Anaesthesia for Medical Students

Anaesthesia for f Medical Students

Pat Sullivan M.D. 1999 Edition Acknowledgements: (

The author gratefully acknowledges the work of William Sullivan MA., M.D., John c Heng MA., Ola Rosaeg M.D., FRCPC, and medical students Susie Quackenbush and Bing Kong for their general suggestions, proofreading and editing skills during the ( preparation of this manual. Special thanks to Robert Elliot M.D., for his assistance in the design of the cover page. (- ( Canadian Cataloguing in Publication Data

Sullivan, Pat

Anaesthesia for medical students

Includes bibliographical references. ISBN 0-9699801-0-8

1. Anesthesiology. I. Ottawa Civic Hospital. Dept. of Anaesthesia 11. Title.

Printed by DocuLink International

O Copyright 1995 by Pat Sullivan. Revised 1999. All rights reserved. No part of ( this book may be reproduced, stored in a retrieval system, or transmitted in any form ( or by any means, electronic, mechanical, photocopying, or otherwise without the written permission of the author. ( ( Published by the Department of Anaesthesia, Ottawa Civic Hospital. Address correspondence to: ( Patrick Sullivan MD, FRCPC ( Department of Anaesthesia c Ottawa Civic Hospital, B310 1053 Carling Avenue Ottawa, Ontario, Canada, K1Y 4E9 ( T:613 - 761 - 4940 F:613 - 761 -5032 ( E: [email protected]~n.ca (

a : Contributing Authors

Dr. Gregory Allen Dr. John Kitts - Assistant Professor Associate Professor Anesthesia Pennsylvania State University University of Ottawa MHAUS Hotline Consultant Vice President Medical Affairs - Department of Anesthesia Ottawa Hospital - Hershey, Pennsylvania ' Dr. Anne Lui - Dr. Wayne Barry Assistant Professor - Assistant Professor University of Ottawa University of Ottawa Department of Anesthesia Department of Anesthesia Ottawa Hospital - Civic Campus - Ottawa Hospital - Civic Campus Dr. John Penning Dr. Greg Bryson Assistant Professor - Assistant Professor University of Ottawa - University of Ottawa Director of the Acute Pain Service Department of Anesthesia Department of Anesthesia - Director Preadmission Unit Ottawa Hospital - Civic Campus - Ottawa Hospital - Civic Campus Dr. Gordon Reid Dr. Robert Cirone Assistant Prsfessor - Staff Anesthesiologist University of Ottawa Department of Anesthesia Director Malignant Hyperthermia St. Joseph's Hospital Investigation Unit Toronto Department of Anesthesia Ottawa Hospital - Civic Campus Dr. Robert Elliot Assistant Professor Dr. Linda Robinson University of Ottawa Assistant Professor Department of Anesthesia University of Ottawa Ottawa Hospital - General Campus Department of Anesthesia Ottawa Hospital - Civic Campus Introduction

Specialists in the fields of medicine and should know. A11 other material is surgery may ask why medical students ~rovidedfor background reading which should be exposed to the specialty of the student may know. The manual is anesthesia. We believe that there are to be used as a primary reference for basic concepts and technical skills that lectures on monitoring in anesthesia, every physician should possess, and that and on acute and chronic pain manage- these concepts and skills are best taught ment. The problem-based tutorial ques- by our specialty. tion will also be on material covered in this manual. Medical school curricula across North America are repeatedly criticized for The student who completes the anest- lacking the teaching of both acute and hesia rotation should have acquired chronic pain management. In addition, confidence in airway management skills students who pursue a career in surgery, including mask ventilation and tracheal emergency medicine or internal medi- intubation, as well as securing intra- cine are expected to have the skills to venous access. Important concepts for manage a patient's airway. However, the student to attain during their rotation they usually have had no formal teach- include: ing in these basic skills. Finally, medical school curricula in North America 1. Preoperative assessment. are rapidly changing. Students are now 2. Basic principles of managing acute asked to commit themselves to a spe- and chronic pain disorders. cialty during the third year of their 3. The appropriate use of local anaes- medical school training. We believe thetic agents. that this process is unfair. We also 4. Analgesic options for women in recognize that a student with no prior labour. exposure to anesthesia is unlikely to 5. Basic neonatal assessment and re- choose anesthesia as a career. suscitation. 6. Intravenous fluid and blood compo- This manual was written with contribut- nent therapy including the potential ing authors from the Departments of complications of a blood product Anesthesia at the Ottawa Civic and transfusion. General Hospitals for medical students spending two weeks of their clinical rotation in the specialty of anesthesia. Six specific objectives are used to focus Patrick Sullivan MD, FRCPC the students reading. The text is high- Assistant Professor lighted by two asterisks (**) for University of Ottawa, material that is essential and that the Resident Program Director student must know, and one asterisks Department of Anesthesia (*) for material which the student University of Ottawa Preface

The first public demonstration of ether macology and resuscitation of acutely was by W.T.G. Morton in the traumatized patients. The importance of Etherdome of the Massachusetts General imparting these skills and knowledge to Hospital in 1846. Ether anaesthesia medical students has been realized by became widely available and would those responsible for medical school soon be followed by chloroform and curricula. Accreditation bodies are nitrous oxide. Surgeons were not demanding that anaesthetists teach med- particular about who poured the ether or ical students. chloroform so long as someone was there to do the job. It was not until the When the new curriculum, founded on early 1920's that physicians began to problem-based learning, was adopted in show interest in anaesthesia as a the Faculty of Medicine at the Univer- specialty. By the end of World War I1 sity of Ottawa, anaesthesia was given the infant specialty was firmly estab- responsibilities in the program. Each lished and university training programs student must spend two weeks in an began. anaesthesia rotation and many anaesthetists participate in small group sessions. The emphasis has traditionally been on Dr. Patrick Sullivan found that an an- postgraduate teaching. Why has aesthesia manual, which would meet the undergraduateanaesthesia teachingbeen needs of medical students submerged in neglected or de-emphasized? It was a new curriculum, was not available. because the medical school curriculum The manual he and his co-authors have was controlled by older, traditional written covers all of the important disciplines that were unwilling to material a medical student must and relinquish time for competing spe- should know. It is best taught by an- cialties. This was complicated by the aesthetists because it falls almost fact that anaesthetists originally worked exclusively in their domain. The only in the operating room, and found it organization of the manual makes it difficult to be freed from that responsi- essential reading for students rotating bility to undertake teaching outside the through anaesthesia who want to operating room. Anaesthesia has optimize their brief exposure to anaes- expanded to include other services thesia, which has so much to offer. which include Intensive Care, Acute and Chronic Pain Services, Malignant Hyperthermia Diagnostic Services, and a Pre-admission Unit. Anaesthetists have developed many skills which are J. Earl Wynands, M.D. valuable to physicians, regardless of Professor and Chairman their discipline. They have become Department of Anaesthesia specialists in applied physiology, phar- University of Ottawa Table of Contents

1. Rotational Objectives ...... 2 . Anaesthesia Overview ...... 3 . Preoperative Evaluation and Risk Assessment ...... 4 . Premedication ...... 5 . Getting Started: A practical approach to the OR ...... 6 . Intubation and Anatomy of the Airway ...... 7 . Intubation Decisions ...... 8 . The Laryngeal Mask Airway ...... 9 . Rapid Sequence Induction ...... 10. Monitoring in Anaesthesia ...... 11. General Intravenous Anaesthetic Agents ...... 12. Muscle Relaxants ...... 13. Inhalational Agents ...... 14. Narcotic Agonists and Antagonists ...... 15. Local and Regional Anaesthetics ...... 16. Acute Pain Mechanisms and Management ...... 17. Chronic Pain ...... 18 . Obstetrical Anaesthesia ...... 19. Basic Neonatal Resuscitation ...... 20 . Intravenous Fluid and Blood Component Therapy ...... 21 . Common Perioperative Problems ...... 22. Managing the Circulation ...... 23 . Oxygen Therapy and Hypoxemia ...... 24 . Unusual Anaesthetic Complications: Malignant Hyperthermia ...... Aspiration Syndrome ...... Allergic Reactions ...... Appendix: Intravenous Access ...... Review Questions ...... Index ...... Notes ...... I' Anaesthesia

)' Rotational Objectives

There are six speclflc knowledge and The student will demonstrate proper ) sk111s obJect1ves4 for the two week airway and ventilatory management of ) anaesthesia rotation: the unconscious patient by:

1. To become aware of anaesthetic a. Describing and identifying basic considerations in the preoperat- oropharyngeal and laryngotracheal ive evaluatlon and preparation of anatomy. the patient. b. Describing the indications, benefits and risks of airway management by This will be accomplished by conduct- mask and endotracheal intubation. ing several preoperative assessments, c. Identifying and stating appropriate including: sizes of masks, oral and nasal airways, laryngoscope blades and a. Taking and recording a pertinent endotracheal tubes. history. d. Identifying and overcoming upper b. Performing an appropriate physical airway obstruction with mask ven- examination, including assessment tilation using various masks, oral of the airway, the respiratory and and nasal airways, jaw thrust and cardiovascular systems, and other or chin lift maneuvers. systems as indicated. e. Successfully preparing appropriate c. Reviewingrelevantlaboratorydata. equipment, positioning and d. Preparing a problem list and intubating several patients with assigning appropriate ASA phy- minimal supervisor intervention. sical status. f. Correctly identifying within 30 sec- e. Prescribing appropriate premedica- onds those patients in whom endo- tion, including continuing relevant tracheal intubation was not succ- current medications, and demon- essful. strating knowledge of the prin- g. Recognizing and discussing the ciples of managing specific medi- need for controlled ventilation cations (eg. insulin,anticoagulants). using physical signs, cardiovascular parameters, respiratory measure- 2. To learn appropriate airway and ments, and/or arterial blood gases. ventllatory management.

Must Know ** Should Know * Page I Anaesthesia for Medical Students h. Discussing the various methods of - examination of the patient. monitoring the adequacy of ventila- - pulse and blood pressure. tion. - urine output. i. Prescribing appropriate parameters - invasive monitoring (CVP, for mechanical ventilation. PCWP, Arterial pressure j. Describing and identifying criteria waveforms, cardiac output). for extubation. To learn local anaesthetlc phar- 3. To acqulre skllls necessary to macology approprlate to general prescribe and conduct approprl- medlclne by: ate fluld and blood component therapy, lncludlng establlshlng Classifying commonly used agents vascular access. according to amide and ester link- age. This will be demonstrated by: Listing commonly used local a. Identifying common sites for anaesthetics for: venous access. - topical use b. Demonstrating skill at establishing - local infiltration venous access by: - peripheral nerve blocks - using sterile technique. - iv (Bier's) block - Successfully inserting several - epidural anaesthesia peripheral catheters of various - spinal anaesthesia calibres. Listing acceptable doses of at - Protecting the venipuncture site least two agents used for topical and immobilizing the catheter. and local infiltration anaesthesia. c. Describing the indications and Describing the diagnostic criteria complications of central venous for, and management of: access. - local anesthetic toxicity. d. Prescribingperioperative fluid and - inadvertent intravascular injec- electrolyte replacement, taking tion of local anaesthetic. into account such factors as NPO - allergic reaction to a local an- status, preoperative bowel prep, aesthetic. NG suction, fever, blood losses, and third space losses. To understand the management e. Discussing perioperative indica- of pain In the peripartum period tions for blood administration, and and the lnltlatlon of neonatal learning rational use of blood resuscltatlon. products, and the potential complications of blood product adminis- This will be demonstrated by: tration. a. Discussingindications, contraindi- f. Correctly interpreting data from cations and adverse effects of the following monitors of volume various modes of obstetrical pain status: relief.

Page 2 Rotational Objectives

- mask analgesia with nitrous c. Chronic low back pain. oxide and/or volatile anaesthe- d. Post herpetic neuralgia. tic agents. e. Cancer pain. - narcotic analgesia (im, or iv). - epidural anaesthesia. ANAESTHESIA CURRICULUM: - spinal anaesthesia. KNOW LEDGEfSKILLSIATTITUDE b. The student will develop skills in assessment and management of the healthy newborn by: - administering oxygen by mask. The following topics will be covered - performing oropharyngeal and either in the manual, or in seminar nasopharyngeal suction. format and problem solving sessions - performing an initial physical during the 12-week surgical - anaes- examination. thesia rotation. - assigning Apgar Scores. - recognizing newborn distress. Preoperative evaluation and preparation. c. The student will be able to Anaesthetic - Surgical risk assessment. describe therapeutic steps necess- Hypoxia . ary to begin neonatal resuscitation. Oxygen Therapy. Intubation-indications/complications. 6. To understand the prlnclples of Principles of mechanical ventilation. acute and chronlc paln manage- Shock. ment. Fluid Therapy. Blood component therapy. This will be achieved through the pro- Acute and Chronic Pain management. vided reading material in the anaesthesia Obstetrical anaesthesia-analgesia. manual, a pain clinic rotation, and a Basic neonatal resuscitation. discussion of modalities for acute pain management including: a. iv narcotic infusions. 1. Airway maintenance maneuvers in b. non-narcotic analgesics. the unconscious patient. c. iv and epidural PCA 2. Artificial airway insertion. (patient controlled analgesia). 3. Mask ventilation. d. peripheral nerve blocks. 4. Endotracheal intubation and extubation. Reading material in the anaesthesia 5. Spontaneous, manual, and con- manual and discussion of the diagnosis trolled modes of ventilation. and management of common chronic 6. Venous cannulation. pain syndromes will focus on: 7. Prescription, identification and administration of blood components, a. Reflex sympathetic dystrophy. including equipment assembly.w b. Fibrositis. 8. Arterial blood gas sampling.w

Should Know * Page 3 4naathaia for Medical Srudenfs

9. Spinal anaesthesia encounters do not have to be devoid of (Lumbar puncture)." reassurance, kindness or a comforting 10. Nasogastric tube insertion." touch. We expect both positive and negative experiences during your rota- ti Skills number 1 to 6 must be tion to be discussed openly with us, to achieved during the rotation. Students ensure the best possible rotation for may acquire skills number 7 to 10 de- future students. pending on clinical opportunity and the students' interest level. Resources: Attitude: Our University of Ottawa Anaesthesia Manual will be distributed to all stud- We hope that your two-week rotation ents, and will be used as the basic ref- will stimulate a thirst for knowledge and erence text for the rotation. Additional understanding of the fascinating physiol- reference material will be available in ogy and pharmacology that occurs in each hospital's anaesthesia library. the patient undergoing surgery. Anaes- thesia is a somewhat unnatural if not Topics covered in this manual have magical state. It is normal to feel tech- been classified as either must know, nically challenged during your rotation should know, or may know material. as you acquire vascular access and Material designated as must know will airway management skills. Each of you be identified by two asterisks (**), and can expect to experience (as all doctors will have a greater emphasis in content have), a humbling but hopefully reward- and weighting in the multiple choice, ing, technical learning curve. You short answer, and OSCE questions at should be aware of your difficulties, the end of the surgical anaesthesia rota- your response to them, and the response tion. Material assigned to the should of your patient and other medical per- know portion of each chapter will be sonnel to your difficulties. We ask that identified by one asterisk (*). All other your eyes and senses not be clouded by topics covered in the manual provide a technical monitors, but rather be open to general background for the student the overall care of the patient. We during their anaesthesia rotation, and are demand a commitment of excellence in topics which the student may know. A your care and concern for the well- passing grade can be achieved with a being of the patient and their family. good comprehension of the must know We expect punctuality and honesty as a material, while an honours mark may be basis of good medicine. awarded to students correctly answering material covered in the should know and While students may view anaesthesia as may know sections of the manual. a specialty with limited patient contact, they should ensure that opportunities for communication with the patient and family do not slip by. Fact-gathering

Page 4 Rotational Objectives

A computerized anaesthesia simulator will be available as anoption during the students rotation. (The simulator The rotation evaluation will be based on includes models of pharmacology, four components. pharmacokinetics, critical incidents, as well as cardiovascular and respiratory I. Participation during problem solv- physiology). ing sessions. 11. One or more examinations using a The hospitals' anaesthesia library and multiple choice format, short main libraries will be available for answer examination format, or reference during the rotation. OSCE examination. 111. A clinical profile record. IV. A review of the anaesthesia simu- Notes: lator problems (optional).

MwKnow ** Should Know * Page 5 Anaesthesia Overview

Modem general anaesthesia is based on iologist uses both skills in clinical the ability to provide adequate analgesia examination and a host of technical and amnesia during surgical procedures. monitors to provide ongoing feedback Neuromuscular-blocking drugs may be on the patient's physiological status and utilized to facilitatesurgical exposure by anaesthetic requirements. Table 2.1 lists providing profound muscle relaxation. options available to the anaesthesiol- The anaesthesiologist attempts to ogist for providing analgesia, amnesia achieve both analgesia and amnesia, and muscle relaxation. with or without muscle relaxation, while maintaining the patient's normal physio- A state of general anaesthesia may be logical functions. The challenge in induced with the injection of anaesthetic anaesthesia is to maintain a balance drugs, or by the inhalation of a mixture between the stress of the surgical proof anaesthetic vapours (figure 2.1). cedure and the cardiorespiratory With general anaesthesia, muscle relax- depressant effects of deepening levels of ants may be used to facilitate both tra- anaesthesia (figure 2.1). The anaesthes- cheal intubation and muscle relaxation. Anaest hesla Surgery Physbbgical Stability Stw End organ homeostasis - psychological - cardiovascular - physiologlcal - respiratory - Blood loss - Cardiovascular stress - neural - Fluid shifts - Respiratory stress - renal - Temperature changes

Figure 2.1: The Anaesthetic - Surgical balance.

Page 6 Chapter 2 Anaesthesia Overview

Muscle relaxants are frequently used to muscles of respiration, positive pressure facilitate surgical access, and are essen- ventilation is frequently used to main- tial for thoracic and abdominal oper- tain normal minute ventilation when ations. As muscle relaxants have no they are given. When muscle relaxants effect on the state of consciousness, are not used, the patient may be allowed additional anaesthetic medications must to spontaneously inhale anaesthetic be given to ensure both amnesia and vapours to maintain the anaesthetic analgesia. The use of muscle relaxants state. If efforts at spontaneous ventila- avoids the need for excessive amounts tion are inadequate, manually assisted or of other anaesthetic agents that would controlled mechanical ventilation may otherwise be required to achieve the be used by the anaesthetist. Controlled same degree of muscle relaxation. mechanical ventilation is generally used Because muscle relaxants also affect the only when the trachea has been intubated. Table 2.1: Anaesthetic Options*. Anaesthetic Options Local Anaesthesia Alone. Local Anaesthesia eg. iv Propofol, midazolam, fentanyl and or music for with intravenous sedation. conscious sedation. Neurolept-analgesia. Used infrequently. Achieved with high doses of droperidol with a opioid (such as fentanyl) for analgesic supplementation. Regional Anaesthesia, eg. Spinal Anaesthesia with or without seda- Epidural Anaesthesia tion. Brachial Plexus Block Intravenous 'Bier' Block Peripheral Nerve Blocks General Anaesthesia. May be combined with regional anaesthesia, peripheral (see figure 2.2) nerve blocks or local anaesthesia. Others Acupuncture Biofeedback techniques (Lamaze) Inhalational agents (eg. Entonox = 5050 mixture of nitrous oxide and oxygen). im, po, iv sedatives, narcotics, neuroleptics, or antiemetics

** Must Know Should Know Page 7 ) Anaesthesia for Medical Students )

Intravenous Anaesthetics or Inhaled Anaesthetic Gases

Induction of General Anaesthesia

Mask Endotracheal tube

No muscle Assisted Controlled relaxants jH Ventilation yon

v Spontaneous Ventilation with ventilation muscle relaxants

Figure 2.2: Establishment of General Anaesthesia.

Spontaneous and assisted ventilation drugs used during general anaesthesia may be used in conjunction with a include antiemetics, neuromuscular tracheal tube, laryngeal mask airway, or blocking agents, and neuromuscular simple face mask (figure 2.2). antagonists.

Modem general anaesthesia uses combinations of medications in an attempt to minimize each drug's side effects, and maximize individual benefits. Hence, rather than using halothane alone -to provide anaesthesia for abdominal surgery, the anaesthetist often chooses a series of medications to match the patient's needs. These medications may include opioids to blunt the pain response to surgery, barbiturates to induce the anaesthetic state, and volatile anaesthetic agents such as nitrous oxide and isoflurane to maintain the anaesthetic state. Other common anaesthetic

Page 8 / CHAPTER 3 1 ' Preoperative

I Evaluation and : Risk Assessment

) GREGBRYSON M.D., FRCPC AND JOHNB. KITTS M.D., FRCPC

-- - Preoperative assessment is essential for safe and effective performance of sur- the safety of anaesthesia. Physicians gery. The preoperative evaluation does who have had no exposure to the spe- not replace the role of the primary care cialty of anaesthesia are ill-equipped to provider, and should not be used to evaluate, prepare, and institute measures address issues that are not relevant to to minimize the patient's risk in the the performance of anaesthesia and perioperative period. This chapter pro- surgery. vides a framework for physicians who need to understand their patients' risk of The preoperative visit should include undergoing a surgical procedure, and the the following steps: measures that can be used to optimize their patients' condition prior to surgery. I. Problem Identification 11. Risk Assessment Preoperative evaluation serves many 111. Preoperative Preparation purposes. First, it offers the anaesthetist IV. Plan of Anaesthetic Technique an opportunity to define the patient's medical and surgical problems, and plan the anaesthetic technique. Sewnd, further investigation, consultation, and treatment can be arranged for patients Identification of the problems a patient whose condition is not optimal. Finally, brings to the operating room is one of the anaesthetist can provide information the most vital, yet easily neglected, and reassurance for the patient during components of the perioperative man- this stressful time. agement of the surgical patient. A system-oriented approach to the patient An organized approach to the preoperat- is helpful in completing a thorough ive evaluation will allow the anaesthetist preoperative assessment. As is the case to perform a focused evaluation of the elsewhere in medicine, the preoperative patient's medical and surgical condition, evaluation should progress through and to address issues relevant to the history (including a review of the

** Must Know Should Know Page 9 Anaesthesia for Medical Students

patient's chart), physical examination, be directly sought. Valvular heart and laboratory investigation. disease presents a special set of concerns to the anaesthetist. This includes Anaesthetic drugs and techniques have unfavourable and even dangerous alter- profound effects on human physiology. ations in haemodynamics brought on by Hence, a focused review of all major the anaesthesia, particularly major organ systems should be completed regional techniques (see chapter 15: prior to surgery. The anaesthetist pays Local and regional anaesthetics). Con- .

special attention to symptoms and dis- sider the risk of subacute bacterial , ease related to the cardiovascular, res- endocarditis (SBE) in these patients. I

piratory, and neuromuscular systems as I they will directly manipulate these sys- Although less common with new anaes- , ' tems during surgery. Because one of thetic drugs, arrhythmias are frequently the goals of the preoperative evaluation seen in the operating room. In the , is to ensure that the patient is in the preoperative visit, identify a past history ; best (or optimal) condition, it is import- of arrhythmia or symptoms suggesting

ant not only to identify symptoms, but the need for a pacemaker. The patient / also to document their severity and to with hypertension will require special ; determine their stability or progress. attention to perioperative antihyper- Patients with unstable symptoms should tensive therapy and fluid and electrolyte

be postponed for optimization prior to balance. I elective surgery. Respirology: Cardlovascular: Cigarette smoke has several adverse Patients with ischemic heart disease are effects, including alteration of mucus at risk for myocardial ischaemia or secretion, clearance, and decrease in infarction in the perioperative period. A small airway calibre. It also may alter thorough history should ascertain the immune response. The chronic whether angina is new or has recently smoker should be encouraged to abstain changed from a previously stable pat- from smoking for at least 8 weeks prior tern. A description of the patient's to the operation,' but stopping smoking exercise tolerance must also be for even 24 hours may produce benefits included. Patients with a history of a in cardiovascular physiology2 and carb- recent myocardial infarction (< 6 oxyhemoglobin levels. months) or unstable angina are poor surgical candidates, with a high risk of Patients with chronic obstructive pulm- significant morbidity or mortality. onary disease (COPD) are at increased risk of perioperative respiratory compl- Assessment of cardiac risk is discussed ications. Anaesthesia, surgery and later in this chapter. As many anaes- postoperative analgesia all predispose thetic agents are also myocardial the patient with COPD to respiratory depressants, a history of congestive depression, atelectasis, retained secret- heart failure or cardiomyopathy should ions, pneumonia and respiratory insuff- Chapter 3 Preoperative Assessment iciency or failure. The patient with papilledema. Pituitary lesions may asthma is at particular risk as manipula- cause endocrine abnormalities. A his- tion of the airway and cold dry anaes- tory of TM's or CVA's suggests signifi- thetic gases are potent triggers of intra- cant cerebrovascular disease. The an- operative bronchospasm. Determine the aesthetist should ask the patient about a presence of cough and the colour and history of seizures, and determine the amount of sputum. Ensure that there is type, frequency and time of last occur- no acute upper respiratory infection. rence. Note any anticonvulsant medications the patient is receiving. The patient's exercise capacity should be evaluated by asking questions such as The patient with a history of spinal cord how they manage around stairs at home, injury is at risk for a number of and walking to local stores. Are they perioperative complications including able to walk several blocks comfortably respiratory failure, arrhythmias, auto- at a normal pace? Do they avoid stairs? nomic hyperreflexia, hyperkalemia, If they routinely uses stairwells, how pathologic fractures and pressure sores. many flights are they able to complete? It is important to document the date and Do they have to rest in the stairwell? Is level of the neurological injury, as the this the result of fatigue, shortness of incidence of many of these complica- breath, or chest pain? tions are dependent on such variables. Patients with lower motor neuron Restrictive lung disease will be lesions of any kind are at risk for worsened by upper abdominal or unusual responses to anaesthetic drugs thoracic surgery, and place the patient at (see chapter 12: Muscle Relaxants - increased risk for perioperative failure. Succinylcholine), and regional anaes- Any disease process which leads to an thesia should be considered only after altered control of breathing (obstructive careful documentation of the patient's sleep apnea, CNS disorders, etc.) may nerve deficits. lead to profound respiratory depression from the drugs used in the perioperative Disorders of the neuromuscular junction period, and may require postoperative such as myasthenia gravis, myasthenic monitoring in a critical care setting. syndrome, etc., will cause unpredictable Potential airway problems are of par- responses to neuromuscular-blocking ticular concern to the anaesthetist, and drugs. Lastly, patients with muscular must always be evaluated (see chapter dystrophies and underlying myopathies 6: Intubation and Anatomy of the Air- are known to have both an increased way). association withmalignant hyperthermia and an increased risk of postoperative Neuromuscular: respiratory failure (see chapter 24: If the patient has an intracranial lesion, Uncommon Anaesthetic Complications - seek early signs and symptoms of raised Malignant Hyperthermia). intracranialpressure such as headaches, nausea, vomiting, confusion and

** Must Know Should Know Page 11 Anaesthesia for Medical Studenis

Endocrlne: than one week in the last six months. Patients with diabetes mellitus require careful management in the perioperative GI-Hepatic: period, as the stress of surgery and peri- Patients with hepatic disease frequently operative fasting can cause marked present problems with fluid and electro- swings in blood glucose. Diabetics lyte imbalance, coagulopathies and frequently have widespread end organ altered drug metabolism. Patients with damage involving the cardiovascular, gastroesophageal reflux (GER), as well nervous and renal systems. as those at risk for GER, are prone to regurgitation of gastric contents and Patients with thyroid disease may ex- aspiration pneumonitis during the perio- perience difficulties under anaesthesia. perative period (see chapters 9 & 24: Profound hypothyroidism is associated Rapid Sequence Induction & Unusual with myocardial depression and exag- Anaesthetic Complications - Aspiration gerated responses to sedative medica- Pneumonitis). These patients should tions. Hyperthyroid patients are at risk receive anti-reflux prophylaxis pre- for perioperative thyroid storm. Thyroid operatively. goitres may compress the airway and involve the recurrent laryngeal nerve Renal: leading to vocal cord palsy. These Disorders of fluid and electrolyte bal- place the patient at risk for airway obst- ance are common in the perioperative ruction. period, and management of any possible electrolyte deficiency or excess may be Patients with phaeochromocytoma are part of the anaesthetic management of particularly challenging for the anaes- the patient. Generally all fluid and thetist, surgeon, and internist involved electrolyte disorders should be corrected in their care. These patients are at risk prior to elective surgery. for extreme swings in blood pressure and heart rate in the perioperative Patients with renal failure, both acute period, and require intensive preoper- and chronic, frequent the OR. The ative therapy with adrenergic blocking anaesthetist must be prepared to deal drugs. Patients at risk for adrenal sup- with their fluid and electrolyte dis- pression (history of exogenous steroid orders, dialysis requirements and altered therapy) may not be able to increase drug metabolism. Pay careful attention their own corticosteroid production to to the patient's dialysis schedule, as match the imposed stress of surgery. important changes in blood volume and The incidence of adrenal suppression is serum potassium levels occur pre- and not predictable, and depends on the post-dialysis. If possible, plan elective potency and frequency of steroid dose surgery so that the patient receives and on the length of steroid therapy. dialysis either the night before surgery, As a general rule, corticosteroid or on the morning of surgery. Patients supplementation is provided for patients with renal insufficiency are at risk for who have required steroids for more deterioration of their renal function, and Chapter 3 Preoperative Assessment

careful attention must be paid to their their age alone. However, every fluid and haemodynamic management in attempt must be made in adequately the perioperative period. diagnosing and treating coexisting disease preoperatively. The risk of defer- Haematologic: ring surgery must be balanced against Anemias of a variety of causes are the potential for the patient returning on common in the patient undergoing sur- an emergency basis. gery. A minimum haemoglobin level of 100 gm/L was traditionally required Emergency surgery in the elderly patient before a patient could undergo elective may lead to a four- to twenty-fold surgery. The dogma regarding an increase in perioperative mortality. adequate haemoglobin level has held Delay in presentation and inadequate less sway in recent years. Now the time for optimizing coexisting disease "transfusion trigger" must be individual- place an increased burden on a patient ized to the patient, bearing in mind the lacking the physiological reserve to chronicity of the anemia, the likelihood tolerate major stress and surgery. of perioperative blood loss, and the patient's co-existent disease (see chapter Medications and Allergies: 20). A detailed list of the patients' medications and allergies is an essential part of Coagulopathles involving clotting fac- the preoperative assessment. Particular tors and platelets, both congenital and attention should be paid to acquired, require careful management. cardiovascular and respiratory medica- Patients with a bleeding tendency are tions, narcotic analgesics, and drugs generally poor candidates for major known to have significant side effects or regional anaesthesia and management drug interactions. must be individualized, depending on the nature of the bleeding problem, the As a general rule, all cardiac and pul- proposed surgery, and the patient's monary medications and most other medical condition. necessary medications should be taken with sips of water at the usual time, up The Elderly: to and including the day of surgery. The elderly have a higher incidence of Possible exceptions to this include age-related coexisting disease as well as coumadin, ASA and NSAID's, insulin both diminished organ function and (adjustment of the dose is needed on the organ reserve. The result is that elderly day of surgery), oral hypogylcemics and patients are generally recognized to be antidepressants. Pay special attention to in a higher perioperative risk group. patients receiving monoamine oxidase Perioperative morbidity and mortality (MAO) inhibitors and amiodarone. are related to the extent of coexisting disease rather than the patient's age Question patients with allergies to drugs alone. Elderly patients should not be carefully on the nature of the reaction refused elective surgery on the basis of and the circumstances under which it

** Must Know Should Know Page 13 Anaesthesia for Medical Students occurred. Many "allergies" are simply on evaluation of the airway, the anticipated drug side effects such as cardiovascular system, the respiratory nausea and vomiting, or adrenaline system, and any other systems identified absorption from local anaesthetic agents. as having symptoms or disease from the True allergies to anaesthetics are history. unusual, but when present, can be fatal. General: Prlor Anaesthetics: A general assessment of the patient's The patient undergoing anaesthesia and physical and mental status is performed. surgery should be carefully questioned Note whether the patient is alert, calm, on their response to previous anaes- and cooperative, or unusually anxious thetics and a family history of problems about their scheduled procedure. Is the with anaesthesia. Investigate any com- patient young and physically fit, or plication or adverse reaction to prior elderly incoherent, emaciated and con- anaesthetics. Document the type of fined to bed? Such obvious differences problem, as well as its management and will dictate the extent and intensity of outcome. In the case of serious peri- the examination and the time required to operative events, consult the old chart to listen to the patient's concerns and pro- complete the history. Seek a family vide reassurance. The patient's mental history of adverse anaesthetic experi- status also influences the type and ence. Malignant hyperthermia and amount of preoperative medication plasma cholinesterase deficiency are two required (if any), and may influence the hereditary disorders that manifest under type of anaesthetic technique used (eg. anaesthesia (see chapter 24: Unusual general vs. regional). Anaesthetic Complications). Upper airway: Problems related to Surgery: Examination of the upper airway must Information about the patient's general be performed on all patients. Identify medical condition and anticipated intra- and document any loose teeth, capped operative problems can be gained from teeth, or bridges. The patient should be an evaluation of the proposed surgery. asked to open their mouth as widely as Careful consideration of the surgical possible, in order to assess temporal procedure will reveal the likelihood of mandibular joint mobility, and allow significant blood or third space loss, visualization of the soft palate, uvula, cardiorespiratory compromise, andlor pharyngeal arches and posterior phar- unusual positioning requirements (prone, ynx. The thyromental distance (the lateral, lithotomy, etc.). This informa- distance from the mentum (lower border tion will be useful in planning venous of the chin) to the thyroid notch, the access, monitoring, and anaesthetic mobility of the C-spine in both flexion technique. and extension, as well as the position of the trachea should all be assessed, as Physlcal Examinatlon: each of these have implications with The physical examination should focus respect to the ease of intubation.

