients with unilateral carotid occlu- tions have less efficacy as established by sion to 5% in patients with significant bilat- evidence/opinion. For Class III interventions, eral stenosis (Naylor, Cuffe, Rothwell, Loftus, evidence and/or general opinion suggests that & Bell, 2003). Accordingly, carotid endarterec- the intervention is not effective. tomy is recommended before or concurrently The strength of the level of evidence for with CABG in patients with symptomatic specific interventions is also identified carotid stenosis and for patients with 80% according to the type or presence of research. unilateral or bilateral carotid stenosis (Eagle For example, Level of Evidence A indicates et al., 2004). that findings from multiple randomized clinical trials or meta-analyses supported use of an Minimally Invasive Myocardial intervention. Level of Evidence B indicates Revascularization that a single randomized trial or a series of Off-pump CABG (OPCAB) has resulted in nonrandomized trials supported an interven- patency rates and survival rates equivalent to tion. Level of Evidence C is assigned to those those seen with traditional CABG (Puskas interventions supported by consensus opin- et al., 2003; Sharony et al., 2004). In addition, ion of experts, case studies, or standard of emerging evidence suggests that neurological- care (Eagle et al., 2004). related risks are lower when off-pump techniques are used to treat patients (Stamou et al., 2002). Currently, OPCAB is used chiefly CABG in Diabetics for low-risk patients with single-vessel disease The connection between diabetes mellitus (Brown et al., 2008). New surgical techniques and CHD is well established. Diabetes pro- such as total endoscopic CABG (TECAB) duces a prothrombotic, inflammatory, and will continue to change the landscape of proliferative state in the vascular endothe- CABG. OPCAB is discussed in more detail in lium and carries a higher risk for restenosis. Chapter 7. Individuals with diabetes tend to have more diffuse coronary disease—a state that favors ■ use of a procedure that can produce complete TRANSMYOCARDIAL LASER revascularization. Regardless of the revascu- REVASCULARIZATION larization procedure used, diabetics have a Despite advances in prevention, medical ther- higher risk of adverse outcomes (BARI Inves- apy, PCI, and CABG, CHD remains the single tigators, 2000). For persons with diabetes, greatest cause of death for Americans (AHA, there is a trend toward lower mortality and 2007). A substantial number of patients with fewer revascularizations with CABG than diffuse CHD have refractory angina despite with PCI. As yet, no studies have compared maximal medical and interventional therapy the outcomes from PCI with DES with the (Horvath & Zhou, 2008). Severe, diffuse CHD 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 32

32 Chapter 3 Indications for Cardiac Surgery

is often not amenable to complete revascular- 2002). The Society of Thoracic Surgeons’ ization, leaving myocardium at risk even after (STS) National Cardiac Database data from such a procedure is attempted. Incomplete 1998 to 2001 indicate perioperative mortality revascularization is a predictor of adverse of 6.4% and 4.2% when TMR is performed events (Horvath & Zhou, 2008). with CABG (Peterson et al., 2003). Options to treat refractory CHD include There remains divergence of opinion as to angiogenesis, genetic therapies, and transmy- the role of TMR (Brown et al., 2008; Horvath ocardial revascularization. These strategies & Zhou, 2008). Nevertheless, the STS has involve various means of creating new path- issued guidelines for the use of TMR in stable ways for blood to reach the myocardium. patients with medically refractory angina (see Transmyocardial laser revascularization Table 3–2). (TMR) is a procedure whereby transmyocardial channels are created from the epi- ■ cardium into the ventricle via a laser. The SURGERY FOR VALVE DISEASE new channels then allow blood from the ven- Valve disease can occur due to congenital or tricle to reach the myocardium directly. acquired factors. Decisions regarding medical Results of trials comparing TMR with med- or surgical management (repair or replace- ical therapy have been mixed, with studies ment) are made by weighing the risk and ben- showing inconsistent sustained symptom efits of each treatment modality. Valve relief with the former technique (Horvath surgery is discussed in detail in Chapter 5. et al., 2001). Early clinical trials of various techniques in ■ the 1980s demonstrated limited benefit, with SURGICAL MANAGEMENT patients experiencing only short-lived relief of OF ARRHYTHMIAS angina and little improvement in exercise tol- Durrer and colleagues (1967) first reported erance (Horvath & Zhou, 2008; Morrow, the successful initiation and termination of a Gersh, & Braunwald, 2005). Advances in laser tachycardia in 1967, when they induced and technology improved these results (Frazier, successfully terminated atrioventricular reen- March, & Horvath, 1999). Since that time, trant tachycardia (AVRT). Advancements in more than 25,000 patients have been treated understanding of arrhythmia initiation and worldwide (Horvath & Zhou, 2008). Two trials propagation as well as surgical techniques failed to show any benefit from this approach created a role for surgical ablation for tach- (Morrow et al., 2005; Saririan & Eisenberg, yarrhythmias (Eckart & Epstein, 2008). The 2003). Several follow-up reports of patients at need for open heart surgery limited this role 43 months and 5 years, however, demonstrated and spurred the development of catheter significantly improved angina symptoms and ablation techniques. Many arrhythmias— reduced hospitalizations; some patients were including atrioventricular nodal reentrant actually angina free at 5 years (Aaberge et al., tachycardia (AVNRT), AVRT, atrial tachycar- 2002; Horvath et al., 2001). dia, atrial flutter, atrial fibrillation (AF), and Perioperative mortality has improved from ventricular tachycardia (VT)—have been the earliest studies to approximately 1% to 5% mapped and ablated using catheter techniques (Frazier et al., 1999). Four-year follow-up data with varying degrees of success (Eckart & indicate a nonsignificant increase in survival Epstein, 2008). For persistent or recurring for TMR compared with an approach relying dysrhythmias, surgical management remains on continued medical therapy (Aaberge et al., an option. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 33

Surgical Management of Arrhythmias 33

Table 3–2 Indications for Transmyocardial Laser Revascularization as Sole Therapy

1. LVEF greater than 30% with CCS Class III or IV angina refractory to medical therapy, CABG, or PCI, reversible ischemia of LV free wall and CHD corresponding to the regions of ischemia. 2. Criteria in number 1 with either LVEF less than 30%, angina refractory to medical therapy or surgical revascularization (e.g., PTCA, stent), history of MI, cardiogenic shock and heart failure, uncontrolled ventricular dysrhythmia, or an area of ischemia that will not respond to CABG. 3. End-stage coronary artery disease for which medical therapy or surgical revascularization is no longer feasible and patient does not have indications for cardiac transplantation. 4. Refractory severe intractable angina. NYHA Class III or IV angina with symptoms refractory to medical therapy at endurable or highest safe dose, viable myocardium not amenable to surgical revascularization (e.g., PTCA, stent, coronary atherectomy, CABG), and the patient has made maximal attempts to stabilize acute conditions (e.g., severe ventricular dysrhythmia, decompensated heart failure, or acute MI).

CABG ϭ coronary artery bypass graft; CCS ϭ Canadian Cardiovascular Society; CHD ϭ coronary heart disease; LVEF ϭ left ventricular ejection fraction; MI ϭ myocardial infarction; NYHA ϭ New York Heart Association; PCI ϭ percutaneous coronary intervention. CCS Class III ϭ Apparent restriction of ordinary activity. CCS Class IV ϭ Angina at rest; patient cannot perform any physical activity without discomfort. NYHA Class III ϭ Patient is comfortable at rest; less than ordinary activity causes fatigue, palpitation, dyspnea, or angina. NYHA Class IV ϭ Inability to carry on any physical activity without discomfort. Symptoms of heart failure or angina may be present even at rest. Decreased comfort with any physical activity. Sources: Aetna, 2008; Bridges et al., 2004; Campeau, 1976; Eckstein et al., 2001.

Atrial Fibrillation catheter ablation, surgery, pacing, and The most important goals of therapy for AF implantable atrial defibrillators. are symptom alleviation and reducing the risk The most important indication for surgical of stroke (Cheng & Arnsdorf, 2007). Much treatment of AF is intolerance to the dys- research attention has been given to deter- rhythmia in patients who have failed pharma- mining the efficacy of rhythm control versus cological therapy. Other indications include rate control in AF. Currently, pharmacologi- paroxysmal atrial flutter or AF unresponsive cal rate control with anticoagulation is the to medical therapy, tachycardia-induced car- most common treatment strategy. Rate con- diomyopathy, patients who are intolerant of trol may be advantageous in that a less antiarrhythmic agents, patients who have a aggressive dosing regimen is associated with a contraindication to long-term anticoagula- lower risk of side effects and there are no tion, and patients with chronic AF who have a proven survival benefits for a rhythm control stroke despite adequate anticoagulation strategy (Voeller, Schuessler, & Damiano, (Voeller et al., 2008). 2008; Wyse et al., 2002). However, pharmaco- Surgical techniques have included left atrial logical therapy is limited in this indication by isolation, the Corridor procedure, pulmonary its inconsistent efficacy and side effects. For vein isolation, atrial transection, and the Maze this reason, strong interest remains in non- and Cox/Maze procedures (Cheng & Arnsdorf, pharmacological approaches to AF, including 2007; Voeller et al., 2008). Procedures that 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 34

34 Chapter 3 Indications for Cardiac Surgery

involve both atria have been most effective in study, pulmonary vein isolation reliably pro- controlling AF (Barnett & Ad, 2006). The duced a return to sinus rhythm (de Lima majority of patients have a surgical procedure et al., 2004). Other studies have not con- for AF in conjunction with another cardiac firmed these results, however, and lone pul- surgery such as a valve surgery (Cheng & Arns- monary vein isolation is not currently dorf, 2007). The most common surgical recommended (Doty et al., 2007; Eckart & approaches to AF are the Cox/Maze III proce- Epstein, 2008). The Cox/Maze III procedure dure and a modification of this technique that remains the standard surgical therapy for AF, uses radiofrequency (RF) ablation instead of although energy ablation is emerging as an surgical incisions (Barnett & Ad, 2006; Cheng effective alternative. & Arnsdorf, 2007; Chiappini, et al., 2004; Doty et al., 2007; Gaynor et al., 2005; Voeller et al., 2008). The Maze procedure interrupts the Surgical Management of Ventricular reentrant pathways required for AF using sur- Tachycardia gical incisions. The original procedure has Ventricular arrhythmias—particularly sus- been modified several times to the current ver- tained VT—are not uncommon in patients sion Cox/Maze III procedure. In addition, the who survive an acute myocardial infarction Cox/Maze IV procedure (Voeller et al., 2008), (AMI); the incidence in this patient popula- which involves the use of RF ablation, is now tion is approximately 3% (Pinto & Josephson, in use. A number of studies have attempted to 2007). Surgery to eradicate ventricular tach- determine whether RF or surgical incision yarrhythmias began in the 1970s with a tech- ablation is more effective; to date, the results nique called endocardial resection (Pagé, have been mixed. 2004). Over time, the initial enthusiasm for In a review of 276 patients who underwent the development of surgical therapies for VT the Cox/Maze I, II, III, and IV procedures, no waned as medical therapies such as mapping, difference in survival was found between the catheter ablation, and implantable devices procedures at a mean follow-up of 5.8 years advanced. The success of various surgical pro- (Gaynor et al., 2005). There was a significantly cedures in preventing VT is counterbalanced greater freedom from AF recurrence with the by the myocardial damage and high intraop- Cox/Maze III and IV procedures compared erative mortality associated with these proce- with the Cox/Maze I and II procedures. The dures (Pagé, 2004; Pinto & Josephson, 2007). results indicated that the Cox/Maze IV proce- Any surgical therapy for VT seems to be most dure further increased freedom from AF at 6 successful if the origin of the arrhythmia is in months; however, the follow-up time was too irreversibly damaged myocardium, which short to compare this procedure with other most commonly occurs after AMI. When versions (Gaynor et al., 2005). Another study patients have diffuse myocardial damage, indicated that the RF procedure results in such as cardiomyopathy, surgical therapies high efficacy and shortened operative time are not successful (Pagé, 2004). (Mokadam et al., 2004). A number of studies The development of multiple-site endocar- have reported that the Cox/Maze IV RF abla- dial and epicardial mapping systems has con- tion procedure is at least as safe and effective tributed greatly to the efficacy of surgical as the Cox/Maze III procedure (Chiappini management of VT. Localization of the site of et al., 2004; Topkara et al., 2006). earliest activation during VT on both the epi- The tissue around the pulmonary veins can cardial and endocardial surfaces allows for produce ectopic beats that trigger AF. In one precise targeting of therapies. Surgical man- 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 35

Ventricular Reconstruction Techniques 35

agement approaches to VT now include map- renders this option available to only a few ping-guided energy ablation, subendocardial patients. Accordingly, other surgical options resection, and ventricular endoaneurysmor- have been developed. Cardiac transplantation rhaphy. Subendocardial resection (SER) is discussed in detail in Chapter 19. involves surgical removal of scar tissue, portions of an aneurysm, or other sites gener- Coronary Revascularization as ating abnormal electrograms. Endoaneurysm- Treatment for Heart Failure orrhaphy involves incising the aneurysm and using a Dacron patch to control the shape Coronary revascularization via CABG or PCI and size of the ventricle (Pagé, 2004). These is known to improve ejection fraction (EF) techniques have achieved mortality and sud- when viable myocardium exists. Revascular- den cardiac death rates that are comparable ization can be used even for patients with an to those achieved with implantable car- EF as low as 10%. CABG for ischemic cardioverter defibrillators (ICDs) (Pagé, 2004). diomyopathy results in improved quality of Indications for surgery for VT are ill life and fewer hospitalizations compared with defined and largely dependent on the sur- medical therapy alone, and in survival rates geon’s judgment. Consensus does exist that superior to transplant for the first 2 years. VT caused by ischemic heart disease is most Revascularization for heart failure is indi- amenable to surgical therapy. Other factors cated for those patients with documented that should be considered when deciding on viable myocardium and no evidence of right the best course of action include the patient’s ventricular dysfunction. Revascularization is response to antiarrhythmic agents, history of not a good option for heart failure patients cardiac arrest, inducibility of the rhythm, with right ventricular dysfunction, signs of need for aneurysm resection, LV end-diastolic right-sided heart failure, or pulmonary hyper- volume, NYHA functional class, and presence tension (Spoor & Bolling, 2008). of mitral valve regurgitation (Pagé, 2004). ■ MITRAL VALVE REPAIR IN DILATED CARDIOMYOPATHY ■ SURGICAL THERAPIES FOR Ventricular failure and dilatation will eventu- HEART FAILURE ally result in mitral regurgitation (MR). MR is Following a myocardial infarction, both the often a pre-terminal event and is associated infarcted and non-infarcted areas undergo with a survival time of 6–24 months (Spoor & pathological changes such as thinning and Bolling, 2008). Early attempts at mitral valve fibrous replacement, which alter the size and replacement in these cases produced high shape of the ventricle and ultimately lead to mortality rates, and the practice was discour- heart failure. Medical therapy can improve aged. Mitral valve repair is discussed in more symptoms and increase lifespan, but it cannot detail in Chapter 5. cure the condition. Mechanical support, such as a ventricular assist device (VAD), has been ■ used as a bridge to transplant and occasion- VENTRICULAR RECONSTRUCTION ally as a bridge to recovery, but is not gener- TECHNIQUES ally regarded as a feasible long-term therapy Ventricular reconstruction techniques are for heart failure. The treatment of choice for based on the principle that the ventricular end-stage heart failure is cardiac transplanta- wall tension is proportional to the left vention, although the shortage of donor hearts tricular radius and pressure and inversely 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 36

36 Chapter 3 Indications for Cardiac Surgery

proportional to the wall thickness (Law of term failure (McCarthy et al., 2004). Other Laplace) (Spoor & Bolling, 2008). By chang- centers have reported similar results (Batista ing the size and shape of the ventricle, these et al., 1997; Franco-Cereceda et al., 2001; Star- techniques seek to reduce wall tension and ling et al., 2000). improve LV function. Specifically, surgical Given that mitral valve repair has been reconstruction techniques attempt to remove shown to improve heart failure, it is unclear or isolate dysfunctional myocardium, reduce whether the results of the Batista procedure the diameter of the ventricle, and restore a are attributable to the surgical reduction in more elliptical ventricular shape (Fang, ventricular size or to the effects of the mitral 2007). Additional goals are to relieve valve repair. Other surgical procedures have ischemia by revascularization if possible, and achieved results superior to the partial left to further reduce ventricular size and volume ventriculectomy. The Batista procedure is no via mitral valve repair (Menicanti & Di longer preformed in most of North America, Donato, 2002). though it is sometimes used in other areas where cardiac transplantation is less available ■ ENDOANEURYSMORRHAPHY (Spoor & Bolling, 2008). One of the earliest approaches to treating ■ GEOMETRIC VENTRICULAR post-infarction aneurysms sought to excise RECONSTRUCTION the aneurysmal area and reapproximate the wall edges, a procedure known as endoa- The Dor procedure, also known as endoven- neurysmorrhaphy. Although this approach tricular circular patch plasty repair, is a attempts to restore more normal ventricular procedure whereby the left ventricle is recon- geography, study data indicate that it does structed using a purse-string suture to isolate not improve LV function (Fang, 2007). nonfunctional segments of myocardium (rather than excising them) and a circular patch to control the shape of the ventricle. ■ PARTIAL LEFT The Dor procedure is usually performed con- VENTRICULECTOMY comitantly with a CABG (Di Donato et al., Batista and colleagues (1996) described a pro- 2001). The first case series report demon- cedure to restore the proper mass-to-diameter strated a significant improvement in LVEF, ratio for the left ventricle. To do so, a section which was maintained at 1-year follow-up. In of the left ventricular wall from the apex to addition, in those patients for whom data the mitral annulus was removed, and the were available, 92% had improved NYHA edges were reapproximated. The mitral valve functional class, and 91% of patients with was repaired or replaced as necessary. ventricular tachycardia were free of VT at Improvements in signs of heart failure and EF 1-year follow-up (Dor, Saab, Coste, Sabatier, have been achieved in more than 150 patients & Montiglio, 1998). Mickleborough, Mer- who have undergone a left ventriculectomy. chant, Inanov, Rao, and Carson (2004) The procedure produces a reduction in LV reported that a similar left ventricular recon- volume and, therefore, a reduction in LV wall struction procedure improved patients’ LVEF stress (Fang, 2007). In a series of North Amer- and NYHA functional class and had low peri- ican patients who underwent this procedure, operative mortality. researchers identified a short-term improve- Another modification of the original Dor ment in EF, reduced heart size, and symptom concept—the surgical anterior ventricular improvement, but a high incidence of long- endocardial restoration (SAVER) procedure— 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 37

Cardiac Transplantation 37

has produced similar results. Studies have Yet another novel device for heart failure is shown that SAVER leads to a significant the mitral valve annuloplasty ring. This new reduction of left ventricular volume and a sig- three-dimensional ring, which improves nificant increase in EF as well as significant mitral valve function and left ventricular reductions in hospitalizations for heart fail- shape (Maisano et al., 2005), is approved for ure. Survival at 18 months was 89%. A major- clinical use in the United States. The mitral ity of patients had concomitant CABG, and valve annuloplasty ring is discussed in more 23% had mitral valve replacement at the time detail in Chapter 5. of the procedure (Athanasuleas et al., 2004; When combined with optimal medical Hernandez et al., 2006). Studies have reported therapy, revascularization via CABG, geomet- consistently favorable results with ventricular ric mitral reconstruction, and left ventricular reconstruction (Athanasuleas et al., 2004; reconstruction have achieved results compa- Mickleborough et al., 2004). rable to transplantation. Spoor and Bolling (2008) list these interventions as first-line sur- ■ DYNAMIC CARDIOMYOPLASTY gical options for heart failure. Ventricular Dynamic cardiomyoplasty (DCMP) is an reconstruction is indicated for patients with innovative technique whereby the latissimus anteroseptal MI with a dilated left ventricle, dorsi muscle is wrapped around the heart. An EF less than 20%, left ventricular dyskinesis, implanted stimulator is then used to stimu- and symptoms of angina, heart failure, or late the muscle to contract in synchrony with arrhythmias, or for asymptomatic patients ventricular contraction. A clinical trial of with inducible ischemia on provocative test- DCMP was terminated early due to limited ing (Fang, 2007). By contrast, this procedure enrollment and borderline clinical improve- is not indicated for patients who have pul- ment (Fang, 2007). Dynamic cardiomyoplasty monary artery systolic pressures greater than is rarely performed in the United States, but it 60 mm Hg, severe right ventricular dysfunc- remains in use in other areas. tion, or regional dyskinesis or akinesis with- The concept of DCMP is spurring research out ventricular dilation (Fang, 2007). into other techniques that may produce ■ favorable results by “girdling” the ventricle. CARDIAC TRANSPLANTATION For example, the ACORN Cardiac Support Transplantation is considered the definitive Device (ACSD; Acorn Medical, Minneapolis, therapy for end-stage heart failure. The prin- Minnesota) is a polyester mesh fabric that is cipal limitation to heart transplantation is wrapped snugly around the ventricles. This the growing gap between the number of device provides passive support to the ventri- potential recipients and the number of avail- cles, which should reduce wall stress and pre- able donor organs. Given this mismatch in vent further remodeling. Another device used supply and demand, selection of recipients to decrease wall stress is the Myocor Myo- becomes an ethical dilemma as well as a clini- splint (Myocor Medical, St. Paul, Minnesota). cal issue (Colucci & Peña, 2007). A centralized With this device, which is currently in clinical organ allocation system has been established trials, transventricular tension bands are in the United States, known as the United placed through the right and left ventricular Network for Organ Sharing (UNOS); it works walls. The tension on these bands can be tai- alongside local committees to assure that the lored to the patient by tightening them indi- scarce donor organs are allocated in an objec- vidually to achieve a 20% reduction in wall tive, equitable, and medically justified way to stress. recipients in the greatest need. Evaluation of 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 38

38 Chapter 3 Indications for Cardiac Surgery

potential candidates is complex and is merely one of many factors considered when directed at selecting those patients with evaluating a patient for transplantation. refractory end-stage heart disease who have Table 3–3 lists the currently accepted indi- the potential to maintain compliance with a cations and contraindications for cardiac complex post-transplant regimen (Nwakanma, transplantation. Cardiac transplantation is Shah, Conte, & Baumgartner, 2008). Factors discussed in more detail in Chapter 19. considered in allocation include the amount of waiting time, the patient’s clinical status, and the geographic distance between the Heart–Lung Transplantation donor hospital and the transplant center Introduced in 1982, heart–lung transplantation (Colucci & Peña, 2007). was used for patients with end-stage cardiopul- The most common refractory heart dis- monary and septic lung disease (Sheikh, Pel- eases leading to transplantation are non- letier, & Robbins, 2008). The procedure reached ischemic cardiomyopathy (45%) and coronary its peak in the 1990s. Since then, however, due artery disease (38%) (Taylor et al., 2007). The to improvements in single- and double- highest mortality rate associated with these lung transplant techniques as well as donor conditions is seen in the first 6 months after allocation to critically ill heart recipients, the diagnosis. There is an increase in mortality number of procedures has declined substan- rate by 3.4% each year. Patient survival had a tially (Sheikh et al., 2008). Today, the most projected half-life (the time at which 50% of common indication for heart–lung transplan- those transplanted remain alive) of 11 years in tation is congenital heart disease with second- 2002 (Taylor et al., 2007). ary pulmonary hypertension (Eisenmenger The goals of transplantation are to improve syndrome). Congenital conditions that may survival and quality of life. As medical therapy lead to Eisenmenger syndrome include atrial has improved both of these outcomes, the and ventricular septal defects, patent ductus role of transplant has become less clear. Most arteriosus, and truncus arteriosus. Other pedi- candidates for transplantation must have atric and neonatal complex congenital heart failed aggressive medical therapy. anomalies have been successfully treated with Efforts to determine who will benefit most heart–lung transplant as well (Sheikh et al., from transplantation have centered on identi- 2008). Additional indications for adult fying predictors of mortality from heart fail- heart–lung transplantation include primary ure. The primary indicator currently is pulmonary hypertension with secondary right severely impaired exercise capacity as demon- heart failure, cystic fibrosis, septic lung disease,

strated by peak VO2 of 10 mL/kg/min or less severe coronary artery disease with end-stage (Colucci & Peña, 2007; Nwakanma et al., lung disease, and parenchymal lung diseases 2008). An additional tool is a prognosis score, with severe right-sided failure such as idio- such as the Heart Failure Survival Score pathic pulmonary fibrosis, lymphangioleiomy- (HFSS) or the Seattle Heart Failure Model omatosis, sarcoidosis, and desquamative (SHFM). These scores use clinical indicators interstitial pneumonitis (Sheikh et al., 2008; to stratify patients into risk categories or sur- Taylor et al., 2007). vival rate categories. Unlike the HFSS, the Recipients are selected on the basis of pro- Seattle model incorporates current medical gressively disabling symptoms and ability to therapy regimens, so it may be more reflective withstand full rehabilitation after the trans- of current practice (Colucci & Peña, 2007). plant (Sheikh et al., 2008). Table 3–4 outlines Although these tools may be useful, they are the generally accepted transplant candidate 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 39

Cardiac Transplantation 39

Table 3–3 Indications and Contraindications for Cardiac Transplantation

Indications ● Severe heart failure refractory to medical therapy ● Severely limiting ischemia not amenable to revascularization ● Recurrent symptomatic ventricular tachyarrhythmias refractory to medical therapy, devices, or surgery ● Cardiac tumors (rare) Diseases Systolic heart failure (EF less than 35%) ● Ischemic ● Dilated ● Valvular ● Hypertensive ● Other Ischemic heart disease with intractable angina ● Refractory to maximal tolerated medical therapy ● Not amenable to revascularization (CABG, PCI, or TMR) ● Unsuccessful revascularization Intractable arrhythmia ● Uncontrolled with implantable cardioverter defibrillator ● Not amenable to electrophysiologic guided therapy ● Not a candidate for ablative therapy Hypertrophic cardiomyopathy: Class IV heart failure symptoms persist despite maximal medical therapy ● Alcohol injection ● Myomectomy ● Mitral valve replacement ● Maximal medical therapy ● Pacemaker therapy Congenital heart disease in which fixed pulmonary hypertension is not a complication ● Cardiac tumor ● Confined to myocardium ● No evidence of distant disease via extensive metastatic workup

Contraindications and Excluded Etiologies Systolic heart failure as a result of ● Amyloidosis ● HIV infection ● Cardiac sarcoma continues 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 40

40 Chapter 3 Indications for Cardiac Surgery

Table 3–3 Indications and Contraindications for Cardiac Transplantation (continued)

Absolute contraindications ● Age greater than 70 years (depending on facility) ● Fixed pulmonary hypertension (unresponsive to pharmacologic therapy) ● Pulmonary vascular resistance greater than 5 Wood units or U/m2 ● Transpulmonary gradient greater than 15 mm Hg ● Systemic illness that will limit survival despite transplantation ● Neoplasm other than skin cancer (less than 5 years’ disease-free survival) ● HIV/AIDS (CD4 count less than 200 cells/mm3) ● SLE or sarcoidosis that has multisystem involvement or is still active ● Any systemic process with a high probability of recurrence in the transplanted heart ● Irreversible renal or hepatic dysfunction Relative contraindications ● Recent malignancy ● Chronic obstructive pulmonary disease (COPD) ● Recent and unresolved pulmonary infarction and pulmonary embolism ● Diabetes mellitus with end-organ damage ● Nephropathy ● Neuropathy ● Retinopathy ● Peripheral vascular or cerebrovascular disease ● Not amenable to surgical or percutaneous therapy ● Asymptomatic carotid stenosis greater than 75% or symptomatic carotid stenosis of less severity ● Active peptic ulcer disease ● Current or recent diverticulitis ● Other systemic illness likely to limit survival or rehabilitation ● Severe obesity or cachexia ● Severe osteoporosis ● Active alcohol or drug abuse ● History of noncompliance or psychiatric illness likely to interfere with long-term compliance ● Psychosocial impairment that jeopardizes the transplanted heart ● Antisocial personality disorder ● Medication noncompliance ● Cigarette smoking ● Inability to rely on alternative caregivers in the event of patient impairment ● Absence of psychosocial support

AIDS ϭ acquired immune deficiency syndrome; CABG ϭ coronary artery bypass grafting; CD4 ϭ cluster of differentia- ϭ ϭ ϭ tion, 4 (tests for T4 helper cells); EF ejection fraction; HIV human immunodeficiency virus; PCI percutaneous coronary intervention; SLE ϭ systemic lupus erythematosus; TMR ϭ transmyocardial laser revascularization. Sources: Colucci, & Peña, 2007; Nwakanma, Shah, Conte, & Baumgartner, 2008; Steinman et al., 2001. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 41

Cardiac Transplantation 41

Table 3–4 Heart–Lung Transplant Recipient Criteria and Contraindications

Criteria Contraindications Life expectancy of less than 18–24 months Absolute Contraindications Disabling symptoms Multiple organ system dysfunction ● Dyspnea, cyanosis Current substance abuse (alcohol, drug, or ● Syncope both) ● Hemoptysis Bone marrow failure ● NYHA Class III or IV Active malignancy Age less than 50 years HIV infection End-stage disease of heart and lungs Progressive neuromuscular disease Untreatable end-stage pulmonary, organ, or vascular disease, or any combination Clinically severe obesity of these Current tobacco use/smoking (must be absti- Disease processes (not all-inclusive) nent for at least one year) ● Irreversible primary PH with HF Noncompliance with other regimens ● COPD with HF Other major organ system disease or infection ● Nonspecific pulmonary fibrosis (e.g., major vascular disease) ● Emphysema with severe HF ● Cystic fibrosis with severe HF or end-stage Collagen vascular disease (scleroderma, SLE, bronchiectasis with compromised cardiac sarcoidosis) if not limited to the lung function Psychosocial history that limits ability to adhere ● Eisenmenger syndrome with irreversible PH to strict pre- and post-transplant regimens and HF Morbid obesity (BMI greater than 40 kg/m2 or ● Severe CAD or cardiomyopathy with greater than 35 kg/m2) with presence of irreversible PH comorbidities ● Noncomplex congenital heart disease Liver or kidney dysfunction (bilirubin greater associated with PH not amenable to lung than 2.5 mg/dL and creatinine clearance less transplantation and repair by standard than 50 mL/minute, respectively) cardiac surgery ● Pulmonary fibrosis with unmanageable PH Inadequate functional status or HF Relative Contraindications ● Congenital heart defect not amenable to standard repair Age (greater than 55–65 years) ● Irreversible right-heart failure from Eating disorder (anorexia, obesity) pulmonary hypertension Peripheral and coronary vascular disease Ventilator support or other conditions associated with limitations in mobility Steroid dependency Chest wall deformity Resistant infection (bacterial or fungal) Lack of social support

CAD ϭ coronary artery disease; COPD ϭ chronic obstructive pulmonary disease; HF ϭ heart failure; NYHA ϭ New York Heart Association; PH ϭ pulmonary hypertension; SLE ϭ systemic lupus erythematosus. NYHA Class III ϭ Patient is comfortable at rest; less than ordinary activity causes fatigue, palpitation, dyspnea, or angina. NYHA Class IV ϭ Inability to carry on any physical activity without discomfort. Symptoms of heart failure or angina may be present even at rest. Decreased comfort with any physical activity. Sources: Aetna, 2008; BlueCross BlueShield of North Carolina, 2008; Mancini, 2008; North Carolina Department of Health and Human Services, Division of Medical Assistance, 2008; Sheikh, Pelletier, & Robbins, 2008; Spiwak, 2008. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 42

42 Chapter 3 Indications for Cardiac Surgery

selection criteria. Contraindications for 2008). ASDs may be closed by patch under heart–lung transplantation are similar to those cardiopulmonary bypass or via percutaneous for heart transplantation (Sheikh et al., 2008). closure using a closure device. Outcomes from surgical closure are good. Adverse events and death are more frequent ■ SURGERY FOR ADULT with medical therapy than with surgical clo- CONGENITAL HEART DISEASE sure, regardless of the patient’s age (Atten- The congenital heart defects most commonly hofer et al., 2005; Laks et al., 2008). Although seen in adults are atrial septal defect (ASD) long-term follow-up has been limited to date, and bicuspid aortic valve (Wiegers & St. John data indicate that for those patients whose Sutton, 2007). As increasing numbers of chil- ASDs are suitable for percutaneous closure, dren with congenital heart defects survive to outcomes are also favorable, showing good adulthood, estimates are that approximately closure, improved functional capacity, and 760,000 adults will be living with congenital improved right and left ventricular perform- heart disease by 2020 (Laks, Marelli, Plunkett, ance (Laks et al., 2008; Wiegers & St. John & Myers, 2008). Most of these patients will Sutton, 2007). Two studies comparing out- have had corrective or palliative surgery in comes with surgical closure to those with per- infancy to minimize the long-term conse- cutaneous closure indicated complete closure quences of congenital defects. For the pur- rates were higher with surgery but signifi- poses of this chapter, this section focuses on cantly fewer complications occurred with management of ASD. percutaneous closure (Berger, Vogel, Alexi- Most ASDs of less than 8 mm close sponta- Meskishvili, & Lange, 1999; Du et al., 2002). neously. For those patients whose defects do not close, the primary cause of symptoms is ■ left-to-right shunting. Data indicate that an HYPERTROPHIC open ASD will increase in diameter over time, CARDIOMYOPATHY leading to increased shunting with age Hypertrophic cardiomyopathy (HCM) is a (McMahon et al., 2002). An ASD is most often common genetic cardiovascular disease char- asymptomatic until the individual reaches acterized by abnormal myocytes leading to adulthood; by age 30 to 40 years, however, AF hypertrophy without dilatation and preserved and reduced exercise tolerance as a result of systolic function (Maron et al., 2003; the defect are usually evident. Chronic left-to- McKenna, 2007; Padera & Schoen, 2008). right shunting may cause right ventricular Hypertrophy is most severe in the ventricular failure, tricuspid regurgitation, atrial arrhyth- septum. This asymmetrical growth usually mias, paradoxical embolization, and cerebral arises at the level of the LV outflow tract, lead- abscesses. Ultimately, irreversible pulmonary ing to subaortic stenosis or asymmetrical hypertension and right-to-left shunting and HCM. In addition, abnormal systolic anterior hypoxia will develop (Laks et al., 2008; motion of the mitral valve contributes to the Wiegers & St. John Sutton, 2007). Surgery is outflow obstruction (Maron et al., 2003; usually recommended before these adverse McKenna, 2007; Padera & Schoen, 2008; van sequelae occur. Surgical repair should be con- der Lee et al., 2005). sidered for patients with an ASD when the HCM has a variable course, although two ratio of pulmonary flow to systemic flow is presentations commonly lead to treatment. greater than 1.5:1, and pulmonary vascular Impaired diastolic filling due to massive resistance is less than 6–8 U/m2 (Laks et al., hypertrophy is usually responsible for signs 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 43

Hypertrophic Cardiomyopathy 43

and symptoms of heart failure, although The LV myectomy reduces anterior mitral sys- obstruction of the LV outflow tract con- tolic motion and MR and reduces the LV out- tributes as well (Maron, 2005; Maron et al., flow tract obstruction (Woo et al., 2005). The 2003; McKenna, 2007; Padera & Schoen, procedure is performed in conjunction with 2008). In addition, HCM is the most common perioperative transesophageal echocardiogra- cause of sudden cardiac death in young adults phy to precisely determine the amount of tis- (Padera & Schoen, 2008). sue to be removed. This procedure has a long Four approaches are employed for treat- history and experience and is well documented ment of HCM: pharmacological therapy, to be safe, provide excellent hemodynamic dual-chamber pacing, surgery, and chemical results, and improve quality of life (Maron, ablation (McKenna, 2007; Padera & Schoen, 2005; Maron et al., 2004; Maron et al., 2003; 2008; van der Lee et al., 2005; Woo et al., McKenna, 2007; Padera & Schoen, 2008; van 2005). Pharmacological therapy is usually the der Lee et al., 2005; Woo et al., 2005; Yacoub, first approach to signs and symptoms of 2005). heart failure; indeed, it is often the only treat- Systolic anterior motion (SAM) of the mitral ment needed in patients without outflow valve has been shown to be a major determi- obstruction (Maron et al., 2003). Beta block- nant of the amount of outflow obstruction. ade is the standard first-line therapy, with ver- Mitral valve replacement (MVR) is often added apamil and disopyramide often being added to the myectomy procedure, depending on the to the treatment regimen to take advantage of degree of SAM and obstruction. their negative inotropic properties (Maron Although successful, surgery is recom- et al., 2003). For a majority of patients, this mended for only some 5% of all patients with course of treatment is effective; a few patients HCM (Maron et al., 2003). Left ventricular develop systolic heart failure, however, and myectomy is recommended for those patients become candidates for heart transplantation. with drug-refractory symptomatic outflow A second treatment approach, dual-chamber obstruction (peak gradients greater than pacing, was introduced in the 1990s. Pacing 50 mm Hg as measured by echocardiography was thought to change the geometry of ven- under resting conditions and/or gradients tricular contraction and lead to reduced LV greater than 50 mm Hg as measured under outflow tract obstruction and symptomatic physiologic exercise). Surgery may also be con- improvement (McKenna, 2007). This proce- sidered in symptomatic patients with dure is currently recommended only for HCM documented outflow obstruction under physi- patients with sinus or AV node dysfunction ologic exercise but in whom resting obstruction (Gregoratos et al., 2002). is either absent or very mild (Maron et al., The mainstay of treatment for patients with 2003). One additional subset of patients may HCM who develop significant drug-refractory benefit from LV myectomy—young, asympto- LV outflow tract obstruction has been surgical matic patients with documented severe outflow LV myectomy and/or mitral valve replacement tract obstruction (gradient 75–100 mm Hg) (Maron, 2005; Maron et al., 2004; Maron et al., (Maron et al., 2003). Surgery is usually not rec- 2003; McKenna, 2007; van der Lee et al., 2005; ommended for asymptomatic or mildly symp- Woo et al., 2005). The myectomy procedure tomatic patients (Maron et al., 2003). MVR is involves excision of a section of subaortic sep- indicated when MR is present in addition to tal muscle that is approximately 3–7 cm long outflow tract obstruction (McKenna, 2007). and 3–12 grams in weight, with or without Finally, a percutaneous alternative for mitral valve replacement (Maron et al., 2004). relieving outflow obstruction is available. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 44

44 Chapter 3 Indications for Cardiac Surgery

Ethanol septal ablation is accomplished by and clots to accumulate in the mediastinal infusing ethanol into the first septal branch space and impair ventricular filling (cardiac of the left anterior descending coronary artery tamponade). via an angioplasty catheter (McKenna, 2007). Reexploration of the mediastinum is indi- Studies of this approach indicate that ethanol cated for signs of tamponade, including a ablation reduces outflow tract obstruction, sudden decrease or cessation of chest tube increases exercise capacity, and improves output, tachycardia, narrowing pulse pres- symptoms (McKenna, 2007; Padera & sure, and decreased cardiac index. Partial Schoen, 2008; van der Lee et al., 2005; Yacoub, resection of the pericardium is known as a 2005). Available data indicate that ethanol pericardial window. In such a procedure, a ablation markedly reduces symptoms but portion of the pericardium is excised to allow results in more complications and requires fluid to drain into the pleural or peritoneal more repeated interventions than myectomy. space and prevent reaccumulation of pericar- Hemodynamic results appear to be better with dial fluid. surgery. The effects of ethanol septal ablation on sudden cardiac death are as yet unknown ■ CARDIAC TUMORS (Maron et al., 2003; van der Lee et al., 2005; Yacoub, 2005). A benign tumor, myxoma accounts for half of Although the number of ethanol ablation all benign cardiac tumors. Approximately 75% procedures is clearly increasing, more research of these masses arise in the left atrium, most into this treatment alternative is warranted. often occurring in individuals between ages Indications for ethanol ablation are similar to 20 and 50 years. Myxomas are more common those for surgical intervention: Patients in women. These tumors cause obstruction of should have severe heart failure symptoms blood flow, which in turn leads to the clinical refractory to pharmacological therapy as well presentation of heart failure, signs of central as a gradient of greater than 50 mm Hg either nervous system (CNS) embolization, and con- at rest or under physiologic exercise (Maron stitutional symptoms such as fever, weight et al., 2003). Left ventricular septal myectomy loss, fatigue, weakness, arthralgia, and myal- remains the gold standard for treatment of gia. Resection of the myxoma is the only effec- outflow tract obstruction (Maron et al., 2004; tive therapy and should be performed early to van der Lee et al., 2005; Yacoub, 2005). prevent embolization (Walkes, Smythe, & Reardon, 2008). Other benign cardiac tumors in adults ■ OTHER CARDIAC SURGERIES: include lipoma and fibroelastoma. Large lipo- PERICARDIAL SURGERY mas are resected when they are symptomatic Bleeding and cardiac tamponade are known because of their potential for obstruction. complications after cardiac surgery. Typi- Papillary fibroelastomas occur on the heart cally, the surgeon leaves the pericardium valves and may cause obstruction or CNS open and places mediastinal chest tubes to embolization; these tumors should also be manage any postoperative bleeding. Despite resected. Primary cardiac malignancies are these precautions, it is still possible for blood extremely rare (Walkes et al., 2008). 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 45

Self-Assessment Questions 45

CASE STUDY

P.S. is a 73-year-old man with a history of angina pectoris and atherosclerotic heart disease. He underwent angioplasty and stenting to the left PDA and an obtuse marginal 2 years ago. He has known aortic stenosis and has been followed with echocardiogram for this condition. P.S. had been doing well until the last several months, when he began notic- ing substernal burning and pain with exercise that was relieved by rest. The patient noted that the pain occurred with any exercise after a meal. The latest echo by his primary care physician reveals an aortic gradient of 80 mm Hg, a jet velocity of 6.5 m/sec (meters per second), and an aortic valve area of 0.5 cm2. Additional history includes hyperlipidemia, hypertension, and a sedentary lifestyle. P.S. is mildly overweight, is not diabetic, does not smoke, and drinks only occasionally. His father was hypertensive; there is no history of aortic valve disease. P.S. takes atorvastatin 10 mg daily, atenolol 25 mg twice daily, aspirin (ASA) 81 mg daily, and a daily vitamin. He has been retired from his mail-carrying position since 1993 and lives at home with his wife. He was referred to a cardiac surgeon for aortic valve replacement. P.S. underwent coronary angiography, which revealed an 85% stenosis in the proximal LAD and another 90% in the first diagonal. A left dominant system with a previously stented PDA was noted, with heavy atherosclerosis that was deemed not bypassable. Ventricular function was normal. Preoperative lab studies were normal. The surgeon estimated that P.S. had a risk of less than 2% for major complications such as heart attack, stroke, and death, and a 4–5% risk of other complications such as pneumonia, bleeding, reoperation, and pacemaker. His surgery was scheduled for the next day. The operative report noted a tricuspid aortic valve, severe aortic stenosis, and advanced calcifications of the aortic valve leaflets. He underwent CABG with a left internal mammary artery graft to the left anterior descending and a radial artery graft to the first diagonal. The aortic valve was replaced. The operation was uneventful, and the patient was transferred to the intensive care unit in stable condition. P.S. had a smooth recovery. He was extubated within 4 hours and transferred to the progressive care unit the next morning. P.S. was discharged to home on postoperative day 6. His discharge instructions included consumption of a low-fat, low-cholesterol diet and outpatient cardiac rehabilitation. P.S. was given an appointment for the hospital’s “Living with Heart Disease” class and was discharged on ASA 325 mg PO once daily, lisinopril 2.5 mg PO once daily at bedtime, metoprolol 50 mg PO twice daily, and atorvastatin 10 mg PO once daily. He was to follow up with his surgeon in 2 weeks and his primary care physician in 4 weeks.

■ SELF-ASSESSMENT QUESTIONS 2. What are the indications for CABG in 1. What is the primary reason for surgery this patient? in the Case Study patient? a. One- or two-vessel disease not a. STEMI involving proximal LAD with LVEF b. Severe aortic stenosis less than 50% or a large amount of c. Coronary artery disease myocardium at risk on noninvasive d. Aortic dissection studies b. Proximal LAD stenosis with one- or two-vessel disease 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 46

46 Chapter 3 Indications for Cardiac Surgery

c. Failed PCI with persistent pain or 7. Which characteristics would indicate hemodynamic instability and severe AS? anatomically feasible a. Mean gradient of 80 mm Hg, jet d. Asymptomatic or mild angina and velocity of 6.5 m/sec, and valve area proximal LAD stenosis and one- or of 0.5 cm2 two-vessel disease b. Mean gradient of 20 mm Hg, jet 3. What are the indications for aortic valve velocity of 2 m/sec, and valve area of 2 replacement? 1.8 cm a. Patients undergoing CABG with mild c. Mean gradient of 35 mm Hg, jet AS when there is evidence that velocity of 3 m/sec, and valve area of 2 progression may be rapid 1.2 cm b. Severe AS and LV systolic d. Mean gradient of 45 mm Hg, jet dysfunction (ejection fraction less velocity of 3 m/sec, and valve area of 2 than 50%) 1.0 cm c. Symptomatic patients with severe AS 8. Which symptoms might indicate the d. Moderate AS undergoing CABG or presence of worsening AS? surgery on aorta or other heart valves a. Sudden cardiac death, AMI, and a 4. Which classification is the indication for diastolic murmur aortic valve replacement? b. Systolic murmur, angina, and a. Class III syncope b. Class IIa c. Angina, syncope, and CHF c. Class IIb d. Syncope, sudden cardiac death, and d. Class I elevated C-reactive protein 5. P.S. would be at high risk for which spe- 9. What are effective therapies for severe cific postoperative complications? AS other than aortic valve replacement? a. Bleeding, ileus, AMI a. Antihypertensives, digoxin, and b. Ileus, pacemaker, prolonged diuretics ventilation b. Diuretics, amiodarone, and lisinopril c. Pacemaker, bleeding, CVA c. Lisinopril, amiodarone, and an ICD d. Pneumonia, ileus, prolonged d. The only effective long-term therapy ventilation for AS is valve repair or replacement. 6. When P.S. asks you why he is being dis- 10. What is the most probable etiology of charged on lisinopril, what do you tell P.S.’s aortic stenosis? him? a. Rheumatic heart disease a. Lisinopril’s antiplatelet actions will b. Degenerative calcification help prevent clotting. c. Bicuspid aortic valve b. Lisinopril is an antianginal agent. d. Papillary muscle dysfunction c. Lisinopril is prescribed because P.S. Answers to Self-Assessment Questions has decreased myocardial function. 1. b 6. d d. Lisinopril provides plaque 2. d 7. a stabilization and antihypertensive therapy. 3. c 8. c 4. d 9. d 5. c 10. b 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 47

References 47

Clinical Inquiry Box

Question: Is ablation of atrial fibrillation in octogenarians during cardiac surgery safe? Reference: Grubitzsch, H., Beholz, S., Dohmen, P. M., Dushe, S., & Konertz, W. (2008). Concomi- tant ablation of atrial fibrillation in octogenarians: An observational study. Journal of Cardiothoracic Surgery, 3(1), 21. Objective: To evaluate the outcomes of octogenarians undergoing atrial fibrillation ablation. Method: Twenty-eight patients aged 80 years or older were evaluated at 3 months, 6 months, 12 months, and annually thereafter for atrial fibrillation duration, prevalence, aortic valve disease, ICU length of stay, and 30-day mortality. Results: Octogenarians were similar to controls regarding AF duration and left atrial diameter. The prevalence of paroxysmal AF, aortic valve disease, ICU stay, hospital stay, and 30-day mortality were increased in octogenarians. After 12 months, 14 octogenarians (82%) and 101 controls (68%, nonsignificant) were in sinus rhythm; 59% who were not taking antiarrhythmic drugs in either group were in sinus rhythm (nonsignificant). Conclusion: Even in advanced age, ablation for atrial fibrillation should be considered for octogenarians. The implication of this study for cardiac surgical nurses is to enhance awareness that the “oldest of old” will continue to be candidates for cardiac surgery and should be considered for surgical strategies such as ablation regardless of age.

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Partial left ventriculectomy to treat end-stage with diabetes who have acute myocardial heart disease. Annals of Thoracic Surgery, 64(3), infarction: Bypass Angioplasty Revasculariza- 634–638. tion Investigation Investigators. The New Eng- Berger, F., Vogel, M., Alexi-Meskishvili, V., & Lange, land Journal of Medicine, 342(14), 989-997. P.E. (1999). Comparison of results and com- Di Donato, M., Sabatier, M., Dor, V., Gensini, G. F., plications of surgical and Amplatzer device Toso, A., & Maioli, M., et al. (2001). Effects of closure of atrial septal defects. Journal of Tho- the Dor procedure on left ventricular dimen- racic and Cardiovascular Surgery, 118(4), sion and shape and geometric correlates of 674–678. mitral regurgitation one year after surgery. BlueCross BlueShield of North Carolina. (2008). Cor- Journal of Thoracic and Cardiovascular Surgery, porate medical policy: Heart–lung transplan- 121(1), 91–96. tation. Retrieved December 29, 2008, from Dor, V., Saab, M., Coste, P., Sabatier, M., & Mon- https://www.bcbsnc.com/services/medical- tiglio, F. (1998). Endoventricular patch plas- policy/pdf/heart-lung_transplantation.pdf ties with septal exclusion for repair of Bridges, C. R., Horvath, K. A., Nugent, W. C., ischemic left ventricle: Technique, results and Shahian, D. M., Haan, C. K., Shemin, R. J., et al. indications from a series of 781 cases. Japanese (2004). The Society of Thoracic Surgeons Journal of Thoracic and Cardiovascular Surgery, practice guideline series: Transmyocardial 46(5), 389–398. laser revascularization. Annals of Thoracic Doty, J. R., Doty, D. B., Jones, K. W., Flores, J. H., Surgery, 77(4), 1494–1502. Mensah, M., & Reid, B. B., et al. (2007). Com- Brown, M. L., Sundt, T. M., & Gersh, B. J. (2008). parison of standard Maze III and radiofre- Indications for revascularization. In L. H. quency Maze operations for treatment of Cohn (Ed.), Cardiac surgery in the adult (3rd ed., atrial fibrillation. Journal of Thoracic and Cardio- pp. 551–572). New York: McGraw-Hill vascular Surgery, 133(4), 1037–1044. Medical. Du, Z. D., Hijazi, Z. M., Kleinman, C. S., Silverman, Campeau, L. (1976). Letter: Grading of angina pec- N. H., Larntz, K., & Amplatzer Investigators. toris. Circulation, 54(3), 522–523. (2002). Comparison between transcatheter Cheng, J., & Arnsdorf, M. F. (2007). Surgical and surgical closure of secundum atrial septal approaches to prevent recurrent atrial fibrilla- defect in children and adults: Results of a mul- tion. Retrieved October 19, 2007, from ticenter nonrandomized trial. Journal of the www.uptodate.com American College of Cardiology, 39(11), 1836–1844. Chiappini, B., Martin-Suàrez, S., LoForte, A., Arpe- sella, G., Di Batolomeo, R., & Marinelli, G. Durrer, D., Schoo, L., Schuilenburg, R. M., & (2004). Cox/Maze III operation versus Wellens, H. J. (1967). The role of premature radiofrequency ablation for the surgical treat- beats in the initiation of and the termination ment of atrial fibrillation: A comparative of supraventricular tachycardia in the study. Annals of Thoracic Surgery, 77(1), 87–92. Wolff–Parkinson–White syndrome. Circulation, 36, 644–662. Colucci, W. S., & Peña, I. L. (2007). Indications and contraindications for cardiac transplan- Eagle, K. A., Guyton, R. A., Davidoff, R., Edwards, tation. Retrieved December 17, 2007, from F. H., Ewy, G. A., & Gardner, T. J. et al. (2004). www.uptodate.com 2004 guideline update for coronary artery bypass graft surgery: A report of the American de Lima, G. G., Kalil, R. A., Leiria, T. L., Hatem, D. M., College of Cardiology/American Heart Associ- Kruse, C. L., & Abrahão, R., et al. (2004). Ran- ation Task Force on Practice Guidelines (Com- domized study of surgery for patients with mittee to Revise the 1999 Guidelines for permanent atrial fibrillation as a result of Coronary Artery Bypass Graft Surgery). Circu- mitral valve disease. Annals of Thoracic Surgery, lation, 110, e340–e437. 77(6), 2089–2094. Eckart, R. E., & Epstein, L. (2008). Interventional Detre, K. M., Lombardero, M. S., Brooks, M. M., therapy for atrial and ventricular arrhythmias. Hardison, R. M., Holubkov, R., & Sopko, G. et al. In L. H. Cohn (Ed.), Cardiac surgery in the adult (2000). The effect of previous coronary artery (3rd ed., pp. 1357–1374). New York: McGraw- bypass surgery on the prognosis of patients Hill Medical. 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 49

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Laks, H., Marelli, D., Plunkett, M., & Myers, J. (2008). graft surgery versus percutaneous coronary Adult congenital heart disease. In L. H. Cohn intervention with multiple stenting for multi- (Ed.), Cardiac surgery in the adult (3rd ed., pp. system disease: A meta-analysis of individual 1431–1463). New York: McGraw-Hill Medical. patient data from randomized clinical trials. Maisano, F., Redaelli, A., Soncini, M., Votta, E., Journal of Thoracic and Cardiovascular Surgery, Arcobasso, L., & Alfieri, O. (2005). An annular 130(2), 512–519. prosthesis for the treatment of functional Mickleborough, L. L., Carson, S., & Ivanov, J. mitral regurgitation: Finite element model (2001). Repair of dyskinetic or akinetic left analysis of a dog bone-shaped ring prosthesis. ventricular aneurysm: Results obtained with a Annals of Thoracic Surgery, 79(4), 1268–1275. modified linear closure. Journal of Thoracic and Mancini, M. C. (2008). Heart–lung transplantation. Cardiovascular Surgery, 121(4), 675–682. Retrieved December 29, 2008, from Mickleborough, L. L., Merchant, N., Ivanov, J., Rao, http://emedicine.medscape.com/article/ V., & Carson, S. (2004). Left ventricular recon- 429188-overview struction: Early and late results. Journal of Tho- Maron, B. J. (2005). Surgery for hypertrophic racic and Cardiovascular Surgery, 128(1), 27–35. obstructive cardiomyopathy: Alive and quite Mokadam, N. A., McCarthy, P. M., Gillinov, A. M., well. Circulation, 111(16), 2016–2018. Ryan, W.H., Moon, M.R., Mack, M.J., et al. Maron, B. J., Dearani, J. A., Ommen, S. R., Maron, (2004). A prospective multicenter trial of bipo- M. S., Schaff, H. V., & Gersh, B. J., et al. (2004). lar radiofrequency ablation for atrial fibrilla- The case for surgery in obstructive hyper- tion: Early results. Annals of Thoracic Surgery, trophic cardiomyopathy. Journal of the Ameri- 78(5), 1665–1670. can College of Cardiology, 44(10), 2044–2053. Morrow, D. A., Gersh, B. J., & Braunwald, E. (2005). Maron, B. J., McKenna, W. J., Danielson, G. K., Chronic coronary artery disease. In D. P. Zipes, Kappenberger, L. J., Kuhn, H J., & Seidman, P. Libby, R. O. Bonow, & E. Braunwald (Eds.), C. E., et al. (2003). American College of Cardi- Braunwald’s heart disease: A textbook of cardiovas- ology/European Society of Cardiology clinical cular medicine (7th ed., pp. 1311–1328). expert consensus document on hypertrophic Philadelphia: Elsevier. cardiomyopathy. European Heart Journal, Naylor, R., Cuffe, R. L., Rothwell, P. M., Loftus, 24(21), 1965–1991. I. M., & Bell, P. R. (2003). A systematic review McCarthy, P. M., Bhudia, S. K., Rajeswaran, J., of outcome following synchronous carotid Hoercher, J., Lytle, B. W., Cosgrove, D. M., & endarterectomy and coronary artery bypass: Blackstone, E. H., et al. (2004). Tricuspid valve Influence of surgical and patient variables. repair: Durability and risk factors for failure. European Journal of Endovascular Surgery, 26(3), Journal of Thoracic and Cardiovascular Surgery, 230–241. 127(3), 674–685. North Carolina Department of Health and Human McKenna, W. J. (2007). Nonpharmacologic treat- Services, Division of Medical Assistance. ment of outflow obstruction in hypertrophic (2008). Heart–lung transplantation. Retrieved cardiomyopathy. Retrieved December 18, December 29, 2008, from http://www 2007, from www.uptodate.com .ncdhhs.gov/dma/Transplant/116.pdf McMahon, C. J., Feltes, T. F., Fraley, J. K., Bricker, Nwakanma, L. U., Shah, A. S., Conte, J. V., & Baum- J. T., Grifka, R. G., Tortoriello, T. A., et al. gartner, W. A. (2008). Heart transplantation. (2002). Natural history of growth of secun- In L. H. Cohn (Ed.), Cardiac surgery in the adult dum atrial septal defects and implications for (3rd ed., pp. 1539–1577). New York: McGraw- transcatheter closure. Heart, 87(3), 256–259. Hill Medical. Menicanti, L., & Di Donato, M. (2002). The Dor Padera, R. F., & Schoen, F. J. (2008). Pathology of procedure: What has changed after fifteen cardiac surgery. In L. H. Cohn (Ed.), Cardiac years of clinical practice? Journal of Thoracic and surgery in the adult (3rd ed., pp. 112–178). New Cardiovascular Surgery, 124(5), 886–890. York: McGraw-Hill Medical. Mercado, N., Wijns, W., Serruys, P. W., Sigwart, U., Pagé, P. L. (2004). Surgery for cardiac arrhythmias. Flather, M. D., & Stables, R. H., et al. (2005). In D. P. Zipes & J. Jalife (Eds.), Cardiac electro- One-year outcomes of coronary artery bypass 57625_CH03_027_052.pdf 4/10/09 11:10 AM Page 51

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Wiegers, S. E., & St. John Sutton, M. (2007). Manage- Yacoub, M. H. (2005). Surgical versus alcohol sep- ment of atrial septal defects in adults. Retrieved tal ablation for hypertrophic obstructive car- October 19, 2007, from www.uptodate.com diomyopathy. Circulation, 112(4), 450–452. Woo, A., Williams, W. G., Choi, R., Wigle, D., Yusuf, S., Zucker, D., Passamani, E., Peduzzi, P., Rozenblyum, E., Fedwick K., et al. (2005). Clin- Takaro, T., Fisher, L. D., et al. (1994). Effect of ical and echocardiographic determinants of coronary artery bypass graft surgery on sur- long-term survival after surgical myectomy in vival: Overview of 10-year results from ran- obstructive hypertrophic cardiomyopathy. Cir- domized trials by the Coronary Artery Bypass culation, 111(16), 2033–2041. Graft Surgery Trialists Collaboration. Lancet, Wyse, D. G., Waldo, A. L., DiMarco, J. P., Domanski, 344(8922), 563–570. M. J., Rosenberg, Y., Schron, E. B., et al. (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. New Eng- land Journal of Medicine, 347(23), 1825–1833. 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 53

Chapter 4 Preoperative Cardiac Surgery Nursing Evaluation

Roberta Kaplow, Sonya R. Hardin, Brenda Hardin-Wike, Timothy E. McMurry

■ INTRODUCTION Preoperative evaluation and preparation of Evidence further indicates that preoperative the patient for cardiac surgery affects postop- patient education results in increased patient erative outcomes and progress. The primary compliance, resulting in decreased length of goal of a presurgical assessment is evaluation hospital stay (Cupples, 1991; Shuldham, of perioperative risk. An in-depth assessment 2001). assists in minimizing surgical risk and poten- Numerous risk assessment tools have been tial morbidity and mortality. The literature developed to predict mortality in patients supports the preoperative optimization of undergoing heart surgery. Some of these scor- a patient’s cardiovascular status as part of ing tools include the Parsonnet, Cleveland the effort to improve patient outcomes Clinic, French, Euro, Pons, and Ontario (Halaszynski, Juda, & Silverman, 2004). An Province Risk scores (Geissler et al., 2000). The evaluative screening identifies special needs Parsonnet score has been found to be predic- that may require modification of the patient’s tive in the oldest of old individuals who require course of treatment before, during, and after cardiac surgery (Chaturvedi, deVarennes, & surgery. Lachapelle, 2007). Prolonged hospital stays and increased mortality are associated with ■ RISK FACTORS OF MORBIDITY higher scores. Table 4–1 presents the criteria utilized in the Parsonnet score. AND MORTALITY FOLLOWING CARDIAC SURGERY ■ The major risk factors for adverse outcomes of NURSING ASSESSMENT cardiac surgery include advanced age, emer- Nursing assessment prior to cardiac surgery gency surgery, previous cardiac surgery, dialysis typically begins during an outpatient visit, dependency, and creatinine level of 2 mg/dL or but may occur during an acute inpatient higher. Preoperative renal insufficiency is an admission. The latter situation may occur in independent risk factor for morbidity and patients with conditions that increase their mortality (Mageed & El-Ghoniemy, 2007). operative risk. The preoperative nursing Research has demonstrated a decreased assessment provides baseline information for incidence of physical and psychological prob- the postoperative period, along with an lems that adversely affect recovery when pre- opportunity to develop a relationship with operative education of patients is completed. the patient. Components of the preoperative

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54 Chapter 4 Preoperative Cardiac Surgery Nursing Evaluation

Table 4–1 Parsonnet Score the nurse evaluate patient and family knowledge as well as determine educational needs Factor Weight related to the planned procedure. Under- standing of the underlying illness, planned Female gender 1 surgical course, and willingness and ability to Comorbidities adhere to the surgical regimen are also evalu- Morbid obesity 3 ated. Put simply, the nurse is responsible for Diabetes 3 the overall assessment of the patient’s physi- Hypertension 3 cal and psychological readiness for surgery. Preoperative IABP 2 Data suggest that cardiac surgery patients Dialysis dependency 2 who receive preoperative education with or Pacemaker dependency 5 without coping strategies as opposed to rou- Left ventricular aneurysm 5 tine preoperative preparation experience less Emergency surgery following PTCA 10 emotional distress, have better physical and Acute renal failure 10 Cardiogenic shock 30 psychological recovery, and experience fewer hypertensive episodes postoperatively (Ander- Ejection Fraction son, 1987). Good (≥ 50%) 0 Baseline information is obtained about the Fair (30–49%) 2 patient’s clinical history, including the type of Poor (< 30%) 4 heart disease, associated symptoms, resource Age availability, stability, and ability to participate < 70 years 0 in care and decision making. The level of 70–74 years 7 resilience will be determined when the nurse 75–79 years 12 ascertains the degree of compensation the >80 years 20 patient has developed. Reoperation During the patient interview, the nurse should seek to discover any information that First 5 Second 10 can affect perioperative risk and postoperative management. Several risk factors have been Risk Scores: Good (0-4); Fair (5-9); Poor (10-14); identified in the literature as influencing the High (15-19); Extremely High (> 20). mortality of cardiac surgery patients. Table 4–2 IABP ϭ intra-aortic balloon pump; PTCA ϭ percutaneous transluminal coronary angioplasty. lists many of these comorbid conditions. Source: Parsonnet, Dean, & Bernstein, 1989. Used with The nurse should also inquire if the patient permission. has any history of gastrointestinal bleeding, peptic ulcer disease, or bleeding diathesis. Any of these conditions may affect the antiplatelet assessment include information from the regimen following revascularization or the patient, family, and medical records, and the choice of a valvular prosthesis. Likewise, the physical exam. nursing evaluation should gather information on the presence of cardiac risk factors as well as Preoperative Patient Interview presence of associated medical diseases, such The purpose of a patient interview is to review as COPD, cerebrovascular or other peripheral past medical and surgical histories and to arterial occlusive disease, and hypertension. conduct a systems evaluation to identify The patient’s baseline sleep patterns should processes that may affect the outcome of a be determined. Patients who undergo coro- patient’s cardiac surgery. The interview helps nary artery bypass grafting (CABG) proce- 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 55

Nursing Assessment 55

Table 4–2 Factors That May Affect Cardiac Surgery Patient Mortality

Alcohol use Tobacco use Diabetes Elevated serum creatinine (2 mg/dL or higher) Chronic airway disease Previous cardiac surgery Recent myocardial infarction Low left ventricular ejection fraction Chronic heart failure Pulmonary hypertension Unstable angina Depression Obesity Hypoalbuminemia Active endocarditis Procedure urgency Ventricular septal rupture Critical preoperative condition Dialysis Advanced age

Sources: Albert & Antman, 2003; Blumenthal et al., 2003; Engelman et al., 1999; Roques et al., 1999.

dures are at risk of developing sleep distur- 4 weeks prior to cardiac surgery, as they are at bances postoperatively. The presence of anxi- great risk for sepsis and respiratory failure. ety and depression should be assessed as well, Enhanced nutrition is also essential to pro- as these psychosocial conditions may develop mote wound healing and meet postoperative in the postoperative cardiac surgery patient metabolic demands (Albert & Antman, 2003). (Hedges & Redeker, 2008). This can be accomplished with dietary enhancement or enteral feeding if no con- Nutrition Evaluation traindications are present. Patients who are undergoing cardiac surgery and who have low The preoperative evaluation should also look body mass index (<20 kg/m2) and hypoalbu- for indicators of nutritional deficiency. In minemia (< 2.5 g/dL) are at increased risk of particular, malnutrition is a risk factor associ- postoperative morbidity and mortality (Engel- ated with significant morbidity and mortality man et al., 1999). Further, patients with in surgical patients. During the nursing eval- hypoalbuminemia are at increased risk for uation, it is essential that all cardiac surgery bleeding, renal failure, and prolonged ventila- patients undergo nutritional screening to tory support. Conversely, patients with a high identify malnourished or at-risk patients so as percentage of body fat have a greater risk for to ensure an adequate nutritional plan is sternal wound and saphenous vein harvest included as part of the patient’s care. site infections and atrial arrhythmias (Albert In addition to the nutritional assessment & Antman, 2003). screens available, unintentional weight loss, protein-calorie malnutrition, laboratory findings (e.g., anemia, hypoalbuminemia, preal- Discharge Planning

bumin, vitamin B12 deficiency), and low body To begin proactive discharge planning, the mass index are among the variables suggest- patient’s living arrangements are assessed. ing nutritional deficiency (Hengstermann, Many patients need assistance at discharge Nieczaj, Steinhagen-Thiessen, & Schulz, 2008; owing to limited social and financial Meyyazhagan & Palmer, 2002). Patients with resources. Early discharge planning alleviates hypoalbuminemia (<2.5 g/dL) should have stressors and anxiety for both the patient and their nutritional status optimized 1 to family (Carroll & Dowling, 2007). 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 56

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Physical Assessment stenosis. Auscultation of the carotid arteries Cardiac Assessment is performed from the base of the neck to the angle of the jaw while breath holding. A bruit For patients undergoing cardiac surgery, the is usually most audible in the upper third of assessment of the cardiovascular system will the carotid near the bifurcation (Cassar, Fin- likely be more extensive than the assessment gernet, & Woodcome, 1997). of the other body systems. Blood pressure, As noted in Chapter 3, perioperative stroke temperature, assessment of peripheral pulses, risk ranges from 2% to 12% with unilateral and weight are recorded. Blood pressure read- carotid occlusion to 5% with significant bilat- ings should be obtained from both arms. eral stenoses (Naylor, Cuffe, Rothwell, Loftus, Blood pressure difference between arms is & Bell, 2003). Accordingly, carotid endarterec- associated with increased morbidity and mor- tomy is recommended before or concurrently tality (Clark & Powell, 2002) and subclavian with CABG in patients who have sympto- artery stenosis (Osborn, Vernon, Reynolds, matic carotid stenosis and for patients who Timm, & Allen, 2002). This condition may have 80% unilateral or bilateral carotid steno- eliminate the possibility of using the internal sis (Eagle et al., 2004). mammary artery for grafting (Fortier, Peripheral vascular assessment is per- Demaria, & Perrault, 2002). It has been sug- formed to help determine the extent of gested that stenting the subclavian artery will peripheral perfusion. Components of this make the vessel suitable for CABG (Rogers & evaluation include determining the presence Calhoun, 2007). and strength of pulses in all extremities, capil- Auscultation of the heart and carotid arter- lary refill time, extremity and nail bed color, ies will provide essential baseline information. and temperature. Calculating the ankle- Heart sounds should be evaluated in terms of brachial index helps evaluate the arterial their rate, rhythm, and presence of extra blood flow to the lower extremities; steps to sounds, murmurs, gallops, or rubs. If the determine this index appear in Chapter 10. patient is noted to have a slow heart rate and The results of this calculation are then used a Mobitz II or complete heart block is noted, to rate degree of peripheral artery disease and insertion of a temporary transvenous pace- will help determine if the saphenous vein is maker wire should be considered (Albert & suitable for use during cardiac surgery (Crea- Antman, 2003). ger & Libby, 2004). Identification of aortic regurgitation (AR) A cardiac assessment further entails deter- is a significant finding, as this condition may mining presence of varicose veins. Presence of be exacerbated during cardiopulmonary significant numbers of lower-extremity vari- bypass and lead to acute left ventricular dis- cosities may indicate the need to use upper- tention (Albert & Antman, 2003). AR is iden- extremity vessels (e.g., radial artery) as tified with the presence of an early diastolic conduits during CABG. Using arm veins for murmur that can be heard at the second and conduits necessitates avoiding placing intra- third intercostal spaces (ICSs) at the right- venous lines in the affected arm (Albert & sternal border and at the second and fourth Antman, 2003). ICSs at the left-sternal border. The murmur of AR usually decreases in intensity Pulmonary Assessment (decrescendo) and disappears before the S1 heart sound (Choudhry & Etchells, 1999). Postoperative pulmonary complications con- A carotid bruit is a sound associated with tribute significantly to morbidity and mortal- turbulent flow and may indicate arterial ity. A thorough pulmonary assessment, 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 57

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including identification of associated risk fac- patients with COPD who are undergoing car- tors, is pivotal so that implementation of diac surgery have preoperative pulmonary strategies to mitigate complications can begin function testing (American Thoracic Society & in a timely fashion (Khan & Hussain, 2005). American College of Chest Physicians, 2003). Lung auscultation provides information about respiratory rate and breath sounds, and Abdominal Assessment the presence of crackles or wheezing. Presence A preoperative abdominal assessment is of crackles indicates fluid in the alveoli, which important to determine the presence of an may require diuresis prior to surgery. Presence abdominal aortic aneurysm (AAA), which is a of decreased breath sounds or adventitious potential contraindication of the use of an sounds may be related to an undiagnosed intra-aortic balloon pump (IABP—discussed condition that may increase the risk of post- in detail in Chapter 10) (Albert & Antman, operative pulmonary complications or to 2003). Abdominal palpation to detect abnor- underlying heart or lung disease. In either mal widening of an aortic pulsation is sug- case, optimizing the patient’s clinical condi- gested to be the most effective method to tion preoperatively is indicated (Khan & Hus- determine presence of an AAA. The width is sain, 2005). compared with the intensity of aortic pulsa- A patient’s smoking history should be tion to establish the presence of an AAA. determined. Studies in which patients under- Findings from palpation, however, are limited going CABG were evaluated suggest that cur- in patients with abdominal obesity. Diagnos- rent smokers are more likely to develop tic evaluation with ultrasound may also be pulmonary complications, require mechani- performed (Lederle & Simel, 1999). cal ventilation longer, and have higher mor- To palpate for presence of an AAA, the tality rates than patients who stopped patient should be positioned supine with smoking either 2 or 6 months prior to surgery knees raised. The abdomen should be (Khan & Hussain, 2005). Further, the inci- relaxed. To locate aortic pulsation, the dence of complications in patients who quit abdomen is palpated a few centimeters from smoking more than 6 months prior to cardiac the umbilicus toward the patient’s head and surgery is similar to the rate in patients who just left of the midline (the umbilicus is the never smoked. indicator of the level of the aortic bifurca- Preoperative cardiac surgery patients tion). Next, both hands are positioned on the should be assessed for preexisting pulmonary abdomen with palms down, and an index fin- disease to help anticipate potential postoper- ger is placed on either side of the pulsating ative conditions. Specifically, a history of pul- area to confirm that it is the aorta (each sys- monary hypertension and COPD are two tole should move the two index fingers apart) predictors of extubation failure in cardiac sur- and to measure the aortic width (Lederle & gery patients (Rady & Ryan, 1999). Patients Simel, 1999). with COPD, bronchitis, poor control of asthma symptoms, productive cough, or poor Neurologic Assessment exercise tolerance are also more likely to A patient who is undergoing cardiac surgery develop postoperative complications (Albert & may develop neurologic impairment during Antman, 2003; Hulzebos, Van Meeteren, De the intraoperative or postoperative period. A Bie, Dagnelie, & Helders, 2003; Jensen & Yang, baseline assessment will help facilitate identi- 2007; Khan & Hussain, 2005). The American fication of changes in neurologic status College of Chest Physicians recommends that (Albert & Antman, 2003). Baseline data can 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 58

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help prevent unnecessary testing that might should be partly based on the patient’s hemo- otherwise be performed to evaluate postoper- dynamic status (Albert & Antman, 2003). ative neurologic symptoms, which, in fact, might have been present preoperatively. The Cardiac History risk for postoperative delirium has been Nursing evaluation includes assessment of the reported to be 11.5% in cardiac surgery current level of symptoms. During the patient patients. Risk factors include cognitive interview, any increase in intensity or fre- impairment, atrial fibrillation, a history of quency of symptoms should be relatively easy peripheral vascular disease, major depression, to uncover. The interview is used to identify and advanced age (Kazmierski et al., 2006). the degree of the patient’s associated functional impairment and to observe for indications that heart function is inadequate during ■ PREOPERATIVE ASSESSMENT exertion. Several classification systems can be OF HEART DISEASE used to assess the functional status of patients Typically, patients undergoing cardiac sur- with heart disease; these systems evaluate gery have coronary artery disease (CAD). In angina, heart failure, and other aspects of fact, increasing numbers of patients who are heart disease. For example, the Canadian Car- undergoing cardiac surgery have decreased diovascular Society’s (CCS) functional classifi- cardiac function and several comorbid condi- cation system is used for the evaluation of tions, and many have undergone interven- angina; the New York Heart Association’s tional procedures for their cardiac condition (NYHA) classification is used to evaluate heart in the past (Albert & Antman, 2003). The risk failure (Campeau, 2002; Hurst, 2007). of surgery in terms of associated morbidity Preoperative evaluation of a patient’s cur- and mortality is logically higher in these rent medical status should include a cardiac patients. history. Specifically, the presence and severity A baseline assessment of underlying heart of symptoms of CAD should be determined. function is essential to help identify those In addition to assessing presence of risk fac- patients who are at risk during the intraoper- tors for CAD (e.g., tobacco, hypertension, dia- ative period. Data specific to heart function as betes, hyperlipidemia), obtaining a list of the well as the presence and extent of comorbidi- patient’s current medications and their usage ties such as diabetes and hypertension should will provide essential information. Severity of be collected. The patient history should pain should be rated on a zero to ten scale. include determination of when cardiac Characteristics of angina patterns should be comorbidities (e.g., myocardial infarction described in terms of onset; location; dura- [MI]) occurred and whether associated com- tion; character; precipitating, aggravating, plications are present (e.g., heart failure, and alleviating factors; and frequency. From ischemia, dysrhythmias) (Beattie & Hurtado, this information, healthcare providers can 2002; Moonesinghe & Kelleher, 2006). decide whether the patient has stable or The relationship between CAD and valvular unstable angina. Existence of a previous or disease is discussed in Chapter 5. Patients recent MI and presence of dysrhythmias or with valvular heart disease are vulnerable to palpitations are also essential pieces of infor- additional intraoperative and postoperative mation. Signs of pulmonary edema or pul- risk. A preoperative cardiac assessment for monary hypertension or other associated these patients should evaluate the impact of cardiovascular, peripheral vascular, or valvu- valvular disease on ventricular function and lar heart disease should be identified as well 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 59

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(Rupert, 2007). The surgeon should be noti- PND is a feeling of shortness of breath that fied of significant findings and if possible pre- awakens the patient. It is usually relieved operative hospital admission is anticipated. when the patient assumes an upright position A committee for the American College of (Mukerji, 1990). Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guide- lines revised these organizations’ guidelines Serological Testing for conducting a preoperative cardiovascular In addition to patient history, preoperative evaluation. Although, strictly speaking, these testing with serological and other diagnostic recommendations are designed for patients methods should be performed. Data from undergoing noncardiac surgery, many of the these tests will help determine surgical and factors may be used as a guideline for patients postoperative risk, and define the presence undergoing cardiac surgery. Three of the or extent of any new or known comorbid major clinical predictors of cardiac risk in the conditions. guidelines are the presence of unstable Laboratory data that may be collected pre- angina, the presence of significant dysrhyth- operatively include complete blood count mias, and recent MI (Eagle et al., 2002). (CBC); coagulation profile; liver, renal, and Dyspnea is another symptom of heart dis- thyroid function; electrolytes; and albumin ease to be evaluated in the preoperative car- level. Identifying the presence of anemia or diac surgery patient; it usually results from infection is an important consideration when inadequate tissue oxygen delivery. Patients evaluating cardiac patients, as there are may report difficult, labored, or uncomfort- always risks of intraoperative bleeding and able breathing. Some of the more common dilutional effects with bypass procedures. causes of dyspnea include heart failure, car- Attaining and maintaining a hematocrit diac ischemia, asthma, COPD, and pneumo- greater than 35% is recommended. In addi- nia. If dyspnea is noted, determination of tion, CBC data will help suggest presence of whether it has a cardiac or pulmonary etiol- an infection from an elevated white blood cell ogy is vital. Indices of a cardiac etiology count. Preoperative treatment of infection include a history of dyspnea on exertion, should be implemented (Albert & Antman, paroxysmal nocturnal dyspnea (PND), orthop- 2003). If CBC results reveal thrombocytope- nea, and chest pain. Physical findings may nia, a decision as to whether the patient

include jugular venous distention, S3 gallop, should receive heparin should be made, as ascites, and peripheral edema. Radiologic stud- thrombocytopenia may be an indication of ies may reveal pleural effusion or cardiomegaly heparin-induced thrombocytopenia (HIT). (Boyars, Karnath, & Mercado, 2004). Dyspnea Further testing must be done to confirm HIT. is commonly observed in patients with valvular If a patient tests positive for HIT, an alterna- disease; it may also be experienced by patients tive anticoagulation method should be con- with ventricular dysfunction. sidered for cardiopulmonary bypass. For Orthopnea is the sensation of breathless- example, bivalirudin (Angiomax®), a direct ness when the patient is lying in a position of thrombin inhibitor, has been used in cardiac rest. It is relieved by sitting or standing. With surgery patients requiring bypass (Pappalardo worsening cardiac disease, orthopnea often et. al., 2007). develops such that the patient needs to elevate Patients will be heparinized during bypass the head of the bed with more than one pillow procedures. Any coagulopathies should be cor- to breathe comfortably while recumbent. rected (e.g., with fresh frozen plasma or platelet 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 60

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transfusion, administration of vitamin K) and monitoring of these data for the cardiac prior to surgery to minimize risk of postopera- surgery patient should begin in the preoperative bleeding (Albert & Antman, 2003). tive setting. Data suggest that presence of Assessment of liver function should be con- hyperglycemia in cardiac surgery patients ducted to help predict how medications, increases mortality, length of stay, and infec- including anesthetic agents, will be metabo- tion rates (Furnary & Wu, 2006). lized (Albert & Antman, 2003). The value in optimizing a patient’s nutritional status preoperatively was discussed earlier; albumin Diagnostic Studies level is one component of that assessment. In addition to laboratory tests, a number of Sometimes patients develop acute renal diagnostic procedures may potentially be per- failure (ARF) following cardiac surgery. One formed for the preoperative cardiac surgery of the risk factors of this complication is pre- patient. Results of these tests will provide existing renal dysfunction. Further, the information about cardiac anatomical and mortality rate of patients who develop post- physiologic issues and pulmonary status, help operative ARF and require hemodialysis is identify those patients who may be at higher reported to be approximately 64%. Patients risk (and the degree of risk) with surgery, alert with normal renal function have a mortality the surgeon that preoperative “fine-tuning” rate of slightly more than 4% (Albert & may be necessary, or suggest that modifica- Antman, 2003). These data speak to the essen- tions of fluids or medications, or both, intra- tial nature of evaluating a patient’s preopera- operatively may be anticipated. Some of the tive renal function. diagnostic procedures that may be performed Although thyroid function tests are not for these purposes include echocardiography, part of the usual preoperative assessment, it computed tomography (CT), magnetic reso- has been suggested that such evaluation may nance imaging (MRI), radionuclide scanning, be warranted in patients with dysrhythmias cardiopulmonary exercise testing, cardiac such as AF. The risks of hyperthyroidism catheterization, and pulmonary function tests (e.g., ischemia, heart failure, rapid ventricular (Albert & Antman, 2003; Moonesinghe & rate associated with the AF) and hypothy- Kelleher, 2006). roidism (e.g., hypometabolism, decreased Echocardiography may be performed to clearance of anesthesia, prolonged mechani- discover any cardiac anatomical irregularities cal ventilation) provide justification of preop- that might affect surgery (Albert & Antman, erative thyroid function assessment in 2003). Results of an echocardiogram (ECG) patients undergoing cardiac surgery (Albert & may reveal conditions such as decreased ejec- Antman, 2003). tion fraction or RV function, presence of aor- Preoperative serum electrolytes should be tic stenosis or insufficiency, or mitral evaluated, particularly potassium and magne- insufficiency. These data may be used to sium levels. Notably, the presence of reevaluate the surgical plan, identify intraop- hypokalemia, hypomagnesemia, or both can erative risk, or devise a plan to optimize the predispose the patient to develop dysrhyth- patient’s clinical status as much as possible mias. Imbalances should be corrected before prior to surgery (Albert & Antman, 2003). surgery to prevent intraoperative complica- Echocardiography may be used to evaluate tions (Albert & Antman, 2003). wall motion and to estimate the pressure Maintaining serum glucose levels within a drop (gradient—a measure of heart valve effi- normal range decreases the rate of cardiac ciency) associated with valvular disease surgery complications. Effective treatment (Moonesinghe & Kelleher, 2006). 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 61

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CT may be performed to identify any car- tion on actual energy expenditure and stroke diac anatomical irregularities that might volume during exercise. The oxygen extrac- affect the surgery outcome (Albert & Antman, tion from each beat is also measured at vary- 2003). Although traditional two-dimensional ing work intensities (Wasserman, Hansen, CT provides some detail of the heart, the Sue, Stringer, & Whipp, 2004). heart is beating—and therefore moving— Cardiac catheterization is considered the during the procedure. By contrast, the newer gold standard for the diagnosis of CAD. In technology of multislice CT angiography pro- the case of the cardiac surgery patient, it is vides three-dimensional images of the heart, performed to evaluate coronary anatomy and which allows for better visualization of the efficacy of cardiac contractility (American beating heart. Presence of arterial blockages, Heart Association, 2008c). Data such as base- heart function, and wall motion may all be line right atrial, pulmonary artery systolic, assessed with this technique (Moonesinghe & diastolic, and occlusive pressures, as well as Kelleher, 2006; Sun, 2007). pulmonary vascular resistance, ejection frac- As part of the preoperative evaluation, MRI tion, and cardiac output, will help determine may be performed to identify any cardiac LV and RV function, augment valve function anatomical irregularities, assess cardiac func- data, and assist with intraoperative and post- tion and perfusion, and evaluate valves and operative hemodynamic management. Admin- blood vessels (Albert & Antman, 2003; Ameri- istration of fluids and vasoactive agents will be can Heart Association, 2008a). Cardiac MRI guided by these data, as will the choice of the (CMR) creates cardiac images while the heart operative procedure itself. A cardiac catheteri- is beating, thereby providing both still and zation may sometimes reveal the presence of a moving images of the heart and major blood LV mural thrombus, which places the patient vessels. Chamber size and damage from MI at risk for a stroke in the intraoperative or may be determined through use of this tech- postoperative period. In patients with valvular nology as well (Moonesinghe & Kelleher, heart disease, cardiac catheterization may be 2006; National Heart Lung and Blood Insti- used to estimate the degree of regurgitation. tute, 2007). Unlike echocardiography, which provides an Radionuclide scanning is performed to indirect measurement of the pressure gradi- help evaluate blood supply to the ent, cardiac catheterization provides for a myocardium, and to identify the extent of direct measurement of this parameter (Albert damage from any previous MI. Intravenous & Antman, 2003; LeBoutillier & DiSesa, 2003; administration of a radionuclide (e.g., thal- Moonesinghe & Kelleher, 2006). lium, technetium) can highlight those areas Pulmonary function tests may be per- of the myocardium that are hypoperfused formed on patients who have preexisting lung from partial or complete arterial occlusion disease (e.g., COPD). As noted earlier in this (American Heart Association, 2008b). chapter, patients with a history of COPD are Cardiopulmonary exercise testing may be at greater risk for developing postoperative performed to assess the heart’s functional complications and requiring prolonged intu- reserve—that is, the amount of work the heart bation. Data from a preoperative arterial is able to do in extraordinary conditions blood gas sample can help guide postopera- (Albert & Antman, 2003). During this evaluative weaning (Albert & Antman, 2003). tion, concomitant cardiac and ventilatory Given that carotid artery stenosis is a risk effects of exercise are assessed. Gas exchange, factor for stroke following CABG, a preopera- heart rate, and blood pressure measurements, tive carotid ultrasound should be considered. along with ECG evaluation, provide informa- Patients with a carotid bruit or a history of 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 62

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cerebrovascular accident are at greater risk for tion of an inotropic agent may be indicated. developing this complication. Assessment of Agents such as dobutamine (Dobutrex®) or the carotid arteries preoperatively may milrinone (Primacor®) may be used because decrease the postoperative risk of stroke of their vasodilator effects (Albert & (Durland et al., 2004; Tarzamni, Afrasyabi, Antman, 2003). Farhoodi, Karimi, & Farhang, 2007). Patients who are undergoing cardiac sur- Beta Blockers gery should receive a preoperative dental Discontinuing beta-adrenergic-blocking examination. In one study, gingivitis and lym- agents can result in a hypersympathetic state phadenopathy were observed in 64% and 42% that could precipitate myocardial ischemia, of patients, respectively, and oral hygiene was infarction, rebound hypertension, tachycar- unsatisfactory in the majority of patients eval- dia, or dysrhythmias (Wiesbauer et al., 2007). uated (Jegier, Smalc, Ciesielski, Jander, & As noted in Chapter 15, the incidence of AF Jegier, 2006). If patients have not had a dental following cardiac surgery varies with the pro- evaluation for several years, an undetected cedure performed. As many as 65% of patients oral infection may potentially be present; who undergo combined CABG/valve surgery such a condition predisposes the patient to and 10% to 40% of patients who undergo adverse postoperative outcomes (Yasny & Sil- CABG alone develop postoperative AF. Identi- vay, 2007). fied risk factors include greater age, history of hypertension or AF, and heart failure. Preop- Medications erative prophylactic administration of beta A comprehensive review of the patient’s cur- blockers has reportedly decreased the inci- rent medication profile and a concomitant dence of AF by 70% to 80% in patients who medical and surgical history are essential to undergo CABG. Some researchers suggest assist with preoperative planning and prevent that sympathetic tone, which is augmented intraoperative and postoperative complica- during cardiac surgery, is diminished when tions. Although some medications may be beta blockers are taken. Results from other studies suggest that administration of amio- withheld before cardiac surgery, many others ® ® are continued or adjusted during the preopera- darone (Cordorone ) or sotalol (Betapace ) tive period, particularly those used to manage may decrease the incidence of AF following CABG, whereas administration of a calcium hypertension or heart disease (Moonesinghe & ® Kelleher, 2006). channel blocker or digoxin (Lanoxin ) does not decrease incidence of AF (Albert & Nitrates Antman, 2003). It has been further suggested Nitrates should be continued up to the time that beta blockers be tapered or changed to of surgery to avoid an ischemic event. Fur- short-acting agents to help patients avoid ther, preoperative intravenous administration potential intraoperative myocardial depres- of a nitrate or other vasodilator (e.g., prosta- sion (Wiesbauer et al., 2007). cyclin, nitric oxide) may be indicated to decrease pulmonary vascular resistance (PVR) Afterload Reducers and enhance RV function in patients with RV It is recommended that patients with mitral dysfunction (Albert & Antman, 2003). regurgitation and heart failure receive an angiotensin-converting enzyme (ACE) Inotropes/Vasodilators inhibitor or sodium nitroprusside (Nipride®) If patients have a history of PVR that results preoperatively to help reduce afterload. These in RV dysfunction, preoperative administra- medications should be titrated to achieve a 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 63

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systolic blood pressure of 90–100 mm Hg versibly inhibits platelet function and has been (Albert & Antman, 2003). shown to increase perioperative blood loss. Data suggest that a preoperative aspirin-free ACE Inhibitors interval of 2–10 days improves platelet func- While most cardiac medications are not held tion and reduces blood loss and transfusion in the preoperative cardiac surgery patient, requirements. However, if the patient is under- ACE inhibitors are typically discontinued 24 going urgent cardiac surgery and has acute to 48 hours before surgery. Continuation of coronary syndrome, aspirin therapy should ACE inhibitors may result in intraoperative continue until the day of surgery (Dunning et hypotension, most notably in patients under- al., 2008; Weightman et al., 2002). going CABG procedures. The key risk associ- Aprotinin (Trasylol®), an anti-fibrinolytic ated with ACE inhibitor discontinuation is agent that works by inhibiting activation of arterial graft spasm and increased require- plasminogen to plasmin, is not recommended ments for vasodilator therapy (Bertrand et al., for routine use in cardiac surgery because of 2001; Moonesinghe & Kelleher, 2006). data indicating a correlation with postoperative renal dysfunction and a likely increase in Calcium Channel Blockers mortality. This agent may be prescribed for Some preclinical studies suggest that calcium patients at particularly high risk of bleeding channel blockers interact with inhalation in an effort to decrease blood loss and the anesthetic agents and some neuromuscular need for blood transfusions during cardiac blocking agents. The clinical significance of surgery. As this issue is currently being these data is low, however. While it is agreed reviewed by the Food and Drug Administra- that calcium channel blockers should be held tion, these recommendations may soon in patients undergoing cardiac surgery, the change (Dunning et al., 2008). optimal timing for stopping these agents Current guidelines established by the remains a point of contention (Murphy & American College of Chest Physicians recom- Wechsler, 2007). mend heparin prophylaxis for high-risk groups. Other data suggest use of low- Anticoagulants molecular-weight heparin (LMWH) as a Medications affecting hemostasis or bleeding bridge for patients receiving chronic anticoag- are discontinued in preparation for cardiac ulation who are undergoing cardiac surgery surgery. Specifically, warfarin (Coumadin®) is (Douketis, Johnson, & Turpie, 2004; Dunning held 2–4 days prior to surgery so that the inter- et al., 2008). Use of LMWH is also associated national normalized ratio (INR) reaches a level with a low risk for thromboembolic and less than 2.0. Patients who are at risk for devel- major bleeding complications (Douketis et oping thrombosis should receive intravenous al., 2004). Usual practice entails discontinu- heparin when the INR reaches subtherapeutic ing unfractionated heparin 4–5 hours before levels (Dunning et al., 2008). Clopidogrel surgery or LMWH 12–24 hours before surgery (Plavix®) is held 7 days before surgery to (Hartsell & Will, 2004). decrease the risk of excessive intraoperative Heparinization during CABG procedures bleeding and transfusion requirements is performed to prevent intraoperative (Moonesinghe & Kelleher, 2006). Clopidogrel thrombosis. Complicating the preoperative is also associated with a two- to five-fold anticoagulation management issue is the increase in risk for surgical reexploration and a fact that extended preoperative use of 30% to 100% increase in blood loss from the LMWH or unfractionated heparin results in chest tube (Dunning et al., 2008). Aspirin irre- a decrease in intraoperative response to 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 64

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heparin—a phenomenon known as heparin edgebase has significant clinical implications resistance or altered heparin responsiveness. for the cardiac surgery patient, no herbal Aside from preoperative heparin infusion, remedies should be taken for at least 2 weeks other identified associated factors of heparin prior to surgery. Garlic, ginseng, echinacea, resistance include infection and use of IABP ginkgo biloba, St. John’s wort, valerian, kava, therapy (Bar-Yosef, Cozart, Phillips-Bute, flavonoids, and grapefruit juice are all known Mathew, & Grocott, 2007). to decrease platelet activity (Hodges & Kam, 2002). Ginseng may also cause hypoglycemia. Hypoglycemics Kava and valerian may cause an enhanced Patients who are taking oral hypoglycemic sedative effect of anesthetic agents. St. John’s agents for type II diabetes should have these wort may cause increased metabolism of agents withheld preoperatively for several many of the drugs used in the perioperative days. The combination of metformin (Glu- period (Ang-Lee, Moss, & Yuan, 2001). caphage®) and sulfonylureas is known to contribute significantly to postoperative ■ MANAGEMENT OF HIGH-RISK morbidity and mortality (Evans, Ogston, PATIENTS Emslie-Smith, & Morris, 2006). Long-acting insulin is usually discontinued preoperatively Ventricular Dysfunction as well. In contrast, insulin glargine (Lan- Preoperative cardiac surgery patients with tus®), a long-acting basal insulin, may be con- heart failure and a history of hypertension, tinued during the surgical period (Marks, ischemia, hypertrophic cardiomyopathy, or 2003). Other patients who receive insulin acute valvular dysfunction are at risk for, and therapy may have their dose withheld on the should be assessed for, ventricular dysfunc- day of surgery, with medication levels being tion (De Marco & McGlothlin, 2005). High regulated based on blood glucose monitoring. morbidity and mortality rates are associated with cardiac surgery in patients who have Statins severe LV dysfunction and clinically signifi- Data suggest that statin therapy should be cant heart failure secondary to ischemic or continued through the day of surgery. A valvular heart disease (Kotlyar et al., 2001). reduction in morbidity and mortality has Patients with LV dysfunction and valvular been reported with ongoing use of such med- disease (e.g., mitral regurgitation, aortic ication (Collard, Body, Shernan, Wang, & stenosis) require preoperative management of Mangano, 2006; Durazzo et al., 2004). their hemodynamic status. Measures required may include administration of nitroprusside Herbal Remedies or an ACE inhibitor or use of IABP therapy to Use of herbal remedies can cause increased stabilize these patients’ condition prior to risk of bleeding and drug interactions. While surgery (Albert & Antman, 2003). Nitroprus- the medication profile obtained during the side has been demonstrated to rapidly stabi- preoperative evaluation should include infor- lize the patient with decompensated heart mation about the use of herbal remedies, failure due to severe LV dysfunction and aor- more is being learned about potential interac- tic stenosis (Khot et al., 2003). tions between these supplements and other Patients with acute tricuspid regurgitation medications every day. As this growing knowl- secondary to infective endocarditis are at 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 65

Summary 65

increased risk for right ventricular dysfunc- teremia or fever after 7–10 days of organism- tion (Nauser & Stites, 2001). The presence of specific antimicrobial therapy, and valve perfo- right ventricular dysfunction also increases ration (Vikram, 2007). patients’ perioperative risk (Mathew, Anand, Addai, & Freels, 2001). Patients should be Severe Aortic Stenosis evaluated for evidence of pulmonary hyper- Patients with severe aortic stenosis who tension, and those with a pulmonary artery develop LV dysfunction have greater intraop- systolic pressure greater than 60 mm Hg erative and postoperative risk. Data suggest, should be treated with agents for lowering however, that performing surgery on these pulmonary vascular resistance. patients is safe (Borowski, Ghodsizad, Severe chronic ventricular dysfunction Vchivkov, & Gams, 2007). The patient with occurs in patients with chronic hypertension, aortic stenosis who develops heart failure and or mitral or aortic valve disease, and in those decreased ejection fraction likely has symp- with prior left ventricular MI. These disorders toms related to increased afterload and alter- affect left ventricular function, leading to left- ations in contractility. If immediate surgery is sided—and ultimately right-sided—heart fail- not required, management may include inter- ure (De Marco & McGlothlin, 2005). ventions to augment cardiac output with a The presence of heart failure may cause sur- positive inotrope infusion (e.g., dobutamine) gery to be delayed while healthcare providers or to decrease peripheral resistance through attempt to improve the patient’s cardiac func- administration of a vasodilator (Carabello, tion and decrease surgical risk. Therapy 2002). focuses on maintaining adequate preload and afterload. Medication or the IABP may be used to augment afterload reduction. In such ■ SUMMARY a case, the nursing evaluation focuses on Patients who present for cardiac surgery identifying and optimizing the patient’s have higher levels of complexity than in the unstable hemodynamic status. past. Often, because of comorbid or concomitant conditions, surgical procedures Infective Endocarditis are combined, creating potentially higher Patients with infective endocarditis (IE) require levels of vulnerability and instability. An in- close monitoring for hemodynamic instability depth preoperative evaluation of the and development of multiple organ dysfunc- patient’s history and cardiac status, along tion. Given that heart failure influences the with collection of laboratory data and possi- prognosis of an individual with IE most signif- bly invasive and noninvasive procedures, is icantly, early surgery should be considered in critical to prevent poor outcomes postoper- those patients with IE, acute mitral or aortic atively. Early detection of potential compli- regurgitation, and signs of heart failure. Other cations can improve outcomes and help indications for urgent surgery include, but are ensure a successful recovery. Critical care not limited to, unstable valve prosthesis, gram- nurses are in a unique position to utilize negative or fungal endocarditis, major clinical inquiry techniques and critical embolism, persistent mobile and large vegeta- thinking skills to uncover those risk factors tion during the first 2 weeks of antimicrobial and data that can redirect interventions to therapy, enlarged vegetations or persistent bac- become more individual specific. 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 66

66 Chapter 4 Preoperative Cardiac Surgery Nursing Evaluation

CASE STUDY

M.J. is a 60-year-old frail female who has four-vessel disease and is scheduled for coronary artery bypass grafting. She is admitted preoperatively for evaluation and to control her blood pressure, as she admits to being forgetful about taking her antihypertensive medications. Her medication profile includes a beta blocker, ACE inhibitor, proton pump inhibitor, Glu- caphage® (metformin), and an antidepressant. M.J. has an allergy to cephalosporins. Her medical history includes type II diabetes for 5 years, atherosclerosis, and alcohol abuse. The patient is very nervous and is concerned about the pain she will experience postoperatively.

Critical Thinking Questions 1. Given the history of this patient, which potential postoperative problems might the nurse expect. 2. Should sleeping medication be given to this patient the night before surgery? 3. Does this patient have a higher risk of bleeding? 4. Which type of antibiotic should be given to this patient prior to surgery to prevent infection given her history? Answers to Critical Thinking Questions 1. Given that she is frail, M.J. might have nutritional deficiencies that could affect her recovery. She is also noncompliant with medication, requiring intervention prior to her cardiac surgery. Diabetes is another risk factor associated with morbidity. 2. Patients can have ischemia with stress. Medication to facilitate sleep the night before surgery can help to decrease stress. At least 40% of patients become ischemic preoperatively if good premedication is not provided (Adams & Antman, 2001). 3. More than likely given her history of alcohol abuse. Laboratory findings would be useful in identifying M.J.’s precise level of risk. 4. Vancomycin is the agent of choice for patients with a penicillin or cephalosporin allergy and to allay concerns about the potential for infection with methicillin-resistant Staphylococcus aureus and S. epidermis (Lemmer, Richenbacher, & Viahakes, 2003).

■ SELF-ASSESSMENT QUESTIONS 2. The nurse is interested in any aspects of 1. During the first preoperative meetings, the cardiac surgery patient’s history the nurse evaluates the patient and fam- that may affect the antiplatelet regimen ily for all the following except after revascularization. Which of the a. understanding of the underlying following histories would be a cause for illness. concern? b. planned course of cardiac surgery. a. Peptic ulcer disease c. ability to comply with surgical b. Overactive bladder disease regimen. c. Migraines d. satisfaction with the facility. d. Fractured tibia 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 67

Self-Assessment Questions 67

3. During the preoperative nutritional 8. A patient scheduled for a CABG will assessment, the nurse should question have blood sent for type and cross- the patient on weight, diet, and food match. Which factor increases the prob- preferences. Which of the following data ability that the patient will have should be reported as being a source of antibodies? concern? a. Previous transfusions a. Unintentional weight loss b. Null parity b. BUN 26 mg/dL c. Steroid utilization c. High-protein diet to lose weight d. MRSA carrier d. Six caffeinated drinks daily 9. The onset of accelerating angina war- 4. A carotid bruit is rants assessment and diagnostic evalua- a. common in individuals older than tion in the pre-cardiac-surgery patient to age 70 years. rule out a myocardial infarction. As a b. loudest in the upper third of the nurse, you know that the best outcome carotid artery. is expected if cardiac surgery occurs c. heard best during normal breathing. within ______hours of the MI. d. an indication of cerebral dementia. a. 4 b. 8 5. Which condition would prevent the use c. 12 d. 24 of an internal thoracic artery? 10. Which of the following patients is at a. Asthma highest risk for right ventricular dys- b. Dental infection function? c. Mastectomy a. A patient with four-vessel disease d. Diabetes b. A patient with a septal aneurysm 6. Atrial fibrillation occurs frequently in c. A patient with mitral valve stenosis patients, especially in those with d. A patient with acute tricuspid a. tricuspid valve disease. regurgitation b. aortic valve disease. c. mitral valve disease. Answers to Self-Assessment Questions d. pulmonic valve disease. 1. d 6. c 7. Which of the following medications 2. a 7. b would you consider holding on the day 3. a 8. a of surgery? a. Proton pump inhibitor 4. b 9. a b. ACE inhibitor 5. c 10. d c. Statin d. Antidepressant 57625_CH04_053_072.pdf 4/10/09 11:09 AM Page 68

68 Chapter 4 Preoperative Cardiac Surgery Nursing Evaluation

Clinical Inquiry Box

Question: How does obesity affect mortality after cardiac surgery? Reference: Rockx, M. A., Fox, S. A., Stitt, L. W., Lehnhardt, K. R., McKenzie, F. N., Quantz, M. A., et al. (2004). Is obesity a predictor of mortality, morbidity and readmission after cardiac surgery? Canadian Journal of Surgery, 47(1), 34–38. Objective: To determine whether obesity is a predictor of mortality, morbidity, or early readmission to hospital. Methods: A retrospective study was undertaken that included 1310 patients who had cardiac surgery between 1999 and 2002 in an academic hospital. Outcome variables such as stroke, reoperation for bleeding, life-threatening cardiac arrest or arrhythmia, new renal failure requiring dialysis, septicemia, mediastinitis, sternal dehiscence, respiratory failure, postoperative myocardial infarction, and low cardiac output necessitating intra-aortic balloon pump use were correlated with body mass index (BMI). Results: An increased BMI was associated with a higher likelihood of readmission to hospital within 30 days of discharge and sternal wound dehiscence. However, an increased BMI did not increase the risk of early postoperative death, stroke, reoperation for bleeding, life-threatening cardiac arrest or arrhythmia, new renal failure requiring dialysis, septicemia, mediastinitis, respiratory failure, postoperative MI, or low cardiac output necessitating IABP use. Conclusion: Obesity was not associated with adverse outcomes after cardiac operations, except for an increased risk of sternal dehiscence and early hospital readmission. Although obesity is often perceived as a major risk factor for cardiac surgery, this study did not find as high a correlation as one might expect. Nurses providing care to obese patients must be aware of the increased risk of sternal dehiscence and the potential for hospital readmission, however, and prevention strategies should be utilized to mitigate these risks.

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Sun, Z. (2007). Multislice CT angiography in Weightman, W. M., Gibbs, N. M., Weidmann, C. R., abdominal aortic aneurysm treated with Newman, M. A., Grey, D. E., Sheminant, M. R., endovascular stent grafts: Evaluation of 2D et al. (2002). The effect of preoperative aspirin- and 3D visualizations. Biomedical Imaging and free interval on red blood cell transfusion Intervention Journal, 3(4), e20. requirements in cardiac surgical patients. Jour- Tarzamni, M. K., Afrasyabi, A., Farhoodi, M., nal of Cardiothoracic and Vascular Anesthesia, Karimi, F., & Farhang, S. (2007). Low preva- 16(1), 54–58. lence of significant carotid artery disease in Wiesbauer, F., Schlager, O., Domanovits, H., Wild- Iranian patients undergoing elective coronary ner, B., Maurer, G., Muellner, M. et al. (2007). artery bypass. Cardiovascular Ultrasound, 5, 3. Perioperative beta-blockers for preventing sur- Vikram, H. R. (2007). Infective endocarditis: Prog- gery-related mortality and morbidity: A sys- nostic stratification and indications for valve tematic review and meta-analysis. Anesthesia & surgery. Indian Heart Journal, 59(2), 118–123. Analgesia, 104, 27–41. Wasserman, K., Hansen, J. E., Sue, D. Y., Stringer, Yasny, J. S., & Silvay, G. (2007). The value of opti- W. W., & Whipp, B. J. (2004). Exercise testing mizing dentition before cardiac surgery. Jour- and interpretation: An overview. In Principles of nal of Cardiothoracic and Vascular Anesthesia, exercise testing and interpretation: Including patho- 21(4), 587–591. physiology and clinical applications (4th ed., pp. 1–10). Philadelphia: Lippincott Williams & Wilkins. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 73

Chapter 5 Heart Valve Surgery

Catherine Drumm, Kristine J. Peterson

■ INTRODUCTION Heart valve surgery is performed to either Valvular heart disease may be caused by repair or replace a failing valve. Cardiac valves either congenital or acquired factors. Congeni- allow for one-way, low-resistance blood flow. tal factors include a bicuspid rather than tricus- The opening and closing of a valve occur pid valve, and other congenital malformations. according to pressure gradients between each For example, a congenital condition found in side of the valve. The valves must open widely adults is Marfan syndrome, a connective tissue to allow for rapid blood movement and mini- disorder. In Marfan syndrome, the chemical mal cardiac work; conversely, they must makeup of the connective tissue supporting the remain tightly closed to prevent backward heart valves is abnormal. As a consequence, the flow of blood. Proper functioning of cardiac valve leaflets may not remain tightly closed, and valves depends on normal fibroelastic tissue the result is a backward flow of blood. This dys- of the valve leaflets, proper number of cusps function increases myocardial workload and of the valve, ability to open and close rapidly, may ultimately lead to an enlarged ventricle. normal-sized ring or annulus, and proper Marfan syndrome is most clinically significant function of chordae tendinae and papillary when the mitral or aortic valve is affected muscles (mitral and tricuspid) (Fann, Ingels, (American Heart Association, 2008). & Miller, 2008; Mihaljevic, Sayeed, Stamou, & Acquired causes of valve disease include Paul, 2008). This chapter describes the vari- ischemic coronary artery disease (CAD), ous valve surgery procedures and their associ- degenerative changes associated with aging, ated care implications. rheumatic changes, infective endocarditis from a bacterial infection, neoplasm, or thrombus (Fann et al., 2008; Hill, 2007; ■ VALVULAR HEART DISEASE Mihaljevic et al., 2008). Valvular heart disease (VHD) is defined The relationship between ischemic CAD according to the valve or valves affected and and VHD is bidirectional. On the one hand, the type of functional alteration. Abnormality myocardial infarction due to CAD can result of the valve is identified as either stenosis in ventricular remodeling (a pathological (narrowing or constriction that creates a pres- change in the shape and size of the ventricle). sure gradient) or regurgitation (incomplete Chordae tendinae, papillary muscle, and the closure of the valve leaflets resulting in a valve annulus may be affected by ischemia as backflow of blood). well, leading to impaired valve function. On

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the other hand, a malfunctioning valve will valve. Nevertheless, patients are educated on cause an increase in myocardial workload and both repair and replacement procedures. Pros can eventually lead to ischemia as a symptom and cons exist for both mechanical and bio- of valve disease. logical valves. Therefore, the surgeon and the Stenosis or regurgitation can occur with patient together decide which type of valve any valve when rheumatic changes are the will be used for replacement. underlying etiology. These changes may be Mechanical valves are believed to be more present for many years before the patient durable than bioprosthetic valves, but require manifests symptoms. Degeneration of valves that patients receive lifelong anticoagulation due to aging occurs when fibrous material therapy. The introduction of International and calcium are deposited in and around Normalized Ratio (INR) self-testing, how- leaflets, resulting in their malfunction. Data ever, should reduce the incidence of throm- suggest that the etiology of aortic valve dis- boembolic and hemorrhagic complications ease is becoming less frequently related to related to the use of mechanical valves rheumatic disease (RD) and more frequently (Thompson et al., 2008). attributable to age-related degenerative changes. In one study, while RD remained the ■ most common cause of aortic stenosis, its AORTIC STENOSIS incidence was found to be decreasing. Con- Aortic stenosis is the most common adult versely, the incidence of valve malfunction as valve lesion in the United States. Its usual a result of degenerative changes was found to causes are a bicuspid valve and degenerative be increasing. Correspondingly, the frequency calcification (Gaasch, 2007a), with the latter of RD, which was the leading cause of aortic etiology being the most frequent cause regurgitation (AR) in this study, was found to (Carabello, 2004; Mihaljevic et al., 2008). be decreasing. The incidence of aortic regurgi- Given that the U.S. population is aging, the tation related to degenerative changes did not incidence of aortic stenosis is increasing. change in this study (Matsumura et al., 2002). Long thought to be a disease of stress and Infective endocarditis occurs when bacteria degenerative changes, the calcification of attach to and destroy the surface of a valve aortic stenosis is now regarded as a prolifera- leaflet or chordae. If a valve is damaged, tive and inflammatory process, similar to immune cells, platelets, and fibrin migrate to atherosclerosis (Carabello, 2004; Mihaljevic the site to initiate healing of the valve. If bac- et al., 2008). teria become trapped under layers of these Aortic stenosis, in which the aortic valve cells, “clumps” of tissue (vegetations) can does not open completely, creates a left ven- develop on the valves and within the heart tricular outflow tract obstruction and muscle, leading to endocarditis. Vegetations increases workload and afterload of the left may also break off and become emboli ventricle (LV). The increase in afterload is (Homma & Grahame-Clarke, 2003). the etiology of the signs and symptoms asso- Decisions about whether to pursue medical ciated with aortic stenosis (LeBoutillier & or surgical management and which type of DiSesa, 2003). surgical management to use, if necessary, are Factors involved in grading the severity of based on the goals of maximizing the life of aortic stenosis include the mean systolic gra- the valve and minimizing complications of dient across the valve, blood velocity, valve treatment (Shemin, 2008). Often the decision area, LV function, and severity of symptoms to repair or replace a valve is made once the (Bonow et al., 2006; Carabello, 2004; Mihalje- surgeon has an opportunity to visualize the vic et al., 2008). Normally the pressures in the 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 75

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LV and the aorta are virtually equal during period, when the disease is already severe. Most systole, meaning there is no aortic systolic patients have left ventricular hypertrophy. Ini- gradient. As the valve opening narrows, how- tially, myocardial contractility and ejection ever, the pressure required to eject blood—and fraction are not affected. Ultimately, however, therefore the pressure in the LV—increases, the patient becomes symptomatic when the LV creating a gradient. The normal aortic valve begins to fail. A systolic murmur may be audi- area is 2.6–3.5 cm2 (Mihaljevic et al., 2008). As ble in the aortic area. Symptoms of heart fail- the valve area narrows and the gradient ure (e.g., crackles, edema) may be present increases, blood velocity increases. Mild aortic (Gaasch, 2007a; LeBoutillier & DiSesa, 2003). stenosis is associated with a mean gradient of Once patients become symptomatic, if jet less than 25 mm Hg, valve area of greater than velocity is greater than 4 m/sec, there is a 1.5 cm2, and jet velocity of less than 3 m/sec. reported event-free survival of 21% (Bonow Severe aortic stenosis is associated with jet et al., 2006). In patients with heart failure, velocity of more than 4 m/sec, mean systolic time from onset of symptoms to death is gradient greater than 40 mm Hg, and a valve 2 years; in those with angina, time from onset area of less than 1.0 cm2 (Bonow et al., 2006; of symptoms to death is 5 years (Mihaljevic Mihaljevic et al., 2008). et al., 2008). Medical therapy may improve Classic signs and symptoms of aortic steno- symptoms of heart failure but is not effective sis include angina, syncope, sudden cardiac long-term therapy for aortic stenosis (Bonow death, and heart failure. Typically, these condi- et al., 2006; Mihaljevic et al., 2008). Table 5–1 tions appear only after a prolonged latent outlines the American College of Cardiology/

Table 5–1 Indications for Aortic Valve Replacement in Aortic Stenosis

Class I 1. Symptomatic patients with severe AS 2. Patients with severe AS undergoing CABG 3. Patients with severe AS undergoing surgery on aorta or other heart valves 4. Severe AS and LV systolic dysfunction (EF < 50%) Class IIa 1. Patients with moderate AS undergoing CABG or surgery on aorta or other heart valves Class IIb 1. Asymptomatic patients with severe AS and abnormal response to exercise (symptoms or fall in blood pressure with exercise) 2. Adults with severe asymptomatic AS if there is a high likelihood of rapid progression (age, calcification, and CAD) or if surgery might be delayed at the time of symptom onset 3. Patients undergoing CABG with mild AS when there is evidence that progression may be rapid 4. Asymptomatic patients with extremely severe AS when expected mortality is 1% or less Class III 1. Not recommended for prevention of sudden death in asymptomatic patients with AS who have none of the Class IIa/IIb indications

AS ϭ aortic stenosis; CABG ϭ coronary artery bypass grafting; CAD ϭ coronary artery disease; EF ϭ ejection fraction; LV ϭ left ventricle. Sources: Bonow et al., 2006; Mihaljevic, Sayeed, Stamou, & Paul, 2008; Vahanian et al., 2007. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 76

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American Heart Association (ACC/AHA) rec- The patient typically remains hospitalized 2 ommendations for aortic valve replacement to 4 days post-procedure (Grube et al., 2007; (AVR) in the presence of aortic stenosis. Lauck, Mackay, Galte, & Wilson, 2008). As discussed in Chapter 3, the AHA classi- Postoperatively, the ICU nurse must be vig- fies recommendations based on the degree of ilant with blood pressure monitoring. Aortic agreement and type and/or amount of available stenosis may result in left ventricular hyper- evidence. The level of recommendation is classi- trophy, increased afterload, and a noncompli- fied as Class I, II, or III. Class I indicates that evi- ant left ventricle. Following valve replacement dence and/or general agreement exists that the for aortic stenosis, the left ventricle may not intervention is effective. Class II refers to con- anticipate the reduction in afterload and conflicting evidence and/or a divergence of opinion tinue to pump hard. Avoiding hypertension is about the efficacy. Class II is further subdivided essential to avoid disrupting suture lines into Class IIa and Class IIb: Class IIa indicates (Khalpey, Ganim, & Rawn, 2008). that evidence/opinion is in favor of efficacy, In other patients, the LV hypertrophy that whereas Class IIb recommendations have less is present may result in outflow obstruction, efficacy as established by evidence/opinion. and postoperative hemodynamic instability Class III refers to evidence and/or general opin- may subsequently occur as a result of preload ion that an intervention is not effective. reduction or if the patient develops bradycar- The strength of the level of evidence is also dia or a heart block. Treatment in this case identified according to the type and/or pres- entails volume repletion, administration of ence of research. For example, Level of Evi- beta blockers, and increasing afterload. Con- dence A indicates that findings from multiple necting intraoperatively placed pacing wires randomized clinical trials or meta-analyses to an external generator may be anticipated supported the use of an intervention. Level of (Khalpey et al., 2008). Evidence B indicates that a single randomized trial or nonrandomized trials supported an ■ intervention. Level of Evidence C refers to AORTIC REGURGITATION consensus opinion of experts, case studies, or When aortic regurgitation is present, there is a standard of care (Eagle et al., 2004). reflux of blood from the aorta into the LV dur- A new option for the treatment of severe ing diastole because the valve leaflets fail to close aortic stenosis in patients who are considered completely and to remain tightly closed during to be at high risk and inoperable is percuta- diastole. Acute aortic regurgitation imposes a neous aortic valve replacement. First large volume load that a normal LV cannot performed in 2002, this investigational proce- accommodate. The sudden increase in end- dure involves insertion of a tri-leaflet biopros- diastolic volume (preload) will result in thesis made from equine pericardium increased left ventricular end-diastolic pressure (Edwards Lifesciences, Irvine, California). The (LVEDP) and decreased cardiac output. Patients device is mounted on a balloon catheter and with concomitant CAD may develop left ventric- delivered through the arterial system via a ular dilation and cardiac failure. Such patients guidewire. After predilatation of the native often present with heart failure. Symptoms of valve, the device is inserted into the midpoint aortic regurgitation depend on the acuity of of the native valve. Placement of the pros- onset, severity of regurgitation, and left ventricu- thetic valve takes place in the cardiac catheter- lar function. As LV dilation occurs over time, ization lab under fluoroscopy. A femoral patients may be asymptomatic for long periods. arterial retrograde or femoral vein antegrade/ Most patients will have an audible diastolic transseptal approach is used for placement. blowing murmur (LeBoutillier & DiSesa, 2003). 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 77

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Causes of aortic regurgitation include con- replacement is not recommended for asymp- ditions that prevent the valve cusps from tomatic patients with chronic aortic regurgi- aligning properly and conditions that dilate tation and good LV function (Mihaljevic et the aortic annular ring. Such conditions al., 2008). A ratio of chamber volume to wall include idiopathic degeneration, calcific aor- thickness and measurements of LV end- tic disease, rheumatic disease, endocarditis, systolic volume are used to guide surgery bicuspid valve, and dissection of the ascend- decisions in chronic aortic regurgitation. ing aorta. Other causes of aortic regurgitation Deteriorating LV function, as indicated by include trauma, chronic systemic hyperten- an ejection fraction (EF) less than 50–55% sion, aortitis of various etiologies, and con- and an end-diastolic dimension greater nective tissue disease such as Marfan than 70 mm or an end-systolic dimen- syndrome, Reiter disease, Ehlers-Danlos sion greater than 50 mm, would indicate syndrome, and rheumatoid arthritis (Bonow need for surgery (Mihaljevic et al., 2008). et al., 2006; Mihaljevic et al., 2008). Most Table 5–2 lists the indications for sur- commonly, aortic regurgitation is seen con- gery for aortic regurgitation. comitantly with aortic stenosis (e.g., aortic Postoperatively, because patients have disease, rheumatoid disease, or degenerative dilated ventricles from the aortic regurgita- disease) (Mihaljevic et al., 2008). tion and its associated aortic insufficiency, they may require administration of intravenous vasodilators. Agents such as milrinone Indications for Aortic Valve Replacement (Primacor®) and dobutamine (Dobutrex®) in Aortic Regurgitation may be indicated for inotropic support and to Patients with acute aortic regurgitation will promote ventricular emptying. The intra- develop hemodynamic instability and LV fail- aortic balloon pump (IABP) also may be used ure. Even small regurgitant volumes will (LeBoutillier & DiSesa, 2003); it is discussed cause a large increase in LVEDP. The result is in detail in Chapter 10. It is often challenging low cardiac output, high LV end-diastolic vol- to optimize a patient’s hemodynamic status umes (LVEDV), and increased heart rate. Any following surgery to correct aortic regurgita- changes in diastolic filling or heart rate can tion (Khalpey et al., 2008). disturb the balance and result in early LV failure (Mihaljevic et al., 2008). ■ Like chronic aortic stenosis, chronic aortic MITRAL STENOSIS regurgitation has a slow, insidious onset and Mitral stenosis, like aortic stenosis, is a condi- progression. Aortic regurgitation may be well tion where the valve leaflets do not open com- tolerated for years. Because it develops slowly, pletely, creating resistance to the forward flow the LV compensates with hypertrophy and an of blood into the LV during diastole. Mitral increase in sympathetic tone to keep the stenosis is predominantly caused by rheumatic LVEDP relatively low and maintain cardiac heart disease (Bonow et al., 2006; Fann et al., output. This change results in a characteristic 2008). Other causes, which are less common, sign of aortic regurgitation, a widened pulse include left atrial myxoma, thrombus, annular pressure (Mihaljevic et al., 2008). If left calcification, endocarditic vegetation, malig- untreated, this process will lead eventually to nant carcinoid syndrome, and metabolic disor- myofibril slippage, ventricular remodeling, ders (Bonow et al., 2006; Fann et al., 2008). and irreversible changes in LV function. Most commonly, rheumatic disease is While acute aortic regurgitation should be acquired in childhood; however, mitral steno- treated with early valve replacement, valve sis does not usually become symptomatic 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 78

78 Chapter 5 Heart Valve Surgery

Table 5–2 Indications for Aortic Valve Replacement in Aortic Regurgitation

Class I 1. Symptomatic patients with severe AR irrespective of LV function (Level B) 2. Asymptomatic patients with chronic, severe AR and LV systolic dysfunction (EF < 50%) (Level B) 3. Chronic pure, severe AR while undergoing CABG or surgery on the aorta or other heart valves (Level C) Class IIa 1. Asymptomatic patients with pure, severe AR and normal LV systolic function but with severe LV dilatation (end-diastolic dimension > 75 mm or end-systolic dimension > 55 mm) (Level B) Class IIb 1. Patients with moderate AR while undergoing surgery on the ascending aorta (Level C) 2. Patients with moderate AR while undergoing CABG (Level C) 3. Asymptomatic patients with severe AR and normal LV function at rest (EF > 50%) when end- diastolic dimension > 70 mm or end-systolic dimension = 50 mm and evidence of progressive LV dilatation, decreasing exercise tolerance, or abnormal hemodynamic response to exercise (Level C) Class III 1. Not indicated for asymptomatic patients with normal LV function at rest (EF > 50%) when dilatation is not moderate or severe based on end-systolic and end-diastolic dimensions (Level B)

AR ϭ aortic regurgitation; CABG ϭ coronary artery bypass grafting; EF ϭ ejection fraction; LV ϭ left ventricle. Sources: Bonow et al., 2006; Vahanian et al., 2007.

until decades later. The valve leaflets gradually and will likely have satisfactory LV function. become thickened and calcified. Often, the These individuals, however, have pulmonary chordae and commissures fuse (Bonow et al., hypertension, right ventricular failure, and 2006; Fann et al., 2008; Todd & Higgin, tricuspid insufficiency. Symptoms of low car- 2005). Left atrial pressure (LAP) rises as the diac output and pulmonary venous conges- disease worsens and a progressively higher tion develop as left atrial and pulmonary gradient develops across the mitral valve. Pul- pressures rise. At first, symptoms may occur monary artery systolic pressure increases as only on exertion. As the valve area narrows, the valve area narrows. Defining characteris- symptoms occur with less exertion, emotional tics of severe mitral stenosis include a gradi- stress, or atrial fibrillation (AF). Dyspnea on ent of greater than 10 mm Hg, LAP greater exertion, paroxysmal nocturnal dyspnea, than 15 mm Hg, valve area less than 1.0 cm2, orthopnea, and fatigue are the first symptoms and pulmonary artery systolic pressure to occur. Once pulmonary hypertension greater than 50 mm Hg (Bonow et al., 2006; develops, right-sided heart failure with Fann et al., 2008). edema, hepatomegaly, ascites, and tricuspid Because of the resistance to the forward regurgitation are seen. The ECG may reveal flow of blood, patients with mitral stenosis right ventricular hypertrophy (LeBoutillier & will not develop volume overload in the LV DiSesa, 2003). 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 79

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Intervention is warranted for symptomatic mal. These factors include patient age at time patients with moderate or severe mitral steno- of replacement, presence of sinus rhythm, sis, and it may be indicated for asymptomatic desire to avoid anticoagulation, contraindica- patients with new-onset AF; in contrast, inter- tions to anticoagulation, high-risk occupa- vention is not usually considered for patients tion or lifestyle, size and condition of the with mild mitral stenosis (Bonow et al., 2006; annulus, comorbidities, and desire to become Fann et al., 2008; Sorrentino, 2007). The pres- pregnant (Gudbjartsson, Absi, & Aranki, ence of pulmonary hypertension, low cardiac 2008). In general, mitral valve repair is better output, and right-sided heart failure warrants suited to treating mitral regurgitation than as further evaluation (Fann et al., 2008). Individ- a therapy for mitral stenosis (Bonow et al., uals with the latter symptoms and concomi- 2006; Gudbjartsson et al., 2008). Table 5–3 tant calculated valve area of less than 1 cm2 lists the indications for mitral valve replace- should undergo surgical correction of the ment and repair in mitral stenosis. mitral valve (LeBoutillier & DiSesa, 2003). Postoperatively, the ICU nurse should assess the patient’s level of pulmonary hyper- Mitral Commissurotomy versus Mitral tension by comparing it with the preoperative Valve Replacement level. The more significant the pulmonary hypertension, the greater the likelihood for Percutaneous mitral balloon valvotomy postoperative right ventricular (RV) failure. (PMBV), also known as commissurotomy, has Increased central venous pressure is an indi- very successfully reduced left atrial gradient, cation of possible RV decompensation increased mitral valve area, and improved (LeBoutillier & DiSesa, 2003). symptoms in patients with mitral stenosis Performing a transesophageal echocardio- (Bonow et al., 2006; Carabello, 2004; Farhat et gram postoperatively will assist in the al., 1998; Sorrentino, 2007). Percutaneous assessment of right and left ventricular intervention is recommended for patients function. Administration of dobutamine or with pliable, noncalcified valves; minimal milrinone in combination with norepineph- chordae fusion; no atrial thrombus; and no rine (Levophed®) may be indicated to mitral regurgitation (Bonow et al., 2006; enhance contractility of the right ventricle Farhat et al., 1998; Sorrentino, 2007). If the and decrease pulmonary vascular resistance patient is a high-risk surgical candidate, (right-sided afterload). Prudent fluid admin- PMBV may be a viable alternative, even if the istration in combination with inotropic valve anatomy is not ideal (Sorrentino, 2007). support should augment cardiac output in Percutaneous intervention has been shown to these patients. As an IABP does not affect right result in more favorable outcomes than closed ventricular function, its postoperative use in surgical commissurotomy (Farhat et al., 1998). patients who have undergone mitral valve Open or surgical commissurotomy is associ- repair is usually not indicated. Use of a right ated with a significantly higher reoperation rate ventricular assist device may be indicated in at 10 years than mitral valve replacement (Fann the immediate postoperative period (Khalpey et al., 2008; Wiegand, 2003). et al., 2008; LeBoutillier & DiSesa, 2003).

Mitral Valve Replacement and Repair ■ Once the decision is reached for surgical MITRAL REGURGITATION intervention, many factors must be consid- In mitral regurgitation, the valve leaflets do ered when deciding which technique is opti- not close tightly, resulting in a backward jet 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 80

80 Chapter 5 Heart Valve Surgery

Table 5–3 Indications for Mitral Valve Repair or Replacement in Mitral Stenosis

Class I Consider mitral valve repair if possible over replacement. 1. Symptomatic (NYHA functional Class III–IV) patients with moderate or severe MS when PMBV is not available or contraindicated due to left atrial thrombus or valve morphology is not favorable for PMBV (Level B). 2. Symptomatic patients with moderate to severe MS and moderate to severe mitral regurgitation should have MVR unless valve repair is possible (Level C). Class IIa 1. MVR is indicated for severe MS and severe pulmonary hypertension (PASP > 60 mm Hg) with NYHA Class I–II symptoms when patients are not candidates for PMBV or repair (Level C). Class IIb 1. Repair may be considered for asymptomatic patients with moderate or severe MS who have had recurrent embolic events while on adequate anticoagulation and who have valve anatomy favorable for repair (Level C). Class III 1. Not indicated for mild MS. 2. Closed commissurotomy should not be done in patients receiving mitral valve repair (open commissurotomy preferred) (Level C).

MS ϭ mitral stenosis; MVR ϭ mitral valve repair; NYHA ϭ New York Heart Association; PASP ϭ pulmonary artery systolic pressure; PMBV ϭ percutaneous mitral balloon valvotomy. Source: Adapted from Bonow et al., 2006.

of blood into the left atrium during ventricu- mitral regurgitation. This is often a pretermi- lar systole. Proper function of the mitral valve nal event and carries a survival time of 6 to 24 depends on a complicated interaction months (Spoor & Bolling, 2008). Alterna- between the mitral leaflets, annulus, chordae tively, mitral regurgitation may progress tendinae, papillary muscles, and the left slowly over time, with symptoms appearing atrium and ventricle (Fann et al., 2008). only when the disease is very advanced. The most common causes of mitral regur- Mitral regurgitation causes an increase in gitation include ischemic CAD, mitral valve LVEDP and a decrease in afterload. An enlarged prolapse syndrome, infective endocarditis, left atrium is likely as well. If mitral regurgita- rheumatic heart disease, mitral annular calci- tion develops suddenly, cardiac output will fication, dilated cardiomyopathy, congenital decrease. Patients may present with signs of anomalies, and collagen vascular disease severe heart failure, and the ECG may reveal (Bonow et al., 2006; Fann et al., 2008). As with findings consistent with ischemia. Patients may other valvular lesions, a sudden cause—such also have AF and associated decrease in cardiac as ruptured papillary muscle or chordae output related to the enlarged left atrium tendinae—will result in acute and severe (LeBoutillier & DiSesa, 2003). mitral regurgitation. As noted in Chapter 3, The decision to perform corrective surgery ventricular failure and dilation will result in is based on a number of factors, such as the 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 81

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degree of mitral regurgitation, severity of A number of methods are used in mitral symptoms, left ventricular function, feasibil- valve repair, including annuloplasty, open ity of valve repair, presence of AF, presence commissurotomy, and primary, anterior, and and degree of pulmonary hypertension, and posterior leaflet repair techniques. Selection patient expectations (Gaasch, 2007b). Severe of the technique is based on the type, extent, mitral regurgitation is characterized by the and location of the defect of the mitral valve. following findings: A preoperative echocardiogram provides the surgeon with these data (Savage & Bolling, ● Jet area Ն 7 mm 2005). ● Regurgitant volume Ն 60 mL/beat Because of the relationships among the ● Regurgitant fraction Ն 50% mitral valve apparatus, ventricular geometry, ● Regurgitant orifice area Ն 0.4 cm2 and ventricular function, mitral valve restora- ● Enlarged left atrium and ventricle tion can improve ventricular function. In a (Bonow et al., 2006; Gaasch, 2007b) procedure known as geometric mitral recon- Asymptomatic patients with severe mitral struction (GMR), an annuloplasty ring is used regurgitation can be safely followed for some to restore a more normal mitral valve time (Gaasch, 2007b; Rosenhek et al., 2006). anatomy; this technique has achieved favor- Care in the immediate postoperative able outcomes. Specifically, GMR has consis- period may be challenging. Upon repair of tently resulted in significant improvements in the mitral valve for mitral regurgitation, the mean EF and a reduction in NYHA sympto- left atrium will no longer be receiving regur- matology (Radovanovic et al., 2002; Spoor & gitant blood from the LV and the patient will Bolling, 2008; Spoor, Geltz, & Bolling, 2006). experience an immediate increase in afterload GMR is indicated for patients with cardiomy- (systemic vascular resistance [SVR]). Further opathy and mitral regurgitation. compounding the potential for cardiac dys- The efficacy of medical therapy for function postoperatively are pulmonary asymptomatic mitral regurgitation is the hypertension and effects of myocardial hiber- topic of ongoing debate; however, diuretics, nation (discussed in Chapter 13) that take digoxin, and arterial vasodilators may be time to be reversed. Patients, therefore, are at used to decrease ventricular size, regurgi- risk for the development of right ventricular tant orifice size, and regurgitant volume failure (LeBoutillier & DiSesa, 2003). (Bonow et al., 2006; Fann et al., 2008). The Patients may require administration of presence of left ventricular enlargement, LV inotropes (e.g., milrinone, dobutamine) or dysfunction, pulmonary hypertension, or IABP therapy to reduce afterload. Combination recurrent AF indicates the need for surgery therapy of milrinone and epinephrine may also (Rosenhek et al., 2006). Table 5–4 outlines be used to accomplish afterload reduction, pro- the indications for surgical correction of vide an inotropic effect, and decrease pul- mitral regurgitation. monary hypertension (Khalpey et al., 2008). Increased mortality after mitral valve sur- Patients should be monitored for right ven- gery has been found among perimenopausal tricular failure. If they develop decreased women. The higher mortality rate is thought blood pressure, cardiac output, pulmonary to be associated with a state of estrogen with- artery pressures, and pulmonary artery occlu- drawal that may trigger inflammatory sive pressure, or elevated central venous pres- responses; these responses may, in turn, sure, right ventricular failure should be potentiate ischemia-reperfusion injury (Song suspected (LeBoutillier & DiSesa, 2003). et al., 2008). 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 82

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Table 5–4 Indications for Surgery for Mitral Regurgitation

Class I 1. Symptomatic patients with severe MR (Level B) 2. Chronic, severe MR and NYHA functional Class II–IV symptoms in the absence of severe LV dysfunction (EF < 30% and/or LV end-systolic dimension > 55 mm) (Level B) 3. Asymptomatic patients with chronic, severe MR and mild to moderate LV dysfunction (EF = 30–60% and/or LV end-systolic dimension ≥ 40 mm) (Level B) 4. MV repair is preferred over MVR for the majority of patients (Level C). Class IIa 1. MV repair for asymptomatic patients with chronic, severe MR and preserved LV function, and when the likelihood of successful repair without residual MR is > 90% (Level B) 2. Asymptomatic patients with chronic, severe MR, preserved LV function, and new-onset atrial fibrillation (Level C) 3. Asymptomatic patients with chronic, severe MR, preserved LV function, and pulmonary hypertension (PASP > 50 mm Hg at rest or > 60 mm Hg with exercise) (Level C) 4. Patients with chronic, severe MR due to primary abnormality of the mitral valve apparatus, NYHA functional Class III–IV symptoms, severe LV dysfunction, and in whom mitral valve repair is highly likely (Level C) Class IIb 1. Patients with chronic, severe MR due to severe LV dysfunction with NYHA functional Class III–IV symptoms despite optimal medical therapy for heart failure (Level C) Class III 1. Not indicated for patients with asymptomatic MR with preserved LV function and doubtful feasibility of repair 2. Not indicated for patients with mild or moderate MR (Level C)

EF ϭ ejection fraction; LV ϭ left ventricular; MR ϭ mitral regurgitation; MVR ϭ mitral valve replacement; NYHA ϭ New York Heart Association; PASP ϭ pulmonary artery systolic pressure. Source: Adapted from Bonow et al., 2006.

Mitral Valve Repair versus Mitral Valve apy. Biologic valves do not require anticoagu- Replacement lation therapy, but they are less durable due Prosthetic valves are categorized as mechani- to their tendency toward early calcification, cal or biologic (tissue) valves. Mechanical tissue degeneration, and stiffening of the valves are manufactured from man-made leaflets. materials such as metal alloys, pyrolite car- Advantages and disadvantages of mitral bon, and Dacron. Biologic valves are con- valve replacement with either a prosthetic or structed from bovine, porcine, and human mechanical valve must be carefully weighed cardiac tissue, although they may contain by the patient. Indications for either type of some man-made materials. Mechanical pros- valve vary by patient characteristics and sur- thetic valves are more durable and last longer geon preference (Gudbjartsson et al., 2008). than biologic valves, but they carry an Because of the disadvantages associated increased risk of venous thrombotic events, with prosthetic valves, surgeons have been necessitating long-term anticoagulation ther- interested in valve repair for some time. The 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 83

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decision to repair a valve as opposed to replac- increased right ventricular systolic pressure ing it depends on the degree of regurgitation, (especially if greater than 55 mm Hg), mitral pathophysiology of the regurgitation, LV or aortic valve disease (that results in elevated function, and ability of the surgeon (Chen & LAP and LVEDP), left-sided heart failure, dilated Cohn, 2008). Good evidence suggests that cardiomyopathy, tricuspid annular dilatation, mitral valve repair, if feasible, results in or pulmonary embolism (Bonow et al., decreased operative mortality, greater increase 2006; Phillips, 2005; Shah & Raney, 2008). Occa- in LV ejection fraction, improved survival, sionally, wires inserted through the valve such as enhanced preservation of LV function, dura- an automatic implantable cardioverter defibrilla- bility of repair, and decreased incidence of tor (AICD) or pacemaker may cause tricuspid venous thrombotic events (Chen & Cohn, regurgitation (Bonow et al., 2006; Shemin, 2008; Flameng, Herijgers, & Bogaerts, 2003; 2008). Following the initial classification, tricus- Gaasch, 2007b). It is postulated that the pid valve disease is addressed according to the improved outcomes are attributable to reten- pathology—either tricuspid stenosis or tricuspid tion of the mitral valve apparatus (leaflets, regurgitation (Phillips, 2005). annulus, chordae, and papillary muscles), Symptoms of tricuspid regurgitation which helps to preserve LV function (Chen & include fatigue, weakness, signs of right-sided Cohn, 2008; Flameng et al., 2003). The benefit heart failure, abnormal venous pulsations, may be less in older patients or patients and often AF. Tricuspid stenosis most often undergoing concomitant CABG (Gaasch, presents with some degree of tricuspid regur- 2007b). Valve repair is currently the treatment gitation as well. It is characterized by signs of of choice for mitral regurgitation (Chen & peripheral venous distention, abnormal Cohn, 2008). venous pulsations, fatigue, malaise, and signs of low cardiac output (Shemin, 2008). ■ TRICUSPID VALVE DISEASE The tricuspid valve has an annular ring and Tricuspid Stenosis three leaflets connected via chordae tendinae Patients with tricuspid stenosis have an to papillary muscles that are integrated with obstruction to blood flow from the right the right ventricle. It is located between the atrium to the right ventricle. The most com- right atrium and ventricle, near the atrioven- mon etiology for tricuspid stenosis is rheu- tricular (AV) node, right coronary artery, and matic heart disease. Other conditions coronary sinus. Its function is to maintain associated with tricuspid stenosis include car- forward flow of blood. cinoid syndrome, endocarditis, and intracardiac tumors. The clinical presentation of tricuspid stenosis is logically consistent with Tricuspid Regurgitation right-sided heart failure—that is, it consists of The functional defects that are seen in tricus- decreased cardiac output, fatigue, anasarca, pid disease are classified as either primary or hepatomegaly, and ascites (Bashore, 2006; secondary. Primary valve disease is caused by Phillips, 2005). conditions that affect valve anatomy— for example, congenital abnormalities, rheu- Surgery for Tricuspid Valve Disease matic disease, infective endocarditis, toxicities, tumor, and blunt trauma. Secondary Surgery for Tricuspid Regurgitation tricuspid disease can result from right ventric- The most common cause of tricuspid regur- ular pathology, pulmonary hypertension, gitation is mitral valve disease; therefore, 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 84

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indications for tricuspid surgery will often be Advances in echocardiography have improved influenced by the extent of mitral valve dis- the effectiveness of preoperative assessment, ease (Shemin, 2008). The clinical picture and intraoperative evaluation of valve function, severity of disease play a major role in deter- and outcomes. Nevertheless, the timing and mining the appropriate management. The pri- choice of techniques for tricuspid surgery mary indication for tricuspid valve repair is remain controversial and largely depend on severe tricuspid regurgitation in patients the surgeon’s experience and judgment requiring surgery for mitral valve disease. Data (Bonow et al., 2006; Shemin, 2008). favor tricuspid replacement or annuloplasty for severe, symptomatic primary tricuspid Surgery for Tricuspid Stenosis regurgitation. Tricuspid replacement is also Surgical procedures for tricuspid stenosis indicated for severe tricuspid regurgitation include closed commissurotomy, open com- when the valvular disease is not amenable to missurotomy, and open valvuloplasty. A com- repair. Less well-established evidence suggests missurotomy entails opening the commissures that tricuspid annuloplasty may be performed (the contact area for the valve leaflets) that have in patients with less than severe tricuspid developed scarring and no longer open to allow regurgitation, when there is pulmonary hyper- blood to flow. Valvuloplasty entails insertion of tension or tricuspid annular dilatation, and a balloon to stretch or enlarge the valve open- when patients are undergoing mitral valve sur- ing; this procedure is used infrequently due to gery. Tricuspid valve replacement or annulo- the concomitant presence of tricuspid regurgi- plasty is not indicated for asymptomatic tation (Bashore, 2006) and inconsistent evi- patients with pulmonary artery (PA) pressures dence supporting its efficacy (Phillips, 2005). less than 60 mm Hg and a normal mitral valve. All of tricuspid stenosis procedures are associ- Surgery is also not indicated for mild primary ated with poor long-term outcomes, as progres- tricuspid regurgitation (Bonow et al., 2006). sive tricuspid regurgitation often develops. Other types of tricuspid repair, including Ultimately, valve replacement may be indicated many annuloplasty techniques to repair a for sustained symptom relief (Phillips, 2005). dilated annulus, have been more successful. In Tricuspid balloon valvotomy for tricuspid such procedures, the tissue that supports the stenosis is no longer recommended because a tricuspid leaflets is sutured so the leaflets significant degree of tricuspid regurgitation adjoin correctly. The net effect is a smaller usually develops following this procedure as opening, thereby allowing the valve to close well (Bonow et al., 2006). completely. Research indicates that tricuspid dilatation may be a better predictor of the need ■ for corrective surgery than the degree of tricus- INFECTIVE VALVE ENDOCARDITIS pid regurgitation (Matsunaga & Duran, 2005). Infective endocarditis is a microbial infection Repair of mitral valve disease may reduce of a blood-contacting structure in the heart the extent of tricuspid disease. As many as 20% or great vessels. It produces fever, heart mur- of patients having surgery for mitral valve dis- mur, signs of heart failure, and bacteremia ease will also receive a tricuspid annuloplasty, and can produce rapid hemodynamic deterio- but only 2% will require a valve replacement ration (Bonow et al., 2006). The characteristic (Shemin, 2008). The surgeon typically consid- sign is vegetation, although ulceration, ers the size and function of the right ventricle, abscesses, and destruction of heart structures degree of pulmonary hypertension, size of the may occur as well. Infective endocarditis can right atrium, and clinical picture when mak- be difficult to diagnose because positive cul- ing decisions about which procedure to select. tures may not be obtained. The Duke Criteria 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 85

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are used to diagnose infective endocarditis in patients who underwent mitral valve repair these cases (Stamou, Petterson, & Gillinov, for infective endocarditis between 1989 and 2008). Medical therapy is usually the first-line 1994. These researchers found an 80% 10-year treatment. survival rate, 9% reoperation rate, 95% rate of Indications for surgery differ; however, NYHA Class I or II function, and very low mortality has been reduced since antimicro- rates of minor mitral regurgitation. Other bial therapy has been supplemented with ear- surgeons have reported good outcomes with lier surgical intervention (Schick, Gaasch, & mitral valve repair for infective endocarditis Sexton, 2007). When surgery is indicated, when tissue is acceptable for repair (Ruttman valve repair has been successful in mitral valve et al., 2005). There is agreement that surgery disease, just as it has in other valve disease. is indicated for those patients with acute Early surgery is more likely to result in a suc- infective valve endocarditis and life-threaten- cessful repair and reduces the risk of infection ing heart failure or cardiogenic shock (Bonow of the prosthesis (Bonow et al., 2006). et al., 2006; Schick et al., 2007; Yee, 2005). Zegdi et al. (2005) reported good long-term Tables 5–5 and 5–6 outline the indications for results from valve repair in a review of surgical treatment of native and prosthetic valve endocarditis, respectively. In general, surgery for native valve infective endocarditis Table 5–5 Indications for Surgery in Native Valve Infective Endocarditis Table 5–6 Indications for Surgery in Class I Prosthetic Valve Infective Endocarditis 1. Acute IE with valve dysfunction resulting in heart failure (Level B) Class I 2. Valve destruction resulting in elevated LVEDP or LAP even if asymptomatic 1. Presence of heart failure (Level B) 3. IE caused by fungal or drug-resistant 2. Dehiscence on fluoroscopy or echocar- organism diography (Level B) 4. Presence of heart block, annular abscess, 3. Presence of increasing obstruction or aortic abscess, destructive penetrating regurgitation (Level C) lesions such as a fistula, or local spread 4. Presence of complications such as of infection (Level B) abscesses (Level C) 5. Staphylococcus aureus as the infectious 5. IE occurring less than 12 months after organism valve replacement Class IIa Class IIa 1. Recurrent emboli or persistent vegeta- 1. Persistent bacteremia or recurrent tions despite appropriate antimicrobial emboli despite appropriate antimicrobial therapy (Level C) therapy (Level C) 2. Relapsing infection (Level C) Class IIb Class III 1. Mobile vegetations larger than 10 mm on the aortic or mitral valve 1. Not indicated in uncomplicated IE at first infection with a sensitive organism IE ϭ infective endocarditis; LAP ϭ left atrial pressure; (Level C) LVEDP ϭ left ventricular end-diastolic pressure. ϭ Sources: Bonow et al., 2006; Horstkotte et al., 2004; IE infective endocarditis. Schick, Gaasch, & Sexton, 2007; Stamou, Petterson, & Sources: Bonow et al., 2006; Horstkotte et al., 2004; Gillinov, 2008. Karchmer, 2007. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 86

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carries a better prognosis than surgery for Table 5–7 Postoperative Goals prosthetic valve infective endocarditis (Sta- and Nursing Interventions mou et al., 2008). 1. Achieve and maintain normal body tem- ■ NURSING MANAGEMENT perature. Monitor and optimize vital signs and hemodynamic status (stroke OF THE PATIENT FOLLOWING volume index, cardiac index, central VALVE SURGERY venous pressure, pulmonary artery occlu- The immediate postoperative period is the sive pressure, systemic vascular resistance, SvO [if available]). most critical for the patient who has under- 2 2. Monitor for presence of dysrhythmias. gone valve surgery. A patent airway must be 3. Monitor drainage from the chest tube. maintained. The patient’s vital signs, hemo- 4. Reposition patient every 2 hours and dynamic status, and level of consciousness increase activity level when stable. should be assessed frequently. In addition, 5. Monitor the patient’s respiratory status, the possibility that the patient may need IV and assure adequate deep breathing and fluids, blood transfusion, titration of vasoac- coughing to prevent atelectasis. tive agents, pain management, and chest tube 6. Monitor for and report any neurologic changes from baseline. maintenance requires vigilance on the part of 7. Maintain adequate renal perfusion. Doc- the nursing staff. Table 5-7 identifies com- ument daily weight and fluid intake and mon nursing goals and interventions. Care of output. the immediate postoperative cardiac surgery 8. Monitor serum electrolytes. patient and monitoring for postoperative 9. Maintain adequate fluid volume; avoid complications are discussed in detail in Chap- preload reduction. ters 8 and 13, respectively. 10. Maintain optimal pain management (less than 4 or according to reasonable patient expectations). ■ COMPLICATIONS OF HEART VALVE SURGERY ● Heart failure (Bossone et al., 2007) While complications of heart valve surgery are ● Neurological complications, stroke, or rare, the ICU nurse should be aware of the transient ischemic attack (Bossone et al., possibility of their development and imple- 2007; Filsoufi, Rahmanian, Castillo, Bron- ment measures to try to prevent their devel- ster, & Adams, 2008; Kolh et al., 2007; opment. Complications of heart valve surgery Mihaljevic et al., 2004; Ngaage et al., 2008) reported in the literature include the follow- ● Respiratory insufficiency (Kolh et al., ing conditions: 2007; Ngaage et al., 2008; Tabata et al., ● Venous thrombotic events (Shuhaiber & 2008) Anderson, 2007) ● AV block (Kolh et al., 2007; Mihaljevic ● Atrial dysrhythmias (Bossone et al., 2007; et al., 2004) Kolh, Kerzmann, Honore, Comte, & ● Myocardial infarction (Kolh et al., 2007; Limet, 2007; Ngaage, Cowen, Griffin, Ngaage et al., 2008) Guvendik, & Cale, 2008) ● Sternal wound infection (Mihaljevic ● Renal insufficiency (Bossone et al., 2007; et al., 2004; Rahmanian et al., 2007; Kolh et al., 2007; Ngaage et al., 2008) Tabata et al., 2008) 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 87

Summary 87

● Bleeding—requiring reexploration in most based on culture and sensitivity reports cases (David, Armstrong, Maganti, & (Tang, Maganti, Weisel, & Borger, 2004). As Ihlberg, 2008; Mihaljevic et al., 2004; with all patients, meticulous hand hygiene is Ngaage et al., 2008; Rahmanian et al., essential to help prevent development of post- 2007; Tabata et al., 2008) operative infection. ● Circulatory failure (Haddad et al., 2007) The potential for postoperative dysrhyth- ● Low cardiac output state (Ngaage et al., mias (most notably, atrial fibrillation) has 2008) been reported. The ICU nurse plays a pivotal ● Gastrointestinal complications (Ngaage role in promptly recognizing dysrhythmia et al., 2008) development, determining the clinical significance and hemodynamic response to them, Two case reports of uncommon complications— and implementing treatment measures. Man- left ventricular–right atrial communication agement of postoperative dysrhythmias is dis- (Frigg, Cassina, Siclari, & Mauri, 2008) and an cussed in detail in Chapter 15. immobilized prosthetic mitral valve (Muruge- Development of venous thrombotic events san, Banakal, & Muralidhar, 2008)—following is likely following valvular surgery, particu- valve surgery have also been described. larly if the patient received a mechanical valve. Ways to prevent complications and strate- Preventive measures include use of sequential gies to improve mortality continue to be compression devices and administration of an examined by researchers. For example, statin anticoagulant in the immediate postoperative therapy has been found to improve morbidity period. When feasible, early ambulation and 30-day mortality in valvular surgery should be initiated (Thompson et al., 2008). patients (Fedoruk, Wang, Conaway, Kron, & Johnston, 2008). ■ SUMMARY The possibility of either a deep sternal Selection of a mechanical or biological pros- wound infection or development of an thetic valve has lifelong implications. These infected valve has been reported as well. patients may require lifestyle modification and Because of the significant impact on morbid- medication therapy for the rest of their lives. ity and mortality following cardiac surgery, Advances in technology in the area of heart prophylactic antibiotic administration both valve surgery offer more options, facilitate less preoperatively and for as long as 48 hours invasive techniques, and potentially may postoperatively is part of the standard of care. improve outcomes. Vigilant postoperative nurs- If an infection is suspected, cultures should ing care is critical to help ensure a good out- be obtained and empiric antibiotic therapy come for the patient who undergoes valve started. Modifications are subsequently made surgery.

