Left Ventricular Assist Device
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Hemodynamic Monitoring and Circulatory Assist Devices
Hemodynamic Monitoring Hemodynamic Monitoring and Circulatory Assist Devices • Measurement of pressure, flow, and oxygenation within the cardiovascular system • Includes invasive and noninvasive measurements (Relates to Chapter 66, – Systemic and pulmonary arterial pressures “Nursing Management: Critical Care,” in the textbook) Hemodynamic Monitoring Hemodynamic Monitoring • Invasive and noninvasive measurements • Invasive and noninvasive measurements (cont’d) (cont’d) – Central venous pressure (CVP) – Stroke volume (SV)/stroke volume index (SVI) – Pulmonary artery wedge pressure (PAWP) – O2 saturation of arterial blood (SaO2) – Cardiac output (CO)/cardiac index (CI) – O2 saturation of mixed venous blood (SvO2) Hemodynamic Monitoring Hemodynamic Monitoring General Principles General Principles • Preload: Volume of blood within ventricle at • Contractility: Strength of ventricular end of diastole contraction • Afterload: Forces opposing ventricular • PAWP: Measurement of pulmonary capillary ejection pressure; reflects left ventricular end‐diastolic – Systemic arterial pressure pressure under normal conditions – Resistance offered by aortic valve – Mass and density of blood to be moved 1 Hemodynamic Monitoring Principles of Invasive Pressure General Principles Monitoring • CVP: Right ventricular preload or right • Equipment must be referenced and zero ventricular end‐diastolic pressure under balance to environment and dynamic normal conditions, measured in right atrium response characteristics optimized or in vena cava close to heart • -
Time-Varying Elastance and Left Ventricular Aortic Coupling Keith R
Walley Critical Care (2016) 20:270 DOI 10.1186/s13054-016-1439-6 REVIEW Open Access Left ventricular function: time-varying elastance and left ventricular aortic coupling Keith R. Walley Abstract heart must have special characteristics that allow it to respond appropriately and deliver necessary blood flow Many aspects of left ventricular function are explained and oxygen, even though flow is regulated from outside by considering ventricular pressure–volume characteristics. the heart. Contractility is best measured by the slope, Emax, of the To understand these special cardiac characteristics we end-systolic pressure–volume relationship. Ventricular start with ventricular function curves and show how systole is usefully characterized by a time-varying these curves are generated by underlying ventricular elastance (ΔP/ΔV). An extended area, the pressure– pressure–volume characteristics. Understanding ventricu- volume area, subtended by the ventricular pressure– lar function from a pressure–volume perspective leads to volume loop (useful mechanical work) and the ESPVR consideration of concepts such as time-varying ventricular (energy expended without mechanical work), is linearly elastance and the connection between the work of the related to myocardial oxygen consumption per beat. heart during a cardiac cycle and myocardial oxygen con- For energetically efficient systolic ejection ventricular sumption. Connection of the heart to the arterial circula- elastance should be, and is, matched to aortic elastance. tion is then considered. Diastole and the connection of Without matching, the fraction of energy expended the heart to the venous circulation is considered in an ab- without mechanical work increases and energy is lost breviated form as these relationships, which define how during ejection across the aortic valve. -
Static and Dynamic Components of Right Ventricular Afterload Are Negatively Associated with Calf Survival at High Altitude1