Page 14 Assessment of the upper airway must sites for major regional anaesthetic include evaluation of the range of techniques (eg. spinal, epidural, or motion of the neck, as well as mouth brachial plexus blocks). opening, dentition, and thryromental distance. The adequacy of visualization Again, the state of health of the patient of the hypopharyngeal structures is used will dictate the intensity of the examin- as an indicator of potential difficulty ation required. The healthy 20-year-old with direct laryngoscopy. A hypo- male undergoing an arthroscopy, pharyngeal class is assigned in an requires a much more abbreviated his- attempt to quantify the degree of diffi- tory, physical examination and chart culty that will be encountered during review when compared to the elderly direct la~~n~oscopy.~~~(See Chapter 6: patient undergoing a major abdominal Anatomy and Assessment of the Air- procedure. way). Laboratory Testing: Lower airway: Obtain preoperative laboratory testing Assess the respiratory rate. Note the only if indicated from the preoperative shape of the thoracic cage, and whether history and physical examination. In or not the patient is relying on their September 1993, the Public Hospital's accessory muscles (e.g., the barrel Act in Ontario was amended so that shaped bronchitic patient vs. the pink mandatory haemoglobin and urine an- emphysemic puffer). Auscultate the alysis were no longer required prior to chest for audible rhonchi on quiet and surgery. Perform these tests and all forced expiration, and identify the pres- other preoperative tests, however, where ence or absence of rales. Note the indicated by the medical status of the presence or absence of cyanosis and patient, or if the patient is considered in clubbing. a population at risk for a specific problem. "Routine or standing" re operative Cardiovascular: tests should be discouraged. Assess the heart rate, rhythm and blood pressure. Identify the location of the Do a CBC for patients in whom there is apical impulse, and whether it is significant blood loss anticipated, sus- abnormally displaced. Assess the level pected haematological disorder (eg. of the JVP, and identify the presence or anaemia, thalassaemia, sickle cell dis- absence of peripheral edema. Identify ease), or recent chemotherapy. Patients the first and second heart sounds and on antihypertensive medications, includ- listen for the presence of heart murmurs, ing diuretics, chemotherapy, renal dis- or a third or fourth heart sound. ease, adrenal or thyroid disorders, must have electrolytes evaluated pre- Anticipate any special invasive pro- operatively. Obtain an electrocardio- cedures, and assess the anatomy for gram (ECG)for patients over 50 years arterial line insertion, central vein of age, or those who have a history of cannulation, intravenous access, and cardiac disease, hypertension, peripheral

** Must Know * Should Know Page 15 Anaesthesia for Medical Shtdents vascular disease, diabetes mellitus, patient's outcome is virtually impossible, renal, thyroid or metabolic disease. and the complexity of this issue has Request chest X-rays prior to cardio- made research studies addressing out- thoracic procedures and for patients come very difficult. Nevertheless, sev- with debilitating COPD, asthma, or a eral studies attempting to determine change in respiratory symptoms in the anaesthesia mortality and morbidity past six months. Perform urine analysis have been c~m~leted~'~It is difficult for patients with diabetes mellitus, renal to separate the contributions of anaes- disease or recent urinary tract infection. thesia and surgery to morbidity and mortality, as patients rarely receive an anaesthetic without undergoing a surgical procedure. Table 3.1 summarizes There are three components that must several studies which have attempted to be considered when evaluating peri- determine the risk of mortality due operative risk: the patient's medical solely to anaesthesia. condition preoperatively, the extent of the surgical procedure, and the risk from Studies on perioperative mortality have the anaesthetic. In general, the major yielded differing results. Differences in contribution to increased risk is that of the definition of outcome variables, the patient's health prior to the pro- study design, and the duration of fol- cedure and the magnitude of the sur- low-up make these results difficult to gery. However, patients presenting for compare. When reviewed critically, surgery often have more fear about their these studies suggest that the often anaesthetic than the surgery itself. quoted number for overall risk of pri- Fortunately, anaesthesia-related morbid- mary anaesthetic mortality for all ity and mortality is rare, but unfortu- patients undergoing all types of surgery nately, not absent. This does, however, is approximately 1:10,000. create its own problems. The combination of infrequent but serious events has The question to which anaesthetists and led one author to state that "Perhaps the the patient need the answer is: "What is most insidious hazard of anaesthesia is the risk of a particular procedure in a its relative safety."' patient with a given medical status receiving a specific anaesthetic tech- Anaesthetic Mortality: nique?" Numerous investigators have attempted to address this very complex The wide variety of surgical procedures question. Most of the work, however, and anaesthetic techniques, combined addresses the operative risk according to with the diversity of a patient's coexist- the patient's preoperative medical status. ing surgical and medical illnesses, produce a number of risk factors that con- Perloperatlve Rlsk Assessment: tribute to overall outcome, and make generalized statements about risk diffi- Perhaps the oldest and simplest method cult. Specific predictions for a single for risk assessment is the American i Chapter 3 Preoperative Assessment

Author Country Year No. in Incidence study of Primary Anaesthetic Mortality Turnbul16 Canada 1980 195,232 15,138 ~ovi-Vivander7 Finland 1980 338,934 1:5,059 Lunn & ~ushin' United Kingdom 1982 108,000 1:10,000 Keenan & ~o~en~United States 1985 163,240 1:10,000 ~iret" France 1986 198,103 1:13,207 Holland1' Australia 1987 550,000 1:26,000 Buck1' United Kingdom 1987 500,000 1: 185,000

Table 3.1 : Estlmates of Prlmary Anaesthetic Mortality

Society of Anesthesiology (ASA) physi- patient classification. Although devel- cal status (table 3.2). The ASA physi- oped as a tool for classifying a patient's cal status classification system was physical condition, the ASA physical originally proposed in 1941, and revised status has been used to stratify patient by Dripps in 196113 to provide a uni- risk. While open to significant criticism form assessment of a patient's preoperat- because of its vague categories and ive physical condition. inconsistencies in its application, the ASA physical status classification has As this system is simple, easy to use, been shown to correlate with peri- and requires no laboratory investiga- operative mortality.ld17 tions, it has now been widely accepted as the standard means of preoperative

Category Description I Healthy patient. I1 Mild systemic disease - no functional limitation. I11 Severe systemic disease - definite functional limitation. IV Severe systemic disease - a constant threat to life. V Moribund patient - not expected to survive with or without an operation for 24 hours. E A suffix E is added to denote an emergency procedure. Table 3.2: ASA Physlcal Status Classlflcatlonhc. 1 ** Must Know Should Know Page I7 Anaesthesia for Medical Shrdents

Operative Mortality (percent)

ASA Class Vercantit4 ~arx" &hent6 orr rest " 1970 1973 1986 1990

I .07 .06 .07 .OO I1 24 .40 .20 .04 nr 1.43 43 1.15 59 IV 7.46 23.4 7.66 7.95 V 938 50.7 ------Table 3.3: ASA Physlcal Status vs. Operative Mortality WO).

Examples of the ASA classification: tors that predicted life-threatening cardiac complications. A scoring system ASA 1: Healthy patient, no medical weighted these factors in their ability to problems. predict adverse cardiac outcome. ASA 2: Controlled hypertension. ASA 3: Emphysema. From these data, Goldman suggested ASA 4: Unstable angina. that patients with a score greater than ASA 5E: Ruptured abdominal aortic 25 be considered only for life-saving aneurysm in shock, under- procedures. Patients scoring 13-25were going emergency surgery. advised to have preoperative medical consultations to lower their morbidity Cardiac Risk: and mortality. Certainly, delaying sur- Several perioperative risk studies have gery until the patient is more stable can attempted to assess which perioperative significantly reduce the cardiac risk cardiac risk factors are important. index. Waiting for 6 months after a Ischaemic heart disease has received the most attention because mortality from a Risk Factor Points perioperative myocardial infarction approaches 50%. Third heart sound or elevated JVP 11 MI within 6 months of surgery 10 In 1977 Goldman published Rhythm other than sinus or PAC's 7 a multifactorial risk index > 5 PVC's per minute 7 for cardiac patients undergo- Age > 70 5 ing non-cardiac procedures18 Emergency procedure 4 (table 3.4). This study, in- Abdominal, thoracic, or aortic surgery 3 volving 1001 patients, ident- Important Aortic stenosis 3 ified, by multivariate analy- Poor medical status 3 sis, nine potential risk Table 3.4: Goldman's Cardlac Rlsk Index i Chapter 3 Preoperative Assessment

Variable Points MI < 6 months pre-op 10 MI > 6 months pre-op 5 CCS Class 4 angina 20 CCS Class 3 angina 10 Unstable angina < 3 months pre-op 10 Pulmonary edema < 1 week pre-op 10 Pulmonary edema ever 5 Critical aortic stenosis 20 Rhythm other than sinus 5 > 5 PVC's per minute 5 Poor medial status 5 Age > 70 years 5 Emergency procedure 10

Table 3.5: Detsky's Multltactorlal Index

myocardial infarct, delaying emergency Using likelihood ratios, Detsky was able procedures (if feasible) and improving a to construct a nomogram relating the patient's poor medical status all signifi- pretest probability of cardiac morbidity cantly decrease the risk. for the surgical procedure to the patient's risk score. This generates an The Goldman index has high specificity overall prediction of the risk of major but low sensitivity when predicting risk. cardiac morbidity or mortality for a Patients with scores of 13 or greater patient of a certain medical status should arouse suspicion. A low score undergoing a specific procedure. correlates with a low probability of poor Although Detsky's risk index is a better outcome. In an attempt to improve the sensitivity of Goldman's index, ~etsky'~ Surgery % Cardiac modified Goldman's criteria to Complications include a wider range of cardiac illness (table 3.5). Detsky Vascular 13.2 also recognized that not all sur- Orthopaedic 13.6 gery carries the same risk, and Thoracic - Abdominal 8.O factored in the surgical pro- Head & Neck 2.6 cedures for the pretest probabil- Minor (TURP, Hernia, ...) 1.6 ity of inducing significant cardiac complications (table 3.6).19 Table 3.6: Detsky's Pretest Probablllty For Type of Surgery

** Must Know Should Know Page 19 Anaesthesia for Medical Students

predictor of cardiac outcome than with invasive haemodynamicmonitoring Goldman's, it still has limitations. and aggressive therapy in an intensive However, a review of the risk factors care unit (ICU) setting for 72 hours fol- described in both these studies alerts the lowing surgery. Cumulatively, these anaesthetist to symptoms or signs of studies suggest considerable benefit in significant disease that may contribute delaying elective surgery for a period of to adverse outcome. 6 months following a myocardial infarction. Before six months, invasive moni- Both Goldman and Detsky identified toring and aggressive postoperative recent myocardial infarction as a risk management, appear essential, for those factor for perioperative cardiac morbid- patients in whom surgery must be per- ity. The perioperative period is charac- formed. terized by haemodynamic changes, alterations inventilation, fluid and electrolyte shifts, and changes in coagulation, all of which place the patient with Premedicatlon: (see also chapter 4) underlying cardiac illness at significant Anaesthetic indications: The risk of infarction. Several important preanaesthetic visit should be designed studies have been conducted over the to alleviate patient anxiety and appre- past 20 years in an attempt to identify hension about the proposed surgery. the likelihood of perioperative reinfarc- However, a benzodiazepine such as tion in patients with a recent ML~" diazepam or lorazepam is also frequent- The goal of these studies was to deter- ly administered orally 1 - 2 hours pre- mine the safest time interval following operatively. This may provide sedation, an MI to proceed with elective surgery, relieve anxiety, and provide a degree of and to direct attention to appropriate amnesia for the events immediately perioperative monitoring and care preceding the operation. (Table 3.7). Patients at risk for GE reflux should In Rao's study, patients were managed receive anti-reflux prophylaxis. This is

Time from infarction Tarhan20 Steen21 Rao22 to Surgery (1972) (1978) (1983)

0 - 3 months 37% 27% 5.8%

3 - 6 months 16% 11% 23%

Greater than 6 months 5.6% 4.1% 1.5%

Table 3.7: Comparlson of Perloperatlve Relnfarctlon Rates e!).

Page 20 Cha~ter 3 Preo~erativeAssessment usually achieved with ranitidine 150 - IV: PLANNINGTEE ANAESTHETIC** 300 mg p~.2 hours pre-operatively. Other agents such as metoclopramide Having identified and evaluated our may be added to promote gastric empty- patient's problems we now ask ourselves ing. Sodium citrate is an effective non- five questions. particulate antacid that may also be used alone or in conjunction with ranitidine. I., Is the patient's condition optimal? Surgical indications: According to the American Heart Association Guidelines, 2. Are there any problems whlch appropriate antibiotic prophylaxis must requlre consultation or speclal be administered for patients at risk for tests? the development of infective endocarditis.= These include patients (For example: In a patient with poorly for whom a bacteremia is likely to controlled angina, a cardiology consult occur as a result of respiratory tract, would be appropriate. You may write: genitourinary, or gastrointestinal tract Consult medicine - cardiology. 'Please interventions. Some patients are at high assess and advise re: optimal peri- risk for the development of operative medical management of postoperative deep vein thrombosis angina in this patient'). (DVT). Prophylactic measures should be used and include low-dose heparin, 3. Is there an alternative procedure intermittent calf compression, or which may be more approprlate? wumadin. Patients who are currently receiving steroids and those who have This is especially important to consider required steroids in the previous six in the high risk patient. For example: months may require supplemental ste- the placement of a suprapubic catheter roids because of adrenal suppression may be more appropriate than a trans- and a blunted response to stress. urethral prostatectomy (T'URP) in a terminal cancer patient with a recent Cu-existing Disease Indications: All stroke, congestive heart failure, and important medications should be wn- obstructive uropathy. Discuss the avail- tinued on the day of surgery. These can able options with the staff anaesthetist be taken orally with sips of water. and the surgeon. Some medications, including insulin, prednisone, coumadin, and broncho- 4. What are the plans for post- dilators, require adjustment of dosage operative management of the and/or alternate routes of administration. pa tlent? Oral hypoglycemics and antidepressants should not be taken on the day of sur- Options include: Monitoring in the gery. It is no longer mandatory to post-anaesthesia care unit (PACU) for discontinue MA0 inhibitors two weeks an initial period of observation, then preoperatively . either return to ward or discharge home

** Must Know Should Know Page 21 Anaesthesia for Medical Students

(e.g., daycare patients). Patients with tension for the last six years, and was significant underlying diseases or having also found to have NIDDM at the time major procedures may remain in a criti- his hypertension was diagnosed. cal care setting overnight for closer observation (eg. PACU, ICU, CCU). Our patient's problem list includes: Consideration should be given to which 1. Elective lower abdominal surgery. form of pain management is most 2. Controlled hypertension. appropriate for the patient post- 3. NIDDM. operatively. . 4. Smoking history 35 pack years. 5. Identified risk factors for CAD. 5. What premedication if any is appropriate? The anaesthetic history should include: 1. A brief history of present illness. Finally, we plan our anaesthetic tech- E.g., "Discomfort in groin for 6 nique (see chapter 2: Anaesthesia months." Overview). This may be: 2. Current medications (including 1. Local anesthesia with 'standby' ASA, alcohol, and illicit drugs if monitoring with or without seda- appropriate). Eg., "Enalapril 10 tion. mg and glyburide 10 mg daily." 2. Regional anesthesia with or with- 3. Allergies and type of reaction. out intraoperative sedation. E.g., "Penicillin: hives." 3. General anesthesia with or without 4. Significant past medical - surgical intubation. If an intubation is history. E.g., "Appendectomy". required the anaesthetist may elect 5. Past anaesthetic history. to control the patient's ventilation, E.g., "No known problems." or allow them to breath spontan- 6. Family history of any anaesthetic eously. If controlled ventilation is problems. E.g., "No known prob- used, the anaesthetist may or may lems." (see chapter 24). not use muscle relaxants. 7. Functional inquiry appropriate to 4. Combined regional anaesthesia the patient, and concentrating on with general anaesthesia. the cardiorespiratory systems. E.g., "Inactive lifestyle, no symp- Discuss with your staff anaesthetist toms of chest pain or coronary when and why we would choose each ischemia!' (See also 9 below re: of these techniques. additional appropriate questions. 8. NPO status. E.g., "Nothing to eat For discussion, let us work through a or drink since last night." patient case. We recently gave an an- 9. Specific questions directed at the aesthetic to a 50-year-old male for an identified problem list, attempting elective repair of his inguinal hernia. to assess the severity of the prob- He admitted to smoking one package of lem, its associated disability, and cigarettes per day, and has done so for the patient's remaining physiologi- the last 35 years. He has had hyper- cal reserve. Chapter 3 Preoperative Assessment

Problem: 35 pack year smoker. Appropriate questions concerning his cardiovascular risk factors would Do you have a cough on most mornings include: or a "smoker's cough"? (i.e. Chronic bronchitis). Have you ever had a heart attack? Do you ever wheeze? Do you ever get chest pains, or leg Have you ever required medications for cramps with exertion? (Angina, claud- your breathing? ication). Does your breathing limit your physical How often? What relieves them? What activity? are they like? What kind of activity would make you Do you ever wake up at night short of short of breath? (A fast walk? One breath? (PND). flight of stairs? Two blocks? etc.). Are you able to sleep with the head of the bed flat? (Orthopnea) Problem: Hypertension. Additional appropriate questions for this When were you first aware that you had patient would include questions regard- high blood pressure? ing gastroesophageal reflux. How often is your blood pressure Do you ever experience acid reflux from checked? your stomach? How often? Has it been well controlled with your medications? Next, a physical examination as describ- What is your usual blood pressure when ed previously should be performed. you see your family doctor? Appropriate laboratory tests for this Problem: NIDDM patient would include a CBC, electrolytes, glucose, and electrocardiogram. How long have you been aware of your diabetes? After discussion with the patient and How has it affected you? (end organs surgeon, a spinal anaesthetic was chosen involved include: eyes, heart, kidneys, for this patient. While a general anaes- peripheral circulation, autonomic and thetic would also be an option, we peripheral nerves). chose a spinal anaesthetic because we How do you monitor your blood sugar? would be able to avoid intubation and Have you ever had to come to the emer- its associated sympathetic stimulation gency because of your diabetes? (increased heart rate and blood pressure), as well as its potential to trigger Identified risk factors for CAD include airway reflexes resulting in broncho- hypertension, smoking history, male spasm. gender, age and diabetes.

** Must Know Should Know Anaeslhesia for Medical Students

References: of incidence and causes. JAMA 253:2372, 1985. Wamer MA, Offord KP, Wamer Tiret L, Desmonts JM, Hatton F, et ME et al. Role of preoperative al: Complications associated with cessation of smoking and other anaesthesia - a prospective study in factors in postoperative pulmonary France. Can J Anaesth 33:336, complications: a blinded prospec- 1986. tive study of coronary artery Holland R. Anaesthetic mortality bypass patients. Mayo Clin Proc in New South Wales. Br J 64:609, 1989 Anaesth 59:834, 1987. Pierce AC, Jones RM: Smoking Buck N, Devlin HB, Lunn JL: and anesthesia: preoperative absti- Report on the confidential enquiry nence and perioperative mortality. into perioperative deaths. The Anesthesiology 6 1576, 1984 Nuffield Provincial Hospitals Mallampati SR, Gatt SP, Gugino Trust, London. The King's Fund LD, et al: A clinical sign to pre- Publishing House, London. 1987. dict difficult tracheal intubation: Dripps RD, Lamont A, Eckenoff A prospective study. Can J JE: The role of anaesthesia in , Anaesth 32429, 1985. surgical mortality. JAMA Samsoon GLT, Young JRB: Diffi- 178:261, 1961. cult tracheal intubation: A retro- Vancanti CJ, VanHouten RJ, Hill , spective study. Anaesthesia RC: A statistical analysis of the 42487, 1987. relationship of physical status to ' Cooper JB, Newbower RS, Kitz postoperative mortality in 68,388 , RJ: An analysis of major errors cases. Anesth Analg 49564,1970. and equipment failures in anaes- Marx GF, Mateo CV, Orkin LR: thesia management: Consider- Computer analysis of post anaes- ations for prevention and detection. thetic deaths. Anesthesiology , Anesthesiology 60:34, 1984. 3954, 1973. Tumbull KW, Fancourt-Smith PF, Cohen MM, Duncan PG, Pope ' Banting GC: Death within 48 WDB, et al: A survey of 112,000 , hours of Anaesthesia at the anaesthetics at one teaching hospi- Vancouver General Hospital. Can tal (1975-83). Can J Anaesth Anaesth Soc J 27:159, 1980. 33:22, 1986. Hovi-Viander M: Death associated Forrest JB, et al: Multicenter with anaesthesia in Finland. Br J study of general anesthesia. 11. Anaesth 52:483, 1980. Results. Anesthesiology 72262, Lunn JN, Mushin WW: Mortality 1990. associated with anaesthesia. Goldman L, Caldera DL, Nuffield Provincial Hospitals Nussbaum SR, et al: Multi-factori- Trust, London. 1982. a1 index of cardiac risk in non Keenan RL, Boyan CP. Cardiac cardiac surgical procedures. N arrest due to anesthesia: A study Engl J Med 297:845, 1977. Chapter 3 Preoperative Assessmenf

19. Detsky AS, Abrams HB, Forbath N, et al: Cardiac assessment for patients undergoing non cardiac surgery: A multifactorial clinical risk index. Arch Intern Med 146:2131, 1986. 20. Tarhan S, Moffitt EA, Taylor WF, et al: Myocardial infarction after general anesthesia. JAMA 220:1451, 1972. 21. Steen PA, Tinker JH, Tarhan S: Myocardial re-infarction after anesthesia and surgery. JAMA 2399566, 1978. 22. Rao TLK, Jacobs KH, El-Etr AA: Re-infarctionfollowinganaesthesia in patients with myocardial infarction. Anesthesiology 59:499, 1983. 23. Dajani AS, Bisno Al, Chung KJ, et al: Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAM264:2919,1990.

Notes:

** Must Know Should Know Page 25 ) Anaesthesia for Medical Students ) Notes:

Page 26 i Prernedication

Most patients scheduled for surgery will part of our preoperative visit is to con- experience some degree of apprehen- vey a reassuring, honest and caring sion. The psychological stress a patient attitude. experiences prior to surgery can be more detrimental than the actual physi- The patient's desire for sedation prior to cal insult of the surgical procedure. a planned surgical procedure is the most Preoperative anxiety may be caused by common reason for prescribing a preop- many factors. Some of the more com- erative medication. We also prescribe mon causes include*: medications preoperatively to avoid potential complications associated with 1. The fear of relinquishing control to the procedure (eg., antibiotics to pre- someone else while under general vent the development of endocarditis in anaesthesia. a patient with valvular heart disease), or 2. The fear of dying during the oper- to continue the patient's current medica- ation. tions for coexisting medical conditions. 3. The fear of experiencing pain postoperatively. Reasons* for prescribing a preoperative 4. The inability to preserve their mod- medication include: esty and dignity during the opera tion. I. Patient-related reasons: 5. The fear of separation from family, 1. Sedation and loved ones. 2. Amnesia 6. The fear of discovering a serious 3. Analgesia problem such as cancer. 4. Antisialogogue effect (to dry oral 7. The fear of surgical mutilation and secretions) an altered body image. 5. Medications to decrease gastric acidity and gastric volume. It is important that time is taken to 6. To facilitate induction of anaes- answer each patient's questions. If you thesia. are unable to answer their questions honestly, then reassure them that their 11. Procedure-related reasons: questions are important to you and that, while you may not know the answer, 1. Antibiotic prophylaxis to prevent you will speak to the attending staff infective endocarditis in susceptible physician and provide them with an patients. answer. Perhaps the most important

** Must Know Should Know Page 27 Anaesthesia for Medical Students

2. Gastric prophylaxis (to minimize the Benzodiazepines are the most frequently risk of gastric aspiration during an- used class of drugs to achieve sedation, aesthesia). relief of anxiety, and amnesia pre- 3. Corticosteroid coverage in patients operatively. Diazepam (5 to 15 mg who are immunosuppressed (see pa.) may be given with sips of water chapter 3). 1% to 2 hours preoperatively. Loraze- 4. To avoid undesired reflexes arising pam (1 to 3 mg) may be given either by during a procedure (e.g., vagal reflex the sublingual or oral route. Lorazepam during eye surgery). provides excellent amnesia and sedation, 5. Anticholinergic agents to decrease but occasionally, patients remain excess- oral secretions and facilitate a ively drowsy after the surgery. Alterna- planned awake intubation with a tively, lorazepam can be reserved for fiberoptic bronchoscope. the very anxious patient who is scheduled for afternoon surgery. The ration- 111. Coexisting Diseases: ale of an early morning premedication with lorazepam is to allow the patient to 1. To continue the patient's own medi- remain calm and relaxed throughout the cations for coexisting diseases. morning without prolonging the (e.g., beta blockers, antihypertensive postoperative recovery time. Midazo- medications, nitrates, anti- lam (0.07 mglkg im., approximately 5 parkinsonian medications etc.) mg in a young healthy 70 kg adult) 2. To optimize the patients status prior provides excellent amnesia, sedation, to the procedure. (e.g., bronchodil- and anxiolysis when given 112 hour ators, nitroglycerine, beta blockers, preoperatively. Midazolam (as a antibiotics etc.) premedication) is not available at all hospitals. The discomfort of an intra- Patients with significant coexisting muscular injection and midazolam's diseases should be given a reduced associated higher costs have generally amount of preoperative sedative medica- made it the third choice of the benzo- tion. The obese patient does not neces- diazepine class. sarily require more preoperative medication. It is safer to underestimate the Opioids such as morphine and required amount of preoperative medica- meperidine provide both sedation and tion. Additional medications can be analgesia. They are appropriate for given intravenously as needed when the patients experiencing pain prior to their patient arrives in the operating room. surgery, (e.g., fractured extremity await- Patients older than 65 years of age ing surgery). Morphine has a better should have a reduced drug dosage. sedative effect than meperidine. Caution should be exercised in prescrib- Troublesome side effects of intramuscu- ing sedatives to patients 75 years of age lar (im.) opioids may occur. These or older, as they may experience excess- include nausea, vomiting, respiratory ive depressant effects from these medi- depression, bradycardia, hypotension, cations. and true allergic reactions. In addition, I Chapter 4 Premedicalion I

) Table 4.1: Premedlcatlon - Drug I Dose I Route Class Comments Diazepam* (Valium) Benzodiazepine 1% to 2 hours preop. with sips of 5 - 15 mgpo. water. Sedation, amnesia, and anxiolysis. Anticonvulsant (regional anaesthesia). Respiratory depression with high doses. Lorazepam* (Ativan) Benzodiazepine Good amnestic and sedative. Best 1 - 3 mgpo. or 6.1. given early for late case. Occasionally excessive postoperative sedation.

Midazolam (Versed) Benzodiazepine 112 to 1 hour preop. Excellent 0.07 mg/kg im. arnnestic, sedative, and anxiolytic. (appmx. 5 md70 kg) Not available in all hospitals. Morphine* Opioid 1 hour preop. Occasional side 5 - 15 mg im. effects include decreased HR, BP, RR, nausea, biliary spasm and allergic reactions. Better sedative than meperidine.

Meperidine* (Demerol) Opioid 1 hour preop. Similar side effects 50 - 100 mg im. as morphine. Perhaps more nausea, and less biliary spasm.

Atropine* Anticholinergic 1 hour preop. Fair drying agent, 0.4 - 0.6 mg im. often significant tachycardia (HR > 100). Avoid in patients with CAD.

Hyoscine (Scopolamine) Anticholinergic 1 hour preop. Excellent drying 0.2 - 0.4 mg im. agent, confusion in elderly, occas. delirium in young. Good amnestic and antiemetic. GI ycopyrrolate Anticholinergic Good drying agent for oral secre- (Robinal) tions, less tachycardia than atro- 0.2 - 0.4 mg im. pine, no confusion. Promethazine Antihistamine 1 hour preop. Good sedative and (Phenergan) antiemetic. Occasional 12.5 - 50 mg im. postoperative delirium.