CASE STUDY

A patient who had childhood rheumatic heart disease is diagnosed with mitral valve prolapse (MVP). The patient has a history of type II diabetes and increased body mass index. She experiences pain during periods of emotional stress and presents with mitral regurgitation (MR) and a murmur that gets more intense during systole. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 88

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Critical Thinking Questions 1. Which medications should this patient take to manage the mitral valve prolapse? 2. Which factors should contribute to the decision to have surgery for repair of the valve defect? Answers to Critical Thinking Questions 1. Most people with mitral valve prolapse who experience symptoms will be prescribed medication to treat chest pain, heart rhythm abnormalities, and/or transient ischemic attack. Medications may include beta blockers for heart rhythm, aspirin, or warfarin (Coumadin®). 2. The severity of the symptoms would significantly factor into the decision as well as the need to perform early repair to prevent valve replacement.

■ SELF-ASSESSMENT QUESTIONS c. Elevated pulmonary artery pressure d. Decreased left atrial pressure 1. A patient with newly diagnosed aortic regurgitation will have which of the 6. The nurse caring for a patient immedi- following? ately following surgical repair of mitral a. Increased pulmonary artery occlusive stenosis should observe for which of the pressure following? b. Decreased sympathetic tone a. Elevated central venous pressure c. Decreased cardiac output b. Pulmonary hypertension d. Widening pulse pressure c. Decreased pulmonary vascular resistance 2. Which type of prosthetic valve requires d. Increased cardiac output long-term anticoagulation therapy? a. Mechanical 7. The nurse caring for a patient immedi- b. Biologic ately following surgical repair of mitral c. Bovine regurgitation should observe for which d. Porcine of the following? a. Increased left atrial pressure 3. Patients who are postoperative aortic b. Increased systemic vascular resistance regurgitation repair may require admin- c. Decreased pulmonary artery systolic istration of which of the following? pressure a. Dopamine (Intropin®) d. Decreased ejection fraction b. Neosynephrine (Phenylephrine®) c. Milrinone (Primacor®) 8. An open surgical procedure that repairs d. Judicious intravenous fluids the valve by suturing the torn leaflets, chordae tendinae, or papillary muscles is 4. The primary symptom of mitral stenosis is called a. chest pain. a. angioplasty. b. hypertension. b. valve replacement. c. exertional dyspnea. c. valvuloplasty. d. syncope. d. coronary artery bypass grafting 5. Patients with mitral stenosis will likely (CABG). present with which of the following signs? a. Decreased ejection fraction b. Elevated left ventricular end-diastolic pressure 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 89

Self-Assessment Questions 89

9. Your patient requires mitral valve 10. Which of the following acute valve dis- replacement and is contemplating which orders is most likely to constitute a med- type of valve to select. Which of the fol- ical emergency? lowing statements would help the a. Mitral valve prolapse patient in the decision-making process? b. Aortic valve stenosis a. “If you receive a mechanical valve, it c. Aortic valve regurgitation will not last as long as a biologic d. Mitral valve stenosis valve.” b. “If you receive a mechanical valve, Answers to Self-Assessment Questions you will need to take a blood thinner 1. d 6. a over the long term.” 2. a 7. b c. “You should probably also consider 3. c 8. c valve repair, as many surgeons have been interested in that procedure.” 4. c 9. b d. “Both types of valves are equally 5. c 10. c good, because the papillary muscles and annulus are retained when either valve is used.”

Clinical Inquiry Box

Question: Does valve replacement in the elderly increase quality of life? Reference: Filsoufi, F., Rahmanian, P. B., Castillo, J. G., Chikwe, J., Silvay, G., & Adams, D. H. (2008). Excellent early and late outcomes of aortic valve replacement in people aged 80 and older. Journal of the American Geriatrics Society, 56(2), 255–261. Objective: To investigate early and late outcomes of aortic valve replacement (AVR) in a cohort of patients aged 80 and older. Method: This retrospective study of consecutive patients undergoing AVR was performed. The study included 1308 patients undergoing AVR; 231 subjects were aged 80 years or older, and 1077 subjects were younger than 80 years of age. Patient characteristics, hospital mortality, morbidity, length of stay, and long-term survival were analyzed. Results: Subjects aged 80 and older were more likely to be female, had a lower body mass index, and presented significantly with more comorbidities, such as heart failure, renal failure, and extensive aortic calcification. Hospital mortality was slightly higher in subjects age 80 and older (5.2%) as compared with 4.5% in those younger than aged 80. Respiratory failure occurred more frequently in those aged 80 and older. Age of 80 and older was not a predictor of hospital mortality. The median length of stay was significantly higher in those aged 80 and older than in those younger than 80 (10 days versus 7 days). Five-year survival was essentially the same for those aged 80 and older within the general U.S. population. Conclusion: AVR will result in good outcomes in patients aged 80 and older, with minimal increase in postoperative mortality and acceptable postoperative morbidity. Respiratory failure is the main postoperative complication in patients aged 80 and older. Implications for nurses are that cardiac surgery is an appropriate intervention for individuals older than age 80. Therefore, the need to provide care to this population will continue to increase over the next 15 years as the U.S. population ages. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 90

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■ REFERENCES Farhat, M. B., Ayari, M., Maatouk, F., Betbout, F., American Heart Association. (2008). Marfan syn- Gamra, H., & Jarrar, M., et al. (1998). Percuta- drome. Retrieved July 30, 2008, from www neous balloon versus surgical closed and open .americanheart.org/presenter.jhtml mitral commissurotomy: Seven-year follow-up ?identifier=4672 results of a randomized trial. Circulation, 97(3), 245–250. Bashore, T. M. (2006). Percutaneous balloon valvuloplasty. In M. J. Kern (Ed.), SCAI interventional Fedoruk, L. M., Wang, H., Conaway, M. R., Kron, cardiology review book (pp. 235–248). Philadel- I. L., & Johnston, K. C. (2008). Statin therapy phia: Lippincott Williams & Wilkins. improves outcomes after valvular heart surgery. Annals of Thoracic Surgery, 85(5), 1521–1526. Bonow, R. O., Carabello, B. A., Chatterjee, K., de Leon, A. C., Faxon, D. P., Freed, M. D., et al. Filsoufi, F., Rahmanian, P. B., Castillo, J. G., Bron- (2006). ACC/AHA 2006 guidelines for the ster, D., & Adams, D. H. (2008). Incidence, management of patients with valvular heart imaging analysis, and early and late outcomes disease: A report of the American College of of stroke after cardiac valve operation. Ameri- Cardiology/American Heart Association Task can Journal of Cardiology, 101(10), 1472–1478. Force on Practice Guidelines (Writing Com- Flameng, W., Herijgers, P., & Bogaerts, K. (2003). mittee to Revise the 1998 Guidelines for the Recurrence of mitral valve regurgitation after Management of Patients with Valvular Heart mitral valve repair in degenerative valve dis- Disease). Circulation, 114(5), e84–e231. ease. Circulation, 107(12), 1609–1613. Bossone, E., Di Benedetto, G., Frigiola, A., Carbone, Frigg, C., Cassina, T., Siclari, F., & Mauri, R. (2008). G. L., Panza, A., Cirri, S., et al. (2007). Valve Unusual complication after aortic valve surgery in octogenarians: In-hospital and replacement. Interactive Cardiovascular & Tho- long-term outcomes. Canadian Journal of Cardi- racic Surgery, 7(1), 149–150. ology, 23(3), 223–227. Gaasch, W. H. (2007a). Indications for and types of Carabello, B. A. (2004). Is it ever too late to operate corrective surgery in severe chronic mitral on the patient with valvular heart disease? regurgitation. Retrieved October 19, 2007, Journal of the American College of Cardiology, from www.uptodate.com 44(2), 376–383. Gaasch, W. H. (2007b). Indications for valve Chen, F. Y., & Cohn, L. H. (2008). Mitral valve replacement in aortic stenosis. Retrieved Octo- repair. In L. H. Cohn (Ed.), Cardiac surgery in the ber 19, 2007, from www.uptodate.com adult (3rd ed., pp. 1013–1029). New York: Grube, E., Schuler, G., Buellesfeld, L., Gerckens,U., McGraw-Hill Medical. Linke, A., Wenaweser, P., et al. (2007). Percuta- David, T. E., Armstrong, S., Maganti, M., & Ihlberg, neous aortic valve replacement for severe aor- L. (2008). Clinical outcomes of combined aortic stenosis in high-risk patients using the tic root replacement with mitral valve surgery. second- and current third-generation self- Journal of Thoracic & Cardiovascular Surgery, expanding core valve prosthesis: Device suc- 136(1), 82–87. cess and 30-day clinical outcome. Journal of the Eagle, K. A., Guyton, R. A., Davidoff, R., Edwards, American College of Cardiology, 50(1), 69–76. F. H., Ewy, G. A., Gardner, T. J., et al. (2004). Gudbjartsson, T., Absi, T., & Aranki, S. (2008). ACC/AHA 2004 guideline update for coronary Mitral valve replacement. In L. H. Cohn (Ed.), artery bypass graft surgery: A report of the Cardiac surgery in the adult (3rd ed., pp. American College of Cardiology/American 1032–1068). New York: McGraw-Hill Medical. Heart Association Task Force on Practice Haddad, F., Denault, A. Y., Couture, P., Cartier, R., Guidelines (Committee to Revise the 1999 Pellerin, M., Levesque, S., et al. (2007). Right Guidelines for Coronary Artery Bypass Graft ventricular myocardial performance index pre- Surgery). Circulation, 110(9), e340–e437. dicts perioperative mortality or circulatory Fann, J. I., Ingels, N. B., & Miller, D. C. (2008). failure in high-risk valvular surgery. Journal of Pathophysiology of mitral valve disease. In the American Society of Echocardiography, 20(9), L. H. Cohn (Ed.), Cardiac surgery in the adult 1065–1072. (3rd ed., pp. 973–1012). New York: McGraw- Hill Medical. 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 91

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Hill, K. M. (2007). Surgical repair of cardiac valves. adult (3rd ed., pp. 826–840). New York: Critical Care Nursing Clinics of North America, McGraw-Hill Medical. 19(4), 353–360. Murugesan, C., Banakal, S., & Muralidhar, K. Homma, S., & Grahame-Clarke, C. (2003). Toward (2008). An unusual complication following reducing embolic complications from endo- mitral valve surgery and use of intra-operative carditis. Journal of the American College of Cardiol- transoesophageal echocardiography. Annals of ogy, 42(5), 781–783. Cardiac Anaesthesia, 11(2), 127–128. Horstkotte, D., Follath, F., Gutschik, E., Lengyel, Ngaage, D. L., Cowen, M. E., Griffin, S., Guvendik, M., Oto, A., Pavie, A., et al. (2004). Guidelines L., & Cale, A. R. (2008). Early neurological on prevention, diagnosis and treatment of complications after coronary artery bypass infective endocarditis: Executive summary. grafting and valve surgery in octogenarians. European Heart Journal, 25(3), 267–276. European Journal of Cardio-Thoracic Surgery, Karchmer, A. W. (2007). Surgical treatment of 33(4), 653–659. prosthetic valve endocarditis. Retrieved Octo- Phillips, B. J. (2005). Tricuspid valve disease: A few ber 19, 2007, from www.uptodate.com points regarding right-sided heart failure. Khalpey, Z. I., Ganim, R. B., & Rawn, J. D. (2008). Internet Journal of Thoracic and Cardiovascular Postoperative care of cardiac surgery patients. Surgery, 7(1). http://www.ispub.com/ostia/ In L. H. Cohn (Ed.), Cardiac surgery in the adult index.php?xmlFilePath=journals/ijtcvs/vol7n1/ (pp. 465–486). New York: McGraw-Hill. tvd.xml Kolh, P., Kerzmann, A., Honore, C., Comte, L., & Radovanovic, N., Mihajlovic, B., Selestiansky, J., Limet, R. (2007). Aortic valve surgery in octo- Torbica, V., Mijatov, M., & Popov, M., et al. genarians: Predictive factors for operative and (2002). Reductive annuloplasty of double ori- long-term results. European Journal of Cardio- fices in patients with primary dilated car- Thoracic Surgery, 31(4), 600–606. diomyopathy. Annals of Thoracic Surgery, 73(3), Lauck, S., Mackay, M., Galte, C., & Wilson, M. 751–755. (2008). A new option for treatment of aortic Rahmanian, P. B., Adams, D. H., Castillo, J. G., stenosis: Percutaneous aortic valve replace- Chikwe, J., Bodian, C. A., & Filsoufi, F. (2007). ment. Critical Care Nurse, 28(3), 40–51. Impact of body mass index on early outcome LeBoutillier, M., & DiSesa, V. J. (2003). Valvular and late survival in patients undergoing coro- and ischemic heart disease. In L. H. Cohn & nary artery bypass grafting or valve surgery or L. H. Edmunds (Eds.), Cardiac surgery in the adult both. American Journal of Cardiology, 100(11), (pp. 1057–1074). New York: McGraw-Hill. 1702–1708. Matsumura, T., Ohtaki, E., Misu, K., Tohbaru, T., Rosenhek, R., Rader, F., Klaar, U., Gabriel, H., Asano, R., Nagayama, M., et al. (2002). Etiol- Krejc, M., Kalbeck, D., et al. (2006). Outcome ogy of aortic valve disease and recent changes of watchful waiting in asymptomatic severe in Japan: A study of 600 valve replacement mitral regurgitation. Circulation, 113(18), cases. International Journal of Cardiology, 2238–2244. 86(2–3), 217–223. Ruttmann, E., Legit, C., Poelzl, G., Mueller, S., Matsunaga, A., & Duran, C. M. (2005). Progression Chevtchik, O., Cottogni, M., et al. (2005). of tricuspid regurgitation after repaired func- Mitral valve repair provides improved out- tional ischemic mitral regurgitation. Circula- come over replacement in active infective tion, 112(9 suppl), I-453–I-457. endocarditis. Journal of Thoracic and Cardiovas- cular Surgery, 130(3), 765–771. Mihaljevic, T., Cohn, L. H., Unic, D., Aranki, S. F., Cooper, G. S., & Byrne, J. G. (2004). One thou- Savage, E. B., & Bolling, S. F. (2005). Overview of sand minimally invasive valve operations: mitral valve repair. In E. B. Savage & S. F. Early and late results. Annals of Surgery, 240(3), Bolling (Eds.), Atlas of mitral valve repair 529–534. (pp. 21–24). Philadelphia: Lippincott Williams & Wilkins. Mihaljevic, T., Sayeed, M. R., Stamou, S. C., & Paul, C. (2008). Pathophysiology of aortic valve disease. In L. H. Cohn (Ed.), Cardiac surgery in the 57625_CH05_073_092.pdf 4/10/09 11:08 AM Page 92

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Schick, E. C., Gaasch, W. H., & Sexton, D. J. (2007). Tang, G. H., Maganti, M., Weisel, R. D., & Borger, Surgery in native valve endocarditis. Retrieved M. A. (2004). Prevention and management of October 19, 2007, from www.uptodate.com deep sternal wound infection. Seminars in Tho- Shah, P. M., & Raney, A. A. (2008). Tricuspid valve racic and Cardiovascular Surgery, 16(1), 62–69. disease. Current Problems in Cardiology, 33(2), Thompson, J. L., Sundt, T. M., Sarano, M. E., 47–84. Santrach, P. J., & Hartzell, H. V. (2008). In- Shemin, R. J. (2008). Tricuspid valve disease. In patient International Normalized Ratio self- L. H. Cohn (Ed.), Cardiac surgery in the adult testing instruction after mechanical heart (3rd ed., pp. 1111–1127). New York: McGraw- valve implementation. Annals of Thoracic Hill Medical. Surgery, 85(6), 2046–2050. Shuhaiber, J., & Anderson, R. J. (2007). Meta-analy- Todd, B. A., & Higgin, K. (2005). Recognizing aor- sis of clinical outcomes following surgical tic and mitral valve disease. Nursing, 35(6), mitral valve repair or replacement. European 58–63. Journal of Cardio-Thoracic Surgery, 31(2), 267–275. Vahanian, A., Baumgartner, H., Bax, J., Butchart, E., Song, H. K., Grab, J. D., O’Brien, S. M., Welke, K. F., Dion, R., Filippatos, G., et al. (2007). Guide- Edwards, F., & Ungerleider, R. M. (2008). Gen- lines on the management of valvular heart dis- der differences in mortality after mitral valve ease: The Task Force on the Management of operation: Evidence for higher mortality in Valvular Heart Disease of the European Soci- perimenopausal women. Annals of Thoracic ety of Cardiology. European Heart Journal, Surgery, 85(6), 2040–2045. 28(2), 230–268. Sorrentino, M. J. (2007). Surgical management of Wiegand, D. L. (2003). Advances in cardiac surgery: mitral stenosis. Retrieved October 19, 2007, Valve repair. Critical Care Nurse, 23(2), 72–91. from www.uptodate.com Yee, C. (2005). The infected heart. Nursing Manage- Spoor, M. T., & Bolling, S. F. (2008). Nontrans- ment, 36(2), 25–30. plant surgical options for heart failure. In Zegdi, R., Debiéche, M., Latrémouille, C., Lebied, L. H. Cohn (Ed.), Cardiac surgery in the adult D., Chardigny, C., Grinda, J., et al. (2005). (3rd ed., pp. 1639–1655). New York: McGraw- Long-term results of mitral valve repair in Hill Medical. active endocarditis. Circulation, 111(19), Spoor, M. T., Geltz, A., & Bolling, S. F. (2006). Flex- 2532–2536. ible versus nonflexible mitral valve rings for congestive heart failure: Differential durability ■ of repair. Circulation, 114 (I suppl), I67–II71. WEB RESOURCES Stamou, S. C., Petterson, G., & Gillinov, A. M. American Association of Cardiovascular and Pul- (2008). Surgical treatment of mitral valve monary Rehabilitation: www.aacvpr.org endocarditis. In L. H. Cohn (Ed.), Cardiac sur- American College of Cardiology: www.acc.org gery in the adult (3rd ed., pp. 1069–1078). New American Heart Association: www.americanheart.org York: McGraw-Hill Medical. Mended Hearts: www.mendedhearts.org Tabata, M., Umakanthan, R., Cohn, L. H., Bolman, National Heart, Lung, and Blood Institute: www R.M., Shekar, P.S., Chen, F.Y., et al. (2008). .nhlbi.nih.gov Early and late outcomes of 1000 minimally The Society of Thoracic Surgeons: www.sts.org invasive aortic valve operations. European Jour- nal of Cardio-Thoracic Surgery, 33(4), 537–541. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 93

Chapter 6 Minimally Invasive Cardiac Surgery

Jenniffer Hughes, Kirsten Platt

■ INTRODUCTION Since 1967, coronary artery bypass grafting sternal wound infection (SWI). Other com- (CABG) surgery has entailed creating a plications associated with traditional CABG median sternotomy incision, creating cardiac are listed in Table 6–1. These and other com- standstill with a cardioplegia solution, and plications associated with CABG provided being connected to a bypass machine to some of the needed motivation to develop maintain oxygenation and perfusion during procedures to perform CABG on a beating cardiac standstill (Ley, 2006). Cardiopul- heart (Chikwe, Donaldson, & Wood, 2006; monary bypass (CPB) refers to the temporary Duhaylongsod, 2000). rerouting of blood from the right atrium to Modern technology made for the advance- the aorta via an oxygenator (bypass machine), ment of surgical instrumentation, and surgi- such that blood flow is circumvented around cal intervention has followed much the same the heart and lungs during the surgical proce- path. After almost a decade of laparoscopic dure. During a CABG, an anastomosis of the procedures being performed in the late 1980s, left internal mammary artery (LIMA) to the cardiac surgeons began to accept minimally left anterior descending artery (LAD) is made invasive cardiac surgery (MICS) in the mid- (Chen-Scarabelli, 2002). While data attest to 1990s (Mack, 2006). Patients undergoing the efficacy of overall medical therapy in MICS either have a small incision to access those patients with left main coronary disease the operative site or undergo the surgical pro- and in those with three-vessel disease with cedure without the use of a bypass machine, decreased left ventricular function, CABG or both. Goals of MICS that have been identi- procedures are not without the risk of com- fied include attaining a patent graft with plications (Duhaylongsod, 2000). equal or better efficacy than is achievable with Traditional CABG surgery is associated traditional CABG procedures, returning to with a prolonged ventilation time (initially baseline activity level faster, and decreasing days; now 8–12 hours), prolonged intensive pain, morbidity and mortality, length of stay care unit (ICU) stay (initially 1 week; now (LOS), and cost (Chikwe et al., 2006; Duhay- 24 hours if the case is uncomplicated), pro- longsod, 2000). Data suggest that MICS longed hospitalization (initially several decreases the need for blood transfusions, weeks; now 1 week), a prolonged rehabilita- LOS, and risk of infection and other compli- tion phase (now 8–12 weeks), and potential cations associated with traditional cardiac

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Table 6–1 Pathophysiologic Changes Associated with a Traditional CABG Procedure

Pathophysiologic Change Etiology

Bleeding and thrombotic complications: ● Activation of platelets and plasma proteins disseminated intravascular coagulation (DIC), ● Patients are heparinized and given supple- heparin-induced thrombocytopenia (HIT), mentary doses during bypass, titrated and thrombosis (HITT) against clotting studies ● Bleeding times after full reversal of heparin do not become normalized for as long as 12 hours after bypass Considerable interstitial fluid shifts ● Increased systemic venous pressure ● Volume loading ● Decreased plasma protein concentration (secondary to dilution and absorption onto the bypass circuit, and the inflammatory response increasing capillary permeability) Increased levels of cortisol, epinephrine, ● Stress of surgery and norepinephrine (remain elevated for at ● Hypothermia least 24 hours) ● Cardiopulmonary bypass ● Nonpulsatile flow Hyperglycemia ● Stress of surgery ● Hypothermia ● Cardiopulmonary bypass ● Nonpulsatile flow

● Decreased circulating triiodothyronine (T3) Stress of surgery ● Hypothermia ● Cardiopulmonary bypass ● Nonpulsatile flow Decreased myocardial compliance ● Myocardial stunning and contractility ● Ischemia ● Edema Decreased myocardial function (for 6 to ● Ischemia-reperfusion injury 8 hours postoperatively) Progressive need for volume resuscitation ● Vasodilation ● Capillary leak Pulmonary edema ● Activation of complement system ● Sequestration of neutrophils in pulmonary vasculature (can mediate increase in capillary permeability, which is compounded by fluid shifts) Pulmonary dysfunction ● Cardiopulmonary bypass decreases the effect of surfactant ● General anesthesia ● Median sternotomy ● Cardiopulmonary bypass increases shunts, decreases compliance and functional residual volume, and can cause acute lung injury continues 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 95

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Table 6–1 Pathophysiologic Changes Associated with a Traditional CABG Procedure (continued)

Pathophysiologic Change Etiology

Ischemic stroke ● Emboli released during the cannulation and clamping of the aorta Hemorrhagic stroke ● Anticoagulation necessary for bypass Impaired renal function ● Hemodilution ● Microemboli ● Catecholamines ● Low perfusion pressure ● Diuretics ● Hypothermia ● Hemolysis Peptic ulceration ● Stress response Endotoxin translocation, adding to the ● Greater permeability of gut mucosa inflammatory response

Sources: Chikwe, Donaldson, & Wood, 2006; Duhaylongsod, 2000; Glenville, 1999; Ley, 2006.

surgery (Ley, 2006). There is also reportedly (CAD); valve repair/replacement (mitral, aor- less trauma and faster recovery with MICS tic, or tricuspid); limited-access and totally than with traditional surgical methods (Sun et endoscopic pulmonary vein isolation and the al., 2006). Data regarding reduction of compli- Maze procedure to treat AF; congenital car- cations of cardiac surgery are somewhat diac defects (e.g., patent ductus arteriosis); inconsistent, however. Scherer and colleagues and thoracic endografting for aortic (2006) reported no difference in the develop- aneurysm disease treatment (Mack, 2006). ment of postoperative atrial fibrillation (AF) Any procedure that is done on the surface of with MICS and traditional CABG procedures. the heart, with the exception of surgery performed to correct atrial septal defects (ASD) ■ MINIMALLY INVASIVE CARDIAC and ventricular septal defects (VSD), can be done without the use of CPB. The advantages SURGERY of this approach are many, while the risks are While no official definition of MICS has been few. There is not only greater patient satisfac- established, it is often defined as cardiac sur- tion because of the decreased level of pain gery without the use of cardiopulmonary associated with MICS, but also decreased hos- bypass (CPB) or sternotomy; rather, smaller pital LOS and resumption of activities of incisions are made (Chikwe et al., 2006; May- daily living (ADLs). field, 2007). MICS also refers to a variety of procedures used to bypass blocked coronary arteries (Cowles, 2008). Types of MICS Procedures With the advent of new surgical instrumen- Several different MICS procedures have been tation, including robotics, MICS is now developed, each of which has its own criteria. becoming the standard in certain patient pop- One of two approaches is used in these sur- ulations. Specifically, MICS can be performed geries: (1) a mini-thoracotomy incision with- for multiple-vessel coronary artery disease out use of CPB or (2) an endoscopic approach 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 96

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with use of CPB. The major types of MICS attached to it. The artery is connected to the procedures that are currently performed LAD or branch below the area of the blockage, include minimally invasive direct coronary and then the artery is reopened (Cowles, 2008). artery bypass (MIDCAB), off-pump coronary The use of MICS as a treatment modality artery bypass (OPCAB, also known as beating- has decreased for patients with single-vessel heart surgery), robot-assisted coronary artery disease. This is related to the efficacy of percu- bypass (RACAB), minimally invasive direct taneous coronary intervention and drug elut- view, and keyhole heart surgery (Cowles, ing stents for treatment of this condition 2008). A number of alternative names for (Mack, 2006). MICS appear in the literature. The right internal mammary artery (RIMA) is used to bypass the RCA, and the LIMA is Minimally Invasive Direct Coronary used to bypass the LAD. The internal mam- Artery Bypass mary artery (IMA) conduits are patent for an MIDCAB, which is an alternative approach to average of 20 years as opposed to the 6-vein traditional CABG, has been performed since conduits, which last for only 6 to 10 years 1996 (Chen-Scarabelli, 2002). Differences (Edgar, Ebersole, & Mayfield, 1999). The MID- between the two approaches are threefold. CAB is performed without CPB; however, a First, the incision size is much smaller for perfusionist is on standby in case there is need MIDCAB; several 3-inch to 5-inch incisions for conversion to a traditional sternotomy. are made between the ribs as compared to a Three approaches may potentially be used 10-inch to 12-inch median sternotomy inci- for the MIDCAB; the specific approach cho- sion in conventional CABG procedures. Sec- sen depends on the surgeon’s preference and ond, because MIDCAB is a beating heart the patient’s anatomy. In all of these proce- procedure, no cardioplegia is instilled to stop dures, the patient is intubated with a double- the heart. Third, because MIDCAB is a beat- lumen endotracheal tube, thereby allowing ing heart surgery and no cardioplegia is for ventilation of the right lung and deflation instilled, CBP is not required for MIDCAB of the left lung, providing more room to procedures. manipulate the heart. MIDCAB procedures are performed on The first approach is performed through a patients with one or two blockages to the left left thoracotomy incision approximately 8 to anterior descending (LAD) coronary artery or 12 cm in length between the fourth and fifth its branches on the front of the heart. Blockage ribs. Rib spreaders are used to spread and ele- of the right coronary artery (RCA) may be vate the rib cage to provide ample space to dis- bypassed as well. MIDCAB surgery is per- sect the IMA. The MIDCAB is performed on a formed without the need for a median ster- beating heart, so it requires the use of a car- notomy. Instead, a smaller mini-thoracotomy diac stabilization device. The stabilizer (see incision is made on the left chest to expose the Chapter 7) provides a direct view, dampens the heart, and part of the costal cartilage is movement of the epicardium, and permits a removed. Once the field is exposed, the nontraumatic grip on the beating heart (Edgar affected artery is temporarily closed off and et al., 1999). The device helps the surgeon iso- freed at the lower end. An opening is made in late the diseased vessel and stabilize the local- the pericardium to expose part of the LAD. ized region of epicardium for anastomosis. The heart’s movement is limited during this In the second approach, a 5- to 8-cm verti- part of the procedure owing to the device cal incision is made on either side of the ster- 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 97

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num, depending on the vessel being bypassed. et al., 1999; Sharony et al., 2006). Despite the Intercostal cartilage is removed from the LIMA and the RIMA being the vessels of third and fourth ribs to provide a better view choice, traditional saphenous vein graft via of the operative site and dissection of the endoscopic approach can be used as well. IMA. This approach can easily be converted to The advantages of MIDCAB include a full sternotomy should the patient require decreased pain secondary to a less invasive CPB (Edgar et al., 1999). surgical approach; earlier mobilization The third approach is strictly used for secondary to decreased pain, shorter LIMA-to-LAD bypass and involves an 8- to LOS in the ICU and hospital, greater cost- 10-cm horizontal incision along the fourth effectiveness, low morbidity and mortality intercostal space. The procedure then follows (Chen-Scarabelli, 2002), no CPB, and the steps in the first approach—the incision decreased infection rates, especially with ster- placement is the only variation. nal wound infections. Disadvantages include A left mini-thoracotomy approach provides the potential change in strategy in the operat- direct visualization of the LAD, with the ing room (OR) if more extensive surgical LIMA being the graft vessel of choice. The intervention is required, including a ster- right mini-thoracotomy approach provides notomy and limited patient and vessel direct visualization of the RCA, with the choices. Table 6–2 lists additional advantages RIMA being the graft vessel of choice (Edgar and disadvantages of the MIDCAB approach.

Table 6–2 Advantages and Disadvantages of the MIDCAB Approach

Advantages Disadvantages

Faster recovery/return to routine ADLs Limited access and exposure to the operative Reduced morbidity/mortality area No risk of sternal wound infection Technical difficulty with beating heart LIMA/RIMA more resistant to atherosclerosis/ Need experienced surgeon increased longevity of patency Increased risk of incomplete revascularization No adverse effects related to CPB No data on long-term patency Lower cost Unable to access/visualize posterior heart for Shorter hospital stay revascularization Decreased blood loss Procedure limits target vessels No aortic manipulation No circulatory support Lower intraoperative morbidity/mortality in Acute graft occlusion and incomplete patients with cardiogenic shock, acute MI, revascularization risk increased or LV dysfunction No cardioplegia Capable of revascularization of multiple-vessel lesions

ADLs ϭ activities of daily living; CPB ϭ cardiopulmonary bypass; LIMA ϭ left internal mammary artery; LV ϭ left ventricular; MI ϭ myocardial infarction; RIMA ϭ right internal mammary artery. Sources: Chen-Scarabelli, 2002; Edgar, Ebersole, & Mayfield, 1999. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 98

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With aortic and mitral valve surgery— Robot-Assisted Coronary Artery Bypass whether repair or replacement is required— Robotic surgery was first envisioned by the CPB and cardioplegia will be used, but the military in the 1980s as an answer to war-time approach is still minimally invasive. The injuries by providing a surgeon in every fox- advantages of minimally invasive valve hole, thus allowing a surgeon to perform life- replacement are essentially the same as with saving surgery from a central location on a MICS, with the exception of the complica- soldier located in a distant Mobile Army Sur- tions of CPB and cardioplegia. These issues gical Hospital (Berlinger, 2006). By 1985, a are discussed in detail in Chapter 7. robot, along with computed tomography (CT) guidance, was used to place a needle for Off-Pump Coronary Artery Bypass a brain biopsy. In 1988, a robot was used to OPCAB (beating heart) procedures may be per- perform prostate surgery. formed on four or five vessels, as compared By the 1990s, robotic surgery was becom- with MIDCAB, where only one or two can be ing more finely tuned. The use of minimally repaired. This procedure entails a median ster- invasive laparoscopic surgery was finding its notomy incision; no bypass machine is limits; laparoscopic instruments were rigid required. With OPCAB, an artery or vein from tools that could only move along two axes— the lower extremities is used to make the up and down, clockwise and counterclock- bypass, and a device restricts heart movement, wise. The need for a more manipulative as the heart continues beating during this pro- surgical intervention was realized with the cedure (Cowles, 2008). Reported benefits of introduction of the ROBODOC® (Integrated OPCAB include reductions in blood loss, need Surgical Systems) and the more developed da for transfusions, inflammatory response, renal Vinci® Surgical System (see Figure 6–1) and insufficiency, ventilatory time, incidence of AF, Computer Motion AESOP and ZEUS systems and LOS in ICU and hospital. It is suggested (Intuitive Surgical). that elderly patients at high risk for surgery The surgical robot consists of a collection might benefit the most from the OPCAB of wristed tools called manipulators. The approach (Mack, 2006). manipulators receive digital instructions OPCAB procedures can be adapted so that from an interfaced computer. The (real-life) the IMA harvesting and bypass can be per- surgeon stays seated at a computer console formed either using a MIDCAB approach with with a three-dimensional display and acts as a small thoracotomy incision or endoscopi- the “driver” of the computer. The surgeon ini- cally (totally endoscopic coronary artery bypass tiates the digital instructions by controlling grafting [TECAB]). An alternative approach is the hand grips. By using the hand grips, the endoscopic atraumatic coronary artery bypass surgeon’s hand movements at the console are grafting (endoACAB). In this combination of then duplicated by the robot, with software both of the aforementioned approaches, the filtering out physiologic hand tremors. IMA is harvested using an endoscopic In 1998, the first robotically assisted CABG approach and the anastomosis is performed was performed using the da Vinci surgical with direct visualization through a small tho- robot. Unaccommodating places are what racotomy incision (Chikwe et al., 2006). robot-assisted surgery is all about—the size of OPCAB is discussed in more detail in the human surgeon hand is not optimal for Chapter 7. maneuvering in tiny spaces (Berlinger, 2006). 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 99

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Figure 6–1 da Vinci® Surgical System. Source: Courtesy of Intuitive Surgical System.

Several surgeons have reported performing factors have constrained the adoption of the successful robotic-assisted anastomoses of robotic approach. First, only a limited num- the left internal thoracic artery to the LAD. ber of facilities in the United States have the Robotics has been used successfully for capability to perform robotic cardiac surgery. repair of ASD and for mitral valve repair. Second, surgeons must undergo an extensive Widespread acceptance of the use of robotics training program before they can perform for these procedures is limited, however, as this type of surgery. Third, this approach is performance of these procedures without expensive: A robotic system can cost more robotic assistance is feasible in many facilities than $1 million, not including the cost of the (Mack, 2006). In addition, a few prohibitive disposable tools required for each surgery. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 100

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Figure 6–2 (Left) Minimally invasive AV surgery incision. (Right) minimally invasive MV surgery incision. Source: Courtesy of the University of Southern California.

Minimally Invasive Direct View valve surgery with either redo-sternotomies or Minimally invasive techniques have also been a minimally invasive approach. The overall developed for the repair or replacement of the hospital mortality in the minimally invasive mitral valve (MVR) and repair or replacement group was 5.6% versus 11.3% in the ster- of the aortic valve (AVR). The incision for an notomy group. In addition, LOS was shorter AVR is located on the right side of the chest and the 5-year survival rate was slightly more below the right clavicle and above the right favorable in the minimally invasive surgery nipple. The incision for the MVR is also group (Sharony et al., 2006). located on the right chest but below the right nipple (Figure 6–2). The main benefit of mini- Endovascular/“Keyhole” Procedures mally invasive direct-view valve surgery is the Subsumed under the heading of “minimally avoidance of a median sternotomy. An invasive procedures” are the endovascular 8-cm incision is made and cartilage is removed techniques known as “keyhole” procedures. to allow for direct visualization of the valves. Traditional endoscopes used for gynecologi- Unlike with the MIDCAB procedure, CPB cal and general surgery are 10 mm in width— and cardioplegia are required because the too large to access the heart through the valve surgery takes place inside the heart intercostal space. Advances in technology rather than in front of it. MICS for valve repair have now made endoscopic heart surgery pos- will use smaller incisions than the traditional sible, however, through the development of CABG approach. As with all minimally inva- 5-mm and 3-mm endoscopes. The 5-mm sive surgeries, LOS, cost, and recovery time are endoscope makes it easy to maneuver between reduced with the direct-view procedures. Mini- the ribs, thereby increasing visibility. This lat- mally invasive procedures are also preferred in ter type of endoscope has been used to close a patients who have undergone a sternotomy in patent ductus arteriosus, eliminating the the past (Mayfield, 2007). One study com- need for a thoracotomy. In addition, a newly pared outcomes of patients who underwent engineered digital camera and processing 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 101

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make pictures taken from the 5-mm scope tions because it is less invasive and CPB is not better than those taken with the 10-mm required. Using this approach, congenital heart scope. The 3-mm endoscopes are designed to defects can be repaired through minimally feel and work like the standard instruments invasive endoscopic techniques. For example, used by cardiac surgeons (Mayfield, 2007). atrial and ventricular septal defects (ASD and Some concerns have arisen regarding key- VSD) can be closed without stopping the heart hole procedures—including, inaccurate depth by using specialized endovascular catheters and perception, less tactile feedback, need for transesophageal echocardiography to repair the experienced assistance, and decreased degrees holes. In some cases, robots are used to assist of motion of the surgeons’ hands. As a result, with the procedure. robotics has been applied to counteract the Endoscopic procedures have another benefit: problems of keyhole procedures (Deeba & They assist in making reentry into the sternum Darzi, 2006). safer. Using this approach, the surgeon can Along with treatment for vessels and valves, readily visualize structures behind the sternum. the keyhole technique known as the Maze Adhesions can form between the heart and the procedure has been used as a treatment for sternum, which can cause damage to the heart AF. The “gold standard” treatment for AF is if reentry is required. Now the adhesions can be the Cox/Maze III procedure. This latter proce- cut with the assistance of the scope prior to a dure entails a number of incisions being second sternotomy, thereby reducing the risk made on the right and left atria, where the of damaging the heart (Mayfield, 2007). term “Maze” refers to the pattern of incisions Endoscopic technology can also be used to made in the atrium. The incisions cause scar- harvest the saphenous vein. Instead of a long ring, which does not conduct electricity, stops incision spanning from the inner thigh to the irregular electrical activity, and eradicates AF. lower leg, the vein can be dissected out using The scarring also prevents future irregular endoscopy. This technique requires smaller electrical signals from developing. The incisions and, therefore, produces less pain Cox/Maze III procedure is performed during (Mayfield, 2007). a CABG procedure, which requires a ster- Endoscopic procedures have made more notomy and CPB. Maze procedures are dis- complex cardiac procedures possible, espe- cussed in detail in Chapter 3. cially with the introduction of robotics. Surgi- A cutting-edge technique for the Maze proce- cal treatment of multiple-vessel disease dure has recently been developed. The Ex-Maze through the smaller incisions had proven dif- is performed endoscopically on the outside of a ficult. Robotics was implemented to facilitate beating heart. An ablation device uses unipolar endoscopic cardiac surgery in these circum- radiofrequency energy with vacuum-main- stances. Harvesting of the IMAs was success- tained contact and suction-controlled saline ful with robotics; vascular anastomosis still perfusion to ensure uniform energy transmis- presents a challenge, however, and robotics is sion and transmural lesion development (Kiser, rarely used for this purpose (Mack, 2006). Wimmer-Greinecker, & Chitwood, 2007). When endoscopy is combined with robotic- Because the procedure is performed on a beat- assisted surgery, the robotic arms and small ing heart, atrial function can be monitored dur- camera are advanced through small incisions ing treatment. Patients can convert to normal made in the intercostal spaces. Motion sen- sinus rhythm during the procedure or within sors are attached to the robotic wrists to con- 6 weeks. The Ex-Maze procedure is safer than trol the instruments. The surgeon sits at the the original techniques, is associated with less console and looks through two lenses (like a postoperative pain, and causes fewer complica- microscope) that display the image from the 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 102

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Table 6–3 Robotic Surgery Procedures specifically is indicated for patients who are at high risk for percutaneous coronary interven- ● Single- and multiple-vessel CABG tion, stent restenosis, or redo-CABG with an ● Mitral valve repair and replacement occluded LAD graft (Calafiore et al., 1997; ● Aortic valve repair and replacement Subramanian, 1997). ● ASD repair ● VSD repair Exclusion Criteria for MICS ● Removal of cardiac tumors A number of exclusion criteria for MIDCAB ● Ablation for treatment of atrial fibrillation are listed in the literature. These contraindica- (Maze procedure) tions are essentially related to the patient’s anatomy and the degree of difficulty antici- ASD ϭ atrial septal defect; CABG ϭ coronary artery bypass grafting; VSD ϭ ventricular septal defect. pated in locating the LAD. If patients have an LAD with a diameter of less than 1.5 mm, a coronary artery with a calcified score greater than 2, or an intramyocardial position of the camera. The computer generates a three- coronary artery requiring surgery, they are not dimensional image of the surgical site, with eligible for MIDCAB (Caimmi et al., 2004). foot pedals controlling the camera. As the While not listed as an exclusion criterion, it surgeon moves, the robotic arms mimic has been suggested that patients with small movements and may even be more precise coronary arteries who need several bypass than the surgeon’s natural hand movement procedures should undergo traditional CABG (Pike & Grundy, 2003). The use of robotics procedure (Cowles, 2008). Morbid obesity is has made multiple-vessel, minimally invasive, regarded as an exclusion criterion by some beating heart CABG possible. This technol- surgeons because of the difficulty of perform- ogy can be used on beating heart as well as ing surgery through the small incisions used during arrested heart procedures. Table 6–3 in minimally invasive surgery (Chikwe et al., outlines procedures that can be performed 2006; Schell, Gundry, & Grichnik, 2001). with robotic assistance. Contraindications for MIDCAB specifically include a lesioned vessel located endomyocar- Inclusion Criteria for MICS dially, concomitant surgical intervention to A select group of patients fit the MIDCAB cri- treat other cardiac disorders, inadequate flow, teria. Those included would be individuals diameter or length of the IMA, and stenosis of with a proximal LAD that is at least 1.5 mm the subclavian artery (Calafiore et al., 1997; in diameter and not calcified (Caimmi et al., Subramanian, 1997). Finally, presence of AF 2004). Other patient eligibility criteria are or COPD is suggested to make surgical care related to the small incision size. If blockage more challenging, such that these conditions of one or two coronary arteries on the exterior are considered contraindications to MICS by of the heart exists, whether the patient is some (Schell et al., 2001). healthy or is at too great a risk for a tradi- A number of exclusion criteria have been tional bypass, MIDCAB may be performed. reported for robotic mitral surgery as well. Patients who are considered viable candidates These contraindications include presence of for OPCAB include those with very low ejec- renal failure, liver dysfunction, bleeding tion fraction, COPD or emphysema, kidney diathesis, severe pulmonary hypertension, sig- disease, or high risk for stroke (Cowles, 2008). nificant aortic or tricuspid valve disease, Other sources suggest MIDCAB surgery recent ischemia or stroke (less than 30 days), 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 103

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and history of right thoracotomy (Kypson & numbers. The family should be notified where Chitwood, 2004). they will be contacted and the anticipated time until visitation after the patient arrives in the ICU. If the patient was not in the hospital prior ■ PREOPERATIVE NURSING CARE to the surgery and did not receive preoperative Preoperative cardiac surgery teaching should education, the family should be prepared be employed, with the patient and family about what to expect with the ICU environ- being educated about the possibility of the ment and visitation guidelines to help reduce MIDCAB procedure evolving into a standard their stress level. Questions should be CABG intervention. Teaching should include addressed, and any anticipated resources (e.g., the participation of not only the patient, but pastoral care) may be provided at this time. also any caregivers. Preoperative teaching for the intended procedure should include a Admission to the ICU: The First review of the potential complications and the 15 Minutes standard of care employed by the facility. Emphasis should be placed on the Patients who are intubated will be sedated and decreased amount of postoperative pain expe- possibly chemically paralyzed. Depending on rienced, but patients should be encouraged to the facility, the anesthesia provider will start a report pain levels honestly to help avoid com- sedation infusion to promote comfort, plications. Specifically, patients should be decrease myocardial oxygen consumption, encouraged to volunteer information regard- and enhance tolerance to the ventilator until ing pain level and efficacy of treatment. Such weaning commences. The anesthesia provider is not always the case, however, and pain will provide a more in-depth report including, management may be inadequate as a result but not limited to, the patient’s past medical (Watt-Watson, Stevens, Garfinkel, Streiner, & history, allergies, intraoperative course, last set Gallop, 2004). of pertinent lab results, volume of crystalloid The value of aggressive pulmonary toileting and colloids given, antibiotics administered and early ambulation cannot be over-empha- and times, urinary output, and, if CPB was sized. The technique of coughing and deep required, the length of time on bypass and the breathing as well as the use of incentive length of time the aorta was cross-clamped. spirometry should be taught in the preopera- While settling the patient after surgery, tive period. maintaining hemodynamic stability is essential. Baseline vital signs should be obtained and all pressure lines zeroed and leveled to the ■ POSTOPERATIVE NURSING CARE phlebostatic axis (see Figure 6–3). In addition Immediate postoperative care of patients who to vital signs, an initial hemodynamic assess- have undergone MICS will follow the same ment should include a review of current med- path as care for those who required a ster- ications, cardiac rhythm, and central venous notomy. Approximately 1 hour prior to the pressure (CVP). If the patient has a pulmonary patient’s arrival to the ICU, the OR nurse usu- artery catheter in place, pulmonary artery ally calls in a report to the admitting ICU pressure (PAP) and pulmonary artery occlusive nurse. After receiving the initial brief report, pressure (PAOP) should be measured. Data the family should be updated. Early contact should be obtained to allow for calculation of

establishes a rapport with family and provides cardiac output (CO), SvO2, and systemic vas- time to obtain information for the admission cular resistance (SVR) (Khalpey, Ganim, & assessment and emergency contact names and Rawn, 2008). PAP readings and waveforms 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 104

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tion profile, and a complete blood count (CBC). If the patient is bleeding, a fibrinogen level may be obtained as well. The patient should also have a portable chest radiograph and an ECG performed. An ECG after a beating heart, minimally invasive procedure is imperative because graft closure secondary to thrombosis, arterial graft spasm, and a kinked conduit are all potential complications. Early graft closure may be manifested as ST-segment elevation, T-wave inversion, and Q waves present in the leads reflective of the revascularized Figure 6–3 The phlebostatic axis myocardium (Edgar et al., 1999). (intersection of the X and Y reference lines). Chest tubes are connected to –20 cm suc- Source: Illustrated by James R. Perron tion and should be assessed for amount and type of drainage, patency, and presence of should be confirmed with the anesthesia clots. If a patient’s blood pressure permits, provider to assess any changes and the PA the head of the bed should be elevated to catheter location should be noted. Fluid and facilitate chest tube drainage. medication infusion rates should be titrated to maintain hemodynamic stability. Among patients who did not have CPB, Secondary Assessment: The Next hypothermia is uncommon. A temperature less 15 Minutes than 35 ºC (95 ºF) is considered hypothermic; After initial stabilization of the MICS patient in such a case, warming techniques should be is achieved and a preliminary patient assess- implemented. Patients who have undergone ment for clinically significant issues (e.g., MICS are routinely hypovolemic and have bleeding, hypotension, hypertension, agita- labile blood pressure, requiring volume repletion, dysrhythmias) is performed, a more tion to achieve hemodynamic stability. The focused head-to-toe assessment is completed. frequency with which vital signs and a hemo- The neurologic assessment is ongoing and dynamic profile are obtained depends on the more complete as the patient emerges from facility guidelines and the patient’s condition. anesthesia. Skin is assessed for temperature, The patient’s height and weight should be color, and location of incisions (procedure entered into the monitoring system database based). Pain should be anticipated, and its to assure accurate calculations based on body level should be assessed with a scale appropri- surface area (e.g., cardiac index). If the ate for the cognitive status of the patient. If a patient is hypothermic, cardiac index values mini-thoracotomy incision was made, pain will be skewed and reflect “cold numbers.” A remains an expected finding. true hemodynamic picture will not be Measures to relieve the thoracotomy inci- reflected until the patient is normothermic. sion pain should be implemented. In the ini- Lab specimens should be collected as pre- tial postoperative period, patients will scribed by unit protocol or as indicated by the receive opioid analgesics. They should also patient’s clinical status. Baseline postoperative be premedicated prior to potentially painful labs will likely include an arterial blood gas, procedures (e.g., chest tube removal), ionized calcium, serum chemistries, coagula- although studies suggest that this care is not 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 105

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Table 6–4 Hemodynamic Parameters

Parameters Normal Values

Systolic and diastolic blood pressure 100–130/60–90 mm Hg Mean arterial pressure 70–105 mm Hg Right atrial pressure (central venous pressure) 0–8 mm Hg Right ventricular pressure 25–30/0–8 mm Hg Pulmonary artery pressure 15–30/6–12 mm Hg Pulmonary artery occlusive pressure 4–12 mm Hg Derived Hemodynamic Parameters Cardiac output/cardiac index 4–8 L/min; 2.5–4.2 L/min/m2 Systemic vascular resistance 770–1500 dyne/sec/cm–5 Pulmonary vascular resistance 20–120 dyne/sec/cm–5 Systemic vascular resistance index 1680–2580 dyne/sec/cm–5 Pulmonary vascular resistance index 69–177 dyne/sec/cm–5 Stroke volume/index 60–130 mL/beat; 30–65 mL/beat/m2 Right ventricular stroke work 8–16 g-m/beat Right ventricular stroke work index 5–10 g-m-m2/beat Left ventricular stroke work 58–104 g-m/beat Left ventricular stroke work index 50–62 g-m-m2/beat Oxygenation Parameters Arterial oxygen saturation 95–100% Mixed venous oxygen saturation 60–80% Arterial oxygen content 17–20 mL/dL Venous oxygen content 12–15 mL/dL Oxygen delivery 900–1150 mL/min Oxygen consumption 200–290 mL/min Oxygen extraction ratio 22–30%

Sources: Blount, 2007; Khalpey, Ganim, & Rawn, 2008; LiDCO, 2008.

provided consistently (Puntillo, 1994). As healthy individuals with healthy hearts. The discussed in Chapter 14, inadequate analge- values most commonly monitored in cardiac sia can result in tachycardia, increased surgery patients are listed in Table 6–4 and peripheral vascular resistance, imbalance covered in more detail in Chapter 9. between oxygen supply and demand, hypox- Managing a patient’s hemodynamic profile emia, pneumonia, and atelectasis. Lower lev- entails evaluating the patient’s clinical condi- els of pain are typically encountered with a tion and past medical and surgical histories minimally invasive procedure. Chest tubes, so the correct decision is made about how to however, can be a source of pain. optimize preload, afterload, and contractility. Depending on comorbidities, hemodynamic ■ HEMODYNAMIC MONITORING values may be skewed. For example, a patient Successful hemodynamic monitoring begins with pulmonary hypertension may have ele- with knowing the normal range for hemody- vated pulmonary artery pressures and CVP namic values. “Normal,” in this case, is a rela- secondary to lung disease. A valuable source tive term, as normal values are based on for a patient’s baseline hemodynamic values 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 106

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Table 6–5 Commonly Used Cardiac Surgery Postoperative Medications

Medication Dosage Range

Vasodilator Medications Nitroglycerin 0.25–3 mcg/kg/min or 10–200 mcg/min Nitroprusside 0.5–10 mcg/kg/min Vasoactive Medications Dobutamine 2–20 mcg/kg/min Dopamine 2–20 mcg/kg/min Epinephrine 1–30 mcg/min Milrinone Loading dose: 50 mcg/kg, then 0.1–0.75 mcg/kg/min Norepinephrine 1–40 mcg/min Phenylephrine 10–500 mcg/min Vasopressin 0.01–0.1 unit/min Antiarrhythmic Medications Amiodarone Loading dose: 150–300 mg (depending on presence or absence of pulse) Maintenance infusion: 1 mg/min ϫ 6 hours; then 0.5 mg/min for the next 18 hours Diltiazem 5–15 mg/hr Lidocaine 1–4 mg/hr

Sources: Albright, Zimmerman, & Selzman, 2002; Bojar & Warner, 1999; Kayser & Schell, 2006; Levy, Bailey, & Deeb, 2002.

is the cardiac catheterization lab report. Try- dysrhythmias (Khalpey et al., 2008). These are ing to maintain a patient with underlying dis- discussed in detail in Chapters 13 and 15. ease within the standard norms is unrealistic Table 6–5 lists some of the medications most and can even be detrimental to the patient. commonly used to optimize hemodynamic For example, a patient with hypertension may status. The goal of therapy is optimal end- not have adequate kidney perfusion with a organ perfusion with hemodynamic stability. MAP of 80 mm Hg, but instead may need a Although hemodynamic parameter goals slightly higher MAP of 90–95 mm Hg to should be individualized, suggested mini- maintain end-organ perfusion. mum values for most patients will likely

The key to hemodynamic stability starts include an SvO2 near 60%, a MAP greater than with maintaining and normalizing heart rate 65 mm Hg, and cardiac index (CI) greater and stroke volume (SV). This goal may be than 2 L/min/m2 (Khalpey et al., 2008). accomplished through the administration and titration of fluids and medications. SV is ■ affected by preload, afterload, and contractil- POSTOPERATIVE COMPLICATIONS ity (Zellinger, 2007); these variables are Postoperative complications of cardiac surgery described further in Chapter 9. in general are discussed in detail in Chapter Some of the more common etiologies of 13. It is essential for the ICU nurse to monitor hemodynamic compromise are myocardial patients who have undergone MICS proce- ischemia, hypothermia, and postoperative dures for development of complications, inter- 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 107

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vene to prevent them from occurring, and catheter with a pacing port, which can pace promptly recognize and treat any complica- the ventricle. Institution-specific equip- tions that develop following cardiac surgery. ment will dictate which pacing options are available. MICS-Specific Complications Lethal arrhythmias, such as ventricular tachycardia (VT) or ventricular fibrillation Some of the complications related to MICS (VF), can also occur in the immediate postop- specifically are felt to be related to the more erative period. Electrolyte imbalance, cardiac technically challenging nature of these proce- irritability from the surgery, and acidosis may dures and to procedure-related stress on the be contributing factors to their development. heart. Complications reported in the litera- Resuscitation of these dysrhythmias should ture include dysrhythmias, hypotension, MI, follow the American Heart Association (AHA) bleeding, brain injury (if intraoperative blood recommendations. Development of VF may flow is decreased), infection, pulmonary com- require opening the patient’s chest at the bed- plications, and bone and muscle surgical site side. Postoperative dysrhythmias are dis- injury (Cowles, 2008). Lung herniation, while cussed in more detail in Chapter 15. rare, has also been reported (Athanassiadi, Bagaev, Simon, & Haverich, 2008). Hypothermia Hypothermia can present a variety of prob- Dysrhythmias lems postoperatively. For example, it can Dysrhythmias are common following cardiac cause bleeding, platelet dysfunction, and gen- surgery. AF can occur in patients with no prior eralized impairment of the coagulation cas- history from electrolyte imbalances, volume cade. It may also stimulate the sympathetic overload, surgical manipulation, or acid–base nervous system, leading to hemodynamic imbalance. Without the atria contracting (atrial instability, dysrhythmias, vasoconstriction, kick), there is a 25–30% loss of cardiac output. hypertension, and increased SVR, thereby Management with an AV nodal blocker such as making the heart work harder to pump. diltiazem (Cardizem®) or metoprolol (Lopres- These effects can increase myocardial oxygen sor®) for rate control, or amiodarone for demand and produce myocardial ischemia rhythm conversion, is recommended. If AF is (Frank, 2001; Khalpey et al., 2008). Controlled accompanied by hemodynamic instability, or if rewarming with any available method (e.g., the patient experiences a rapid ventricular forced warm-air device, fluid warmer) is an response that does not respond to pharmaco- essential nursing intervention. logic therapy, synchronized cardioversion is Shivering is another problem associated recommended (Fuster et al., 2006). with hypothermia. If a patient is shivering, The patient who underwent valve surgery there is a twofold to threefold increase in oxy-

or a Maze procedure may develop bradycar- gen consumption (seen as a decrease in SvO2) dia or heart block as a result of intraopera- and CO2 production. Shivering also causes tive manipulation around the conduction adrenergic stimulation and discomfort (Bhat- system (Ishikawa et al., 2007). Such a patient tacharya, Bhattacharya, Jain, & Agarwal, 2003). may have epicardial pacing wires in place For all these reasons, controlling shivering is from surgery, so the heart can be temporarily important. One of the few effective agents to controlled. If pacing wires were not placed treat postoperative shivering is meperidine during the procedure, transcutaneous pac- (Demerol®) (Kranke, Eberhart, Roewer, & ing pads or transvenous pacing wires may be Tramèr, 2002). placed (Lemmer, Richenbacher, & Vlahakes, Rewarming the patient causes vasodilation, 2003). Another option is a pulmonary artery resulting in decreasing blood pressure and 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 108

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filling pressures. Administration of volume et al., 2006; Kapoor et al., 2008). In addition, and vasopressors may be indicated. Postopera- other factors should be considered while tive cognitive impairment due to cerebral weaning the patient off ventilatory support, hyperthermia has been reported in patients such as surgical technique used (on-pump who are warmed too quickly following cardiac versus off-pump; CPB may lead to capillary surgery (Borger & Rao, 2002). Hypothermia is leak), patient age, comorbidities, length of more prevalent in patients who have under- time in the operating room, intraoperative gone on-pump procedures. course, and presence of any postoperative complications. Weaning from mechanical ventilation following cardiac surgery is dis- Bleeding cussed in detail in Chapter 11. Postoperative bleeding is a risk with any cardiac surgery, including a minimally invasive ■ RECOVERY FROM MICS approach. The risk increases if the procedure is performed on CBP, as higher doses of Patients who undergo MICS procedures tradi- heparin are administered. Hemodilution, fib- tionally have a quicker and less complicated rinolysis, and hypothermia are also risk fac- recovery than patients who undergo conven- tors for postoperative bleeding. tional CABG procedures. Table 6–6 summa- When assessing chest tube drainage, rizes the recovery associated with these patency as well as the consistency and color of procedures. drainage should be noted. Dark blood will usually indicate venous or older blood; bright ■ SUMMARY red blood is usually arterial or fresh blood. If Minimally invasive cardiac surgery, with all an off-pump patient is bleeding, it is generally of its benefits, provides a viable option for surgical in nature. Postoperative bleeding is the patient who meets the criteria established discussed in more detail in Chapter 13. for this type of procedure. The major benefit is the decreased level of pain associated with MICS, which leads to early ambulation and ■ POSTOPERATIVE VENTILATORY better pulmonary toileting. Decreased inci- SUPPORT dence of postoperative complications related Patients who undergo MICS may be extu- to CPB and aortic cross-clamping, intraoper- bated in the operating room. If not, they can ative anticoagulation, cardioplegia, and ster- generally be weaned from the ventilator rela- nal wound infections have all been tively quickly (3–6 hours). Patients may be documented. weaned from mechanical ventilation when The cardiac surgery ICU nurse takes on certain criteria, which may vary among facili- many roles when caring for this type of ties, are met. In general, these conditions may patient: educator, advocate for the patient include the patient being awake and coopera- and family, and collaborator with the multi- tive, dissipation of neuromuscular blocking disciplinary team. agent effects (usually manifested with a sus- Robotic surgery, while still in its infancy, tained head lift), hemodynamic stability, continues to evolve. Indeed, with continued absence of dysrhythmias, ABG values within training on the part of the surgeon and the the physiological range, normal chest radi- development of new equipment, a new era of ograph findings, normothermia, no evidence cardiac surgery is yet to unfold. While MICS of bleeding once the sternum has been closed, is not an innovative new treatment for cardiac chest tube drainage less than 100 mL/hr, and disease, it is certainly an attractive new urine output more than 1 mL/kg/hr (Chikwe approach to a traditional procedure. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 109

Summary 109

Table 6–6 Recovery from Cardiac Surgery

Time to Return LOS in ICU LOS in Hospital to Normal Activities

MIDCAB 1 day 3 days 2 weeks OPCAB 1 day 5–7 days 2–3 months Traditional CABG 1–3 days* 5–10 days 2–3 months

*Data vary regarding definition of prolonged ICU stay, ranging from > 2 or 3 days. CABG ϭ coronary artery bypass grafting; ICU ϭ intensive care unit; LOS ϭ length of stay; MIDCAB ϭ minimally invasive direct coronary artery bypass; OPCAB ϭ off-pump coronary artery bypass. Sources: Abrahamyan, Demirchyan, Thompson, & Hovaguimian, 2006; Atoui, Ma, Langlois, & Morin, 2008; Cowles, 2008.

CASE STUDY

A 70-year-old patient came to the emergency department with chest pain, shortness of breath, and nausea. He reported having multiple similar episodes over the last month, with the symptoms normally resolving with rest after 30 minutes. Today, the symptoms continued for more than 2 hours, and his wife forced the patient to seek treatment. He rated his pain as an 8 on a 0 to 10 scale. He also reported a history of COPD, 50-pack-year smoking history, chronic renal insufficiency, diet-controlled diabetes, and transient ischemic attack. The patient was immediately evaluated. Oxygen was applied, an IV established, and labs obtained, including a CBC, chemistry panel, PT/PTT, CK-MB, troponin, and arterial blood gas. Sublingual nitroglycerin was administered 3 times with no relief of pain; 2 mg of IV morphine was given, which decreased the patient’s pain from an 8 to a 6. A 12-lead ECG

revealed ST elevation in leads I, aVL, V3, V4, V5, and V6, indicating an anterior lateral wall MI. The patient was taken to the catheterization lab. Cardiac catheterization revealed a proximal occlusion of the LAD with good collateral circulation. The right coronary and the circumflex arteries had 10% occlusion, and the patient’s ejection fraction was 40%. He was deemed not to be a candidate for angioplasty or stent placement because of a tortuous arterial anatomy. A MIDCAB procedure was scheduled owing to the patient’s comorbidities. Preoperative education was performed by the ICU nurse on the evening before surgery was scheduled. Early the next morning, the patient underwent a MIDCAB procedure with a mini- thoracotomy approach under general anesthesia. The surgeon anastomosed the LIMA to the LAD; no cardiopulmonary bypass was required. The patient was transported to the ICU, hooked to hard-wire monitoring, and placed on a ventilator. He had an intra-arterial catheter, left pleural chest tube to a drainage collection device at –20 cm suction, and urinary catheter. Initial labs were obtained and the assessment completed. Hemodynamic data were as follows: heart rate 90; sinus rhythm

with no ectopy; BP 112/64 (80); PA 32/20 (24); CVP 13; CO 3.5; CI 1.9; SVR 1554; SvO2 70; SpO2 100%; temperature 36.0 °C; urinary output. 180 mL; and CT drainage 50 mL. A portable chest radiograph and ECG were obtained. The patient was extubated within 2 hours after his arrival to the ICU. A postoperative angiography revealed a patent graft. The patient’s postoperative course was uneventful, and he was discharged home on postoperative day 5. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 110

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Critical Thinking Questions 1. Which postoperative test will provide the necessary information about this patient’s graft status, including the patency of the graft? 2. If graft occlusion has occurred, which ECG findings will be present in this case? 3. Why is diltiazem ordered postoperatively? Answers to Critical Thinking Questions 1. 12-lead ECG 2. The patient will likely manifest ST-segment elevation, T-wave inversion, and the pres-

ence of Q waves in leads V1–V5, indicating changes in the anterior wall—that is, the area of the heart that was revascularized. 3. One of the causes of graft closure is IMA graft vasospasm. Administration of a calcium channel blocker helps to prevent postoperative spasm of the graft vessel.

■ SELF-ASSESSMENT QUESTIONS 4. An advantage of robotic surgery over other forms of MICS may include: 1. Which of the following is not an advan- a. experience is not as essential since the tage of MICS over traditional CABG? surgeon is not actively doing the a. Shorter operative time procedure b. Breastbone not retracted b. there is a decreased chance of blood c. Less blood loss loss d. Better cosmetic results c. cosmetic results 2. A patient who has undergone a MID- d. lower risk of infection CAB procedure asks you when he should 5. Which of the following statements is be able to return to work. Which of the true regarding MICS procedures? following time frames should you give a. No bone cartilage is removed. him? b. The ascending aorta is manipulated. a. 4–5 days after discharge from c. Use of a cardiac stabilizer is required. hospital d. The heart temporarily loses b. 2 weeks pericardial support. c. 2–3 months d. 6–10 months 6. Valve procedures require cardiopulmonary bypass because 3. Which of the following statements is a. of the anatomic location involved. true regarding minimally invasive valve b. of surgeon preference. surgery? c. there is less risk of postoperative a. It doesn’t require being placed on a bleeding. bypass machine. d. comorbidities associated with valve b. There is a decreased chance of disease. infection. c. Patients who are obese may be good candidates for this approach. d. It is the ideal approach for patients with multiple forms of valve disease. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 111

Self-Assessment Questions 111

7. Which of the following is a potential c. Male, age 63, mitral valve manifestation of a patient experiencing regurgitation, EF 60%, plays golf postoperative shivering following 3 times a week MICS? d. Female, age 40, s/p bilateral

a. Increased SvO2 mastectomy, 3-vessel CAD b. Decreased CVP 10. A benefit of the Cox/Maze III procedure c. Increased pCO2 for atrial fibrillation is d. Decreased sympathetic stimulation a. this procedure uses ablation so 8. One advantage associated with endovas- return of AF is unlikely. cular “keyhole” procedures is b. this procedure does not require the a. increased accuracy of depth patient to go on cardiopulmonary perception. bypass. b. less experience is required because the c. incisions are made on both atria to procedure is less invasive. stop irregular electrical activity. c. increased degree of motion of the d. no sternotomy incision is required. surgeon’s hands. d. enhanced visibility. Answers to Self-Assessment Questions 9. Which of the following patients is a 1. a 6. a good candidate for MICS? 2. b 7. c a. Male, age 80, 70% circumflex 3. b 8. d occlusion, inpatient, cardiogenic shock b. Female, age 50, morbid obesity, day 2 4. d 9. c s/p inferior lateral MI, IABP 5. c 10. c

Clinical Inquiry Box

Question: Do patients who undergo minimally invasive cardiac surgery have better outcomes or quality of life? References: Yamada, T., Ochiai, R., Takeda, J., Shin, H., & Yozu, R. (2004). Comparison of early postoperative quality of life in minimally invasive versus conventional valve surgery. Journal of Anes- thesia, 17(3), 171–176. Objective: To evaluate the quality of life in patients who undergo minimally invasive cardiac surgery. Method: Two groups of patients were included in the study—66 who underwent MICS and 50 who underwent conventional cardiac surgery (CCS). Patients had either aortic or mitral valve surgery. Results: Shorter hospitalization, less pain medication use, and a lower incidence of delirium were found with the MICS group as compared with the CCS group. Members of the MICS group were able to take food earlier and have a urinary catheter removed before members of the CCS group. Conclusion: Earlier recovery from MICS procedure as compared to CCS allows for improved quality of life through the early reinstitution of daily activities. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 112

112 Chapter 6 Minimally Invasive Cardiac Surgery

■ REFERENCES tages, and limitation. Critical Care Nurse, 22(5), Abrahamyan, L., Demirchyan, A., Thompson, M. E., 44–58. & Hovaguimian, H. (2006). Determinants of Chikwe, J., Donaldson, J., & Wood, A. J. (2006). morbidity and intensive care unit stay after Minimally invasive cardiac surgery. British Jour- coronary surgery. Asian Cardiovascular Thoracic nal of Cardiology, 13(2), 123–128. Annals, 14(2), 114–118. Cowles, R. A. (2008). Minimally invasive heart sur- Albright, T. N., Zimmerman, M. A., & Selzman, gery. Retrieved August 21, 2008, from C. H. (2002). Vasopressin in the cardiac sur- www.nlm.nih.gov/medlineplus/ency/article/ gery intensive care unit. American Journal of 007012.htm Critical Care, 11(4), 326–330. Deeba, S., & Darzi, A. (2006). Cardiac robotics: A Athanassiadi, K., Bagaev, E., Simon, A., & Haverich, A. review and St. Mary’s experience. International (2008). Lung herniation: A rare complication in Journal of Medical Robotics and Computer Assisted minimally invasive cardiac surgery. European Surgery: MRCAS, 2(1), 16–20. Journal of Cardiothoracic Surgery, 33(5), 774–776. Duhaylongsod, F. G. (2000). Minimally invasive Atoui, R., Ma, F., Langlois, Y., & Morin, J.-F. (2008). cardiac surgery defined. Archives of Surgery, Risk factors for prolonged stay in the intensive 135(3), 296–301. care unit and the ward after cardiac surgery. Edgar, W. F., Ebersole, N., & Mayfield, M. G. Journal of Cardiac Surgery, 23(2), 99–106. (1999). MIDCAB. American Journal of Nursing, Berlinger, N. T. (2006). Robotic surgery: Squeezing 99(7), 40–46. into tight places. New England Journal of Medi- Frank, S. M. (2001). Consequences of hypothermia. cine, 345(20), 2099–2101. Current Anaesthesia and Critical Care, 12(2), 79–86. Bhattacharya, P. K., Bhattacharya, L., Jain, R. K. & Fuster, V., Ryden, L. E., Cannom, D. S., Crijns, H. J., Agarwal, R. C. (2003). Post anaesthesia shiver- Curtis, A. B., Ellenbogen, K. A., et al. (2006). ing (PAS): A review. Indian Journal of Anaesthe- ACC/AHA/ESC 2006 guidelines for the man- sia, 47(2), 88–93. agement of patients with atrial fibrillation: Blount, K. (2007). Hemodynamic monitoring. In Executive summary. Circulation, 114(7), 700–752. R. Kaplow & S. R. Hardin (Eds.) Critical care Glenville, B. (1999). Minimally invasive cardiac sur- nursing. Synergy for optimal outcomes. Sudbury, gery offers ways of reducing complications of MA: Jones & Bartlett. coronary artery bypass grafts. British Medical Bojar, R. M., & Warner, K. G. (1999). Cardiovascu- Journal, 319(7203), 135–136. lar management. In R. M. Bojar & K. G. Ishikawa, S., Obayashi, T., Kawasaki, A., Suzuki, Y., Warner. Manual of perioperative care in cardiac Neya, K., Ohki, S., et al. (2007). Septal-superior surgery (3rd ed., pp. 213–334). Malden, MA: exposure in mitral valve surgery with radiofre- Blackwell. quency ablation. ANZ Journal of Surgery, Borger, M. A., & Rao, V. (2002). Temperature man- 77(1–2), 40–42. agement during cardiopulmonary bypass: Kapoor, P. M., Kakani, M., Chowdhury, U., Choud- Effect of rewarming rate on cognitive dysfunc- hury, M., Lakshmy, R., & Kiran, U. (2008). tion. Seminars in Cardiothoracic and Vascular Early goal-directed therapy in moderate to Anesthesia, 6(1), 17–20. high-risk cardiac surgery patients. Annals of Caimmi, P., Fossaceca, R., Lanfranchi, M., Cardiac Anaesthesia, 11(1), 27–34. Kapetanakis, E. I., Verde, A., Panella, A., et al. Kayser, S. R., & Schell, H. M. (2006). Vasoactive (2004). Cardiac angio-CT scan for planning medications. In H. M. Schell & K. A. Puntillo MIDCAB. Heart Surgery Forum, 7(2), E113–E116. (Eds.), Critical care nursing secrets (2nd ed., pp. Calafiore, A., Teodori, G., Di Giammarco, G., Vit- 173–184). St. Louis: Mosby. tola, G., Iaco, A., Iovino, T., et al. (1997). Mini- Khalpey, Z. I., Ganim, R. B., & Rawn, J. D. (2008). mally invasive coronary bypass grafting on a Postoperative care of cardiac surgery patients. beating heart. Annals of Thoracic Surgery, 63(6 In L. H. Cohn (Ed.), Cardiac surgery in the adult suppl), 572–575. (pp. 465–486). New York: McGraw-Hill. Chen-Scarabelli, C. (2002). Beating-heart coronary Kiser, A. C., Wimmer-Greinecker, G., & Chitwood, artery bypass graft surgery: Indication, advan- W. R. (2007). Totally extracardiac Maze proce- 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 113

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dure performed on the beating heart. Annals of Scherer, M., Sirat, A. S., Dogan, S., Aybek, T., Thoracic Surgery, 84(5), 1783–1785. Moritz, A., & Wimmer-Greinecker, G. (2006). Kranke, P., Eberhart, L. H., Roewer, N., & Tramèr, Does totally endoscopic access for off-pump M. R. (2002). Pharmacological treatment of cardiac surgery influence the incidence of postoperative shivering: A quantitative sys- postoperative atrial fibrillation in coronary tematic review of randomized controlled tri- artery bypass grafting? A preliminary report. als. Anesthesia & Analgesia, 94(2), 453–460. Cardiovascular Engineering: An International Jour- Kypson, A., & Chitwood, W. R. (2004). Robotically nal, 6(3), 118–121. assisted cardiac surgery. Indian Heart Journal, Sharony, R., Grossi, E. A., Saunders, P. C., 56(5), 618–621. Schwartz, C. F., Ursomanno, P., Ribakove, Lemmer, J. H., Richenbacher, W. E., & Vlahakes, G. G. H., et al. (2006). Minimally invasive reoper- J. (2003). Complications involving the heart ative isolated valve surgery: Early and mid- and lungs. In J. H. Lemmer, W. E. Richen- term results. Journal of Cardiac Surgery, 21(3), bacher, & G. J. Vlahakes, Handbook of patient 240–244. care in cardiac surgery (6th ed., pp. 116–167). Subramanian, V. (1997). Less invasive arterial Philadelphia: Lippincott Williams & Wilkins. CABG on a beating heart. Annals of Thoracic Levy, J. H., Bailey, J. M., & Deeb, G. M. (2002). Surgery, 63(6), S30–S34, S68–S71. Intravenous milrinone in cardiac surgery. Sun, H.-S., Ma, W.-G., Xu, J.-P., Sun, L.-Z., Lu, F., & Annals of Thoracic Surgery, 73(1), 325–330. Zhu, X.-D. (2006). Minimal access heart sur- Ley, S. J. (2006). Postoperative management of the gery via lower ministernotomy: Experience in cardiac surgery patient. In H. M. Schell & K. A. 460 cases. Asian Cardiovascular & Thoracic Puntillo (Eds.), Critical care nursing secrets (2nd Annals, 14(2), 109–113. ed., pp. 113–121). St. Louis: Mosby. Watt-Watson, J., Stevens, B., Garfinkel, P., Streiner, LiDCO. (2008). Normal hemodynamic parameters. D., & Gallop, R. (2004). Relationship between Retrieved December 12, 2008 from http://lidco-ir nurses’ knowledge and pain management out- .co.uk/html/clinical/nph.asp comes for their postoperative cardiac patients. Journal of Advanced Nursing, 36(4), 535–545. Mack, M. J. (2006). Minimally invasive cardiac surgery. Surgical Endoscopy, 20(suppl 2), Zellinger, M. (2007). Cardiac surgery and heart S488–S492. transplant. In R. Kaplow & S. R. Hardin (Eds.), Critical care nursing: Synergy for optimal outcomes Mayfield, W. R. (2007). Minimally invasive cardiac (pp. 229–242). Sudbury, MA: Jones and surgery. Heart Surgery Forum. Retrieved Decem- Bartlett. ber 12, 2007, from www.hsforum.com/ stories/story. Pike, N. A., & Grundy, S. R. (2003). Robotically ■ WEB RESOURCES assisted cardiac surgery: Minimally invasive Minimally invasive valve surgery: www.youtube techniques to totally endoscopic heart surgery. .com/watch?v=y4pHVQvBhx0 Journal of Cardiovascular Nursing, 18(5), 382–388. Minimally invasive aortic valve surgery: www .youtube.com/watch?v=wT23obEeVlM Puntillo, K. (1994). Dimensions of procedural pain and its analgesic management in critically ill Minimally invasive robotic cardiac surgery: surgical patients. American Journal of Critical www.youtube.com/watch?v=phs8CG0iTyI& Care, 3(2), 116–122. feature=related Schell, R. M., Gundry, S. B., & Grichnik, K. P. Minimally invasive direct coronary artery bypass (2001). Anesthesia for minimally invasive car- (MIDCAB): www.youtube.com/watch?v=V4vv diac surgery. In F. G. Estafanous, P. G. Barash, SAwaBtU & J. G. Reves (Eds.), Cardiac anesthesia (pp. Hybrid Maze procedure: www.youtube.com/ 673–702). Philadelphia: Lippincott Williams & watch?v=ubxVAqoENwI Wilkins. 57625_CH06_093_114.pdf 4/10/09 11:06 AM Page 114 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 115

Chapter 7 Cardiopulmonary Bypass and Off-Pump Coronary Artery Bypass

Julie Miller

■ INTRODUCTION For years, nurses have cared for patients who Schmaderer, 1998), more readmissions (Duits, have undergone traditional coronary artery Boeke, Taams, Passchier, & Erdman, 1997), bypass grafting (CABG) surgery, in which the poor psychological outcomes (Boudrez & De patient is placed on a cardiopulmonary bypass Backer, 2001), and worse quality of life (Duits circuit. Since 1990, however, nurses have seen et al., 1997). Factors predictive of increased an increase in the number of patients under- anxiety include being female, having to wait going off-pump coronary artery bypass for surgery, pain prior to surgery, concerns (OPCAB) surgery, in which the surgeon sews over returning to work, prior anxiolytic or anti- the grafts onto the beating heart. Nursing care depressant use, and difficulty sleeping (Gal- of patients who have received the CABG and lagher & McKinley, 2007). Nurses must assess OPCAB procedures has a number of similari- patients’ anxiety levels throughout the hospi- ties and differences. talization and seek to understand the best As recently as 15 years ago, coronary patient-specific approach in countering their bypass surgery patients spent 2 to 3 days on a stress. The provision of realistic information ventilator, sedated, with a pulmonary artery about what to expect through every step of the catheter (PAC) in place and multiple vasoac- care delivered and effective pain management tive drips infusing to maintain optimal are crucial in decreasing anxiety levels. hemodynamic status. Today, a patient under- Despite the need to address anxiety levels, going CABG or OPCAB may be discharged the hemodynamic challenges, constant obser- from the operating room extubated, without vation for potential complications and need for a PAC, and be transferred from the ICU to a the astute critical care nurse remain the same. progressive care unit within 12 hours of sur- This chapter will explore the similarities and gery. Regardless of the short stay, patients differences in the care of the traditional on- remain critically ill when transferred from pump coronary artery bypass grafting (CABG the ICU. Nurses are often faced with the chal- or ONCAB) patient compared to the patient lenge of patients and families who are anx- who undergoes off-pump bypass (OPCAB). ious over the potential for death throughout ■ the course of hospitalization. POTENTIAL COMPLICATIONS Anxiety during the preoperative and post- OF BYPASS SURGERY operative periods has been correlated with Stroke, infection, bleeding, dysrhythmias, poor outcomes such as increased pain levels myocardial infarction, gastrointestinal dysfunc- (Nelson, Zimmerman, Barnason, Nieveen, & tion, renal failure, and death are all potential 115 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 116

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complications for the bypass surgery patient, aortic balloon pump therapy is discussed in whether the procedure is performed with the detail in Chapter 10. On rare occasions, a on- or off-pump technique. The risk for atrio- patient’s heart does not restart following CPB. ventricular heart block is present in both types of bypass procedures, and both types of ■ OFF-PUMP CORONARY patients will have epicardial pacing wires ARTERY BYPASS placed. Nursing challenges for bypass surgery OPCAB is performed either through a median patients include ensuring hemodynamic sta- sternotomy incision or via a thoracotomy inci- bility, monitoring for and treating cardiac sion, also known as minimally invasive direct dysrhythmias, balancing the need to ade- coronary artery bypass (MIDCAB). Robotic- quately medicate for pain while guarding assisted coronary artery bypass (ROBOCAB) against oversedation and respiratory compli- surgery is another type of off-pump procedure cations, and monitoring for and intervening that is done through a minimally invasive to prevent the myriad of potential postopera- approach. Minimally invasive surgery is dis- tive complications. cussed in detail in Chapter 6. ONCAB patients undergo surgery while their In OPCAB, the surgeon sews the grafts onto heart is not beating. In this procedure, through the beating heart using specialized instru- a median sternotomy incision, the heart is ments to stabilize the myocardial tissue where stopped using cardioplegia solution. Oxygen the surgeon is sewing the graft (St. Andre & needs are met by cannulating the aorta and DelRossi, 2005). These instruments, known as placing the patient on the cardiopulmonary stabilizers, are similar in shape to the sewing bypass (CPB) circuit. ONCAB carries a higher foot for a sewing machine (see Figure 7–1). risk of aortic dissection and embolization Studies have noted that patients undergo- because of the cannulation of the aorta for ing OPCAB receive fewer grafts than those bypass procedures (Wijeysundera et al., 2005). undergoing ONCAB. This pattern may lead Heparin is utilized to maintain patency of to a higher reintervention rate for OPCAB the CPB circuit and to reduce the risk of patients (Sedrakyan, Wu, Parashar, Bass, & microemboli formation. Heparin-induced Treasure, 2006). The risk for aortic dissection thrombocytopenia (HIT) and bleeding are potential complications for all patients receiving heparin. In addition, the CPB circuit can contribute to the development of systemic inflammatory response syndrome (SIRS) and microemboli (Bruins et al., 1997). Moderate hypothermia is utilized during the ONCAB procedure to decrease myocardial oxygen demand. The postoperative rewarming process contributes to vasodilation and can worsen the effects of SIRS. As part of the ONCAB procedure, the bypass grafts are sewn onto the heart and aorta while the heart is not beating. When the surgery is completed, the heart is restarted and the CPB circuit withdrawn. There is a risk that the patient will not be able to be weaned from CPB and may require an intra-aortic balloon pump Figure 7–1 Stabilizer used in OPCAB. (IABP) or pacemaker postoperatively. Intra- Source: Illustrated by James R. Perron 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 117

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with OPCAB is less than traditional CABG, Assessment for postoperative bleeding is however (Shekar, 2006). Approximately 50 of essential, especially given that mediastinal 1000 (5%) patients undergoing off-pump reexploration rates for bypass surgery bypass procedures may need to be converted patients are as high as 5% (Raja, 2005). Bleed- to on-pump procedures (Sedrakyan et al., ing in these patients can be attributed to 2006). This possibility should be discussed CPB, hypothermia, fibrinolytic agents admin- with the patient and family during preopera- istered during the procedure, heparin rever- tive teaching. sal, and loose anastomoses. As OPCAB was OPCAB is performed on a patient with developed, concern was voiced that these either mild hypothermia or normothermia. patients would have more bleeding due to Hypothermia contributes to postoperative the risk of sewing onto the beating heart. In bleeding by causing impairment in the clot- fact, data from randomized controlled trials ting cascade. It is theorized that less bleeding suggest that OPCAB patients experience less occurs with mild hypothermia as compared to bleeding postoperatively than ONCAB the moderate hypothermia (30–34 ºC) utilized patients (Raja, 2005). in the ONCAB procedure. Mild hypothermia In all post-bypass patients, assessment for does help reduce myocardial oxygen demand bleeding is necessary. The mediastinal and and may be beneficial to both ONCAB and pleural tubes must be monitored hourly for OPCAB patients (St. Andre & DelRossi, 2005). amount and quality of drainage, including assessment for clots. Monitoring for narrowing of pulse pressure is performed, as this ■ COMPLICATIONS OF ON-PUMP finding could indicate cardiac tamponade in SURGERY VERSUS OFF-PUMP the post-bypass patient. SURGERY Heparin is utilized to maintain vessel Off-pump coronary artery bypass grafting, patency and prevent thrombus formation dur- also known as a beating heart procedure, was ing OPCAB, but the amount is about one-third developed partly to offset the risk of postop- to one-half the dose used in traditional CABG erative alterations associated with on-pump (Zenati, 2005). Because heparin is utilized in procedures. Specifically, patients who both on- and off-pump procedures, it is imper- undergo OPCAB are felt to be less likely to ative that the nurse assess all post-bypass develop cerebral hypoperfusion, emboliza- patients for bleeding, check lab data for pres- tion, and inflammatory response associated ence of a coagulopathy, and assess for HIT. with on-pump procedures (Abu-Omar, Bal- Protamine is a polypeptide isolated from acumaraswami, Pigott, Matthews, & Taggart, salmon sperm (Arslan, Tarhan & Yilmaz, 2004; Demaria et al., 2002; Fearn et al., 2001). 2005). It is utilized in both on- and off-pump Recent work has found that the cytokine and procedures to bind heparin and reverse its chemokine production is similar in ONCAB anticoagulant effect (Stafford-Smith et al., and OPCAB, but biomarkers such as eco- 2005). In one study, researchers estimated that taxin, macrophage inflammatory protein-1 protamine caused adverse events in approxi- beta (MIP-1β), and interleukin-12 (IL-12) mately 2.6% of cardiac surgery patients (Kim- were found more prevalent in the setting of mel, Sekeres, Berlin, Goldberg, & Strom, ONCAB. Although more research needs to be 1998). Risk factors for protamine reactions conducted on the inflammatory response include being a diabetic patient who uses pro- most often seen in ONCAB, OPCAB does tamine-containing insulin, previous drug appear to produce less of an inflammatory reaction, and allergy to protamine or fish. An response, which can improve cardiopul- estimated 39% of bypass surgery patients have monary outcomes (Castellheim et al., 2008). these risk factors (Kimmel et al., 1998). 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 118

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A minor protamine reaction may result in Patients who undergo bypass procedures hypotension and an increase in pulmonary may develop postoperative temporary meta- artery pressures (St. Andre & DelRossi, 2005). bolic, hemodynamic, and neurohormonal This effect is more common in patients who changes (Hedges & Redeker, 2008). For exam- have diabetes, perhaps related to their use of ple, in one study, on- and off-pump cardiac protamine-containing insulin. Anaphylaxis has surgery patients were evaluated at 24-hour been associated with administration of prota- intervals. Both groups of patients had elevated mine, and the affected patient may suffer car- cardiac markers and white blood cell, neu- diac arrest. Any adverse reaction to protamine trophil, and monocyte counts postoperatively; increases the risk of mortality for both ONCAB the levels were consistently and significantly and OPCAB patients (Welsby et al, 2005). higher in the on-pump group. In addition, the The critical care nurse must be vigilant in hematologic abnormalities persisted longer in monitoring for protamine reactions, including the on-pump group. Patients who underwent assessing the patient for different presentations OPCAB had less of a rise in serum lactate lev- of these reactions. Massive systemic vasodila- els. Those whose peak lactate level was greater tion is manifested by hypotension, decreased than 4.0 mmol/L were more likely to develop systemic vascular resistance (the amount of postoperative morbidities, including those work the heart must do to eject blood), and hemodynamic, pulmonary, and renal in nature increased cardiac output (the amount of blood as well as myocardial infarction. The same ejected by the heart every minute). Acute pul- group of patients had a greater tendency monary vasoconstriction will lead to an toward hypoxic episodes, were intubated increase in pulmonary artery pressures (PAP) longer, had a higher length of stay, and con- with subsequent right ventricular failure. The sumed more hospital resources. Three patients hemodynamic profile in this type of reaction in the on-pump group required postoperative will reveal bradycardia, decreased cardiac out- use of the IABP (Warang et al., 2007). put, elevated PAP, and elevated systemic and Hemodynamic alterations may occur after pulmonary vascular resistance. cardiac surgery. In one study, patients who In recent years, studies have tested new drugs underwent OPCAB developed a postoperative suggested as candidates to replace protamine increase in pulmonary artery pressure and a for reversing heparin and improve the safety of concomitant drop in cardiac output (Do et al., the bypass procedure for all CABG patients. 2002). In another study, patients receiving on- Unfortunately, none of these drugs has demon- pump cardiac surgery developed a decrease in strated a superior safety profile as compared to cardiac output and increase in SVR. These protamine during clinical trials (Stafford-Smith hemodynamic effects were attributed to the et al., 2005). As a consequence, heparin–prota- transient decline in triiodothyronine concen- mine remains the only drug combination trations that is associated with CABG. approved for use in the CPB circuit. Patients who received thyroid hormone peri- Recent studies have evaluated a direct operatively demonstrated improvement in car- thrombin inhibitor, bivalirudin (Angiomax®), diac output and SVR (Klemperer et al., 1995). as a replacement for heparin anticoagulation ■ for CPB and OPCAB. These studies indicate HEMODYNAMIC MONITORING that bivalirudin can be used safely in patients In the initial postoperative period for both with heparin allergy or increased risk for HIT ONCAB and OPCAB patients, the primary (Koster et al., 2006; Koster et al., 2007). Nurs- focus is hemodynamic stability. The first ing care for a patient receiving bivalirudin 6 hours postoperatively tends to be when includes astute monitoring of lab data and the patient is the most vulnerable and for bleeding. unstable. 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 119

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Cardiac dysfunction tends to manifest as 1% to 2% (Shekar, 2006). Nursing interventions decreased compliance and contractility from for both OPCAB and ONCAB patients include the pressure-overloaded myocardial tissue. A assessment for and prevention of these adverse pressure-overloaded ventricle will have events and preoperative teaching that includes reduced compliance and be stiff, which will a discussion of these potential risks. result in a decreased ejection fraction, cardiac OPCAB was developed to try to minimize output, and contractility. the risks of the cardiopulmonary bypass cir- Preoperative ischemia and duration of the cuit (Verma et al., 2004). A meta-analysis operative procedure contribute to instability in revealed a reduced incidence of stroke, atrial patients who undergo either on- or off-pump fibrillation, and infections with OPCAB as procedures. In the ONCAB patient, hemody- compared to ONCAB (Sedrakyan et al., 2006). namic instability is related to effects from the Women undergoing bypass surgery are at a CPB circuit and the cold potassium cardiople- higher risk for complications. Recent studies gia used to reduce myocardial oxygen demand. have also shown that OPCAB benefits women In contrast, manipulation of the beating heart by reducing their intraoperative and postoper- for OPCAB leads to decreased compliance and ative morbidity and mortality rates (Puskas et contractility (St. Andre & DelRossi, 2005). al., 2007). The off-pump bypass is technically A patient who has had valve replacement is more challenging than ONCAB, and critics typically volume overloaded (St. Andre & Del- cite this difference as a factor that complicates Rossi, 2005). In both ONCAB and OPCAB the process of setting up randomized con- surgeries, fluid needs may be higher than trolled studies and comparing outcomes for expected; thus the critical care nurse will need on- and off-pump procedures. Many studies to assess all interventions for their effect on that focus on OPCAB are observational, mak- hemodynamics to ensure adequate preload. ing the ability to generalize the results diffi- Hemodynamic profiles of cardiac surgery cult (Wijeysundera et al., 2005). patients are discussed in detail in Chapter 9.

Cognitive Decline ■ RISKS OF ON-PUMP SURGERY Cognitive decline has been noted in patients VERSUS OFF-PUMP SURGERY who have undergone coronary artery bypass. It A number of risks are associated with coronary had been theorized that this decline in func- artery bypass surgery, whether it is performed tion was related to the CPB circuit. In a recent on an on- or off-pump basis. Specifically, study comparing ONCAB, OPCAB, and healthy stroke, atrial fibrillation, acute renal failure, patients, however, researchers determined acute liver failure, bleeding, infection, and that the rate of cognitive decline in both types death have all been associated with on- and off- of surgery was the same. In this study, OPCAB pump surgery. proponents had theorized there would be less The ONCAB procedure and the CPB circuit cognitive decline without CPB. Demographic have shown to increase the risk for develop- data revealed that cognitive decline was pres- ment of acute renal failure, stroke, liver failure, ent prior to surgery in both the ONCAB and atrial fibrillation, and bleeding (Sedrakyan OPCAB groups at a higher level than in the et al., 2006). Use of the CPB circuit has also healthy patients (Selnes et al., 2007). At this been associated with the development of time, the decline in cognitive function does microemboli and SIRS. SIRS occurs in OPCAB not appear to be related to CPB. Cognitive patients, albeit to a lesser degree than in decline in patients undergoing coronary artery ONCAB patients (Raja, 2005). The risk of death bypass surgery will require more study to for both OPCAB and ONCAB is approximately determine the contributing factors. 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 120

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Table 7–1 Steps for Performing the Allen Test

Step 1: Simultaneously locate the radial and ulnar artery; palpate and compress them with three digits. Step 2: Maintaining compression on the radial and ulnar arteries, ask the patient to clench and unclench the hand 10 times. Step 3: Release pressure from the ulnar artery and monitor the time it takes for flushing to return to the palm, thumb, and nail beds. Step 4: If the amount of time it takes for flushing to return is greater than 6 seconds, this means that collateral flow is impaired. The radial artery should not be used as a graft.

Source: Asif & Sarkar, 2007.

Graft Occlusion for 6 months have produced patency rates Both on- and off-pump procedures utilize the similar to those for other arterial grafts at saphenous vein and arterial conduits for 5 years (Desai et al., 2007; Hayward et al., grafts. Saphenous vein harvesting is accom- 2007; Sajja, Mannam, & Sompalli, 2005). plished endoscopically, which reduces the Patient Assessment pain and scarring associated with the histori- Ongoing preoperative and ongoing postopera- cal harvest approach of an inner thigh to tive assessments are crucial for patients under- ankle incision (O’Hanlon, 2000). Vein grafts going radial artery harvest. In the preoperative are implanted in a reverse direction relative to phase, the nurse performs a detailed assessment their valves and have a higher occlusion rate of the patient’s history, activity level, and collat- when compared to the left internal thoracic eral ulnar blood flow to the affected hand(s). artery grafts (Desai et al., 2007). Collateral blood flow to the hand is most com- Arterial grafts include the left internal tho- monly assessed by using the Allen test. Specifi- racic artery, radial artery, and, less commonly, cally, the Allen test is used to assess the the right internal thoracic artery. The intratho- adequacy of blood supply to the hand through racic arteries, also known as mammary arteries, the ulnar artery. Table 7–1 outlines the perform- are used to bypass the anterior coronary circu- ance and evaluation criteria included on the lation and require only one anastomosis. The Allen test. The literature varies in interpretation elimination of anastomosis to the ascending of an Allen test, with 5 to 9 seconds being con- aorta may reduce emboli, which might other- sidered a positive result (Desai et al., 2007; Gur- wise cause stroke (St. Andre & DelRossi, 2005). buz, Findik, Cui, & Aytac, 2007; Hayward et al., Arterial grafts have been shown to decrease the 2007). The recommended contraindication for need for revascularization and reduce short- radial graft harvest is a positive Allen test (the and long-term mortality; approximately 80% of red color of the palm returns) in greater than these grafts are still patent 8 years after 6 seconds (Asif & Sarkar, 2007). A positive Allen implantation (St. Andre & DelRossi, 2005). test has been reported to have a predictive value The radial artery, which was first utilized as of 53%, which means there is a need to investi- a graft in the 1970s, has regained popularity as gate collateral flow further. a graft in recent years due to its long patency Techniques to more closely examine collat- duration (Hayward, Hare, Gordon, Matalanis, eral flow include the use of Doppler flow mea- & Buxton, 2007). Improved harvest tech- surements, thumb systolic pressure, finger-pulse niques for radial artery grafts and the use of plethysmography, and pulse oximetry (Asif & calcium channel blockers intraoperatively and Sarkar, 2007). Some sources suggest that the ® postoperatively (e.g., diltiazem [Cardizem ]) Allen test could give a false-negative result and 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 121

Summary 121

that, regardless of the results, it is always ered loosely with a gauze dressing and mandatory to have a preoperative ultrasound wrapped with a compressive wrap for 24 study if radial artery harvesting is being consid- hours (Schouchoff & Belhumeir, 2000). ered (Agrifoglio et al., 2005). Postoperative assessment of the affected Patients who perform manual labor, are extremity includes the amount and quality of physically active with their hands, have suf- drainage, signs and symptoms of infection, fered a stroke with upper limb involvement, and the six P’s for diminished arterial blood have peripheral vascular disease, Raynaud’s flow (i.e., pain, pulselessness, pallor, paresthe- disease, or experienced a traumatic injury to sia, paralysis, and polar [cold]). Patients should the affected side should not be considered can- be made aware that they may experience loss of didates for radial artery harvest (Desai et al., motor strength and numbness on the affected 2007; Hayward et al., 2007; Serricchio et al., extremity. These symptoms usually resolve in 1999; Shah et al., 2007). Additionally, smok- most patients 6 months postoperatively. ing, diabetes, hypertension, and hyperlipi- Patients who smoke report higher levels of sen- demia have been associated with diminished sory loss but no difference in motor function radial artery graft patency rates. Recent data compared to nonsmokers (Shah et al., 2007). suggest that patients with peripheral vascular disease are more likely to have early occlusion Compartment Syndrome of a radial artery graft (Desai et al., 2007). The literature reports a rare occurrence of com- Data from one small prospective study sug- partment syndrome in the vein donor limbs for gest that radial artery graft patency rates are coronary artery bypass (James, Friedman, Scher, decreased in the OPCAB population (Gurbuz & Hall, 2002). Nursing assessment of the donor et al., 2007). Desai and colleagues (2007) report limb should include assessment for diminished that women are more likely to have longer blood flow. Like their counterparts undergoing graft patency with radial artery grafts when radial artery harvesting, vein graft donors should compared to saphenous vein grafts for non-left have the six P’s assessed. Early symptoms of anterior descending bypasses. Although more compartment syndrome include severe pain and studies on this topic are necessary, the current tenderness on passive stretch. This assessment evidence points to women benefiting from may be masked by the use of sedation and nar- complete arterial revascularization instead of cotic analgesia in the early postoperative period. vein grafting and to patients with peripheral The demonstrated decrease in complica- vascular disease benefiting from vein grafts. tions with OPCAB has had the benefit of reducing the cost of performing CABG Radial Artery Harvesting (Raja, 2005). Other factors contributing to In the early development of radial artery har- the reduction in cost for OPCAB are vesting, it was recommended that the non- shorter lengths of stay in the ICU, shorter dominant hand be the site of harvest owing intubation times, and decreased use of to fear of hand ischemia. Shah and colleagues blood products due to diminished blood (2007) suggest that harvesting of radial arter- loss (Bayrak et al., 2007). Despite the ies from the dominant hand can be accom- mounting evidence that OPCAB has some plished safely with minimal adverse effects for advantages over ONCAB, the majority of the patient, as hand ischemia is actually a rare bypass surgeries performed in the United occurrence. Depending on surgeon prefer- States remain on-pump procedures. ence, the radial artery donor site may or may not have a drain placed. If a drain is placed, it ■ SUMMARY is usually removed when drainage is less than Nursing care of both on- and off-pump coro- 20 mL for 8 hours. The incision will be cov- nary artery bypass patients continues to 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 122

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advance as evidence mounts regarding the with the use of off-pump procedures has also risks and advantages of each procedure. On- been documented. As the techniques and uti- and off-pump patients remain at risk for a lization of off-pump surgery continue to myriad of complications. Patients who evolve, so will the skill and practice of the undergo off-pump procedures tend to experi- expert cardiac surgery nurse. Care of these ence a lower incidence of stroke, infection, patients will continue to be highly challeng- and atrial fibrillation; a notable cost savings ing and rewarding.

CASE STUDY

A 49-year-old female is scheduled for off-pump bypass surgery utilizing the left internal mammary artery, radial artery, and saphenous veins for grafts. She is 4 days post inferior wall myocardial infarction. Her coronary angiogram showed three-vessel disease with multiple distal stenoses. The patient has a history of hypertension and type II diabetes. She smoked in her twenties but has been smoke free for 20 years.

Critical Thinking Questions 1. Identify three teaching points important for this patient. 2. Discuss the use of radial artery grafts in women. 3. Compare and contrast the advantages/disadvantages of on- and off-pump coronary artery bypass surgery. Answers to Critical Thinking Questions 1. a. Discuss the risks and possible complications of CABG. b. Discuss lifestyle changes and medications needed postoperatively to help ensure long graft survival. Education should be provided on medications, dietary modifications, management of diabetes and high blood pressure, and stress reduction. c. Discuss the graft site locations and the postoperative care. 2. Arterial grafts are typically recommended given that they have been found to have longer patency durations than saphenous veins. Given its superior quality, the length of function- ality of the radial artery is thought to decrease the need for repeat operations. Studies report that 5-year survival among women who received a radial artery graft was significantly better than among women who did not receive such a graft (Lawton et al., 2005). 3. a. Off-pump CABG does not require that the patient’s heart be stopped and that a heart–lung machine be used. Instead, the surgeon uses a stabilizer to hold the tissue in place while the heart is still beating. b. Off-pump CABG usually reduces the need for blood transfusion during the procedure and results in shorter hospital stays. c. A lower rate of complications is seen with off-pump CABG. Patients are less likely to experience stroke, memory impairment, or decreased ability to concentrate.

■ SELF-ASSESSMENT QUESTIONS b. Liver failure, bleeding, and decreased cognitive function 1. Off-pump bypass has been associated c. Stroke, infection, and atrial with reduced rates for which of the fol- fibrillation lowing complications? d. SIRS, renal failure, and microemboli a. Renal failure, sepsis, and death formation 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 123

Self-Assessment Questions 123

2. Patients with which of the following b. Increased SVR, decreased pulmonary characteristics are more likely to have a artery pressures, and hypertension protamine reaction? c. Hypotension and increased SVR and a. Allergy to fish cardiac output b. Renal failure, on dialysis d. Increased pulmonary artery pressures c. Type II diabetes, taking Glucophage and decreased SVR and cardiac output d. Bleeding disorder 7. Narrowing pulse pressures and clots in 3. Contraindications to radial artery graft the mediastinal tubes could indicate harvest include which of the following? ______in both on- and off-pump coro- a. Allen test of 18 seconds in the nary artery bypass patients. nondominant hand a. bleeding b. Male patient who lays tile for a living b. cardiac tamponade c. Female patient with a history of c. protamine reaction Raynaud’s disease d. systemic inflammatory response d. All of the above syndrome 4. Surgeons may opt to use which of the 8. The cost reductions noted with OPCAB following agents for anticoagulation in have been linked to the CPB circuit for patients with a previ- a. increased use of blood products. ous history of heparin-induced throm- b. endoscopic harvest of saphenous vein bocytopenia? grafts. a. Enoxaparin c. use of cardioplegia. b. Bivalirudin d. decreased complication rates. c. Heparin 9. Off-pump patients have a reduced inci- d. Protamine sulfate dence of AV blocks and do not have 5. A patient has been admitted for OPCAB. epicardial pacing wires placed intraoper- Your preoperative assessment reveals atively. cool and pale fingertips. The patient a. True reports weakness from a previous stroke b. False in the donor arm. The surgeon is at the 10. SIRS has been identified in both on- and bedside requesting that the patient sign off-pump bypass patients. A factor that the consent form. What should you do? could worsen the systemic vasodilation a. Encourage the patient to sign and associated with SIRS is witness the signature. a. rewarming the patient. b. Perform the Allen test to assess for b. prolonged hypothermia. collateral flow from the ulnar artery. c. fluid resuscitation. c. Ask to speak to the surgeon in private d. administration of vasopressors. regarding your assessment findings. d. Explain the procedure to the patient, Answers to Self-Assessment Questions including its potential risks and benefits. 1. c 6. a 6. Protamine reactions in coronary artery 2. a 7. b bypass patients present with which of 3. d 8. d the following signs and symptoms? 4. b 9. b a. Decreased SVR, hypotension, and increased cardiac output 5. c 10. a 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 124

124 Chapter 7 Cardiopulmonary Bypass and Off-Pump Coronary Artery Bypass

Clinical Inquiry Box

Question: Is there a difference in sleep patterns postoperatively between on-pump and off-pump CABG? Reference: Hedges, C., & Redeker, N. S. (2008). Comparison of sleep and mood in patients after on-pump and off-pump coronary artery bypass surgery. American Journal of Critical Care, 17(2), 133–139. Objective: To examine sleep and mood of patients having cardiac surgery with the on- and off- pump techniques. Methods: After the second postoperative night while staying on a cardiac step-down unit, 129 cardiac surgery patients were asked to complete the Pittsburg Sleep Quality Index, a sleep diary, and the Profile of Mood States tool. Subjects wore wrist actigraphs for measuring movement at night. The sample consisted of 48 patients who underwent on-pump surgery and 81 patients who underwent off-pump surgery. Results: There was no significant difference between groups on subjective sleep characteristics, mood disturbance, or preoperative sleep quality. Off-pump CABG was associated with less movement as measured by the actigraphs, indicating fewer awakenings. There was no length of sleep difference between the groups. No gender-related difference in outcomes was noted in either the on-pump or off-pump group. Conclusion: Given that this study was limited by the small sample size, further studies are needed to examine the differences in sleep between on- and off-pump patients. Relationships among sleep and mood should be examined in relation to other variables, such as acuity level, comorbidities, type of cardiac surgery, history of sleep apnea, and characteristics of the hospital environment such as staffing ratios. Cardiac nurses should be aware of the importance of sleep in all cardiac surgery patients. Regardless of whether an on-pump or off-pump surgical approach is used, they should provide interventions that promote sleep in postoperative patients.

■ REFERENCES Asif, M., & Sarkar, P. K. (2007). Three digit Allen Abu-Omar, Y., Balacumaraswami, L., Pigott, D. W., test. Annals of Thoracic Surgery, 84, 686–687. Matthews, P. M., & Taggart, D. P. (2004). Solid Bayrak, S., Özsöyler, I., Yetkin, U., Pamuk B., and gaseous cerebral microembolization dur- Yakut, N., Karahan, N., et al. (2007). Compari- ing off-pump, on-pump, and open cardiac sur- son of beating heart coronary artery surgery gery procedures. Journal of Thoracic and and conventional CABG with regard to cost Cardiovascular Surgery, 127(6), 1759–1765. effectiveness. Internet Journal of Thoracic Cardio- Agrifoglio, M., Dainese, L., Pasotti, S., Galanti, A., vascular Surgery, 10(2). Retrieved December 12, Cannata, A., Roberto, M., et al. (2005). Preop- 2007 from http://www.ispub.com/ostia/ erative assessment of the radial artery for coro- index.php?xmlFliePath=journals/ijtcvs/vol10n2/ nary artery bypass grafting: Is the clinical Allen cabg.xml test adequate? Annals of Thoracic Surgery, 79(2), Boudrez, H., & De Backer, G. (2001). Psychological 570–572. status and the role of coping style after coro- Arslan, Y., Tarhan, A., & Yilmaz, M. (2005). Life threat- nary artery bypass surgery: Results of a ening protamine reactions in cardiac surgery: prospective study. Quality Life Research, 10(1), Literature review with a case report. Internet 37–47. Journal of Thoracic Cardiovascular Surgery, 7(1). Bruins, P., te Velthuis, H., Yazdanbakhsh, A. P., Retrieved December 12, 2007, from http:// Jansen, P., van Hardevelt, F., de Beaumont, E., www.ispub.com/ostia/index.php et al. (1997). Activation of the complement ?xmlFilePath=journals/ijtcvs/vol7n1/ system during and after cardiopulmonary protamine.xml bypass surgery: Postsurgery activation involves 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 125

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C-reactive protein and is associated with post- Hedges, C., & Redeker, N. S. (2008). Comparison of operative arrhythmia. Circulation, 96(10), sleep and mood in patients after on-pump and 3542–3548. off-pump coronary artery bypass surgery. Castellheim, A., Hoel, T. N., Videm, V., Fosse, E., American Journal of Critical Care, 17(2), 133–140. Pharo, A., Svennevig, J. L., et al. (2008). Bio- James, T., Friedman, S. G., Scher, L., & Hall, M. marker profile in off-pump and on-pump (2002). Lower extremity compartment syn- coronary artery bypass grafting surgery in low- drome after coronary artery bypass. Journal of risk patients. Annals of Thoracic Surgery, 85(6), Vascular Surgery, 36(5), 1069–1070. 1994–2002. Kimmel, S. E., Sekeres, M. A., Berlin, J. A., Ellison, Demaria, R. G., Carrier, M., Fortier, S., Roland G., N., DiSesa, V. J., & Strom, B. L. (1998). Risk Martineau, R., Fortier, A., et al. (2002). factors for clinically important adverse events Reduced mortality and strokes with off-pump after protamine administration following car- coronary artery bypass grafting surgery in diopulmonary bypass. Journal of the American octogenarians. Circulation, 106(12 suppl 1), College of Cardiology, 32(7), 1916–1922. I5–I10. Kimmel, S. E., Sekeres, M. A., Berlin, J. A., Gold- Desai, N. D., Naylor, C. D., Kiss, A., Cohen, E. A., berg, L. R., & Strom, B. L. (1998). Adverse Feder-Elituv, R., Miwa, S., et al. (2007). Impact events after protamine administration in of patient and target-vessel characteristics on patients undergoing cardiopulmonary bypass: arterial and venous bypass graft patency: Risks and predictors of under-reporting. Jour- Insight from a randomized trial. Circulation, nal of Clinical Epidemiology, 51(1), 1–10. 115(6), 684–691. Klemperer, J. D., Klein, I., Gomez, M., Helm, R. E., Do, Q., Goyer, C., Chavanon, O., Couture, P., Ojamaa, K., Thomas, S. J., et al. (1995). Thy- Denault, A., & Cartier, R. (2002). Hemody- roid hormone treatment after coronary-artery namic changes during off-pump CABG sur- bypass surgery. New England Journal of Medicine, gery. European Journal of Cardio-Thoracic Surgery, 333(23), 1522–1527. 21(3), 385–390. Koster, A., Dyke, C. M., Aldea, G., Smedira, N.G., Duits, A. A., Boeke, S., Taams, M. A., Passchier, J., & McCarthy, H. L., Aronson, S., et al. (2007). Erdman, R. A. (1997). Prediction of quality of Bivalirudin during cardiopulmonary bypass in life after coronary artery bypass graft surgery: patients with previous or acute heparin- A review and evaluation of multiple, recent induced thrombocytopenia and heparin anti- studies. Psychosomatic Medicine, 59(3), 257–268. bodies: Results of the CHOOSE-ON trial. Fearn, S. J., Pole, R., Wesnes, K., Faragher, E. B., Annals of Thoracic Surgery, 83(2), 572–577. Hooper, T. L., & McCollum, C. N. (2001). Cere- Koster, A., Spiess, B., Jurmann, M., Dyke, C. M., bral injury during cardiopulmonary bypass: Smedira, N. G., Aronson, S., et al. (2006). Emboli impair memory. Journal of Thoracic and Bivalirudin provides rapid effective and reliable Cardiovascular Surgery, 12(6), 1150–1160. anticoagulation during off-pump coronary Gallagher, R., & McKinley, S. (2007). Stressors and revascularization: Results of the EVOLUTION anxiety in patients undergoing coronary artery OFF trial. Anesthesia & Analgesia, 103(3), 540–544. bypass surgery. American Journal of Critical Care, Lawton, J. S., Barner, H. B., Bailey, M. S., Guthrie 16(3), 248–257. T. J., Moazami N., Pasque M. K., et al. (2005). Gurbuz, A. T., Findik, O., Cui, H., & Aytac, A. Radial artery grafts in women: Utilization and (2007). Radial artery graft use and off-pump results. Annals of Thoracic Surgery, 80(2), 559–563. coronary artery bypass surgery outcomes. Asian Nelson, F. V., Zimmerman, L., Barnason, S., Cardiovascular Thoracic Annals, 15(2), 106–112. Nieveen, J., & Schmaderer, M. (1998). The rela- Hayward, P. A., Hare, D. L., Gordon, I., Matalanis, G., tionship and influence of anxiety on postoper- & Buxton, B. F. (2007). Which arterial con- ative pain in the coronary artery bypass graft duit? Radial artery versus free right internal patient. Journal of Pain Symptom Management, thoracic artery: Six year clinical results of a 15(2), 102–109. randomized controlled trial. Annals of Thoracic O’Hanlon, J. V. (2000). Minimally invasive saphe- Surgery, 84(2), 493–497. nous vein harvesting. Critical Care Nursing Quarterly, 23(1), 42–46. 57625_CH07_115_126.pdf 4/10/09 11:06 AM Page 126

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Puskas, J. D., Kilgo, D. D., Kutner, M., Pusca, S. V., St. Andre, A. C., & DelRossi, A. (2005). Hemody- Lattouf, O., & Guyton, R. (2007). Off-pump namic management of patients in the first 24 techniques disproportionately benefit women hours after cardiac surgery. Critical Care Medi- and narrow the gender disparity in outcomes cine, 33(9), 2082–2093. after coronary artery bypass surgery. Circula- Verma, S., Fedak, P. W., Weisel, R. D., Szmitko, P. E., tion, 116(suppl I), I192–I199. Badiwala, M. V., & Bonneau, D. (2004). Off- Raja, S. G. (2005). Pump or no pump for coronary pump coronary artery bypass surgery: Funda- artery bypass: Current best available evidence. mentals for the clinical cardiologist. Texas Heart Institute Journal, 32(4), 489–501. Circulation, 109(10), 1206–1211. Sajja, L. R., Mannam, G., & Sompalli, S. (2005). Warang, M., Waradkar, A., Patwardhan, A., Extrafascially harvested radial artery in CABG: Agrawal, N., Kane, D., Parulkar, G., et al. Technique of harvest, complications, and mid- (2007). Metabolic changes and clinical out- term angiographic patency. Journal of Cardiac comes in patients undergoing on and off Surgery, 20(5), 440–448. pump coronary artery bypass surgery. Indian Schouchoff, B., & Belhumeir, J. (2000). Radial Journal of Thoracic Cardiovascular Surgery, 23(1), artery: An alternative revascularization con- 9–15. duit. Critical Care Nursing Quarterly, 23(1), Welsby, U., Newman, M. F., Phillips-Bute, B., 28–34. Messier, R. H., Kakkis, E. M., & Stafford- Sedrakyan, A., Wu, A. W., Parashar, A., Bass, E. B., Smith, M. (2005). Hemodynamic changes after & Treasure, T. (2006). Off-pump surgery is protamine administration: Association with associated with reduced occurrence of stroke mortality after coronary artery bypass surgery. and other morbidity as compared with tradi- Anesthesiology, 102(2), 308–314. tional coronary artery bypass grafting: A meta- Wijeysundera, D. M., Beattie, W. S., Djaiani, G., analysis for systematically reviewed trials. Rao, V., Borger, M. A., Karkouti, K., et al. Stroke, 37(11), 2759–2769. (2005). Off-pump coronary artery surgery for Selnes, O. A., Grega, M. A., Bailey, M. M., Pham, L., reducing mortality and morbidity: Meta- Zeger, S., Baumgartner, W. A., et al. (2007). Neu- analysis of randomized and observational rocognitive outcomes 3 years after coronary studies. Journal of the American College of Cardiol- artery bypass graft surgery: A controlled study. ogy, 46(5), 872–882. Annals of Thoracic Surgery, 84(6), 1885–1896. Zenati, M. A. (2005). Off pump coronary artery Serricchio, M., Gaudino, M., Tondi, P., Gasbarrini, bypass (OPCAB). Retrieved December 22, A., Gerardino, L., Santoliquido, A., et al. 2007, from http://www.ctsnet.org/sections/ (1999). Hemodynamic and functional conse- clinicalresources/adultcardiac/expert_ quences of radial artery removal for coronary tech.html artery bypass grafting. American Journal of Car- diology, 84(11), 1353–1356. ■ WEB RESOURCES Shah, S. A., Chark, D., Williams, J., Hessheimer, A., Huh, J., Wu, Y., et al. (2007). Retrospective Off-Pump Video: In a Webcast from Memorial analysis of local sensorimotor deficits after Hermann Heart and Vascular Institute in radial artery harvesting for coronary artery Houston, TX, cardiovascular and thoracic sur- bypass grafting. Journal of Surgery Research, geons Miguel Gomez, M.D., and Donald Gib- 139(2), 203–208. son, M.D., give the general public a rare Shekar, P. S. (2006). Cardiology patient page: On- glimpse into the operating room to view sur- pump and off-pump coronary artery bypass gery “off pump,” on a beating heart. URL: grafting. Circulation, 113(4), e51–e52. http://video.google.com/videoplay?docid=901 4695099760440284&q=on+pump+and+off Stafford-Smith, M., Lefrak, E. A., Qazi, A. G., Welsby, I. J., Barber, L., Hoeft, A., et al. (2005). CABG Video for Patient and Families: http:// Efficacy and safety of heparinase I versus prot- www.brightcove.tv/title.jsp?title=627018303& amine in patients undergoing coronary artery channel=537078573 bypass grafting with and without cardiopulmonary bypass. Anesthesiology, 103(2), 229–240. 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 127

Chapter 8 Recovery from Anesthesia

Toni Patrice Johnson

■ INTRODUCTION According to the American Heart Association should include pertinent information regard- (AHA, 2008), more than 6.9 million cardiac ing the surgical procedure, any intraoperative procedures were performed in the United complications or events, hemodynamic and States in 2005. Of these procedures per- ventilatory status, cardiopulmonary bypass formed, 699,000 total open-heart procedures (CPB) time, recent laboratory data, type and were reported (AHA, 2009). Thousands of car- amount of intravenous fluids and blood diac surgery patients have enjoyed speedy products administered, reversal of anticoagu- recovery times, thanks to advances in surgical lants, pertinent medical and surgical history, techniques, anesthetic agents, and postopera- preoperative status, location of intravenous tive medications. More importantly, improve- lines and invasive catheters, vasopressor and ments in anesthetic techniques have allowed inotropic agents used, and current infusion patients to transition quickly from the inten- rates. Additional information includes use of sive care unit (ICU) for the immediate postop- mechanical cardiac assist devices, presence of erative period to a general unit and then pacing wires, length of surgery, estimated home in increasingly shorter periods of time. blood loss, intraoperative intake and output, Given these trends, ICU nurses must be assid- patient position on the OR table, location of uous in the care of these patients. This chap- drains and dressings, and anesthetic and ter focuses on care in the immediate reversal agents administered. Table 8–1 lists postoperative period. the more common anesthetic agents used. In addition to the information provided by the anesthesia provider, an extensive preoper- ■ HAND-OFF COMMUNICATION ative evaluation is conducted prior to cardiac Postoperative care begins immediately after surgery. Details of this evaluation are the patient is transferred from the operating described in Chapter 4. Information about room (OR). Following cardiac surgery, existing comorbidities, cardiac disease, patients are typically transferred to the ICU tobacco use, nutritional status, medication for monitoring, hemodynamic stabilization, history, preoperative cardiac status, and any assessment for complications, and possibly optimizing that might have taken place prior extubation. Vital information is exchanged in to surgery will help the ICU nurse anticipate the hand-off communication between the the patient’s immediate postoperative course anesthesia provider and the ICU nurse. Data and potentially required interventions. By way

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Table 8–1 Anesthetic Agents/ A patient’s comorbidities may also help the Adjuncts Commonly Used in Cardiac ICU nurse anticipate problems in the imme- Surgery diate postoperative period. For example, patients with a history of conditions such as Intravenous Induction Agents valvular disease, recent myocardial infarction (MI), arterial hypertension, diabetes, previous Propofol (Diprivan®) Etomidate (Amidate®) cardiac surgery, chronic peripheral vascular Thiopental sodium (Pentothal®) disease, involvement of three or more vessels, Methohexital (Brevital®) elevated serum creatinine, ejection fraction less than 40%, or COPD are more likely to Neuromuscular Blocking Agents require prolonged mechanical ventilation Rocuronium (Zemuron®) (Suematsu et al., 2000). Vecuronium (Norcuron®) If the patient underwent CPB, the potential Succinylcholine (Anectine®) for a systemic inflammatory response with ® Atracurium besylate (Tracrium ) associated hemodynamic effects should be ® Mivacurium chloride (Mivacron ) anticipated. As described in Chapter 13, the cis-Atracurium (Nimbex®) inflammatory response may be related to the Doxacurium (Raplon®) Pancuronium (Pavulon®) surface of the CPB circuit being in contact Tubocurarine with blood or reperfusion injury associated Metocurine with aortic cross-clamping (Laffey, Boylan, & Cheng, 2002). Analgesics/Sedatives ® Fentanyl (Sublimaze ) ■ Sufentanil (Sufenta®) IMMEDIATE POSTOPERATIVE Alfentanil (Alfenta®) CARE ® Remifentanil (Ultiva ) The foremost objectives when caring for a car- Morphine sulfate diac surgery patient in the immediate postop- Midazolam (Versed®) Lorazepam (Ativan®) erative period are maintenance of cardiac perfusion and maximization of tissue perfu- Inhalation Agents sion (Baltimore, 2001; Smartt, 2004). Goals of the first hour of care include stabilization of Isoflurane (Forane®) Sevoflurane (Ultane®) hemodynamic, oxygenation, and thermoregu- Enflurane (Ethrane®) latory status. Postoperative care requires Halothane (Fluothane®) assessment of physiologic parameters and hemodynamic monitoring, as well as assess- Sources: Dozier, 2007; Savino & Cheung, 2008. ment, prompt recognition, and treatment of potential complications that are related to either patient comorbidities, effects of anesthesia, or the surgical procedure itself. of illustration, as discussed in Chapter 5, the Control of the cardiac surgery patient’s hemodynamic profile and resultant interven- blood pressure in the immediate postopera- tions indicated for patients who undergo car- tive period is important. The ICU nurse diac surgery for valvular disease will vary with should monitor for hypertension to avoid the pathophysiology of each of the respective associated complications such as bleeding, disorders (e.g., aortic insufficiency versus myocardial ischemia, dysrhythmias, stroke, or stenosis) (Khalpey, Ganim, & Rawn, 2008). graft dehiscence. Initial management of 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 129

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hypertension may entail administration of chest expansion, and respiratory rate, depth, opioids, sedatives, or both. However, infusion effort, and rhythm. If the patient remains on of a vasodilator may be required if initial ther- mechanical ventilation, assessment of tube apies are not effective in controlling hyperten- placement by the markings on the endotra- sion (Karski et al., 2001). cheal tube should be noted, and ventilator settings (e.g., mode, fractional inspired oxygen [FiO ], rate, tidal volume, positive end-expira- ■ 2 ASSESSMENT tory pressure [PEEP], pressure support, alarm The nurse performs a detailed physical assess- settings) should be verified as applicable. Typi- ment. ECG monitoring of heart rate and cal ventilator settings in the immediate post- rhythm is performed. The patient’s hemody- operative period following cardiac surgery are namic profile (e.g., blood pressure, pulmonary discussed in Chapter 11. Once these data are artery pressures, pulmonary artery occlusive obtained, the patient’s respiratory status can pressure [PAOP], central venous pressure be correlated with pulse oximetry and ABG [CVP], cardiac output/index, and systemic vas- results. A baseline chest radiograph should be cular resistance [SVR]); temperature; and pulse obtained to verify placement of the endotra- oximetry are evaluated. Additional invasive cheal tube (2 to 3 cm above the carina), monitoring (e.g., mixed venous saturation) may catheters, wires, or any other devices that were be monitored as well. The ICU nurse can then inserted in the OR. The presence of any post- correlate these findings with an assessment of operative atelectasis, pneumothorax, or other peripheral perfusion. If temporary pacing wires common respiratory complication following are present, they should be checked to ensure cardiac surgery can also be determined proper function for emergent temporary pac- (Khalpey et al., 2008). ing. A baseline postoperative ECG should be Types and number of drainage catheters attained to determine presence of ischemia, will vary based on the operative procedure infarction, conduction abnormalities, or graft and approach used. If a minimally invasive spasm (Khalpey et al., 2008). approach is used, a small-diameter catheter Assessment of neurologic status typically will be noted. If the patient had a sternotomy includes level of consciousness, degree of ori- but the pleural space is not opened, the entation, pupil size and reaction, and ability to patient will have a mediastinal chest tube, or a move extremities. A more in-depth neurologic chest tube in the mediastinal and pleural assessment may follow later in the postopera- spaces will be present (Baltimore, 2001). tive period. Inherent in a neurologic assess- Tubes are connected to –20 cm of wall suc- ment is an initial and ongoing assessment of tion. The ICU nurse should assess the pain. If the patient is able to self-report the amount, color, and viscosity of initial opera- level of pain, that is the most reliable indicator. tive and subsequent drainage. Patency of the The ICU nurse should differentiate incisional catheters must be maintained at all times. If pain from anginal pain. If the patient is cogni- the patient is experiencing bleeding, then vol- tively impaired and cannot self-report, use of a ume repletion, treatment of the underlying valid and reliable behavioral pain rating scale cause (if possible), and monitoring of the should be used. Management of pain in the patient’s coagulation profile are indicated postoperative cardiac surgery patient is dis- (Baltimore, 2001). Surgical reexploration may cussed in detail in Chapter 14. be indicated if blood loss exceeds 200 mL/hr An initial respiratory assessment typically for 4 hours, 300 mL/hr for 3 hours, 400 mL/hr includes auscultation of breath sounds, oxy- for 2 hours, or 500 mL/hr for 1 hour (Khalpey gen delivery mode, presence of symmetrical et al., 2008; St. Andre & DelRossi, 2005). 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 130

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If a mediastinal chest tube becomes clotted, mechanical ventilation time; and promoting a cardiac tamponade may ensue. Signs and quicker, uneventful recovery from anesthesia. symptoms may include sudden decrease or Typically, shorter-acting agents—although cessation of mediastinal bleeding, dyspnea, more costly—result in earlier extubation and decreased cardiac output (CO) and hypoten- reduced postoperative stays (Myles & McIlroy, sion, tachycardia, low-voltage QRS on ECG, 2005). It is important for the ICU nurse to increased CVP, altered mental status, cyanosis recognize signs and symptoms, multisystem or pallor, anxiety, and restlessness (Talmor & effects, and postoperative nursing implica- Lisbon, 2005). Other signs and symptoms are tions of commonly used anesthetic agents described in Chapter 13. administered during surgery. Preventive measures include positioning the patient on the side with the head of the bed elevated 30 degrees, to facilitate Induction Agents drainage of the catheters. Until the condi- Combinations of intravenous agents are tion is treated, the ICU nurse should administered to augment the effects of inhala- administer volume to help counteract the tion agents. Classifications of these agents decrease in preload from the associated include barbiturates (e.g., thiopental sodium, decrease in diastolic filling pressures of the methohexital), nonbarbiturates (e.g., etomi- tamponade. Administration of afterload date, propofol), and tranquilizers (e.g., mida- reducers (i.e., vasodilator) may help pro- zolam, lorazepam) (Dozier, 2007; Savino & mote contractility (Baltimore, 2001). Car- Cheung, 2008). diac tamponade management is discussed Barbiturates depress the central nervous in detail in Chapter 13. system (CNS). Thiopental sodium, for exam- An initial assessment of the patient’s fluid ple, causes cardiovascular depression and neg- and electrolyte status should be performed ative inotropy, resulting in hypotension, upon admission to the ICU. In addition to decreased CO, and peripheral vascular resist- the output from drains, a correlation between ance. Barbiturates also cause respiratory the patient’s hemodynamic status and the depression, which puts the patient at risk for intraoperative intake and output of fluids apnea, airway obstruction, and, at higher should be made. The ICU nurse should antici- doses, loss of laryngeal reflexes; the latter pate third spacing of fluid in the immediate effect puts the patient at risk for aspiration postoperative period (Khalpey et al., 2008). (Dozier, 2007; Savino & Cheung, 2008). Other Evaluation of serum electrolytes should be side effects may include headache, emergence included in the initial assessment, as imbal- delirium, prolonged somnolence, and nausea. ances may be anticipated. Anticipated alter- Nursing considerations include monitoring ations and management of fluid and for the prolonged effects of thiopental, which electrolytes in the postoperative cardiac surgery could persist for as long as 36 hours (Schick, patient are discussed in detail in Chapter 17. 2004). Etomidate is a hypnotic agent with no analgesic effects. It is considered the agent of ■ ANESTHETIC AGENTS choice in patients with cardiovascular insta- “Balanced” anesthesia or “fast-tracking” is bility. When this agent is used, it is less likely generally employed to facilitate early extuba- to cause hypotension. Heart rate, contractil- tion of the cardiac surgery patient while con- ity, and CO remain stable, and negative comitantly decreasing anxiety, pain, length of inotropic effects are negligible with etomidate ICU stay, and complications; minimizing (Savino & Cheung, 2008; Schick, 2004). Some 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 131

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patients may develop postoperative nausea which generally manifest during the immedi- and vomiting (PONV), hiccoughs, involun- ate postoperative period. Inhalation agents tary tremors, or suppressed adrenal function typically do not possess analgesic properties. following administration of etomidate They are eliminated through the lungs; the (Dozier, 2007). amount of time it takes depends on the Propofol (Diprivan) is a sedative that is pri- patient’s CO. Patients will require oxygen marily used as an induction agent. Compared therapy and encouragement to cough and with barbiturates, it causes less myocardial deep breathe (Dozier, 2007). Hemodynamic depression. Hypotension seen following monitoring is essential given the sensitization propofol administration is felt to be related to catecholamines associated with many of to arterial and venous dilation (Savino & these inhalation agents. Cheung, 2008). An infusion of propofol is Because some of the inhalation agents are fat generally initiated en route to the ICU and soluble and are absorbed into adipose tissue, discontinued 10 to 15 minutes prior to venti- elimination and recovery times are longer when lator weaning. The maintenance infusion rate these agents are given. Further, patients with is 50 to 150 mcg/kg/min. Propofol has a low higher percentages of body fat will have a incidence of postoperative side effects and is longer recovery time when administered fat sol- less likely to cause PONV than etomidate. It uble inhalation agents. Prompt management of allows the patient to quickly regain con- pain and PONV are other vital ICU nursing sciousness with minimal residual CNS effects, responsibilities at this time (Dozier, 2007). allowing for early extubation. As propofol has Sevoflurane and halothane have depressant no analgesic properties, postoperative anal- effects on the respiratory system. Additionally, gesics will be required (Drain, 2003). smooth bronchial muscles, laryngeal, and pha- Benzodiazepines are used as adjuncts to ryngeal reflexes are blunted by these agents, induction agents prior to cardiac surgery. placing the patient at risk for aspiration. Midazolam (Versed®) may also be used post- Sevoflurane and halothane side effects may operatively for sedation in the patient who include decreased responsiveness to oxygena- remains intubated. This agent can cause res- tion and ventilation and elevated carbon diox- piratory depression and mild vasodilation, ide levels. Halothane decreases mucociliary but it minimizes PONV (Couture, May, function for as long as 6 hours, which O’Brien, & Smith, 2006). Nursing considera- increases the patient’s risk for atelectasis and tions include monitoring of vital signs and pneumonia. Its cardiovascular effects include oxygen saturation. If severe, respiratory myocardial depression and peripheral vasodila- depression may be reversed by administering tion. Two benefits of halothane are the associated flumazenil (Romazicon®) (Dozier, 2007). low incidence of PONV and its bronchodilator properties, making this agent useful in patients with pulmonary disease (Dozier, 2007). Sevoflu- Inhalation Agents rane does not appear to irritate the respiratory Inhalation agents cause circulatory depres- system or to sensitize the heart to cate- sion and hypotension as a result of vasodila- cholamines, although it may cause hypotension tion and decreased contractility (Savino & by decreasing afterload (Dozier, 2007). Cheung, 2008). They may be administered Enflurane and isoflurane may cause laryn- either alone or in combination with intra- gospasm, coughing, and breath holding. venous anesthetics (Schick, 2004). Nursing These side effects predispose the patient to considerations include monitoring for ven- non-cardiogenic pulmonary edema. Attri- tricular ectopy, fibrillation, and tachycardia, butes of isoflurane include that it is not 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 132

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associated with increased cardiac sensitiza- tem) (Savino & Cheung, 2008); as a conse- tion to catecholamines, stabilizes the cardio- quence, their effects will be prolonged in vascular system, and has the least related patients with severe liver disease. increase in cerebral blood flow (Dozier, 2007). Return paralysis can occur during the early Enflurane has residual CNS depressant postoperative period. The ICU nurse should effects, which manifest during the postopera- observe for a descending trend in minute ventive period. Other effects include decreased tilation, which can be caused by inadequate blood pressure, stroke volume, and SVR, and reversal of the NMBA. Nondepolarizing increased heart rate; this medication also sen- agents are reversed with anticholinesterase sitizes the heart to catecholamines. Enflurane drugs (e.g., neostigmine [Prostigmin®]). Depo- causes mild coronary vasodilation and puts larizing NMBAs cannot be pharmacologically the patient at increased risk for development reversed because they are metabolized by of junctional rhythms (Savino & Cheung, pseudocholinesterase, an endogenous enzyme. 2008). A benefit of enflurane is the low associ- It is essential that the ICU nurse realize ated incidence of PONV (Dozier, 2007). Nurs- that NMBAs have no amnestic or analgesic ing considerations include anticipation of properties, nor do they cause a loss of con- delayed awakening and extubation. sciousness. Analgesics must be administered Isoflurane augments the effects of nonde- to the postoperative cardiac surgery patient polarizing muscle relaxants. It is a coronary despite the patient’s inability to quantify pain artery vasodilator that is associated with levels (Dozier, 2007). Medications to achieve increased coronary perfusion (Savino & Che- decreased level of consciousness or amnesia ung, 2008). Isoflurane and halothane can must similarly be administered if those effects cause postoperative shivering, with an associ- are desired in the postoperative cardiac sur- ated increase in myocardial oxygen demand gery patient. (Weinbroum & Geller, 2001).

Opioids Neuromuscular Blocking Agents Intravenous opioids are used as analgesics or Neuromuscular blocking agents (NMBAs) are as induction agents. When administered, these used as adjuncts to inhalation agents to pro- medications decrease the response and percep- vide relaxation of skeletal muscles, facilitate tion to pain. The most frequently used opioid intubation, and decrease shivering (Savino & in cardiac surgery is fentanyl. Nursing consid- Cheung, 2008). These agents are classified as erations include monitoring for bradycardia, either depolarizing or nondepolarizing which may be treated with atropine or gly- agents. NMBAs that are commonly adminis- copyrrolate (Robinul®). PONV is a common tered during cardiac surgery include rocuro- side effect of opioids and is of clinical concern. nium, vecuronium, and succinylcholine. Succinylcholine is an example of a depolariz- ■ POSTOPERATIVE CARE ing NMBA; rocuronium and vercuronium are examples of nondepolarizing agents and are Hemodynamic Management short- to medium-acting agents, respectively. The primary goal of care for the cardiac sur- Rocuronium, cis-atracurium, doxacurium, gery patient in the immediate postoperative and vecuronium have no cardiovascular side period is optimization of hemodynamic status effects and, therefore, are useful in cardiac to help achieve a balance between oxygen sup- surgery. These agents are eliminated by the ply and demand. This goal can best be accom- hepatic system (as opposed to the renal sys- plished by maintaining an adequate CO. 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 133

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As described in Chapter 9, CO is affected by of medications that cause vasodilation, or a patient’s preload, afterload, and contractil- fever (Khalpey et al., 2008). ity. Preload refers to the heart’s filling pres- Once a patient’s preload and afterload have sures, reflected as the amount of volume been optimized, if CO is inadequate, adminis- returning to the right and left sides of the tration of an inotropic agent to augment con- heart. It is evaluated by measuring central tractility may be considered. Agents such as venous pressure (CVP) and PAOP, respec- milrinone or dobutamine increase CO by aug- tively. Afterload refers to the amount of work menting contractility and decrease afterload the heart must do to eject blood. Typically, by causing vasodilation (Khalpey et al., 2008). left-sided afterload (SVR) is evaluated most Chapter 12 discusses inotropic agents in often. These two parameters can be evaluated more detail. and manipulated by the ICU nurse to opti- As described in Chapter 13, although mize a patient’s hemodynamic profile. acceptable postoperative hemodynamic val- Causes of alterations in preload in the post- ues will vary with the patient’s cardiac history, operative cardiac surgery patient include optimal hemodynamic parameters in a post- vasodilation from a systemic inflammatory operative cardiac surgery patient include a CI response associated with CPB procedures, of more than 2 L/min/m2, PAOP of approxi- medications, vasodilation from rewarming, mately 15 mm Hg, CVP less than 15 mm Hg, bleeding, third spacing, and urinary output. mean arterial pressure (MAP) more than Volume repletion is indicated for patients 65 mm Hg, systolic blood pressure (SBP) in with decreased preload. The decision of the range of 90–140 mm Hg, and systemic whether to use crystalloids or colloids for vascular resistance index in the range of fluid resuscitation remains unresolved given 1400–2800 dyne/sec/cm–5/m2 (Khalpey et al., the pros and cons of each option. If volume 2008). resuscitation alone is inadequate to maintain filling pressures and CO in a patient who has Alterations in Heart Rate and Rhythm adequate pump function and vasodilation, Postoperative dysrhythmias can be antici- consideration should be given to adding an pated in the postoperative cardiac surgery infusion of a vasopressor (e.g., neosynephrine, patient. The most common dysrhythmias are vasopressin, methylene blue) (Khalpey et al., atrial in origin; ventricular dysrhythmias and 2008). Chapter 12 discusses vasopressor ther- bradycardic rhythms are possible as well. Dys- apy in more detail. rhythmias may or may not manifest in the An increase in afterload may be related to initial postoperative period. If present, how- postoperative hypertension, use of medications ever, dysrhythmias may cause hemodynamic that cause vasoconstriction, hypothermia, pain, instability. If the patient has a clinically sig- anxiety, hypovolemia, or postoperative pump nificant dysrhythmia, then pharmacologic failure. Infusion of a vasodilator (e.g., nitro- control of rate, rhythm, or both, may be indi- prusside, nitroglycerin, nicardipine) is indicated cated. Management of alterations in heart for patients who are hypertensive or who have rate and rhythm is discussed in detail in inadequate pump function but with individual- Chapters 12 and 15. specific normal blood pressure (Khalpey et al., 2008). Vasodilator therapy is discussed in more detail in Chapter 12. Postoperative Nausea and Vomiting A decrease in afterload may be caused by Postoperative nausea and vomiting is a com- vasodilation from the CPB-associated sys- mon occurrence in the immediate postopera- temic inflammatory response, administration tive period, primarily due to the medications 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 134

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Table 8–2 Multimodal Management Thermoregulation (Hypothermia) of Postoperative Nausea and Vomiting According to American Society of PeriAnes- thesia Nursing (ASPAN, 2006) standards, Dexamethasone postoperative nursing considerations include 5-HT3 receptor antagonists the identification of patients at risk for H1 blockers hypothermia and application of passive and Scopolamine patch active warming devices (e.g., bonnet, cotton Droperidol blankets, socks, forced air warming device). NK1 antagonists Hydration Patients are considered hypothermic if they Pain and comfort management have a temperature of less than 96.8 °F (36 °C) (ASPAN, 2006). Others define postop- Sources: Ali, Taguchi, Holtmann, & Kurz, 2003; ASPAN, 2006. erative hypothermia as a temperature less than 95 °F (35 °C) (Khalpey et al., 2008). Fac- tors affecting the development of hypothermia include patient age, health status, surgical procedure, exposed body areas, dura- administered intraoperatively. PONV increases tion of anesthesia or surgery, ambient room the risk of pulmonary aspiration, disrupts sur- temperature, prepping and irrigation solu- gical repairs secondary to retching, increases tions, administration of cool IV fluids, and postoperative bleeding, and causes electrolyte peripheral vascular disease (Dozier, 2007). disturbances (e.g., hypokalemia, hyponatremia, The postoperative cardiac surgery patient hypochloremia), dehydration, and esophageal should be monitored every 30 minutes until rupture and tears (Couture et al., 2006). PONV normothermic. Adjusting ambient room tem- can be minimized by assessing for risk factors perature or warming oxygen may also be ben- (e.g., age, gender, history of PONV or motion eficial (Bräuer et al., 2004; Frank, 2000). sickness, and use of volatile anesthetics and Attaining and maintaining postoperative opioids) in the preoperative phase and by normothermia is vital, as inadvertent postop- implementing preventive strategies utilizing a erative hypothermia has been linked to multimodal approach (see Table 8–2). adverse effects. Overall, postoperative patients Administering prophylactic antiemetics admitted from the OR with a core tempera- that affect different receptor sites in the ture less than 36 °C have prolonged mechani- brain has been shown to decrease the inci- cal ventilation, shivering, and increasing dence of PONV. Medications that may be oxygen consumption. Hemodynamic effects used to treat PONV include ondansetron of hypothermia include increased SVR and (Zofran®), promethazine (Phenergan®), and greater likelihood of developing dysrhyth- prochlorperazine (Compazine®). If PONV is mias, hypertension, tachycardia, decreased not relieved following two doses of antiemet- preload, impaired contractility, or coronary ics, it should be reported to the anesthesia graft spasm (Khalpey et al., 2008; Lemmer, provider (Dozier, 2007). If it is not con- Richenbacher, & Vlahakes, 2003). traindicated or if the cause of PONV is Hypothermia alters drug metabolism, caus- hypotension, hydration may also be effective ing delays in patients’ emergence from anes- in reducing the occurrence of PONV (Ali, thesia. It also causes a disruption of the Taguchi, Holtmann, & Kurz, 2003). Patients coagulation pathway, increasing the need for who are vomiting should be positioned to blood transfusions. Hypothermia leads to prevent aspiration (Dozier, 2007). delays in wound healing, which increases sus- 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 135

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ceptibility to surgical site infections, and shiv- in the ICU from the OR (Baltimore, 2001). ering, which increases myocardial oxygen Upon determination that the patient is ready demand and consumption (Silvestry, 2008; for extubation, the patient’s mouth should be St. Andre & DelRossi, 2005; Talmor & Lisbon, suctioned and the tube-securing device is 2005). removed. The cuff on the endotracheal tube is deflated with a syringe. The presence of an air Postoperative Respiratory Management leak must then be ascertained; such a leak In addition to managing a patient’s hemody- may be either heard or felt. The patient is namic status, respiratory management is instructed to take a deep breath and cough, another pivotal role of the ICU nurse in the with the tube being removed toward the end immediate postoperative cardiac surgery of the cough. Supplemental humidified oxy- period. Unless the patient was “fast-tracked” gen is applied (Dozier, 2007). Placement on and extubated in the OR, short-term mechan- low-flow oxygen such as nasal cannula is ical ventilation is employed until anesthetic common practice. agents have been eliminated. Early extubation should be a goal for all patients. Stir-up Regime Weaning and extubation protocols vary Cardiac surgery patients require the “stir-up among facilities. Nevertheless, these processes regime” in the immediate postoperative are generally based on adequate muscle period if they received an inhalation agent as strength, pulmonary function, and hemody- part of their anesthesia, as these agents cause namic stability (Baltimore, 2001; Smartt, 2004). respiratory depression and are eliminated As discussed in Chapter 11, extubation criteria with ventilation. The stir-up regime is accom- typically include presence of a heart rate less plished by elevating the head of the bed and than 140, respiratory rate less than 25, nor- encouraging deep breathing and coughing at mothermia, and absence of ischemia and infu- regular intervals. This practice facilitates sion of vasoactive agents. The patient should be movement of the inhalation agent from an alert and cooperative (i.e., able to respond to area of higher concentration (the patient’s commands). Presence of a cough and gag reflex lungs) to an area of lower concentration are important, as the patient must be able to (room air), which is how the agent will be maintain a patent airway following extubation. eliminated (Dozier, 2007). The patient must also demonstrate adequate muscle strength by sustaining a head lift for at least 5 seconds. Other weaning criteria include Complications Related to Extubation ability to breathe spontaneously and ade- Complications following extubation are fairly quately while maintaining adequate oxygen sat- uncommon but may include laryngospasm, uration and arterial blood gas values. noncardiogenic pulmonary edema, bron- Physiologic parameters that may be measured chospasm, hypoventilation, and hypoxia. to assess potential readiness for extubation include a negative inspiratory force (NIF) of at Laryngospasm and Noncardiogenic Pulmonary Edema least 20–25 cm H2O, minute volume no greater than 10 L/min, and vital capacity 10–15 mL/kg Laryngospasm is a partial or complete block- (Hemant, Chacko, & Singh, 2006; Khalpey age of air flow into and out of the lungs et al., 2008). owing to spasms of the vocal cord (Fodale et Typically, cardiac surgery patients are extu- al., 2004). Causes include aspiration, suction- bated within 4 to 12 hours after their arrival ing, and histamine release associated with 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 136

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some medications. Signs of laryngospasm Bronchospasm include “rocking” respirations, wheezing, stri- Bronchospasm can occur as a result of con- dor, dyspnea, use of accessory muscles, and striction of bronchial smooth muscles after tachypnea. The patient should be encouraged extubation. It resolves quickly after airway to cough, as this action may be effective in irritants are eliminated. Symptoms include eradicating a partial obstruction (Dozier, wheezing, dyspnea, and tachypnea. Treatment 2007). involves administration of a bronchodilator Patients can have laryngospasm during and humidified oxygen. In severe cases, mus- extubation, which can trigger noncardiogenic cle relaxants, lidocaine, epinephrine, or hydro- pulmonary edema. Noncardiogenic pul- cortisone may be administered to relax the monary edema occurs following an acute air- airway (Carlson, 2004). way obstruction, such as when the patient forcefully inspires against a closed glottis, Hypoventilation and Hypoxia thereby creating an increase in intrathoracic Hypoventilation is common in the immediate pressure and resulting in pulmonary edema postoperative period. It may result from the (Van Kooy & Gargiulo, 2000). Protein and anesthetic agents administered or the surgical fluid accumulate and extravasate into the procedure itself. Treatment entails eradicat- alveoli without an associated increase in ing the underlying cause. If the underlying PAOP (Colucci, 2008). Symptoms of this con- cause is related to opioid administration, dition, which typically have a rapid onset, then treatment may include administration include agitation, tachypnea, tachycardia, of naloxone (Narcan®) for patients with shal- decreased oxygen saturation, and pink, frothy low or slow respirations. Institutional policy sputum. Crackles will be audible. varies regarding use of opioid antagonists Prompt recognition and treatment of both (Dozier, 2007). laryngospasm and noncardiogenic pul- Hypoxemia is defined as oxygen saturation monary edema are crucial; indeed, the patient less than 90%. Hypoxemia can have numerous may require reintubation until these prob- undesired sequelae, including cardiac dys- lems resolve. Treatment of laryngospasm gen- rhythmias and myocardial ischemia. Signs erally involves positive-pressure breathing and symptoms may include cyanosis, agita- with a bag-valve-mask device with 100% oxy- tion, somnolence, tachycardia, bradycardia, gen and mandibular support. If these meas- hypertension, and hypotension. Depending ures prove ineffective, succinylcholine can be on the severity of the symptoms or hypox- administered intravenously. Lidocaine may be emia, reintubation and mechanical ventila- effective in preventing a laryngospasm. tion may be required (Dozier, 2007). Noncardiogenic pulmonary edema manage- Inadequate reversal of NMBAs’ effects can ment involves maintenance of a patent airway, cause hypoventilation and hypoxia after extu- supplemental oxygen, and administration of a bation. Extubation of a patient who is par- diuretic. Mechanical ventilation with PEEP tially paralyzed increases the individual’s risk may be required in severe cases (Marley & of developing postoperative complications. Riess, 2004). Chest radiograph may reveal Residual respiratory muscle weakness can findings consistent with pulmonary edema. cause airway obstruction, hypoventilation, Treatment of noncardiogenic pulmonary and an impaired response to hypoxia. Cardiac edema includes supplemental oxygen, respira- surgery patients are at increased risk if they tory support, and diuretics (Dozier, 2007). receive a long-acting NMBA whose action is 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 137

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inadequately reversed with anticholinesterase Malignant Hyperthermia agents. Re-paralysis can occur when an Malignant hyperthermia (MH) is a genetic, NMBA has a longer half-life than the reversal life-threatening disorder that is triggered by agents. If this problem occurs, the patient will certain anesthetic agents, depolarizing skele- demonstrate weak, shallow respirations and tal muscle relaxants, and stress. With this poor chest rise; anxiety and restless may condition, a defect in the sarcoplasmic reticu- become apparent as well. Treatment involves lum leads to a buildup of excess calcium in administration of additional doses of a rever- the mycoplasm. This results in sustained sal agent, respiratory support, and temporary skeletal muscle contraction that is intense reintubation until muscle strength is and prolonged, leading to a hypermetabolic regained. state of heat production. During weaning and extubation, opioids The onset of MH usually occurs during should be used judiciously. Opioids decrease induction of anesthetic agents. Halothane, respiratory effort, oxygen saturation, and respi- enflurane, isoflurane, desflurane, and succinyl- ratory rate and depth. Pain management is of choline are the most common triggering agents. concern; however, small doses of short-acting The triggering of events is characterized by mus- analgesics (e.g., dexmedetomidine [Pre- cle rigidity of the jaw (masseter rigidity), tachyp- cedexTM]) may be recommended (Khalpey et al., nea, tachycardia, elevated CO2 level, cyanosis, 2008). Complications that arise after extuba- respiratory and metabolic acidosis, elevated tion can be minimized by recognizing and serum creatine phosphokinase (CPK), and treating respiratory emergencies and by adher- hyperkalemia. Late signs include temperature ing to weaning and extubation criteria elevation, bleeding from venipuncture sites, and (Haghenbeck & Keeler, 2003). rhabdomyolysis. MH typically manifests in the OR but it can develop within 24 hours postoperatively (Litman & Rosenberg, 2005). ■ POTENTIAL POSTOPERATIVE Treatment of MH includes discontinuance of triggering agents and immediate intra- COMPLICATIONS venous administration of dantrolene sodium The ICU nurse plays a pivotal role in prevent- (Dantrium®) 2.5 mg/kg (up to a maximum ing or promptly identifying and treating post- dose of 10 mg/kg). Dantrolene inhibits the operative complications. Among the more release of calcium. Once the loading dose is common complications seen in the immedi- administered, dantrolene is infused at a dose ate postoperative period are hemodynamic of 1 mg/kg every 4 hours for at least 48 hours compromise, respiratory insufficiency, neuro- (Dozier, 2007). logic issues, and hematological problems. Hyperventilation, administration of 100% Some complications are related to patient oxygen, body surface area cooling, administra- comorbidities; others are related to the surgi- tion of sodium bicarbonate, maintenance of cal procedure itself. These complications and fluid and electrolyte balance, and treatment of the associated ICU nursing responsibilities associated conditions (e.g., hypertension, dys- are discussed in detail in Chapters 13 and 16. rhythmias) are also essential interventions in Potential complications related to effects of the setting of MH. Lab data that may be anesthesia are addressed in this section. One obtained include arterial glood gas, serum unique complication related to the surgical electrolytes, liver enzymes, renal function procedure is covered here as well. studies, blood counts, and coagulation profile 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 138

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(Dozier, 2007). Effective management involves should be used when administering prota- prompt recognition, guidance of the multidis- mine sulfate to patients who may be at ciplinary team, and expert direction from the increased risk of allergic reaction—specifically, Malignant Hyperthermia Association of the individuals who have previously undergone United States (MHAUS). procedures such as coronary angioplasty or CPB, diabetics who have been treated with Pseudocholinesterase Deficiency protamine insulin, patients who are allergic to fish, and men who have had a vasectomy or Prolonged mechanical ventilation after cardiac are infertile and may have antibodies to prot- surgery may be caused by a deficiency in amine. Patients undergoing prolonged proce- pseudocholinesterase. A small percentage of dures involving repeated doses of protamine patients lack this enzyme, which is responsible should be subject to careful monitoring of for metabolizing medications such as succinyl- clotting parameters. A rebound bleeding choline. Patients with pseudocholinesterase effect may occur as long as 18 hours postop- deficiency who receive these medications eratively (Hepner & Castells, 2003). exhibit prolonged responses to these medications, can have sustained skeletal muscle paralysis, and remain apneic for as long as 48 hours ■ SUMMARY after administration. Management involves emotional support and mechanical ventilation Although much progress has been made with until the effects of the medication are com- respect to the postoperative care of the car- pletely eliminated (Dozier, 2007). diac surgery patient, critical thinking and caring practices of the ICU nurse are primary determinants of positive outcomes. The ini- Protamine Sulfate Allergic Reactions tial hours following cardiac surgery are tenu- Protamine sulfate is administered as a reversal ous. The patient’s preoperative status, the agent for heparin. If it is given too rapidly, intraoperative course, and the effects of anes- severe hypotension and anaphylactic reac- thesia all contribute to the complexity of the tions may result. Consequently, caution patient’s profile.