Published September 29, 2016 Static and dynamic components of right ventricular afterload are negatively associated with calf survival at high altitude1 J. M. Neary,*2 R. D. Brown,† T. N. Holt,‡ K. R. Stenmark,† R. M. Enns,§ M. G. Thomas,§ and F. B. Garry‡ *Department of Animal and Food Sciences, College of Agricultural Sciences and Natural Resources, Texas Tech University, Lubbock 79409-2141; †Division of Pediatric Critical Care, School of Medicine, University of Colorado Denver, Aurora 80045; ‡Integrated Livestock Management, Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 1678 Campus Delivery, Fort Collins 80523-1678; and, §Department of Animal Sciences, The College of Agricultural Sciences, Colorado State University, Fort Collins 80523-1171. ABSTRACT: The purposes of this study were to pulse pressures (P = 0.03) at 3 mo of age than calves evaluate mean, systolic, and diastolic pulmonary that survived to 7 mo. Calves presumed to have died arterial pressures; pulmonary arterial pulse pres- tended to have greater systemic oxygen extraction sures; and systemic oxygen extraction fraction as fractions at 3 mo of age than calves that survived (P risk factors for the survival of suckling calves on one = 0.13). Diastolic pressure was not associated with ranch located at an altitude of 2,730 m in Colorado, survival (P = 0.27). Mean pulmonary arterial pres- USA. A prospective cohort study of 58 calves was sure is predominantly determined by static resistance performed. Pulmonary arterial pressures and sys- attributable to distal pulmonary arterial remodeling. temic oxygen extraction were measured when calves Pulse pressure and systolic pulmonary arterial pres- were approximately 3 mo (86 ± 7 d) and 7 mo (197 sure represents the dynamic or oscillatory resistance ± 6 d) of age. -
Quantitative Electrocardiography for Prediction Of
QUANTITATIVE ELECTROCARDIOGRAPHY FOR PREDICTION OF POSTOPERATIVE ATRIAL FIBRILLATION AFTER CARDIAC SURGERY by FLORIAN RADER, M.D. Submitted in partial fulfillment of the requirements For the degree of Master of Science Clinical Research Scholars Program CASE WESTERN RESERVE UNIVERSITY January 2010 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of Florian Rader, M.D. candidate for the Master of Science degree*. (signed) Regis E. McFadden (chair of the committee) Eugene H. Blackstone, M.D. Ottorino Costantini, M.D. Neal Dawson, M.D. (date) 10-28-2009 *We also certify that written approval has been obtained for any proprietary material contained therein. 2 Table of Contents List of Tables 4 List of Figures 5 Acknowledgments 6 List of Abbreviations 7 Abstract 9 Text Background and Significance 10 Specific aims 12 Methods 13 Results 21 Discussion 46 Limitations 54 Conclusions 54 References 55 3 List of Tables: Table 1: Patient characteristics 24 Table 2: Clinical predictors of postoperative atrial fibrillation 37 Table 3: ECG predictors of postoperative atrial fibrillation 38 4 List of Figures: Figure 1: Relationship of anatomic and ECG changes with POAF 11 Figure 2: Patient flow chart 22 Figure 3: Occurrence of POAF by days after surgery 33 Figure 4: Occurrence of POAF by surgery type 34 Figure 5: ROC curve of final prediction model 35 Figure 6: Calibration curve of final prediction model 36 Figure 7: Adjusted Co-plots of ECG predictors 39 Figure 8: Unadjusted and adjusted co-plot of P wave amplitude 41 Figure 9: Nomogram of final prediction model 42 Figure 10: Nomogram of prediction model with pre-op variables 43 Figure 11: Calibration curve of model without ECG predictors 45 Figure 12: Left atrial sizes by P wave amplitude in aVR 48 Figure 13: Correlation matrix (P wave amplitude, aVR, and left atrial volume) 49 5 Acknowledgments: I thank Dr. -
Chapter 9 Monitoring of the Heart and Vascular System
Chapter 9 Monitoring of the Heart and Vascular System David L. Reich, MD • Alexander J. Mittnacht, MD • Martin J. London, MD • Joel A. Kaplan, MD Hemodynamic Monitoring Cardiac Output Monitoring Arterial Pressure Monitoring Indicator Dilution Arterial Cannulation Sites Analysis and Interpretation Indications of Hemodynamic Data Insertion Techniques Systemic and Pulmonary Vascular Resistances Central Venous Pressure Monitoring Frank-Starling Relationships Indications Monitoring Coronary Perfusion Complications Electrocardiography Pulmonary Arterial Pressure Monitoring Lead Systems Placement of the Pulmonary Artery Catheter Detection of Myocardial Ischemia Indications Intraoperative Lead Systems Complications Arrhythmia and Pacemaker Detection Pacing Catheters Mixed Venous Oxygen Saturation Catheters Summary References HEMODYNAMIC MONITORING For patients with severe cardiovascular disease and those undergoing surgery associ- ated with rapid hemodynamic changes, adequate hemodynamic monitoring should be available at all times. With