** Must Know Should Know Page 29 Anacs~hesiafor Medical Students

morphine, and to a lesser extent all does not cross the blood brain barrier other opioids, may cause biliary spasm. and causes less tachycardia than atro- Opioids should be used with caution in pine. patients with known cholelithiasis. Other special premeditations include: Drugs with both antiemetic and sedative oxygen, antibiotics, steroids, qualities, are often used in combination antihistamines, H-2 blockers, beta with an opioid to avoid nausea and to blockers, calcium channel blockers, enhance the sedative effects of the nitroglycerine, bronchodilators, ant- opioid. Promethazine is one such drug acids, desmopressin, insulin, etc. Ask (antihistamine - phenothiazine class), your staff anaesthesiologist when and and is given in a dose of 125 to 50 mg why they would prescribe these im. together with the opioid. Dimen- medications. hydrinate (~ravol9also possesses sedative and antiemetic qualities. It is given General contraindications* to the use of in a dose of 12.5 to SO mg im. with the a prernedication include: opioid (e.g., 'Demerol 75 mg with gravol 50 mg ism. in one syringe one 1. Allergy or hypersensitivity to the hour preoperatively 9. drug. 2. Upper airway compromise, or respir- Anticholinergics may be given with atory failure. morphine or meperidine to avoid the 3. Hemodynamic instability or shock. potential opioid-induced bradycardia. 4. Decreased level of consciousness or An anticholinergic agent may also be increased intracranial pressure. used if an awake fiberoptic intubation is 5. Severe liver, renal, or thyroid dis- planned. The use of an anticholinergic ease. in these patients causes decreased secre- 6. Obstetrical patients. tions from oral salivary glands, thereby 7. Elderly or debilitated patients. facilitating both absorption of topical anaesthetics and visualization of the Notes: airway by a fiberoptic scope. Both hyoscine and atropine cross the blood brain barrier. Hyoscine (0.2 - 0.4 mg im.) has been associated with confusion in the elderly and postoperative delirium in young patients. Atropine (0.4 - 0.6 mg im.) rarely causes clinical mental confusion. However, it is less effective in drying secretions than hyoscine and causes a greater tachycardia (which is undesirable in the patient with coronary artery disease). Glycopyrrolate (0.2 - 0.4 mg im.) is a good drying agent. It

Page 30 Getting Started (A Practical Approach to the OR)

Medical students, beginning their rota- make sure that any information that tion in anaesthesia, will undoubtedly was missing (eg. Hb, ECG, etc.) at feel unsure of their role and what they the time of the preoperative visit is ought to do to assist the anaesthes- now available and on the anaesthetic iologist. As anaesthesiologists we record. observe many operations, however, we 3. Monitors attached including an recognize that passively watching a ECG, blood pressure cuff, and pulse procedure does not give us the under- oximeter to start with. (See chapter standing or skills required to perform it. 10: Monitoring in Anaesthesia). Accordingly, the more active a role you 4. Establish an intravenous. Prepare take in the anaesthetic management of your intravenous equipment before the patient, the more you will get out of the patient arrives. the rotation, in terms of understanding, 5. Record the patients initial vital signs sense of accomplishment, and develop- on the anaesthesia record. ment of technical skills. Naturally, you should not attempt to perform tasks for The above tasks will occupy the first 5 which you have little knowledge or to 10 minutes of your time following supervision. Of all the specialties, the patients arrival in the OR. A pre- anaesthesia is one of the few which can anaesthetic check list can be used to offer intensive one-on-one teaching, and ensure that YOU are ready when the you should try to take as much advan- patient arrives to the operating room. tage of this as possible. There are many ways anaesthetists What can I do when the patient arrives ensure that everything is checked and to the operating room? ready to proceed safely with anaesthesia. Whatever system that is used, it Every patient undergoing general, should be simple yet comprehensive, regional, or monitored anaesthesia care and one that will be followed wnsist- requires*: ently. One such method can be recalled by using the abbreviation 'SAM'. If you 1. A safe transfer from their bed to the check with SAM before you give an operating room table. anaesthetic, things should proceed 2. An anaesthetic record removed smoothly. from the chart and placed on the anaesthesia clipboard. Check to What does SAM stand for?

** Must Know Should Know Page 31 Anaeslhesia for Medical Sluden/s

SAM* (really SAMMM') stands for: B. Anaesthesla Machlne:

S Suctlon checked and functioning. 1. Oxygen and nitrous oxide pipeline A Airway equipment checked and pressures should be at 40-60 psi. prepared. (This includes checking 2. Check that an adequate amount of that you have a functioning and oxygen is present in the reserve backup laryngoscope, an appropriate cylinder on the back of the sized endotracheal tube and stylet, machine. By turning the cylinder oropharyngeal airways, as well as an on, the pressure can be read from oxygen source and manual resuscita- the pressure gauge on the front of tion bag). the machine. An oxygen reserve M Machine checked. (see anaesthesia cylinder (E tank) has a full pressure machine checkout procedure and of 2200 psi. The amount in the make sure you know how to check oxygen tank varies directly with its your machine. You can go to the pressure. Hence, a reading of 1100 operating room before or after sche- psi indicates the tank is half full. A duled procedures to explore the full E tank contains approximately machine. Ask your staff anaesthe- 660 liters of oxygen. tist to go through this procedure 3. Turn the reserve cylinder on the with you). back of the machine off after check- M Monltors available and functioning. ing it, to prevent a possible leak M Medications prepared and labelled. from draining the oxygen from the You should know where the emerg- tank. ency drugs are kept and location of 4. Test that the flowmeters for 02and the difficult intubation cart. N20 are functioning by increasing and decreasing the oxygen and You will notice that the last thing that nitrous oxide flows. Ensure that the SAM has you do is check your medica- flowmeter bobbins move freely and tions. If you follow this routine, in this do not stick. Turn the nitrous oxide order, you will never put a patient to off. sleep and then discover, for instance, 5. The vaporizer should be filled, that their ECG is abnormal, or that a turned off, and the filling port laryngoscope is unavailable. closed. 6. The oxygen bypass flush valve Anaesthesla Machine Checkout should release a flush of oxygen Procedure (Modified from CAS 1989; when it is activated by pressing the 36, 6 suppl. 82-7.) flush button on the front left-hand side of the machine. A. Gas Plpeilnes: Secure connections 7. The oxygen fail-safe device should between terminal units (medical gas be functioning, and will produce a outlet) and machine. shrill Ritchie whistle if the oxygen pipeline is temporarily disconnected from the wall or ceiling source. Chapter 5 Getting Started

8. Check for the oxygen analyzer 5. Pressurize the circuit and check for which will be located on the respir- leaks. (Fill the circuit with fresh atory gas monitor or mounted on gas, occluding the outlet while pres- the machine as a separate unit. It surizing the circuit to 30 cm H20. should be turned on and calibrated, The circuit should maintain a pres- if this has not been done recently. sure of 30 cm H20 with a fresh-gas. 9. The 02 and N20 proportioning inflow of less than one liter per device prevents the delivery of less minute). than 30% oxygen, and greater than 6. Ensure the high pressure relief valve 70% N20, and can be tested by is functioning. (The circuit should varying the 02 and N20 flows develop a leak when the pressure is through the flowmeter. sustained above 75 cm H20. By 10. The common fresh gas outlet occluding the end of the circuit and located on the front left-hand side squeezing the reservoir bag, a pres- of the machine releases anaesthetic sure of greater than 75 cm H20 can gases from the flowmeters, be created. When this is done, the vaporizer and flush valve. high pressure release valve will open preventing any further increase C. Breathing Clrcult: in pressure in the circuit). 1. The two most common anaesthesia 7. Unidirectional valves are function- circuits used for adult anaesthesia ing. (Watch the valves open and are the circle circuit and the Bain close smoothly as you take a test circuit. An anaesthesia circuit breath through the mask and anaes- functions to take the anaesthetic thetic circuit) gases from the machine to and from 8. Check that the soda lime is fresh the patient. The circle circuit con- and that the canister is full, tains a soda lime canister to absorb the exhaled carbon dioxide, an D. Vacuum system: inspiratory and expiratory valve to Suction is connected and working. direct the flow of gases, and light weight corrugated tubing to trans- E. Scavenging System: port the gases. A sample port near Correctly connected to patient cir- the patient end of the circuit is used cuit. for analysis of the respiratory gases. These include inspired and expired F. Ventllator functioning. oxygen, carbon dioxide, nitrous (Test the ventilator using the 2 Litre oxide and volatile anaesthetic gas reservoir bag as a set of test lungs. tensions. Once the system has been filled 2. Connect the anaesthesia circuit to with fresh gas, turn the ventilator common fresh gas outlet. on. With the fresh gas flows at < 1 3. Turn the oxygen flowmeter on. Umin, the bellows should continue 4. Check for fresh gas exiting at the to refill as the ventilator cyles. The face mask. maximal accepted leak is 1 Umin).

** Must Know Should Know Page 33 Anaesthesia for Medical Students

" SAMMM" Preanaesthetlc Check Llst Suction Tonsillar tip connected to suction tubing and suction J functioning. Airway's Laryngoscope, blades, Em,syringe, stylet, oral and 4 nasal airways, tape, mask and manual resuscitation bag. Machine Wall-source DHSS medical gas pipelines connected, 4 N20 & 02 cylinder and pipeline pressures OK, Machine tumed on, flowmeters functioning, 02flush functioning, N20 and 02 proportioning device functioning, Oxygen pipeline disconnect (Ritchie) whistle functioning. - Vaporizer Full and turned off. 4 - Circuit Assembled, valves functioning, and circuit leak less J than 1 L / min at 30 cm H20 pressure. - Ventilator Disconnect alarm functioning, and test ventilation leak J of less than 1 L / min. Monitors Capnograph connected to circuit and functioning. 4 ECG, BP cuff, oximeter, peripheral nerve stimulator, and temperature probe monitors available and working. Meds Intravenous fluids and equipment for starting i.v. 4 prepared. Emergency medications as per staff anaesthesiologist where appropriate, (eg. atropine, ephedrine, succinylcholine etc.). Intubation and Anatomy of the Airway

The goal of assessing a patients rotate forward freely such that the space airways* preoperatively is to attempt to created between the tragus of the ear identify potential problems with main- and the mandibular condyle is approxi- taining, protecting, and providing a mately one fingerbreadth in width. patent airway during anaesthesia. The assessment is performed with the aid of The opening aperture of the patient's a physical examination and a review of mouth should admit at least 2 fingers the patients history and anaesthetic between their teeth. Note any loose, records. capped, or missing teeth as well as any bridge work on the teeth. If the open- The '1-2-3' test** is used to assess ing is less than 2 fingerbreadths, it will several factors that may affect decisions be difficult to insert the laryngoscope concerning the patient's airway manage- blade, let alone visualize the larynx. ment. The first component of the test is used to identify any restricted mobility With the patient's tongue maximally of the temporomandibular joint (TMJ). protruded, the structures visualized Ask the patient to sit up with their head should include: the pharyngeal arches, in the neutral position and open their uvula, soft palate, hard palate, tonsillar mouth as wide as possible. Note the beds, and posterior pharyngeal wall. mobility of the mandibular condyle at Technical difficulties with intubation the TM joint. The condyle should should be anticipated when only the

Fig.6.1: 1 = TMJ mobillty. Fig. 6.2: 2 = Mouth opening.

++ Must Know + Should Know Page 35 Anaesthesia for Medical Students

Adults who have less than 3 fingerbreadths (or < 65 cm) between their mentum and thyroid notch may have either an anterior larynx or a small mandible, which will make intubation difficult.

Next, evaluate the mobility of the cervical spine. This is performed by asking the patient to flex and extend their neck. They should be able to perform this without discomfort. Disease of the G spine (RA, OA, previous injury or surgical fusion) may limit neck extension, Flg.6.3: which may create difficulties during 3 = Thyromentai distance. attempts to intubate. This is certainly true if the atlanto-occipital joint is tongue and soft palate are visualized in involved, as restriction of this joints a patient during this above maneuver'. mobility may impair one's ability to The third component of this test visualize the larynx. assesses the patient's thyromental distance. 'Ihe thyromental distance is With the patient sitting upright with measured from the thyroid notch to the their head in the neutral position, mouth mentum (lower border of the chin). opened as wide as possible, and the

Table 6.1: Hypopharyngeal Classlflcation used In predlctlng a difficult Intubatlon. ) Chapter 6 Intubalion and Anatomy of the Airway j

Figure 6.4: Classification of the hypopharynx on the basis of the visible anatomy. Class I - 1v2.

tongue maximally protruded, the airway conscious sedation, or the use of a can be classified according to the stmc- laryngeal mask rather than an endo- tures visualized in the hypopharynx2 tracheal tube. (figure 6.4, table 6.1). In those patients who have a class I hypopharyngeal Finally one should try to ascertain view, adequate exposure of the glottis whether there could be any difficulty during direct laryngoscopy should be with the lower airway (glottis, larynx, easily achieved. As the hypopharyngeal and trachea). This is particularly im- class number increases, so does the portant in patients who have had a difficulty one anticipates in performing previous airway injury, or surgery on intubation using direct laryngoscopy. their airway such as a tracheostomy. We can predict that a patient with a Observe the patient for hoarseness, class IV hypopharynx, a full set of stridor, or a previous tracheostomy scar teeth, a restricted thyromental distance suggesting a potential underlying tra- and restricted atlanto-occipital extension cheal stenosis. will be difficult to intubate using direct laryngoscopy. Patients who have a Figure 65illustrates the visualization of restricted airway may require techniques the laryngeal structures at the time of other than direct laryngoscopy to secure laryngoscopy. Just as the visualization an airway. Choosing regional or local of the hypopharyngeal structures has anaesthesia, rather than general anaes- been classified, the extent to which thesia, is one way to avoid the need for laryngeal structures may be visualized intubation. Other airway management has also been graded from I to IV. options include "awake" intubation with While there is not a perfect correlation topical anaesthesia and intravenous between the hypopharyngeal class and

** Must Know Should Know Page 37 I Anaesthr~iafor Medical Students ,)

Laryngeal Grade

Figure 6.5: Laryngeal visualization and grading during direct laryngoscopy. (Grades I - IV). Adapted with permission from Cormack R.S., Lehane J. I Anesthesia 39:1105 - 11,1984. the laryngeal grade, we anticipate that a (AO) extension. We describe this as patient with a class one hypopharyngeal the sniffing position. This enables one view and no other identified airway to align the axes of the patient's mouth, abnormalities will have a grade I laryn- pharynx, and larynx permitting direct geal view. Similarly a class IV hypo- visualization of the larynx during pharyngeal view is a predictor of diffi- laryngoscopy (figures 6.6, 6.7, 6.8). culty visualizing laryngeal anatomy. Atlanto-occipital extension alone The technique of tracheal intubation increases the angle between the axes of involves five steps* *. the pharynx and the larynx. By con-

I. Positioning the patient. Axis of the 11. Opening the patients mouth. ( Axis Mouth 111. Performing laryngoscopy. IV. Insertion of the ElT through the vocal cords and removing the laryngoscope. V. Confirmation of correct placement, and securing the E?T tube.

I. Posltlonlng the patlent When preparing to intubate a patient, Figure 6.6: Poor alignment of the their head and neck should be pos- axes of the mouth, pharynx, and itioned using a combination of both larynx in the neutral position. cervical flexion and atlanto-occipital Chapter 6 Intubation and Anatomy of the Airway

Figure 6.8: Alignment of the axes of Figure 6.7: Alignment of the axes of the airway with cervical flexion and A0 the pharynx and larynx produced with extension, permitting visualization of cervical flexion. the larynx with direct laryngoscopy. trast, the combination of cervical flexion in ensuring a successful intubation (fig- of the neck with A0 extension results in ures 6.9, 6.10). This is especially true the alignment of the axes of the pharynx in obese or pregnant patients, or those and larynx. patients in whom you anticipate a difficult intubation. It is good practice to Optimizing the position of the patients make sure that your first attempt at head and neck before attempting intubation is your best. laryngoscopy is an important initial step

Flg. 6.9: Inadequate (suplne) Flg. 6.10: Optlmlzed posltlonlng posltlonlng for Intubatlon. for lntubatlon wlth cervlcal flexlon. ** Must Know Should Know Page 39 Anaesfhesia for Medical Shtdenfs

Flg. 6.12: Modlfled sclssors Fig. 8.11: Scissors technlque. technique.

Repeat attempts at intubation should be 11. Opening the patlent's mouth avoided unless there is something that The next step in performing intubation can be done differently to improve one's is to open the mouth. Take the laryngo- chance of success. Persistent repeat scope in your left hand as you stand attempts at intubation traumatize the directly behind the patient's head. The patients airway, interrupt and delay both right hand is used to open the patient's oxygenation and ventilation, and place mouth and, later, to advance the Em. the patient at risk of significant morbid- Mouth opening can be accomplished by ity and mortality. using the right hand to open the patients teeth (e.g., the scissors tech- If you are having difficulty, retreat, nique, as illustrated in figures 6.11 and regroup, and resume manual mask venti- 6.12), or by placing the operators right lation and oxygenation. Call for help hand on the patient's occiput to rotate and allow the patient to recover from the occiput backward and create A0 any sedative - relaxant medications that extension (see figures 6.13 and 6.14). have been given. No more than three Using the scissors maneuver the index attempts should be made at intubation. finger pulls the upper right incisors Discuss with your staff anaesthetist towards the operator, and serves to open what other options are available for the mouth, extend the atlanto-occipital patients whom you anticipate will be (AO) joint, and protect the teeth and difficult to intubate, or the patient in lips. At the same time, the thumb whom attempts at intubation have depresses the lower mandible, further failed. opening the mouth. One can modify this technique by opening the patient's Chapter 6 Infubafionand Anatomy of the Airway 1

Flg. 8.13 and 6.14: Rlght hand controlling atlantoscclpltal ) extenslon and facllltatlng mouth openlng prlor to laryngoscopy.

) Figure 6.15: Illustrates the position of the curved laryngoscope blade, which ) displaces the tongue to the left. Upward and forward traction brings the larynx into view. Adapted with permission from Finucane B.T., Santora A.H. In: iples of Airway Management. EA. Davis Co.,Philadelphia 1988.

** Musf Know Should Know Page 41 Anaesthesia for Medical Students mouth using one's right middle finger to tongue into the back of the oropharynx, depress the lower teeth (figure 6.12). If as this will also obscure your vision. the clinician chooses the extraoral tech- Once the tip of the blade lies at the base nique of mouth opening, their right of the tongue (just above the epiglottis), hand is placed on the patient's occiput apply firm, steady upward and forward and the patient's head is rotated into the traction to the laryngoscope. The direc- sniffing position. With this movement, tion of force should be at 45' from the the mandible drops and the mouth horizontal. Once the laryngoscope is opens. This method of mouth opening properly positioned at the base of the is more suitable for the edentulous tongue, avoid rotating it, as this action patient than the scissors technique. might exert pressure on the upper teeth and damage them. Damage to the im- 111: Laryngoscopy mobile upper maxillary teeth is more The third step involves insertion of the common than to the lower mandibular laryngoscope into the mouth (figure teeth, which are free to move forward 6.15). The tip of the laryngoscope with the jaw during laryngoscopy. blade is advanced to the base of the Figures 6.15 and 6.17 illustrate how the tongue -by rotating its tip around the larynx is more visible if the blade of the tongue (figure 6.17). The laryngoscope laryngoscope moves the tongue to the blade should follow the natural curve of left of the mouth and out of the line of the oropharynx and tongue. The blade vision. should be inserted to the right of the tongue's midline, so that the tongue Students learning the technique of moves toward the left and out of the laryngoscopy have a common tendency line of vision. Avoid pushing the to adopt a stooped posture, which posi-

Glosso- Eplglottlc Ugament

Figure 6.16: The glottis and epiglottis. Adapted with permission from Finucane B.T., Santora A.H. Principles of airway management. FA Davis Co. Philadelphia 1988. Chapter 6 Intubation and Anatomy of the Airway

tions their face within inches of the the epiglottis. Try to visualize this patient's. This posture limits the power anatomy as well as possible when you that can be used by the arms, making perform laryngoscopy. laryngoscopy technically more difficult to perform. Try to maintain a good IV: Insertlon of the ETT posture during laryngoscopy. This Intubation is performed with the iefC allows the arms to exert traction on the hand controlling the laryngoscope blade, laryngoscope, rather than attempting to while the right hand opens the mouth lift the laryngoscope with the wrists. and then passes the ElT tip through the laryngeal inlet. When a limited laryn- The larynx is located at the level of the geal view is encountered (grade 111 - IV 4& to 6& cewical vertebrae in adults. It larynx), the epiglottis can be used as a consists of numerous muscles, cartilages landmark for guiding the E?T through and ligaments. The large thyroid carti- the hidden vocal cords. The tip of the lage shields the larynx and articulates E'LT is passed underneath the epiglottis inferiorly with the cricoid cartilage. and anterior to the esophageal inlet. 'lbo pyramidal shaped arytenoid carti- Recall that the glottis lies anterior to the lages sit on the upper lateral borders of esophagus (or above the esophagus the cricoid cartilage. The aryepiglottic during laryngoscopy). When the epi- fold is a mucosal fold ruming from the glottis partially obscures the view of the epiglottis posteriorly to the arytenoid glottis, an assistant may be used to cartilages. The cuneiform cartilages apply cricoid pressure. This maneuver appear as small flakes within the margin moves the larynx posteriorly and helps of the aryepiglottic folds (fig. 6.16). to bring the vocal cords into view. A malleable stylet, shaped so that it forms The adult epiglottis resembles the shape a distal anterior J curve, can also be of a leaf, and functions like a trap door helpful in guiding the E?T tip through for the glottis. In figure 6.16, the trap the laryngeal inlet. When you have had door' is shown in both its open and a limited view of the Em passing closed positions. The epiglottis is through the vocal cords, the Ford attached to the back of the thyroid carti- Maneuver can help you to visually lage by the thyroepiglottic ligament and confirm its correct placement in the to the base of the tongue by the glosso- glottis. One performs this maneuver by epiglottic ligament. The covering mem- displacing the glottis posteriorly using brane is termed the glossoepiglottic downward pressure on the ETT prior to fold, and the valleys on either side of withdrawing the laryngoscope. This this fold are called valleculae. The maneuver is useful in the patient with a valleculae are a common site for the grade 111 or IV larynx for whom diffi- impaction of sharp swallowed objects, culty was encountered visualizing the such as fish bones. When performing glottic structures. laryngoscopy, one should advance the tip of the curved laryngoscope's blade to The cuff of the ETT should be observed the base of the tongue at it's union with passing through the vocal cords and

1 ** Must Know * Should Know Page 43 Anaesthesia for Medical Sludenb

a. Introduction of the larygoscope blade b. The tongue obscun the laryngeal using left wrist rotation. view due to inadequate advancement of the larygoscope blade .

. . . c. The tip of larygoscope blade is d. Laryngeal blade inserted too deep, properly positioned at the base of pushing epiglottis over laryngeal inlet. tongue. The blade is lifted forward

e. Laryngeal blade inserted to the left f. Laryngoscope blade inserted too far, of midline, with tongue obscuring with visualization of the esophageal inlet. visualization of the larynx. Figure 6.17: Laryngoscopy. Adapted with permission from Lui PL. inciples and Procedures in Anesthesiology. J.B. Lippincott Co. 1992

Page 44 Chapter 6 Intubation and Anatomy of the Airway should lie just inferior (2 to 3 cm) to lung fields may reveal bronchospasm or the cords. As soon as you withdraw the evidence of an endobronchial intubation, laryngoscope blade from the mouth, but cannot be relied on as absolute note the length of the ETT at the lips proof that the tube is correctly position- using the centimetre markers on the ed in the trachea. ElT. This may prove to be useful if the endotracheal tube moves from its If the tube is positioned in the tracheal original position. The usual distance lumen and the patient is breathing spon- from the tip of the ETT to the mouth is taneously, the reservoir bag will fill and approximately 21 to 24 cm in adult empty with respiration. If the patient is males, and 18 to 22 cm in adult awake they will not be able to vocalize females. The usual distance for a nasal- with an ETT positioned in the tracheal ly intubated adult male (from the tip of lumen. On an 'A-P'CXR the tip of the the Ento the naris) is 25 cm. The E'IT should be located between the ElT cuff is inflated with enough air to midpoint of the thoracic inlet and the create a seal around the ETT during carina. positive pressure ventilation. A cuff leak may be detected by listening at the Decreased air entry to one lung field patient's mouth, or over their larynx. may indicate that the ElT is in a main- stem bronchus (usually the right main- V: Confirmation of correct stem bronchus). In this situation, the ETT placement. patient may become increasingly Immediate absolute proof that the ElT hypoxic, or continue to cough. You is in the tracheal lumen may be may suspect an endobronchial intubation obtained by observing the ETT passing when you observe one side of the chest through the vocal cords, observing car- moving more than the other with venti- bon dioxide (ETCOJ returning with lation. In this situation, the airway each respiration, or by visualizing the pressures will be higher than normal tracheal lumen through the ETT using a (greater than 25 cm H20), and an fiberoptic scope. Indirect confirmation abnormally distant tube position at the that the trachea is intubated with a patient's lips will be noted. tracheal tube includes: listening over the epigastrium for the absence of "IF IN DOUBT TAKE IT OUT:"** breath sounds with ventilation, observ- This is prudent advice for anyone who ing the chest to rise and fall with posi- has just intubated a patient and is tive pressure ventilation, and listening to unsure and unable to confirm the tube's the apex of each lung field for breath placement. It is better to be safe by sounds with ventilation. There are, removing the ElT, resuming mask however, numerous reports of physi- ventilation with 100% oxygen, stabiliz- cians auscultating "distant breath ing the patient, and calling for help, sounds" in each lung field, when the than to risk hypoxic injury and gastric ETT was, in fact, incorrectly placed in aspiration. the esophagus. Hence, listening to the

+* Must Know + Should Know Page 45 1 Anaesthesia for Medical Students

"IF IN DOUBT LEAVE IT IN:"** This advice applies to the clinician who is considering extubating a patient who has been intubated for a period of time. When the clinician has concerns as to whether the patient can be safely extubated (see chapter 7: extubation criteria), it is generally safer to delay extubation, continue to support ventilation, ensuring hemodynamic stability, analgesia, and oxygenation, than to prematurely extubate the patient. Figure 6.19: 0topharGgeal 1 Upper elrwey obstruction**: airway restoring airway patency. ) The most common cause of an upper ) airway obstruction in an unconscious Excluding intubation, simple man- ' supine patient is from the tongue falling euvers** to overcome upper airway 1 back into the hypopharynx (figures 6.18 obstruction in the unconscious supine ) and 6.19). In the unconscious state patient, include: there is a decrease in the tone of 1 muscles attaching the tongue to the 1. Clearing the airway of any foreign ) mandible, hyoid bone and epiglottis. material. The respiratory efforts of the uncon- 2. Using a chin lift maneuver. 1 scious patient tend to pull the tongue 3. Using a jaw thrust maneuver. i backward causing further airway ob- 4 Inserting an oral andlor nasal , struction. Finally in the unconscious airway. patient the epiglottis tends to fall down- 5. Positioning the patient on their side ward, also increasing upper airway in the semi-prone recovery posi- , obstruction. tion.

References:

1. Mallampati SR, Gatt SP, Gugino LD, et al: A clinical sign to predict difficult tracheal intubation: A prospective study. Can J Anaesth 32:429,1985.

2. Samsoon GLT, Young JRB: Diffi- cult tracheal intubation: A retro- Figure 6.18: Obstructed airway spective study. Anaesthesia in the unconscious supine patient. I 42:487,1987. Page 46 ~ Intubation Decisions

In chapter 6, we reviewed the technical should prepare equipment and medica- skills required for tracheal intubation in tions for tracheal intubation. adults. In this chapter we present four clinical cases as an illustration of the Most open cholecystectomies today are process used when deciding to intubate. performed under general anaesthesia with tracheal intubation. While it may A clinician will readily recognize that be possible to provide regional anaes- the comatose patient with a severe head thesia (e.g., epidural anaesthesia) for injury will need tracheal intubation for this procedure most anaesthetists today airway protection, maintenance, and will opt to provide general anaesthesia. hyperventilation. However, the need to The rationale for this decision includes: intubate a dyspneic patient with chronic obstructive lung disease and a recent 1. A high abdominal incision with the respiratory infection is not so readily need for muscle relaxation. apparent. Tables 7.1 and 7.2 list com- 2. Surgical retractors which may impair mon criteria anaesthesiologists use to spontaneous ventilation. evaluate a patient's need for intubation. 3. A moderately obese patient who will The individual criteria are not absolute have difficulty breathing spontan- indications. They are to be used eously when lying supine, due to the together, in the context of the patient's surgical retractors restricting the clinical presentation, in formulating a muscles of respiration. decision concerning the patients need 4. Epidural anaesthesia used by itself for intubation. would require a high level of block to provide adequate anaesthesia. Case Studies on intubation decisions: This could impair the patients intercostal and abdominal muscles of Case 1: respiration, resulting in respiratory On the first day of your rotation, you insufficiency. are scheduled to assist with anaesthesia in the general surgical room. The first In the early days of anaesthesia, ether or patient is a moderately obese forty year chloroform was administered through a old female who is scheduled for an face mask during spontaneous respir- open cholecystectomy. What kind of ation for this procedure. Ether produced anaesthesia should we provide for this marked muscle relaxation when used patient? You ponder whether you with minimal doses of muscle relaxants

** Musf Know Should Know Page 47 1 Anaesthesia for Medical Students i)

Table 7.1 Objectlve Crlterla for Intubatlon wlth or wlthout ventllatlon* (Oxygenatlon I Ventllatlon / Mechanlcs) I. Oxygenatlon Pa02 < 70 mm Hg with Fi02 = 70% (A double flow puritan oxygen setup with 15 Umin x 2, provides a total of 30 Umin of oxygen flow to the patient, minimizing entrainment of room air; see figure 233, table 23.2). A-a DO2 gradlent > 350 mm Hg. Recall the normal A-a DO2 gradient is s 15 mm Hg, and increases up to 37 with increasing age (Nunn Applied Respiratory Physiology 3rd Edition p. 248) Use an arterial blood gas sample, and alveolar gas equation to calculate A-a DO2 gradient; where: PA02 = (Pa - P,)x Fi02 - PaCO2l0.8 11. Ventllatlon RR > 35 1 mln in adults (muscles fatigue, at these rates). PaC02 > 60 in normal adults. PaC02 45 In status asthmatlcus, and rising despite maximum medical management (must use other objective and subjective criteria as well) Respiratory acidosis with pH < 7.20 In COPD patients. 111. Mechanics VC < 15 mL / kg (Normal vital capacity = 70 mL per kg or approximately 5 litres; a vital capacity of 15 mL / kg is needed to cough effectively and clear secretions). NIF > -25 cm HZ0 (Normal negative inspiratory force (NIF) is approximately -80 to -100 cm H20).

(e.g., curare 6 mg). Respiratory de- muscle relaxants were not available to pression was accepted. When the ether the anaesthetist during these early years. was discontinued the patient recovered Today, by contrast, we routinely plan their muscle strength and increased their general anaesthesia with intubation, ventilation to match metabolic needs. muscle relaxation, and controlled mech- Pulse oximeten, end tidal carbon diox- anical ventilation for patients undergo- ide monitors, nerve stimulators, mechan- ing an open cholecystectomy. This ical ventilators, and antagonists for allows the anaesthetist to produce pro- Chapter 7 Intubation Decisions

Table 7.2 Subjective Criteria for Intubatlon and (or) ventllatlon* (Protect I Provide I Malntaln I T.B.T.)