CASE STUDY

A 52-year-old patient with a history of coronary artery disease, hypertension, hyperlipidemia, and mitral regurgitation underwent coronary artery bypass grafting with a left internal mammary artery graft and mitral valve repair. Her intraoperative course was unremarkable. Postoperatively, the patient was admitted to the ICU extubated with a mediastinal tube and chest tube that were draining bloody fluid, and on a nitroglycerin infusion. Her admission vital signs were BP 132/74; HR 92; RR 24; temperature 97.5 °F; CVP 11; PAP 32/16; PAOP 10 mm Hg; cardiac output 4.1 L/min; and cardiac index 2.7 L/min/m2. The patient’s initial postoperative course was uneventful. Two hours after admission, the ICU nurse recorded the following vital signs and hemodynamic data: BP 86/48; HR 120; RR 28; CVP 22; PAP 36/22; PAOP 23; cardiac output 3.2 L/min; and cardiac index 2.5 L/min/m2. The ICU nurse also noted a decrease in the drainage from the mediastinal and 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 139

Self-Assessment Questions 139

chest tubes. The patient reported feeling short of breath and that “something was just not right.” She appeared anxious and pale, as compared to her baseline postoperative status. The ICU nurse initiated a fluid bolus and alerted the cardiac surgeon. A bedside echocardiogram was performed, and a large pericardial effusion and a clot were noted. The patient returned to the OR for clot evacuation and relief of the cardiac tamponade. Subsequently, the patient returned to the ICU in stable condition. The remainder of her initial postoperative course was uneventful.

Critical Thinking Questions 1. Why was this patient at risk for the development of cardiac tamponade? 2. Why is diagnosis of cardiac tamponade challenging in the postoperative cardiac surgery patient? 3. Why was a fluid bolus indicated with the patient’s hemodynamic profile? Answers to Critical Thinking Questions 1. During cardiac surgery, the pericardial sac is entered and is usually not sutured back together before chest closure. This leaves a communication between the heart and the mediastinum, which can lead to the potential accumulation of blood or fluid (Lemmer et al., 2003; St. Andre & DelRossi, 2005). The accumulation compresses the atria, restricts venous return to the heart and ventricular filling, and results in a decrease or cessation of preload, causing a potential precipitous fall in CO (Massé & Antonacci, 2005). Early tamponade is usually a result of persistent mediastinal bleeding not being evacuated by chest tubes, as is what occurred in this case. 2. Diagnosis may be difficult because hypotension, tachycardia, and elevated filling pressures are common in cardiac surgery patients in the most immediate postoperative period. In addition, some of the other characteristic symptoms of cardiac tamponade— for example, muffled heart sounds, pulsus paradoxus, and neck vein distention—are not helpful in making the diagnosis in the cardiac surgery patient. 3. The pathophysiology of cardiac tamponade entails fluid accumulation around the cardiac chambers, which causes a restriction of diastolic filling, with an impact on cardiac output. This patient manifested clinically significant hemodynamic instability as a result of the cardiac compression caused by pericardial fluid. While preparation is being made to correct the underlying cause, supportive management includes augmenting preload and minimizing the hypotensive episode.

■ SELF-ASSESSMENT QUESTIONS 2. Your postoperative cardiac surgery patient has the following vital signs: BP 152/96; 1. Which of the following patients is most HR 104; RR 18; temperature 97.2 °F. likely to require prolonged ventilatory Which of the following medications is ini- support? A patient with: tially indicated? a. an elevated BUN a. Morphine b. two-vessel disease b. Nitroglycerin c. an ejection fraction of 45% c. Labetalol d. arterial hypertension d. Nicardipine 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 140

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3. Your postoperative cardiac surgery patient c. SVO2 76% has decreased drainage from the mediasti- d. CVP 12 mm Hg nal chest tube. Vital signs are as follows: 8. Which of the following postoperative BP 88/50; HR 106; RR 24, CVP 12; cardiac cardiac surgery patients has criteria sug- output 3.1 L/min. Which of the following gesting readiness to wean from mechani- actions is indicated initially? cal ventilation? A patient with: a. Milk the chest tube a. BP 104/60; HR 144; temperature 97.5 °F b. Raise the head of bed to 45 degrees b. a positive cough and gag reflex, NIF c. Administer a fluid bolus 25 cm H2O, receiving low-dose d. Prepare for echocardiogram norepinephrine 4. Your postoperative cardiac surgery c. new ST-segment elevation but no patient received an inhalation agent as Q waves, sustained head lift for 10 part of general anesthesia. Which of the seconds, vital capacity 10 mL/kg following developments should the ICU d. minute ventilation 8 L/min, nurse anticipate? RR 24, HR 136 a. Hyperventilation 9. Your postoperative cardiac surgery b. An initial reduced need for analgesics patient was recently extubated and c. Peripheral vasoconstriction develops “rocking respirations,” wheez- d. Ventricular ectopy ing, tachypnea, and dyspnea. Which of 5. You are caring for a postoperative car- the following is initially indicated? diac surgery patient who has been in the a. Bag-valve-mask ventilation ICU for the past hour. The patient was b. Administration of succinylcholine not extubated in the OR. You note a c. Administration of a nebulized decrease in the patient’s minute ventila- bronchodilator tion since admission. You suspect d. Immediate reintubation a. development of postoperative atelectasis. 10. Which of the following ABG results b. presence of pseudocholinesterase should the ICU nurse anticipate in a deficiency. patient with malignant hyperthermia? c. inadequate reversal of the a. pH 7.30; pCO2 50; pO2 60; SaO2 90; neuromuscular blocker. HCO3 25 d. hepatic dysfunction. b. pH 7.50; pCO2 30; pO2 50; SaO2 85; 6. Which of the following patients would HCO3 18 benefit from an infusion of a vasodilator c. pH 7.55; pCO2 45; pO2 71; SaO2 93; in the immediate postoperative period HCO3 34 following cardiac surgery? A patient with: d. pH 7.29; pCO2 38; pO2 68; SaO2 92; a. normotension and inadequate pump HCO3 19 function Answers to Self-Assessment Questions b. inadequate volume repletion and adequate pump function 1. d 6. a c. cardiopulmonary bypass-related 2. a 7. a systemic inflammatory response 3. c 8. d d. inadequate cardiac output and 4. d 9. a optimized preload and afterload 5. c 10. a 7. Which of the following is an expected hemodynamic effect of hypothermia? a. SVR 1700 dyne/sec/cm–5 b. Heart rate 58 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 141

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Clinical Inquiry Box

Question: Can postoperative cardiac surgery patients be admitted to the ICU and have acceptable outcomes? Reference: Sino, C. A., & Martich, G. D. (1999). Who goes to the ICU postoperatively? Chest, 115(5 suppl), 125S–129S. Objective: To evaluate the outcomes of postoperative admission to the ICU following cardiac surgery. Method: This study included an evidence-based review of the available clinical literature, direct observation of facilities utilizing a rapid recovery program following cardiac surgery, and informal collaboration with colleagues who use the ICU for immediate postoperative management of cardiac surgery patients. Results: Most of the evaluations that were performed involved care of patients following coronary artery revascularization procedures. Efficacy of ICU admission was evaluated based on time to extubation, length of stay in the ICU and hospital, incidence of postoperative complications including reintubation and ICU readmission, patient satisfaction, and resource savings. Conclusion: Only limited data are available from controlled clinical trials. Those data suggest that postoperative admission of cardiac surgery patients can result in rapid recovery and decreased resource utilization and costs, while maintaining high levels of quality of care and patient satisfaction. These outcomes are not apparently related to the patient’s preoperative risk. A multidisciplinary approach can result in shortened postoperative stays in the ICU following cardiac surgery.

■ REFERENCES Baltimore, J. (2001). Perianesthesia care of cardiac Ali, S. Z., Taguchi, A., Holtmann, B., & Kurz, A. surgery patients: A CPAN review. Journal of (2003). Effect of supplemental pre-operative PeriAnesthesia Nursing, 16(4), 246–254. fluid on postoperative nausea and vomiting. Bräuer, A., Weyland, W., Kazmaier, S., Trostdorf, U., Anesthesia, 58(8), 780–784. Textor, Z., Hellige, G., et al. (2004). Efficacy of American Heart Association (AHA). (2005). Open- postoperative rewarming after cardiac surgery. heart surgery statistics. Retrieved May 1, 2008, Annals of Thoracic and Cardiovascular Surgery, from www.americanheart.org/presenter 10 (3), 171–177. .jhtml?identifier=4674 Carlson, K. (2004). Perianesthesia complications. American Heart Association (AHA) (2008). Heart In D. M. DeFazio Quinn & L. Schick (Eds.), disease and stroke statistics—2008 update. PeriAnesthesia nursing core curriculum: Preopera- Retrieved February 1, 2009, from http://www tive, phase I and phase II PACU nursing .americanheart.org/presenter.jhtml?identifier (pp. 658–661). St. Louis, MO: Saunders. =3037327 Colucci, W. S. (2008). Noncardiogenic pulmonary American Heart Association (AHA) (2009). Open edema. Retrieved October 23, 2008, from Heart Surgery Statistics. Retrieved February 1, http://patients.uptodate.com/topic.asp?file 2009, from http://www.americanheart.org/ =hrt_fail/12162 presenter.jhtml?identifier=4674 Couture, D. J., May, J. P., O’Brien, D., & Smith, A. B. American Society of PeriAnesthesia Nurses (2006). Therapeutic modalities for prophylac- (ASPAN). (2006). Standards of perianesthesia tic management of postoperative nausea and nursing practice. Cherry Hill, NJ: Author. vomiting. Journal of PeriAnesthesia Nursing, 21 (6), 398–403. 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 142

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Dozier, T. (2007). Care of the postanesthesia bacher, & G. Vlahakes, Handbook of patient care patient. In R. Kaplow & S. R. Hardin (Eds.), Crit- in cardiac surgery (6th ed., pp. 116–167). ical care nursing: Synergy for optimal outcomes (pp. Philadelphia: Lippincott Williams & Wilkins. 649–666). Sudbury, MA: Jones and Bartlett. Litman, R. S., & Rosenberg, H. (2005). Malignant Drain, C. B. (2003). Basic principles of pharmacol- hyperthermia. Journal of the American Medical ogy. In C. B. Drain (Ed.), PeriAnesthesia nursing: Association, 293(23) 2918–2924. A critical care approach (pp. 326–328). St. Louis, Marley, R. A., & Riess, C. A. (2004). Respiratory MO: Saunders. care. In D. M. DeFazio Quinn & L. Schick Fodale, V., Praticò, C., Leto, G., Caminiti, V., (Eds.), PeriAnesthesia nursing core curriculum: Pre- Mazzeo, A. T., & Lucanto, T. (2004). Propofol operative, phase I and phase II PACU nursing relieves post-extubation laryngospasm in (pp. 526–531). St. Louis, MO: Saunders. obstetric anesthesia. International Journal of Massé, L., & Antonacci, M. (2005). Low cardiac Obstetric Anesthesia, 13(3), 196–197. output syndrome: Identification and manage- Frank, S. M. (2000). Warmed humidified inspired ment. Critical Care Nursing Clinics of North Amer- oxygen accelerates postoperative rewarming. ica, 17(4), 375-383. Journal of Clinical Anesthesia, 12(4), 283–287. Myles, P. S., & McIlroy, D. (2005). Fast-track car- Haghenbeck, K. T., & Keeler, K. D. (2003). Care of diac anesthesia: Choice of anesthetic agents the cardiac surgical patient. In C. B. Drain (Ed.), and techniques. Seminars in Cardiothoracic and PeriAnesthesia nursing: A critical care approach (pp. Vascular Anesthesia, 9 (1), 5–16. 473–505). St. Louis, MO: Saunders. Savino, J. S., & Cheung, A. T. (2008). Cardiac anes- Hemant, H. R., Chacko, J., & Singh, M. K. (2006). thesia. In L. H. Cohn (Ed.), Cardiac surgery in the Weaning from mechanical ventilation— adult (pp. 281–314). New York: McGraw-Hill. Current evidence. Indian Journal of Anaesthesia, Schick, L. (2004). Anesthetic agents and adjuncts 50(6), 435–438. In D. M. DeFazio Quinn & L. Schick (Eds.), Hepner, D. L., & Castells, M. C. (2003). Anaphy- PeriAnesthesia nursing core curriculum: Preopera- laxis during the perioperative period. Anesthe- tive, phase I and phase II PACU nursing sia and Analgesia, 97(5), 1381–1395. (pp. 390–431). St. Louis, MO: Saunders. Karski, J. M., Djaiani, G. N., Carroll, J., O’Brien, W., Silvestry, F. E. (2008). Overview of the postopera- Bailey, K., Cheng, D. C., et al. (2001). A clinical tive management of patients undergoing car- evaluation of postoperative alfentanil infusion diac surgery. Retrieved September 16, 2008, in cardiac surgical patients: Effects on hemo- from www.utdol.com/online/content/topic dynamics, sedation and shivering. Pain, Symp- .do?topicKey=cc_medi/22438&linkTitle tom Control and Palliative Care: The Internet =Perioperative%20myocardial%20infarction&s Journal of Anesthesiology, 5(2). http://www.ispub ource=preview&selectedTitle=1~150&anchor .com/ostia/index.php?xmlFilePath=journals/ =13# ijpsp/vol1n2/alfena.xml Smartt, S. L. (2004). Cardiovascular surgery. In Khalpey, Z. I., Ganim, R. B., & Rawn, J. D. (2008). D. M. DeFazio Quinn & L. Schick (Eds.), Peri- Postoperative care of cardiac surgery patients. Anesthesia nursing core curriculum: Preoperative, In L. H. Cohn (Ed.), Cardiac surgery in the adult phase I and phase II PACU nursing (pp. 532–578, (pp. 465–486). New York: McGraw-Hill. 720–762). St. Louis, MO: Saunders. Laffey, J., Boylan, J., & Cheng, D. (2002). The sys- St. Andre, A., & DelRossi, A. (2005). Hemodynamic temic inflammatory response to cardiac sur- management of patients in the first 24 hours gery. Anesthesiology, 97(1), 215–252. following cardiac surgery. Critical Care Lemmer, J., Richenbacher, W., & Vlahakes, G. Medicine, 33(9), 2062–2083. (2003). Postoperative complications involving Suematsu, Y., Sato, H., Ohtsuka, T., Kotsuka, Y., the heart and lungs. In J. Lemmer, W. Richen- Araki, S., & Takamoto, S. (2000). Predictive 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 143

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risk factors for delayed extubation in patient ■ WEB RESOURCES undergoing coronary artery bypass grafting. Dr. Bernadine Healy takes a tour of the hospital. Heart Vessels, 15(5), 214–220. The operating room is a virtual beehive during Talmor, D., & Lisbon, A. (2005). Management of the heart surgery and afterward in the intensive postoperative cardiac surgical patient. In care unit. URL: http://video.google.com/ M. Fink, E. Abraham, J. Vincent, & P. Kochanek videosearch?hl=en&q=postoperative%20 (Eds.), Textbook of critical care (5th ed., cardiac%20surgery&um=1&ie=UTF-8&sa pp. 1955–1967). Philadelphia: Elsevier Saunders. =N&tab=wv#q=Navigating%20the%20hospital Van Kooy, M. A., & Gargiulo, R. F. (2000). Postob- %20part%203&hl=en&emb=0 structive pulmonary edema. American Family Cardiac tamponade: While not taken on a postop- Physician, 62(2), 401–404. erative cardiac surgery patient, this video Weinbroum, A. A., & Geller, E. (2001). Flumazenil demonstrates a swinging heart due to fluid in improves cognitive and neuromotor emer- high tension within the pericardial space gence and attenuates shivering after and subsequent echocardiogram following halothane-, enflurane- and isoflurane-based treatment. URL: http://video.google.com/ anesthesia. Canadian Journal of Anesthesia, videosearch?hl=en&q=postoperative%20 48(10), 963–972. cardiac%20surgery&um=1&ie=UTF-8&sa =N&tab=wv#q=cardiac%20tamponade%20&hl =en&emb=0&start=0 57625_CH08_127_144.pdf 4/10/09 11:07 AM Page 144 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 145

Chapter 9 Hemodynamic Monitoring

Mary Zellinger

■ INTRODUCTION ■ ESSENTIALS OF HEMODYNAMIC Hemodynamic monitoring of the patient after MONITORING cardiac surgery is a routine part of the imme- Monitoring assists in determining changes in diate postoperative care. Data obtained during fluid status and cardiac performance at the ear- this period guide the clinician in initiating the liest possible time so that treatment fluctua- optimal intervention to ensure a smooth tions in three factors that affect cardiac recovery. Hemodynamics, or the study of the output—preload, afterload, and contractility dynamics of blood circulation, can be assessed (see Box 9–1)—can be quickly addressed. through both invasive and noninvasive mech- New monitoring devices and techniques are anisms; the ultimate goal is to determine the introduced annually to the critical care arena, adequacy of cardiac output (the amount of each of which has the goal of increasing accu- blood ejected by the heart each minute). This racy and decreasing invasiveness of monitoring. chapter reviews the essentials of hemody- It is imperative for the clinician to incorporate namic monitoring in the patient who has data from a variety of sources when assessing undergone cardiac surgery. Both basic and the hemodynamic picture so as not to rely on a newer technologies are discussed. single—and potentially misleading—parameter. Box 9–1 Hemodynamic Monitoring Terms and Definitions

Preload: the volume of blood either in the right atrium or in the left ventricle at the end of diastole or the beginning of systole. Preload is quantified with central venous pressure (CVP) and pulmonary artery occlusive pressure (PAOP), respectively; these parameters reflect a patient’s volume status. The end-diastolic volume (EDV) is related to the amount of stretch of the sarcomeres. Preload is a reflection of all of the elements that affect tension of the chamber wall at the end of filling (diastole). Afterload: the amount of work the heart must do to eject blood; the impedance or resistance to ventricular contraction. Afterload reflects all of the elements that affect tension of the myocardial wall during systole. Contractility: the ability of the myocardial muscle to shorten itself or the amount of strength produced by the myocardium when it ejects blood. It is influenced by neural factors and certain metabolic states (e.g., hypoxia, hypercarbia, or decrease in pH). Cardiac output: the amount of blood ejected by the heart each minute.

Sources: Norton, 2001; Rothe, 2003.

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■ INITIAL POSTOPERATIVE Figure 6–3 in Chapter 6). The transducers are ASSESSMENT then zero-balanced, establishing atmospheric Following cardiac surgery, the ICU nurse will pressure as zero. Leveling at the phlebostatic connect the patient to the bedside monitor axis is performed to eradicate the effects of upon receipt from the operating room. The hydrostatic forces on the hemodynamic pres- ECG leads are connected to the bedside moni- sures (AACN, 2004). A square wave test is per- tor from the transport monitor, and heart rate formed to ensure responsiveness (see Box 9–2 and rhythm are assessed. The pulse oximetry and Figure 9–1a). Proper setup and functioning probe is connected to the finger, earlobe, or of the monitoring system itself are essential to forehead. Pulse oximetry is a simple, noninva- obtain accurate values, regardless of the specific sive method of monitoring the percentage of parameter being measured. A number of hemoglobin that is saturated with oxygen. The variables—such as the number of stopcocks, the length of the tubing, the responsiveness of the target oxygen saturation (SpO2) is 95% or greater in a patient without a history of COPD. tubing, and the presence of air bubbles—can influence the accuracy of the readings. Preparing Hemodynamic Equipment Vital Signs and Hemodynamic After elevating the head of the bed, the trans- Assessment ducers are leveled at the phlebostatic axis, which An initial assessment of vital signs and hemo- is located at the fourth intercostal space, mid- dynamic parameters (see Box 9–3) is obtained, point of the anterior–posterior diameter (see ensuring that the latter are assessed at end-

Box 9–2 Square Wave Test

A square wave test (also referred to as a fast flush or dynamic response test) is performed to assure that the waveforms that appear on the monitoring screen accurately reflect pulmonary artery pressures (AACN, 2004). It is accomplished by pulling and releasing the pigtail or squeezing the button of the flush device so that the flow through the tubing is increased (from 3 mL/hr obtained with a pressure bag inflated to 300 mm Hg). This causes a sudden rise in pressure in the system, such that a square wave is generated on the monitor oscilloscope. An acceptable response is the pressure waveform reverting to baseline within one to two oscillations. If the response is lacking in shape, amplitude, or time to return to baseline, the ICU nurse should troubleshoot the system until an acceptable response is achieved (McGhee & Bridges, 2002). If an underdamped or overdamped waveform is present, hemodynamic measurements will not be accurate. It is recommended that a square waveform test be performed when the system is being initially set up, at least once a shift, after opening the catheter system (e.g., for rezeroing, blood sampling, or changing tubing), and whenever the pressure waveform appears to be damped or distorted (AACN, 2004). An overdamped waveform is sluggish and has an exaggerated or falsely widened and blunt tracing. It will cause the patient’s systolic blood pressure (SBP) to be recorded as falsely low and the diastolic blood pressure (DBP) to be recorded as falsely high. Causes of an overdamped waveform include the presence of large bubbles in the system, loose connections, no or low fluid in the flush bag, low pressure of the flush solution pressure bag, or a kink in the catheter (AACN, 2004) (see Figure 9–1b). An underdamped waveform consists of an over-response, which is seen as an exaggerated, narrow, artificially peaked tracing. In this case, the waveform overestimates the patient’s SBP and underestimates the DBP. Causes of an underdamped waveform include the presence of small bubbles in the system, the pressure tubing being too long, or a defective transducer (AACN, 2004) (see Figure 9–1c). 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 147

Initial Postoperative Assessment 147

expiration. Readings are obtained at this tionships among the amount of volume point in the respiratory cycle to eliminate the infused and lost in the operating room, base- effects of changes in intrathoracic pressure line postoperative vital signs, and hemody- that occur with breathing (McGhee & namic status are assessed. Setting monitor Bridges, 2002). The frequency of obtaining alarm limits specific to the patient’s baseline subsequent sets of vital signs and hemody- profile, and ensuring these alarms are acti- namic parameters varies by facility and vated, are crucial at this stage. according to the patient’s clinical status. Depending on unit-specific protocols and, Patient Assessment perhaps, physician order, in addition to A complete baseline physical assessment is baseline hemodynamic values, cardiac out- then completed. While the primary nurse is put/index may be measured. From cardiac performing the baseline assessment, a num- output/index and invasive pressure data, sev- ber of concomitant essential activities related eral hemodynamic calculations can be per- to the patient’s hemodynamic status are performed, yielding valuable information about formed. These activities are listed in Box 9–4. cardiac performance. A comprehensive head-to-toe assessment The ICU nurse will check the vasoactive will enable the nurse to evaluate several indices drips and other fluids infusing to verify their to determine the overall adequacy of perfusion. type, infusion status, and dosages. The rela- A complete neurological assessment may

Figure 9–1a Square wave test.

Figure 9–1b Overdamped waveform.

Figure 9–1c Underdamped waveform. Source: Illustrations by James R. Perron 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 148

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Box 9–3 Hemodynamic Parameters and Normal Values

Parameters Normal Values Systolic and diastolic blood pressure 100–130/60–90 mm Hg Mean arterial pressure 70–105 mm Hg Right atrial pressure (central venous pressure) 0–8 mm Hg Right ventricular pressure 25–30/0–8 mm Hg Pulmonary artery pressure 15–30/6–12 mm Hg Pulmonary artery occlusive pressure 4–12 mm Hg Derived Hemodynamic Parameters Cardiac output/cardiac index 4–8 L/min / 2.5–4.2 L/min/m2 Systemic vascular resistance 770–1500 dyne/sec/cm–5 Pulmonary vascular resistance 20–120 dyne/sec/cm–5 Systemic vascular resistance index 1680–2580 dyne/sec/cm–5 Pulmonary vascular resistance index 69–177 dyne/sec/cm–5 Stroke volume/index 60–130 mL /beat/ 30–65 mL/beat/m2 Right ventricular stroke work 8–16 g-m/beat Right ventricular stroke work index 5–10 g-m-m2/beat Left ventricular stroke work 58–104 g-m/beat Left ventricular stroke work index 50–62 g-m-m2/beat Oxygenation Parameters Arterial oxygen saturation 95–100% Mixed venous oxygen saturation 60–80% Arterial oxygen content 17–20 mL/dL Venous oxygen content 12–15 mL/dL Oxygen delivery 900–1150 mL/min Oxygen consumption 200–290 mL/min Oxygen extraction ratio 22–30%

Sources: Blount, 2007; Khalpey, Ganim, & Rawn, 2008; LiDCO, 2008.

Box 9–4 Postoperative Cardiac Surgery Initial Admission Responsibilities

Assessment of Chest Drainage System ● Connect chest drainage system to suction. ● Note and record the amount of drainage from the OR. Correlate these findings with the patient’s baseline hemodynamic profile. Assessment of Fluid Status ● Compare intraoperative intake and output with baseline hemodynamic profile and vital signs to help determine fluid volume status. Diagnostics ● Obtain lab samples per protocol (e.g., electrolytes, ABG, CBC, coagulation profile) and other diagnostic procedures (e.g., 12-lead ECG to check for potential intraoperative or postoperative ischemia, chest radiograph to verify endotracheal tube placement and assess for presence/ degree of pneumothorax). 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 149

Blood Pressure Monitoring 149

prove challenging if the patient has not been ative diuresis of 200–400 mL/hr owing to the reversed from general anesthesia or is receiv- effects of hemodilution and osmotic agents ing a continuous infusion of an anesthetic sometimes administered during cardiopul- agent or sedation. Some hospital protocols monary bypass (Lee & Sladen, 2002; Stafford- require the anesthetic agent or sedation infu- Smith & Newman, 2006), urinary output may sion be weaned and temporarily discontinued not be indicative of perfusion for the first sev- in the immediate postoperative period so that eral hours after the surgery. Following the ini- appropriate neurological function can be con- tial few hours postoperatively, urinary output firmed. The infusion can then be restarted should be at least 0.5 mL/kg/hr. until the ventilator weaning process begins. An awake and alert patient is one indicator of ■ adequacy of cardiac output. BLOOD PRESSURE MONITORING Extremity movement, warm skin, and pal- In the immediate postoperative period, main- pable pulses indicate acceptable perfusion, taining hemodynamic stability is the priority. unless obstructive peripheral vascular disease Intra-arterial pressure monitoring provides for is present and limits perfusion to the distal the direct measurement of arterial blood pres- extremities. Assessment of heart sounds will sure, and in many clinical situations is more provide additional information about cardiac accurate than the auscultatory measurement. function and any valve dysfunction. The pres- Variables such as cuff size can influence indi- ence of extra heart sounds, although normal rect (noninvasive) pressure readings. Indirect in certain situations, warrants further investi- pressure readings can underestimate actual

gation. An S3 or S4 heart sound may be a sign systolic pressures by several mm Hg in of decreased ventricular compliance. The hypotensive patients (Borrow & Newburger, presence or sudden absence of murmurs may 1982; Cloud, Rajkumar, Kooner, Cooke, & Bul- indicate changes in native or prosthetic valve pitt, 2003). This difference occurs because of function. Placing the head of the bed between the Korotkoff sounds produced by blood flow. 30 and 45 degrees and observing for jugular As blood flow diminishes, the sound becomes vein distention will reinforce other findings less audible, to the point that the faint early of right-sided heart failure or fluid overload. sounds may be missed. Indirect measurement Breath sounds should be auscultated in all of blood pressure, whether obtained manually fields, noting any areas that are diminished or or with a noninvasive automated pump, pro- abnormal. Pulmonary congestion may be vides the best estimate of SBP but underesti- indicative of pulmonary dysfunction from the mates DBP when the patient is at rest (Griffin, surgical process, be the effect of complica- Robergs, & Heyward, 1997). tions from mechanical ventilation, or occur as Intra-arterial monitoring is indicated in sit- a result of cardiac dysfunction. uations when the patient’s condition necessi- Urinary output is another indication of ade- tates close hemodynamic observation. quacy of cardiac output, although it may Patients who undergo mechanical manipula- sometimes misrepresent the adequacy of per- tion of the heart as in cardiac surgery, those fusion to the kidneys. Postoperatively, cardiac who receive drug therapy, and those in whom surgery patients should be evaluated for renal an intra-aortic balloon pump (IABP; dis- insufficiency if urinary output is less than cussed in Chapter 10) is used will all require 0.5 mL/kg/hr for 2 to 3 consecutive hours and frequent assessment of arterial pressure post- serum creatinine levels are increasing (Lem- operatively. An intra-arterial line will also mer, Rickenbacker, & Vlahakes, 2003). Given assist in assessing perfusion associated with that cardiac surgery patients may exhibit a rel- dysrhythmias. When an intra-arterial catheter 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 150

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Box 9–5 Mean Arterial Pressure Calculation

Systolic blood pressure ϩ (Diastolic blood pressure ϫ 2) MAP ϭ 3 For example, if the patient’s blood pressure is 120/80, the MAP can be calculated as follows: ϩ ϫ 120 (80 2) ϭ 3 120 ϩ 160 280 or ϭ 3393 mm Hg

is in place in a peripheral artery, the SBP read- exhales. Pulsus alternans is an indicator of ings may be falsely elevated because of the the presence of severe ventricular systolic amplitude of the waveform. However, mean failure (Weber, 2003) and can be a sign of arterial pressure (MAP) and DBP data are several conditions, including cardiac tam- accurate (Griffin et al., 1997). ponade, which is a concern following cardiac MAP is the driving force for peripheral surgery. blood flow and the preferred pressure to be Complications associated with an intra- evaluated in unstable patients. On the moni- arterial catheter include ischemia or throm- tor screen, it appears as a digital readout adja- bosis of the affected extremity, infection, and cent to the displayed blood pressure, usually bleeding. Prolonged hyperextension of the in parentheses. MAP can also be calculated by wrist can cause nerve conduction deficits. the nurse using the formula given in Box 9–5. Close assessment for proper positioning and MAP readings do not change as the pressure for signs of any complications related to waveform moves distally along the arterial indwelling intra-arterial catheters (e.g., pres- tree. This pressure is measured electronically ence of paresthesias, redness, extremity tem- by first integrating the area under the arterial perature and color) is an essential nursing pressure waveform and then dividing by the responsibility and should be included in rou- duration of the cardiac cycle. Many clinical tine assessments (Srejic & Wenker, 2003). conditions may be reflected by changes in the arterial waveform. ■ Pulsus alternans (see Figure 9–2) is CENTRAL VENOUS PRESSURE believed to be a sign of decreased myocardial MONITORING contractility. A paradoxical pulse is an exag- Because of the lack of supportive data on cur- geration of the normal variation in the pulse rent use of pulmonary artery catheters during the inspiratory phase of respiration, (PACs), central venous pressure (CVP) in which the pulse becomes weaker as the catheters are being used more often in the person inhales and stronger as the person cardiac surgical population. In one study,

Figure 9–2 Pulsus alternans. Source: Illustrated by James R. Perron 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 151

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researchers compared low-risk patients RV or LV dysfunction, valve disease (mitral, undergoing coronary artery bypass grafting tricuspid), pulmonary hypertension, atrial with CVP with patients undergoing the same fibrillation, high pericardial pressures (such procedure with a PAC. Patients who had sur- as seen in tamponade), high intrathoracic gery with a PAC in place had higher weight pressure (such as seen in pneumothorax or gain and longer intubation time. Further, it is with positive pressure ventilation), and high also speculated that the PAC may be associ- intra-abdominal pressure. A low CVP value is ated with increased morbidity and resource most often indicative of hypovolemia or a utilization (Stewart, Psyhojos, Lahey, Levit- decrease in cardiac output (Kazerooni & sky, & Campos, 1998). Circumstances in Gross, 2003). Volume repletion with a crystal- which a PAC may be used include patients loid, colloid, blood, or blood product, along with pulmonary hypertension, low cardiac with identifying and treating the source of output, or predicted postoperative hemody- fluid loss, will resolve the problem. The most namic instability following cardiac surgery common sources of hypovolemia are overzeal- (Handa, Kyo, & Miyao, 2003). ous diuresis, third spacing, and hemorrhage, It can be anticipated that patients will man- but causes may also include diaphoresis and ifest a decrease in blood and plasma volume vasodilation. CVP readings are influenced by within the first 24 hours following cardiac the relationships among intravascular volume surgery. Etiologic factors for this phenome- status, ventricular compliance, and intratho- non include the patient’s underlying cardiac racic pressure. As a consequence, trending disease, medications (preoperative, anesthe- data and correlating them with the patient’s sia, and vasoactive agents), procedure- clinical status is more likely to optimize the induced hypothermia, rewarming, and patient’s hemodynamic status than evaluat- bleeding. There is no reported agreement on ing and treating just one isolated numeric which data should be used to guide fluid ther- value. apy in these patients. Filling pressures (i.e., To further help assure the accuracy of CVP CVP and pulmonary artery occlusive pressure) readings, pressure waveforms are read at end- are often misleading as signs of optimal left expiration. Reading the tracing at this point ventricular filling, especially in patients with minimizes the influence of intrathoracic alterations in ventricular compliance (Boldt, pressure on the values. 2005). In a landmark study, significant varia- In addition to aligning the transducer to tions were reported in hemodynamic data the phlebostatic axis and interpreting the following cardiac surgery. Because hemody- waveforms at end-expiration, analysis of namic reference data had not been previously waveform morphology is essential when the reported and great variability existed among nurse is collecting hemodynamic data. A the participants in this study, it remains diffi- typical CVP tracing consists of three waves cult to use hemodynamic data as the sole and two descents. An “a” wave represents basis for treatment decisions; indeed, using contraction of the right atrium and corre- acceptable values to guide treatment may sponds with the P wave on an ECG tracing. result in over-treatment of some patients An “a” wave will not be seen in patients with (Sloth et al., 2008). Rather, correlating hemo- tricuspid stenosis, right ventricular hyper- dynamic data with the patient’s clinical pres- trophy, pulmonary hypertension, pul- entation may be the most advantageous monary stenosis, or atrial fibrillation. Giant course of action. “a” waves may be visible if the right atrium Causes of elevated CVP readings may is attempting to eject blood into the right include hypervolemia, increased venous tone, ventricle through a closed tricuspid valve, as 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 152

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Table 9–1 Complications Associated with CVP Catheters

Pneumothorax (usually occurs during catheter placement) Thrombus Infection Air embolism Adjacent vessel perforation Catheter shearing and embolization Thrombophlebitis Extravasation of fluid or medication into the mediastinum, pericardium, retroperitoneum, or pleural cavity Hemothorax Vascular injuries (e.g., local hematoma, arterial laceration, perforation of the superior vena cava, pericardial perforation) Figure 9–3 CVP waveform. Arterial puncture Subpleural hematoma Source: Illustrated by James R. Perron Uncontrolled venous bleeding

occurs in tricuspid stenosis (Mathew & Sources: Gerhardt & Skeehan, 2007; Savolainen et al., 2004. Newman, 2001). Pericardial constriction may be reflected by a prominent “a” wave. A “c” wave is produced with bulging of the from the right atrium (causing an associated tricuspid valve into the right atrium at the decrease in right atrial pressure) into the RV start of ventricular systole. It corresponds (Mathew & Newman, 2001) (see Figure 9–3). An with the start of the QRS complex on an ECG attenuated “Y descent” may be seen in tricuspid tracing (Mathew & Newman, 2001). A large stenosis, reflecting obstruction to right atrial “c” wave may be present in patients who have emptying. tricuspid regurgitation. The nurse must keep in mind that alter- The “X descent” represents atrial relaxation ations in waveforms may result in inaccurate and corresponding displacement of the tri- numeric displays and that analysis of the cuspid valve during ventricular systole waveforms is essential to obtain accurate (Mathew & Newman, 2001). Absence of the hemodynamic data. “X descent” may be present in patients who Table 9–1 lists complications associated have tricuspid regurgitation. with use of a CVP catheter. Some of these A “v” wave represents filling of the right complications are site dependent—for exam- atrium with a closed tricuspid valve. It corre- ple, pneumothorax is associated with internal sponds to the area immediately following the jugular or subclavian insertion sites but not T wave on an ECG tracing. A giant “v” wave may external jugular or femoral site use. be seen where an acute increase in pressure in the The risk of vascular injuries may be right ventricle occurs (Muehlschlegel, Dobija, & reduced with use of real-time ultrasound Lobato, 2007), as is seen in patients who have tri- imaging during catheter insertion. Infectious cuspid regurgitation. Pericardial constriction complications may be minimized when steps may be reflected by a prominent “v” wave. to prevent infection are taken—and such steps Finally, a “Y descent” represents opening of should be part of every hospital’s protocol. the tricuspid valve. At this time, blood is flowing Preventive strategies include hand hygiene, 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 153

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maximal barrier precautions, chlorahexidine good overall indicator of pulmonary skin antisepsis, optimal catheter site selec- artery pressures. Conditions such as tion, use of antibiotic-impregnated catheters, COPD, acute respiratory distress syn- and daily review of catheter necessity (Barbi- drome, and pulmonary hypertension are eto & Mark, 2006). likely to increase PAS pressure. ● The PAD reflects pressure in the area between the pulmonic and aortic valves. ■ MONITORING USING A If there is no obstruction to blood flow, PULMONARY ARTERY CATHETER PAD is a good indicator of LV function. A PAC may be used to assess cardiac function, ● The pressure in the pulmonary artery is cardiac output/index, and intracardiac pres- dynamic; it increases when blood is sures (Vender & Szokol, 2002). Achieving a car- ejected from the right ventricle and then diac index in the range of 2.5–4.2 L/min/m2 is decreases until the next ejection of a goal for most postoperative cardiac surgery blood. The mean pulmonary artery pres- patients. Obtaining these hemodynamic data sure is the continuous average of the directly from the LV would be ideal. Unfortu- pressure in the pulmonary artery during nately, because of the potential for both dam- one complete cardiac cycle (from the age to the left ventricular wall and start of ejection of blood to the next) dysrhythmias, it is not possible to directly (Costanzo, 2008). monitor these pressures on a continuous basis. ● The PAOP, obtained by inflating the Left atrial pressure is an alternative parame- PAC balloon, reflects the pressure ter to evaluate, as this pressure is the earliest between the tip of the PAC and the aor- indicator of left ventricular preload if no tic valve. Because it assesses less surface obstruction to flow is present (e.g., mitral area, the PAOP is more reflective of left stenosis). The line may be used for direct ventricular function than is the PAD. In vasoactive medication infusion when the drug most circumstances, the PAOP is administered may be deleterious if routed thought to closely equate to left atrial through the pulmonary system before reaching pressure and left ventricular end-dias- the left heart. However, because the possibility tolic pressure (LVEDP) or LV preload. of tamponade with catheter removal and entry Fluid therapy and titration of vasoactive of air or catheter dislodgement exist while the agents are based on these data. In some condi- catheter is in place, a left atrial pressure line is tions, the PAOP is reported as greater than not a routine choice for most clinicians. LVEDP—for example, in mitral valve disease, A PAC may be the next choice because it increased pulmonary vascular resistance, use of sits in the pulmonary artery and would pro- positive-pressure ventilation with associated vide an earlier indication of changes in the LV increase in intrathoracic pressure, tachycardia, than a CVP line. With no obstruction to flow, and COPD. In other conditions, the PAOP is pulmonary artery pressure (PAP) will indi- reported as less than LVEDP—for example in rectly reflect left atrial pressure and approxi- the presence of aortic regurgitation, a noncom- mate value of left ventricular end-diastolic pliant left ventricle, or pulmonary embolism pressure (left-sided preload). Values obtained (Tuman, Carroll, & Ivankovitch, 1989). with a PAC include pulmonary artery systolic Normally, the PAD is slightly higher than (PAS), pulmonary artery diastolic (PAD), pul- the PAOP, and the normal correlation is less monary artery mean (PAM), and PAOP. than 5 mm Hg (Marini & Leatherman, 2005). ● The PAS reflects pressure measured from To obtain the PAOP, the balloon must be the tricuspid to the mitral valve and is a inflated, which increases the potential risk of 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 154

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pulmonary artery rupture, pulmonary infarc- right-to-left shunt; this condition also results tion, pulmonary thrombosis or embolism, in an underestimation of CO. Tricuspid and pulmonary artery hemorrhage. Obtaining regurgitation causes underestimation of PAOP readings may not be performed rou- the CO because the injectate will reflux back tinely but may be done if an acute change in into the right atrium and prevent adequate the patient’s clinical status or PAD occurs, or mixing. if no correlation between the PAD and PAOP In patients with a left-to-right shunt, exists. Unit-specific protocols for obtaining increased right heart volume dilutes the injec- hemodynamic data should be followed. tate, resulting in an overestimation of CO. When obtaining PAOP readings, balloon Temperature of the injectate, injectate tech- inflation time should be minimized. The bal- nique, minimal manipulation of the injectate- loon should be inflated slowly to avoid migra- filled syringe, time between measurements, tion of the catheter into a smaller pulmonary and lack of obstruction to a smooth injection artery or vessel rupture. The balloon should be must be confirmed and the patient’s body left deflated at all other times (Marino, 2006). position assessed to ensure accuracy of measurements. The monitor must be preset with the gauge of the PAC in place and the amount ■ CARDIAC OUTPUT of injectate to be infused (5 mL or 10 mL). In MEASUREMENT addition, forward flow—so that adequate mix- The PAC also allows measurement of cardiac ing occurs—is important (Gawlinski, 2004). output (CO) via thermodilution or the Dysrhythmias, such as atrial fibrillation, will assumed Fick method. A bolus of either nor- prevent thorough mixing. Thus the trend in

mal saline or D5W is injected into the RA CO values obtained is extremely important to (proximal) port. The fluid mixes with the monitor. blood as it travels past the tricuspid valve, through the RV, and into the PA. The overall temperature of the mixed blood and injectate Continuous Cardiac Output is measured by the thermistor (a temperature- Potential causes of errors in obtaining inter- sensing device) at the tip of the catheter. The mittent measurements of CO have been dis- amount of time it takes the cooler blood to cussed. Continuous cardiac output (CCO) pass the thermistor is used to calculate CO. catheters use a tracer that is not cool but The longer it takes for the cooler blood to warm; a 10-cm thermal filament is placed on pass, the lower the CO. An electronic display the outside of the catheter at the level of the of the time–temperature curve and calculated RV. The filament warms the catheter every numerical CO value are displayed on the 30–60 seconds, with low levels of heat energy monitor. being transferred to the blood that is adjacent Several variables must be assessed to assure to the filament. The same process is used to the accuracy of the CO displayed. Accuracy of determine CO as with the intermittent injec- CO results is essential because many of the tate method. The only difference is that with hemodynamic calculations listed earlier and this technology CO is calculated based on the subsequent therapeutic modalities are based amount of time it takes the warmed blood on accurate CO determination (Gawlinski, to pass the thermistor instead of cooled 2004). Intracardiac shunts produce shunting blood. The CO value is averaged over of cold injectate into the left heart, which 3–6 minutes, and a numeric display of the cal- decreases PA cooling and lowers the peak of culated value appears on the monitor screen the time–temperature curve, as seen with a (Headley, 1997). 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 155

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Benefits of contour cardiac output include waveform is typically recorded from an intra- avoidance of individual variations in the vol- arterial catheter, although noninvasive record- ume and speed of infusion of the tracer bolus, ings have also been used. The efficacy of and the fact that CO is based on a time- arterial pulse contour-based CO technology weighted average versus a single instantaneous has been demonstrated in patients who under- measurement. Drawbacks include the expense went coronary artery bypass grafting proce- and lack of data supporting improved patient dures (de Waal, Kalkman, Rex, & Buhre, 2007). outcomes with its use (Headley, 1997). Three of the currently available pulse contour cardiac output systems use intra-arterial waveform analysis. The PiCCOTM system uses ther- Alternative Methods to Determine modilution for calibration and requires femoral Cardiac Output or axillary arterial catheterization. It incorporates Even as the incorporation of goal-directed use of a catheter with a thermistor on the tip. The therapy using CO or similar parameters to catheter records aortic pressure waveforms, and guide intravenous fluid and inotropic therapy CO is then calculated using a formula based on continues to increase, other, less invasive the area under the systolic portion of the wave- options for monitoring CO are being adopted form (Button et al., 2007). Data from several stud- in many practices. Technologies that are ies have led some researchers to question the based on arterial pressure can provide CO correlation between CO measurements obtained determinations and measure other clinically using this technology and the intermittent injec- important variables, such as stroke volume tate method in hypothermic patients, including variation (SVV), pulse pressure variation those undergoing cardiopulmonary bypass and (PPV), and systolic pressure variation (SPV). patients with an upper-body warming device in Clinical use of these parameters is emerging use (Böttiger et al., 1995; Ong, Gillies, & Bel- as a means for determining the patient’s abil- lomo, 2004; Spackman & Abenstein, 1993). ity to respond to changes in fluid levels. SVV When the PiCCO system is used, it is suggested occurs due to changes in intrathoracic pres- that the arterial waveform be calibrated preop- sure during spontaneous breathing; blood eratively and that recalibration be avoided pressure decreases during inhalation and until the patient is admitted to the ICU (Rauch increases during exhalation. The opposite et al., 2002). changes are observed when a patient is receiv- The second pulse contour cardiac output ing positive pressure ventilation. system available is LiDCOTM, which uses lithium dilution for calibration and arterial Arterial Pulse Contour CCO pulse wave analysis from PulseCOTM. The radial Arterial pulse contour CCO monitoring esti- or brachial artery is used as the access site. With mates CO based on pulse contour analysis; it this technique, a small dose of intravenous is an indirect method based on analysis of the lithium chloride is administered. Cardiac out- arterial pressure pulsation waveform. This put is then determined by a dilution curve technology relies on the concept that the con- made by a lithium-sensitive electrode that is tour of the arterial pressure waveform is attached to the intra-arterial catheter ( Jonas & proportional to stroke volume. The arterial Tanser, 2002). pressure waveform is used to calculate CO, FloTracTM/VigileoTM, the third method of stroke volume variance, intrathoracic vol- pulse contour analysis, does not employ a cal- umes, and extravascular lung water. These ibration process to improve monitor preci- data are then used to predict response to fluid sion but instead uses a formula or algorithm therapy (Uchino et al., 2006). The arterial to continually update a constant that is used 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 156

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to determine CO (Compton, Zukunft, Hoff- Pulse Pressure Variation mann, Zidek, & Schaefer, 2008). The FloTrac PPV is “the difference between the maximum sensor and Vigileo monitor together consti- and minimum values of the arterial pulse tute the FloTrac system. As with the other pressure during one mechanical breath pulse contour cardiac output systems, SVV divided by the mean of the two values” may be calculated. Data used to calculate SVV (Berkenstadt et al., 2005, p. 721). Reports sug- include the patient’s blood pressure, age, gen- gest that variations in PPV can accurately pre- der, and body surface area. The patient’s CO dict response to fluid therapy in patients with is determined from the stroke volume and shock and in surgical procedures. Upon eval- heart rate. An accurate arterial pressure wave- uating the Frank-Starling curve, an increase form is essential for accurate contour cardiac in preload is associated with a decrease in output determination. Any factor that may PPV; conversely, a decrease in preload is asso- alter the tracing (e.g., dysrhythmias, hypoten- ciated with an increase in PPV and contractil- sion, equipment issues) may affect the results. ity. It has been suggested that PPV is more Recently, a study was conducted to com- accurate in predicting fluid response than pare the efficacy of these three pulse contour CVP and PAOP, SPV, and SVV (Michard, cardiac output systems in determining CO in Lopes, & Auler, 2007). patients who have undergone cardiac surgery. The data suggest that each of the methods is Systolic Pressure Variation comparable to using a PAC with the intermit- SPV is “the difference between the maximum tent injectate method (Button et al., 2007). and minimum systolic blood pressure during one mechanical breath” (Berkenstadt et al., Stroke Volume Variation 2005, p. 721). It can reportedly indicate SVV produces data on changes in preload that decreases in CO from blood loss and predict a occur with mechanical ventilation. It is “the dif- patient’s response to volume repletion. This ference between the maximum and minimum parameter is used to estimate circulating vol- stroke volume during one mechanical breath ume (Gouvêa & Gouvêa, 2005). relative to the mean stroke volume” (Berken- In a study of patients in the ICU who stadt et al., 2005, p. 721). SVV monitoring can underwent coronary artery bypass grafting, provide data that suggest whether a patient’s researchers determined that PPV and SPV stroke volume will improve with volume reple- were both able to predict whether a patient tion (Reuter, Felbinger, Kilger, et al., 2002). would respond to volume repletion with an Currently, there are conflicting data regard- increase in CO. While PPV was demonstrated ing the ability of SVV to predict response to to be superior to SPV at predicting response fluid therapy. Reuter and colleagues (Reuter, to fluid therapy, the researchers concluded Felbinger, Schmidt, et al., 2002) determined that both PPV and SPV were far superior to that SVV predicted preload responsiveness in CVP and PAOP data (Kramer, Zygun, Hawes, cardiac surgery patients. Conversely, Wiese- Easton, & Ferland, 2004). nack and colleagues (2003) reported that SVV did not predict an increase in CO or stroke volume in cardiac surgery patients. Possible Doppler Methods explanations for the discrepancies in results Doppler-based methods use ultrasound and include differences in tidal volumes used and the Doppler effect to determine CO. When differences in the cardiac stability of the two ultrasound waves strike moving objects, the groups of patients (Pinsky, 2003). waves are reflected back to their source at a 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 157

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different frequency, which is directly related and oxygen consumption (the amount of oxy- to the velocity of the moving objects and the gen used by the tissues) ( Jesurum, 2004). angle at which the ultrasound beam strikes Mixed venous blood represents the amount these objects. Proper probe placement is of oxygen in the systemic circulation after the essential when using these methods to moni- blood’s passage through the tissues. Venous tor CO. Several different Doppler-based oxygen saturation data reflect tissue oxygena- methods may be used to measure CO, each of tion and cardiopulmonary function and can which uses a slightly different site in the body be used to discover whether a patient is clini- for measuring blood flow (Berton & Cholley, cally deteriorating. It has been suggested that

2002). Data suggest that ultrasound determi- changes in SvO2 may occur prior to changes nation of CO correlates with data from a PAC in other aspects of the hemodynamic profile and central venous saturation percentage ( Jesurum, 2004).

(Knobloch et al., 2005). Normal SvO2 is in the range of 60% to 80%. Trends and changes in oxygen delivery, oxygen consumption, or tissue oxygenation may Electrical Bioimpedence be identified by reviewing data related to Electrical bioimpedence is a noninvasive venous oxygen saturation. These data can also method to determine CO. Using this technol- be used to determine the efficacy of interven- ogy, CO is measured based on changes in tions implemented to optimize these vari- impedance that occur as blood is ejected from ables as well as procedures performed by the the left ventricle into the aorta and is calcu- ICU nurse while caring for a postoperative lated from changes in thoracic impedance. cardiac surgery patient ( Jesurum, 2004). With With this method, changes in thoracic blood continuous digital readout of SvO2 measure- volume during the cardiac cycle can be used to ments, early recognition and prompt inter- calculate CO. This technique is a successful vention to eradicate effects of poor tissue method of monitoring CO because the algo- oxygenation can be implemented by the ICU rithm eliminates the impedance due to body nurse. Causes of changes in SvO2 are many tissue and lung volume changes, instead using and include most variables affecting preload, only the change in thoracic blood volume for afterload, and contractility. Although not spe- CO determination. An alternative approach cific to any one factor, any change in SvO2 uses a specially designed endotracheal tube to alerts the ICU nurse to quickly investigate. measure electrical impedance changes in the ascending aorta (Ramsay, 2006). Central Venous Oxygen Saturation ■ ASSESSMENT OF OXYGENATION Newer catheters that allow for assessment of central venous oxygen saturation (ScvO ) are PARAMETERS 2 being used in some cardiac surgical programs as Venous Oxygen Saturation the transition away from PACs continues. With In addition to direct pressure measurements this monitoring approach, a blood sample is and CO assessment, other hemodynamic data obtained from a central venous catheter and is

may assess a patient’s condition following car- analyzed. A normal ScvO2 is 70% or greater. If diac surgery. Another type of PAC provides for the value is less than 70%, it indicates that the continuous monitoring of venous oxygenation tissues are extracting more oxygen than is

saturation (SvO2). SvO2 reveals the association normal and that the tissues do not perceive that between oxygen delivery (the amount of oxy- their oxygen needs are being met (Goodrich, gen that is carried to the tissues each minute) 2006; Rivers, Ander, & Powell, 2001). 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 158

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There is some concern that ScvO2 may not of any dysrhythmia may affect a patient’s accurately reflect global hypoxia. ScvO2 and hemodynamic status and requires rapid SvO2 values are not equivalent, but trends in intervention. The etiology and management both values are similar enough to allow them of postoperative dysrhythmias are discussed to be substituted for each other. Both levels in detail in Chapter 15. have been shown to be correlated with patient After assessing heart rate, an adequate outcomes, and both respond rapidly to stroke volume should be ensured. Variables changes in blood flow and oxygenation (Rein- that influence stroke volume—preload, after- hart, Rudolph, Bredle, Hannemann, & Cain, load, and contractility—often are affected in 1989). In any event, changes in trends are the intraoperative and postoperative periods. more important to track than any change in For example, preload may be decreased as the one parameter. patient undergoes the rewarming process, which may lead to vasodilation. Bleeding from chest tubes or third spacing that results ■ POSTOPERATIVE HEMODYNAMIC from the inflammatory process may also ASSESSMENT decrease preload, resulting in a decrease in The ICU nurse caring for a postoperative car- CO. Postoperative bleeding is always a con- diac surgery patient must be aware of both nor- cern for the cardiac surgical patient. Blood mal and baseline parameter values so that any loss will decrease the oxygen-carrying capacity clinical deterioration or improvement in the to vital organs and tissues (Gespard, 2006). patient may be promptly noted. Some patients, Logically, decreased circulating volume will because of their comorbidities or their disease decrease preload, stroke volume, and CO. process (such as valve disease), may require The causes of postoperative bleeding are higher filling pressures postoperatively to many. For instance, the cardiopulmonary maintain an adequate cardiac output/index. bypass circuit may cause platelet destruction An adequate cardiac index in the range of as the blood circulates through it, in addition 2.5–4.2 L/min/m2 will be sustained by nor- to decreasing levels of clotting factors. Inade- malizing heart rate and stroke volume as soon quate hemostasis from incomplete heparin as possible. Many variables may affect heart reversal or excessive protamine administra- rate and rhythm in the postoperative period. tion is another potential cause of altered The most common causes in the postopera- hemostasis, as is a surgical bleed from a tive cardiac surgery patient include hypov- suture site. olemia and pain, both of which should be If chest tube drainage exceeds 100 mL/hr addressed promptly. Despite sedation, the for more than 3 hours, 200 mL/hr for 3 hours, nurse should assess for other signs and symp- or 300 mL in the first hour following surgery, toms that indicate the presence of pain. Pain the surgeon should be notified. Transfusion assessment and management are discussed in of blood or blood products may be ordered if detail in Chapter 14. the coagulation studies are outside of the nor- Dysrhythmias that may be seen in the mal range or if the patient’s hematocrit level is postoperative period include atrial fibrilla- low. If the patient is hypertensive, the blood tion, premature ventricular contractions, and pressure must be decreased to prevent stress ventricular tachycardia; the latter two dys- on the suture sites, which may cause further rhythmias may occur due to electrolyte bleeding. The patient may need to undergo imbalance. All of the dysrhythmias may arise surgical reexploration. Decreases in blood as a result of cardiac irritability from opera- pressure, cardiac filling pressures, and urinary tive manipulation. Ventricular fibrillation, output are signs of hypovolemia that must be although rare, may also occur. The presence evaluated. Adjustments to volume administra- 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 159

Summary 159

tion are frequently necessary as well. Volume ■ SUMMARY repletion is accomplished by administration The number of cardiac surgical patients with of isotonic crystalloids (e.g., lactated Ringer’s pulmonary artery catheters has decreased or normal saline) or colloids (e.g., albumin, worldwide. Interestingly, data have not sup- blood, or blood products) as determined by ported the assertion that any specific hemo- the patient’s lab results. Conversely, if preload dynamic monitoring technique affects indices are too high, diuretics, vasodilators patient outcomes (Nesbitt, 2006). Although (e.g., nitroglycerin), or both may be used. little published evidence exists to associate An increased afterload may result from use of patient monitoring with improved severe left ventricular dysfunction, hypov- clinical outcomes, this lack of evidence does olemia, vasoconstriction, hypothermia, or not necessarily equate to a lack of benefit. increased catecholamine stimulation from Thus catheters will still be used, albeit with the surgical procedure. Along with volume- caution. related interventions and use of a warming ICU nurses play a pivotal role in monitor- blanket, arterial vasodilator administration ing the postoperative hemodynamic status of may be beneficial in such cases. A decreased patients following cardiac surgery. They afterload may be the result of significant must obtain accurate data, integrate those vasodilation from warming; this condition monitoring data with information gained by may be treated with administration of an assessing the patient’s clinical status, and use agent that causes vasoconstriction. clinical judgment to select the best interven- Decreased contractility in the postoperative tions to optimize the patient’s status given period may be the result of an increase or the patient’s current condition and past med- decrease in preload, an increase in afterload, ical history. Having expertise helps to ensure or factors that affect myocardial contractility that obtained parameters are not reflecting directly (e.g., ischemia, right or left ventricular nonphysiologic events such as patient turn- failure, and aneurysms). Electrolyte imbal- ing, artifact, and inaccurate leveling, and that ance and tamponade may also alter contrac- values are assessed at end-expiration. The tility. In such a scenario, preload and ICU nurse with high levels of critical judg- afterload are optimized while other interven- ment and clinical inquiry competencies will tions to treat the underlying cause are com- use accurate information and evidence-based pleted. If indicated, administration of positive guidelines to determine when activities can inotropic agents is initiated. If afterload be clustered or when oxygen consumption is reduction is needed, an IABP is added. The too high to do so. IABP can increase CO by as much as 1 liter By definition, the cardiac surgical patient and may be necessary to support the patient always has underlying cardiac pathology that through an acute event. IABP therapy is dis- will have a major impact on postoperative cussed in detail in Chapter 10. The use of recovery. Monitoring that incorporates a clin- biventricular pacing has also been reported to ical evaluation, review of physiology, and improve contractility following bypass proce- expected responses relative to the type of car- dures (Bakhtiary et al., 2007). diac surgery performed is essential. Invasive If blood builds up inside the mediastinum, catheters may be used to augment—but not cardiac tamponade may occur, resulting in replace—monitoring for subtle changes. The physical compression of the heart, limitation expert ICU nurse validates signs and inter- of diastolic filling time, and a decrease in CO. venes quickly. Each of these competencies is Cardiac tamponade and several other postop- essential to achieve an optimal patient out- erative complications are discussed in detail come following cardiac surgery. in Chapter 13. 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 160

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CASE STUDY

A 76-year-old male patient, with a history of MI and angioplasty to the left anterior descending artery 3 years ago, is admitted to the ICU after on-pump cardiac surgery. Triple bypass was completed on the LAD, circumflex, and right coronary artery. At the time of admission, the patient data were as follows: BP 101/70; MAP 80 mm Hg; HR 110; PAS 22 mm Hg; PAD 9 mm Hg; PAOP 7 mm Hg; CVP 5 mm Hg; temperature 35.4 °C; CI 2.2 L/min/m2; Hct 26%.

Critical Thinking Questions 1. What else should be part of this patient’s initial admission assessment? 2. Which of the parameters given in the case study may indicate hypovolemia? 3. What are the best options for fluid replacement for this patient? 4. What are two reasons why tachycardia might occur in the immediate postoperative period? Answers to Critical Thinking Questions 1. Following cardiac surgery, the ICU nurse will connect the patient to the bedside monitor upon receipt from the operating room. The ECG leads are connected to the bedside monitor from the transport monitor, and heart rate and rhythm are assessed. The pulse oximetry probe is connected to either the finger, earlobe, or forehead. Pulse oximetry is a simple, noninvasive method of monitoring the percentage of hemoglobin

that is saturated with oxygen. The target oxygen saturation (SpO2) is 95% or greater. 2. CVP 5 mm Hg 3. Fluid bolus with normal saline 4. Tachycardia may arise as a result of cardiac irritability from intraoperative manipulation, electrolyte imbalance, pain, or anxiety.

■ SELF-ASSESSMENT QUESTIONS c. 1–4 mm Hg. d. 4–8 mm Hg. 1. Pulsus alternans is indicative of a. left ventricular systolic dysfunction. 4. You suspect that the tip of the PA b. left ventricular diastolic dysfunction. catheter has slipped from the PA to the c. right ventricular systolic dysfunction. RV. Two changes on the waveform that d. right ventricular diastolic dysfunction. might indicate this dislodgement are a. higher diastolic pressure and 2. Causes of an increased CVP may include presence of a dicrotic notch. a. hypervolemia, mitral regurgitation, b. lower diastolic pressure and absence and third spacing. of a dicrotic notch. b. ascites, pulmonary hypertension, and c. higher diastolic pressure and absence diuresis. of a dicrotic notch. c. cardiac tamponade, pneumothorax, d. lower diastolic pressure and presence and third spacing. of a dicrotic notch. d. hypervolemia, pneumothorax, and tricuspid stenosis. 5. Positive inotropic therapy to improve cardiac output includes 3. An acceptable correlation between the a. IABP, milrinone, and labetalol. PAD and PAOP, with the PAD being b. dobutamine, milrinone, and IABP. higher, is c. digoxin, atenolol, and IABP. a. 3–8 mm Hg. d. IABP, metoprolol, and dobutamine. b. 1–2 mm Hg. 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 161

Self-Assessment Questions 161

6. A large “v” wave seen on the PAOP wave d. percentage of lactic acid remaining in tracing may indicate the blood, assessed upon return to a. mitral regurgitation. the right side of the heart after b. mitral stenosis. passage through the systemic c. tricuspid regurgitation. circulation and tissues. d. tricuspid stenosis. 9. Interventions to increase preload include 7. The presence of a paradoxical pulse is a. crystalloids, blood, and epinephrine. often indicative of b. nitroglycerin, crystalloids, and a. ARDS. furosemide. b. hypertrophic cardiomyopathy. c. epinephrine, norepinephrine, and c. mitral stenosis. furosemide. d. cardiac tamponade. d. crystalloids, blood, and nitroglycerin.

8. SvO2 represents the 10. The PAD would not reflect left ventricu- a. percentage of oxygen remaining in lar pressure in the presence of the blood, assessed upon return to a. mitral stenosis. the right side of the heart after b. tricuspid stenosis. passage through the systemic c. pulmonic stenosis. circulation and tissues. d. tricuspid regurgitation. b. percentage of oxygen removed from the blood, assessed upon return to Answers to Self-Assessment Questions the right side of the heart after 1. a 6. a passage through the systemic 2. d 7. d circulation and tissues. c. percentage of lactic acid removed 3. c 8. a from the blood, assessed upon return 4. b 9. a to the right side of the heart after 5. b 10. a passage through the systemic circulation and tissues. Clinical Inquiry Box

Question: Does the level of experience of a critical care nurse affect the hemodynamic decision making in postoperative cardiac surgery patients? Reference: Currey, J., & Botti, M. (2006). The influence of patient complexity and nurses’ experience on haemodynamic decision-making following cardiac surgery. Intensive and Critical Care Nursing, 22(4), 194–205. Objective: To uncover the decision-making utilized by critical care nurses during the first 2 hours after cardiac surgery. Specifically, a nurse’s level of experience and complexity of decision making were investigated. Methods: This descriptive study used continuous nonparticipant observation of clinical practice for a 2-hour period after cardiac surgery. Observations were recorded in field notes, and semistruc- tured interviews occurred among 28 nurses and were audio recorded. Content analysis of the observation and interview data were performed. Results: Experience of the nurses and support of colleagues were associated with higher-quality decision making. These two factors—nurses’ utilization of evidence for practice and the experience levels of both nurses and their colleagues—are critical for the delivery of quality patient care. Conclusion: These findings suggest staffing units with experienced nurses is essential, especially to ensure that new nurses have individuals to use as resources in the decision-making process. 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 162

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■ REFERENCES monitoring devices in patients undergoing American Association of Critical-Care Nurses cardiac surgery. British Journal of Anaesthesia, (AACN). (2004). Pulmonary artery pressure 99(3), 329–336. measurement practice alert. Retrieved August Cloud, G. C., Rajkumar, C., Kooner, J., Cooke, J., & 14, 2008, from www.aacn.org/WD/Practice/ Bulpitt, C. W. (2003). Estimation of central Docs/PAP_Measurement_05-2004.pdf aortic pressure by sphygmoCor(r) requires Bakhtiary, F., Dogan, S., Dzemali, O., Ackermann, H., intra-arterial peripheral pressures. Clinical Sci- Kleine, P., Schächinger, V., et al. (2007). Impact ence, 105(2), 219–229. of different pacing modes on left ventricular Compton, F. D., Zukunft, B., Hoffmann, C., Zidek, contractility following cardiopulmonary bypass. W., & Schaefer, J. H. (2008). Performance of a Pacing and Clinical Electrophysiology, 30 (9), minimally invasive uncalibrated cardiac output TM TM 1083–1090. monitoring system (FloTrac /Vigileo ) in Barbieto, A., & Mark, J. (2006). Arterial and central unstable haemodynamically unstable patients. venous pressure monitoring. Anesthesiology British Journal of Anaesthesia, 100(4), 451–456. Clinics, 24(4), 717–735. Costanzo, L. S. (2008). Cardiovascular physiology. Berkenstadt, H., Friedman, Z., Preisman, S., Kei- In L. S. Costanzo. Physiology cases and problems dan, I., Livingstone, D., & Perel, A. (2005). (3rd ed., pp. 47–56). Philadelphia: Lippincott Pulse pressure and stroke volume variations Williams & Wilkins. during severe haemorrhage in ventilated dogs. de Waal, E. E., Kalkman, C. J., Rex, S., & Buhre, W. F. British Journal of Anaesthesia, 94 (6), 721–726. (2007). Validation of a new arterial pulse- Berton, C., & Cholley, B. (2002). Equipment review: contour based cardiac output device. Critical New techniques for cardiac output measure- Care Medicine, 35(8), 1904–1909. ment: Oesophageal Doppler, Fick principle Fink, M. P. (2003). Monitoring techniques and com- using carbon dioxide, and pulse contour plications in critical care. In N. A. Norton, R. R. analysis. Critical Care, 6(3), 216–221. Bollinger, A. E. Chang, S. F. Lowry, S. J. Mulvi- Blount, K. (2007). Hemodynamic monitoring. In R. hill, H. I. Pass, et al. (Eds.), Essential practice of sur- Kaplow & S. R. Hardin (Eds.), Critical care nurs- gery (pp. 113–118). New York: Springer. ing: Synergy for optimal outcomes (pp. 139–159). Gawlinski, A. (2004). Measuring cardiac output: Sudbury, MA: Jones and Bartlett. Intermittent bolus thermodilution method. Boldt, J. (2005). Volume therapy in cardiac surgery. Critical Care Nurse, 24(5), 74–78. Annals of Cardiac Anaesthesia, 8(2), 104–116. Gerhardt, M. A., & Skeehan, T. M. (2007). Monitor- Borrow, K. M., & Newburger, J. W. (1982). Noninva- ing the cardiac surgery patient. In F. A. Hens- sive estimation of central aortic pressure using ley, D. E. Martin, & G. P. Gravlee (Eds.), oscillometric method of analysing systemic A practical approach to cardiac anesthesia artery pulsatile blood flow: Comparative study (pp. 104–141). Philadelphia: Lippincott of indirect systolic, diastolic, and mean Williams & Wilkins. brachial artery pressure with simultaneous Gespard, K. J. (2006). The red blood cell and alter- direct ascending aortic pressure measure- ations in oxygen transport. In C. Porth, Essen- ments. American Heart Journal, 103 (5), 879–886. tials of pathophysiology (2nd ed., pp. 211–228). Böttiger, B. W., Rauch, H., Böhrer, H., Motsch, J., Philadelphia: Lippincott Williams & Wilkins. Soder, M., Fleischer, F., et al. (1995). Continu- Goodrich, C. (2006). Continuous central venous ous versus intermittent cardiac output mea- oximetry monitoring. Critical Care Nursing Clin- surement in cardiac surgical patients ics of North America, 18(2), 203–209. undergoing hypothermic cardiopulmonary Gouvêa, G., & Gouvêa, F. G. (2005). Measurement bypass. Journal of Cardiothoracic and Vascular of systolic pressure variation on a Datex AS/3 Anesthesia, 9(4), 405–411. monitor. Anesthesia & Analgesia, 100(6), 1864. Button, D., Weibel, L., Reuthebuch, O., Genoni, M., Griffin, S. E., Robergs, R. A., & Heyward, V. H. Zollinger, A., & Hofer, C. K. (2007). Clinical (1997). Blood pressure measurement during evaluation of FloTrac/VigileoTM system and exercise: A review. Medicine and Science in Sports two established continuous cardiac output and Exercise, 29(1), 37–74. 57625_CH09_145_164.pdf 4/10/09 11:06 AM Page 163

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Rauch, H., Muller, M., Fleischer, F., Bauer, H., Mar- Spackman, T. N., & Abenstein, J. P. (1993). Contin- tin, E., & Böttiger, B. W. (2002). Pulse contour uous cardiac output may be more accurate analysis versus thermodilution in cardiac sur- than bolus thermodilution output during the gery patients. Acta Anaesthesiologica Scandinav- use of an upper-body warming blanket. Anes- ica, 46(4), 424–428. thesiology, 79(3A), 473A. Reinhart, K., Rudolph, T., Bredle, D. L., Hanne- Srejic, U., & Wenker, O. C. (2003). “A-line” or mann, L., & Cain, S. M. (1989). Comparison of “intra-arterial catheters.” Internet Journal of central-venous to mixed-venous oxygen satu- Health, 3(1). http://www.ispub.com/ostia/ ration during changes in oxygen supply/ index.php?xmlFilePath=journals/ijh/vol3n1/ demand. Chest, 95(6), 1216–1221. aline.xml Reuter, D. A., Felbinger, T. W., Kilger, E., Schmidt, C., Stafford-Smith, M., & Newman, M. F. (2006). Lamm, P., & Goetz, A. E. (2002). Optimizing What effects do hemodilution and blood fluid therapy in mechanically ventilated transfusion during cardiopulmonary bypass patients after cardiac surgery by on-line moni- have on renal outcomes? Nature Clinical Prac- toring of left ventricular stroke volume varia- tice Nephrology, 2(4), 188–189. tions: Comparison with aortic systolic Stewart, R. D., Psyhojos, T., Lahey, S. J., Levitsky, S., & pressure variations. British Journal of Anaesthesia, Campos, C. T. (1998). Central venous catheter 88(1), 124–126. use in low-risk coronary artery bypass grafting. Reuter, D. A., Felbinger, T. W., Schmidt, C., Kilger, E., Annals of Thoracic Surgery, 66(4), 1473–1496. Goedje, O., Lamm, P., et al. (2002). Stroke vol- Tuman, K. J., Carroll, G. C., & Ivankovitch, A. D. ume variations for assessment of cardiac (1989). Pitfalls in interpretation of pulmonary responsiveness to volume loading in mechani- artery catheter data. Journal of Cardiothoracic cally ventilated patients after cardiac surgery. Anesthesia, 3(5), 625–641. Intensive Care Medicine, 28(4), 392–398. Uchino, S., Bellomo, R., Morimatsu, H., Sugihara, Rivers, E. P., Ander, D. S., & Powell, D. (2001). Cen- M., French, C., Stephens, D., et al. (2006). Pul- tral venous oxygen saturation monitoring in monary artery catheter versus pulse contour the critically ill patient. Current Opinions in Crit- analysis: A prospective epidemiological study. ical Care, 7(3), 204–211. Critical Care, 10(6), R174. Rothe, C. (2003). Toward consistent definitions for Vender, J. S., & Szokol, J. W. (2002). Hemodynamic preload and afterload—revisited. Advances in assessment in the critically ill patient. In M. J. Physiology Education, 25(1–4), 44–45. Murray, D. B. Coursin, R. G. Pearl, & D. S. Savolainen, H., Takala, J., Widmer, M., Heller, G., Prough (Eds.). Critical care medicine: Periopera- Carrell, T., Schmidt, J., et al. (2004). Severe vas- tive management (2nd ed., pp. 122–136). cular complications of central venous line. Philadelphia: Lippincott Williams & Wilkins. International Journal of Angiology, 13(3), Weber, M. (2003). Pulsus alternans: A case study. 109–112. Critical Care Nurse, 23(3), 51–54. Sloth, E., Lindskov, C., Lorentzen, A.-G., Nygaard, Wiesenack, C., Prasser, C., Rodig, G., & Keyl, C. M., Kure, H. H., & Jakobsen, C-J. (2008). Car- (2003). Stroke volume variation as a continuous diac surgery patients present considerable parameter of cardiac preload using pulse con- variation in pre-operative hemodynamic vari- tour analysis in mechanically ventilated patients. ables. Acta Anaesthesiologica Scandinavica, 52(7), Anesthesia & Analgesia, 96(5), 1254–1257. 952–958. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 165

Chapter 10 Intra-aortic Balloon Pump

Barbara Hutton-Borghardt

■ INTRODUCTION The intra-aortic balloon pump (IABP) is a cardiac surgery patients (Ahmad, 2006). mechanical device that is temporarily used to Worldwide, it is estimated that 100,000 IABP improve cardiac function. In many situations, catheters are inserted annually (Stenz, 2006). the IABP is life-saving in its ability to stabilize A description of how an IABP improves car- patients as they await procedures such as diac function appears in Box 10–1. heart transplant, coronary artery bypass graft- ■ ing (CABG), or percutaneous coronary inter- COMPONENTS OF AN IABP ventions (PCI) such as PTCA/stent placement The IABP consists of two main parts: (1) a (Tommaso, 2002). double-lumen catheter with an inflatable bal- An IABP may be further indicated in the loon attached to the distal end and (2) a con- management of cardiogenic shock (Reid & Cot- sole that regulates the inflation and deflation trell, 2005). Medications such as vasodilators of the balloon. One lumen of the balloon and inotropes are used initially to improve car- catheter is attached to a pressure-transducer diac function. If they are not effective, the IABP device that monitors the patient’s arterial aor- may be used alone or with pharmacotherapy to tic pressure; the other lumen (with the bal- assist left ventricular (LV) function and loon) is attached to a gas reservoir. The improve cardiac output (CO) (Stenz, 2006). console allows for appropriate timing of bal-

Since its introduction in the late 1960s, loon inflation and houses the helium (or CO2) IABP has become a widely used device in pre- tanks. The tanks contain the gas that will be operative, intraoperative, and postoperative used to inflate the balloon during therapy.

Box 10–1 Goals of IABP Therapy

The IABP achieves its goals of stabilizing cardiac function by several mechanisms:

● It improves cardiac function (cardiac output) by decreasing left ventricular end-diastolic volume (preload). ● It improves myocardial oxygen supply by increasing blood flow to the coronary arteries. ● It decreases myocardial oxygen demand by decreasing left ventricular wall tension. ● It stabilizes cardiac function in patients with dysrhythmias and myocardial ischemia.

Source: Laurent & Shinn, 2005.

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Additionally, the console has a monitor that emptying decreases preload (or end-diastolic displays the arterial waveforms, electrocardio- volume) and myocardial oxygen demand. The gram (ECG), and balloon-pressure wave- tension caused by the pressure of blood on forms. Waveforms assist practitioners in the left ventricle as it ejects blood (afterload) determining whether the timing of balloon is diminished as well, further decreasing inflation/deflation is appropriate and allow myocardial oxygen demand and increasing for any necessary adjustments to be made CO and ejection fraction (EF). Systolic blood (Metules, 2003). pressure is noted to be lower with the reduction in afterload (Metules, 2003). Secondary effects of the IABP placement Physiology of Balloon Function result from the improvement in cardiac func- The IABP is timed to inflate and deflate in tion as well. Heart rate, pulmonary artery opposition to the cardiac cycle. The goal of diastolic (PAD), and pulmonary artery occlu- inflation of the IABP balloon is to enhance sive pressures (PAOP) are decreased; mean perfusion. The balloon inflates at the begin- arterial pressure (MAP), CO, and perfusion ning of diastole and deflates before ventricular to vital organs are increased (Laham & systole, a process known as counterpulsation. Aroesty, 2008). To correlate the inflation and deflation to the ECG, the balloon begins to inflate in the mid- ■ dle of the T wave and to deflate before the end INDICATIONS FOR IABP THERAPY of the QRS complex (Ahmad, 2006). The IABP is used in a variety of clinical situa- Inflation of the balloon at the beginning of tions, such as in cardiogenic shock. Cardio- diastole displaces blood upward toward the genic shock is a complication in approximately aortic root and augments the diastolic pressure 7.5% of patients with an acute myocardial between the balloon and the aortic origin. The infarction (AMI) and carries a mortality rate in increase in diastolic pressure, which is known the range of 70% to 80%. Early revasculariza- as diastolic augmentation, forces blood back tion with angioplasty, fibrinolysis, or bypass into the coronary arteries, which are normally surgery is initiated to improve mortality in perfused during diastole. Consequently, blood such circumstances (Hochman et al., 2006). In flow to the coronary arteries is increased, with a the case of the patient with cardiogenic shock, resultant improvement in myocardial oxygen the IABP may be used to reduce myocardial supply. IABP inflation further causes a ischemia and improve cardiac function, espe- decrease in heart rate and afterload and cially as the patient is prepared for a revascu- enhances LV function. Ischemia of the myocar- larization procedure (Metules, 2003). Data dial muscle is diminished or relieved with the suggest that the use of the IABP in reducing ensuing improved CO (Boehmer & Popjes, ischemia in AMI can preserve and prevent the 2006). During inflation, blood is also pushed loss of viable myocardial muscle and improve forward to the periphery. In this way, blood survival rates in cardiogenic shock (Lindholm flow is increased below the inflated balloon, et al., 2003). In post-MI patients, persistent which may enhance perfusion of the renal ischemia and reinfarction may also be pre- arteries and systemic blood vessels (Paul & Ras- vented through use of an IABP (Duvernoy & musson, 2007). Bates, 2005). Deflation of the balloon immediately For patients with unstable angina who are before systole occurs pulls blood forward receiving maximum medical therapy but who away from the left ventricle, allowing for still experience chest pain/discomfort, the more complete emptying. This enhanced LV IABP has been successful in reducing or 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 167

Indications for IABP Therapy 167

entirely eliminating symptoms. The patient’s enable these patients to ambulate as they condition can be stabilized in preparation for await transplant (Boehmer & Popjes, 2006). surgery or revascularization procedure Refractory ventricular dysrhythmias may (Ahmad, 2006; Laham & Aroesty, 2008). also be responsive to IABP therapy. Poor LV In post-MI patients, structural damage, function, coupled with an increase in afterload such as a ventriculoseptal defect (VSD) or and increased myocardial oxygen demand, will mitral regurgitation may occur. The IABP produce ventricular stretching. Ventricular can help hemodynamically stabilize these stretching increases irritability, resulting in dif- patients until surgical repair can be per- ficult to treat dysrhythmias. The use of the formed. With a VSD, there is an abnormal IABP improves coronary blood flow, thereby opening between the right and left ventri- helping to reduce irritability. Additionally, cles. Because pressure is higher in the left because the IABP decreases preload and after- ventricle than in the right ventricle, blood is load, the ventricle will be less distended, which shunted into the right ventricle, resulting in further decreases irritability and arrhythmo- a lower CO and right ventricular failure. The genicity (Fotopoulos et al., 1999). decrease in afterload produced by the IABP It is often difficult to wean postoperative decreases the right-to-left shunt (Thiele on-pump cardiac surgery patients from car- et al., 2003). diopulmonary bypass (CPB) due to preexist- Mitral regurgitation in post-MI patients is ing poor cardiac function and the effects of often due to papillary muscle dysfunction or CPB itself. Placing patients on CPB involves rupture. The papillary muscles, which are stopping the heart, usually with the use of a located in the mid- to lower ventricles, are cold electrolyte solution (cardioplegia), and connected to the valve leaflets by the string- inducing a controlled state of ischemia. In the like cordinae tendinae. When left ventricular postoperative period, the myocardial muscle systole occurs, the papillary muscles contract is stunned and may need assistance to func- and pull on the cordinae. This action pre- tion effectively (Dixon, Santamaria, & Camp- vents the mitral valve leaflets from inverting. bell, 2005; Henke & Eigsti, 2003). The IABP In the setting of papillary muscle dysfunc- stabilizes the hemodynamic profile of these tion, the mitral valve becomes incompetent cardiac surgery patients and allows them to and regurgitant blood flow occurs. Blood is be weaned more slowly with less risk of organ then forced back up into the left atrium dur- damage from a failing heart. Myocardial stun- ing ventricular systole, increasing the pres- ning is discussed in detail in Chapter 13. sure in that chamber. The increased left atrial Preoperative use of the IABP in patients pressure is transmitted into the pulmonary who are considered at high risk for cardiac vasculature, causing pulmonary congestion surgery has been shown to lower the postop- and edema. Use of the IABP to decrease after- erative mortality rate and shorten intensive load can diminish this regurgitant blood care recovery (Christenson, Cohen, Miller, flow, thereby relieving pulmonary congestion Ohman, & Urban, 2002). High-risk patients as the patient awaits surgical repair (Antman include those with two of the following char- et al., 2004). acteristics: poor LV function (EF less than The IABP may be essential to assist cardiac 30%), unstable angina, left main coronary function in patients with end-stage cardiac artery stenosis of greater than 70%, and disease or damage while they are awaiting undergoing a redo bypass procedure (Chris- transplant (i.e., as a bridge to transplant). The tenson, Simonet, & Schmuziger, 2000). IABP may be used on a longer basis—as long Other indications for use of IABP therapy as 6 months—in these instances. Its use may include progressive heart failure, prevention 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 168

168 Chapter 10 Intra-aortic Balloon Pump

of restenosis of the coronary artery in a post- catheter is inserted into either the right or left PTCA procedure, need for cardiac support femoral artery. It is threaded up into the during noncardiac surgery (Stone et al., descending aorta so that the tip of the 2003; Tremper, 2006), right ventricular fail- catheter is located 1 to 2 centimeters below ure, and septic shock (Kern, King, Douglas, & the subclavian branch of the aortic arch and Franch, 2004). above the branches of the renal arteries (Kern In a worldwide study known as the Bench- et al., 2004; Metules, 2003) (see Figure 10–1). mark Registry, more than 16,000 patients who In bridge-to-transplant patients, the catheter had undergone IABP support were evaluated. is usually inserted in the subclavian fossa, The most common indications for initiating with the distal end being located above the IABP therapy were to provide hemodynamic renal arteries (Boehmer & Popjes, 2006). support during or after a cardiac catheteriza- Traditionally, the balloon catheter is tion procedure, cardiogenic shock, postopera- inserted through an introducer sheath, tive cardiac surgery in which CPB was used, although many newer catheters are designed preoperative cardiac support in high-risk to be sheathless. The latter design results in a patients, and unstable angina refractory to smaller-diameter catheter in the femoral medical therapy (Ferguson et al., 2001). artery, decreasing the chance of ischemic complications to the lower extremity (Erdo- ■ CONTRAINDICATIONS TO IABP gan et al., 2006). THERAPY The catheter may be inserted under fluoroscopy, which facilitates direct visualization—a Contraindications to the use of the IABP are key consideration in ensuring proper placement few and can be divided into absolute and rela- of the catheter. If fluoroscopy is not used, a radi- tive contraindications. Absolute contraindica- ograph film will be checked immediately follow- tions are those in which the patient should ing the procedure (Little, 2004). When viewed, not receive IABP therapy; they include abdom- the tip of the catheter should be located at the inal aortic aneurysm, aortic dissection, aortic second or third intercostal space. Proper posi- insufficiency, and irreversible brain damage tioning is essential, as a catheter placed too high (Little, 2004). Relative contraindications are will obstruct blood flow to the subclavian artery, those in which the potential risk of using the which supplies the head and upper extremities. IABP must be weighed against the potential A catheter placed too low can obstruct blood benefit; they include patients with peripheral flow to the renal arteries (Zellinger, 2007). vascular disease, coagulopathies or thrombocytopenia, terminal diseases, and end-stage cardiomyopathies that are not suitable for transplant (Little, 2004; Tremper, 2006).

■ INSERTION OF AN IABP Insertion of an IABP catheter may be performed at the bedside in the ICU, in the catheterization lab, or in the operating room. Generally, institutional policy requires an informed consent to be signed and reviewed for completeness prior to insertion. Figure 10–1 Inflated balloon catheter After preparation of the area and adminis- in descending aorta. tration of a local anesthetic, the balloon Source: Illustrated by James R. Perron 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 169

Timing 169

After the catheter is secured in place, a ster- balloon. In such a case, the trigger must be ile dressing is applied to the insertion site. restored or a different trigger selected for the The patient’s ECG tracing is displayed on the pump to work. console’s monitor; review of the ECG is The arterial waveform displayed on the important to maintain proper triggering of console’s monitor is used to identify whether the pump. The central lumen of the balloon the timing of inflation and deflation is accu- catheter is attached to a pressure-monitoring rate. Balloon inflation should start at the device with continuous flush to monitor the beginning of diastole; deflation occurs just arterial pressure waveform. The balloon before systole. Initially, the inflation fre- lumen is attached to the gas reservoir of the quency is set at 1:2 (every other beat assisted) IABP console. so that the unassisted and assisted waveforms Upon its initial setup and every hour there- can be compared. Later, the frequency may be after, the balloon will be inflated with a switched to 1:1 (every beat assisted) if the syringe, or by the autofill function on some patient’s status requires this timing. As the consoles, with the appropriate volume of patient’s condition improves, the frequency

helium or CO2. Helium is beneficial, espe- may be weaned to 1:2, 1:3, 1:4, or 1:8 before cially with faster heart rates, because it is IABP therapy is discontinued.

lighter in density than CO2 and can travel To confirm that the timing of inflation and faster in and out of the balloon circuit. How- deflation is correct, specific characteristics are ever, in the event helium is released into the observed on the arterial waveform. First, it is descending aorta (e.g., from a leak or balloon necessary to become familiar with the normal rupture), the gas will rapidly move to the cere- arterial waveform, noting the dicrotic notch bral and coronary vasculature—an immedi- (see Figure 10–2). Next, the arterial waveform ately fatal complication (Little, 2004). Carbon of a patient receiving IABP therapy is dioxide, while slower in moving through the observed. The unassisted systole, the dicrotic balloon circuit, has the advantage of being a notch signifying closure of the aortic valve, more soluble gas and may cause less harm and the unassisted aortic end-diastolic pres- and decreases the potential for gas embolism sure should be identified (see Figure 10–3). development should the gas leak into the Following the dicrotic notch of an assisted bloodstream via a ruptured or torn balloon beat will be diastolic augmentation. The (Metules, 2003). Balloon volume size varies dicrotic notch should form a distinct “V” from 30 to 34 mL for a smaller adult to 50 mL shape between the unassisted systole and the for a larger adult. Most balloons used are 40 augmented diastolic, indicating that pressure mL in size (Quaal, 2005). increased in the aortic root during balloon inflation. Following the augmented diastolic is the assisted end-diastolic pressure, which is ■ TIMING lower than the unassisted diastolic pressure Correct timing of balloon inflation and defla- because deflation of the balloon results in tion is imperative to achieve the optimal ben- lower aortic pressure. efit. Usually, the ECG is used to trigger the Balloon inflation is optimal when (1) a sharp pump: The pump identifies the “R” wave to “V” is noted at the dicrotic notch and (2) fol- signify ventricular systole. Other triggers, lowing the dicrotic notch, the augmented dias- such as an arterial pressure waveform or pacer tolic is as high as or higher than the previous spikes, may also be used (Metules, 2003). If systolic blood pressure. Balloon deflation is the designated trigger is not noted, the pump optimal when (1) the assisted end-diastolic will not initiate inflation and deflation of the pressure is lower, usually by 5 to 10 mm Hg, 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 170

170 Chapter 10 Intra-aortic Balloon Pump

mm Hg 120

Dicrotic Notch 100

80 Figure 10–2 Normal arterial waveform. Source: Illustrated by James R. Perron

Unassisted Systole

Diastolic Augmentation mm Hg 140 Assisted Systole

120

100 Dicrotic Notch 80

Unassisted Aortic Assisted Aortic End Diastolic Pressure End Diastolic Pressure Figure 10–3 Arterial waveform of IABP patient, 1:2 counterpulsation. Source: Illustrated by James R. Perron

than the unassisted aortic end-diastolic pres- ous consequences, especially when inflation is sure and (2) the assisted systolic blood pressure not timed correctly (Pantalos et al., 2003). is 5 to 10 mm Hg lower than the unassisted sys- Timing errors occur when there is early or tolic pressure (Tremper, 2006). late inflation or early or late deflation of the balloon. With early balloon inflation, the balloon inflates before closure of the aortic valve. This Timing Errors action forces the valve to close early, resulting Although most IABPs have automatic timing, in aortic regurgitation and subsequent reduc- it is essential that continuous monitoring be tion in stroke volume, as well as increases in maintained. Often, manual adjustments to end-diastolic volume and myocardial oxygen optimize timing are needed. With timing demand. In such a case, the arterial waveform errors, not only are patients not receiving opti- will lose its characteristic “‘V” shape before mal benefit, but they may also suffer deleteri- diastolic augmentation (see Figure 10–4). 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 171

Timing 171

mm Hg Unassisted Systole 140 Diastolic Augmentation

120 Assisted Systole

100

60 Assisted Aortic End Diastolic Pressure Figure 10–4 Arterial waveform with early balloon inflation. Source: Illustrated by James R. Perron mm Hg Unassisted Systole 140 Diastolic Augmentation Assisted Systole 120

100

Dicrotic 80 Notch

60 Assisted Aortic End Diastolic Pressure Figure 10–5 Arterial waveform with late balloon inflation. Source: Illustrated by James R. Perron With late inflation, the balloon inflates later balloon deflates later than the optimal time, than the appropriate time after closure of the its volume decreases as the aortic valve opens aortic valve, with resultant lower augmented instead of before it opens. This results in the diastolic and coronary perfusion pressures. As loss of the afterload reduction benefit; it may a result, the IABP’s key benefit—improving also increase afterload (and myocardial oxygen blood and oxygen supply to the coronary demand) as the inflated balloon impedes the arteries—is lost or reduced. On the waveform, ejection of blood from the left ventricle. The the peak of the augmented diastolic will be waveform will reveal a widened augmented farther away from the dicrotic notch and will diastolic wave and a slow rise of the next be lower, instead of higher, than the unas- assisted systole (see Figure 10–7). sisted systolic (see Figure 10–5). Most IABP consoles have a display for the Normally, balloon deflation occurs just balloon pressure waveform. This waveform before the beginning of systole. If it occurs too represents the pressure as gas is propelled in far before the onset of systole, however, the and out of the balloon catheter. Monitoring patient’s diastolic pressure will rise, leading to this waveform is beneficial as it will assist the increases in afterload and myocardial oxygen ICU nurse in determining whether the balloon demand. The arterial waveform reveals a sharp is functioning effectively (Quaal, 2005) (see drop-off in the augmented diastolic curve, fol- Figure 10–8). Caregivers may find it necessary lowed by a “U”-shaped curve before the next to follow the specific manufacturer’s direc- systolic upstroke (see Figure 10–6). When the tions for many settings on such devices, as 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 172

172 Chapter 10 Intra-aortic Balloon Pump

mm Hg Diastolic Augmentation 140 Assisted Systole

120

Unassisted Aortic 100 End Diastolic Pressure

80 Assisted Aortic End Diastolic Pressure 60 Figure 10–6 Arterial waveform with early balloon deflation. Source: Illustrated by James R. Perron

Unassisted Systole mm Hg 140 Diastolic Augmentation

120 Prolonged Rate of Rise of Assisted Systole 100 Widened Appearance 80 Assisted Aortic End Diastolic Pressure 60 Figure 10–7 Arterial waveform with late balloon deflation. Source: Illustrated by James R. Perron

C C D D

B E B E

A F A' F A

Figure 10–8 IABP waveform. A = Balloon Pressure baseline; B = Rapid inflation; C = Peak inflation artifact; D = Balloon Pressure Plateau (balloon is completely inflated); E = Rapid deflation; F = Balloon deflation artifact; A' = Return to baseline (balloon completely deflated) Source: Illustrated by James R. Perron 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 173

Complications of IABP Therapy 173

Box 10–2 IABP Therapy Waveform Definitions

Dicrotic notch: An area on the downstroke of the arterial waveform that results from the slight pressure increase created by closure of the aortic valve. Diastolic augmentation: The increase in pressure in the aorta above the balloon catheter that results with balloon inflation during diastole. It increases perfusion in the coronary arteries and myocardial oxygen supply. Unassisted aortic end-diastolic pressure: The pressure in the aorta at the end of diastole when counterpulsation via the balloon pump has not assisted that cardiac cycle. Assisted aortic end-diastolic pressure: The pressure in the aorta at the end of diastole when counterpulsation has assisted the cardiac cycle. It is usually lower than the unassisted end-diastolic pressure. Unassisted systole: The systolic aortic pressure when counterpulsation has not assisted the cycle. Assisted systole: The systolic aortic pressure when counterpulsation has assisted the cardiac cycle. It is usually lower than the unassisted systole due to the action of balloon deflation.

Source: Laurent & Shinn, 2005.

consoles offered by different companies may cular disease (Hurwitz & Goodman, 2005). have unique properties. Limb ischemia can occur while the catheter is Refer to Box 10–2 for definitions related to in place or within hours of its removal and is IABP therapy. related to presence of a clot at the catheter site. Thrombectomy is usually required to treat this complication (Marino & Sutin, 2006). ■ COMPLICATIONS OF IABP Other vascular complications include THERAPY bleeding or hemorrhage from the insertion Although the mortality rate associated with site, perforation of the femoral artery, superfi- the use of the IABP is low, the rate of compli- cial or deep vein thrombosis, stroke, aortic cations is reported to range from 2% to 40% dissection or perforation, and compartment (Boehmer & Popjes, 2006; Stenz, 2006; Trem- syndrome (Kern et al., 2004; Tremper, 2006). per; 2006). In the largest study of IABP use, Vascular complications can result in severe the complication rate was 7%, with major consequences, to the point that the patient complications occurring in only 2.8% of cases may require an amputation, thrombectomy, (Ferguson et al., 2001). blood transfusions, or vascular surgery The most prevalent complications are vascu- (Boehmer & Popjes, 2006; Stone et al., 2003). lar in nature, with the most common being Mortality rates associated directly with the lower-limb ischemia below the insertion site. use of the IABP are reported to be less than Fortunately, catheter sizes are becoming 1% (Ferguson et al., 2001; Stone et al., 2003). smaller and many do not require a sheath for Balloon-related complications can occur as placement (Erdogan et al., 2006). Over the well. Balloon rupture will result in the release

years, smaller catheter size and sheathless of a helium or CO2 bolus into the blood- introducers have helped to reduce complica- stream, as the gas will no longer be contained tion rates (Boehmer & Popjes, 2006). Some within the balloon circuit. Blood noted within patients, however, are more prone to limb the gas tubing, inability to maintain augmen- ischemia. Especially vulnerable populations tation, and low pressure/gas alarms are indica- include the elderly, diabetics, females, obese tors of possible balloon rupture (Boehmer & patients, and individuals with peripheral vas- Popjes, 2006). Balloon rupture is more likely to 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 174

174 Chapter 10 Intra-aortic Balloon Pump

occur in patients with atherosclerosis, in have IABP therapy discontinued intraopera- whom the balloon will be inflating against tively if it was used to stabilize the patient’s rough calcium deposits in the aorta (Laurent & condition in the preoperative period. Unless Shinn, 2005). complications occur, the IABP is removed Balloon migration within the aorta is also after a period of weaning. The ICU nurse, possible. If the balloon migrates upward, while monitoring the patient on an ongoing blood supply to the upper extremities and basis, is often the first to assess readiness for head may be compromised. If the balloon weaning (Krau, 1999). Although the orders migrates downward, blood supply to the renal for weaning will be instituted by a physician arteries will be impaired (Tremper, 2006). or mid-level provider, the ICU nurse is The ICU nurse should monitor for a variety responsible for determining the patient’s tol- of other complications when an IABP is used. erance to the weaning process. Some of the Infection at the insertion site or in the sys- parameters that may suggest readiness for temic circulation may occur due to the pres- weaning are listed in Box 10–3. ence of an indwelling catheter; red blood cell Weaning from the IABP involves decreasing hemolysis and thrombocytopenia are possible the frequency of assisted beats, decreasing the due to the action of the balloon on blood volume in the balloon over time, or both. Fre- components as they pass through the aorta quency weaning involves switching from 1:1 (Tremper, 2006). Other complications cited (every beat assisted by IABP) to 1:2 (every in the literature include spinal cord ischemia, other beat assisted). Switching from a 1:1 to visceral ischemia, renal failure, and peripheral 1:2 ratio provides the most marked decrease neuropathy (Marino & Sutin, 2006). in blood flow to the coronary arteries—more than switching from 1:2 to 1:3 or 1:4, or from 1:4 to 1:8 (Krau, 1999). As a consequence, the ■ WEANING FROM IABP THERAPY patient who is weaned in this manner will The IABP is a temporary device that is usually require frequent monitoring, especially dur- discontinued postoperatively. Occasionally, ing the first stage of weaning. some patients who are awaiting cardiac trans- Volume weaning involves gradually reduc- plant may have it in place longer. Others may ing the amount of gas in the balloon. Usually,

Box 10–3 Parameters for IABP Weaning

● Stable hemodynamic parameters: Stable on low doses of vasoactive medications; MAP Ͼ 65– 70 mm Hg; PAOP Ͻ 18 mm Hg; cardiac index Ͼ 2.0 L/min/m2; SVR Ͻ 2000 dynes/sec/cm–5; Ͼ urine output 0.5 mL/kg/hr; SvO2 60–80%. ● No unstable dysrhythmias: Heart rate should be normal or near normal without dysrhythmias that compromise hemodynamic parameters. ● Low or normal serum lactate levels. ● Normal electrolyte levels. ● Acceptable hemoglobin/hematocrit levels. ● No chest pain/discomfort or dyspnea. ● No mental status changes indicative of poor cerebral perfusion.

ϭ ϭ ϭ MAP mean arterial pressure; PAOP pulmonary artery occlusive pressure; SvO2 mixed venous oxygen saturation; SVR ϭ systemic vascular resistance (afterload). Sources: Krau, 1999; Quaal, 2005. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 175

Troubleshooting the IABP 175

the volume is lowered by 20% with each timing, dysrhythmias that result in low reduction. Because there is an increased risk stroke volume, hypotension or low vascular of thrombus formation in the balloon folds, resistance, balloon leak or rupture, incorrect volume weaning is not recommended as read- balloon catheter placement or balloon migra- ily as frequency weaning. Volume weaning, tion, inappropriate balloon size, and balloon however, may be better tolerated by patients not fully opened. who do not tolerate frequency weaning (Krau, If the balloon or balloon catheter is found 1999). Weaning is successful when the patient to be faulty, it should be removed as soon as is able to remain hemodynamically stable possible (within 30 minutes) to avoid throm- with IABP therapy off. bus development on an idle catheter (Trost & Anticoagulation used during IABP therapy Hillis, 2006). Most consoles have an alarm should be tapered and ultimately discontin- system that warns providers when there is a ued prior to catheter removal. Frequency of gas leak or a rapid loss of gas. Slow leaks may balloon inflation can be set to 1:8 while the be the result of a hole in the balloon or a loose heparin effect is allowed to wear off (Trost & connection in the gas tubing. A rapid loss of Hillis, 2006). gas, in contrast, is usually the result of Once the catheter is removed, pressure balloon rupture or a disconnected gas circuit. should be applied to the site for 30 to 45 min- In this scenario, the gas line should be utes, followed by application of a sterile pres- clamped off immediately. If blood is noted in sure bandage for 2 to 4 hours (Quaal, 2005). the balloon catheter or gas circuit, it is recom- After placement of the pressure bandage, the mended that the pump be stopped immedi- patient should be checked for bleeding every ately because the balloon or catheter has a 30 minutes for 2 to 4 hours, then every 2 leak (Reid & Cottrell, 2005). Continuing to hours for 24 hours. Monitoring should con- pump will introduce gas into the blood- firm that a hematoma is not developing stream, producing an air embolus. under the bandage, as hematomas can be a significant source of blood loss. The patient Faulty Trigger should be instructed to keep the head of the On occasion, the ECG trigger may not func- bed at 30 degrees or less, with no flexion of tion properly. Common causes of a faulty the leg for at least 8 hours following IABP trigger include poor electrode placement, low catheter removal (Quaal, 2005). ECG voltage, faulty electrode pads or cables, dysrhythmias, and other equipment’s inter- ■ TROUBLESHOOTING THE IABP ference with the ECG signal (Tremper, 2006). With the IABP, as with any mechanical device, If the problem cannot be easily rectified, problems may occur that need to be switching to the arterial pressure trigger will addressed promptly. Often it is best to refer be necessary until the problem can be solved. to the manufacturer’s troubleshooting guide, as it contains a complete reference of prob- Autofill Failure lems likely to be encountered. A few of the The autofill feature on the IABP maintains most common problems are discussed here. the volume of gas within the balloon. Should this feature not function, an autofill alarm Low Diastolic Augmentation will sound. The cause of this problem could Poor augmentation occurs in approximately be an insufficient amount of gas in the tank 39% of unsuccessful IABP attempts (Ferguson or occlusion of the gas outlet. The amount of et al., 2001). Potential causes of low diastolic gas in the tank should be checked and the augmentation include incorrect balloon tank replaced as needed. Also, the provider 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 176

176 Chapter 10 Intra-aortic Balloon Pump

should assess for and correct any kinks or ● Bleeding at the Insertion Site. Check the leaks in the tubing and ensure that the valve dressing and under the patient’s thigh on the tank is in the open position (Tremper, for bleeding every 2 hours. Check for 2006). hematoma development under dressing. In the event of pump failure or if pumping ● Anemia and Thrombocytopenia. Obtain needs to be stopped, the IABP balloon should a daily CBC. Transfuse platelets and red be manually inflated with a syringe every blood cells as indicated. 5 minutes. The syringe should be filled with a ● Infection. Monitor for signs and symp- volume of gas that is 10 mL less than balloon toms of infection: temperature Ͼ 101 ЊF, capacity so as to prevent thrombus formation WBC count greater than 10,000 cells/ (Weil, 2007). mm3, chills, mental status changes. If ICU nurses caring for a patient receiving infection is suspected, send specimens for IABP therapy must be knowledgeable about peripheral blood, urine, and sputum cul- the potential complications that can occur tures. Culture the IABP port as well. during catheter/balloon insertion and Change the insertion site dressing accord- removal and during therapy. They must ing to facility policy and examine the skin equally be aware of management strategies around site for redness, increased temper- and preventive measures to implement to ature, or purulent drainage. Institute avoid or minimize associated morbidity. antibiotics promptly as prescribed Patients receiving IABP therapy need to have (Quaal, 2005; Reid & Cottrell, 2005). continuous monitoring, and the nurse-to- ● Catheter Migration. Monitor the patient ratio is encouraged to be 1:1. Often, patient’s pulses, skin color, and tempera- these patients are critically ill and have com- ture; assess for altered sensation in the plex problems related to their condition as left upper extremity every 1–2 hours. well as the difficulties experienced by depen- Report urine output of less than 0.5 dence, even for a few days, on highly special- mL/kg/hr, increasing BUN/creatinine, ized equipment. Box 10–4 lists nursing or flank pain. Assess the patient for interventions required by the patient who is increased abdominal girth or discomfort receiving IABP therapy. with absent bowel sounds. Monitor the level of consciousness and evaluate the patient for unilateral neurological ■ MONITORING FOR impairment. Obtain a chest radiograph COMPLICATIONS OF IABP and anticipate repositioning or reinser- THERAPY tion of the catheter if migration is sus- ● Limb Ischemia. Perform peripheral vas- pected (Quaal, 2005). cular checks, including checking pulses, ● Aortic Dissection. This complication capillary refill time, skin color, and tem- occurs in 1% to 4% of IABP insertions. perature of lower extremities. Distal Assess the patient for abdominal, back, pulses should be checked at least every 4 intrascapular, or shoulder pain, usually hours until the patient is discharged. of sudden onset. The pain may be Patients should be instructed to notify described as “tearing.” Other symptoms the nurse if they note any changes in cir- include increased abdominal girth and culation (Reid & Cottrell, 2005). absent or unequal peripheral pulses with 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 177

Monitoring for Complications of IABP Therapy 177

Box 10–4 Nursing Interventions for the Patient Receiving IABP Therapy

Pre-insertion Interventions ● Provide as calm an environment as possible because the patient will likely be overwhelmed. ● Provide reassurance that the IABP therapy is temporary. ● Explain the procedure and the steps to help ensure safety (as time permits). ● Allow families to participate in discussions and to express concerns. ● Ascertain that consent is signed and complete if required. ● Obtain a 12-lead ECG; insert a urinary catheter. ● Assist with the insertion of invasive lines such as an arterial line and a pulmonary artery catheter. ● Obtain baseline hemodynamic readings: HR, RR, BP, MAP, PAP, PAOP, CVP, CO or CI, SVR, and urine output. ● Obtain baseline blood work: ABG, mixed venous blood gas, chemistries with BUN/creatinine, CBC with platelets and differential, coagulation profile, and type and crossmatch. ● Perform a peripheral vascular assessment, including checking ankle-brachial index,* skin temperature, presence and strength of pulses, and capillary refill in lower extremities. ● Monitor for the presence of a left radial pulse. Inform the physician if the pulse is lost so that the catheter can be repositioned.

Post-insertion Interventions ● Monitor and record hemodynamic measurements every 15 to 30 minutes until the patient is stable, then hourly and PRN. ● Obtain an ECG and chest radiograph daily and PRN. ● Titrate vasopressors/inotropic agents as required to desired hemodynamic parameters. Hemo- dynamic stability is essential to maintain optimal perfusion to the limb. ● Maintain IV fluid therapy as ordered to maintain an acceptable preload. ● Assess for pain/discomfort, anxiety, and mental status changes hourly. ● Document IABP settings hourly; include the assisted and unassisted pressures. ● Print and document the arterial waveform tracing every 12 hours and PRN with changes. ● Assess for presence and strength of distal pulses, indices of adequate limb perfusion, and sensorimotor function of both lower extremities every 15 minutes for 1 hour, then 30 minutes for 1 hour, and then hourly or according to unit protocol. ● Assess the ankle-brachial index every 4 hours. ● Monitor for the presence of a left radial pulse. Loss of pulse indicates that the catheter has migrated upward, is occluding the left subclavian artery, and requires repositioning. ● Maintain and titrate the heparin infusion to desired anticoagulation as ordered. Obtain coagulation studies 6 hours after dosage changes or follow the facility protocol. ● Obtain daily blood work: chemistries, CBC with platelets, coagulation profile, ABG, lactate level, and mixed venous blood gas. ● Monitor respiratory status: Assess breath sounds every 4 hours. Maintain oxygen and/or ventilator therapy. Encourage coughing and deep breathing/incentive spirometry every 2 hours. Keep the head of bed at a 30- to 45-degree angle to prevent aspiration. Perform chest physiotherapy when the patient is logrolled. continues 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 178

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Box 10–4 Nursing Interventions for the Patient Receiving IABP Therapy (continued)

● Maintain NPO or clear liquids as tolerated. If tolerated, maintain tube feedings via feeding tube. Check residual every 4 hours and notify the physician if it is greater than 200 mL. ● Prevent skin breakdown related to immobility. Maintain the patient on bed rest, with sedation if needed. Encourage the patient not to flex the hip on affected side. Use a leg immobilizer if necessary. If tolerated, logroll the patient every 4 hours; perform meticulous skin care. Provide passive range-of-motion exercises for the lower extremity without a catheter and for upper extremities every 4 hours. *To check ankle-brachial index: ● With patient supine and at rest, apply blood pressure cuff around both ankles and arms. ● Inflate blood pressure cuffs above patient’s normal systolic blood pressure (SBP). ● Deflate blood pressure cuffs. Obtain blood pressure readings using a Doppler and record SBP measurements from the arms and ankles. ● Divide ankle systolic pressure by the highest arm pressure; this will yield an ABI value for each leg. An index value of 0.9 to 1.3 is considered normal. Values greater than the normal range indicate the presence of some degree of peripheral vascular disease. Presence of mild, moderate, or severe peripheral vascular disease warrants reevaluation of vein selection for cardiac surgery.

ABG ϭ arterial blood gas; ABI ϭ ankle-brachial index; BP ϭ blood pressure; BUN ϭ blood urea nitrogen; CBC ϭ complete blood count; CI ϭ cardiac index; CO ϭ cardiac output; CVP ϭ central venous pressure; ECG ϭ electrocardiogram; HR ϭ heart rate; MAP ϭ mean arterial pressure; PAOP ϭ pulmonary artery occlusive pressure; PAP ϭ pulmonary artery pressure; RR ϭ respiratory rate; SVR ϭ systemic vascular resistance (afterload). Sources: Creager & Libby, 2004; Laurent & Shinn, 2005; Little, 2004; Marino & Sutin, 2006; Quaal, 2005; Reid & Cot- trell, 2005. Vascular Disease Foundation, 2009.

concomitant decreased blood pressure ■ SUMMARY and urine output. Obtain a CT scan or Care of the patient receiving IABP therapy is MRI if dissection is suspected. Treat- complex and challenging. Patients require ment consists of prompt surgical repair prompt intervention for problems and empa- (Hurwitz & Goodman, 2005; Reid & thy for their critical illness. For the ICU Cottrell, 2005). nurse, additional instruction both in theory ● Compartment Syndrome. This compli- and in hands-on experience is required to be cation may occur during therapy or after able to maintain and troubleshoot the com- removal of the catheter. The patient plex IABP apparatus. Management of this should be assessed for increased girth, device is accomplished while balancing evi- tenderness, pain, loss of sensation, pres- dence-based care that involves critical think- sure, paresthesia, or paralysis of the ing and decision making, preventing and affected extremity. The leg may also detecting complications, and providing emo- develop pallor when elevated if compart- tional support to patients and families who ment syndrome is present. Treatment are experiencing one of the most vulnerable may involve a fasciotomy (Reid & Cot- times in their lives. trell, 2005). 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 179

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CASE STUDY

M.H. is a 63-year-old male with a history of diabetes, hypertension, and coronary artery disease who presented to the emergency department with crushing substernal chest pain radiating down his left arm, without relief from sublingual nitroglycerin. Based on his ECG findings and serum troponin levels, the diagnosis of acute anterior wall MI was made and the patient was admitted to the ICU. Although he was initially stable, within hours after his admission, M.H.’s blood pressure began to drop; he also developed bibasilar crackles and low urine output. A pulmonary artery catheter was inserted. Despite appropriate interventions and vasoactive agents, however, the patient’s condition continued to deteriorate. It was noted that M.H. was becoming confused at this time. Owing to his instability, he was taken to the cardiac catheterization lab, where an IABP catheter was inserted via the right femoral artery. The patient underwent coronary angiography and rotational atherectomy with intercoronary stent placement for a high-grade lesion in the LAD. After M.H.’s readmission to the ICU, the initial frequency of balloon inflation and deflation was at a 1:1 ratio. In the next few hours, his condition stabilized, with the patient showing improvements in vital signs, urine output, and mental status. Over the next 2 days, M.H. was weaned from vasoactive agents; weaning from the IABP also commenced. By day 4, the IABP had been successfully removed. On day 7 of hospitalization, M.H. was transferred out of the ICU to a progressive care unit and then to the general unit; 1 week later, he was discharged from the hospital with frequent follow-up appointments scheduled.

Critical Thinking Questions 1. Identify and discuss M.H.’s risk factors, and explain how these factors led to his current diagnosis of acute MI. 2. During M.H.’s IABP therapy, the diastolic augmentation is noted to be low. Discuss why diastolic augmentation is a critical factor for this patient. Describe the possible reasons for this outcome, and identify the interventions that will be required. 3. M.H. will require support and teaching for his recovery phase. Identify and discuss the major areas for teaching that will be needed, including medications and lifestyle alterations. Answers to Critical Thinking Questions 1. M.H.’s history of diabetes is a significant risk factor for CAD because hyperglycemia causes vascular damage. Approximately two-thirds of all persons with diabetes will die from complications of heart or vascular disease (Morton, 2005). Hypertension confers a three to four times greater risk of developing CAD. Current criteria for the diagnosis of hypertension are a systolic blood pressure greater than 120 mm Hg or a diastolic blood pressure greater than 80 mm Hg. In the setting of hypertension, changes occur to the vessel wall possibly by sheer stress and endothelial dysfunction (Henri & Rugg, 2006). M.H.’s history of CAD raises significant suspicion that his symptoms are related to a serious cardiac event. Often such a patient will have stable angina with predictable 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 180

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pain on exertion (when the heart’s oxygen demand rises), which later changes with thrombus formation in the coronary artery to unstable angina or AMI. 2. Diastolic augmentation is an important function of the IABP. For M.H., diastolic augmentation increases blood flow into the coronary arteries during diastole. This increases blood flow to the heart muscle, resulting in relief from ischemia and improved function of the left ventricle. In addition, because preload and afterload are diminished, forward flow (cardiac output) is improved, resulting in improved hemodynamic parameters. Reasons for low diastolic augmentation include the following issues: ● Incorrect timing of balloon inflation and deflation. To correct this problem, read- just the timing according to the arterial waveform. ● Leak in the balloon catheter. Occasionally balloons can rupture or tear. This problem warrants prompt changing of the balloon catheter. ● Leak in the gas circuit resulting in poor inflation. Check all connections from the catheter to the gas cylinder and tighten them as necessary. ● Balloon not unwrapped completely. This issue results in poor or incomplete opening of the balloon. Check the position of the catheter with an x-ray. Attempt to inflate the balloon with an appropriate-sized syringe. If this measure is unsuccessful, the catheter will need to be replaced. ● Poor cardiac function or low vascular resistance. If appropriate, add positive inotropic agents and vasoactive agents. ● Dysrhythmias such as atrial fibrillation or ventricular tachycardia that result in low stroke volume. To correct these conditions, administer antiarrhythmics as ordered, and improve oxygen and electrolyte imbalances. 3. Some of the major areas for teaching may include the following topics: ● Control hyperglycemia and blood pressure through diet and exercise. A diet that is low in cholesterol and saturated fats with an increase in fiber is recommended. M.H. should also continue to follow the dietetic recommendations and carbohy- drate limitations of his diabetic diet. ● Attend smoking cessation programs (if appropriate). ● Use stress reduction techniques. ● Engage in weight reduction (if appropriate) through diet and exercise. An exercise program that is physician guided and increases over time as the patient tolerates more activity is the most appropriate strategy. Medications for M.H. that will require teaching as to mechanisms of action, side effects, and contraindications may include these agents: ● Lipid-lowering medications to reduce cholesterol levels. ● Nitrates to relieve symptoms of chest pain and lower blood pressure. ● Antiplatelet medications to reduce the inflammatory response involved in coronary artery thrombus formation. ● Beta-adrenergic blocking agents. These agents block sympathetic stimulation by epinephrine and norepinephrine on beta receptors. They lower heart rate, contractility, and blood pressure, which in turn decrease myocardial oxygen demand. In addition, they exert an antiarrhythmic effect. ● Angiotensin-converting enzyme (ACE) inhibitors to lower blood pressure and decrease the work of the heart. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 181

Self-Assessment Questions 181

● Calcium channel blockers to cause coronary artery and systemic vasodilation, decrease contractility of the heart, blood pressure, heart rate, and conduction through the AV node. All of these effects can decrease myocardial oxygen demand. These agents also dilate coronary arteries, which helps to increase myocardial oxygen supply and have a negative inotropic effect on the heart muscle. M.H.’s patient education should include recognition of warning signs and symptoms for progressing angina and symptoms of LV dysfunction that may occur after an MI. Early treatment of these symptoms may result in improved survival and quality of life.

■ SELF-ASSESSMENT QUESTIONS 5. If the balloon’s inflation/deflation cycle 1. Positive effects of IABP therapy include must be stopped temporarily, which which of the following? action must be taken by the nurse? i. Decreased afterload a. Administer a heparin bolus. ii. Decreased preload b. Flush the catheter with saline every iii. Decreased stroke volume 2 hours. iv. Increased coronary artery c. Inflate the balloon manually every perfusion 5 minutes with a syringe. a. iv only b. i and ii d. Remove the balloon catheter. c. i, ii, and iv d. iii and iv 6. Indications for IABP use include all of 2. If the ECG is not sufficient as a trigger, the following except which of the following should be used as a. postoperative cardiopulmonary a trigger? bypass. a. T-P interval b. cardiogenic shock after acute b. Pacer spikes myocardial infarction. c. T wave c. mitral regurgitation with papillary d. Arterial waveform muscle dysfunction. d. uncomplicated myocardial 3. The most common complication that infarction. results from the use of IABP therapy is a. lower limb ischemia. 7. Which of the following is considered b. aortic dissection. an absolute contraindication to IABP c. bleeding. therapy? d. infection. a. Heart failure b. Aortic insufficiency 4. The urine output of a patient receiving c. Peripheral vascular disease IABP therapy has suddenly dropped to d. Myocardial infarction less than 0.5 mL/kg/hr over the past 2 hours. A complication of IABP therapy 8. The effectiveness of the timing of bal- that should be suspected is loon inflation and deflation can be a. infection. assessed by b. anemia. a. arterial pressure waveform. c. catheter migration. b. daily lactate level. d. balloon rupture. c. urine output. d. daily ECG. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 182

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9. After removal of the catheter, the nurse b. The augmented diastolic wave will be should expect all of the following except higher than the previous systolic and a. explaining to the patient mobility coronary artery perfusion will be limitations (not to flex affected leg) decreased. for the next 8 hours. c. The augmented diastolic wave will be b. holding pressure on the site of lower than the previous systolic and catheter removal for 30 to 45 coronary artery perfusion is minutes. decreased. c. checking the site every 2 hours only if d. The augmented diastolic wave will be blood is noted on the dressing. higher than the previous systolic and d. continuing to check the site every 30 coronary artery perfusion will be minutes for 1 hour, then every 2 increased. hours for the next 24 hours. 10. If the diastolic augmentation is low dur- Answers to Self-Assessment Questions ing IABP therapy, which of the following 1. c 6. d observations will be made? 2. d 7. b a. The augmented diastolic wave will be lower than the previous systolic and 3. a 8. a coronary artery perfusion will be 4. c 9. c increased. 5. c 10. c

Clinical Inquiry Box

Question: Does the use of IABP prior to cardiac surgery ensure better outcomes? Reference: Dyub, A. M., Whitlock, R. P., Abouzahr, L. L., & Cinà, C. S. (2008). Preoperative intra- aortic balloon pump in patients undergoing coronary bypass surgery: A systematic review and meta-analysis. Journal of Cardiac Surgery, 23(1), 79–86. Objective: To assess the effectiveness of preoperative IABP placement in high-risk patients undergoing coronary bypass surgery as evidenced by hospital mortality and IABP-related complications (bleeding, leg ischemia, aortic dissection). Methods: A meta-analysis was conducted using a random effects model. Studies were chosen that met the following criteria: randomized controlled trials (RCT) and cohort studies with controls; adults (older than 18 years of age) undergoing elective or urgent coronary bypass surgery; and documentation of at least hospital mortality. The treatment was defined as insertion of IABP before surgery. The control groups consisted of patients who did not receive IABP therapy preoperatively and those who received IABP therapy either intraoperatively or postoperatively. The outcome variables for the analysis were hospital mortality and IABP-related complications (e.g., bleeding, leg ischemia, aortic dissection). Results: Ten publications fulfilled the eligibility criteria (four were RCTs and six were cohort studies with controls). Both statistical and clinical heterogeneity were noted among the included studies. A total of 1034 patients received preoperative IABP; 1329 did not receive preoperative IABP. The overall risk for hospital mortality in patients treated with preoperative IABP was 41%. Broken down by type of study, the risk of hospital mortality was 18% in RCT and 54% in cohort studies (studies following patients over a period of time). Overall, 3.7% (13 of 349) of patients who received preoperative IABP developed either limb ischemia or hematoma at the IABP insertion site, and most of these complications improved after discontinuation of IABP therapy. Conclusion: Evidence from this meta-analysis supports the use of preoperative IABP in high-risk patients to reduce hospital mortality. Implications for nurses are that preoperative IABP therapy poses an increased risk of mortality and hence these individuals will more than likely present with higher acuity. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 183

References 183

■ REFERENCES Fotopoulos, G. D., Mason, M. J., Walker, S., Jepson, Ahmad, I. (2006). Overview of the intraaortic bal- N. S., Patel, D. J., Mitchell, A. G., et al. (1999). loon pump. Care of the Critically Ill, 22(4), Stabilisation of medically refractory ventricu- 95–98. lar arrhythmia by intra-aortic balloon counterpulsation. British Heart Journal, 82(1), 96–100. Antman, E. M., Anbe, D. T., Armstrong, P. W., Bates, E. R., Green, L.A., Hand, M. et al. (2004). Henke, K., & Eigsti, J. (2003). Bypass injury: Impli- ACC/AHA guidelines for the management of cations of cardiopulmonary bypass. Dimensions patients with ST-segment elevation myocardial in Critical Care Nursing, 22(2), 64–70. infarction: Executive summary. Journal of the Henri, H. C., & Rugg, P. (2006). Hypertension: American College of Cardiology, 44, (3)674–719. Context and management. In E. J. Topol, R. M. Boehmer, J. P., & Popjes, E. (2006). Cardiac failure: Califf, E. N. Prystowsky, J. D. Thomas, & P. D. Mechanical support strategies. Critical Care Thompson (Eds.), Textbook of cardiovascular Medicine, 34(suppl 9), 268–277. medicine (3rd ed., pp. 88–108). Philadelphia: Lippincott Williams & Wilkins. Christenson, J. T., Cohen, M., Miller, M. F., Ohman, E. M., & Urban, P. M. (2002). Trends Hochman, J. S., Sleeper, L. A., Webb, J. G., Dzavik, in intraaortic balloon counterpulsation: Com- V., Buller, C. E., Aylward, P., et al. (2006). Early plications and outcomes in cardiac surgery. revascularization in acute myocardial infarc- Annals of Thoracic Surgery, 74(4), 1086–1090. tion complicated by cardiogenic shock. New England Journal of Medicine, 295(21), Christenson, J. T., Simonet, F., & Schmuzilger, M. 2511–2515. (2000). Economic impact of preoperative intraaortic balloon pump therapy in high-risk Hurwitz, L., & Goodman, P. (2005). Intraaortic bal- coronary patients. Annals of Thoracic Surgery, loon pump location and aortic dissection. 70(2), 510–515. American Journal of Radiology, 184(4), 1245–1246. Creager, M. A., & Libby, P. (2004). Peripheral artery diseases. In D. P. Zipes et al. (Eds.), Braunwald’s Kern, M. J., King, S. B., Douglas, J. S., & Franch, R. heart disease (7th ed., pp. 1437–1461). Philadel- H. (2004). Cardiac catheterization, coronary phia: Elsevier Saunders. angiography and coronary blood flow and pressure measurements, intraaortic balloon Dixon, B., Santamaria, J., & Campbell, D. (2005). counterpulsation, indications and contraindi- Coagulation activation and organ dysfunction cations. In V. Fuster, R. W. Alexander, & R. A. following cardiac surgery. Chest, 128(1), O’Rourke (Eds.), Hurst’s the heart (11th ed., pp. 229–236. 481–544). New York: McGraw-Hill. Duvernoy, C. S., & Bates, E. R. (2005). Management Krau, S. D. (1999). Successfully weaning the intra- of cardiogenic shock attributable to acute aortic balloon pump patient: An algorithm. myocardial infarction in the reperfusion era. Dimensions in Critical Care Nursing, 18(3), 1–7. Journal of Intensive Care Medicine, 20(4), 188–198. Laham, R. J., & Aroesty, J. M. (2008). Intraaortic balloon pump counterpulsation. Retrieved Erdogan, H. B., Goksedef, D., Erentug, V., Polat, A., July 26, 2008, from www.uptodate.com Bozbuga, N., Mansuroglu, D., et al. (2006). In which patients should sheathless IABP be Laurent, D., & Shinn, J. A. (2005). Acute heart fail- used? An analysis of vascular complications in ure and shock. In S. L. Woods, E. S. Sivarajan 1211 cases. Journal of Cardiac Surgery, 24(4), Froelicher, S. Underhill Motzer, & E. J. Bridges 342–346. (Eds.), Cardiac nursing (5th ed., pp. 659–688). Philadelphia: Lippincott Williams & Wilkins. Ferguson, J. J., Cohen, M., Freedman, R. J., Stone, G. W., Miller, M., Joseph, D. L., et al. (2001). Lindholm, M. G., Aldershvile, J., Sundgreen, C., Jor- The current practice of intra-aortic balloon gensen, E., Saunamaki, K., & Boesgaard, S. counterpulsation: Results from the Bench- (2003). The effect of early revascularization on mark Registry. Journal of the American College of cardiogenic shock complicating acute myocar- Cardiology, 38(5), 1456–1462. dial infarction: A single center’s experience. European Journal of Heart Failure, 5(1), 73–79. 57625_CH10_165_184.pdf 4/10/09 11:08 AM Page 184

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Little, C. (2004). Your guide to the intra-aortic bal- Tommaso, C. L. (2002). Support for percutaneous loon pump. Nursing, 34(12), 32cc1–32cc4. coronary interventions: IABP, CPS and Marino, P. L., & Sutin, K. M. (2006). Acute heart beyond. In D. A. Morrison & P. W. Serruys failure syndromes. In P. L. Marino & K. M. (Eds.), High-risk cardiac revascularization and clin- Sutin, The ICU book (3rd ed., pp. 255–276). ical trials (pp. 469–478). New York: Informa New York: Wolters Kluwer Health. Health Care. Metules, T. (2003). IABP therapy: Getting patients Tremper, R. S. (2006). Home study program: Intra- treatment fast. RN, 66(5), 56–62. aortic balloon pump therapy: A primer for Morton, P. G. (2005). Acute myocardial infarction. perioperative nurses. AORN Journal, 84(1), In P. G. Morton, D. K. Fontaine, C. M. Hudak, 33–35, 37–40, 42, 44. & B. M. Gallo (Eds.), Critical care nursing: A holis- Trost, J., & Hillis, D. L. (2006). Intra-aortic balloon tic approach (8th ed., pp. 422–447). Philadel- counterpulsation. American Journal of Cardiol- phia: Lippincott Williams & Wilkins. ogy, 97(9), 1391–1398. Pantalos, G. M., Gillars, K. J., Dowling, R. D., Etoch, Vascular Disease Foundation. (2009). The Ankle- S. W., Koenig, S. C., McMahan, A. M., et al. Brachial index. Retrived February 25, 2009 (2003). Intraaortic balloon pump (IABP) tim- from www.vdf.org/diseaseinfo/pad/ankle ing errors in adult patients. ASAIO cardiopul- brachial.php monary abstracts. ASAIO Journal, 49(2), 155. Weil, K. M. (2007). On guard for intra-aortic bal- Paul, S., & Rasmusson, K. D. (2007). Heart failure. loon pump problems. Nursing, 37(7), 28. In R. Kaplow & S. Hardin (Eds.), Critical care Zellinger, M. (2007). Cardiac surgery and heart nursing: Synergy for optimal outcomes (pp. transplant. In R. Kaplow & S. Hardin (Eds.), 197–208). Boston: Jones and Bartlett. Critical care nursing: Synergy for optimal outcomes Quaal, S. (2005). Circulatory assist devices. In D. L. (pp. 229–242). Boston: Jones and Bartlett. M. Weigand & K. K. Carlson (Eds.), AACN procedure manual for critical care (5th ed., ■ pp. 362–380). St. Louis, MO: Elsevier Saunders. WEB RESOURCES Reid, M. B., & Cottrell, D. (2005). Nursing care of Intra-aortic balloon pump transport: This short patients receiving intra-aortic balloon coun- video demonstrates the proper procedure to terpulsation. Critical Care Nurse, 25(5), 40–49. safely load and transport a patient who has Stenz, R. (2006). Intra-aortic balloon counterpulsa- IABP therapy in place. http://video.google.com/ tion. Anesthesia and Intensive Care Medicine, 7(9), videoplay?docid=7160026936252015006& 335–336. q=IABP&ei=widCSOiZMoO8rwKAsYSOCQ& hl=en Stone, G. W., Ohman, E. M., Miller, M. F., Joseph, D. L., Christenson, J. T., Cohen, M., et al. Avoid Hazards of IABP (FDA): http://www.fda (2003). Contemporary utilization and out- .gov/cdrh/medicaldevicesafety/tipsarticles/ comes of intra-aortic balloon counterpulsa- balloonpump.html tion in acute myocardial infarction. Journal of Hazard video: http://video.google.com/videosearch?hl the American College of Cardiology, 41(11), =en&q=IABP&um=1&ie=UTF8&sa=N&tab=wvhl 1940–1945. =en&sitesearch=&q=intraaortic%20balloon% Thiele, H., Lauer, B., Hambrecht, R., Boudriot, E., 20pump Sick, P., Niebauer, J., et al. (2003). Short- and IABP information: http://www.cprworks.com/ long-term hemodynamic effects of intra-aortic IABP.html balloon support in ventricular septal defect complicating acute myocardial infarction. American Journal of Cardiology, 92(4), 450–454. 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 185

Chapter 11 Mechanical Ventilation After Cardiac Surgery

Mary Jane Bowles

■ INTRODUCTION Mechanical ventilation may be essential in the arterial blood gases and radiographic find- postoperative management of patients under- ings. They must be able to identify complica- going cardiac surgery and cardiopulmonary tions of patients on mechanical ventilation bypass. Prior to the 1990s, patients were and implement measures to prevent morbidi- mechanically ventilated until the morning ties associated with therapy so optimal after surgery before weaning was attempted. patient outcomes can be attained. In more recent decades, the need for cost con- tainment has resulted in “fast-tracking” ■ PREDICTORS OF PROLONGED patients by implementing early weaning pro- MECHANICAL VENTILATION tocols and reversible sedation. This strategy Several preoperative and postoperative factors has been reported to lead to shorter mechani- have been identified as predictors of the need cal ventilation times and ICU stays for cardiac for prolonged mechanical ventilation follow- surgery patients. Other reported benefits of ing cardiac surgery. earlier extubation include improved preload, decreased hemodynamic compromise, and decreased neurologic compromise (in elderly Preoperative Predictors patients) (Kern et al., 2001). Preoperative predictors of prolonged mechani- The majority of patients are extubated cal ventilation include the presence of valvular within 24 hours following coronary artery disease, recent myocardial infarction, arterial bypass grafting (CABG) procedures. However, hypertension, diabetes, previous cardiac sur- prolonged mechanical ventilation may occur gery, chronic peripheral vascular disease, in as many as 50% of cardiac surgery patients involvement of three or more vessels, surgical (Yende & Wunderink, 2002). priority, elevated serum creatinine, age (greater Nurses in the ICU who are caring for than 75 years), gender (females have a higher patients who underwent cardiac surgery in risk than males), impaired left ventricular the immediate postoperative phase must have function (ejection fraction less than 40%), and an understanding of the pathophysiology of COPD (Doering, Imperial-Perez, Monsein, & the lungs, use of mechanical ventilation, Esmailian, 1998; Hammermeister, Burchfield, weaning protocols, and ability to interpret the Johnson, & Grover, 1990; Kern et al., 2001; clinical significance of diagnostic tests such as Natarajan, Patil, Lesley, & Ninan, 2006;

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Pappalardo et al., 2004; Thompson et al., 1997; required prolonged ventilation (more than 72 Tu, Jaglal, & Naylor, 1995; Wong et al., 1999). hours) experienced sepsis, endocarditis, gastrointestinal bleeding, stroke, renal failure, or Postoperative Predictors deep sternal wound infection (Durham & Gold, 2008). A higher mortality rate is also Postoperative predictors include hypoxia, associated with patients who require pro- decreased mentation, excessive postoperative longed ventilation. bleeding, renal or cardiovascular failure, need for intra-aortic balloon pump (IABP), parenteral nutrition, inotropic therapy, acute res- ■ PATHOPHYSIOLOGY piratory distress syndrome (ARDS), pulmonary OF THE LUNGS edema, and prolonged surgical or bypass time The main function of the respiratory system (Guller et al., 2004; Kern et al., 2001; Thomp- is to transport air into the lungs so that oxy- son et al., 1997; Wong et al., 1999). gen can enter the body and carbon dioxide Other researchers have reported CABG can be eliminated. Air enters the nose or patients (aged 65 years or older) who required mouth and moves through the trachea into 6 to 12 hours of postoperative mechanical the bronchi and then into each lung. Once air ventilation have higher mortality in compari- is in the lungs, gas exchange occurs in the son to those patients requiring less than approximately 300 million alveoli. Oxygen 6 hours of mechanical ventilation (Peterson and carbon dioxide can cross between the et al., 1999). Other predictors for prolonged lung capillaries and the alveolar spaces, allow- mechanical ventilation include duration of ing gas exchange to occur. The nasal passages surgery, perioperative heart failure, serum and bronchi warm and moisten the air before glucose level, postoperative transfusion, and it enters the alveoli as a method of preventing PaO2/FiO2 ratio (Suematsu et al., 2000). damage to delicate alveolar structures. The mechanism of breathing involves the Delays Related to Bypass Complications diaphragm and the intercostal muscles. Dur- Several clinical conditions, when present, ing normal breathing, inspiration is an active are likely to result in failure of ventilator process and expiration is a passive process. weaning. When these conditions are com- Inspiration involves contraction of the pounded with complications associated diaphragm and the intercostal muscles to with cardiopulmonary bypass, ventilation allow for the movement of air into the respi- time may be prolonged due to a decrease in ratory tract. The diaphragm and intercostal surfactant production, potential for pul- muscles then relax during expiration. monary microemboli, and interstitial fluid The respiratory center, which is located in accumulation in the lungs. Further, red the medulla oblongata (the lower part of the blood cell damage in the pump circuit may brain stem), receives neural, chemical, and potentially occur, decreasing the number of hormonal signals that can control the rate oxygen-carrying capacity cells (Alsoufi, and depth of movements of the diaphragm 2006; Khalpey, Ganim, & Rawn, 2008). and other respiratory muscles. An increase in carbon dioxide or a decrease in oxygenation, for example, will increase the rate or depth of ■ COMPLICATIONS OF PROLONGED breathing. Injury, medications, and disease VENTILATION processes can affect the respiratory center’s Prolonged use of mechanical ventilation is ability to respond to changes in carbon diox- not without risk. In one study, patients who ide or oxygen, resulting in respiratory com- 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 187

Assessment of Readiness for Weaning 187

promise. The use of mechanical ventilation of heart failure (e.g., increase in pulmonary may be needed in these circumstances. artery occlusive pressure or decrease in car- The autonomic nervous system is also diac output or mixed venous saturation) involved in breathing. The parasympathetic (Hanneman, 2004). nervous system may stimulate bronchoconstric- A number of clinical conditions have been tion, whereas stimulation of the sympathetic found to influence the ability to wean by nervous system may cause bronchodilation. affecting either the capacity of or the demand on the respiratory system. In addition to hemodynamic instability and electrolyte ■ ASSESSMENT OF READINESS imbalances, the presence of an acid–base FOR WEANING imbalance, volume overload, alterations in While many postoperative cardiac surgery mental status, myocardial ischemia, new- patients are extubated prior to their admis- onset dysrhythmia, or need for vasopressors sion to the ICU and many others remain on may delay weaning from mechanical ventila- mechanical ventilation for only a few hours tion (Eskandar & Apostolakos, 2007). after surgery, all intubated patients should be Electrolyte imbalances can decrease muscle evaluated for their readiness for weaning. contractility and, therefore, may influence Despite the relatively short amount of time success with weaning. Specifically, phospho- during which patients are intubated postop- rus, calcium, magnesium, and potassium eratively, it has been reported that as many as deficits should be corrected prior to attempt- 20% of patients experience difficulty with ing to wean the patient from mechanical ven- weaning. A number of criteria have been sug- tilation (Eskandar & Apostolakos, 2007). gested for the ICU nurse to use to determine A patient’s mental status should be ade- patient readiness, including the patient’s gen- quate enough to allow for maintenance of a eral physiologic and hemodynamic stability, patent airway and ability to cooperate with pulmonary mechanics, adequacy of gas coughing and deep breathing to prevent post- exchange, ability to breathe spontaneously, extubation respiratory compromise and com- and mental status (Hanneman, 2004). plications (Eskandar & Apostolakos, 2007).