the ability to measure and record almost all vital physi- ologic parameters, the development of acute hemodynamic changes may be observed and corrective action may be taken in an attempt to correct adverse hemodynamics and improve outcome. Although outcome changes are difficult to prove, it is a rea- sonable assumption that appropriate hemodynamic monitoring should reduce the incidence of major cardiovascular complications. This is based on the presumption that the data obtained from these monitors are interpreted correctly and that thera- peutic decisions are implemented in a timely fashion. Many devices are available to monitor the cardiovascular system. These devices range from those that are completely noninvasive, such as the blood pressure (BP) cuff and ECG, to those that are extremely invasive, such as the pulmonary artery (PA) catheter. To make the best use of invasive monitors, the potential benefits to be gained from the information must outweigh the potential complications. -
Dynamic Auscultation
TOP 10 TAKEAWAYS… Jane A. Linderbaum MS, APRN, CNP, AACC Assistant Professor of Medicine Department of cardiovascular disease No Disclosures No off-label discussions 73% of survey respondents identified a need for improved knowledge of CV pathophysiology #10 CARDIAC CIRCULATION, KNOW IT AND LOVE IT The Cardiac Cycle The heart sounds • S1 Mitral (and tricuspid) valve closure Soft if poor EF, loud if good EF • S2 Aortic and pulmonary valve closure Loud if aortic (pulm) pressure • S3 – means “restrictive” filling • S4 – means “abnormal” filling Listening Posts for Auscultation AV – 2nd RICS PV – 2nd LICS MV – 5-6th LICS @ the apex TV – 5-6th LICS parasternal 83% of survey respondents identified themselves as early career in clinic/hospital consult practices # 9 COMMON SYSTOLIC MURMURS YOU WILL DIAGNOSE AND MANAGE MITRAL REGURGITATION MR Treatment • Treat underlying conditions • Consider MV repair when possible at experienced center • Consider MV replacement before ventricle dilates and/or function decreases MITRAL VALVE PROLAPSE Mitral Valve Prolapse Pearls • CHANGE in Murmur (from click-murmur or isolated late sys murmur to holosystolic without audible click) • Skeletal deformities in up to 50% • Upright posture enhances auscultation of the mid-late systolic murmur • May develop severe MR, refer for additional testing as patient may be candidate for mitral valve repair • Murmur may INCREASE with Valsalva • Typically do not require SBE prophylaxis Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy • Vigorous LV apical impulse – sustained -
How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability to Handle Additional Volume Loads
003 1 -3998/87/2205-053 1 $02.00/0 PEDIATRIC RESEARCH Vol. 22. No. 5, 1987 Copyright (c) 1987 International Pediatric Research Foundation. Inc 1'rinrc.d in LI. S ,4 How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads RONALD I. CLYMAN, CHRISTINE ROMAN, MICHAEL A. HEYMANN, AND FRANCOlSE MAURAY Cardiovasc~clarRe.search In.sriru[e and the Departments of Pediatrics. Univc.rsity of Calijornia; and Mr. Zion Hospilal and Medical Ccwter, Sun Francisco. Calijbrnia ABSTRACT. A model of patent ductus arteriosus in pre- Bishop et a/. (I) and Stone el al. (2) used the maximal level of mature lambs was created to examine the lamb's ability to cardiac output reached during a rapid infusion of fluid as a handle the volume load imposed by a patent ductus arte- measure of cardiac performance during a volume load. The riosus and to determine the lamb's ability to handle any response to volume loading improves with maturation (3-7). additional volume load. Fifteen preterm lambs I133 -C 2 (2 Full-term newborn lambs respond to volume loading with a SD) days gestation, term 145 days], whose ductal diameter limited increase in stroke volume, compared with adult sheep. could be regulated with a mechanical occluder, were studied The left ventricle of the full-term newborn lamb is capable of to determine the independent effects of ductus patency and developing greater force than the left ventricle of the preterm a saline volume load (50 ml/kg over 3 min) on left ventric- lamb (with closed ductus) at comparable filling volume and ular output and its distribution. -
Navigating Preload Assessment