I. Real or impending airway obstruction. (e.g., epiglottitis, thermal bums, mediastinal tumours, etc.). 11. Protection of the airway. (e.g., decreased level of consciousness, drug overdose, etc.). 111. "Tracheal bronchial toilet." For patients who are unable to clear their secretions, the ETT provides a direct access for suctioning secretions, (e.g., COPD patient with pneumonia.) IV. To provide positive pressure ventllatlon during general anaesthesia. Additional indications for intubation under general anaesthesia include: long procedure anticipated, difficult mask ventilation, operative site near patients airway, thoracic cavity opened, muscle relaxants required, and if the patient is in a difficult position to maintain mask anaesthesia. V. Clinical signs of respiratory failure and fatigue. (e.g., diaphoresis, tachypnea, tachycardia, accessory muscle use, pulsus paradoxus, cyanosis, etc.). VI. Shock not immediately reversed with medical treatment (i.e. not responding to medical management in the first 35 - 45 minutes).

Normal respiratory muscles use approximately 2 - 5 % of the cardiac output, in shock states this may increase to up to 15 - 20 %, stealing from other organs in vital need of oxygen such as the heart and brain. Dogs subjected to septic shock conditions, die much earlier if they are allowed to breathe on their own, when compared to dogs who are intubated and ventilated. found muscle relaxation during the endotracheal tube, checking the anaes- procedure, protect the airway from asp- thesia machine, and preparing the anaes- iration of gastric contents, and provide thetic medications. good ventilation and oxygenation. The anaesthetist can also administer potent Case 2: anaesthetic drugs, such as opioids and Having recently completed your anaes- volatile anaesthetic agents (e.g., iso- thesia rotation, you are working in the flurane) to minimize the stress of the emergency department, when a pale surgical procedure. Accordingly, you diaphoretic 50 year old man stumbles should plan to assist by preparing the through the door and collapses in front

** Must Know Should Know Page 49 Anaesthesia for Medical Students of the receptionist. The patient is risks of aspirating gastric contents. The quickly placed on a bed and taken to E'IT also provided a route for the resuscitation room. Unable to find administrating epinephrine, which a pulse, the emergency physician im- played an important role in this man's mediately applies chest paddles, iden- resuscitation. tifies a chaotic rhythm on the monitor, and defibrillates at 200, then 300 and Later, a classmate asks why you didn't finally 360 joules, in rapid succession. give any medications to intubate the Unfortunately, the patient fails to patient. You explain that patients with respond. You are at the head of the bed profound cardiovascularcollapse requir- and have initiated manual ventilation ing emergent intubation, do not need with an Ambu bag and mask. Chest any anaesthetic medications such as compressions are initiated, while a nurse thiopental or succinylcholine to perform attempts, unsuccessfully, to insert an tracheal intubation. In fact the adminis- intravenous catheter. Should you pro- tration of thiopental could have a detri- ceed to intubate the patient? mental result by further depressing his already compromised myocardium. If The emergency physician appreciates your colleague asks what other medica- your help and asks you to proceed with tions can be given through the EIT, tell tracheal intubation. After placing the him to remember the word NAVEL'. Em, you confirm its position, secure it, This stands for the drugs: Naloxone, and continue with controlled ventilation. Atropine, Ventolin, Epinephrine, and At your suggestion, 10 mls of 1:10,000 Lidocaine, all of which can be given epinephrine is injected down the Em through an E'IT. and propelled to the lungs and central circulation with subsequent ventilation. Case 3: The cardiac rhythm changes to a coarser Later, another clinical clerk asks for form of ventricular fibrillation. Repeat your opinion regarding a 68 year old defibrillation at 360 joules converts the man with known COPD. He is evaluat- man's rhythm to a sinus tachycardia ing this patient in the emergency room with a systolic pressure of 110 mm Hg. because he is feeling more short of Frequent ventricular premature beats breath than usual. Your colleague was (VPB's) are noted, and lidocaine 100 mg ready to send him home on antibiotics is given through the now secure intra- but hesitated after seeing his arterial venous. An infusion of lidocaine is blood gases (ABGs). He is concerned started and arrangements are made for that this man may need to be intubated the patient's transfer to the CCU. because his PaCO, is so high. On room air his ABGs were pH = 734, PaCO, = The resuscitation of this patient could 65, PaO, = 54, HCO, = 34. How would have proceeded with mask ventilation you assess and treat this patient. and chest compressions. By choosing to intubate this patient, we were able to The patients ABGs demonstrate protected the patient's lungs from the hypoxemia and an acute on chronic

Page 50 Chapter 7 Iniubation Decisions respiratory acidosis with metabolic When you examine him you find that compensation. You review his old chart his breathing is laboured at 28 breaths and note that his HCO, was 33 and his per minute with a prolonged expiratory PaO, was 59 mrn Hg at the time of phase and a surprisingly quiet chest. discharge 4 months previously. This, He is diaphoretic, clammy, and has you suggest, probably represents his difficulty catching his breath to talk. optimal blood gas values. You com- His vital signs reveal a HR of 130 bpm, plete your evaluation by examining the BP = 1801100, with a pulsus paradoxus patient noting a RR = 22 per minute, of 35 mm Hg, and maximal use of his HR = 90 bpm, BP = 160185, and diffuse accessory muscles. The emergency mild rhonchi throughout the chest with physician orders salbutamol with no significant (i.e. < 10 mm Hg) pulsus ipratropium bromide by nebulization. paradoxus. You also note that the An intravenous is established, ABGs are patient is able to talk without stopping drawn, ECG, oximetry, and BP monitor- frequently to catch his breath, and that ing is initiated, and a portable CXR is he is not vigorously using his accessory ordered. Your classmate thinks you muscles of respiration. Reviewing his better intubate him now. Do you agree? other lab tests you note a Hb = 170, WBC = 12,000, and an ECG which is As the ABGs and CXR return, the unchanged from his former cardiogram. patient is noted to have become increas- The CXR demonstrates hyperinflation ing drowsy, while little clinical im- with basal bullae, but gives no evidence provement has occurred. The ABGs on of cardiac failure or pulmonary infec- face mask oxygen at 8Umin reveal pH tion. The patient admits to having = 7.10, PaO, = 66, PaCO, = 120, and a stopped his bronchodilators in the last HCO, = 36. The emergency physician week. After clinical and subjective orally intubates the patient using topical improvement with salbutamol aerosol lidocaine anaesthesia to the (ventolinQ) and ipratropium bromide hypopharnyx and glottis, and initiates (atrovent@), the patient is discharged hyperventilation at 20lmin in order to home with a prescription for his inhalers 'blow off the carbon dioxide. The and a follow-up visit with his family nurse reports that the patients systolic practitioner. pressure is now 65 mm Hg, and his cardiac monitor is showing sinus Case 4 tachycardia at 120lmin with multiple Four weeks later you are completing ventricular premature beats (VPB's). your emergency rotation when the Your classmate reviews the CXR and patient in the case 3 returns. You are states that he believes the patient has a alarmed at his ill appearance. His wife pneumothorax on the left side. How are accompanies him and relates that he you going to manage the patient? 'caught a cold' a week ago and has been getting progressively worse. He has Before rushing to insert a needle been unable to eat or sleep for the last thoracotomy and chest tube for a poss- day because of his shortness of breath. ible tension pneumothorax, you review

** Must Know Should Know Page 51 Anaesthesia for Medical Students the patient's status. Although he has respiratory acidosis, with a pH of 7.20 become unresponsive to verbal stimula- or less, indicates that the patient is no tion, his trachea is in the midline, and longer able to compensate. His condi- you are able to manually ventilate him tion was likely precipitated by his recent without excessive airway pressures. chest infection superimposed on his The emergency physician orders 100 mg former severe COPD. PaCO, levels of lidocaine i.v., and asks you to take over greater than 95 mm Hg become increas- ventilation while he reviews the chest ingly anesthetic, (MAC CO, = 245, see radiograph. A repeat CXR is ordered to chapter 14 re: MAC definition). The verify the ElT position. A fluid bolus decreased level of consciousness may be of 1000 mL of ringer's lactate increases accounted for by the low blood pressure the patient's blood pressure to 100 rnm and the high arterial carbon dioxide Hg systolic. The VPB's remain but are tension. now unifocal and less frequent. A mechanical ventilator is set up to pro- This case illustrates several common vide ventilation, with an inspired 0, problems. The patient presented in an concentration of SO%, a tidal volume of extreme condition, following an illness 850 mL, an intermittent mandatory which likely resulted in significant ventilatory (IMV) rate of 12, and 5 cm dehydration. Upon his arrival in the of positive end expiratory pressure emergency department, his cardiorespir- (PEEP). atory system was being maximally stressed. Following intubation, his Arrangements are made to transfer the blood pressure fell precipitously. patient to the ICU. Review of the Patients with cardiorespiratory initial CXR shows the previous basilar decompensation who require urgent bullae, but no evidence of a intubation will often demonstrate a fall pneumothorax. The second CXR shows in blood pressure following intubation. the ElTtip to be correctly positioned in This occurs irrespective of whether the mid trachea. sedative drugs are given prior to intubation. The fall in blood pressure Your classmate was correct about the may be due to: patient requiring intubation. Clinical 1. The sedative drugs given. examination, and ABG analysis con- 2. The removal of endogenous catechol- firmed that the patient was indeed in amines by treating the condition that acute respiratory failure. Analysis of caused the patient to decompensate the ABGs revealed a severe acute on (i.e., removing the work of breathing chronic respiratory acidosis. Often we from patient). have no background information regard- 3. Decreasing venous return to the heart ing the patient's usual PaCO, and HCO, due to positive pressure ventilation. levels. In patients with COPD who may 4. All of the above, plus the unmasking retain carbon dioxide, we rely on the pH of a significant underlying hypo- more than the CO, to guide our man- volemia or concurrent illness (e.g., agement (as in case 3). A primary myocardial infarction).

Page 52 Chapter 7 Intubation Decisions

The occurrence of multiple ventricular larger En. Endotracheal tubes less premature beats may reflect an irritable than 6 mm do not have distal inflatable myocardium secondary to hypercapnia, cuffs. This decreases the risk of post hypotension, and hypoxemia. Another intubation swelling and stridor, as a explanation for the appearance of the result of trauma from the En. VPB's may be the result of an acutely induced hypokalemia. Mechanical Example: A 10 year old child would hyperventilation may result in a pre- generally use a 6.0 mm cuffed En, cipitous drop in the PaCO, level. The uncuffed tubes are generally used for sudden lowering of PaCO, will rapidly patients age 8 and less. increase the patients pH and shift Kt 6 yr. old child = 55or 6 uncuffed ETT into the cells, creating an acute extra- Term newborn = 35 ElT cellular hypokalemia. The differential Premature infant = 25 - 3.0 EIT diagnosis of this patient's acute hypotension, dysrhythmias, and abnor- Potential Complications of mal CXR includes a tension Intubation*: pneumothorax. In this case, the emerg- Direct injury can be caused by either ency physician correctly interpreted the the laryngoscope, or the ETT. The lips, lucency on the CXR as chronic basilar tongue, pharynx, larynx and trachea are bullae, and avoided the potential disas- all susceptible to injury. Damage to the trous consequences of a needle teeth may be caused by the laryngo- thoracostomy and chest tube insertion in scope, or by biting on the EIT or this patient (i.e., risk of a broncho- tonsillar suction tip. Damage to the pleural-cutaneous fistula). teeth, though rare, is still the most frequent problem resulting in litigation In retrospect, this patient fulfilled sev- against anaesthetists. Damaged teeth eral criteria for intubation (Tables 7.1 can fragment and may be aspirated by and 7.2). This emergency was best met the patient. by first supporting his ventilation. As this patient's condition is likely to The patient who experiences a sore require prolonged ventilatory support, throat following their operation (with this is most easily accomplished by tracheal intubation), may obtain some endotracheal intubation. relief with throat lozenges. This discomfort rarely persists for more than 24 Typlcal Endotracheal tube slzes* hours. Beware of the patient who Adult male 8.0, 85, and 9.0 mm recalls a severely sore throat on previ- Adult female 7.0, 7.5, and 8.0 rnrn ous operations. They may have a restricted airway, and their larynx may ETT slze calculation for children: have been traumatized because they Size (mm) = age14 + 4. were difficult to intubate. Inserting the ETT through the larynx can injure the The presence of a soft distal cuff on the vocal cords or even dislocate the FIT is equivalent to having a 112 size arytenoid cartilages. Patients with

** Must Know Should Know Page 33 Anaesthesia for Medical Students

arthropathies, such as rheumatoid arthri- impairment of chest excursion, and tis, may have an arthritic involvement increases the chance of regurgitation of the arytenoids, creating a 'functional and pulmonary aspiration. laryngeal stenosis'. If symptomatic, they may note hoarseness or pain on Criteria for extubation*: speaking. Always consider these The criteria for extubation are generally patients to be at an increased risk for the reverse of those for intubation. The vocal cord and arytenoid injury, use a patient should not require an E'IT for smaller En,and take extra care during airway provision, protection, mainten- intubation. ance or tracheobronchial toilet, and should meet criteria for adequate oxy- If the E'IT is too short it may result in genation, ventilation, and lung mech- accidental extubation. Excessive ad- anics. The condition that initially vancement of the EIT into the trachea required intubation should be corrected may result in an endobronchial prior to extubation. The patient should intubation. Prolonged E'IT placement be able to protect their airway, i.e., they may lead to vocal cord granulomas or must be awake with a gag and cough tracheal stenosis. Although a cuffed reflex. They should be hemo- ETT will protect against gastric aspir- dynamically stable, and their RR should ation, they do bypass the bodies natural be greater than 8/min, and less than humidifying and warming mechanisms, 35lmin. Respiratory muscles will and afford a potential conduit for fatigue with prolonged rates greater than pathogens to enter the lung. 35 breaths per minute. Oxygenation should be adequate, which means a Upon inserting the ElT, a patient is PaO, of at least 60 mm Hg on an subjected to a significant sympathetic inspired oxygen concentration of 50% stress, which may precipitate or less. This should be at accompanied tachycardia, dysrhythmias, and with evidence of adequate ventilation myocardial ischemia. Pediatric patients with a PaCO, of less than 50 mm Hg. have a relatively higher parasympathetic Vital capacity should be greater than 15 tone than adults. Hence tracheal mUkg (- 1 litre in a 70 kg patient), intubation of infants and children may with a tidal volume of greater than 5 result in a significant bradycardia. In mUkg and the negative inspiratory both adult and paediatric patients, medi- force (NIF) should be more negative cations are commonly given prior to than -25 cm H,O. The vital capacity, intubation in an attempt to minimize tidal volume, and NIF can be measured these reflexes. at the bedside with simple spirometry equipment. The most serious complication of tracheal intubation is an unrecognized esophageal intubation. The resulting gastric distension with ventilation, subjects the patient to hypoxia, hypercarbia, The Laryngeal Mask Airway (LMA)

IV11at is the differecrtce between a LMA isoflurane because the il~ternaldiameter and a traclteal tube*? of the LMA is relatively large compared The laryl~gealmask airway is a special- to an ETT. ized airway device made of wide bore PVC tubing, which incorporates a distal Does the LMA protect the patient inflatable non-latex laryngeal cuff against gastric aspiration*? (figure 8.1). The LMA is inserted No. Should gastroesophageal reflux without special equipment, in the back occur, the LMA will 1101 prevent gastric of the patient's pharynx with the soft contel~tsfrom entering the trachea. (see laryngeal cuff resting above the vocal chapter 24: Ul~usualAnaesthetic Com- cords at the junction of the larynx and plications: Aspiration Pneumonitis, and esophagus. An endotracheal tube (En) chapter 9: Perioperative Aspiration generally requires a laryl~goscopefor its Risk: The Rapid Sequence Induction). il~sertionillto the trachea. Unlike a LMA, the ElT passes through the vocal Wltich patients woi~ldbe si~itablefor cords with its tip positioned in the mid general annesthesia wit11 a LMA? trachea. Patients who have no identified risk factors for aspiration (see chapter 9), A foreign body in the trachea, such as and who do not require intubation and an endotracheal tube, evokes an inteuse col~trolledventilation, are suitable can- reflex. This results in an increase in didates for the LMA. It may be diffi- heart rate, blood pressure al~da cough cult to obtain an adequate seal using a reflex. The anaesthetist routinely ad- face mask in patiel~tswith no teeth or ministers poteut anaesthetic agents such with a full beard. The LMA is particu- as opioids al~dmuscle relaxants to blunt larly useful in these patients, providing or abolish this reflex. The tracheal a good seal and an unobstructed ainvay. "foreign body" reflex does not result from the il~sertiol~of a LMA because it i"lticlt patients are not suitable for a does not enter the trachea. Therefore, LMA? the LMA can be positioned with mini- 1. Patients with risk factors for gastric mal amounts of anaesthetic agents (e.g., aspiration. propofol alone). Mailltellance of anaes- The comatose patient in the emerg- thesia can be easily achieved by sponta- ency department with a presumed neous respiration of a mixture of anaes- drug overdose and intermittent thetic gases such as nitrous oxide and airway obstruction, would not be a

** Must KIIOW Should Kno\v Page 55 Anaesthesia for Medical Students

Table 8.1: Advantages and Disadvantages of a LMA and Endotracheal Tube. I 1

LMA ETT Provides airway protection against 1 ~e~u~~~aesthetid'shands, gastric aspiration. when compared to a face mask Allows for tracheal suctioning. alone. Allows positive pressure ventilation Provides a better airway in the without increasing the risk of gastric unconscious patient than a face distension and aspiration. mask alone. Can often be positioned with minimal anaesthetic drugs (e.g., Propofol alone, i.e., no "Foreign body in trachea reflex") DISAD LMA ETT I I Doesn't protect against gastric as- Muscle relaxants are usually require piration. for intubation. Positive pressure ventilation with Technically more difficult to insert airway pressures of > 20 cm H20 and position compared to LMA. results in increasing gastric * Trauma and positioning complica- insufflation and risks pulmonary tions e.g., endobronchial intubation. aspiration of gastric contents. (see chapter 8). Laryngospasm can occur with the "Foreign body in trachea reflex": LMA in place. This may result in resulting in an undesired reflex sym complete airway obstruction. pathetic stimulation (see text). Laryngospasm can occur when the E'IT is removed.

good candidate for the LMA, as 3. Patients with limited mouth opening. they are at high risk for gastric asp- (e.g., wired jaw, TMJ disease) iration. 4. Patients with a cervical vertebrae or 2. Patients with oropharyngeal or laryngeal cartilage fracture. retropharyngeal pathology, or 5. Patients requiring positive pressure foreign bodies in the hypopharynx. ventilation with airway pressures of Examples include peritonsillar greater than 20 cm H20 (e.g., abscess, Ludwig's angina, epiglot- patients with significant restrictive titis, and trauma to the mouth. or obstructive airway disease, trendelenburg position, laparoscopy). Chapter 8 The Laryngeal Mask Airway

B. With the neck flexed and head upwards againet the hard extended, the mask is advanced palate as it is advanced into dong the posterior pharyngeal w

C. A wrzectly positioned LMA. The cuff D. When medypositioned the LMA should be inflated without holding on cuff does not push the epiglottis to the LMA. downward, or obstruct the glottis.

Figure 8.1: Positioning of the Laryngeal Mask Airway. Adapted with from Brain AIJ., The lntavont Laryngeal Mask Instruction ManuaL Second Edition 1991.

" Must Know Should Know Page 57 Anaesflresia for Medical Sfude~tts

Figure 8.2: A number 4 (top) and number 3 (bottom) laryngeal mask airway.

How do you position a LMA? be used to induce anaesthesia. Propofol The laryngeal mask is positioned after is the preferred induction agent as it is the induction of general anaesthesia. superior to thiopental for reducing The laryngeal mask should be lubri- laryngeal irritability and laryngospasm cated, and the cuff valve checked. It is during LMA insertion. If thiopental is recommended that the cuff is fully used for LMA insertion, the use of deflated prior to insertion. Our experi- succinylcholine will facilitate its inser- ence, however, has been that a small tion and prevent laryngospasm. amount of air in the cuff (6 - 10 mL in an adult cuff) facilitates its insertion. After general anaesthesia is induced, the The patient is placed in the supine posi- patient's mouth is opened by creating tion with their head and neck oriented atlanto-occipital extension of the neck in the usual 'sniffing position' used for in combination with forward displace- intubation. ment of the jaw. The tip of the LMA is inserted into the mouth, and pressed up Anaesthesia is typically induced with against the hard palate as it is advanced the use of propofol. Other agents such into the pharynx with the right hand. as thiopental, ketamine or halothane can The cuff of the tube is guided along the Cka~ler 8 Tlte Larvneeal Mask Airwav

) posterior pharyngeal wall, and inserted oxygenate or ventilate the patient, with j as far as possible into the pharynx. secondary hypercarbia and hypoxemia. ) Stridor, a high pitched inspiratory sound As an aid to advancing the laryngeal produced by an upper airway obstruc- ) cuff past the tongue, it is recommended tion, may be noted during laryngo- ) that the right index finger be positioned spasm. Occasionally a muscle relaxant, at the tube-cuff interface guiding the such as a small dose of succinylcholine, ) cuff into the pharynx, while the palm of is needed to break the laryngospasm and ) the right hand pushes the proximal end permit positive pressure ventilation and ) of the LMA into the pharynx. Resis- oxygenation. tance is felt when the cuff is positioned at the upper esophageal sphincter. An ) assistantmay help by holding the mouth open, or by lifting the jaw forward to ) open the hypopharyngeal space. The black line running longitudinally along ) the LMA tube should be facing the upper lip. Once in this position, the ) cuff is inflated with air, causing the ) LMA to rise out of the mouth a little as it settles into its correct position. ) ) How do you remove the LMA? ) The LMA can be left in place until the patient is awake enough to remove it. ) Alternatively the LMA can be removed by the anaesthetist as the patient is emerging from anaesthesia, or while ) they are under deep anaesthesia and ) breathing spontaneous1y. The cuff may be deflated before removing it. How- Figure 8.3: LMA Sizes and weights. ) ever, if left inflated, the cuff removes # 1: for wt. c 6.5 kg. ) any upper airway secretions as it is # 2: for wt. 6.5 - 25 kg. ) taken out. Deflating the cuff risks hav- # 3: for wt: 25 kg. up to adult females ing secretions stimulate the vocal cords # 4: for adult males ) with the potential for laryngospasm. References: ) Deflation of the LMA cuff in the lightly 1. Brain AIJ. The laryngeal mask - a anaesthetized patient may result in new concept in airway management. ) laryngospasm because of stimulation of Br J Anaesth 1983; 55:801-5. the vocal cords by secretions. Laryngo- 2. Fischer JA, Ananthanarayan C, spasm** is an involuntary reflex closure Edelist G. Role of the laryngeal of the glottis by adduction of the vocal mask in airway management. Can J j cords. It may result in the inability to Anaesth 39:l-3; 1992.

i ** Must Know Sltould KIIOW Page 59 Rapid Sequence Induction

A 'rapid sequence induction'* is used ness, and tracheal intubation with a when a patient requires general anaes- cuffed Em. thesia who has been identified as having risk factors for gastric aspiration (see Without a cuffed tracheal tube, the table 9.1). All patients are at risk of patient is at risk of pulmonary aspiration aspirating gastric contents when general of gastric contents. Cricoid pressure is anaesthesia is induced, because it applied by an assistant with the induc- impedes the patient's protective airway tion of anaesthesia. It's purpose is to reflexes. For this reason, all patients reduce the risk of passive regurgitation requiring elective surgery are asked to and aspiration before an endotracheal abstain from eating solid foods for at tube can be placed. Cricoid pressure is least 8 hours, and clear liquids, for at only released when the tracheal tube least 4 hours prior to their procedure. cuff has been inflated, and the tube Should gastric contents reflux into the position confirmed by auscultation of hypopharynx during the general anaes- both lung fields and measurement of thetic, the use of a cuffed endotracheal carbon dioxide in the exhaled gases tube prevents it from entering the lungs. (ETCOJ.

Technique for Rapid Sequence* The predisposing factors for gastric aspiration include a depressed level of 1. Prepare for CeneralAnesthesia. The consciousness (4 LOC), impaired airway suction is checked, on and under the reflexes, abnormal anatomical factors, patient's pillow. Airway equipment is decreased gastroesophageal (GE) checked. An appropriately sized Em sphincter competence, increased intra- with a stylet is prepared. A gastric pressure, and delayed gastric laryngoscope and laryngoscope blade emptying. Patients who have any of is checked. The machine is checked, these predisposing risks for gastric the monitors applied, and the aspiration, and who require a general medications are prepared and anaesthetic, should have measures taken labelled. to prevent aspiration during the perioperative period. The three key com- 2. If a nasogastric tube is in place, suc- ponents of a rapid sequence induction tion and remove it, or leave it open are: preoxygenation, the application of to drainage. cricoid pressure with loss of conscious-

Page 60 i Anaestlaesia for Medic&/Students \

Table 9.1: Aspiration : Predisposing Factors and Preventative Measures** & LOC - Drug overdose (e.g., ETOH) - Head injury - Anaesthesia - CNS Pathology - Trauma or shock states . . Impaired Airway - Prolonged Tracheal intubation - Myopathies Reflexes - Local anaesthesia to the airway - CVA - & LOC

Abnormal - Zenkers Diverticulum - Esophageal stricture Anatomy

& GE - NG tube - Hiatus Hernia Competence - Elderly patient - Obesity - Pregnancy - Curare

t Intragastric - Pregnancy - Large abdominal Pressure - Obesity tumours - Bowel Obstruction - Ascites

Delayed Gastric - Narcotics - Pregnancy Emptying - Anticholinergics - Renal Failure - Fear, Pain, Labour - Diabetes - Trauma

Prevention - Preoperative Fasting - NG tube to empty - H2 Antagonists (&acidity) stomach prior to 1 Antacids (4 acidity) induction - Metoclorpropamide (t motility) - Cricoid Pressure - Antiemetics on induction of - Regional or Local anaesthesia general anaesthesia rather than General - Extubation awake Anesthesia (GA) on side

about the role of ketamine or propofol relaxant for a rapid sequence induction? as alternatives to thiopental when anaes- When would a muscle relaxant other thesia is induced. Why is succinyl- than succinylcholine be chosen for a choline the most commonly used muscle rapid sequence induction?

Page 62 1 Chapter 9 Rapid Sequence Induction 1

) For a discussion of the consequences of pulmonary aspiration see chapter 24: ) Uncommon Anaesthetic Complications - ) Aspiration.

J Notes:

** Must Know * Should Know Page 63 Monitoring in Anaesthesia

Inspection, palpation, percussion and Monltorlng auscultation are the cornerstones of monitoring in anaesthesia. In addition, Current Canadian guidelines to the numerous technical monitors are used to Practice of Anaesthesia and patient improve our understanding of the monitoring are: patients physiological status and minimize the patients anaesthetic risk. 1. An anaesthetist present. "The only indispensable monitor is the pres- ANAESTHETIC DEPTH*: ence at all times, of an appropriately trained and experienced phys- Patients undergoing surgery with local ician." or regional anaesthesia are able to 2. A completed preanaesthetic provide verbal feedback regarding their checklist. (Current history and well being. When we induce a state of physical documented, appropriate general anaesthesia, the onset of laboratory investigations reviewed, anaesthesia is signalled by the lack of pre-anaesthesia evaluation com- response to verbal commands and the pleted, ASA classification recorded, loss of a 'blink' reflex when the eyelash and npo policy observed if it is an is lightly touched. Inadequate anaes- elective procedure). thesia may be signalled by facial 3. An anaesthetic record. Every grimacing to a painful stimulus or by patient receiving general anaes- movement of an arm or leg. In the case thesia, major regional anaesthesia, of full paralysis with muscle relaxants, or monitored intravenous conscious inadequate anaesthesia is suggested by sedation, should have their HR and hypertension, tachycardia, tearing or BP measured at least every 5 min- sweating. Excessive anaesthetic depth utes, unless impractical. The time, may be signalled by cardiac depression dose, and route of all drugs and manifesting as bradycardia and fluids should be charted. hypotension. In the patient who has not 4. Oxygenation, ventilation, circula- been given muscle relaxants and is tion, and temperature are continual- breathing spontaneously, excessive ly evaluated both clinically and anaesthetic depth may result in hypo- quantitatively. (Continual is ventilation with hypercapnia (increasing defined as 'repeated regularly'). PaCOJ and hypoxemia . Chapter 10 Monitoring in Anaesthesia

the mid trachea. The right internal jugular vein has been cannulated and displays a pulmonary artery catheter passing through the right atrium (I), right ventricle (2), and the pulmonary artery (3).

** Must Know Should Know Page 65 ST Segment 0.0 mm

158/82 Arterial (114) Pressure rJ 4 32lO 27/14 (19) 12 Central Right Pulmonary Pulmonary Venous Ventricular Artery Capillary Pressure Pressure Pressure Wedge Pressure

Figure 10.3: Hernodynamic monitoring. Central venous pressure, right ventricular pressure, pulmonary artery pressure, and pulmonary capillaty wedge pressure tracings \ from positions 1,2,3 and 4 in figure 10.1.

Page 66 1 Chapter 10 Monitoring in Anaesthesia 1 I. OXYGENATION: system has electrodes positioned on the Oxygenation is monitored clinically by right arm, left arm, and chest position. providing adequate illumination of the Lead I1 is usually monitored with a patient's colour and by pulse oximetry. three lead system, as the axis of this The inspired oxygen concentration vector is similar to the P-wave axis. (FiOJ is quantitatively monitored dur- Identification of P waves in lead I1 and ing all general anaesthetics using an it's association with the QRS complex is oxygen analyzer. Each analyzer is useful in distinguishing a sinus rhythm equipped with an audible low oxygen from other rhythms. The chest elec- concentration alarm. trode is usually placed in the left anterior axillary line at the fifth interspace 11. VENTILATION: and is referred to as the V5 precordial Ventilation is monitored clinically by lead. A five lead electrode system adds verification of a correctly positioned a right leg and left leg electrode and endotracheal tube as well as by observ- allows monitoring of vectors I, 11, 111, ing chest excursions, reservoir bag dis- AVR, AVL, AVF and V5 (see figure placement, and breath sounds over both 10.1) Today's anaesthesia monitors are lung fields. Ventilation is quantitatively capable of analysis of the ST segment monitored using end tidal carbon diox- as an indicator of myocardial ischemia. ide @?'KO3 analysis as well as an Depression or elevation of the ST seg- audible disconnection alarm on all ment may be indicative of myocardial mechanically ventilated patients. The ischemia or infarction respectively. measurement of expired gas volumes Over 85% of ischemic events occurring and the ability to perform arterial blood in the left ventricle during surgery can gas analysis are useful adjuncts in be detected by monitoring the ST seg- assessing the adequacy of both oxygen- ments of leads I1 and V5. ation and ventilation. BP Measurement: The simplest 111. CIRCULATION: method of blood pressure (BP) determi- The circulation is monitored clinically nation estimates the systolic blood pres- by using one or more of: palpation of sure by palpating the return of the arter- the pulse, auscultation of heart sounds, ial pulse as an occluding BP cuff is a-arterial pressure monitoring, deflated. Other methods include doppler pulse monitoring, or oximetry. auscultation of the Kortokoff sounds Quantitative evaluation of the circula- with cuff deflation. This allows both tion includes an audible electrocardio- systolic (SBP) and diastolic (DBP) gram (ECG) signal, and arterial blood pressure measurements. The mean pressure measurements at least every 5 arterial pressure (MAP) can be est- minutes. imated from this as the MAP = DBP + 1/3(SBP - DBP). The ECG: A three or five lead electrode system is used for ECG monitoring in the operating room. A three lead

** Must Know Should Know Page 67 > naesthesia for Medical Students rable 10.1: Normal values for a healthy adult undergoing general anaesthesia*. ------Systolic Blood Pressure SBP 85 - 160 mmHg Diastolic Blood Pressure DBP 50 - 95 mmHg Heart Rate HR 50 - 100 bpm Respiratory Rate RR 8 - 20 rpm Oxygen saturation by pulse oximetry Sp02 95 - 100 % End tidal carbon dioxide tension ETCO, 33 - 45 mmHg Skin appearance warm, dry Colour pink Temperature 36 - 37.5 O C Urine production 2 0.5 ml. kg-'. min" Central Venous Pressure CVP 1 - 10 mmHg Pulmonary Artery Pressure PAP (mean) 10 - 20 mmHg Pulmonary Capillary Wedge Pressure PCWP 5-15 mmHg Mixed venous oxygen saturation Sv02 75 % Cardiac Output CO 4.5 - 6 1- mid'.