General Physiologic and Hemodynamic Pulmonary Mechanics Stability Evaluation of certain parameters is suggested The patient’s overall condition should be to evaluate patient readiness to wean— assessed, as a number of conditions may namely, vital capacity, minute ventilation (or potentially influence the success of weaning volume), respiratory rate, tidal volume, and from mechanical ventilation. Presence of negative inspiratory pressure (or force) (Han- excessive bleeding or an electrolyte imbalance neman, 2004; Soo Hoo & Park, 2002). may affect the patient’s ability to oxygenate or eliminate carbon dioxide (Hanneman, 2004). ● Vital capacity is the amount of air that Similarly, if the patient is not hemodynami- can be exhaled forcibly following a full cally stable—a common finding in the post- inspiration (Steltner et al., 2004). operative cardiac surgery patient—success ● Minute ventilation is the volume of gas with weaning may be impaired. The ICU exchange (inhaled and exhaled) in nurse should assess vital signs and hemody- 1 minute. It is measured by multiplying namic parameters, and evaluate the patient respiratory rate and tidal volume (Sey- for presence of dysrhythmias, tachycardia, mour, Halpern, Christie, Gallop, & bradycardia, weak peripheral pulses, and signs Fuchs, 2008). 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 188

188 Chapter 11 Mechanical Ventilation After Cardiac Surgery

● Respiratory rate is the number of breaths atelectasis and pneumonia (Silvestry, 2008). taken by a patient in a minute. Aggressive pulmonary toileting and pain ● Tidal volume refers to the amount of air management are needed post-extubation to inhaled by the patient during a normal prevent further respiratory compromise. breath (versus a forced inhalation.) If Atelectasis is discussed in more detail in tidal volume is too low, it is surmised Chapter 13. that the patient will develop atelectasis post-extubation. Left Ventricular Failure ● Negative inspiratory pressure refers to Persistent left ventricular failure after cardiac the amount of negative pressure that the surgery causes an increase in hydrostatic patient generates during a forced inspi- pressure, with resultant fluid extravasation ration when working against an obstruc- into alveoli. Interstitial fluid in the alveoli tion to flow (Soo Hoo & Park, 2002). It is inhibits oxygen transfer, increases shunting, a reflection of the patient’s ability to decreases compliance, increases secretions, take a deep breath and generate a cough and facilitates atelectasis that can progress to that is strong enough to clear secretions. pneumonia (Salenger, Gammie, & Vander The ICU nurse should be mindful that Salm, 2003). these physiologic weaning parameters are Pleural Effusion not perfect predictors of a patient’s success Postoperative cardiac surgery patients may with successful extubation. Rather, when also develop a pleural effusion, usually on the assessed in combination with the other crite- left side. Although the specific etiology of this ria discussed in this section, these data will condition is not known, contributing factors provide some insight into the patient’s con- are thought to include volume overload, dition and possible tolerance to breathing hypoalbuminemia, inflammation of the peri- without mechanical support (Soo Hoo & cardium and pleura (postpericardiotomy Park, 2002). syndrome), atelectasis, pneumonia, and pulmonary embolism (Khalpey et al., 2008). Respiratory Physiologic Issues Development of a pleural effusion may lead Infrequently, a postoperative patient may to hypoxia, thereby affecting the success of require prolonged ventilator support for more weaning from mechanical ventilation. than several days. Failure to wean has two pri- A small pleural effusion is common in the mary causes: failure of gas exchange at the alve- early postoperative course following CABG olar level and failure to ventilate adequately. procedures. It occurs with less frequency in patients who have undergone mitral or aortic Atelectasis valve replacement surgery, and typically One of the most common reasons for defi- occurs more commonly on the left side than ciency in gas exchange in the postoperative on the right side. Effusions may necessitate cardiac surgery patient is atelectasis. Atelecta- thoracentesis or occasionally placement of a sis affects as many as 70% of cardiac surgery chest tube. Pleural effusions can present with patients. It usually results from single-lung different symptoms depending on the size of ventilation and associated intraoperative the effusion. Typically, the ICU nurse can intentional lung collapse (Sladden & expect to percuss dullness or decreased reso- Berkowitz, 1993). Pain from median ster- nance and to auscultate diminished or notomy or thoracotomy incisions inhibits inaudible breath sounds or a pleural friction deep breathing efforts, which can result in rub. Pleural effusions rarely result in an 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 189

Assessment of Readiness for Weaning 189

increased mortality rate or increased lengths side more likely to be affected (Abd et al., 1989). of stay (Heffner, 2008). This complication is Because the phrenic nerve is responsible for discussed in more detail in Chapter 13. diaphragmatic contraction, when partial injury of one or both phrenic nerves occurs, lower lobe Phrenic Nerve Injury atelectasis—particularly on the left side—may result in delay of weaning or decreased ability to Another potential cause of weaning failure is clear secretions after extubation. In one study, phrenic nerve injury. During cardiac surgery, the researchers did not find difference in dura- cold preservation techniques for myocardial tion of mechanical ventilation time or hospital protection are often utilized—one study lengths of stay between patients with unilateral reported the incidence of phrenic nerve injury and bilateral phrenic nerve injury (Dimopoulou ranges from 10% to 85% of cardiac surgery et al., 1998). patients (Dimopoulou et al., 1998). The use of ice slush has been associated with phrenic nerve injury (Dimopoulou et al., 1998; McGar- Arterial Blood Gas vey, Cheung, & Stecker, 2006) and, therefore, Another method of evaluating the effective- has been suggested as a measure that should ness of breathing and determining readiness be avoided (Dimopoulou et al., 1998). for weaning from mechanical ventilation fol- Other factors have also been implicated in lowing cardiac surgery is by obtaining an arte- the development of phrenic nerve injury. They rial blood gas (ABG). An ABG provides data include use of the left internal mammary with which to evaluate the patient’s condition artery (Abd, Braun, Baskin, O’Sullivan, & and the need for potential intervention; specif-

Alkaitis, 1989; DeVita, Robinson, Rehder, Hat- ically, it includes pH, PaO2, SaO2, PaCO2, and tler, & Cohen, 1993), preexisting diabetes HCO3 levels. Accurate interpretation will assist (Efthimiou, Butler, Benson, & Westaby, 1991), in determining the patient’s acid–base balance low preoperative cardiac performance (Abd et and any required interventions. Table 11–1 al., 1989), and surgical technique (Benjamin, lists normal values for an ABG. Cascade, Rubenfire, Wajszczuk, & Kerin, 1982). Data are not consistent, however, regarding Acid–Base Disorders these factors’ implications for phrenic nerve The pH is a measurement of acidity and alka- injury (Dimopoulou et al., 1998). linity of the blood. If a patient has an acidic Phrenic nerve injury may be associated with pH, a decrease in myocardial contractility, either unilateral or bilateral paralysis. Most vascular response to catecholamines, and cases have unilateral involvement, with the graft response to effects and actions of certain

Table 11–1 Components and Normal Values of Arterial Blood Gas

ABG Component Normal Value

pH 7.35–7.45 PaO2 80–100 mm Hg PaCO2 35–45 mm Hg HCO3 22–26 mEq/L SaO2 94–100% Base excess –2 to +2 (A negative base excess indicates a base deficit in the blood.) 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 190

190 Chapter 11 Mechanical Ventilation After Cardiac Surgery

medications may result. An alkalotic pH may Signs and symptoms of respiratory acidosis result in interference with tissue oxygenation, are respiratory, neurological, and cardiovascu- normal neurological functioning, and normal lar in nature. Respiratory symptoms may muscular functioning. include dyspnea, respiratory distress, and shallow respirations. Headache, restlessness, com- RESPIRATORY ACIDOSIS bativeness, hallucinations, and confusion are The definition of respiratory acidosis is a neurological symptoms. If CO2 levels continue pH of less than 7.35 with a PaCO2 greater to increase, symptoms can progress to stu- than 45 mm Hg. It is important to treat a porousness, constricted pupils, drowsiness, respiratory acidosis, because its presence seizures, and coma. Cyanosis may be present if increases the minute ventilation required to the acidosis is accompanied by hypoxemia normalize pH (Eskandar & Apostolakos, (Adrogué & Madias, 1998a; Hayes, 2005). 2007). Table 11–2 lists common causes of Cardiac response to acidosis includes respiratory acidosis in the postoperative car- flushed warm skin, bounding pulses, diac surgery patient. diaphoresis, tachycardia, dysrhythmias, cen-

Table 11–2 Causes of Respiratory Acidosis

Impaired Respiratory Muscle Function Related to: ● Neuromuscular blocking agents Pulmonary Disorders ● Atelectasis ● Pneumonia ● Pneumothorax ● Pulmonary edema ● Pulmonary embolism

Increased CO2 Production ● Shivering ● Sepsis Hypoventilation Secondary to: ● Pain ● Sternal incision ● Residual anesthesia ● Awakening with inadequate analgesia and impaired respiratory mechanics ● Opioid side effects User Error ● Inappropriate ventilator settings ● Hypoventilation during transfer from the operating room

Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, 2007; Gothard, Kelleher, & Haxby, 2003. 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 191

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tral and peripheral cyanosis, and pulmonary gospasm, confusion, and blurred vision are hypertension. In severe cases, decreased car- common neurologic symptoms. Cardiac diac output, hypotension, peripheral edema, symptoms may include chest pain, ischemic dysrhythmias, and prerenal azotemia may changes on ECG, peripheral vasoconstriction, develop (Adrogué & Madias, 1998a). Treat- dysrhythmias, and palpitations. The patient ment for respiratory acidosis entails treating often experiences dry mouth, diaphoresis, the underlying cause of hypoventilation and muscle twitching, weakness, and tetanic increasing ventilation. spasms of the arms and legs; some patients may also develop seizures (Adrogué & Madias, RESPIRATORY ALKALOSIS 1998b; Edgren, 2008). Respiratory alkalosis is defined as a pH greater Treatment of respiratory alkalosis focuses on eradicating the underlying cause. The than 7.45 with a PaCO2 less than 35 mm Hg. Conditions that cause hyperventilation can patient must be monitored for respiratory result in respiratory alkalosis. Table 11–3 lists muscle fatigue and acute respiratory failure. If common causes of respiratory alkalosis in the these situations occur, temporary reinstitution postoperative cardiac surgery patient. of mechanical ventilation may be indicated. Respiratory alkalosis is associated with both nervous and cardiac system sequelae. METABOLIC ACIDOSIS Lightheadedness, dizziness, agitation, numb- Metabolic acidosis is defined as a bicarbon- ness or tingling of the extremities, laryn- ate level less than 22 mEq/L and a pH less

Table 11–3 Causes of Respiratory Alkalosis

Hypoventilation Secondary to: ● Anxiety or fear ● Pain or generalized discomfort Increased Oxygen Demand ● Fever ● Sepsis Pulmonary Disorders ● Pneumonia ● Pulmonary edema Medications ● Respiratory stimulants User Error ● Inappropriate ventilator settings ● Hyperventilation during transfer from OR

Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, 2007; Gothard, Kelleher, & Haxby, 2003; Rimailho, Goldstein, & Vincent, 1985. 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 192

192 Chapter 11 Mechanical Ventilation After Cardiac Surgery

Table 11–4 Causes of Metabolic Table 11–5 Causes of Metabolic Acidosis Alkalosis

Hemodynamics Loss of Acids ● Decreased cardiac output ● Nasogastric suctioning ● Inadequate systemic perfusion ● Excessive administration of diuretics ● Decreased cardiac function ● Hypochloremia

● Decreased peripheral perfusion Hypokalemia ● Hypotension Massive Transfusion (from citrate) ● Hypovolemia ● Vasoconstriction from hypothermia Sources: Chikwe, Beddow, & Glenville, 2006; Gothard, Kelleher, & Haxby, 2003. Physiologic Conditions (increasing acids) ● Sepsis preventing further hypoxemia and hypoxia ● Renal failure from developing. If renal failure is the etiol- ● Regional ischemia ogy of the metabolic acidosis, the ICU nurse ● Diabetic ketoacidosis should attempt to attain and maintain nor- movolemia, administer diuretics based on the ● Anaerobic metabolism patient’s hemodynamic profile, and possibly Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, support the patient during dialysis or 2007; Gothard, Kelleher, & Haxby, 2003. hemofiltration (Gothard et al., 2003). Treat- ment may also entail administration of than 7.35. Table 11–4 lists possible causes of sodium bicarbonate (depending on the sever- metabolic acidosis in the postoperative car- ity of the acidosis or pH level), treatment of diac surgery patient. the patient’s hypothermia, and initiation of Metabolic acidosis symptoms arise in rela- measures to optimize the patient’s hemody- tion to the neurologic, cardiovascular, gas- namic profile (Gerhardt, 2007). trointestinal, and respiratory systems. Headache, confusion, restlessness progressing METABOLIC ALKALOSIS to lethargy, stupor, and coma are possible. Metabolic alkalosis is defined as a bicarbon- Kussmaul respirations occur when the body ate level greater than 26 mEq/L with a pH attempts to maintain a normal pH by blow- greater than 7.45. Table 11–5 lists conditions

ing off CO2. Cardiac dysrhythmias; decreased that may cause a metabolic alkalosis in the cardiac contractility and cardiac output; postoperative cardiac surgery patient. hypotension; warm, flushed skin; nausea and Metabolic alkalosis symptoms are prima- vomiting; insulin resistance; and hyper- rily associated with the neurologic and mus- kalemia may also be observed (Adrogué & culoskeletal systems. Dizziness, headache, Madias, 1998a). lethargy, stupor, disorientation, delirium, The ICU nurse should attempt to identify seizures, and coma may be expected. Muscu- the underlying cause of the metabolic acido- loskeletal symptoms may include weakness, sis. Hypoxia of any tissues will produce meta- muscle cramps, muscle twitching, and tetany. bolic acids from anaerobic metabolism even if The patient can progress to respiratory

the PaO2 is normal. The only way to treat aci- depression—evidenced as hypoventilation and dosis is to restore tissue perfusion, thereby hypoxemia—and may develop supraventricu- 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 193

Assessment of Readiness for Weaning 193

lar or ventricular dysrhythmias. Electrolyte respiratory distress syndrome). Because the imbalances associated with metabolic alkalo- desaturated blood has not been exposed to sis include hypokalemia, hypocalcemia, hypo- ventilated alveoli, increasing oxygen delivery magnesemia, and hypophosphatemia. Of will not correct the resultant hypoxia. Instead, note, patients with a mild to moderate meta- correction of the underlying pathology is nec- bolic alkalosis have few or no symptoms. essary to resolve this condition. However, if the bicarbonate level is severe (greater than 40 mEq/L), symptoms will likely A-a Gradient develop (Adrogué & Madias, 1998b). In addition to assessing acid–base balance, Treatment of metabolic alkalosis can be another assessment criterion that may be used ® difficult. Acetazolamide (Diamox ) is com- to determine patient readiness to wean from monly given after cardiac surgery when excess mechanical ventilation is calculation of the diuretics have been administered. It may take Alveolar-arterial oxygen gradient (A-a gradient), hours to days to resolve the alkalosis. Aceta- a method of measuring IPS. This calculation zolamide blocks the action of carbonic anhy- determines the difference between the percent- drase, thereby promoting renal excretion of age of alveolar oxygen entering the alveoli and sodium, potassium, phosphorus, bicarbonate, the percentage of oxygen diffusing into the and water. Renal excretion of potassium and arterial blood. The result of this calculation will phosphorus may be excessive with acetazo- aid the clinician in assessing for the presence of lamide therapy, however. In severe cases, IV dysfunction in oxygenation as well as the administration of hydrochloric acid may be degree of IPS (Marini & Wheeler, 2005). The necessary. The ICU nurse should be aware of higher the A-a gradient, the more severe the the fluid load associated with this therapy problem with oxygen reaching the blood. If (Adrogué & Madias, 1998b). If an electrolyte the shunt is too extensive, the patient is not disturbance occurs in conjunction with ther- ready for weaning from mechanical ventilation. apy for metabolic alkalosis, repletion accord- Hypoventilation during cardiac surgery ing to facility protocol is indicated (Gothard results in atelectasis, increasing A-a gradient. et al., 2003). As the alveoli reexpand postoperatively, the A-a gradient normalizes (Ͻ 300 mm Hg), Intrapulmonary Shunt revealing the patient’s readiness for weaning Intrapulmonary shunt (IPS) is the percentage (Markou, Myrianthefs, & Baltopoulos, 2004). of cardiac output that does not participate in The formula for calculating an A-a gradient gas exchange. This blood passes through the is complex. Fortunately, Internet sources offer lungs but is not exposed to ventilated alveoli, calculator programs installed to facilitate the so gas exchange does not take place; as a con- process. The ICU nurse would need to insert

sequence, the blood leaves the lungs in a the local barometric pressure PB (which is pre- desaturated state. IPS can occur as a result of set at 760 mm Hg), PaO2 and PaCO2 data a number of conditions (e.g., collapsed or from the ABG, and the patient’s FiO2 level. fluid-filled alveoli) and is a major cause of Once the nurse clicks the “Calculate A-a hypoxemia in the ICU. A frequent cause of gradient” button, the result appears (Global- IPS following cardiac surgery is atelectasis RPh.com, 2008). A-a gradient calculation (Magnusson & Spahn, 2003). A normal shunt has been criticized for its complexity, its is in the range of approximately 2–5%. Some age-dependent nature, and its relationship with

patients, however, may have a shunt as high FiO2 in patients with constant ventilation/ as 40% or 50% (e.g., patients with acute perfusion mismatch (Markou et al., 2004). 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 194

194 Chapter 11 Mechanical Ventilation After Cardiac Surgery

PaO2 /FiO2 Ratio If not extubated in the OR, the patient is A suggested alternative to the A-a gradient placed on mechanical ventilation upon that is easy to calculate and considered a reli- arrival to the ICU. The mode of ventilation able indicator of gas exchange is the and settings used will depend on the patient’s clinical status. Cardiac surgical PaO2/FiO2 (P/F) ratio (Markou et al., 2004). This ratio is an index of oxygenation that is patients have multiple risk factors for post- commonly used by clinicians because of its operative respiratory dysfunction. Most patients are resilient and will be weaned from ease in calculation. A PaO2/FiO2 ratio of less than 200 is associated with a significant mechanical ventilation within 24 hours; 5% will require prolonged support (Chikwe, Bed- shunt. Criticisms of the PaO2/FiO2 ratio include the fact that it is affected by changes dow, & Glenville, 2006).

in PaCO2 and SvO2, it is reportedly not equally sensitive across the entire range of Initial Postoperative Ventilator Settings FiO2, and it cannot provide information For patients who remain on mechanical venti- about the functional status of the lungs based lation in the postoperative period, the set- on interventions to augment oxygenation tings used should be based on a plan (e.g., positive end-expiratory pressure [PEEP], intended to optimize gas exchange, decrease lateral or prone positioning) (Marini & work of breathing, and minimize complica- Wheeler, 2005). tions associated with positive-pressure ventilation (Chikwe et al., 2006). Table 11–6 shows PaO /(FiO ϫ Mean P ) 2 2 aw the initial ventilator settings. ϫ Another oxygenation index, PaO2/(FiO2 mean P , where P is mean airway pressure), aw aw Patient Monitoring takes into account the effects of PEEP. It has been widely used in neonatal and pediatric When the patient is admitted to the ICU, the venues, but has not been well adapted for use nurse should auscultate breath sounds to in the adult population as yet (Hess & Kac- confirm good bilateral air entry and absence marek, 2002). In a study of cardiac surgery of bronchospasm. The postoperative cardiac ϫ surgery patient will be monitored with pulse patients, data suggested that PaO2/(FiO2 oximetry and potentially with capnometry mean Paw) measurements may be more reliable than other oxygenation measurements in (end tidal carbon dioxide [ETCO2]) (Khalpey reflecting intrapulmonary shunt (El-Khatib & et al., 2008). These noninvasive monitoring Jamaleddine, 2004). devices provide the ICU nurse with continuous estimates of the patient’s oxygenation and ventilation status, respectively and will ■ POSTOPERATIVE MECHANICAL likely expedite the weaning process. For VENTILATION capnography, an infrared gas analyzer is Prolonged mechanical ventilation following placed in the exhalation port of the ventilator cardiac surgery is associated with increased or closest to the endotracheal tube. The nor-

ICU and hospital lengths of stay, resource mal ETCO2 is 2–6 mm Hg less than the use, costs, and poorer physiologic outcomes PaCO2. Researchers have found continuous, (Natarajan et al., 2006). Results of “fast-track” noninvasive monitoring of SpO2 and ETCO2 programs have shown that postoperative to be a reliable means of weaning patients intubation can be safely limited to 4 to 8 from mechanical ventilation after cardiac hours (Doering, Esmailian, & Laks, 2000). surgery if adjustments are made for the 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 195

Weaning Criteria 195

Table 11–6 Initial Postoperative Ventilator Settings

SIMV, Assist Control, Pressure Support Ventilation, or Pressure Mode Control

FiO2 Range = 0.4–1.0. Depends on the patient’s ABG results and SpO2 measurements. It is modified to the lowest level while maintaining SpO2 levels at least 92% or what is reasonable according to the patient’s baseline and past medical history. Tidal volume 8–12 mL/kg ideal body weight. Tidal volume may be increased to decrease carbon dioxide levels, and vice versa. Tidal volume may also be adjusted to maintain pH within appropriate limits for the patient. It may also be adjusted to maintain peak inspiratory pressure less than 35 cm H2O. Rate 8–18 breaths/minute. Respiratory rate may be increased to decrease carbon dioxide levels. Minute volume 100–120 mL/kg/min. Minute volume may be increased by increasing the rate, the tidal volume, or both to decrease carbon dioxide levels.

PEEP 5–10 cm H2O. PEEP levels may be increased to improve oxygenation.

Pressure support 5–10 cm H2O. Inspiratory:expiratory 1:2. If a patient has difficulty with oxygenation, the ratio may be (I:E) ratio changed to either 1:1 or 2:1 (inverse I:E ratio). Inspiratory flow rate 30–60 L/min.

ABG = arterial blood gas; PEEP = positive end-expiratory pressure; SIMV = synchronized intermittent mandatory ventilation. Sources: Chikwe, Beddow, & Glenville, 2006; Herlihy, Koch, Jackson, & Nora, 2008; Khalpey, Ganim, & Rawn, 2008; Lytle & Brown, 2008.

PaCO2–ETCO2 gradient that can occur at must be awake, oriented, able to cooperate high ventilatory rates (Thrush, Mentis, & with instructions, and triggering the ventila- Downs, 1991). tor by taking spontaneous breaths (Heijmans, Maessen, & Roekaerts, 2004). The patient should also demonstrate ade- ■ WEANING CRITERIA quate muscle strength as demonstrated by Anesthesia traditionally utilizes short-acting either a strong hand grasp or a sustained head anesthetic agents so that the patient will wake lift for 5 seconds (Lytle & Brown, 2008). A up quickly. The ICU nurse assesses the chest radiograph should be reviewed prior to patient for readiness to wean on an ongoing extubation to ascertain the presence of any basis. indicators that may indicate the patient Initiating the weaning process commences might not tolerate extubation. Lab values when the patient is hemodynamically stable, (e.g., electrolytes, lactate level) should be normothermic, and adequately resuscitated; within normal ranges. The ABG results does not have any clinically significant dys- should be at or close to the patient’s baseline rhythmias; is draining less than 100 mL/hour or normalized. from the chest tube; is not shivering; and is The patient should be normothermic on minimal vasoactive support. The patient before weaning is attempted, as shivering 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 196

196 Chapter 11 Mechanical Ventilation After Cardiac Surgery

causes an increase in carbon dioxide produc- the least effective method of weaning and no tion. Shivering following hypothermic car- added benefit existed between pressure sup- diopulmonary bypass (CPB) causes a twofold port and spontaneous breathing trials to threefold increase in oxygen consumption (Hemant, Chacko, & Singh, 2006). and predisposes the patient to develop respi- Regardless of the method used, once the ratory and metabolic acidosis (Bhattacharya, patient has satisfactory ABG results and has Bhattacharya, Jain, & Agarwal, 2003). demonstrated the ability to breathe independently without signs of distress, extubation can be considered. In addition to assessment ■ WEANING FROM MECHANICAL of pulmonary mechanics, if the patient is able VENTILATION to maintain a patent airway and manage secre- Weaning may be accomplished in several differ- tions, the patient is considered ready to be ent ways, depending on the mode of ventilation extubated if the criteria in Box 11–1 are met. and the patient’s condition. The first goal is to The ICU nurse plays a pivotal role in assess- wean the patient as tolerated while maintaining ing tolerance to weaning. Signs and symp- Ն a SpO2 92–94% on FiO2 .40 and PEEP 5 cm toms that would indicate poor tolerance to H2O. If the patient is receiving pressure sup- weaning include a respiratory rate of 35 or port, as the patient’s respiratory effort greater; SpO2 less than 90%; heart rate greater increases, pressure support levels can be gradu- than 140; systolic or diastolic blood pressure ally titrated down (Heijmans et al., 2004; higher than 180 or 90 mm Hg, respectively; Khalpey et al., 2008). and presence of agitation, diaphoresis, or anx- Once physiologic parameters have been met, the amount of support the patient Box 11–1 Readiness for Extubation receives from the ventilator is gradually Criteria decreased or else the patient undergoes a Ն spontaneous breathing trial with either pres- NIP –25 cm H2O sure support or a t-piece. If using pressure RR Յ 25 bpm support, the patient is placed on 5 cm H O HR Ͻ 140 2 Յ with no preset breaths to be delivered. The Minute volume (VE) 10 L/min Vital capacity (VC) Ն 10–15 mL/kg patient’s minute volume and respiratory rate should remain within clinically acceptable Cardiac status: limits. The patient will remain on these set- ● No signs of ischemia tings (if tolerated) for 30 minutes, at which ● Not receiving vasopressor therapy or low point an ABG is obtained. dose inotropic agents An alternative to a spontaneous breathing Neurologic status: trial for weaning is to gradually and incremen- ● Alert tally decrease the amount of support from ● Able to respond to commands pressure support ventilation or the synchro- ● Cough and gag reflex nized intermittent mandatory ventilation ● Able to protect airway and clear secretions (SIMV) rate. Data suggest that patients who ● Able to sustain a head lift for at least are weaned with spontaneous breathing trials 5 seconds are successfully extubated two to three times ϭ ϭ earlier than patients who are weaned with NIP negative inspiratory pressure; RR respiratory rate. Sources: Hanneman, 2004; Hemant, Chacko, & Singh, either of the alternative methods (Esteban et 2006; Khalpey, Ganim, & Rawn, 2008. al., 1995). Further, SIMV has been found to be 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 197

Post-Extubation Care 197

iety (Khalpey et al., 2008). Further, if the wean and extubation. The physiologic index patient has an inadequate minute volume, is determined by assessing the minute fre- tidal volume, episodes of apnea lasting more quency of spontaneous ventilation (f ) and than 25 seconds, mental status changes, a dividing this value by the tidal volume (Vt) in

decrease in SpO2 to less than 92%, or ETCO2 liters. When this index is high, it reflects a greater than 55 mm Hg, the trial is stopped, clinical picture of a patient with rapid, shal- the patient is restored to the prior ventilator low breathing. When f/Vt is less than 105, settings, and an ABG is obtained. It has been 78% of patients can be weaned and extubated recommended that spontaneous breathing successfully. When f/Vt is greater than 105, trials be attempted hourly until weaning is 95% of patients cannot be weaned and extu- successful (Lytle & Brown, 2008). bated successfully. A Vt of 325 mL is a good When ABG results are obtained and are threshold value for predicting weaning suc- within the appropriate range, collaboration cess or failure (Yang & Tobin, 1991). with the physician regarding extubation is indicated. If the ABG results are not accept- ■ able, the patient should be placed back on the POST-EXTUBATION CARE previous support settings and reassessed in an Upon extubation, the patient is assessed for a hour (Lytle & Brown, 2008). patent airway and absence of laryngeal edema. Researchers have compared intubation The ICU nurse should ask the patient to times using SmartCare™, a knowledge-based speak a few words. Afterward, the patient system for automated weaning with conven- should be placed on a humidified face mask

tional physician-controlled weaning after set to deliver a FiO2 10% greater than what off-pump coronary artery bypass. No com- was received when the patient was on

plications or increase in reintubations mechanical ventilation. The FiO2 level may be occurred with this computer-driven weaning titrated down according to SpO2 values, system, and SmartCare reduced the duration which should initially be maintained above of mechanical ventilation (Kataoka et al., the range of 97% to 98%. After the initial post-

2007). Many factors associated with cardiopul- extubation period, FiO2 can be titrated to monary bypass would need to be studied maintain SpO2 at least 95% for the first 2 to before the use of SmartCare could be routinely 3 days. After that point, a nasal cannula can

recommended in this population, however. be used to maintain SpO2 at least 90% Another study evaluated the Siemens Servo (Salenger et al., 2003). 300A ventilator, which has an automode Extubation failure in postoperative cardiac function allowing for automated weaning surgery patients has a reported overall inci- from mechanical ventilation. Data suggest dence of 5%. The incidence is 14% among that the automode decreased ventilation patients with COPD; it is 10% for those with a time by 2 hours, decreased peak airway pres- history of stroke. Other identified risk factors sure during spontaneous ventilation, and of extubation failure include renal failure, improved patients’ cardiac index (Hendrix, IABP requirement, longer surgical time, and Kaiser, Yusen, & Merk, 2006). longer time on bypass (Khalpey et al., 2008). In a qualitative study of cardiothoracic patients, four nursing dimensions of care Weaning from Prolonged Ventilation emerged as critical issues during the immedi- In long-term weaning, the physiologic index ate post-extubation period: clinical physiologic is a reliable predictive indicator of failure to data, communication, early physical activities, 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 198

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and available resources. Specifically, ICU inflammatory drugs with the serine protease nurses identified these four aspects of care as inhibitor activity of Aprotinin in combination their responsibility (De Beer, Nel, & Arries, with leukocyte-reduction filters. The last com- 2002). bination has been shown to improve post- Post-extubation, the ICU nurse should ini- bypass lung performance by reducing tially observe for laryngospasm for as long as 1 inflammatory response and its sequelae hour and stridor for as long as 24 hours—both (Olivencia-Yurvati, Ferrara, Tierney, Wallace, & conditions may result in the need for reintu- Mallet, 2003). bation. Prophylactic administration of dexamethasone has been shown to be effective in ■ decreasing the incidence of post-extubation SUMMARY stridor in patients who are at risk for develop- Caring for patients following cardiac surgery ing laryngeal edema (Lee, Peng, & Wu, 2007). is often challenging. While many patients are After cardiac surgery, many patients will admitted to the ICU having already been have decreased breath sounds secondary to extubated, others require management with lower lobe atelectasis (Khalpey et al., 2008). mechanical ventilation for either a short or For this reason, the critical care nurse must prolonged period of time. Mechanical venti- frequently evaluate the patient in terms of lation is suggested to be associated with— work of breathing, respiratory rate, use of and may even cause—lung damage and many accessory muscles, and expiratory phase of other complications (Pappalardo et al., breathing. Nursing care must include encour- 2004). aging mobility, use of incentive spirometry, Prolonged use of mechanical ventilation is bronchial hygiene, and frequent auscultation correlated with increased mortality rate. The of breath sounds. Chest physiotherapy will mortality rate can be 50% or more in patients promote lung expansion, mobilize secretions, who develop acute lung injury or acute respira- encourage coughing, and prevent the side tory distress syndrome (El-Chemaly, Abreu, & effect of retained secretions, which might oth- Krieger, 2003). The cardiac surgery ICU erwise cause atelectasis and potentially pneu- nurse must continuously assess the post-car- monia (Salenger et al., 2003). diac surgery patient for tolerance to therapy, One of the sequelae of bypass procedures is prevent complications associated with activation of the inflammatory response, mechanical ventilation, minimize the effects which can cause marked pulmonary dysfunc- of the patient’s comorbidities and the proce- tion (Khalpey et al., 2008). A variety of inter- dure-associated complications, and assess ventions are being studied for their potential the patient’s readiness for and tolerance of to mitigate the deleterious effects of bypass weaning from mechanical ventilation. procedures that can cause delays in weaning Although the majority of patients are from mechanical ventilation. These interven- quickly weaned from mechanical ventilation tions include use of a leukocyte filtration to and extubated, extubation failure must be reduce the effects of cardiopulmonary bypass; minimized or recognized promptly. Using intraoperative use of heparin-bonded circuits high levels of clinical judgment and caring designed to prevent complement activa- practices will affect the ICU nurse’s ability to tion and subsequent increase in neutrophil optimize outcomes of the postoperative car- activation; and use of antioxidants and anti- diac surgery patient. 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 199

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CASE STUDY

A 65-year-old, moderately obese female has a 3-year history of coronary artery disease with a stent placed in her right coronary artery 18 months prior to her current admission. Her history includes elevated cholesterol, hypertension, and diet-controlled diabetes. The patient is being treated with 325 mg aspirin daily, atorvastatin (Lipitor®), and an angiotensin-converting enzyme (ACE) inhibitor. The patient presented with nausea and vomiting as well as “heaviness” in her chest. She had a recent bout with bronchitis and had not been feeling well for 2 days, but felt her condition was related to the bronchitis. Upon her admission, a 12-lead ECG revealed ST-segment elevation in leads II, III, and aVF. The patient reported her chest pain to be 7 out of 10; she was treated with sublingual nitroglycerin, which decreased the pain to 5 out of 10. Initial electrolytes and complete blood count were within normal limits although troponin I was elevated. Cardiac catheterization revealed the following: ● Severe triple vessel coronary artery disease. ● The right coronary artery (RCA) had 90% dominant obstruction. ● The left anterior descending (LAD) coronary artery had 80% obstruction. ● The aortic and mitral valves were normal without significant stenosis or regurgitation. The patient was scheduled for coronary artery bypass grafting. The left internal mammary artery was used to bypass the LAD, and radial arteries were used to bypass the remaining blockages. The intraoperative course was uneventful, and the patient was admitted to the ICU postoperatively.

Critical Thinking Questions 1. For which post-extubation complications should the ICU nurse assess on this patient? 2. Which pulmonary interventions will be necessary to facilitate respiratory functioning in this patient? 3. What are possible pulmonary complications from cardiac surgery? 4. How would the nurse assess for a positive Hoover sign? 5. How should you assess for air leak syndrome? Answers to Critical Thinking Questions 1. In the post-extubation patient, the nurse should initially observe for laryngospasm for as long as 1 hour and stridor for as long as 24 hours; either of these complications may result in the need for reintubation. After cardiac surgery, the patient would be expected to have decreased breath sounds secondary to lower lobe atelectasis. The patient will need frequent assessment in terms of work of breathing, respiratory rate, use of accessory muscles, and the expiratory phase of breathing, which can indicate compromised pulmonary function. 2. Nursing care must include mobility and bronchial hygiene, and frequent auscultation of breath sounds. Bronchial hygiene will promote lung expansion, mobilize secretions, and prevent retention of secretions that cause atelectasis and potentially pneumonia. This care should include pulmonary toileting of effective coughing and 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 200

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incentive spirometry. Incentive spirometry has only limited effectiveness, however, because many patients are unable to cooperate adequately to use it correctly. 3. Potential pulmonary complications include phrenic nerve injury, pulmonary atelectasis, pleural effusions, and air leak syndrome. 4. A positive Hoover sign indicates a pleural effusion. To assess for this condition, the nurse should observe the patient for an asymmetric expansion of the thoracic cage. With a positive Hoover sign, the nurse will note a lagging expansion on the affected side where the pleural effusion is located. 5. Assess the patient for symptoms of a sensation of fullness in the chest, pleuritic chest pain that may radiate to the shoulders, dyspnea, coughing, hoarseness, and dysphagia. Crepi- tus in the neck due to associated subcutaneous emphysema may be present. Upon auscultation, a crackling sound may be heard over the heart during systole (Hamman sign).

■ SELF-ASSESSMENT QUESTIONS c. CI of 2.6 L/min/m2 1. An initial set of blood gas results are as d. MAP of 75 mm Hg 5. After 8 hours in the ICU, your patient follows: pH = 7.31; PCO2 = 50 mm Hg; has received 4 units of PRBCs, 2 units of and HCO3 = 22 mEq/L. What is the correct interpretation of these results? FFP, and 6 units of platelets. Chest tube a. Uncompensated respiratory acidosis output is minimal and the patient has b. Compensated respiratory acidosis remained hemodynamically stable. The c. Uncompensated metabolic acidosis patient is again being evaluated for extu- ϭ d. Compensated metabolic acidosis bation. She is alert, respiratory rate 7, ϭ 2. Based on the post-cardiac surgery ABG and PaCO2 75 mm Hg. You should results given in Question 1, which of the anticipate following is the potential cause? a. a decrease in tidal volume. a. Bleeding b. an increase in rate. b. Hypoventilation c. proceeding with extubation. c. Hyperglycemia d. administering opioids. d. Preexisting cardiac history 6. After reassessment, the patient has the 3. Which of the following criteria would following characteristics: alert and coop- indicate that the patient is not ready for erative, NIP –20 cm H2O, minute vol- extubation? ume 10 L/min, vital capacity 14 L/kg, a. Minute volume of 3 L/minute hemodynamically stable, chest tube b. Vital capacity Ն 10–15 mL/kg draining minimal. Your assessment of c. Negative inspiratory pressure of the patient is that she is a. ready for extubation. –20 cm H2O d. Respiratory rate of 24 bpm b. not ready for extubation. 4. After 4 hours of mechanical ventilation, Answers to Self-Assessment Questions your patient is stable on a FiO2 of 0.30, rate of 4, and pressure support of 5 cm 1. a 4. a

H2O. Which of the following indicators 2. b 5. b would deter extubation? 3. a 6. b a. Chest tube draining of 225 mL/hr b. Temperature of 37.0°C 57625_CH11_185_204.pdf 4/14/09 1:04 PM Page 201

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Clinical Inquiry Box

Question: Is there a difference in pulmonary complications following on-pump versus off-pump cardiac surgery? Reference: Groeneveld, A. B., Jansen, E. K., & Verheij, J. (2007). Mechanism of pulmonary dysfunction after on-pump and off-pump cardiac surgery: A prospective cohort study. Journal of Cardiotho- racic Surgery, 2(1). http://www.cardiothoracicsurgery.org/content/2/1/11 Objective: To investigate whether there are differences in pulmonary complications between on- pump and off-pump cardiac surgical approaches. Methods: The study enrolled 31 patients who underwent on-pump surgery and 8 patients who underwent off-pump surgery. Data collected included postoperative pulmonary leak index (PLI), extravascular lung water (EVLW), transfusion history, radiographs, and ventilatory and gas exchange variables. Results: There was no significant difference between PLI, EVLW, transfusion of red blood cell (RBC) concentrates, occurrence of atelectasis, ventilatory variables, and duration of mechanical ventilation. The PLI was significantly correlated to the number of RBC concentrates infused. Conclusion: Cardiopulmonary bypass does not cause lung vascular injury. Atelectasis is the major factor contributing to pulmonary dysfunction. Therefore, nurses must be vigilant in their assessment of postoperative patients’ pulmonary status and implement measures to prevent or treat this pulmonary complication.

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Thrush, D. N., Mentis, S. W., & Downs, J. B. (1991). als of weaning from mechanical ventilation.

Weaning with end-tidal CO2 and pulse oxime- New England Journal of Medicine, 324(21), try. Journal of Clinical Anesthesia, 3(6), 456–460. 1445–1450. Tu, J. V., Jaglal, S. B., & Naylor, C. D. (1995). Multi- Yende, S., & Wunderink, R. (2002). Causes of pro- center validation of a risk index for mortality, longed mechanical ventilation after coronary intensive care unit stay, and overall hospital artery bypass surgery. Chest, 122(1), 245–252. length of stay after cardiac surgery. Steering Committee of the Provincial Adult Cardiac Care Network of Ontario. Circulation, 91(3), ■ WEB RESOURCES 677–684. Respiratory assessment: http://www.youtube.com/ Wong, D. T., Cheng, D. C., Kustra, R., Tibshirani, watch?v=IepL5u5lAtE R., Karski, J., Carroll-Monro, J., et al. (1999). Mechanical ventilation tutorial: http://www Risk factors of delayed extubation, prolonged .ccmtutorials.com/rs/mv/ length of stay in the intensive care unit, and Patient education guides on mechanical ventila- mortality of patients undergoing coronary tion: http://www.chestnet.org/patients/ artery bypass graft with fast-track cardiac guides/mech_vent/ anesthesia: A new cardiac risk score. Anesthesi- Ventilator case studies: http://www.ventworld ology, 91(4), 936–944. .com/education/casestudies.asp Yang, K. L., & Tobin, M. J. (1991). A prospective study of indexes predicting the outcome of tri- 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 205

Chapter 12 Pharmacologic Support Following Cardiac Surgery

Timothy E. McMurry, Roberta Kaplow, and Sonya R. Hardin

■ INTRODUCTION As described in Chapters 8 and 13, hemody- action of some of these medications and their namic compromise following cardiac surgery sometimes burdensome side effect profiles, the is common and challenging to manage. The ICU nurse needs a high level of clinical judg- etiology of the instability may be the patient’s ment to help optimize the patient’s outcome. underlying cardiac disease, postoperative filling pressures, dysrhythmias, decreased ven- ■ tricular compliance, loss of vasomotor tone, AGENTS USED TO MANAGE increased capillary permeability, excessive POSTOPERATIVE HYPERTENSION bleeding, increased urinary output, inflam- Hypertension may occur in as many as 60% of matory response to cardiopulmonary bypass postoperative cardiac surgery patients (Tal- (CPB), poor myocardial protection during mor & Lisbon, 2005). This condition is fre- aortic cross-clamping, pulmonary edema, car- quently linked to vasoconstriction (Silvestry, diac tamponade, or ventricular dysfunction. 2008). Development of hypertension, vaso- Even though the surgery has been completed, constriction, or both may be due to decreased there may not be an immediate improvement oxygen levels or inflammatory responses to in contractility in some patients (Salenger, CPB (Salenger et al., 2003; Silvestry, 2008). Gammie, & Vander Salm, 2003). Hypertension leads to increased afterload In the care of the postoperative cardiac sur- with resultant metabolic acidosis, increased gery patient, the ICU nurse must be aware of systemic vascular resistance (SVR), decreased the intricate balance between physiological cardiac output (CO), and increased myocar- data and the medications utilized to treat and dial oxygen consumption (Katz, 2007). As prevent complications. This chapter discusses noted in Chapters 8 and 13, potential causes several medications used in the immediate of increased afterload include hypothermia, postoperative setting, including their mecha- hypovolemia, hypercarbia, inadequate rewarm- nism of action, therapeutic uses, and side ing, volume overload, cardiogenic shock, pain, effects. In addition, nurse precautions that are and anxiety. The latter two causes arise as a utilized in the delivery of care are described. result of increased sympathetic nervous sys- Many of the medications profiled in this chap- tem stimulation (Khalpey, Ganim, & Rawn, ter have a number of mechanisms of action and 2008; Talmor & Lisbon, 2005). If vasocon- indications. Because of the potential for inter- striction is extreme, patients are at risk of

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developing life-threatening hypertension and higher doses, afterload. Patients with high decreased CO (Khalpey et al., 2008). Control- preload benefit because NTG lowers pulling hypertension is also important after car- monary artery pressure (PAP) and central diac surgery to reduce bleeding from surgical venous pressure (CVP) via its vasodilatory sites and enhance CO. Refer to Table 12–1 for action. NTG also decreases SVR and a summary of medications used to treat pulmonary vascular resistance (PVR) hypertension following cardiac surgery. (Salenger et al., 2008). Whenever ischemia is suspected postoperatively, NTG may be Vasodilators ordered because of its ability to dilate the coronary arteries and increase coronary blood Vasodilators are the agents of choice to flow. This agent also decreases pulmonary decrease hypertension in the immediate post- congestion and myocardial oxygen consump- operative cardiac surgery patient (Katz, tion (Katz, 2007). 2007). Vasodilators are utilized to control In addition to treating hypertension, hypertension, reduce afterload, and prevent decreasing preload or afterload, and treating angina pectoris, myocardial infarction (MI), myocardial ischemia, NTG is also used on a and heart failure, all of which could occur in short-term basis (24 to 48 hours) to prevent the postoperative cardiac surgery patient. spasm of internal mammary arteries in the These agents may also be used in postopera- postoperative period. tive cardiac surgery patients who have normal blood pressure despite poor pump function (Khalpey et al., 2008). Agents may DOSAGE dilate either the arterial or venous system, or Infusion rates for NTG may be set as low as both. The most commonly used vasodilators 5–10 mcg/min. The rate is titrated in 10-mcg in this patient population are nitroglycerin increments until a mean arterial pressure (NTG, Tridil®), nitroprusside (Nipride®), (MAP) goal has been attained. Titration to nicardipine (Cardene®), and fenoldopam effect can occur as often as every 5 to 10 min- mesylate (Corlopam®). utes owing to the short half-life of NTG. This Care must be taken to correct hypovolemia agent has an immediate onset of action and in hypertensive patients prior to administer- the drug effects last 30 minutes (Katz, 2007). ing a vasodilator. Abrupt, life-threatening hypotension may develop when vasodilators SIDE EFFECTS are used and there is an inadequate volume to One potential side effect of NTG is hypoxia— fill the vasculature. The ICU nurse should a condition caused by the drug’s inhibition of always be prepared to administer a rapid fluid pulmonary arterial vasoconstriction, which in bolus when starting any vasodilator, should turn increases blood flow through poorly oxy- hypotension occur. As with all vasoactive genated lung areas (Katz, 2007; Massé & agents, use of the smallest dose necessary to Antonacci, 2005). Other side effects that are accomplish the desired effect is recom- often reported with NTG administration mended. The risk of side effects escalates with include lightheadedness, headache, hypoten- higher infusion rates. sion, tachycardia, dizziness, and flushing of Nitroglycerin the face and neck (Doucet et al., 2000; Silver, 2002). Although rare, methemoglobinemia HEMODYNAMIC EFFECTS AND INDICATIONS has been reported as being associated with NTG has many uses in postoperative cardiac intravenous administration of NTG (Ander- surgery patients. It decreases preload and, in son, Woodside, Spencer, & Hunter, 2004). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 207

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Table 12–1 Antihypertensive Agents Used in Postoperative Cardiac Surgery Patients and Hemodynamic Effects

Mechanism Hemodynamic Agent Dose of Action Effects

Vasodilators Nitroglycerin (Tridil®) 5–10 mcg/min; Venous and arterial Decreases preload and titrated in 10-mcg vasodilation (dose afterload (dose increments every dependent). Increases dependent). Decreases 5 to 10 minutes. coronary blood flow, PAP, CVP, SVR, PVR, dilates coronary arteries. myocardial oxygen consumption. Nitroprusside 0.3 mcg/kg/min; Smooth muscle relaxant; Decreases SVR and (Nipride®) titrate every arterial vasodilation. PVR; increases venous 10 minutes up to Generates nitric oxide. capacitance, decreases 10 mcg/kg/min. coronary vascular resistance. Nicardipine Infusion at 5 mg/hr. Blocks flow of calcium. Peripheral vascular and (Cardene®) Dose may be slowly Acts directly on arterioles. coronary vasodilation increased by Also been shown to dilate and lower blood 2.5 mg/hr to a the coronary vasculature. pressure. maximum of 15 mg/hr. Once blood pressure endpoint is reached, a maintenance infusion may be run at 3 mg/hr. Fenoldopam mesylate Initial dose of 0.03– Selective dopamine-1- Vasodilator; increases (Corlopam®) 0.1 mcg/kg/min. receptor agonist and renal blood flow; Titration in moderately binds to decreases SVR and increments of 0.05– alpha2 receptors. PVR and enhances 0.1 mcg/kg/min cardiac output. every 5–15 min, to maximum of 1.6 mcg/kg/min, to achieve desired blood pressure. Doses must be administered as a continuous infusion. Should not be used for more than 48 hrs. continues 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 208

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Table 12–1 Antihypertensive Agents Used in Postoperative Cardiac Surgery Patients and Hemodynamic Effects (continued)

Mechanism Hemodynamic Agent Dose of Action Effects

Beta Blockers Esmolol (Brevibloc®) Loading dose: Cardioselective beta- Decreases heart rate, 500 mcg/kg IV bolus adrenergic receptor blood pressure, over 1 minute. blocker. Inhibits effects contractility, and Maintenance dose: of beta1 receptors. cardiac output. 50 mcg/kg/min over Inhibits beta2 receptors 4 min. If additional at higher doses. dosing is required after 5 min, use same loading dose followed by 100 mcg/kg/min over 4 min. May continue to titrate by increasing the maintenance dose in 50 mcg/kg/min increments until desired endpoint or maintenance dose of 200 mcg/kg/min is reached. When endpoint is reached, loading dose should be eliminated or titration may take place every 10 min. Labetalol 10 mg IV over Non-cardioselective (Normodyne®, 2 minutes. adrenergic blocking agent. Trandate®) Additional 10mg Exerts inhibitory effects to 20 mg doses on beta1, beta2, and every 10 min up to alpha1 receptors. a maximum of 300 mg in 24 hours may be given. ACE Inhibitors Enalaprilat (Vasotec®) 0.625 to 1.25 mg, Prevents conversion of Vasodilation; infused over 5 min. angiotensin I to decreases SVR. Additional doses, angiotensin II (a potent up to a maximum vasoconstrictor) by of 5 mg every inhibiting ACE in the 6 hours, may be pulmonary and systemic administered. vascular endothelium. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 209

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Table 12–1 Antihypertensive Agents Used in Postoperative Cardiac Surgery Patients and Hemodynamic Effects (continued)

Mechanism Hemodynamic Agent Dose of Action Effects

ARBs No specific ARB Dosage is drug Blocks production of The adrenal-related recommendations dependent. angiotensin II from blockage results in a noted in literature. sources of angiotensin II decrease in aldosterone other than the liver (i.e., levels, thereby leading blood vessels, in the to increased excretion adrenals, and within all of sodium and water other tissues.) from kidneys. Calcium Channel Blockers Nicardipine See page 207 under vasodilators. Clevidipine 1–2 mg/hr via Smooth muscle relaxant Decreases MAP and (Cleviplex®) continuous infusion. and arterial vasodilator. SVR. Dose may be doubled in 90- second intervals. Once blood pressure begins to approach goal, incremental dosing should be every 5–10 min and be less than double the dose. A maximum initial dose is 16 mg/hr. Total 24-hr dosing should not exceed 21 mg/hr. Selective Dopamine- 1-Receptor Agonist Fenoldopam Mesylate See page 207 under vasodilators.

Sources: Cheung et al., 1999; Katz, 2007; Khalpey et al., 2008; Lemmer, Richenbacher, & Vlahakes, 2003; Levy, Tanaka, & Bailey, 2008; Micromedex Online, 2008; Salenger et al., 2008; Singla et al., 2008. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 210

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NURSING IMPLICATIONS SIDE EFFECTS Abrupt discontinuation of NTG can cause Administration of nitroprusside may produce coronary vasospasm. For this reason, close reflex tachycardia, hypotension, and renal dys- monitoring of rhythm, blood pressure, and function. Rarely, patients may develop a hemodynamic parameters is warranted when decreased platelet count or hypothyroidism the infusion is stopped. The drug dosage used (thiocyanate impairs iodine transport). Owing depends on the desired effect, the patient’s to its dilation of the pulmonary arterioles, blood pressure, and hemodynamics, bearing nitroprusside can decrease arterial oxygen in mind that increasing coronary blood flow content and cause—or worsen—any existing may improve cardiac function. The advan- ventilation/perfusion mismatch. Methemo- tages of NTG are its ease of titration and globinemia may also occur, which will short half-life. decrease the blood’s oxygen-carrying capacity (Benowitz, 2004). Cerebral vasodilation with Nitroprusside resultant increased intracranial pressure may HEMODYNAMIC EFFECTS AND INDICATIONS occur. Nitroprusside may also inhibit platelet Nitroprusside is a smooth muscle relaxant function (Massé & Antonacci, 2005). that is used to control hypertension and An excessive amount of cyanide in the reduce afterload (SVR and PVR). A powerful plasma (more than 80 ng/mL) following arterial vasodilator, it lowers blood pressure nitroprusside administration—as a conse- by generating nitric oxide. Nitroprusside also quence of overdosage or depletion of endoge- increases venous capacitance and decreases nous thiosulfate (which converts cyanide to coronary vascular resistance (Katz, 2007; thiocyanate)—may result in nausea, disorien- Salenger et al., 2008). tation, confusion, psychosis, weakness, muscle spasm, or convulsions. These symptoms DOSAGE are related to the effects of thiocyanate toxicity (Habal, 2008). Metabolic acidosis may be For afterload reduction, initial doses as low as the first sign of cyanide toxicity. Thiocyanate 0.3 mcg/kg/min should be used and slowly levels should be monitored daily (Massé & titrated (every 10 minutes) up to 10 mcg/ Antonacci, 2005); excess amounts can be kg/min to maintain the blood pressure within removed with dialysis. specified limits. Nitroprusside has an immediate onset of action (the peak effect occurs in 2 minutes), and its effects dissipate rapidly NURSING IMPLICATIONS (within 3 minutes) when the infusion is dis- Nitroprusside can cause sudden, life-threat- continued (Katz, 2007; Massé & Antonacci, ening hypotension if its use is not closely 2005). It rapidly reduces blood pressure and is monitored. Care should be taken not to flush converted in the body to cyanide and then or initiate new medications in lines that con- thiocyanate when administered in doses tain nitroprusside, as doing so can result in greater than 10 mcg/kg/min. Its adverse abrupt hypotension. When nitroprusside is effects can be attributed mainly to excessive discontinued, the line should be aspirated hypotension and excessive cyanide accumula- and then flushed to avoid this possibility. tion; thiocyanate toxicity may also occur, Like NTG, nitroprusside can cause pul- especially in patients with renal impairment. monary vasodilation with shunting of blood Typically, this effect occurs more often in to atelectatic areas of the lung, resulting in patients who receive an infusion over a period lowered oxygen saturation and a need for of 72 to 96 hours (Massé & Antonacci, 2005). higher oxygen delivery. This effect is usually 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 211

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seen immediately and can be dose dependent. is reached. When the endpoint is reached, the If it occurs, another therapy may be chosen. loading dose should be eliminated or titra- Increasing positive end-expiratory pressure tion may take place every 10 minutes rather (PEEP) is helpful in resolving atelectasis. than every 5 minutes (Micromedex Online, 2008). Because esmolol has a short half-life, it Beta Blockers is a practical choice for treating patients with a labile blood pressure (Khalpey et al., 2008). Depending on the etiology of hypertension, a beta blocker may be considered part of the SIDE EFFECTS pharmacological arsenal to combat this complication. The net effects of beta blockers are Side effects commonly associated with a decrease in heart rate, blood pressure, con- esmolol include bradycardias, chest pain, tractility, and CO. Beta blockers are discussed hypotension, confusion, headache, dizziness, in detail later in this chapter. agitation, dyspnea, wheezing, fatigue, consti- pation, and nausea and vomiting. Serious, but Esmolol (Brevibloc®) less common side effects include seizures, MECHANISM OF ACTION bronchospasm, and pulmonary edema (Micromedex Online, 2008). Esmolol is an ultra-short-acting, cardioselective, beta-adrenergic receptor blocker. It NURSING IMPLICATIONS inhibits the effects of beta1 receptors. At Logically, any patient who requires an agent higher doses, this agent inhibits beta2 receptors located in bronchial musculature and that causes beta-receptor stimulation should blood vessels (Micromedex Online, 2008). not receive beta-blocker therapy (Khalpey et al., 2008). Esmolol is contraindicated in patients INDICATIONS with cardiogenic shock, hemodynamic compromise, second- or third-degree heart block, Esmolol is indicated for postoperative hyper- first-degree heart block (if the PR interval is tension. It is also indicated as part of the greater than 0.24 sec) (Khalpey et al., 2008), or management of acute MI, intraoperative hyper- severe sinus bradycardia. Caution should be tension, and intraoperative and postoperative exercised when this agent is administered to tachyarrhythmias, including supraventricular patients with heart failure, bronchospastic dysrhythmias (Micromedex Online, 2008). disease, atrial fibrillation (AF) with associated hypotension, diabetes, renal impairment, or DOSAGE hyperthyroidism. Because esmolol may For postoperative hypertension, the dose of require large volumes of fluid for its adminis- esmolol is 500 mcg/kg, given as an IV bolus tration, thought should be given as to administered over 1 minute. This bolus whether it is the appropriate drug for patients should be followed by a maintenance dose of who may not be able to tolerate this excessive 50 mcg/kg/min given over 4 minutes. If addi- fluid intake. tional dosing is required after 5 minutes, the The ICU nurse should monitor heart rate, same loading dose followed by 100 mcg/ blood pressure, and for signs of heart failure kg/min may be infused over 4 minutes. This in patients receiving esmolol. Similarly, titration may continue by increasing the patients with diabetes should have their maintenance dose in 50 mcg/kg/min incre- blood glucose monitored on a regular basis. ments until the desired therapeutic endpoint Sudden withdrawal of therapy should be or a maintenance dosage of 200 mcg/kg/min avoided (Micromedex Online, 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 212

212 Chapter 12 Pharmacologic Support Following Cardiac Surgery

Labetalol (Normodyne®, Trandate®) ure, ischemic heart disease, liver disease, peripheral vascular disease (PVD), or hyper- MECHANISM OF ACTION thyroidism. Monitoring by the ICU nurse Labetalol is a nonselective, adrenergic block- should include heart rate, blood pressure, and ing agent that exerts inhibitory effects on signs of heart failure. Similarly, patients with beta1, beta2, and alpha1 receptors (Khalpey et diabetes should have their serum glucose al., 2008; Micromedex Online, 2008). monitored on a regular basis. Sudden withdrawal of therapy should be avoided INDICATIONS (Micromedex Online, 2008). As with esmolol, Labetalol is used on an off-label basis for any patient who requires an agent that causes postoperative hypertension. Data suggest it is beta-receptor stimulation should not receive effective when used on postoperative vascular beta-blocker therapy (Khalpey et al., 2008). surgery patients. Angiotensin-Converting Enzyme DOSAGE Inhibitors For postoperative hypertension, patients Enalaprilat (Vasotec®) receive 10 mg intravenously over 2 minutes. If additional doses are needed, 10 to 20 mg may HEMODYNAMIC EFFECTS be given every 10 minutes, up to a maximum Angiotensin-converting enzyme (ACE) dose of 300 mg in a 24-hour period. inhibitors act on the renin–angiotensin– aldosterone system (RAAS). Specifically, they SIDE EFFECTS prevent the conversion of angiotensin I to When labetalol is administered, no adverse angiotensin II (a potent vasoconstrictor) by effects or hemodynamic consequences have inhibiting ACE in the pulmonary and systemic been reported (Orlowski, Vidt, Walker, & vascular endothelium, resulting in vasodila- Haluska, 1989). When it is given for on-label tion (Levy, Tanaka, & Bailey, 2008). These conditions, serious side effects have included agents cause a decrease in SVR and typically bronchospasm, hyperkalemia, and ventricular have little effect on heart rate. With the dosage dysrhythmias. Commonly experienced side described below, patients should experience effects include bradycardias, edema, orthosta- improvements in both blood pressure and CO tic hypotension, diaphoresis, increased liver (Lemmer, Richenbacher, & Vlahakes, 2003). enzymes, dizziness, paresthesias, elevated renal function tests, dyspnea, wheezing, and INDICATIONS fatigue (Micromedex Online, 2008). ACE inhibitors may be administered early after cardiac surgery to patients with mild left NURSING IMPLICATIONS ventricular (LV) dysfunction, even in the face Like esmolol, labetalol is contraindicated in of moderate renal impairment (Manché, patients with cardiogenic shock, second- or Galea, & Busuttil, 1999). third-degree heart block, or severe sinus bradycardia. It is also contraindicated in DOSAGE patients with bronchial asthma or COPD. The initial dose of enalaprilat is 0.625 to Caution should be exercised when labetalol is 1.25 mg, infused over 5 minutes. Additional administered to patients with heart failure, doses, up to a maximum of 5 mg every 6 hours, bronchospastic disease, diabetes, heart fail- may be administered (Lemmer et al., 2003). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 213

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SIDE EFFECTS ARBs do not increase potassium levels or The most common side effects with enalapri- cause many of the side effects associated with lat are cough, hyperkalemia, and renal failure. ACE inhibitors. They are utilized predomi- The cough is thought to occur due to the nately for hypertension management and accumulation of bradykinin in the lung and require blood pressure monitoring after their vasculature (Levy et al., 2008). Hyperkalemia initiation. Both ACE inhibitors and ARBs are occurs when aldosterone is inhibited second- contraindicated in patients with bilateral ary to the inhibition of angiotensin II. In one renal artery stenosis. study, hypotension and a transient decline in renal function occurred; these conditions Calcium Channel Blockers were corrected with dopamine (Manché et al., Nicardipine 1999). Rare side effects such as dysgeunia (altered sense of taste) and neutropenia can HEMODYNAMIC EFFECTS be serious complications, however. The ICU As the classification connotes, nicardipine nurse should observe for signs of onset of blocks the flow of calcium. It acts directly on these complications and anticipate possible arterioles to cause peripheral vascular and discontinuation of the medication if they coronary vasodilation and lower blood occur. pressure. It has little effect on contractility or atrioventricular (AV) node conduction. NURSING IMPLICATIONS Nicardipine has also been shown to dilate the For patients who have a history of renal insuf- coronary vasculature (Khalpey et al., 2008; ficiency and who are receiving enalaprilat, Lemmer et al., 2003; Levy et al., 2008). Admin- nurses should monitor serum creatinine lev- istration did not affect ventricular preload or els (Lemmer et al., 2003). Meticulous moni- afterload or CO despite significant decreases toring of the patient’s hemodynamic profile in blood pressure (Cheung et al., 1999). and hourly measurement of urinary output may help avoid the development of renal fail- INDICATIONS ure sometimes associated with ACE Nicardipine is indicated for postoperative inhibitors. In any event, caution should be hypertension. used when administering ACE inhibitors to patients with significant LV dysfunction (Manché et al., 1999). DOSAGE Therapy is initiated at an infusion rate of Angiotensin-Receptor Blockers 5 mg/hr. The dose may be slowly increased by 2.5 mg/hr to a maximum of 15 mg/hr. Once Angiotensin-receptor blockers (ARBs) influ- the blood pressure endpoint is reached, a ence the RAAS by blocking production of maintenance infusion may be run at 3 mg/hr angiotensin II from sources of angiotensin II (Micromedex Online, 2008). other than the liver. The blocking of angiotensin receptors occurs on blood vessels, in the adrenals, and within all other tissues. SIDE EFFECTS The adrenal-related blockage results in a The most common side effects of nicardipine decrease in aldosterone levels, thereby leading are headache, hypotension, nausea, vomiting, to increased excretion of sodium and water peripheral edema, headache, dizziness, and from the kidneys. tachycardia. Serious adverse events that have 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 214

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been reported include angina, MI, and a rare patients at infusion rates of 4–6 mg/hr. The dysrhythmia (Micromedex Online, 2008). total 24-hour dosing should not exceed an average of 21 mg/hr because of lipid load NURSING IMPLICATIONS restrictions (Micromedex Online, 2008). Because of nicardipine’s potential to cause negative inotropic effects, especially in SIDE EFFECTS patients with heart failure, portal hyperten- Reported side effects of clevidipine include sion, or significant LV dysfunction, caution headache, sinus tachycardia, hypotension, nau- should be exercised when administering this sea, vomiting, and dizziness (Singla et al., agent with a beta blocker. Close blood pres- 2008). Other side effects that have been sure and heart rate monitoring are required reported include AF and acute renal failure. during therapy. Nicardipine is contraindi- Although rare, cardiac arrest, MI, hypotension, cated in patients with advanced aortic steno- and reflex tachycardia have occurred with use sis. Diastolic pressure and afterload reduction of this agent (Micromedex Online, 2008). may worsen rather than improve myocardial oxygen balance (Micromedex Online, 2008). NURSING IMPLICATIONS Clevidipine (Cleviplex®) Administration of clevidipine is contraindi- HEMODYNAMIC EFFECTS cated in patients with an allergy to soy or egg products or with alterations in lipid metabo- Clevidipine is a newly FDA-approved, ultra- lism (e.g., hyperlipidemia). It is also con- short-acting intravenous calcium channel traindicated in patients with severe aortic blocker. It functions as both a smooth muscle stenosis because clevidipine may reduce relaxant and an arterial vasodilator (Singla et al., myocardial oxygen delivery secondary to after- 2008). This agent causes a decrease in MAP load reduction. Caution should be exercised and SVR, but it does not reduce filling pres- when administering clevidipine concomitantly sures (Micromedex Online, 2008). with a beta blocker. Heart failure symptoms may be exacerbated due to this agent’s nega- INDICATIONS tive inotropic effects. Patients may develop Clevidipine is used to treat postoperative hypotension and reflex tachycardia when hypertension without impairing cardiac func- rapid titration takes place in an effort to tion. In one study of postoperative cardiac increase the dosage. Rebound hypertension surgery patients, treatment with this calcium may develop following extended infusions of channel blocker was effective in 91.8% of clevidipine (Micromedex Online, 2008). patients (Singla et al., 2008). Clevidipine is prepared in a phospholipid emulsion. Any unused medication must be DOSAGE discarded after 4 hours of spiking the stopper. The initial dose of clevidipine is 1–2 mg/hr When a patient is receiving clevidipine, the via continuous infusion. The dose may be ICU nurse should continuously monitor doubled in 90-second intervals. Once the heart rate and blood pressure during the infu- patient’s blood pressure begins to approach sion and until vital signs become stable. the goal, incremental dosing should be less Blood pressure monitoring should continue frequent (every 5–10 minutes) and be less for a minimum of 8 hours following discon- than double the dose. A maximum initial tinuation of clevidipine if the patient is not dose of 16 mg/hr is recommended, and a converted to another antihypertensive agent. therapeutic effect is achieved for most Patients should also be monitored for 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 215

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exacerbation of heart failure symptoms diac dysrhythmias, heart failure, MI, and (Micromedex Online, 2008). serum creatinine elevation (Micromedex Online, 2008). Selective Dopamine-1-Receptor Agonists NURSING IMPLICATIONS Fenoldopam Mesylate Caution should be used when fenoldopam is HEMODYNAMIC EFFECTS administered to patients who are concomi- Fenoldopam mesylate is a dopamine-1-recep- tantly receiving beta blockers or in patients

tor agonist. The dopamine-1 (D1) receptors with hypokalemia, hypotension, liver are located in the coronary, mesenteric, and disease, tachycardia, or glaucoma. During renal vasculature; when stimulated, they administration of this agent, the ICU nurse cause vasodilation (Levy et al., 2008). should monitor blood pressure, heart rate,

Fenoldopam also moderately binds to alpha2 and serum electrolytes, particularly potas- receptors, which results in lowered SVR and sium (Micromedex Online, 2008). PVR and enhanced CO. This agent has rapid action as a vasodilator and increases renal ■ AGENTS USED TO MANAGE blood flow (Lemmer et al., 2003). POSTOPERATIVE LOW CARDIAC OUTPUT AND HYPOTENSION INDICATIONS Some degree of myocardial depression, low Fenoldopam is indicated for the treatment of CO, and hypotension is common in the severe postoperative hypertension (Micro- immediate postoperative period following medex Online, 2008). It is believed to be cardiac surgery. These conditions can be especially useful in patients with renal insuffi- related to preexisting cardiac disease, post- ciency when it is administered in the prescribed ischemic dysfunction, or reperfusion injury dose range. Fenoldopam causes an increase (Levy et al., 2008). in glomerular filtration rate, renal blood Low CO following cardiopulmonary bypass flow, and sodium excretion (Lemmer et al., (CPB) procedures is primarily due to LV dys- 2003; Levy et al., 2008). function. This LV dysfunction may occur secondary to cardioplegic arrest, decreased DOSAGE preload, loss of vasomotor tone, intraoperative The initial dose of fenoldopam is 0.03–0.1 mcg/ blood loss, increased capillary permeability, kg/min. Titration can occur in increments of increased urinary output from hypothermia, 0.05–0.1 mcg/kg/min every 5–15 minutes, to dysrhythmias, or intraoperative MI (Aranki, a maximum of 1.6 mcg/kg/min, to achieve Cutlip, & Aroesty, 2008). Low cardiac output the desired blood pressure. The doses must be syndrome (LCOS), which may occur in post- administered as a continuous infusion; operative cardiac surgery patients, is a no bolus administration should be per- decrease in CO secondary to a brief episode of formed. Fenoldopam should not be used for myocardial dysfunction (Massé & Antonacci, more than 48 hours (Lemmer et al., 2003; 2005). Micromedex Online, 2008). Contributing factors to postoperative hypotension include hypovolemia, vasodila- SIDE EFFECTS tion (relative hypovolemia), anemia, pneu- Possible adverse effects of fenoldopam include mothorax, hemothorax, cardiac tamponade, hypotension, tachyarrhythmias, flushing, nau- electrolyte imbalance, hemorrhage, metabolic sea, vomiting, dizziness, headache, angina, car- alterations, and dysrhythmias. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 216

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Effective treatment of low CO and hypoten- Any patient receiving an adrenergic agonist sion depends on quickly identifying the causes should be continuously assessed for hypov- and initiating the appropriate treatment. olemia, which may occur even after adequate Detrimental complications can occur even volume repletion. Adrenergic agonists are with brief periods of hypotension, so aggres- often referred to as sympathomimetics, reflect- sive and prompt intervention is warranted. ing their ability to activate adrenergic receptors When low CO or hypotension is accompa- by direct receptor binding, promotion of nor- nied by low CVP and pulmonary artery occlu- epinephrine (NE) release, blockade of NE reup- sive pressure (PAOP), volume resuscitation is take, and inhibition of NE inactivation. needed to correct hypovolemia. A combina- Adrenergic agonists are classified as either tion of crystalloids, colloids, and blood prod- catecholamines or non-catecholamines. ucts may be used for this purpose. An Catecholamines include epinephrine (Adrena- in-depth discussion of volume resuscitation line®), norepinephrine (Levophed®), dopamine appears in Chapter 17. (Intropin®), and dobutamine (Dobutrex®). An If hypotension persists after volume resusci- example of a non-catecholamine is phenyle- tation, significant vasodilation may occur. In phrine (Neosynephrine®). this scenario, adrenergic agonists or vasopres- Adrenergic agonists are notable for their sors may be required to normalize blood pres- specificity, with the various agents acting on

sure if the patient has normal pump function alpha1, alpha2, beta1, beta2, or a combination and remains unresponsive to volume repletion of these receptors (see Table 12–2). The precise alone (Khalpey et al., 2008). Pharmacologic ability of a drug to selectively activate certain intervention is also suggested to begin once receptors to the exclusion of others is depends the patient has adequate filling pressures and on the dosage, however. Clinical activation of

acid–base and electrolyte balance has been alpha1 receptors results in vasoconstriction. achieved (Massé & Antonacci, 2005). Activation of alpha2 receptors inhibits NE As many as 40% of postoperative cardiac release. When beta1 receptors are activated, surgery patients require vasopressor support, patients experience a positive inotropic effect and as many as 20% require inotropic support (increased force of contraction), increased (St. Andre & DelRossi, 2005). Patients who blood pressure, heart rate, CO, and impulse have poor LV function or CO may require conduction through the AV node. Activation

inotropic support to augment contractility. of beta2 receptors can also have positive In these patients, volume repletion, adminis- inotropic (increase in contractility) and tration of vasodilators, pacing, or any combi- chronotropic (increase in heart rate) effects on nation of these may not be adequate (Khalpey the heart and cause peripheral vasodilation et al., 2008; Silvestry, 2008). Typically, (especially in skeletal and muscle vasculature).

patients who improve with inotropic support When beta2 receptors in the lung are stimu- are those with a cardiac index (CI) less than lated, bronchodilation occurs. 2 2 L/min/m with an optimal heart rate, car- Stimulation of dopamine-1 (D1, post- diac rhythm, filling pressures, afterload, and synaptic) receptors, by contrast, causes direct

absence of tamponade (Silvestry, 2008). vasodilation. Stimulation of dopamine- 2 (D2, pre-synaptic) receptors causes vasodilation by inhibiting the release of NE (Salenger et al., Adrenergic Agonists 2003). Adrenergic agonists are used to normalize Use of adrenergic agonists is typically initi- blood pressure when all known causative fac- ated in the operating room during cardiac tors are corrected but hypotension persists. surgery, and patients can be weaned from 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 217

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Table 12–2 Adrenergic Receptors and Effects when Stimulated

Adrenergic Receptor Type Effects when Stimulated

β 1 Increased heart rate, blood pressure, contractility (increased inotropic effect), cardiac output, conduction velocity, and automaticity β 2 Bronchodilation α 1 Vasoconstriction α 2 Vasodilation by inhibition of norepinephrine release

D1, post-synaptic Direct vasodilation

D2, pre-synaptic Vasodilation by inhibition of norepinephrine release

V1 (on vascular smooth muscle) Increased peripheral vascular resistance and vasoconstriction of capillaries and arterioles

Sources: Katz, 2007; Salenger et al., 2003.

their agents rapidly after recovery from anes- SVR. Phenylephrine is also valuable in patients thesia. These drugs are titrated so as to main- with a high CI who are profoundly vasodi- tain blood pressure within the ordered lated. A decrease in CO is seen with use of this parameters—typically a MAP of more than 65 agent, and either an increase or a decrease in mm Hg or a systolic blood pressure (SBP) of heart rate may be seen (Micromedex Online, at least 90 mm Hg. Higher pressures may be 2008; Salenger et al., 2003). required to perfuse organs when patients have a history of extreme hypertension, carotid DOSAGE artery disease, PVD, or renal dysfunction Phenylephrine should be started at a dose (Khalpey et al., 2008). relative to the clinical situation. Effects are Six adrenergic agonists are typically used often seen immediately. The dose range is after cardiac surgery: phenylephrine, norepi- 2–200 mcg/min (St. Andre & DelRossi, 2005). nephrine, epinephrine, vasopressin (antidiuretic hormone), dopamine, and dobutamine. SIDE EFFECTS These medications are used to elevate blood Because of its vasoconstrictor activity, pressure for patients in hypotensive states. phenylephrine causes hypoperfusion to tissues and end organs, which can lead to vis- Phenylephrine ceral and renal ischemia. It also causes an HEMODYNAMIC EFFECTS AND INDICATIONS increase in myocardial oxygen consumption Phenylephrine is a vasoconstrictor that is and may exacerbate metabolic acidosis often used after cardiac surgery to manage (Salenger et al., 2003). Other reported side mild to moderate hypotension. It causes vaso- effects include hypertension, MI, tach-

constriction by activating alpha1 receptors; no yarrhythmias, ventricular dysrhythmias, and other adrenergic receptors are stimulated. The pulmonary edema (Micromedex Online, vasoconstrictor effects lead to an increase in 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 218

218 Chapter 12 Pharmacologic Support Following Cardiac Surgery

NURSING IMPLICATIONS alpha1-receptor stimulation (Katz, 2007). The patient should receive adequate volume Norepinephrine exacerbates hyperglycemia resuscitation prior to receiving phenylephrine and metabolic acidosis; the latter effect is or receiving a significantly increased dose of related to an increase in lactate production this agent. Phenylephrine is contraindicated (Salenger et al., 2003). for use in patients with severe hypertension and tachycardia. Caution should be exercised NURSING IMPLICATIONS when administering this drug to patients High doses and long-term use of norepineph- with bronchial asthma, diabetes, or hyperten- rine cause decreased perfusion to the skin and sion. Monitoring of blood pressure and heart can lead to tissue necrosis and limb loss. rate is advisable (Micromedex Online, 2008). Patients should be assessed regularly for cyanosis, decreased capillary refill time, and Norepinephrine diminished peripheral pulses, all of which are HEMODYNAMIC EFFECTS AND INDICATIONS signs of decreased perfusion (Margereson, Norepinephrine is a powerful vasopressor and 2003). They should receive adequate volume resuscitation prior to receiving this therapy or adrenergic agonist that stimulates alpha1 and receiving a significantly increased dose of beta1 receptors, causing vasoconstriction, increased inotropic effects, and cardiac stimu- norepinephrine.

lation. A small amount of beta2-receptor stimulation occurs as well. Norepinephrine is Epinephrine classified as a vasopressor and an inotrope HEMODYNAMIC EFFECTS AND INDICATIONS (Levy et al., 2008; Salenger et al., 2003). It is Epinephrine stimulates alpha1, beta1, and beta2 typically used in profound hypotension when receptors (Levy et al., 2008). While not typically volume repletion is inadequate; it can also be administered in other situations in postopera- administered concomitantly with fluid resus- tive patients, this powerful catecholamine may citation if the patient’s blood pressure and be used after cardiac surgery as an inotrope to CO are significantly impaired (Katz, 2007). In improve cardiac function and enhance stroke addition, norepinephrine is the most com- volume (SV), as an adrenergic agonist and mon treatment for vasodilatory hypotension/ vasopressor for refractory hypotension, or as a shock associated with CPB (Aranki, Cutlip, & positive chronotropic agent to increase heart Aroesty, 2008). rate in bradycardia (Massé & Antonacci, 2005). Epinephrine is also useful in the cardiac arrest DOSAGE situation owing to its ability to enhance auto- Norepinephrine is initially started at maticity (Katz, 2007). 2–20 mcg/min and titrated so as to reach the desired response, usually a MAP of at least DOSAGE 70 mm Hg (Katz, 2007; Salenger et al., 2003). Epinephrine’s effects on different adrenergic receptors vary with the dosage used. At low SIDE EFFECTS doses (less than 0.02 mcg/kg/min), epineph-

The most clinically significant side effects rine causes stimulation of beta2 receptors experienced by the postoperative cardiac sur- with resultant vasodilation and relaxation of gery patient are an increase in myocardial the bronchial smooth muscle. At higher doses

workload and oxygen consumption. End- (0.008–0.06 mcg/kg/min), beta1 stimulation organ damage (e.g., damage to the kidneys results in an increased blood pressure, CO, and and mesentery) may also occur secondary to contractility. At doses of 0.5–4.0 mcg/min, 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 219

Agents Used to Manage Postoperative Low Cardiac Output and Hypotension 219

positive chronotropic effects are noted. At the occurs in patients who receive epinephrine highest dosage (more than 2 mcg/min), within the first 6–8 postoperative hours and

alpha1-receptor stimulation causes vasocon- usually disappears within a few hours of epi- striction. The blood pressure effects of epinephrine’s discontinuation (St. Andre & Del- nephrine vary in postoperative cardiac surgery Rossi, 2005). patients. In particular, patients who are postoperative CPB demonstrate inconsistent NURSING IMPLICATIONS hemodynamic responses to epinephrine While on epinephrine, the patient must be mon- administration. Variable responses in CO, itored closely for tachycardia and signs of heart rate, and MAP have been reported myocardial ischemia—administration of this (Salenger et al., 2003; Silvestry, 2008). agent will increase PVR, SVR, lactate, and myocardial oxygen consumption. Adequate oxy- SIDE EFFECTS genation should be maintained and the patient When higher doses of epinephrine are admin- monitored for signs of ischemia, given that epi- istered, patients may develop atrial or ventric- nephrine increases myocardial oxygen demand. ular ectopy and tachyarrhythmias owing to The ICU nurse should be prepared to beta1-receptor stimulation. The higher the quickly wean the patient from insulin if the dose, the more likely that atrial or ventricular epinephrine drip is reduced or discontinued. ectopy and tachyarrhythmias will be seen Hyperglycemia usually resolves within a few (Katz, 2007; Salenger et al., 2003). hours (6 or fewer) after the epinephrine Epinephrine can raise the serum glucose infusion is discontinued (St. Andre & Del- levels so profoundly that insulin drips should Rossi, 2005). be anticipated. Higher than normal doses of While increasing blood pressure and CO/CI insulin may be required to maintain adequate are goals of therapy, vasodilators may be nec- glycemic control. The hyperglycemia is attrib- essary to control elevated blood pressure utable to increased gluconeogenesis and the when epinephrine must be used at high doses stress response to epinephrine administration to maintain CO. Similarly, when epinephrine (Katz, 2007). Hyperglycemia typically occurs is infused at higher doses, alpha1 stimulation in patients who receive epinephrine within the causes an increase in myocardial workload, first 6–8 postoperative hours and usually dis- SVR, and PAOP (Katz, 2007). appears within a few hours after epinephrine Adrenergic agonists—including epinephrine— is discontinued (St. Andre & DelRossi, 2005). cause vasoconstriction, such that significant Patients receiving epinephrine may also tissue damage can occur if extravasation of develop metabolic acidosis; serum bicarbon- these agents into the subcutaneous tissue ate levels are typically between 17 and occurs. Decreased blood flow to tissue as a 21 mEq/L, although a serum bicarbonate result of vasoconstriction may lead to tissue level of 15 mEq/L has been reported. This death. Immediate treatment with an appro- metabolic acidosis may occur secondary to priate agent should be utilized promptly after the inadequate metabolism and lactate extravasation of adrenergic agonists is sus- buildup that occurs in response to beta1 stim- pected or identified. Epinephrine should be ulation. It is not related to hypoperfusion, as given ideally via a central line to limit the risk patients’ cardiac performance is acceptable of extravasation. when the acidosis develops. CO and mixed venous saturation levels also remain within Vasopressin acceptable parameters (Katz, 2007). As with CPB frequently causes the release of vaso- hyperglycemia, metabolic acidosis typically pressin, antidiuretic hormone, that may 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 220

220 Chapter 12 Pharmacologic Support Following Cardiac Surgery

contribute to post-bypass vasoconstriction. tion (VF) or pulseless ventricular tachycardia Data indicate that vasopressin levels may (VT) (Katz, 2007). diminish as hypotension continues. This Vasopressin may be effective in milrinone- finding suggests that the body may have a related hypotension (Gold et al., 2000); milri- limited supply of vasopressin that is none is discussed later in this chapter.

exhausted with the initial bout of hypoten- Vasopressin stimulates V1 receptors on vascu- sion (Levy et al., 2008). lar smooth muscle, which causes an increase Approximately 10% of cardiac surgery in peripheral vascular resistance and vasocon- patients develop vasodilatory shock (Argen- striction of capillaries and arterioles (Katz, ziano et al., 1998). Features of vasodilatory 2007). shock include decreased MAP, organ hypop- Vasopressin increases secretion of corti- erfusion, lactic acidosis, decreased SVR, and cotropin, a hormone produced by the anterior maldistribution of blood volume. End-organ pituitary gland that stimulates the adrenal failure is the ultimate outcome if the condi- cortex. The adrenal cortex produces cortisol, a tion is not reversed (Albright, Zimmerman, & major hormone responsible for blood pres- Selzman, 2002). sure regulation.

HEMODYNAMIC EFFECTS AND INDICATIONS DOSAGE Vasopressin is used to treat vasodilatory The dosage of vasopressin needed to achieve shock following CPB procedures in patients vasoconstrictor effects is 0.01–0.1 unit/min with profound hypotension (MAP less than by continuous IV infusion (Albright et al., 70 mm Hg) despite fluid resuscitation, after- 2002; Katz, 2007). load reduction, inotropic therapy, and norepinephrine administration. Postoperative CPB SIDE EFFECTS patients who have protracted hypotension Side effects of vasopressin are rare but include demonstrate poor vascular smooth-muscle end-organ damage from vasoconstriction, response to catecholamines. Vasopressin, leading to hypoperfusion, hyponatremia, and when administered in high doses, promotes increased SVR. All of these effects occur sec- contraction of vascular smooth muscle, which ondary to the drug’s vasoconstriction effects in turn causes vasoconstriction of the capil- (Katz, 2007). laries and small arterioles and can increase MAP (Albright et al., 2002). It is also believed that some patients have low vasopressin con- NURSING IMPLICATIONS centrations, such that exogenous administra- Extreme caution should be used in patients tion may improve these patients’ clinical with vascular disease who are receiving vaso- status (Aranki et al., 2008; Raja & Dreyfus, pressin because of the potential for extreme 2004). The postoperative cardiac surgery vasoconstriction associated with this agent. patients with vasodilatory shock who benefit The ICU nurse should monitor for a number most from vasopressin are those with a of adverse effects in the postoperative cardiac deficiency and those with a low ejection frac- surgery patient, including decreased CO, tion (EF) who take ACE inhibitors (Argen- chest pain, myocardial ischemia, ventricular ziano et al., 1998). dysrhythmias, bronchoconstriction, meta- Vasopressin also has indications in cardiac bolic acidosis, tremors, gastrointestinal arrest situations as an early substitute for epi- infarction, abdominal cramping, and water nephrine in patients with ventricular fibrilla- intoxication (Albright et al., 2002). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 221

Agents Used to Manage Postoperative Low Cardiac Output and Hypotension 221

Dopamine and Dobutamine stimulates D1 and D2 receptors when adminis- The use of dopamine and dobutamine is tered in doses less than 8 mcg/kg/min required in many postoperative cardiac sur- (Albright et al., 2002; Salenger et al., 2003). gery patients even when careful attention is paid to intraoperative myocardial protection. DOSAGE Prolonged surgery, myocardial edema, Renal vasodilation occurs due to stimula- advanced age, reperfusion injuries, and poor tion of dopaminergic receptors at doses of preoperative cardiac function are all factors 0.5–3.0 mcg/kg/min. At an infusion rate of

that put the patient at higher risk for low CO 4–10 mcg/kg/min, beta1 stimulation is seen. postoperatively. Both dopamine and dobuta- Positive inotropic and chronotropic effects mine cause an increase in CO and heart rate lead to an increase in heart rate, blood pres- (Silvestry, 2008). sure, contractility, and CO. At doses exceed-

Before these agents are administered, ing 10 mcg/kg/min, alpha1 stimulation CO/CI should be high enough to sustain end- occurs, along with associated vasoconstric- organ perfusion and deliver adequate tion and increased SVR. While receptor stim- amounts of oxygen to tissues. This criterion ulation overlap occurs at these higher should be judged subjectively for each patient infusion rates, the dopaminergic effect is lost based on adequate urine output, normal cap- (Salenger et al., 2003). Dopamine’s effect on illary refill time, appropriate mentation, ade- renal perfusion in terms of long-term out- quate blood pressure, warm skin temperature, comes remains controversial (Massé & and lack of acidosis. Objectively, CI should be Antonacci, 2005). This agent should be more than 2 L/min/m2 before use of started at a low dose and doses titrated dopamine and dobutamine is considered; upward slowly to achieve the desired effect. normal CI in the nondiseased heart is in the 2 range of 2.5–4.5 L/min/m . When preload has SIDE EFFECTS been optimized and SV remains low, poor Common side effects of dopamine include contractility is the likely etiology and chest pain, hypertension, palpitations, tach- inotropes are indicated. Adding inotropes will yarrhythmias, headache, anxiety, dyspnea, increase the amount of contractile force and oliguria, nausea, and vomiting. Serious side result in an improved SV and CO/CI. effects include ectopic beats (including ven- Dopamine tricular dysrhythmias), widening QRS com- HEMODYNAMIC EFFECTS AND INDICATIONS plex, and gangrenous disorder (Micromedex Online, 2008). Like epinephrine, dopamine’s effects on different adrenergic receptors vary with dosage. NURSING IMPLICATIONS Dopamine stimulates alpha1, beta1, and beta2 receptors, resulting in either vasoconstriction Systolic pressures are often elevated with or positive inotropic and chronotropic effects dopamine use, making it a poor choice in

(Levy et al., 2008). Stimulation of beta2 recep- patients with pulmonary hypertension. tors is less than that seen with the other adren- Dopamine is also contraindicated in patients ergic agents. Dopamine is used to increase with tachyarrhythmias. Caution should be blood pressure, CO, and perfusion through the exercised when administering this agent to renal vasculature. At higher doses, this drug patients with angina, hypovolemia, or ventric- has vasopressor properties, as it stimulates the ular dysrhythmias (Micromedex Online, release of endogenous NE. Dopamine also 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 222

222 Chapter 12 Pharmacologic Support Following Cardiac Surgery

Like epinephrine, dopamine causes vaso- discontinued, allowing for rapid titration constriction, such that significant tissue dam- of the drug. The dose is 2–20 mcg/kg/min age can result if extravasation into the (Katz, 2007). subcutaneous tissue occurs. Decreased blood flow to tissue from vasoconstriction may lead SIDE EFFECTS to tissue sloughing and death. Immediate While administering dobutamine, the ICU infiltration with an appropriate agent (e.g., nurse should observe for hypotension, tachy- ® phentolamine [Regitine ] 10–15 mL) to the cardia, ventricular dysrhythmias, and myocar- ischemic area should be implemented dial ischemia (Katz, 2007; Khalpey, Ganim, & promptly after extravasation of adrenergic Rawn, 2008; Leyh et al., 2003). Other reported agonists is suspected or identified. side effects include angina, dyspnea, tach- Dobutamine yarrhythmias, hypertension, and headache (Micromedex Online, 2008). Of note, dobuta- HEMODYNAMIC EFFECTS AND INDICATIONS mine is less likely to cause dysrhythmias than Dobutamine is a synthetic catecholamine and other positive inotropic agents.

positive inotrope that acts primarily as a beta1 agonist. It causes an increase in CO/CI, while NURSING IMPLICATIONS lowering SVR and increasing heart rate (Massé Like other agents in this category, dobuta- & Antonacci, 2005). It achieves these effects by mine should not be given to hypovolemic increasing contractility and causing peripheral patients. Monitoring of blood pressure, heart vasodilation (Khalpey et al., 2008). Dobuta- rate, PAP, PAOP, CVP, CO, SVR, and urinary mine causes minimal amounts of alpha1- output should be performed on an ongoing receptor stimulation and a small amount of basis to determine the drug’s efficacy and the beta2-receptor stimulation (Salenger et al., patient’s tolerance of therapy. Evaluation of 2003). This agent is useful when patients have the patient’s ECG and electrolyte status low CO with high SVR or PVR and cannot tol- should also be performed on a regular basis erate vasodilators to decrease afterload. Dobu- (Micromedex Online, 2008). tamine administration also results in enhanced coronary blood flow and decreased LV preload and afterload—more so than is Phosphodiesterase Inhibitors noted with dopamine (Salenger et al., 2003; Another category of medications that may be Silvestry, 2008). used to treat low CO after cardiac surgery Patients with high pulmonary pressures comprises the phosphodiesterase (PDE) (e.g., those who have undergone mitral valve inhibitors. Two direct phosphodiesterase replacement), with or without a history of pul- inhibitors—inamrinone (formerly amrinone, monary hypertension, and with low heart Inocor®) and milrinone (Primacor®)—are rates may benefit more from dobutamine than especially well-known agents. from dopamine. This preference arises because dobutamine administration is associated with Inamrinone a decrease in pulmonary artery pressure, left HEMODYNAMIC EFFECTS AND INDICATIONS ventricular stroke work index, CI, PAOP, and Inamrinone increases CO with its inotropic SVR (Micromedex Online, 2008). effects as well as its vasodilating systemic and pulmonary vasculature (Salenger et al., 2003). DOSAGE It enhances CO by directly inhibiting phos- The onset of action of dobutamine is rapid, phodiesterase from metabolizing cyclic and it is rapidly cleared (2–3 minutes) when adenosine monophosphate (cyclic AMP) in 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 223

Agents Used to Manage Postoperative Low Cardiac Output and Hypotension 223

myocardial cells. An increase in cyclic AMP the drug and to monitor cardiac function causes an increase in the amount of calcium hours after the drug has been discontinued. that moves into cells through ion channels, thereby resulting in a more forceful contrac- SIDE EFFECTS tion (inotropic effect). Inamrinone may cause thrombocytopenia and Inamrinone also produces venous and arte- has largely been replaced by milrinone because rial vasodilation, and decreases SVR, PVR, and of this effect. Occasional side effects that have LV preload (PAOP), while minimally affecting been reported include nephrogenic diabetes myocardial oxygen demand (Levy et al., 2008; insipidus, elevated liver function tests, fever, Silvestry, 2008). All of these effects contribute flu-like symptoms, and exacerbation of an to an improvement in CO/CI (Khalpey et al., underlying dysrhythmia (DiDomenico, 2001). 2008). The drug has little effect on heart rate, however (Levy et al., 2008). Inamrinone also NURSING IMPLICATIONS produces vasodilation in vascular smooth Patients receiving inamrinone may require muscle by decreasing intracellular calcium concomitant administration of an adrenergic concentration. This effect causes relaxation of agonist owing to the profound vasodilation the vasculature and ventricles, thereby that occurs with use of this drug (Katz, 2007). increasing stroke volume and CO/CI and lowering afterload (Levy et al., 2008; Massé & Milrinone Antonacci, 2005). In addition, inamrinone HEMODYNAMIC EFFECTS AND INDICATIONS promotes myocardial relaxation and improves Milrinone is a positive inotrope with vasodila- coronary skeletal muscle and mesenteric tor properties. Its administration will cause a blood flow (Salenger et al., 2003). decrease in SVR and PVR, making it an ideal Inamrinone is indicated for the manage- agent for patients with RV failure. Milrinone ment of ventricular failure in the postopera- also decreases coronary vascular resistance tive cardiac surgery patient (Katz, 2007). and, therefore, has a highly favorable effect on Because of its vasodilator properties, this myocardial oxygen consumption (Salenger et agent is useful in the management of al., 2003). patients with pulmonary vasoconstriction Like inamrinone, milrinone enhances CO and right ventricular (RV) dysfunction by directly inhibiting phosphodiesterase from (Levy et al., 2008). metabolizing cyclic AMP in myocardial cells. An increase in cyclic AMP causes an increase in DOSAGE the amount of calcium that moves into cells A loading dose of 0.75 mg/kg of inamrinone through the ion channels, thereby resulting in should be administered over a period of 2–3 a more forceful contraction (inotropic effect). minutes. It is followed by a continuous infu- Milrinone also produces venous and arte- sion of 10–30 mg/kg/min. Additional loading rial vasodilation, and decreases SVR, PVR, and doses at 0.75 mg/kg may be administered as LV preload (PAOP), while minimally affecting clinically indicated, although the total daily myocardial oxygen demand (Levy et al., 2008; dose should not exceed 10 mg/kg/day. Silvestry, 2008). All of these actions con- The peak effect of inamrinone occurs tribute to an improvement in CO/CI (Khalpey within 10 minutes of administration. The et al., 2008). The drug has little effect on heart duration of the drug’s effect is dose depend- rate, however (Levy et al., 2008). It also pro- ent, lasting approximately 30 minutes to duces vasodilation in vascular smooth muscle 2 hours. Inamrinone has a long half-life, mak- by decreasing intracellular calcium concentra- ing it important to slowly wean patients from tion. This effect causes relaxation of the 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 224

224 Chapter 12 Pharmacologic Support Following Cardiac Surgery

vasculature and ventricles, thereby increasing electrolyte imbalance is present. Patients SV and CO/CI and lowering afterload (Levy receiving milrinone should also be observed et al., 2008; Massé & Antonacci, 2005). In for hypotension during therapy. Patient addition, milrinone promotes myocardial improvement may be reflected by increased relaxation and improves coronary skeletal CO, decreased PAOP, and favorable changes muscle and mesenteric blood flow (Salenger in clinical indices. See Table 12–3 and et al., 2003). Box 12–1 for a summary of medications used Milrinone is indicated for the management to treat low cardiac output syndrome and of ventricular failure in the postoperative car- hypotension following cardiac surgery. diac surgery patient (Katz, 2007). Because of its vasodilator properties, it is a valuable Other Agents Used to Control option in the management of patients with Postoperative Hypotension pulmonary vasoconstriction and RV dysfunc- ® tion (Levy et al., 2008). Methylene Blue (Urolene Blue ) HEMODYNAMIC EFFECTS AND INDICATIONS DOSAGE Methylene blue is an inhibitor of nitric oxide, A loading dose of 50–75 mcg/kg of milrinone which is released in large quantities in should be followed by a continuous infusion patients following CPB. Nitric oxide produces at a rate of 0.25–0.75 mcg/kg/min (Salenger profound vasodilation and vasoplegia et al., 2003). Milrinone has a rapid onset of (hypotension with normal or high CO, low action, and its effects last 2–4 hours following CVP, low PAOP, and low peripheral vascular titration or discontinuation (Katz, 2007). Mil- resistance) (Katz, 2007). Methylene blue is rinone has a shorter half-life (36 minutes) indicated in vasodilatory shock in the imme- than inamrinone (Levy, Bailey, & Deeb, 2002), diate postoperative CPB period. Despite its and may be weaned more quickly than inam- frequent use for this indication, vasodilatory rinone. This half-life is still longer than that shock is not currently an FDA-approved on- for dobutamine, making PDE inhibitors more label indication for methylene blue challenging to titrate (Levy et al., 2008). (Micromedex Online, 2008).

SIDE EFFECTS DOSAGE VT or supraventricular tachycardia (SVT) may The dosage of methylene blue is 1–2 mg/kg, occur when milrinone is given, owing to the administered as a slow IV push (Katz, 2007; drug’s proarrhythmic properties. Hypoten- Micromedex Online, 2008). In one study, the sion should be anticipated related to the dose was administered over 20 minutes (Leyh vasodilatory properties of milrinone (Salenger et al., 2003) et al., 2003). SIDE EFFECTS NURSING IMPLICATIONS The two main side effects of methylene blue Patients receiving milrinone may require con- administration are hypertension and a brief comitant administration of an adrenergic period of factitious low oxygen saturation on agonist to counteract the profound vasodila- pulse oximetry (Katz, 2007). Other reported tion that occurs (Katz, 2007). Aggressive side effects include hypertension, hypoten- replacement of potassium and magnesium sion, abdominal pain, dizziness, headache, are recommended as well, because the dys- confusion, nausea, vomiting, and diarrhea. rhythmias are more likely to occur when an Serious adverse events reported include 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 225

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Table 12–3 Select Agents Used to Manage Postoperative Low Cardiac Output and Hypotension and Hemodynamic Effects

Mechanism Hemodynamic Agent Dose of Action Effects Adrenergic Agonists β Epinephrine 0.008–0.06 mcg/kg/min Stimulation of 1 Increased contractility (Adrenaline®) by continuous IV infusion receptors and stroke volume, and cardiac stimulation. 0.5–4.0 mcg/min by Increased heart rate. continuous IV infusion β Less than 0.02 mcg/kg/ Stimulation of 2 Vasodilation and min by continuous receptors relaxation of the IV infusion bronchial smooth muscle. α Greater than 2 mcg/min Stimulation of 1 Vasoconstriction; by continuous IV infusion receptors increased SVR. α Norepinephrine 2–20 mcg/min by Stimulation of 1 Vasoconstriction; (Levophed®) continuous IV infusion receptors increased SVR; decreased cardiac output; increase or decrease in heart rate. β Stimulation of 1 Increased inotropic receptors effects and cardiac stimulation. Dopamine 0.5–3.0 mcg/kg/min Stimulation of Renal vasodilation. (Intropin®) dopaminergic receptors β 4–10 mcg/kg/min by Stimulation of 1 Increased heart rate, continuous IV infusion receptors blood pressure, contractility, and cardiac output. α Greater than 10 mcg/ Stimulation of 1 Vasoconstriction; kg/min receptors increased SVR.

Less than 8 mcg/kg/min Stimulation of D1 Vasodilation. by continuous IV infusion and D2 receptors β Dobutamine 2–20 mcg/kg/min by Stimulation of 1 Increased cardiac (Dobutrex®) continuous IV infusion receptors (increased output/cardiac index, contractility) and and heart rate; peripheral decreased SVR and vasodilation PAOP (more so than dopamine), pulmonary artery pressure, left ventricular stroke work index, enhanced coronary blood flow. continues 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 226

Table 12–3 Select Agents Used to Manage Postoperative Low Cardiac Output and Hypotension and Hemodynamic Effects (continued)

Mechanism Hemodynamic Agent Dose of Action Effects Adrenergic Agonists (cont.) Dobutamine Minimal amounts Vasoconstriction. ® α (Dobutrex ) (cont.) of 1 stimulation Small amount of Relaxation of the β 2 receptor bronchial smooth stimulation muscle. α Phenylephrine 2–200 mcg/min by Activation of 1 Vasoconstriction; (Neosynephrine®) continuous IV infusion receptors increased SVR; decreased cardiac output; increase or decrease in heart rate.

Vasopressin 0.01–0.1 unit/min by Stimulates V1 Contraction of vascular (antidiuretic continuous IV infusion receptors smooth muscle, which hormone) causes vasoconstriction of the capillaries and small arterioles and can increase mean arterial pressure. Phosphodiesterase (PDE) Inhibitors Inamrinone (Inocor®) Loading dose: 0.75 mg/kg PDE inhibitor; venous Increased cardiac administered over 2–3 min. and arterial output/cardiac index Maintenance: 10–30 mg/ vasodilation; and stroke volume; kg/min by continuous vasodilation in decreased SVR, PVR, infusion of. vascular smooth and PAOP; promotes Additional loading doses muscle by decreasing myocardial relaxation at 0.75 mg/kg may be intracellular calcium and improves coronary administered. Total daily concentration. skeletal muscle, and dose should not exceed mesenteric blood flow. 10 mg/kg/day. Milrinone Loading dose: PDE inhibitor; Increased cardiac output/ (Primacor®) 50–75 mcg/kg. positive inotrope cardiac index and stroke Maintenance dose: and vasodilator. volume; decreased SVR, 0.25–0.75 mcg/kg/min PVR, and PAOP; pro- by continuous infusion. motes myocardial relaxation and improves coronary skeletal muscle, and mesenteric blood flow. Other agent Methylene Blue 1–2 mg/kg, administered Inhibitor of nitric Vasodilation. (Urolene Blue®) as a slow IV push oxide

PAOP = pulmonary artery occlusive pressure; PVR = pulmonary vascular resistance; SVR = systemic vascular resistance. Sources: Albright et al., 2002; Katz, 2007; Khalpey et al., 2008; Levy et al., 2008; Massé & Antonacci, 2005; Micromedex Online, 2008; Salenger et al., 2003; Silvestry, 2008; St. Andre & DelRossi, 2005.

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Box 12–1 Vasoactive Agents Used to Manage Postoperative Low Cardiac Output and Hypotension and Hemodynamic Effects

Agent MAP PAP PAOP CO/CI SVR PVR

Epinephrine + +/– +/– + +/– +/– Norepinephrine ++ ++ ++ + ++ ++ Dopamine +/– +/– +/– + +/– +/– Dobutamine +/– – – + – – Phenylephrine ++ ~ + ~ ++ ++ Vasopressin ++ – ~~++ –/~ Inamrinone – – – + – – Milrinone – – – + – – Methylene Blue + + ~~++ CI ϭ cardiac index; CO ϭ cardiac output; MAP ϭ mean arterial pressure; PAOP ϭ pulmonary artery occlusive pressure; PAP ϭ pulmonary artery pressure; PVR ϭ pulmonary vascular resistance; SVR ϭ systemic vascular resistance. + ϭ increase; – ϭ decrease; ~ ϭ no change Sources: Albright et al., 2002; Katz, 2007; Khalpey et al., 2008; Levy et al., 2008; Massé & Antonacci, 2005; Micromedex Online, 2008; Salenger et al., 2003; Silvestry, 2008; St. Andre & DelRossi, 2005.

cardiac dysrhythmias, malignant hyperther- cantly within 12 hours after administration of mia, and methemoglobinemia (Micromedex methylene blue to patients with vasoplegia Online, 2008). following CPB (Leyh et al., 2003).

NURSING IMPLICATIONS Dexamethasone (Decadron®) Following administration of methylene blue, The inflammatory process and the sequelae the ICU nurse should observe for hyperten- that occur as a result of CPB surgery have been sion, urine discoloration, and transiently low the focus of several studies (Whitlock, Rubens, oxygen saturation on pulse oximetry. The last Young, & Teoh, 2005). CPB stimulates a sys- effect typically lasts less than 10 minutes temic inflammatory response, with an associ- (Katz, 2007) and results from interference ated release of pro-inflammatory mediators. with light absorption. If the patient’s oxygen The results include development of hemody- saturation is in question during this time, namic instability (Bruins et al., 1997). evaluation with an arterial blood gas should Despite supportive data, and possibly because be performed (Touma, 2007). The ICU nurse the data are not consistent (Chaney, Nikolov, should anticipate immediate increases in SVR Blakeman, Bakhos, & Slogoff, 1998), the use of and MAP and the need to significantly lower steroids remains controversial in cardiac surgery the infusion rate of norepinephrine (Leyh et al., patients. Their mechanism of action and the 2003). The ICU nurse should also monitor pathophysiologic changes that occur during methemoglobin levels, complete blood count cardiac surgery have been cited as justifications results, and blood pressure during adminis- for their administration in this scenario. In one tration of methylene blue. Caution should be study, patients who received preoperative and exercised when this agent is administered to postoperative doses of steroids experienced less patients with renal impairment or G6PD defi- systemic inflammation as compared with ciency (Micromedex Online, 2008). In one patients who did not receive prophylactic study, serum lactate levels decreased signifi- steroids (Kilger et al., 2003). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 228

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Any postoperative cardiac surgery patient SIDE EFFECTS exhibiting protracted vasodilatory shock A number of clinically significant adverse reac- should be suspected of having adrenal insuffi- tions have been reported in association with ciency. In a stressed patient (e.g., a cardiac sur- dexamethasone administration. These reactions gery patient), a low or normal cortisol level include, but are not limited to, dysrhythmia, can be assumed to be associated with adrenal bradycardia, cardiac arrest, cardiomyopathy, insufficiency (Khalpey et al., 2008). Adrenal heart failure, circulatory collapse, edema, insufficiency responds to steroids, which raise myocardial rupture (if administered to a patient cortisol levels. Cortisol plays a vital role in following MI), thromboembolism, depression, regulating blood pressure by increasing the emotional instability, euphoria, headache, sensitivity of the vasculature to endogenous increased intracranial pressure, seizure, adrenal epinephrine and norepinephrine. In the suppression, diabetes mellitus, hyperglycemia, absence of normal cortisol levels, widespread metabolic alkalosis, sodium retention, abdomi- vasodilation occurs secondary to the effects of nal distention, gastrointestinal (GI) hemorrhage pro-inflammatory mediators. A cosyntropin or perforation, nausea, hepatomegaly, gluco- stimulation test can be performed for diagno- suria, and pulmonary edema (Uptodate.com sis of adrenal insufficiency. In the meantime, Lexi Corp, 2008). intravenous dexamethasone may be administered (Khalpey et al., 2008). NURSING IMPLICATIONS

MECHANISM OF ACTION The ICU nurse should monitor hemoglobin, potassium, and glucose levels, and evaluate Steroids decrease inflammation by suppress- for occult blood loss when caring for a patient ing neutrophil migration, decreasing produc- who is receiving steroids. If the patient is tion of pro-inflammatory mediators, and receiving concomitant calcium channel block- reversing the increase in capillary permeabil- ers, these agents may decrease the metabolism ity (Uptodate.com Lexi Corp, 2008). of steroids. Steroid therapy should, therefore, be monitored to determine its efficacy. INDICATIONS Caution should be exercised if steroids are Steroids are used in cases involving postoper- administered to patients with diabetes melli- ative hemodynamic instability associated tus, as hyperglycemia related to alteration in with a CPB-induced inflammatory response. glucose production/regulation may occur. Caution should also be exercised when DOSAGE administering steroids to patients with GI The dosage of dexamethasone for treatment disease because of the risk of perforation. In of shock (e.g., related to adrenal insufficiency patients with renal disease, fluid retention that is responsive to steroid therapy) is 4–10 may develop when steroids are given. Patients mg IV. This dose may be repeated as needed. with a history of a seizure disorder should be For shock that is unresponsive to steroids, the monitored closely, as adrenal crisis in con- dose is 1–6 mg/kg IV or up to a maximum of junction with steroid therapy may precipitate 40 mg. Doses may be repeated every 2–6 hours seizures. Withdrawal and discontinuation of a while shock persists. Each dose should be corticosteroid should be done slowly, with administered over a span of 5–10 minutes. gradual tapering of the dose (Uptodate.com (Uptodate.com Lexi Corp, 2008). Lexi Corp, 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 229

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Hydrocortisone (Solu-Cortef ®) to, hypertension, edema, headache, delirium, hallucinations, seizure, mood swings, bruis- MECHANISM OF ACTION ing, hypokalemia, hyperglycemia, Cushing’s As described earlier, steroids decrease inflam- syndrome, sodium and water retention, mation by suppressing neutrophil migration, abdominal distention, ulcerative esophagitis, decreasing production of pro-inflammatory and immunosuppression (Uptodate.com Lexi mediators, and reversing the increase in capil- Corp, 2008). lary permeability (Uptodate.com Lexi Corp, 2008). NURSING IMPLICATIONS As with dexamethasone, withdrawal and dis- INDICATIONS continuation of hydrocortisone should be Hydrocortisone is used in cases involving done slowly, with gradual tapering of the dose postoperative hemodynamic instability (Uptodate.com Lexi Corp, 2008). The nursing associted with a CPB-induced inflammatory implications described earlier for dexametha- response. sone apply to patients receiving hydrocortisone as well. DOSAGE The dosage of hydrocortisone is based on the ■ AGENTS USED TO PREVENT indication. For acute adrenal insufficiency, OR CONTROL POSTOPERATIVE the recommended dose is 100 mg IV bolus, DYSRHYTHMIAS then 300 mg/day in divided doses every As discussed in Chapter 15, postoperative dys- 8 hours. Alternatively, the drug may be admin- rhythmias are common in cardiac surgery istered as a continuous infusion for 48 hours. patients. Several potential etiologic factors If hydrocortisone is being administered to have been identified, including preexisting counteract the stress of surgery in patients cardiac conditions (e.g., pericarditis), atrial who have adrenal insufficiency, the dose is infarction, ischemia, or enlargement; respira- 100–150 mg/day (50 mg every 8–12 hours) for tory complications; electrolyte imbalance 2–3 days. The dose should be diluted to 50 (e.g., hypokalemia, hyperkalemia, hypomag- mg/mL and administered over a period of 30 nesemia); surgical trauma (intraoperative seconds to several minutes, depending on the injury to the atrium, inadequate cardioprotec- dose (Uptodate.com Lexi Corp, 2008). tion during CPB); hypothermia; hyperadren- In one study, patients received 100 mg of ergic state; acid–base imbalance; anxiety; and hydrocortisone preoperatively. Postopera- pain (Bharucha & Marinchak, 2007). Prior to tively, the patients received 10 mg/hr for intervening with pharmacotherapy, any 24 hours, 5 mg/hr for 24 hours, 3 ϫ 20 mg/day, underlying causes should be treated (Massé & and 3 ϫ 10 mg/day (Kilger et al., 2003). Antonacci, 2005). Atrial and ventricular dysrhythmias, as well as bradyarrhythmias and SIDE EFFECTS tachyarrhythmias, may be experienced by car- Side effects that are reported as being related diac surgery patients. to administration of hydrocortisone include The most common antiarrhythmic medica- insomnia, diabetes mellitus, epistaxis, and tions used in the immediate postoperative arthralgia. Rare but potentially life-threaten- phase are categorized as Class I, II, III, or IV ing adverse events include, but are not limited agents. Class I agents are sodium channel 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 230

230 Chapter 12 Pharmacologic Support Following Cardiac Surgery

Box 12–2 Categories of Antiarrhythmic Therapy

Category Mechanism of Action

Class I Sodium channel blockers Class II Beta blockers Class III Delays repolarization; prolongs action potential Class IV Calcium channel blockers

blockers and include quinidine (Quinaglute®), A wide array of medications is used to treat procainamide (Pronestyl®), disopyramide atrial dysrhythmias after cardiac surgery. The (Norpace®), lidocaine (Xylocaine®), propafenone particular medication selected will depend on (Rythmol®), flecanide (Tambocor®), and the drug’s mechanism of action, the sus- encainide (Enkaid®). Class II agents are beta pected cause of the dysrhythmia, and the blockers and include metoprolol (Lopressor®) drug’s side effect profile. and sotalol (Betapace®). Class III agents delay Prior to initiating treatment of AF, three repolarization and include amiodarone (Cor- criteria are considered. First, determination is darone®), ibutilide (Corvert®), and sotalol. made as to whether the patient is hemody- Class IV agents include the calcium channel namically stable or unstable with the presence blockers diltiazem (Cardizem®) and verapamil of AF. The ICU nurse can identify the pres- (Calan®) (see Box 12–2). The agents used ence of hemodynamic compromise by assess- most often for postoperative cardiac surgery ing for hypotension, altered mental status, patients are discussed here and are summa- presence of chest pain, shortness of breath, rized in Table 12–4. poor peripheral perfusion, decreased urinary output, signs of impaired CO, or increased Agents Used to Manage Atrial preload (Khalpey et al., 2008). Dysrhythmias Next, precipitating factors should be identified. These conditions may include ischemia, As noted in Chapter 15, AF is a common dys- increased sympathetic tone, electrolyte or rhythmia that may occur in postoperative car- acid–base imbalance, or pulmonary disorders diac surgery patients. Its reported incidence (Khalpey et al., 2008). ranges from 10% to 65% in such patients. The Lastly, the goal of therapy (rate or rhythm incidence varies with type of procedure per- control) needs to be decided. The ultimate formed, with 20–40% of patients who have goal is hemodynamic stability (Khalpey et al., undergone coronary artery bypass grafting 2008). Agents that may be used to control (CABG) procedures, as many as 50% of rate include beta blockers, calcium channel patients who have undergone valve surgery, blockers, and possibly digoxin. and as many as 60% of patients who have undergone combination surgical procedures Class II Agents being affected by this complication. The onset of occurrence is 1–3 days following surgery Metoprolol (Aranki et al., 2008; Khalpey et al., 2008). Metoprolol is currently recommended as Given that most patients remain in the ICU first-line therapy for AF. Treatment with a for 24 hours or less, AF may not appear until beta blocker or amiodarone (which is dis- after the patient leaves the ICU. cussed later in this chapter) has an efficacy 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 231

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Table 12–4 Agents Used to Manage Postoperative Dysrhythmias

Mechanism Dysrhythmia Agent Dose of Action

Atrial Fibrillation Metoprolol PO: Initial dose of 50 mg, Class II cardioselective followed by additional beta blocker. doses of 25 mg until heart rate is less than 100 beats/min. IV: 5–15 mg (usually 5 mg) over 2.5 minutes. Additional doses may be given at 7.5-minute intervals. Carvedilol PO: 6.25 mg BID. Class II cardioselective Patients with heart beta blocker. failure: 3.125 mg PO daily. Amiodarone IV: 150 mg given over Class III but possesses 10 minutes, followed by properties in all four a 24-hour infusion given categories of agents. at a rate of 1 mg/min for Blocks potassium the first 6 hours and at a channels, which pro- rate of 0.5 mg/min for longs the duration of the next 18 hours, if the action potential required. and decreases membrane excitability. Slows heart rate by depressing SA node. Increases refractoriness of AV node. Decreases impulse conduction by indirectly blocking sodium channels, and blocking beta- adrenergic receptors. Increases atrial and ventricular refractoriness. Inhibits alpha-adrenergic receptors. Ibutilide IV: For patients who Class III antiarrhythmic. weigh ≥ 60 kg: 1 mg over 10 min. For patients who weigh less < 60 kg: 0.01 mg/kg over 10 min. A second dose of equal strength may be administered over 10 min if conversion does not take place with initial dose. continues 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 232

232 Chapter 12 Pharmacologic Support Following Cardiac Surgery

Table 12–4 Agents Used to Manage Postoperative Dysrhythmias (continued)

Mechanism Dysrhythmia Agent Dose of Action

Atrial Fibrillation Sotalol PO: For AF prevention: Classes II and III. (cont.) 80 mg BID. Dose may be Non-cardioselective increased in 3 days to beta blocker. 120 mg and then to 160 mg BID if no QT prolongation. Diltiazem IV: Initial bolus: Class IV. Blocks calcium 0.25 mg/kg over ion influx during 5-10 min. depolarization of cardiac Subsequent bolus: and vascular smooth 0.35 mg/kg over 5–10 min. muscle. after 15 minutes if needed. Decreases vascular Maintenance infusion: resistance and causes 5–15 mg/hr. relaxation of the vascular smooth muscle, resulting in a decrease in blood pressure. Negative inotropic effect. No specific ACE Dose is drug dependent. Agents that act on the inhibitor or ARB Renin–Angiotensin– recommendations Aldosterone System. It noted in literature. is not clear how angiotensin inhibition helps prevent development of AF. Digoxin IV or PO: Loading dose May control ventricular 0.25 mg every 2 hrs up to rate. Slows conduction a maximum of 1.5 mg. at the AV node and PO maintenance dose: is increases refractory 0.125–0.375 mg daily. period. Positive IV maintenance dose: inotrope. 0.125–0.25 mg daily. Decreases sympathetic response and renin– angiotensin system effect. Adenosine IV Initial dose: 6 mg rapid Transient depression of IV push followed by LV function. 20 mL normal saline. Slows SA node impulse Subsequent IV doses: formation. 12 mg IV push followed Slows conduction by 20 mL normal saline. through the AV node. Two subsequent doses Can interrupt reentry may be given. pathways through the AV node. Coronary vasodilation. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 233

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Table 12–4 Agents Used to Manage Postoperative Dysrhythmias (continued)

Mechanism Dysrhythmia Agent Dose of Action

Atrial Fibrillation Dexamethasone Anti-inflammatory IV Decreases effect of (cont.) dose: 0.75–9 mg over activation of the com- 5–10 min. daily in divided plement system follow- doses every 6 hrs. ing CPB. Decreases release of pro-inflammatory mediators. Hydrocortisone Anti-inflammatory IV Decreases effect of dose: 15–240 mg IV activation of the com- every 12 hrs. plement system following CPB. Decreases release of pro-inflammatory mediators. Ventricular Amiodarone VF, pulseless VT Initial See description in AF. Dysrhythmias bolus: 300 mg IV push. A maximum of 2.2 g may be given in 24 hrs. Continuous infusion: 1 mg/min for the first 6 hrs and at a rate of 0.5 mg/min for the next 18 hours, if required. Lidocaine VF, pulseless VT Initial Class I antiarrhythmic bolus: 1–1.5 mg/kg. agent. Subsequent bolus doses: 0.5–0.75 mg/kg every 5–10 min. Continuous infusion: 1–4 mg/min. Maximum dose is 3 mg/kg in 24 hrs. Sotalol PO: 80 mg BID. If Classes II and III. necessary, may increase Non-cardioselective dose to 240–320 mg/day. beta blocker.

AF ϭ atrial fibrillation; CPB ϭ cardiopulmonary bypass; VF ϭ ventricular fibrillation; VT ϭ ventricular tachycardia. Sources: Bharucha & Marinchak, 2007; Engelman et al., 1995; Katz, 2007; Khalpey et al., 2008; Levy et al., 2008; Micromedex Online, 2008; Uptodate.com Lexi Corp, 2008. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 234

234 Chapter 12 Pharmacologic Support Following Cardiac Surgery

rate of 52–65% in terms of reducing the fre- SIDE EFFECTS quency of AF (Aranki et al., 2008). Side effects of metoprolol include bradycardia, AV block, heart failure symptoms, and HEMODYNAMIC EFFECTS widening QRS complexes. Other potential As the name of the category connotes, beta- side effects include hypotension and bron- adrenergic receptor blockers decrease tissue chospasm (Lúcio et al., 2004). response to catecholamines (especially epinephrine and NE). Beta blockers are classified NURSING IMPLICATIONS as either cardioselective or non-cardioselective Valve replacement surgeries make patients based on whether they exert their efforts on prone to heart block; metoprolol is con- alpha receptors, beta1 receptors, beta2 recep- traindicated in these cases. Metoprolol should tors, or a combination of these (Levy et al., be used with caution in patients with COPD 2008). Metoprolol is a Class II antiarrhythmic and asthma because it may lead to airway and a cardioselective beta blocker. It has a constriction. Likewise, it should be used with negative inotropic effect and decreases heart caution in patients with ongoing pump dys- rate, contractility, CO, and blood pressure. function, as immediate correction does not occur postoperatively. INDICATIONS On rare occasions, beta blockers may mask Metoprolol is used to decrease the workload signs of hypoglycemia in patients with dia- of the heart by reducing heart rate and pro- betes (Levy et al., 2008). Caution should be phylactically to prevent AF or atrial flutter exercised when administering these agents to after cardiac surgery. In addition to promot- patients with hypotension or heart failure ing rate control for AF (Fuster et al., 2006), (Fuster et al., 2006). this drug may be used for rhythm conversion If patients do not convert to normal sinus (Khalpey et al., 2008). Beta blockers, because rhythm or become clinically unstable, synchro- of their mechanism of action, are not particu- nized cardioversion (SCV) may be performed larly effective in the treatment of dysrhyth- once rate control has been achieved. SCV typi- mias related to catecholamine stimulation cally will not be effective until rate control has (Levy et al., 2008). Typically, these agents are been attained in this patient population, as used in the period after the initial 24 postop- intense adrenergic activity is occurring at this erative hours, as myocardial function has gen- time. Patients should be considered for antico- erally improved by that time (St. Andre & agulation therapy despite their postoperative DelRossi, 2005). status if AF persists for more than 48 hours (St. Andre & DelRossi, 2005). DOSAGE Carvedilol (Coreg®) Metoprolol may be administered either intravenously or orally. The initial oral dose is HEMODYNAMIC EFFECTS 50 mg, followed by additional doses of 25 mg Carvedilol is a non-cardioselective beta until the patient’s heart rate is less than blocker. By blocking beta receptors, it 100 beats/min (Khalpey et al., 2008). The decreases heart rate, blood pressure, contrac- intravenous dose is 5–15 mg (usually 5 mg) tility, and CO, thereby decreasing myocardial administered over 2.5 minutes. Additional workload. This drug also blocks alpha recep- doses may be given at 7.5-minute intervals. tors, causing arterial vasodilation. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 235

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INDICATIONS increased risk of renal impairment secondary to While carvedilol is primarily prescribed in the hypotension in patients with a systolic blood management of hypertension and heart fail- pressure less than 100 mm Hg. Chest pain may ure, data suggest that it is more effective in develop in patients with Prinzmetal’s variant preventing postoperative AF in cardiac sur- angina. Carvedilol may also cause or exacer- gery patients than either metoprolol or bate adrenal insufficiency in those patients atenolol (Celik, Iyisoy, Celik, Gunay, & Isik, with PVD. 2008; Merritt, 2003). Its use for atrial dys- The ICU nurse should monitor heart rate rhythmias is a non-FDA-labeled indication and blood pressure while the patient remains (Micromedex Online, 2008). on carvedilol therapy. Renal function test data should be evaluated in patients with ischemic heart disease. The ICU nurse should DOSAGE anticipate a decrease with any signs of heart The dosage of carvedilol for patients with failure or angina (Micromedex Online, 2008). hypertension is 6.25 mg orally twice daily. The dosage for patients with heart failure is Class III Agents 3.125 mg orally daily. Amiodarone MECHANISM OF ACTION SIDE EFFECTS Amiodarone, while placed in the Class III cat- Side effects of carvedilol include hypotension, egory of drugs, is unique in that it possesses bradycardia, hyperglycemia, dizziness, diar- properties in all four categories of agents rhea, and fatigue. Serious but rare adverse described earlier. It creates its antiarrhythmic events that have been reported include heart effect by blocking potassium channels, which block, worsening heart failure, asthma with prolongs the duration of the action potential status asthmaticus, Stevens-Johnson syn- and decreases membrane excitability. Amio- drome, and aplastic anemia (Micromedex darone slows heart rate by depressing sinoa- Online, 2008). trial (SA) node automaticity (the heart’s inherent ability to initiate a beat) and NURSING IMPLICATIONS increases refractoriness of the AV node (Levy Carvedilol is contraindicated in patients with et al., 2008). This agent also decreases impulse second- or third-degree heart block, bronchial conduction by indirectly blocking sodium asthma, cardiogenic shock, severe sinus channels, blocking beta-adrenergic receptors bradycardia (if the patient does not have a (causing beta blockade), increasing atrial and pacemaker), decompensated heart failure ventricular refractoriness, and inhibiting being treated with an inotrope, sick sinus syn- alpha-adrenergic receptors and calcium chan- drome, or hepatic impairment (Micromedex nels, producing antianginal effects. The Online, 2008). It should be used with caution vasodilatory effects, including coronary in patients with diabetes, as carvedilol may vasodilation, further contribute to its potentiate insulin-induced hypoglycemia and antianginal effects (Brantman & Howie, 2006; hinder glucose level upturn. It may also exac- Levy et al., 2008). Collectively, these actions erbate hyperglycemia in patients with heart make amiodarone one of the most effective failure. As noted earlier, the drug may mask antiarrhythmic agents in postoperative car- symptoms of hypoglycemia. There is an diac surgery patients (Katz, 2007). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 236

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INDICATIONS and haloperidol) and in the presence of elec- Amiodarone is used in postoperative cardiac trolyte imbalance, pulmonary disease, and surgery patients to convert AF, and in the man- hepatic disease. Electrolyte imbalance may agement of VF and VT. It has replaced dilti- result in diminished drug efficacy or a dys- azem as the treatment of choice for SVT (Levy rhythmia. Patients with hepatic disease will et al., 2008). Amiodarone is generally recom- demonstrate decreased drug clearance. Pul- mended if a beta blocker or calcium channel monary toxicity (e.g., acute respiratory dis- blocker is ineffective in the management of a tress syndrome, pulmonary fibrosis or patient with AF (Fuster et al., 2006). infiltrates, and pneumonitis) has been reported as well (Micromedex Online, 2008).

DOSAGE Ibutilide The dosage of amiodarone for AF is 150 mg MECHANISM OF ACTION given intravenously over 10 minutes, followed by a 24-hour infusion given at a rate of Ibutilide is a Class III antiarrhythmic agent 1 mg/min for the first 6 hours and at a rate of (Bharucha & Marinchak, 2007). 0.5 mg/min for the next 18 hours, if required. INDICATIONS SIDE EFFECTS Ibutilide may be used to attempt to convert AF Amiodarone is associated with a wide array of to normal sinus rhythm if SCV has not proved side effects, including pulmonary and liver successful (Bharucha & Marinchak, 2007). toxicity with its long-term use. Myocardial depression and heart block may develop as DOSAGE well. If the drug is administered too quickly, For patients who weigh at least 60 kg, the significant hypotension may result (Khalpey dosage of ibutilide is 1 mg. If patients weigh et al., 2008). less than this amount, the dosage is 0.01 mg/kg. Either dose is administered over NURSING IMPLICATIONS 10 minutes. A second dose of equal strength With intravenous administration of amio- may be administered over 10 minutes if con- darone, a patient’s heart rate and blood pres- version does not take place upon completion sure may decrease. Minimal change is noted of the initial dose (Bharucha & Marinchak, in the QRS and QT complexes (QTc), however 2007; Khalpey et al., 2008). The half-life of (Levy et al., 2008). The hypotension seen in ibutilide is 2 to 12 hours, with an average of 6 postoperative cardiac surgery patients is typi- hours (Bharucha & Marinchak, 2007). cally temporary. If the patient experiences sustained or clinically significant bradycardia SIDE EFFECTS during that time, the epicardial pacing wires The primary side effect noted with ibutilide is can be used to reestablish a normal heart rate development of torsade de pointes. The risk (Katz, 2007). of developing torsade de pointes is increased The ICU nurse should closely monitor if ibutilide is given in combination with amio- patients on amiodarone for AV block, brady- darone (Bharucha & Marinchak, 2007; cardia, electrolyte imbalance, hypotension, LV Khalpey et al., 2008). Other significant side dysfunction, and new or worsened arrhyth- effects include, but are not limited to, mias. Amiodarone should be used with cau- monomorphic VT, SVT, hypotension, QT tion in conjunction with QTc-prolonging prolongation, AV block, and bradycardia drugs (e.g., quinidine, sotalol, erythromycin, (Bharucha & Marinchak, 2007). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 237

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NURSING IMPLICATIONS increased in 3 days to 120 mg and then to Administration of ibutilide is contraindicated 160 mg BID if the response is inadequate and in patients with a QT complex greater than no associated undue QT prolongation (not 440 milliseconds. The ICU nurse should mon- greater than 520 milliseconds) occurs. The itor patients who are receiving this Class III onset of action for sotalol is 1–2 hours, with a drug for development of QT prolongation, peak effect being noted in 2.5 to 4 hours. The torsade de pointes, and heart block. Prior to duration of effect is 8–16 hours; the half-life and during therapy, patients should have any is 12 hours (Bharucha & Marinchak, 2007). hypokalemic and hypomagnesemic conditions corrected. Patients should not receive SIDE EFFECTS concomitant therapy with another agent that A number of side effects have been reported can cause QT prolongation (Bharucha & Mar- in conjunction with administration of sotalol. inchak, 2007). These include, but are not limited to, bradycardia, chest pain, palpitations, fatigue, dizzi- Sotalol ness, dyspnea, hypotension, edema, confusion, MECHANISM OF ACTION headache, sleep disturbances, bleeding, upper Sotalol has both Class II and Class III mecha- respiratory problems, nausea, and vomiting nisms of action. As a beta blocker, it is non- (Bharucha & Marinchak, 2007).

cardioselective; it affects both beta1 and beta2 receptors. Net effects include a decrease in NURSING IMPLICATIONS heart rate and AV node conduction and an Monitoring of QT complexes, serum magne- increase in AV node refractoriness. As a Class sium and potassium levels, and ECG reports is III agent, sotalol prolongs the atrial and ven- recommended when this drug is used. Sotalol tricular action potentials (Bharucha & Marin- is contraindicated for patients with bronchial chak, 2007). asthma, bradycardias (sinus, Mobitz II, or complete heart block, unless the patient has a pace- INDICATIONS maker), prolonged QT complex, cardiogenic Sotalol was initially indicated to help prevent shock, heart failure, or a creatinine clearance development of AF after cardiac surgery in less than 40 mL/min. Patients with diabetes patients who were not candidates for the who are receiving sotalol may develop hypo- usual beta-blocker therapy. The 2004 glycemia, although the therapy may mask the ACC/AHA guidelines for postoperative CABG symptoms of a decreased serum glucose level. patients, however, downgraded this recom- Patients who are receiving concomitant cal- mendation, as the efficacy of sotalol in pre- cium channel blocker therapy should be venting AF is not well established based on observed for bradycardia or heart block devel- the most recent data (Bharucha & Marinchak, opment. Those receiving concomitant therapy 2007). with other agents that can prolong QT com- Sotalol may also be indicated in the treat- plexes are at increased risk for this complica- ment of life-threatening ventricular dysrhyth- tion given the additive effect exerted by sotalol mias (Bharucha & Marinchak, 2007; Levy et (Bharucha & Marinchak, 2007). al., 2008). Class IV Agents DOSAGE Two calcium channel blockers sometimes If used for AF prevention, the dosage of used in postoperative cardiac surgery patients sotalol is 80 mg PO BID. This dose may be are diltiazem and verapamil. Both slow the 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 238

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ventricular response in patients with AF, rate is reached prior to completing the initial atrial flutter, or SVT (Davison et al., 1985). bolus. The bolus should be followed by a con- However, verapamil is seldom used because of tinuous infusion at 5–15 mg/hr (Levy et al., its negative inotropic effects (Levy et al., 2008); this rate may be titrated to maintain 2008). There are no convincing data that cal- the heart rate within the prescribed parame- cium channel blockers prevent development ters. Conversion to normal sinus rhythm is of AF after cardiac surgery, and they are not commonly seen after administration of dilti- typically prescribed for that reason. Diltiazem azem; however, the primary goal when this may be administered to help decrease agent is used is rate control. ischemic events. Calcium channel blockers may be effective in controlling the ventricular SIDE EFFECTS rate associated with AF, but are reportedly AV block may occur with diltiazem use. This not as effective as beta-blocker therapy side effect occurs more often in patients who (Bharucha & Marinchak, 2007). have undergone valve operations, and particu- Diltiazem larly those involving the mitral valve. In this case, diltiazem therapy should be placed on MECHANISM OF ACTION hold (Mooss et al., 2000). Other side effects Diltiazem blocks calcium ion influx during commonly observed with this calcium chan- depolarization of cardiac and vascular smooth nel blocker include bradycardias, heart fail- muscle (Levy et al., 2008). It decreases vascular ure, peripheral edema, dizziness, and resistance and causes relaxation of the vascu- headache. Cardiac dysrhythmias are rare side lar smooth muscle, resulting in a decrease in effects (Micromedex Online, 2008). blood pressure (Micromedex Online, 2008). A negative inotropic effect occurs as well, as con- NURSING IMPLICATIONS tractile strength is regulated by calcium ions Diltiazem can be safely administered to flowing in and out of the cell. patients with marginal blood pressure if it is given slowly. Reduction of heart rate will INDICATIONS improve diastolic filling, which will in turn Diltiazem is used to lower the ventricular improve CO and reduce myocardial workload response in AF, atrial flutter, and SVT when after rate control is achieved. If the patient is the ventricular rate is greater than 100 beats on vasodilators to treat hypertension, consid- per minute. It may also be used for rhythm eration should be given to lowering the dose conversion (Khalpey et al., 2008). In addition, or stopping the vasodilators altogether prior diltiazem may be used to prevent vasospasm to administering diltiazem, as co-administra- in patients with internal mammary grafts by tion may potentiate a hypotensive effect. relaxing vascular smooth muscle and stabiliz- When administering diltiazem with adrener- ing the vessel. gic agonists, the ICU nurse should continuously monitor the patient’s heart rate and DOSAGE blood pressure. An initial bolus of 0.25 mg/kg, followed by Diltiazem may increase the effects of anes- 0.35 mg/kg after 15 minutes if needed, is typi- thetics. Patients who were taking diltiazem pre- cally ordered. Doses should be administered operatively may not awaken as quickly or may over a course of 5–10 minutes. The medication be more difficult to arouse after receiving this can be slowed or stopped if a reduction in medication during the first 24 hours following blood pressure is noted or if the target heart cardiac surgery (Micromedex Online, 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 239

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Agents Acting on the Renin–Angiotensin– therapy for this indication (Bharucha & Mar- Aldosterone System inchak, 2007). The renin–angiotensin–aldosterone system (RAAS) is implicated in the causal pathway of HEMODYNAMIC EFFECTS AF. Inhibition of this pathway with ACE Digoxin slows conduction at the AV node and inhibitors and ARBs may, therefore, prevent increases the refractory period (Levy et al., occurrence of AF (Manché et al., 1999). Data 2008). It also has a positive inotropic from trials and observations suggest that ACE effect and causes a decreased sympathetic inhibitors and ARBs may decrease the inci- response and renin–angiotensin system effect dence of postoperative AF in patients who (Micromedex Online, 2008). have undergone CABG (Arnsdorf & Podrid, 2006). In one meta-analysis, preoperative and INDICATIONS postoperative administration of an ACE Digoxin may be considered in the treatment inhibitor significantly decreased the incidence of postoperative AF in patients with poor of postoperative AF following CABG (Mathew ejection fraction, heart failure, or other con- et al., 2004). These data are not consistent, traindications to beta-blocker therapy (Fuster however. Other investigators have reported et al., 2006; Khalpey et al., 2008). However, no significant reduction in postoperative AF neither preoperative nor postoperative following cardiothoracic surgery (Coleman, administration of digoxin has been shown to Makanji, Kluger, & White, 2007). decrease the development of AF. Digoxin may It is not clear how angiotensin inhibition add to the effectiveness of beta blockers or helps prevent development of AF. One calcium channel blockers if monotherapy hypothesis is that it helps control risk factors with either type of agent proves effective for for AF, heart failure, and hypertension (Arns- rate control (Bharucha & Marinchak, 2007; dorf & Podrid, 2006). Another suggested Fuster et al., 2006). Oral digoxin is not indi- mechanism focuses on the decrease in atrial cated as monotherapy for treatment of parox- stretch in the setting of increased left atrial ysmal AF (Fuster et al., 2006). pressure. Administration of ACE inhibitors and ARBs cause improved ventricular func- DOSAGE tion and a decrease in left atrial pressure, The loading dose of digoxin for AF is 0.25 mg thereby decreasing triggers for the develop- IV or orally every 2 hours up to a maximum of ment of AF (Webster, Fitzpatrick, Nicholls, 1.5 mg. The maintenance dose is 0.125– Ikram, & Wells, 1985). ACE inhibitors such as 0.375 mg orally daily or 0.125–0.25 mg IV enalaprilat and ARBs (e.g., losartan [Cozaar®]) daily. The half-life of digoxin is typically 38–48 do not currently have an FDA-approved indi- hours but is longer in patients with impaired cation for AF, but rather are used on an off- renal function (Khalpey et al., 2008). Digoxin label basis for this condition (Micromedex should be administered over a period of at Online, 2008). least 5 minutes (Micromedex Online, 2008).

Other Agents to Treat Atrial SIDE EFFECTS Dysrhythmias Side effects associated with digoxin include ® Digoxin (Lanoxin ) nausea, vomiting, anorexia, diarrhea, Digoxin may be effective in controlling the headache, and visual disturbances. Cardiac ventricular rate associated with AF, but is dysrhythmias may also occur (Micromedex reportedly not as effective as beta-blocker Online, 2008). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 240

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NURSING IMPLICATIONS reentry pathways through the AV node. Several drugs (e.g., amiodarone) increase Adenosine produces coronary vasodilation, serum digoxin levels (Khalpey et al., 2008). possibly related to its action on smooth mus- Caution should be exercised when adminis- cle receptors (Micromedex Online, 2008). tering digoxin to any patient with acute MI, AV block, electrolyte imbalance (e.g., INDICATIONS hypokalemia, hypocalcemia, hypercalcemia, Adenosine is indicated for the treatment of hypomagnesemia), hypoxia, severe bradycar- paroxysmal SVT (Micromedex Online, 2008). dia, heart failure, pulmonary disease, VT, The drug is also used on an off-label basis to Wolff-Parkinson-White syndrome, renal dis- counteract an etiology of narrow or wide QRS ease, sick sinus syndrome, or premature ven- complex supraventricular tachyarrhythmias tricular contractions (Micromedex Online, (Micromedex Online, 2008). 2008). The ICU nurse should observe the patient’s blood pressure, heart rate, and car- DOSAGE diac rhythm during and following adminis- The initial dose of adenosine is 6 mg delivered tration of digoxin. Evaluation of renal via rapid IV administration. This dose should function and electrolyte status should ideally be followed by infusion of 20 mL of normal be made prior to administration. saline. Administration should take place as The therapeutic range for digoxin levels is close to the hub as possible. Two subsequent 0.8–2 ng/mL; levels should be obtained imme- doses of 12 mg each (maximum dose) may be diately prior to administering the next dose of administered, if needed. Adenosine has an the drug (Micromedex Online, 2008). The ultra-short half-life (less than 10 seconds) determination of digoxin toxicity is based (Micromedex Online, 2008). more on the presence of a “dig toxic” rhythm rather than exclusively on blood levels. Indications for digoxin immune Fab SIDE EFFECTS (Digibind®) include presence of ventricular Side effects that have been reported following dysrhythmias, bradyarrhythmias, second- or adenosine’s termination of the tachycardic third-degree heart block, or hyperkalemia rhythm include chest pain, lightheadedness, (greater than 5.0 mEq/L). If the patient has flushing, nausea, headache, and dyspnea. Seri- bradycardia and Digibind is not available, ous adverse events that have been reported atropine may be indicated. Extreme caution include bradycardias, dysrhythmias, heart should be exercised in patients who have block, and bronchospasm (in patients with received digoxin and who require cardiover- asthma) (Micromedex Online, 2008). sion, as digoxin potentiates the effects of electricity and the patient may develop a “dig NURSING IMPLICATIONS toxic” rhythm. Prior to administration of adenosine, the ICU nurse should alert the patient to anticipate “a Adenosine (Adenocard ®) strange sensation.” Monitoring of the patient MECHANISM OF ACTION during treatment should include continuous Adenosine produces no negative inotropic cardiac monitoring and vital signs. A rapid effects, although transient depression of LV decrease in heart rate with a brief episode (6 sec- function does occur. The latter effect slows onds) of ventricular asystole should be antici- SA node impulse formation, slows conduc- pated. For this reason, emergency resuscitative tion through the AV node, and can interrupt equipment should be immediately available 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 241

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during administration of adenosine. A baseline a 33% lower incidence of postoperative AF and repeat ECG are also recommended. when they received preoperative and postop- Administration of adenosine is contraindi- erative steroids (Halonen et al., 2007). cated in patients with second- or third-degree heart block, symptomatic bradycardia, or sick MECHANISM OF ACTION sinus syndrome. Caution should be exercised when administering this agent to patients As previously described, steroids decrease with hypertension, hypotension, MI, unstable inflammation by suppressing neutrophil angina, or bronchoconstrictive disorders migration, decreasing production of pro- (Micromedex Online, 2008). It is also recom- inflammatory mediators, and reversing mended that adenosine administration be the increase in capillary permeability (Uptodate avoided in heart transplant recipients, revas- .com Lexi Corp, 2008). Levels of complement, cularized patients, and individuals with AF or C-reactive protein complex, the number of atrial flutter (Khalpey et al., 2008). white blood cells, and the amount of pro- inflammatory mediators—all of which serve as Dexamethasone (Decadron®) indicators of an inflammatory response—are higher in patients who develop AF as com- The use of steroids as a prophylactic measure pared with patients who remain in normal for development of postoperative AF follow- sinus rhythm after cardiac surgery (Halonen ing cardiac surgery is based on the mecha- et al., 2007). It has been suggested that intra- nism of action of steroids and the operative inflammation may contribute to the pathophysiologic changes that occur during development of AF; dexamethasone, as an the intraoperative and postoperative periods. anti-inflammatory agent, may help prevent Activation of the complement system occurs AF from developing (Uptodate.com Lexi during CPB and during the first few postoper- Corp, 2008). ative days. In addition, increasing levels of C-reactive protein supplement activation of the complement system. Activation of the INDICATIONS complement system is associated with devel- Prophylactic administration of dexametha- opment of postoperative dysrhythmias (Bru- sone may prevent development of AF associ- ins et al., 1997). Steroid administration has ated with cardiac surgery. been shown to decrease this effect as well as the release of pro-inflammatory mediators (Engelman et al., 1995). DOSAGE Data are not consistently supportive of While not recommended specifically for steroid use despite studies suggesting these prevention of postoperative AF, the anti- agents’ efficacy. In one study, patients inflammatory dose of dexamethasone is received a preoperative dose of steroids, fol- 0.75–9 mg/day, given in divided doses every lowed by additional doses for the first 6 hours. The drug should be administered as 24 postoperative hours. A significant differ- an IV bolus over 5–10 minutes (Uptodate.com ence in the incidence of postoperative AF was Lexi Corp, 2008). reported between patients who did and did In one study, patients received 1 g of not receive steroids—21% and 51%, respec- methylprednisolone preoperatively. This ini- tively (Prasongsukarn et al., 2005). tial dose was followed by dexamethasone In another study, patients who underwent 4 mg every 6 hours for 24 hours following CABG, aortic valve replacement, or both had surgery (Prasongsukarn et al., 2005). 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 242

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SIDE EFFECTS of hydrocortisone preoperatively. This was A number of clinically significant adverse reac- followed by 1 mg every 8 hours for 3 days tions have been reported to be associated with (Halonen, et al., 2007). dexamethasone administration. These side effects were listed in the section addressing SIDE EFFECTS management of postoperative hypotension. Side effects that are reported as being related to administration of hydrocortisone are delin- NURSING IMPLICATIONS eated in the section addressing postoperative Because steroids have a large number of phys- hypotension. iologic effects, additional data are necessary before recommending their routine use in NURSING IMPLICATIONS prevention of postoperative cardiac surgery As with dexamethasone, withdrawal and dis- dysrhythmias. Withdrawal and discontinua- continuation of hydrocortisone should be tion of a corticosteroid should be done done slowly, with gradual tapering of the dose slowly, with gradual tapering of the dose (Uptodate.com Lexi Corp, 2008). The other (Uptodate.com Lexi Corp, 2008). The other nursing implications described earlier apply nursing implications described in the section here as well. on hypotension apply here as well. Hydrocortisone (Solu-Cortef ®) Agents Used to Treat Postoperative Ventricular Dysrhythmias MECHANISM OF ACTION VF, VT, and torsade de pointes may occur As described earlier, steroids decrease inflam- after heart surgery. The development of mation by suppressing neutrophil migration, paroxysmal VT is common following cardiac decreasing production of pro-inflammatory surgery—its incidence ranges from 17% to mediators, and reversing the increase in capil- 97%. This dysrhythmia is usually an indica- lary permeability (Uptodate.com Lexi Corp, tion of intraoperative ischemia–reperfusion 2008). Levels of complement, C-reactive pro- injury, electrolyte abnormalities (e.g., tein complex, the number of white blood hypokalemia and hypomagnesemia), or an cells, and the amount of pro-inflammatory increase in sympathetic stimulation (Aranki mediators—all of which are indicators of an et al., 2008; Khalpey et al., 2008). inflammatory response—are higher in The incidence of sustained VT, VF, and tor- patients who develop AF as compared with sade de pointes ranges from 1% to 3% (Aranki patients who remain in normal sinus rhythm et al., 2008). The presence of sustained VT after cardiac surgery (Halonen et al., 2007). (i.e., VT lasting for more than 30 seconds or associated with significant hemodynamic INDICATIONS compromise) requires a more aggressive man- Prophylactic administration of hydrocorti- agement approach. In addition to treating the sone is intended to prevent development of underlying cause, administration of inotropes AF associated with cardiac surgery. should be minimized. Pharmacologic intervention with amiodarone or lidocaine may be DOSAGE implemented. SCV should be performed if When administered as an anti-inflammatory sustained VT causes significant compromise agent, the recommended dose is 15-240 mg IV (Khalpey et al., 2008). every 12 hours (Uptodate.com Lexi Corp, VF should be treated with immediate defib- 2008). In one study, patients received 100 mg rillation. Following the initial shock, car- 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 243

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diopulmonary resuscitation should be per- diopulmonary resuscitation, and epinephrine formed. This procedure should be followed by (Uptodate.com Lexi Corp, 2008). administration of epinephrine and an antiarrhythmic such as amiodarone or lidocaine DOSAGE (American Heart Association, 2006). For VF or pulseless VT, the initial dose is Torsade de pointes is usually associated 1–1.5 mg/kg. Additional bolus doses may be with an intraoperative MI in patients with administered every 5–10 minutes at a dose of risk factors such as intraoperative hemody- 0.5–0.75 mg/kg. The bolus dose is followed by namic instability, increased sympathetic activ- an infusion of 1–4 mg/min if indicated. The ity, or metabolic derangements (Aranki et al., maximum dose in a 24-hour period is 2008). It is often terminated by correcting low 3 mg/kg. magnesium levels or by removing the The onset of action for a bolus dose of lido- causative agent (if the dysrhythmia was initi- caine is 45–90 seconds. The duration of ated in response to a medication that causes action is 10–20 minutes (Uptodate.com Lexi prolongation of the QT complex). Corp, 2008).

Amiodarone SIDE EFFECTS Amiodarone was discussed earlier in the sec- A number of side effects have been reported tion on atrial dysrhythmias. The dosage for related to lidocaine administration. These VF or pulseless VT is an initial bolus of 300 effects include dysrhythmias, bradycardia, mg IV push. A maximum dose of 2.2 g may be cardiovascular collapse, heart block, hypoten- administered in 24 hours. If indicated, a con- sion, seizures, somnolence, slurred speech, tinuous infusion may be initiated. drowsiness, confusion, dizziness, metallic taste, bronchospasm, dyspnea, and respira- Lidocaine tory depression or arrest (Uptodate.com Lexi MECHANISM OF ACTION Corp, 2008).

Lidocaine is a Class I antiarrhythmic agent. It NURSING IMPLICATIONS controls cardiac rate and rhythm by blocking Patients need to receive continuous cardiac the sodium channels, thereby decreasing the monitoring while receiving lidocaine therapy. duration of the action potential (Katz, 2007; Lidocaine should be used with caution in Levy et al., 2008). It also blocks the initiation patients with severe liver dysfunction, as this and conduction of nerve impulses by decreas- condition increases the risk of lidocaine toxicity. ing membrane permeability to sodium ions. Caution should also be taken when lidocaine is This latter effect inhibits depolarization and administered to patients with Wolff-Parkinson- blocking of conduction (Uptodate.com Lexi White syndrome, heart failure, hypovolemia, Corp, 2008), which includes slowing conduc- shock, or severe respiratory depression. Lido- tion in the ischemic myocardium (Levy et al., caine is contraindicated for patients with severe 2008). Lidocaine also inhibits automaticity of heart block unless the patient has a pacemaker conduction tissue by intensifying the electri- (Uptodate.com Lexi Corp, 2008). Patients cal stimulation threshold of the ventricle and should be monitored for development of neuro- the His–Purkinje system. logic toxicity during therapy.