NAVIGATING PRELOAD ASSESSMENT CHOOSING THE RIGHT PATHWAY Cecilia Baylon & Sarah Neville LEARNING OBJECTIVES • Explain the relationship between preload and fluid responsiveness (FR) • Review the different methods of assessing preload and FR • Analyze the current research in regard to their use in the critical care setting O2 demand CARDIAC OUTPUT Respiratory Lung Muscle Compliance Patient’s Venous Vessel Diameter Function Pre-existing Alveoli Return (Peripheral Medical Perfused? Vascular Condition Blood Work of Resistance) Viscosity Breathing Total Alveoli Thickness of Circulating Ventilated? Alveolar-Capillary Membrane Volume Aortic Physical Tidal Volume etc Impedence Activity Respiratory Vital Capacity Rate Functional Resid. Capac V/Q Emotional Diffusion pH, PC02 Matching Contractility Preload Temperature Stress 2,3 DPG Afterload Ventilation ie: pain PaCO2 Oxygen ALVEOLAR Hgb Hgb Level GAS EXCHANGE Affinity METABOLIC STROKE HEART RATE DEMANDS Pa02 Oxygen VOLUME ARTERIAL OXYGEN transported SATURATION in blood Sa02 ARTERIAL OXYGEN CARDIAC OUTPUT CONTENT OXYGEN OXYGEN SUPPLY DEMAND BALANCE End organ perfusion OXYGEN SUPPLY & DEMAND (HEMODYNAMIC) FRAMEWORK CONTRACTILITY PRELOAD AFTERLOAD STROKE VOLUME X HEART RATE CARDIAC OUTPUT EOP FRANK-STARLING’S LAW FRANK-STARLING’S LAW • “the force of ventricular ejection is directly related to…” VOLUME IN THE VENTRICLE AT END-DIASTOLE (PRELOAD) AMOUNT OF MYOCARDIAL STRETCH PLACED ON THE VENTRICLE AS A RESULT Urden, Stacy, Lough (2018), p. 214 Ejection Phase Hyperinotropy Contractility Norminotropy -
Quick Guide to Cardiopulmonary Care
Edwards Clinical Education Quick Guide to Cardiopulmonary Care 4th Edition This reference guide is presented as an aide to guide medical personnel by Edwards Lifesciences. The information in this reference guide has been compiled from available literature. Although every effort has been made to report faithfully the information, the editors and publisher cannot be held responsible for the correctness. This guide is not intended to be, and should not be construed as, medical advice. For any use, the product information guides, inserts and operation manuals of the various drugs and devices should be consulted. Edwards Lifesciences and the editors disclaim any liability arising directly or indirectly from the use of drugs, devices, techniques or procedures described in this reference guide. Note: Algorithms and protocols included in this book are for educational reference only. Edwards does not endorse or support any one specific algorithm or protocol. It is up to each individual clinician and institution to select the treatment that is most appropriate. ISBN 978-0-615-96605-2 Quick Guide to Cardiopulmonary Care 4th Edition Editors William T. McGee, MD, MHA, FCCP, FCCM Critical Care Medicine Associate Professor of Medicine and Surgery University of Massachusetts Medical School Caulette Young, BSN, RN, CCRN, CHSE Clinical Nurse Consultant John A. Frazier, BS, RN, RRT Sr. Manager Edwards Lifesciences Previous edition editor Peter R. Lichtenthal, M.D. Previous editions contributors and reviewers Diane K. Brown, RN, MSN, CCRN Barbara “Bobbi” Leeper, MN, RN, CCRN Quick Guide to Cardiopulmonary Care Pertinent clinical information dedicated to the critical care clinician The intent of the Quick Guide is to provide a ready reference for hemodynamic monitoring and oxygenation assessment of the critically ill. -
Cardiovascular Effects of Mechanical Ventilation
Cardiovascular Effects of Mechanical Ventilation G. J. DUKE Intensive Care Department, The Northern Hospital, Epping, VICTORIA ABSTRACT Objective: To review the cardiovascular effects of spontaneous breathing and mechanical ventilation in healthy and pathological states. Data sources: A review of articles published in peer-reviewed journals from 1966 to 1998 and identified through a MEDLINE search on cardiopulmonary interaction. Summary of review: Respiration has a hydraulic influence upon cardiovascular function. Pulmonary and cardiac pathology alter this interaction. Spontaneous inspiration increases right ventricular (RV) preload and left ventricular (LV) afterload. Mechanical ventilation with positive pressure (MV) reduces LV preload and afterload. The influence of MV upon the cardiovascular