Table 10.2: Derived Cardio~ulmonarvValues: 1 Body Surface Area (BSA) Normal Values: , Mean Arterial Pressure MAP = 80 - 120 mmHg MAP = DBP + 113 Pulse pressure Cardiac Index (CI) = COIBSA CI = 2.5 - 4.0 L. min". mq2 Systemic Vascular Resistance SVR = 1200 - 1500 dynes-cm-secSs SVR = MAP - CVP x 79.9

Pulmonary Vascular Resistance PVR = 100 - 300 dynes-cm-sec" PVR = PAP(mean) - PCWP x 79.9

Stroke Volume = CO x 1000 SV = 60 - 90 ml. bear1 HR

Alveolar Oxygen Tension PAO, = 110 mmHg (Fi02= 0.21) PAO, = (P, - P,,)Fi02- PaC0dR.Q. (where P, = 760, Pm= 47, R.Q. = 0.8)

' Alveolar-arterial oxygen gradient A-a02 gradient < 10 mmHg (FiO, = 0.21 A-a02 = PAO~- Pao,

Arterial Oxygen Content (Ca02) CaO, = 21 mI.100ml" = (SaOJ(Hb x 134) + PaO, x 0.0031 Chapter 10 Monitoring in Anaesthesia

Automated non-invasive BP measurements are routinely performed intraoperatively using a microprocessor- Procedures frequently requiring direct controlled oscillotonometer such as a arterial pressure monitoring include Dinamape. These units have replaced major cardiac, thoracic, vascular and routine BP measurements by neurosurgical procedures. Arterial line auscultation or palpation techniques. placement is also indicated in pro- They automatically inflate the BP cuff cedures requiring induced hypotension to occlude the arterial pulse at preset or induced hypothermia. Patients with time intervals. The cuff pressure is co-existing diseases, including signifi- sensed by a pressure transducer. cant cardiopulmonary disease, severe Repeated step deflations provide oscilla- metabolic abnormalities, morbid obesi ty, tion measurements which are digitalized and major trauma, may also require and processed as the cuff is deflated. perioperative arterial line placement. Rapid, accurate (+ 9 mmHg) measurements of SBP, DBP, MAP and HR can A central venous pressure (CVP) cath- be obtained several times a minute. eter provides an estimate of the right Artifacts can occur with patient move- atrial and right ventricular pressures. ment, arrhythmias, or blood pressure The CVP reflects the patients blood fluctuations due to respiration. volume, venous tone, and right ventricular performance. Serial meas- When automated non-invasive BP urements are much more useful than a measurements are unsuccessful, simple single value. The HR, BP, and CVP auscultation or palpation techniques can response to a volume infusion (100 - be used with a manual cuff. Automated 500 ml of fluid) is a very useful test of BP measurements are routinely per- right ventricular performance. CVP formed every 3 to 5 minutes during monitoring is useful in patients undergo- general anaesthesia. Repeated rapid ing procedures associated with large measurements for prolonged periods of fluid volume shifts. Shock states, mass- time are not recommended due to a ive trauma, significant cardiopulmonary small risk of a compressive peripheral disease or the need for vasoactive medi- nerve injury. cations are other indications for using a CVP catheter. lnvasive monitoring of the circulation may include the use of an arterial, cen- Unlike a CVP catheter that lies in the tral venous, or pulmonary artery cathe- superior vena cava, the pulmonary ter. An arterial line is established with artery catheter (PAC) passes through a small (20 - 22 gauge) catheter in a the right atrium and right ventricle and peripheral artery. The radial artery at rests in a branch of one of the pulmon- the wrist is the most common site for an ary arteries (see figure 10.1). Inflation arterial catheter insertion. The femoral, of a plastic cuff at the tipof the catheter brachial, and dorsalis pedis arteries are allows occlusion of the proximal pul- alternative sites for arterial line inset- monary artery and measurement of the

** Must Know Should Know Page 69 Anoesthesio for Medical Shtdenh distal pressure. This distal (back) pres- peripheral nerve stimulator must be sure is referred to as the pulmonary immediately available. artery wedge pressure (PCWP) and reflects the left atrial filling pressure. Cyanosb: Thermodilution calculations of cardiac Cyanosis has been defined historically output are performed by injecting a as the presence of 5 grn/dL of fixed volume of cool fluid into the right deoxygenated hemoglobin (deoxy Hb). atrial port and measuring the tempera- When the hemoglobin level is 15gm/dL ture change over time from a thermistor and 5 gm/dL of this Hb releases oxygen probe at the distal tip of the PA cathe- to the tissues, the oxygenated hemo- ter. A sample of blood taken from the globin portion (OxyHb) is 10 gm/dL. distal tip of the PA catheter can be Hence the oxygen saturation is: analyzed to determine the mixed venous SaO, = OxyHb 1 (OxyHb + DeoxyHb) oxygen saturation (SvO,). Detailed SaO, = 10 1 (10 + 5) = 66% analysis of the patient's blood and fluid requirements, as well as the adequacy of An oxygen saturation of 66% corres- oxygen transport can be made with the ponds to an arterial oxygen tension of measurements obtained from a PA cath- approximately 35 mmHg (see oxygen eter. The results of manipulating the dissociation curve figure 10.4). Should patient's hemodynamic parameters with the patient become anemic, however, ionotropic agents, vasopressors, vaso- the oxygen tension (PaO,) at which dilators, diuretics, fluids or blood prod- cyanosis is detected will be even lower. ucts, can then be followed. Assume for example that the patient's Hb is now 10 gm/dL. The saturation at Figures 10.2 and 103 illustrate typical which we will detect cyanosis (ie., cardiorespiratory variables monitored when the DeoxyHb = 5 gm/dL) will be: during general anaesthesia. Tables 10.1 SaO, = OxyHb / (OxyHb + DeoxyHb) lists normal cardiorespiratory values SaO, = 5 / (5 + 5) = 50% during general anaesthesia for a healthy An oxygen saturation of 50% corre- adult. Table 10.2 lists formulas used in sponds to an oxygen tension (PaOJ of calculating common cardiorespiratory only 27 mmHg! values. We now recognize that under optimal IV. TEMPERATURE: lighting conditions with no excessive A temperature monitor must be readily skin pigmentation and a normal hemo- available to continuously measure tem- globin level, the earliest that cyanosis perature. Temperature monitoring is can be appreciated is at an oxygen mandatory if changes in temperature are saturation of approximately 85%. This anticipated or suspected. corresponds to a PaO, of 55 rnmHg. At a SaO, of 70% most clinicians will be An EKG with defibrillator, as well able to detect cyanosis (PaO, of apptox- resuscitation and emergency drugs must imately 40 mmHg). be immediately available. In addition a Chapter 10 Monitoring in Anaesthesia

p ght Shift in curve: Hb Uremia Ci tthosis Hypoxemi a Anemia

Hypophosphatemia Banked blood 27 40 60 Aadosis

Figure 10.4: The oxyhemoglobin dissociation curve. The running man I generates heat, carbon dioxide, and acid shifting the curve to the right, and \enhancing oxygen release to his tissues.

Pulse Oximetry*: an audible tone, which varies with the Pulse oximetry allows beat to beat ana- percent saturation, allows an auditory lysis of the patient's oxygenation status. assessment of the patients oxygenation Oximetry is based on the differences in status. light absorption by hemoglobin as it binds and releases oxygen. Red and Pulse oximetry (SpOJ includes meas- infra-red light frequencies are trans- urements of oxyHb, deoxyHb, metHb, mitted through a translucent portion of and carboxyHb. An over estimation of tissue, such as the finger tip or earlobe. the true measured oxygen saturation The signal is filtered to isolate pulsatile (SaOJ may occur in the presence of changes in light absorption. Micropro- significant carbon monoxide poisoning cessors are then used to analyze the (e.g., a bum victim). Oximeters may amount of light absorbed by the two become inaccurate or unable to deter- wave lengths of light, and this is com- mine the oxygen saturation when the pared with an empiric table of measured tissue perfusion is poor (e.g., shock. values to determine the concentration of states or cold extremities), when move- oxygenated and deoxygenated forms of ment occurs, when dysrhythmias are hemoglobin. Once the concentrations of present, or when there is electrical inter- oxyHb and deoxyHb have been deter- ference (e.g., electrosurgical cautery mined, the oxygen saturation can be unit). calculated. Current pulse oximeters have numeric LED displays for the The oxyhemoglobin dissociation curve heart rate and percent saturation. A describes a sigmoidal shape (see figure pulse plethysmograph allows visual 10.4). A decrease in PaO, of less than analysis of the pulse waveform, while 60 mrnHg (corresponding to a SpO, of

** Must Know Should Know Page 71 voestkesio for Medico1 Students

Real time capnograpgh with Trend speed recording at 25 mm/sec. I recarder speed at 12.5 mm/sec. Expiratory phase occurs from 1- 3. Inspiratory phase occurs from 3 - 1. 1 - 2: Alveolar C02 increases in concentration during expiration. 2 - 3: Alveolar plateau. C02 level peaks at 3 and is recorded as the ETC02. 3 - 4: Inspiratory phase begins, and C02 rapidly decreases.

'Curare cleft' indicates a decreasing neuromuscular block. This is always seen in the right 113 of the plateau.

Spontaneous patient ventilation efforts interposed between mechanical ventilations. "Patient fighting the ventilator."

Cardiogenic oscillations. The patient's cardiac stroke volume displaces small volumes of alveolar gas with each heart beat. Interesting, but of no significance.

Esophageal intubation. The initial ETC02 measurement is abnormally low, and rapidly falls to zero with subsequent ventilations.

An exponential decrease in ETC02. This may occur with severe hyperventilation, massive pulmonary embolism, or circulatory arrest. Also observed when the patient is cooled to induce profound hypothermia.

Obstructive airway disease results in an unequal emptying of the alveoli, and a rising alveolar plateau. The ETC02 measurement will greatly underestimate the arterial PaC02. A rapid fall in the ETC02 value to zero may indicate a patient disconnection from the ventilator. An accidental patient extubation, kinked ETI' or blocked sample line, are other possible causes.

Figure 10.5: Capnography. A normal capnogram, and its four components are represented in the top figure. Examples of diagnostic capnograms are included.

Page 72 Chapter I0 Monitoring in Anaeslhesia

90%) results in a rapid fall in the Measurement of ETCO, involves sampl- oxygen saturation. The lower limit of ing the patient's respiratory gases near acceptable oxygen saturation is 90% as the patients airway. A value is pro- this represents an arterial oxygen duced using either an infrared gas ana- tension just above hypoxic values. lysis, mass spectrometry, or raman scat- tering technique (see figure 10.2 and End-Tidal CO, Monltorlng 105). Provided the inspired CO, value Definitions: is near zero (no rebreathing of COJ, the Capnometry: Is the measurement of ETCO, value is a function of the CO, the carbon dioxide (COJ concentration production, alveolar ventilation and during inspiration and expiration. pulmonary circulation. Capnogram: Refers to the continuous display of the CO, concentration During general anaesthesia the PaCO, to waveform sampled from the patient's ETCO, gradient is typically about 5 airway during ventilation. mmHg. In the absence of significant Ca pnogra phy : Is the continuous moni- ventilation perfusion abnormalities and toring of a patient's capnogram. gas sampling errors, an ETCO, value of 35 mmHg will correspond to a PaCO, End-tidal C0,monitoring is standard for value of approximately 40 mmHg. all patients undergoing general anaes- Increases or decreases in ETCO, values thesia with mechanical ventilation. It is may be the result of either increased an important safety monitor and a valu- CO, production or decreased C0, elim- able monitor of the patient's physiologic ination (see table 103). status. Examples of some of the useful information that capnography is able to Monltorlng Neuromuscular function: provide include*: In order to quantify the depth of 1. Confirmation of tracheal intubation. neuromuscular blockade, electo- 2. Recognition of an inadvertent esoph- myography is commonly employed ageal intubation. during anaesthesia. This involves the 3. Recognition of an inadvertent ex- application of two electrodes over an tubation or disconnection. easily accessed peripheral nerve. The 4. Assessment of the adequacy of venti- ulnar nerve is the most common nerve lation and an indirect estimate of used for monitoring neuromuscular Pa CO,. function during general anaesthesia. 5. Aids the diagnosis of a pulmonary Other nerves that may be used include embolism (e.g., air or clot). the facial nerve and the common 6. Aids the recognition of a partial peroneal nerve. The electrodes are airway obstruction (e.g., kinked attached to a nerve stimulator, which Em. applies an electrical impulse to the 7. Indirect measurement of airway reac- nerve. By attaching a strain gauge to tivity (eg., bronchospasm). the muscle being stimulated, the muscle 8. Assessment of the effect of cardio- response to stimulation may be observed pulmonary resuscitation efforts. or measured. Ulnar nerve stimulation

** Must Know Should Know Page 73 / Lnaesfhesia for Medical Sfudenfs j rable 103: Etiologies of increased or decreased ETC0,values (Modified from Gilber HC, Vendor JS. Monitoring the Anesthetized Patient. In Clinical Anesthesia. Second Edition 1993. JB Lippincott Co. Philadelphia). Increased ETCO, Decreased ETCO, I Changes in CO, Production I I I Hyperthermia Hypothermia Sepsis, Thyroid storm Hypometabolism Malignant Hyperthermia Muscular Activity Changes in CO, Elimination I Hypoventilation Hyperventilation Rebreathing Hypoperfusion Embolism results in the contraction of the abductor A pure depolarizing block produces a pollicis muscle and a twitch in the uniform reduction in the height of a thumb. Up to 70% of the single twitch, TOF stimulus, and tetanus neuromuscular receptors may be stimulation. If excessive amounts of blocked by a neuromuscular blocking succinylcholine are given (> 5-6 drug before a change in the twitch mgkg), the block may begin to height can be observed. When 90% of resemble a non-depolarizing block and the receptors are blocked, all observable is said to be a phase I1 block (see succ- twitches are eliminated. inylcholine). Tetanus stimulation of a nerve will demonstrate a continued Common methods of stimulation of the weak contraction in the presence of a nerve include a single twitch stimulus, depolarizing block, but will progressive- four twitch stimuli, (each separated by ly fade with a non-depolarizing block. 112 second) referred to as a train-of-four stimulus (TOF), or a continuous stimu- In the case of a non-depolarizing block- lus referred to as a tetanus stimulation. ade, there is an increasing reduction in The intensity of neuromuscular blockade each of the four TOF twitches. The and type of blockade (i.e., depolarizing ratio of height of the fourth to first versus a non-depolarizing blockade) can twitch (i.e., the TOF ratio) is less than be characterized by the response to 0.7 in a non-depolarizing block. Also these different type of stimuli. Clinical both the single twitch and the TOF relaxation will occur when a single stimulus, will be increased following a twitch or first twitch of a TOF stimulus, tetanus stimulation. This is referred to is reduced by 75% to 95% of its orig- as post-tetanic facilitation, and only inal height (see figure 10.6). occurs with a non depolarizing block. I Chapter 10 Monitoring in Anaesthesia i The intensity of non-depolarizing When all twitches disappear r 90% of neuromuscular blockade can be esti- all receptors are occupied. For pro- mated by the height and number of cedures requiring muscle relaxation twitches that are present following a attempts are made to maintain one TOF stimulus. When the first twitch is twitch present with a TOF stimulus. reduced in height by 75%, the fourth Reversal of a neuromuscular block will twitch disappears. With an 80% reduc- be easily accomplished if all four tion in height of the first twitch both the twitches of the TOF are present, and third and fourth twitches are lost, and will be difficult or impossible if one or with a 90% reduction in the first twitch no twitches are observed. the remaining three twitches disappear.

Single %itch Stimulus 11l1 Train of Four Stimulus (TOF) ( Train of Four Ratio (T4lTI) = 0.4

Tetanus Stimulation Tetanus Fade

Post tetaNc facilitation L+ I-. Depolarizing neummuscular block. (eg. Succinylcholine 2 mgfltg)

1 minute 1. Block established within 1 minute. b 2. No fade with tetanus stimulation. S - 8 minutca 3. No post tetanic facilitation. 4. Block cannot be reversed. 5. TOF ratio > 0.4 I Non Depolarizing neummuscular block. (eg. Atncurium 0.4 mgflt) 2-25mlnutcs + 1. Blockestablished over 2 - 2.5 mlnutes. 4 40 minutes 2. Fades with tetanus slimulation 3. Post tetanic faciUtalion present 4. Revemes with anticholinesteraseagents, 5. TOF ratio < 0.7.

Figure 10.6 Assessing neuromuscular function. Characteristics of a depolarizing and non-depolarizing neummuscular block.

** Must Know Should Know Page 73 ) Anaesthesia for Medical Students j Notes: Intravenous Anaesthetic Agents

For over forty years, the ultra short Classification: acting thiobarbiturate, sodium thio- Intravenous anaesthetic - hypnotic pental, has been the intravenous induction agent of choice. Thiopental's Physical Chemical Properties: popularity is currently being challenged Thiopental is a highly lipid soluble by a new akylphenol class of drug compound, that is supplied as a yellow called propofol. Propofol's rapid metab- powder with a sulphuric smell and a olism and elimination, as well as its bitter taste. When combined with anti-emetic properties, are welcome sodium carbonate, it becomes water features to the specialty of anaesthesia. soluble. It is bacteriostatic in water and Ketamine is infrequently used as an has a pH of 10.6 to 10.8. When intravenous induction agent due to its injected, sodiumcarbonate is neutralized unpopular psychological side effects. and the thiopental is converted to its Despite this, it continues to play an lipid soluble non ionized form (pKa = important role in anaesthesia due to its 7.6, i.e. 40% ionized at pH = 7.4). unique cardiorespiratory pharmaco- Thiopental is highly protein bound by dynamics. albumen (75%), which prevents its precipitation out of solution in vivo. In this chapter we shall present three commonly used intravenous anaesthetic induction agents: thiopental, propofol, and ketamine. For each of these drugs we shall highlight its physical properties, pharmacokinetics, pharmacodynamics, dosage, indications and contraindications. Other adjuvant intravenous anaesthetic agents such as midazolam and droperidol are also presented. Opioid analgesics and neuromuscular I Figure 11.1: Sodium thiopentothd. I blocking agents are presented in the following chapters.

A. Sodium Thiopental (Pentothala) Supplied: Thiopental is supplied in the Definition: form of a yellow powder, dissolved in Ultra short acting barbiturate water and sodium carbonate to make a

** MYE~Know Should Know Page 77 j Lnacsthcsia for Medical Sludents i 25% solution (25 mg/ml). It is stable glands comprise the vessel rich group*. as a solution at room temperature for a They receive 75% of the cardiac output, period of 2 weeks. even though they constitute only 10% of body mass. After reaching its peak Structure Activity Relationship: serum level within these vessel rich organs, thiopental is then distributed to CH3 at N-1: shortens the duration the muscles, fat and the vessel poor (eg. methohexital) group of organs (see figure 11.2). 'Ihe S substitution at C-2: muscle group receives just less than markedly shortens the 20% of the cardiac output (second only duration of narcosis to the vessel rich group), and constitutes C-5 substitution with branched chains: approximately 50% of the body mass. increases potency and While peak serum concentrations of toxicity thiopental are reached within seconds of the injection, the fat group and vessel Pharmacokinetics: (i.e., What happens poor group (e.g., bone, and cartilage) to the drug with respect to uptake, dist- may require hours before peak levels are ribution, metabolism, and excretion.) achieved. The longer time for thiopental to reach peak levels in these An intravenous dose of 3 - 5 mgkg compartments is due to the lower results in loss of consciousness. The perfusion rates of the vessel poor time required to render the patient un- organs. conscious is generally 30 to 60 seconds following administration. This time has been referred to as the 'arm-brain' circulation time. It is the time required for the drug to pass from the site of injection to the brain as it passes through the right heart, pulmonary circulation, and left heart. When no other drugs are given, the anaesthetic state persists for 5 to 10 minutes. The patient awakes 1 1 1 4 16 64 256 after this period of time not because the 16 4 drug has been metabolized ('I%= 5 - 12 Logarithmic Time Scale (minutes) hours), but rather because the thiopental has moved away from the brain and is Figure 11.2 Distribution of thiopentothal in the vessel rich and entering the more slowly perfused vessel poor groups over time, organs. Hence, the termination of following a rapid intravenous action of the drug is due to its 're- injection. (Modified with permission distribution' from the brain to other from Miller RD., Anesthesia 3rd Ed. tissues and organs. Churchill Livingstone 1990). \ 1 The brain, liver, kidney's, and adrenal Chapter 11 Intravenous Anaesthetic Agents

Sulphur containing drugs, acidosis, and cardiovascular depression from high non steroidal anti-inflammatory drugs doses of thiopental, other antiepileptic (NSAIDS) may displace thiopental from drugs are used (e.g., a benzodiazepine albumen. This results in an increase in class of drug). free thiopental which increases the anaesthetic potency and toxicity. Liver Elevated intracranial pressure (ICP) can and renal disease may be associated be quickly reduced by administering with lower albumen levels, also raising thiopental. The improvement in ICP is free serum thiopental concentrations. transitory and would require excessive amounts of thiopental to maintain. The Metabolism occurs primarily in the liver use of high doses of barbiturates in with approximately 10 to 15% of the patients with persistently elevated ICP, remaining drug level being metabolized has not been shown to improve their per hour. A desulfuration reaction overall outcome. The reduction of ICP occurring in the liver produces pento- from thiopental is a result of cerebral barbital, which then undergoes oxidative vasoconstriction, reduced cerebral metabolism yielding two compounds metabolism and oxygen requirements. with no anaesthetic activity. Less than This is associated with a decrease in one per cent of the administered cerebral blood volume. The overall thiopental is excreted unchanged in the effect is an improvement in cerebral urine. perfusion pressure (CPP), as the decrease in ICP is generally greater than Pharmacodynamics: (i.e., What the drug the decrease in mean arterial pressure does in the body.) (MAP).

CNS: Barbiturates, including thiopental, interact with chloride ion channels by alter- Thiopental has an anti-analgesic effect, ing the duration they spend in an 'open since low doses may decrease a patients state'. This facilitates inhibitory pain threshold. neurotransmitters such as gama amino butyric acid (GABA), as well as block- Intraocular pressure (IOP) decreases up ing excitatory neurotransmitter actions to 25% with 3 - 5 magof thiopental. such as glutamic acid. The decrease in IOP persists for 3 to 5 minutes. Thiopental will decrease both cerebral ) electrical and metabolic activity. CVS: ) Hence, it can be used to stop seizure Thiopental causes a dose related 3 activity in an emergency situation. To depression of myocardial function as maintain depression of cerebral electri- measured by cardiac output (CO), stroke ) cal activity, very high doses of volume (SV), and blood pressure. ) thiopental are required. To maintain Coronary blood flow, heart rate, and seizure control and avoid significant myocardial oxygen uptake all increase )

Must Know Should Know Page 79 lnaesthesia for Mcdical Shtdcnts following administration of thiopental. limited to 4 m&. Venous tone decreases (decreased preload) and contributes to the increase in Dose and Administration: HR, and decrease in BP. Little change Thiopental must be used with caution in in the total peripheral resistance occurs patients suffering from a shock state. following thiopental administration. This was quickly appreciated by the anaesthetists caring for the casualties of RESP: pearl harbour. They presented to the Induction of anaesthesia with thiopental operating room in shock states second- may be associated with 2 or 3 large arily to massive blood loss. The admin- breaths followed by apnea. The duration istration of the usual sleep dose of of apnea following a 'sleep' dose of thiopental of 3 to 6 magfor induction thiopental is usually less than one min- of anaesthesia resulted in their rapid ute. There is a dose related depression demise. For a frail elderly lady who of the respiratory response to hyper- has fractured her hip, a dose of 25 to 50 carbia and hypoxia. Laryngospasm may mg (05 - 1 mag) may be all that is occur with induction, especially at light required for the induction of anaes- levels of anaesthesia and with airway thesia. For short procedures (eg. cardio- manipulation. Bronchoconstriction may version) a dose of 2 mglkg is generally be associated with thiopental, but is sufficient. much more commonly seen following the combination of a small dose of Indications: thiopental with airway manipulation or 1. Sole anaesthetic agent for brief surgi- intubation. As with any general an- cal procedures (less than 15 minutes). aesthetic agent, the functional residual 2. For induction of anaesthesia, prior to capacity (FRC) is reduced with the administration of other anaesthetic induction of anaesthesia by up to 20%. agents. 3. For control of convulsive states. GI: 4. For the supplementation of regional Enzyme induction may occur with pro- anaesthesia, or low potency an- longed high dose therapy, as in barbitu- aesthetic agents such as N20. rate induced comas. Hypoalbuminemia will result in an increase in unbound Contraindications to Thiopental*: (free) thiopental and an increase in the I. ABSOLUTE: potency of thiopental. 1. Lack of knowledge of the drug. 2. Lack of resuscitative equipment. GUPregnancyIFetus: 3. Inability to maintain a patent airway. Thiopental has little or no effect on the 4. Complete absence of suitable veins. kidney's or gravid uterus. Although 5. Allergy or hypersensitivity to bar- thiopental rapidly crosses the placenta to biturates. reach the fetus, it has no significant 6. Status asthmaticus. effect on the fetus when used for cesar- 7. Porphyria (Varigate Porphyria, or ean section provided the dose used is Acute Intermittent Porphyria) Chaprcr 11 Infravcnous Anaesrheric Agents

11. RELATIVE: 1. Hypotension or shock. 2. Severe cardiovascular disease. 3. Severe liver disease. 4. Myxedema.

Side Effects and Toxicity: An extravascular injection of thiopental will usually not cause any serious long term sequelae, provided the concentration of the solution injected is 5 25%. With more concentrated solutions, an extravascular injection may cause severe pain on injection as well as subsequent tissue necrosis. If a solution of a 25% Figure 11.3: Propofol. thiopental is injected accidentally into an artery, severe pain, vascular spasm, loss of digital pulses, gangrene, and permanent nerve damage may occur. If an intra-arterial injection does occur, the offending iv should be kept in place, and 5 to 10 mL of 1% plain lidocaine administered through it. Consideration should be given for systemic heparin administration (to prevent thrombosis), and for administering some form of sympathetic block (eg. stellate ganglion block) to reduce the sympathetic tone of Time (minutes) the injured area. Figure 11.4: Simulated time course of whole-blood levels of propofol Other side effects not mentioned above following an induction dose of 2.0 include allergic reactions, which may mglkg. (With permission from manifest as a skin rash, pain on injec- Miller RD., Anesthesia 3rd Ed. tion, urticaria, angioedema, broncho- Churchill Livingtone, 1990.) spasm, laryngospasm, and cardiovascular collapse. 1% propofol (10 mg/mL) 10% soyabean oil B. Propofol (DiprivanB) 2.25% glycerol Definition: 1.2% purified egg phosphatide Intravenous anaesthetic - hypnotic Classification: Akylphenol Propofol is a highly lipid soluble oil Phvsical Chemical Properties: that is combined with glycerol, egg, and soyabean oil for intravenous administra-

** Must Know * Should Know Page 81 Lnaesthesia for Medical Shcdena

:ion. It's appearance is similar to that of blood vessels remain responsive to C02 2% milk, as the solution that is used to during a propofol infusion. Cerebral dissolve it is similar to total parenteral metabolic rate is decreased up to 36%. nutrition (TPN) solutions. It has a pH Propofol appears to have neither epilep- of 7 and is supplied in 20 mL ampules tic nor anticonwlsant properties. with a concentration of 10 mg/ml. RESP: Pharmacokinetica: The respiratory rate is decreased with TIA initial distribution = 2 - 8 minutes. the induction of anaesthesia, and ap- 'l?4 redistribution = 30 - 60 minutes. proximately one quarter of patients 'l?4 elimination = 4 - 7 hours. become apneic at induction. The period of apnea depends on the dose given, the Following a single bolus injection, peak speed of injection, and concomitant use serum concentrations are reached rapid- of an opioid. The frequency of apnea is ly. Propofol's high lipid solubility greater than that seen following results in a quick transfer to the brain thiopental. Maintenance anaesthesia and rapid onset (one 'arm-brain' circula- (100 mcg/kg/min iv) with propofol tion time). Recovery from a single results in a decreased tidal volume and bolus injection results from both redis- increased respiratory rate. At this same tribution and elimination. Propofol is infusion rate the ventilatory response to metabolized in the liver, yielding water C02 is depressed similar to that caused soluble inactive conjugated compounds by administration of 1 MAC (0.76%) which are excreted by the kidney. Less halothane. Unlike halothane, however, than 2% of propofol is excreted doubling the infusion rate of propofol unchanged in the urine and feces. Pro- does not result in a marked increase in pofol is cleared from the blood faster depression of the C02 response curve. than hepatic blood flow, which suggests that extrahepaticmetabolismandelimin- cvs: ation may be occurring in the lungs. Systolic, mean and diastolic blood pressure are reduced 25-40% with an induc- Pharmacodvnamics: tion dose of 2-2.5 mg/kg. Cardiac output, stroke volume and systemic CNS: vascular resistance are all decreased Unlike barbiturates, propofol is not with induction by 15-20%. The antanalgesic. At low (subhypnotic) decrease in blood pressure is believed to concentrations, propofol can provide be secondary to both myocardial de- both sedation and amnesia. Patients pression and vasodilation. Heart rate report a general sense of well being on may increase, remain the same, or awakening from propofol anaesthesia. decrease following propofol. Concomi- lntracranial and intraocular pressure are tant administration of an opioid tends to both decreased by propofol. Cerebral result in a greater reduction in heart perfusion pressure undergoes a small rate, cardiac output, and arterial pres- decrease with propofol. The cerebral sure.