INDICATIONS Sotalol Lidocaine is indicated for management of VF Sotalol was discussed previously in the sec- or pulseless VT following defibrillation, car- tion addressing management of atrial 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 244

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dysrhythmias. The initial dosage for manage- Agents to Treat Electrolyte Imbalances ment of ventricular dysrhythmias is 80 mg Correcting electrolyte imbalances is para- given orally on a twice-daily basis. If mount in preventing and correcting all dys- necessary, this dose may be increased to rhythmias. The goal of treatment is to lower 240–320 mg/day. It is suggested to allow the heart rate, thereby reducing the workload 3 days between dose adjustments to allow for on the heart and promoting conversion back a steady-state plasma concentration to be to sinus rhythm as soon as possible. As attained and to monitor QT intervals. Most described in Chapter 17, numerous factors patients require 160–320 mg/day in divided related to cardiac surgery put the patient at doses to help ensure effectiveness. However, risk for developing postoperative acid–base for patients with refractory ventricular dys- and electrolyte disturbances. These factors rhythmias, doses as high as 480–640 mg/day include anesthesia, induced hypothermia, may be required. When these higher doses are physiologic effects of CPB techniques, shock considered, clinicians should determine that resulting in renal insult, cardioplegia, rapid the potential benefits of sotalol administra- fluid and electrolyte shifts across fluid com- tion outweigh the risks (Uptodate.com Lexi partments following CPB, stress associated Corp, 2008). with surgery, intraoperative volume repletion, hemodilution, and the rewarming process Agents to Treat Postoperative that follows hypothermia (Margereson, 2003; Bradycardia Pezzella, Ferraris, & Lancey, 2004). An in- As described in Chapter 15, bradycardia and depth discussion of the management of the heart blocks may develop postoperatively common electrolyte imbalances experienced after cardiac surgery (Brister & Lenkei-Ker- by postoperative cardiac surgery patients win, 2005). Cold cardioplegia, valve repair, appears in Chapter 17. hypothermia, MI, medications (e.g., beta blockers, calcium channel blockers, digoxin, ■ OTHER AGENTS THAT MAY BE or amiodarone), and surgical trauma near the REQUIRED IN POSTOPERATIVE SA and AV nodes may all be causative factors. The most common bradyarrhythmias include CARDIAC SURGERY PATIENTS complete heart block, sinus node dysfunc- Naloxone (Narcan®) tion, and junctional rhythms (Aranki et al., MECHANISM OF ACTION 2008). Naloxone is an opioid antagonist. It has the A normal rate is typically restored within greatest affinity for the mu receptor but com- 24–48 hours after cardiac surgery, with epi- petes for the mu, kappa, and sigma opiate cardial, transvenous, or transcutaneous pac- receptor sites in the central nervous system ing being used in the interim (Khalpey et al., (Micromedex Online, 2008). 2008; Zevola, Raffa, & Brown, 2002). Some patients require permanent pacemaker placement after surgery to maintain a normal rate INDICATIONS and rhythm (Morris & St. Claire, 1999). It is Naloxone may be indicated if hypoventilation important to aggressively treat bradycardia or is present following narcotic administration. heart blocks that depress cardiac function; When this problem occurs, small doses of otherwise, they may quickly lead to cardio- naloxone should be enough to stimulate genic shock. respiration. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 245

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DOSAGE (defined as loss of more than 500 mL of blood For reversal of opioid-induced respiratory in the first postoperative hour) following car- depression, the dose is 0.4–2 mg IV. It may be diac surgery is reported to range from 3% to repeated every 2 to 3 minutes as needed until 14% (Bowman et al., 2008). Postoperative the desired effect is achieved (Micromedex bleeding may be surgical in origin, related to Online, 2008). platelet dysfunction from exposure to CPB circuitry, or attributable to inadequate SIDE EFECTS heparin reversal at the end of CPB (Mullen- Fortino & O’Brien, 2008; Talmor & Lisbon, Side effects associated with use of naloxone 2005). Depending on the etiology of the include cardiac dysrhythmias, hypertension, bleeding, pharmacologic intervention may be hypotension, VF, pulmonary edema, and warranted. hepatotoxicity (Micromedex Online, 2008). Protamine Sulfate NURSING IMPLICATIONS MECHANISM OF ACTION Care should be taken to closely monitor for Protamine sulfate combines with heparin to continued hypoventilation owing to the rela- form an inactive salt. This salt has no antico- tively short half-life of naloxone as compared agulation activity (Caravati, 2004). to some narcotics. The dose should be titrated to patient effect. The ICU nurse should monitor blood pressure, heart rate, INDICATIONS and respiratory rate following administration Protamine sulfate is indicated for patients of naloxone. In addition, a decline in opioid with a postoperative coagulopathy that is due medication effects should be anticipated to inadequate heparin reversal (Katz, 2007). (Micromedex Online, 2008). DOSAGE ■ PROPHYLACTIC ANTIBIOTICS The dosage is 1 mg of protamine sulfate for every 100 units of heparin that needs to be Data suggest a 50% incidence of postoperative reversed, up to a maximum dose of 50 mg. infection in patients who have undergone This dose is administered over 10 minutes. CPB and who did not receive prophylactic Heparin is neutralized within 5 minutes of antibiotic therapy. Administration of prophy- administration and the effect lasts for 2 hours lactic antibiotics preoperatively and continu- (Katz, 2007). ing for 24 hours postoperatively significantly decreases postoperative infection rates. No added benefit is reported when antibiotics are SIDE EFFECTS continued for additional time. Antibiotic Side effects of protamine sulfate administra- selection is area and facility specific (Salenger tion include hypotension, elevated PAP (from et al., 2003). pulmonary vasoconstriction secondary to a non-immunologic reaction), bradycardia, and non-cardiogenic pulmonary edema (Katz, ■ AGENTS USED TO CONTROL 2007; St. Andre & DelRossi, 2005). POSTOPERATIVE BLEEDING A protamine reaction may manifest in any As discussed further in Chapter 13, the inci- of several ways. If this medication is adminis- dence of excessive postoperative bleeding tered too quickly, a Type I reaction occurs: 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 246

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Hypotension develops as a result of histamine While a protamine reaction is more likely release, with resultant decreases in SVR and to occur in the OR, administration of prota- PVR. These effects can be reversed with mine also may take place in the ICU if the administration of an alpha-receptor agonist. patient experiences inadequate heparin rever- A Type II reaction is either an anaphylactic sal. If a protamine reaction occurs, in addi- or anaphylactoid reaction with associated tion to administration of an alpha-receptor hypotension, tachycardia, bronchospasm, agonist to increase SVR, management strate- flushing, and pulmonary edema. This reac- gies that may be implemented include admin- tion is often related to immunoglobulin E or istration of the following therapies: 500 mg G (IgE or IgG) causing release of histamine, intravenous calcium chloride to increase SVR leukotrienes, and kinins. The release of these and promote contractility; an inotropic agent substances results in capillary leak, hypoten- (e.g., low-dose epinephrine, dobutamine, sion, and pulmonary edema. Type II reactions inamrinone, milrinone) to decrease PVR; a may occur within the first 10–20 minutes (or vasodilator (e.g., nitroglycerin, nitric oxide) to more) following administration of protamine. decrease preload and PVR; aminophylline to A Type III reaction causes catastrophic pul- manage wheezing; and heparin to reverse a monary vasoconstriction, with associated protamine reaction (Bojar, 2004). increases in pulmonary artery pressure, hypotension (secondary to peripheral vasodi- Recombinant Activated Factor VII lation), decreased left atrial depression, right (NovoSeven®) ventricular dilation, and myocardial depres- MECHANISM OF ACTION sion. This kind of reaction is hypothesized to Recombinant activated factor VII activates the result from activation of various mediators of extrinsic pathway of the coagulation system. the inflammatory response. Complement This action stimulates the generation of activation leads to leukocyte aggregation, thrombin and leads to a subsequently rapid which causes pulmonary edema; the arachi- correction of the patient’s prothrombin time donic acid pathway stimulates production of (Khalpey et al., 2008). Factor VII also expe- thromboxane, which causes constriction of dites platelet activation and ultimate fibrin pulmonary vasculature. The latter effect sub- clot formation (Bowman et al., 2008). sides in approximately 10 minutes (Bojar, 2004). INDICATIONS As described further in Chapter 13, recombi- NURSING IMPLICATIONS nant activated factor VII may prove helpful in Patients with allergies to fish have a high risk achieving hemostasis in cardiac surgery of the anaphylactoid type of protamine reac- patients, thereby reducing their transfusion tion, as protamine sulfate is made of a protein requirements (Enomoto & Thorborg, 2005). found in fish sperm. In addition, caution It is administered to patients with clotting should be used when administering prota- deficiencies or antibodies to replacement of mine to men who are infertile or who have factors. Factor VII is used frequently in an off- undergone a vasectomy, as anti-protamine label manner following cardiac surgery—in antibodies may be present in these individuals this case, postoperatively in coagulopathic (Katz, 2007). There is also a 30- to 50-fold patients who received blood and blood prod- increased risk of protamine reaction in ucts. More data are needed before recom- patients who take NPH insulin (Bojar, 2004). mending its widespread use in the cardiac 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 247

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surgery population, however (Katz, 2007). If administering recombinant activated factor this clotting factor is administered to cardiac VII to patients with advanced atheroscle- surgery patients who do not have hemophilia, rotic disease, coagulopathies, or septicemia factor VII deficiency, or factor VIII deficiency, because of the increased risk of thrombotic this practice would be considered off-label use events associated with use of this medica- at this time (Micromedex Online, 2008). tion (Micromedex Online, 2008). Aminocaproic Acid (Amicar®) DOSAGE No dosage data are available that are specifi- MECHANISM OF ACTION cally applicable to the cardiac surgery patient Aminocaproic acid is an anti-fibrinolytic without a history of hemophilia, factor VII agent. It works by preventing plasminogen deficiency, or factor VIII deficiency. The from binding to fibrin, thereby stopping the smallest possible dose or a single dose of activation of plasmin and preventing clot 2.4–4.8 mg or 45 mcg/kg is suggested for con- breakdown (Katz, 2007). sideration (Johnson, Ross, & Moores, 2007). In one study, when 1.2 mg was administered INDICATIONS to postoperative cardiac surgery patients, sig- Aminocaproic acid is indicated for patients nificant improvements in intractable bleeding with postoperative bleeding that occurs sec- were reported (Romagnoli et al., 2006). ondary to fibrinolysis. Administration takes place via a slow IV push. DOSAGE SIDE EFFECTS The dose of aminocaproic acid is 4–5 g Serious adverse effects that have been administered over 1 hour, followed by a con- reported with recombinant activated factor tinuous infusion at a rate of 1 g/hr for VII use include ischemic heart disease, MI, 8 hours or until bleeding is controlled (Katz, SVT, arterial thromboembolism, bleeding, 2007). coagulopathies, venous thromboembolism, cerebral artery occlusion, cerebral ischemia, SIDE EFFECTS acute renal failure, and pulmonary embolism Side effects of aminocaproic acid include (Micromedex Online, 2008). thrombocytopenia, dysrhythmias, and thrombosis formation; all of these side effects are NURSING IMPLICATIONS rare (Katz, 2007). Reported serious adverse The ICU nurse must carefully observe for events include bradyarrhythmias, hypoten- and anticipate thromboembolic complica- sion, renal failure, and rhabdomyolysis tions when the patient receives recombinant (Micromedex Online, 2008). activated factor VII (Katz, 2007). Monitor- ing of coagulation profile results (i.e., NURSING IMPLICATIONS prothrombin time, activated partial throm- Administration of aminocaproic acid is con- boplastin time, platelets, and international traindicated in patients with coagulopathies. normalized ratio), obtaining factor VII lev- This medication should be used with caution els, and assessing for decreased postopera- in patients with cardiac, hepatic, or renal tive bleeding are all steps that should be insufficiency. A definitive diagnosis of pri- taken to determine the efficacy of this treat- mary fibrinolysis must be made before admin- ment. Caution should be exercised when istering aminocaproic acid. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 248

248 Chapter 12 Pharmacologic Support Following Cardiac Surgery

Aminocaproic acid should not be adminis- each of which has its own side effect profile. tered rapidly. The ICU nurse should monitor An understanding of the pharmacologic the patient’s complete blood count and agents used in the immediate postoperative coagulation profile prior to and after ther- period is essential. Part of the role of the ICU apy. Evaluation for bradycardia, hypoten- nurse is to stay current with data regarding sion, thrombosis, dyspnea, pulmonary pharmacologic agents used in the manage- embolism, and renal function tests should ment of postoperative cardiac surgery be conducted as well (Micromedex Online, patients. Implementation of recommenda- 2008). tions published in updates and Black Box Warnings issued by the Food and Drug ■ SUMMARY Administration (FDA) is essential to help Patients who undergo cardiac surgery may assure patient safety and optimal patient out- develop several alterations in their hemody- comes (see Table 12–5). The ICU nurse must namic profile and their cardiac rate and be vigilant in managing the complexities asso- rhythm in the immediate postoperative ciated with administration of these agents period. Alterations in preload, afterload, and and use clinical judgment to help ensure opti- CO may be treated with a variety of agents, mal patient outcomes. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 249

Summary 249

Table 12–5 Black Box Warnings Issued by the FDA

Agent Black Box Warning

amiodarone HCL (Cordarone®) Grapefruit juice decreases absorption of the medication. Skin can turn a gray-blue color. Regular blood work for thyroid problems should be planned. beta blockers (oral dosage forms): Abrupt withdrawal may result in angina pectoris, the metoprolol, (Lopressor®) occurrence of MI, and ventricular arrhythmias. Gradual reduction over several weeks is recommended. ibutilide (Corvert®) Continuous ECG monitoring and personnel trained in identification and treatment of acute ventricular arrhythmias are required due to the potential for fatal arrhythmias. Patients with atrial fibrillation of more than 2–3 days must be adequately anticoagulated for ≥ 2 weeks. nitroprusside (Nipride®) Medication must be diluted. Frequent blood pressure monitoring required due to hypotension. Cyanide toxicity can occur; therefore monitoring of acid-base balance and venous oxygen concentration is needed. norepinephrine (Levophed®), Infiltration requires the use of phentolamine mesylate dopamine (Intropin®) (Regitine®) as soon as possible to treat extravasation. phenylephrine (Neosynephrine®) The complete contents of the package insert should be reviewed prior to prescribing. sotalol (Betapace®) ECG monitoring required when starting medication. Adjust dosage in renal impairment. Creatinine clearance should be calculated prior to dosing.

Source: www.fda.gov. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 250

250 Chapter 12 Pharmacologic Support Following Cardiac Surgery

■ SELF-ASSESSMENT QUESTIONS tricular response and a history of a 30% ejection fraction? 1. Which of the following agents would be a. Digoxin most useful to treat postoperative hyper- b. Metoprolol tension in a cardiac surgery patient with c. Diltiazem a labile blood pressure? d. Amiodarone a. Nitroprusside 6. You are caring for a patient with a fail- b. Methylene blue ing right ventricle and elevated pul- c. Nitroglycerin monary vascular resistance. Which of d. Esmolol the following agents is indicated? 2. Which of the following should the ICU a. Nitroglycerin nurse anticipate when caring for a b. Milrinone patient receiving dobutamine? c. Nitroprusside a. Coronary ischemia d. Nicardipine b. Increased myocardial oxygen 7. Which of the following measurements consumption should indicate to the ICU nurse the c. Increased afterload need to temporarily hold off on admin- d. Methemoglobinemia istering nitroprusside to a patient with 3. Your patient is receiving methylene blue. hypertension? You note a decrease in SpO2 on the a. SVR 1600 dyne/sec/cm–5 pulse oximeter. Which of the following b. PAOP 10 mm Hg actions is indicated? c. MAP 95 mm Hg a. Increase the FIO2 d. CVP 1 mm Hg b. Immediately stop the infusion 8. Which of the following arterial blood c. Obtain an arterial blood gas gas results should indicate to the ICU d. Collaborate with the physician for nurse the presence of a complication nitric oxide administration related to nitroprusside administration? 4. Your postoperative cardiac surgery a. 7.25/pCO2 42/pO2 73/SaO2 patient develops atrial fibrillation. Meto- 93%/HCO 17 prolol is prescribed. Which of the fol- 3 b. 7.49/pCO2 31/pO2 81/SaO2 lowing conditions should prompt the 95%/HCO 25 ICU nurse to question the order? 3 c. 7.50/pCO2 39/pO2 68/SaO2 a. The patient underwent a combined 91%/HCO 31 CABG and valve repair procedure. 3 d. 7.25/pCO2 52/pO2 70/SaO2 b. The patient has a first-degree AV 93%/HCO 23 block with a PR interval of 0.28 3 9. You are caring for a patient with second. advanced aortic stenosis and postopera- c. The patient has a cardiac index of tive hypertension. The ICU nurse should 2.7 L/min/m2 on a milrinone question use of which of the following infusion. medications? d. The patient was taking digoxin a. Nitroprusside preoperatively. b. Nicardipine 5. Which of the following agents should be c. Clevidipine considered for rate control in a patient d. Enalaprilat with atrial fibrillation with a rapid ven- 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 251

Self-Assessment Questions 251

10. Your postoperative cardiac surgery Answers to Self-Assessment Questions patient is receiving an epinephrine infu- 1. d 6. b sion. For which of the following condi- 2. a 7. d tions should the ICU nurse observe? 3. c 8. a a. Respiratory acidosis b. Hyperglycemia 4. b 9. b c. Adrenal insufficiency 5. a 10. b d. Afterload reduction

Clinical Inquiry Box

Question: What is the postoperative impact of intraoperative administration of catecholamines to adult elective cardiac surgery patients based exclusively on the clinical judgment of the anesthesiologist? Reference: Fellahi, J.-L., Parienti, J.-J., Hanouz, J.-L., Plaud, B., Riou, B., & Quattara, A. (2008). Perioperative use of dobutamine in cardiac surgery and adverse cardiac outcome. Anesthesiology, 108(6), 979-987. Objective: To determine the clinical outcome of catecholamine administration based on clinical judgment. The endpoints for this study were major cardiac morbidity and mortality. Methods: Consecutive patients (nonrandomized; n ϭ 657) were divided into two groups. One group received catecholamines; the other (control group) did not. Ninety percent of the patients who received catecholamines had also received dobutamine. The endpoint of major cardiac morbidity was defined as any one of the following conditions: (1) sustained ventricular arrhythmia that required treatment; (2) need for postoperative intra-aortic balloon pump therapy; or (3) postoperative myocardial infarction. The endpoint of overall mortality was defined as death during the patient’s hospitalization. Results: Of the 657 patients, 84 (13%) received catecholamines either intraoperatively or during the first few postoperative hours. The incidence of major cardiac morbidity was 30% among the patients who received catecholamines compared with 9% among the patients who were in the control group. No patients required intra-aortic balloon pump therapy. A clinically significant relationship between catecholamine administration and ventricular arrhythmias was identified. The relationship between catecholamine administration and myocardial infarction was not statistically significant. The authors noted, however, that only low-risk patients were evaluated in this study. The overall mortality in the patients who received catecholamines was 8%, as compared with 1% in the control group. The relationship between catecholamine administration and mortality did not achieve statistical significance. Conclusion: Intraoperative administration of dobutamine to low-risk cardiac surgery patients who undergo cardiopulmonary bypass, when use of that therapy is based solely on the clinical judgment of the cardiac anesthesiologist, is associated with major cardiac morbidity. ICU nurses caring for postoperative cardiac surgery patients who received intraoperative catecholamines should anticipate the possibility of a major cardiac event in the immediate postoperative period. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 252

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Effectiveness of metoprolol in preventing Pezzella, A. T., Ferraris, V. A., & Lancey, R. A. (2004). atrial fibrillation and flutter in the postopera- Care of the adult cardiac surgery patient: Part tive period of coronary artery bypass graft sur- II. Current Problems in Surgery, 41(6), 526–574. gery. Arquivos Brasileiros de Cardiologia, 82(1), Prasongsukarn, K., Abel, J. G., Jamieson, W. R., 37–41. Cheung, A., Russell, J. A., Walley, K. R., et al. Manché, A., Galea, J., & Busuttil, W. (1999). Toler- (2005). The effects of steroids on the occur- ance to ACE inhibitors after cardiac surgery. rence of postoperative atrial fibrillation after European Journal of Cardiothoracic Surgery, 15(1), coronary artery bypass grafting surgery: A 55–60. prospective randomized trial. Journal of Tho- Margereson, C. (2003). Postoperative care follow- racic and Cardiovascular Surgery, 130(1), 93–98. ing cardiothoracic surgery. In C. Margereson Raja, S. G., & Dreyfus, G. D. (2004). Pharmacologic & J. Riley (Eds.), Cardiothoracic surgical nursing manipulation of systemic inflammatory trends in adult nursing (pp. 129–204). Boston, response after cardiac surgery. Internet Journal MA: Blackwell. of Thoracic and Cardiovascular Surgery, 6(2). Massé, L., & Antonacci, M. (2005). Low cardiac Retrieved November 19, 2008 from http:// output syndrome: Identification and manage- www.ispub.com/ostia/index.php?xmlFilePath ϭ ment. Critical Care Nursing Clinics of North Amer- journals/ijtcvs/vol6n2/response.xml ica, 17(4), 375–386. Romagnoli, S., Bevilacqua, S., Gelsomino, S., Mathew, J. P., Fontes, M. L., Tudor, I. C., Ramsay, J., Pradella, S., Ghilli, L., Rostagno, C., et al. Duke, P., Mazer, C. D., et al. (2004). A multi- (2006). Small-dose recombinant activated fac- center risk index for atrial fibrillation after tor VII (NovoSeven®) in cardiac surgery. Anes- cardiac surgery. Journal of the American Medical thesia & Analgesia, 102(5), 1320–1326. Association, 291(14), 1720–1729. Salenger, R., Gammie, J. S., & Vander Salm, T. J. Merritt, J. (2003). Comparison of effectiveness of (2003). Postoperative care of cardiac surgical carvedilol versus metoprolol or atenolol for patients. In L. H. Cohn & L. H. Edmunds, Jr. atrial fibrillation appearing after coronary (Eds.), Cardiac surgery in the adult (pp. 439–469). artery bypass grafting or cardiac valve opera- New York: McGraw-Hill. tion. American Journal of Cardiology, 92(1), Silver, M. (2002). Summary of common heart fail- 735–736. ure drugs. In M. Silver, Success with heart failure: Micromedex Online. Retrieved May 28, 2008, from Help and hope for those with congestive heart failure www.micromedex.com (pp. 87–104). Cambridge, MA: Da Capo Press. Mooss, A. N., Wurdeman, R. L., Mohiuddin, S. M., Silvestry, F. E. (2008). Overview of the postopera- Reyes, A. P., Sugimoto, J. T., Scott, W., et al. tive management of patients undergoing car- (2000). Esmolol versus diltiazem in the treat- diac surgery. Retrieved September 16, 2008, ment of postoperative atrial fibrillation/atrial from www.utdol.com/online/content/topic flutter after open heart surgery. American Heart .do?topicKeyϭcc_medi/22438&linkTitle Journal, 140(1), 181–188. ϭPerioperative%20myocardial%20infarction& ϭ ϭ Morris, D. C., & St. Claire, D. (1999). Management source preview&selectedTitle 1~150& ϭ of patients after cardiac surgery. Current Prob- anchor 13# lems in Cardiology, 24(4), 161–228. Singla, N., Warltier, D. C., Ghandi, S. D., Lumb, P. D., Mullen-Fortino, M., & O’Brien, N. (2008). Caring Sladen, R. N., Aronson, S., et al. (2008). Treat- for a patient after coronary artery bypass graft ment of acute postoperative hypertension in surgery, Nursing, 38(3), 46–52. cardiac surgery patients: An efficacy study of clevidipine assessing its postoperative antihy- Orlowski, J. P., Vidt, D. G., Walker, S., & Haluska, J. F. pertensive effect in cardiac surgery-2 (1989). The hemodynamic effects of intra- (ESCAPE-2), a randomized, double-blind, venous labetalol for postoperative hyperten- placebo-controlled trial. Anesthesia & Analgesia, sion. Cleveland Clinic Journal of Medicine, 56(1), 107(1), 59–67. 29–34. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 255

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St. Andre, A. C., & DelRossi, A. (2005). Hemody- ■ WEB RESOURCES namic management of patients in the first Federal Drug Administration: http://www.fda.gov/ 24 hours after cardiac surgery. Critical Care Safety-related drug labeling changes: http://www Medicine, 33(9), 2082–2093. .fda.gov/medwatch/safety.htm Talmor, D., & Lisbon, A. (2005). Management FDA Safety News (recalls and safety alerts and of the postoperative cardiac surgical patient. preventing medical errors): http://www In M. Fink, E. Abraham, J. Vincent, & .accessdata.fda.gov/scripts/cdrh/cfdocs/psn/ P. Kochanek (Eds.), Textbook of critical care (5th index.cfm ed., pp. 1955–1967). Philadelphia: Elsevier Saunders. Adverse event reporting system (case reports): http://www.fda.gov/cder/aers/extract.htm Touma, R. N. (2007). Factitious pulse oximeter desaturation with methylene blue injection in Herbal–drug interaction poster: http://www sentinel lymph node biopsy. Chest, 132(4), 696. .coloradopatientsafety.org/Herbal-Drug -Poster.pdf Uptodate.com Lexi Comp. (2008). Lidocaine: Drug information. Retrieved November 19, 2008, Scientific Review of Alternative Medicine: from www.utdol.com/online/content/topic http://www.sram.org/ .do?topicKeyϭdrug_l_z/143999&selectedTitle National Center for Complementary and Alterna- ϭ50~150&sourceϭsearch_result tive Medicine: http://nccam.nih.gov/ Webster, M. W., Fitzpatrick, M. A., Nicholls, M. G., Clinical drug trials (lists studies by drug interven- Ikram, H., & Wells, J. E. (1985). Effect of tion): www.clinicaltrials.gov enalapril on ventricular arrhythmias in con- Micromedex Online: www.micromedex.com gestive heart failure. American Journal of Cardi- ology, 56(18), 566–569. Whitlock, R. P., Rubens, F. D., Young, E., & Teoh, K. H. (2005). Pro: Steroids should be used for cardiopulmonary bypass. Journal of Cardiotho- racic and Vascular Anesthesia, 19(2), 250–254. Zevola, D., Raffa, M., & Brown, K. (2002). Using clinical pathways in patients undergoing cardiac valve surgery. Critical Care Nurse, 22(1), 31–50. 57625_CH12_205_256.pdf 4/10/09 11:07 AM Page 256 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 257

Chapter 13 Postoperative Complications of Cardiac Surgery and Nursing Interventions

Beverly Jones

■ INTRODUCTION More than 600,000 coronary artery bypass the healthcare team’s awareness of the high- grafting (CABG) and valve procedures are per- risk patient for whom more aggressive ther- formed in the United States annually (Sil- apy may be warranted and alerts caregivers to vestry, 2008). Patients who become candidates the potential for postoperative complications for cardiac surgery present with a number of (Adams, Filsoufi, & Antman, 2005). This comorbidities. Some of these comorbidities chapter describes the most common postop- are directly related to the need for surgery, erative complications associated with cardiac whereas others are attributable to age or other surgery and the ICU nursing management of noncardiac issues. An extensive presurgical these complications. evaluation should always be performed, as discussed in Chapter 4. From these data and the ■ RISK FACTORS FOR patient’s condition, management of the patient’s complex problems may take place POSTOPERATIVE before, during, and following cardiac surgery. COMPLICATIONS Despite the trend toward cardiac surgery The incidence of postoperative complications being performed on older persons and those after cardiac surgery is reported according to with more complex health issues, the 30-day the specific complication, presence of comor- mortality associated with these types of pro- bidities, and patient-related factors (e.g., age). cedures continues to decline (Brown et al., Multiple cardiac surgery databases have been 2008). The overall mortality rate is now developed that compile information and reported to be less than 5%. For patients allow for calculating risk factors for postoper- undergoing their first cardiac surgery proce- ative complications. Table 13–1 lists the most dure, the mortality rate is 1–2%, even among common risk factors that have been shown to those patients who experience postoperative have predictive value for postoperative com- complications (St. Andre & DelRossi, 2005). plications and higher rates of mortality. An important focus for the patient under- In one study, risk of predetermined compli- going cardiac surgery is an assessment of car- cations was evaluated among participants of diac risk. Calculation of risk potential affords the Medicare program. Patients who sus- patients and their families insight into the tained postoperative cardiac surgery compli- risk of complications and possible mortality cations tended to be older than 75 years, of the surgical procedure. It also heightens female, and non-Caucasian, and had a history

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Table 13–1 Risk Factors of procedure, or cardiopulmonary bypass (CPB). Postoperative Complications Examples of the latter two causes are effects of anesthesia, transient left ventricular (LV) Older age (greater than 65 years) dysfunction, increased capillary permeability, Emergent need for procedure (versus urgent hypothermia, bleeding, and infection (Sil- need) vestry, 2008). Reoperations Advances in surgical management, critical care, technology, understanding of CPB Preexisting preoperative comorbidities: renal dysfunction (dialysis dependent), COPD, hypothermia, and pharmacologic manage- diabetes, cerebrovascular disease, peripheral ment have positively influenced postoperative vascular disease, heart failure, acute myocar- management and outcomes, allowing for dial infarction, pulmonary hypertension more complex surgeries, operations on older CABG-valve surgery persons, and consideration of patients with Low ejection fraction multiple comorbidities as surgical candidates. Pulmonary dysfunction Data further suggest that postoperative strict glycemic control is correlated with lower mor- Preoperative use of intra-aortic balloon pump bidity and mortality rates (Talmor & Lisbon, Sources: Grover, Shroyer, & Hammermeister, 1996; 2005). Kurki &, Kataja, 1996; Tu, Jaglal, & Naylor, 1995; Tuman, McCarthy, March, Najafi, & Ivankovich, Despite all the improvements in cardiac 1992. surgery, a few complications continue to be associated with a mortality rate of 50% or greater. Even as ever more technological of heart failure, COPD, acute myocardial advances emerge, it is important to identify infarction (MI), cardiogenic shock, atrial fib- the deleterious side effects of CPB, circulatory rillation (AF) or flutter, ventricular fibrilla- arrest, hypothermia, and aortic cross-clamp- tion (VF), nonsustained tachycardia, valve ing, as they can cause physiologic abnormali- disease, or type I diabetes. The overall inci- ties in major organs that may persist in the dence of complications was 13.64%; 10.99% of postoperative period. Knowledge and early patients developed one complication, and identification of potential postoperative com- 2.64% developed two or more complications plications are essential to successful patient (Brown et al., 2008). outcomes from cardiac surgery. Another study evaluated older patients (mean age of 79 years) with an elevated body ■ mass index (BMI). The incidence of postoper- CARDIAC COMPLICATIONS ative complications was 23.1% in this patient Adequate cardiac function is the most piv- group (Maurer, Luchsinger, Wellner, Kukuy, otal factor associated with recovery from & Edwards, 2002). cardiac surgery. Patients with low cardiac Complications of cardiac surgery have neg- output (CO) have a higher mortality risk. ative and variable effects on patient out- Hence, the ICU nurse plays a vital role in comes. They can occur as a result of change in preventing or identifying and then treating cardiac performance from preexisting comor- cardiac complications. bidities, preoperative preparation for surgery, Hemodynamic compromise in the cardiac the surgical procedure itself, intraoperative surgery patient is challenging to manage, as care, or any combination of these factors (St. the status of such patients tends to be labile Andre & DelRossi, 2005). in the immediate postoperative period. The Postoperative complications may occur sec- etiology of hemodynamic compromise is mul- ondary to patient comorbidities, the surgical tifactorial. It may be caused by the patient’s 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 259

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underlying cardiac disease, factors that affect perfusion include tachycardia, diminished CO (e.g., filling pressures, dysrhythmias), peripheral pulses, delayed capillary refill time decreased ventricular compliance, loss of (CRT), decreased urinary output, hypoten- vasomotor tone, increased capillary perme- sion, and (possibly) metabolic acidosis ability, excessive bleeding, increased urinary (Margereson & Riley, 2003). output, inflammatory responses to CPB, poor One of the primary foci of caring for a post- myocardial protection during aortic cross- operative cardiac patient is obtaining a bal- clamping, pulmonary edema, cardiac tam- ance between oxygen supply and demand so ponade, or ventricular dysfunction. The that oxygen delivery to the tissues can be factor that influences decreased cardiac per- enhanced without stressing the heart as it formance most in the immediate postopera- recovers from surgery (Khalpey, Ganim, & tive period, however, is the underlying Rawn, 2008). Optimal hemodynamic parame- preoperative cardiac pathology. Even though ters in a postoperative cardiac surgery patient surgery has been performed, the patient will include a CI of greater than 2 L/min/m2, pul- not experience an immediate improvement in monary artery occlusive pressure (PAOP) of contractility (Salenger, Gammie, & Vander approximately 15 mm Hg, central venous Salm, 2003). pressure (CVP) less than 15 mm Hg, mean In addition to the inflammatory response of arterial pressure (MAP) greater than 65 mm CPB, data suggest that a release of inflamma- Hg, systolic blood pressure (SBP) in the range tory mediators occurs in patients who undergo of 90–140 mm Hg, left atrial pressure (LAP) cardiac surgery without bypass, contributing in the range of 5–15 mm Hg, systemic vascu- to these individuals’ postoperative hemody- lar resistance index in the range of namic instability. Secretion of prostaglandins 1400–2800 dyne/sec/cm–5/m2, and heart rate and other pro-inflammatory mediators less than 100 bpm. The patient should also (cytokines) stimulates release of nitric oxide, have warm, well-perfused extremities and leading to profound vasodilation (Scollan-Bor- urine output greater than 0.5 mL/kg/hr. ing, 2005). Nitric oxide causes resistance to These goals, however, should be individual- vasopressors by preventing vessels of some ized based on the patient’s comorbidities and patients from vasoconstricting. A decrease in clinical status (Khalpey et al., 2008; Salenger vasopressin levels further contributes to a rela- et al., 2003). tive hypovolemia despite normal intravascular volume (Bridges & Dukes, 2005). When decreased ventricular function is Low Cardiac Output present, compensatory mechanisms such as To help ensure oxygen delivery, CO (the sympathetic nervous system (SNS) stimula- amount of blood ejected by the heart each tion and endogenous catecholamine produc- minute) must be adequate (Salenger et al., tion cause an increase in heart rate, 2003). A related parameter to CO is cardiac contractility, and vasoconstriction. In turn, index (CI), the amount of blood ejected by the both preload and afterload increase (Talmor heart each minute in relation to a patient’s & Lisbon, 2005). Initially, these compensatory body surface area. Adequate tissue perfusion factors will improve CO and blood pressure, is dependent on satisfactory CO. Cardiac out- albeit usually at the cost of increasing put and index are functions of stroke volume myocardial oxygen consumption, which can (SV, the amount of blood ejected by the heart exacerbate myocardial ischemia. The compen- with each beat) and heart rate. SV depends on satory mechanisms are temporary, however; myocardial contractility, preload (the amount when they are exhausted, poor tissue perfu- of volume returning to the right or left side of sion will ensue. Initial signs of poor tissue the heart), and afterload (the amount of work 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 260

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the heart has to do to eject blood) (Massé & provides data on the balance between oxygen Antonacci, 2005; Silvestry, 2008). supply and demand. Lab data that will help Low cardiac output syndrome (LCOS) is support a diagnosis of low CO include a often seen after cardiac surgery and is associ- metabolic acidosis or increasing base deficit ated with increased morbidity and mortality. on arterial blood gas and an elevated serum The reported incidence of this condition is 6%, lactate level (Massé & Antonacci, 2005). 12%, and 23% for patients with a LV ejection Management of the patient with low CO fraction (LVEF) greater than 40%, between depends on the underlying cause, hemody- 20% and 40%, and less than 20%, respectively. namic profile, and patient assessment find- LCOS has been defined as the need for admin- ings. Low CO is usually brief in duration. Use istration of inotropic therapy for more than of fluids, vasopressors, and inotropic agents 30 minutes or for intra-aortic balloon pump will vary based on whether the patient has low (IABP) therapy; it is a common complication preload or cardiac index and whether the SVR following aortic valve surgery (Maganti, Rao, is elevated or low (Aranki, Cutlip, & Aroesty, Borger, Ivanov, & David, 2005). 2008; Liu & Gropper, 2002). If inotropic sup- Postoperative cardiac surgery patients may port is required, the chosen drug’s efficacy develop LCOS due to a transient decrease in must be carefully monitored, as inotropic perfusion due to LV dysfunction. Cardiac agents increase myocardial workload and arrest from cardioplegia with resultant metabolic rate (Massé & Antonacci, 2005). myocardial stunning and diastolic dysfunc- Epinephrine, norepinephrine (Levophed®), tion, decreased preload, increased afterload, dopamine (Intropin®), or dobutamine dysrhythmias, and MI have also been impli- (Dobutrex®) may be administered if contrac- cated etiologies for LCOS. The ultimate tility (EF) is below the expected values for the results are an imbalance between oxygen sup- patient. These agents may have decreased ply and demand and a metabolic acidosis efficacy in patients with chronic systolic dys- (Aranki, Cutlip, & Aroesty, 2008; Massé & function due to downregulation of beta Antonacci, 2005; Talmor & Lisbon, 2005). receptors. Use of a phosphodiesterase The ICU nurse must monitor for signs and inhibitor (e.g., milrinone [Primacor®]) may be symptoms of impaired CO. These include a more effective means to augment contrac- altered mental status, hypotension, decreased tility in this group of patients (Talmor & Lis- MAP, narrow pulse pressure, tachycardia, bon, 2005). If vasodilation is the cause of the decreased peripheral pulses, increased CRT, LCOS, administration of a vasoconstrictor cool extremities, poor perfusion, oliguria, or (e.g., phenylephrine [Neosynephrine®], nor- anuria (Massé & Antonacci, 2005; Mullen- epinephrine, or vasopressin) is warranted Fortino & O’Brien, 2008). (Talmor & Lisbon, 2005).

If monitoring equipment is available, SvO2 If afterload is elevated, administration of levels will be lower than normal in the setting nitroprusside (Nipride®) or IABP therapy may

of LCOS. SvO2 (i.e., mixed venous oxygen sat- be indicated (Aranki et al., 2008; Massé & uration) is the percentage of hemoglobin sat- Antonacci, 2005). Regardless of the cause of urated with oxygen in the pulmonary artery low CO, the primary goal of management will after blood has circulated systemically and focus on decreasing metabolic demand. Inter- oxygen has been extracted based on cellular ventions such as preventing hyperthermia,

need. Normal SvO2 values are in the range of administering sedation and analgesia, 70–75%. If SvO2 is less than 70%, it indicates decreasing work of breathing with mechani- that cells are sensing hypoperfusion or an cal ventilation, and preventing or treating

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and acid–base imbalances may need to be need to be given to correct coagulopathies considered (Massé & Antonacci, 2005). usually caused by CPB. If bleeding is not present, bolus administration of isotonic crystalloids (e.g., 0.9% normal Preload Issues saline, lactated Ringer’s solution) or colloid Preload refers to the amount of volume (e.g., 5% albumin, hetastarch [up to 2 L]) returning to the right or left heart at the end may be used to optimize preload, usually to a of filling (diastole). It may be assessed by CVP PAOP of 18–20 mm Hg. Administration of and PAOP, which are the filling pressures of inotropic agents is not recommended for the right and left heart, respectively. PAOP is patients with decreased preload (Khalpey et al., a reflection of left ventricular end-diastolic 2008; Marino, 2006; St. Andre & DelRossi, pressure (LVEDP), from which estimates of 2005). Patients with a history of ventricular left ventricular end-diastolic volume can be hypertrophy or diastolic dysfunction usually made (Silvestry, 2008). The majority of require a higher preload (Khalpey et al., 2008). patients are admitted to the ICU from the OR Volume requirements may decrease after the with alterations in preload despite having a patient has been removed from positive pres- positive fluid balance. The volume, however, sure ventilation, as this change is often associ- is not in the intravascular space; instead, ated with an increase in venous return owing much of the fluid is located in the intersti- to the decrease in intrathoracic pressure tium or other third space (e.g., pleural cavity). (Khalpey et al., 2008). Vasodilation is reported Adequate preload is essential to maintain as the major contributor to a decrease in pre- a satisfactory CO and tissue perfusion. load in the initial postoperative period. Vol- Decreased preload in the immediate postoper- ume repletion typically occurs most within ative cardiac surgery patient can result from the first 5 hours following surgery (St. Andre several factors, including excessive fluid output & DelRossi, 2005). from diuresis or hypothermia, vasodilation A therapeutic endpoint for volume resusci- during rewarming, inadequate intraoperative tation may be the MAP. The goal of a MAP in fluid resuscitation, intraoperative or postoper- the range of 70–80 mm Hg is suggested. ative bleeding, loss of vasomotor tone, infusion Tachycardia is not believed to be an appropri- of vasodilator agents, decreased LV compli- ate indicator of adequacy of preload, given the ance, or capillary leak leading to third spacing many preoperative and intraoperative factors of fluid (Khalpey et al., 2008; Massé & that can affect the correlation between heart Antonacci, 2005; Silvestry, 2008). rate and hypovolemia (St. Andre & DelRossi, The type and amount of fluid resuscitation 2005). Ongoing monitoring of the patient’s required will be based on the patient’s history, hemodynamic profile must take place con- the amount and type of fluid lost, and the comitantly with volume repletion. Care must hematocrit level. If the patient experiences be taken not to overstretch the ventricle with excessive postoperative bleeding, transfusion excessive volume, as an impaired CO may of blood and blood products should be initi- ensue (Massé & Antonacci, 2005). ated while the source of the blood loss is being determined. The hemoglobin requirement should be determined by the patient’s cardiac Cardiac Dysrhythmias status, age, and other clinical issues Dysrhythmias often occur after cardiac sur- pertinent to the situation (Ferraris et al., gery, as discussed in detail in Chapter 15. AF 2007). Coagulation factors such as fresh is the most frequently encountered dysrhyth- frozen plasma and cryoprecipitate may also mia, occurring in as many as 50% of patients 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 262

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(Auer et al., 2005). It usually occurs on the Table 13–2 Common Causes of second and third postoperative days and, Dysrhythmias Following Cardiac Surgery therefore, may not manifest while the patient is in the ICU. Ventricular dysrhythmias are Cardiac Problems less common and may be indicative of Preexisting heart disease myocardial dysfunction or injury (Tineli et al, Poor intraoperative myocardial protection 2005). Dysrhythmias following cardiac surgery may result from a number of etiologies Myocardial ischemia (Table 13–2). Respiratory Issues Dysrhythmias can compromise CO when Hypoxia they interfere with diastolic filling. If a distur- Hypocarbia/hypercarbia bance in heart rhythm is present, prompt Endotracheal tube misplacement identification and close assessment of the patient are essential. Assessment of the patient Pneumothorax with cardiac dysrhythmias following cardiac Electrolyte Disturbances surgery requires evaluation of the rhythm and Hypokalemia its effects on systemic perfusion, as well as Hyperkalemia evaluation of precipitating factors. Treatment Hypomagnesemia is based on whether the goal of therapy is to control the rate or to convert the rhythm. Surgical Trauma Pharmacologic management of dysrhythmias Atriotomy is discussed in detail in Chapters 12 and 15. Ventriculotomy Surgical correction near the conduction Diastolic Dysfunction system Diastolic dysfunction may result from Medications impaired systolic relaxation, stiffness of the Digoxin left ventricle, or decreased diastolic stretching Vasoactive medications or compliance. Dysfunction commonly occurs as a result of aortic stenosis with LV Other hypertrophy or poorly preserved intraopera- Hypothermia tive myocardial protection. Patients with Disorders in acid–base balance postoperative decreased ventricular compli- Anxiety ance will have diastolic dysfunction (Salenger Pain et al., 2003; Silvestry, 2008). This complica- Anemia tion often persists for at least 3 hours follow- Rebound adrenergic tone ing CABG (Ekery et al., 2003). If the left ventricle becomes stiff during filling (dias- Source: Brister & Lenkei-Kerwin, 2005. tole), it may not be able to fill completely. As a result, fluid may back up to the lungs, and heart failure may ensue. edema or inadequate coronary blood flow, graft A number of intraoperative and postopera- occlusion or thrombosis from MI or ischemia, tive etiologic factors of ventricular dysfunc- MI from an air embolism or graft vasospasm, tion have been identified. They include and cardiac tamponade (Silvestry, 2008). inadequate myocardial protection during aor- The consequence of diastolic dysfunction is tic cross-clamping, intraoperative pulmonary low CO with a small left ventricle. The hemo- 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 263

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dynamic picture is one of elevated PAOP and Management of RV failure includes provid- low CO. Treatment of diastolic dysfunction ing sufficient preload, reducing right ventric- includes volume administration to maximize ular afterload (pulmonary vascular resistance, preload and administration of vasodilators. PVR), and maintaining systemic blood pres- Patients with diastolic dysfunction from sure. Volume repletion is essential to opti- decreased LV compliance will require a higher mize left heart function. Care must be taken, PAOP to maintain adequate preload than do however, to avoid overdistention of the right patients with a reduced preload from the other ventricle (Khalpey et al., 2008). Inotropic sup- etiologies listed earlier. Because the ventricle port may be required; the key is to use med- has decreased compliance in this case, the ications that provide ventricular support PAOP may be elevated despite the need for without increasing PVR. Milrinone is com- additional preload (Silvestry, 2008; St. Andre & monly used in the treatment of RV failure, as DelRossi, 2005). Infusion of an inotropic agent this agent increases contractility and causes with either a catecholamine (e.g., dopamine) or vasodilation without increasing PVR (Khalpey other agent to augment CO may also be et al., 2008). required. Milrinone, a phosphodiesterase In the case of severe RV failure, inhaled inhibitor, or nicardipine (Cardene®), a calcium nitric oxide or a prostaglandin E infusion channel blocker, may cause relaxation of the may be warranted. These medications cause ventricle and may be of benefit in patients with dilation of the pulmonary vasculature, diastolic dysfunction (Salenger et al., 2003). If thereby reducing PVR (Khalpey et al., 2008; the patient does not respond to traditional Vlahakes, 2005). therapies, an echocardiogram should be obtained to determine the presence of valvular Decreased Myocardial Contractility incompetence or cardiac tamponade (Silvestry, Contractility is the shortening of myocardial 2008). fibers during systole (ventricular emptying) and the force produced by the myocardium to Low Cardiac Output due to Right eject blood. It is evaluated with EF by echocar- Ventricular Failure diography (Massé & Antonacci, 2005). Although most low output failure following Cardiac contractility may be impaired post- cardiac surgery is attributable to LV failure, operatively due to such factors as hypoxia, occasionally the right ventricle fails. Etiology acidosis, electrolyte imbalance, narcotics, of this complication may include ischemia, anesthesia, transient ischemic/reperfusion infarction, or increased PVR. Preexisting con- injury, impaired preoperative function (EF ditions such as pulmonary hypertension, aor- less than 35%), inadequate intraoperative tic stenosis, mitral valve disease, tricuspid myocardial protection, duration and extent of regurgitation, or right ventricular hypertro- postoperative hypothermia, CPB time (espe- phy can also lead to postoperative right ven- cially if longer than 120 minutes), tampon- tricular (RV) failure. Inadequate output of the ade, valve function, or myocardial ischemia or right ventricle leads to decreased filling of the infarction (Khalpey et al., 2003; Massé & left ventricle, LV output, and poor systemic Antonacci, 2005; Salenger et al., 2003; perfusion. The right ventricle then becomes St. Andre & DelRossi, 2005). distended, with RV failure being the ultimate Myocardial function usually declines outcome. The diagnosis of RV failure is based approximately 5 hours after surgery, possibly on the presence of elevated CVP and low as a result of reperfusion from cardio- PAOP and CO (Khalpey et al., 2008). plegia arrest. This effect usually lasts about 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 264

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24 hours, though the duration and extent of impaired ventricular function related to diminished function may be influenced by myocardial stunning is reported to terminate any recent ischemic events, intraoperative within 1–2 days and is not affected by preload course, and degree of dysfunction preopera- or afterload manipulation (Kloner, Przyklenk, & tively (St. Andre & DelRossi, 2005). Decreased Kay, 1994). contractility may require inotropic support Hibernating myocardium is a condition of with vasoactive medications to support car- impaired LV function when the patient is at diac function. Both inotropic and vasodilator rest; it reflects a chronic reduction in blood support with medications such as dobuta- flow. Heart function can be partially or totally mine, dopamine, milrinone, and epinephrine, normalized by improving blood flow or decreas- used alone or in combination, may prove ing oxygen demand (Shavelle, 2006). Myocar- effective in improving cardiac contractility dial hibernation is considered a compensatory (Khalpey et al., 2003; Salenger et al., 2003). or protective mechanism to safeguard the Epinephrine, however, is associated with the capacity and integrity of the myocardium dur- development of temporary but significant ing times of decreased blood flow (Schipke & hyperglycemia, metabolic acidosis, and Birkenkamp-Demtröder, 2001). increased serum lactate when used in the initial 6–8 postoperative hours. These effects Increased Systemic Vascular Resistance usually resolve in 12 hours (St. Andre & (Afterload) DelRossi, 2005). As with preload, right- and left-sided after- In addition to titrating medications accord- load can be evaluated to help determine caring to the patient’s hemodynamic profile, the diac performance. Right-sided afterload is ICU nurse must monitor for signs and symp- reflected by PVR; left-sided afterload is toms of inadequate perfusion related to the reflected by SVR. Most of the discussion in impaired contractility. Evaluation of cardiac this section refers to left-sided afterload. index, hypotension, mottling, end-organ dys- Afterload is determined by intraventricular function (e.g., inadequate urinary output), systolic pressure and the thickness of the ven- and presence of a metabolic acidosis is vital. tricular wall. The latter factor is minimally Urinary output may be increased in the initial affected with cardiac surgery. SBP will have postoperative period, however, so it is consid- the greatest effect on afterload and, therefore, ered a less reliable indicator of poor perfusion SV and myocardial oxygen demand. By (St. Andre & DelRossi, 2005). decreasing afterload, CO will improve (Salenger et al., 2003). Myocardial Stunning and Hibernation Increased SVR is also often a compensatory Cardiovascular research has led to the identifi- result of the SNS response to low CO. cation of two important phenomena: myocar- Increased SVR may be poorly tolerated in a dial stunning and myocardial hibernation. patient with already poor myocardial function. Myocardial stunning is a period of impaired Hypertension occurs in as many as 60% of contractility following temporary ischemia, in postoperative patients (Talmor & Lisbon, which the dysfunction persists despite return of 2005) and is often associated with vasocon- blood flow (Shavelle, 2006; Wang et al., 2003). striction (Silvestry, 2008). Development of Myocardial stunning may occur after CPB, hypertension, vasoconstriction, or both may and postoperative cardiac dysfunction (i.e., be related to decreased oxygen levels in the decreased ventricular function) is often attrib- muscle with concomitant metabolic acidosis uted to its effects (Wang et al., 2003). The or inflammatory responses to CPB (Salenger 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 265

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et al., 2003; Silvestry, 2008). Other potential a vasoconstrictor agent such as phenylephrine causes of increased afterload include or norepinephrine (Khalpey et al., 2008; hypothermia, hypovolemia, hypercarbia, Salenger et al., 2003; Silvestry, 2008). If inadequate rewarming, volume overload, car- patients do not respond to this therapy, vaso- diogenic shock, pain, and anxiety. The latter pressin administration may be attempted. two etiologies result from increased SNS Finally, methylene blue administration may stimulation (Khalpey et al., 2008; Talmor & be considered, as this agent inhibits nitric Lisbon, 2005). If vasoconstriction is extreme, oxide production (Aranki et al., 2008; Sil- the patient is at risk of developing life-threat- vestry, 2008). ening hypertension and decreased CO (Khalpey et al., 2008). Mechanical Issues Treatment of increased afterload may entail administration of vasodilator therapy A number of mechanical issues can con- with medications such as sodium nitroprus- tribute to the development of hemodynamic side, nitroglycerin (Tridil®), or milrinone. compromise in the postoperative cardiac sur- Sodium nitroprusside is the treatment of gery patient. These complications include car- choice (Silvestry, 2008; St. Andre & DelRossi, diac tamponade, coronary artery graft spasm, 2005). Given that vasodilators cause a prosthetic valve regurgitation, pneumotho- decrease in preload, concomitant administra- rax, and hemothorax (Silvestry, 2008). tion of fluids may be required to maintain Cardiac Tamponade adequate intravascular volume during their use. As the potential for abrupt hypotension During cardiac surgery, the pericardial sac is exists when nitroprusside is administered, fre- entered and is usually not sutured back quent blood pressure monitoring is essential, together before chest closure. This leaves a especially during rewarming (Silvestry, 2008). communication between the heart and medi- In severe cases of LV failure, IABP counterpul- astinum, which can lead to the potential accu- sation may be used to reduce afterload. IABP mulation of blood or fluid (Lemmer, therapy is discussed in detail in Chapter 10. Richenbacher, & Vlahakes, 2003; St. Andre & DelRossi, 2005). The accumulation compresses the atria, restricts venous return to the Decreased Systemic Vascular Resistance heart and ventricular filling, and results in a While an increase in afterload is common fol- decrease or cessation of preload, causing a lowing cardiac surgery, some patients develop potential precipitous fall in CO (Massé & a decreased SVR postoperatively. This condi- Antonacci, 2005). Early tamponade is usually tion, which is also referred to as vasodilatory a result of persistent mediastinal bleeding not shock, is associated with a CO that is either being evacuated by chest tubes. normal or increased (Aranki et al., 2008). The Cardiac tamponade is one of several poten- incidence of vasodilatory shock is reported to tial complications that may result in ventricular range from 5% to 8%. Patients who are at dysfunction (Silvestry, 2008), and typically higher risk for the development of a occurs within the first 12 postoperative hours decreased SVR are those who have a low EF (St. Andre & DelRossi, 2005). Diagnosis may (less than 35%) and those with end-stage be difficult because hypotension, tachycardia, heart failure requiring assist device insertion. and elevated filling pressures are common sce- Vasodilatory shock may be caused by an narios in most immediate postoperative inflammatory response to CPB (Silvestry, cardiac surgery patients. In addition, some of 2008). Its treatment entails administration of the other characteristic symptoms of cardiac 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 266

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tamponade (e.g., muffled heart sounds, pul- Table 13–3 requires prompt intervention, sus paradoxus, and neck vein distention) are including a bedside echocardiogram (Talmor not helpful in the cardiac surgery patient. & Lisbon, 2005). The patient may need to While the patient may experience equaliza- return to the OR for clot evacuation or bleed- tion of intracardiac pressures (CVP equal with ing site repair. When an echocardiogram is PAOP or PAD), other signs and symptoms not feasible or there is impending cardiac will likely suggest the presence of cardiac tam- arrest, emergency mediastinal exploration is ponade prior to this manifestation (St. Andre warranted for accurate diagnosis (Mullen- & DelRossi, 2005). Heightened awareness for Fortino & O’Brien, 2008; Talmor & Lisbon, tamponade should be present when the 2005). Box 13–1 lists the steps undertaken in patient develops the signs and symptoms an emergency resternotomy. listed in Table 13–3. Coronary Vasospasm Continuous hypotension that does not respond to fluid administration and the pres- A frequently unrecognized cause of sudden ence of signs and symptoms listed in cardiovascular collapse in the early postoperative period is coronary vasospasm. This complication usually presents itself as acute Table 13–3 Signs and Symptoms hypotension, ST-segment elevation in multi- of Cardiac Tamponade ple leads, and low CO. All types of coronary grafts are implicated in the development of Sudden decrease or cessation of mediastinal coronary vasospasm—saphenous vein grafts, bleeding arterial conduits, and normal cardiac vessels Dyspnea alike (St. Andre & DelRossi, 2005). The etiol- Low cardiac output with hypotension ogy of coronary graft spasm is not completely Narrowing pulse pressure understood. Several hypotheses have proposed Inappropriately fluctuating MAP release of platelet thromboxane A2, increased alpha-adrenergic tone, hypothermia, or elec- Increased central venous pressure trolyte imbalances of magnesium or calcium Low cardiac output/index as possible causes (Lemmer et al., 2003). Sudden oliguria Vasospasm usually resolves on its own. If it Altered mental status does not, treatment is aimed at supporting Diaphoresis hemodynamic instability and administration Dysrhythmias, including tachycardia of vasodilators (Saxena, Konstantinov, Cyanosis or pallor Koniuszko, Singh, & Newman, 2006). Anxiety Myocardial Ischemia and Infarction Restlessness Low-voltage QRS on ECG Myocardial ischemia, whether transient or leading to MI, may occur after cardiac surgery. Electrical alternans on ECG The risk of postoperative myocardial ischemia “Water bottle heart” and cardiac or MI is greater given the increased age, enlargement on chest radiograph comorbidities, extent of coronary artery dis- Hepatomegaly ease, and degree of LV dysfunction that car- ECG ϭ electrocardiogram; MAP ϭ mean diac surgery patients tend to have prior to arterial pressure. surgery (Moosbauer, Hofer, & Gombotz, Sources: Kaplow & Reid, 2006; St. Andre & DelRossi, 2007). Specific risk factors for MI include car- 2005; Talmor & Lisbon, 2005. diomegaly, long CPB time, redo surgery, and 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 267

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Box 13–1 Emergency Resternotomy patient’s risk for developing ischemia second- Procedures ary to an imbalance between oxygen supply and demand. Increased SNS activity is also 1. Alert the surgeon and operating team. associated with increased platelet aggregation 2. Obtain an emergency chest opening tray. and decreased fibrinolytic activity, both of 3. Obtain an electrocautery device, and which contribute to coronary thrombosis apply the ground pads to the patient’s development (Aboyans, Frank, Nubret, skin to prevent a Bovie burn. 4. Set up sterile suction. Lacroix, & Laskar, 2008). 5. Obtain personal protective equipment, The incidence of postoperative MI has been sterile gowns, antiseptic solution, and reported to range from 7% to 26% (Aboyans et drapes. al., 2008; Fransen, Diris, Maessen, Hermens, 6. Remove the dressing. & van Dieijen-Visser, 2002; Gilchrist, 2001). 7. Pour antiseptic on the patient’s skin. The incidence specifically for patients who 8. Place sterile towels on the patient’s skin. have undergone CABG is reported to be in the 9. Assist the surgeon by supplying wire cutters or a scalpel. range of 2% to 4% (Silvestry, 2008). Patients 10. Open the wound down to the sternum may be started on aspirin, clopidogrel, or with the scalpel. both within the initial few postoperative 11. Cut the sternal wires with the wire hours to reduce prevalence of MI (St. Andre & cutters. DelRossi, 2005). 12. Place the sternal retractor to expose the Mechanisms for myocardial ischemia heart. include reperfusion injury from poor myocar- 13. Assist with controlling bleeding and suctioning, if needed. dial protection with cardioplegia, incomplete 14. Assist in irrigation of mediastinum with revascularization, coronary vasospasm, or warm saline or antibiotics. coronary artery or intracoronary embolism 15. Assist in closing the sternum. (Khalpey et al., 2008). MI may also occur in 16. Apply a dressing to the incision, securing the early postoperative period related to clo- the epicardial pacer wires and chest tube sure of a bypass graft (Lemmer et al., 2003). sites. The diagnosis of MI is initially determined 17. Assess the patient’s cardiovascular and by ECG changes (e.g., the presence of Q waves hemodynamic status every 15 minutes until stable. or ST elevation) and the presence of elevated 18. Monitor coagulation and hematology cardiac markers (troponin I or creatine kinase laboratory studies as needed. [CK-MB]). ST segment changes are common in 19. Monitor chest tube drainage. the immediate postoperative period after cardiac surgery and are usually not clinically significant. Other suspect ECG findings include CABG combined with another cardiac surgical new bundle branch block, ventricular dys- procedure (Aranki et al., 2008). rhythmias, or complete heart block (Khalpey In one study, predictive factors for postop- et al., 2008). Development of new Q waves is erative MI included female gender, combined indicative of MI even in the presence of normal valvular surgery and preoperative renal fail- cardiac markers. When evaluating cardiac ure, LVEF less than 40%, pulse pressure markers, it is important to account for the ele- greater than 70 mm Hg, and faster heart rate. vation in the patient’s baseline levels due to the The last factor is felt to be related to the cor- surgical injury to the heart (Wu, 1998). relation between heart rate and sympathetic Troponin I is a myocardial protein that is a tone. As the SNS is highly activated during very sensitive and specific marker for myocar- cardiac surgery, this condition increases the dial damage. Elevation of troponin I to more 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 268

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than 15–20 mcg/L within 12 hours and a Cardiac Arrest peak of more than 35 mcg/L at 24 hours are Cardiac arrest is the most serious complica- indicative of MI (Gensini et al., 1998). Follow- tion in postoperative cardiac surgery patients. ing an MI, troponin I levels peak in 36 hours Low CO and sepsis are the leading causes of and remain elevated longer than CK-MB lev- cardiac arrest in this population. Mechanical els (Lemmer et al., 2003). Of note, troponin factors such as tamponade and coronary levels are usually elevated after cardiac sur- artery graft occlusion are also causes of sud- gery, making diagnosis of MI difficult in these den cardiac arrest in hemodynamically stable patients. For this reason, it has been recom- patients during the immediate postoperative mended that troponin I levels not be used for period (Anthi et al., 1998). definitive MI diagnosis after cardiac surgery Basic and advanced cardiac life support (Abramov et al., 2006). protocols set forth by the American Heart CK-MB levels can also be used in the diag- Association should be initiated in any patient nosis of MI. Some release of CK-MB isoen- who experiences cardiac arrest (St. Andre & zymes occurs in most patients who undergo DelRossi, 2005). As resuscitation efforts are cardiac surgery. However, if a cardiac surgery started, evaluation for potential causes— patient has an intraoperative MI, the CK-MB including those unique to cardiac surgery peak level will be higher and the elevation will patients—should begin. Checking the posi- last longer. Data suggest that in a patient who tion of the endotracheal tube, signs of hypov- has undergone CABG surgery, peak postoper- olemia, patient temperature, chest tube ative CK-MB levels of less than 20 U/L with drainage, proper ventilator functioning, no ECG changes indicate no significant results from chest radiograph (for widened myocardial injury. If CK-MB levels exceed 50 mediastinum, tension pneumothorax, or tam- U/L or are five times the upper limit of nor- ponade), arterial blood gas, and electrolytes mal or greater, MI is suggested (Aranki et al., may help identify the underlying cause of car- 2008; Lemmer et al., 2003). Most recent data diac arrest. Noting the infusion rates of suggest that troponin levels are more useful vasoactive agents may provide additional for detecting necrosis and should be used to clues. Treating and reversing the cause is the either supplement or replace CK-MB mea- priority here, with concomitant high-quality surements (Aranki et al., 2008). cardiopulmonary resuscitation (CPR) being a Data also suggest that troponin T may be pivotal part of this care. used for up to 2 days postoperatively to diag- Many patients will experience pulseless nose an MI. In one study, CK-MB levels were electrical activity in the postoperative cardiac almost normal by day 2 after cardiac surgery surgery scenario (St. Andre & DelRossi, 2005). (Abdal Aziz, Ali, Roberts, & Al Khaja, 2000). If, however, the underlying rhythm requires Patients with suspected MI or persistent defibrillation, this procedure (which is out- ischemia follow the same course as uncompli- lined in Box 13–2) can be accomplished with cated postoperative patients, with beta block- internal defibrillation. ade and intravenous nitroglycerin being Adequate cardiac function has been identi- administered to them if the blood pressure fied as the most critical factor affecting recov- permits (Khalpey et al., 2008; Lemmer et al., ery from cardiac surgery (Silvestry, 2008). 2003). Serial troponin and CK-MB levels Continuous monitoring of the patient’s should be obtained and monitored as well as hemodynamic status by the ICU nurse is 12-lead ECG for the presence of new Q waves. essential. Evaluation of the patient’s cardiac IABP therapy is suggested to diminish rate and rhythm, blood pressure, hemody- inotrope use, infarct size, and myocardial oxy- namic profile data, chest tube drainage, uri- gen demand (Khalpey et al., 2008). 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 269

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Box 13–2 Internal Defibrillation Preoperative identification of patients Procedure with pulmonary risk factors should facilitate provision of proper perioperative interven- 1. Follow the procedure for open tion. Presence of preoperative risk factors sternotomy. such as tobacco use, age older than 65 years, 2. Follow the procedures for advanced obesity, diabetes, preexisting pulmonary dis- cardiac life support (ACLS). ease (e.g., COPD), heart failure, and LV dys- 3. Prepare the defibrillator for internal defibrillation by gathering sterile internal function place the patient at higher risk for defibrillation paddles. postoperative pulmonary complications 4. Assist with positioning the internal (Mullen-Fortino & O’Brien, 2008). Identifi- paddles on the heart. cation and early intervention can prevent the a. One paddle is placed over the right incidence of most postoperative pulmonary atrium or right ventricle. dysfunction (Margereson & Riley, 2003). b. The other paddle is placed over the Cardiac surgery patients are especially apex of the heart. 5. Charge the defibrillator paddles (5–20 prone to pulmonary complications as a joules). result of several procedure-related factors: 6. Verify providers are clear of the patient use of general anesthesia, need for a median and all equipment before defibrillation. sternotomy incision, cooling for myocardial 7. Assess the patient’s cardiac rhythm for protection, use of CPB, and harvest of the conversion and presence of pulse. internal mammary artery (IMA), which 8. If needed, repeat the defibrillation, requires pleural dissection (Wynne & Botti, following advanced cardiac life support guidelines. 2004). Developing an understanding of the 9. Assist with transport to the operating postoperative changes in pulmonary func- room or closure at the bedside. tion, routine pulmonary management, and 10. Monitor the patient’s neurologic, contributory factors of pulmonary dysfunc- cardiac, and pulmonary status until tion allows for the early identification and stable. management of such problems.

Postoperative Effects on Pulmonary Function nary output, and lab data, combined with ongoing patient assessment, will provide the The development of pulmonary dysfunction valuable data required to titrate vasoactive after cardiac surgery is associated with infusions to help attain and maintain optimal inconsistencies in gas exchange, ventilation/ hemodynamic function. perfusion mismatch, and pulmonary shunting. Patients will often manifest signs including shortness of breath and decreased oxygen ■ PULMONARY COMPLICATIONS saturation (Mullen-Fortino & O’Brien, 2008). Postoperative pulmonary complications are Cardiac surgery patients are at risk for noted to be primary contributors to increased developing postoperative pulmonary compli- morbidity for the cardiac surgery patient (Sil- cations due to increased age, comorbidities, vestry, 2008). The incidence of pulmonary and the surgical procedure itself. In one dysfunction following CABG ranges between study, patients who were hypoalbuminemic 30% and 60% (Mullen-Fortino & O’Brien, had a higher incidence of pulmonary dysfunc- 2008). Most patients are able to tolerate pul- tion, nosocomial infections including pneu- monary dysfunction without major disrup- monia, and increased duration of mechanical tion in oxygenation and ventilation. ventilation than patients with normal albumin 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 270

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levels (Rady, Ryan, & Starr, 1997). In a study group (29.5 ± 3.8) had the highest incidence of the “oldest old” patients, the effect of an of pulmonary complications following car- elevated BMI was evaluated on development diac surgery (Maurer et al., 2002). Table of complications. Patients in the lowest BMI 13–4 lists other factors contributing to group (20.8 ± 1.6) and the highest BMI higher risk of pulmonary dysfunction.

Table 13–4 Factors Contributing to Development of Pulmonary Dysfunction after Cardiac Surgery

Contributing Factors Effects on Pulmonary System

General anesthesia Decreased central respiratory drive leading to Paralytics decreased use of respiratory muscles. Narcotics Upward shift of diaphragm. Supine positioning Chest wall relaxation. Changes in compliance of chest wall.

Cardiopulmonary bypass Pulmonary edema from fluid overload and hemodilution. Interstitial pulmonary edema from a systemic inflammatory response, which produces capillary leak. Complement activation, release of cytokines, and neutrophil activation, which cause increased endothelial permeability. Insufficient alveolar distention to activate production of surfactant, which may lead to alveolar collapse, retention of secretions, and atelectasis.

Cooling for myocardial protection Phrenic nerve injury.

Median sternotomy incision and chest tubes Chest wall splinting, which reduces the patient’s ability to take deep breaths.

Use of IMA for coronary artery bypass conduit Use of IMA requires pleural dissection, which causes a potential decrease in chest wall compliance.

Sternal or thoracotomy incisional pain Decreased respiratory muscle use. Obesity Age Diaphragmatic injury Smoking history History of COPD, heart failure

IMA = internal mammary artery. Sources: Taggart, 2000; Wynne & Botti, 2004. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 271

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Atelectasis Patients with small pleural effusions (less Atelectasis occurs in the dependent parts of than 500 mL) are usually asymptomatic. Small the lungs, most commonly in the left lower pleural effusions will likely resolve on their lobe, in most patients who have had anesthe- own (Mullen-Fortino & O’Brien, 2008; Talmor sia. Incidence is reported to be as high as 70% & Lisbon, 2005). Preexisting lung disease and of cardiac surgery patients, and the complica- moderate to large effusions (occupying more tion typically occurs secondary to single-lung than 50% of the lung) may cause dyspnea. In ventilation and deliberate intraoperative lung this situation, a thoracentesis or chest tube collapse as part of the procedure (Silvestry, insertion is indicated (Mullen-Fortino & 2008). The development of atelectasis is asso- O’Brien, 2008; Talmor & Lisbon, 2005). ciated with decreased lung compliance, impaired oxygenation, and development of Phrenic Nerve Injury some degree of lung injury (Weissman, 2004). Phrenic nerve injury with diaphragmatic dys- These adverse effects continue into the post- function has been documented in 10–85% of operative period and can have a substantial postoperative cardiac surgery patients. The impact on patient recovery. primary etiology of this complication is cold Techniques or devices that encourage injury to the phrenic nerve from use of iced patients to inspire deeply are beneficial. The slush in the pericardial region (Dimopoulou aim of therapy is to produce a large and sus- et al., 1998). The phrenic nerve may also be tained increase in the transpulmonary pres- injured in the takedown of the IMA (Tripp & sure, thereby distending the lung and Bolton, 1998). Unilateral nerve injuries pro- reexpanding the collapsed alveoli. Several duce few respiratory symptoms, and patients methods, such as deep breathing exercises, can usually be extubated without difficulty. incentive spirometry, and chest physiother- In contrast, bilateral phrenic nerve injury may apy, have been shown to be helpful in reex- cause paradoxical breathing, tachypnea, and pansion of the collapsed lung units (Wynne & carbon dioxide retention when attempts are Botti, 2004). Vigorous pulmonary toileting made at extubation. Chest radiograph may along with early ambulation are generally reveal an elevated hemidiaphragm at end- effective therapies for the postoperative car- expiration with spontaneous ventilation; the diac surgery patient who is recovering from elevation will not be apparent while the atelectasis. patient is mechanically ventilated owing to the effects of the positive pressure ventilation. Pleural Effusion Treatment may involve plication of the Postoperative pleural effusions, which com- diaphragm, which attempts to stabilize the prise a collection of fluid in the pleural space, diaphragmatic muscle and prevents paradoxi- are common in postoperative cardiac surgery cal motion with breathing (Mertens, 2006). patients, occurring in 41–87% of these indi- Phrenic nerve injury is discussed in more viduals (Mullen-Fortino & O’Brien, 2008). detail in Chapter 11. Typically, the effusion develops in the immediate postoperative period (the first 24 hours) Pneumothorax (Talmor & Lisbon, 2005) and can be visual- A pneumothorax may occur after cardiac sur- ized on chest radiograph. The effusion is usu- gery because of direct injury to the lung dur- ally present in the left lower lobe and is small ing surgery, central venous cannulation, or in size, but can also be bilateral (Heidecker & barotrauma during positive pressure ventila- Sahn, 2006). tion. It is usually noted in the immediate 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 272

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postoperative period and is considered a surgery. Prolonged mechanical ventilation is residual effect of surgery (Talmor & Lisbon, often necessitated by cardiac dysfunction, 2005). The overall incidence of pneumothorax continual postoperative bleeding, neurologic after cardiac surgery is approximately 1–2%, complications, acute renal failure, surgical although the incidence following CABG with reexploration, or need for blood transfusions IMA harvesting is as high as 5.3% (Weissman, (Weissman, 2004). In these patients, contin- 2004). The incidence may also increase in ual attempts at extubation are made; failure patients with bullous lung disease or in those to wean after 24 hours is usually due to diffi- requiring high levels of positive end-expiratory culty with oxygenation, ventilation, or both. pressure (PEEP). A pneumothorax typically When weaning failure occurs, cardiac and vol- presents on the left side of the chest and ume status are optimized, metabolic abnor- occurs when the left parietal pleura is opened malities corrected, narcotics and sedation and the left IMA is dissected. This complica- reduced, and nutrition is initiated. tion is managed by connecting the chest tube One important goal in the mechanically

to suction (Talmor & Lisbon, 2005). ventilated patient is reduction of the FiO2 to A tension pneumothorax can develop less than 0.50. Prolonged exposure to FiO2 quickly in patients who are placed on greater than 0.50 has been shown to cause mechanical ventilation. This complication harmful effects on the lungs (e.g., through usually arises after the patient develops a production of oxygen free radicals); for this

right pneumothorax if the right parietal reason, using the lowest FiO2 to achieve an pleura is accidentally cut (Talmor & Lisbon, acceptable oxygen saturation is important 2005). In this situation, the patient acutely (Peruzzi & Shapiro, 2002). Addition of PEEP

decompensates. Although breath sounds may may allow for a decrease in FiO2 and improve be diminished, it may be difficult to assess oxygenation. Patients who develop fluid over- given ventilator sounds and various alarms in load may need aggressive diuresis over a the unit. Other signs and symptoms of ten- course of days to decrease interstitial lung sion pneumothorax can include distended water or pleural effusion. Patients who are neck veins, hypotension, and tracheal devia- ventilated for 10–14 days with multiple tion away from the collapsed lung. If the unsuccessful attempts at weaning may patient is hemodynamically unstable and a require a tracheostomy. In one study of tension pneumothorax is suspected, decom- patients requiring prolonged mechanical ven- pression with a 16-gauge needle at the second tilation, 99% were ultimately successfully intercostal space, midclavicular line, is indi- weaned and 85% were discharged (Engoren, cated. A rush of air and an improvement in Buderer, & Zacharias, 2000). Care of the hemodynamics confirm the diagnosis patient requiring prolonged ventilation is (Goodrich, 2005). A chest radiograph should addressed in detail in Chapter 11. be obtained to assess the involved structures and the severity of the tension pneumotho- Acute Respiratory Distress Syndrome rax. Treatment also includes placement of a and Acute Lung Injury chest tube, usually at the fifth intercostal Acute respiratory distress syndrome (ARDS) space, anterior axillary line, for the residual is an extreme form of acute lung injury (ALI) pneumothorax (Weissman, 2004). that is characterized by inflammation of the lung parenchyma and increased microvascu- Prolonged Mechanical Ventilation lar permeability, which causes leakage of fluid A small number of patients will require pro- into the alveolar space, hypoxemia, increased longed mechanical ventilation after cardiac work of breathing, and pulmonary infiltrates 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 273

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on chest radiograph. Both ARDS and ALI notomy or thoracotomy sites are at risk for usually occur after the first 24 hours follow- developing pneumonia if the pain interferes ing cardiac surgery (Talmor & Lisbon, 2005). with effective coughing and deep breathing ARDS is an uncommon complication after (Silvestry, 2008). cardiac surgery but can be associated with a One key way to prevent postoperative high mortality rate—as high as 15% to 70% pneumonia is to follow evidence-based guide- (Talmor & Lisbon, 2005). The reported inci- lines for managing ventilator-associated dence of ARDS following cardiac surgery is pneumonia. These guidelines can be accessed less than 2%, however (Silvestry, 2008). Previ- from the American Association of Critical- ous cardiac surgery, shock, and number of Care Nurses’ Web site, in the “Practice Alerts” blood products received are important predic- section. tive factors for this complication (Milot et al., 2001). CPB has been implicated as a causative ■ HEMATOLOGIC COMPLICATIONS factor in ARDS because the extracorporeal circulation stimulates a systemic inflamma- Bleeding and Coagulopathies tory response and release of cytokines and Bleeding is a common postoperative scenario endothelial-derived factors (e.g., nitric oxide). in the cardiac surgery patient population. The Treatment of ARDS is mainly supportive, incidence of excessive bleeding is reported to but maintaining adequate oxygenation is the range from 3% to 14%, with reexploration primary goal. The use of smaller tidal vol- being required in as many as 5% of patients umes (6 mL/kg) and PEEP have been associ- (Bowman et al., 2008). The etiology of post- ated with lower mortality (Sakr et al., 2005). operative bleeding may be surgical, related to Data support the use of smaller tidal volumes platelet dysfunction from exposure to CPB in patients with established ALI or ARDS. circuitry, or associated with inadequate ARDS specifically in cardiac surgery patients heparin reversal at the end of CPB (Mullen- has not been studied, however. Data are also Fortino & O’Brien, 2008; Talmor & Lisbon, not available on the efficacy of smaller tidal 2005). Excessive bleeding is defined as loss of volumes to prevent these complications from more than 500 mL of blood in the first post- developing (Talmor & Lisbon, 2005). operative hour. If excessive bleeding is present, the source Pneumonia must be quickly identified. Possible sources Postoperative pneumonia may develop after include, but are not limited to, anastomoses the first 24 hours following cardiac surgery. sites—that is, a branch of the saphenous veins, Patients at high risk are those who require IMAs, cannulation sites, or sternal wire sites. mechanical ventilation for more than 48 If the bleeding is quite excessive or an hours or who develop diaphragmatic dysfunc- anatomic source has been identified or sus- tion (Talmor & Lisbon, 2005). As discussed in pected, treatment entails emergently return- Chapter 11, patients with persistent LV failing the patient to the OR (Salenger et al., ure are also at higher risk for pneumonia. Per- 2003). sistent LV failure after cardiac surgery An estimated 30% of patients who undergo ultimately results in extravasation of fluid CABG require blood transfusion (Silvestry, into the alveoli. Interstitial fluid in the alveoli 2008). Cardiac surgery patients are transfused decreases compliance, increases secretions, with 10–25% of all blood products used in the and facilitates atelectasis, which may then United States every year (Whitlock, Crowther, & progress to pneumonia (Salenger et al., 2003). Ng, 2005). Preoperative risk factors for bleed- Patients with incisional pain from ster- ing include use of pharmacologic agents that 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 274

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cause platelet dysfunction (e.g., ASA, clopidi- Table 13–5 Potential Causes of ® ® grel [Plavix ], dipyridamole [Aggrenox ], Bleeding in the Postoperative Cardiac ® abciximab [ReoPro ], and tirofiban [Aggras- Surgery Patient tat®]) and agents that prevent clotting (e.g., ® warfarin [Coumadin ], heparin, enoxaparin Surgical bleeding ® [Lovenox ]). Other patients at higher risk for Platelet dysfunction/depletion postoperative bleeding include those with Hypotension inherited disorders of coagulation (e.g., Von Deficiency/depletion of plasma clotting Willebrand’s disease, hemophilia) or acquired factors coagulopathies (e.g., from end-stage renal dis- Residual effects of heparin due to incomplete ease, hepatic impairment) (Adams, Manson, reversal with protamine Turner, Sindram, & Lawson, 2007). In these Hemodilution cases a hematologist should be involved with the case prior to surgery. Hypothermia Excessive postoperative bleeding has also Increased fibrinolytic activity been associated with the following risk fac- Consumption coagulopathy

tors: previous cardiac surgery, preoperative Sources: Mullen-Fortino & O’Brien, 2008; Silvestry, cardiogenic shock, emergency cardiac surgery, 2008; St. Andre & DelRossi, 2005; Talmor & Lisbon, female gender, small BMI, older age, periph- 2005. eral vascular disease, lower preoperative hemoglobin, and renal insufficiency (Maurer should return to the OR for exploration. Typ- et al., 2002; Silvestry, 2008, Whitlock et al., ical indications for surgical reexploration are 2005). Patients who have been identified as blood loss greater than 200 mL/hr for being at higher risk for requiring blood trans- 4 hours, 300 mL/hr for 3 hours, 400 mL/hr for fusions typically have the following character- 2 hours, or 500 mL/hr for 1 hour (St. Andre & istics: (1) advanced age; (2) preoperative DelRossi, 2005). anemia or small body size; (3) preoperative Packed red blood cells, platelets, cryopre- use of antiplatelet or antithrombotic drugs; cipitate, and fresh frozen plasma should be (4) redo operations or complex procedures; administered to correct abnormalities in (5) emergency operations; and (6) noncardiac hemoglobin, platelets, fibrinogen, and coagu- comorbidities (Ferraris et al., 2007). Table 13–5 lation factors, respectively, if the cause is lists surgery-specific factors that can cause thought to stem from an acquired coagulopa- excessive bleeding in the postoperative cardiac thy. Medications that improve platelet func- surgery patient. tion (e.g., desmopressin [DDAVP®]) or prevent Postoperative bleeding in the ICU setting is fibrinolysis (e.g., aminocaproic acid [Amicar®]) categorized as either surgical (bleeding vessel, may also help in improving postoperative anastomosis, or other suture line) or nonsur- coagulopathy (Levi & Mannucci, 2007; Sil- gical (coagulopathy). General guidelines for vestry, 2008). Protamine sulfate is adminis- excessive mediastinal bleeding are character- tered to neutralize the heparin given during ized by continuous chest tube output of CPB; its potential side effects include brady- greater than 200 mL/hr for 2 hours. When cardia, hypotension, and pulmonary vasocon- bleeding exceeds these guidelines, efforts striction secondary to a non-immunologic must be made to determine whether the reaction (St. Andre & DelRossi, 2005). Prota- bleeding is correctable by replacement of mine sulfate reactions are described in detail coagulation factors or whether the patient in Chapter 12. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 275

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A newer medication that may help in the caused by platelet-activating, heparin-depend- patient with a perioperative coagulopathy is ent antibodies. The platelet activation effect factor VIIa. In the past, recombinant activated leads to excessive thrombin generation, which factor VII was used only for treatment of evolves into the hypercoagulable state. HIT bleeding episodes in patients with deficiencies develops in approximately 1% of all inpatients of factor VII or IX or hemophilia who devel- receiving heparin, with its incidence depend- oped bleeding following an invasive proce- ing on heparin type, length of treatment, and dure. This therapy works by expediting patient population (rates are higher in surgi- platelet activation and ultimate fibrin clot cal patients than in medical patients) (Adams formation (Bowman et al., 2008). Current evi- et al., 2007). Patients undergoing cardiac sur- dence suggests that factor VIIa may be helpful gery are at a higher risk for HIT secondary to in achieving hemostasis in cardiac surgery the large systemic dose and long exposure to patients, thereby reducing transfusion unfractionated heparin required for intraop- requirements (Enomoto & Thorborg, 2005). erative systemic anticoagulation (Selleng, After deficiencies in coagulation factors are Markentin, & Greinacher, 2007). corrected, if bleeding persists (greater than The diagnosis of HIT should be considered 300 mL/hr for 2 hours), urgent reexploration when the platelet count falls to less than may be warranted. In one study, administra- 150,000 mm3 or by greater than 50% of the tion of recombinant activated factor VII baseline count between 5 and 14 days of expo- resulted in a significant decrease in chest tube sure. Laboratory testing with platelet factor- output, blood and blood product administra- 4/heparin enzyme-linked immunosorbent tion, and need for reexploration. Reported assay (ELISA) antibody and serotonin release incidence of thrombosis in this patient group assay are necessary to identify whether the was 11.1% (Bowman et al., 2008). patient has acquired the antibodies (Levy & Hursting, 2007). Heparin-Induced Thrombocytopenia Clinical signs and symptoms may include Thrombocytopenia affects some 23–41% of all venous or arterial thromboses and skin lesions. critically ill patients (Napolitano, Warkentin, Correlation of laboratory data with clinical Almahameed, & Nasraway, 2006). This condi- symptoms is important for an accurate diag- tion has numerous etiologies in cardiac sur- nosis. When HIT is suspected, all heparin gery patients. Factors such as effects of the products must be discontinued, including use CPB circuitry (e.g., mechanical destruction of of heparin-coated vascular access catheters. A platelets), hemodilution, platelet dysfunction, non-heparin anticoagulant—such as arga- depletion of platelets, intravascular devices, troban, a direct thrombin inhibitor to prevent use of IABP therapy, and effects of medica- new thrombosis—should be administered, even tions (e.g., antibiotics, antiarrhythmics) are when confirmatory lab results are not yet avail- common causes of thrombocytopenia in this able (Cypher, 2006). Careful and thorough population. A multitude of medications used assessment for areas of new thrombosis, evalu- in the cardiac surgery setting can also cause ation of skin temperature, color, CRT, sensa- thrombocytopenia. One medication of signif- tion, and peripheral pulses is essential. icance is heparin, which is used to counteract Ongoing evaluation for signs and symptoms exposure of the blood to the surfaces of the of stroke, MI, pulmonary embolism, and renal CPB machines (Matthai, 2005). impairment is equally necessary. Heparin-induced thrombocytopenia (HIT) Postoperative care should include use of is a prothrombotic disorder of coagulation measures to prevent venous thrombotic 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 276

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events, including early mobility (ambulation renal perfusion and subsequently lead to if possible), isometric exercises, sequential postoperative renal failure (Mehta et al., compression devices, graduated compression 2006). stockings, or combinations of these interven- Administration of renal dose dopamine tions (Mullen-Fortino & O’Brien, 2008). remains controversial, as data do not support improved survival or prevention of renal failure with this therapy. Efficacy data on the use ■ RENAL COMPLICATIONS of dopaminergic-receptor agonists (e.g., The incidence of postoperative renal compli- fenoldopam [Cloropam®] and dopexamine cations is reported as high as 30% (Mullen- [Dopacard®]) are inconsistent. Studies inves- Fortino & O’Brien, 2008; Silvestry, 2008; tigating the use of diuretics (loop or osmotic) Talmor & Lisbon, 2005). Renal failure has have failed to demonstrate improved survival; been correlated with poor quality of life, a indeed, use of these medications may place higher mortality rate, and a longer length of the patient at greater risk for renal failure stay (LOS). development by exacerbating any existing Preoperative risk factors for development of reduction in preload (Talmor & Lisbon, renal failure include poor cardiac function, 2005). type I diabetes, advanced atherosclerosis, The ICU nurse plays a pivotal role in help- increased age, moderate to advanced heart ing to prevent postoperative renal dysfunc- failure, prior revascularization or CPB proce- tion. Prevention can best be accomplished dure, preoperative hyperglycemia (greater by maintaining adequate renal perfusion than 300 mg/dL), decreased creatinine clear- through optimization of preload and CO ance, hypoalbuminemia, and elevated creati- (Talmor & Lisbon, 2005). Another preven- nine levels (1.4–2 mg/dL). Intraoperative risk tive measure is avoiding administration of factors include prolonged CPB time (3 hours nephrotoxic agents whenever possible or longer), use of contrast agents, and ventric- (Silvestry, 2008). Collaboration with the ular dysfunction (Mullen-Fortino & O’Brien, physician and critical care pharmacist to 2008; Rady et al., 1997; Silvestry, 2008; Talmor determine whether use of alternative thera- & Lisbon, 2005). Development of renal failure pies, such as angiotensin-converting enzyme is believed to be related to renal artery vaso- (ACE) inhibitors or aminoglycosides, is fea- constriction, intraoperative hypothermia, and sible as indicated. loss of blood flow while on CPB (Silvestry, 2008). Fortunately, only a small percentage ■ (1% to 5%) of patients with postoperative renal GASTROINTESTINAL failure requires dialysis or other renal replace- COMPLICATIONS ment therapy (Mehta et al., 2006; Silvestry, Gastrointestinal (GI) complications are rare 2008; Talmor & Lisbon, 2005). in cardiac surgery patients, occurring in only In one study, patients who required dialysis 2% of individuals who undergo such proce- after cardiac surgery were older by 7 years dures (Andersson, Nilsson, Brandt, Hoglund, than those who did not. Other risk factors & Andersson, 2005; Talmor & Lisbon, 2005). identified in this study included history of The likelihood of a patient manifesting a GI diabetes, COPD, peripheral or cerebrovascu- complication in the ICU is small, as most lar disease, heart failure, previous CPB or early complications are reported to occur on valve surgery, CPR, recent MI, and cardio- postoperative days 6 and 7—well after the genic shock. The last two conditions are asso- patient has likely been discharged from the ciated with decreased CO, which can decrease ICU (Talmor & Lisbon, 2005). 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 277

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Most GI complications are difficult to diag- deficits, stupor, coma, and new onset of nose because of their atypical symptoms, the seizures are other reported complications fol- many different underlying diseases that cause lowing CPB. The incidence of neurologic them, and the inability of patients to accu- complications has been reported to be rately describe their symptoms. All of these between 2% and 16% in this patient popula- factors may delay diagnosis or treatment. Pro- tion (Silvestry, 2008; Talmor & Lisbon, 2005). longed mechanical ventilation, septic shock, In one study, most patients with preoperative and renal complications have been shown to hypoalbuminemia were found to be at be strong predictors of GI complications increased risk for development of postopera- (D’Ancona et al., 2003). tive neurologic complications (Rady et al., Overall, the mortality rate is 50% among 1997). Neurologic complications following patients who experience serious GI complica- cardiac surgery are discussed in detail in tions, with the most likely cause of GI compli- Chapter 16. cations being perioperative visceral or splanchnic hypoperfusion. Hypoperfusion is ■ SYSTEMIC INFLAMMATORY likely to stem from low CO, which produces RESPONSE TO CARDIAC SURGERY vasoconstriction, hypoxia, and hypoperfusion of the splanchnic bed with resultant intestinal Cardiac surgery elicits a powerful inflamma- ischemia. This complication is probably attrib- tory response that can have serious effects. utable to the increased age of cardiac surgery Inflammation is the body’s response to the candidates, the longer and more complex pro- disruption within the tissues and involves a cedures performed during cardiac surgery, and series of controlled humoral and cellular reac- the increased prevalence of atherosclerosis in tions. Nonspecific activators of the immune these surgical candidates (Filsoufi et al., 2007). response include trauma to the tissues during Other GI complications include ileus, upper surgery, blood transfusions, and hypother- GI bleeding from gastritis or peptic ulcer dis- mia. A specific activator of this response is ease, acute pancreatitis, cholecystitis, and acute CPB, which affects the immune system in sev- hepatic failure (Lemmer et al., 2003; Mullen- eral different ways. First, the surface of the Fortino & O’Brien, 2008). CPB circuit causes activation of the immune The ICU nurse should monitor the patient system when blood comes in contact with the for presence and changes in bowel sounds, foreign surfaces of the circuit. Second, aortic abdominal pain or distention, nausea, and cross-clamping causes reperfusion injury to vomiting. Diagnostic lab tests (e.g., complete the brain, kidneys, liver, heart, and lungs (Laf- blood count, metabolic panel) and abdominal fey, Boylan, & Cheng, 2002). radiograph may be obtained if GI complica- The systemic inflammatory response is tions are suspected (Mullen-Fortino & characterized by the release of pro-inflamma- O’Brien, 2008). tory factors such as interleukins 6 and 8 (IL-6 and IL-8) and tumor necrosis factor (TNF). The amount released correlates with the ■ NEUROLOGIC COMPLICATIONS development of postoperative complications Postoperative cardiac surgery patients may (Chello et al., 2006). The inflammatory develop any of a wide range of neurologic response seems to be most evident in the set- complications. Neurocognitive insufficiency ting of postoperative pulmonary and cardiac may occur in as many as 80% of these dysfunction, where it causes acute lung injury patients. Stroke, transient ischemic attack, and global myocardial dysfunction with sub- decline in intellectual function, memory sequent peripheral vasodilation. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 278

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Current recommendations for treatment most patients with preoperative hypoalbu- call for supportive care until the inflamma- minemia were found to be at increased risk tory response resolves. Much research is evolv- for development of postoperative infectious ing in this area, with treatment modalities complications (Rady et al., 1997). In another such as stress-dose steroids, aprotinin (Trasy- study, while no statistically significant differ- lol®), atorvastatin (Lipitor®), and improved ences among groups were found, patients circuit biocompatibility being explored (Laf- with the highest BMI had a higher incidence fey et al., 2002). of sternal wound infections. These manifesta- Aprotinin is the most potent anti-fibri- tions occurred within 30 days of surgery nolytic agent that is used to decrease postop- (Maurer et al., 2002). Education of those erative cardiac surgery bleeding; it also has patients with high BMI should include strict anti-inflammatory properties. Specifically, monitoring for signs of infection. aprotinin decreases neutrophils and The ICU nurse should monitor the patient macrophage activation, and it reduces release for purulent discharge from the wound, fever, and activation of pro-inflammatory mediators increased pain or tenderness of the chest wall, (McEvoy, Reeves, Reves, & Spinale, 2007). or an unstable sternum. In addition to adher- Given the relationship between inflammation ing to facility-specific wound care policies, and hemostasis, aprotinin is indicated for use administration of prophylactic antibiotic ther- in postoperative cardiac surgery patients apy for 48 hours and tight glycemic control (Levy, Tanaka, & Bailey, 2008). Its use for this help to minimize the likelihood of infections purpose is controversial, however (McEvoy et (Mullen-Fortino & O’Brien, 2008). Wound al., 2007). care is discussed in detail in Chapter 18. Whenever blood is exposed to an artificial surface, thrombus development is likely. For ■ SUMMARY this reason, anticoagulation is required during bypass procedures. To avoid additional The initial 24 hours following cardiac surgery anticoagulation, the use of heparin-coated is a challenging and tenuous time. Patients circuits has been proposed. These devices are have high levels of vulnerability and instabil- designed to decrease coagulation and dimin- ity in the initial postoperative period. While ish the associated inflammatory response, there is some degree of predictability in terms although their efficacy has not been consis- of the postoperative trajectory, the trends tently demonstrated (Taneja & Cheng, 2006). toward increasing age and number of preoperative comorbidities in these patients have increased the level of complexity associated ■ INFECTIOUS COMPLICATIONS with this population. Most patients, despite Postoperative infections include bacteremia, their initial instability, are discharged from pneumonia, urinary tract infections, and the ICU within 24 hours, often in 15–20 wound infections. Wound infections follow- hours (St. Andre & DelRossi, 2005). ing cardiac surgery are classified as either The role of the ICU nurse cannot be superficial or deep (mediastinitis). Although overemphasized in terms of these providers’ wound infections are rare in cardiac surgery influence in reducing the likelihood of critical patients, their development results in events associated with postoperative compli- increased morbidity, longer LOS, and higher cations. High levels of clinical judgment and costs. Identified risk factors for this complica- caring practices are essential competencies. tion include increased BMI, diabetes, COPD, Prevention and prompt recognition of post- prolonged surgery (greater than 90 minutes), operative complications are pivotal to help and use of bilateral IMA grafts. In one study, ensure optimal patient outcomes. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 279

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CASE STUDY

An 82-year-old male is brought to the ED via ambulance after a brief loss of consciousness that caused him to fall. He is now alert and oriented ϫ 3 with a negative neurological exam. The patient states that he has a 3-month history of chest pain that increases with activity and resolves with rest. He also reports shortness of breath (SOB) that has become progressively worse, to the point that he cannot make it to the top of the stairs at his home without feeling “winded.” The patient also states he has been very healthy all of his life and does not seek medical care on a routine basis, although he takes a baby aspirin because heart attacks run in the family. The patient is divorced but has two grown children who live nearby and check in on him weekly. He reports a history of tobacco use for 30 years but has recently cut his smoking down to 1–2 cigarettes per day because of his increasing SOB.

Testing CT scan of brain: Negative for bleed or stroke 12-Lead ECG: Sinus rhythm, HR 80, left ventricular hypertrophy (The patient was admitted for observation and additional testing.) Echocardiogram (TEE): Severe aortic stenosis with valve area 0.5 cm2 (critical aortic stenosis) with severe left ventricular hypertrophy; moderate mitral regurgitation; no pulmonic stenosis or insufficiency; no tricuspid stenosis or insufficiency. Cardiac catheterization: Left anterior descending artery with 99% occlusion; right coronary artery with 80% occlusion; obtuse marginal with 85% occlusion; severe triple vessel disease with critical aortic stenosis; EF 70%. Because of the severity of symptoms, the critical aortic stenosis, and LAD occlusion, surgery is scheduled for the next morning. The intraoperative course is uneventful, and the patient receives a tissue aortic valve and a three-vessel coronary artery bypass. Postopera- tively, the patient is transported to the ICU. Admission vital signs are as follows: BP: 102/65 mm Hg (via arterial line) HR: 102 bpm, sinus tachycardia, no ectopy RR: 12 breaths/min (ventilator rate set at 12) Temperature: 95.4 °F (35.2 °C) PAP: 20/9 (11) mm Hg CVP: 7 mm Hg CI: 2.3 L/min (CO 4 L/min) SVR: 1300 dyne/sec/cm–5 The patient is receiving milrinone 0.375 mcg/kg/min, NTG 0.1 mcg/kg/min, and an insulin infusion at 4 units/hr.

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Laboratory Data Hgb: 10.2 g/dL PTT: 45.2 sec Hct: 31.7% PT: 16.8 sec K: 3.5 mEq/L INR: 1.4 Mg: 1.9 mg/dL Platelets: 96,000/mm3 Glucose: 270 mg/dL

Critical Thinking Questions 1. What is a first priority for this patient? a. Replacement of electrolytes b. Pain medication c. Application of a warming blanket to correct the hypothermia d. Administer 0.9% NS to correct the low blood pressure 2. The patient is at higher risk for postoperative complications because of which of the following risk factors? a. Severely depressed left ventricular function b. Gender c. Presence of moderate mitral regurgitation d. Aspirin taken within 7 days prior to surgery

Postoperative 30 Minutes BP: 90/43 mm Hg PAP: 18/7 (11) mm Hg CVP: 4 mm Hg Chest tube outputs: mediastinal: 175 mL in container; pleural: 100 mL in container

Critical Thinking Questions 3. The ICU nurse is concerned about the increasing chest tube output and knows this patient is at risk for bleeding after cardiac surgery due to a. aspirin use. b. decreased platelet count. c. hypothermia. d. all of the above. 4. The cardiac surgeon is notified of the chest tube output. Protamine sulfate 25 mg is prescribed. Which of the following lab values should be evaluated to determine efficacy of this intervention? a. PT/INR b. Hemoglobin c. aPTT d. Magnesium

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CVP: 18 mm Hg CI: 1.5 L/min/m2 Chest tube outputs: mediastinal: 180 mL in container; pleural: 100 mL in container

Critical Thinking Questions 5. Which of the following is the likely etiology of the patient’s condition at this time? a. Tension pneumothorax b. Pleural effusion c. Cardiac tamponade d. Bleeding 6. Based on the patient’s condition, which of the following interventions should the ICU nurse anticipate? a. Preparation for emergency resternotomy b. Replacement of electrolytes c. Administration of adenosine (Adenocard®) d. Insertion of an additional chest tube The patient develops ventricular tachycardia with no pulse. The chest is immediately opened at bedside by the surgeon.

Critical Thinking Questions 7. Which of the following interventions is indicated at this time? a. Connection of epicardial pacing wires to external pacemaker box b. Internal defibrillation c. Administration of blood products d. Chest closure 8. How many joules should the nurse prepare to defibrillate with? a. 360 joules b. 5–20 joules c. 160 joules d. 200–300 joules The patient returns to normal sinus rhythm. Post-resuscitation, 1 L of clot is evacuated from the chest. The patient’s condition stabilizes, and he returns to the OR for washout and sternal closure. He receives intraoperative blood product replacement and returns to the ICU in stable condition. The remainder of his postoperative course is uneventful and he is discharged home after 10 days. Answers to Critical Thinking Questions 1. c (Hypothermia in the cardiac surgery patient can cause increased myocardial oxygen demand, depression of ventricular function, and coagulopathy.) 2. d (Use of aspirin within 7 days of surgery and female gender are risk factors for postoperative complications. The patient did not have evidence of depressed left ventricular function based on his diagnostic test data.) 3. d (Decreased platelet count, use of aspirin, and hypothermia all can increase perioperative bleeding.) 4. c (Protamine sulfate reverses the effects of heparin. Large amounts of heparin are used for the cardiopulmonary bypass circuit and to systemically anticoagulate the patient.) 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 282

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5. c (The nurse should be concerned about cardiac tamponade due to the sudden cessation of bleeding, tachycardia, narrow pulse pressure, and low cardiac index.) 6. a (Prepare for emergency sternotomy to relieve the tamponade. If time and the patient’s hemodynamic profile allow, obtain an echocardiogram to confirm the diagnosis and guide the procedure. If time does not allow, emergency resternotomy is indicated.) 7. b (The nurse should obtain the paddles for internal defibrillation because the chest is open. Immediate defibrillation is indicated.) 8. b (Energy in the range of 5–20 joules is used for internal defibrillation. It takes less energy when the paddles are directly on the heart because the electricity does not have to permeate chest skin, bone, muscle, and fat.)

Clinical Inquiry Box

Question: Does the length of storage time for red blood cells affect patient outcomes post cardiac surgery? Reference: Koch, C. G., Li, L., Sessler, D. I., Figueroa, P., Hoeltge, G. A., Mihaljevic, T., et al. (2008). Red- cell storage and complications of cardiac surgery. New England Journal of Medicine, 358(12), 1229–1239. Objective: To evaluate the correlation of cardiac surgery complications and the length of time during which transfused cells are stored. Method: A retrospective study was conducted to evaluate the complications in patients who had a coronary artery bypass grafting, heart valve surgery, or both over an 8-year period. Com- plications were correlated with the length of time during which blood had been stored prior to administration. Results: Complications such as higher rates of in-hospital mortality, longer periods of intubation, renal failure, and sepsis were associated with patients who received blood that was stored for an average of 20 days. Conclusion: Nurses should be aware that complication rates may be increased in patients who receive red blood cells that were stored for more than two weeks. Critical care nurses are in a position to review the latest research and propose policy changes such as limiting the age of stored blood for transfusion.

■ REFERENCES Abdel Aziz, T. A., Ali, M. A., Roberts, D. G., & Al Abramov, D., Abu-Tailakh, M., Fireger, M., Ganiel, Khaja, N. (2000). Troponin T as a marker of A., Tuvbin, D., & Wolak, A. (2006). Plasma tro- infarction during coronary bypass surgery. ponin levels after cardiac surgery vs after Asian Cardiovascular and Thoracic Annals, 8(1), myocardial infarction. Asian Cardiovascular Tho- 19–23. racic Annals, 14(6), 530–535. Aboyans, V., Frank, M., Nubret, K., Lacroix, P., & Adams, D. H., Filsoufi, F., & Antman, E. M. (2005). Laskar, M. (2008). Heart rate and pulse pres- Medical management of the patient undergo- sure at rest are major prognostic markers of ing cardiac surgery. In D. P. Zipes, P. Libby, R. early postoperative complications after coro- O. Bonow, & E. Braunwald (Eds.), Braunwald’s nary artery bypass surgery. European Journal of heart disease (7th ed., pp. 1993–2020). Philadel- Cardio-thoracic surgery, 33(6), 971–976. phia: Elsevier Saunders. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 283

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Milot, J., Perron, J., Lacasse, Y., Letourneau, L., Scollan-Boring, S. (2005). Cardiovascular surgery, Cartier, P., & Maltais, F. (2001). Incidence and the systemic inflammatory response, and cor- predictors of ARDS after cardiac surgery. ticosteroids. Progress in Cardiovascular Nursing, Chest, 119(3), 884–888. 20(3), 127–128. Moosbauer, W., Hofer, A., & Gombotz, S. (2007). Selleng, K., Markentin, T., & Greinacher, A. (2007). Prevention and management of cardiac dys- Heparin induced thrombocytopenia in inten- function during and after cardiac surgery. In sive care unit patients. Critical Care Medicine, J. L. Atlee, A. Gullo, G. Sinagra, & J.-L. Vincent 35(4), 1165–1176. (Eds.), Perioperative critical care cardiology (2nd Shavelle, D. M. (2006). Pathophysiology of ed., pp. 225–241). Milan: Springer. stunned or hibernating myocardium. Mullen-Fortino, M., & O’Brien, N. (2008). Caring Retrieved September 28, 2008, from for a patient after coronary artery bypass graft www.utdol.com/online/content/topic.do surgery, Nursing, 38(3), 46–52. ?topicKey=chd/46551&linkTitle=Stunned%20 Napolitano, L., Warkentin, T., Almahameed, A., & myocardium&source=preview&selected Nasraway, S. (2006). Heparin induced throm- Title=2~37&anchor=3#3 bocytopenia in the critical care setting: Diag- Silvestry, F. E. (2008). Overview of the postopera- nosis and management. Critical Care Medicine, tive management of patients undergoing car- 34(12), 2898–2911. diac surgery. Retrieved September 16, 2008, Peruzzi, W. T., & Shapiro, B. A. (2002). Respiratory from www.utdol.com/online/content/topic care. In M. J. Murray, D. B. Coursin, R. G. .do?topicKey=cc_medi/22438&linkTitle= Pearl, & D. S. Prough (Eds.), Critical care medi- Perioperative%20myocardial%20infarction& cine: Perioperative management (2nd ed., pp. source=preview&selectedTitle=1~150&anchor 428–446). Philadelphia: Lippincott Williams & =13# Wilkins. St. Andre, A., & DelRossi, A. (2005). Hemodynamic Rady, M. Y., Ryan, T., & Starr, N. J. (1997). Clinical management of patients in the first 24 hours characteristics of preoperative hypoalbumine- following cardiac surgery. Critical Care mia predict outcome of cardiovascular sur- Medicine, 33(9), 2062–2083. gery. Journal of Parenteral and Enteral Nutrition, Taggart, D. P. (2000). Respiratory dysfunction after 21(2), 81–90. cardiac surgery: Effects of avoiding cardiopul- Sakr, Y., Vincent, J. L., Reinhart, K., Groeneveld, J., monary bypass and the use of bilateral inter- Michalopoulos, A., Sprung, C. L., et al. (2005). nal mammary arteries. European Journal of High tidal volume and positive fluid balance Cardio-thoracic Surgery, 18(1), 31–37. are associated with worse outcome in acute Talmor, D., & Lisbon, A. (2005). Management of lung injury. Chest, 128(5), 3089–3091. the postoperative cardiac surgical patient. In Salenger, R., Gammie, J. S., & Vander Salm, T. J. M. Fink, E. Abraham, J. Vincent, & P. Kochanek (2003). Postoperative care of cardiac surgical (Eds.), Textbook of critical care (5th ed., patients. In L. H. Cohn & L. H. Edmunds, Jr. pp. 1955–1967). Philadelphia: Elsevier (Eds.), Cardiac surgery in the adult (pp. 439–469). Saunders. New York: McGraw-Hill. Taneja, R., & Cheng, D. C. (2006). Con: Heparin- Saxena, P., Konstantinov, I. E., Koniuszko, M., bonded cardiopulmonary bypass circuits Singh, T., & Newman, A. J. (2006). Persistent should be routine for all cardiac surgical severe vasospasm in off-pump coronary artery patients. Anesthesia & Analgesia, 103(6), bypass surgery: The value of intraluminal 1365–1369. stenting. Journal of Thoracic and Cardiovascular Tineli, R. A., Silva, R. A., Jairo, L., Menezes, P. L., Surgery, 131(1), 237–238. Rodrigues, A. J., Vicente, W. V., et al. (2005). Schipke, J. D., & Birkenkamp-Demtröder, K. Atrial fibrillation and cardiac surgery: A never (2001). Another view of myocardial hiberna- ending and always controversial history. tion. International Journal of Cardiology, 79(1), Revista Brasileira de Cirurgia Cardiovascular, 13–17. 20(3), 323–331. 57625_CH13_257_286.pdf 4/10/09 11:08 AM Page 286

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Tripp, H., & Bolton, J. (1998). Phrenic nerve injury Weissman, C. (2004). Pulmonary complications following cardiac surgery: A review. Journal of after cardiac surgery. Seminars in Cardiothoracic Cardiac Surgery, 13(3), 218–223. and Vascular Anesthesia, 8(3), 185–211. Tu, J. V., Jaglal, S. B., & Naylor, C. D. (1995). Multi- Whitlock, R., Crowther, M., & Ng, H. (2005). Bleed- center validation of a risk index for mortality, ing in cardiac surgery: Its prevention and intensive care unit stay, and overall hospital treatment—An evidence based review. Critical length of stay after cardiac surgery. Steering Care Clinics, 21(3), 589–610. Committee of the Provincial Adult Cardiac Wu, A. H. (1998). Cardiac troponin I. In A. H. Wu, Care Network of Ontario. Circulation, 91(3), Cardiac markers (pp. 209–245). Totowa, NJ: 677–684. Humana Press. Tuman, K. J., McCarthy, R. J., March, R. J., Najafi, Wynne, R., & Botti, M. (2004). Post-op pulmonary H., & Ivankovich, A. D. (1992). Morbidity and dysfunction after cardiopulmonary bypass. duration of ICU stay after cardiac surgery: A American Journal of Critical Care, 13(5), 384–393. model for preoperative risk assessment. Chest, 102(1), 36–44. ■ WEB RESOURCES Vlahakes, G. J. (2005). Right ventricular failure following cardiac surgery. Coronary Artery Disease, Median sternotomy: http://www.youtube.com/ 16(1), 27–30. watch?v=r7RsB0BA4EI Wang, X., Wei, M., Kuukasjärvi, P., Laurikka, J., IABP complications: http://www.youtube.com/ Järvinen, O., Rinne, T., et al. (2003). Novel watch?v=X4gWT3u0FqQ pharmacological preconditioning with diazox- Heparin-induced thrombocytopenia: http://www ide attenuates myocardial stunning in coro- .youtube.com/watch?v=_LVHEW8vH-E nary artery bypass grafting. European Journal of Sepsis development and progression: http:// Cardiothoracic Surgery, 24(6), 967–973. www.youtube.com/watch?v=HoxoeP-l5Uw 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 287

Chapter 14 Pain Management

Susan Lynch

■ INTRODUCTION Pain is one of the most significant problems tle to no progress has been made in reducing for patients requiring surgery. Although it is the incidence of postoperative cardiac surgery recognized as a major healthcare issue for all pain (Gelinas, 2007a). One possible contribu- patients, pain continues to be poorly man- tor to inadequate pain management is the aged. It is estimated that 50–70% of patients lack of reassessment following administra- experience moderate to severe pain following tion of analgesics. In one study, only 4.4% of surgery despite advances in care (Pogatzki- pain activities entailed reassessment of effi- Zahn, Zahn, & Brennen, 2007). cacy of an analgesic intervention (Bucknall, Cardiac surgery patients are no different. In Manias, & Botti, 2007). one study, patients who underwent cardiac or Other data support that while there is a abdominal vascular surgery experienced mod- high prevalence of patients reporting moder- erate pain that did not lessen over the first ate to severe levels of pain after cardiac sur- few postoperative days (Puntillo & Weiss, gery, those individuals receive only a small 1994). It has been reported that more than percentage of their prescribed/allotted anal- 77% of cardiac surgery patients recall having gesic dosage. Some patients receive less than postoperative pain (Gelinas, 2007a). Surveys half of the amount of analgesic that was pre- of cardiac surgery patients at one academic scribed (Maxam-Moore et al., 1994; Puntillo medical center reflected lower than antici- & Weiss, 1994; Watt-Watson & Stevens, 1998; pated ratings; pain management specifically Watt-Watson, Stevens, Garfinkel, Streiner, & was identified as an area of concern. These Gallop, 2001; Watt-Watson et al., 2004). findings included excellent clinical outcomes Presence of pain following cardiac surgery and high levels of technical expertise at the has implications for optimal recovery. Patients center (Cutshall et al., 2007). The data also have reported pain while turning, coughing corroborate other research findings of cardiac and deep breathing, using the incentive surgery patients’ memories of postoperative spirometer, moving or turning in bed, and get- pain while in the ICU (Maxam-Moore, Wilkie, ting up (Gelinas, 2007a; Milgrom et al., 2004). & Woods, 1994; Meyerson, Thelin, Gordh, & Pain management requires effective and Karlsten, 2001). efficient assessment, treatment, and evalua- Although significant numbers of research tion by all members of the healthcare team, studies support presence of postsurgical pain with nurses playing a critical role. Nurses are issues and advances in pain management, lit- crucial in advocating for patients who are

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experiencing pain, to help assure that those ■ PAIN PHYSIOLOGY patients receive the best possible symptom Pain physiology can be described in relation management. To be an effective advocate, to four distinct steps in the process of pain nurses must be able to recognize pain, be perception: transduction, transmission, per- available, be ready to act, be empathetic ception, and modulation. Pain physiology instead of judgmental, and be willing to edu- related to the perception of pain begins with cate not only the patient but also the health- the initial tissue injury, whether real or per- care team (St. Marie, 2002). ceived. Transduction occurs when the injury causes the release of mediators by stimulating ■ WHAT IS PAIN? the nociceptors or free nerve endings to cause Pain is defined by the International Associa- the release of more mediators. Transmission tion for the Study of Pain (IASP) as “an occurs when the neurotransmitters activate unpleasant and emotional experience associ- the action potential, causing the information ated with actual or potential tissue damage, to travel along the primary neuron and to or described in terms of such damage” (IASP, synapse with the secondary neuron in the 2008, p. 34). Pain was first defined by the sub- dorsal horn of the spinal cord. Perception committee on Taxonomy of IASP in 1979, occurs as the brain processes the information. and this definition continues to be used in The spinal cord sends the information carried the literature (Gelinas, 2007b; IASP, 2008; by the free nerve ending to the thalamus, and Lome, 2005). Multiple factors—including pre- the information is then sent to the cortical vious pain experience, culture, mood, and areas of the brain where pain is perceived. coping skills—influence an individual’s pain Modulation, the final step, occurs when stimuli experience (Spacek, 2006). “The patient’s are either enhanced or inhibited by the hypo- experience of pain is seen as involving far thalamus, pons, and somatosensory cortex so more than a localized sensation; it encom- as to process and transmit a pain sensation passes what this sensation means to him” (Li, 2008; Lome, 2005). Figure 14–1 depicts (McCaffery, 1972, p. 7). the pain physiology process. Pain is subjective (IASP, 2008). The ■ patient’s self-report of pain is the most reli- TYPES OF PAIN able indicator of its presence. Pain is There are two major classifications of pain: described as “whatever the person says it is nociceptive and neuropathic. and exists whenever he says it does” (McCaf- Nociceptive pain occurs with direct stimula- fery, 1972, p. 8). However, it is important to tion of pain receptors. Examples of this type of note that the inability to communicate does pain include tissue injury or inflammation. not mean the patient is not experiencing pain. Nociceptive pain can be further classified as The use of the word “says” does not mean the either somatic or visceral. Somatic pain refers to patient must verbalize existence of pain. All the stimulation of pain in the cutaneous and patient behaviors—whether voluntary or deep layers of skin. Patients are able to localize involuntary, verbal or nonverbal—may indi- this pain, which often comprises acute pain cate presence of pain (McCaffery, 1972). Mea- due to surgery. Visceral pain refers to pain sures must be taken to appropriately assess resulting from infiltration or compression of and treat patients who may not be able to ver- the abdominal or thoracic viscera. It is often bally report pain (Gelinas, 2007b; IASP, 2008; difficult for patients to localize visceral pain Michaels, Hubbartt, Carroll, & Hudson-Barr, because the pain is referred to another part of 2007; Spacek, 2006). the body (Goldstein & Morrison, 2005). 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 289

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Transduction Injury

Nocireceptors Release Neurotransmitters

Neurotransmitters Activate Firing of More Nocireceptors

Transmission Information Sent via Nerve Fibers to Dorsal Horn of the Spinal Cord

Spinal Cord Sends Info via Spinothalmic Tract to Thalamus

Perception of Pain Thalamus Sends to Cortical Areas of Brain to Process Information

Modulation Inhibit or Enhance the Stimuli to Transmit a Pain Stimulus Figure 14–1 Pathophysiology of pain.

Postoperative cardiac surgery patients are occur either centrally or peripherally. It is likely to experience pain from a variety of caused by nerve damage. Examples of this sources. Incisions from sternotomy, thoraco- type of pain include diabetic neuropathy and tomy and graft sites, required invasive proce- phantom pain (Chong & Brandner, 2006; dures, tissue retraction and dissection, Gelinas, 2007b). turning, and presence and removal of chest Pain can also be categorized according to tubes are some of the identified etiologies whether it is acute or chronic. Acute pain is (Cohen et al., 1993; Gelinas, 2007a; Heye, described as having a recent onset or resulting 1991; Mehta & Kumar, 2004; Meyerson et al., from an ongoing injury, likely has a limited 2001; Mueller et al., 2000; Valdix & Puntillo, duration, and is often easier to treat. Chronic 1995; Watt-Watson & Stevens, 1998). In one pain persists beyond the time of tissue healing study, patients who were having painful pro- and does not have a definable cause, as often cedures (e.g., chest tube removal) were not there may be behavioral and emotional com- premedicated for pain; these patients subse- ponents (Hamill-Ruth & Marohn, 1999; quently reported moderate to high levels of Spacek, 2006). Acute and chronic pain can be pain (Puntillo, 1994). visualized as a continuum instead of two dis- Neuropathic pain is primarily caused by a tinct categories (Spacek, 2006). The duration dysfunction in the nervous system that can of pain is considered when determining 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 290

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whether the pain should be classified as acute chronic pain. One hypothesis for this phe- or chronic. Acute pain typically lasts no more nomenon suggests that a neurophysiologic than 30 days, whereas chronic pain lasts 3–6 link results in glial activation following months (Gelinas, 2007b). For patients who nerve or tissue injury. The signaling mole- undergo cardiac surgery, healthcare providers’ cules involved in glial activation are ATP; focus remains on acute, nociceptive pain. CX3CL (fractalkine); CCL1 (monocyte Unfortunately, cardiac surgery patients are chemotactic protein-1); the pro-inflammatory also at risk for developing chronic pain. Over cytokines interleukin 1-beta (IL-1β), inter- time, the patient’s pain characteristics may leukin 6 (IL-6), tumor necrosis factor alpha evolve from acute, nociceptive pain to chronic, (TNF-α), and substance P (SP); and glutamate neuropathic pain in origin caused by the nerve (Marchand, Perretti, & McMahon, 2005). damage associated with sternal incisions and Nevertheless, individuals need early cessation retractions. Approximately 30–44% of patients of pain to prevent them from progressing to a who undergo thoracotomy exhibit chronic state of chronic pain. Clearly, early recogni- pain 6 months to a year after surgery has been tion and treatment of acute pain is of prime reported (Cerfolio, Bryant, Bass, & Bartolucci, importance. 2003; Jensen & Andersen, 2004). The risk of developing chronic pain seems to be reduced ■ if postoperative pain is adequately managed PAIN ASSESSMENT (Markman & Philip, 2007; Pogatzki- Zahn et Pain assessment is a critical part of a nurse’s al., 2007), placing greater emphasis on the total assessment of all patients. This state- need for control of pain in acute periods. ment was universally accepted and validated In another study of cardiac surgery by the Joint Commission (2004) standard for patients, persistent pain from any site (lasting pain assessment, which states, “A comprehen- at least 2 months postoperatively) was experi- sive pain assessment is conducted as appro- enced by 29% of patients; 25% had persistent priate to the individual’s condition and the sternotomy pain. Other sites of pain included scope of care, treatment and services pro- the shoulder, back, and neck. Pain intensity vided” (www.jointcommission.org). In the level in these patients was mild, with 7% of 2004 Joint Commission standards, PC.8.10 the study participants reporting that the pain reads, “When pain is identified, the patient is interfered with activities of daily living. There assessed and treated by the organization or was no significant difference in the incidence referred for treatment” (Alcenius, 2004, p. 12). in those patients who received postoperative To meet the standards for pain assessment, high thoracic epidural anesthesia and opioids organizations are expected to perform screen- (Ho, Royse, Royse, Penberthy, & McRae, ing and intensive assessment. Screening 2002). should be conducted in the initial assessment These findings were corroborated in to be able to determine the patient’s need. another study of cardiac surgery patients. Typically, screening will ask a question related Patients who reported moderate to severe to the patient’s present pain state and history pain postoperatively were the same patients of pain. The progression to an intensive who reported chronic post-sternotomy pain assessment is determined by the screening. more frequently (Lahtinen, Kokki, & Hyny- Evaluation of pain needs to focus on several nen, 2006). domains, including the pain’s location, inten- Individuals who experience uncontrolled sity, quality, and duration; relief measures; acute pain for long periods of time are known and the patient’s perception of an acceptable to have a greater probability of developing pain level. Recommendations include using 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 291

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pain assessment tools that are age and ability visual analog scale (VAS), numerical rating, appropriate (Alcenius, 2004). verbal rating, faces rating, and behavioral observation scales (Dunwoody et al., 2008). Numeric rating scales are commonly used due Preoperative Baseline Assessment to their ease of administration and under- To optimally manage pain for surgical standing. With such tools, patients are asked patients, nurses should obtain a thorough to rate the severity of their pain on a scale of 0 preoperative health history, encompassing (representing “no pain”) to 10 (representing topics related to the patient’s current and the “worst imaginable pain”) (Bertagnolli, past experiences with pain. Many factors can 2004; Dunwoody et al., 2008; Li, 2008). VASs, affect a patient’s response and perception of numeric rating scales, and verbal rating scales pain—for example, fatigue, sleep deprivation, are all valid, reliable, and appropriate for clini- fear, anxiety, depression, anger, misinforma- cal use (Dunwoody et al., 2008; Williamson & tion, altered mental status, educational level, Hoggart, 2005). Identification of the best pain cultural background, ethnic background, and assessment tool for the patient preoperatively pain experience (Hamill-Ruth & Marohn, can assist the patient to provide the most reli- 1999). Past experiences will alert the nurse to able information using the scale postopera- factors that may directly affect the patient’s tively, thereby resulting is more effective pain response to the current treatment, including management (Gelinas, 2007b). medications that have been effective in the past, Duration of pain includes questions con- acceptable pain levels, concerns about pain, and cerning the timing of when the pain starts, educational needs. Discussions focusing on the how long it lasts, and which factors alleviate it. patient’s expectations can assist the nurse and Patients are also asked about factors that the patient to jointly develop a plan of care aggravate the pain. Additionally, determining related to pain that has desirable predicted out- if any associated factors exist can assist the comes (Dunwoody, Krenzischek, Pasero, Rath- nurse in developing a more comprehensive mell, & Polomano, 2008). treatment plan. For example, do nausea and The pain assessment process includes mul- vomiting accompany the pain? Treatment tiple components, such as initial assessment, may need to include measures to control these treatment, reassessment, and evaluation. associative factors. Determining how the pain Optimal goals include adequate pain manage- affects the individual’s activities of daily living ment, manageable side effects, and assurance provides supplemental information about of safety (Dunwoody et al., 2008). Dimen- how the pain interferes with normal function- sions of the assessment should include the ing. Treatment strategies then can be aimed at pain’s location, description, intensity, dura- specific challenges the patient faces related to tion, alleviating and aggravating factors, asso- daily life events (St. Marie, 2002). ciative factors, and impact on life. To identify Although a considerable amount of the location and obtain a description of the research on pain has been conducted over the pain, the nurse should ask patients to describe past several decades, cardiac surgery patients the pain in their own words and to point to have been the focus of only a small percentage where the pain occurs (St. Marie, 2002). of these studies. In such investigations, the Intensity or severity of pain is typically focus has tended to be on pain intensity, with measured by one of the available assessment other important pain factors not being cov- tools. The choice of pain assessment instru- ered. Mueller and colleagues (2000) evaluated ment typically depends on the characteristics cardiac surgery patients’ pain and found that of the individual patient. Options include a pain intensity was highest during the first 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 292

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2 postoperative days and lowest on days 3 and attempts must be made to obtain a patient 7. Age was the only demographic variable that self-report of pain. Explanation as to the diffi- affected pain in this study; patients older culty of obtaining a self-report should be doc- than age 60 had lower pain intensity scores umented, and further investigation should on the second postoperative day than did ensue. A search for the potential cause of pain patients younger than age 60. Pain location is conducted, with the provider assuming that varied, with patients reporting more shoulder pain is present. Observation of behaviors is pain on day 7. Pain distribution did not vary the best approach when the patient is unable in this study. to make a self-report. Pain behaviors, however, do not always accurately depict pain intensity. Family reports of patient pain may Pain Assessment in Patients Who also be considered, as family members can Are Unable to Communicate often identify subtle changes in the patient’s Assessment of pain for patients who are status. However, discrepancies do exist unable to communicate can pose a challenge between patient self-reports and reports given for nurses. It cannot be assumed that non- by other observers, such that severity of pain communicative patients are not in pain. may not be accurately reported. Therefore, Instead, these patients must be assessed and one must consider all aspects of an assess- treated appropriately for pain (Erdek & ment and perhaps perform an analgesic trial, Pronovost, 2004; Gelinas, Fillion, Puntillo, monitoring the patient’s response to the med- Viens, & Fortier, 2006). ication (Herr et al., 2006). Utilization of a behavioral observation pain assessment tool may be necessary based on ■ the patient’s condition. Behavioral assess- MANAGEMENT OF PAIN ment tools have been created to measure Adequate pain management is essential for those patient behaviors labeled as being the well-being of all patients and may even be indicative of the presence of pain. Examples considered a fundamental human right of tools that have been tested in acute care (Brennan, Carr, & Cousins, 2007). The conse- settings with acute pain and that have the quences of inadequate pain management most reliable and valid data to date include encompass physiologic, psychological, social, the Checklist of Nonverbal Pain Indicators and economic ramifications. Physiologically, (CNPI), the Behavioral Pain Scale (BPS), and unrelieved pain results in many adverse the Critical-Care Pain Observation Tool effects, including increased heart rate, sys- (CPOT). Typically, behaviors observed include temic vascular resistance, and circulating cat- facial expressions, body movements, ease of echolamines. These effects place patients at breathing, vocalization, and/or muscle ten- greater risk for myocardial ischemia, stroke, sion. Points are given for observed behaviors and bleeding. Additionally, chronic pain in each category, resulting in a pain score that results in decreased mobility, decreased sleep, can be compared to the results obtained with immune dysfunction, dependence of medica- more traditional pain assessment tools (Herr tion, and codependence on family members. et al., 2006). In terms of psychological effects, studies have The American Society for Pain Manage- shown that patients with chronic pain are ment Nursing recommends that a hierarchi- four times more likely to suffer from depres- cal approach for assessment be used. First, all sion and anxiety. Social and economic consid- 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 293

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erations include the inability or decreased by local anesthetics and some anticonvulsants ability to work, which directly affects the indi- such as phenytoin (Dilantin®). Opioids also vidual’s socioeconomic status and also has an are used to inhibit both synapses at the dorsal impact on unemployment, disability, and use horn. Additionally, nonpharmacologic inter- of government benefits (Brennan et al., 2007). ventions such as massage and application of heat or cold may inhibit transmission of pain- related messages. The final strategy in pain ■ PHASES OF PAIN management is to enhance the inhibition of The patient experiences pain through three the pain sensation. Opioids are the agents of phases: anticipation, presence, and aftermath. choice in such a case, as they will affect both The nurse’s responsibility is to intervene and the primary and secondary neurons. Tricyclic assist the patient with each pain phase antidepressants can have the same effect by (McCaffery, 1972). interfering with serotonin uptake and pri- During the anticipation phase, interven- mary neuron transmission (Lome, 2005). tions should focus on education and the Opioids, non-opioids, and other analgesics reduction of anxiety. Anxiety has shown to used as adjuvant therapies are the mainstays in increase the intensity of pain scores. Anxiety pain management (Cadden, 2007). Treatment can often be relieved by knowing that pain modalities may differ, depending on whether may occur and developing a plan to manage the goal is treating acute versus chronic pain, it. This goal is best accomplished if these or nociceptive versus neuropathic pain. issues are discussed preoperatively prior to Traditionally, pain management strategies the occurrence of pain (Gallager & McKinley, have applied the World Health Organization’s 2007; McCaffery, 1972). (WHO) cancer pain treatment ladder in The presence of pain is the phase where attempts to manage postoperative pain. This interventions can directly affect the patient’s ladder suggests that the first step should level of comfort and pain intensity. Physiolog- include treatment options using non-opioids ically, the management of pain revolves with or without adjuvants. Step two entails around altering the source and perception of utilizing opioids for mild to moderate pain. pain and blocking the transmission of pain Step three entails continuing opioid use for impulses within the nervous system. Different moderate to severe pain. Postoperative pain pharmacologic and nonpharmacologic agents reaches its highest level initially after the sur- perform differently in relation to the pathol- gery, but then rapidly improves (Li, 2008; ogy of pain. One strategy is to block or limit Rosenquist & Rosenburg, 2003). the effect of local mediators at the site of In one study, Reimer-Kent (2003) devel- injury and decrease inflammation. Non- oped a pain management guideline using the steroidal anti-inflammatory drugs (NSAIDs) WHO ladder to prevent pain following car- are able to block specific mediator production diac surgery. Under this guideline, most such as prostaglandin, thereby decreasing patients received acetaminophen around the inflammation. Other medications such as clock, 89% of patients received an NSAID, and clonidine (Catapres®) block the release of epi- all patients received intermittent morphine. nephrine from the nerve fibers. A second The morphine was converted from an intra- strategy involves limiting transmission to the venous medication to an oral preparation on secondary neurons in the dorsal horn. The the second postoperative day. The amount of action potential can be blocked or inhibited morphine administered declined significantly 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 294

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by the second postoperative day. Effective Table 14–1 summarizes these recommenda- pain relief was reported in 95% of the patients tions for pain management in conjunction in this study. with cardiothoracic surgery. Evidence-based guidelines must direct Intravenous opioids are the preferred efforts to manage postoperative pain related method for managing patients who undergo to site-specific surgeries. Rosenquist and coronary artery bypass grafting (CABG) sur- Rosenburg (2003) gathered a multidiscipli- gery. These medications can be delivered via nary group to review and grade the evidence nurse- or patient-controlled methods. The use and then provide recommendations along of patient-controlled analgesia (PCA) devices these lines. An algorithmic approach to pain allows for small doses of opioids to be deliv- assessment was developed, with a flow dia- ered by the patient. Patients are able to main- gram outlining the key considerations prior tain a more stable blood concentration level to, during, and after the treatment of pain. with this approach, which may provide better Site-specific pain management recommenda- pain control (Roediger, Larbuisson, & Lamy, tions were provided regarding the use of phar- 2006; Rosenquist & Rosenburg, 2003). In one macologic and nonpharmacologic therapy. study, most postoperative cardiac surgery

Table 14–1 Summary of Site-Specific Pain Treatment Recommendations

Thoracotomy Coronary Artery Bypass Grafting

Preferred treatment Pharmacologic Pharmacologic Epidural Intravenous ● Opioids ● Opioids Regional local anesthetics ● NSAIDs Nonpharmacologic Nonpharmacologic Application of cold None identified TENS Cognitive (patient dependent) Common usage Pharmacologic Pharmacologic PO, IM, IV opioids, and NSAIDs PO, IM opioids, and NSAIDs IV PCA opioids IV PCA opioids Intrathecal opioids Intrathecal opioids Intrathecal local anesthetics Nonpharmacologic Nonpharmacologic Cognitive (patient dependent) None identified Comments If there is a risk of or actual If there is a risk of or actual bleeding, bleeding, avoid NSAIDs. avoid NSAIDs. If there is renal hypoperfusion, avoid all NSAIDs. Rarely Used Epidural Regional local anesthetics

NSAID ϭ nonsteroidal anti-inflammatory drug; PCA ϭ patient-controlled analgesia; TENS ϭ transcutaneous electrical nerve stimulation. Source: Rosenquist & Rosenburg, 2003. 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 295

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patients received hourly intermittent dosages and enhanced pulmonary function (Stenseth of morphine sulfate. Oral analgesics— et al., 1996). primarily acetaminophen with oxycodone— Data are not consistent regarding the bene- were prescribed as well (Maxam-Moore et al., fits of thoracic epidural anesthesia. In one 1994). Morphine has been used effectively as study involving cardiac surgery patients, par- opioid analgesia in other postoperative car- ticipants received either (1) thoracic epidural diac surgery patients (Coventry, Siffleet, & analgesia in combination with general anes- Williams, 2006). thesia, which was followed by postoperative NSAIDs delivered intravenously have also patient-controlled thoracic epidural analge- been identified as a preferred method of pain sia, or (2) general anesthesia, followed by PCA management for CABG patients (Rosenquist with intravenous morphine. No differences & Rosenburg, 2003). Their use in conjunction between these two groups were observed in with opioids in the majority of other surgical terms of pain relief, pulmonary function, procedures is well established. NSAIDs have ambulation, level of sedation, length of stay, been found to relieve pain more effectively or quality of recovery. The study authors did and to decrease the use of opioids (Roediger conclude, however, that thoracic epidural et al., 2006). Data suggest that administering anesthesia decreases stress response and pain NSAIDs results in reduced pain scores, less scores (Hansdottir et al., 2006). The major opioid requirements, and no differences in concern when using that method of pain mortality or incidence of serious side effects management is the potential for development (Bainbridge, Cheng, Martin, & Novick, 2006). of an epidural hematoma. When this strategy However, NSAID use has been limited in is used, the ICU nurse must monitor for and cardiac surgery patients due to these medica- report lower extremity motor weakness tions’ potential for troublesome side effects. (Mehta & Kumar, 2004). The actual occurrence of side effects tends to The use of intrathecal morphine has been depend on whether the medication inhibits reported to be effective in the management of cyclo-oxygenase 1 or 2 (COX-1 or COX-2), or postoperative cardiac surgery pain. In one both. Serious side effects, including sternal study, patients undergoing on-pump bypass wound infections, myocardial ischemia, who received intrathecal morphine prior to infarction, stroke, and pulmonary embolus, induction of general anesthesia were extu- have been reported with the use of COX-2 bated earlier and had a shorter ICU length of inhibitors; as a consequence, these medica- stay than did a comparison group of patients tions are not recommended for patients who did not receive the intrathecal injection deemed to have an increased cardiac risk prior to induction (Yapici et al., 2008). (Bainbridge et al., 2006; Roediger et al., 2006). Epidural and local anesthetics are the pre- ■ ferred methods for managing pain in patients PAIN SEQUELAE who are undergoing a thoracotomy (Rosen- If postoperative pain is not well controlled, quist & Rosenburg, 2003). Agreement exists complications such as pneumonia and that epidural use in these patients provides an chronic pain may occur. This possibility has excellent method for pain control during the encouraged the evaluation of other options to acute pain phase (Jensen & Andersen, 2004; assist with the control of pain. Local anes- Pennefather, Akrofi, Kendall, Russell, & thetic agents may prove effective if they are Scawn, 2004; Tan, Guha, Scawn, Pennefather, injected into the nerves prior to sternal & Russell, 2004). Other reported benefits of wound closure (Barr, Tutungi, & Almeida, epidural analgesia include earlier extubation 2007; Markman & Philip, 2007). However, the 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 296

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use of other types of local injections has not a significant decrease in anxiety and pain shown to be equally beneficial. One study compared to patients who rested. No differ- examined the use of lidocaine injections in ence was reported in opioid use between these the skin prior to a thoracotomy; the results two groups, however (Sendelbach, Halm, did not show any decrease in postoperative Doran, Miller, & Gaillard, 2006). pain (Cerfolio et al., 2003). In another study, A study in patients who underwent CABG patients with shoulder pain following a tho- surgery revealed a correlation between use of racotomy procedure had bupivacine injected slow, deep breathing with medications during in the intrapleural space; no effective pain painful procedures such as chest tube relief was noted (Pennefather et al., 2005). removal and a decrease in pain scores imme- Epidural use has been limited in other cardiac diately after the procedure and 15 minutes surgery patients due to concerns about later (Friesner, Curry, & Moddeman, 2006). hypotension, decreased coronary perfusion, In a study of postoperative cardiac surgery and potential hematoma formation after patients, those who used TENS experienced heparinization (Barr et al., 2007; Markman & less pain related to coughing and improved Philip, 2007). chest wall mechanics, tidal volume, and vital Nonpharmacologic interventions to assist capacity (Cipriano, Carvalho, Bernardelli, & with the pain control range from relaxation Peres, 2008). techniques, application of cold to the surgical Massage therapy has been implemented to site, and use of transcutaneous electrical promote comfort and reduce pain in cardiac nerve stimulation (TENS). The success of surgery patients. It has been suggested pro- relaxation techniques typically is patient viding massage helps decrease pain and anxi- dependent, although results appear to be bet- ety in these patients and may be used as an ter if preoperative teaching has occurred alternative intervention when other nursing (Rosenquist & Rosenburg, 2003). Unfortu- and medical treatments are not effective in nately, to date nonpharmacologic methods of helping with these symptoms (Anderson & pain control have been only minimally Cutshall, 2007). addressed in research on cardiac surgery patients. ■ Use of music as a pain management REASSESSMENT OF PAIN approach has been studied and shows some The aftermath of the pain experience focuses promise. In a review of studies from 1995 on the nurse’s evaluation of pain. The plan of through 2007, 42 studies were conducted to care is reviewed, and assessment is refocused assess the efficacy of music as a means of pain to determine if the interventions assisted with control, with roughly half showing pain pain reduction. Reassessment of pain entails a reduction might be achieved with this comparison of the pain exhibited after the method. Of the 42 studies, 7 were conducted intervention versus the pain observed at the with cardiothoracic surgery patients (Nilsson, initial assessment (McCaffery, 1972). Atten- 2008). A study of postoperative cardiac sur- tion must be given by nurses to reassess gery patients using music during rest in con- patients after any treatment to determine junction with medications showed a efficacy. reduction in anxiety and pain as compared to Little research has been conducted in the rest and medications alone (Voss et al., 2004). areas of reevaluation of pain and the measure- In a later study, cardiac surgery patients who ment tools used to determine the patient’s received music interventions also experienced level of comfort. One study, however, found a 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 297

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significant lack of reassessment by nurses. Its When studying pain differences reflective authors propose that knowledge, time, and of gender, gender personality traits are meas- workload may be factors that limit effective ured in relation to pain. For example, persons reassessment. Interestingly, these researchers identified with more feminine characteristics found that nurses tended to be more focused (women) report experiencing more pain than on surgical incision pain and, therefore, did men. Additionally, it is reported that men— not consider other complaints of pain as a that is, those persons with more masculine priority, resulting in a delay in treatment traits—report a higher tolerance of pain (Bucknall et al., 2007). It is crucial that nurses (Bernardes et al., 2008). Gender-related differ- be aware of the potential gap in pain control ences exist among pain beliefs, expectations, measures that result from periods of and behaviors. Gender role expectations can increased and uncontrolled pain due to lack account for males predominately underre- of timely reevaluation (Polomano, Dun- porting pain and women being more apt to woody, Krenzischek, & Rathmell, 2008). verbalize pain. Additionally, males demonstrate greater pain endurance, whereas women report a lower threshold and toler- ■ SPECIAL CONSIDERATIONS ance, resulting in their greater willingness to Pain is a unique individualized experience. report pain (Wise et al., 2002). Similarly, stud- Nevertheless, some elements that affect the ies suggest that women were more likely to response to pain management techniques experience severe pain and on a more frequent may apply across certain groups of people. basis. In a study of cardiac surgery patients, Recognition of these special considerations female patients rated their pain on a VAS may assist the nurse with managing an indi- higher than did their male counterparts vidual’s pain. The special considerations for (Meehan, McRae, Rourke, Eisenring, & Impe- pain management discussed here are gender rial, 1995). Some differences in the reports of differences, cultural influences, and older age. pain between males and females may be related to the issue of willingness to make a self-report: Males and females have differing Gender behaviors regarding the expression and Research has shown that there are differences response to pain (Miller & Newton, 2006). in the way males and females perceive and These data on gender differences have been experience pain. Both biological and psy- corroborated through studies in other chosocial factors are important to consider in patients who have undergone cardiac surgery. this respect. Biological factors include hor- Compared to males, females more frequently mone and cardiovascular status (Wise, Price, report less improvement in pain scores or Myers, Heft, & Robinson, 2002). Other bio- higher pain intensity (Decker & Perry, 2003; logical factors may relate to the type of stimu- Puntillo & Weiss, 1994; Valdix & Puntillo, lus and neural receptor differences (Giles & 1995; Watt-Watson et al., 2004; Yorke, Walker, 2000). Psychosocial factors encom- McLean, & Wallis, 2004), report lower health- pass individual expectations, emotions, and related quality of life after cardiac surgery social learning (Giles & Walker, 2000; Wise et (Gjeilo, Wahba, Klepstad, Lydersen, & al., 2002). Societal norms in how children of Stenseth, 2008), and experience a more diffi- both genders are raised, for example, play a cult recovery (Vaccarino et al., 2003). part in their pain experience (Bernardes, Conclusions regarding gender differences Keogh, & Lima, 2008). and recovery from cardiac surgery are not 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 298

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consistent. King (2000), for example, reported difficult in the literature, with many of the fewer differences between males and females terms being used interchangeably. The term in terms of short-term recovery following car- “race” in the literature has been debated as diac surgery. whether it is a biological or social concept. It has also been reported that gender- Typically, race is predominantly used to col- related biases may arise related to receipt of lect data regarding health disparities. There is medical treatment. Women have been found no globally accepted definition of race; how- to receive less pain medication. One reason ever, the National Institutes of Health has for this difference may be related to the gen- adopted the use of five racial categories to col- der of the observer and perception of the per- lect its data (Ezenwa, Ameringer, Ward, & Ser- son’s pain (Bernardes et al., 2008; Miller & lin, 2006). Newton, 2006). It has also been shown that By comparison, “ethnicity” refers to a women who present with pain in association group of people who share ancestry, social with anxiety tend to receive less medical background, culture, and traditions that are attention than when the pain is without emo- sustained over a period of time and provide a tional attachment (Bernardes et al., 2008). sense of identity for group members. Typi- Differences between males and females in cally, self-identification is the best approach the response to analgesia have been docu- to assigning individuals to a particular ethnic mented in the literature. Some studies show group (Lasch, 2002). greater morphine potency but slower onset of Finally, “culture” seems to be derived from pain relief in females. Additionally, it has been behavioral and attitudinal norms in relation found that NSAIDs have refractory effects in to belief systems. Culture is viewed as a factor women when doses exceed 800 mg. Pharmaco- influencing healthcare practices and illness kinetics may play a role in these differences, beliefs. In terms of the pain experience, then, although studies to date have not shown any culture affects all areas related to pain, significance in clinical practice. One explana- including expression, reporting, and manage- tion may be that the differences are related to ment (Lasch, 2002). the specific drugs, rather than to whole cate- Given that there are differences in the way gories of drugs (Giles & Walker, 2000). these terms are used and studied, findings in Greenspan and colleagues (2007) suggest the this arena must be reviewed carefully. For need to address numerous variables in terms of example, a study of low back pain found that how they influence gender-related pain immigrated Latinos in New York showed pain response. These variables include comorbidi- responses more similar to the responses of a ties, culture, disability, medications, coping, New England Latino group than to the and physical variables. To be able to appropri- responses of a group from Puerto Rico. It was ately respond to an individual’s pain experi- concluded that the pain response is shaped by ence, nurses need to be sensitive to various culture (Morris, 2001). societal norms and communication patterns Questions often arise as to whether race, related to gender and recognize the potential ethnicity, and culture affect how different differences in reports of pain and their own groups biologically experience pain or how potential biases (Miller & Newton, 2006). the factors influence the perception of pain. Additionally, culture can influence how the caregiver assesses and treats the pain of per- Race, Ethnicity, and Culture sons from different ethnic backgrounds. Distinguishing differences among the defini- Authors of several studies have reported tions of race, ethnicity, and culture has proved that minorities are at higher risk for under- 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 299

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treatment of pain (Lasch, 2002). Although resulting in a longer duration of action not studying cardiac surgery patients specifi- (Burgess & Burgess, 2008; Goldstein & Morri- cally, significant differences have been son, 2005). For this reason, care must be reported in terms of the amount of narcotic taken when prescribing, administering, and analgesics administered to patients who were monitoring the effects of pain medications in white as compared to those who were His- the elderly population (Goldstein & Morri- panic or black (Bernabei et al., 1998; Bonham, son, 2005). 2001; Ng, Dimsdale, Rollnik, & Shapiro, Assessment is crucial for managing pain in 1996; Ng, Dimsdale, Shragg, & Deutsch, the older patient. The pain scale chosen is 1996; Todd, Deaton, D’Amato, & Goe, 2000; important to the individual functioning of Todd, Samaroo, & Hoffman, 1993). In these the older patient, and the same scale should cases, patients who were white received higher be used consistently when assessing a partic- amounts of narcotics than did patients of ular patient to ensure reliability of the results other races. A systematic review of studies in (Goldstein & Morrison, 2005). Trying differ- this area reveals further disparities in pain ent scales to determine the best fit for indi- management related to ethnicity and race in vidual patients is a good strategy. Often, the United States (Cintron & Morrison, older patients have more success using 2006). Consistent with these data, a relation- simple word scales, such as “none,” “mild,” ship between race and ethnic background and “moderate,” and “severe,” than with a prescriptions given for PCA has been identi- numeric scale or a VAS. Often, if the older fied (Ng, Dimsdale, Rollnik, & Shapiro, 1996; patient has any cognitive impairment, rating Salamonson & Everett, 2005). The lesson for pain may be difficult. The FACES scales, critical care nurses is that care must be taken which seems to be easily used, often produces to acknowledge potential differences related unreliable results with the elderly. The faces to race, ethnicity, and culture in how pain is are often seen by these individuals as repre- experienced, including the awareness that senting moods like sadness instead of pain, people are individuals with individual needs. which results in understated pain intensity (Burgess & Burgess, 2008). Additional challenges in using pain scales The Elderly Population in the elderly population relate to vision and Pain management is complex with all hearing loss, which are more prevalent in patients—but it may be even more complex in older individuals. It is critical that the nurse the elderly population. This difference may be assess for these deficits and utilize assistive explained by elderly patients’ tendency to devices as appropriate. underreport pain, difficulty communicating, For the patient with vision impairment, it and caregiver biases regarding the use of pain might be best to use a verbal reporting scale; medication in the older patient (Goldstein & in contrast, hearing-impaired patients may Morrison, 2005). prefer to use a printed scale that they can Although there may be no changes in the point or gesture toward. Depending on the perception of pain in the older patient, some severity of cognitive impairment, using a physiologic changes do occur with aging that yes/no question with a behavioral observation need to be considered when utilizing pain scale may be the best option. Studies have medications. In particular, physiologic found that using a family member’s or nurse’s changes related to kidney and liver function judgment of the pain often leads to underesti- may affect the way the older patient can mation of the actual pain experienced (Gold- metabolize and eliminate pain medication, stein & Morrison, 2005). 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 300

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The older patient’s view of pain and pain more often than were younger patients. In management is also considered a barrier to contrast, Decker and Perry (2003) reported the effective assessment and treatment of higher levels of self-reported pain in older pain. Many older patients may fear addiction patients. to painkillers and, therefore, underreport their pain. Preparing patients for pain management ■ SUMMARY following surgery provides nurses with a unique opportunity to educate patients and Adequate pain assessment and management their families about pain, tolerance, depen- for cardiac surgery patients are pivotal in dence, addiction, the patient’s disease process, helping ensure a successful outcome. This and other pain control techniques (Goldstein & complex process involves timely assessment, Morrison, 2005). intervention, reassessment, and evaluation of Treatment strategies for the older patient pain management strategies. The relationship can include medication regimens in which the of traditional pain treatment strategies and patient does not have to request treatment. their impact on pain physiology places the Options to consider may include nerve nurse in a better position for advocating for blocks, epidural analgesia, and around-the- the best treatment strategy for patients. The clock dosing of pain medications. Opioids are care focus needs to address not only the acute the most widely utilized therapy with surgical postoperative period, but also the potential patients, though their dosing needs to be con- for development of chronic pain. sidered carefully. Typically, if communication Nurses can best address their patients’ pain deficits are present, nurses may be fearful by employing a thorough and systemic of postoperative delirium and withhold approach to pain assessment and treatment. opioids. Nevertheless, even though these Recognizing the importance of reassessment medications may potentially contribute to and evaluation can have a direct impact on postoperative delirium, recent studies suggest the patient’s experience and satisfaction that patients with higher pain scores and regarding the nursing care provided. Knowl- uncontrolled pain are more likely to develop edge that assessment techniques may need to delirium (Burgess & Burgess, 2008). be adjusted when providing care to nonverbal The level of postoperative pain following and elderly patients may allow for more opti- cardiac surgery in relation to age has been mal pain control. Acknowledging the differ- investigated; results have been inconsistent, ences in pain perception related to gender and however. In one study, patients older than age culture will allow the nurse to recognize 60 received less analgesic therapy than younger trends and avoid biases when dealing with patients (Celia, 2000). Yorke, McLean, and different groups of people. Recognizing the Wallis (2004) found that older postoperative individual and subjective nature of the pain cardiac surgery patients received less analgesic experience will aid in maximizing positive therapy and were refused pain medication outcomes for pain management. CASE STUDY

A 79-year-old Hispanic female’s admission status is post myocardial infarction, with preparations being made for CABG. The nurse takes the presurgical initial health history. During the course of this interaction, the nurse notes that the patient predominantly speaks Span- ish, but can also speak English. Her daughter is available at the bedside. The patient reports a medical history of adult onset diabetes controlled with oral agents and chronic pain due 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 301

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to arthritis. The physical assessment is unremarkable. The daughter adds that the patient has a history of anxiety. Current medications include aspirin daily, Diabeta® prior to meals, multivitamin daily, ibuprofen twice a day, Ambien® as needed at night for sleep, and Xanax® as needed every 12 hours for anxiety.