system (CVS), particularly in critically ill patients, depends upon the mode of ventilation and the pre-existing cardiac and respiratory status. The influence of these factors is reviewed. Consideration of these parameters will enable the clinician to predict the likely effect of MV and develop strategies to minimise adverse events. Conclusions: Mechanical ventilation has an adverse effect upon the CVS in healthy subjects and in patients with pulmonary pathology, particularly in the presence of preload-dependent LV dysfunction or afterload-induced RV dysfunction. Mechanical ventilation may benefit cardiac function in patients with respiratory failure and afterload-dependent or exercise-induced LV dysfunction. (Critical Care and Resuscitation 1999; -
6 Heart Sounds
Chapter 6 / Heart Sounds 141 6 Heart Sounds CONTENTS PRINCIPLES OF SOUND FORMATION IN THE HEART FIRST HEART SOUND (S1) CLINICAL ASSESSMENT OF S1 AND COMPONENTS SECOND HEART SOUND (S2) NORMAL S2 ABNORMAL S2 CLINICAL ASSESSMENT OF S2 OPENING SNAP (OS) THIRD HEART SOUND (S3) CLINICAL ASSESSMENT OF S3 FOURTH HEART SOUND (S4) CLINICAL ASSESSMENT OF S4 REFERENCES PRINCIPLES OF SOUND FORMATION IN THE HEART In the past, many theories have been advanced to explain the origins of sounds during the cardiac cycle. These included simple concepts of sound originating from the actual contact of valve cusps upon closure. When it was realized that the strength of contraction of the left ventricle had a significant effect on the intensity of the first heart sound, the myocardial theory of the origin of the sound was postulated. Some even had suggested extracardiac origin of sounds such as the third heart sound. It is now, however, well established by several investigators and accepted that the formation of all sounds in the heart can be explained by a “unified concept” (1–10). It is a common experience to hear sound produced when a pipe half-filled with water is moved back and forth, splashing the water against the two palms of the hands held against the ends of the pipe. We have all heard banging sounds sometime produced in the water pipes of the plumbing systems of our homes when air is introduced into the plumb- ing. In both examples, the mechanism of sound production is the same. When the moving column of water in either case comes to sudden stop or marked deceleration, the energy of the column dissipates and in the process generates vibration of the pipes as well as the column of water. -
Effect of Afterload Reduction in Patients with Ventricular and Physiological Pacing
Br Heart J: first published as 10.1136/hrt.51.3.292 on 1 March 1984. Downloaded from Br Heart J 1984; 51: 292-7 Effect of afterload reduction in patients with ventricular and physiological pacing M BEEN, D P DE BONO, H C MILLER, W S HILLIS From the Departments of Cardiology, Royal Infirmary, Edinburgh, and Stobhill Hospital, Glasgow suAlMARY The effect of afterload reduction was studied in a group of patients who remained breath- less or tired after permanent ventricular pacing. Haemodynamic measurements were made before and after giving hydralazine 20 mg intravenously using a triple lumen thermodilution catheter and cuff blood pressure recordings during ventricular pacing at the standard rate of 71/min or an increased rate of 88/min and physiological pacing. Increasing the ventricular pacing rate had no effect on cardiac output as stroke volume fell. Hydralazine produced a greater rise in cardiac output than physiological pacing alone, although peak values were obtained by combining the two. Ven- tricular pacing produced intermittent large left and right atrial pressure peaks. Physiological pacing produced no such peaks, and mean right and left atrial pressures fell. Hydralazine did not significantly alter atrial pressures. These findings show that in these patients, most of whom had a low cardiac output, afterload reduction with ventricular pacing increased resting cardiac output more than physiological pacing alone. Nevertheless, persistence of high filling pressures despite afterload reduction may limit the potential therapeutic benefit. Care should be taken in extrapolating these data to other patient groups. Technical improvement in dual chamber pacing sys- ical pacing is still controversial.