Page 82 Chapter 11 Intravenous Anaesthetic Agents

OTHERS: cardiac output (severe aortic or mitral Propof01 neither precipitates histamine stenosis, IHSS, pericardial release, nor triggers malignant tamponade) and those in shock states. hyperthermia. Propofol has no effect on muscle relaxants and is associated with C. Ketamine (KetalarB) a low incidence of nausea and vomiting. Pain on injection is more common than DefinitionIClassi fication: with thiopental, especially if given in a Dissociative Anaesthetic Agent small vein in the hand. The discomfort at injection can be decreased by the Physical Chemical Properties: administration of a small dose of lido- Ketamine is chemically related to the caine with propofol, or by administering psychotropic drug phencyclidine (PCP), propofol through a fast flowing more and cyclohexamine. It is water soluble proximal intravenous catheter. and is 10 times more lipid soluble than thiopental. It exists as two enantiomers Intravenous Induction Dose: s (+) and r (-) ketamine, and is supplied An induction dose of 2.5 - 3.0 mglkg is as a 50:50 mixture. It has a pH of 35 - used for healthy unpremedicated 55and is supplied as a clear colourless patients. When an opioid, or a solution of 10 and 50 mg/mL. premeditation has been given, the induction dose is reduced to 15-2.0 mg/kg. In elderly patients the induction dose should be reduced to s 1mgkg of propofol.

Infusion rates of 50-150 mcg/kg/min in combination with nitrous oxide and opioids, can be used for maintenance of anaesthesia. ( Figure 11.5: Ketamine. I Intravenous conscious sedation for operative procedures with local anaesthesia can be facilitated with propofol infu- Pharmacokinetics: sions of 25 - 75 mcgkglmin. Ketamine may be given iv, im, po, or pr. Extensive first pass metabolism and Contraindications to Pro~ofol*: decreased absorption necessitates the 1. Allergy (egg allergy). administration of higher doses when 2. Lack of resuscitation equipment or given by the oral or rectal routes. Keta- knowledge of the drug. mine undergoes biotransformation in the 3. Inability to maintain a patent airway. liver, yielding eight metabolites. The 4. Conditions in which precipitous re- most significant metabolite is nor- ductions in blood pressure would not ketamine (also known as Metabolite I), be tolerated; in patients with a fixed which has 113 the potency of ketamine,

** Must Know * Should Know Page 83 lnaesfheria for Medical Studenfs and subsequently undergoes hydoxyl- due to different mechanisms, with the ation, conjugation, and excretion in the analgesic effects resulting from an inter- liver. action between ketamine and central or Following administration, there is rapid spinal opiate receptors. absorption and distribution to the vessel rich group (see thiopental), with CNS: recovery of consciousness probably Ketamine anaesthesia produces a cata- secondary to its redistribution to other leptic state during which nystagmus as tissues. Over 90% of an im. injection well as intact corneal and pupillary light is bioavailable. Hepatic metabolism is reflexes may be observed. There is a required for elimination, with less than generalized increase in muscle tone and 5% of the administered drug recovered purposeful movements, and vocalization in the urine unchanged. There is a three may occur. Unpleasant dreams, hal- phase exponential decline in ketamine lucinations, or frank delirium may occur levels with a 'I% distribution of 24 with ketamine, especially if the patient seconds, a l%redistribution of 4.7 is young, female, and large doses of minutes, and 'I% elimination of 22 ketamine are given rapidly. The inci- hours. dence of delirium is decreased with the concomitant administration of a benzo- Mechanism of Action: diazepine (eg. diazepam or midazolam), Three current theories about ketamines and by giving small doses slowly. The mechanism of action are: overall incidence of delirium in the 15 1. N. Methvl Aspartate receptor theory. to 35 year old population is approxi- NMA receptors may represent a mately 20%. subgroup of the sigma (a) opiate receptors (the PCP site),' that block Intracranial pressure is not increased spinal pain reflexes. with ketamine provided ventilation is 2. Opiate receptor theory. Ketamine adequate. Intraocular pressure may or may have some affinity for opiate may not increase with ketamine. receptors but its effects cannot be reversed with naloxone. RESP: 3. ~iscellaneousreceptor theory. Ketamine provides general anaesthesia Ketamine interacts with muscarinic, while preserving laryngeal and cholinergic, and serotonergic pharyngeal airway reflexes. Despite receptors. this, there are reports of pulmonary aspiration of gastric contents during Ketamine was originally thought to ketamine anaesthesia when an artificial cause a 'functional and electrophysio- airway is not used. Ketamine is associ- logical dissociation between the ated with mild respiratory depression in thalamoneocortical and limbic systems'. healthy patients following 2 mag Ketamine is a potent analgesic at sub- intravenously. The C02response curve anaesthetic plasma concentrations. Its is shifted to the left with its slope analgesic and anaesthetic effects may be unchanged (similar to opiates). Func- Chapter I2 Intravenous Anaesthetic Agents

tional residual capacity (FRC), minute succinylcholine and curare, are ventilation (VA,and tidal volume (V,), enhanced by ketamine. are preserved as is hypoxic pulmonary vasoconstriction (HPV). In dogs, keta- ENDO: mine is as effective as halothane or Ketamine's sympathetic stimulation will enflurane in preventing bronchospasm. result in an increase in blood glucose, Changes in the respiratory pattern may plasma cortisol, and heart rate. be observed with periods of prolonged apnea, resulting in hypoxic episodes. Dosage: Increased secretions occur with ket- im: 5 - 10 mag amine, and can be limited with the prior iv: 1 - 2 mgfltg (To limit the risk of administration of an anticholinergic, delirium following ketamine, it should such as atropine or glycopyrrolate. be injected at a rate of s 40 mdminute).

cvs: Intramuscular injections in children of 9 Ketamine produces both a central sym- - 13 mgkg produce surgical anaesthesia pathetic stimulation and a direct nega- within 3 - 4 minutes with a duration of tive ionotropic effect on the heart. The 20 - 25 minutes. Peak plasma levels are central sympathetic stimulation results reached approximately 15 minutes fol- in an increase in HR, BP, SVR, pul- lowing an im injection. With iv admin- monary artery pressures (PAP), coronary istration a dissociated state is noted in blood flow (CBF) and myocardial oxy- 15 seconds, and intense analgesia, gen uptake (MV02). Pulmonary vascu- amnesia and unconsciousness occur lar resistance (PVR) is unchanged if within 45 - 60 seconds. A dose of 1 - ventilation is controlled. If the normal 2 mgkg will produce unconsciousness sympathetic nervous system is blocked for 10 - 15 minutes, analgesia for 40 or exhausted, ketamine may cause direct minutes, and amnesia for 1 - 2 hours. myocardial depression. Subsequent iv doses of 113 to 112 the initial dose may be required. GI: Anorexia, nausea, and vomiting are Indications for ketamine*: minimal. 1. Sole anaesthetic for diagnostic and surgical procedures. GU/Placenta/Fetus: 2. For induction of anaesthesia prior Placental transfer does occur, but neona- to the use of other anaesthetic tal depression has not been observed if agents. the ketamine dose is limited to s 1 3. To supplement regional anaesthetic mgfltg. or local anaesthetic techniques. 4. For anaesthetic induction in the MSK: severe asthmatic patient or the At the neuromuscular junction, there is patient with cardiovascular collapse an increase in skeletal muscle tone, and requiring emergency surgery. the effects of muscle relaxants, such as

** Must Know Should Know Page 85 Lnaesthesia for Medical Students

Contraindications to ketamine: muscle relaxant effects are due to an 1. Lack of knowledge of the drug. increase in the concentration of a 2. Lack of resuscitative equipment. glycine inhibitory neurotransmitter. 3. Inability to maintain a patent air- Facilitation of the effects of GABA way. results in the sedative and anti- 4. Allergy or hypersensitivity to convulsant effects of benzodiazepines. ketamine. Benzodiazepines are highly lipid soluble 5. History of psychosis. and highly protein bound. In patients 6. Cerebrovascular disease. with reduced albumen levels (e.g., cir- 7. Patients for whom hypertension is rhosis, renal insufficiency,malnutrition), hazardous. the decreased plasma binding may result (eg. severe hypertension, in an increase in free drug concentra- aneurysms, heart failure, etc.) tion, and an increase in drug related toxicity. Other side effects and toxicity: Benzodiazepines are metabolized in the Respiratory depression may occur and liver by hepatic microsomal enzymes. should be managed with ventilatory The metabolites are conjugated with support. Ketamine has a wide margin glucuronic acid and excreted by the of safety, and in cases of relative over- kidneys. Elimination half times range doses (up to 10 times the usual dose) from 1 - 4 hours for midazolam there has been a protracted though com- (Versed@), to 10 - 20 hours for loraz- plete recovery. epam (Ativana), and 21 - 37 hours for diazepam (Valium@). Other adJuvant intravenous Midazolam and diazepam are the two anaesthetic agents: most commonly used benzodiazepines during operative procedures. Benzodiazepines: Features which result in the popularity of benzodiazepines as Midazolam (Versed@): adjuvant intravenous anaesthetic agents Midazolam's most common use intra- include: operatively is to provide intravenous sedation, amnesia, and to reduce 1. Ability to produce amnesia. anxiety. A dose of 0.5 to 3 mg intra- 2. Minimal cardiorespiratory venously (up to 0.1 mglkg) is effective depressant effects. for intravenous conscious sedation. 3. Anticonvulsant activity. Higher doses of 0.2 - 0.4 mgkg may be 4. Low incidence of tolerance and used to induce anaesthesia. Midazolam dependence. has a more rapid onset, greater amnestic effect and less postoperative sedative Benzodiazepines inhibit the actions of effects than diazepam. Pain on injection glycine and facilitate the actions of the and subsequent thrombophlebitis is less inhibitory neurotransmitter gamma am- likely with midazolam than with inobutyric acid (GABA). Benzo- diazepam. Midazolam's duration of diazepines antianxiety and skeletal action is less than diazepam's, but

Page 86 Cha~ter 11 Intravenous Anaesthetic Aeenfs almost 3 times that of thiopental. It is sedation recurs, infusions of 0.1 to 0.4 supplied for intravenous use as a clear mglhour may be used. Flumazenil is liquid in concentrations of 1 to 5 generally well tolerated. The most mglml. common side effect is nausea, and this is seen in only 4 % of patients. Diazepam: Diazepam has 1/2 to 1/3 the potency of Droperidol: midazolam. A dose of 1 - 10 mg is Butyrophenones such as droperidol and effective for intravenous conscious haldol are classified as major sedation. Higher doses of 0.15 to 15 tranquilizers. Droperidol is more com- magare used to induce anaesthesia. monly used in the perioperative period Diazepam has a high incidence of pain than is haldol, because it has a shorter on intravenous injection, as well as a duration of action, and has less signifi- high incidence of subsequent phlebitis. cant alpha adrenergic antagonist effects An emulsion of diazepam (DiazemulsCO) so marked reductions in blood pressure is available and has a lower incidence are unlikely. Droperidol acts at the of venous irritation and phlebitis. postsynaptic receptor sites to decrease DiazemulsB contains a diazepam the neurotransmitter function of emulsoid of soybean oil, egg lecithin, dopamine. It is used in the operating and a glycerol solution (similar to suite as an antiemetic and as an propofol), however, it is more costly adjuvant to opioid analgesia than plain diazepam. (neuroleptanalgesia). Droperidol is a powerful antiemetic, inhibiting dop- Benzodiazepine Antagonists: aminergic receptors in the Flumazenil (Anexate@) is an imidazo- chemoreceptor trigger zone of the benzodiazepine that specifically ant- medulla. The usual dose of droperidol agonizesbenzodiazepine'scentraleffects as an antiemetic is 0.25 to 2.5 mg iv. by competitive inhibition. The mean Adverse side effects are dose related. elimination half life of flumazenil is approximately one hour, considerably Extrapyramidal reactions are seen in shorter than most benzodiazepines. approximately 1% of patients and are Hence, repeat administration or infu- due to its antagonism of dopamine. For sions may be required when benzodiaze- this reason, droperidol is contraindicated pines with a longer T% elimination are in patients with known Parkinson's being antagonized. disease. Other adverse reactions include Flumazenil is supplied as a colourless orthostatic hypotension, and dysphoric liquid in a concentration of 0.1 mg per reactions resulting in increased anxiety mL. The usual initial dose is 0.2 mg iv and an agitated state. Abnormal sleep over 15 seconds. If the desired level of patterns in the first 24 hours following consciousness is not obtained within 60 the administration of 1.25 mg of droper- seconds of administration, repeated idol have been reported in healthy doses of 0.1 mg can be given every patients undergoing minor surgical minute up to a maximum of 2 mg. If procedures. Droperidol may be admin-

** Must Know Should Know Page 87 4naesthesia for Medical Studenk istered in higher doses with an opioid such as fentanyl to produce an anaesthetic state referred to as neuroleptanalgesia. This is characterized by a trance like immobility and an appearance of tranquility. The intense analgesia produced with neuroleptanalgesia allows a variety of minor procedures to be performed (e.g., bronchoscopy, or cystoscopy). The disadvantages of this form of anaesthesia include a prolonged central nervous system depression and postoperative dysphoric reactions. For these reasons, neuroleptanalgesia is only rarely administered today.

Notes: 1 ) Muscle Relaxants

Neuromuscular physiology*: muscle resulting in a muscular contrac- The neuromuscular junction consists of: tion. Acetylcholine's action is rapidly (< 15 milliseconds) terminated as it 1. A motor nerve ending with diffuses away from the muscles end mitochondria and acetylcholine ves- plate, and is hydrolysed by acetyl- icles (prejunctional). cholinesterase. 2. A synaptic cleft of 20 - 30 nm in width containing extracellular fluid. Muscle relaxants produce skeletal 3. A highly folded skeletal muscle muscle paralysis by interfering with membrane (postjunctional). acetylcholine at the neuromuscular 4. Nicotinic cholinergic receptors junction. Fortunately, involuntary located on both the presynaptic muscles such as the heart are not (nerve) and postsynaptic (muscle) affected by neuromuscular blocking membranes. drugs.

Skeletal muscle contraction involves an intricate series of events. As a nerve impulse is generated, an action potential travels down the nerve to the neurornuscular junction (NMJ) (see figure 12.1). The action potential results in the release of acetylcholine from the nerve endings into the synaptic cleft. The acetylcholine diffuses across to the muscles nicotinic cholinergic receptors causing a change in the membranes permeability to ions. The altered membrane permeability results in a Figure 12.1: The neuromuscular sodium and potassium flux across the junction. Ach = Acetylcholine; muscle membrane. This flux of ions AChE = acetylcholinesterase; JF = decreases the muscles transmembrane junctional folds; M = mitochondria; electrical potential. When the resting V = Vesicle. (With permission from transmembrane potential decreases from Drachman DB; Myasthenia gravis. -90 mV to -45 mV, an action potential \N Engl J Med 298:136-142,1978). spreads over the surface of the skeletal

1 ** Must Know Should Know Page 89 inae$thesia for Medical Students ) Classlflcation*: Non Depolarizing Muscle Relaxants: Muscle relaxants may be classified Non-depolarizing neuromuscular block- according to their duration of action ing drugs compete with acetylcholine (short, intermediate, or long), and on the for the cholinergic nicotinic receptor. basis of the type of neuromuscular As the concentration of muscle relaxant block they produce. A non-competitive increases at the NMJ, the intensity of depolarizing muscle relaxant such as muscle paralysis increases. Anticholin- succinylcholine cannot be antagonized. esterase agents inhibit the break down The termination of succinylcholine's of acetylcholine. This results in an activity is dependent on hydrolysis by increase in the concentration of plasma cholinesterase. All other cur- acetylcholine at the NMJ. Anaesthesio- rently used muscle relaxants are com- logists exploit this pharmacological petitive non-depolarizing agents. Their action by administering ~tplcholin- activity does not result in depolarization esterase agents such as neostigmine and --.. . ----. .. of the motor end-plate or muscle fibre, edrophonium to competitively 'reverse' and their action can be reversed by the the effects of a non-depolarizing administration of an anticholinesterase neuromuscular blockade. agent such as neostigmine or edrophonium. Mlvacurlum: Mivacurium is a new short-acting non-depolarizing neuro- Cholce of muscle relaxant: muscular blocking drug which, like Considerations for choosing a muscle succinylcholine undergoes hydrolysis by relaxant include*: plasma cholinesterase. Patients who 1. Duration of action of relaxant, and have deficiencies in the quality or quan- duration of required muscle relax- tity of plasma cholinesterase will have a ation. prolonged duration of action with both 2. Route of excretion. mivacurium and succinylcholine (see 3. Tendency to release histamine. succinylcholine, p.93). The effective 4. Cardiopulmonary side effects result- dose to produce a 95% reduction in the ing from administration. Potential twitch height (ED,) is 0.08 m&g (see adverse reactions include brady- chapter 10: Monitoring Neuromuscular cardia, tachycardia, bronchospasrn Function). Intubation with a non-depo- and hypotension. larizing muscle relaxant is typically 5. The ability to reverse the accomplished by the administration of 2 neuromuscular block. to 3 times the EDQ5. Intubation with 6. Cost. mivacurium can be performed approxi- 7. Contraindications to any specific mately 2 - 2.5 minutes after administer- muscle relaxant. ing twice the EDB. With rapid injection Table 12.1 summarizes the duration of of an intubating dose of mivacurium, a action of some commonly used muscle transient fall in blood pressure may be relaxants, and the extent to which they observed secondary to the release of depend on renal excretion. histamine. Special infusion pumps are 1 Chapter 12 Muscle Relarants )

Brand Name Block Duration % Time to Intubating (Trade Name) (mins.) , dependent intubation Dose Concentration on renal (90%block) (mgkg) excietion at 2 x ED,

Succinylcholine Non Short 0 < 60 sec 1-2 (Anectine) Competitive 5 - 10 20 mg/ml (Depolarizing) Mivacurium Competitive 25 - 30 0 2 - 3 min 0.16 - .30 (Mivacron) Non - 2mgiml Depolarizing Vecuronium Inter- 10 - 25 2.5 - 3 min .07 - 0.10 (Norcuron) mediate ' 10 mgtvial 45 - 60 Rocumnium 25 - 80 secs 0.6 (Zemuron) 30 - 45 10 mglml

Cisatracurium 20 - 60 0 3.3 min 0.1 (Nimbex) 10 mg/ml

Pancuronium Long 60 - 80 3 - 8 min .06 - ,lo (Pavulon) 60 - 75 1 - 2 mg/ml Doxacurium 50 - 130 60 - 80 3 - 10 min 0.05 (Nuromax) 1 mg/ml ) Table 12.1: Properties of neuromuscular blocking agents.

) frequently utilized in the operating room one of 10 isolated isomer of it's ) to deliver opioid analgesics, sedatives, predescesor atracurium. It undergoes or muscle relaxants. These pumps hydroiysis in the plasma by a non- allow for both continuous infusions and enzymatic process referred to as ) bolus doses to be administered. Con- Hoffman elimination, and by an ester tinuous infusions of 5 - 10 mcgkglmin hydrolysis reaction. Significant hista- ) of mivacurium may be used to maintain mine release resulting in hypotension, a stable neuromuscular blockade during tachycardia, and bronchospasm, that the procedure. may occur after rapid administration of Cisatracurium: Cisatracurium is atracurium is not seen with ) classified as an intermediate-acting cisatracurium. This lack of histamine ) neuromuscular blocking drug, and is release, is the main advantage of I ** Muslfiow Should Know Page 91 \naerthesia for Medical Students

:isatracurium over it's parent compound vantage is it's ability to quickly induce atracurium. The EDg5of cisatracurium a neuromuscular block, making it suit- is 0.05 mglkg. A stable neuromuscular able for a rapid induction and intubation block can be achieved using an infusion sequence. It has an ED, of approxi- of cisatracurium' at a rate of 1 - 5 mately 0.3 m&g. The onset time (i.e. mcg/kg/min. Cisatracurium is an ideal time to 90% depression of TI twitch agent for patients with renal or hepatic height) for an intubating dose of ro- insufficiency requiring muscle curonium (i.e. 2 x EDgs) is 60 - 80 relaxation. seconds. By contrast, vecuronium has a much slower onset time of 150 - 200 Vecuronium: Vecuronium is an inter- seconds. Rocuronium's onset time is mediate-acting neuromusc~larblocking comparable to the onset time following agent. It is a popular agent because it 1.5 mglkg of s~ccinylcholine(50 - 70 does not' produce any undesirable seconds). Hence, rocuronium matches cardiovascular side effects even when succinylcholine's onset time, and avoids administered rapidly in large doses. Its its potential side effects. Nevertheless, ED, is 0.05 mg/kg. The onset time for it must be remembered that the duration neuromuscular relaxation following 2 x of action of this dose of succinylcholine the ED, is 150 - 200 seconds. This can is only 8 - 12 minutes, compared to 35 be shortened by the administration of a - 45 minutes for rocuronium. Continu- small 'priming' dose (0.01 mag) of ous infusions in the range of 4 - 16 vecuronium, followed by 2 - 4 times the mcglkglmin. can be used to maintain a ED,. This can achieve conditions stable neuromuscular block. This suitable for intubation in approximately should be reduced by 30 - 50% when 90 seconds from the time of administra- administered in the presence of 1% tion. The duration of neuromuscular isoflurane (similar to all other block'will be increased to more than 1 neuromuscular relaxants). hour if a larger dose is used for intubation. Continuous infusions of 0.5 Paneoronium: Pancuronium is a long- - 1.5 mcglkglmin have been used to acting neuromuscular blocking drug. maintain a stable neuromuscular block Administration of pancuronium is fre- during the procedure. quently associated with a modest (< 15%) increase in heart rate, blood pres- Racuronium: This new intermediate sure, and cardiac output. The increase acting non-depolarizing neuromuscular in heart rate is due to its blockade of relaxant may replace atracurium, vec- the cardiac muscarinic receptors, as well uronium, and mivacurium as the relax- as an inhibition of catecholamine re- ant of choice for short and intermediate uptake by sympathetic nerves. Pancur- procedures. It has just recently been onium administration does not result in released, and has a duration of action, histamine release. The ED, of pan- route of metabolism, and lack of hemo- curonium is 0.06 m&g. Pancuronium dynamic side-effects similar to that of is much more dependent on renal excre- vecuronium. Rocuronium's major ad- tion than the other clinically used

Page 92 Chapter 12 Muscle Relaxants

) muscle relaxants. A prolonged neuromuscular blocking agent that is neuromuscular block will result when clinically used. Depolarizing muscle I pancuronium is administered to patients relaxants bind and depolarize the end- ) with renal failure or insufficiency. plate cholinergic receptors. By contrast, non-depolarizing muscle relaxants com- ' d - Tebocurare: The muscle petitively block the action of ) paralyzing properties of curare were acetylcholine. The initial depolarization well know to South American natives can be observed as irregular, generalized who used this drug to immobilize and fasciculations occurring in the skeletal ) kill animals with blowgun darts. In muscles. 1942 Griffith and Johnson in Montreal introduced the medical world to the Succinylcholine (AnectineB) ) paralyzing properties of curare. Since Classification: ) the early 1990's curare has been Non-competitive depolarizing unavailable in Canada, and is now only neuromuscular blocking agent. of historical interest. In the 1980's ) curare was most frequently used to _Phvsical-Chemical: ) attenuate the muscle fasciculations and Succinylcholine physically resembles postoperative myalgias associated with two acetylcholine molecules linked end the administration of succinylcholine. to end. It has two quaternary ammon- ) A small 'pretreatment' dose of curare (3 ium cations which interact with the mg per 70kg) was administered approxi- anionic sites on the muscle end plate ) . mately 3 minutes prior to the adminis- receptors. ) tration of succinylcholine, and was ) appreciated for it's excellent Ninety percent of succinylcholine 'defasciculating' properties. Today, undergoes hydrolysis by plasma ) anesthesiologists who wish to attenuate cholinesterase (psuedocholinesterase) 1 the muscle fasculations and postop before it reaches the neuromuscular myalgia's seen with succinylcholine junction. After binding to the end plate ' administer a small (- 1/10 intubating muscle receptors and causing skeletal ) dose) of a non-depolarizing muscle muscle relaxation, it diffuses out of the relaxant 3 minutes prior to NMJ. Outside the NMJ, succinyl- succinylchole (eg., rocuronium 5 mg per choline is again exposed to plasma 70 kg). cholinesterase and the remaining 10% is 1 hydrolysed. The metabolites of suc- Depolarizing Muscle Relaxants: cinylcholine are excreted in the urine. 1 Succinylcholine is the most frequently Peak effect is reached within 60 seconds ) used muscle relaxant that is adminis- of administration, and the neuro-muscu- tered outside the operating room by a lar blocking effects of succinyl-choline i non-anaesthetist physician. Hence a typically dissipate over the next 5 to 10 detailed discussion of its properties is minutes. ,, included in this chapter. Succinyl- choline is the only depolarizing i 1 ** Mut Know Slrould Know Page 93 naesthesia for Medical Students

'hase I and Phase I1 Blocks: 5. ~es~onseto a tetanus stimulus fades ;uccinylcholine produces a 'prolonged during the stimulus rcetylcholine (Ach) effect'. It combines 6. The neuromuscular block can be with the Ach receptor to depolarize the reversed with anticholinesterase :nd plate, resulting in a generalized agents iepolarization (seen as succinylcholine induced fasciculations). The membrane The presence of a normal amount of remains depolarized and unresponsive active plasma cholinesterase is essential until succinylcholine diffuses away from to terminate the effects of succinyl- the endplate (due to a concentration choline. In certain conditions, the levels gyadient). This initial neuromuscular of plasma cholinesterase may be low, block is referred to as a phase I block. and this is referred to as a quantitative If large amounts of succinylcholine are decrease in cholinesterase levels. The given (eg. 4 6 mg/kg), a different consequences of a low plasma neuro-muscular- block may occur. This cholinesterase level are generally of block is referred to as a phase I1 block. little significance. In patients with Clinically this may occur when repeated severe liver disease with plasma doses of succinylcholine are given, or cholinesterase levels as low as 20% of when succinylcholine infusions are normal, the duration of a neuromuscular used. A phase I1 block has features block resulting from the administration which resemble a neuromuscular block of succinylcholine increases threefold that is produced by non-depolarizing (eg. 5 to 15 minutes). Liver disease, muscle relaxants. The actual mechan- cancer, pregnancy, and certain drugs ism of a phase I1 block is unknown. such as cyclophosphamide, phenylzine, and monoamine oxidase inhibitors have p:all been associated with low 1. Similar response to a single twitch cholinesterase levels. 2. No post-tetanic facilitation 3. Train of four (TOF) ratio > 0.7 Abnormalities in plasma cholinesterase 4. Muscle fasciculations prior to paral- activity are inherited. Patients may ysis have normal plasma levels of 5. Decreased amplitude, but sustained cholinesterase, with a severely impaired response to tetanic stimulus enzyme activity. This is referred to as 6. The neurornuscular block is increased a qualitative decrease in plasma ,when cholinesterase inhibitors are cholinesterase. Plasma cholinesterase administered enzyme activity is genetically determined by four alleles identified as the Characteristics of Phase I1 Blocks: silent or absent allele (s), the usual 1. Decreased response to a single twitch allele (u), the dibucaine allele (d), and 2. Post-tetanic facilitation present the fluoride allele (f). The normal 3. Train of four (TOF) ratio < 0.7 plasma cholinesterase genotype is EuEu. 4. No fasciculations with onset of paral- Patients with abnormal cholinesterase ysis activity are otherwise healthy and can I Clzapter 12 Muscle Relarants ) ) be identified only by a specific blood pressure, changes in pH, PaCO,, mean test that identifies the genotype and arterial pressure, and a direct effect ' enzyme activity. The sixteen possible from the extraocular muscles. A normal ) genotypes are expressed as ten possible IOP is 10 - 20 mmHg. An increase in ) phenotypes. Six of these ten IOP under anaesthesia is undesirable in phenotypes are associated with a patients with an injury that disrupts the ) marked reduction in the hydrolysis of globe's integrity. These patients are at ) succinylcholine. Patients with the risk of vitreous extrusion and damage to genotype EaEa have a marked reduction the eye if the IOP increases. While suc- ) in the hydrolysis of succinylcholine. cinylcholine increases IOP, crying, ) These patients will have a prolonged straining, or coughing can result in neuromuscular block that can be much greater increases of up to 50 increased from ten minutes to several mmHg. Increases in intracranial pres- ) hours following a normal intubating sure (ICP) of up to 10 mmHg may 1 dose of 1 - 2 mg/kg of succinylcholine. occur following succinylcholine admin- The EaEa genotype has a frequency of istration. The mechanism of the approximately 1:3200. increase in ICP is thought to be due to ) the central mobilization of blood that The treatment of postoperative paralysis results from succinylcholine's general- ' secondary to deficiencies in plasma . ized muscle contractions. ) cholinesterase activity includes con- ) trolled ventilation, reassurance, and REP: . sedation. Blood samples should be A progressive paralysis from eyelids to / taken to confirm the diagnosis and the jaw, limbs, abdominal, intercostal ) identify the enzyme genotype. Immedi- and diaphragmatic muscles follows the ate family members should be tested to administration of succinylcholine. ) determine their genotypes and suscepti- ) bility. Medical alert bracelets should be cvs: worn by any patient with a significant Succinylcholine stimulates both the reduction in their plasma cholinesterase nicotinic and muscarinic cholinergic activity. autonomic receptors. As a consequence of muscarinic cholinergic stimulation, harmacodvnamics: bradycardia, dysrhythmias, and sinus 1 b: arrest may be observed. This vagal ) Succinylcholine has no known effect on response is prominent among children 1 consciousness, pain threshold or cerebral and, after repeated doses, in adults. It function. An increase in intraocular may be inhibited with anticholinergics pressure (IOP) begins within 1 min of such as atropine. administration of succinylcholine. A peak rise in IOP of 6-10 mmHg occurs GI: at 2-4 minutes, and subsides by 6 min- Succinylcholine iincreases the intra- I utes. Factors that may increase IOP gastric in proportion to the intensity of include: an increase in central venous the muscle fasciculations in the abdo-

** Mud Know * Should Know Page 95 i inaesthesia for Medical Students nen. It can be limited with prior use of patients may respond with an on-depolarizing muscle relaxant. abnormally high tone in masseter muscle following succinylcholine. GZf : These patients are said to have devel- Succinylcholine does not rely on renal oped a masseter muscle spasm, and may excretion. It's metabolites, succinic acid represent a subgroup of patients suscep- and choline, however, are excreted by tible to malignant hyperthermia. the kidney. Patients with renal failure may have pre-existing hyperkalemia, Hyperkalemia following succinyl- and ma,y be susceptible to succinylcholine* *: choline-induced hyperkalemia. A few cholinergic receptors are located along skeletal muscle membranes out- The usual serum potassium response side of the NMJ. The receptors are following succinylcholine is a transient called extrajunctional cholinergic and brief increase in the extracellular receptors. The numbers of these Kt concentration of - 0.5 meq/L. receptors increase dramatically over a Generally patients with K+ concentra- period of 24 hours whenever nerve tions of r 5.5 meq/L should not receive impulse activity to the muscle is inter- succinylcholine, and all but emergency rupted. Acute disruption of nerve activ- procedures should be delayed. Succ- ity to skeletal muscle occurs in patients inylcholine does not cross the placenta who have sustained third degree burns because of its low fat solubility and its or traumatic paralysis (paraplegia, ionized state. quadriplegia). Administration of succinylcholine to these patients will result MSK: in an abnormally high flux of potassium Succinylcholine has no direct effect on out of the muscle cells because of the the uterus or other smooth muscles. increased number of receptors. An Myalgias following the administration acute rise in the serum potassium to of succinylcholine are infrequent in levels as high as 13 meq/L following children, the geriatric population, and succinylcholine may result in sudden pregnant patients. The incidence of cardiac arrest. Succinylcholine is abso- succinylcholine myalgias can be lutely contraindicated in these patients. decreased with prior administration of a The administration of a non-depolariz- non-depolarizing muscle relaxant such ing muscle relaxant in these patients as curare (3 mgl70kg). Fasciculations does not result in a hyperkalemic result in the release of myoglobin into response because the receptors are sim- the serum (myoglobinemia). The excre- ply blocked and not depolarized. tion of myoglobin into the urine (myoglobinuria) is more common in children, and can be decreased with prior treatment with non-depolarizing muscle relaxants. Succinylcholine increases the masseter muscle tone in the jaw. Some

Page 96 1 Chapter 12 Muscle Relavnnts

) Patients who are at risk of a hyper- 3. Myotonia: Patients with myotonia kalemic response following the adminis- congenita, myotonia dystrophica, and ) tration of succinylcholine include: paramyotonia congenita may all develop a severe, generalized 1. Patients with extensive third degree contracture if given succinylcholine. ) burns. Succinylcholine should be The use of a depolarizing muscle ) avoided if the injury is more than.24 relaxant such as succinylcholine in hours old, and for 6 months follow- these patients may result in a second- ) ing the healing of the bum injury. ary generalized contracture of the ) 2. Patients with nerve damage or skeletal muscles, and prevent airway ) neuromuscular diseases such as mus- maintenance and ventilation. cular dystrophy are susceptible to ) hyperkalemia and cardiac standstill 4. Familial Periodic Paralysis: ) with succinylcholine. The degree of ~uccin~lcholinecan precipitate a hyperkalemia appears to be related to generalized contracture and should be ) the degree and extent of muscle avoided in these patients. affected. ) 3. Severe intra-abdominal infections. Dosage & Administration: 4. Severe closed head injury. Intubating dose: ) 5. Upper motor neuron lesions. With curare pretreatment: 1 1.5 - 2 mg/kg intravenously: ) Specific Diseases: Without curare pretreatment: ) 1. Myasthenia Gravis - All muscle re- 1 - 1.5 mglkg iv. ) laxants are best avoided, if possible, in patients with myasthenia gravis. Infusion: ) These patients behave as if partially An infusion may be used for short pro- ) curarized. They are very sensitive to cedures to maintain a stable non-depolarizing muscle relaxants, neuromuscular block. Recommended ) and may be sensitive or resistant to rates for infusion are 50 - 150 ) depolarizing muscle relaxants. mcg/kg/min.