Critical Thinking Questions 1. Name the top priorities of your treatment plan regarding pain management? 2. Which factors may predispose the patient toward poor pain control postoperatively? 3. Which strategies could you implement to promote the best postoperative pain control? The patient undergoes a CABG due to a left main artery blockage. She arrived to the ICU on a ventilator, with invasive hemodynamic monitoring, midsternal chest tubes, intravenous fluids, and vasopressor infusing. Morphine sulfate 1–2 mg/hr is ordered as needed for pain. The patient’s vital signs are stable, with appropriate hemodynamic parameters. Weaning from the ventilator and vasopressors has commenced without difficulty. The surgeon and the anesthesiologist prefer to have the patient extubated as soon as possible. As the patient begins to wake up, you notice her grimacing and her respiratory rate increases. You decide you need to further assess her and treat her for pain.

Critical Thinking Questions 4. Which assessment technique provides the best evaluation of the patient’s current pain? 5. Which factors should be considered when planning for treatment of this patient’s pain? You treat the patient with the lower range of the ordered dose of morphine sulfate. When reassessed after 30 minutes, the patient shakes her head “no” when asked if the pain is relieved.

Critical Thinking Question 6. What should be the nurse’s next steps? Answers to Critical Thinking Questions 1. The patient’s pain will be adequately managed to a level below 4 on a 1–10 scale. The patient will be able to state preoperatively the plan of care regarding the treatment of pain and management of potential side effects. 2. Gender, age, history of chronic pain, culture, and history of anxiety. 3. Preoperative education regarding expectations related to pain and the strategies to treat pain is essential. Review of pain assessment scales to determine the best method for individual patients allows patients to best report their pain postoperatively. 4. All attempts should be made for the patient to self-report her pain. Use of visual or numeric analogue scale allows the patient to point to the number that corresponds with her pain level. 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 302

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5. Attempt to identify the location of the pain by having the patient point to that area. You should ensure that the pain is surgical and not related to chronic pain of arthritis. Should the patient’s NSAID medication be restarted? What is her history of medication response? Which doses previously had relieved the pain? The patient’s experience with chronic pain may require a larger dose of pain medication now. Is the patient exhibiting any signs of anxiety? If so, this may contribute to her current pain experience. What is the time frame related to extubation? If extubation will occur in the near future, you may need to consider a lower opioid dose and other adjuvant strategies. 6. Consider re-treating the patient with the PRN morphine sulfate as prescribed. Con- sider seeking treatment for anxiety if the assessment suggests that anxiety may be contributing to her pain. If the patient’s pain remains uncontrolled, consider a PCA. The lower basal dose may be more effective in controlling the patient’s pain, plus it will allow the patient to remain awake and able to participate in her care. Additionally, assess the possibility of restarting NSAIDs for the patient’s arthritis and new inflammatory processes as soon as deemed appropriate. NSAIDs are appropriate treatment options for CABG patients, though they are not often used immediately postoperatively due to their potential to enhance bleeding.

■ SELF-ASSESSMENT QUESTIONS of injury to the skin, which is perceived by the person owing to 1. Which of the following is the most triggers located in the brain. important assessment for the nurse to d. Pain physiology is subjective and determine that a patient is experiencing categorized as acute or chronic, with pain? the differentiation related to how a. Measurement of increased blood long the patient has exhibited the pressure symptoms. b. Observation of grimacing to touch c. Patient’s report of pain 3. A nurse is caring for a patient who is 5 d. Patient guarding the surgical area days status post CABG surgery. Which of the following best describes the type 2. Which of the following statements by of pain this patient is experiencing? the nurse best explains the concept of a. Acute, neuropathic pain pain physiology? b. Acute, nociceptive pain a. Pain physiology is a complex series of c. Chronic, neuropathic pain steps that includes tissue injury, d. Chronic, nociceptive pain which then triggers a reaction that results in the transmission of 4. The nurse can best ascertain the severity impulses to the spinal cord and brain, of pain by asking the patient to producing the perception of the pain. a. describe the pain. b. Pain is caused by actual events that b. discuss the timing and duration of cause injury to the tissues, which the pain. results in the brain perceiving the c. rate the pain on a scale of 0 to 10. stimulus of pain. d. report relief of pain after treatment. c. Pain physiology is truly a physiologic phenomenon that occurs as a result 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 303

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5. Which of the following is the best 9. A nurse is caring for a male patient who method to assess pain in a nonverbal requires cardiac surgery. Which of the patient? following statements by the nurse indi- a. Family observations cates an understanding of gender differ- b. Physiologic changes ences related to pain? c. FACES pain scale a. “Because males have a faster d. Behavioral assessment tool metabolism compared to females, 6. Which of the following strategies would males may require a higher dose of best suit the pain experience phase of opioids to control their pain.” anticipation? b. “Observation of other indicators and a. Education behaviors of pain is warranted because b. Continual reassessment males often underreport pain.” c. Pharmacologic management c. “Caregiver perceptions regarding pain d. Relaxation exercises perception need to be recognized 7. Which of the following pharmacologic because males have a lower threshold combinations is the preferred treat- for pain and complain more often ment method for patients having a than do females.” thoracotomy? d. “Gender differences have been linked a. Intravenous opioids and NSAIDs primarily to physiologic processes, b. Intravenous PCA-delivered opioids and men may require more aggressive and local anesthetics treatment than females.” c. Epidural opioids and local 10. Which of the following issues is the anesthetics most challenging in the treatment of d. Epidural opioids and NSAIDs pain in the elderly? 8. Which of the following statements best a. Communication impairment may explains why NSAIDs are limited in car- limit objective assessment data. diac surgery patients? b. Physiologic changes related to kidney a. The potential for serious side effects and liver function may alter dosing with NSAID administration guidelines. outweighs the benefits of these c. Fear of addiction may limit the medications’ use. patient’s report of pain. b. There have been reports d. Caregiver biases may lead to the under of neurological changes in treatment of pain in elderly patients. elderly patients after NSAID Answers to Self-Assessment Questions administration. 1. c 6. a c. The inflammatory process is 2. a 7. c necessary for healing to occur. 3. b 8. a d. The amount of opioids used postoperatively is unchanged 4. c 9. b regardless of NSAID administration. 5. d 10. a 57625_CH14_287_308.pdf 4/10/09 11:09 AM Page 304

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Clinical Inquiry Box

Question: Do certain activities postoperatively induce more pain than other activities? Reference: Milgrom, L., Brooks, J. A., Qi, R., Bunnell, K., Wuestefeld, S., & Beckman, D. (2004). Pain levels experienced with activities after cardiac surgery. American Journal of Critical Care, 13(2), 116–125. Objective: To describe pain levels associated with five postoperative activities following cardiac surgery. Methods: A secondary, descriptive analysis design was used for a subset of 711 patients undergoing cardiac surgery. The patients were divided into four groups: Group 1 consisted of those patients who had undergone single (aortic or mitral) valve replacement; group 2 patients underwent an on- pump CABG procedure; group 3 patients had an off-pump CABG procedure; and group 4 patients had undergone multiple cardiac surgeries. On postoperative days 1–6, the 711 patients were asked to rate their pain following five activities: rest while lying in bed, coughing, deep breathing or using an incentive spirometer, movement or turning in bed, and getting up to a chair or to walk. Analysis was focused on comparing pain levels for the postoperative day, activity, and type of surgery. Pain scores before and after chest tube removal and extubation were analyzed. Results: Pain scores were higher on earlier postoperative days. The highest pain level was reported during coughing. As time progressed, pain lessened significantly. Changes in pain reported with coughing and deep breathing or using the incentive spirometer were significant over time between some surgery groups. The removal of chest tubes was a significant event in decreasing the pain associated with activities such as being at rest, coughing, and getting up. Conclusion: Pain was present on postoperative day 6 in all patient groups, which indicates a need for nurses to critically evaluate pain and provide measures that will bring about relief. While nurses should certainly treat each patient individually, there is important information to be applied from this study. Although the level of pain did diminish over the 6-day period in all groups, nurses need to respond more aggressively to control pain. The removal of chest tubes resulted in a significant decrease in pain level with activities, and may be a point in the recovery trajectory at which to consider the timing of education.

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Todd, K. H., Samaroo, N., & Hoffman, J. R. (1993). Yapici, D., Altunkan, Z. O., Atici, S., Bilgin, E., Ethnicity as a risk factor for inadequate emer- Doruk, N., Cinel, I., et al. (2008). Postoperative gency department analgesia. Journal of the effects of low-dose intrathecal morphine in American Medical Association, 269(12), coronary artery bypass surgery. Journal of Car- 1537–1539. diac Surgery, 23(2), 140–145. Vaccarino, V., Lin, Z. Q., Kasl, S. V., Mattera, J. A., Yorke, J., McLean, B., & Wallis, M. (2004). Patients Roumanis, S. A., Abramson, J. L., et al. (2003). perceptions of pain management after cardiac Gender differences in recovery after coronary surgery in an Australian critical care unit. artery bypass surgery. Journal of the American Heart & Lung: The Journal of Acute and Critical College of Cardiology, 41(2), 307–314. Care, 33(1), 33–41. Valdix, S., & Puntillo, K. (1995). Pain, pain relief and accuracy of their recall after cardiac sur- ■ gery. Progress in Cardiovascular Nursing, 10(3), WEB RESOURCES 3–11. American Academy of Pain Management: www Voss, J. A., Good, M., Yates, B., Baun, M. M., .aapainmanage.org/ Thompson, A., & Hertzog, M. (2004). Sedative Pain Management Nursing: http://www.pain music reduces anxiety and pain during chair managementnursing.org/ rest after open heart surgery. Pain, 112(1–2), American Pain Society: www.ampainsoc.org/ 197–203. National Pain Foundation: www.national Watt-Watson, J., & Stevens, B. (1998). Managing painfoundation.org/default.asp pain after coronary artery bypass surgery. Car- International Association for the Study of Pain diovascular Nursing, 12(3), 39–51. (IASP): www.isap-pain.org/ Watt-Watson, J., Stevens, B., Garfinkel, P., Streiner, American Society for Pain Management Nursing D., & Gallop, R. (2001). Relationship between (ASPMN): www.aspmn.org/ nurses’ pain knowledge and pain management National Pain Education Council: www.npecweb.org/ outcomes for their postoperative cardiac patients. Journal of Advanced Nursing, 36(4), Daily Pain Diary: www.americangeriatrics.org/ 535–545. education/daily_pain_diary.pdf Watt-Watson, J., Stevens, B., Katz, J., Costello, J., Inside look at chronic pain: www.or-live.com/ Reid, G., J., & David, T. (2004). Impact of pre- distributors/nlm-flash/chp_1867/rnh operative education on pain outcomes after .cfm?id=704 coronary artery bypass graft surgery. Pain, Transcutaneous electrical nerve stimulation 109(1–2), 73–85. (TENS): www.intelihealth.com/IH/ihtIH/ Williamson, A., & Hoggart, B. (2005). Pain: A WSIHW000/8513/34968/363973.html?d review of three commonly used pain scales. =dmtContent Journal of Clinical Nursing, 14(7), 798–804. Wise, E. A, Price, D. D., Myers, C. D., Heft, M. W., & Robinson, M. E. (2002). Gender role expectations of pain: Relationship to experimental pain perception. Pain, 96(3), 335–342. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 309

Chapter 15 Postoperative Dysrhythmias

Roberta Kaplow and Dawn B. Adams

■ INTRODUCTION Patients may have dysrhythmias prior to sur- ment), respiratory complications, electrolyte gery or develop them postoperatively. Indeed, disturbances (e.g., hypokalemia, hyper- dysrhythmias are a common complication kalemia, hypomagnesemia), surgical trauma following cardiac surgery. The origins of such (inadequate cardioprotection during bypass dysrhythmias often include the atrium, atri- procedures), hypothermia, hyperadrenergic oventricular (AV) node, and ventricle. This state, acid–base imbalance, anxiety, or pain chapter discusses the most commonly (Bharucha & Marinchak, 2007). encountered postoperative dysrhythmias, The overall reported incidence of premature including their incidence, etiology, and sug- beats, tachydysrhythmias, and bradydysrhyth- gested management. mias is reported to be 30–50% in patients who Dysrhythmias may compromise cardiac have undergone coronary artery bypass grafting output (CO) when they interfere with dias- (CABG) procedures (Brister & Lenkei-Kerwin, tolic filling. It is essential that the nurse work- 2005). The incidence is higher in patients who ing in the ICU with postoperative cardiac have undergone valve surgery or CABG in com- surgery patients be proficient in identifying bination with valve surgery. In fact, patients in and possibly eradicating potential causes as one study who had undergone CABG, valve and well as promptly recognizing potentially life- CABG, and valve-only procedures had a threatening dysrhythmias. Assessment of the reported dysrhythmia incidence of approxi- patient requires evaluation of cardiac rhythm, mately 90%, 100%, and 50%, respectively its effects on systemic perfusion, and etiologic (Dewar, Rosengarten, Blundell, & Chiu, 1985). factors. ■ ATRIAL DYSRHYTHMIAS ■ ETIOLOGY Atrial dysrhythmias are the most commonly Several potential etiologic factors related to encountered rhythm abnormalities encoun- postoperative cardiac surgery dysrhythmias tered in the postoperative CABG patient. have been identified. Dysrhythmias in this Their incidence is reported to be as high as patient population may result from cardiac 50% in patients undergoing valve replace- problems (e.g., pericarditis, atrial infarction or ments (Hogue, Creswell, Gutterman, & ischemia, injury to the atrium during surgery, Fleisher, 2005). Atrial dysrhythmias that may fluid overload-induced acute atrial enlarge- develop in the postoperative cardiac surgery

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patient may include sinus tachycardia, prema- Ganim, & Rawn, 2008; Maisel, Rawn, & Steven- ture atrial contractions, atrial fibrillation son, 2001). The majority of patients with new- (AF), and atrial flutter. onset AF convert back to normal sinus Sinus tachycardia is a common dysrhyth- rhythm (NSR) within 6 to 8 weeks postopera- mia following surgery in general, with cardiac tively (Khalpey et al., 2008). It has been sug- surgery being no exception. It can be attrib- gested that patients who develop AF uted to the normal stress response. As a gen- following cardiac surgery are more likely to eral guideline, treatment of sinus tachycardia have other complications, including myocar- should focus on ameliorating its underlying dial infarction (MI), heart failure, or respira- cause. Etiology of sinus tachycardia may tory failure (Almassi et al., 1997). include pain, fever, anxiety, anemia, medica- The pathophysiology of AF involves the tions (e.g., catecholamines, pancuronium), rapid release of multiple impulses from the hypermetabolic state (e.g., sepsis), or an atrium to the AV node; however, the AV node increase in adrenergic tone (e.g., in a patient can respond to only a few of these impulses. taking a beta blocker preoperatively). The In AF, the patient’s heart does not contract presence of sinus tachycardia is not likely to with maximum efficiency. The rapid quiver- cause adverse effects if the patient has normal ing of the atria may result in hemodynamic left ventricular (LV) function, and treatment compromise from decreased atrial filling and is usually not indicated (Brister & Lenkei- the atrial kick that can normally contribute as Kerwin, 2005). much as 20% of CO. In patients with normal Premature atrial contractions may also LV function, however, AF is generally well tol- develop in the postoperative cardiac surgery erated (Brister & Lenkei-Kerwin, 2005). patient. These abnormal beats are usually not Because the blood lingers in the atria with AF, clinically significant and rarely require treat- small clots may develop, which place the ment. However, they may signal the develop- patient at risk for stroke. Development of AF ment of atrial tachydyshythmias in this may lead to increased length of hospital stay patient population (Brister & Lenkei-Kerwin, and greater use of resources (Aranski et al., 2005). Although not consistently defended in 1996; Archbold & Zaman, 2000). the literature, consideration may be given to Treatment of AF focuses on control of rate administering magnesium sulfate in the and rhythm. Ultimately, intervention to bring immediate postoperative period to prevent or about a conversion from AF to NSR is most treat atrial tachydysrhythmias (Piotrowski & desirable. Numerous approaches have been Kalus, 2004). employed, including use of antiarrhythmic AF is a common dysrhythmia that may agents, synchronized cardioversion (SCV), occur in the postoperative cardiac surgery and surgical interventions (e.g., Cox-Maze III, patient. Its reported incidence ranges from Ex-Maze procedure, or cryoablation). The 10% to 65% in this patient population. The Cox-Maze III procedure has a success rate of incidence varies with type of procedure per- 75–97% and is often performed during the formed, with 20–40% for patients who have repair of a mitral valve (Ghavidel et al., 2008). undergone CABG procedures developing AF In addition, a variety of ablative techniques and as many as 50% of patients who have that electrically separate the pulmonary veins undergone valve surgery experiencing this from the atria have been used to ensure that complication. The onset of occurrence is 1 to impulses are not conducted. While ablative 3 days following surgery (Archbold & Zaman, methods do not have as high a success rate as 2000; Brister & Lenkei-Kerwin, 2005; Creswell, some other surgical approaches, they are sim- Schuessler, Rosenbloom, & Cox, 1993; Khalpey, pler, are cost-effective, and have a 57–70% cor- 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 311

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rection rate (Jais et al., 2004). Surgical treat- genital heart defects, changes in elasticity of ment of AF is discussed in more detail in the atrial wall lead to increased atrial Chapters 3 and 6. excitability. Conduction pathways other than the heart’s normal pathway develop in the refashioned tissue, with the ultimate result Risk Factors for Postoperative being AF or flutter (Furer, Gomes, Love, & Atrial Dysrhythmias Davendra, 2005). Knowing the factors that Many studies have attempted to determine the predispose the patient to developing AF, the etiology of AF in the postoperative cardiac sur- nurse will attempt to anticipate the occur- gery patient. A patient’s demographic data rence of this complication and will be pre- and medical history provide insight into the pared to quickly respond to the dysrhythmias probability of postoperative dysrhythmias. and convert the patient to NSR. The primary predictor of postoperative AF is Another factor thought to contribute to AF age. As the body ages, structural and size is hypomagnesemia (Archbold & Zaman, 2000; changes of the atria predispose the individual Miller et al., 2005). Hypomagnesemia may be to develop atrial dysrhythmias (Sethares, attributed to the effects of hemodilution and Seifert, & Smith, 2008). Other risk factors beta-adrenergic-mediated mechanisms. Data include pericarditis, previous cardiac surgery, remain inconsistent regarding the correlation increased adrenergic tone, electrolyte deple- between AF and low magnesium levels. Results tion (e.g., potassium, magnesium), valvular of a meta-analysis suggest that prophylactic heart disease, atrial enlargement, and preoper- preoperative administration of magnesium ative atrial dysrhythmias (Creswell et al., 1993; may decrease the incidence of postoperative AF Fuster & Ryden, 2001; Maisel et al., 2001). without increasing either morbidity or hospi- A detailed preoperative history is important tal length of stay (Miller et al., 2005). Prophy- in preventing postoperative dysrhythmias. laxis for AF should include magnesium sulfate Analysis of the ECG will reveal the presence of 2 g IV after cardiopulmonary bypass and on preexisting conditions such as left ventricular the first postoperative morning. In addition, hypertrophy, which is also believed to be a metoprolol 25–50 mg PO or by nasogastric precursor to postoperative dysrhythmias tube may be started 8 hours after surgery (Hogue et al., 2005). The preoperative ECG (Piotrowski & Kalus, 2004). also plays a role in later care, serving as a basis In another study, Baldwin and Heland for comparison postoperatively. Chronic dis- (2000) noted the incidence of dysrhythmias orders such as those previously mentioned are to be approximately 20% in postoperative car- thought to contribute to AF through their diac surgery patients. The dysrhythmias were effects of remodeling of atrial tissue (Sethares reported to be related to removal of a pul- et al., 2008). If AF is present, its rate should be monary artery catheter. The most life-threat- controlled and its duration identified. If AF ening of the dysrhythmias reported was has been present for less than 6 months, it is nonsustained ventricular tachycardia (VT), likely that conversion to NSR can be obtained which occurred in 2% of the cases. postoperatively (Piotrowski & Kalus, 2004). Remodeling of the myocardium occurs in Intraoperative Factors Contributing to patients who experience long periods of vol- Postoperative Atrial Dysrhythmias ume or pressure elevation. The tension Manipulation of the heart during surgery exerted on myocardial cells causes a reconfig- and changes in the fluid and electrolyte com- uration of the muscle fibers. For patients with position of the blood may also influence the a previous history of chronic disease or con- incidence of postoperative dysrhythmias. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 312

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Techniques used to stop the heart from beat- Atrial Dysrhythmias Following Cardiac ing and to isolate the surgical area may be Transplant contributing factors to this complication. For Following cardiac transplantation, the ECG on-pump procedures, the heart must be may reveal two P waves. In orthotopic heart cooled and induced into arrest. Electrolyte- transplantation, part of the right atrium of rich cardioplegic solutions are infused into the diseased heart remains attached to the the heart to allow the surgeon to work on a aorta and the donor heart is connected at this stabilized, nonbeating organ with this surgi- juncture. White-Williams and Grady (2008) cal approach (Guo-Wei, 1997). delineated other sources to explain this phe- Creswell, Alexander, Ferguson, Lisbon, nomenon of the two P waves’ appearance. If and Fleisher (2005) reported a correlation the donor P wave has the smaller height of between atrial ischemia and prolonged car- the two waves, it indicates that the leftover dioplegia. Moreover, with the utilization of sinus node of the removed heart is regulating on-pump procedures, an inflammatory the spread of the impulse onto the AV node response that releases histamine during use and His bundle of the donor heart. The wave- of the aortic cross-clamp is associated with form may be misinterpreted as complete AF and flutter development (Fayaz, Pugh, heart block. Balachandran, Sudheer, & Hall, 2005). In the cardiac transplant patient, postopera- During the intraoperative period, fluid bal- tive AF incidence is the same as in other cardiac ance and electrolyte composition in the blood surgical procedures. Concern for electrolyte are altered. Patients receive fluid boluses, and replacements related to volume resuscitation is electrolyte shifts occur with loss of blood and also similar. Balance of potassium, magnesium, the bypass procedure. Oftentimes, the elec- and calcium must be tightly controlled (Wade, trolyte shifts result in decreased levels of Reith, Sikora, & Augustine, 2004). potassium, magnesium, calcium, and pH, which are all essential to electrical conduction (Martin & Turkelson, 2006). Management of Postoperative Data from another study suggest that the Atrial Dysrhythmias temperature of systemic cooling during Several treatment strategies for the manage- bypass procedures contributes to the development of AF have been reported. When a post- ment of AF after CABG surgery. Data from operative cardiac surgery patient develops AF, this study also confirm that increasing age is hemodynamic stability status, possible under- a significant contributor to the incidence of lying causes, and goals of treatment are all key AF in the postoperative cardiac surgery popu- considerations that need to be identified lation (Adams et al., 2000). Other identified promptly. possible etiologic factors of AF that have been Atrial fibrillation can decrease CO by 25–30%. identified in the literature include atrial Establishment of hemodynamic stability should stretch from volume overload, increased sym- be the principal goal of therapy. Signs of hemo- pathetic tone, ischemia, pericarditis, sympa- dynamic compromise may include hypotension, thomimetic agents (e.g., bronchodilators, mental status changes, decreased urine output, inotropes), respiratory conditions (e.g., pneu- impaired peripheral perfusion, chest pain, and monia, pulmonary embolism, atelectasis), signs of decreased CO or increased filling pres- metabolic/acid–base/electrolyte disturbances, sures (Khalpey et al., 2008). and surgical manipulation (Khalpey et al., Hemodynamic stability may need to be 2008; Stamou, Hill, & Sample, 2001). attained by controlling rate, rhythm, or both; 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 313

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the former is usually all that is required and is Although varying by procedure type, the the preferred method to treat AF (Fuster & overall decrease in risk for postoperative AF Ryden, 2001). The pharmacologic agents used development with prophylactic beta-blocker to prevent or treat postoperative dysrhyth- administration has been reported to be 72% mias are discussed in detail in Chapter 12. (Andrews, Reimold, Berlin, & Antman, 1991). Agents that are used to control heart rate Studies of patients who are undergoing CABG include beta blockers, calcium channel block- revealed that their risk for this complication ers, and digoxin. Digoxin may be effective in decreased from 40% to 20% when prophylactic controlling the ventricular rate associated beta-blocker therapy was implemented. Simi- with AF, but is reportedly not as effective as larly, patients having valve surgery had a beta-blocker therapy (Bharucha & Marin- decrease in risk from 60% to 30% (Fuster & chak, 2007). Ryden, 2001; Maisel et al., 2001). Metoprolol (Lopressor®) is recommended Amiodarone (Cordarone®) has been used pro- as first-line therapy for most patients. Dilti- phylactically to prevent atrial dysrhythmias, azem (Cardizem®), administered as an IV though its efficacy in this indication is not as bolus and followed by an infusion, is the cal- high as that for some other medications. Toxici- cium channel blocker of choice. Calcium ties (e.g., pulmonary toxicity, thyroid, or liver dys- channel blockers are generally used if beta function) should be considered if amiodarone is blockers are contraindicated. Digoxin may be being used in this manner (Khalpey et al., 2008). contemplated for patients with contraindica- Amiodarone prolongs both the duration and tions for beta-blocker therapy (e.g., patients the refractory period of the myocardial cell with low ejection fraction) (Khalpey et al., action potential. It possesses mild alpha, beta, 2008). Data suggest that digoxin is less effec- and calcium channel blocking effects, which tive as a prophylactic measure (Thompson, have been shown to be effective in decreasing Hirsch, & Pearson, 2002). incidence of AF (Stamou et al., 2001). As noted Antiarrhythmic agents used to convert the in Chapter 12, amiodarone is generally recom- patient from AF include metoprolol, dilti- mended if a beta blocker or calcium channel azem, ibutilide (Corvert®), and amiodarone. blocker proves ineffective in the conversion of Ibutilide is administered if SCV does not con- AF (Fuster et al., 2006). vert the rhythm. This medication is given as a Sotalol (Betapace®), another beta blocker, bolus and may be repeated once. The ICU has also been evaluated for prophylaxis of AF nurse must monitor the patient for develop- in cardiac surgery patients. Data initially sug- ment of torsade de pointes if ibutilide is used gested that sotalol was as effective an agent as (Khalpey et al., 2008). amiodarone (Wurdeman, Mooss, Mohiuddin, Prophylaxis for AF usually entails use of beta & Lenz, 2002). However, the 2004 ACC/AHA blockers, which should be resumed as soon as guidelines for postoperative CABG patients possible postoperatively. The efficacy of meas- reflected a downgrading of the recommenda- ures aimed at preventing postoperative AF is tion, as the efficacy of sotalol to prevent AF is enhanced when beta blockers are initiated pre- not well established based on the most recent operatively (Maisel et al., 2001). Contraindica- data (Bharucha & Marinchak, 2007). tions to beta blocker use include hemodynamic In addition to the use of beta blockers to compromise, use of inotropes, and presence of treat AF postoperatively, research supports heart block (i.e., first-degree heart block with a the use of treating paroxysmal AF with ® PR interval greater than 0.24 second, second- carvedilol (Coreg ). Carvedilol blocks alpha1 or third-degree heart block). receptors and has a vasodilator effect, so that 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 314

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its use results in little change in the hemody- ment of atrial flutter, and this medication namic profiles of patients. Postoperative parox- should be used with caution when the origin ysmal AF, which is often seen in patients of of the tachyarrhythmia is unclear, as it may advanced age, may be prevented with carvedilol produce ventricular fibrillation (VF) in (Tsuboi, Kawazoe, Izumoto, & Okabayashi, patients with coronary artery disease and AF 2008). Carvedilol may be used to control the with a rapid ventricular response in the set- ventricular rate of AF. ting of pre-excited tachycardias. Adenosine Patients who developed AF during their should be avoided in patients with severe postoperative cardiac surgery trajectory and bronchial asthma (American College of Cardi- remain in AF for more than 24 hours or have ology, American Heart Association, & Euro- persistent incidents of AF should receive anti- pean Society of Cardiology, 2003). coagulant therapy. These individuals may be discharged home on oral anticoagulant ther- ■ apy even if they convert to NSR prior to dis- VENTRICULAR DYSRHYTHMIAS charge. If patients have atrial enlargement, Three dysrhythmias of ventricular origin have they remain at risk for development of recur- been reported in the postoperative cardiac rent paroxysmal AF (Brister & Lenkei-Kerwin, surgery patient: premature ventricular con- 2005; Khalpey et al., 2008). The patient who tractions, VT, and VF. Premature ventricular underwent CABG is also at increased risk for contractions usually do not require interven- stroke development (Fuster & Ryden, 2001). tion if the patient has normal LV function In 2005, the American College of Chest Physi- and electrolyte levels. Either or both of these cians released evidence-based clinical practice etiologies require correction if LV or elec- guidelines for the prevention and manage- trolyte abnormalities are present. For exam- ment of postoperative AF after cardiac sur- ple, alterations in potassium or magnesium gery (McKeown & Gutterman, 2005). The use levels may be the underlying cause that would of atrial pacing for prevention of postopera- require optimization (Brister & Lenkei-Ker- tive AF has been noted in the literature win, 2005). In one study of postoperative car- (Greenberg, Katz, Iuliano, Tempesta, & diac surgery patients, administration of Solomon, 2000). In this study, the use of beta supplemental magnesium decreased the fre- blockade and atrial pacing decreased length quency of postoperative ventricular dysrhyth- of hospital stay by 22%. mias and increased stroke volume in the early If the patient has hemodynamic instability postoperative period (England, Gordon, accompanying rhythm disturbances, SCV Salem, & Chernow, 1992). should be performed. The clinician should fol- Ventricular dysrhythmias are less common low advanced cardiac life support (ACLS) pro- than dysrhythmias of atrial origin in patients tocols for dysrhythmia management, as having undergone cardiac surgery and may be delineated by the American Heart Association. indicative of myocardial dysfunction. Parox- If the patient develops supraventricular ysmal VT occurs in 17% to 97% of patients; its tachycardia (SVT) without symptoms of development is believed to be related to reper- hemodynamic compromise following cardiac fusion. Non-paroxysmal monomorphic or surgery, adenosine (Adenocard®) may be polymorphic VT or VF occurs in 1% to 3% of administered. Adenosine should not be used in patients (Aranki, Cutlip, & Aroesty, 2008). patients with atrial flutter, those who under- Predictors of postoperative VT or VF that went cardiac transplant, or those who have have been identified include age younger than been partially revascularized (Khalpey et al., 65 years, female gender, body mass index less 2008). Adenosine is not effective in the treat- than 25 kg/m2, unstable angina, ejection frac- 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 315

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tion less than 50%, pulmonary hypertension, used for defibrillation depends on how the systemic hypertension, prolonged cardiopul- energy is delivered—monophasic or biphasic, monary bypass (CPB), or need for inotropic although the latter is presently more common. agents, intra-aortic balloon pump (IABP), or both (Ascione, Reeves, Santo, Khan, & ■ BRADYARRHYTHMIAS Angelini, 2004; Yeung-Lai-Wah et al., 2004). Risk factors for development of monomor- Postoperatively, cardiac surgery patients may phic VT include a history of MI, heart failure, develop bradyarrhythmias such as sick sinus or decreased LV function. Development of syndrome, Mobitz II, or complete heart block polymorphic VT (i.e., torsade de pointes) is (Brister & Lenkei-Kerwin, 2005). AV block believed to be associated with perioperative may occur in patients who have undergone MI and other risk factors (e.g., hemodynamic surgery to repair an aortic, mitral, or tricuspid instability, increased sympathetic activity, valve. Development of this complication is metabolic derangements). In one study, believed to be related to surgical injury and patients who developed VT or VF had a signif- edema (Silvestry, 2008). Presence of a heart icantly higher postoperative mortality rate as block may also be associated with an inferior compared to patients who did not develop wall MI. Etiologic factors that have been iden- ventricular dysrhythmias (24.6% versus 1.5%) tified include medications (e.g., digoxin, (Aranki et al., 2008). amiodarone, calcium channel blockers, and beta blockers) and certain surgical approaches (Khalpey et al., 2008). Management of Postoperative Ventricular Dysrhythmias Management of Bradyarrhythmias Ventricular tachycardia associated with Management of bradyarrhythmias usually hemodynamic stability may be treated by entails use of a temporary pacemaker. The ameliorating the underlying cause, including epicardial wires that are oftentimes left in ruling out ischemia, replacing electrolytes, place following the initial cardiac surgery are and avoiding inotropic therapy (Khalpey used for this purpose (Zevola, Raffa, & et al., 2008). In addition, a bolus of an antiar- Brown, 2002). Transcutaneous or transve- rhythmic agent (e.g., amiodarone, lidocaine nous pacing or a pulmonary artery catheter ® [Xylocaine ], or sotalol) may be administered. with a pacing port may also be used (Khalpey Once converted, the patient may be main- et al., 2008). Rarely do bradyarrhythmias per- tained with a continuous infusion of the sist. However, in the fewer than 5% of patients antiarrhythmic that was instrumental in the who do not experience resolution, permanent chemical conversion of the dysrhythmia. If pacemaker implantation is required (Morris VT persists despite administration of antiar- & St. Claire, 1999). rhythmic agents or if VT is associated with hemodynamic instability, concomitant SCV ■ MANAGEMENT OF and antiarrhythmic administration may be indicated (Brister & Lenkei-Kerwin, 2005; DYSRHYTHMIAS FOLLOWING Khalpey et al., 2008). CARDIAC TRANSPLANT VF should be treated with immediate defib- A significant difference exists in the pharma- rillation per ACLS protocol, cardiopulmonary cological management of dysrhythmias fol- resuscitation, administration of epinephrine lowing cardiac transplant and the approaches and antiarrhythmic agents, and eradication of used in patients who undergo other open heart the underlying cause. The amount of energy surgical procedures and develop postoperative 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 316

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dysrhythmias. Digoxin is not as effective on wires emplaced. Generally, the ventricular and the SA and AV node of the transplanted heart atrial wires exit the skin to the left and right owing to the interruption in the nerve path- of the sternum, respectively. It is essential for ways from the incisions, which reduce the the ICU nurse to secure the leads to the heart’s response to the autonomic nervous patient’s chest or abdomen, have a pacemaker system (Wade et al., 2004). Bradycardia may generator with new batteries readily available, develop as a consequence of the incision and ensure that all wiring and connections made in the SA node during surgery. Atropine are tight and free of fraying. The ends of the will not be effective in this instance because of pacer wires should be covered, insulated, and the severing of the vagus nerve. protected with a clean, dry dressing. Gloves Management with a pacemaker should be should be worn when handling the wires, and the primary treatment (Wade et al., 2004). other electrical appliances should be kept Pacemakers also give the patient the needed away from the ends to prevent electrical interatrial kick and augment CO. Isoproterenol ference (Rushton & Kalpin, 2004). (Isuprel®), milrinone (Primacor®), and dobut- ® amine (Dobutrex ) may be used to increase ■ SUMMARY heart rate and improve the electrical stimulation of the newly implanted heart (Wade et Nurses caring for patients who have under- al., 2004; White-Williams & Grady, 2008). gone cardiac surgery must understand which patients are at risk for the development of dysrhythmias, know how to identify these ■ EPICARDIAL PACEMAKERS dysrhythmias, be able to prevent their occur- During surgery for CPB or valvuloplasty, pac- rence, and implement early treatment to cor- ing electrodes are attached directly to the rect any irregular rhythm that does arise. atria, the ventricles, or both. Wires are While it may be difficult to isolate the under- inserted in the event that the patient develops lying cause of a postoperative dysrhythmia, bradycardia, AF, or junctional rhythm, all of correction of possible etiologies is an essential which require better conduction control to component of successful management. As resolve. The wires are then secured to the epi- part of the clinical patient assessment, the cardium and brought out through the skin. ICU nurse should note the duration of the Depending on the surgeon’s preference, the dysrhythmia as well as any associated hemo- patient may have one or two sets of pacing dynamic effects (Atlee, 1997).

CASE STUDY

A 53-year-old male is admitted to the ICU immediately following aortic valve repair. His history includes calcific aortic valve disease and dilatation of the ascending aorta due to Ehlers-Danlos syndrome. Ehlers-Danlos syndrome is a rare, inheritable, connective tissue disease in which patients usually have a history of bruising and hyperextendability of joints (history of being double jointed). The patient underwent an aortic valve replacement with tissue (Starr) prosthesis and came off bypass without difficulty. On the third postoperative day, when he had left the intensive care unit and was making excellent progress mobilizing, he had further episodes of syncope and developed palpitations. The patient was noted to have atrial fibrillation with a rate of 124. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 317

Self-Assessment Questions 317

Critical Thinking Questions 1. Which factors might predispose this patient to new-onset atrial fibrillation? 2. Which prophylactic treatment could have been utilized to reduce the incidence of rhythm problems? 3. What is the best method to manage atrial fibrillation postoperatively in this patient? Answers to Critical Thinking Questions 1. Aortic valve repair. 2. Statins. 3. Agents that are used to control rate include beta blockers, calcium channel blockers, and digoxin. Metoprolol is recommended as first-line therapy for most patients. Dilti- azem is the calcium channel blocker of choice.

■ SELF-ASSESSMENT QUESTIONS 5. Which of the following patients with an arrhythmia should receive anticoagulant 1. Treatment of premature atrial contrac- therapy? tions is considered because this condition a. A patient who had six-beat runs of is associated with an increased risk of ventricular tachycardia a. ventricular tachycardia. b. A patient who has one episode of b. atrial tachyarrhythmias. atrial fibrillation within 2 hours of c. bradycardia. surgery d. sinus arrhythmia. c. A patient who remained in atrial 2. Which of the following postoperative fibrillation for more than 24 hours cardiac surgery patients is most likely to d. A patient who had bradycardia develop atrial fibrillation? preoperatively a. A 35-year-old male undergoing a 6. If the patient develops supraventricu- heart transplant lar tachycardia following cardiac sur- b. A 45-year-old male undergoing triple gery, which medication should be bypass surgery administered? c. A 65-year-old female undergoing a. Metoprolol aneurysm repair b. Epinephrine d. An 88-year-male undergoing aortic c. Adenosine valve surgery d. Amiodarone 3. Remodeling of the myocardium occurs in 7. Premature ventricular contractions in patients who experience long periods of postoperative cardiac surgery patients a. volume or pressure elevation. are most likely to occur due to alter- b. intraoperative ischemia. ations in levels of c. postoperative arrhythmia. a. sodium. d. postoperative hypoxia. b. calcium. 4. In orthotopic heart transplantation, the c. hemoglobin. ECG may reveal d. magnesium. a. two P waves. 8. The first line of treatment for ventricu- b. a prolonged P-R interval. lar fibrillation should be c. elevated T wave. a. administration of epinephrine. d. an inverted QRS. b. immediate defibrillation. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 318

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c. cardiopulmonary resuscitation. c. the wires are removed immediately d. antiarrhythmic agents. upon entering the ICU to prevent 9. Symptomatic bradycardia may develop electrical injury. in the postoperative cardiac surgery d. the wires are connected to a patient. Which intervention should be pacemaker generator at all times expected? until their removal. a. Atropine b. Epinephrine Answers to Self-Assessment Questions c. Pacemaker 1. b 6. c d. Ventilation 2. d 7. d 10. Epicardial pacing wires should be man- 3. a 8. b aged by ensuring that a. a transparent occlusive dressing is 4. a 9. c smoothly laid across the chest to 5. c 10. b secure the wires to the skin. b. the ends of the pacer wires are covered, insulated, and protected with a clean, dry dressing.

Clinical Inquiry Box

Question: Which interventions can reduce the incidence of postoperative atrial fibrillation? Reference: Patti, G., Chello, M., Candura, D., Pasceri, V., D’Ambrosio, A., & Covino, E., et al. (2006). Randomized trial of atorvastatin for reduction of postoperative atrial fibrillation in patients undergoing cardiac surgery: Results of the ARMYDA-3 (Atorvastatin for Reduction of MYocardial Dysrhythmia After cardiac surgery) study. Circulation, 114(14), 1455–1461. Objective: To identify whether statin therapy as an intervention lowers the incidence of postoperative atrial fibrillation (AF) after cardiac surgery. Method: A randomized controlled trial was conducted with 200 patients undergoing elective cardiac surgery with cardiopulmonary bypass. Subjects had no previous statin treatment or history of AF. Patients were randomized to atorvastatin 40 mg/day (n ϭ 101) or placebo (n ϭ 99) starting 7 days before cardiac surgery. Outcome variables measured were incidence of postoperative AF, length of stay, 30-day major adverse cardiac and cerebrovascular events, and postoperative C-reactive protein (CRP) variations. Results: Atorvastatin significantly reduced the incidence of AF versus placebo. Length of stay was longer in the placebo versus atorvastatin arm. Peak CRP levels were lower in patients without AF, irrespective of their randomization assignment. Atorvastatin treatment conferred a 61% reduction in risk of AF, whereas high postoperative CRP levels were associated with increased risk of AF. The incidence of major adverse cardiac and cerebrovascular events at 30 days was similar in both arms of the study. Conclusion: Treatment with atorvastatin 40 mg/day initiated 7 days before surgery significantly reduces the incidence of postoperative AF after elective cardiac surgery with cardiopulmonary bypass and shortens hospital stay. Nurses in the ICU caring for postoperative cardiac surgery patients should advocate for the use of a statin to improve patient outcomes. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 319

References 319

■ REFERENCES Baldwin, I. C., & Heland, M. (2000). Incidence of Adams, D. C., Heyer, E. J., Simon, A. E., Delphin, E., cardiac dysrhythmias in patients during pul- Rose, E. A., Oz, M. C., et al., (2000). Incidence monary artery catheter removal after cardiac of atrial fibrillation after mild or moderate surgery. Heart & Lung, 29(3), 155–160. hypothermic cardiopulmonary bypass. Critical Bharucha, D. B., & Marinchak, R. A. (2007). Care Medicine, 28(2), 309–311. Arrhythmias after cardiac surgery: Atrial fibril- Almassi, G. H., Schowalter, T., Nicolosi, A. C., lation and atrial flutter. Retrieved April 16, Aggarwal, A., Moritz, T. E., Henderson, W. G., 2008, from http://www.utdol.com/online/ et al. (1997). Atrial fibrillation after cardiac content/topic.do?topicKey=carrhyth/43828& surgery: A major morbid event? Annals of selectedTitle=1~150&source=search_result Surgery, 226(4), 501–511. Brister, S. J., & Lenkei-Kerwin, S. C. M. (2005). American College of Cardiology, American Heart Common ward complications and manage- Association, & European Society of Cardiol- ment. In D. C. H. Cheng & D. E. Tirone (Eds.), ogy. (2003). ACC/AHA/ESC guidelines for the Perioperative care in cardiac anesthesia and surgery management of patients with supraventricular (pp. 429–434). Philadelphia: Lippincott arrhythmias: Executive summary. Journal of the Williams & Wilkins. American College of Cardiology, 42(8), Creswell, L. L., Alexander, J. C., Ferguson, T. B., Lis- 1493–1531. bon, A., & Fleisher, L. A. (2005). Intraoperative Andrews, T. C., Reimold, S. C., Berlin, J. A., & interventions: American College of Chest Antman, E. M. (1991). Prevention of supraven- Physicians guidelines for prevention and man- tricular arrhythmias after coronary artery agement of postoperative atrial fibrillation bypass surgery: A meta-analysis of randomized after cardiac surgery. Chest, 12(suppl. 2), control trials. Circulation, 84(5 suppl), 236–244. S28–S35. Aranki, S., Cutlip, D., & Aroesty, J. (2008). Early Creswell, L. L., Schuessler, R. B., Rosenbloom, M., cardiac complications of coronary artery & Cox, J. L. (1993). Hazards of postoperative bypass graft surgery. Retrieved December 6, atrial arrhythmias. Annals of Thoracic Surgery, 2008, from http://www.utdol.com/online/ 56(3), 539–549. content/topic.do?topicKey=correvas/7991& Dewar, M. L., Rosengarten, M. D., Blundell, P. E., & linkTitle=Ventricular%20tachyarrhythmias& Chiu, R. C. (1985). Perioperative Holter moni- source=preview&selectedTitle=9~150&anchor toring and computer analysis of dysrhythmias =13#13 in cardiac surgery. Chest, 87(5), 593–597. Aranski, S. F., Shaw, D. P., Adams, D. H., Rizzo, R. J., England, M. R., Gordon, G., Salem, M., & Cher- Couper, G. S., & VanderVliet, M. (1996). Pre- now, B. (1992). Magnesium administration dictors of atrial fibrillation after coronary and dysrhythmias after cardiac surgery: A artery surgery: Current trends and impact on placebo-controlled double-blind randomized hospital resources. Circulation, 94(3), 390–397. trial. Journal of the American Medical Association, Archbold, R. A., & Zaman, A. G. (2000). Magne- 268(17), 2395–2402. sium for atrial fibrillation after coronary Fayaz, K. M., Pugh, S., Balachandran, S., Sudheer, artery bypass graft surgery: Its role in aetiology P. S., & Hall, J. E. (2005). Histamine release and prevention. Critical Care and Resuscitation, during adult cardiopulmonary bypass. Anaes- 2(4), 260–268. thesia, 60(12), 1179–1184. Ascione, R., Reeves, B. C., Santo, K., Khan, N., & Furer, S. K., Gomes, J. A., Love, B., & Davendra, M. Angelini, G. D. (2004). Predictors of new (2005). Mechanism and therapy of cardiac malignant ventricular arrhythmias after coro- arrhythmias in adults with congenital heart nary artery surgery: A case-control study. Jour- disease. Mount Sinai Journal of Medicine, 72(4), nal of the American College of Cardiology, 43(9), 263–269. 1630–1638. Fuster, V., & Ryden, L. E. (2001). ACC/AHA/ESC Atlee, J. L. (1997). Perioperative cardiac dysrhyth- guidelines for the management of patients mias: Diagnosis and management. Anesthesiol- with atrial fibrillation. Journal of the American ogy, 86(6), 1397–1424. College of Cardiology, 38(4), 1–69. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 320

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Fuster, V., Ryden, L. E., Cannom, D. S., Crijns, H. J., McKeown, P. P., & Gutterman, D. (2005). Executive Curtis, A. B., Ellenbugen, K. A., et al. (2006). summary: American College of Chest Physi- ACC/AHA/ESC guidelines for the manage- cians guidelines for the prevention of postop- ment of patients with atrial fibrillation: A erative atrial fibrillation after cardiac surgery. report of the American College of Cardiology/ Chest, 128(2 suppl), 1S–5S. American Heart Association Task Force on Miller, S., Crystal, E., Garfinkle, M., Lau, C., Practice Guidelines and the European Society Lashevsky, I., & Connolly, S. J. (2005). Effects of Cardiology Committee for Practice Guide- of magnesium on atrial fibrillation after car- lines (Writing committee to revise the 2001 diac surgery: A meta-analysis. Heart, 91(5), guidelines for the management of patients 618–623. with atrial fibrillation). Journal of the American Morris, D. C., & St. Claire, D. (1999). Management College of Cardiology, 48(4), 854–906. of patients after cardiac surgery. Current Prob- Ghavidel, A. A., Javadpour, H., Shafiee, M., lems in Cardiology, 24(4), 161–228. Tabatabaie, M-B., Raiesi, K., & Hosseini, S. Piotrowski, A. A., & Kalus, J. S. (2004). Magnesium (2008). Cryoablation for surgical treatment of for the treatment and prevention of atrial chronic atrial fibrillation combined with tachyarrhythmias. Pharmacotherapy, 24(7), mitral valve surgery: A clinical observation. 879–895. European Journal of Cardio-Thoracic Surgery, Rushton, S., & Kalpin, P. (2004). Cardiovascular 33(6), 1043–1048. surgery. In L. Davis (Ed.), Cardiovascular nursing Greenberg, M. D., Katz, N. M., Iuliano, S., Tem- secrets (pp. 223–239). St. Louis, MO: Elsevier pesta, B. J., & Solomon, A. J. (2000). Atrial pac- Mosby. ing for the prevention of atrial fibrillation after Sethares, K., Seifert, P. C., & Smith, H. (2008). Care cardiovascular surgery. Journal of the American of patients undergoing cardiac surgery. In College of Cardiology, 36(6), 1416–1422. D. K. Moser & B. Riegel (Eds.), Cardiac nursing: Guo-Wei, H. (1997). Coronary endothelial func- A companion to Braunwald’s heart disease tion in open heart surgery. Clinical and Experi- (pp. 951–976). St. Louis, MO: Saunders Elsevier. mental Pharmacology and Physiology, 24(12), Silvestry, F. E. (2008). Overview of the postopera- 955–957. tive management of patients undergoing car- Hogue, C. W., Creswell, L. L., Gutterman, D. D., & diac surgery. Retrieved December 5, 2008, Fleisher, L. A. (2005). Epidemiology, mecha- from http://www.utdol.com/online/content/ nisms, and risks: American College of Chest topic.do?topicKey=cc_medi/22438#11 Physicians guidelines for the prevention and Stamou, S., Hill, P., & Sample, G. (2001). Preven- management of postoperative atrial fibrillation of atrial fibrillation after cardiac surgery: tion after cardiac surgery. Chest, 128 (suppl 2), The significance of postoperative oral amio- S9–S16. darone. Chest, 120(6), 1936–1941. Jais, P., Hocini, M., Hsu, L. F., Sanders, P., Scavee, Thompson, A. E., Hirsch, G. M., & Pearson, G. J. C., Weerasooriya, R., et al. (2004). Technique (2002). Assessment of new onset postcoronary and results of linear ablation at the mitral artery bypass surgery atrial fibrillation: Cur- isthmus. Circulation, 110(19), 2996–3002. rent practice pattern review and the develop- Khalpey, Z. I., Ganim, R. B., & Rawn, J. D. (2008). ment of treatment guidelines. Journal of Clinical Postoperative care of cardiac surgery patients. Pharmacy & Therapeutics, 27(1), 21–37. In L. H. Cohn (Ed.), Cardiac surgery in the adult Tsuboi, J., Kawazoe, K., Izumoto, H., & (pp. 465–486). New York: McGraw-Hill. Okabayashi, H. (2008). Postoperative treat- Maisel, W. H., Rawn, J., & Stevenson, W. G. (2001). ment with carvedilol, a β-adrenergic blocker, Atrial fibrillation after cardiac surgery. Annals prevents paroxysmal atrial fibrillation after of Internal Medicine, 135(12), 1061–1073. coronary artery bypass grafting. Circulation Martin, C. G., & Turkelson, S. L. (2006). Nursing Journal, 72(4), 588–591. care of the patient undergoing coronary artery Wade, C. R., Reith, K. K., Sikora, J. H., & Augustine, bypass grafting. Journal of Cardiovascular Nurs- S. M. (2004). Postoperative nursing care of the ing, 21(2), 109–117. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 321

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cardiac transplant recipient. Critical Care Nurs- ■ WEB RESOURCES ing Quarterly, 27(1), 17–28. Anesoft rhythm recognition: www.anesoft.com/ White-Williams, C., & Grady, K. L. (2008). Care of FreeStuff/rhythm/rhythm.html patients undergoing cardiac transplantation. A guide to reading and understanding EKG inter- In D. K. Moser & B. Riegel (Eds.), Cardiac nurs- pretation: http://students.med.nyu.edu/erclub/ ing: A companion to Braunwald’s heart disease (pp. ekghome.html 998–1021). St. Louis, MO: Saunders Elsevier. EKG Library: www.ecglibrary.com/ Wurdeman, R. L., Mooss, A. N., Mohiuddin, S. M., ECG Learning Center: www.library.med.utah & Lenz, T. L. (2002). Amiodarone vs sotalol as .edu/kw/ecg/ prophylaxis against atrial fibrillation/flutter after heart surgery. Chest, 121(4), 1203–1210. University of Wisconsin–Madison’s self-study ECG manual: www.fammed.wisc.edu/medstudent/ Yeung-Lai-Wah, J. A., Qi, A., McNeill, E., Abel, J. G., pcc/ecg/ecg.html Tung, S., Humphries, K. H., et al. (2004). New- onset sustained ventricular tachycardia and fibrillation early after cardiac operations. Annals of Thoracic Surgery, 77(6), 2083–2088. Zevola, D., Raffa, M., & Brown, K. (2002). Using clinical pathways in patients undergoing cardiac valve surgery. Critical Care Nurse, 22(1), 31–50. 57625_CH15_309_322.pdf 4/10/09 11:06 AM Page 322 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 323

Chapter 16 Neurologic Complications

Myra F. Ellis

■ INTRODUCTION Neurologic complications following cardiac advances of cardiopulmonary bypass (CPB) surgery are considered severe because they and other improvements, as well as increased affect mortality and, for survivors, quality of life expectancy for the population as a whole, life. In addition, neurologic complications dra- have allowed the benefits of cardiac surgery to matically increase the length of hospitalization be offered more frequently to older patients and costs associated with cardiac surgery with more comorbidities (Ferguson, Hammill, (Eagle et al., 2004). They occur in an estimated Peterson, DeLong, & Grover, 2002). Unfortu- 1% to 6% of postoperative cardiac surgery nately, elderly patients are at increased risk for patients (Albert & Antman, 2003), with an pathophysiologic stress—including neurologic increased incidence being noted in older dysfunction—following cardiac surgery. patients (Silvestry, 2008). Neurologic compli- Postoperative stroke is a leading cause of cations are the second leading cause of mor- death following CPB. The incidence of stroke bidity and mortality in postoperative cardiac has been reported to range from 0.4% to 14% surgery patients; heart failure is the leading in studies, with the variability being attributed cause (McGarvey, Cheung, & Stecker, 2008). to differences in patient populations, surgical Postoperative neurologic complications procedure, and data collection methods. have been attributed to patient-specific fac- Increased rates of stroke and encephalopathy tors, emboli, hypoperfusion, and metabolic are attributed to increased numbers of high- derangements. Rates of neurologic complica- risk patients undergoing cardiac surgery tions are increasing, despite numerous (McKhann, Grega, Borowicz, Baumgartner, & advances in cardiac surgery (Newman et al., Selnes, 2006). 2006). Estimates of cognitive impairment The incidence of negative sequelae from range from 20% to 70% during the first post- neurologic complications is reported to be operative week, and approximately 10% to approximately 8.4%. In one study, length of 40% of these patients continue to exhibit cog- ICU stay for patients who experienced these nitive impairment 6 weeks after surgery complications increased from 3 days to 6–8 (Bruce, Smith, Yelland, & Robinson, 2008). days; the length of hospital stay increased by Studies suggest that elderly patients with 50% (Talmor & Lisbon, 2005). The death rate comorbidities and cardiovascular disease may from neurologic complications in the 1970s benefit more from surgical treatment than was 7.2%, increased to 20% by the mid 1980s, from medical management. Technological and continues to rise (Newman et al., 2006).

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This chapter discusses the incidence and with a significant increase in the need for extent of neurologic complications following intermediate- and long-term care following cardiac surgery, offers evidence-based strate- hospital discharge (Roach et al., 1996). The gies for prevention of these undesirable financial cost of a perioperative stroke is esti- sequelae, and describes nursing management mated to be in the range of $90,000–$228,000, of patients with adverse neurologic outcomes. as a result of lost productivity and increased costs of care (Eagle et al., 2004). ■ DESCRIPTION AND INCIDENCE OF NEUROLOGIC COMPLICATIONS Type II Neurologic Deficits Neurologic complications cover a wide range Type II neurologic deficits are more prevalent of disorders, from debilitating stroke or coma than Type I deficits, occurring in 3% of to encephalopathy, delirium, and neurocogni- patients (Silvestry, 2008). Type II injuries also tive dysfunction. Adverse cerebral outcomes carry important implications for both long- can be divided into two types: Type I and and short-term disability and are associated Type II. Type I deficits include stroke and with increased length of hospital stay, higher major focal neurologic deficits, transient hospital costs, and an increased likelihood of ischemic attacks (TIA), stupor, and coma. discharge to rehabilitation or extended care Type II deficits include new decline in intel- facilities (Roach et al., 1996). A 53% incidence lectual function, confusion, agitation, disori- of abnormal neurocognitive function at dis- entation, memory deficits, and seizure charge was reported in a study of patients without evidence of focal deficit. The undergoing coronary artery bypass grafting reported incidence of adverse cerebral out- (CABG) with CPB. In this study, 24% of comes varies widely, from 0.4% to 80%, patients continued to have neurologic abnor- depending on how the deficit is defined malities at 6 months after their cardiac surgery, (Eagle et al., 2004; Silvestry, 2008; Talmor & and 42% reported cognitive decline at 5 years Lisbon, 2005). following the surgery (Newman et al., 2001). Other neurologic complications have also been reported following cardiac surgery, ■ RISK FACTORS FOR NEUROLOGIC including injuries to the brachial plexus, COMPLICATIONS phrenic nerve, cranial nerves, other peripheral nerves, and visual pathways. These injuries A number of risk factors have been implicated occur less frequently and are usually less seri- in adverse neurologic outcomes. These factors ous, but nevertheless contribute to overall incorporate a combination of patient risk fac- patient discomfort and morbidity (Grocott, tors, intraoperative variables, and postopera- Clark, Homi, & Sharma, 2004). tive events. Importantly, the additive effect of variables significantly increases a patient’s risk. Identification of risk factors has led to Type I Neurologic Deficits predictive models that allow stroke probabil- Data from the largest prospective study of ity to be calculated for individual patients adverse cerebral outcomes following cardiac (McKhann et al., 2006). Risk factors are sum- surgery reveal that Type I neurologic deficits marized in Table 16–1. occur in 3.1% of patients and are responsible for a 21% mortality rate in this population. In addition, Type I deficits contribute to the (rel- Predictors for Type I and II Deficits atively long) average stay of 11 days in the ICU Increasing age, especially greater than 70 years, and 25 days in the hospital, and are associated is a strong predictor for both Type I and Type II 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 325

Risk Factors for Neurologic Complications 325

Table 16–1 Significant Risk Factors for Type I and Type II Neurologic Outcomes

Risk Factors Types I and II Advanced age, especially greater than 70 years History of pulmonary disease History of hypertension Existing hypertension Type I Moderate to severe proximal aortic atherosclerosis History of neurologic deficit Diabetes mellitus History of unstable angina Use of left ventricular venting procedure Use of intra-aortic balloon pump Type II History of excessive alcohol consumption Postoperative dysrhythmias Prior cardiac surgery

Sources: Newman et al., 2006; Roach et al., 1996; Salenger, Gammie, & Vander Salm, 2003.

deficits. A history of significant hypertension tricular assist device, peripheral vascular dis- has also been linked to both types of adverse ease (PVD), renal failure, left main coronary neurologic outcomes following cardiac surgery stenosis, emergent operation, number of aor- (Roach et al., 1996). In addition, patients under- tic anastamoses, reoperations, and use of a going combined open chamber procedures and non-membrane oxygenator have also been coronary artery surgery are at greatest risk for implicated as increasing the patient’s risk of adverse neurologic outcomes; these complica- developing a Type I deficit in various studies tions are equally divided between Type I (Salenger, Gammie, & Vander Salm, 2003). and Type II deficits (Newman et al., 2006). Predictors for Type II Deficits Predictors for Type I Deficits Factors that are associated with Type II Moderate to severe proximal aortic atheroscle- deficits include preoperative substance abuse rosis, as identified by intraoperative palpation, (e.g., alcohol consumption), dysrrhythmias, is the single greatest marker for a Type I neu- hypertension, prior CABG, PVD, metabolic rologic deficit. The risk for Type I deficits conditions, and heart failure. Although a increases fourfold in the presence of aortic recent study linked aortic atherosclerosis to lesions, with these kinds of complications delirium (Rudolph et al., 2005), earlier studies being more prevalent in older patients (Roach did not show a strong correlation between the et al., 1996). Atherosclerotic emboli are likely two, suggesting an etiology related to pathol- mobilized by manipulation of the aorta. Other ogy of the microcirculation in the brain, significant risk factors that have been identi- rather than embolization (Hogue, Palin, & fied include history of neurologic abnormali- Arrowsmith, 2006). Other factors linked to ties such as stroke or TIA, diabetes mellitus, Type II deficits include certain genetic factors history of unstable angina, and use of an (Mathew et al., 2007). Type II deficits are seen intra-aortic balloon pump (IABP) (Roach et more commonly in patients who have experi- al., 1996). Perioperative hypoperfusion, non- enced periods of hypoperfusion or hypoten- pulsatile flow, intraoperative use of a left ven- sion (Grocott, Homi, & Puskas, 2005). 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 326

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■ UNDERLYING PATHOPHYSIOLOGY a biomarker known as N-methyl-D-aspartate The precise mechanisms of cerebral injury fol- (NMDA) receptor antibody (NR2Ab) is pre- lowing cardiac surgery are not fully under- dictive of severe neurologic adverse events stood. Numerous factors inherent to cardiac after CPB. “Patients with a positive NR2Ab surgery play a role in adverse neurologic out- test (2.0 ng/mL) preoperatively were nearly 18 comes. These complications have been attrib- times more likely to experience a postopera- uted primarily to the effects of CPB. Reported tive neurologic event than patients with a mechanisms are the embolization of gas and negative test” (Bokesch et al., 2006, p. 1432). particulate matter, inadequate cerebral perfu- A number of strategies have been suggested to sion, and large fluctuations in hemodynamic minimize patients’ risk of experiencing neuro- parameters (Ganushchak, Fransen, Visser, logic deficits following cardiac surgery. de Jong, & Maessen, 2004). Patients who undergo cardiac surgery expe- Avoiding Injury rience a profound systemic inflammatory response, especially when CPB is used Many strategies to reduce complications dur- (Bhimji, Estabrooks, & Price, 2007). One of ing cardiac surgery focus on avoiding injury. the effects of the systemic inflammatory As previously stated, atherosclerosis is an response related to CPB is the development of important predictor of stroke. The surgeon clots. CPB activates the intrinsic and extrinsic can identify high-risk patients intraopera- pathways of the coagulation system second- tively with the use of epiaortic ultrasound or ary to factors including hypothermia, pumps transesophageal echocardiogram (TEE) to propelling blood through the circuit, and modify cannulation sites and avoid atheroma exposure of blood to the artificial surfaces of (fatty deposits in arteries). Single cross-clamp the bypass circuit (Day & Taylor, 2005). These technique and the use of an internal mam- conditions may contribute to neurologic mary artery–Y (IMA-Y) graft for proximal injury, although data on this point are incon- anastomosis to avoid aortic manipulation are clusive (Newman et al., 2006). also intraoperative strategies to minimize Cognitive decline has been linked to surger- atheroembolism (Stamou, 2006). In patients ies other than cardiac procedures, albeit at a with severe atherosclerosis, other options for lower rate. Notably, exposure to general anes- surgery may be employed, such as off-pump thetic agents may contribute to cognitive coronary artery bypass grafting (OPCAB) or decline. In addition, postoperative hyperther- replacement of the ascending aorta under mia and cerebral edema have been linked to deep hypothermic circulatory arrest. Other poor neurologic outcomes, although these strategies shown to reduce neurologic injury complications may be an effect of processes include emboli reduction with the use of cell that resulted in cerebral injury itself, rather saver to process shed mediastinal blood, post- than being directly responsible for the neuro- pump arterial filters, and acid–base balance logic deficit (Grocott & Yoshitani, 2007). management with the Alpha-stat method (Hogue et al., 2006). Hyperglycemia, hypotension, and hyperthermia during rewarming ■ STRATEGIES FOR have all been linked to adverse neurologic NEUROPROTECTION DURING outcomes, and should be avoided (Grocott & CARDIAC SURGERY Yoshitani, 2007). Careful preoperative screening can help iden- OPCAB has been proposed as a means of tify patients who are at higher risk for devel- decreasing the incidence of adverse neuro- oping neurologic complications. For example, logic outcomes following cardiac surgery. It 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 327

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seems logical that avoiding CPB—the pro- 2006; Stamou, 2006), with an estimated posed etiology for much of the neurologic 5000–35,000 postoperative cardiac surgery damage—would improve outcomes. However, patients developing a stroke annually (Albert & conflicting results with this strategy have Antman, 2003; Stamou, 2006). The incidence been reported from clinical trials, and the appears to be increasing—a trend that is largest randomized controlled trial failed to attributed to the higher acuity of surgical can- show any significant reduction in stroke rate didates (McKhann et al., 2006). or incidence of neurocognitive dysfunction The majority of postoperative strokes are (Bucerius et al., 2003). The American College evident in the first 24 to 48 hours after sur- of Cardiology (ACC) does not find enough gery in patients who initially awaken without evidence to conclude that OPCAB is better for neurologic deficits (Henke & Eigsti, 2003; limiting neurologic deficits (Eagle et al., 2004; Hogue, Murphy, Schechtman, & Dávila- Barriero & Baumgartner, 2006). OPCAB is Román, 1999). Data from one study suggest discussed in detail in Chapter 7. that 42% of strokes are present on awakening from surgery and an additional 20% become Minimizing Injury evident on the first postoperative day (Likosky et al., 2003). Other strategies to reduce neurologic compli- Most of the strokes following cardiac sur- cations focus on minimizing the extent of gery are ischemic in nature (Henke & Eigsti, injury. These measures include rapid treat- 2003). A small percentage (5%) of patients ment of atrial fibrillation (AF) and early iden- with ischemic strokes, however, experience tification of and intervention for ischemic hemorrhagic alteration or conversion. brain lesions. Some evidence suggests that Intracranial hemorrhage with associated clin- increasing blood pressure to increase cerebral ical significance is rare following cardiac sur- blood flow may help to minimize infarction gery (McGarvey et al., 2006). Strokes that size (McKhann et al., 2006). occur later in the postoperative period are more often associated with dysrhythmias, ■ DIAGNOSIS AND TREATMENT especially AF, valve surgery, or use of a ven- OF CENTRAL NERVOUS SYSTEM tricular assist device (McKhann et al., 2006). INJURY An estimated 30% of patients who develop a stroke following cardiac surgery are believed Nurses who care for postoperative cardiac to have had carotid artery disease present. surgery patients should be able to recognize Intraoperative cerebral microembolization those patients who are at increased risk for during CABG has been suggested to be the central nervous system injury and differenti- most common etiology (Albert & Antman, ate between the various types of neurologic 2003). In one study, 10 predictors that were deficits. Care includes interval assessments of present preoperatively were identified as neurologic function and changes to the plan increasing the risk of stroke: female gender, of care to enhance neurologic recovery. age, aortic surgery, previous stroke, critical preoperative state, poor ventricular function, Stroke diabetes, peripheral vascular disease, unstable Stroke is a devastating complication follow- angina, and pulmonary hypertension. Other ing cardiac surgery. Its incidence ranges from risk factors that have been identified include 0.8% to 6% in this population (Arrowsmith, redo surgery, valve surgery, calcified aorta, Grocett, & Newman, 2000; Ganushchak et al., duration of CPB, renal failure, low cardiac 2004; McGarvey et al., 2005; McKhann et al., output syndrome (LCOS), hypertension, 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 328

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postoperative AF, recent myocardial infarc- related events (McKhann et al., 2006). Unfor- tion (MI), left ventricular dysfunction, and tunately, MRI is often impractical in postop- smoking (John et al., 2000; McGarvey et al., erative cardiac surgery patients due to the 2008; McKhann et al., 2006; Ricotta, Faggioli, presence of metallic implants such as valves, Castilone, Hassett, & Brener, 1995). Patients defibrillators, pacemakers, or surgical metal who develop postoperative AF have a twofold (e.g., epicardial pacing wires). An alternative to fivefold greater risk of having a stroke imaging modality, head computed tomogra- (Mullen-Fortino & O’Brien, 2008). Patients phy (CT), can be used in such cases (Mc- with LCOS are also at greater risk. The Khann et al., 2006). increased risk of stroke is believed to be Neurologic assessments of cardiac surgery related to blood pressure variability, which in patients should be conducted at regular inter- turn increases the risk of thrombus formation vals in the postoperative period. This review and cerebral hypoperfusion (Hogue et al., includes assessment of the patient’s level of 1999). As previously suggested, postoperative consciousness (LOC) and motor movement. cardiac surgery patients who develop a stroke As mentioned earlier, medications given dur- have higher mortality rates and longer hospi- ing the intraoperative period can make accu- tal stays (Anyanwu, Filsoufi, Salzber, Bron- rate assessment more difficult. If deficits are ster, & Adams, 2007). suspected, a full neurologic assessment Suspicion for stroke occurs when the should be performed. The National Institutes patient fails to awaken, move extremities, fol- of Health Stroke Scale (NIHSS) outlines a low commands after discontinuation of seda- complete evaluation for stroke. The NIHSS tion, or any combination of these in the first assessment includes LOC, best gaze, visual 6 postoperative hours (McKhann et al., 2006). fields, facial palsy, motor function of arms The onset of focal findings such as facial and legs, limb ataxia, sensory, best language, droop, hemiparesis, aphasia, visual distur- dysarthria, extinction, and inattention (NIH, bances, or pupil change may also indicate 2003). stroke. Assessment is often difficult in the immediate postoperative period, however, Treatment of Stroke and is confounded by the patient’s emergence The treatment of stroke is primarily support- from anesthesia and the effects of postopera- ive in the immediate phase and aims to pre- tive medications. vent secondary complications (Young et al., Diagnosis of stroke is made based on the 1998). Monitoring the patient’s neurologic, presence of focal deficits in the physical exam hematologic, and respiratory status is essen- and brain imaging results (Adams et al., tial. Nursing care is guided by the specific 2007). Clinical signs of catastrophic stroke neurologic deficits observed in the patient. may include fixed and dilated pupils, postur- More generally, the ACC and other groups ing, Cushing’s syndrome (hypertension with have published evidence-based guidelines for bradycardia), and persistent coma (Young, the management of stroke patients (Adams et Bratina, Hickenbottom, Demchuk, & Wein, al., 2007). 1998). Patients suspected of having a stroke should be evaluated by a neurologist and OXYGENATION SUPPORT undergo brain imaging. Supporting adequate tissue oxygenation is Brain magnetic resonance imaging (MRI)— important in patients who are experiencing specifically, diffusion-weighted imaging—is cerebral ischemia. Patients with acute stroke the most accurate neuroimaging technique may have abnormal breathing patterns and available; it is able to detect microemboli- may need increased support to prevent 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 329

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hypoxia, which can worsen brain injury. more than 180 mm Hg is associated with Hypoxia may be caused by airway obstruc- adverse outcomes (Adams et al., 2007). Blood tion, aspiration, pneumonia, or atelectasis. pressure should be maintained within a range Endotracheal intubation may be necessary if that is adequate to maintain cerebral perfu- concerns arise about airway protection or the sion, yet does not exacerbate neurologic dam- patient’s ability to maintain adequate oxy- age. Deleterious effects of hypertension may genation. Pneumonia is among the leading include vasogenic edema (permeation of complications of stroke (Adams et al., 2007), intravascular fluid and proteins into the cere- so optimal nursing management includes bral extracellular space), disruption of the measures to prevent ventilator-associated blood–brain barrier, or an increase in myocar- pneumonia. Oxygen saturation levels of at dial oxygen consumption (Young et al., 1998). least 92% should be maintained (McGarvey et Aggressive treatment of hypertension may al., 2008). disrupt autoregulation. Care should be taken to gradually decrease BP to a specified target, TEMPERATURE MANAGEMENT as the other extreme—hypotension—worsens neurologic outcome. In the majority of stroke Increased body temperature is associated with patients, BP declines several hours after the increased morbidity and mortality in acute onset of stroke symptoms without any med- stroke patients (Adams et al., 2007). It is ical intervention (Adams et al., 2007). Con- important to assess these patients for sources versely, some evidence suggests that increased of hyperthermia, which may be related to BP following embolic stroke can improve brain injury or secondary infections. In such cerebral blood flow and limit ischemic effects cases, patients may benefit from measures that (McKhann et al., 2006). lower their body temperature. Interventions to Periods of hypotension should be similarly accomplish this goal may include the adminis- avoided so as to maintain adequate cerebral tration of antipyretics and application of cool- perfusion. If necessary, this goal can be ing devices (McGarvey et al., 2008). accomplished by administering fluid boluses. Hypothermia protects against cerebral A vasopressor may be added if fluid therapy is ischemia. Data suggest that a 1 °C decrease in not sufficient (McGarvey et al., 2008). brain temperature is associated with a 7% decrease in cerebral metabolic rate. Con- GLYCEMIC CONTROL versely, even a mild increase in brain tempera- Hypoglycemia may mimic symptoms of ture (1–2 °C) can be harmful (Nussmeier, stroke and may exacerbate brain injury. Initial 2005). Although the neuroprotective benefits assessment of the patient upon presentation of hypothermia are well known, currently no of stroke symptoms should include measure- evidence exists to support induced hypother- ment of serum glucose and correction of mia as an intervention in the setting of acute hypoglycemia. stroke (Adams et al., 2007; Rees, Beranek- Conversely, hyperglycemia is associated Stanley, Burke, & Ebrahim, 2007). with poorer outcomes following stroke and should be avoided (McGarvey et al., 2008). HEMODYNAMIC STATUS Researchers hypothesize that hyperglycemia Blood pressure (BP) control is crucial in increases the infarct size associated with a stroke patients. Increased BP is common in stroke and elevates cerebral lactate levels, the acute phase of stroke, with systolic BP which results in acidosis of brain tissue and (SBP) greater than 160 mm Hg being noted in decreases the function of the mitochondria 60% of these patients; elevation of SBP to of the penumbra (an ischemic area that 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 330

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is still viable, located adjacent to the area pneumonia, venous thrombotic events, uri- affected by the stroke). Hyperglycemia is also nary tract infections, and skin breakdown reported to disrupt the blood–brain barrier, (Young et al., 1998). which puts the patient at risk of developing cerebral edema; this complication, in turn, promotes brain cell death in the stroke- Encephalopathy and Delirium affected area. All of these factors influence Postoperative cardiac surgery patients are at morbidity and mortality following a stroke greater risk for not only a stroke, but also (Paolino & Garner, 2005). encephalopathy. “Encephalopathy” is a The goal of glycemic control therapy should generic term that refers to several types of be to maintain serum glucose in the range of brain dysfunction. This term has been used 80 to 140 mg/dL (Adams et al., 2007). Others synonymously with confusion, delirium, suggest that serum glucose levels should not lethargy, depression, disorientation, halluci- exceed 110 mg/dL (Capes, Hunt, Malmberg, nations, transient ischemic attacks, mental Pathak, & Gerstein, 2001). Careful titration status changes, combativeness, and agitation. and control of serum glucose levels are key The incidence of this complication has been nursing measures, and are usually best accom- reported to range from 8.4% to 32%. Patients plished with an insulin infusion. who develop postoperative encephalopathy have worse outcomes, increased length of ASPIRIN hospital stay (8 days versus 14 days in one Although studies have failed to confirm the study), and higher mortality rates—as much efficacy of anticoagulation following CABG, as threefold higher—than patients who do not and fibrinolysis is contraindicated in patients develop this neurologic complication (Henke & who have undergone this surgical procedure, Eigsti, 2003; McKhann et al., 2006). Postop- administration of aspirin may decrease neuro- erative encephalopathy may be related to the logic complications following CABG and development of microemboli, cerebral edema improve outcomes following stroke. If not secondary to the inflammatory response, contraindicated, aspirin is recommended in inadequate temperature regulation, or cere- postoperative cardiac surgery patients bral hypoperfusion (Henke & Eigsti, 2003). (McGarvey et al., 2008). Risk factors that have been identified for the development of postoperative encephalopathy Prevention of Secondary Complications include age and history of stroke, hyperten- Stroke following cardiac surgery increases sion, diabetes, and carotid bruit. Signs and both ICU and overall hospital length of stay. symptoms typically manifest after extubation Patients who experience this neurologic com- has taken place (McKhann et al., 2006). plication are at increased risk for secondary Delirium is a “disturbance of consciousness complications and have a threefold to sixfold with inattention that is accompanied by increased risk of death. Mortality rates in the changes in cognition or perceptual distur- range of 14% to 30% have been reported in bance and has an acute onset with a fluctuat- hospitalized patients who follow this course ing course” (Chang, Tsai, Lin, Chen, & Liu, (Bucerius et al., 2003; McGarvey et al., 2008). 2008, p. 568). It is the most common neuro- Anticipation of complications allows the ICU logic complication following cardiac surgery nurse to develop a plan of care to reduce the and may be the most difficult to manage risk of stroke and its sequelae. Common sec- (Sockalingam et al., 2005). This condition ondary complications include aspiration, develops over the course of hours to days and 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 331

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may be life-threatening. An estimated 3% to In one study, the signs and symptoms of 73% of postoperative cardiac surgery patients delirium did not appear until the second or develop delirium (Chang et al., 2008). The third postoperative day in the ICU. More than incidence is higher in those patients with pre- 70% of patients who developed delirium had existing psychological disorders, substantial their symptoms diminish within 24 hours of prior alcohol use, left ventricular ejection frac- transfer from the ICU (Chang et al., 2008). tion less than 30%, advanced age (greater than 65 years), or cerebral artery disease, and in Treatment of Delirium those individuals who undergo an emergent There are four main aspects of managing procedure (Chang et al., 2008). Anesthesia, delirium: (1) identify and treat underlying sedation, time in circulatory arrest greater causes; (2) provide environmental and sup- than 30 minutes, and intraoperative hypother- port measures; (3) administer drug therapy mia (less than 25 °C) are noted intraoperative aimed at treating symptoms; and (4) conduct causes. Etiologies of delirium in postoperative regular evaluations of the effectiveness of patients include sleep deprivation, renal or treatment (Sockalingam et al., 2005). hepatic failure, cardiogenic shock, AF, massive blood transfusions (more than 1 L), bilirubin IDENTIFICATION AND TREATMENT greater than 2 mg/dL, hypoalbuminemia, low OF THE CAUSE hematocrit, acute infection, dehydration, and Delirium after cardiac surgery is common and thyroid disorders (Chang et al., 2008; Khalpey, multifactorial. As a consequence, it is impor- Ganim, & Rawn, 2008). tant for ICU nurses to recognize patients who Symptoms of delirium include an inability to are at risk of developing this neurologic com- maintain attention, disturbance of conscious- plication and adjust their care to reduce or ness, cognitive deficits, memory impairment, prevent postoperative delirium. Recom- disorientation, inappropriate speech, and per- mended measures include creating an envi- ceptual changes (Chang et al., 2008). Focal neu- ronment that promotes sleep so the patient’s rologic findings are not present in delirium. sleep cycle can be reestablished and avoiding These changes are acute and not associated the use of medications that may promote the with preexisting psychiatric disorders. Early development of delirium (e.g., benzodi- detection and treatment of delirium are impor- azepines) (Khalpey et al., 2008). tant aspects of the nursing care of postopera- In patients experiencing postoperative delir- tive cardiac surgery patients and may limit this ium, a thorough examination must be made to complication’s severity or prevent it altogether. identify and allow for correction of possible Agitation often accompanies postoperative causes. The underlying causes of delirium may delirium. It is defined as extreme motor or be metabolic derangements including elec- vocal behavior that is disruptive, is unsafe for trolyte disorders, drug or alcohol withdrawal, the patient and staff, or interferes with the nutritional deficiencies, or medications. Several delivery of patient care and medical therapies. drugs frequently prescribed for cardiac patients Examples of agitation in hospitalized patients are associated with neuropsychiatric changes, may include screaming, shouting, moaning, including beta blockers, calcium channel block- combativeness (e.g., biting, kicking, hitting, ers, angiotensin-converting enzyme (ACE) scratching), pulling out tubes and disconnect- inhibitors, diuretics, antiarrhythmics, and ing monitoring devices, and getting out of lipid-lowering agents (Sockalingam et al., bed. Delirium and agitation often present 2005). Careful review of medications with together and may be difficult to distinguish. emphasis on new medications is warranted 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 332

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whenever delirium presents. Attempts should dol®) is a first-generation, high-potency neu- be made to avoid use of drugs that impair real- roleptic and is considered to be the drug of ity, such as benzodiazepines or barbiturates, in choice in the treatment of delirium in the postoperative patients. ICU. The American Psychiatric Association Analgesics are often associated with mental (APA) recommends starting treatment with status changes. Undertreatment of pain, how- 1–2 mg every 2–4 hours as needed, with titra- ever, may contribute to increased stress and tion to higher doses in patients who continue sleep deprivation, thereby exacerbating post- to demonstrate agitation. In rare circum- operative delirium. The ICU nurse should stances, a continuous infusion of haloperidol closely monitor patients to avoid adverse may be necessary (APA, 1999). Haloperidol effects from analgesics. Special care should be has been linked to cardiac dysrhythmias, given to administering narcotics in the elderly including torsade de pointes (Perrault, population, as glomerular filtration rate Denault, Carrier, Cartier, & Belisle, 2000). decreases with age (Demeure & Fain, 2006). Patients receiving antipsychotic therapy should have ECG monitoring, including meas- ENVIRONMENTAL AND SUPPORTIVE MEASURES urement of the QT interval (see Box 16–1). A Environmental interventions include mini- QT interval of greater than 450 milliseconds or mizing or eliminating factors that exacerbate more than 25% over baseline warrants close delirium. In the ICU, patients are frequently monitoring and possibly a reduction or discon- exposed to interruptions in sleep patterns, tinuation of haloperidol, although QT prolon- noise, and excessive environmental stimula- gation may not always precede dysrhythmias tion (Vena, 2007). Transfer to a progressive (Sockalingam et al., 2005). care unit should be made as soon as medically Treatment of delirium with benzodi- feasible and often results in abatement of azepines is reserved for patients who are expe- delirium-related symptoms. In addition, care riencing withdrawal from alcohol or should be taken to reduce sensory impair- sedative-hypnotics. Patients who are unable ment and to return patients’ glasses or hear- to tolerate high doses of antipsychotic med- ing aids as soon as practical. In all cases, ications may benefit from combined benzodi- nurses should focus on providing patients azepine therapy (APA, 1999). Multivitamin with reorientation and reassurance. replacement should be implemented for In extreme cases of agitation, restraints patients with a deficiency in vitamin B. In may be needed to ensure the patient’s safety. extreme cases of delirium and agitation with Attendance at the bedside by family members hypercatabolic conditions, measures such as or sitters is preferable to the use of physical paralysis, sedation, intubation, and mechani- restraints. Sitters may participate in orienting cal ventilation may be required (APA, 1999). activities by talking to the patient, engaging Newer antipsychotic agents such as risperi- in frequent touch, and making eye contact. done (Risperdal®), olanzepine (Zyprexa®), and quetiapine (Seroquel®) may have fewer cardiac DRUG THERAPY and extrapyramidal complications. To date, few studies have evaluated their use in cardiac Pharmacologic interventions are often necessary surgery patients (Sockalingam et al., 2005). in patients with postoperative delirium, especially when agitation is present. Despite the prevalence of postoperative delirium, only a lim- Seizures ited number of agents to treat this complication Seizures are a rare neurologic complication have been studied in postoperative patients. following cardiac surgery, occurring in 0.5% The drugs most commonly used to treat to 3.5% of patients following CABG (McGar- delirium are antipsychotics. Haloperidol (Hal- vey et al., 2008). They most often accompany 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 333

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Box 16–1 Measuring QT Intervals

QT RR (the number of seconds between R waves)

Each small box in ECG paper equals 0.04 seconds. Each large box equals 0.20 seconds. QT complex

cerebral insult from hypoxia or emboli (air or patients need more information about what particulate). Seizures may also be caused by the effects of surgery are and what to expect hypoxemia, hyponatremia, hypoglycemia, during recovery (Jaarsma, Kastermans, stroke, or medication overdoses, especially Dassen, & Philipsen, 1995; Theobald & overdoses of lidocaine (Xylocaine®) or pro- McMurray, 2004). To ensure that such educa- cainamide (Pronestyl®) (McGarvey et al., tion is provided, the ICU nurse should pre- 2008). A thorough examination for contribut- pare patients and families for the possibility ing factors, evaluation by a neurologist, CT that the patient may experience some cogni- scan, and electroencephalogram (EEG) tive decline and reassure them that most should be performed, and administration of patients experience improvement in these anticonvulsant therapy should be considered symptoms if they do occur. In addition, both (Young et al., 1998). An EEG is recommended patients and families should be taught about for patients who are unresponsive 18 to 24 subtle changes and symptoms for which to hours after surgery to determine if seizure observe. activity is occurring without motor manifestations (McGarvey et al., 2008). Anxiety and Depression Early studies of postoperative cardiac surgery Cognitive Decline patients suggest that the presence of anxiety Cognitive decline is commonplace following and depression may have a negative effect on cardiac surgery, with its reported incidence outcomes. Aside from their physiologic ranging from 45% to 80% (Bernet, Grapow, & impact in the immediate postoperative Zerkowski, 2004; Carrascal et al., 2005; New- period, these conditions are reported to have man et al., 2001; Talmor & Lisbon, 2005). negative effects on long-term quality of life. Typical cognitive disturbances include mild Both the immediate and long-term effects difficulty with memory, problem solving, may increase the risk of death following car- attention, and ability to learn. Most patients diac surgery (Pignay-Demaria, Lespérance, report improvement of symptoms in 1 or Demaria, Frasure-Smith, & Perrault, 2003). 2 months. Data suggest a correlation between the pres- Several studies evaluating postdischarge ence of symptoms of depression and the recovery in cardiac surgery patients show that chance of hospital readmission for cardiac 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 334

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issues within 6 months of discharge following disorders. Initial data suggest that psycholog- CABG (Saur et al., 2001). Other data indicate ical intervention with an antidepressant, psy- that unstable angina, MI, redo CABG, angio- chotherapy, psychosocial management, or plasty, or death may result secondary to any combination of these measures should be depressive symptoms (Baker, Andrew, employed, with the selection of a specific Schrader, & Knight, 2001; Perski et al., 1998; therapy being based on the patient’s clinical Scheier et al., 1999). It has been further sug- manifestations. Implementation of any of gested that depressive symptoms have as sig- these measures may result in decreased hospi- nificant an effect on cardiac surgery outcomes tal length of stay, analgesic use, and post- as having a low ejection fraction (less than operative morbidity. Administration of 35%) or being of female gender (Connerney, benzodiazepines should be done prudently, Shapiro, McLaughlin, Bagiella, & Sloan, 2001). owing to the increased risk of delirium associ- Anxiety has variable effects on postopera- ated with use of these medications. Tricyclic tive cardiac surgery outcomes. Differences antidepressants and monoamine oxidase that have been reported are typically attrib- inhibitors are contraindicated in patients uted to anxiety type—that is, state or trait. In with coronary artery disease because of their one small study, for example, patients with cardiovascular side-effect profiles. Caution preoperative anxiety had higher associated should also be taken when administering morbidity and mortality rates, whereas serotonin reuptake inhibitors, as some of patients with trait anxiety did not experience these agents may interact with cardiac med- postoperative adverse events related to this ications (Pignay-Demaria et al., 2003). The disorder (Stengrevics, Sirois, Schwartz, Fried- ICU nurse should collaborate with members man, & Domar, 1996). of the multidisciplinary team to help assure Depression occurs commonly after cardiac early recognition and prompt management of surgery and may last for 2 to 3 months. anxiety and depression in postoperative car- Although it may be severe in rare cases, diac surgery patients. depression is usually mild, disappears spontaneously, and is treated short term. Patients ■ OTHER NEUROLOGIC INJURIES who reported a higher level of satisfaction Although central neurologic complications with discharge teaching were less likely to receive more attention and have a greater experience postoperative depression (Davies, impact on patient recovery, several other neu- 2000). rologic complications associated with cardiac In another study of patients admitted for surgery bear mentioning. These include, but CABG surgery, 92% had mild preoperative are not limited to, injuries to the brachial anxiety and 8% had major anxiety. Each of plexus, phrenic nerve, and recurrent laryngeal these patients was readmitted to the hospital nerve. The incidence of these injuries varies, within 6 months of discharge. In that same and these conditions may be underrepre- study, 72% of CABG surgery patients had sented in studies that examine postoperative depression preoperatively and were readmit- complications (Grocott et al., 2004). ted to the hospital. Depressive symptoms worsened in some of these patients, but most patients with preoperative depression experi- Brachial Plexus Injury enced a resolution or reduction of their symp- The brachial plexus includes divisions of the toms after CABG (Murphy et al., 2008). fifth and eighth cranial nerves and the first Anxiety and depression occur more com- thoracic nerve; it forms the peripheral nerves monly in patients with a history of psychiatric that innervate structures of the upper extrem- 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 335

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ities. The brachial plexus passes over the first patient who experiences this type of injury, rib and under the clavicle, with cords that collaboration with a physical therapist is indi- pass downward into the axilla (Gray, 2000). cated to augment the patient’s strength and The location and structure of the brachial flexibility (McGarvey et al., 2008). plexus make it susceptible to injury by direct puncture, stretch, fractures, or displacement Phrenic Nerve Neuropathy of the first rib. Damage to one or both phrenic nerves may Several prospective studies on cardiac sur- occur during cardiac surgery. This complica- gery patients reported a 2% to 15% incidence tion, which is usually related to the applica- of injuries to the brachial plexus and identi- tion of topical hypothermia or surgical fied risk factors for this type of complication. trauma during left IMA dissection (Grocott et Pertinent etiologic factors include sternal al., 2004), occurs in 1% to 30% of patients retraction, first rib fractures, use of IMA (McGarvey et al., 2008). The phrenic nerve retractors, IMA dissection, positioning during traverses the thoracic cavity to provide deen- surgery, central venous catheter placement, ervation to the diaphragm. The left phrenic and advanced patient age (Grocott et al., nerve runs between the lung and mediastinal 2004; McGarvey et al., 2008). aspect of the pleura along the pericardium. Sensory and motor symptoms associated The right phrenic nerve is deeper in the tho- with this type of injury will vary, depending on racic cavity, running lateral to the right sub- the site of the nerve damage. Brachial plexus clavian vein (Gray, 2000). injury often presents as paresthesia of the Diagnosis of phrenic nerve damage may be fourth and fifth digits on the affected side and made by chest radiograph, fluoroscopy, discoordination of an upper extremity, but spirometry, ultrasound, or nerve conduction may also cause pain and weakness. The pres- studies. The reported incidence of phrenic ence of pain is consistent with a peripheral nerve dysfunction ranges from 26% to 70%, injury; in contrast, the presence of confusion, depending on the method used for diagnosis cranial nerve involvement, or hemiparesis is (Grocott et al., 2004). Postoperative atelecta- typically consistent with a central injury sis makes diagnosis more difficult. (McGarvey et al., 2008). Patients often report Paralysis of the diaphragm results in symptoms several days postoperatively. These immobility or paradoxical movement of the subtle injuries may be overlooked owing to the affected side. Unilateral phrenic nerve palsy is emphasis placed on more serious issues in the usually associated with minimal symptoms immediate postoperative period. Any patient because of the recruitment of accessory mus- complaints suggestive of brachial plexus dam- cles. The most common complaints include age should be reported to the surgeon, and a nocturnal orthopnea or dypsnea on exertion. full assessment of motor and sensory function Phrenic nerve neuropathies generally resolve should be performed for the muscles affected in 3 months to 1 year following cardiac sur- by the brachial plexus. gery, but may take 2 years or longer to subside The symptoms of brachial plexus injuries completely (McGarvey et al., 2008). In patients may persist for several months, but generally with underlying lung disease (e.g., COPD), the resolve without treatment (Grocott et al., consequences may be more serious. Deteriora- 2004). In rare cases, prolonged recovery with tion in lung function and extended hospital residual symptoms has been reported. It is stays have been reported in these individuals important to reassure patients that brachial (Grocott et al., 2004). plexus injury is generally transient—most Bilateral phrenic nerve paralysis is a rare patients are symptom-free at discharge. In any and serious complication of cardiac surgery 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 336

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that carries a significant associated mortality. stridor, and signs of airway obstruction. In The first indication may be difficulty in wean- postoperative cardiac surgery patients, these ing the patient with normal lung function symptoms are often attributed—erroneously— from mechanical ventilation. Bilateral phrenic to cardiac or respiratory dysfunction. It is neuropathy has a much longer recovery time. essential that the ICU nurse identify these These patients may compensate with acces- symptoms both correctly and promptly to sory muscle use during the day, but experience avoid patient decompensation and reintuba- respiratory insufficiency at night. Prolonged tion (Hamdan et al., 2002). ventilatory support may be necessary (Grocott A definitive diagnosis is made by perform- et al., 2004; McGarvey et al., 2008). ing laryngoscopy in a spontaneously breathing patient. Recovery following unilateral Recurrent Laryngeal Nerve Neuropathy vocal cord paralysis usually takes 8 to 12 months. Most patients recover with conserva- The left recurrent laryngeal nerve lies in close tive treatment, but occasionally patients may proximity to the parietal pleura as it encircles require reintubation, tracheostomy, vocal the aortic arch (Gray, 2000). Vocal cord paral- cord medialization (an implant to provide ysis as a result of injury to this nerve is less bulk to the vocal cord), or any combination of common than injury to the brachial plexus or these measures (Grocott et al., 2004). phrenic nerve, with a reported incidence in the range of 1% to 2% (Hamdan, Moukarbel, Farhat, & Obeid, 2002). Laryngeal Nerve Injury The left recurrent laryngeal nerve may be IMA harvesting may cause injury to the ante- injured during cardiac surgery if the pleura is rior intercostal nerves. Symptoms may opened and large amounts of ice slush are include numbness, tenderness, pain with light placed in the pleural cavity. Other sources of touch, or persistent burning pain over the injury to the left recurrent laryngeal nerve sternum or left anterolateral aspect of the include tracheal intubation, central line place- chest wall. Although symptoms typically ment, surgical dissection, and trauma from resolve within 4 months, in some patients the TEE probe (Grocott et al., 2004). symptoms may last as long as 28 months For the nurse caring for postoperative car- (McGarvey et al., 2008). diac surgery patients, it is important to observe patients with a weak or ineffective cough, respiratory insufficiency, or hoarse- Other Peripheral Neuropathies ness following extubation, as these may be Other, less common peripheral neuropathies indications of recurrent laryngeal nerve neu- have also been reported. Horner’s syndrome, ropathy and not laryngeal edema. Dysphagia, (characterized by miosis, ptosis, and anhydrosis change in voice quality, inefficient cough, and [inability to sweat]) is thought to result from throat clearing are often associated with vocal damage to the cervical sympathetic chain. Such cord paralysis. Patients in whom this compli- damage occurs from a first rib fracture. Injury cation is suspected should remain NPO until to the saphenous nerve during saphenous vein further evaluation is performed, as these harvest may result in neuralgia that presents patients are at risk for aspiration and pneu- as anesthesia, hyperesthesia, and pain along the monia (Hamdan et al., 2002). medial side of the operative leg and foot. Endo- Patients with unilateral vocal cord paralysis scopic vein harvesting has reduced the inci- may demonstrate respiratory insufficiency, dence of this injury (Grocott et al., 2004). 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 337

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■ SUMMARY ensure effective symptom management. Pre- Despite advances in cardiac surgery, neuro- ventive strategies may include maintaining logic complication rates are increasing. ICU adequate blood pressure, avoiding develop- nurses caring for postoperative cardiac surgery ment of shock, preventing infection, and patients should be able to recognize which administering albumin (Chang et al., 2008). patients are at increased risk for these compli- Although management of neurologic complications and plan their care so as to prevent cations is primarily supportive in nature, early these complications from occurring, minimize recognition and prompt intervention may the associated detrimental effects, and help minimize complications (Silvestry, 2008).

CASE STUDY

Mrs. S. is a 78-year-old patient who was admitted for elective three-vessel CABG and mitral valve replacement for mitral regurgitation. Her medical history was significant for intermittent atrial fibrillation, diabetes, hypertension, and transient ischemic attacks. Her intraoperative course was uneventful, and Mrs. S. was extubated and weaned off inotropic therapy on the day of surgery. She was transferred to the progressive care unit on postoperative day 1. Her medications included metoprolol 25 mg PO q12h (hold for systolic BP < 90 or HR < 50), furosemide 40 mg PO q12h, and atorvastatin 20 mg qhs. On postoperative day 2, Mrs. S. reported feeling “funny.” The nurse detected several subtle neurologic changes from the morning assessment. She was less responsive, had some difficulty with speech, and demonstrated a slight right facial droop. Her BP and serum glucose were checked to rule out hypotension or hypoglycemia as causes; both were found to be within the patient’s normal limits. The nurse alerted the house officer. The nurse initiated a “stroke code.” The members of the team quickly responded to offer rapid assessment and recommendations for care. Mrs. S.’s neurologic status was assessed utilizing the NIHSS. She was alert and oriented, and had normal pupil function, normal motor and sensory function, a slight right facial droop with normal sensation, and dysarthria. She was transferred to the ICU for further evaluation and treatment. Mrs. S. was hemodynamically stable and experiencing no respiratory difficulty. She was transported to the radiology department for a noncontrast CT scan. The CT scan showed no evidence of hemorrhage. Her recent surgery made her ineligible for fibrinolytic therapy. Mrs. S. returned to the ICU, and a dopamine infusion was started to increase her blood pressure and cerebral perfusion. The patient had a BP of 110/70 mm Hg, which was lower than her admission BP of 170/80 mm Hg. A goal BP of 160 mm Hg was achieved with a dopamine infusion rate of 5 mcg/kg/min. Mrs. S.’s neurologic changes resolved after initiation of the dopamine. An NPO restriction was maintained until the patient’s ability to swal- low could be assessed, and a small-bore feeding tube was inserted for enteral feedings. Mrs. S.’s serum glucose was 210 mg/dL; an insulin infusion was started and the cardiac surgery insulin protocol initiated. On postoperative day 5, Mrs. S. was weaned off the dopamine infusion without any changes in neurologic function. She was subsequently transferred to the progressive care unit. Her clinical status continued to improve, and she was discharged home on postoperative day 8. 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 338

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Critical Thinking Questions 1. Why was a dopamine infusion initiated in this patient when her blood pressure was recorded at 110/70 mm Hg? 2. Which risk factors did Mrs. S. have that put her at risk for a postoperative stroke? 3. Which factors contributed to Mrs. S.’s outcome? 4. Why was an insulin infusion an important aspect in Mrs. S.’s plan of care? Answers to Critical Thinking Questions 1. In addition to avoiding hypertension in patients who experience a stroke, periods of hypotension should be avoided to maintain cerebral perfusion. 2. Mrs. S. underwent a CABG procedure. Intraoperative cerebral microembolization during CABG is believed to be the most common etiology for postoperative stroke. Other factors that put this patient at higher risk include her female gender, age greater than 65 years, and history of atrial fibrillation, and diabetes. 3. Mrs. S. recognized a change in her clinical status and alerted the nurse, who immediately summoned the stroke team. A stroke team is a multidisciplinary group with specialized training and experience in stroke care. The physicians on a stroke team have typically received additional preparation to care for patients with a stroke. Patients who are managed by a stroke team often experience better outcomes. 4. Hypoglycemia may mimic symptoms of stroke and may exacerbate brain injury. Initial assessment at the presentation of stroke symptoms should include measurement of serum glucose and correction of hypoglycemia. In addition, hyperglycemia is associated with poorer outcomes following stroke and should be avoided (McGarvey et al., 2008). It has been suggested that hyperglycemia increases the infarct size associated with a stroke and elevates cerebral lactate levels, which results in acidosis of brain tissue and decreases the function of the mitochondria of the penumbra (an ischemic area that is still viable, located adjacent to the area affected by the stroke). Hyper- glycemia is also reported to disrupt the blood–brain barrier, which puts the patient at greater risk of developing cerebral edema; this complication, in turn, promotes brain cell death in the stroke-affected area. All of these factors affect morbidity and mortality following a stroke.

■ SELF-ASSESSMENT QUESTIONS c. increased number of transfusions during surgery. 1. Which of the following is not a risk fac- d. both a and b. tor for neurologic complications following cardiac surgery? 3. Haloperidol is the drug of choice for a. Increased age management of postoperative delirium b. Hypertension not related to substance abuse. The c. Previous stroke nurse should monitor the ECG to detect d. Previous myocardial infarction which side effect? a. QTc prolongation 2. The rate of stroke is increasing in car- b. First-degree AV block diac surgery patients. This trend most c. Ventricular dysrhythmias likely reflects the d. Ischemic changes a. increased age of patients. b. increased number of high-risk patients. 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 339

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4. Neurologic complications in cardiac sur- c. maintaining SBP > 180 mm Hg. gery patients result in d. thrombolytic therapy. a. increased cost of hospitalization. 9. Patients report a lower incidence of b. increased length of stay. postoperative depression with which of c. increased mortality. the following interventions? d. all of the above. a. Antidepressant therapy with 5. An example of a Type II neurologic serotonin inhibitors deficit is b. Discharge teaching that includes a. delirium. realistic expectations of recovery b. agitation. c. Discharge to a long-term facility c. transient ischemic attack. d. Preoperative administration of d. cognitive decline. haloperidol 6. Which of the following peripheral nerve 10. Which of the following is not a risk fac- deficits is not associated with cardiac tor for both Type I and Type II neuro- surgery? logic deficits following cardiac surgery? a. Brachial plexus injury a. Combined open chamber procedures b. Left recurrent laryngeal neuropathy and CABG c. Phrenic nerve dysfunction b. Age d. Sciatic nerve injury c. Diabetes mellitus 7. Atherosclerotic aorta, which increases d. Hypertension risk for Type I neurologic deficits, may be detected intraoperatively by Answers to Self-Assessment Questions a. epiaortic scanning. 1. d 6. d b. TEE. 2. d 7. d c. palpation of the aorta. d. all of the above. 3. a 8. b 8. Management of postoperative stroke 4. d 9. b includes 5. b 10. c a. systemic hypothermia. b. glycemic control. 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 340

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Clinical Inquiry Box

Question: Does the timing of a postoperative stroke after a CABG determine the patient’s rehabilitation needs? Reference: Lisle, T. C., Barrett, K. M., Gazoni, L. M., Swenson, B. R., Scott, C. D., Kazemi, A., et al. (2008). Timing of stroke after cardiopulmonary bypass determines mortality. Annals of Thoracic Surgery, 85(5), 1556–1563. Objective: The purpose of this study was to evaluate the mortality and rehabilitation needs of individuals having a stroke subsequent to CABG. Methods: Consecutive cardiac surgery charts were reviewed. Among the 7201 patients, 202 patients had developed stroke postoperatively. Stroke was classified as early or late. An early stroke occurred within 24 hours after the surgery; a late stroke occurred more than 24 hours after the surgery. Data were collected on patient characteristics, intraoperative variables and outcomes, postoperative course, stroke severity, and discharge status. The relationship between the timing of stroke and discharge status was analyzed with logistic regression. Results: In this study, 2.8% of the patients had a stroke. Incidence of early stroke (within 24 hours after surgery) was 22.8% (46 of 202 patients); incidence of late stroke (more than 24 hours after surgery) was 77.2% (156 of 202 patients). Factors found to be independently associated with stroke-related death included early stroke within 24 hours postoperatively and preoperative chronic renal insufficiency. Those individuals surviving an early stroke had greater rehabilitation needs. Discussion: An early stroke is associated with a higher risk of death and rehabilitation needs. Strategies to prevent a postoperative stroke are needed. Meticulous assessment by the ICU nurse is essential for rapid identification and treatment of stroke.

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Salenger, R., Gammie, J. S., & Vander Salm, T. J. Stengrevics, S., Sirois, C., Schwartz, C. E., Fried- (2003). Postoperative care of cardiac surgical man, R., & Domar, A. (1996). The prediction patients. In L. H. Cohn & L. H. Edmunds, Jr. of cardiac surgery outcome based upon preop- (Eds.), Cardiac surgery in the adult (2nd ed., pp. erative psychological factors. Psychology and 439–469). New York: McGraw-Hill. Health, 11(4), 471–477. Saur, C. D., Granger, B. B., Muhlbaier, L. H., For- Talmor, D., & Lisbon, A. (2005). Management of man, L. M., McKenzie, R. J., Taylor, M. C., et al. the postoperative cardiac surgery patient. In (2001). Depressive symptoms and outcome of M. Fink, E. Abraham, J.-L. Vincent, & P. coronary artery bypass grafting. American Jour- Kochanek (Eds.), Textbook of critical care (5th nal of Critical Care, 10(1), 4–10. ed., pp. 1955–1967). Philadelphia: Saunders. Scheier, M. F., Matthews, K. A., Owens, J. F., Theobald, K., & McMurray, A. (2004). Coronary Schulz, R., Bridges, M. W., Magovern, G. J., et artery bypass graft surgery: Discharge plan- al. (1999). Optimism and rehospitalization ning for successful recovery. Journal of after coronary artery bypass graft surgery. Advanced Nursing, 47(5), 483–491. Archives of Internal Medicine, 159(8), 829–835. Vena, C. (2007). Sleep disturbances in the ICU. In Silvestry, F. E. (2008). Overview of the postopera- R. Kaplow & S. R. Hardin (Eds.), Critical care tive management of patients undergoing car- nursing: Synergy for optimal outcomes (pp. 53–66). diac surgery. Retrieved September 1, 2008, Sudbury, MA: Jones and Bartlett. from www.utdol.com/online/content/topic Young, M. A., Bratina, P., Hickenbottom, S., Dem- .do?topicKey=cc_medi/22438&selectedTitle chuk, A., & Wein, T. (1998). Neurologic com- =12~150&source=search_result plications after coronary artery bypass Sockalingam, S., Parekh, N., Bogoch, I. I., Sun, J., grafting. Journal of Cardiovascular Nursing, 13(1), Mahtani, R., Beach, C., et al. (2005). Delirium 26–33. in the postoperative cardiac patient: A review. Journal of Cardiac Surgery, 20(6), 560–567. Stamou, S. C. (2006). Stroke and encephalopathy after cardiac surgery: The search for the Holy Grail. Stroke, 37(2), 284–285. 57625_CH16_323_344.pdf 4/10/09 11:08 AM Page 344 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 345

Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

Carol Isaac MacKusick

■ INTRODUCTION Numerous factors increase the cardiac sur- Matfin & Porth, 2005). The term “fluid” refers gery patient’s predisposition for postopera- to both water and electrolytes found in the tive fluid and electrolyte imbalances, body. Electrolytes are substances that develop including anesthesia, induced hypothermia, a positive (cation) or negative (anion) electri- physiologic effects of cardiopulmonary cal charge when dissolved in water (Matfin & bypass (CPB) techniques, shock resulting in Porth, 2005). renal insult, cardioplegia, rapid fluid and elec- Fluids are found in both the intracellular trolyte shifts across fluid compartments fol- and extracellular compartments of the body. lowing CPB, stress associated with surgery, Intracellular fluid (ICF) accounts for approxi- intraoperative volume repletion, hemodilu- mately two-thirds of all body fluids. It is tion, the rewarming process that follows located primarily in skeletal muscle mass and hypothermia, or other comorbidities (Mar- provides nutrients for daily cellular metabo- gereson, 2003; Pezzella, Ferraris, & Lancey, lism. ICF contains high levels of potassium 2004). This chapter provides an overview of and phosphorus, and has a moderate amount some of the common acid–base and fluid and of magnesium and proteins (Margereson, electrolyte imbalances, treatments for these 2003). Extracellular fluid (ECF) is further alterations, and the ICU nurse’s role in caring divided into intravascular fluid (plasma) and for these patients in the immediate postoper- interstitial fluid (between the cells). ECF is ative period. The chapter concludes with a more easily lost than ICF because of its loca- brief look at acute renal failure (ARF) and its tion. Electrolyte values that are reported reflect treatment implications as they relate to the plasma levels and are generally considered rep- patient who has undergone cardiac surgery. resentative of ECF status (Speakman & Weldy, 2001). ■ FLUID AND ELECTROLYTE DISTRIBUTION ■ FACTORS AFFECTING FLUID Slightly more than half of the average adult’s VOLUME DISTRIBUTION body weight is made up of fluid—55% to 60% Fluid balance and homeostasis are main- of body weight in men, 50% to 55% of body tained by several body systems, including the weight in women, and slightly less in older heart, lungs, endocrine system, and renal sys- adults (Holte, Sharrock, & Kehlet, 2002; tem. Additionally, the pituitary, adrenal, and

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346 Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

parathyroid glands all play important roles in serum sodium concentration in the postopera- maintaining fluid balance and composition. tive period. Increased production of renin and Without a properly functioning cardiovascu- aldosterone leads to sodium retention and lar system, blood could not be pumped to the potassium excretion (Holte et al., 2002). Cortisol, kidneys. The renal system requires approxi- which is secreted in response to stress, con- mately 25% of cardiac output (CO) for ade- tributes to postoperative fluid homeostasis by quate function to occur. A mean arterial maintaining capillary integrity and by inhibiting pressure (MAP) less than 70 mm Hg results in the production of stress-related inflammatory shunting of the blood supply away from the mediators, thereby decreasing postoperative kidneys (Parker, 2006). fluid shifts (Holte et al., 2002). Without proper lung function, blood is Following CPB, the body experiences an inadequately oxygenated, carbon dioxide is increase in ECF volume (by 20% to 30%), not removed through exhalation, and insensi- sodium retention, and potassium excretion. ble water loss does not occur. The lungs act as The estimated amount of fluid buildup is 800 the first line of defense against acid–base mL for each hour the patient is on CPB. COP imbalances. Without all three body systems decreases by an estimated 50% over this same functioning in harmony, acid–base, fluid, and period (Pezzella et al., 2004). electrolyte disturbances will occur. Fluid exchange takes place between the ■ intracellular and extracellular compartments ACID–BASE IMBALANCES according to differences in hydrostatic pres- Acid–base balance is determined by the arte- sure and colloid osmotic pressure (COP). rial blood pH (hydrogen ion concentration; Surgery causes a decrease in COP by causing normal range 7.35–7.45), arterial carbon diox-

increased capillary permeability, which results ide (pCO2; normal range 35–45 mm Hg), par- in fluid shifts from the vasculature to the tial pressure of oxygen (pO2) in arterial blood interstitium (Holte et al., 2002). (normal range 80–100 mm Hg), and bicar-

The endocrine system causes sodium and bonate (HCO3) value (normal range 22–26 water retention and potassium excretion by mEq/L). Table 17–1 provides a brief overview stimulating production of antidiuretic hormone of arterial blood gas (ABG) values and their (ADH) in response to surgical trauma. ADH interpretive implications. secretion causes the kidneys to reabsorb water The human body desires to maintain a with a subsequent decrease in diuresis and state of homeostasis at all times. When

Table 17–1 Arterial Blood Gas Values and Interpretation

Lab Parameter Normal Value Results and Implications

pH 7.35–7.45 < 7.35 ϭ acidosis > 7.45 ϭ alkalosis If compensation is suspected and the pH is within normal limits, look at the “end” where the pH falls: Is it closer to the acidosis side or the alkalosis side? ϭ HCO3 22–26 mEq/L < 22 metabolic acidosis > 26 ϭ metabolic alkalosis ϭ pCO2 35–45 mm Hg < 35 respiratory alkalosis > 45 ϭ respiratory acidosis ϭ pO2 80–100 mm Hg < 80 possible hypoxemia 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 347

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changes in pH occur, buffer systems are acti- Acidosis vated to assist the body to normalize pH. As Respiratory Acidosis changes in pH occur, cellular responses are Respiratory acidosis may occur in the immedi- stimulated immediately. When the cellular ate postoperative period following cardiac sur- responses are inadequate to handle the result- gery and is a direct result of inadequate ant change in pH, the respiratory system will ventilation or sedation (Pezzella et al., 2004; provide compensation; if needed, the renal Sinclair, 2006). Table 17–2 lists common system will activate its compensatory mecha- causes of respiratory acidosis in the postopera- nisms as well. ABG changes that are primarily tive cardiac surgery patient. Evaluation of driven by the kidneys may take days to ABG results and observation for signs and appear, whereas changes caused by the respi- symptoms are essential roles of the ICU nurse. ratory system will occur in a matter of min- Signs and symptoms of respiratory acidosis utes (MacKusick, 2007). ABG interpretation may include dizziness, confusion, weakness, is discussed in detail in Chapter 11.

Table 17–2 Common Causes of Respiratory Acidosis in the Postoperative Cardiac Surgery Patient

Central respiratory depression ● Cardiac arrest with resultant cerebral hypoxia ● Obesity ● Use of opiates, sedatives, or anesthesia Pulmonary issues ● Acute respiratory distress syndrome ● Aspiration, pneumonia, and/or airway obstruction ● Asthma ● Atelectasis ● Bronchospasm or laryngospasm ● Pneumothorax ● Pulmonary edema ● Pulmonary embolism ● Restrictive lung diseases

Increased CO2 production ● Shivering ● Sepsis Hypoventilation secondary to the following conditions: ● Pain ● Sternal incision ● Residual anesthesia ● Awakening with inadequate analgesia and impaired respiratory mechanics Side effects of opiates Other ● Inadequate mechanical ventilation (user error) ● Inadequate ventilation/perfusion ratio (decreased ventilation) ● Neuromuscular blocking agents

Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, 2007; Gothard, Kelleher, & Haxby, 2003. 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 348

348 Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

palpitations, tetany, convulsions, or ventricu- warm, flushed skin from peripheral vasodila- lar fibrillation. Of note, ventricular fibrillation tion. CO may decrease, and myocardial con- is more likely to occur during the intraopera- tractility is depressed (Porth, 2005a). Because tive or immediate postoperative period of the contractility issues commonly associ- (Wilkins & Wheeler, 2003). ated with metabolic acidosis and the poten- Treatment of respiratory acidosis will vary tial for hyperkalemia, the ICU nurse should according to the cause, but generally focuses monitor for dysrhythmias in patients who on improving the patient’s ventilation/perfu- develop this imbalance. Table 17–3 lists com- sion (V/Q) status. Conventional interventions mon causes of metabolic acidosis seen in the performed by the ICU nurse include frequent postoperative cardiac surgery patient. pulmonary hygiene and encouraging turning, Metabolic acidosis is generally classified as coughing, and deep breathing. Titration of having either a high or normal anion gap. sedation may be indicated if it will not cause Bicarbonate and chloride are considered the excessive patient discomfort. If the patient is major anions in the body. In cases where a on mechanical ventilation, respiratory acidosis metabolic acidosis is accompanied by a loss of can be corrected by increasing the patient’s bicarbonate, a normal anion gap metabolic minute ventilation; this goal can be accom- acidosis state is present. The most common plished by increased the preset rate or tidal vol- causes of normal anion gap acidosis include ume. If the patient is not on mechanical renal tubular acidosis, excessive administra- ventilation and conventional interventions are tion of isotonic solutions, and diarrhea not successful in correcting the respiratory aci- (Parker, 2006). In cases where the concentra- dosis, depending on the patient’s clinical sta- tion of anions increases (thereby destroying tus and ABG results, intubation and the electrical neutrality of the body), a high mechanical support may be required (Lemmer, anion gap acidosis is said to exist (Hertford, Richenbacher, Vlahakes, & Behrendt, 2003). McKenna, & Chamovitz, 1989). Lactic acidosis, renal failure, and diabetic ketoacidosis Metabolic Acidosis (DKA) are the most common causes of high Because a state of electrical neutrality must be anion gap acidosis. maintained within the body at all times, patients with a metabolic acidosis must retain Alkalosis a positive (cation) ion to adjust for the increasing bicarbonate. This goal is accom- Respiratory Alkalosis plished by the renal system, which accumu- Some form of hyperventilation is typically the lates positively charged potassium ions. cause of a respiratory alkalosis (Adrogué & Hyperkalemia frequently accompanies a Madias, 1998). Table 17–4 lists common metabolic acidosis (unless the metabolic aci- causes of respiratory alkalosis seen in the dosis is caused by lactic acidosis or diarrhea). postoperative cardiac surgery patient. Respi- It has been suggested that when acid (hydro- ratory alkalosis is usually seen as a later com- gen ion) levels are high in the blood, the body plication in the postoperative cardiac surgery attempts to compensate by causing muscles patient, arising as a compensatory mecha- to take up the excess hydrogen. In order to nism (e.g., in response to diuretic therapy) maintain neutrality, in exchange for the (Pezzella et al., 2004). hydrogen ions, potassium is transferred into Signs and symptoms of respiratory alkalo- the blood. Signs and symptoms of metabolic sis may include lightheadedness, inability to acidosis may include headache, confusion, concentrate, headache, numbness and tin- drowsiness, nausea and/or vomiting, and gling of the extremities, tinnitus, palpitations, 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 349

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Table 17–3 Common Causes of Metabolic Acidosis in the Postoperative Cardiac Surgery Patient

Hemodynamics ● Decreased cardiac output ● Inadequate systemic perfusion ● Decreased cardiac function ● Decreased peripheral perfusion ● Hypotension ● Hypovolemia ● Vasoconstriction from hypothermia Physiologic conditions (increasing acids) ● Sepsis ● Renal failure ● Renal tubular acidosis ● Regional ischemia ● Diabetic ketoacidosis ● Splanchnic ischemia ● Anaerobic metabolism

Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, 2007; Gothard, Kelleher, & Haxby, 2003; Pezzella, Ferraris, & Lancey, 2004.

Table 17–4 Common Causes of Respiratory Alkalosis in the Postoperative Cardiac Surgery Patient

Hypoventilation secondary to the following conditions: ● Anxiety or fear ● Pain or generalized discomfort Increased oxygen demand as a result of the following conditions: ● Fever ● Bacteremia (especially with gram-negative organisms) ● Sepsis Pulmonary disorders ● Pneumonia ● Pulmonary edema ● Pulmonary embolism ● V/Q mismatch (increased ventilation, decreased perfusion) Medications: Respiratory stimulants User error ● Inappropriate ventilator settings ● Hyperventilation during transfer from OR

Sources: Chikwe, Beddow, & Glenville, 2006; Gerhardt, 2007; Gothard, Kelleher, & Haxby, 2003; Rimailho, Goldstein, & Vincent, 1985. 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 350

350 Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

Table 17–5 Common Causes of Metabolic Alkalosis in the Postoperative Cardiac Surgery Patient

Adrenal disorders: hyperaldosteronism Hypokalemia Hypochloremia Excessive diuretic administration Nasogastric suctioning Overuse of potassium wasting drugs (e.g., increased use of thiazide diuretics) Vomiting Massive transfusions (from citrate)

Sources: Chikwe, Beddow, & Glenville, 2006; Gothard, Kelleher, & Haxby, 2003.

dry mouth, sweating, chest pain, or nausea results in a hypokalemic state. Signs and and vomiting. Late stage signs and symptoms symptoms of metabolic alkalosis include poor may include loss of consciousness or seizures skin turgor (from fluid loss). Treatment is (Adrogué & Madias, 1998). The neurologic aimed at restoring fluid balance and correct- symptoms may be caused by a hypocalcemic ing the underlying disorder. state, which is commonly seen with a respiratory alkalosis. This acid–base disturbance can ■ cause an increase in protein binding of ion- ELECTROLYTE IMBALANCES ized calcium (the amount of calcium not Electrolyte imbalances are frequently seen in bound to protein and available for use by the postoperative cardiac surgery patients. The body). Treatment is aimed at correcting the ICU nurse should recognize normal values, underlying cause. signs, and symptoms associated with these imbalances, and implement appropriate inter- Metabolic Alkalosis ventions to correct the imbalances. Table 17–6 Common causes of metabolic alkalosis in the lists the common electrolytes and their associ- postoperative cardiac surgery patient are pre- ated normal values. sented in Table 17–5. Like respiratory alkalosis, metabolic alkalosis is usually seen later in the postoperative cardiac surgery patient, act- Potassium Imbalances ing as a compensatory mechanism (Pezzella et Fluctuations in potassium levels are common al., 2004). Patients often have concomitant following cardiac surgery and can affect car- hypokalemia and hypocalcemia; these under- diac automaticity and conduction (Khalpey, lying conditions must be simultaneously cor- Ganim, & Rawn, 2008; Pezzella et al., 2004). rected. The relationship between potassium Potassium works with sodium to help main- and hydrogen ions was explained in the sec- tain fluid balance within the body, with kid- tion on metabolic acidosis. In the case of a ney regulation being the mechanism that metabolic alkalosis, while the underlying governs the balance (Flanagan, Devereaux, physiologic principles remain the same, the Abdallah, & Remington, 2007). The potas- opposite effect occurs. With a metabolic alka- sium found in the extracellular fluid is losis, as the hydrogen ion concentration responsible for neuromuscular function and increases in the blood, potassium ions move plays a major role in myocardial contractility, into the cells to maintain neutrality. This function, and rhythm (Rose & Post, 2000a). 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 351

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Table 17–6 Electrolyte Reference Values

Electrolyte Normal Value*

Potassium 3.5–5.0 mEq/L Sodium 135–145 mEq/L Magnesium 1.8–2.4 mg/dL† Phosphorus 2.5–4.5 mg/dL Calcium 8.5–10.5 mg/dL‡

*Normal value markers may vary according to facility. Figure 17–1 Hyperkalemia—peaked T Always check with your local laboratory if unsure of wave. the normal values for any laboratory finding. Source: Illustrated by James R. Perron †Serum magnesium may also be reported in millimoles per liter (mmol/L). In these cases, normal values would be in the range of 0.65–1.1 mmol/L. Patients with progressive hyperkalemia will ‡Serum calcium can be reported as total calcium, ionized calcium, or non-ionized calcium. The value pro- present with ventricular dysrhythmias and vided in the table is for the total calcium. A normal may develop nausea, paresthesias, muscle ionized calcium value is in the range of 4.4–5.3 weakness, cramps, or paralysis (muscle weak- mg/dL. ness first appears in the larger muscles and the myocardium). These signs and symptoms are directly related to the effect of the elevated Hyperkalemia potassium on the cellular membrane poten- The major causes of hyperkalemia in the post- tial. Respiratory failure may also occur as a operative cardiac surgery patient are result of hyperkalemia (Margereson, 2003). decreased urinary output, cardioplegia, Treatment of moderately elevated serum potas- decreased insulin levels, metabolic acidosis, sium levels may include sodium polystyrene diabetes, and hemolysis of red blood cells sulfonate (Kayexalate®). Kayexalate acts by ex- (Khalpey et al., 2008; Margereson, 2003; changing sodium ions for potassium ions in the Pezzella et al., 2004). Oliguric or anuric renal gastrointestinal (GI) tract, thereby allowing for failure, or failure to excrete and metabolize elimination of excess potassium in the stool. potassium through the kidneys may occur Before Kayexalate is administered, however, it postoperatively as well (Parker, 2006). Many must be known if a patient can tolerate an cardiac medications can cause hyperkalemia increase in serum sodium (Kozar & Moore, 2006). (e.g., angiotensin-converting enzyme [ACE] Emergent renal replacement therapy is an inhibitors, potassium-sparing diuretics, beta option to lower serum potassium levels in those blockers, unfractionated heparin, and patients who do not respond to conservative digoxin). Massive blood transfusions are also therapy. With severe hyperkalemia, 10 units of

associated with higher levels of potassium. regular insulin with one ampule of D50W, cal- Evidence of hyperkalemia may be noted in cium gluconate (if no cardiac symptoms the electrocardiogram (ECG). Peaked T waves related to the hyperkalemic state are present), (see Figure 17–1), a widening QRS complex, a beta agonist, or sodium bicarbonate may be and a prolonged PR interval may be noted administered. These interventions are tempo- (Montague, Ouellette, & Buller, 2008). Car- rary in nature, but will provide almost imme- diac arrest may occur at any point if potas- diate lowering of potassium levels and allow sium levels continue to increase (Roth & time for the patient to be prepared for dialysis Patel, 2003). therapy (Margereson, 2003). 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 352

352 Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

Hypokalemia Sodium Imbalances The major causes of hypokalemia in cardiac Sodium is the major extracellular ion found surgery patients include brisk diuresis, rapid in the body; its concentration normally correction of hyperglycemia with insulin, ranges between 135 and 145 mEq/L. Sodium adrenal hyperreactivity, vomiting, alkalosis, is directly responsible (in conjunction with and hypothermia (Margereson, 2003; Pezzella potassium and the sodium potassium ATPase et al., 2004). Patients may also present with a pump) for maintaining the fluid balance in dilutional hypokalemia (Leier, Dei Cas, & the body, ensuring appropriate water distri- Metra, 1994). bution, and maintaining the ECF volume sta- Hypokalemia is associated with increased tus (Rose & Post, 2000b). ventricular dysrhythmias and hypertension (Whelton et al., 1997), a prolonged PR inter- Hypernatremia val, U-wave development as the T wave flat- Hypernatremia is a relatively uncommon phe- tens, and ST-segment depression (Diercks, nomenon, but is associated with a 40–60% (or Shumaik, Harrigan, Brady, & Chan, 2004). greater) mortality rate. This imbalance occurs Figure 17–2 illustrates the development of when there is a gain of sodium in excess of U waves in the hypokalemic patient. water or a loss of water in excess of sodium. In Hypokalemia will typically manifest as the postoperative cardiac surgery patient, it is muscle weakness, fatigue, hypotension, and most commonly seen in conjunction with absent or diminished bowel sounds (Margere- hyperventilation. Hypernatremia may also son, 2003). It is frequently accompanied by develop secondary to dehydration from fever, metabolic alkalosis and hypomagnesemia. diabetes, or use of osmotic diuretics (Mar- Ventricular dysrhythmias and syncope are gereson, 2003). likely to develop as well (Leier et al., 1994). Signs and symptoms of hypernatremia may Treatment for hypokalemia involves include thirst, fever, restlessness, weakness, replacement of potassium, either orally or dry oral mucosa or tongue, poor skin turgor, intravenously. If concomitant hypomagne- and disorientation with possible progression semia exists, initial correction of magnesium to lethargy, stupor, or coma (Howanitz & levels is required (Leier et al., 1994). Typically, Howanitz, 2007). Depending on the cause, serum potassium levels will increase by treatment focuses on either increasing water 0.1 mEq/L for each 2 mEq of potassium within the body or removing sodium from it replacement administered (Pezzella et al., (Kang, Kim, & Oh, 2002; Margereson, 2003). 2004). Postoperative cardiac surgery patients with a severe hypernatremia (greater than 150 mEq/L) may experience an acid–base imbalance that is difficult to correct. In this situation, use of tromethamine (Tham®) to treat metabolic acidosis is recommended instead of sodium bicarbonate, as the latter therapy may increase sodium levels further and cause central nervous system effects (Pezzella et al., 2004). Hyponatremia Figure 17–2 Hypokalemia—U wave. Hyponatremia commonly arises when cells Source: Illustrated by James R. Perron swell as water enters them. This swelling can 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 353

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progress to the point that it eventually leads les, and muffled heart sounds (Flanagan et al., to cellular rupture. Common causes of 2007). Because of their fluid volume status, hyponatremia include use of certain medica- these patients also present with low hemoglo- tions (e.g., thiazide diuretics, nonsteroidal bin and hematocrit levels (Flanagan et al., anti-inflammatory drugs [NSAIDs]), pneu- 2007). monia, and acute respiratory failure. Signs Treatment of hyponatremia includes and symptoms may include headache, nausea replacement of fluid in patients with hypo- and vomiting, generalized muscle weakness, volemic hyponatremia, water restriction in and fatigue. CO may be decreased as well hypervolemic or normovolemic hypona- (Leier et al., 1994). Cheyne-Stokes respirations tremia, and management of associated adre- and respiratory failure may accompany severe nal and ADH imbalances as appropriate. For hyponatremia (Rai, Whaley-Connell, McFar- those patients with volume overload, treat- lane, & Sowers, 2006). Only rarely will a post- ment includes a loop diuretic agent, fluid operative cardiac surgery patient develop restriction to less than 1000 mL/day, and pos- hyponatremia in the absence of hyper- itive inotropic agents (Leier et al., 2004). Dur- glycemia, however (Pezzella et al., 2004). ing treatment, close monitoring and accurate Hyponatremia may be seen in patients who intake and output records should be main- are either hypovolemic, normovolemic, or tained, and the nurse should monitor the hypervolemic. Most often, this type of sodium patient’s vital signs closely to assess for rapid imbalance is seen in patients with severe heart fluid changes (Flanagan et al., 2007). The level failure, in whom a decrease in CO triggers the of sodium replacement depends on the extent release of ADH, which in turn causes hyper- of loss; infusions of 3% or 5% sodium must be volemia. Patients who are hypovolemic may closely monitored. Rapid changes in level of develop hyponatremia secondary to brisk consciousness indicate worsening cerebral diuresis, excess insensible loss from the skin edema. or GI tract, or glucocorticoid deficiency. Those who are normovolemic may develop Magnesium Imbalances hyponatremia secondary to hypokalemia, Magnesium is an electrolyte that plays a key medications, or hypothyroidism. Patients role in cellular function. Some researchers with hypervolemia may develop hypona- have suggested that magnesium is equally as tremia secondary to renal failure or heart fail- responsible for ensuring appropriate electri- ure (Margereson, 2003). cal conduction in the heart as is potassium The patient with hypervolemia-associated (Henke & Eigsti, 2003). Magnesium helps hyponatremia will present with changes in maintain cellular permeability and neuro- mental status, restlessness, anxiety, decreased muscular excitability, and it is intrinsically urinary output, weight gain, peripheral and involved in the appropriate utilization of ATP dependent edema (including pitting edema; (Pezzella et al., 2004). Levels of this ion are see Figure 17–3), hypertension, jugular vein regulated by GI absorption and renal excre- distention, shortness of breath, diffuse crack- tion; the normal range is 1.8–2.4 mg/dL.

1+ 2+ 3+ 4+

2 mm 4 mm 6 mm 8 mm Figure 17–3 Pitting edema. Source: Illustrated by James R. Perron 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 354

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Hypermagnesemia with atrial and ventricular dysrhythmias. Hypermagnesemia is most likely to occur in Affected patients may present with depres- patients with decreased renal function. The sion, muscle weakness, coronary spasm, con- patient with an elevated magnesium level will fusion, and irritability. Tetany, delirium, and present with lethargy, muscle weakness, seizures are also possible (Margereson, 2003). dilated pupils, nausea, vomiting, diarrhea, Hypomagnesemia is often accompanied by anorexia, muscle weakness, decreased or hypophosphatemia, hypocalcemia, and absent bowel sounds, and hypotension hypokalemia. The action of the parathyroid (Margereson, 2003). Initially the patient will gland and hormone release will be inhibited present with hypotension and shallow respi- in cases where the serum magnesium falls rations, followed by periods of apnea (Hoff- below 1.0 mg/dL (Hoffman, 2002). Changes man, 2002). Ventricular dysrhythmias, will appear on the ECG tracing, including bradycardia, a prolonged PR interval, com- nonspecific T wave changes, appearance of plete heart block, and cardiac arrest are not U waves, prolonged QT intervals, widened uncommon in patients whose magnesium QRS complex, ST-segment depression, peaked levels exceed 2.5 mg/dL (Henke & Eigsti, T waves, and torsade de pointes. Ventricular 2003; Margereson, 2003). ectopy, paroxysmal supraventricular tachycar- Magnesium levels greater than 10 mg/dL dia, premature ventricular contractions, and (particularly 15 mg/dL) are usually fatal. atrial and ventricular fibrillation are likely to Treatment for symptomatic hypermagne- occur as well (Margereson, 2003; Pezzella et semia includes an infusion of insulin and glu- al., 2004). Finally, insulin resistance may cose as well as intravenous calcium gluconate, occur in patients with severe hypomagne- which acts as a magnesium antagonist. Cal- semia, making serum glucose levels hard to cium gluconate rapidly reverses cardiac dys- control (Rodriguez-Hernández, Gonzalez, rhythmias or respiratory depression directly Rodriguez-Morán, & Guerrero-Romero, related to hypermagnesemia. The ICU nurse 2005). should prepare to administer 10–20 mEq of Treatment entails magnesium repletion. If calcium gluconate over 10 minutes or follow magnesium is to be given intravenously, the facility policy in cases of life-threatening patient’s renal function should be determined hypermagnesemia. Patients who develop this prior to its administration to help avoid electrolyte imbalance will also require fluid refractory hypermagnesemia (Phillips, 2004). resuscitation and loop diuretics. Mechanical Additionally, during infusions of magnesium, ventilation may be required for those individ- urinary output should be closely monitored. uals with severe respiratory depression, and a If urinary output decreases to less than temporary pacemaker may be required in 100 mL over 4 hours, the infusion of magne- patients who experience severe bradycardia. sium should be discontinued and the surgeon Hemodialysis may be required if the patient’s notified. The actions of magnesium as a cal- renal function is inadequate (Hoffman, 2002). cium channel blocker, as a regulator of intracellular potassium, and in the activation of Hypomagnesemia ATP explain the antiarrhythmic effects of this Hypomagnesemia is a common clinical prob- electrolyte (Pezzella et al., 2004). lem in postoperative cardiac surgery patients, Protection of the patient’s overall condi- especially in those individuals who develop tion remains a high priority in a hypomagne- hemodilution following CPB or who receive semic patient. Seizure precautions should be diuretics (Margereson, 2003; Pezzella et al., implemented, the airway and respiratory sta- 2004). This electrolyte imbalance is associated tus should be continually monitored, and 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 355

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falls precautions implemented for those indi- polyuria, polydipsia, shortened QT segments, viduals who have an altered mental status. and depressed T waves. Nonspecific dysrhythmias, bradycardia, and first-, second-, or Calcium Imbalances third-degree heart block may develop. Bundle The majority (greater than 99%) of the body’s branch blocks may also be seen. If left calcium is found in the skeletal system. Most untreated, the patient with severe hypercal- of the remaining calcium is found inside cells, cemia may develop psychosis or lethargy that with only 0.1–0.2% of this remaining 1% being leads to coma (Ziegler, 2001). found in the extracellular fluid (Matfin & Calcitonin may be given intravenously as a Porth, 2005). A normal serum calcium level is treatment for hypercalcemia; it enhances uri- in the range of 8.5–10.5 mg/dL in individuals nary calcium excretion and decreases bone with a normal pH and normal serum albumin resorption of this electrolyte (Matfin & Porth, levels. For every 1 g/dL decrease in serum albu- 2005). Glucocorticoids have also been used suc- min, there is an approximate 0.75–1.0 mg/dL cessfully in cases of hypercalcemia; however, decrease in total calcium. For every 0.1 unit results will not be seen for 5 to 7 days with this rise in pH, there is an approximate 0.16 mg/dL therapy, and patients may develop increased decrease in total calcium (Matfin & Porth, risks for hyperglycemia and sodium and water 2005). Assessment of total calcium level retention (Jacobs & Bilezikian, 2005). requires pH and serum albumin evaluation. Hypocalcemia In cases of protein malnutrition or other issues affecting serum albumin, an ionized cal- Hypocalcemia occurs when serum calcium is cium level is a more accurate indicator of cal- less than 8.5 mg/dL. At a minimum, measure- cium status than total calcium level. Ionized ment of ionized calcium level is needed to calcium is the calcium that is not bound to pro- confirm a diagnosis of hypocalcemia, and tein; its normal range is from 4.4 to 5.3 mg/dL these data should always be reviewed in con- (Fukagawa, Kurokawa, & Papadakis, 2008). junction with the acid–base status of the Adequate levels of ionized calcium are essential patient. A patient with a low serum calcium for cardiac performance (Khalpey et al., 2008). but normal ionized calcium is typically asymptomatic, and is referred to as having Hypercalcemia pseudohypocalcemia. Three basic causes exist for hypercalcemia: Development of hypocalcemia is expected increased intestinal absorption, increased following CPB, hemodilution, low CO, or bone resorption, and decreased elimination administration of citrated blood (Khalpey et (Matfin & Porth, 2005). Decreased elimina- al., 2008). Packed red blood cells, for example, tion of calcium is seen generally with medica- are conditioned with citrate to prevent their tion use, or when decreased availability of coagulation. When citrate combines with cal- physiologic calcium is present (such as with cium, hypocalcemia can occur. This effect acidosis). Medications that increase serum generally does not occur during normal blood calcium levels include thiazide diuretics and transfusions because citrate has adequate lithium carbonate, both of which decrease time to metabolize in the liver; only in cases renal calcium excretion. Some estrogens also of faster than normal blood transfusions or increase calcium levels. cases of liver dysfunction does this citrate– Patients with hypercalcemia will present calcium binding become a potential problem. with altered mental status, fatigue, weakness, Cardiac surgery patients who develop sepsis lethargy, anorexia, nausea, vomiting, consti- are also predisposed to hypocalcemia (Mor- pation, decreased renal function or ARF, gan, Mikhail, & Murray, 2005). 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 356

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Patients with hypocalcemia may report a prolonged QT interval, shortness of breath, numbness or tingling of the fingers and toes. and dysrhythmias ranging from bradycardia Muscle cramps, spasms, tremors, twitching, to asystole. Heart sounds may be muffled and abdominal and intestinal cramps are com- (Khalpey et al., 2008). mon. Bowel sounds are hyperactive. Because of Acute hypocalcemia should be promptly the increased neuromuscular activity, hypocal- corrected with administration of 10% calcium cemic patients who are left untreated may gluconate. This medication may be given develop seizures, laryngospasm, and bron- either as an intravenous push over 5 to chospasm. These spasms may lead to laryngeal 10 minutes or mixed in 0.9% normal saline for stridor, which will eventually necessitate intu- infusion according to facility policy. bation if the calcium level is not adequately treated (Litwack, 2003). Auscultation of breath Phosphorus Imbalances sounds may reveal inspiratory and expiratory Phosphorus is mainly an intracellular anion, wheezing. In approximately 70% of patients accounting for approximately 1% of the total with hypocalcemia, positive Trousseau’s and body weight of adults (Matfin & Porth, 2005). Chvostek’s signs are present. Trousseau’s sign These ions play integral roles in the repair of is considered positive when an inflated blood cells and tissues, and are crucial ions in the pressure cuff elicits a carpopedal spasm (see production of ATP (Parker, 2006). Phospho- Figure 17–4). Chvostek’s sign is considered rus is excreted through the kidneys; as kidney positive when tapping of the facial nerve elicits function declines, phosphorus levels are likely facial muscle movement (Parker, 2006). to increase (Porth, 2005b). As is the case with Cardiac complications associated with calcium, hormonal regulation is provided hypocalcemia include a decrease in myocar- through the parathyroid gland (Weinman et dial contractility and CO. Symptoms of al., 2007). A normal serum phosphorus is in hypocalcemia will likely include hypotension, the range of 2.5–4.5 mg/dL.