Myasthenic Syndrome: The Eaton- Indications: Lambert Syndrome is a proximal 1. Skeletal muscle relaxation during muscle myopathy associated with a endotracheal intubation carcinoma of the bronchus. Unlike 2. Abdominal operations of short dur- myasthenia gravis, muscle fatigue ation decreases with exercise, and the eye- 3. Prior to electroconvulsive therapy lids are less affected. These patients (ECT), to prevent the possibility of are unusually sensitive to both depo- seizure induced injury (e.g., vertebral larizing and non-depolarizing muscle fracture) relaxants. 4. Emergency treatment for laryngospasm

** Must Know Should Know Page 97 naesfhesiafor Medical Students

reversal, to block these unwanted muscarinic effects. Common combina- ibsolufe tions of anticholinergic and anti- .. Inability to maintain an airway cholinesterase agents used to reverse a !. Lack of resuscitative equipment neuromuscular block are atropine 0.01 b. Known hypersensitivity or allergy mg/kg with edrophonium (TensilonB) I. Positive history of Malignant 0.5 - 1.0 mg/kg, or glycopyrrolate 0:01 Hyperthermia rnglkg with neostigmine (ProstigminB) 5. Myotonia (M.Congenita, M. Dystro- 0.05 - 0.07 mg/kg intravenously. phica or Paramyotonia congenita) 6. Patients identified as being at risk Timing of reversal: of a hyperkalemic response to suc- There are numerous methods of assess- cinylcholine (see above). ing the depth of neuromuscular blockade. The most common of these' Relative: include the train of four (TOF) stimulus, 1. Known history of plasma tetanus stimulus, and the train of four cholinesterase deficiency (TOF) ratio. The train of four stimulus 2. Myasthenia Gravis (TOF) applies four brief electrical stim- 3. Myasthenic Syndrome uli of 2 Hz each over a period of 2 4. Familial Periodic Paralysis seconds. The train of four ratio, 5. Open eye injury (T4/Tl), is the ratio of the twitch response of the fourth stimulus (T4) to Reversal of neuromuscular blockade: the first stimulus (TI). In most circum- Muscle relaxation produced by non- stances, adequate muscle relaxation for depolarizing neuromuscular agents may surgery occurs when only one of the be "reversed" by anticholinesterase four twitches is observed. This corre- agents such as edrophonium and neo- sponds to a r 90% blockade of the NMJ stigmine. These agents prevent the receptors. One must consider the inten- ' .breakdown of acetylcholine in the NMJ. sity and anticipated duration of The increased concentration of neuromuscular block before attempting acetylcholine at the NMJ competes with to antagonize it. Reversal may be un- the muscle relaxant allowing the successful if only one of the four receptor once again to become respon- twitches is present. With inadequate sive to the release of acetylcholine from reversal of muscle relaxation, the patient the nerves. will have a weak hand grip, be unable to' cough effectively, and unable to The increased concentrations of sustain lifting their head from their acetylcholine also stimulate the pillow for 5 seconds. Treatment of muscarinic cholinergic receptors, result- inadequate reversal includes supportive ing in bradycardia, salivation, and ventilation, sedation, analgesia, and increased bowel peristalsis. Anti- adequate time for the neuromuscular cholinergic agents such as atropine and block to dissipate. glycopyrrolate are administered prior to

Page 98 Inhalational Anaesthetic Agents

The intravenous anaesthetic agents inhalational anaesthetic agents such that introduced in chapter 11 (propofol, very accurate concentrations can be ketamine, and thiopentothal) are fre- delivered to the patient by simply set- quently used to induce the anaesthetic ting the vaporizer dial at the desired state. To maintain the anaesthetic state, concentration. volatile anaesthetic agents are commonly vaporized and delivered to the patient The role of inhalational anaesthetic through the anaesthetic machine and drugs in current anaesthetic practice is anaesthetic circuit. This volatile vapour changing. The introduction of potent is then delivered to the lungs where it intravenous agents, including muscle diffuses across the alveolar capillary relaxants, opioids, benzodiazepines, membrane and is dissolved in the blood. propofol, and intravenous infusion tech- The blood then carries it to the brain niques have decreased the need for high and other organs in the body. doses of inhalational agents. In anaesthesia, a number of different agents Intravenous drugs are typically delivered representing different classes of drugs according to a specific number of milli- are chosen to minimize the side effects grams or micrograms per kilogram of of any one agent and capitalize on each body tissue. Inhalational agents on the agent's benefits. other hand are administered according to a specific concentration. The concen-' Inhalational agents are compared to one tration of a gas is expressed as a per- another according to their minimal centage of the volume of anaesthetic gas alveolar concentration** or "MAC" to the total volume of the gas mixture. values. The MAC value of an ihhalat- For example if we deliver 2 literslmin. ional agent is the alveolar concentration of oxygen and 4 literslmin. of nitrous in oxygen at one atmosphere of pressure oxide (N20) to a patient, the concentra- that will prevent 50% of the subjects tion of N20 is 4/(2 + 4) = 66%. If we from making a purposeful movement in want to add a 1% concentration of response to a painful stimulus such as a isoflurane to this mixture we would surgical incision. The MAC value can have to add approximately 60 ml of a be considered the effective dose in 50% saturated isoflurane vapour to the 6 of the subjects or the ED,. Knowledge liters of fresh gas flow (0.01 x 6000 ml of the MAC value allows one to com- = 60 ml). Modem anaesthetic pare the potencies of different inhalat- vaporizers are able to vaporize liquid ional agents. The MAC values of dif-

** Must Know * Should Know Page 99 rrnesflresia for Yedical Sfuderr~s 1

Cable 13.1: Factors whlch alter anaesthetic re' ulren~ents(MAC). 1 Increased MAC 1 No change In MAC Decreased MAC 1 -- Hyperthermia Gender Increasing age Chronic drug Duration of anaesthesia Hypothermia abuse: Ethanol Carbon dioxide tensions: Severe hypotension Acute use of PaC0,21 - 95 mmHg Other anaesthetic agents: amphetamines Metabolic acid-base status opioids, benzodiazepines Acute drug intoxication: Ethanol Pregnancy Hypothyroidism Other drugs: clonidine, reserpine ferent anaesthetic agents are additive. The rapidity with which the anaesthetic Nitrous oxide is the only inhalational state is reached depends on how quickly agent that is routi~lelycombined with the anaesthetic inhalational agent another inhalational agent such as iso- reaches the brain to exert its partial flurane, enflurane, or halothane. It is pressure effects. necessary to establish an anaesthetic Factors determining how quickly the depth equivalent to 1.2 to 1.3 of the inhalational agent reaches the alveoli MACvalue. The added 20 - 30% MAC include: depth of anaesthesia will prevent move- 1. The inspired concentration of anaes- ment in 95% of patients. The MAC thetic gas being delivered by the value of N20is 105%, which is approx- anaesthetic machine (concentration imately one-hundred-fold greater than effect). the other inhalational agents. Because 2. The gas flow rate through the anaes- the recommellded millimum concentra- thetic machine. tion of oxygen delivered during general 3. The amount of alveolar ventilation anaesthesia is 30%, the maximum con- (V, = Respiratory Rate x Tidal Vol- centration on N20is 70% (approximate- ume). ly 0.7 MAC). Hence, nitrous oxide I~lcreasing any of these factors will alone is unable to provide adequate result in a faster rise in the alveolar anaesthesia. Opioid a~lalgesics,benzo- concentratio~lof the inhalational agent. diazepines, or other inhalational agents may be added to supplement the nitrous Factors determining how quickly the oxide. Table 13.1 lists factors that inhalational agent reaches the brain increase or decrease the MAC values. from the alveoli in order to establish Table 13.2 lists differences in inhal- anaesthesia include: ational agents as well as their MAC 1. The rate of blood flow to the brain. values, with and without nitrous oxide. 2. The solubility of the inhalational agent in the brain. Chapter 13 Inhalational Anaesthetic Agents

6 Anaesthetic Tension Cascade

alveolar concentration of inhaled anaesthetic agent provides a reasonable estimate of brain anaesthetic tension and anaesthetic depth.

,---c------Delivered Concentration 8h Nvmlar a Brain

Fresh gas flow rate = 4 Umin.

I 1' 1 5 10 15 lime Elapsed in minutes

Figure 13.1 and 13.2: The anaesthetic tension cascade over time. Note the difference in anaesthetic tension in the alveoli and brain compared to the set vaporizer concentration being delivered. Increasing either the fresh gas flow rate or anaesthetic concentration will result in a faster delivery of the aled anaesthetic agent to the brain.

3. The difference in the arterial and The cascade of anaesthetic partial pres- venous concentrations of the inhalat- sures starts at the vaporizer. The gas ional agent. from the vaporizer is diluted by exhaled Increasing any of these factors will gas to form the inspired gas. With a hasten the onset of anaesthesia. circle system, a fresh gas flow of 4 - 5 Patients with low cardiac output states liters per minute will raise the inspired (eg. shock states) may have a rapid rise anaesthetic tension close to the in the alveolar partial pressure of an vaporizer's delivered concentration. As inhalational anaesthetic agent. This will the body continues to take up the result in a more rapid onset in anaes- inhaled anaesthetic gas, the alveolar thesia, with possible exaggerated anaesthetic tension will remain below cardiorespiratory depressant effects. the inspired anaesthetic tension for

** Must Know Should Know Page 101 L~~aes/lresiafor Medical Slude~lls many hours. The brain can be co~lsider- oxide are released and flood the alveoli, ed the final step in the anaesthetic cas- diluting the oxygen present in the cade. The brain tension will approach alveoli. When only room air is admin- the alveolar tension within 8 to 10 ministered at the end of the anaesthetic, the utes of any change. Monitoring the dilution of oxygen may be sufficient to alveolar end-tidal concentration of the create a hypoxic mixture, and result in inhaled anaesthetic agent provides a hypoxemia. Other factors contributing reasonable estimate of the brain anaes- to hypoxemia at the end of anaesthesia thetic tension (see figure 13.1 and 13.2). include respiratory depression due to anaesthetic agents, residual neuromus- Nitrous Oxide: cular blockade, and pain with splinted Nitrous oxide is an inert, inorganic, col- respirations. The administration of ourless, tasteless, and odourless gas. It 100% oxygen at the end of an anaes- has a rapid onset and a quick recovery thetic may avoid hypoxemia resulting of 3 to 10 minutes due to its low solu- from any of these causes. bility in blood. Its low potency (MAC = 105%) limits the amount that can be Finally, closed air spaces will expand in administered, and its usefulness when the presence of nitrous oxide due to the high concentrations of oxygen are differences in solubility of nitrogen and required. Myocardial depression is nitrous oxide. With the administration usually minimal in healthy patients, of 66% N20, a closed air space will however significant cardiovascular de- expand 2 times in volume over a period pression may occur in patients with of approximately 15 minutes. For this coexisting myocardial dysfunction or in reason N20 is contraindicated in patients in a shock state. patients with a pneumothorax, closed loop bowel obstruction, air embolism, or Nitrous oxide is 34 times more soluble any other closed air space in the body. than nitrogen. This property results in three special anaesthetic phenomena. At Nitrous oxide undergoes very little the begirlrling of anaesthesia, N20 metabolism and is excreted uncha~lged leaves the alveoli much faster than by the lu~lgs. nitrogen can leave the body tissues to fill the space left by N20. The result is The most conlrno~llyused inhalational an increase in the concentratio~lof other agents today are nitrous oxide, iso- gases in the alveoli (oxygen, and other flurane, enflurane, and halothane. The inhalational agents). This increase in latter three are synthetic, colourless concentratio~lspeeds the onset in inhala- liquids that are non flammable and tional anaesthetic effect, and is referred administered as a vapour from a to as the sccond gns cffcct. vaporizer on the anaesthesia machine. A dose-related depression of cardio- Diffusion hypoxin may result at the end respiratory function is common to each of the anaesthetic. As nitrous oxide is of these inhalational agents. All three discontinued, the body stores of nitrous produce smooth muscle relaxation, and this property has been exploited to Hnlothnne: produce bronchodilation in patients with Halothane is the agent of choice for an status asthmaticus, and uterine relax- inhalational anaesthetic induction,and is ation in patients with a retained pla- the most common inhalational agent centa. Halothane, enflurane, and iso- used in paediatric anaesthesia. flurane are all contraindicated in Halothane decreases myocardial con- patients with malignant hyperthermia. tractility, slows the heart rate, and decreases cardiac conduction. The Isoflurnne: myocardium is sensitized to cate- Isoflurane is the most common inhala- cholamines in the presence of halothane, tional agent used for adult anaesthesia resulti~lg in severe ventricular dys- in North America. It has a MAC value rhythmias if the body releases cate- of 1.16%, and has the fastest uptake and cholamines (stress), or if exogenous washout times of these three inhala- catecholamines such as epiilephrine are tional agents. It is not as well tolerated administered. Cerebral blood flow as halothane for an inhalational anaes- increases secondary to cerebral thetic illduction because of its pungent vasodilation and may result in an odour and tendency to irritate the air- undesired increase in intracra~iialpres- ways. These irritating effects nlay sure. result in coughing and breath-holding if isoflurane is administered too quickly. Halothane's popularity in adult anaes- Isofluraile is the preferred agent for thesia has declined because of its impli- neurosurgical procedures as it causes the cation in causingpostoperative hepatitis. least increase in cerebral blood flow and "Halothane hepatitis" is believed to intracranial pressure. Isoflurane has the occur in approximately 1 in 10,000 least depressant effect on the halothane anaesthetics and presents as myocardium. The reduction in blood postoperative fever, jaundice, pressure is accompanied by a similar eosinophilia, and occasionally extensive reduction in vascular resistance such hepatic necrosis and death. Hepatitis that there is little change in cardiac following isoflurane and enflurane expo- output. In certain patients (especially sure is very rare, as is hepatitis in the young healthy patients), isoflurane may paediatric population following any produce a significant sinus tachycardia. inhalational agent (including halothane). 111 a small percentage of patients with There is a ten fold difference in metab- corollary artery disease, isoflurane may olism of these three inhalatioilal agents. cause vasodilatio~l of the distal The maill route of excretioil is through endocardia] vessels, and result in a the lungs, but approximately 20% of 'coronary steal'. A coronary steal is halothane is metabolized by the liver. produced when blood is diverted away By contrast 2% of enflurane and only from the collateral dependent ischemic 0.2% of isoflurane undergoe metabolism regions of the heart to the areas of by the P, enzyme system. Both aller- vasodilation. The significance of this gic and metabolic mechanisms may be observation is still debated. active in producing hepatitis following

Should KIIOIV Page 103 Lt~acslhesiafor Medical Slirde~~~s rnble 13.2: Cornpal-ison of three conlnl ~ninhnlationnl annesthetic agents. I I I 1 I I lsofiurane MAC in Oxygen* 1.16% 1 MAC In 70% N20 I 0.50% I CNS Causes the lowest Increases ICP and Increases ICP. increase in ICP of Potential to cause the 3 agents when CNS excitation and ventilation is seizures at high controlled concentrations.

Resp. Irritating to the Good for inhalational Depresses ainvays, and more inductions, and is respiration more difficult to use lor less irritating to the than halothane or inhalational ainvays. Decreases isoflurane. induction. tidal volume, and Decreases tidal minute ventilation, volunie and minute accompanied by an sentilation, increase in the ( accompanied by an respiratory rate. I increase in the respiratoly rate. cvs Increases heart rate. Depresses BP, HR, Depresses cardiac Decreases BP and I CO and conduction. function more than CO. Potential to Sensitizes the halothane or create a 'coronary myocardium to isoflurane. adrenaline induced I dysrhythmias. I Neuron~uscular Potentiates niuscle Potentiates muscle Potentiates muscle relaxan ts relaxants less than relaxants. lsoflurane or I Enflurane.

Other Most common agent Halothane Hepatitis Second choice agent used in adult association in adulls. in adult anaesthesia anaesthesia. Cheapest agent of the in Nonh America. three. exposure to halothane, Repeated Enflurane: exposures to halothatle over a short Enflurane has a MAC of 1.68%, more ~eriodof time have also beeti thought to than twice that of halothane's MAC contribute to halothalie hepatitis in value of 0.75%. Enflurane is a potent patients. cardiorespiratory depressant, decreasing both respiratory drive and cardiac function to a greater extent than halothane. Desflurane and Scvoflurane: Unlike halothane or isoflurane, Desflurane and sevoflurane are two vol- enflurane produces abnormal electro- atile anaesthetics which have been encephalographic (EEG) patterns recently introduced in Canada. Both resembling seizure activity. This is have low solubilities in blood, only observed in some patients during approaching that of nitrous oxide, so in- deep enflurane anaesthesia with lowered duction and emergence from anaesthesia PaC02 levels secondary to mechanical is rapid. Cardiovascular, respiratory, hyperventilation. Occasionally tonic neurological and neuromuscular effects clonic movements under enflurane an- of both agents are similar to those of aesthesia have been observed. Despite isoflurane. the lack of documented adverse postoperative sequelae in these patients, Desflurane is unique in that it boils at enflurane is best avoided in patients room temperature (22.8'C). Because of with a history of a seizure disorder. this physical property, desflurane requires a special heated and electroni- cally controlled vaporizer to administer it safely. Desflurane has a MAC value in oxygen of 6% compared to sevoflurane which has a MAC value of 2% in oxygen. Desflurane has a pungent odour, and like isoflurane can cause coughing and breath holding if administered too rapidly. Sevoflurane is more pleasant smelling and is well suited for inhalational induction of anesthesia.

Sevoflurane, like enflurane, is metabolized in the liver yielding inorganic fluoride. Approximately 3% of sevoflurane is broken down in this fashion. Minutes oE Administration Is is degraded by the chemicals used to absorb the patients' C02 in their Figure 13.3. For potent anaestheti cs, solubil- patient's breathing circuit. Production ity determines the increase in the alveolar of a renal toxin called "compound A" at (Fd) anaesthetic concentration toward the low fresh gas flows has lead to the re- concentration inspired (F,): the least soluble commendation that sevoflurane be ad- anaesthetic (desflurane) shows the most rapid ministered with a minimum of two liters increase; the most soluble anaesthetic (halothane) shows the least rapid increase. of fresh gas flow. In contrast, des- Reproduced with permission. Eger 11, flurane is the least metabolized of the Edmond I. New Inhaled Anesthetics. volatile anesthetics (0.02%), and is Anesthesiology 80:906-922, 1994 ideally suited for use in low flow anaesthetic techniques.

** Musl Know Should Know Poge I05 innestheria Tor Medical Students jevoflurane and Desflurane have had a Our g- goals are to naj~rimpact on our anesthetic pactice. administer enough anaesthetic that the While structurally similar to their par- patient's awareness and their pain znts Halothane and Isoflurane, the sub- response to surgery is suppressed. Our stitution of a couple of key chlorine goal is to provide adequate anaesthesia atoms with fluorine atoms results in (inhibit awareness) yet at the same time their lower observed solubilities. This avoid a relative anesthetic overdose. translates clinically into a more rapid induction and recovery from anesthesia. We can use the knowledge that the MAC values of the individual inhal- Sevoflurane, unlike isoflurane, does not ational agents are additive. have an unpleasant smell, and is well tolerated in adults for inhalational Let's assume our patient is under gen- induction of anesthesia. Using high eral anaesthesia and is receiving end- concentrations of Sevoflurane at induc- tidal concentrations of 63% nitrous tion (5 - 8%, with or without nitrous oxide with 0.4% isoflurane. We can oxide), the patient can be taken from an calculate the relative contributions of awake state to an anesthetized state with these inhalational agdnts to the patients as little as one vital capacity breath. anaesthetic. Anesthesia sufficient for laryngeal mask placement and intubation can be 63 % Nitrous oxide (MAC = 105 %) achieved after three to five minutes of :. 631105 = 0.60 MAC breathing a high concentration of Sevoflurane. 0.4 % Isoflurane (MAC = 1.16 %) :. 0.4 / 1.16 = 0.35 MAC Desflurane is not suitable for __0.95 MAC inhalational induction due to it's irritating and pungent properties. When As stated earlier we generally provide given rapidly in high concentrations 1.2 - 1.3 times the MAC value to (6% or more) it may result in coughing, achieve adequate anaesthesia in 95% of breath-holding, laryngospasm, tachy- patients. In addition to the inhalational cardia, and hypertension. Unlike agents this patient is receiving, heishe Sevoflurane, Desflurane is essentially probably has also received a preoperat- inert with only 0.02% undergoing ive sedative, and intraoperative intra- metabolism. Very low fresh gas flow venous agents such as an opioid, benzo- anesthesia can be safely practiced with diazepine, and general anaesthetic in- Desflurane, limiting the increased cost duction agent (e.g., propofol). These of Desflurane when compared to will also contribute to the depth of Halothane and Isoflurane. anaesthesia for this patient. Repeated assessments for inadequate anaesthesia Clinical Note: or excessive depth of anaesthesia are How do we know if the patient is re- made during the surgery, and correspon- ceiving enough anaesthetic? ding corrective adjustments in the an-

Page 106 ) Cl~npter 13 In/ralationa/ Annestlretic Agents. 1 aesthetic depth are made. These are ) based on the patients vital signs, tearing, i or obvious movement (see chapter 10; 1 monitoring in anaesthesia).

) References: ) 1. Miller R.D. editor. Anesthesia third ) edition. Churchill Livingstone Inc. ) 1990. ) 2. Barash PG, Cullen BF, Stoelting RK., editors. . Clinical Anesthesia ) second edition. J.B. Lippincott Co., ) Philadelphia 1993. 3. Elliot RD. What can gas monitoring ) tell us? Winterlude symposium on ) monitoring and equipment. Univer- 1 sity of Ottawa 1994. 1 ) Notes:

** Must Know * Slrould Know Page 107 inaesthesia for Medical Students 1 Narcotic Agonists and Antagonists

Opium is derived from the dried juice mediation of the analgesic and anaes- of the poppy plant, which contains over twenty plant alkaloids, including morphine, and codeine. An opiate refers to ' p Mu) receptor any preparation from, or derivative of, Analgesia, respiratory depression, opium. A narcotic refers to any sub- euphoria, physical dependence stance that produces both analgesia and stupor, and includes both opium alka- K (Kappa) receptor loid derivatives and synthetic analgesic compounds. Analgesia, sedation, respiratory depression, miosis In this chapter, we shall present 5 com- . a (Sigma) receptor monly used intraoperative anaesthetic narcotics: morphine, meperidine, Dysphoria, hallucinations, fentanyl, sufentanil, and alfentanil. tachypnea, tachycardia Chapter 16 reviews other narcotic and non narcotic analgesic agents useful in managing acute postoperative pain. The thetic properties of narcotics. The properties of naloxone, a pure narcotic effects of stimulation of mu (p), kappa antagonist are presented at the end of (K), and sigma (a) receptors are sum- this chapter. marized in the table below. Features common to all narcotics Site of Action: include a dose related depression of Opioid receptors are predominately respiration, sensorium, and pain percep- located in the brain stem, spinal cord, tion. They are rapidly distributed and gastrointestinal tract. Narcotics through the body following intravenous exert their analgesic action by interact- injection. Hepatic metabolism is the ing with opioid receptors in the brain- primary route of elimination and the stem (amygdala, corpus striatum, peri- majority of inactive metabolites are aqueductal gray matter, and medulla), excreted unchanged in the urine. A and in the substantia gelatinosa in the systems review of the other spinal cord. Three classes of opioid pharmacodynamic properties of nar- receptors are primarily involved with cotics is presented below.

Page 108 j 1 Chapter 14 Narcotic Agonists and Antagonisls CNS: in both the blood pressure and SVR. Opioids produce both sedation and Synthetic opioids, such as fentanyl and interfere with the sensory perception of its related congeners, are less likely to painful stimuli, Although large doses of release histamine. Opioids produce opioids produce unconsciousness, they bradycardia by stimulating the vagal are generally incapable of providing nucleus in the brainstem. Meperidine, complete anaesthesia, and cannot guar- unlike other narcotics, does not produce antee total amnesia. Dysphoric reac- bradycardia and may cause significant tions rather than euphoria may occur cardiac depression due to its direct when opioids are administered to negative ionotropic activity. patients who are not experiencing pain. Stimulation of the chemoreceptor trigger GIIGU: zone by narcotics may result in nausea Narcotics slow gastrointestinal mobility and emesis. and may result in constipatibn or postoperative ileus. All narcotics RESP: increase biliary tract tone and may Narcotics result in a depression of the precipitate biliary colic in patients with respiratory rate and minute ventilation cholelithiasis. By increasing the tone of accompanied by an increase in the tidal the bladder sphincter, opioids may pre- volume. The result is a slow deep cipitate postoperative urinary retention. respiratory pattern. The extent of res- Other, less common, side effects of piratory depression is dose related and opioids includes anaphylactic reactions, reversible with the narcotic antagonist bronchospasm, chest wall rigidity, and naloxone. An increase in minute venti- puritis. lation normally corrects any increase in arterial carbon dioxide tension. Nar- Fentanyl, sufentanil, and alfentanil are cotics depress this response and elevated the most common narcotic agents used levels of PaC02 may accompany the during induction and maintenance of administration of narcotics. anaesthesia. This is due to their rapid onset, and predictable duration of cvs : action. Opioids have little to no myocardial depressant effects even when adminis- Morphine may be used in the peri- tered in high doses. Supplementation operative period to provide long lasting with either nitrous oxide or benzo- analgesia. It should be administered diazepines may depress cardiac output. slowly at a rate not exceeding 5 mg per Narcotics decrease systemic vascular minute to avoid excessive histamine resistance (SVR) by either decreasing release. sympathetic outflow or, in the case of morphine and meperidine, by direct Meperidine is less commonly used for release of histamine. Morphine and induction and maintenance of anaes- meperidine's tendency to release hista- thesia because of its negative ionotropic mine produces vasodilation with a fall activity. Hallucinations and nausea are

** Must Know * S/~ouldKnow Page 109 Anaesthesia for Medical Studen&

Table 14.1: Comparison of common intraoperative narcotic agonist potencies and doses. The 'low dose' schedule represents typical doses administered in divided increments intravenously for perioperative analgesia with inhalational agents when extubation is planned at the end of the procedure. The 'moderate dose' schedule represents opioid doses used in combination with a nitrous oxide - relaxant technique, when extubation of the patient is planned within the next four hours. The 'high dose' technique is used to induce anaesthesia in patients for whom prolonged postoperative ventilation is planned. more common with meperidine than due to its redistribution from the CNS with morphine. Normeperidine is an to other tissue sites in the body. active metabolite of meperidine, which has only half of meperidine's analgesic Sufentanil is the most potent narcotic activity. Normeperidine may cause that is in clinical use today. It has a CNS excitation. In patients receiving much smaller volume of distribution large amounts of meperidine for pro- than fentanyl, and is ideally suited for longed periods of time, or in patients intravenous infusion techniques during with renal insufficiency, normeperidine longer procedures. Infusion rates of 0.1 levels may rise significantly and seizure to 0.5 mcg/kg/hr are appropriate for activity may result. anaesthesia with a? inhalational anaesthetic agent (balanced anaesthesia). Fentanyl is much more potent than morphine, and because of its high lipid Alfentanil has a rapid onset and rapid solubility, it has a rapid onset in action. recovery and is ideally suited for short Fentanyl's short duration of action is procedures requiring intense analgesia.