Figure 17–4 Test for hypocalcemia. Source: Illustrated by James R. Perron 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 357

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Hyperphosphatemia tion (Mailhot & Richardson, 2006). The most Hyperphosphatemia is defined as a serum common cause of hypophosphatemia is phosphorus level greater than 4.5 mg/dL, but increased renal elimination of this ion, as is becomes clinically significant when phospho- seen with respiratory alkalosis or postopera- rus levels exceed 5.0 mg/dL (Patterson, 2008). tive stress (Margereson, 2003). Almost all cases of hyperphosphatemia are a Signs and symptoms of severe hypophos- direct result of decreased renal function. phatemia include paresthesias; severe, pro- When the glomerular filtration rate (GFR) found, and progressive muscle weakness; falls below 50 mL/min, the kidneys are no tremors; muscle pain and tenderness; longer able to adequately metabolize phos- lethargy; confusion; anxiety; and apprehen- phorus (Parker, 2006). Respiratory acidosis sion. If this condition is left untreated, the and DKA may also lead to hyperphos- patient will develop hypoxia and bradycardia. phatemia. It is suggested that the relationship Hypotension will be present, and stroke vol- between a respiratory acidosis and hyperphos- ume will be decreased. Muscle weakness will phatemia is twofold. First, a sudden rise in eventually lead to acute respiratory failure carbon dioxide levels can lead to an elevation from decreased contraction of the diaphragm in phosphorus levels. Second, presence of a (Margereson, 2003). Seizures and coma may respiratory acidosis causes phosphorus to also be present. Hemolytic anemia as well as move from the intracellular to extracellular leukocyte and platelet dysfunction will be fluid compartment. Presence of a metabolic noted. Respiratory rate decreases as phospho- acidosis, as seen in DKA, is associated with rus levels decrease. However, if the hypophos- hyperphosphatemia (Patterson, 2008). phatemia is related to presence of respiratory Signs and symptoms of hyperphosphatemia alkalosis, tachypnea will be present. Hypomag- may include altered mental status, delirium, nesemia and hypercalcemia are oftentimes seizures, paresthesias (especially around the present in conjunction with hypophos- mouth or in the fingers and toes), and tetany. phatemia (Mailhot & Richardson, 2006; Positive Trousseau’s and Chvostek’s signs, Matfin & Porth, 2005). hypotension, and cardiac dysrhythmias may Treatment for severe hypophosphatemia also be present. Heart sounds may be muffled, requires intravenous replacement of phos- and a pericardial friction rub may be present, phorus. The precise therapy employed indicative of potential heart failure. The QT depends on the patient’s renal status, as one interval is often prolonged. phosphorus preparation is built on sodium If kidney function is adequate, normal and the other relies on potassium. For the saline infusions may help return the serum patient with adequate renal function, potas- phosphorus to baseline. If the patient is sium phosphate may be administered; symptomatic, emergent renal replacement sodium phosphate should be administered to therapy may be indicated (Parker, 2006). those patients with decreased renal function. Should a heart block or flaccid paralysis Hypophosphatemia develop, the infusion of phosphorus should Patients with a serum phosphorus level less be immediately discontinued, as these symp- than 1.0 mg/dL are considered severely com- toms indicate rebound hyperphosphatemia. A promised. Because of the key role that phos- patient with severe hypophosphatemia may phorus plays with ATP, a sharp decrease in also be more prone to infection. Conse- phosphorus levels results in cell energy deple- quently, a complete blood count should be 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 358

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performed on the postoperative cardiac sur- Assessment gery patient to provide information about the Hypovolemia is common postoperatively, but presence of bleeding and possible infection. often proves difficult to assess. FVD is generally gauged as mild, moderate, or severe. Mild ■ FLUID BALANCE AND VOLUME FVD represents a loss of approximately 2% of MANAGEMENT total body weight; moderate FVD entails an Fluids shift on an as-needed basis between approximately 2–5% body weight loss; and compartments to maintain homeostasis. This severe FVD involves a greater than 8% body fluid exchange is partly affected by osmolar- weight loss (Matfin & Porth, 2005). ity, and hence by electrolyte concentrations Signs and symptoms of FVD and hypo- (Margereson, 2003). Shifts between compart- volemia include decreased capillary refill time, ments occur as the body seeks to maintain an central venous pressure (CVP), and urinary appropriate cation and anion distribution as output; dizziness; increased osmolality, spe- well as optimal fluid levels in each compart- cific gravity, thirst sensation in conscious ment. Frequently, alterations in fluid volume patients, hemoglobin and hematocrit, and status accompany electrolyte imbalances. For blood urea nitrogen (BUN) to serum creati- the nurse caring for the postoperative cardiac nine ratio (usually greater than 30:1); postural surgery patient, either hypovolemia or hyper- or prolonged hypotension; tachycardia; weak volemia may represent worsening of a pre- and thready pulse; and decreased vein filling. existing medical condition or may be related A urinary output rate that is less than 0.5 to the surgical procedure and associated mL/kg/hr is indicative of severe FVD and interventions. In either case, it is important to inadequate renal perfusion. Assessment of recognize the implications of alterations in skin turgor reveals skin that does not “spring” fluid volume status and to determine appro- back, but rather remains in the tented posi- priate courses of treatment. tion; dry oral membranes; and a tongue that appears shrunken, with fissures. Severe FVD is also accompanied by confusion, upper body Hypovolemia weakness, and speech difficulties. Hypovolemia, which is also known as fluid Shock develops when FVD is left untreated. volume deficit (FVD), results when both water In such cases, hypotension becomes severe and electrolytes are lost together. This condi- and perfusion to vital organs is compromised tion is not the same as dehydration, which (Matfin & Porth, 2005; Wilkins & Wheeler, results from water loss alone (and, therefore, 2006). leads to hypernatremia). An isotonic fluid volume deficit indicates that electrolyte levels Treatment remain essentially unchanged (Matfin & Treatment of hypovolemia depends on the Porth, 2005). cause of the FVD. Hypoxia is likely to develop Common causes of fluid losses in the post- in cases of shock; oxygen should be adminis- operative cardiac surgery patient include tered to maintain adequate saturation blood loss, fever, and third spacing of fluid (Wilkins & Wheeler, 2006). The goal of FVD (Parker, 2006). Hypovolemic shock results treatment is to expand plasma volume until a when circulating blood volume falls to such a desired MAP has been attained and sustained. low level that vital organs are not perfused When planning for delivery of replacement adequately, causing irreversible damage to fluids, daily fluid losses and intraoperative these organs (Wilkins & Wheeler, 2006). fluid loss must also be accounted for and 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 359

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added into the replacement. A fever greater support to augment CO. Finally, patients who than 101 °F (38.3 °C) increases the daily fluid underwent repair for mitral regurgitation may requirement by approximately 500 mL. If the develop postoperative right ventricular failure patient is not severely hypotensive, the fluid and, therefore, require inotropic administra- replacement plan may be based on an tion (Khalpey et al., 2008). assumption that 50% to 80% of the fluid loss Ongoing debate surrounds the use of crys- will be replaced over 12 to 24 hours; in cases talloids versus colloids for fluid resuscitation. where severe hypotension or shock exists, vol- As their name connotes, isotonic crystalloid ume repletion must take place much more solutions contain the same concentration of quickly (Sue & Bongard, 2008). The vasodila- electrolytes as interstitial fluid, along with a tion that occurs with rewarming following high percentage of water (Margereson, 2003). CPB may necessitate administration of addi- Commonly used isotonic replacement fluids tional fluid to maintain adequate cardiac out- include 0.9% normal saline and lactated put (Margereson, 2003). Ringer’s (LR) solution. Factors driving the use of crystalloid therapy Fluid Challenge include their ready availability in the ICU and For the patient who has developed oliguria and their low cost. Other considerations with crys- who has a urinary output of less than talloid administration for volume repletion 0.5 mL/kg/hr, a fluid challenge should be antici- include their tendency to cause decreased blood pated. The goal of a fluid challenge is to replen- viscosity, increased urinary output with associ- ish the intravascular volume. A supplemental ated sodium and potassium excretion, and dose of fluid (e.g., 250 mL) is administered over increased peripheral blood flow, thereby a short period of time (e.g., 15 minutes). Admin- improving tissue perfusion (Margereson, 2003). istration of fluid challenges may avert use of A negative aspect of isotonic crystalloid inotropic agents, which are associated with administration is that approximately 75% of tachycardia and increased myocardial oxygen the volume moves out of the vascular space, consumption (Margereson, 2003). with half being lost to the circulating volume The fluid needs will differ for patients based shortly after crystalloid administration. Fur- on their history, comorbidities, and the surgi- ther, one of the components of crystalloids cal procedure performed. In addition, used for fluid repletion in postoperative car- patients’ hemodynamic profiles and tolerance diac surgery patients is sodium. If excessive to fluid will vary. For example, as discussed in amounts of sodium are administered, the Chapter 5, postoperative patients who under- patient’s osmolarity may become elevated and went valve repair for aortic stenosis will ini- water may be drawn from cells, resulting in tially continue to have left ventricular cellular dehydration. Some providers prefer to hypertrophy following surgery. This condition alternate administration of 0.9% normal may result in outflow obstruction and subse- saline with administration of LR in an effort quent postoperative hemodynamic instability to avoid this excessive sodium load. Adminis- from preload reduction. Treatment will tration of LR, however, can result in hyper- include volume repletion. Conversely, postop- kalemia, especially in patients with renal erative patients who underwent repair for aor- dysfunction (Margereson, 2003). tic regurgitation will likely require vasodilator Administration of hypotonic crystalloids therapy. Patients who underwent repair for may occasionally result in cerebral edema or mitral stenosis will likely need prudent fluid seizures. Administration of glucose-containing

administration in combination with inotropic solutions for volume repletion (e.g., D5W) can 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 360

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cause dilutional hyponatremia or hyper- associated with FVD, except that either weight glycemia with hyperosmolarity and osmotic gain may occur or weight may remain stable in diuresis, as such solutions do not contain any conjunction with third spacing. electrolytes (Margereson, 2003). Third spacing occurs in two phases. The Following CPB, patients develop a low COP first phase mimics FVD (except for the weight secondary to a systemic inflammatory loss), and the second (recovery) phase mimics response. Colloids such as albumin, plasma hypervolemia. In the postoperative cardiac protein fraction, or fresh frozen plasma can surgery patient, third spacing is most likely to raise COP. Unlike crystalloids, colloids arise as a result of vasodilation, hypothermia, remain in the intravascular space for an or hyperemia (increased amount of blood) to extended period of time, allowing for the the tissue bed (Khalpey et al., 2008). Treat- osmotic force to promote movement of water ment is aimed at moving the fluid from the back into the intravascular space from the third space to the cellular compartments as interstitium (Margereson, 2003). well as forcing diuresis. During the initial Although they are more expensive than stage, treatment with LR is generally consid- crystalloids, colloids may be preferred follow- ered appropriate unless other alterations in ing cardiac surgery, as crystalloid therapy may electrolyte balance are present. The goal decrease COP and increase the risk of pul- remains to provide adequate circulating vol- monary edema. In some patients, colloid ume to maintain an optimal blood pressure administration may improve the patient’s and urinary output until the recovery phase hemodynamic profile and improve balance begins (Hammon, 2008). between oxygen supply and demand (Mar- gereson, 2003). Hypervolemia Healthcare providers should remember Fluid weight gain with subsequent diuresis that most colloids do not contain clotting should be anticipated following CPB. Hyper- factors or contribute to oxygen-carrying volemia, which is also known as fluid volume capacity (Margereson, 2003). In addition, excess (FVE), occurs when water and serum some of the protein molecules do eventually sodium are proportionately increased in the leak into the interstitium. When this phe- body. Common causes of FVE include exces- nomenon occurs, the oncotic pull may pro- sive intake of fluids that cannot be removed mote third spacing of fluid. (e.g., as occurs in renal failure or heart failure, The efficacy of fluid challenges is tradition- or following administration of fluids at an ally assessed based on improvements in the excessive rate), excessive sodium intake, or patient’s hemodynamic profile and physical inadequate sodium and water elimination assessment findings. It is suggested that evalu- (e.g., secondary to heart, renal, or liver fail- ation for respiratory changes associated with ure). In the postoperative cardiac surgery CVP and blood pressure be made, as these patient, hypervolemia is most commonly changes reflect changes in filling pressures sec- related to excessive fluid administration intra- ondary to pleural pressure (Holte et al., 2002). operatively, most notably in patients with Third Spacing either preexisting renal dysfunction, heart failure, or hypoalbuminemia (Kerns, 2006). Third spacing refers to the movement of fluids from the vascular space to a part of the body Assessment where exchange with the rest of ECF is Patients with FVE will manifest weight gain; decreased, resulting in alterations of capillary peripheral edema; distended peripheral veins; membrane permeability (Khalpey et al., 2008). jugular venous distention; increased CVP; Symptoms of third spacing will mimic those crackles; decreased dilutional BUN, hemoglo- 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 361

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bin, and hematocrit; and bounding pulses. In and pro-inflammatory mediators. Release of cases of severe FVE, pulmonary edema, these substances leads to decreases in renal ascites, or pleural effusion may develop blood flow and glomerular filtration rate (Matfin & Porth, 2005). Patients may also (Khalpey et al., 2008). During CPB, attempts develop hypertension, cough, and dependent to protect the kidneys focus on ensuring edema. Some patients may report visual blur- hemodilution, returning to a pulsatile flow as

ring or headache, and an S3 heart sound is a soon as possible, and reestablishing a normal common finding (Parker, 2006). body temperature as quickly as possible (Henke & Eigsti, 2003). Treatment The incidence of ARF in patients undergo- For patients who do not have preexisting ing cardiac surgery is approximately 30%. Of renal dysfunction, diuresis is attempted to these patients, 1% to 5% may require dialysis normalize volume status when hypervolemia therapy (Silvestry, 2008; Talmor & Lisbon, occurs. Electrolyte balance must be carefully 2005). Patients who had a myocardial infarc- monitored during this time to avoid poten- tion may have resultant renal impairment or tially life-threatening complications of rapid acute tubular necrosis (ATN) from the diuretic therapy. For the patient with ARF, ischemia. Patients who are older, have dia- renal replacement therapy (usually through betes mellitus, or who have a history of heart hemodialysis or continuous renal replace- failure are more likely to develop ARF follow- ment therapy [CRRT]) will be necessary to ing a cardiovascular event (Campbell, 2003; maintain an appropriate fluid volume state. Henke & Eigsti, 2003). Other individuals at Fluid restriction to less than 1000 mL/day is higher risk include those with poor underly- typically implemented as well. ing cardiac performance, advanced atherosclerosis, and preexisting decreased GFR. The Glycemic Issues amount of time spent on CPB and intraopera- Postoperative cardiac surgery patients may tive instability are also predictors of the devel- have comorbidities that include either type I opment of postoperative renal impairment or II diabetes mellitus. During times of (Silvestry, 2008). increased stress, serum glucose levels become Renal perfusion must be maintained in all more labile, and the patient with or without a patients. Urinary output should be at least 0.5 history of diabetes is more likely to exhibit mL/kg/hr. For these goals to be met, satisfac- hyperglycemia or hypoglycemia. The fluctua- tory CO and blood pressure are essential. tions in blood glucose levels will also result in Maintaining them at appropriate levels can be alterations in fluid and electrolyte status. accomplished by delivering volume repletion Tight glycemic control is essential to help to keep up with urinary output, which is typi- ensure improved patient outcomes (Talmor & cally 200–300 mL/hr following CPB. If uri- Lisbon, 2005). nary output is maintained with use of diuretics, renal perfusion is considered adequate (Khalpey et al., 2008). ■ ACUTE RENAL FAILURE AND RENAL INSUFFICIENCY Unfortunately, some postoperative cardiac Azotemia surgery patients may have sustained renal Azotemia is the buildup of nitrogenous waste damage from ischemia or decreased blood products from protein metabolism; these flow. CPB causes an increased secretion of wastes are normally eliminated by urination catecholamines, renin, angiotensin II, aldos- (Broscious & Castagnola, 2006; Dirkes & terone, vasopressin, atrial natriuretic peptide, Kozlowski, 2003). The patient with azotemia 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 362

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will demonstrate increasing serum creatinine The most common cause of ARF is ATN, a and BUN levels, and GFR will decrease. As form of intrarenal ARF (Richard, 2001). GFR continues to decline, FVE will develop. ARF results in alterations in electrolyte bal- Uric acid levels may also rise, resulting in ance, acid–base and fluid volume status, nitro- symptoms of gouty arthritis or joint and soft genous waste accumulation, and decreased tissue pain (Dirkes & Kozlowski, 2003). production of erythropoietin. In the majority of cases, an insult occurs, resulting in multi- Acute Renal Failure ple organ damage and affecting the ability of the kidneys to function appropriately. Acute renal failure may be recognized by a Management of ARF will vary based on the sudden, rapid deterioration in renal function. etiology and the degree of renal injury Despite new treatment strategies and (MacKusick, 2007). improved surveillance methods, the number The predominant cause of ARF in postop- of patients who develop ARF is increasing, erative cardiac surgery patients is ATN. The and mortality rates remain greater than 50% majority of cases of ATN result in suppres- (Ronco, Kellum, Mehta, Bellomo, & Palevsky, sion of bone marrow, endocrine disturbance, 2002). Elderly patients and individuals with a coagulopathy, and cardiovascular dysfunc- history of previous CPB procedures, type I tion as normal homeostasis can no longer be diabetes mellitus, renal disease, or heart fail- maintained (MacKusick, 2007). Prolonged ure prior to admission seem to be most pre- hypotension and hypovolemic shock are the disposed to development of ARF (Campbell, most common causes of ATN. Renal cellular 2003; Khalpey et al., 2008; Mullen-Fortino & death begins to occur when MAP falls below O’Brien, 2008; Silvestry, 2008). 75 mm Hg (Richard, 2001). The extent of the One study evaluated patients who under- renal damage may be estimated by determin- went CPB procedures for development of ing the length of time of renal ischemia, with ARF. Patients who were identified to be at ischemia of 25 minutes or less generally caus- greater risk for postoperative renal dysfunc- ing reversible mild injury, ischemia of 40–60 tion included those with heart failure, type I minutes causing damage that will take the diabetes mellitus, preoperative hyperglycemia kidneys 2 to 3 weeks to recover from, and (greater than 300 mg/dL), preoperative serum ischemia lasting longer than 1–1.5 hours creatinine in the range of 1.4–2.0 mg/dL, and causing irreversible damage (Richard, 2001). aged 70–95 years. Perioperative factors that As ischemia progresses, the renal tubular cells increased patient risk included CPB time of at swell and become necrotic (MacKusick, 2007). least 3 hours and ventricular dysfunction (Talmor & Lisbon, 2005). These factors result Assessment in either renal artery vasoconstriction, The patient with ATN will present with olig- hypothermia, atheroembolic disease, or loss uria or anuria, elevated BUN and serum of pulsative blood flow (Silvestry, 2008). creatinine, and isosthenuria (a condition in Three types of ARF exist, and diagnosis is which urinary osmolality approximates based on the point of initial renal insult: plasma osmolality). Oliguria is generally ● Prerenal: injury occurring before the defined as urinary output less than 400 mL kidney over a period of 24 hours; anuria is defined as ● Intrarenal: intrinsic to the kidney urinary output less than 100 mL in 24 hours. ● Postrenal: injury occurring after the Patients should be closely monitored for life- kidney threatening alterations in electrolyte levels. 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 363

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Frequent laboratory testing will be necessary bleeding (Campbell, 2003; Dirkes & to monitor serum electrolytes and complete Kozlowski, 2003). The mortality rate during blood count. FVE will develop, and the the oliguric stage is greater than 50% (Ronco patient will present with its associated signs et al., 2002). Approximately half of all and symptoms. patients with ARF do not present with olig- The patient with ATN will progress uria (MacKusick, 2007). through the stages of AFR in a relatively pre- During the oliguric/anuric stage, the dictable pattern. Initiation is the first stage; it patient needs to be closely monitored for is followed by oliguria, diuresis, and then alterations in electrolyte status and prepared recovery. The last two stages will typically not for renal replacement therapy to remove be managed in the ICU and, therefore, are not waste products and excess fluid, and to return within the scope of this chapter. The total electrolytes to near normal levels. length of time from onset of renal damage to recovery can last from months to 1 year. Treatment Morbidity and mortality rates are significantly Initiation Stage increased in postoperative cardiac surgery The initiation stage of ARF begins when the patients who develop renal dysfunction renal insult occurs and lasts from a few hours (Khalpey et al., 2008). The most essential pre- to a few days. Initial signs and symptoms of vention measure and treatment intervention renal impairment are noticed, and the cause for ARF is maintaining adequate renal perfu- of ARF is investigated. Initial signs and symp- sion (Talmor & Lisbon, 2005). Nursing inter- toms generally include a decrease in urinary ventions focus on maintaining strict intake output, crackles, muffled heart sounds, devel- and output and monitoring oxygen saturation, opment of a new heart murmur or S3 gallop, vital signs, and fluid volume status. Prevention and an increase in body weight indicating of further ischemia is necessary to prevent FVE (MacKusick, 2007). additional renal damage from occurring. Because third spacing and significant diuresis Oliguric Stage are common following CPB, a fluid challenge Oliguria is a decrease in urinary volume to less will likely be initiated. Urinary output should than 400 mL/24 hours. The diminished uri- be maintained at a rate of at least 0.5 mL/kg/hr. nary output seen with ATN occurs when shock The patient’s hemodynamic profile must be or dehydration leads to inadequate perfusion optimized, and use of nephrotoxic agents of the kidneys. The oliguric stage generally should be avoided (Khalpey et al., 2008). If the lasts from 1 to 2 weeks (Richard, 2001). patient progresses to oliguria or anuria, renal Laboratory data will indicate a decrease in replacement therapy will be required. GFR, an increase in serum creatinine and Both hemodialysis and CRRT act via the BUN, and an elevation in the electrolytes principles of osmosis, diffusion, and filtra- excreted by the renal system (potassium, tion. CRRT has the added advantage of being sodium, and phosphorus). Laboratory data able to slowly and safely provide for ultrafil- must be closely monitored, because a fre- tration and thereby help remove excess fluid quent cause of death during the oliguric stage over a slower period of time. This gradual is cardiac arrest secondary to hyperkalemia action is beneficial when cardiac performance (Richard, 2001). is compromised and the patient cannot As azotemia progresses, the patient is at tolerate rapid fluctuations in fluid volume increased risk for developing infection and GI status (Jaski & Miller, 2007). Cardiac failure 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 364

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intrinsically leads to hemodynamic instabil- alterations in fluid and electrolyte balances ity, making CRRT an optimal choice for the may be present from previous surgery, previ- postoperative cardiac surgery patient in ARF ous comorbid conditions, or a combination (DiMuzio, 2008). of these factors. While receiving CRRT, the patient must be Nurses caring for postoperative cardiac sur- closely monitored for alterations in fluid and gery patients should also be aware of the electrolyte status, as well as cardiac, respira- manifestations of acute renal failure and its tory, GI, and neurologic function. Successful treatment options. The primary methods of CRRT results in removal of fluid and toxins, prevention and treatment of ARF for cardiac clearer breath sounds, improved CO, and sta- surgery patients entail interventions that bilization in vital signs (DiMuzio, 2008). optimize filling pressures and cardiac output (Talmor & Lisbon, 2005). Patients usually receive diuretic therapy starting on the first ■ SUMMARY postoperative day. This therapy typically con- Caring for postoperative cardiac surgery tinues until the patient’s preoperative weight patients requires extensive knowledge, skill, has been reestablished (Mullen-Fortino & and sound critical thinking that allow the O’Brien, 2008). The ICU nurse plays a pivotal critical care nurse to perform patient assess- role in attaining and maintaining fluid and ment and management in a rapidly chang- electrolyte balance and optimizing patient ing environment. Life-threatening outcomes.

CASE STUDY

A patient with a history of diabetes mellitus, acute coronary syndrome, tobacco use (one pack per day for 25 years), and hypertension with renal failure is admitted with chest pain. An echocardiogram and cardiac catheterization are performed. Their results indicate left ventricular hypokinesis and an ejection fraction of 22% on echocardiogram and three-vessel disease on cardiac catheterization. The patient undergoes three-vessel CABG surgery, with grafts being taken from the left internal mammary artery and saphenous vein. Cardiopul- monary bypass and aortic cross-clamp times are 180 minutes and 124 minutes, respectively. Postoperative ICU admission vital signs are 88/56, HR 112, RR 14, temperature 101.2 °F, CVP 1 mm Hg, and PAOP 6 mm Hg.

Critical Thinking Questions 1. Based on these clinical data, how would you classify the patient’s fluid status? 2. Which risk factors are present in association with this patient’s condition? 3. What should the initial management include? 4. The patient receives 2 L of crystalloid solution over the next 2 hours with no change being noted in the patient’s status. An orientee questions you why the patient’s hemodynamic status has not changed. How should you respond? 5. Given this patient’s history and condition, which electrolyte imbalance is he at risk for developing? 6. If the electrolyte imbalance identified in Question 5 develops, which ECG tracing findings should the ICU nurse anticipate? 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 365

Self-Assessment Questions 365

Answers to Critical Thinking Questions 1. This patient’s clinical picture is consistent with fluid volume deficit. 2. Risk factors in this patient include fever, intraoperative blood loss, and third spacing of fluid. 3. Management of fluid volume deficit includes expansion of intravascular volume to prevent prolonged hypotension, shock, and their sequelae. There remains ongoing debate regarding use of crystalloids versus colloids for volume repletion. Because crystalloids are typically readily available in the ICU, initial management will likely begin with 0.9% normal saline or lactated Ringer’s solution. Because the patient is vasodilated, concomitant administration of norepinephrine may be indicated to avoid the negative sequelae of prolonged hypotension. 4. Approximately 75% of crystalloid volume moves out of the circulating volume/ vascular space. 5. This patient is at risk for developing hyperkalemia secondary to hemolysis of red blood cells during bypass, cardioplegia, metabolic acidosis from the history of renal failure, and diabetes. 6. The patient with hyperkalemia may develop peaked T waves. This will be followed by a prolonged PR interval, absent P waves, and eventual degradation of the QRS complex.

■ SELF-ASSESSMENT QUESTIONS 3. A patient has the following arterial blood gas results following cardiac sur- 1. Which of the following is an effect of gery: pH 7.54/pCO 44/pO 83/SaO surgery that can cause alterations in 2 2 2 94%/HCO 30. Which of the following fluid volume in the postoperative car- 3 electrolyte abnormalities should the ICU diac surgery patient? nurse anticipate? a. Increase in colloid osmotic pressure a. Hypokalemia b. Decrease in hydrostatic pressure b. Hyperchloremia c. Impaired renin production c. Hypophosphatemia d. Secretion of cortisol d. Hypermagnesemia 2. Which of the following is a potential 4. A patient who underwent cardiac sur- cause of respiratory acidosis in the post- gery had excessive intraoperative bleed- operative cardiac surgery patient? ing, requiring rapid transfusion with a. Reversal of neuromuscular blocking multiple units of packed red blood cells. agents Which of the following acid–base distur- b. Shivering bances should the ICU nurse anticipate? c. Diabetes a. Respiratory alkalosis d. Hypotension b. Metabolic acidosis c. Respiratory alkalosis d. Metabolic alkalosis 57625_CH17_345_370.qxp:57625_CH17_345_370 3/22/10 11:07 AM Page 366

366 Chapter 17 Fluid and Electrolyte Imbalances Following Cardiac Surgery

5. Which of the following ECG changes is 8. A patient’s QT intervals are shortening associated with a hypomagnesemic and the T waves are depressed. Which of state? the following lab values should the ICU a. Narrowing QRS complex nurse anticipate? b. Progressive lengthening of PR a. K 3.0 mEq/L interval b. Mg 1.4 mg/dL c. Flattened T wave c. Phos 5.2 mg/dL d. Presence of U wave d. Ca 12.6 mg/dL 6. Your postoperative cardiac surgery 9. Which of the following values, if sus- patient has the following lab results: Na tained, is indicative of fluid volume 142 mEq/L; K 4.7 mEq/L; Mg 12.4 deficit? mg/dL; Phos 2.8 mg/dL; Ca 9.2 mg/dL. a. MAP 55–60 mm Hg Administration of which of the follow- b. U/O 0.3–0.4/kg/hr ing is indicated? c. CVP 0–1 mm Hg a. 250 mL 5% albumin d. Heart rate 110–120 beats/min b. 1 mEq/kg sodium bicarbonate 10. Which of the following lab results c. 20 mEq calcium gluconate should the ICU nurse anticipate when d. Albuterol via nebulizer caring for a patient with hypokalemia? 7. The patient’s wife requests an explana- a. Phos 4.8 mg/dL tion for the intervention described in b. Ca 7.8 mg/dL Question 6. Your best response is c. Na 151 mEq/L a. “To prevent dehydration that can d. Mg 1.3 mg/dL occur with his current condition.” b. “To correct an associated acid–base Answers to Self-Assessment Questions imbalance he developed from the results of his blood work.” 1. d 6. c c. “To treat any respiratory depression 2. b 7. c associated with his electrolyte 3. a 8. d imbalance.” 4. d 9. b d. “To prevent wheezing from 5. d 10. d developing in association with his lab values.” 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 367

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Clinical Inquiry Box

Question: When should a nurse expect to see postoperative atrial fibrillation in the cardiac surgery patient? Reference: Scherr, K., Jensen, L., Smith, H., & Kozak, C. (2007). Atrial fibrillation following cardiac surgery: A retrospective cohort series. Progress in Cardiovascular Nursing, 21(1), 7–13. Objective: This study was designed to identify the incidence and time of onset of atrial fibrillation (AF) in the postoperative cardiac surgery patient. Method: Data were obtained on demographic, preoperative, perioperative, and postoperative risk factors for postoperative AF, documented episodes of AF, and clinical outcomes through a retrospective chart review of 1078 adults who underwent cardiac surgery. Results: Researchers found that 39.6% of the patients in the study had postoperative atrial fibrillation. Of these individuals, more than half had undergone valve surgery. The peak onset of AF occurred on the second postoperative day. Predictors for AF included greater age, history of AF, combined cardiac valve and coronary artery bypass grafting surgery, and high magnesium levels on the third postoperative day. Conclusion: Although multiple factors are associated with atrial fibrillation, the nurse should be vigilant in monitoring magnesium levels in cardiac surgery patients and should be aware that AF is most likely to occur on the second postoperative day.

■ REFERENCES Flanagan, J., Devereaux, K., Abdallah, L., & Rem- Adrogué, H. J., & Madias, N. E. (1998). Manage- ington, R. (2007). Interpreting laboratory val- ment of life-threatening acid–base disorders: ues in the rehabilitation setting. Rehabilitation Second of two parts. New England Journal of Nursing, 32(2), 77–84. Medicine, 338(2), 107–111. Fukagawa, M., Kurokawa, K., & Papadakis, M. A. Broscious, S., & Castagnola, J. (2006). Chronic kid- (2008). Fluid and electrolyte disorders. In S. J. ney disease: Acute manifestations and role of McPhee, M. A. Papadakis, & L. M. Tierney critical care nurses. Critical Care Nurse, 26(4), (Eds.), Current medical diagnosis and treatment 17–28. (pp. 757–784). New York: McGraw-Hill. Campbell, D. (2003). How acute renal failure puts Gerhardt, M. A. (2007). Postoperative care of the the brakes on kidney function. Nursing, 33(1), cardiac surgical patient. In F. A. Hensley, D. E. 59–64. Martin, & G. P. Gravlee (Eds.), A practical approach to cardiac anesthesia (pp. 261–288). Chikwe, J., Beddow, E., & Glenville, B. (2006). Car- Philadelphia: Lippincott Williams & Wilkins. diac intensive care. In J. Chikwe, E. Beddow, & B. Glenville (Eds.), Cardiothoracic surgery (pp. Gothard, J., Kelleher, A., & Haxby, E. (2003). The 127–250). New York: Oxford University Press. early postoperative management of patients undergoing cardiac surgery. In J. Gothard, A. Diercks, D., Shumaik, G., Harrigan, R., Brady, W., Kelleher, & E. Haxby, Cardiovascular and tho- & Chan, T. (2004). Electrocardiographic mani- racic anaesthesia: Anaesthesia in a nutshell (pp. festations of electrolyte abnormalities. Journal 78–94). St. Louis: Elsevier Health Sciences. of Emergency Medicine, 27(2), 153–160. Hammon, J. W. (2008). Extracorporeal circulation. DiMuzio, C. (2008). CRRT spells success against In L. H. Cohn (Ed.), Cardiac surgery in the adult acute renal failure in critically ill patients. (pp. 349–414). New York: McGraw-Hill. American Nurse Today, 3(5), 9–17. Henke, K., & Eigsti, J. (2003). Implications of car- Dirkes, S. M., & Kozlowski, C. (2003). Renal assist diopulmonary bypass. Dimensions of Critical device therapy for acute renal failure. Nephrol- Care Nursing, 22(2), 64–70. ogy Nursing Journal, 30(6), 611–620. 57625_CH17_345_370.pdf 4/10/09 11:07 AM Page 368

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Weinman, E. J., Biswas, R. S., Peng, Q., Shen, L., Wilkins, I., & Wheeler, D. (2003). Preventing, rec- Turner, C. L., Xiaofei, E., et al. (2007). Parathy- ognizing, and treating postoperative compli- roid hormone inhibits renal phosphate trans- cations. Surgery, 21(1), 14–20. port by phosphorylation of serine 77 of Wilkins, I., & Wheeler, D. (2006). Recognizing and sodium–hydrogen exchanger regulatory fac- treating postoperative complications. Founda- tor-1. Journal of Clinical Investigations, 117(11), tion Years, 2(6), 244–250. 3412–3420. Ziegler, R. (2001). Hypercalcemic crisis. Journal of Whelton, P. K., He, J., Cutler, J., Brancati, F. L., the American Society of Nephrology, 12(suppl 1), Appel, L. J., Follmann, D., et al. (1997). Effects S3–S9. of oral potassium on blood pressure: Meta analysis of randomized controlled clinical trials. Journal of the American Medical Association, ■ WEB RESOURCE 277(20), 1624–1632. Water and electrolyte balance: http://www .youtube.com/watch?v=vvGyHBWcQQU 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 371

Chapter 18 Wound Care

Mary Zellinger and Vicki Morelock

■ INTRODUCTION Assessment and care of postoperative surgical diac surgery. Port-access and robotic surgeries sites will have a profound impact on patient approach the heart through the left chest wall outcomes after cardiac surgery. Surgical site in the case of coronary artery bypass and infections (SSIs) of the sternum and underly- through the right chest wall for mitral valve ing mediastinum occur in 0.4% to 4% of repair or replacement. patients who undergo such procedures (Eagle In minimally invasive bypass, ports for the et al., 2004; Engelman et al., 2007). Infections left internal mammary artery (LIMA) harvest can lead to significant morbidity, warranting are placed in the third, fifth, and seventh an increased length of hospitalization and intercostal spaces (ICSs), with a fourth higher financial costs at best, and patient slightly larger working port (2 to 3 inches) for mortality at worst. Observant practitioners the anastomosis located in the fourth or fifth must routinely assess for factors that may ICS. Minimally invasive valve procedures may potentially slow surgical wound healing, and utilize a mini-right thoracotomy (third ICS follow strict and consistent protocols in car- for aortic and fourth ICS for mitral valve) or a ing for these incisions. This chapter describes hemisternotomy (upper for aortic valve proce- the wound care that is required for the post- dures and lower for mitral valve procedures) operative cardiac surgery patient and explores (Rosengart et al., 2008). Each of these proce- the pivotal role the ICU nurse plays in pre- dures has the potential to result in the com- venting potentially fatal complications associ- plication of infection. ated with SSIs. ■ CONDUITS ■ INCISION SITES The internal mammary artery (IMA) is an Surgical access options in cardiac surgery ideal conduit to use for bypass grafting, patients have greatly increased in the past sev- although other conduits may be used as well. eral years. Midline sternotomy access is still The IMA does not have valves as the vein the most common access and is used for grafts do, so there is no obstruction to flow. patients who are operated on with or without In addition, arteries are more vasoresponsive the aid of cardiopulmonary bypass (CPB). The than veins. The IMA is taken down from the lengths of these incisions can range from 6 to chest wall during on-pump, off-pump, and 10 inches. Mini-thoracotomy incisions of minimally invasive surgery and does not approximately 2 inches are also used in car- require a separate incision for removal.

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The radial artery is another frequently used Preoperative Risk Factors conduit. It can be removed without fear of Preoperative assessment of risk factors for diminishing blood flow to the hand if the wound complications is imperative, and early ulnar artery is functioning adequately. and sustained attention to these risk factors is Removal of the radial artery typically requires mandatory. Table 18–1 lists the most com- a 2- to 4-inch incision. Because of its visibility, mon preoperative risk factors. it may be easily monitored in the postopera- The presence of diabetes may impede tive period. wound healing by leading to a compromised The gastroepiploic artery is rarely used as a immune system. Both chemotaxis and phago- conduit during cardiac surgery because of the cytosis play a role in the development of a high chance of contamination that may occur wound infection. If serum glucose levels when the abdominal cavity is open at the remain elevated, both processes will be com- same time as the sternum. promised (Turina, Fry, & Polk, 2005). Chemo- The saphenous vein is often removed from taxis is the oriented movement toward or away the leg when the other arteries are not avail- from a chemical stimulus—in this case, the able or when additional grafts are needed. process by which white cells are attracted to The saphenous vein may be removed via a the site of an infection. Phagocytosis is the 3- to 6-inch incision for quick use in an emergency, or it may be removed using two or three small (1.5 to 2.5 cm) incisions via endo- Table 18–1 Preoperative Risk Factors scope (Crouch et al., 1999). The saphenous for Wound Complications vein is the most commonly used graft, even though the grafts become occluded in 12% to Diabetes 27% of patients in the first year, with half of Advanced age those occlusions occurring within the first Obesity month. Annual occlusive rates for saphenous Large breast size veins range between 2% and 4%, and only 69% COPD (i.e., emphysema) Urgent or emergent CABG repeat operations of patients will experience a 10- to 12-year Steroids period free of reoperations or coronary angio- Preoperative hospital stay of greater than plasty (Vorp, Maul, & Nieponice, 2005). 5 days While saphenous veins are the most com- Poor nutrition monly utilized grafts, arterial grafts are the Venous impairment preferred conduits. Arterial grafts have better Renal failure long-term patency, but are short in length, Certain medications Jaundice have a small diameter, and have limited avail- Decreased mobility/activity ability, resulting in the need for multiple Dehydration grafts. Respiratory disease Infection Anemia ■ RISK FACTORS FOR WOUND Smoking COMPLICATIONS Pain Several factors put patients at greater risk for Decreased immunity developing postoperative wound complica- CABG ϭ coronary artery bypass grafting. tions. These risk factors can be categorized as Sources: DeBaun, 2007; Paul et al., 2007. preoperative, intraoperative, or postoperative. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 373

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ingestion of bacteria by these white cells. Intraoperative Risk Factors Delayed macrophage introduction and dimin- Intraoperative risk factors also affect the ished leukocyte migration, which cause a pro- potential for postoperative problems related longed inflammatory phase, interfere in the to wound healing. Use of both IMAs is associ- wound healing process (Streeter, 2006). Unfor- ated with increased chance of infection tunately, a large number of patients presenting because these arteries provide the major for surgery are unaware of their diabetic status source of blood supply to the sternum. The and, therefore, may have an uncontrolled removal of the IMA significantly devascular- serum glucose level preoperatively. izes the sternal half from which it is taken. Advanced age may also diminish wound Surgical technique and adherence to sterile healing. Evidence suggests that inherent dif- technique certainly have critical implications ferences in cellular structure and function, for for incision and mediastinum status. Other example, may impair tissue repair and regen- potential offending factors include the num- eration in older patients (Eagle et al., 2004; ber of bypass grafts used, excessive use of elec- Pittman, 2007). Comorbidities are more com- trocautery or bone wax, prolonged operative mon among the elderly as well, and any of time, and the need for blood transfusions. these may affect wound healing (Pittman, The last factor increases the risk of infection 2007). incrementally based on the number of units Obesity is a risk for sternal infections transfused (Banbury, Brizzio, Rajeswaran, because of the increased force applied to the Lytle, & Blackstone, 2006; Eagle et al., 2004; line of closure in these patients, which affects Keib & Pelham, 2006). the quantity, aggregation, and orientation of An increase in the number of coronary collagen fibers. In addition, undue pressure artery grafts, which can prolong surgical time, on the wound may lead to ischemia of the increases the likelihood of infection. Long surrounding tissues (Ridderstolpe, Gill, Gran- cardiopulmonary pump runs, long surgical feldt, Åhlfeldt, & Rutberg, 2001). procedure times (greater than 4 hours), and COPD and emphysema may present prob- any infractions in sterile technique are all lems because effective wound healing known to increase the risk for infection requires adequate oxygenation, hemoglobin (Eagle et al., 2004; Haycock, Laser, Keuth, & for oxygen transport, and adequate tissue Montefour, 2005; Keib & Pelham, 2006; Man- perfusion (Ragheb & Buggy, 2004). These gram et al., 1999). Hypothermia, which is conditions may not be present with COPD or used for cardiac protection during surgery, emphysema. needs to be corrected quickly in the immedi- Protein-calorie malnutrition and the result- ate postoperative period, as prolonged ant body composition changes are additional hypothermia increases the risk for infection. considerations that may delay wound healing. Rewarming can be carried out using warming The local ability to supply oxygen to the heal- blankets, fluid warmers, and radiant heat ing wound process is inhibited by peripheral lamps (Streeter, 2006). vascular disease, previous radiation, chronic In rare cases, periods of ischemia may lead inflammation, or any combination of these to the development of myocardial or pul- conditions (Streeter, 2006). monary edema (Marshall & Barash, 2004). Prior VAD insertion and preoperative The edematous organ may prohibit closure of inotropic support have been identified as risk the chest wall without causing a pressure factors for orthotopic heart transplants (Fil- tamponade and, subsequently, a significant soufi et al., 2007). decrease in cardiac index (the amount of 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 374

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Aorta

Pericardium Superior Vena Cava Rubber Dam Right Atrium (cut for viewing)

Right Ventricle

Sternal Edges

Fascia Mediastinal Space

Figure 18–1 Rubber dam. Source: Adapted from Zellinger, M. & Lienberger, T. (1991). Use of the rubber dam after open heart surgery. Critical Care Nurse, 11(8), 24–27.

blood ejected by the heart Ϭ body surface periods of cardiopulmonary resuscitation area). This complication may warrant leaving (CPR) (Keib & Pelham, 2006). Other postop- the chest cavity open after the procedure for a erative risk factors include autotransfusion of period of several days to allow for cardiac mediastinal blood, low cardiac output (CO; recovery. During this time, the sternal open- the amount of blood ejected by the heart each ing is covered by an impermeable piece of rub- minute), sternal instability, and infections ber latex called a “rubber dam” (Zellinger & arising from sites other than the sternal inci- Leinberger, 1991) (see Figure 18–1). sion. For example, a patient with a tra- While the mediastinum is left open in such cheostomy is at greater risk for poor wound cases, it does not remain exposed. The rubber healing because of the close proximity of the dam is securely sutured to the skin edges, cov- surgical incision to the tracheal stoma, which ered with gauze that has been soaked in povi- is colonized by bacteria. In such a case, the done-iodine, and then covered with a sterile sternal wound should be protected from the dressing. The initial dressing change should be tracheostomy by dressings. performed with the surgeon in attendance so that the site can be assessed and evaluated together with the ICU nurse, thereby preventing ■ WOUND INFECTIONS unnecessary additional site exposures. All dress- CLASSIFICATION ing changes are done with strict aseptic tech- An infection that occurs within 30 days of a nique. The need for and presence of this rubber surgical procedure is considered an SSI, dam does not increase the risk of sternal infec- according to the definition established by the tion (Pokorny, Koldjeski, & Swanson, 2003). Centers for Disease Control and Prevention (see Box 18–1) (Mangram et al., 1999). Postoperative Risk Factors Numerous classifications of SSIs have been In the immediate postoperative period, risk developed. Most often, they are classified as factors for wound infection include early either superficial or deep, although a more chest reexploration, need for transfusion of structured approach utilizing numerous clas- more than five units of blood, prolonged sification types has been proposed in the liter- mechanical ventilation time, and prolonged ature (Vlajcic, Zic, Stanec, & Stanec, 2007). 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 375

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Box 18–1 Criteria for Defining Surgical Site Infections

Superficial Incisional SSI ● Infection occurs within 30 days after surgery ● Involvement of only the skin and subcutaneous tissue of the incision ● Dehiscence of superficial incision ● Stable sternum ● At least one of the following: ● Purulent drainage from the incision ● Organisms isolated from an aseptically obtained culture of incision’s tissue or fluid ● Presence of signs and symptoms of infection of incision (e.g., pain, tenderness, swelling, redness, heat) ● Diagnosis of superficial SSI is made by the physician or mid-level provider Deep Incisional SSI ● Infection occurs within 30 days after surgery (if no implant was left in place) or 1 year (if an implant was left in place and infection appears to be related to surgery) ● Exposed fascia and muscle of incision ● Exposed bone with a stable or unstable wired sternum ● Exposed necrotic or fractured bone, unstable, heart exposed ● Exposed bone with a stable or unstable wired sternum or exposed necrotic or fractured bone, unstable, heart exposed with the presence of septicemia ● Inflammation of the sternum ● Presence of at least one of the following: ● Purulent drainage from the deep incision (e.g., mediastinum) ● Dehiscence of deep incision ● Deep incision opened by surgeon because of presence of either fever > 38Њ C, localized pain, or tenderness ● Presence of an abscess or other signs of deep incision infection ● An abscess or other sign of infection of the deep incision is discovered ● Diagnosis of deep SSI is made by the physician or mid-level provider Notes: 1. If there is presence of both superficial and deep SSIs, it should be reported as a deep incisional SSI. 2. If there is an infection with drainage to an organ/space related to the surgery, it should be reported as a deep incisional SSI. Organ/Space SSI ● Infection occurs within 30 days after surgery (if no implant was left in place) or 1 year (if an implant was left in place and infection appears to be related to surgery) ● Infection entails any anatomical structure (e.g., organ, space) aside from the incision ● Presence of at least one of the following: ● Purulent drainage from a drain in the organ/space ● Organisms isolated from an aseptically obtained culture of incision’s tissue or fluid

Sources: Jones et al., 1997; Mangram et al., 1999; Vlajcic, Zic, Stanec, & Stanec, 2007 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 376

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Superficial Wound Infections wound infection often requires a total Superficial wound infections are classified as sternectomy and an omentum pedicled flap, Type 1. These wound infections involve only along with an advanced flap of the pectoralis the skin or subcutaneous tissue around the major (Athanassiadi, Theakos, Benakis, incision and occur within 30 days of surgery. Kakaris, & Skottis, 2007; Vlajcic et al., 2007). They may be identified by purulent drainage, isolated organisms upon culture; signs and Septicemia symptoms of purulent infection such as pain, A Type 4 infection is characterized by the tenderness, swelling, redness or heat, or puru- presence of a Type 2 or 3 wound infection lent drainage; diagnosis of an SSI by the along with septicemia. Treatment of such an healthcare provider; or any combination of infection involves radical debridement, these (Sweene, Lindholm, Borowiec, & Carls- delayed closure, and aggressive intravenous son, 2004). antibiotic therapy (Vlajcic et al., 2007).

Sternal Wound Dehiscence ■ PREVENTION OF SURGICAL SITE Sternal wound dehiscence is associated with a INFECTION Type 2 infection. A Type 2 infection is further Appropriate incisional care must be initiated classified into one of three subcategories: in the preoperative phase and includes a vari- ● Type 2A: a sterile viable bone ety of necessary interventions. Preoperative ● Type 2B: a nonviable bone in the pres- prevention of SSIs begins with a meticulous ence of sternal osteitis (inflammation) in handwashing campaign (Haycock et al., 2005; the upper two-thirds of the sternum Mangram et al., 1999). In addition, a multi- ● Type 2C: a nonviable bone in the pres- tude of preventive strategies (listed in ence of sternal osteitis in the lower third Box 18–2) are incorporated into any cardiac of the sternum surgical program to decrease the risk of postoperative complications. A Type 2 sternal wound infection could require any number of interventions, ranging Local Collagen-Gentamicin from debridement and rewiring to flap surgery (Rand et al., 1998; Vlajcic et al., 2007). The use of local collagen-gentamicin has been found to reduce the incidence of sternal wound infections (SWIs) caused by all major Mediastinitis clinically important microbiological agents, Deep wound infections that occur within 30 including coagulase-negative Staphylococcus days of a procedure and involve the deep soft (CoNS). Given the cost of this intervention, tissue (i.e., the fascia and muscle) warrant a centers may want to limit its use to adult car- diagnosis of mediastinitis, which is consid- diac surgery patients who have diabetes, a ered a Type 3 sternal wound infection. Typi- BMI greater than 25 kg/m2, or both (Friberg, cally, purulent drainage, dehiscence of the 2007). If a patient has a suspected infection surgical site, fever, pain, tenderness at the site, prior to an elective operation, the infection and evidence of infection will be noted. A source and site need to be identified and diagnosis of a deep incisional infection will be treated before the patient undergoes surgery. made (Horan, Gaynes, Martone, Jarvis, & Elective surgery should be postponed until Emori, 1992). Treatment of a Type 3 sternal the infection has resolved. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 377

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Box 18–2 Strategies for Preventing Surgical Site Infections

● Identify and treat infections before the patient undergoes an elective operation. ● Minimize hair removal at or around the incision site. Use clipping instead of shaving when hair removal is needed. ● Bathe the patient with an antiseptic solution at least the night before surgery. ● Clean the incision site of any gross contaminants and then prep the skin with chlorhexidine gluconate, povidone-iodine, or alcohol-containing products prior to making the incision. ● Use local collagen-gentamicin. ● Use additional fixation wires at the lower sternum.

Sources: Eagle et al., 2004; Friberg, 2007; Friberg, Dahlin, Soderquist, Kallman, & Svedjeholm, 2006; Mangram et al., 1999.

Hair Removal remove the microbial burden on the skin and It is recommended to not remove hair preop- to maintain a greater residual activity hours eratively unless the hair at or around the inci- after the skin is prepared (Mangram et al., sion site might interfere with the surgical 1999). In addition, some promising results procedure. If hair removal is necessary, hair have been obtained in using CHG to reduce should be removed with electrical clippers drug-resistant Acinetobacter and methicillin- rather than the traditional shaving method. resistant Staphylococcus aureus (MRSA) counts Clipping is recommended to be performed (DeBaun, 2007). immediately prior to the operation (Mangram Two methods are currently used to prepare et al., 1999). patients’ skin: ● The rinse-off method, which uses a CHG Preoperative Skin Cleansing 4% solution or presoaked scrub packets ● The no-rinse method, which uses CHG Cleansing the patient’s skin at least the night 2% presoaked preparation cloths before surgery is imperative. In particular, removing gross contaminants by showering To lower the microbial count, it is recom- or bathing, and then cleansing the skin with a mended to apply the antiseptic several times. preparation that lowers microbial skin bur- Studies comparing these two methods have den, has proven to be effective in lowering the shown some positive results with the no-rinse incidence of SSIs (Eagle et al., 2004; Edmis- method (Edmiston et al., 2007; Ryder, 2007). ton, Seabrook, Johnson, Paulson, & Beau- With this method, the patient takes an initial soleil, 2007; Haycock et al., 2005; Mangram et shower to wash any gross contaminants off al., 1999). the skin and to enhance comfort. After a min- Several antimicrobial preparations are cur- imum of 1 hour, the no-rinse method cloth is rently available: chlorhexidine gluconate used to prepare the skin. It is recommended (CHG), povidone-iodine, alcohol, and tri- that the no-rinse method be used at least once closan (an antibacterial chemical). Recent the evening before and again the morning of reports in the literature suggest that CHG is surgery. It is then followed by the skin prepa- the superior product in terms of its ability to ration in the operating room (DeBaun, 2007). 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 378

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MRSA Prophylaxis gram-negative organisms. In such a case, it is Staphylococcus aureus is a frequent offender in recommended that an aminoglycoside be sternal wound infections. The nares are used in addition to the glycopeptide. known to be colonized with S. aureus in Prophylaxis is accomplished by administer- 20–30% of the healthy population (Mangram ing one preoperative dose and one postopera- et al., 1999). Mupirocin (Bactroban®) oint- tive dose (Engelman et al., 2007). Correctly ment, a topical antibiotic, is effective in treat- timing the preoperative antibiotic dose is ing nasal colonization, including some essential so that a bactericidal concentration resistant strains of this pathogen. Mupirocin, of the drug is present in the patient’s serum given intranasally, is recommended preopera- and tissues by the time the skin incision is tively for all cardiac surgical patients (Engel- made (Haycock et al., 2005). With the man et al., 2007). It is administered by the cephalosporins, the dose needs to be adminis- patient for a period up to 5 days to reduce any tered within 30 minutes of the time the inci- nasal colonization involving S. aureus. Treat- sion is made. It is best accomplished by the ment should begin at least 1 day preopera- anesthesiologist after induction of anesthesia. tively and may extend into the postoperative The surgeon should confirm that the antibi- period until the treatment is complete (Cimo- otic dosing has occurred prior to the scalpel chowski et al., 2001). being in hand. If the length of the operative procedure exceeds 3 hours, redosing is mandated based on cephalosporin pharmacoki- Preoperative Antibiotic Administration netics. If the combination of a glycopeptide Preoperative antibiotic administration should and an aminoglycoside is used, the medica- be performed for all cardiac surgical patients tions are usually administered over a 60- to to reduce their risk of postoperative infection 90-minute period (dependent on dosage) (Eagle et al., 2004). This measure reduces the (Eagle et al., 2004; Engelman et al., 2007; incidence of infection fivefold; S. aureus has Mangram et al., 1999). been identified as the infective organism in more than 50% of all SSIs (Engelman et al., 2007). A cephalosporin is the preferred pro- Glycemic Control phylactic agent of choice for cardiac surgery According to a 2004 consensus statement by procedures in populations who do not have a the American College of Endocrinology (ACE), high incidence of MRSA. Data suggest that strict glycemic control entails maintaining a prophylaxis with glycopeptides, such as van- critically ill (e.g., immediate postoperative car- comycin (Vancocin®), is more effective in pre- diac surgery) patient’s serum glucose at a level venting infection by methicillin-resistant up to 110 mg/dL. For patients who are not organisms, but is less effective in countering critically ill (e.g., cardiac surgery patients who methicillin-sensitive organisms (Coskun & are preparing for discharge and are healing at Aytac, 2006). One or two doses of a glycopep- home), the recommendation is that prepran- tide in combination with a cephalosporin are dial serum glucose should be 110 mg/dL, up reasonable when a healthcare facility has a to a maximum of 180 mg/dL (ACE, 2004). “high incidence” of MRSA, the patient is espe- Attaining these goals improves healing poten- cially susceptible to colonization, or the tial and lessens the risk of mediastinitis (Eagle patient is having a prosthetic valve or vascular et al., 2004; Haycock et al., 2005). Appropriate graft inserted (Engelman et al., 2007). glycemic control is accomplished by assessing

If a patient is allergic to cephalosporins, a the patient preoperatively for elevated HbA1c glycopeptide should not be used as a sole levels, noting any history of diabetes, and agent, as it does not provide any coverage for checking for any elevated serum glucose. If a 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 379

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patient’s HbA1c level is greater than 8%, the respective facility. Regardless of which proto- risk for morbidity and mortality is known to col is followed, serum glucose levels should be be significantly increased (Peter, Cox, & Evans, checked frequently (e.g., every 1 to 2 hours 2008). Ideally, achieving adequate glycemic during this time frame) to adjust the insulin control before the patient’s admission for sur- infusion. No evidence-based guidelines have gery will lower the risk for infection (Furnary been established regarding the ideal frequency et al., 2003). for serum glucose testing (Buonocore, 2008). If patients have elevated serum glucose lev- Box 18–3 provides sample orders for ensuring els, they should be treated with a continuous glycemic control. intravenous insulin infusion immediately Once the patient is being advanced on a prior to, during, and immediately following diet, serum glucose targets should be adjusted surgery in the postanesthesia care unit and the to 150 mg/dL as a mean target (110 mg/dL ICU. The literature does not include any stud- preprandial; 180 mg/dL maximum serum ies that have compared protocols for insulin glucose) (Buonocore, 2008; Kazlauskaite & infusions specifically in postoperative cardiac Fogelfeld, 2003). The patient is then transi- surgery patients. It is suggested that published tioned from the intravenous insulin back to protocols in the literature be reviewed, and the oral agent, subcutaneous injections, or that one be selected that is appropriate for the both (Streeter, 2006). If serum glucose levels

Box 18–3 Sample Postoperative Orders to Ensure Adequate Glycemic Control

1. Treatment for Elevated Blood Glucose (BG > 140 mg/dL): Begin insulin infusion. Insulin infusion: 125 units of regular insulin in 250 mL 0.9% normal saline (1 mL of solution ϭ 0.5 unit of insulin). Bedside BG monitoring hourly until the patient is within the target range for two consecutive readings; then obtain BG every two hours. If the BG is above or below the targeted range, resume hourly readings. (If using an arterial line specimen, do so consistently while the patient is on the insulin infusion). When a nondiabetic patient has BG < 100 mg/dL for two consecutive measurements, discontinue insulin infusion. Target BG range on insulin infusion: 80 mg/dL to 110 mg/dL. Step 1: Calculate insulin infusion rate: (BG – 60) ϫ 0.04 (multiplier) ϭ units of insulin per hour (ϫ 2 to determine milliliters per hour). Adjusting the multiplier: BG greater than target range: Increase multiplier by 0.01. BG within target range: No change in multiplier. BG less than target range: Decrease multiplier by 0.01. 2. Treatment for Low Blood Glucose (BG < 80 mg/dL): ϭ ϫ ϭ (a) BG 60–79 mg/dL: Give D50W using this formula: (100 – BG) 0.3 mL D50W IV push. Adjust the multiplier per protocol. ϫ ϭ (b) BG < 60 mg/dL: Give D50W using this formula: (100 – BG) 0.3 mL D50W IV push. Decrease insulin infusion to 50% of current infusion rate. Recheck BG in 30 minutes: BG > 80 mg/dL: Decrease multiplier by 0.01; then return to step 1 of the formula. For example, if you have been using the Step 1 formula (BG – 60) ϫ 0.04, you are now going to use the multiplier 0.03 instead of 0.04 (you have dropped the multiplier by 0.01). BG ϭ 60–80 mg/dL: Repeat step 2a. BG < 60 mg/dL: Notify physician and repeat step 2b.

Source: Emory University Hospital, Atlanta, GA. Cardiac Surgery Postoperative (ICU/PACU) Orders. Used with permission. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 380

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remain elevated, consultation with an closure, neutrophils migrate toward the fibrin endocrinologist to attain tighter glycemic clot at the margins of the incision and fill in control is advisable. the incisional space. During the proliferative phase, new capillaries are formed, and fibrin, Avoiding Potentially Contaminated collagen, and growth factors spread across the Sources wound bed. Basophils (white blood cells) migrate to the incision borders and multiply. Reestablishing the skin barrier can prevent During the maturation phase, collagen the onset of superficial infections. Diabetes, matrix development furthers wound closure. obesity, and renal failure are all conditions As keratinization occurs, the skin thickness that can delay wound closure. Dressings are returns to normal (Streeter, 2006). Recent not the only way to protect the incision site, studies have found that placement of addi- however. ECG wires are known to be a source tional fixation wires at the lower sternum, of infection; disposable leadware is now avail- along with prophylaxis with a local collagen- able and should be considered for SSI preven- gentamicin, decreases the incidence of deep tion (Jancin, 2004). Blood pressure cuffs have sternal wound infections (Friberg et al., 2006). also been noted to be infection sources, and After waiting the designated time stated in disposable cuffs are now available. Individual the protocol (see Box 18–4 for an example), per- stethoscopes should be cleansed with alcohol forming appropriate hand hygiene, and don- after each individual patient assessment. It is ning clean gloves, the nurse should remove and imperative that the nurse assess the incision discard the dressing. Initially, the incision site regularly and protect the incision as it heals. may appear slightly red around the edges. The edges should be well approximated, with mini- Postoperative Dressings mal tension evident. The surrounding tissue Postoperative incisional dressing assessment should display no inflammation, hematoma, should be performed upon admission and swelling, erythema, skin discoloration, or every 4 hours thereafter until the patient is warmth, and it should not cause pain when pal- transferred out of the ICU. To minimize the pated. Several variables, if present, need to be risk of infection, most cardiac surgical centers documented and brought to the attention of opt to keep the initial dressing on the incision the surgeon; the variables indicative of an infec- for 24 to 48 hours, as per CDC recommendation are listed in Table 18–2. tions (Mangram et al., 1999). If the patient is experiencing a coagulopathy, a small amount of blood or blood-tinged Table 18–2 Variables Indicative fluid may drain from the incisional site. The of Infection dressing may be reinforced unless it becomes saturated, at which time it should be changed A nonapproximated incision using sterile technique. Excessive pain and tenderness Redness, odor, or swelling Evaluation of the Incision Site Wound breakdown Phases of Incision Healing Exudate (Note the amount—none, minimal, moderate, heavy leakage through the An incision goes through three major phases bandage—and type—serous/straw-colored as it heals. During the inflammatory phase, fluid or serosanginous/red fluid, as well as after the incision is made, a cascade of clot- any frank blood or pus [creamy yellow or ting and immune responses produces inflam- green].) mation at the incision site. After incisional 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 381

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Box 18–4 Procedure: Incision Care Following Cardiac Surgery

Purpose: To reduce the potential for nosocomial infections while patients are in the hospital having cardiac surgery. Equipment ● Chlorhexidine (CHG) 2% preop no rinse cloth ● Towels ● Disposable linen savers or bed pad if scrubs are used ● 4 ϫ 4 sterile dressings ● Tape ● Sterile gloves for dressing change (if incision is less than 48 hours old and the dressing is saturated) ● Sterile water or NS (if incision is less than 48 hours old and the dressing is saturated)

After Surgery 1. Dressings are to remain on for 48 hours. When heavily stained with blood, they are to be changed using sterile technique. (This procedure is to be done by RNs and LPNs only.) a. Don clean gloves and a mask, remove the old incision dressing, and dispose of it into the proper receptacle; remove the dirty gloves. b. Open the 4 ϫ 4 packages and retain them in a sterile manner. c. Put on sterile gloves using the proper procedure. d. Use chlorhexidine (CHG) 2% preoperative, no-rinse cloth to cleanse the area around the incision. Cleanse the incision gently. e. Cover incision with sterile 4 ϫ 4 pads and cover with paper tape. f. Write the date, time, and initials on the tape. 2. After 48 hours, dressings are to be removed. 3. If the patient is unable to shower, bathe the incision daily with one package of CHG 2% preoperative, no-rinse disposable cloths. Cleanse the incision gently. 4. If the wound still has some drainage, reapply a dressing using clean technique; the patient may require only spot dressings in areas where oozing is occurring. Change these PRN. 5. Give the patient a CHG shower daily if there is no chest tube (traditional or flexible silastic drain [e.g., Blake]).Use CHG 2% preoperative, no-rinse disposable cloths in the shower.

Source: V. Morelock & M. Zellinger, Emory University Hospital, Atlanta, GA. Procedure: Incision Care, Cardiac Surgery. Used with permission.

Saphenous vein graft infections occur more If unresolved, these infections can lead to the frequently in obese patients. Drainage of non- need for further interventions, including skin infected serosanginous fluid from leg inci- grafts, vascular procedures, or even amputa- sions is common. Oftentimes, the drainage tions (Alam, Kowalski, & Sample, 1999). results from an underlying hematoma that has liquefied and is draining out of the neigh- ■ boring skin incision. The presence of ery- NURSING RESPONSIBILITIES TO thema, induration, and undue tenderness to ENHANCE WOUND HEALING palpation indicate infection. In such cases, The radial artery site is easy to assess because the patient may require a dilation and curet- of its visibility. Assessment should always tage procedure, followed by open packing of include color, capillary refill time, tempera- the wound and administration of antibiotics. ture, and presence of an ulnar artery pulse. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 382

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Assessment for an underlying incision addition, the patient and family will deal with hematoma is imperative, as its presence may the consequences of a loss in the patient’s pro- impede blood flow to the hand and lead to ductivity. In particular, the patient may be out loss of function. Elevation of the arm and of work for an extended period of time. The affected hand on pillows will help decrease patient’s functional status may be decreased, any edema. such that the individual requires assistance to The multitude of factors that may poten- complete activities of daily living and with tially affect wound healing should be exam- transportation to and from the many visits to ined for each individual patient. Providing for physicians, clinics, or EDs (Kirkland, Briggs, optimal wound healing, eliminating any Trivette, Wilkinson, & Sexton, 1999). The rate underlying causative or contributory factors, of ICU admissions is 60% higher among and stimulating positive physiologic factors infected patients than among uninfected required for the healing process are essential patients (Kirkland et al., 1999). ICU nursing interventions. Optimizing the patient’s nutritional status, including assur- Impact of Postoperative Infection ing that the patient is consuming a diet with adequate protein and caloric intake, trace In an attempt to quantify the impact of post- metals, and vitamins, is equally essential. Col- operative infection, the Agency for Healthcare laboration with a dietitian is recommended. Research and Quality (AHRQ) reviewed The ICU nurse should also assess the patient safety indicators to identify injuries patient’s emotional and psychosocial status. among patients from 994 hospitals in Depression makes it difficult for a patient to 28 states. In this study, a total of 7.45 million be fully compliant with treatment regimens, hospital discharge abstracts were reviewed. which may potentially inhibit wound healing. The researchers found that failure in the Assuring adequate pain control helps process of care can precipitate postoperative enhance the patient’s willingness to be active infection, and that infection is associated with and ability to adhere to treatment regimens. an overall increase of 9.58 extra hospital days, If the patient has an elevated serum glucose $38,000 to $40,000 in excess charges, and a level, close monitoring to maintain tight 4.31% mortality rate (Zhan & Miller, 2003). glycemic control to promote wound healing Reducing the potential for any SSI to occur is required. Renal or liver insufficiency also is a paramount concern with any surgical pro- requires correction, as both of these condi- cedure. Approximately 500,000 SSIs occur in tions will impede healing. Finally, ICU nurses conjunction with the estimated 27 million sur- must implement measures to optimize perfu- gical procedures performed in the United sion and oxygenation and promote early States annually (Barnett, 2007). The Deficit ambulation, as feasible. Reduction Act, passed in 2005, allows the Cen- ters for Medicare and Medicaid Services (CMS) to adjust payments downward for patients ■ WOUND INFECTION SEQUELAE experiencing hospital-acquired infections; this When wound infections occur, they can be provision took effect in October 2008. As of devastating. Most SSIs are identified on a October 1, 2008, the Centers for Medicare and post-hospitalization basis. They can require Medicaid Services no longer reimburses for frequent outpatient and emergency depart- hospital-acquired conditions such as SSIs— ment (ED) visits, radiology services, lab work, specifically, mediastinitis after CABG surgery home health services, hospital readmissions (CMS, 2008) or flap surgery due to an SSI. for treatment, and possibly, further surgery. In Hospitals are now paid at the “without compli- 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 383

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cations rate” when such SSI-related events Table 18–3 Sternal Wound Infection occur, instead of the “with complications” Predictor Scale (SWIPS) higher rate that they had been receiving in the past (Barnett, 2007). The impact of this change Variable Weight in billing practice on hospitals’ financial status could be considerable. Preoperative SSIs affect numerous parties: the patient, Smoking 9 insurance companies, medical caregivers, and Diabetes mellitus hospitals. There has been increasing focus on IDDM 7 preventing SSIs as one element of the Insti- NIDDM 5 tute for Healthcare Improvement’s (IHI) ini- COPD 8 Preoperative ICU stay 4 tiatives in the “Protect 5 Million Lives from Obesity (> 30 kg/m2)4 Harm” campaign (McCannon, Hackbarth, & Advanced age (> 70 years) 3 Griffin, 2007). Sex (male) 1 The general trend is toward surgical Impaired immune response 8 patients who are increasingly sicker and have Intraoperative more complex comorbidities. Many of these patients are elderly (older than 80 years). Bilateral IMA 6 Single IMA 3 When these patients get SSIs, increasing Long operative time (> 4 hr) 7 numbers of them are infected with resistant Reexploration for bleeding 6 strains of microbes (e.g., MRSA and van- Long cardiopulmonary 6 comycin-resistant enterococcus [VRE]). bypass time (> 2 hr) Postoperative ■ WOUND INFECTION PREDICTION Hypoperfusion/hypotension 8 The CDC’s National Nosocomial Infection Ventilator support (> 48 hr) 6 Surveillance (NNIS) system predicts the risk Pharmacologic support of SSI based on three factors: length of Dopamine/dobutamine only 2 All others 6 surgery, wound class, and the patient’s Ameri- Postoperative CPR 7 can Society of Anesthesiology (ASA) score Hypoxemia 5 (Hollenbeak et al., 2000). This system has not Banked blood transfusions 3 been adapted specifically for cardiac surgery, CPR ϭ cardiopulmonary resuscitation; IDDM ϭ however. insulin-dependent diabetes mellitus; IMA ϭ internal The first scale to predict surgical wound mammary artery; NIDDM ϭ non-insulin-dependent infections in CABG patients was developed in diabetes mellitus. 1998 (Hussey, Leeper, & Hynan, 1998; Trout- Source: Hussey, Leeper, & Hynan, 1998. man, Hussey, Hynan, & Lucisano, 2001). This scale, which is known as the Sternal Wound Infection Predictor Scale (SWIPS), consists of has suggested that these two newer scoring weighted predictors related to the preopera- systems outperform the NNIS risk index tive, intraoperative, and postoperative phases (Paul et al., 2007). The Society of Thoracic of care (see Table 18–3). Surgeons (STS) has recently developed a score Validation of other risk score assessment that predicts the risk for infection following tools for mortality such as the EuroSCORE CABG, which includes both preoperative and (Nashef et al., 1999) and the Society of Tho- intraoperative scores and takes several vari- racic Surgeons risk scores (Fowler et al., 2005) ables into account. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 384

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Currently, mediastinitis occurs in 0.04% to flammatory mediators. In recent years, CoNS 4.0% of cardiac surgical patients, with more has been identified as the most common than 50% of these infections involving Staphy- causative agent of SWI (Friberg, 2007). lococcus aureus and epidermidis. The 1-year Mediastinitis can develop as early as 7 to mortality rate of those patients with deep 10 days following a cardiac surgical proce- sternal infections is as high as 22%—far dure. Patients have often been discharged higher than the 0.6% mortality rate in home before any sign of this infection occurs. patients who do not develop infections (Hol- Oftentimes, the first sign is significant serous lenbeak et al., 2000). drainage that appears 4 to 5 days postoperatively. Patients experience fever, chills, pain, and leukocytosis within 2 to 5 days after the ■ MANAGEMENT OF WOUND onset of infection. Erythema may form on INFECTIONS the outside borders of the incision and Sternal Wound Infections is often first seen at the xiphoid process. Sternal wound infections may be superficial, Occasionally, a section of the incision may involving only the skin and subcutaneous fat, dehisce and purulent drainage will exude or they may be deep, involving the sternum from the site. and underlying structures. Superficial infec- More commonly, mediastinitis becomes tions are characterized by drainage from the evident later in the postoperative course, usu- wound and local inflammation, even as the ally within 30 days after surgery. Patients underlying sternum remains stable (see often develop sternal pain, become lethargic, Box 18–1). In this instance, removal of the and demonstrate unwillingness to do many overlying skin sutures, culture of the activities that they were doing previously. The drainage, administration of antibiotics, and incision then begins to drain purulent fluid local dressings are often effective interven- and will separate. Upon assessment, the nurse tions. These wounds respond well to vacuum- often finds that the sternum is unstable, with assisted closure therapy and may heal without the borders rubbing against each other. Pain any further surgery (Agarwal et al., 2005). will be worse with respiration. Fever, chills, Reconstructive surgery can be avoided in clin- and leukocytosis are evident. ically stable patients with the use of vacuum- Treatment of mediastinitis depends on the assisted closure (Chen et al., 2008). stage of the infectious process at the time of diagnosis. If identified early, the sternum is not destroyed—success may be achieved with Mediastinitis prompt surgical intervention, debridement of Bacterial mediastinitis starts when the inva- the sternal edges, copious irrigation of the sion of a pathogen causes an inflammatory mediastinum, placement of retrosternal irriga- response. The invading bacteria proliferate, tion and drainage catheters, rewiring of the and the body forms a thick layer of fibrin in an sternum, and closure of the fascia and attempt to encapsulate the foreign agents. An skin. Appropriate intravenous antibiotic ther- area of dead space forms underneath the ster- apy is given for a minimum of 7 days. The num as the infection expands through sinus results of a gram stain are utilized to identify tracts that have formed. The patient develops the appropriate antibiotic to infuse through fever, and the systemic inflammatory response an irrigating catheter, with the fluid being causes production of leukocytes and proin- directed to exit via drainage catheters. The irri- 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 385

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gation continues for 3 to 5 days, until the home with the drains in place. The drains drainage is sterile as confirmed by culture. remain in place until the daily drainage vol- Although frequently successful, this treatment ume becomes small; they may then be method can have serious complications—for removed in the physician’s office. Early example, erosion of the catheters into medi- aggressive use of muscle flaps in serious mediastinal structures and systemic toxicity from astinitis is considered the optimal approach absorption of the irrigating antibiotic. For (Vlajcic et al., 2007). these reasons, this procedure is reserved for Several long-term complications are associ- specific groups of patients (Lemmer, Richen- ated with mediastinitis. Notably, patients bacher, & Vlahakes, 2003). have a significant increase in mortality during More longstanding, advanced infections the first year and subsequent 4 years. The are associated with large amounts of suppura- potential for other nosocomial infections, tive fluid in the mediastinum, loss of integrity including systemic infections, is increased as of the sternum, and diffuse cellulitis of the well. Patients may develop sepsis and organ skin and subcutaneous tissue. Patients with system failure. Identifying mediastinitis early such infections may require opening of the allows for earlier treatment and is associated sternum and debridement of necrotic tissue, with a better prognosis (Vlajcic et al., 2007). exposure and draining of the mediastinum, For patients who have a relatively unevent- and packing of the wound with moist gauze. ful postoperative course, discharge may occur Vacuum-assisted closure therapy can be used on the third or fourth postoperative day. as a bridge between debridement and closure Many infections do not become evident until of the wound. It can assist in decreasing over- after the patient has been discharged, which all wound edema, reduce bacterial counts in makes early diagnosis of sternal infection and the wound, and reduce the time to closing the mediastinitis after cardiac surgery difficult. In wound (Agrawal et al., 2005). After control of some patients, fever, leukocytosis, and a posi- the infection is achieved and a healthy- tive blood culture will be the first manifesta- appearing bed of granulation tissue forms, tions of a hidden infection that will become secondary closure is performed with or with- obvious only later. The most common early out a muscle flap (Vlajcic et al., 2007). sign is fluid drainage from the wound; sternal The most frequently used approach to instability usually develops subsequently. treating serious mediastinitis is a single-stage Clear and thorough patient education procedure in which radical debridement of reviewing the appearance of a normally heal- the sternum and cartilage is performed with ing incision is of utmost importance in recog- advanced muscle flaps, using the pectoralis nizing postoperative wound infections. The major and/or rectus muscles (Eagle et al., patient and family members must be 2004). Depending on the degree of sternal instructed to frequently observe the incision resection required, the remaining bone tissue for any changes in status and to call the sur- may or may not be approximated. Soft silastic geon’s office if changes or questions arise (see drains are placed beneath the muscle flaps Box 18–5). Given the trend toward earlier hos- and connected to gentle suction. Often per- pital discharge following cardiac surgery, formed by a plastic surgeon, this procedure fewer SSIs will be detected prior to patient may be associated with decreased morbidity discharge. Without careful supervision and and mortality and a decreased length of hos- intervention, the physical and financial costs pital stay. The patient may be discharged of these infections will increase. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 386

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Box 18–5 Patient/Family Discharge Education Regarding Incision Care

Emphasize the following points when explaining wound care at home: ● Shower daily with soap and water. ● Avoid sitting in bathtub. ● A dressing is needed only if drainage is present. ● Remove any dressings applied during hospitalization on the day after going home. ● Inspect the wound daily using a mirror. If you see any redness, irritation, swelling, tenderness, or unusual drainage, contact the surgeon or surgeon on call. Optimal Patient Outcomes ● Patient can perform appropriate incision care. ● Patient has no signs and symptoms of infection. ● Patient can list signs and symptoms of infection. ● Patient modifies lifestyle to reduce risk factors that may impede wound healing.

■ SUMMARY potentially catastrophic complication. Sternal wound infections occur in a small per- Although a sternal wound infection is not centage of patients who undergo cardiac sur- likely to develop while the patient is in the gery. There is a high associated cost in terms ICU postoperatively, initiation of preventive of morbidity, mortality, and length of hospi- measures must begin while the patient is in talization, and financial costs if they develop. the early phase of recovery. The ICU nurse has A number of predictive variables have been a pivotal role in preventing sternal wound identified that put the patient at greater risk infections and beginning the essential patient for development of a sternal wound infection, and family education that must be accom- and a number of preventive strategies must be plished to help ensure optimal postoperative implemented to avoid development of this outcomes are attained.

CASE STUDY

A 79-year-old patient with a history of smoking one pack of cigarettes per day, diabetes, obesity, and inactivity due to peripheral vascular disease was admitted to the emergency department with chest pain. The patient was taken for a cardiac catheterization, where it was determined that emergency cardiac surgery was necessary. The surgeon performed a quadruple coronary artery bypass. Because of the patient’s peripheral vascular disease, both internal mammary arteries were used as conduits. The surgery lasted 4 hours, after which time the patient was admitted to the ICU on epinephrine and milrinone (Primacor®) infusions to augment cardiac output. Initial arterial blood gas

results were as follows: pH 7.23, pCO2 51 mm Hg, pO2 89 mm Hg. Copious endotracheal secretions were noted. The initial chest tube drainage was 350 mL for the first hour and 300 mL for the second hour. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 387

Self-Assessment Questions 387

Critical Thinking Questions 1. What were some of the preoperative risk factors present for development of a sternal wound infection? 2. Which predictive factors for the development of wound infection are present postoperatively? 3. How frequently should the incision dressing be changed in the postoperative period? 4. What are four preventive strategies that the ICU nurse should incorporate into the care plan to prevent postoperative wound contamination? Answers to Critical Thinking Questions 1. Diabetes, advanced age, obesity, tobacco (possibility of COPD) and emergent CABG procedure. 2. Low cardiac output and use of both internal mammary arteries. Use of both IMAs is associated with an increased risk of infection because these arteries provide the major source of blood supply to the sternum. 3. If a rubber dam is present, the initial dressing change should be performed with the surgeon in attendance so that the site can be assessed and evaluated by both physician and nurse simultaneously, thereby avoiding unnecessary site exposures. For all open chest wounds sterile dressing changes are performed every 24 hours. If the patient has a closed chest incision, the initial dressing change occurs 48 hours postoperatively. If needed the dressing is reapplied and changed every 24 hours. All dressing changes must be done with strict aseptic technique. 4. (1) Postoperative incisional dressing assessments should be performed upon the patient’s admission to the ICU and every 4 hours thereafter until the patient transfers out of the ICU. (2) To minimize the risk of infection, keep the initial dressing on the incision for 24 to 48 hours, as per CDC recommendations. (3) The multitude of factors affecting wound healing should be examined for each individual patient. Provid- ing for optimal wound healing, eliminating any underlying causative and/or contributory factors, and stimulating the positive physiologic factors required for the healing process are essential nursing interventions. (4) Optimizing the patient’s nutritional status, assuring that the patient is ingesting a diet with adequate protein and caloric intake, trace metals, and vitamins is equally essential.

■ SELF-ASSESSMENT QUESTIONS 2. The most common infectious organism found in mediastinitis is 1. Preoperative risk factors for mediastini- a. Staphylococcus aureus. tis include b. Staphylococcus epidermidis. a. Asian race, Marfan syndrome, and c. Enterococcus. advanced age. d. gram-negative Serratia. b. advanced age, chest pain, and emphysema. 3. Postoperatively, a sterile dressing should c. emphysema, advanced age, and male be kept on gender. a. 72 to 96 hours. d. advanced age, emphysema, and b. 8 to 12 hours. infection. c. 12 to 24 hours. d. 24 to 48 hours. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 388

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4. Discharge education should incorporate c. a diet that contains adequate protein, a. characteristics of a normal and caloric intake, trace metals, and abnormal healing incision. vitamins. b. self-treatment procedures for d. strict glycemic control. infection. 8. Continuous intravenous insulin infu- c. normal lab results from sions should be used perioperatively hematological lab studies. a. to maintain serum glucose less than d. referral to online resources. 180mg/dL. 5. An initial indication of infection may b. in all patients who are hyperglycemic, include whether they have a history of a. serous drainage, increased chest tube diabetes or not. drainage, and bradycardia. c. while adjusting the infusion by b. serous drainage, fever, and pain. checking serum glucoses every 3 to 4 c. leukocytosis, bradycardia, and hours and following the established hypertension. protocol of the institution. d. hypertension, decreased chest tube d. but lower doses may be needed drainage, and serous drainage. because patients experience an 6. A prophylactic antibiotic regimen insulin sensitivity. should consider which of the following 9. All of the following statements about measures? mediastinitis are true except a. Adding a glycopeptide to the a. it may begin with serous drainage a cephalosporin, such as vancomycin, few days postoperatively and can for two to three doses postoperatively progress to purulent drainage, and a is appropriate in patients who have portion of the wound may dehisce. received a prosthetic valve or vascular b. bilateral IMAs, prolonged ICU stay, graft. decreased cardiac output, and b. Routine postoperative antibiotic autotransfusion are all factors that regimen should be no longer than lessen the patient’s risk for infection. 72 hours. c. mediastinitis is a deep sternal c. A glycopeptide, such as vancomycin, incisional infection that affects fascia provides adequate broad-spectrum and bone, occurring within 5 to 30 coverage and can be used as a solo days postoperatively. prophylactic agent. d. diabetes, renal failure, increased age, d. The initial dose of antibiotic should large breast size, and obesity all be timed to provide a bactericidal increase a patient’s risk of developing concentration in the tissues and the mediastinitis. serum before the incision is made, Answers to Self-Assessment Questions and is usually given 30 to 60 minutes prior to incision. 1. d 6. d 7. All of the following factors promote 2. a 7. a wound healing except 3. d 8. b a. renal failure or liver failure. 4. a 9. b b. adequate pain control to promote 5. b ambulation and respiratory exercises. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 389

References 389

Clinical Inquiry Box

Question: What is the incidence of sternal wound infections? Reference: Strecker, T., Rösch, J., Horch, R. E., Weyand, M., & Kneser, U. (2007). Sternal wound infections following cardiac surgery: Risk factor analysis and interdisciplinary treatment. Heart Surgery Forum, 10(5), E366–E371. Objective: To evaluate the outcomes of interventions utilized in the treatment of complicated median sternotomy wounds. Methods: In a retrospective review covering a three-year period, 3016 consecutive open-heart surgery patients were evaluated. The majority of patients (65.6%) underwent coronary artery bypass grafting (CABG). The remainder received surgery for artificial heart implantation, cardiac transplantation, aorta reconstruction or replacement, cardiac valve replacement, or combined CABG and valve replacement. Results: Of the 3016 subjects, only 2.1% developed sternal wound infections. Treatment of the infections consisted of debridement, irrigation, and rewiring in 56 cases. Vacuum-assisted closure therapy was utilized in 34 patients, and 19 patients eventually required reconstructive surgery with either rectus abdominis or pectoralis major flaps. Significant risk factors for the development of a surgical site infection included diabetes mellitus, rethoracotomy, duration of operation, and, interestingly, the time of operation (morning versus afternoon). Discussion: In this study, a decreased risk of infection was associated with first position on the OR schedule. Although vacuum-assisted closure therapy is useful in preventing reconstructive surgery, a small percentage of patients will require flap surgery. The type of flap will depend on the location of the infection and the availability of muscle for the closure of the wound. Nurses should be aware that hospitals in the future might decide to schedule cardiac surgery only as the first case, especially for those patients at the highest risk for surgical site infection.

■ REFERENCES after cardiovascular surgery. Journal of the Agarwal, J. P., Ogilvie, M., Wu, L. C., Lohman, R. F., American College of Surgery, 202(1), 131–138. Gottlieb, L. J., Franczyk, M., et al. (2005). Vac- Barnett, T. E. (2007). The not-so-hidden costs of uum-assisted closure for sternal wounds: A surgical site infections. AORN Journal, 86(2), first-line therapeutic management approach. 249–258. Plastic and Reconstructive Surgery, 116(4), Buonocore, D. (2008). Treatment of hyper- 1035–1040. glycemia. Critical Care Nurse, 28(6), 72–73. Alam, H. B., Kowalski, C., & Sample, G. A. (1999). Centers for Medicare and Medicaid Services Saphenous vein graft infection: A fatal compli- (CMS). (2008). Hospital acquired conditions. cation of postoperative mediastinitis. Chest, Retrieved September 9, 2008, from 116(6), 1816–1818. http://www.cms.hhs.gov/HospitalAcqCond/ Athanassiadi, K., Theakos, N., Benakis, G., Kakaris, 06_Hospital-Acquired_Conditions.asp S., & Skottis, I. (2007). Omental transposition: Chen, Y., Almeida, A. A., Mitnovetski, S., Goldstein, The final solution for major sternal wound J., Lowe, C., & Smith, J. A. (2008). Managing infection. Asian Cardiovascular Thoracic Annals, deep sternal wound infections with vacuum- 15(3), 200–203. assisted closure. Australiasian Journal of Surgery, Banbury, M. K., Brizzio, M. E., Rajeswaran, J., Lytle, 78(5), 333–336. B. W., & Blackstone, E. H. (2006).Transfusion increases the risk of postoperative infection 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 390

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Cimochowski, G. E., Harostock, M. D., Brown, R., (2005). Clinical predictors of major infections Bernardi, M., Alonzo, N., & Coyle, K. (2001). after cardiac surgery. Circulation, 112(9 suppl), Intranasal mupirocin reduces sternal wound 1358–1365. infection after open heart surgery in diabetics Friberg, O. (2007). Local collagen-gentamicin for and nondiabetics. Annals of Thoracic Surgery, prevention of sternal wound infections: The 71(5), 1572–1579. LOGIP trial. Acta Pathologica, Microbiologica et Coskun, D., & Aytac, J. (2006). The decrease in Immunologica Scandinavica, 115(9), 1016–1021. healthcare-associated methicillin-resistant Friberg, O., Dahlin, L.-G., Soderquist, B., Kallman, Staphylococcus aureus infections and savings J., & Svedjeholm, R. (2006). Influence of more from glycopeptides use. Infection Control and than six sternal fixation wires on the incidence Hospital Epidemiology, 27(10), 1131–1132. of deep sternal wound infection. Thoracic Car- Crouch, J. D., O’Hair, D. P., Keuler, J. P., Barragry, diovascular Surgery, 54(7), 468–473. T. P., Werner, P. H., & Kleinman, L. H. (1999). Furnary, A. P., Gao, G., Grunkemeier, G. L., Wu, Y., Open versus endoscopic saphenous vein har- Zerr, K. J., Bookin, S. O., et al. (2003). Continu- vesting: Wound complications and vein qual- ous insulin infusion reduces mortality in ity. Annals of Thoracic Surgery, 68(4), 1513–1516. patients with diabetes undergoing coronary DeBaun, B. (2007). New alcohol-free 2% CHG solu- artery bypass grafting. Journal of Thoracic Car- tion reduced bacterial counts of drug-resistant diovascular Surgery, 125(5), 1007–1021. Acinetobacter and MRSA by 99.9%. AORN, Haycock, C., Laser, C., Keuth, J., & Montefour, K. 87(5), 925–933. (2005). Implementing evidence-based practice Eagle, K. A., Guyton, R. A., Davidoff, R., Edwards, findings to decrease postoperative sternal F. H., Ewy, G. A., Gardner, T. J., et al. (2004). wound infections following open heart sur- ACC/AHA 2004 guideline update for coronary gery. Journal of Cardiovascular Nursing, 20(5), artery bypass graft surgery: A report of the 299–305. American College of Cardiology/American Hollenbeak, C. S., Murphy, D. M., & Koenig, S., Heart Association Task Force on Practice Woodward, R. S., Dunagan, W. C., & Fraser, Guidelines (Committee to Update the 1999 V. S. (2000). The clinical and economic impact Guidelines for Coronary Artery Bypass Graft of deep chest surgical site infections following Surgery). Circulation, 110(9), 1168–1176. coronary artery bypass graft surgery. Chest, Edmiston, C., Seabrook, G., Johnson, C., Paulson, 118(2), 397–402. D., & Beausoleil, C. (2007). Comparative of a Horan, T. C., Gaynes, R. P., Martone, W. J., Jarvis, new and innovative 2% chlorhexidine glu- W. R., & Emori, T. G. (1992). CDC definitions conate–impregnated cloth with 4% chlorhexi- of nosocomial surgical site infections, 1992: A dine gluconate as topical antiseptic for modification of CDC definitions of surgical preparation of the skin prior to surgery. Ameri- wound infections. Infection Control and Hospital can Journal of Infection Control, 35(2), 89–96. Epidemiology, 13(10), 606–608. Engelman, R., Shahian, D., Shemin, R., Guy, T. S., Hussey, L. C., Leeper, B., & Hynan, L. S. (1998). Bratzler, D., Edwards, F., et al. (2007). Society Development of the Sternal Wound Infection of Thoracic Surgeons practice guidelines Prediction Scale. Heart & Lung, 27(5), 326–336. series: Antibiotic prophylaxis in cardiac sur- Jancin, B. (2004). Antibiotic resistant pathogens gery, part II: Antibiotic choice 2007. Annals of found on 77% of ECG lead wires. Cardiology Thoracic Surgery, 83(4), 1569–1576. News, 2(3), 14. Filsoufi, F., Rahmanian, P. B., Castillo, J. G., Pin- Jones, G., Jurkiewicz, M. J., Bostwick, J., Wood, R., ney, S., Broumand, S. R., & Adams, D. H. Bried, J. T., Culbertson, J., et al. (1997). Man- (2007). Incidence, treatment strategies and agement of the infected median sternotomy outcome of deep sternal wound infection after wound with muscle flaps. The Emory 20-year orthotopic heart transplant. Journal of Heart experience. Annals of Surgery, 225(6), 766–778. and Lung Transplantation, 26(11), 1084–1090. Kazlauskaite, R., & Fogelfeld, L. (2003). Inpatient Fowler, V. G., O’Brien, S. M., Muhlbaier, L. H., management of diabetes and hyperglycemia. Corey, G. R., Ferguson, T. B., & Petersen, E. D. Disease-a-Month, 49(6), 377–420. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 391

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Keib, C. N., & Pelham, J. C. (2006). Mediastinitis Ragheb, J., & Buggy, D. J. (2004). Tissue oxygen

following coronary artery bypass graft surgery: tension (PTO2) in anaesthesia and periopera- Pathogenesis, clinical presentation, risks, and tive medicine. British Journal of Anaesthesia, management. Journal of Cardiovascular Nursing, 92(4), 464–468. 21(6), 493–499. Rand, R. P., Cochran, R. P., Aziz, S., Hofer, B. O., Kirkland, K. B., Briggs, J. P., Trivette, S. L., Wilkin- Allen, M. D., Verrier, E. D., et al. (1998). son, W. E., & Sexton, D. J. (1999). The impact Prospective trial of catheter irrigation and of surgical-site infections in the 1990s: Attrib- muscle flaps for sternal wound infection. utable mortality, excess length of hospitaliza- Annals of Thoracic Surgery, 65(4), 1046–1049. tion, and extra costs. Infection Control and Ridderstolpe, L., Gill, H., Granfeldt, H., Åhlfeldt, Hospital Epidemiology, 20(11), 725–730. H., & Rutberg, H. (2001). Superficial and deep Lemmer, J. H., Richenbacher, W. E., & Vlahakes, G. sternal wound complications: Incidence, risk J. (2003). Handbook of patient care in cardiac sur- factors, and mortality. European Journal of Car- gery. Philadelphia: Lippincott Williams & dio-thoracic Surgery, 20(6), 1168–1175. Wilkins. Rosengart, T. K., Feldman, T., Borger, M. A., Vassil- Mangram, A. J., Horan, T. C., Pearson, M. L., Silver, iades, T. A. Jr., Gillinov, A. M., Hoercher, K. J., L. C., Jarvis, W. R., & Hospital Infection Con- et al. (2008). Percutaneous and minimally trol Practices Advisory Committee. (1999). invasive valve procedures: A scientific state- Guideline for prevention of surgical site infec- ment from the American Heart Association tion, 1999. Infection Control & Hospital Epidemi- Council on Cardiovascular Surgery and Anes- ology, 20(4), 250–278. thesia, Council on Clinical Cardiology, Func- Marshall, K. E., & Barash, P. G. (2004). Myocardial tional Genomics and Translational Biology ischemia monitoring: A sequential systems Interdisciplinary Working Group, and Quality approach. ASA Refresher Courses in Anesthesiol- of Care and Outcomes Research Interdiscipli- ogy, 32(1), 135–144. nary Working Group. Circulation, 117(13), McCannon, C. J., Hackbarth, A. D., & Griffin, F. A. 1750–1767. (2007). Miles to go: An introduction to the 5 Ryder, M. (2007). Improving skin antisepsis: 2% no- Million Lives campaign. Joint Commission Jour- rinse CHG cloths improve antiseptic persistence on nal on Quality and Patient Safety, 33(8), 477–484. patient skin over 4% CHG rinse-off solution. Poster Nashef, S. A., Roques, F., Michel, P., Gauducheau, presented at Association for Professionals in E., Lemeshow, S., & Salamon, R. (1999). Euro- Infection Control and Epidemiology (APIC), pean system for cardiac operative risk evalua- June 2007. tion (EuroSCORE). European Journal of Streeter, N. B. (2006). Considerations in prevention Cardiothoracic Surgery, 16(1), 9–13. of surgical site infections following cardiac Paul, M., Raz, A., Leibovici, L., Madar, H., Holinger, surgery: When your patient is diabetic. Journal R., & Rubinovitch, B. (2007). Sternal wound of Cardiovascular Nursing, 21(3), 14–20. infection after coronary artery bypass graft Sweene, C. L., Lindholm, C., Borowiec, J., & Carls- surgery: Validation of existing risk scores. Jour- son, M. (2004). Surgical-site infections within nal of Thoracic and Cardiovascular Surgery, 133(2), 60 days of coronary artery by-pass graft sur- 397–403. gery. Journal of Hospital Infection, 57(1), 14–24. Peter, R., Cox, A., & Evans, M. (2008). Management Troutman, S., Hussey, L. C., Hynan, L., & Lucisano, of diabetes in cardiovascular patients. Heart, K. (2001). Sternal Wound Infection Prediction 94(3), 369–375. Scale: A test of the reliability and validity. Pittman, J. (2007). Effect of aging on wound heal- Nursing and Health Sciences, 3(1), 1–8. ing current concepts. Journal of Wound, Ostomy Turina, M., Fry, D. E., & Polk, H. C. (2005). Acute and Continence Nursing, 34(4), 412–417. hyperglycemia and the innate immune system: Pokorny, M. E., Koldjeski, D., & Swanson, M. Clinical, cellular, and molecular aspects. Criti- (2003). Skin care intervention for patients hav- cal Care Medicine, 33(7), 1624–1633. ing cardiac surgery. American Journal of Critical Care, 12(6), 535–544. 57625_CH18_371_392.pdf 4/10/09 11:10 AM Page 392

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Vlajcic, Z., Zic, R., Stanec, S., & Stanec, Z. (2007). ■ WEB RESOURCES Algorithm for classification and treatment of Centers for Medicare and Medicaid Services poststernotomy wound infections. Scandina- (CMS): http://www.cms.hhs.gov/ vian Journal of Plastic Reconstructive Surgery and Deficit Reduction Act: http://www.cbo.gov/ Hand Surgery, 41(3), 114–119. ftpdocs/70xx/doc7028/s1932conf.pdf Vorp, D. A., Maul, T., & Nieponice, A. (2005). Mole- Institute for Healthcare Improvement: http:// cular aspects of vascular tissue engineering. www.ihi.org/ihi Frontiers in Bioscience, 10, 768–789. Guideline for the Prevention of Surgical Site Infec- Zellinger, M., & Lienberger, T. (1991). Use of the tion, 1999: http://www.cdc.gov/ncidod/dhqp/ rubber dam after open heart surgery. Critical gl_surgicalsite.html Care Nurse, 11(8), 24–27. Zhan, C., & Miller, M. R. (2003). Excess length of stay, charges, and mortality attributable to medical injuries during hospitalization. Jour- nal of the American Medical Association, 290(14), 1868–1874. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 393

Chapter 19 Bridge to Transplant and Cardiac Transplantation

Rachel S. Ball, Kathy Halabicky, Laurie Hartman, Erin Lindstrom, and Tracey Romans

■ INTRODUCTION ■ MANAGEMENT OF HEART The American Heart Association (AHA) esti- FAILURE mates that nearly 5 million Americans are cur- When patients are diagnosed with HF, they rently living with heart failure (HF); typically are started on diuretics or ultrafiltra- approximately 550,000 new cases are diagnosed tion techniques to assist with volume over- in the United States each year (AHA, 2007) and load. When their clinical status declines and more than 287,000 people die from HF annu- these measures are no longer effective, these ally (AHA, 2008). Over the past 10 years, med- patients may be admitted to the ICU in car- ical advances have greatly increased treatment diogenic shock requiring inotropic (e.g., options for people living with heart failure. In dobutamine [Dobutrex®], dopamine [Intropin®], particular, mechanical circulatory support tech- milrinone [Primacor®], inamrinone [Inocor®]) nology has emerged as a life-saving option for or mechanical support (e.g., ventricular assist patients with acute and chronic heart failure device [VAD], intra-aortic balloon pump that is not amenable to maximal therapy. [IABP]). If the patient requires ongoing hospi- In the United States, 257 facilities currently talizations for HF and management strategies have the ability to perform heart transplants. are not beneficial, consideration should be The Organ Procurement and Transplantation given for heart transplantation (McCalmont & Network (OPTN) reported that 2684 patients Ohler, 2008). IABP therapy and pharmaco- were awaiting such transplants in March logic interventions for HF are discussed in 2008. In 2007, 2030 heart transplants were Chapters 10 and 12, respectively. performed in this country. As of December 5, 2008, there were 2705 waitlisted candidates ■ for a heart transplant (OPTN, 2008). An esti- CRITERIA FOR HEART mated 10% to 15% of these patients will die TRANSPLANTATION each year while awaiting a heart transplant A patient may become a candidate for a heart (McCalmont & Ohler, 2008). transplant based on specific criteria. The This chapter reviews the management of patient may have terminal HF that has not heart failure as the patient moves through the responded to medical therapy or cardiomy- trajectory of illness toward transplantation. opathy (ischemic, nonischemic, idiopathic, The role of the critical care nurse is discussed or valvular). In addition, the predicted 1-year during the various phases of illness through survival rate for the patient should be the transplant process and beyond. 50%. Another proposed physiologic criterion

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is a maximum oxygen consumption of less rate < 40 mL/min), severe PVD or CVD, than 14 mL/kg/min with associated restric- uncontrolled diabetes/poor glycemic control

tions on activities of daily living (if the patient (i.e., HbA1c > 7.5%), active peptic ulcer disease, is not receiving beta-blocker therapy) or less amyloidosis, current or recurrent diverticuli- than 12 mL/kg/min if the patient is receiving tis, severe mental illness or psychosocial insta- beta-blocker therapy (Colucci & Piña, 2008). bility, demonstrated noncompliance with Other criteria include labile fluid balance and medical regimens, no social support, and renal function that are not related to lack of active use of alcohol, drugs, or tobacco adherence with the medical regimen. The (McCalmont & Ohler, 2008). potential candidate must be emotionally sta- Patients must be evaluated for their degree ble and have sources of social support of renal dysfunction, as anti-rejection medica- (McCalmont & Ohler, 2008). tions (especially calcineurin inhibitors [CNIs], As their condition continues to deteriorate, discussed later in this chapter) are nephro- patients with HF will be evaluated for a match toxic. Individuals with severe pulmonary with the criteria for heart transplantation. Both hypertension may develop right heart failure, absolute and relative contraindications to heart which is associated with immediate death fol- transplant have been reported in the literature. lowing transplant because the donor heart Relative contraindications to heart trans- will not pump effectively. Peptic ulcer disease plant include age greater than 65 years, is a contraindication because the steroid ther- reversible pulmonary hypertension (pul- apy required as part of the transplant process monary vascular resistance [PVR] less than may impair postoperative healing. Patients 400 dyne/sec/cm–5 while receiving vasodilator with hepatic failure are not candidates therapy), reversible hepatic or renal dysfunc- for transplant because many of the post- tion, HIV positive status, asymptomatic transplant medications are hepatotoxic and peripheral vascular disease (PVD) or cere- these individuals have a higher risk of develop- brovascular disease (CVD), insulin-dependent ing coagulopathies. Patients with amyloidosis diabetes mellitus requiring high doses of are at greater risk for post-transplant recur- insulin, receiving therapy for a psychiatric dis- rence, as their disease may spread to other order, body mass index (BMI) greater than 35 organs. Persons with severe mental illness or a kg/m2, and cachexia (BMI < 20 kg/m2). These history of noncompliance with medical regi- last two conditions are associated with poor mens are at risk for rejection if they do not postoperative healing and recovery (McCal- consistently follow the required anti-rejection mont & Ohler, 2008). HIV positive patients are therapy regimen (McCalmont & Ohler, 2008). evaluated based on their overall health status, anticipated long-term survival, and presence of ■ infectious disease, and must have a stable MECHANICAL CIRCULATORY CD4+ count to be considered viable candidates SUPPORT for heart transplant (Pelletier et al., 2004). Because the number of transplant candidates Absolute contraindications to heart trans- exceeds the number of available organs, lead- plant include advancing age, severe pul- ing to protracted times spent on the waitlist, monary hypertension (PVR Ն 400 dyne/sec/ a patient’s clinical status will likely decline cm–5), irreversible hepatic dysfunction (i.e., while awaiting a new heart, and medications cirrhosis, bilirubin > 2.5 mg/dL, or transami- may become ineffective. Patients will then be nase levels higher than twice the normal val- evaluated for mechanical circulatory support ues), irreversible renal dysfunction (i.e., as the wait continues; this care is termed creatinine > 3 mg/dL, glomerular filtration “bridge to transplant.” 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 395

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Mechanical circulatory support has three Abiomed pumps (Danvers, Massachusetts), primary functions: bridge to transplant, TandemHeart PTVA® (CardiacAssist, Inc.), bridge to recovery, and destination therapy. and extracorporeal membrane oxygenation Short-term, temporary devices are often used (ECMO). TandemHeart PTVA® and ECMO as a bridge to recovery in the setting of acute are particularly useful in the setting of acute cardiogenic shock or cardiopulmonary arrest. cardiogenic failure because of the relative ease Under these circumstances, circulatory assis- of their placement if experienced personnel tance provides immediate hemodynamic sup- are available. All of these short-term devices port, restoring blood flow to vital organs require anticoagulation, generally with while decompressing the heart, thereby help- heparin. Figures 19–1, 19–2, and 19–3 show a ing the patient avoid pulmonary edema and left ventricular assist device (LVAD), right minimizing cardiac workload so as to maxi- ventricular assist device (RVAD), and a biven- mize the individual’s chances of recovery. tricular assist device (BiVAD), respectively.

Types of Short-Term Assist Devices Abiomed Pumps Examples of short-term assist devices com- Abiomed produces two blood pumps, called monly used in emergent situations include the BVS 5000 and the AB 5000, that are

Superior Superior Vena Vena Cava Aorta Cava Aorta Pulmonary Artery Pulmonary Artery

Pulmonary Veins Pulmonary Veins Pulmonary Veins Pulmonary Veins LA LA RA RA LV LV RV RV

Descending Descending Inferior Inferior Aorta Aorta Vena Vena Cava Cava

RVAD LVAD

Figure 19–1 Left ventricular assist Figure 19–2 Right ventricular assist device. device. Source: Illustrated by Lydia Lemmond Source: Illustrated by Lydia Lemmond 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 396

396 Chapter 19 Bridge to Transplant and Cardiac Transplantation

Aorta Superior Vena Cava Pulmonary Artery

LA Pulmonary Veins Pulmonary Veins RA

LV RV

Descending Inferior Aorta Vena Cava

RVAD LVAD

Figure 19–3 Biventricular assist device. Source: Illustrated by Lydia Lemmond

designed for temporary mechanical circula- rate as high as 5 L/min. Abiomed’s newer tory support (see Figure 19–4). These pumps pump, the AB 5000, has improved durability can be used for left, right, or biventricular and shorter tubing, which improves patient support. Both models require sternotomy for mobility, allowing for rehabilitation and direct access to and cannulation of the heart ambulation. and great vessels. The BVS 5000 consists of a pump with an atrial chamber that fills with TandemHeart PTVA blood through gravity-assisted drainage, and The TandemHeart PTVA also offers tempo- a ventricular chamber that returns blood to rary circulatory assistance. In contrast to the the body pneumatically (utilizing movement Abiomed pumps, this device utilizes a cen- of compressed air). The chambers are sepa- trifugal pump and is inserted percutaneously rated by two trileaflet valves. This pump can (see Figure 19–5). Under fluoroscopic guid- produce blood flow (“cardiac output”) at a ance in the cardiac catheterization laboratory, 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 397

Mechanical Circulatory Support 397

(A)

(B) Figure 19–4 Two Abiomed blood pumps—(A) BVS 5000 and (B) AB 5000. Source: Illustrated by James R. Perron 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 398

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Figure 19–5 The TandemHeart PTVA—this device utilizes a centrifugal pump and is inserted percutaneously. Source: Illustrated by James R. Perron 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 399

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a drainage cannula is inserted into the most of their previous cardiac function, thus femoral vein up the inferior vena cava, into allowing for the removal of the assist device. the right atrium, across the inter-atrial sep- Patients with acute viral myocarditis, for tum, and into the left atrium. The pump example, often experience improved cardiac withdraws oxygenated blood from the left function once the initial inflammatory atrium, propels it via a magnetically driven, processes within the cardiac muscle have six-bladed impeller through the outflow port, resolved. Many patients, however, have and returns it to the femoral artery via an chronic irreversible HF such that long-term arterial cannula. The pump is capable of mechanical support, transplant, or both will delivering blood flow at a rate as high as 4 be necessary. L/min. The TandemHeart support has been Recovery of heart function is assessed by used successfully in postcardiotomy cardio- briefly decreasing the amount of support pro- genic shock patients (those who have devel- vided by the device (e.g., decreasing device oped HF as a result of heart surgery or a heart blood flow to 2 L/min) and monitoring the attack) and as a bridge to a definitive therapy. patient’s hemodynamic parameters. If this It can be readily removed if native function brief trial is well tolerated, a surface echocar- returns. diogram is obtained during a trial of decreased support to more accurately assess valve and Extracorporeal Membrane Oxygenation ventricular function. Depending on the results ECMO is a technique of partial cardiopul- of these trials, plans are made for device monary bypass (CPB) that was initially devel- removal followed by appropriate medical ther- oped to treat reversible neonatal respiratory apy if there has been adequate recovery of failure. The equipment typically used for cardiac function, or for transition to a longer- standard CPB in open heart surgery has been term implanted device, heart transplant, or modified to reduce hemolysis, thrombus for- both if poor cardiac function persists. mation, and risk of air embolus. ECMO can provide support for days or weeks. With this Long-Term Mechanical Circulatory technique, blood is continuously withdrawn Support from any large central vein and pumped into a gas exchanger that oxygenates hemoglobin Longer-term mechanical circulatory support and removes carbon dioxide. The oxygenated is accomplished with the class of devices gen- blood is then pumped into any large artery erally termed VADs. VADs are implanted (see Figure 19–6). The heart and lungs are mechanical pumps that are used in patients bypassed, providing both hemodynamic and with end-stage heart disease. VADs assist the respiratory support. The blood oxygenation weakened heart by pumping blood through- provided by this method is a distinct advan- out the body. They were originally designed tage of ECMO. to stabilize HF patients until a donor heart became available, a strategy referred to as “bridge to transplant.” Alternatively, they may Short-Term Mechanical Circulatory be used in patients who are not candidates for Support or have declined heart transplant, in which Following placement of a short-term circula- case their use is termed “destination therapy.” tory assist device (e.g., a VAD) and a period of Research supports the use of VADs as desti- hemodynamic stability, the patient’s heart nation therapy. In 2001, the Randomization function and need for continued support are Evaluation of Mechanical Assistance for the assessed. Some patients will regain some or Treatment of Congestive Heart Failure 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 400

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Oxygen Supply

Heat Exchanger

Blood Flow Bridge Membrane Lung Fluid (Nutrition)

Servoregulator

Pump

Blood Flow

Heparin Infusion Pump

Pulse Ox Figure 19–6 ECMO Pulse Ox. Source: Illustrated by James R. Perron

(REMATCH) trial compared the outcomes ■ VENTRICULAR ASSIST DEVICES with LVAD devices for destination therapy VADs can provide left, right, or biventricular and the outcomes with medical therapy. Rose support. The most common scenario involves and colleagues (2001) noted that survival the use of LVAD to counteract left ventricular rates at 1 year were better in the LVAD dysfunction. Mechanisms for movement of patients than in the medical therapy patients blood vary among the different types of (52% versus 25%, respectively). In addition to pumps. In general, blood is drained from the realizing a survival benefit, patients on LVAD apex of the left ventricle to the pump via the gained energy and vitality as a result of inflow cannula. It is returned to the body via improved organ perfusion, and they reported an outflow cannula, which is attached to the overall increased quality of life. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 401

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aorta. The pump is housed in the pre- that powers the device is large and noisy, so peritoneal space of the abdomen, near the transport of the device is tedious. Use of this stomach. A percutaneous drive line that is BiVAD requires initial anticoagulation with tunneled across the pre-peritoneal space to heparin, followed by warfarin (Coumadin®) the left side of the body carries the electrical and antiplatelet therapy, which means that cable and air vent to the electrical controller bleeding complications are increased when outside the patient’s body. The risk of pump this type of pump is used. One important infection is reduced by tunneling the cable advantage is the Thoratec BiVAD’s innovative across the abdomen, thereby increasing the design, which places the blood chambers distance from the pump to the exit site and external to the body, allowing for placement allowing the body to form a natural seal of this device in smaller patients. around the cable. Table 19–1 compares the various types of Heartmate XVE VADs. The Heartmate XVE is another type of implanted, long-term pump with pulsatile blood flow. It is used for left ventricular (LV) VAD Selection Criteria support and is FDA approved for both desti- Selection criteria for patients requiring VAD nation therapy and bridge to transplant. therapy are rigorous. As part of patient evalua- Because this model is a larger pump, patient tion, a battery of lab and diagnostic tests are selection criteria include the requirement that performed to determine eligibility for the the patient’s body surface area (BSA) be device. Cardiologists, social workers, nurses, greater than 1.5 m2. As a consequence, the VAD coordinators, and the cardiac surgeon Heartmate XVE device is used more fre- collaborate to determine the appropriateness quently in males. The surface of the device is of the device for the patient and decide on the coated with a unique texture, allowing plan of care. The surgeon determines the type antiplatelet therapy to consist of aspirin of support required (i.e., LVAD, RVAD, or alone. This is an important advantage because BiVAD). LVAD recipients must have adequate it means there is a decreased risk of throm- right ventricular (RV) function to achieve a boembolism with this device (Bojar, 2005). successful outcome because the LVAD is Bleeding risks are also minimized because dependent on blood flow from the right ventri- warfarin therapy is not required. cle. If RV failure is present, patients’ length of stay, post-implantation morbidity/mortality, Heartmate II and costs are increased (Decoene et al., 2004). The Heartmate II is an axial (continuous) In such cases, temporary biventricular support flow LVAD device that is more compact than may be initiated, with discontinuation of the the Heartmate XVE, so it can be used in RVAD if the right ventricle has recovered. patients who have smaller frames (BSA of 1.3–2.3 m2). This device is FDA approved for use as a bridge to transplant; approval for des- Types of VADs tination therapy is expected. Clinical trials of Biventricular Support this device by the manufacturer have demon- The Thoratec BiVAD can be used for biven- strated its superior durability in comparison tricular support. In the patient with biventric- with pulsatile pumps (Haft et al., 2007). In ular failure, this pump affords a chance for addition, the Heartmate II generates less recovery to transplant that an LVAD cannot. noise and has a smaller percutaneous lead Unfortunately, the portable mechanical driver than the Heartmate XVE. These features are 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 402

402 Chapter 19 Bridge to Transplant and Cardiac Transplantation Continuous flow (axial) 1.2 Antiplatelet therapy and heparin Temporary support and bridge to recovery Percutaneous placement by cardiology Patients must remain in bed with no mobility Partial support LVAD right ventricular assist Abiomed Pulsatile flow 1.2 Antiplatelet therapy and initial heparin followed by warfarin Temporary support and bridge to recovery Flexible design for biventricular support Cannot be discharged Extracorporeal design limits mobility LVAD, RVAD, or BiVAD Total Total left ventricular assist device; RVAD ϭ Pulsatile flow 1.7 Antiplatelet therapy and initial heparin followed by warfarin Bridge to transplant Biventricular support Large console limits mobility System not designed for hospital discharge Total orthotopic heart Pulsatile flow 1.5 Antiplatelet therapy and initial heparin followed by warfarin Bridge to transplant Three-year durability Large size limits application to small people LVAD left ventricular; LVAD ϭ Pulsatile flow 1.2 Antiplatelet therapy and initial heparin followed by warfarin Bridge to transplant Flexible design for biventricular support Large portable driver system impairs active lifestyle LVAD, RVAD, or BiVAD body surface area; LV ϭ Heartmate Artificial Continuous flow (axial) 1.3 Antiplatelet therapy and initial heparin followed by warfarin Destination and bridge to transplant Permits nontethered ambulation Approved for patient discharge Quiet operation Small percutaneous lead Fixed motor speed with risk of LV suction events LVAD biventricular assist device; BSA ϭ Heartmate II XVE Thoratec Novacor Heart (TAH) (AB 5000) TandemHeart Pulsatile flow 1.5 ASA only Destination and bridge to transplant Permits nontethered ambulation Approved for patient discharge No warfarin required Limited durability Large device LVAD aspirin; BiVAD ϭ ϭ ) 2 device. Type of blood flow BSA limitation (m ASA Anticoagulation Indications for use Positive aspects Negative aspects Support design Table 19–1Table Assist Devices Ventricular 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 403

Ventricular Assist Devices 403

appreciated by patients. The Heartmate II complications. The most common compli- pump requires anticoagulation with heparin/ cations are bleeding, hypovolemia, tampon- warfarin as well as antiplatelet therapy, so the ade, organ failure (e.g., kidney, liver), stroke, risk of postoperative bleeding is increased air embolism, need for inotropic support for when this device is used. RV failure, sepsis, driveline infection, and device failure (McCalmont & Ohler, 2008; Total Artificial Heart Piccione, 2000). Infusion of inotropes may A total artificial heart (TAH) is a treatment be required until the patient becomes hemo- alternative for patients with biventricular fail- dynamically stable following insertion of ure who are hospitalized candidates for heart the device (McCalmont & Ohler, 2008). transplant. An example of such a device is the Dobutamine at 3–5 mcg/kg/min or milri- SynCardia CardioWest. It replaces the func- none at 0.125–0.375 mcg/kg/min are com- tion of both ventricles and the four heart monly used in the postoperative period to valves. The CardioWest device is implanted in provide RV support. the patient’s chest and attached to the atria. Table 19–2 provides general infection con- Tubes from the CardioWest ventricles control guidelines for VADs. Bleeding in the tinue from the patient’s chest to a power-gen- immediate post-insertion period is common erating console. The TAH can deliver cardiac owing to the frequent use of aspirin and war- output (CO) as high as 9.5 L/min. It report- farin in HF patients preoperatively for edly augments renal and hepatic blood flow severely depressed LV function, coronary and improves survival of heart transplant artery disease, dysrhythmias, or any combina- patients with preoperative biventricular fail- tion of these conditions. ure (McCalmont & Ohler, 2008). Because LVAD function depends on adequate flow from the right ventricle, patients Postoperative Complications are monitored closely for signs of right heart VAD placement is a major surgical proce- failure. Pulmonary artery catheters (PACs) are dure with significant risk for postoperative inserted preoperatively for close monitoring

Table 19–2 General Infection Control Guidelines

Dressings over drive-line exit sites must be kept clean and dry at all times. Sterile dressing changes to the drive-line exit site must be performed at least daily. Dressing should be changed more frequently when increased drainage is observed. Immobilize the drive-line or exit cannulas with abdominal binders continuously. This prevents trauma to the exit site and helps to develop tissue ingrowth around the drive line, which promotes formation of a skin barrier. Trauma to exit sites significantly increases the risk of infection. Remove monitoring lines as soon as possible to decrease the risk of infection. Notify the physician of a change in the patient’s temperature (<36 °C [96.9 °F] or >38.5 °C [101.4 °F]) or other signs and symptoms of drive-line infection (e.g., redness, increase in drainage, foul odor, or skin separation from drive line). Ensure adequate nutrition (maintain albumin > 2.5 g/dL). This is essential for the healing process to occur.

Source: Adapted with permission from Kaplow & Hardin, 2007, p. 216. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 404

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of right-sided function (right atrial pressure, Table 19–3 Safety Precautions central venous pressure). at Discharge Nitric oxide (NO) has been shown to improve RV function by selective pulmonary Maintain a method to obtain a backup gener- vasodilation, which in turn improves LV fill- ator in case of power failure. ing, CO, and systemic arterial pressure (Idrees Notify the local electricity provider of the use et al., 2008). NO delivered postoperatively can of life support equipment. be continued until the chest is closed and RV Use a transport power base unit to and from stability is achieved (McCalmont & Ohler, the hospital. 2008). Avoid immersion in water (e.g., do not sit in a Respiratory therapy can help promote pul- tub of water). monary vasodilation by making ventilator Avoid static electricity (e.g., touching a com- adjustments that allow for permissive hyper- puter screen). carbia. Prevention of hypoxia is also impor- Never disconnect both batteries simultaneously. tant to avoid pulmonary vasoconstriction Protect the vent filter from water. (Hoskote et al., 2004). Cardiopulmonary resuscitation varies depen- The patient who has undergone LVAD ding on the model of LVAD used. placement is at risk for the development of Do not engage in excessive jumping or con- renal failure (Topkara et al., 2006). Baseline tact sports. renal dysfunction is common in the HF popu- Do not let children sit on the patient’s chest. lation, and renal function may transiently worsen in the postoperative period. Because No exposure to MRI is allowed. renal failure or severe renal insufficiency is Pregnancy is not permitted. generally a contraindication to heart trans- LVAD ϭ left ventricular assist device; MRI ϭ magnetic plant, care must be taken to minimize injury resonance imaging. to the kidneys in this patient population. Diligent intake and output surveillance and medication administration are necessary so that the kidneys can recover for the impend- of the device can be ensured through hand ing heart transplant. pumping, switching power sources, emer- Transient hepatic dysfunction due to con- gency interventions, or a combination of gestion associated with HF and intraoperative these. Extra batteries should always be avail- transfusions may occur. Supportive care able (Mason & Konicki, 2003). Table 19–3 including maintenance of appropriate fluid lists the safety precautions required of the balance is usually sufficient to correct this patient who is discharged to home with an problem (McBride et al., 2001). LVAD. Requirements for Being Discharged with an LVAD ■ HEART TRANSPLANTATION Patients who return home with an LVAD Although many patients can be supported require extra education to ensure the safety of with either medical management or a VAD, this therapy. A grounded, three-pronged plug another cohort of patients would benefit outlet near the patient’s sleeping site will be from receiving a heart transplant. As men- required for the patient to switch to the tioned previously, however, the number of power source during sleep. In the event of bat- potential transplant recipients far exceeds the tery or generator failure, ongoing functioning number of available donors. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 405

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There are two approaches to performing a progress and decision making. Heart failure heart transplant. With the orthotopic patients who have been bridged to transplant approach, the recipient’s heart is replaced with an LVAD may benefit from enhanced with a donor heart. With the heterotopic end-organ perfusion preoperatively and, approach, the recipient’s heart is left in place therefore, better tolerate the stress of the and the donor heart is “piggybacked” to the heart transplant procedure and its aftermath right side of the recipient’s heart. This latter (Goldstein, Smego, & Michler, 2006). approach is rarely used. Donor and harvest factors may also influ- Donor hearts are typically placed either with ence postoperative course. For example, the the Lower and Shumway method (the donor efficacy of the strategies utilized to maintain heart is anastomosed to the left atrium, right hemodynamic stability in the donor after atrium, pulmonary artery, and aorta), atrial brain death will affect the donor heart’s func- cuff technique (anastamoses are made at the tion (Poston & Griffith, 2004). inferior and superior vena cavae), or the het- Duration of the cold ischemia of the erotopic (end-to-end anastamoses of the donor donated heart will also be relevant to the superior vena cava, pulmonary artery, and recipient’s recovery. Cold ischemic time aorta). Regardless of which technique is refers to the amount of time from cross- employed, denervation of the donor heart clamping of the donor with subsequent results in a higher heart rate, orthostatic removal and immersion of the heart in iced hypotension, and the inability to experience saline until removal of the cross-clamp after angina in the transplant recipient. The patient it has been implanted into the patient has a median sternotomy incision and is (Anderson, 2008a). The maximum cold placed on CPB during the transplant proce- ischemic time is 6 hours, and preferably dure (Wade, Reith, Sikora, & Augustine, 2004). should be less than 4 hours. Younger organs Once the transplant procedure is com- tolerate relatively longer ischemic times; pleted, pacing wires are secured. The patient older organs tolerate shorter ischemic times may require inotropic support to be removed (Russo et al., 2007). from CPB. If the patient has elevated pul- The surgical technique used may also influ- monary artery pressures, nitric oxide may be ence the patient’s outcome. For example, the used to decrease PVR. The patient’s systemic bicaval technique (attachment of the donor vascular resistance will not be affected by the heart with anastamoses in the superior and use of NO; hypotension should not ensue. inferior vena cavae) has been found to Once the patient is successfully removed from improve patient survival, atrial geometry CPB and the donor heart is functioning, the (non-fluoroscopic imaging system), and patient is transferred to the ICU for recovery hemodynamics as well as to decrease valvular (Wade et al., 2004). insufficiency, dysrhythmias, pacing requirements, vasopressor requirements and hospital ■ CARE IN THE IMMEDIATE stay when compared with biatrial technique (attachment of donated heart to recipient POSTOPERATIVE PERIOD atrial “cuffs”) (Morgan & Edwards, 2005). Factors Influencing Patient Recovery Patients who receive transplants via the After the transplantation procedure is com- bicaval technique are less likely to develop plete, the heart recipient’s postoperative care mitral or tricuspid regurgitation, atrial and course will vary depending on many fac- thrombus, or tachydysrhythmias because tors. Comorbidities such as renal or pul- atrial anatomy is maintained with this tech- monary dysfunction will affect both patient nique (Wade et al., 2004). 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 406

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Postoperative Care to permit visualization of accumulating Once admitted to the ICU, heart transplant blood and rapid mediastinal exploration, patients typically remain on mechanical venti- should it be required. lation for 12–48 hours and remain in the ICU The ICU nurse should observe the patient for 2–3 days. The overall reported ICU mor- for tachycardia, chest tube drainage greater tality is less than 5% in this population. The than 100 mL/hr, cardiac index less than 2 most common morbidities (and their inci- 3 L/min/m , falling hemoglobin and hemat- dence) are infection, especially pulmonary ocrit levels, decreased mixed venous saturation (10%); pulmonary hypertension with right (SvO2), and increasing oxygen requirements. heart dysfunction (10%); nodal dysrhythmias Results of coagulation profiles and platelet (5%); bleeding (24%); hyperacute rejection count should be evaluated as well. Hypoten- (less than 1%); and pain (8–10%) (Jaffe & sion and decreasing pulmonary artery and Samuels, 2003; Wade et al., 2004). central venous pressures are late signs of The immediate postoperative period can be bleeding. If the patient is to be transfused with quite challenging for both patients and blood or blood products, cytomegalovirus nurses. While the immediate postoperative (CMV)-negative patients must receive CMV- recovery after a heart transplant generally negative products (Wade et al., 2004). progresses without complication, patients Strategies employed for bleeding are the may demonstrate high levels of vulnerability same as those used in other cardiac surgery and low levels of stability. Clinical issues and patients. These interventions include aggressive implications specific to the recovery from transfusion of blood products (e.g., fresh frozen anesthesia and CPB are discussed in detail in plasma, cryoprecipitate) as indicated; use of Chapter 8. Hemodynamic monitoring and plasminogen inhibitors (e.g., aminocaproic acid ® care for the patient on mechanical ventila- [Amicar ]) and factor VII; administration of tion, including weaning and extubation, are additional protamine sulfate, desmopressin ® ® described in Chapters 9 and 11, respectively. (DDAVP ), or aprotinin (Trasylol ); and early Early weaning and extubation is the goal for reexploration (Wade et al., 2004). all heart transplant patients (Wade et al., 2004). Postoperative complications related to Hypovolemia CPB are discussed in detail in Chapter 13; Post-transplant hypovolemia has the same those specific to heart transplantation are dis- etiology in heart transplant recipients as it cussed next. does in other cardiac surgery patients who have undergone CPB. CPB causes increased Bleeding capillary permeability, with resultant third Postoperative bleeding is a common problem spacing of fluid. Intraoperative use of diuret- in all cardiac surgery patients, including those ics and initial high post-CPB urinary output who have undergone heart transplant. Post- further contribute to the postoperative heart operative bleeding may be related to transplant patient’s hypovolemic state. Hypo- hypothermia, administration of heparin for volemia, in turn, results in a decrease in pre- CPB, preexisting hepatic dysfunction from load and cardiac function (Wade et al., 2004). HF and associated low CO, surgical-site tissue The ICU nurse must observe heart trans- trauma, and platelet destruction from CPB plant recipients for hypotension; decreased pul- (Wade et al., 2004). For this reason, the ster- monary artery, pulmonary artery occlusive, and notomy wound is often left open, covered central venous pressures; decreased urinary out- with a sterile, occlusive, transparent dressing put; and decreased cardiac output/index. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 407

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Hematocrit levels may be elevated as a conse- Hypertension quence of hemoconcentration. Patients may Prevention and prompt detection and man- manifest hypotension more so than might be agement of hypertension following heart expected after receiving narcotics or sedation transplantation are essential to prevent surgi- (Wade et al., 2004). cal site dehiscence. Administration of nitro- Treatment of hypovolemia focuses on vol- prusside may be indicated (Wade et al., 2004). ume repletion. This goal may be accomplished through administration of either a Pulmonary Hypertension crystalloid or a colloid, depending on facility Pre-emptive protective maneuvers are fre- protocol. As discussed in Chapter 17, the quently successful in avoiding right heart fail- debate over the efficacy of crystalloid versus ure. Pulmonary artery catheters are placed in colloid therapy continues. The ICU nurse all heart transplant patients. NO is frequently must carefully monitor the patient’s vital utilized to selectively dilate the pulmonary signs, urinary output, and hemodynamic pro- vasculature without decreasing systemic file both during and following volume resus- blood pressure (Wolfgang, Bauer, & Podesser, citation. Development of fluid overload can 2006); its administration has been shown to cause dilation of the right ventricle and pul- decrease the incidence of RV dysfunction in monary edema, which can be life-threatening patients with pulmonary hypertension (Arde- (Cohn, 1997; Wade et al., 2004). Fluid resusci- hali, Laks, et al., 2001). Other agents that tation is discussed in detail in Chapter 17. dilate the pulmonary vasculature (e.g., nitroglycerin [Tridil®], sodium nitroprusside Right Heart Failure [Nipride®], prostaglandin E-1 [PGE1], and Right heart failure is a major cause of morbid- prostacyclin [PGH2]) may cause hypotension ity and mortality in the post-heart transplant and, therefore, are used less often in post- period. The left ventricle is generally able to heart transplant patients. tolerate increased afterload (the amount of Patients are generally weaned from NO on work the heart must do to eject blood). How- the first postoperative day or later, depending ever, the implanted right ventricle is not physi- on the overall clinical picture and their degree ologically adapted to overcome high afterload of hemodynamic stability. NO has a very as would be encountered with pulmonary short half-life, and patients are weaned from it hypertension, which develops frequently in very slowly (over hours). Rebound pulmonary HF patients. Opposed by high pulmonary hypertension and acute RV dysfunction are pressures or pulmonary vascular resistance, likely if use of NO is abruptly discontinued or the implanted right ventricle dilates readily weaning proceeds too quickly. Acidosis, hyper- and fails. This chain of events is difficult to carbia, and hypoxemia increase pulmonary reverse once it begins. Further, right heart vascular resistance. Patients are, therefore, dilation alters septal position and function, hyperventilated to achieve a pH in the range of

which in turn interferes with LV function 7.45–7.49 and a pCO2 in the range of 30–35 (Stobierska-Dzierzek & Brook, 2001). High mm Hg. Hypoxemia must be avoided (Arde- preoperative pulmonary artery pressure (PAP) hali, Hughes, et al., 2001). may predict increased risk for development of this syndrome; however, normal PAP does not Chronotropy (Rate) Issues preclude it. Right heart failure is characterized Tachycardia, which decreases ventricular fill- by an elevated central venous pressure, edema, ing time and hence the risk of RV dilation, is and hepatomegaly (Taegtmeyer, 2006). achieved with an atrial pacer set to the AAI 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 408

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mode (atria paced, atria sensed, inhibited) pressure greater than 65 mm Hg. Vasopressin and a rate of 100–120 beats per minute via is thought to cause less constriction of the epicardial pacing wires. The AAI mode is pulmonary vasculature, is associated with selected because transplanted hearts generally lower arrhythmogenicity, and increases have intact conduction systems (unlike in glomerular filtration rate. For these reasons, valve surgery patients, who are susceptible to it is used preferentially either alone or with temporary heart blocks). Utilization of the norepinephrine (Kee, 2003). heart’s intrinsic conduction system promotes ventricular synchrony, which stabilizes the Allograft Dysfunction septum in a manner that facilitates LV and Post-transplant cardiac function depends on RV function. Tachycardia is also achieved a number of factors, including donor and har- pharmacologically with isoproterenol vest factors, cold ischemic time, surgical tech- (Isuprel®), which also dilates pulmonary vas- nique, condition of the donor heart, and culature; dobutamine; and dopamine. preservation techniques (McGiffin, Kirklin, Naftel, & Bourge, 1997; Morgan & Edwards, Contractility (Inotropy, Force 2005; Poston & Griffith, 2004; Russo et al., of Contractions) Issues 2007; Wade et al., 2004). Poor cardiac func- Inotropic agents such as dopamine, dobuta- tion is an early cause of allograft failure mine, and milrinone are used to support RV (Anderson, 2008a). and LV function. Milrinone is frequently LV systolic dysfunction is categorized as given at a dose of 0.125–0.375 mcg/kg/min either early or late. Early LV dysfunction and has the added benefit of promoting pul- occurs either intraoperatively or in the imme- monary vascular dilation. If these pharmaco- diate postoperative period. Late LV dysfunc- logical interventions (which are described in tion develops weeks to years following a heart detail in Chapter 12) are not successful in pre- transplant. The most common cause of both venting or ameliorating right heart failure, early and late LV dysfunction is allograft insertion of an intra-aortic balloon pump (see rejection. If LV dysfunction develops within Chapter 10) or right ventricular assist device days of the transplant, it typically occurs sec- may be necessary. ondary to one of three etiologies: hyperacute rejection, reperfusion injury, or a suboptimal Hypotension donor heart (Anderson, 2008a). As in other cardiac surgery populations, blood pressure variability is common in patients REPERFUSION INJURY DURING SURGERY who have received heart transplants. Hypoten- Allograft dysfunction may be caused by reper- sion decreases coronary artery perfusion, fusion ischemia, prolonged cold ischemic which is undesirable in all cardiac surgery time (greater than 5 hours), or both. This con- patients and may contribute to right heart dition may be only a temporary complication failure in the heart transplant patient. Treat- (myocardial stunning), and resolve after 12 to ment is directed at the underlying mechanism. 24 hours after heart transplant. The heart Vasodilation may be exacerbated by med- does sustain ischemic injury when such dys- ications such as milrinone. Decreasing the function occurs, despite the short duration dose of vasodilator medications, if feasible, (Anderson, 2008a). may mitigate hypotension. Vasopressors such as norepinephrine (Levophed®) and vaso- SUBOPTIMAL DONOR HEART pressin (antidiuretic hormone [ADH]) are As is well known, the number of heart trans- often required to maintain a mean arterial plant candidates far exceeds the number of 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 409

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donor hearts available. Consequently, some donor heart may not be accustomed to pump- transplant programs have been accepting ing against such a high pulmonary artery “suboptimal” donors (e.g., patients older than pressure. Management of pulmonary hyper- 63 years of age, hearts with mild left ventricu- tension may include administration of a lar hypertrophy). These hearts have typically vasodilator (e.g., nitroglycerin) with an been treated with higher doses of inotropic inotrope (e.g., dobutamine or milrinone). If agents or vasopressors or have LV dysfunction the patient’s pulmonary artery systolic pres- (Anderson, 2008a). sure exceeds 50 mm Hg, administration of

LV systolic dysfunction is treated with intravenous prostaglandin E1 and prostacy- inotropic support and appropriate fluid clin may be considered (Wade et al., 2004). administration. Dopamine, dobutamine, or Inhaled nitric oxide is another agent that may milrinone may be used to increase CO with- be used to decrease pulmonary vascular resist- out associated increases in systemic vascular ance without diminishing SVR (Kieler-Jenson, resistance (SVR). Each of these inotropic Lundin, & Ricksten, 1995; Wade et al., 2004). agents is discussed in detail in Chapter 12. IABP therapy may be initiated if high doses of Rhythm Disturbance and inotropes are required to maintain LV func- Electrocardiograph Changes tion; IABP therapy is discussed in detail in Development of cardiac dysrhythmias is com- Chapter 10. Monitoring of the patient’s vital mon following heart transplant. For patients signs and hemodynamic profile is essential who undergo transplants, the likelihood of while any of these therapies is being used such abnormalities in heart rhythm is higher (Wade et al., 2004). in the immediate postoperative period. Such If the patient’s SVR is elevated, an associ- dysrhythmias may result from surgical ated decrease in CO may ensue. An elevated trauma to the sinoatrial (SA) and atrioventric- SVR may be managed with administration of ular (AV) nodes, ischemia, suture lines, rejec- a vasodilator such as nitroglycerin or nitro- tion, and transplant vasculopathy (TV) prusside. (Rothman & Eisen, 2008). On rare occasions, a patient’s SVR may be low following heart transplant. This condition BRADYCARDIA is believed to be related to use of angiotensin- Bradycardia may occur in the immediate converting enzyme (ACE) inhibitors for heart postoperative period. This complication failure, release of proinflammatory mediators affects as many as 50% of orthotopic heart as occurs with CPB, or decreased levels of transplant patients, typically taking the form vasopressin. Low SVR may be treated with a of SA node dysfunction. SA node dysfunction vasopressor such as norepinephrine or epi- occurs as a result of ischemia, intraoperative nephrine (Adrenaline®). If neither of these manipulation of the SA node, perinodal medications is effective in reversing the deficit, atrial tissue, SA artery trauma, or pretrans- vasopressin may be given (Landry et al., 1997; plant use of amiodarone (Cordarone®) (Roth- Wade et al., 2004). All of these agents are dis- man & Eisen, 2008). Whereas bradycardia cussed in detail in Chapter 12. immediately following surgery has little RV dysfunction following heart transplan- prognostic significance, late-onset bradycar- tation is likely due to pulmonary hyperten- dia may be an indicator of organ rejection or sion and can be difficult to manage. Patients TV (Rothman & Eisen, 2008). with HF have chronic high left atrial pressure. Atropine sulfate is not effective in denerva- Following the transplant, pulmonary hyper- tion of the sympathetic and parasympathetic tension and RV failure can occur because the nerves. Bradycardia may be treated with 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 410

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administration of a beta1-receptor agonist dose reduction of inciting medications as (e.g., dobutamine or isoproterenol). It has appropriate. also been suggested that administration of Treatment of atrial dysrhythmias is dis- theophylline or terbutaline (Brethine®) may cussed in detail in Chapter 15. Of note, increase heart rate in heart transplant patients digoxin (Lanoxin®) is not effective in the den- who develop bradycardia (Rothman & Eisen, ervated heart. Caution should be exercised 2008; Wade et al., 2004). when treating atrial dysrhythmias with beta Clinically significant bradycardia will typi- blockers or calcium channel blockers (Wade cally be treated with epicardial pacing. Dual- et al., 2004). Radiofrequency ablation has chamber pacing is preferred so that the been used to treat atrial flutter in heart trans- patient’s cardiac output can be augmented plant patients (Rothman & Eisen, 2008). from the atrial kick (Rothman & Eisen, 2008; Stecker, Strelich, Chugh, Crispell, & Mc- SUPRAVENTRICULAR TACHYCARDIA Anulty, 2005; Wade et al., 2004). Types of supraventricular dysrhythmias that have been reported in orthotopic transplant ATRIAL DYSRHYTHMIAS patients include AV reentrant tachycardia, The incidence of atrial fibrillation (AF) in Wolff-Parkinson-White syndrome, and non- heart transplant patients ranges from 0.33% paroxysmal atrial tachycardia (Rothman & to 24% (Ahmari et al., 2006; Khan et al., 2006; Eisen, 2008). The incidence of supraventricu- Rothman & Eisen, 2008). AF usually occurs lar tachycardia (SVT) is reported to be within the first 2 postoperative weeks; later approximately 1.3% (Khan et al., 2006). SVT development is associated with higher mor- has been treated successfully with radiofre- tality rates (Rothman & Eisen, 2008). It has quency ablation (Rothman & Eisen, 2008). been suggested that AF is attributable to surgical insult in this patient population (Cui, VENTRICULAR DYSRHYTHMIAS Tung, Kobashigawa, Laks, & Sen, 2001; Khan Premature ventricular contractions may occur et al., 2006). in as many as 100% of orthotopic heart trans- The incidence of atrial flutter ranges from plant patients early in the postoperative 2.8% to 15% in heart transplant recipients period. The incidence decreases over time, (Ahmari et al., 2006; Khan et al., 2006; Roth- however (Rothman & Eisen, 2008). man & Eisen, 2008). Atrial flutter usually Paroxysmal ventricular tachycardia (VT) develops late in a patient’s post-transplant decreases in incidence after the initial postop- course (Rothman & Eisen, 2008). It is believed erative period. There may be a correlation to result from rejection, which causes between VT, rejection, and TV (Rothman & increased cardiac fibrosis (Cui et al., 2001; Eisen, 2008). Non-paroxysmal ventricular Khan et al., 2006), but may occur if rejection dysrhythmias are rare in the postoperative has not occurred (Rothman & Eisen, 2008). heart transplant patient. Development is usu- Rejection-associated atrial flutter may be ally related to severe TV or allograft rejection caused by impairment in atrial conduction (Rothman & Eisen, 2008). and refractoriness, alteration in atrial hemodynamics, and decreased ventricular function, CONDUCTION DELAYS all of which occur with rejection (Rothman & Right bundle branch block (RBBB) is a com- Eisen, 2008). mon ECG finding post-transplant, but has no Atrial dysrhythmias may be ameliorated by clinical or prognostic significance (Golshayan maintenance of normal electrolytes (potas- et al., 1998). This condition may be encoun- sium > 4 mEq/L, magnesium > 2 mg/dL) and tered in as many as 70% of orthotopic trans- 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 411

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plant patients (Rothman & Eisen, 2008). 2004). The required equipment and nursing Development of a RBBB may be associated care for the latter procedure are discussed in with prolonged donor ischemic time and sev- Chapter 13. eral rejection episodes. Etiologic factors may include RV hypertrophy from elevated pul- Renal Dysfunction monary artery pressures or right bundle dam- In the immediate post-transplant period and age during endomyocardial biopsy procedures following CPB, the patient’s urinary output (Rothman & Eisen, 2008). will be increased. Once these effects have worn AV node function remains intact following off, it is important that urinary output be a heart transplant. As a consequence, high- maintained at a rate of at least 0.5 mL/kg/hr. degree AV block is rare in post-transplant Renal function requires preservation because patients, especially in the early postoperative of the nephrotoxic immunosuppression period. Late development carries an increased agents that will be administered to prevent mortality rate (Rothman & Eisen, 2008). rejection of the donated heart. The ICU nurse must maintain adequate renal perfusion with Cardiac Tamponade Cardiac tamponade may develop either grad- Table 19–4 Signs and Symptoms ually or suddenly in patients who have under- of Cardiac Tamponade gone heart transplantation. It results from fluid accumulating in the pericardial sac, Sudden decrease or cessation of chest tube which causes compression of the atria, restric- drainage tion of venous return to the heart and ventric- Dyspnea ular filling, and results in a decrease or Low cardiac output with hypotension cessation of preload and a potential precipitous decline in CO (Massé & Antonacci, Narrowing pulse pressure 2005). Early tamponade may also result from Inappropriately fluctuating mean arterial persistent mediastinal bleeding not being pressure evacuated by chest tubes or clot formation. Increased central venous pressure The diagnosis of cardiac tamponade may be Low cardiac output/index difficult in heart transplant recipients because Sudden oliguria hypotension and tachycardia are common sce- Altered mental status narios in the immediate postoperative period. Diaphoresis When caring for these patients, the ICU nurse Dysrhythmias, including tachycardia should maintain patency of chest tubes, moni- Cyanosis or pallor tor vital signs and hemodynamic profiles, and observe for signs and symptoms including Anxiety those listed in Table 19–4. Restlessness If cardiac tamponade develops, initial man- Low-voltage QRS on ECG agement should include volume resuscitation Electrical alternans on ECG to optimize filling pressures (being careful “Water bottle heart” and cardiac enlarge- not to overload the right ventricle), and initia- ment on chest radiograph tion and titration of inotropes (if blood pres- Hepatomegaly sure is not responsive to fluid resuscitation). Sources: Kaplow & Reid, 2006; St. Andre & DelRossi, Diagnosis is made by echocardiogram. Defini- 2005; Talmor & Lisbon, 2005; Wade, Reith, Sikora, & tive treatment entails surgical intervention or Augustine, 2004. emergent bedside sternotomy (Wade et al., 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 412

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fluids, vasoactive agents, or combinations of intubated, a continuous infusion of either these to maintain a mean arterial pressure in morphine or fentanyl is typically adminis- the range of 60–80 mm Hg. Monitoring of tered. The narcotic should be titrated so that hourly urinary output and all renal function the patient is easily arousable to verbal stimuli tests should be performed by the ICU nurse as and able to follow simple commands. Once well (Wade et al., 2004). the patient has been extubated, use of acetaminophen and oral narcotics (e.g., oxycodone) Psychosocial Conditions is preferred. Nonsteroidal anti-inflammatory In addition to all of the physiologic stressors drugs (NSAIDs) are avoided given the com- associated with heart transplantation, a vari- pounded risk of nephrotoxicity when these ety of psychosocial conditions may surface in medications are utilized in conjunction with the postoperative period. Patients are typi- CNIs (e.g., tacrolimus [Prograf®], cyclosporine cally and predictably euphoric and relieved [CsA, Sandimmune®]) to prevent rejection that they were recipients of a long-awaited (Wade et al., 2004). organ. However, depression, anxiety, confusion, and delirium may develop in a few post- Nutrition operative days. It is common for the patient to inquire about the donor and to experience A clear liquid diet is initiated at the time of difficulty coping with the knowledge that a extubation and advanced as tolerated. death was associated with the organ procure- Because many heart transplant recipients are ment. Patients may manifest violent out- malnourished preoperatively with little nutri- bursts, attempt to climb out of bed, tional reserve, caloric intake is followed inappropriately yell at staff, or have halluci- closely and enteral feeding is initiated readily nations. Maintaining patient safety during for patients who are not meeting caloric this time is essential (Wade et al., 2004). The requirements. All transplant patients are fol- etiology and specific management of these lowed by a registered dietitian. neurocognitive disorders are discussed in detail in Chapter 16. Maintaining a calm, Activity reassuring environment and demonstrating a Coughing, deep breathing, and early ambula- high level of caring practices are essential for tion are important in heart transplant recipi- optimal psychological patient outcomes. ents, as in all postoperative patients. Physical and occupational therapy services are con- ■ PROGRESSION OF CARE sulted for all transplant patients, and a pro- Transfer to a progressive care unit occurs gram of progressive activity is undertaken as when the patient is extubated, hemodynami- soon the patient’s status permits. Patients are cally stable, and no longer receiving any encouraged to assume gradually increasing vasoactive medications. The expectation responsibility for their self-care needs. throughout the hospitalization period and beyond is that patients will participate Rejection actively and fully in their own recovery. Rejection occurs when T cells recognize the implanted heart tissue as foreign and mount Pain Management an immune response targeted at eliminating Transplant patients’ requirements for pain it. The immune response leads to inflamma- medications vary. Back, shoulder, and chest tion, cell damage, and death. If left unchecked, discomfort are common. While the patient is progressive decline in organ function ensues. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 413

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Three types of rejection are distinguished: immunosuppression, which is usually accom- hyperacute, acute, and chronic. Hyperacute plished with a steroid pulse or OKT3 (Linden- rejection is rare, but is caused by an feld et al., 2004a). antigen–antibody reaction. It may occur Rejection is prevented by ongoing adminis- within minutes to hours after a transplant tration of immunosuppressive agents. Proto- and is often fatal. Acute rejection occurs when cols for immunosuppression are facility surface cell antigens of the donor heart are specific. The components of standard recognized as being “non-self.” This type of immunosuppression are a corticosteroid, a rejection usually occurs within the first few CNI, and an antiproliferative agent. Some weeks after a transplant, but may occur years facilities may also prefer induction therapy later. Chronic rejection is manifested by accel- with antilymphocyte antibody for the first erated graft vasculopathy and typically does few weeks following a transplant, reflecting not occur within the first year of a transplant the increased risk of acute rejection during (Anderson, 2008a; Wade et al., 2004). this time (Wade et al., 2004). Despite use of immunosuppressive medica- The treatment of rejection depends on the tions, rejection is a relatively common occur- histologic grade and the clinical situation. rence. In one study, 35–45% of recipients had Mild rejections (grade 1A, grade 1B, or low at least one episode of acute rejection in the grade 2) are treated by optimizing the first year after transplant. Rejection rates were immunosuppression regimen in current use. higher in those receiving CsA plus mycophe- Moderate rejections (advanced grade 2, grade nolate mofetil (MMF) than tacrolimus plus 3A, and low grade 3B) are usually treated with MMF. Rates of rejection were higher in augmented immunosuppression. Severe rejec- women than in men, and decreased with tion (grade 4) is typically treated by administer- advancing recipient age (Taylor et al., 2007). ing high doses of intravenous corticosteroids, Risk factors for rejection include previous anti-3 globulin (ATG), or polyclonal antibodies episodes of rejection, young patient age, (e.g., OKT3) and by optimizing the initial female gender, female donor, positive CMV immunosuppression regimen (Taylor, 2007). serology, prior infections, OKT3 induction, and hemodynamic compromise (Kubo et al., 1995; Michaels et al., 2003). Immunosuppression Patients experiencing rejection may be The term “immunosuppression” is used in asymptomatic, or they may demonstrate dys- the organ transplant setting to describe meth- rhythmias, a ventricular gallop, or increased ods by which the transplant recipient’s central venous pressure (Snell, Randolph, & immune system is prevented from “attacking” Artig-Brown, 2007). A myocardial biopsy is the newly implanted organ. Given that rejec- needed for definitive diagnosis. Complica- tion is mediated almost entirely by T cells, tions of myocardial biopsy include pneu- with B cells playing a lesser role, immunosup- mothorax, cardiac perforation, and tricuspid pressants target T-cell function in a variety of valve injury. Surveillance biopsies are ways (Oka & Yoshimura, 1996). obtained weekly for the first month after Immunosuppression regimens generally transplant, every 2 weeks for the second and consist of two phases—induction and third months, monthly through the ninth maintenance—with intensification of treat- month, at the one-year anniversary, and then ment or addition of new agents for episodes every 6 months. Biopsies are obtained more of rejection. The particular strategy employed frequently if episodes of rejection occur. varies by surgeon preference, facility practice, Rejection is treated with an intensification of and patient factors, but is uniformly initiated 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 414

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at the time of transplant. A discussion of the gen (something “other than self,” such as most commonly used immunosuppressant transplanted heart tissue). Clonal expansion medications follows. of that specific T cell then ensues as the body attempts to eradicate the foreign substance. Corticosteroids The signaling process that initiates replication Corticosteroids (e.g., methylprednisolone of this cell is mediated by cellular calcineurin [Medrol®]) are useful in all phases of immuno- and extracellular interleukin 2 (IL-2). CNIs suppression (induction, maintenance, and block this pathway, thereby inhibiting clonal management of acute rejection), as these expansion of T cells. This type of immunosup- agents suppress nearly all mechanisms of pression is highly effective, but significant immunity. Corticosteroids act directly on cell toxicities—most notably nephrotoxicity—limit DNA to influence transcriptional regulation, their use in the post-transplant setting. Other which alters the expression of genes involved significant toxicities include new-onset dia- in immune and inflammatory responses (Lin- betes mellitus, hyperkalemia, hypomagne- denfeld et al., 2004b). Through this mecha- semia, and dyslipidemia. The incidence of nism, corticosteroids affect the number and hypertension and hyperlipidemia is reportedly distribution of leukocytes, their ability to sig- lower with tacrolimus than with CsA; a higher nal other immune cells, and their functional incidence of diabetes is noted with tacrolimus, ability (e.g., decreased phagocytosis, inhibition however (Wade et al., 2004). of secretion of inflammatory substances) Because a significant proportion of heart (Smith, 2002). transplant patients have baseline renal dys- Short-term use of these drugs is associated function (and possibly additional insult fol- with hyperglycemia and lability of mood; oth- lowing CPB), CNIs are more often included in erwise, corticosteroids are generally well toler- maintenance therapy rather than being used as ated. Long-term use is associated with induction therapy. The nurse should monitor multiple toxicities, including osteoporosis, renal function tests and intake and output. chronic adrenal suppression, infection, fluid Levels (troughs) are followed daily until stable, and sodium retention, cataract formation, and then periodically. Because CNIs are metab- peptic ulcer development, and cosmetic olized by the cytochrome P450 3A enzyme sys- effects. Side effects that are detrimental to car- tem, drug interactions are common and can diovascular health include hypertension, dys- significantly alter drug levels. Ketoconazole, lipidemia, and diabetes. For this reason, diltiazem, fluconazole, erythromycin, and itra- research related to immunosuppression in conazole may increase CNI levels; isoniazid, heart transplant recipients has focused on reg- phenobarbital, phenytoin, and rifampin may imens that minimize corticosteroid exposure decrease CNI levels (Kobashigawa, 1999; Wade (Smith, 2002). Administration of a prophylac- et al., 2004).

tic H2 blocker may prevent gastrointestinal bleeding. Patients should have bedside blood Monoclonal Antibodies glucose testing at least every 6 hours to moni- Muromonab-CD3 (OKT3) is a murine tor for hyperglycemia (Wade et al., 2004). (mouse-derived) monoclonal antibody targeted at a specific “marker” on the surface of Calcineurin Inhibitors T cells that (1) transiently activates and elimi- The CNI category of anti-rejection agents nates nearly all T cells from peripheral circula- includes tacrolimus and CsA. These drugs pre- tion, and (2) renders remaining or subsequent vent T-cell proliferation. Specifically, a T cell T cells incapable of activation (Smith, 2002). becomes activated when it encounters an anti- OKT3 may be used as induction therapy, par- 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 415

Progression of Care 415

ticularly in patients with renal dysfunction rienced a higher incidence of antibody-medi- who would not tolerate CNIs. It is adminis- ated rejection. As a result, OKT3 has been tered intravenously during the first 14 post- replaced by other agents for early rejection transplant days (Wade et al., 2004). Response prophylaxis in many centers. to therapy can be assessed by measurement of Daclizumab (Zenapax®) and basiliximab CD3-expressing lymphocytes. (Simulect®) are other monoclonal antibodies Because OKT3 initially activates T cells used to suppress the immune system. These through binding of the monoclonal antibody two agents target only the IL-2 receptor; as a with the CD3 surface protein, side effects are consequence, they inhibit only activated those associated with cytokine release. These T cells, rather than all T cells. IL-2 receptor side effects may range from common, minor antagonists (IL-2Ras) are being used to a flu-type symptoms (e.g., fever, chills, and greater extent for induction therapy. These minor pulmonary or gastrointestinal [GI] monoclonal antibodies are also administered symptoms) to life-threatening symptoms for the first 14 days post-transplant (Wade et (e.g., bronchospasm, tachycardia, bradycardia, al., 2004). encephalopathy, seizures, renal insufficiency, In a comparison of basiliximab and OKT3 and graft thrombosis). Symptoms from a as induction agents after heart transplant, “first dose response” are termed cytokine researchers found that both agents had simi- release syndrome and include decreased lar efficacy. However, basiliximab was associ- myocardial contractility, hypotension, coro- ated with shorter ICU length of stay nary vasospasm, increased capillary perme- post-transplant (Vaqueriza et al., 2006). ability, chest pain, alterations in bronchial In another comparison study, heart trans- and GI smooth muscle control, dyspnea, plant patients received MMF, CsA, and pred- wheezing, myalgias, arthralgias, headache, nisone with or without basiliximab. In this and weakness. A life-threatening infection study, survival and renal function were not (especially CMV), and Epstein-Barr virus affected by the addition of basiliximab. The (EBV)-related lymphoproliferative disorder 1- and 3-year rates of acute rejection, however, may also develop in some patients (Sayegh, were improved with basiliximab therapy 2008; Sevmis et al., 2005; Smith, 2002). (Rosenbaum et al., 2006). OKT3 significantly decreases the patient’s More recently, a systematic review of clini- lymphocyte count, so there is an increased risk cal trials evaluating IL-2Ras failed to demon- of lymphoma and vascular rejection when this strate that these agents are effective in medication is given to heart transplant improving survival of heart transplant patients (Wade et al., 2004). Interestingly, the patients or in decreasing the incidence of car- 22nd report of the Registry of the Interna- diac allograft rejection. The authors of this tional Society for Heart and Lung Transplan- meta-analysis concluded that use of these tation reported that patients who received agents remains uncorroborated (Møller, OKT3 as part of an induction regimen had Gustafsson, Gluud, & Steinbrüchel, 2008). higher rejection rates during the first year ® after transplant than both patients who Mycophenolate Mofetil (Cellcept ) received polyclonal antibody or IL-2 induction MMF is an antiproliferative agent that and patients who received no antibody induc- inhibits an enzyme that is necessary for DNA tion (Taylor et al., 2005). These data were later synthesis. All cells other than B cells and corroborated by Stehlik and colleagues (2006), T cells can use alternative pathways that do who reported that heart transplant patients not require this enzyme for DNA production; who received OKT3 for more than 7 days expe- consequently, they are not affected by the 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 416

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drug. MMF is used concomitantly with CNIs, group at the 3-month mark. The 1-year sur- corticosteroids, or both. Side effects are largely vivors who received MMF were less likely to gastrointestinal in nature, although leukope- develop rejection, experienced fewer cases of nia may occur as well (Meiser et al., 1999). steroid-resistant rejection requiring cytolytic therapy, and had more patients weaned off ® Azatriaprine (Imuran ) steroids by 1 year. Renal function was better Azatriaprine (AZA) is another antiprolifera- for the MMF-treated group; they had higher tive agent that may be used to prevent rejec- creatinine clearance and lower serum creati- tion following a heart transplant. A large nine levels (Hamour, Lyster, Burke, Rose, & randomized comparative study was con- Banner, 2006). ducted between MMF and AZA. Data from Regardless of which antiproliferative agent this study initially revealed no differences in is used, the nurse should monitor complete terms of rejection prevention. However, 72 blood counts to evaluate for presence of asso- patients in the study were unable to take oral ciated myelosuppression (Wade et al., 2004). medications (MMF was not available in intravenous form at the time); 75% of these patients Polyclonal Antibodies had not previously received any study drug and Polyclonal antibodies used for immunosup- were given AZA. These 72 patients had a high pression in heart transplant patients include (56%) mortality or retransplant rate. The thymoglobulin (Sangstat®; rabbit ATG) and MMF-treated group had an 11% reduction in lymphocyte immune globulin (Atgam®; ATG, treated rejection episodes and a 34% reduction antithymocyte globulin [horse]). Whereas in biopsy-proven rejection associated with OKT3 is a monoclonal antibody directed at a hemodynamic compromise. In addition, the specific protein found on T cells, thymoglobu- MMF-treated group had a statistically lower lin contains antibodies that bind with multi- 12-month post-transplant mortality rate (6.2% ple T-cell antigens. It is produced by collecting versus 11.4%). Further, during the first 12 and purifying the sera from rabbits or horses months post-transplant, among the remaining that have produced antithymocyte antibodies 578 patients enrolled in the study, there were in response to immunization with human thy- no deaths in the MMF-treated patients as com- mocytes. Proposed mechanisms of action pared to 12 deaths (32%) in the AZA-treated include depletion of circulating T cells, modu- patients. Hemodynamic compromise was expe- lation of cell surface receptor molecules, and rienced by both groups of patients. The induction of apoptosis (programmed cell researchers concluded that MMF was more death) of activated T cells (Smith, 2002). It has effective in preventing and successfully treat- been suggested that these polyclonal antibod- ing rejection. The patients receiving MMF ies’ lymphocytotoxicity may also have a role in experienced more diarrhea, esophagitis, and preventing organ rejection. Both thymoglobu- opportunistic infections than did the AZA- lin and lymphocyte immune globulin are treated patients; the AZA-treated patients expe- administered for the first 14 days post- rienced more leukopenia than the MMF transplant (Wade et al., 2004). recipients (Kobashigawa et al., 1998). Side effects unique to thymoglobulin In a more recent study, heart transplant include anti-antibody reactions that can render patients received induction therapy with rab- the drug ineffective; serum sickness, which bit ATG followed by steroids, CsA, and either results from anti-antibody–drug complexes; MMF or AZA. One-year survival rates and and increased risk of malignancy, possibly LVEF were similar for the two groups. How- related to profound inhibition of T cells ever, CsA levels were lower in the MMF-treated (Smith, 2002). Patients are also at risk for ana- 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 417

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phylaxis; acetaminophen (Tylenol®) and be administered early in the post-transplant diphenhydramine (Benadryl®) are adminis- period as a means to delay initiation of CNIs, tered as premedications to prevent this allergic thereby avoiding the nephrotoxicity concerns reaction. The nurse should also monitor the associated with the latter medications. While complete blood count and subsets of T cells fluid retention is clinically demanding when during therapy for any patient who receives TOR inhibitors are given, renal and cardiac these polyclonal antibodies (Wade et al., 2004). function may be maintained using this approach (Griffith, Augustine, & Wade, Targets of Rapamycin Inhibitors 2003). Sirolimus has significant renal toxicity Sirolimus (Rapamune®) and everolimus (Cer- and also causes dyslipidemia. Impaired tican®, currently in clinical trials) are rela- wound healing has been documented in some tively new agents that block T-cell patients (Knight et al., 2007). proliferation through a mechanism similar Nursing monitoring of patients receiving to, but distinct from, the mechanism underly- TOR inhibitors includes assessment of coming CNIs’ activity. These agents block the sig- plete blood count data to evaluate for devel- naling necessary for T-cell growth and clonal opment of myelosuppression and to monitor expansion via inhibition of serine-threonine sirolimus levels (Wade et al., 2004). kinase mammalian TOR (mTOR) (Lindenfeld et al., 2004a). They are powerful inhibitors of growth factor-induced proliferation of lym- Infectious Disease Following Heart phocytes (Formica et al., 2004). Transplant Targets of rapamycin (TOR) inhibitors are Infection is a primary complication following the focus of intense research. Data comparing a heart transplant and is a common cause of everolimus or sirolimus and AZA suggest sim- morbidity and mortality in this patient popu- ilar survival rates among patients. However, lation (Bethea, Yuh, Conte, & Baumgartner, studies have shown that incidence of CMV or 2003). Interventions to prevent development cardiac allograft vasculopathy is higher in of infection are essential. AZA-treated patients than in everolimus- Heart transplant patients are at increased treated patients (Eisen et al., 2003; Keogh, risk for development of infection for a num- 2002). In a later study, everolimus was more ber of reasons. For example, anti-rejection effective than AZA in preventing rejection in medications, especially when used in combi- heart transplant patients. In the everolimus- nation, uniformly increase the risk of infec- treated patients, there was a lower incidence tion and malignancy. Transplant recipients and severity of cardiac allograft vasculopathy are also at risk for common hospital-acquired and major adverse cardiac events 4 years after infections as well as opportunistic infections transplant than in the AZA-treated patients (e.g., Pneumocystis carinii, yeast, fungus). Reac- (Eisen, 2006). tivation of old infections, such as CMV, toxo- The ultimate role of TOR inhibitors in the plasmosis, herpes simplex (HSV), varicella immunosuppressant armamentarium and zoster (VZV), or EBV poses another threat: their impact on long-term outcomes remain Primary infection by these organisms is not to be determined. Currently, these agents are “cured,” but rather is controlled by a compe- typically used as adjuncts to other medica- tent immune system. Reactivation of infections or as a rescue therapy if toxicities limit tion does not occur in the immunocompetent the use of other classes of immunosuppres- patient because T and B cells are constantly sants in heart transplant patients. It has also circulating and immediately respond to been suggested that these medications might any renewed activity of these latent organisms. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 418

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T and B cell function in the immunocompro- The most common pneumonia-causing mised patient, however, is diminished; thus bacteria found in heart transplant patients in reactivation of these infections will not be the immediate postoperative period (the first curtailed by a weakened immune system month) are gram-negative bacilli (GNB). (Bethea et al., 2003). Staphylococcus epidermidus, Staphylococcus aureus, Other common sources of nosocomial and GNB are the organisms most commonly infection include invasive lines, catheters, and linked to sternal wound infections and medi- devices; surgical incisions; and mechanical astinitis. Urinary tract infections in this ventilation equipment. An infectious organ- patient population are often caused by GNB, ism may also be present in the allograft (Wade enterococcus, or Candida albicans. et al., 2004). After the first month, pneumonia may Meticulous nursing care is essential to pre- develop secondary to CMV, HSV, or P. carinii vent this potentially lethal complication. Pre- pneumonia (PCP). Cutaneous infections with ventive measures are crucial in this regard; HSV, VZV, atypical Mycobacterium species, or they include meticulous handwashing; Cryptococcus may develop as well (Bethea et al., administration of antibiotic, antiviral, and 2003). antifungal agents (the choices will be facility specific); and discouraging visitation by per- Infection Prophylaxis sons with colds or flu, or by persons who Several well-established procedures to mini- recently received a live vaccine. Invasive lines, mize infectious risks exist. First, the heart catheters, and devices should be managed donor is screened for HIV, hepatitis B virus using aseptic technique and removed as early (HBV), hepatitis C virus (HCV), CMV, and Tox- as possible. When feasible, early ambulation oplasma gondii. Likewise, the heart recipient is should be encouraged. Data do not support screened before transplant for antibodies to use of protective isolation garb when caring CMV, toxoplasmosis, HIV, HSV, VZV, HBV, for post-transplant patients (Walsh et al., HCV, T. gondii, endemic fungi, and EBV. Pres- 1989). As discussed in Chapter 18, strict ence of antibodies indicates previous infection glycemic control decreases the risk of deep and confirms the risk for reactivation of these sternal wound infection. While the patient is infections in the setting of immunosuppres- intubated and on mechanical ventilation, evi- sion. The patient also receives a tuberculin dence-based interventions should be imple- skin test (Bethea et al., 2003). Prophylactic mented to prevent ventilator-associated medications are used to prevent reactivation pneumonia (VAP). Guidelines to prevent VAP of a latent infection when appropriate. may be found on the American Association of To prevent de novo (new infection in recipi- Critical-Care Nursing’s Web site in the “Prac- ent) infections with PCP, patients receive tice Alerts” section. trimethoprim-sulfamethoxazole (Bactrim®), Assessment for and prompt recognition of dapsone, or inhaled pentamadine (Nebu- presence of signs and symptoms is equally pent®). Nystatin (Mycostatin®) or clotrima- important. These may include fever, hypoten- zole (Mycelex®) is administered to prevent sion, tachycardia, increased cardiac output/ Candida infection. Ganciclovir (Cytovene®) is cardiac index, decreased systemic vascular administered to prevent CMV infection; the resistance, increased oxygen requirements, patient will be discharged home on acyclovir mental status changes, elevated white blood (Zovirax®). Patients are also placed on routine cell count, and changes in the incision endocarditis precautions (Bethea et al., 2003). (e.g., purulent drainage, redness, swelling) Although these regimens are highly effective (Wade et al., 2004). in preventing infectious complications, infec- 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 419

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tion remains a significant cause of mortality Post-transplant Surveillance through the 1-year mark following transplant Because the transplanted heart is denervated (Taylor et al., 2007). (the nerve supply has been cut), the transplanted heart will not receive autonomic nerv- Transplant Vasculopathy ous system or vagal nerve stimulation. As a result, the patient’s heart rate will be higher Transplant vasculopathy (TV) refers to allo- than normal. Transplant recipients will also graft coronary artery disease (ACAD) in the have physiologically altered responses to transplanted heart. It is the leading cause of stress; the denervated heart is unable to com- death in patients after the first 5 years follow- pensate with an increase in heart rate to ing a heart transplant (Bethea et al., 2003). TV maintain cardiac output. This lack of in transplant recipients is distinguished from response makes orthostatic hypotension diffi- CAD in other populations in that it results in cult to manage. Further, angina is not experi- diffuse luminal narrowing rather than dis- enced in response to ischemia. Dyspnea on crete lesions. Therefore, it is often not exertion may increase, although early signs of amenable to percutaneous or surgical inter- rejection or TV may be absent. vention. Another difference is the absence of Surveillance is implemented to screen for the collateral circulation (Bethea et al., 2003). TV development of any or all of these problems. An remains the predominant barrier to long- ECG, surface or transesophageal echocardio- term survival following a heart transplant gram (TEE), stress test, and left heart catheteri- (Aranda & Hill, 2000). zation are performed at regular intervals in all The etiology of TV may be either immuno- patients who undergo a heart transplant logic or non-immunologic. Examples of non- (Bethea et al., 2003; Wade et al., 2004). immunologic factors leading to development of TV include the age of the donor, hyperlipi- ■ demia, and CMV infection (Bethea et al., OUTCOMES AFTER HEART 2003). Development of TV may begin weeks TRANSPLANT following transplant and evolve at a subtle, yet The Registry of the International Society for rapid pace, resulting in complete obliteration Heart and Lung Transplantation’s 24th Official of the lumen of coronary vessels and allograft Adult Heart Transplantation Report provided failure due to ischemia (Bethea et al., 2003). detailed data on outcomes following trans- At present, the best treatment for TV is plant; these data are summarized in Table 19–5. retransplantation, because the coronary lumi- Currently, graft half-life (the time at which 50% nal damage tends to be diffuse. The need for a of all transplant recipients remain alive) is prudent lifestyle and preventive measures are 10 years. emphasized to include smoking cessation, Kaplan-Meier curves show a steep decline in control of hypertension, and cholesterol survival during the first 6 months following reduction (with diet and medications). heart transplant, then a linear decline. Survival Statins and calcium channel blockers have during the first 6 to 12 months after transplant been shown to decrease the incidence of TV is improving, but has not changed beyond that (Bethea et al., 2003; Wenke et al., 2003). point in patient recovery. Causes of death vary Several medications—sirolimus, everolimus, by time after transplant. In the first 30 days and MMF—have been shown to decrease the post-transplant, in order of decreasing fre- incidence of both vasculopathy and rejection quency, graft failure, multi-organ failure, and (Patel & Kobashigawa, 2004). More research is non-CMV infection caused 67% of deaths. From needed in this area, however. 31 to 365 days post-transplant, non-CMV 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 420

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Table 19–5 Outcomes Within One Year Following Transplant, 2000–2003, and Within Ten Years Following Transplant, 1994–2006

Within 1 Year Within 10 Years

Hypertension 76.8% 98% Renal dysfunction All 31.7% 14% Abnormal creatinine < 2.5 mg/dL 22.1% Creatinine > 2.5 mg/dL 7.8% 8% Long-term dialysis 1.5% 5% Renal transplant 0.3% 1% Hyperlipidemia 68.7% 93% Diabetes 30.2% 37% Coronary artery vasculopathy 7.0% 53%

Sources: Anderson, 2008b; Taylor et al., 2005, 2007.

infection (33%), graft failure (18%), and acute Infection Avoidance rejection (12%) are the leading causes of death. Because infection poses one of the greatest After 5 years, TV and late graft failure explain threats to the transplant patient, avoidance 30% of deaths, followed by malignancies (22%) and recognition of infection constitute a and non-CMV infections (10%). In summary, major focus of teaching. Common signs of non-CMV infection is the leading single cause infection are reviewed and patients are of death from 6 months through 10 years instructed to call if they develop any of these postoperatively. Transplant vasculopathy signs. Response to infection will be blunted (confirmed) and “graft failure” collectively in the immunosuppressed patient, so signs cause more deaths than infection in this of infection may be nonspecific (e.g., patient population (Taylor et al., 2007). malaise, “don’t feel right”). Patients are advised to avoid people who have received ■ PATIENT TEACHING live vaccines, and to check with their trans- The complexity of transplant care and the plant provider before receiving any immu- consequences of noncompliance make effec- nization. Other routine practices include tive patient teaching critically important. proper handwashing, avoiding contact with Adherence to mandated care regimens is more people who are ill, observing standard food likely if patients understand why these prac- hygiene procedures, and avoiding stagnant tices are important. For this reason, several water, gardening, and digging. Patients fre- educational strategies are used to relay infor- quently assume that the risk of gardening mation and confirm understanding. Methods can be avoided if their hands are protected of teaching include provision of printed infor- with gloves; in reality, the risk with garden- mation, verbal instruction from multidiscipli- ing relates to inhalation of spores mobilized nary team members, opportunities to practice by manipulation of dirt. Finally, patients are skills, demonstration, and return demonstra- encouraged to avoid any unnecessary med- tion. Patients are also provided with contact ical procedures in the first 6 months after information so they can call with questions. transplant. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 421

Patient Teaching 421

Activity Exercise As part of patient teaching, the nurse must Transplant patients are prescribed a specific review the anticipated schedule of return vis- exercise program by physical therapists. This its. Clearance to return to work or school or program is implemented during hospitaliza- to resume driving will depend on each indi- tion and continued upon discharge. Patients vidual’s progress. Physical restrictions include are also referred for cardiac rehabilitation. no lifting, pulling, or pushing of any item Teaching includes information regarding weighing more than 10 pounds for the first transplanted heart physiology. 6 weeks post-transplant. This is followed by The transplanted heart responds differ- orders not to lift, pull, or push anything ently to exercise than does a native heart. For weighing more than 25 pounds for at least instance, the resting heart rate is higher 12 weeks. Patients are also provided with a because of the lack of vagal innervation. Heart MedicAlert® bracelet. rate is slower to increase with exercise, and slower to return to baseline following physical exertion. In addition, the maximal heart Nutrition rate is lower in a transplanted heart. Nutritional counseling is provided as patient When engaging in exercise, transplant education. Patients should consume a diet patients are advised to warm up and cool low in sodium, potassium, cholesterol, and down for 7 to 10 minutes, and to self-monitor saturated fat. They are instructed to avoid perceived exertion and degree of dyspnea. nutritional supplements except as directed by They are taught to monitor for other subjec- their transplant team. tive symptoms such as dizziness, unusually An increase in acute (grade 3A) rejection heavy perspiration, nausea, and a general has been noted in late post-transplant sense of fatigue. patients (more than 1 year post-transplant) Long-term physical activity is important to who started taking nutritional supplements ensure favorable results following heart trans- that contained echinacea, zinc, or coenzyme plantation. Studies suggest that hyperten- Q10. In a study examining this phenome- sion, hyperlipidemia, doubts about expected non, the patients had no hemodynamic benefits, side effects of immunosuppressant compromise, subtherapeutic levels of anti- therapy, perceived negative sense of well- rejection medication, or rejection episodes in being, poor self-efficacy, continued cigarette the 6 months preceding the acute rejection. smoking, and obesity are associated with a The rejection persisted despite steroid pulse lower level of physical activity among women therapy, suggesting that the rejection was who receive heart transplants (Evanelista, resistant to steroids. It was noted that each Dracup, Doering, Moser, & Kobashingawa, of the supplements involved stimulates 2005; Franklin, Swaim, & Shepard, 2003; immunologic activity by destroying levels of Kobashingawa et al., 1999; Yates, Price- IL-2, IL-6, tumor necrosis factor, interferon, Fowlkes, & Agrawal, 2003). Exercise training and natural killer cells and by altering in heart transplant patients has also been cytochrome P450 pathways. It was suggested found to increase capacity for physical work that nurses amend their screening proce- (Kobashigawa et al., 1999). Further, data sug- dures to include nutritional supplements gest that endurance and strength training by such as “power bars,” which may contain at heart transplant patients may improve muscle least one of these supplements (Boguszewski function and aerobic performance, decrease et al., 2006). side effects of immunosuppression agents, 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 422

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and control risk factors associated with car- prescribed. The consequences of noncompli- diac allograft vasculopathy (Marconi & Mar- ance (whether intentional or inadvertent) may zorati, 2003). be devastating. Every effort is made to ensure that the patient understands the dosing and Sexual Activity administration regimen for all medications to be taken. Printed information should be pro- Issues related to sexuality are also included in vided to patients listing each medication pre- discharge teaching; specific instructions are scribed along with its mechanism of action, provided, as well as opportunity to discuss side effects, interactions, dosing schedule, and concerns. Sexual activity may be resumed as procedures to be followed for missed doses. soon as the patient feels ready. For 6 weeks, Due to the risk of interactions or com- patients should avoid putting weight on their pounded toxicities, patients are instructed not arms and chest. Sexual activity may be aerobic to take any over-the-counter medication with- and should be approached as such, with out clearance from the transplant provider. appropriate warm-up (e.g., foreplay) and cool- Exceptions to this rule include acetamino- down (e.g., cuddling) periods being employed. phen, acetylsalicylic acid, docusate sodium Patients should be given the opportunity to (Colace®), senna, loperamide (Immodium®), discuss other sexuality-related issues, such as and bismuth subsalicylate (Kaopectate®). anxiety, lack of desire, and body image con- New prescriptions from non-transplant- cerns, and should be reassured that these con- care providers should also be cleared by the cerns are not unusual. They should be invited transplant team. Patients are instructed to to speak openly about their concerns and ask avoid all NSAIDs. Herbal teas, medications, questions as they arise. Finally, all patients are and other nutritional supplements should strongly encouraged to avoid pregnancy due also be cleared with the transplant team. to the theoretical and documented risk to the fetus prenatally and later in life (Skotzko, Stowe, Wright, Kendall, & Dew, 2001; Subra- ■ SUMMARY maniam & Robson, 2008). The ICU nurse plays a pivotal role in optimizing outcomes of patients and families Other Instructions during HF exacerbations and the wait for a heart transplant. High levels of critical Other instructions included in discharge thinking are required to care for the patient teaching include recommendations regarding on inotropic or mechanical support. Evalu- pet care, travel, and procedure for contacting ating the patient’s candidacy for transplant the donor family. Sunscreen use is encouraged and supporting the patient and family as due to risk of photosensitivity and increased they await availability of a suitable donor risk of skin cancer associated with immuno- heart require high levels of clinical inquiry suppressive medications. Skin squamous cell and caring practices. The ICU nurse also has carcinoma is a significant cause of morbidity a role as a facilitator of learning as the and mortality in organ transplant patients patient and family learn about management (Ulrich, Degen, Patel, & Stockfleth, 2008). strategies for HF and about the transplant process. Bridge to transplant therapy Medications requires the nurse to provide realistic infor- Transplant patients are prescribed multiple mation to both patients and families about medications that must be taken exactly as the percentage of patients (20–40% [Leeper, 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 423

Summary 423

2006]) who may die while receiving VAD tive period. The ICU nurse must monitor for, therapy either due to complications or while promptly recognize, and treat the significant awaiting a heart transplant. complications that can affect short-, interme- Post-transplant patients have a high degree diate-, and long-term survival following heart of vulnerability in the immediate postopera- transplantation.

CASE STUDY

A 19-year-old college football player presented to the ED with chest pain, dyspnea, and fatigue. Six months ago, he was diagnosed with non-ischemic cardiomyopathy, thought to be related to a viral illness. At the time of his diagnosis, an echocardiogram revealed an ejection fraction of 13% with severe mitral regurgitation (MR), tricuspid regurgitation (TR), and moderate pulmonary hypertension. The patient was started on Coumadin® for his heart wall motion abnormalities and discharged home on metoprolol (Lopressor®), furosemide (Lasix®), and lisinopril (Prinivil®). Several days after his discharge, he developed aphasia. MRI confirmed a stroke. The patient’s speech returned to normal within 24 hours with no other deficits. Aside from an embolic stroke and heart failure, the patient has no other significant past medical history. At the time of his hospital admission, the patient reported that he had been doing well at home up until 1 week ago, when he began to experience poor appetite, fatigue, and worsening dyspnea. The night prior to admission, he began having nonradiating, constant chest pain with no aggravating or alleviating factors. He denied associated lightheadedness, palpitations, or lower extremity edema. He was admitted to the hospital with the concern of worsening heart failure.

Examination Physical findings at the time of the patient’s admission showed a normal neurologic exam. Vital signs were within normal limits, with the exception of a heart rate of 120. Jugular vein

distention (JVD) was noted. Breath sounds were clear throughout. Examination revealed S1 and S2 heart sounds, with a holosystolic murmur best heard at the apex. The patient’s abdomen was soft with normal bowel sounds; the liver edge was not palpable. The patient had moderate lower extremity edema. Bilateral lower extremities were cool to the touch, with 1+ pedal pulses.

Pertinent Laboratory Results Na ϭ 135 mEq/L, K ϭ 4.3 mEq/L, BUN ϭ 17 mg/dL, Cr ϭ 1.3 mg/dL WBC ϭ 7.9 mm3, Hgb ϭ 13.2 g/dL TCK ϭ 215 units/L, CKMB ϭ 2.1 ng/mL, troponin ϭ 0.06 ng/mL BNP ϭ 275 pmol/L

Diagnostics An ECG revealed sinus tachycardia, normal axis, normal intervals, left ventricular hypertrophy by voltage criteria, and no ST or T wave changes. A chest radiograph revealed an 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 424

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enlarged cardiopericardial silhouette. There was demonstration of diffuse airspace opaci- ties, likely representing mild pulmonary edema. No effusions or pneumothorax was identified. Cardiac MRI revealed marked cardiomyopathy of both the left and right sides of the heart secondary to cardiomyopathy. The patient had global hypokinesis and a markedly reduced ejection fraction of 13.6%. Right heart catheterization results were as follows: RA 27, RV 57/27, PA 57/33, PA mean 43, PAOP 25, CO 3.3 L/min, and CI 1.3 L/min/m2.

Impression/Diagnosis The right heart catheterization and echocardiogram results were consistent with worsening heart failure, biventricular fluid overload, and worsening cardiac output.

Decision Making The patient was transferred to the ICU for closer hemodynamic monitoring. A pulmonary artery catheter was inserted, and the patient was started on milrinone at 0.25 mcg/kg/min for low cardiac indices. The infusion was titrated up to 0.5 mcg/kg/min. The patient was placed on a fluid restriction, diuresis with intravenous furosemide was begun, and a heparin infusion was initiated. This patient is a 19-year-old male with non-ischemic cardiomyopathy of 6 months’ duration, who had an acute exacerbation of his heart failure symptoms and became inotrope dependent with unsatisfactory hemodynamics and resting symptoms. His cardiac indices remained less than 2 L/min/m2 on high-dose milrinone therapy. In addition, he had a significantly elevated resting heart rate at 120 beats per minute. Based on these findings, the patient was at risk for death from progressive heart failure and ventricular dysrhythmias. It was recommended that he undergo evaluation for heart transplantation, with left ventricular assist device (LVAD) therapy serving as a bridge to heart transplant.

Critical Thinking Questions 1. How are patients selected for VAD therapy? 2. What are potential complications when using an LVAD? 3. Why was milrinone utilized for this patient? Answers to Critical Thinking Questions 1. Selection criteria for patients requiring VAD therapy are rigorous; a battery of labs and diagnostic tests are performed to determine eligibility for this therapy. Cardiolo- gists, social workers, nurses, VAD coordinators, and the cardiac surgeon collaborate to determine the patient’s eligibility and develop a plan of care. The surgeon determines the type of assist device support required. LVAD recipients must have adequate right ventricular function to have a successful outcome because the LVAD is dependent on blood flow from the right ventricle. If right ventricular failure is present, then length of hospital stay, post-implantation morbidity/mortality, and cost are all increased (Decoene et al., 2004). In such cases, temporary biventricular support may be initiated, with discontinuation of the RVAD if right ventricular recovery occurs. 2. LVAD placement is a major surgical procedure that carries a significant risk for postoperative complications. The most common complications are bleeding, hypo- 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 425

Self-Assessment Questions 425

volemia, tamponade, organ damage (i.e., renal failure, liver failure), stroke, device failure, need for inotropic support for right ventricular failure, sepsis, and drive-line infection (Piccione, 2000). Bleeding in the immediate postoperative period is common due to the frequent use of aspirin and Coumadin® in HF patients preoperatively for severely depressed left ventricular function, coronary artery disease, or dysrhythmias. 3. Inotropic agents such as dopamine, dobutamine, and milrinone are used to support right and left ventricular function. Milrinone is frequently administered at a dose of 0.125–0.375 mcg/kg/min and has the added benefit of promoting pulmonary vascular dilation.

■ SELF-ASSESSMENT QUESTIONS 4. Which statement by a heart transplant candidate indicates a need for additional 1. What are the possible postopera- education? tive complications following LVAD a. “I am looking forward to living implantation? without coronary artery disease a. Bleeding and hypervolemia following the transplant.” b. Stroke and reflex tachycardia b. “My HbA is 7% this week; I’m doing c. Left ventricle failure and bleeding 1c well.” d. Tamponade and left ventricular c. “I am surprised I will have to stay on depression Lipitor® (atorvastatin calcium) for 2. Your patient has a history of right ven- the rest of my life.” tricular failure and requires support d. “My wife and I will have to find from a ventricular assist device. Which another hobby to share because I can of the following devices will most likely no longer garden.” be utilized? 5. The patient with which preoperative a. Heartmate VE hemodynamic profile is at risk for devel- b. TandemHeart opment of right heart failure following c. Thoratec transplant? d. Heartmate XVE B/P PAP CVP PAOP 3. For which of the following patients would a. 163/71 25/10 3 4 a heart transplant be contraindicated? b. 132/74 42/26 10 12 a. A 47-year-old patient with early-stage c. 88/50 30/20 16 15 Alzheimer’s disease d. 140/82 34/15 4 14 b. A 68-year-old patient with unstable 6. Your postoperative heart transplant diabetes mellitus patient develops atrial fibrillation. c. A 28-year-old patient with protein Which of the following should not be calorie malnutrition used? d. A 32-year-old patient who received a. Amiodarone the hepatitis B vaccine b. Digoxin c. Calcium channel blocker d. Cardioversion 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 426

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7. Your postoperative heart transplant b. A patient who underwent heart patient develops sinus bradycardia with transplantation using the biatrial mental status changes. Which of the fol- technique lowing medications is least likely to be c. A patient who was supported on a used initially? left ventricular assist device a. Isoproterenol (Isuprel®) preoperatively b. Atropine sulfate (Atropine®) d. A patient who had preoperative left c. Epinephrine (Adrenalin®) ventricular dysfunction ® d. Dopamine (Intropin ) 10. A postoperative cardiac transplant 8. Which of the following increases pul- patient will be unable to manifest which monary vascular resistance? of the following conditions? a. Alkalosis a. Angina b. Nitric oxide b. Reflex tachycardia c. Nitroglycerin c. Vasovagal response d. Hypoxemia d. Decreased cardiac output 9. Which of the following patients is most Answers to Self-Assessment Questions likely to have a more challenging immediate postoperative heart transplant 1. d 6. b recovery? 2. c 7. b a. A patient who received a heart with a 3. a 8. d cold ischemic time of 4 hours 4. a 9. b 5. b 10. d

Clinical Inquiry Box

Question: What is the incidence of ventricular dysrhythmia in VAD therapy? Reference: Bedi, M., Kormos, R., Winowich, S., McNamara, D., Mathier, M., & Murali, S. (2007). Ventricular arrhythmias during left ventricular assist device support. American Journal of Cardiology, 99(8), 1151–1153. Objective: To identify the incidence, risk factors, and clinical significance of ventricular dysrhythmias with ventricular assist device therapy. Method: A descriptive study was conducted in 111 patients who received LVAD support as a bridge to cardiac transplant. Data were collected on the frequency of ventricular dysrhythmia (ventricular fibrillation, sustained ventricular tachycardia, or nonsustained ventricular tachycardia). Risk factors for the development of ventricular dysthythmia were analyzed. The mortality rate was compared for those individuals who had ventricular dysrhythmias and those patients who were dysrhythmia free. Results: Ventricular dysrhythmias occurred in 24 patients (22%) during device support. Ischemic heart disease was the cause of heart failure in 71% of patients with ventricular dysrhythmias, compared to 45% of patients without dysrhythmias. The mortality rate was significantly higher during LVAD support in the group with dysrhythmias (33%) in contrast to the mortality rate in those patients without dysrhythmias (18%). The earlier the dysrhythmias occurred, the higher the potential for mortality. Conclusion: Early occurrence of ventricular dysrhythmias after VAD therapy initiation predicts a higher mortality rate. Nurses need to be vigilant in assessing for ventricular dysrhythmias for timely interventions. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 427

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vasodilation of septic shock. Circulation, 95(5), Humoral rejection in cardiac transplantation: 1122–1125. Risk factors, hemodynamic consequences and Leeper, B. (2006). Advanced cardiovascular con- relationship to transplant coronary artery dis- cepts. In M. Chulay & S. M. Burns (Eds.), ease. Journal of Heart and Lung Transplantation, AACN essentials of critical care nursing (pp. 22(1), 58–60. 431–461). New York: McGraw-Hill. Møller, C. H., Gustafsson, F., Gluud, C., & Stein- Lindenfeld, J., Miller, G., Shakar, S., Zolty, R., brüchel, D. A. (2008). Interleukin-2 receptor Lowes, B., & Wolfel, E. (2004a). Drug therapy antagonists as induction therapy after heart in the heart transplant recipient: Part II: transplantation: Systematic review with meta- Immunosuppressive drugs. Circulation, analysis of randomized trials. Journal of Heart 110(24), 3858–3865. and Lung Transplantation, 27(8), 835–842. Lindenfeld, J., Miller, G. G., Shakar, S. F., Zolty, R., Morgan, J., & Edwards, N. (2005). Orthotopic car- Lowes, B. D., Wolfel, E. E., et al. (2004b). Drug diac transplantation: Comparison of outcome therapy in the heart transplant recipient: using biatrial, bicaval and total techniques. Part I: Cardiac rejection and immunosuppres- Journal of Cardiac Surgery, 20(1), 102–106. sive drugs. Circulation, 110(24), 3734–3740. Oka, T., & Yoshimura, N. (1996). Immunosuppres- Marconi, C., & Marzorati, M. (2003). Exercise after sion in organ transplantation. Journal of Phar- heart transplantation. European Journal of macology, 71(2), 89–100. Applied Physiology, 90(3–4), 250–259. Organ Procurement and Transplantation Network Mason, V. F., & Konicki, A. J. (2003). Left ventricu- (OPTN). (2008). Retrieved December 11, 2008, lar assist devices as destination therapy. AACN from www.optn.org. Clinical Issues: Advanced Practice in Acute and Crit- Patel, J. K., & Kobashigawa, J. A. (2004). Immuno- ical Care, 14(4), 488–497. suppression, diagnosis, and treatment of car- Massé, L., & Antonacci, M. (2005). Low cardiac diac allograft rejection. Seminars in Thoracic and output syndrome: Identification and manage- Cardiovascular Surgery, 16(4), 378–85. ment. Critical Care Nursing Clinics of North Amer- Pelletier, S. J., Norman, S. P., Christensen, L L., ica, 17(4), 375–383. Stock, P. G., Port, F. K., & Merion, R. M. McBride, L. R., Naunheim, K. S., Fiore, A. C., John- (2004). Review of transplantation in HIV son, R. G., Moroney, D. A., Brannan, J. A., et al. patients during the HAART era. Clinical Trans- (2001). Risk analysis in patients bridged to plants, 63-82. transplantation. Annals of Thoracic Surgery, Piccione, W. (2000). Left ventricular assist device 71(6), 1839–1844. implantation: Short- and long-term surgical McCalmont, V., & Ohler, L. (2008). Cardiac trans- complications. Journal of Heart and Lung Trans- plantation: Candidate identification, evalua- plantation, 19(8), S89–S94. tion, and management. Critical Care Nursing Poston, R., & Griffith, B. (2004). Heart transplanta- Quarterly, 31(3), 216–229. tion. Journal of Intensive Care Medicine, 19(1), McGiffin, D. C., Kirklin, J. K., Naftel, D. C., & 3–12. Bourge, R. C. (1997). Competing outcomes Rose, E. A., Gelijns, A. C., Moskowitz, A. J., Heitjan, after heart transplantation: A comparison of D. F., Stevenson, L. W., Dembitsky, W., et al., eras and outcome. Journal of Heart and Lung for the Randomized Evaluation of Mechanical Transplantation, 16(2), 190–198. Assistance for the Treatment of Congestive Meiser, B. M., Pfeiffer, M., Schmidt, D., Reichen- Heart Failure (REMATCH) Study Group. spurner, H., Ueberfuhr, P., Paulus, D., et al. (2001). Long-term use of a left ventricular (1999). Combination therapy with tacrolimus assist device for end-stage heart failure. New and mycophenolate mofetil following cardiac England Journal of Medicine, 345(20), transplantation: Importance of mycophenolic 1435–1443. acid therapeutic drug monitoring. Journal of Rosenbaum, D., Mitchell, J., Adams, B., Paul, M., Heart and Lung Transplantation, 18(2), 143–149. Kaiser, P., Meyer, D., et al. (2006). Does basilix- Michaels, P. J., Espejo, M. L., Kobashigawa, J., Ale- imab decrease acute rejection and improve jos, J. C., Burch, C., Takemoto, S., et al. (2003). renal function in cardiac transplant recipients 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 430

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at mid-term follow up? Journal of Heart and era. Journal of Heart and Lung Transplantation, Lung Transplantation, 25(2 suppl), S166. 25(2 suppl), S132–S133. Rothman, S. A., & Eisen, H. J. (2008). Arrhythmias Stobierska-Dzierzek, B., & Brook, R. H. (2001). The following cardiac transplantation. Retrieved evolving management of acute right-sided December 8, 2008, from http://www heart failure in cardiac transplant recipients. .utdol.com/online/content/topic/do Journal of the American College of Cardiology, ?topicKey=hrt_tran/2409&selectedTitle 38(4), 923–931. =9~150&source=search_result. Subramaniam, P. & Robson, S. (2008). Heart trans- Russo, M., Chen, J., Sorabella, R., Martens, T., Gar- plant and pregnancy. O & G Magazine, 10(3), rido, M., Davies, R., et al. (2007). The effect of 32–35, 24. ischemic time on survival after heart trans- Taegtmeyer, H. (2006). Heart failure. In T. A. Miller plantation varies by donor age: An analysis of (Ed.), Modern surgical care: Physiologic foundations the United Network for Organ Sharing data- and clinical applications (3rd ed., pp. 663–670). base. Journal of Thoracic and Cardiovascular Boca Raton, FL: CRC Press. Surgery, 133(2), 554–559. Talmor, D., & Lisbon, A. (2005). Management of Sayegh, M. H. (2008). Major side effects associated the postoperative cardiac surgical patient. In with OKT3. Retrieved December 12, 2008, M. Fink, E. Abraham, J. Vincent, & P. from http://www.uptodate.com/patients/ Kochanek (Eds.), Textbook of critical care (5th content/topic.do?topicKey=renltran/13043 ed., pp. 1955–1967). Philadelphia: Elsevier Sevmis, S., Emiroglu, R., Karakayali, M., Yagmur- Saunders. dur, A., Dalgic, G., Moray, G., et al. (2005). Taylor, D. O. (2007). The role of heart transplanta- OKT3 treatment for steroid-resistant acute tion. In P. M. McCarthy & J. B. Young (Eds.), rejection in kidney transplant. Transplantation Heart failure: A combined medical and surgical Proceedings, 37(7), 3016–3018. approach (pp. 228–254). Malden, MA: Blackwell. Skotzko, C. E., Stowe, J. A., Wright, C., Kendall, K., Taylor, D., Edwards, L, Boucek, M., Trulock, E., & Dew, M. A. (2001). Approaching a consen- Aurora, P., Christie, J., et al. (2007). Registry of sus: Psychosocial support services for solid the International Society for Heart and Lung organ transplantation programs. Progressive Transplantation: Twenty-fourth official adult Transplantation, 11(3), 163–168. heart transplant report—2007. Journal of Heart Smith, S. (2002). Immunosuppressive therapies in and Lung Transplantation, 26(8), 769–781. organ transplantation. Retrieved November 6, Taylor, D., Edwards, L., Boucek, M., Trulock, E., 2007, from http://www.medscape.com/ Deng, M., Keck, B., et al. (2005). Registry of the viewarticle/437182 International Society for Heart and Lung Snell, L., Randolph, S., & Artig-Brown, T. (2007). Transplantation: Twenty-second official adult Home nutrition in the transplant patient. In heart transplant report—2005. Journal of Heart C. S. Ireton-Jones & M. H. DeLegge (Eds.), and Lung Transplantation, 24(8), 945–955. Handbook of home nutrition support (pp. 353–388). Topkara, V. K., Dang, N. C., Barili, F., Cheema, F. Sudbury, MA: Jones and Bartlett. H., Martens, T. P., George, I., et al. (2006). Pre- St. Andre, A., & DelRossi, A. (2005). Hemodynamic dictors and outcomes of continuous veno- management of patients in the first 24 hours venous hemodialysis after implantation of a following cardiac surgery. Critical Care left ventricular assist device. Journal of Heart Medicine, 33(9), 2062–2083. and Lung Transplantation, 25(4), 404–408. Stecker, E., Strelich, K., Chugh, S., Crispell, K., & Ulrich, C., Degen, A., Patel, M. J., & Stockfleth, E. McAnulty, J. (2005). Arrhythmias after ortho- (2008). Sunscreens in organ transplant topic heart transplantation. Journal of Cardiac patients. Nephrology Dialysis Transplantation, Failure, 11(6), 464–472. 23(6), 1805–1808. Stehlik, J., Kroury, G., Renlund, D. G., Gilbert, E. Vaqueriza, D., Delgado, J. F., Sanchez, V., Renes, E., M., Stringham, J. C., Seaman, J. T., et al. Escribano, P., Cortina, J., et al. (2006). Com- (2006). Antibody-mediated rejection of the parison of basiliximab and OKT3 as induction cardiac allograft-outcomes in the post OKT3 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 431

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agents after heart transplant. Journal of Heart ■ WEB RESOURCES and Lung Transplantation, 25(2 suppl), S167. Cardiac surgery: http://www.youtube.com/ Wade, C. R., Reith, K. K., Sikora, J. H., & Augustine, watch?v=qVYiGdQKP4s S. M. (2004). Postoperative nursing care of the Ventricular assist device: http://www.youtube cardiac transplant recipient. Critical Care Nurse .com/watch?v=DLV6kIfvSDA Quarterly, 27(1), 17–30. Life on the transplant list: http://www.youtube Walsh, T. R., Guttendorf, J., Dummer, S., Hardesty, .com/watch?v=xS7v4M-VmGw R. L., Armitage, J. M., Kormos, R. L., et al. Innovations in heart and lung transplantation: (1989). The value of protective isolation proce- http://www.youtube.com/watch?v= dures in cardiac allograft recipients. Annals of BxwQxI6n0bE Thoracic Surgery, 47(4), 539–544. Deciding whether to have transplant surgery: Wenke, K., Meiser, B., Thiery, J., Nagel, D., Von http://www.youtube.com/watch?v= Scheidt, W., Krobot, K., et al. (2003). Simvas- Q0qQX6Ps79c tatin initiated early after heart transplantation: 8-year prospective experience. Circulation, Orthotopic heart transplant: www.youtube 107(1), 93–97. .com/watch?v=N7etGEtdCCk Wolfgang, D., Bauer, M., & Podesser, B. (2006). ECMO: www.youtube.com/watch?v=Psci-wZKN_s Nitric oxide in cardiac transplantation. Phar- macological Reports, 58(suppl), 145–152. Yates, B. C., Price-Fowlkes, T., & Agrawal, S. (2003). Barriers and facilitators of self-reported physical activity in cardiac patients. Research in Nurs- ing Health, 26(6), 459–469. 57625_CH19_393_432.pdf 4/10/09 11:07 AM Page 432 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 433

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ACORN cardiac support device: A polyester extremities. Results of this calculation are mesh fabric that is wrapped snugly around used to rate the degree of peripheral artery the ventricles. It provides passive support to disease and to determine if the saphenous the ventricles, which should reduce wall stress vein is suitable for use during cardiac surgery. and prevent further remodeling. Annuloplasty: Surgical repair of an ineffec- Afterload: The resistance against which the tual heart valve. left ventricle must pump to move blood for- Aortic regurgitation: Incomplete closure of ward. The pressure of the arterial systemic cir- the aortic valve leaflets, resulting in a back- culation produces afterload. Smooth muscle flow of blood. There is a reflux of blood from tone in the arterioles can increase the resist- the aorta into the left ventricle (LV) during ance to blood flow and increase afterload. diastole because the valve leaflets fail to close Medications can alter the amount of resist- completely and remain tightly closed during ance that arteriolar smooth muscle generates. diastole. Acute aortic regurgitation imposes a Allograft: The transfer of an organ from one large volume load on the LV, which a normal person to another. The donor is not a twin, heart cannot accommodate. The sudden but is of the same species. increase in end-diastolic volume (preload) will Allograft coronary artery disease (ACAD): result in increased left ventricular end-dias- Development of coronary artery disease in tolic pressure (LVEDP) and decreased cardiac heart transplant patients. It can be described output. Aortic regurgitation is identified by based on the degree of stenosis of the affected the presence of an early diastolic murmur vessel(s). ACAD is often associated with graft that can be heard at the second and third failure. intercostal spaces at the right sternal border and the second and fourth intercostal spaces Alveolar-arterial oxygen gradient (A-a gra- at the left sternal border. The murmur of aor- dient): A method of measuring intrapul- tic regurgitation usually decreases in intensity monary shunt. The calculation is the and disappears before S . difference between the concentration of alve- 1 olar oxygen entering the alveoli and the con- Aortic stenosis: Narrowing or constriction of centration of oxygen diffused into the arterial the aortic valve that creates a pressure gradi- blood. ent. The aortic valve does not open completely, which creates a left ventricular Ankle-brachial index: An assessment used outflow tract obstruction and increases both to evaluate arterial blood flow to the lower

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the workload and afterload of the left ventri- moses are made in the superior and inferior cle. The calcification of aortic stenosis is vena cavae. regarded as a proliferative and inflammatory Biologic valves: Valves that are constructed process, similar to atherosclerosis. from bovine, porcine, and human cardiac Arterial pulse contour continuous cardiac tissue. output monitoring: A method that estimates Biventricular assist device (BiVAD): A type cardiac output by use of pulse contour analy- of mechanical support for the heart. It is used sis; it is an indirect method based on analysis when both the right and left ventricles are of the arterial pressure pulsation waveform. failing. Blood is drained from each ventricle The key underlying concept is that the con- through cannulae to centrifugal pumps, tour of the arterial pressure waveform is pro- which provide circulatory support in severely portional to stroke volume. The arterial decompensated heart failure patients until a pressure waveform is used to calculate cardiac heart transplant can be performed. A BiVAD output, stroke volume variance, intrathoracic is typically used when a left ventricular assist volumes, and extravascular lung water. These device does not provide sufficient circulatory data may predict response to fluid therapy. support. Assisted aortic end-diastolic pressure: The Bridge to recovery: Use of a mechanical cir- pressure in the aorta at the end of diastole culatory device (ventricular assist device when counterpulsation has assisted the car- [VAD]) to support circulation in patients with diac cycle. It is usually lower than the unas- heart failure. If myocyte damage is not perma- sisted end-diastolic pressure. nent, myocardial cells may regain their ability Assisted systole: The systolic aortic pressure to function. The VAD supports the patient when counterpulsation has assisted the car- until heart function improves and is adequate diac cycle. It is usually lower than the unas- without mechanical support. sisted systole due to the action of balloon Bridge to transplantation: Use of a mechan- deflation. ical circulatory device (ventricular assist Atrial cuff technique (bicaval technique): A device [VAD]) to support circulation in method used during heart transplantation in patients with severe heart failure until a which the donated heart is attached to the donor heart becomes available and a trans- recipient’s atrial “cuffs.” plant can be performed. Atrial septal defect (ASD): An opening Cardiac allograft vasculopathy: See coronary between the right and left atria. Oxygenated artery vasculopathy. blood leaves the left atrium and returns to the Cardiac catheterization: An invasive diag- right atrium through this opening rather nostic test whereby a catheter is inserted and than continuing forward to deliver oxygen to advanced into the heart chambers or coronary cells, organs, muscles, and tissues throughout arteries. It reveals information about the the body. blood pressure of the heart and the heart’s Balloon valvotomy/valvuloplasty: Use of a ability to pump, blood flow in the heart balloon to stretch open a narrowed heart chambers, presence and degree of narrowing valve or to break adhesions in a scarred valve. of the coronary arteries, and valve function. Beating heart surgery: See off-pump coronary Cardiac output (CO): A measure of the artery bypass. amount of blood that is ejected by the heart Bicaval technique: A method used during each minute. It is affected by the individual’s heart transplantation in which the anasta- preload, afterload, and contractility. 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 435

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Cardioplegia: A method of intentionally Central venous oxygen saturation (ScvO2): arresting the heart’s motion with infusion of A method used to determine how much oxy- a solution to facilitate performance of cardiac gen the tissues are extracting. It entails analy- surgery. The solution contains potassium (to sis of a blood sample from a central venous decrease myocardial oxygen consumption catheter. and the rate of anaerobic metabolism while Cold ischemia time: The time from cross- the heart is ischemic), magnesium (to clamping of the donor heart, with subsequent decrease myocardial oxygen consumption), excision and immersion of the heart in iced calcium (to decrease the chance of reperfusion saline, to removal of the cross-clamp after the injury), procaine (vasodilator and antiar- donor heart’s implantation in the recipient. rhythmic; may decrease dysrhythmias follow- Commissurotomy: A procedure that opens ing aortic cross-clamping), bicarbonate (to commissures (the contact area for the valve counter the metabolic acidosis that occurs leaflets), which have developed scarring and secondary to anaerobic metabolism while the do not open to allow blood to flow. heart is in arrest), hypothermia (decreases myocardial oxygen consumption and increases Contractility: The rate and ability of the the heart’s tolerance to ischemia), mannitol myocardial muscle to shorten itself, or the (to decrease edema related to hypothermia amount of strength evidenced by the and ischemia, and may minimize reperfusion myocardium when it ejects blood. It is influ- injury), dextrose (to counter edema due to enced by heart rate, neural factors, and certain hypothermia and ischemia, and for continued metabolic states. energy production), amino acids (for energy Coronary artery bypass grafting (CABG): production, may minimize reperfusion injury, See surgical revascularization. and has a role as a scavenger for oxygen free Coronary artery vasculopathy (CAV): A type radicals), and oxygenated blood (to optimize of stenosis caused by plaque in the coronary the heart’s metabolic environment and mini- arteries. The lesions contain inflammatory mize reperfusion injury). The patient’s circu- cells (including T cells). CAV is a major cause lation is diverted to a heart–lung machine of long-term morbidity and mortality in heart that takes over the function of these two transplant patients who survive past the first organs. The heart is isolated from the body year. Innate and adaptive immune responses with cross-clamping of the aorta. A cold car- result in development of vascular lesions. dioplegic solution is then instilled to Cox/Maze III procedure: A modification of a decrease myocardial oxygen consumption procedure that interrupts the reentrant path- and increase the heart’s tolerance to ways required for atrial fibrillation using sur- ischemia, thereby preventing heart damage gical incisions. The Cox/Maze III procedure during the procedure. remains the standard surgical therapy for Cardiopulmonary bypass (CPB): The tem- atrial fibrillation. It entails a number of inci- porary rerouting of blood from the right sions being made on the right and left atria. atrium to the aorta via an oxygenator (bypass “Maze” refers to the pattern of incisions made machine), thereby bypassing the heart and in the atrium. The incisions cause scarring, lungs during the surgical procedure. which does not conduct electricity, stops irreg- Carotid bruit: A sound associated with tur- ular electrical activity, and eradicates atrial fib- bulent blood flow that may indicate arterial rillation. The scarring also prevents future stenosis. irregular electrical signals from developing. 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 436

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Cox/Maze IV procedure: A procedure that technique, DCMP is rarely used in the United uses radiofrequency ablation to eradicate States, though it remains in use in other atrial fibrillation. areas. Deep sternal wound infection: Infection of Dynamic response test: See square wave test. the sternum and underlying structures. Ejection fraction (EF): The percentage of Destination therapy: Use of a ventricular blood volume of the left ventricle that is assist device in patients with severe heart fail- ejected with each contraction. A normal ejec- ure who are not candidates for or have tion fraction is approximately 65–70%. declined heart transplant. Electrical bioimpedence: A noninvasive Diastolic augmentation: The increase in method to determine cardiac output. Using pressure in the aorta above the balloon this technology, cardiac output is identified catheter that results with balloon inflation by changes in impedance that take place as during diastole. This phenomenon increases blood is ejected from the left ventricle into perfusion in the coronary arteries and the aorta and is calculated from changes in myocardial oxygen supply. thoracic impedance. Change in thoracic Dicrotic notch: When referring to an intra- blood volume during the cardiac cycle can be aortic balloon pump or intra-arterial pressure used to calculate cardiac output. monitoring, an area on the downstroke of the Endoaneurysmorrhaphy: A procedure that arterial waveform that results from the slight involves excising an aneurysm and reapproxi- pressure increase created by closure of the mating the wall edges using a Dacron patch aortic valve. to control the shape and size of the ventricle. Dor procedure: Also known as endoventricu- It is used to treat ventricular tachycardia. lar circular patch plasty repair. A procedure Although this approach attempts to restore whereby the left ventricle is reconstructed more normal ventricular geography, data using a purse-string suture to isolate non- indicate that it does not improve LV function. functional segments of myocardium (rather Endoscopic atraumatic coronary artery than excising them) and a circular patch to bypass grafting (EndoACAB): A combina- control the shape of the ventricle. The Dor tion of both two methods to perform off- procedure is usually performed concomi- pump coronary artery bypass grafting. The tantly with a coronary artery bypass graft. internal mammary artery is harvested using Drug-eluting stent (DES): A metal tube or an endoscopic approach, and the anastomosis “scaffold” inserted into a coronary artery fol- is performed with direct visualization lowing dilation of the vessel with a balloon through a small thoracotomy incision. (balloon angioplasty). The tube is coated with Endovascular/“keyhole” procedure: A type a drug to prevent reblockage (restenosis) of of minimally invasive procedure. It entails use the vessel. of a small (5-mm or 3-mm) endoscope to Dynamic cardiomyoplasty (DCMP): An access the heart through the intercostal space. innovative technique whereby the latissimus The 5-mm scope makes it easy to maneuver dorsi muscle is wrapped around the heart. An between ribs, increasing visibility, and has implanted stimulator is then used to stimu- been used to close a patent ductus arteriosus, late the muscle to contract in synchrony with thereby eliminating the need for a thoraco- ventricular contraction. Due to the borderline tomy. The digital camera and processing clinical improvement associated with this make pictures from the 5-mm scope better 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 437

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than the pictures provided by the traditional used to restore a more normal mitral valve surgical 10-mm scope. The 3-mm scopes are anatomy that has achieved favorable out- designed to feel and work like standard comes. GMR has consistently resulted in sig- instruments used by cardiac surgeons. nificant improvements in ejection fraction. It Endoventricular circular patch plasty is indicated for patients with cardiomyopathy repair: See Dor procedure. and mitral regurgitation. Ethanol septal ablation: A procedure for Graft closure: Failure of the harvested vein relieving outflow obstruction symptoms that (graft) to maintain patency, usually due to is accomplished by infusing ethanol into the platelet aggregation. Antithrombotic therapy first septal branch of the left anterior is initiated to prevent this complication of descending coronary artery via an angioplasty coronary artery bypass surgery. catheter. This technique reduces outflow tract Heterotopic method: A heart transplanta- obstruction, increases exercise capacity, and tion technique utilizing end-to-end anasta- improves symptoms. moses of the donor to the superior vena cava, Ex-Maze procedure: A cutting-edge technique pulmonary artery, and aorta. The donor heart for the Maze procedure. It is performed endo- is placed “piggyback” to the recipient heart. scopically on the outside of a beating heart. This method may be used in patients with The ablation device uses unipolar radiofre- severe pulmonary hypertension or if there is a quency energy with vacuum-maintained con- mismatch between the donor and recipient tact and suction-controlled saline perfusion to heart size. It is rarely used. ensure uniform energy transmission and trans- Hypertrophic cardiomyopathy (HCM): A mural lesion development. Because the proce- common genetic cardiovascular disease char- dure is performed on a beating heart, atrial acterized by abnormal myocytes leading to function can be monitored during treatment. hypertrophy without dilatation and preserved Patients can convert to normal sinus rhythm systolic function. Hypertrophy is most severe during the procedure or within 6 weeks. The in the ventricular septum. It is asymmetrical Ex-Maze procedure is less invasive and does and usually occurs at the level of the LV out- not require cardiopulmonary bypass. It is safer, flow tract, leading to subaortic stenosis or associated with less postoperative pain, and asymmetrical HCM. In addition, abnormal has fewer complications. systolic anterior motion of the mitral valve Extracorporeal membrane oxygenation contributes to the outflow obstruction. (ECMO): Use of a machine that can provide Hypothermia: A decrease in internal (core) oxygen to the blood while it is circulating out- body temperature below normal values. side of the body. Blood is removed from the Often, a temperature less than 95 °F (35 °C) body via a catheter, pumped through a is considered hypothermia. machine to be oxygenated by an artificial Infective endocarditis: A condition that lung, and returned to the body through occurs when bacteria attach to and destroy another catheter. The heart and lungs are the surface of a valve leaflet or chordae. If a bypassed, providing both hemodynamic and valve is damaged, immune cells, platelets, and respiratory support. Blood oxygenation is a fibrin migrate to the site to initiate healing of distinct advantage with this technique. the valve. If bacteria become trapped under Fast flush: See square wave test. layers of these cells, “clumps” of tissue (called Geometric mitral reconstruction (GMR): A vegetations) can develop on the valves and procedure in which an annuloplasty ring is within the heart muscle (endocarditis). Vege- tations may break off and become emboli. 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 438

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Internal mammary artery (IMA): An artery the abdomen, near the stomach. A percuta- in the chest located adjacent to the left ante- neous drive line that is tunneled across the rior descending coronary artery. There is one pre-peritoneal space to the left side of the IMA on either side of the sternum. This artery body carries an electrical cable and air vent to is resistant to cholesterol buildup (atheroscle- the electrical controller outside the patient’s rosis), which makes it a good choice for use as body. a graft in coronary artery bypass surgical Lower and Shumway method: A method procedures. used during heart transplantation in which Intra-aortic balloon pump (IABP): A the donor heart is anastomosed to the left mechanical device that is used to improve car- atrium, right atrium, pulmonary artery, and diac function on a temporary basis. It increases aorta. blood flow, oxygen delivery to the heart, and Maze procedure: See Cox/Maze III procedure. cardiac output, and decreases the amount of Mean arterial pressure (MAP): The driving work the heart must do to eject blood through force for peripheral blood flow and the pre- a process called counterpulsation. ferred pressure to be evaluated in unstable Intrapulmonary shunt (IPS): The percent- patients. It is measured electronically by first age of cardiac output that does not partici- integrating the area under the arterial pres- pate in gas exchange. This portion of blood sure waveform and then dividing by the dura- passes through the lungs but is not exposed tion of the cardiac cycle. to ventilated alveoli, so gas exchange does not Mechanical assist device: A device used to take place and the blood leaves the lungs support cardiac function over the short or desaturated. long term. Mechanical circulatory support International Society of Heart and Lung has three primary functions: bridge to trans- Transplantation (ISHLT) grading system: plantation, bridge to recovery, and destina- The standardized cardiac biopsy system that tion therapy. Short-term, temporary devices is used to grade acute heart rejection. are often used as bridge to recovery in the set- Keyhole procedures: See endovascular/“key- ting of acute cardiogenic shock or cardiopul- hole” procedures. monary arrest. Under these circumstances, Left-to-right shunting: Diversion of blood circulatory assistance provides immediate from the left heart to the right heart, rather hemodynamic support, restoring blood flow than forward into the systemic circulation. to vital organs while decompressing the heart, Oxygenated blood from the arterial circula- avoiding pulmonary edema, and minimizing tion mixes with deoxygenated blood from the cardiac workload to maximize the patient’s venous system. Chronic left-to-right shunting chances of recovery. may cause right ventricular failure, tricuspid Mediastinitis: Inflammation of the medi- regurgitation, atrial arrhythmias, paradoxical astinum; an uncommon but severe complica- embolization, and cerebral abscesses. tion following cardiac surgery. Its incidence is Left ventricular assist device (LVAD): A reportedly higher in patients who have under- type of mechanical support for the left ventri- gone grafting with bilateral internal mam- cle. Blood is drained from the apex of the left mary arteries. ventricle to a pump via an inflow cannula. It Minimally invasive cardiac surgery is returned to the body via an outflow can- (MICS): An alternative approach to coronary nula, which is attached to the aorta. The artery bypass graft surgery that entails use of pump is housed in the pre-peritoneal space of a laparoscopic procedure to perform cardiac 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 439

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surgery. MICS has also been defined as car- dient. The narrowing creates resistance to the diac surgery without the use of cardiopul- forward flow of blood into the left ventricle monary bypass or sternotomy; rather, smaller during diastole. incisions are made. MICS also refers to vari- Mitral valve annuloplasty ring: A three- ous procedures used to bypass blocked coro- dimensional ring that improves mitral valve nary arteries. function and left ventricular shape. Minimally invasive direct coronary artery Myocardial revascularization: Restoration bypass (MIDCAB): An alternative approach of blood supply to the myocardium. It may be to traditional coronary artery bypass grafting accomplished by either percutaneous inter- (CABG). Differences between the two vention or surgery. approaches are threefold. First, the incision Myectomy: A procedure that involves exci- size is much smaller for MIDCAB; several 3- sion of a section of sub-aortic septal muscle inch to 5-inch incisions are made between the approximately 3–7 cm long and 3–12 g in ribs as compared to a 10-inch to 12-inch weight, with or without mitral valve replace- median sternotomy incision in conventional ment. Left ventricular myectomy is recom- CABG procedures. Second, because MIDCAB mended for patients with drug-refractory is a beating heart procedure, no cardioplegia symptomatic outflow obstruction (peak gra- is instilled to stop the heart. Third, because dient > 50 mm Hg under resting conditions MIDCAB is a beating heart surgery and no and/or gradient > 50 mm Hg measured). cardioplegia is instilled, cardiopulmonary Surgery may also be considered in sympto- bypass (CBP) is not required for MIDCAB matic patients with documented outflow procedures. MIDCAB procedures are per- obstruction under physiologic exercise but formed on patients with one or two blockages with absent or very mild resting obstruction. to the right coronary artery, left anterior One additional subset of patients may benefit descending coronary artery, or its branches on from LV myectomy: young, asymptomatic the front of the heart. patients with documented severe outflow Minimally invasive direct view: Techniques tract obstruction (gradient 75–100 mm Hg). that were developed to repair or replace the Myxoma: A benign cardiac tumor. It causes mitral valve and repair or replace the aortic obstruction of blood flow, which leads to the valve. The main benefit of minimally invasive clinical presentation of heart failure, signs of direct view valve surgery is the avoidance of a central nervous system (CNS) embolization, median sternotomy. An 8-cm incision is made and/or constitutional symptoms such as and cartilage removed to allow for direct visu- fever, weight loss, fatigue, weakness, arthral- alization of the valves. gia, and myalgia. Tumor resection is the only Minute ventilation: The volume of gas effective treatment. exchange (inhaled and exhaled) in one Negative inspiratory pressure: Also referred minute. It is measured by multiplying respira- to as negative inspiratory force. The amount tory rate and tidal volume. of negative pressure that the patient generates Mitral regurgitation: Incomplete closure of during a forced inspiration when working the mitral valve leaflets, resulting in a back- against an obstruction to flow. It is a reflec- flow of blood into the left atrium during vention of a patient’s ability to take a deep breath tricular systole. and generate a cough that is strong enough to Mitral stenosis: Narrowing or constriction clear secretions. of the mitral valve that creates a pressure gra- 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 440

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Nitric oxide (NO): A product that is released the left ventricle. In this procedure, a section by endothelial cells. It produces vasodilation of the left ventricular wall from the apex to and increased vascular permeability. the mitral annulus is removed, and the edges Off-pump coronary artery bypass are reapproximated. Improvements in signs of (OPCAB): Also known as a beating heart pro- heart failure and ejection fraction have been cedure. This type of minimally invasive car- achieved with this technique. Because other diac surgery entails a median sternotomy or surgical procedures have achieved results thoracotomy incision; no bypass machine is superior to those produced with the partial required. The surgeon sews the grafts onto left ventriculectomy, this procedure is no the beating heart using specialized instru- longer in use in most of North America; how- ments to stabilize the myocardial tissue. ever, it is still used in other areas where car- OPCAB may be performed on patients need- diac transplantation is less readily available. ing four or five vessels repaired, as compared Percutaneous mitral balloon valvotomy with minimally invasive direct coronary artery (PMBV): See commissurotomy. This technique bypass (MIDCAB), where only one or two ves- has very successfully reduced left atrial gradi- sels can be repaired. With OPCAB, an artery ent, increased mitral valve area, and improved or vein from the lower extremities is used to symptoms of mitral stenosis. make the bypass. Percutaneous transluminal coronary Orthotopic heart transplant: A heart trans- angioplasty (PCTA): A technique that uses plant approach that entails replacing the an arterial catheter and various mechanical recipient heart with the donor heart. means to increase the diameter of diseased Overdamped waveform: A situation in coronary arteries, thereby improving blood which a pressure waveform is sluggish and flow. has an exaggerated or falsely widened and Pericardiectomy: Surgical removal of part of blunt tracing. It will cause the patient’s sys- the membrane that surrounds the heart (peri- tolic pressure to be recorded as falsely low and cardium). It is usually performed to treat the diastolic pressure to be recorded as falsely inflammation and prevent collection of fluid high. in the pericardial sac (between the peri- Oxygen consumption: The amount of oxy- cardium and heart), which can cause hemody- gen used by the body’s tissues. namic compromise from poor cardiac filling and emptying. Oxygen delivery: The amount of oxygen that is carried to the body’s tissues each minute. Phlebostatic axis: An anatomic landmark located at the fourth intercostal space, mid- PaO /FiO ratio: An index of oxygenation. A 2 2 point of the anterior–posterior diameter. Lev- PaO /FiO ratio of less than 200 is associated 2 2 eling at the phlebostatic axis is performed to with a significant intrapulmonary shunt. eradicate the effects of hydrostatic forces on Papillary fibroelastoma: A benign cardiac the hemodynamic pressures. tumor that occurs on the heart valves and Phrenic nerve injury: A complication follow- may cause obstruction or central nervous sys- ing cardiac surgery with cardiopulmonary tem (CNS) embolization. bypass. The extent of injury can range from Paroxysmal nocturnal dyspnea (PND): A neuropathy to paralysis of the diaphragm. It feeling of shortness of breath that awakens is often reported to be attributed to the use of the patient. It is usually relieved when the hypothermia, application of ice slush around patient assumes an upright position. the heart, and harvesting of the internal Partial left ventriculectomy: A procedure to mammary artery that occur during surgery. restore the proper mass-to-diameter ratio for 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 441

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Postcardiotomy cardiogenic shock: Heart and stronger as the person exhales. It is an failure that develops as a result of heart sur- indicator of the presence of severe ventricular gery or a heart attack. systolic failure and decreased myocardial Preload: The pressure found in the left ventri- contractility. cle at the end of diastole. It is sometimes Right-to-left shunting: The flow of blood referred to as left ventricular end-diastolic pres- from the right to left side of the heart, usually sure. Right-sided preload is the pressure found through an opening between the two atria or in the right atrium at the end of diastole. ventricles. Great vessels in the chest may be Prosthetic valves (mechanical valves): affected as well. Right-to-left shunting can be Valves that are manufactured from man- attributed to a patent foramen ovale, espe- made materials such as metal alloys, pyrolite cially with conditions that increase right carbon, and Dacron. Mechanical prosthetic atrial pressure (e.g., tricuspid stenosis). An valves are more durable and last longer than example is a patient with an atrial septal biologic valves. defect. The affected patient may have periods of cyanosis. Pulmonary hypertension: High blood pressure in the arteries that supply the lungs and Right ventricular assist device (RVAD): A right side of the heart. It develops when these type of mechanical support for the right ven- vessels become constricted or obstructed, tricle. Blood is drained through a pump from which slows blood flow. The result is an the right ventricle to the pulmonary artery. increase in pressure in the pulmonary arteries, Robot-assisted coronary artery bypass making it more difficult for the right ventricle (RACAB): A cutting-edge surgical technique. to eject blood to the pulmonary arteries. Unaccommodating places is what robot- Pulmonary stenosis: Narrowing or constric- assisted surgery is about; the human surgeon tion of the pulmonic valve that creates a pres- is not optimized for tiny spaces. In RACAB, sure gradient. the surgical robot consists of a collection of wristed tools called manipulators, which Pulse oximetry: A noninvasive method of receive digital instructions from an interfaced monitoring the percentage of hemoglobin computer. The surgeon, who is seated at a that is saturated with oxygen. computer console with a three-dimensional Pulse pressure variation (PPV): An alterna- display, acts as the “driver” of the computer. tive, less invasive method of evaluating car- The surgeon initiates the digital instructions diac output. It may be used as a means for by controlling the hand grips. By using the determining the patient’s ability to respond hand grips, the surgeon’s hand movements at to fluid. PPV is the difference between the the console are then duplicated in the robot, maximum and minimum values of the arte- with software filtering out physiologic hand rial pulse pressure during one mechanical tremors. breath divided by the mean of the two values. Saphenous vein: A vein in the patient’s leg In the evaluation of the Frank-Starling curve, that runs near the leg’s surface. It is used as a an increase in preload causes a decrease in graft for coronary artery bypass procedures. PPV; decreasing preload causes an increase in There are actually two saphenous veins in the PPV and contractility. leg—the great (large) and small veins. When Pulsus alternans: An exaggeration of the harvested for bypass procedures, long inci- normal variation in the pulse during the sions are usually made. Almost directly upon inspiratory phase of respiration, in which the harvest, the surface of the saphenous vein pulse becomes weaker as the person inhales becomes vulnerable to platelet aggregation 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 442

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because of the loss of the vascular endothe- mechanical breath relative to the mean stroke lium. For this reason, patients require volume. antithrombotic therapy to prevent graft Subendocardial resection (SER): A proce- closure. dure that involves surgical removal of scar tis- Square wave test: Also referred to as a fast sue, portions of an aneurysm, or other sites of flush or dynamic response test; a test that is abnormal electrograms. It is used to treat ven- performed to assure that the waveforms that tricular tachycardia. appear on the monitoring screen accurately Superficial sternal wound infection: An reflect pressures. It is accomplished by pulling infection involving only the skin and subcuta- and releasing the “pigtail” or squeezing the neous fat. It is characterized by drainage from button of the flush device so that the flow the wound and local inflammation while the through the tubing increases (from 3 mL/hr underlying sternum remains stable. obtained with a pressure bag inflated to 300 Surgical anterior ventricular endocardial mm Hg). The sudden rise in pressure in the restoration (SAVER): A procedure that is a system generates a square wave on the moni- modification of the original Dor procedure. It tor oscilloscope. is associated with a significant reduction of Stabilizer: A device used in minimally inva- left ventricular volume and a significant sive cardiac surgery that provides a direct view increase in ejection fraction as well as signifi- of the operating field, dampens the movement cant reductions in hospitalizations for heart of the epicardium, and permits the surgeon to failure. maintain a nontraumatic grip on the beating Surgical revascularization: Also known as heart. The device helps the surgeon isolate the coronary artery bypass grafting (CABG). Use diseased vessel and stabilizes the localized of arterial or venous vessels to create a new region of epicardium for anastomosis. pathway for blood to reach the coronary Steroid pulse: Administration of large doses arteries, thereby “bypassing” a stenosis. of steroids over a short period of time to treat Sympathomimetics: Agents that activate heart transplant rejection. adrenergic receptors by direct receptor bind- Stroke volume: The amount of blood ejected ing, promotion of norepinephrine (NE) by the left ventricle with each contraction. release, blockade of NE reuptake, and inhibi- Stroke volume is affected by the amount of tion of NE inactivation. blood in the ventricle and by the force of con- Systolic pressure variation (SPV): An alter- traction of the ventricle. It can also be native, less invasive method of evaluating car- affected if the aortic valve restricts flow out of diac output. It may be used as a means for the left ventricle. determining the patient’s ability to respond Stroke volume variation (SVV): An alterna- to fluid. SPV is the difference between the tive, less invasive method of evaluating car- maximum and minimum systolic blood pres- diac output. It may be used as a means for sure during one mechanical breath. determining the patient’s ability to respond Tidal volume: The amount of air inhaled to fluid. SVV occurs due to changes in during a normal breath (versus a forced intrathoracic pressure during spontaneous inhalation). breathing. It produces data on changes in preload that occur with mechanical ventilation. Total artificial heart (TAH): A treatment SVV is the difference between the maximum alternative for patients with biventricular fail- and minimum stroke volume during one ure who are hospitalized candidates for heart transplant. A TAH replaces the function of 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 443

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both ventricles and the four heart valves. It is Unassisted aortic end-diastolic pressure: implanted in the patient’s chest and attached The pressure in the aorta at the end of dias- to the atria. Tubes from the ventricles con- tole when counterpulsation via the balloon tinue from the patient’s chest to a power- pump has not assisted that cardiac cycle. generating console. The TAH can deliver car- Unassisted systole: The systolic aortic pres- diac output at a rate as high as 9.5 L/min. It sure when counterpulsation has not assisted reportedly augments renal and hepatic blood the cycle. flow and improves survival of heart trans- Underdamped waveform: A situation in plant patients with preoperative biventricular which a pressure waveform has an over- failure. response, revealed visually as an exaggerated, Totally endoscopic coronary artery bypass narrow, and artificially peaked tracing. In this (TECAB): A method of performing off-pump case, the waveform overestimates the patient’s coronary artery bypass grafting. It entails systolic pressure and underestimates the dias- using endoscopy, as opposed to the mini- tolic pressure. mally invasive direct coronary artery bypass Valvuloplasty: A procedure that entails inser- (MIDCAB) approach, which uses small thora- tion of a balloon to stretch or enlarge the cotomy incisions. valve opening. Transmyocardial laser revascularization Venous oxygenation saturation (SvO ): A (TMR): A procedure whereby transmyocar- 2 method used to determine how much oxygen dial channels are created from the epicardium the tissues are extracting. Venous oxygen sat- into the ventricle via a laser. The channels uration reveals the association between oxy- then allow blood from the ventricle to reach gen delivery (the amount of oxygen that is the myocardium directly. carried to the tissues each minute) and oxy- Transplantation: The surgical removal of a gen consumption (the amount of oxygen diseased heart and replacement with a healthy used by the tissues). donor heart. Ventricular assist device (VAD): A device Transplant vasculopathy: Accelerated coro- used for longer-term mechanical circulatory nary artery disease in the transplanted heart. support. This implanted mechanical pump is Tricuspid regurgitation: Incomplete closure used in patients with end-stage heart disease. of the tricuspid valve leaflets, resulting in a VADs assist a weakened heart by pumping backflow of blood. blood throughout the body. Tricuspid stenosis: Narrowing or constric- Ventricular reconstruction: Techniques tion of the tricuspid valve, which creates a that are based on the principle that the ven- pressure gradient. tricular wall tension is proportional to the left Tricuspid valve: The heart valve that is ventricular radius and pressure and inversely located between the right atrium and ventri- proportional to the wall thickness (Law of cle, near the atrioventricular (AV) node, right Laplace). By changing the size and shape of coronary artery, and coronary sinus. Its func- the ventricle, these techniques seek to reduce tion is to maintain forward flow of blood. The wall tension and improve left ventricular tricuspid valve has an annular ring and three function. Specifically, surgical reconstruction leaflets connected via chordae tendinae to techniques remove or isolate dysfunctional papillary muscles that are integrated with the myocardium, reduce the diameter of the ven- right ventricle tricle, and attempt to restore a more elliptical ventricular shape. Additional goals are to 57625_CH20_GLOS_433_444.pdf 4/10/09 11:08 AM Page 444

444 Glossary

relieve ischemia by revascularization if possi- organs, muscles, and tissues. A VSD also ble, and to further reduce ventricular size and results in an increase in ventricular workload volume via mitral valve repair. because greater volumes of blood are being Ventricular septal defect (VSD): An open- circulated; this effect ultimately leads to heart ing in the wall (septum) between the right failure. and left ventricles. The result of this opening Vital capacity: The amount of air that can be is the return of oxygenated blood in the left exhaled forcibly following a full inspiration. ventricle to the right ventricle, rather than the Zero balance: A process of establishing blood continuing forward into the systemic atmospheric pressure as zero to obtain accu- circulation to deliver oxygen to the cells, rate hemodynamic values. 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 445

Index

Boxes, figures, and tables are denoted by b, f, and t following cardiac surgery and, 264–265 the page number. hemodynamic monitoring and, 105–106, 133, 145, 158–159 A hypertension and, 205 hypotension and, 216, 220 AAA. See Abdominal aortic aneurysm IABP and, 166, 167 AACN Synergy Model for Patient Care mitral regurgitation and, 80, 81 clinical judgment, 1, 8 reducers, 62–63, 130, 206, 210, 213 competencies and patient needs, 9, 10 RV failure and, 263 nursing expertise, 4 stroke volume and, 259–260 patient characteristics, 6 venous oxygenation saturation and, 157 A-a gradient (alveolar-arterial oxygen gradient), 193 ALI (acute lung injury), 272–273 Abdominal aortic aneurysm (AAA), 24, 57, 95, 168 Alkalosis, 191–193, 348–350 Abdominal assessment, 57 Allen test for graft occlusion, 120–121, 120t ABG. See Arterial blood gas Allograft, 433. See also Cardiac transplantation Abiomed pumps, 395–396, 397, 397f, 402 cardiac allograft vasculopathy, 417 Ablation for arrhythmias, 32, 33–34, 47, 410 coronary artery disease (ACAD), 419, 422, 433 ACE inhibitors. See Angiotensin-converting enzyme definition, 433 inhibitors dysfunction, 408–409 Acid–base imbalances, 189–193, 346–350 infection in, 418 Acidosis, 190–192, 347–349 Allograft dysfunction, 408–409 ACORN Cardiac Support Device, 37, 433 Alveolar-arterial oxygen gradient (A-a gradient), Action potential phases, 19f, 20, 20b 193, 433 Acute lung injury (ALI), 272–273 American College of Cardiology (ACC)/ American Acute myocardial infarction (AMI), 3, 166 Heart Association (AHA) Acute pain, 289–290 aortic valve replacement recommendations, 76 Acute renal failure (ARF), 361–364 Task Force on Practice Guidelines, 28–31, 59 assessment of, 362–363 American College of Chest Physicians initiation stage, 363 COPD patients, recommendations for, 57 oliguric stage, 363 heparin prophylaxis recommendations, 63 preexisting conditions and, 60 American Heart Association (AHA), 393. See also treatment of, 363–364 American College of Cardiology (ACC)/ Acute respiratory distress syndrome (ARDS), 272–273 American Heart Association (AHA) Adenosine (Adenocard), 240–241, 314 American Society for Pain Management Nursing, 292 Adrenaline. See Epinephrine American Society of Anesthesiology wound infection Adrenergic agonists, 216–222, 217t, 225–226 prediction score, 383 Adult congenital heart disease, 42 AMI. See Acute myocardial infarction Afterload, 433 Aminocaproic acid (Amicar), 247–248, 406 anesthesia and, 131 Amiodarone (Cordorone) aortic stenosis and, 74, 76 black box warning, 249 cardiac output measurements and, 20–21 bradycardia, treatment of, 409

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446 Index

as Class III agent, 235–236 Arterial pulse contour CCO, 155–156, 434 minimally invasive surgery, use after, 106, 107 ASD (atrial septal defect), 42 postoperative dysrhythmias, management of, 62, Aspirin, 63, 330 231, 233, 313 Assisted aortic end-diastolic pressure, 169–170, 434 ventricular dysrhythmias, management of, 242, 243 Assisted systole, 170–172f, 171, 173b, 434 Amrinone. See now Inamrinone Atelectasis, 188, 271 Anesthesia, recovery from, 127–143 Atorvastatin (Lipitor), 278 alterations in heart rate and rhythm, 133 Atrial cuff technique, 405, 434 anesthetic agents, 127, 128, 128t, 130–132 Atrial dysrhythmias. See also specific dysrhythmias balanced anesthesia, 130 agents used in management of, 230, 239–242 extubation, complications related to, 135–137 cardiac transplantation and, 312, 410 “fast-tracking” anesthesia, 130 intraoperative factors, 311–312 hand-off communication, 127–128 postoperative, 309–314, 318 hemodynamic management, 132–133 Atrial fibrillation (AF) hypothermia, 134–135 cardiac transplantation and, 410 immediate postoperative care, 128–129 coronary artery bypass grafting (CABG) and, 62 induction agents, 130–131 Cox/Maze procedure for, 33–34 inhalation agents, 131–132 drug treatment for, 230–236, 238, 239 malignant hyperthermia (MH), 137–138 incidence and time of onset of, 367 neuromuscular blocking agents, 63, 108, 128, 132, Maze procedure for, 33–34, 101, 107 136–137, 190, 347 minimally invasive cardiac surgery (MICS) nursing assessment, 129–130 and, 107 opioids, 132, 137 neurologic complications and, 327 postoperative care, 128–129, 132–137 on- and off-pump coronary bypass surgery, 119 postoperative complications, 137–138 postoperative, 87, 310–314 postoperative nausea and vomiting (PONV), 131, preoperative nursing evaluation, 62 133–134 reduction of, 318 protamine sulfate allergic reaction, 138 strokes and, 33 pseudocholinesterase deficiency, 138 surgical management of, 32, 33–34, 47, 101 respiratory management, 135 Atrial flutter, 314, 410 stir-up regime, 135 Atrial septal defect (ASD), 42, 434 thermoregulation, 134–135 Atrioventricular nodal reentrant tachycardia Aneurysms, 23–24, 57 (AVNRT), 32 Angina, 58, 166–167 Atrioventricular reentrant tachycardia (AVRT), 32 Angiotensin-converting enzyme (ACE) inhibitors, 23, Atropine, 132 62, 63, 208, 212–213, 232 Autonomic receptors and cardiovascular function, 21, Angiotensin-receptor blockers (ARBs), 209, 213, 232 22, 22t Angiotensin II, 23, 212, 213 AV block Ankle-brachial index, 56, 177–178b, 433 bradyarrhythmias and, 315 Annuloplasty, 37, 81, 84, 433, 437, 439 as cardiac surgery complication, 86 ANP (atrial natriurectic protein), 23 conduction delays and, 411 Antibiotics, 245, 378 digoxin and, 240 Anticoagulants, 54, 63–64, 117–118, 314. See also diltiazem and, 238 specific drugs ibutilide and, 236 Anxiety and depression in postoperative patients, 55, metoprolol and, 234 115, 333–334 Azatriaprine (AZA, Imuran), 416 Aortic aneurysm, 24, 57, 95, 168 Azotemia, 361–362 Aortic dissection, 107, 117–118, 176, 178 Aortic regurgitation (AR), 56, 74, 76–77, 78, 78t, 433 B Aortic stenosis, 60, 64, 65, 74–76, 75t, 214, 262, 263, 433 Aortic valve replacement, 75–77, 75t, 78, 78t, 188 Balanced anesthesia, 130 Aprotinin (Trasylol), 63, 278, 406 Balloon valvotomy/valvuloplasty, 79, 80t, 84, AR. See Aortic regurgitation 434, 440 ARBs. See Angiotensin-receptor blockers Barbiturates, 130 ARDS (acute respiratory distress syndrome), 272–273 Basiliximab (Simulect), 415 ARF. See Acute renal failure Beating heart surgery, 312. See also Minimally invasive Arrhythmias. See Dysrhythmias cardiac surgery (MICS); Off-pump coronary Arterial blood gas (ABG), 189–193, 189t, 346, 346t artery bypass (OPCAB) 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 447

Index 447

Benzodiazepines, 131 Bridge to transplantation, 35, 167, 168, 394–404, 422, Beta blockers. See also specific drugs 426, 434 as antihypertensive agents, 208, 211–212 Bronchospasm, 136 black box warning, 249 cardiac transplantation, use after, 410 C dysrhythmias, management of, 230–232, 234–235, 313 CABG. See Coronary artery bypass grafting hypertrophic cardiomyopathy, treatment of, 43 Calcineurin inhibitors (CNI), 414 postoperative treatment of aortic stenosis, 76 monoclonal antibodies and, 415 preoperative nursing evaluation and, 62 mycophenolate mofetil and, 416 Betapace. See Sotalol nephrotoxicity concerns with, 394, 417 Bicarbonate NSAIDs and, 412 arterial blood gas values and, 346 Calcium channel blockers. See also specific drugs cardioplegia and, 435 cardiac transplantation, use after, 120, 410 epinephrine use and, 217 dysrhythmias, management of, 237–238 metabolic acidosis and, 191, 348 effect of, 19 metabolic alkalosis and, 192–193 postoperative dysrhythmias, management Bicaval technique, 405, 434 of, 313 Bicuspid aortic valve, 42 postoperative hypertension, management of, 209, Biologic valves, 82, 434 213–215 Bioprosthetic valves, 74, 85–86. See also Heart valve preoperative nursing evaluation and, 62, 63 surgery Calcium imbalances, 355–356 Bivalirudin (Angiomax), 118 Cardene. See Nicardipine Biventricular assist device (BiVAD), 395, 396f, 401, Cardiac allograft vasculopathy, 417, 420t, 422, 435 402t, 434 Cardiac arrest, 268–269 Biventricular support, 401 Cardiac catheterization, 60, 61, 106, 168, 434 Black box warnings, 249t Cardiac complications of cardiac surgery, Bleeding. See also Hemorrhage 258–269 agents used to control postoperative, 245–248 cardiac arrest, 268–269 cardiac surgery and, 44 coronary vasospasm, 266 cardiac transplantation and, 406 decreased myocardial contractility, 263–264 coagulopathies and, 261, 273–275 decreased systemic vascular resistance, 265 hematologic complications of cardiac surgery, diastolic dysfunction, 262–263 261, 273–276, 274t dysrhythmias, 261–262 heparin-induced thrombocytopenia (HIT), emergency resternotomy procedures, 267 275–276 increased systemic vascular resistance (afterload), herbal remedies and, 64 264–265 history of, 54 internal defibrillation procedure, 268, 269 with intra-aortic balloon pump (IABP) use, low cardiac output, 259–261, 263 173, 176 mechanical issues, 265–266 minimally invasive cardiac surgery (MICS) myocardial ischemia and infarction, 266–268 and, 108 myocardial stunning and hibernation, 264 on- and off-pump coronary bypass surgery, 117 preload issues, 259, 260, 261, 263, 265 postoperative anesthesia assessment, 129 right ventricular failure, low cardiac output postoperative hemodynamic assessment, 158–159 due to, 263 Blood flow through heart and major blood vessels, tamponade, 265–266 15–16, 17, 23–24 Cardiac cycle, 16, 16f, 150, 153, 157, 166 Blood pressure. See also Hypertension; Hypotension Cardiac history of patient, 58–59 monitoring, 149–150 Cardiac output measurements, 154–157, 434 systemic control of, 23 alternative methods to determine, 155–156 Brachial plexus injury, 334–335 arterial pulse contour CCO, 155–156 Bradycardia continuous cardiac output (CCO), 154–155 agents used to treat postoperative, 244–245 doppler methods, 156–157 bradyarrhythmias, 315 electrical bioimpedance, 157 cardiac transplantation and, 409–410 output, preload and afterload, 20–21 minimally invasive surgery and, 107 pulse pressure variation (PPV), 156 Brethine (Terbutaline), 410 stroke volume variation (SVV), 156 Bridge to recovery, 35, 395, 434 systolic pressure variation, 156 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 448

448 Index

Cardiac surgery, 27–52. See also specific procedures indications for, 35, 37–42, 39–40t, 43 adult congenital heart disease, 42 infection prophylaxis, 418–419 arrhythmias, surgical management of, 32–35 infectious disease following, 417–419, 420 bleeding after, 44 mechanical circulatory support, 394–400 cardiac transplantation, 37–42 medications, patient instructions, 422 cardiac tumors, 44–45 mitral valve replacement and, 37 coronary artery bypass grafting (CABG), nutrition, 412, 421 indications for, 28–31, 35 outcomes after, 419–420, 420t dynamic cardiomyoplasty (DCMP), 37 pain management, 412 endoaneurysmorrhaphy, 36 patient recovery, factors influencing, 404–405 geometric ventricular reconstruction, 36–37 patient teaching, 420–422 heart failure, 35 postoperative care, 404–405 hypertrophic cardiomyopathy (HCM), 42–44 procedures for, 36, 404–405, 434, 437, ischemic heart disease, 27–28 438, 440 minimally invasive myocardial revascularization, 31 progression of care following, 412–419 mitral valve repair in dilated cardiomyopathy, 35 psychosocial condition following, 412 mortality risk factors, 55t pulmonary hypertension after, 407, 409 partial left ventriculectomy, 36 rejection, 412–413 pericardial surgery, 44 renal dysfunction, 411–412 preoperative cardiac surgery nursing evaluation, rhythm disturbances and electrocardiograph 53–72 changes, 409–411 tamponade, 44 right heart failure after, 407 transmyocardial laser revascularization (TMR), sexual activity after, 422 31–32, 33 skin cancer prevention after, 422 valve disease, 32 surveillance, post-transplant, 419 ventricular reconstruction techniques, 35–36 transplant vasculopathy (TV), 419 Cardiac tamponade ventricular assist devices (VAD), 400–404 as cardiac surgical complication, 265–266, 266t, wound complications, risk factors for, 268, 403 373, 389 cardiac transplantation and, 411 Cardiac tumors, 44–45 chest tubes and, 130 Cardiogenic shock monitoring and treatment for, 44, 117, 139, 150, carvedilol and, 235 215, 216, 411t esmolol and, 211 postoperative hemodynamic assessment, 159, 266t heart valve surgery and, 85 pulmonary artery catheter removal and, 153 IABP use in, 165, 166 Cardiac transplantation, 393–431 labetalol and, 212 activity after, 412, 421–422 mechanical circulatory support and, 395, 399 allograft dysfunction, 408–409 postoperative care and, 205, 244, 258, 265 bleeding, 406 sotalol and, 237 cardiac allograft vasculopathy, 417, 422, 435 Cardiomyopathy cardiac tamponade following, 411 hypertrophic cardiomyopathy (HCM), 42–44 cardiomyopathy, 38 mitral valve repair in, 35 chronotropy (rate) issues, 407–408 Cardioplegia. See also Cardioprotection contractility issues, 408 atrial dysrhythmias and, 313 contraindications for, 39–40t bradycardia and, 244 criteria for, 393–394 in CABG, 93 definition of, 443 definition of, 435 dysrhythmias, management following, 312, 315–316 fluid and electrolyte imbalances and, 244, 345, exercise, 421–422 351, 365 heart failure management, 393 IABP and, 167 heart-lung transplantation, 38, 42 LCOS and, 260 hypertension after, 407 minimally invasive surgery and, 96, 97t, 98, 100, hypertrophic cardiomyopathy, 43 108, 439 hypotension after, 408 myocardial function and, 263–264 hypovolemia, 406–407 myocardial ischemia and, 267 IABP use and, 167, 174 ONCAB and, 116, 119 immediate postoperative care, 404–405 Cardioplegic arrest, 215 immunosuppression following, 413–417 Cardioplegic solution, 312, 435 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 449

Index 449

Cardioprotection. See also Cardioplegia MICS and, 102 cardiac contractility and, 263 phrenic nerve neuropathy and, 335 cold preservation for, 189 postoperative complications risk factor, 258, 269, dysrhythmias and, 262t, 309 276, 278 inadequate, 205, 229, 259 preoperative assessment and, 57, 59 infections and, 373 wound complications risk factor, 372, 373, 383 postoperative management and, 221 Chronic pain, 289–290, 292 pulmonary complications and, 269, 270t CK-MB (creatine kinase) levels, 267, 268 Cardiopulmonary bypass (CPB), 6, 27, 42, 56, 59, 93, Class I agents for dysrhythmias, 229–230, 243 115, 435. See also Coronary artery bypass Class II agents for dysrhythmias, 229–230, 234–235 grafting (CABG) Class III agents for dysrhythmias, 229–230, 235–237 Cardiovascular anatomy and physiology, 13–26, 13f Class IV agents for dysrhythmias, 229–230, 237–238 blood flow through heart and major blood vessels, Clevidipine (Cleviplex), 209, 214–215 15–16, 17, 17f, 23–24 Clinical judgment processes, 2–4 cardiac lymphatic system, 16–17 data management, 3 cardiac output, preload and afterload, 20–21 decision analysis, 4 chambers and valves of heart, 13–16, 14f information processing, 2–3 coronary arteries, 16 intuition, 3–4 disorders of major blood vessels, 23–24 Clonidine (Catapres), 293 electrical control of cardiac muscle, 18–20, 19f Clopidogrel (Plavix), 63 external control of heart, 21 CMV. See Cytomegalovirus point of maximal impulse, 14–15 CNI (calcineurin inhibitors), 414 pressure of blood in major blood vessels, 17, 18f CNPI (Checklist of Nonverbal Pain Indicators), 292 systemic circulation, 21–23 Cognitive decline after cardiac surgery, 119, 326, 333 systemic control of blood pressure, 23 Cold, use in pain management, 296 Cardizem. See Diltiazem Cold ischemia time, 405, 435 Carotid aortic stenosis, 61–62 Colloid therapy, 359–360 Carotid bruit, 56, 61–62, 435 Commissurotomy, 79, 84, 435. See also Heart valve Carotid disease, coronary artery bypass grafting surgery (CABG) in patients with, 31 Communication in patient care, 8–9 Carvedilol (Coreg), 231, 234–235, 313–314 Compartment syndrome, 121, 178 Catapres (Clonidine), 293 Computer Motion AESOP and ZEUS systems, 98 Catecholamines, 216. See also specific agents Conduction delays after cardiac transplantation, acid–base disorders and, 189 410–411 afterload and, 159 Conduits, wound care of, 371–372. See also Wound care anesthesia and, 131–132 Congenital heart disease, 42 diastolic dysfunction and, 263 Continuous cardiac output (CCO), 154–155 pain management and, 292 Continuous Renal Replacement Therapy (CRRT), renal function and, 95, 361 363–364 Catheter migration with IABP, 176 Contractility CCO (continuous cardiac output), 154–155 acid–base disorders and, 189 Cellcept. See Mycophenolate mofetil anesthesia and, 130, 131, 133, 134 Central venous oxygen saturation, 157–158, 435 aortic stenosis and, 65, 75 Central venous pressure (CVP) monitoring, 150–153, calcium imbalances and, 356 152f, 152t cardiac catheterization and, 61 Cerebral hyperthermia, 108 carvedilol and, 234 Certican (Everolimus), 417, 419 decreased myocardial, 263–264 Chambers and valves of heart, 13–14, 14f, 15–16 defined, 435 Checklist of Nonverbal Pain Indicators (CNPI), 292 dobutamine and, 222, 260, 408 Chest tubes, 104–105, 108, 130, 158, 274 dopamine and, 221, 260, 408 Chronic obstructive pulmonary disease (COPD) epinephrine and, 218, 260 anesthesia and, 128 hemodynamic monitoring and, 105, 106, 119, 145, cardiac transplantation and, 40, 41 150, 156, 157, 160 dyspnea and, 59 mechanical ventilation and, 187, 192 hemodynamic monitoring and, 146, 153 metoprolol and, 234 labetalol and, 212 milrinone and, 263, 408 mechanical ventilation and, 185, 197 mitral valve replacement and, 79 metoprolol and, 234 nicardipine and, 213 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 450

450 Index

potassium imbalances and, 350 Cox/Maze IV procedure, 33–34, 101, 436 protamine sulfate and, 246 CPOT (Critical-Care Pain Observation Tool), 292 sympathetic stimulation and, 21 Critical care, 1–11 COPD. See Chronic obstructive pulmonary disease clinical judgment processes, 2–4 Cordorone. See Amiodarone common trajectories, 6–10 Coreg. See Carvedilol communicating findings, 7–8 Corlopam. See Fenoldopam mesylate day-to-day practice in, 5–10 Coronary angiography, 17 dying and, 10 Coronary arteries, 16 goal-oriented decisions, 9 Coronary artery bypass grafting (CABG) interventional approaches, 9 ACC/AHA indications for, 29–30t investigation of problems, 7 ACE inhibitors and, 63 mobilization of team, 8 anesthesia and, 128, 133 relationship-centered caring in, 4–5 atrial fibrillation (AF) following, 62 surveillance, 7 bleeding after, 273 team decision making, 8–9 cognitive decline after, 119 trending and knowing patients in, 6 compartment syndrome, 121 Critical-Care Pain Observation Tool (CPOT), 292 complications of, 115–116, 269, 326, 340, 346 CRRT (Continuous Renal Replacement Therapy), concomitant carotid disease and, 31 363–364 diabetics and, 31 Crystalloid therapy, 359–360 extubation following, 185 CT scans, 61 graft occlusion after, 120–121 Culture, pain management and, 298–299 heart failure and, 35 CVP (central venous pressure) monitoring, 150–153, hemodynamic monitoring, 118–119 152f, 152t heparin use in, 63–64, 116 Cytomegalovirus (CMV), 406, 418 IABP use in, 167 indications for, 27, 28–31 D mechanical ventilation, prolonged after, 186 medical therapy compared, 27–28 Daclizumab (Zenapax), 415 minimally invasive myocardial revascularization, 31 Data collection and management, 3, 5, 7–8 off-pump CABG (OPCAB) compared, 31, 98, 102, da Vinci Surgical System, 98, 99, 99f 109, 116–121, 201 DCMP (dynamic cardiomyoplasty), 37, 436 pain management, 294–295 Decadron. See Dexamethasone pathophysiologic changes associated with, 93, Decision analysis model, 4 94–95t Deep breathing techniques percutaneous coronary intervention (PCI) for coughing, 103, 135, 271, 273, 287 compared, 28 in pain management, 296 peripheral vascular assessment for, 56 Deep sternal wound infection, 87, 186, 380, 418, 436 pleural effusion following, 188 Defibrillation, internal, 268, 269b pneumothorax following, 272 Delirium pulmonary complications of, 269, 346 drug therapy for, 332 recovery from, 109 environmental and supportive measures for, 332 sleep disturbances following, 54–55 postoperative, 58, 330–332 stroke risk and, 61–62 treatment of, 331–332 systemic inflammatory response following, 95, Dental evaluation, preoperative, 62 128, 133, 198 Depression and anxiety in postoperative patients, 55, total endoscopic CABG (TECAB), 31 115, 333–334 Coronary artery vasculopathy, 417, 420t, 422, 435 DES. See Drug-eluting stents Coronary heart disease (CHD), 27, 31–32. See also Desmopressin (DDAVP), 406 Cardiac surgery Destination therapy, 385, 399–400, 401, 436 Coronary vasospasm, 266 Dexamethasone (Decadron), 227–228, 233, 241–242 Corticosteroids, 414 Diabetes, 31, 372. See also Glycemic control Cortisol, 94t, 220, 228, 346 Diagnostic studies, 60–62 Corvert. See Ibutilide Dialysis after cardiac surgery, 276, 363–364 Coughing and deep breathing procedures, 103, 135, Diastolic augmentation, 166, 169, 170, 175, 436 271, 273, 287 Diastolic dysfunction as complication of cardiac Coumadin. See Warfarin surgery, 262–263 Cox/Maze III procedure, 33–34, 101, 435 Diastolic murmur, 56 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 451

Index 451

Dicrotic notch, 169, 171, 436 Class IV agents for, 229–230, 237–238 Digoxin (Lanoxin), 62, 232, 239–240, 313, 410 electrical control of cardiac muscle, 18–20 Dilantin (Phenytoin), 293 epicardial pacemakers, 316 Dilated cardiomyopathy, 35 heart valve surgery complications and, 87 Diltiazem (Cardizem), 107, 230, 232, 238, 313 IABP use and, 167 Diprivan (Propofol), 131 medications, preoperative assessment of, 62 Discharge minimally invasive cardiac surgery (MICS) and, 107 education regarding incision care, 386 pacing options, 107, 116, 315, 316 with LVAD, requirements for, 404 postoperative, 158, 262t, 309–321 planning, 55–56 preoperative assessment of heart disease, 58 Disopyramide (Norpace), 43, 230 surgical management of, 32–35 Dobutamine (Dobutrex) thyroid function, 60 anesthesia recovery and, 133 tricuspid regurgitation, 64–65 aortic stenosis and, 65 ventricular dysrhythmias, 233, 242–244 cardiac transplantation, use after, 316, 408, 409, 410 heart failure management, 393 E heart valve surgery, use after, 77, 79 postoperative management with, 106, 216, 217, Echinacea, 64 221, 222, 225–226, 227 Echocardiography, 60, 104 preoperative nursing evaluation, 62 ECMO. See Extracorporeal membrane oxygenation Documentation systems, 9 Ehlers-Danlos syndrome, 77 Dopamine (Intropin) Ejection fraction (EF) cardiac contractility and, 264 aortic regurgitation and, 77 cardiac transplantation and, 393, 408, 409 aortic stenosis and, 65 diastolic dysfunction, treatment of, 263 coronary revascularization and, 35 heart failure management, 393 defined, 20, 436 low cardiac output, treatment of, 260 digoxin and, 239 postoperative use, 106, 216, 221–222, 225, 227, ECG analysis of, 60 249, 264 hemodynamic monitoring and, 60, 119 renal complications, 276 IABP and, 166 wound infection predictor, 383 low cardiac output and, 260 Dopamine-1-receptor agonist, 215 OPCAB and, 102 Dopexamine (Dopacard), 276 vasopressin and, 220 Doppler methods for cardiac output measurement, Elderly population. See Older patients 156–157 Electrical conduction, 18–20, 19f, 157, 436 Dor procedure, 36, 436 Electrical control of cardiac muscle, 18–20 Drainage catheters, 129–130 Electrolyte imbalances. See Fluid and electrolyte Drug-eluting stents (DES), 27, 28, 436 imbalances; specific electrolytes Drugs. See Pharmacologic support following cardiac Emergency resternotomy procedures, 267b surgery; specific drugs Enalaprilat (Vasotec), 208, 212–213 Dual-chamber pacing, 43 Encainide (Enkaid), 230 Duke Criteria for diagnosis of infective endocarditis, Encephalopathy and delirium, 330–332 84–85 Endoaneurysmorrhaphy, 36, 436 Dynamic cardiomyoplasty (DCMP), 37, 436 Endocarditis, 74, 80, 84–86, 85t Dynamic response test. See Square wave test Endoscopic atraumatic coronary artery bypass Dyspnea, evaluation of, 59 grafting (EndoACAB), 98, 436 Dysrhythmias. See also specific dysrhythmias Endovascular/“keyhole” procedures, 100–102, ablation for, 32, 33–34, 47, 410 436–437 agents used in management of, 32, 34–35, Endoventricular circular patch plasty repair. See Dor 229–244, 231–233t procedure anesthesia, recovery from, 133 Enflurane, 131–132 atrial dysrhythmias, 230, 239–242, 309–314 Enkaid (Encainide), 230 cardiac surgery complications and, 261–262 Epicardial pacemakers, 316 cardiac transplantation and, 315–316, 407–411 Epidural and local anesthetics, 295–296 categories of antiarrhythmic therapy, 230b Epinephrine (Adrenaline), 216, 218–219, 225, 227 Class I agents for, 229–230, 243 Esmolol (Brevibloc), 208, 211 Class II agents for, 229–230, 234–235 Ethanol septal ablation, 44, 437 Class III agents for, 229–230, 235–237 Ethnicity, pain management and, 298–299 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 452

452 Index

Etomidate, 130–131 Geometric mitral reconstruction (GMR), 81, 437 Everolimus (Certican), 417, 419 Geometric ventricular reconstruction, 36–37 Exercise testing, 61 Gingivitis, 62 Ex-Maze procedure, 101, 437 Ginkgo biloba, 64 External control of heart, 21 Ginseng, 64 Extracorporeal membrane oxygenation (ECMO), 395, Glucose (serum level). See also Diabetes; Glycemic 399, 400, 400f, 437 control Extubation. See also Weaning from mechanical beta blocker use and, 211, 212, 235, 237 ventilation clinical judgment in evaluating, 2 bronchospasm, 136 epinephrine and, 219 complications related to, 135–137 hypoglycemia and, 338 hypoventilation and hypoxia, 136–137 hypomagnesemia and, 354 laryngospasm and noncardiogenic pulmonary management of, 329–330, 361, 378–379 edema, 135–136 mechanical ventilation predictor, 186 post-CABG, 185 monitoring of, 60, 64, 382 post-extubation care, 197–198 steroid use and, 228, 414 postoperative respiratory management, 135 wound care and, 372–373, 382 readiness criteria, 196 Glycemic control fluid and electrolyte imbalances and, 361 F infection and, 378–380, 418 sample postoperative orders to ensure, 379b Factor VII. See Recombinant activated factor VII strokes and, 329–330 Family wound complications and, 372 education regarding incision care, 386 Glycopyrrolate (Robinul), 132 postoperative nursing care, 103 GMR (geometric mitral reconstruction), 81 Fast flush. See Square wave test Goal-oriented decisions, 9 “Fast-tracking” anesthesia, 130 Graft closure, 104 Fenoldopam mesylate (Corlopam), 206, 207, 215, 276 Graft occlusion after coronary artery bypass surgery, Fentanyl, 412 120–121, 437 Fibroelastoma, 44 Flavonoids, 64 H Flecanide (Tambocor), 230 FloTrac/Vigileo system, 155–156 Hair removal from surgical site, 377 Fluid and electrolyte imbalances, 345–370 Haloperidol (Haldol), 332 acid–base imbalances, 346–350 Halothane, 131 acute renal failure and renal insufficiency, 361–364 HCM (hypertrophic cardiomyopathy), 42–44 anesthesia, recovery from, 130 Heart block, 107, 116, 313, 410–411 arterial blood gas values and interpretation, 346, 346t Heart disease, preoperative assessment of, 58–64 electrolyte imbalances, 350–358 cardiac history, 58–59 fluid and electrolytes distribution, 345 diagnostic studies, 60–62 fluid balance and volume management, 358–361 medications, 62–64 fluid volume distribution, factors affecting, 345–346 serological testing, 59–60 postoperative hemodynamic assessment, 159 Heart failure reference values for electrolytes, 351, 351t cardiac surgery for, 35 Frank Starling law, 20–21 cardiac transplantation for, 393, 407 coronary revascularization for, 35 G dynamic cardiomyoplasty (DCMP), 37 endoaneurysmorrhaphy, 36 Garlic, 64 geometric ventricular reconstruction, 36–37 Gas embolism, 169 low cardiac output and, 263 Gastroepiploic artery, 372 management of high-risk patients and, 65 Gastrointestinal problems mechanical ventilation and, 188 bleeding, history of, 54 mitral valve repair in dilated cardiomyopathy, 35 complication of cardiac surgery, 276–277 partial left ventriculectomy, 36 Gender. See also Women ventricular reconstruction techniques, 35–36 pain management and, 297–298 Heart–lung transplantation, 2, 38, 41t, 42. See also postoperative myocardial ischemia and Cardiac transplantation infarction, 267 Heartmate II, 401, 402, 403 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 453

Index 453

Heartmate XVE, 401, 402 minimally invasive surgery, 108 Heart transplantation. See Cardiac transplantation on- and off-pump coronary bypass surgery, 117–118 Heart valve surgery, 73–92 protamine sulfate and, 117–118, 138, 245–246, anesthesia and, 128 274, 406 aortic regurgitation, 56, 74, 76–77, 78 resistance, 64 aortic stenosis, 65, 74–76 VAD use, 401, 403 aortic valve replacement, 75–78, 188 Herbal remedies, 64 complications of, 86–87 Heterotopic method, 405, 437 echocardiography, 60 Hibernation of myocardium, 264 elderly patients, 89 HIT (heparin-induced thrombocytopenia), 275–276 infective valve endocarditis, 74, 80, 84–86 Hydrocortisone (Solu-Cortef), 229, 233, 242 mitral regurgitation, 79–83 Hyperadrenergic state, 229, 309 mitral stenosis, 77–79 Hypercalcemia, 355 mitral valve, 35, 37, 43 Hypercarbia, 205, 265, 404, 407 mitral valve annuloplasty ring, 37 Hyperkalemia, 351, 351f mitral valve replacement (MVR), 35, 37, 43, 80, Hypermagnesemia, 354 82–83 Hypernatremia, 352 pleural effusion following, 188 Hyperphosphatemia, 357 postoperative care, 86, 86t Hypertension, 205–215, 207–209t, 264 preoperative assessment of heart disease, 58 Hyperthermia, 108, 137–138, 227, 260, 326, 329 tricuspid valve disease, 83–84 Hyperthyroidism, 60 valvular heart disease (VHD), 32, 73–74 Hypertrophic cardiomyopathy (HCM), 42–44, 437 Hematologic complications of cardiac surgery, 261, Hypervolemia, 360–361 273–276, 274t Hypoalbuminemia, 55 Hemodynamic monitoring, 145–164 Hypocalcemia, 355–356, 356f anesthesia, recovery from, 132–133 Hypoglycemia, 64, 338 blood pressure monitoring, 149–150 Hypokalemia, 352, 352f cardiac output measurements, 154–157 Hypomagnesemia, 311, 314, 354–355 central venous pressure (CVP) monitoring, 150–153 Hyponatremia, 352–353 diastolic dysfunction as complication of cardiac Hypophosphatemia, 357–358 surgery, 263 Hypotension, 215–229, 217t, 226–227t, 227b, 408 equipment, preparation of, 146 Hypothermia essentials of, 145 afterload and, 205, 265 initial postoperative assessment, 146–149 anesthesia and, 134–135 low cardiac output as complication of cardiac bradycardia and, 244 surgery, 260 defined, 437 minimally invasive cardiac surgery (MICS), hemodynamic monitoring and, 107–108 105–106 hypokalemia and, 352 ONCAB and OPCAB, 118–119 hypovolemia and, 360 oxygenation parameters, assessment of, 157–158 neurologic complications and, 326, 329, 331 postoperative assessment, 148, 148b, 158–159 ONCAB and, 116 preload issues as complication of cardiac surgery, 261 postoperative care and, 108, 265 pulmonary artery catheter (PAC), monitoring renal complications and, 276 using, 150, 151, 153–154, 156, 407 Hypotheses, 2, 7 square wave test, 14, 146, 146b Hypothyroidism, 60 terms and definitions, 145b Hypoventilation and hypoxia, 136–137 vital signs and hemodynamic assessment, 105t, Hypovolemia, 358–360 146–148, 148t assessment of, 358 Hemorrhage, 111, 173, 215, 228. See also Bleeding cardiac transplantation and, 406–407 Hemothorax, 152t, 215, 265 fluid challenge, 359–360 Heparin third spacing, 360 altered heparin responsiveness, 64 treatment of, 358–359 American College of Chest Physicians prophylaxis recommendations, 63 I bypass procedures, 59–60 coated circuits in bypass devices, 278 IABP. See Intra-aortic balloon pump coronary artery bypass grafting (CABG), 63–64, 116 Ibutilide (Corvert), 230, 231, 236–237, 249, 313 induced thrombocytopenia (HIT), 275–276 IMA. See Internal mammary artery 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 454

454 Index

Immunosuppression following cardiac indications for, 166–168, 393 transplantation, 413–417 infections with, 176 Imuran (Azatriaprine), 416 insertion of, 168–169, 168f Inamrinone, 222–223, 224, 226, 227, 246, 393 limb ischemia, 173, 176 Incision sites, wound care for. See Wound care low diastolic augmentation, 175 Induction agents for anesthesia, 130–131 management of high-risk patients and, 65 Infections. See Wound care monitoring for complications of, 176, 178 Infectious complications of cardiac surgery, 278, nursing interventions for patients on, 177–178b 417–419, 420 ONCAB and, 116 Infective endocarditis, 437 physiology of balloon function, 166 heart valve surgery, 74, 80, 84–86 postoperative low cardiac output, treatment of, 260 preoperative management of, 65 preoperative use of, 182 tricuspid regurgitation from, 64–65, 83 timing issues, 169–173 Inflammatory response to cardiac surgery. See troubleshooting, 175–178 Systemic inflammatory response to cardiac waveforms with, 170–172f, 173b surgery weaning from, 174–175, 174b Inhalation agents for anesthesia, 131–132 Intra-arterial pressure monitoring, 149–150 Insulin Intrapulmonary shunt (IPS), 193–194, 438 carvedilol and, 235 Intrathecal pain management, 295 epinephrine and, 219 Intropin. See Dopamine magnesium imbalances and, 354 Intuition model, 3–4 metabolic acidosis and, 192 Investigation of problems, 7 potassium imbalances and, 351, 352 Ischemic heart disease. See also Cardiac surgery preoperative assessment and, 64, 394 cardiac history, 58–59 protamine reactions and, 117–118, 138, 245 coronary artery bypass grafting (CABG), stroke treatment and, 330 indications for, 28–31 wound care and, 379 medical therapy vs. surgical revascularization, 27–28 Internal defibrillation procedure, 268, 269b mitral regurgitation and, 80, 167 Internal mammary artery (IMA), 438 percutaneous vs. surgical revascularization, 28 CABG and, 93 preoperative assessment of, 58–64 diltiazem and, 238 surgery for, 27–28 MIDCAB and, 96 transmyocardial laser revascularization (TMR), neurologic complications and, 189, 326 31–32, 33 nitroglycerin and, 206 valvular heart disease and, 73–74 phrenic nerve injuries and, 189 Isoflurane, 131–132 preoperative assessment and, 56 Isoproterenol (Isuprel), 408, 410, 416 pulmonary complications and, 269 wound care and, 371–372 J International Association for the Study of Pain (IASP), 288 Joint Commission standard for pain assessment, 290 International Normalized Ratio (INR) self-testing, 63, 74, 247 K Intra-aortic balloon pump (IABP), 77, 81, 165–184, 438 abdominal aortic aneurysm and, 57 Kava, 64 afterload reduction with, 166, 167, 265 Keyhole procedures. See Endovascular/“keyhole” anemia and thrombocytopenia, 176 procedures aortic dissection, 176, 178 autofill failure, 175–176 L bleeding with, 173, 176 cardiac transplantation and, 408 Labetalol (Normodyne, Trandate), 208, 212 catheter migration, 176 Lanoxin. See Digoxin compartment syndrome, 178 Laryngeal nerve injury, 336 complications of therapy with, 173–174 Laryngospasm and noncardiogenic pulmonary components of, 165–166 edema, 135–136 contraindications to, 168 Left-to-right shunting, 42, 154, 438 errors in timing, 170–173 Left ventricular assist device (LVAD), 395, 395f, faulty trigger, 175 396f, 438 goals of, 165b Left ventricular end-diastolic pressure. See Preload 57625_CH21_INDX_445_462.pdf 4/20/09 9:50 AM Page 455

Index 455

Left ventricular myectomy, 43 minimally invasive cardiac surgery (MICS) and, 108 Levophed. See Norepinephrine patient monitoring, 194–195 LiDCO system, 155 phrenic nerve injury, 189 Lidocaine (Xylocaine), 230, 233, 242, 243, 333 pleural effusion, 188–189 Limb ischemia, 173, 176 pneumothorax and, 271–272 Lipitor (Atorvastatin), 278 post-extubation care, 197–198 Lipomas, cardiac, 44 prolonged mechanical ventilation, 185–186, 197, 272 Liver function, 60, 404 pulmonary mechanics, 187–188 Local anesthetics, 295–296 readiness for weaning, assessment of, 187–194, 196b Local collagen-gentamicin use in prevention of respiratory physiologic issues, 188–189 infection, 376 weaning from, 195–197 Lopressor. See Metoprolol Mediastinitis, 376, 384–386, 438 Low cardiac output Medications. See Pharmacologic support following agents used in management of, 215–229, 217t, cardiac surgery; specific drugs 226–227t, 227b Metabolic acidosis, 191–192, 192t, 348, 349, 349t as complication of cardiac surgery, 259–261, 263 Metabolic alkalosis, 192–193, 192t, 350, 350t Lower and Shumway method, 405, 438 Methylene blue (Urolene Blue), 224, 226, 227, 265 Lung pathophysiology, 186–187 Metoprolol (Lopressor), 230, 231, 234, 249, 313 LVAD. See Left ventricular assist device MH (malignant hyperthermia), 137–138 Lymphatic system, 16–17 MICS. See Minimally invasive cardiac surgery Lymphocyte immune globulin (Atgam; ATG, MIDCAB. See Minimally invasive direct coronary antithymocyte globulin [horse]), 416 artery bypass Milrinone (Primacor) M cardiac transplantation and, 316, 408, 409 dysrhythmias, management of, 316 Magnesium imbalances, 311, 314, 353–355 heart failure management and, 393 Malignant hyperthermia (MH), 137–138, 227 heart valve surgery and, 77, 79, 81 MAP. See Mean arterial pressure postoperative use, 106, 133, 222–224, 226, 227, Marfan syndrome, 73, 77 260, 263–265 Massage therapy in pain management, 296 preoperative nursing evaluation, 62 Maze procedure. See Cox/Maze III procedure Minimally invasive cardiac surgery (MICS), 93–113, Mean arterial pressure (MAP), 438 438–439 calculation of, 150, 150b benefits of, 93, 95 cardiac tamponade and, 411 bleeding after, 108 IABP and, 166 definition of, 93 nitroglycerin and, 206 dysrhythmias, 107 postoperative monitoring of, 105, 133, 148, 259 endovascular/”keyhole” procedures, 100–102 renal function and, 346, 412 exclusion criteria for, 102–103 vasopressin and, 226, 408 hemodynamic monitoring, 105–106, 105t Mechanical assist device. See Mechanical circulatory hypothermia, 107–108 support ICU admission following, 103–104 Mechanical circulatory support, 394–400 inclusion criteria for, 102 cardiac transplantation and, 393 indications for, 95 long-term, 399–400 minimally invasive direct coronary artery bypass short-term, 395, 399 (MIDCAB), 96–98, 97t, 102, 103, 109, 116 Mechanical valves, 74, 85–86. See also Heart valve minimally invasive direct view, 100 surgery myocardial revascularization, 31 Mechanical ventilation after cardiac surgery, 185–204 off-pump coronary artery bypass, 98 acid–base disorders, 189–193 outcomes and quality of life after, 111 anesthesia recovery and, 129 pathophysiologic changes associated with CABG, arterial blood gas (ABG), 189–193 93–95 atelectasis, 188 postoperative complications, 95, 106–108 delays related to bypass complications, 186 postoperative medications, 106t, 107 general physiologic and hemodynamic stability, 187 postoperative nursing care, 103–105 initial postoperative ventilator settings, 194, 195t postoperative ventilatory support, 108 intrapulmonary shunt, 193–194 preoperative nursing care, 103 left ventricular failure, 188 recovery from, 108, 109t lung pathophysiology, 186–187 robot-assisted coronary artery bypass, 98–99 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 456

456 Index

secondary assessment after procedure, 104–105 National Nosocomial Infection Surveillance (NNIS), 383 serological testing, 104 Nausea and vomiting, postoperative (PONV), 131, types of, 95–102, 100f 133–134, 134t Minimally invasive direct coronary artery bypass Negative inspiratory pressure, 135, 187, 188, 439 (MIDCAB), 96–98, 97t, 102, 103, 109, 116, 438 Neosynephrine. See Phenylephrine Minimally invasive direct view, 9, 100, 439 Neurologic complications, 323–343. See also specific Minorities, pain management and, 298–299 complication Minute ventilation, 132, 187, 190, 348, 439 anesthesia recovery and, 129 Minute volume, 135, 196, 197 avoidance of injury, 326–327 Mitral regurgitation, 79–83, 82t, 439 description and incidence of, 277, 324 afterload reducers and, 62–63 diagnosis and treatment of, 327–336 hypovolemia and, 359 minimizing injury, 327 IABP therapy and, 167 neuroprotection strategies during cardiac surgery, ventricular dysfunction and, 35, 64 326–327 Mitral stenosis, 77–79, 80t, 359, 439 pathophysiology of, 326 Mitral valve annuloplasty ring, 37, 439 predicators for, 324–325 Mitral valve disease preoperative nursing evaluation, 57–58 annuloplasty ring, 37, 439 risk factors for, 324–325, 325t cardiac transplantation and, 37 Type I neurologic deficits, 324–325 cardiomyopathy and, 35, 43 Type II neurologic deficits, 324–325 HCM and, 43 Neuromuscular blocking agents (NMBAs) for high pulmonary pressures, drug treatment for, 222 anesthesia, 63, 108, 128, 132, 136–137, management of high-risk patients, 65 190, 347 mitral regurgitation, 35, 62–64, 79–83, 167, 359 Neuropathic pain, 288, 289 mitral stenosis, 77–79, 359 Nicardipine (Cardene), 206, 207, 209, 213–214 mitral valve prolapse, 80, 87–88 NIHSS (National Institutes of Health Stroke mitral valve repair vs. mitral valve replacement, 37, Scale), 328 80, 80t, 82–83 Nitrates, 62 percutaneous mitral balloon valvotomy (PMBV), Nitric oxide (NO), 404, 407, 409, 440 79, 80 Nitroglycerin (NTG, Tridil), 206, 207, 210, 265 pleural effusion following surgery for, 188 Nitroprusside (Nipride) robotic surgery, exclusion criteria for, 102–103 black box warning, 249 tricuspid valve disease and, 84 cardiac complications, treatment of, 260, 265 MMF. See Mycophenolate Mofetil (Cellcept) hypertension, management of, 206, 207, 210–211 Monoclonal antibodies, 414–415 preoperative nursing evaluation, 62–63 Morphine, 128, 293, 295, 298, 412 pulmonary hypertension, treatment of, 407 Mortality rate of cardiac surgery, 257 NMBAs (neuromuscular blocking agents) for MRI scans, 61 anesthesia, 132, 136–137 MRSA prophylaxis, 378 Nociceptive pain, 288–289 Murmur differentiation, 15b, 17 Noncardiogenic pulmonary edema, 136 Muromonab-CD3 (OKT3), 414–415 Nonsteroidal anti-inflammatory drugs (NSAIDs), Music in pain management, 296 293, 295, 412, 422 Mycophenolate mofetil (MMF, Cellcept), 415–416, 419 Norepinephrine (Levophed) Myectomy, 43–44, 439 black box warning for, 249 Myocardial contractility, decreased, 263–264. See also heart valve surgery and, 79 Contractility low cardiac output and hypotension, treatment of, Myocardial ischemia and infarction, 266–268 216, 217, 218, 225, 227, 265, 408 Myocardial oxygen consumption, 29, 103, 205, 206, postoperative use, 106 217, 219, 223, 259 Normodyne (Labetalol), 208, 212 Myocardial revascularization, 31, 32, 439 Norpace (Disopyramide), 43, 230 Myocardial stunning and hibernation, 81, 264 Novacor, 402 Myocor Myosplint, 37 NTG. See Nitroglycerin Myxomas, 44, 439 Nutrition evaluation, 55 N O Naloxone (Narcan), 244–245 Obesity and cardiac surgery risk, 55, 68 National Institutes of Health Stroke Scale (NIHSS), 328 Off-pump coronary artery bypass (OPCAB) 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 457

Index 457

cognitive decline after, 119 Papillary fibroelastoma, 44, 440 compartment syndrome, 121 Parasympathetic system, 21, 187, 409 conversion to on-pump procedure, 117 Paroxysmal nocturnal dyspnea (PND), 59, 440 defined, 440 Paroxysmal ventricular tachycardia (VT), 314, 410 graft occlusion after, 120–121 Parsonnet risk score, 53, 54, 54t hemodynamic monitoring, 118–119 Partial left ventriculectomy, 36, 440 minimally invasive surgery and, 31, 102, 108 Patent ductus arteriosis, 38, 95, 100, 436 neurologic complications, avoidance of, 326–327 Patient education on-pump surgery compared, 117–118, 119–121, 201 cardiac transplantation and, 420–422 potential complications of bypass surgery, on incision care, 386, 386b, 404t 115–116, 326, 346 Patient interview, preoperative, 54–55 procedure for, 116–117 PDE. See Phosphodiesterase inhibitors sleep patterns after, 124 Peaked T waves, 351 stabilizer use in, 117 Percutaneous coronary intervention (PCI), 28, 35 OKT3 (muromonab-CD3), 414–415 Percutaneous mitral balloon valvotomy (PMBV), 79, Older patients 80, 440 heart valve surgery in, 89 Percutaneous transluminal coronary angioplasty pain management in, 299–300 (PTCA), 27, 440 risk assessment in, 53, 54 Pericardiectomy, 44, 440 ONCAB. See Coronary artery bypass grafting (CABG) Peripheral neuropathies, 336. See also specific nerve OPCAB. See Off-pump coronary artery bypass injuries Opioids Peripheral vascular assessment, 56 pain management, 293, 294–295 PGE1 (prostaglandin E-1), 407 use in anesthesia, 132, 137 PGH2 (prostacyclin), 407 Organ Procurement and Transplantation Network Pharmacologic support following cardiac surgery, (OPTN), 393 205–255 Orthopnea, 59 black box warnings, 249t Orthotopic heart transplant, 312, 373, 405, 409, bleeding, agents use to control, 245–248 410, 440 catecholamines, intraoperative administration Overdamped waveform, 146, 147f, 440 of, 251 Oxygenation parameters, assessment of, 157–158, 440 commonly used, 106 Oxygen-carrying capacity, 158, 186, 210, 360 dysrhythmias, agents used in management of, Oxygen consumption, 29, 103, 205, 206, 217, 219, 229–244, 231–233t 223, 259 hypertension, agents used in management of, Oxygen delivery, 27, 59, 129, 157, 193, 210, 214, 259 205–215, 207–209t low cardiac output and hypotension, agents P used in management of, 215–229, 217t, 226–227t, 227b PAC. See Pulmonary artery catheter other agents required, 244–245 Pacemakers, 107, 116, 315, 316 prophylactic antibiotics, 245 Pain management, 287–308 Phenylephrine (Neosynephrine), 216, 217–218, 226, anesthesia recovery and, 137 227, 249, 265 assessment of pain, 290–292 Phenytoin (Dilantin), 293 cardiac transplantation and, 412 Phlebostatic axis, 103, 104, 104f, 151, 440 elderly population and, 299–300 Phosphodiesterase (PDE) inhibitors, 222–224, 226 gender and, 297–298 Phosphorus imbalance, 356–358 management techniques, 292–293, 294t Phrenic nerve injury, 189, 271, 335–336, 440 pain, defined, 288 Physical assessment, 56–58 patients unable to communicate, assessment of, 292 abdominal assessment, 57 phases of pain, 293–295 anesthesia recovery, 129 physiology of pain, 288, 289f cardiac assessment, 56 postoperative, 103, 104–105, 287–308 neurologic assessment, 57–58 preoperative baseline assessment of pain, 291–292 pulmonary assessment, 56–57, 59 race, ethnicity, and culture, 298–299 PiCCO system, 155 reassessment of pain, 296–297 Pitting edema, 353, 353f sequelae of pain, 295–296 Plavix (Clopidogrel), 63 special considerations of, 297–300 Pleural effusion, 188–189, 271 types of pain, 288–290 PMBV (percutaneous mitral balloon valvotomy), 79 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 458

458 Index

PMI (point of maximal impulse), 14–15 cardiac history, 58–59 PND (paroxysmal nocturnal dyspnea), 59 diagnostic studies, 60–62 Pneumonia discharge planning, 55–56 anesthesia and, 131 heart disease, assessment of, 58–64 dyspnea and, 59 high-risk patients, management of, 64–65 hypoxia and, 329 infective endocarditis, 65 mechanical ventilation and, 188, 198, 418 medications, 62–64 neurologic complications and, 336 nursing assessment, 53–58 postoperative care and, 7, 105, 269, 273, 278 nutrition evaluation, 55 sodium imbalances and, 353 obesity, 55, 68 Pneumothorax, 271–272 older patients, risk assessment of, 53, 54 Point of maximal impulse (PMI), 14–15 patient interview, 54–55 Polyclonal antibodies, 416–417 physical assessment, 56–58 PONV. See Nausea and vomiting, postoperative risk factors of morbidity and mortality following Postcardiotomy cardiogenic shock, 399, 441 cardiac surgery, 53, 54 Postoperative complications of cardiac surgery, serological testing, 59–60 257–286 ventricular dysfunction, 64–65 cardiac complications, 258–269, 262t, 266t Pressure of blood in major blood vessels, 17, 18f emergency resternotomy procedures, 267 Primacor. See Milrinone gastrointestinal complications, 276–277 Primary pulmonary hypertension, 38 hematologic complications, 273–276, 274t Procainamide (Pronestyl), 230, 333 infectious complications, 278 Propafenone (Rythmol), 230, 249 internal defibrillation procedure, 268, 269 Prophylactic antibiotics, 245 neurologic complications, 277 Propofol (Diprivan), 131 pulmonary complications, 269–273, 270t Prostacyclin (PGH2), 407 red blood cell storage time, 282 Prostaglandin E-1 (PGE1), 407 renal complications, 276 Prosthetic valves, 54, 74, 85, 441 risk factors for, 257–258, 258t Protamine sulfate, 117–118, 138, 245–246, systemic inflammatory response, 277–278 274, 406 Potassium imbalance, 314, 350–352 Pseudocholinesterase deficiency, 138 PPV. See Pulse pressure variation PTCA (percutaneous transluminal coronary Preload angioplasty), 27 aortic regurgitation and, 76 Pulmonary artery catheter (PAC), 150, 151, 153–154, aortic stenosis and, 76 156, 403–404, 407 cardiac surgery complication, 259, 260, 261, 263, 265 Pulmonary assessment, 56–57, 59, 129 cardiac tamponade and, 411 Pulmonary complications of cardiac surgery, 269–273 defined, 20–21, 441 acute respiratory distress syndrome and acute hemodynamic monitoring and, 105–106, 119, 133, lung injury, 272–273 145, 153, 158, 159 atelectasis, 271 hypothermia and, 134 factors contributing to, 269–270, 270t hypovolemia and, 406 phrenic nerve injury, 271 IABP and, 167 pleural effusion, 271 inamrinone and, 223 pneumonia, 273 mechanical ventilation and, 185 pneumothorax, 271–272 milrinone and, 223 prolonged mechanical ventilation, 272 nitroglycerin and, 206 Pulmonary function testing, 57, 61 PPV and, 156 Pulmonary hypertension, 441 protamine sulfate and, 246 cardiac transplantation and, 407, 409 renal complications and, 276 heart–lung transplantation and, 38 RV failure and, 263 heart valve surgery and, 79, 81 stroke volume variation and, 156 as postoperative complication, 264 venous oxygenation saturation and, 157 preoperative nursing evaluation, 57, 65 ventricular dysfunction and, 65 primary, 38 Premature atrial contractions, 310 Pulmonary mechanics, 187–188 Premature ventricular contractions, 314 Pulmonary stenosis, 151, 441 Preoperative cardiac surgery nursing evaluation, 53–72 Pulmonary vascular resistance (PVR), 42, 62, 153, 263, anesthesia and, 127–128 264, 394. See also Afterload aortic stenosis, 65 PulseCO, 155 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 459

Index 459

Pulse oximetry, 120, 129, 146, 160, 194, 224, 227, Rewarming 400f, 441 afterload and, 265 Pulse pressure variation (PPV), 155, 156, 441 electrolyte imbalances and, 244, 345, 359 Pulsus alternans, 150, 150f, 441 methods of, 373 neurologic complications and, 326 Q ONCAB and, 116 postoperative care and, 107 QT intervals, 332, 333b preload and, 133, 158, 261 Quinidine (Quinaglute), 230, 249 Rheumatic heart disease, 74, 77–78, 80 Q waves, 267 Rheumatoid disease, 77 Right bundle branch block (RBBB), 410–411 R Right heart failure after cardiac transplantation, 407 Right-to-left shunt, 42, 154, 167, 441 RAAS (renin–angiotensin–aldosterone system), 212, Right ventricular assist device (RVAD), 395f, 396f, 213, 239 401, 402t, 424, 441 Race, pain management and, 298–299 Right ventricular failure, low cardiac output due Radial artery harvesting, 120, 121, 372 to, 263 Radionuclide scanning, 61 Risk assessment models, 53, 54 Rapamune (Sirolimus), 417, 419 Robinul (Glycopyrrolate), 132 Recombinant activated factor VII, 246–247, 275 ROBODOC, 98 Recovery from anesthesia. See Anesthesia, recovery from Robot-assisted procedures Recurrent laryngeal nerve, 336 coronary artery bypass, 98–99, 441 Red blood cell storage time, 282 endoscopy and, 101–102, 102t Registry of the International Society for Heart and Rocuronium, 132 Lung Transplantation, 419 Rubber dams, 374, 374f Regurgitation. See Aortic regurgitation (AR); Mitral RVAD. See Right ventricular assist device regurgitation; Tricuspid regurgitation Rythmol (Propafenone), 230, 249 Reiter disease, 77 Rejection of cardiac transplant, 412–413, 421. See also S Cardiac transplantation Relaxation techniques, 296 St. John’s wort, 64 Renal dysfunction Sangstat (Thymoglobulin), 416 acute renal failure and renal insufficiency, 60, Saphenous vein, 441–442 361–364 coronary vasospasm and, 266 azotemia, 361–362 MICS and, 97, 101, 120 cardiac transplantation and, 411–412 neurologic complications and, 336 complications of cardiac surgery, 276 preoperative assessment and, 55, 56 preoperative nursing evaluation of, 53, 60 wound care and, 372, 381 renal insufficiency and failure, 107, 149 SAVER (surgical anterior ventricular endocardial VAD use and, 404 restoration) procedure, 36–37 Renin, 23, 212, 213, 239, 346, 361 Seizures, 332–333 Renin–angiotensin–aldosterone system (RAAS), 212, Selective Dopamine-1-Receptor Agonists, 207, 209, 213, 239 215, 276 Respiratory acidosis, 190–191, 190t, 347–348, 347t Septicemia, 376 Respiratory alkalosis, 191, 191t, 348–350, 349t SER. See Subendocardial resection Respiratory management, postoperative, 135 Serological testing, 59–60, 104 Resternotomy procedures, emergency, 266, 267b Sevoflurane, 131 Revascularization. See also Coronary artery bypass Sexual activity after cardiac transplantation, 422 grafting (CABG) Shivering, 107 arterial grafts and, 120, 121 Simulect (Basiliximab), 415 cardiac complications and, 267 Sinus tachycardia, 214, 310 DCMP and, 37 Sirolimus (Rapamune), 417, 419 diabetes and, 31 SIRS. See Systemic inflammatory response to cardiac for heart failure, 35 surgery IABP and, 166–167 Skin cancer prevention, 422 ischemic heart disease and, 27–28 Sleep patterns renal complications and, 276 on- and off-pump coronary bypass surgery, 124 transmyocardial laser, 31–32, 33t preoperative, 54–55 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 460

460 Index

SmartCare system for automated ventilator cardiac output and, 155, 259 weaning, 197 defined, 20, 442 Smoking history enflurane and, 132 heart transplantation criteria and, 394 epinephrine and, 218, 225t preoperative assessment and, 57, 58, 127 exercise testing and, 61 pulmonary complications and, 269 hemodynamic stability and, 106 radial artery grafts and, 121 hypophosphatemia and, 357 strokes and, 328 IABP and, 170, 175, 180 Society of Thoracic Surgeons wound infection risk inamrinone and, 223, 226t scores, 383 index, 86t, 105t, 148b Sodium bicarbonate postoperative hemodynamic monitoring and, 158 hyperkalemia, treatment of, 351 variation (SVV), 155, 156, 442 malignant hyperthermia (MH), treatment of, 137 ventricular dysrhythmias and, 314 metabolic acidosis, treatment of, 137 Stroke volume variation (SVV), 155, 156, 442 Sodium channel blockers, 229–230, 243 ST segment changes, 28, 104, 266, 267, 352, 354 Sodium imbalances, 352–353 Subendocardial resection (SER), 35, 442 Sodium nitroprusside. See Nitroprusside (Nipride) Succinylcholine, 132 Sodium-potassium pump, 18, 20 Superficial sternal wound infections, 375, 375b, 376, Solu-Cortef (Hydrocortisone), 229, 233, 242 384, 442 Somatic pain, 288 Supraventricular tachycardia, 224, 314, 354, 410 Sotalol (Betapace) Surgical anterior ventricular endocardial restoration black box warning, 249 (SAVER) procedure, 36–37, 442 dysrhythmias, management of, 230, 232, 233, 236, Surgical revascularization, 27–28, 33t, 442. See 237, 243–244, 313 Coronary artery bypass grafting (CABG) preoperative nursing evaluation, 62, 323 Surgical site infections (SSIs). See Wound care SPV. See Systolic pressure variation SVV. See Stroke volume variation Square wave test, 14, 146, 146b, 147f, 442 Sympathetic nervous system, 21, 23, 107, 187, SSIs (surgical site infections). See Wound care 205, 259 Stabilizer, 96, 116, 116f, 122, 442 Sympathomimetics, 216, 312, 442. See also specific drugs Statin therapy, 64, 87. See also specific drugs SynCardia Cardio, 403 Stents, 27, 28 Systemic circulation, 21–23 Sternal incision site. See also Wound care Systemic control of blood pressure, 23 dehiscence, 376 Systemic inflammatory response to cardiac surgery, infections, 55, 87, 93, 278, 384, 389 277–278 Sternal Wound Infection Predictor Scale (SWIPS), anesthesia recovery and, 118, 133 383, 383t CABG and, 95, 128, 133, 198 Steroid pulse, 413, 421, 442 cardiac complications and, 259 Stir-up regime, 135 dysrhythmias and, 312 Stress-dose steroids, 278 hemodynamic monitoring and, 158 Stroke hypertension and, 205 aspirin use and, 330 neurologic complications and, 326, 350 atrial fibrillation (AF) and, 33 ONCAB and, 116, 117, 119 CABG in patients with carotid disease, 31 postoperative complications and, 259, 264, 265, glycemic control and, 329–330 270, 273, 360 hemodynamic status and, 329 pulmonary dysfunction and, 198 neurologic complications of cardiac surgery, 115, steroid use and, 227–228, 229 277, 323, 327–330, 340 Systemic vascular resistance, 23, 81, 264–265. See also on- and off-pump coronary bypass surgery, 119 Afterload oxygenation support, 328–329 Systolic murmur, 75 perioperative risk of, 56 Systolic pressure variation (SPV), 155, 156, 442 preoperative risk assessment of, 61–62 secondary complications, prevention of, 330 T temperature management, 329 treatment of, 328–330 TAH. See Total Artificial Heart Type I neurologic deficit, 324–325 Tambocor (Flecanide), 230 Stroke volume Tamponade. See Cardiac tamponade arterial pressure waveform and, 434 TandemHeart PTVA, 395, 396, 398f, 399, 402 arterial pulse contour CCO and, 155, 156, 434 Targets of rapamycin (TOR) inhibitors, 417 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 461

Index 461

Task Force on Practice Guidelines (ACC/AHA), Troponin I, 267–268 28–31, 59 Troponin T, 268 TECAB (total endoscopic CABG), 31 TV (transplant vasculopathy), 419 Temporary pacemakers, 315 TENS (transcutaneous electrical nerve U stimulation), 296 Terbutaline (Brethine), 410 Unassisted aortic end-diastolic pressure, 169–170, Theophylline, 410 170–172f, 173b, 434, 443 Thermoregulation, 134–135 Unassisted systole, 169–171, 170–172f, 172b, 173b, Thiopental sodium, 130 434, 443 Third spacing of fluid, 130, 133, 261, 358, Underdamped waveform, 146b, 147f, 443 363, 406 United Network for Organ Sharing (UNOS), 37 Thoracotomy, 294 Urinary output Thoratec BiVAD, 401, 402 fluid imbalances and, 359, 360, 361, 362, 363 Thymoglobulin (Sangstat; rabbit ATG), 416 magnesium imbalances and, 354 Thyroid function, 60, 118 postoperative care and, 103, 133, 149, 158, 205, Tidal volume 213, 215, 222, 230, 259 anesthesia recovery, 129 potassium imbalances and, 351 ARDS and ALI and, 273 sodium imbalances and, 353 definition of, 442 Urolene Blue. See Methylene blue minute volume and, 439 U waves, 352 respiratory acidosis, treatment of, 348 stroke volume variation and, 156 V TENS use and, 296 ventilator settings and, 195t VADs. See Ventricular assist devices weaning from mechanical ventilation and, Valerian, 64 187–188, 197 Valve replacement. See also Heart valve surgery; TMR. See Transmyocardial laser revascularization specific valves TOR (targets of rapamycin) inhibitors, 417 aortic valve, 75–78, 188 Torsade de pointes, 242–243 atrial dysrhythmias after, 309 Total Artificial Heart (TAH), 402, 403, 442–443 atrial fibrillation following, 241 Totally endoscopic CABG (TECAB), 31, 443 fluid overload and, 119 Trandate (Labetalol), 208, 212 heart block following, 234 Transcutaneous electrical nerve stimulation minimally invasive surgery for, 98 (TENS), 296 mitral valve, 35, 43, 80, 82–83 Transesophageal echocardiogram, 79 pleural effusion following, 188 Transmyocardial laser revascularization (TMR), postoperative activities, 304 31–32, 33t, 443 wound infection, 389 Transplantation. See Cardiac transplantation; Valves and chambers of heart. See also Heart valve Heart–lung transplantation surgery; specific procedures involving valves Transplant vasculopathy (TV), 419, 443 adult congenital heart disease, 42 Trasylol. See Aprotinin anatomy and physiology, 13–14, 15–16 Tricuspid regurgitation hypertrophic cardiomyopathy and, 43 congenital heart failure and, 42 murmur differentiation, 17 defined, 83, 443 Valvular heart disease (VHD). See Heart valve hemodynamic monitoring and, 152, 154 surgery mitral stenosis and, 78 Valvuloplasty, 84, 316, 443 postoperative care and, 405 VAP (ventilator-associated pneumonia), 418 RV failure and, 263 Vasodilators, 206–207, 210–211 surgery for, 83–84 Vasopressin, 219–220, 226, 227, 408 ventricular dysfunction and, 64–65 Vasotec (Enalaprilat), 208, 212–213 Tricuspid stenosis Vecuronium, 132 defined, 83, 443 Vegetations in endocarditis, 65, 74, 84 hemodynamic monitoring and, 151–152 Venous oxygen saturation, 157, 443 murmur differentiation and, 15–16 Venous thrombotic events, 87 surgery for, 84 Ventilator-associated pneumonia (VAP), 418 Tricuspid valve disease, 83–84, 443 Ventilatory support. See Mechanical ventilation after Tridil. See Nitroglycerin cardiac surgery 57625_CH21_INDX_445_462.pdf 4/20/09 9:21 AM Page 462

462 Index

Ventricular assist devices (VADs), 402t, 443 criteria for defining surgical site infections, 375 cardiac transplantation and, 393, 400–404, 408 critical inquiry, 389 discharge with LVAD, requirements for, 404 discharge education regarding incision care, 386, infection control guidelines, 403 386b, 404t postoperative complications, 403–404, 426 evaluation of incision site, 380–381 selection criteria for, 401 glycemic control, 378–380 types of, 401–403 hair removal, preoperative, 377 use of, 35 heart valve surgery and, 87 Ventricular dysfunction, preoperative management impact of postoperative infection, 382–383 of, 64–65 incision sites, 371, 375b, 381b Ventricular dysrhythmias. See also specific dysrhythmias intraoperative risk factors for wound agents used to treat postoperative, 233, 242–244 complications, 373–374 cardiac transplantation and, 410 local collagen-gentamicin use in prevention of, 376 management of postoperative, 315 management of wound infection, 384–386 postoperative, 314–315 mediastinitis, 376, 384–386 VAD therapy, 426 MRSA prophylaxis, 378 Ventricular fibrillation (VF), 242–243, 314–315 nursing responsibilities to enhance wound Ventricular reconstruction techniques, 35–36, healing, 381–382 443–444 nutritional assessment, preoperative, 55 Ventricular septal defect (VSD), 38, 95, 101, 444 phases of incision healing, 380 Ventricular tachycardia (VT), 32, 34–35, 242, 314–315 postoperative dressings, 380 Verapamil, 43, 230 postoperative risk factors for, 374 Vessels and blood flow through heart, 15–16 potentially contaminated sources, avoiding, 380 disorders of major blood vessels, 23–24 prediction of wound infection, 383–384, 389 pressure of blood in major vessels, 17 preoperative risk factors for, 372–373, 372t VHD (valvular heart disease). See Heart valve surgery prevention of surgical-site infection, 376–381, 377b Visceral pain, 288 procedure for incision care, 381 Vital capacity, 135, 187, 296, 444 risk factors for wound complications, 372–374 VT. See Ventricular tachycardia septicemia, 376 sequelae of wound infection, 382–383 W skin cleaning, preoperative, 377 sternal wound dehiscence and infections, 55, 87, Warfarin (Coumadin), 63, 401, 403 93, 278, 376 Weaning from mechanical ventilation superficial wound infections, 375, 376 assessment of readiness for, 187–194 ventricular assist devices and, 403–404, 403t criteria for, 195–196 process of, 196–197 X from prolonged ventilation, 197 Women Xylocaine. See Lidocaine arterial revascularization vs. vein grafting in, 121 bypass surgery risk and, 119 Z mitral valve surgery mortality in perimenopausal, 81 pain management and, 297–298 Zenapax (Daclizumab), 415 postoperative myocardial ischemia and Zero balance, 146, 444 infarction, 267 Wound care, 371–392 antibiotic administration, preoperative, 378 classification of, 374–376 conduits, 371–372