Page 110 Chapter 14 Narcotic Agonists and Antagonists

) It has a small volume of distribution With the exception of using a single 1

and does not accumulate in significant ' ' mcg/kg bolus intravenous injection ) amounts in the body. An intravenous during induction of general anesthesia, ) loading dose of 15 - 30 mcglkg i.v. may intravenous bolus administration of ) be followed with an intravenous infu- remifentanil should only be used in sion rate of 0.25 to 1.5 mcg/kg/min to intubated patients during general maintain analgesic plasma levels. Intra- anesthesia. Remifentanil is ideally ) venous intermittent bolus doses of 5 - suited for administration with an intra- 10 mcglkg iv may be used to respond to venous infusion pump. Infusion doses ) varying intensities of surgical stimula- of 0.1 - 2 ug/kg/min with supplemental ) tion, while the infusion rate is adjusted. bolus doses of 0.5 - 1 ug/kg are recom- Discontinuation of the infusion 15 - 20 mended during general anesthesia with ) minutes prior to the end of the surgical 66% nitrous oxide in healthy adults. ) procedure permits rapid'patient awaken- ) ing for extubation. The rapid offset in action means that within 5 - 10 minutes after stopping an ) Remifentanil: infusion there will be no residual anal- ) gesic activity. Patients who are antici- Remifentanil is the newest addition to pated to have postoperative pain, must ' our clinically available opioids. It is have other measures (local anesthesia, ) classified as an ultra-short acting opioid NSAID's, long acting opioid administra- ) agonist, and has both a rapid onset and tion, etc.), instituted to avoid sudden peak effect. Adverse side effects such pain after discontinuing a remifentanil ) as hypotension, bradycardia, muscle infusion. ) rigidity, and respiratory depression or arrest, may be more pronounced with Narcotic Antagonists*: ) remifentanil compared to other opioids Naloxone (Narcan@) is a pure narcotic ) because of it's rapid onset of action. antagonist, which competes with opioids ) These side effects are dose and rate of at the mu, delta, kappa and sigma administration dependant and can be receptors. Naloxone is supplied in ) reversed with naloxone. ampules of 0.02 mg/ml, 0.4 mg/ml, and 1 1 mg/ml. The 0.4 mg/ml and 1 mg/ml Remjfentanil should only be adminis- ampules should be diluted with saline to ) tered by persons specifically trained in provide a concentration of 0.04 to 0.05 ) the use of anesthestic drugs, and in the mg/ml for ease of administration. ) recognition and management of it's adverse effects. Immediate measures Naloxone reaches its peak effect within ) including the ability to establish and 1 - 2 minutes of intravenous administra- ) maintain a patent airway and institute tion, and has a duration of 30 to 60 controlled ventilationand cardio-respira- minutes. Perioperative surgical patients, ) tory resuscitation must be available with evidence of excessive sedation or when administering remifentanil. respiratory depression secondary to opioids, may be given small incremental

** Must Know Should Know Page Ill ) Anaertltesia for Medical Students doses of naloxone of 40 mcg Notes: Sudden reversal of the analgesic effects of opioids, however, may result if high doses of naloxone are given. The subsequent abrupt return of pain can result in hypertension, tachycardia, pulmonary edema, ventricular dysrhythmias, and cardiac arrest. Continuous infusions of 3 to 10 mcglkg/hr of naloxone may be required if sedation or respiratory depression recur.

References:

1. Bailey PL, Stanley. Narcotic intravenous anesthetics. In: Anesthesia. Third edition. Miller RD., ed. Churchill Livingstone Inc. 1990.

2. Hickle RS. Administration of general anesthesia. In: Clinical anaesthesia procedures of the Massachusetts General Hospital. Third edition. Firestone LL, Lebowitz PW, Cook CE., ed. Little, Brown and Company 1988.

3. Barash PG, Cullen BF, Stoelting RK. Opioids. In: Clinical anesthesia. Second edition. JB Lippincott Co., 1993.

Notes:

Page 112 Local and Regional Anaesthesia Ann Lui M.D., FRCPC

INTRODUCTION ibly block impulse conduction in nerve fibers. The molecular structure of most Local and regional anaesthesia plays an local anaesthetics consists of an aro- important role in modern anaesthetic matic group linked to a hydrophillic management. This form of anaesthesia amine by either an amide link (amino may be used as an alternative to general amides) or an ester link (amino esters). anaesthesia, or may be used in combina- Esters are hydrolysed in the blood by tion with general anaesthesia in the hope plasma cholinesterase with the form- of reducing the severity of the perioper- ation of paraaminobenzoic acid, a ative surgical stress response. While metabolite to which some patients are numerous local anaesthetics (LA) are available for use by the clinician, this chapter will focus on three commonly used LA'S; Lidocaine, bupivicaine, and chlorprocaine. These three agents illustrate differences in the classification, potency and duration of local anaesthetics. Understanding these agents provides a basis for understanding other local anaesthetic agents that you may use in the future.

LOCAL ANAESTHETICS

Over the next two clinical years you are likely to encounter and use local anaesthetics in many clinical settings. Minor procedures in the emergency room, Figure 15.1: Hydrolysis of an ester topical application for eye examination, local anaesthetic by plasma and local infiltration for diagnostic and cholinesterase. Amide local therapeutic procedures, are a few com- anaesthetics undergo metabolism in the mon uses of local anaesthetic agents. liver. Adapted with permission from Tucker, GT. Biotransformation and toxicity of local anaesthetics. Acta Local anaesthetics are drugs that revers- \fhaesthesiol. Beig., [Supp.];123,1975J

** Musl Know Should Know Page 113 ,) Anaesthesia for Medical Students 1 allergic. Unlike ester local anaesthetics, penetrated the nerve membrane, LA'S amides areemetabolized in the liver and that bind strongly to the membranes are rarely associated with allergic reac- protein globules will inhibit sodium flux tions. across the nerve membrane for a long period of time. Clinically, we observe Mechanism of Action* a long duration of action when the protein binding of a LA is strong. The mechanism of action of local anaesthetics is not fully understood but most The onset of action of the LA is primar- likely involves a dynamic interaction ily influenced by its pKa. The pKa can with the sodium channel on the axo- be thought of as the pH at which 50% plasmic (inner surface) of the nerve of the LA is in the charged cationic membrane. form (BHt) and 50% is in the "n- charged (B) base form. The nerve cell relies on concentration (BHt r. B + Ht ) gradients of ions across its membranes, andselective permeation of ions through When a local anaesthetic is injected into its membranes as a basis for maintaining tissues, it establishes an equilibrium an electrical potential and generating an between its two forms (BHt, and B) electrical impulse. The generation of which depends on the local pH. In nerve impulses is dependent on the flow order for the LA to move through the of specific ionic currents through chan- tissues and nerve sheath, it must be in nels that span the nerve membrane. its uncharged base form. Hence, the lower the pKa the higher the concentra- The nerve membrane consists of a fluid tion of base form and the faster the lipid bilayer interspersed with protein onset of action. In humans, the starting globules. Local anaesthetics act by base form is almost always less than passing through the nerve membrane to 50% since pKa's are in the range of 7.5 attach or block the sodium conducting to 8.9 and tissue pH is normally 7.4. ion channels thereby inhibiting impulse Conversely, if you are injecting a local generation. anaesthetic into an infected area with a low pH, the local anaesthetic is ineffec- We will now discuss factors that affect tive because most of the LA will be in how fast the local anaesthetic acts the charged form and unable to pen- (onset), how well it blocks impulse etrate the nerve membrane. generation (potency), and how long it will last (duration). In summary:

Agents with a high lipid solubility will Lipid solubility influences potency. penetrate the nerve membrane easily. Protein binding influences duration. Hence very lipid soluble agents will And Pka influences onset of action. move in easily and will appear to be more potent as an anaesthetic. Having Many local anaesthetics have been syn-

Page 11 4 1 Chapter 15 Local and Regional Anaesthesia ) ) thesized since the initial use of the nat- agement for labour and delivery. Such urally.occurring cocaine for ophthalmic a block can provide excellent pain con- ) procedures. Still a search for the "ideal" trol (sensory nerve block), yet it still ) drug with the lowest toxicity and best allows the patient to move and push clinical profile continues. The clinical during labour (minimal motor nerve properties that are important include blockade). Hence, bupivicaine's ability ) potency, onset of action and duiation of to provide a differential nerve blockade ) action. Table 15.1 lists some of the together with its relatively long duration commonly used local anaesthetics and of action makes it a common choice for ' their clinical properties. Sensory nerves, epidural pain management in the obstet- ) motor nerves, and autonomic nerves may rical patient. ) all be blocked to varying degrees by local anaesthetics. Lidocaine provides a faster onset (about ) 10 minutes) but shorter duration (about ) Bupivicaine has the ability to produce a 1 - 2 hours), as compared with bupiv- differential nerve blockade when used icaine, which has an onset time of up to ) in dilute concentrations. This form of 30 minutes and a duration of 2 or more ) blockade is especially advantageous in hours. Memorizing the relative potencies ) obstetrical patients requiring pain man- of the drugs is generally not necessary

0.1 - 0.5 % (Epidural) 0.5 - 0.75 % (Spinal) 1 Table 15.1: Properties of three commonly used local anaesthetics wdh the manufacturer's 1 recommended marimum dose for single injection. The marimum dose may be increased by the ) addition of a vasoconstrictor such as epinephrine. The maximum recommended doses with epinephrine are reported in brackets. 1 ** Musl Know Should Know Page 115 ) Anaesthesia for Medical Students ) as the more potent anaesthetic agents are local anaesthetic is rapidly injected into, commercially supplied in lower concen- or near blood vessels. To avoid these trations (eg. 0.5% bupivicaine with a systemic side effects, inject slowly, potency of 8, versus 2% lidocaine with aspirate to check for intravascular entry, a relative potency of 2). consider adding a vasoconstrictor like epinephrine, to retard vascular absorp- Toxicity of Local Anaesthetics tion, and do not exceed the maximum recommended dosage. How safe are local anaestheti&? We can distinguish the toxic effects of these Most clinicians have difficulty recalling agents according to their local and sys- the maximum safe dose when temic effects. administering a local anaesthetic. For- tunately, the local anaesthetics are com- Local toxicities of these agents include mercially prepared such that the bottle direct injury to nervous tissue with the highest concentration of drug (neurotoxicity), and direct injury to contains less than the maximum dosage muscle tissue (myotoxicity). The use of for the average 70 kg adult. For preservatives in the local anaesthetic example lidocaine's highest concentra- solution (eg. para-aminobenzoic acid), tion for regional anaesthesia is 2% (20 and the use of a vasoconstrictor such as mg/mL). One vial's volume of 20 mL epinephrine may increase a LA'S poten- (total 400 mg) is within the limit of the tial neuro- and myo- toxicities. Direct maximum dosage, if epinephrine is pres- injection of a LA into a nerve will result ent in the lidocaine. Generally, if the in immediate severe pain and will result volume of the local anaesthetic with in pathologic damage to the nerve. If epinephrine is restricted to a maximum excruciating pain is experienced on of one bottle (20 mL) per adult patient, injection of a local anaesthetic near a the clinician will remain within the safe nerve, the injection should be immedi- limit for the total allowable dose. The ately stopped and the needle solution can be diluted (with preserv- repositioned. Injection of LA's into ative free saline) if a greater volume of muscles may result in histological local anaesthetic is required. changes in the tissues. These are, however, generally transient, reversible and The potential for systemic toxicity of clinically insignificant. local anaesthetics increases with the concentration of the local anaesthetic in Systemic toxicities involve the central the blood. Absorption of LA's in the nervous system, the cardiovascular sys- blood can be decreased by the addition tem, and the respiratory system. Figure of a vasoconstrictor such as epinephrine 15.2 shows the positive relationship or phenylephrine. Typical concentra- between symptoms of systemic toxicity tions of epinephrine that are used are and increasing plasma levels of lido- 1:100,00 to 1:200:000. A 1:200,000 caine. Systemic complications are more concentration of epinephrine has 5 likely to occur when a large dose of mcg/mL of epinephrine, or 0.1 mL of

Page 116 1 Chapter 15 Local and Regional Anaesthesia

I - Cardiovascular collapse

I Unconsciousness

I Numbness of the tongue

Figure 152: Relationship of signs and pptoms of local maesthetic toxicity to plasma concentrations of lidocaine. With permission from Covino B.O., Clinical pharmacology of local anaesthetics. In Neural Blockade. Cousins MJ, \ Bridenbaugh (Eds.) 2nd edition J.B. Lippincott 1980. ) epinephrine (1 mg/mL concentration) severe cases, this may be observed as a ) added to 20 mL of LA. sudden loss of consciousness, respiratory arrest, or cardiovascular arrest. ) The uptake of local anaesthetics into the When the clinician administers a large ) blood will be accelerated if injected in dose of a local anaesthetic, the patient the proximity of 'major blood vessels should be closely monitored by main- ' (fig. 15.3). Intercostal nerve blocks ) result in the highest peak local anaes- Intercostal Nerve Block thetic blood concentrations, whereas 4 infiltrative injection achieves the lowest Epidural Anaesthesia ) peak serum levels, provided direct intra- 4 ) vascular injection is avoided. Femoral/Brachial Plexus Block 4 ) The potential for systemic toxicity is Peripheral Nerve Block ) very real. High concentrations of LA in 4 1 the blood may result in a spectrum of Local Infiltration symptoms reflecting an initial excitation ) of the CNS followed by CNS, respira- Fig. 15.3: Regional blocks in decreasing ) tory, and cardiovascular depression. In order of systemic absorption and the potential for systemic toxic reactions.

1 ** Must Know Should Know Page 11 7 Anaafhesia for Medical Students . )

Table 15.2: Treatment of Acute Local Anaesthetic Toxicity**

Ensure a clear airway. Utilize manoeuvres such as suctioning, chin lift, jaw thrust, insertion of oral and nasal airways, and positioning the patient in the lateral decubitus position.

Ensure adequate ventilation. Manually assist or control the patient's breathing using an Ambu bag and mask unit. Avoid respiratory acidosis secondary to hypoventilation, as this will increase the local anaesthetic uplake and toxicity. If unable to control ventilation by mask, consider intubation (may require succinylcholine 1 mg/kg iv).

Provide supplemental oxygen. Ensure the patient is receiving supplemental oxygen. Set the ambu bag oxygen flow at 8 to 10 Vmin.

Assess the heart rate and Treat bradycardia with atropine. Initial dose of 1 mg iv., fol- rhythm, apply monitors. lowed by 0.5 mg iv every 5 mins. to a max, of 3 mg. Use epinephrine as per ACLS guidelines for profound cardiovascular collapse. Consider early electrical cardioversion for arrhythmias.

Assess the blood pressure and If the patient is hypotensive, place them in the trendelenburg perfusion (determine respon- position. Administer an initial fluid bolus of 500 to 1000 ml of siveness). saline or ringer's lactate. Support blood pressure with ephedrine 5 - 10 mg, or phenylephrine 50 mcg iv prn every 2 - 3 minutes.

Stop seizures. Protect the patient from physical injury during a seizure. Con- sider administering 5 - 10 mg of diazepam iv, or 50 mg of sodium thiopental to stop the seizure.

taining verbal contact, as well as by administration. In the case of LA toxic- continuous ECG monitoring, pulse ity and life threatening arrhythmias, oximetry, and blood pressure readings. bretylium is the agent of choice. Epine- phrine can be used if indicated, accord- Management of CNS, respiratory, and ing to the ACLS guidelines. cardiovascular toxicity * * begins with the ABCs (airway, breathing, and circu- REGIONAL ANAESTHESIA lation) followed by the ACLS recommendations for resuscitation. The only Many studies have examined the bene- deviation in the algorithm is the avoid- fits of regionaI over general anaesthesia. ance of the use of Class Ia and Ib anti- Still, there is continuing controversy arrhythmia such as procainamide, regarding the best type of anaesthetic. quinidine, and Iidocaine. These agents are themselves local anaesthetics. Perhaps, what type of anaesthetic is Hence, any local anaesthetic induced chosen may not be as important as how arrhythmia will be exacerbated by their well the anaesthetist administers it.

Page 118 ) ~ha~ter15 Local and RegionalAnaesthesia . 1

Table 15.3: Reported Benefits of Regional ~naesthesia

Benefits ' Importance

Decreased perioperative nausea and , Decreased hospital stay, emesis improved patient satisfaction

Reduced perioperative blood loss Orthopaedic surgery for total hip arthroplasty, prostatic surgery.

educed perioperative stress indicators Decreased catecholamines

Ability to monitor CNS status during Detection of myocardial the procedure ischemia, monitoring CNS status during prostatic surgery (TURP syndrome) and carotid artery surgery

Improved vascular perfusion Improved perioperative patency of vascular grafts (eg. Femoral - popliteal vascular graft)

Reduced deep vein thrombosis Reduced incidence of pulmonary embolism

Reduced perioperative pulmonary Reduced incidence of complications atelectasis, pneumonia

Reduced perioperative analgesic Decreased costs and side effects requirements (pre-emptive analgesia) of other anaesthetic agents

) Table 15.3 summarizes some of the topical anaesthesia, infiltrative anaes- ) benefits of regional anaesthesia. thesia, intravenous regional anaesthesia, peripheral neural blockade, and central It is convenient to distinguish how local neural blockade. I anaesthetics can be administered. The j various routes of administration include:

** Must Know * ShouMKnow Page 119 i Anaesthesia for Medical Students

Topical Anaesthesia may dilute the solution to give the ~ol- ume required to cover the area. There are various preparations of local anaesthetics available for topical use. Intravenous Regional Anaesthesia They must be able to penetrate the sur- "Bier Block" face (either mucous membrane or skin). Cocaine 4% or 10% is often used for This technique is very useful for anaes- anaesthetizing nasal mucosa. As this is thetizing the distal arm or leg for pro- the only local anaesthetic that inhibits cedures of 1 hour or less. ECG, BP, noradrenaline uptake resulting in its and oximetry monitors are applied prior catecholamine effects it has vasocon- to performing the block. An intraven- stricting properties that "shrink" the ous is secured in the non-operative mucosa and effect sohe hemostasis extremity for prn drug administration during procedures. ~idocaine2% jelly is and emergency use. A second small Gsed for intra urethral procedures and intiavenous is inserted in the distal catheter insertion. extremity for injection of the LA. A tourniquet is applied to the limb and In Canada, EMLA (a 1:l eutectic mix- tested for its ability to abolish the ex- ture of 25 mg lidocaine and 25 mg tremities pulse by maintaining a pres- prilocaine per gram of cream) is avail- sure of 100 mm Hg above the systolic able in 5g or 30g tubes for application BP. The limb is elevated, wrapped with on the skin. The cream must be applied an elastic bandage (esmarch) to ex- under an occlusive dressing (e.g., tegaderm@) for more than 60 minutes to achieve dermal analgesia to a depth of 3mm. About 5 to 10% of the drug is absorbed systemically. EMLA is an effective topical anaesthetic for intravenous catheter insertion, blood sampling and minor skin surgery (e.g., laser treatment, wart removal). This preparation'is not recommended for use on mucous membranes.

Infiltrative Anaesthesia Figure 15.4: Intravenous regional anaesthesia commonly referred to as Also referred to as local infiltration, this a 'BierBlock'. Wihpermisrwn from technique involves injection of local Covino BG., Lambert DH. In: anaesthetic intradermally, subcutaneously Anestheswlogy principles and or in the tissue within the vicinity of the procedures. Lui PL. (ed.) JB \Lippincott Co. 199t. area of surgery. When large areas are d involved, avoid using more than one bottle of local anaesthetic. Instead, one

Page 120 ) Chaprer 15 Local and Regional Anaesrh& ) anguinate the limb, and the tourniguet is 1. Avoid intraneural injection. j inflated. The esmarch bandage is 2. Avoid neurotoxic agents. ) removed, loss of arterial pulse con- ) firmed, and a solution of 0.25 - 0.5% An intraneural injection can be detected lidocaine plain (without preservative) is when patients complain of excruciating ) slowly injected in the operative limb's pain in the distribution of the affected ) iv, (max. 3 mg/kg). The local anaes- nerve at the start of the injection. Stop thetic diffuses from the venous vascular and withdraw the needle if this occurs. ) bed into the tissues to provide operative Intraneural injection of less than 0.5 ml ) anaesthesia within 5 minutes. Care must of solution can raise intraneural pres- ) .be taken to ensure proper function of the sures to ischemic levels resulting in tourniquet if success is to be achieved permanent damage. Use an atraumatic ) and a sudden iv infusion of lidocaine is needle; one specifically designed for ) to be avoided. A minimum of 20 min- nerve blockade, the nerve tends to "roll utes tourniquet time'is needed to allow off" the blunt end of these needles, ' adequate tissue uptake of the local an- rather than being impaled. ) aesthetic to avoid toxic reactions on ) deflation of the tourniquet. The tech- Most preservatives contained in the nique is illustrated in figurk 15.4. local anaesthetic solutions have the ) potential to be neurotoxic. All solutions ) Peripheral Nerve Blockade selected for peripheral nerve block (including the normal saline used for dilut- Local anaesthetics can be deposited ing the solutions) should, therefore, be close to individual nerves (e.g., the ulnar free of preservatives as indicated on nerve, median nerve, or femoral nerve), the bottle. or to the nerve plexus (e.g., brachial plexus and lumbosacral plexus). A thor- Central Neural Blockade ough knowledge of the anatomy of the peripheral nervous system is important Central neural blockade refers to either to locate the site of injection as well as epidural or spinal anaesthesia. Epidural to determine whether the technique will anaesthesia involves injecting drugs into provide adequate anaesthesia for the the epidural space, which lies between surgical site. There are many well illus- the ligamentum flavum and the dura trated texts and workshops that describe mater, exterior to the spinal fluid. Spi- each nerve or plexus block that can be nal anaesthesia involves passing a used as a guide. The most devastating needle through the epidural space, complication of peripheral nerve block- through the dura and into the CSF ade is nerve injury which can be mini- (intrathecal) space, see figure 15.5 and mized if two cardinal rules* are 15.6. practiced: In spinal anaesthesia, the local anaesthetic is injected into the subarachnoid

* Should Know Page 121 Anaesthesia for Medical Students

Needle In Subarachnold Space

Needle in Epidural Space

Ugamentum Flavum

Filum Terminale

Figures 15.5 and 15.6: Sagittal and cross sections demonstrating the relationship of the epidural space to the subarachnoid space. Both epidural and spinal needle placement is shown. Adapted with permission from Raj Pl? In: Handbook of regional anesthesia. Churchill Livingstone inc. 1985.

Page 122 ) Chapter 15 Local and Regional ~nakhesia ). ) space (CSF containing space), where it requires 5 - 10 times the amount of LA is in direct contact with the "bare" nerve that would be used for spinal anaesthe- ' roots. By contrast, local anaesthetics sia. ) administered in the epidural space must ) pass through the myelin sheaths Continuous infusions of local anaes- .covering the nerve roots. The dura acts thetics and .opioids into. the epidural 1 as a barrier to epidural LA'S moving into space can be used intraoperatively and ) the CSF space. Local anaesthetics that continued postoperatively. Both spinal contact the nerves directly, as in spinal and epidural anaesthesia affect motor, ) anaesthesia, produce a very rapid and sensory and sympathetic nerves in the ) intense nerve block. By contrast, neural axis. Nerve blockade of the epidural anaesthesia has a slower onset sympathetic nervous system results in ) because the nerves are, in a sense insu- vasodilation, which in turn decreases

) lated, and it produces a less intensk venous'return, stroke volume and car- ' 1. block. Epidural anaesthesia typically diac output. If this produces

Table 15.4: Spinal and Epidural Anaesthesia ContraindicationsL Complications Patient refusal Inadequate anaesthesia Lack of resuscitative equipment Excessive anaesthesia Lack of knowledge of procedure - 'High block' with potential Coagulopathy respiratory insufficiency and Previous back surgery (relative) cardiovascular collapse. Raised intracranial pressure Sympathetic blockade (hypotension) Fixed cardiac output: Dural puncture (headache) - severe aortic or mitral stenosis Injury: - IHSS -.muscles, ligaments, bone Pre-existing neurologic disease (back pain) - ALS, Multiple sclerosis - nerve root or spinal cord (nerve deficit) - epidural vien (epidural hematoma) - anterior spinal artery (nerve deficit) Infection: - bone (osteitis) - epidural space (epidural abscess) - CSF (meningitis) Inadvertent intravascular injection of local anaesthetic: see text re: local anaesthetic toxicity.

1 ** Musl Know Should Know Page 123 . .... Anaesthesia for Medical Students hypotension, it is first treated with fluid Injury to the muscles, ligaments, and boluses and, if necessary a sympatho- bone may result in transient discomfort, mimetic drug such as ephedrine (see that can be treated with oral analgesics chapter 22). and rest. An injury to a nerve root or the spinal cord is very rare. The awake Sympathetic blockade of the cardio- patient will experience severe pain if the accelerator fibres at levels T1 to T4 can spinal cord or a nerve root is touched, result in unopposed vagal effects causing at which point the clinician should bradycardia, or even asystole. Progress- reposition the needle, to avoid perma- ive bradycardia and hypotension under nent injury. As the spinal cord termin- spinal anaesthesia are warning signs that ates between the 1st and 2nd lumbar suggest the block may be reaching the vertebral body in adults, insertion of an cardioaccelerator fibres. A combination epidural or spinal needle in the low of intravenous fluids, atropine, lumbar region (i.e., L3 - L4) reduces the ephedrine, or phenylephrine ought to be. ' risk of direct damage to the spinal used to treat these hemodynamic abnor- cord. malities as soon as they are recognized. Whenever the dura is punctured, there is Nevertheless, misconceptions and un- a' risk that the patient will develop a warranted concern about complications postural headache, referred to as a of epidural and spinal anaesthesia are. "dural pu~ictureheadache". The dura is common in both the lay and medical intentionally punctured when per-- profession. The risks of a life threaten- forming spinal anaesthesia, it may be ing or debilitating complication occur- inadvertent]y punctured with an epidural ring after epidural or spinal anaesthesia needle if the needle is advanced past the are probably less than the risks we take epidural space. The chance of a dural when we ride in our car. Table 15.4 puncture headache varies with the size lists the contraindications and potential and type of needle used, direction of the complications of central neural blockade. bevel, and age of the patient. For instance, young patients who have their The discomfort experienced with the dura punctured with a large bore (16 ga. performance of an epidural or spinal epidural needle) have about a 60% block is comparable to that experienced chance of developing a headache. This when an intravenous is inserted. If headache may be quite debilitating and inadequate local anaesthesia is used to persist for two or more weeks. Some- perform the block, or if musculoskeletal times another procedure called an abnormalities are present, finding the "epidural blood patchn is required to epidural or intrathecal space may be treat this headache. more difficult. In this situation, pain may be experienced from injury to the The risk of an inadvertent dural punc- adjacent muscles, ligaments, bone, nerve ture when an epidural is performed is roots, or spinal cord. approximately 1:100 to 1:200 patients. Young patients having a dural puncture

Page 124 Chapter 15 Local and Regional Anaesthesia

for spinal anaesthesia with a small two greatest causes of morbidity and needle (eg. 27 ga. needle) have a 1 - 3 mortality in pregnant patients having a ). % chance of developing a headache. general anaesthetic are aspiration of ) ~lderl~patients do not seem to be prone gastric contents and the failure to to this complication. intubate, both of which are avoided by using regional anaesthesia. ) Permanent neurologic damage following ) central neural blockade is very rare. References: This can dccur if: direct nerve trauma ) occurs, infection is introduced into the 1. Cousins MJ, Bridenbaugh PO. (ed.) ) .spinal canal, a neurotoxic drug is Neural Blockade in Clinical iiijected by mistake, or an epidural. Anesthesia and Management of

) hematoma develops and compresses the Pain. ' Second Edition. JB .nerve roots. Historically there are Lippincott Co.1988. 1 reports of paraplegia following the use of epidural or spinal anaesthetics con- 2. Miller RD. (ed) Anesthesia. Third ) taminated with neurotoxic chemicals or Edition. Churchill Livingstone Inc. ) with bacteria. Despite this, the currently 1990. available local anaesthetics are safe ' when used in' the appropriate doses. Notes: Although extra care should be taken when inserting an epidural or spinal anaesthetic in the patient with low back pain,'this is not a contraindication to performing the block. Moreover, the incidence of postoperative low back pain in patients who had regional as compared to general anaesthesia is not significantly different. In fact, patients with chronic back pain problems benefit from epidural injections of local anaesthetics and steroids.

Undoubtedly, some risk is associated with any form of anaesthesia. Still the risks of general anaesthesia are greater than those for central neural blockade in some cases. For example, epidural or spinal anaesthesia are preferred to general anaesthesia for caesarean sections. This is because we recognize that the

Should Know Page 125 Acute Pain Management

JOHN PENNINGM.D., FRCPC

specialists in pain management regard intramuscular opioid administration as a The last few decades has brought vast technique that provides inferior pain improvements in the understanding and control when compared to other tech- management of acute pain. Many new niques currently available. and effective treatment modalities are now available, including patient con- This discrepancy between recommended trolled analgesia (PCA) and administra- and actual pain management techniques, tion of neuraxial (epidural or spinal) spurred the American Agency for Health opioids. Anaesthesiologists are highly Care Policy and Research Development knowledgeable in opioid pharmacology, towards developing clinical practice and are experts at spinal and epidural guidelines for acute pain -management. drug delivery. In the 1980's, acute pain This extensive work involved the review services were developed under the direc- of thousands of articles and consultation tion of the departments of anaesthes- with hundreds of leading world experts. iology and nursing, at leading centres The results were published in February throughout the world. We have learned 1992 under the title: "cute Pain Man- that acute painmanagement is attainable agement: Operative or Medical Pro- and that the optimization of acute pain cedures and ~rauma'". This well management leads to better patient regarded clinical practice guideline outcome and shorter hospital stays. promises to set the standard in pain Poorly controlled acute pain is causally management for 1990's. related to perioperative morbidity and mortality. The investment in acute pain We will now proceed with a review of management has been cost effective for some basic neurophysiology of acute both hospitals and society as a whole. pain. Following this, we shall review the principles of analgesia therapy with Despite remarkable progress in certain PC& neuraxial opioids and non centres in the management of acute steroidal anti-inflammatory drugs pain, intramuscular morphine or (NS AIDS). meperidine on an as needed @.rn.) basis remain the most popular form of acute postoperative pain management at most Canadian hospitals. Even so,

Page 126 Chapter 16 Acute Pain Management

Nociception refers to the detection, transduction and transmission of A goal of all health care providers noxious stimuli. Substances generated should be to provide optimal acute pain from thermal, mechanical or chemical management. Indeed, some of the mor- tissue damage, activate free nerve end- bidity and mortality that patients experi- ings, which we refer to as nociceptors. ence after trauma or major surgery may These peripheral afferent neurons have be the final result of the pathological their cell body located in the dorsal root disturbances that are initiated by severe ganglion and send axonal projections and poorly controlled acute pain. into the dorsal horn and other areas of the spinal cord (figure 16.1). Synapses Patients with large chest wall or abdo- occur with a second order afferent minal incisions, who do not receive neuron, as well as with regulatory adequate acute pain control, experience interneurons. In addition, synapses significant chest, abdominal and occur with the cell bodies of the sym- diaphragmatic muscle splinting that pathetic nervous system and ventral limits their ability to breathe deeply and motor nuclei, either directly or through to cough. This impairs their ability to the internuncial neurons. These circuits clear airway secretions. The patient is are important for understanding the rendered prone to atelectasis (collapse reflex sympathetic and motor responses of segmental lung regions), which that result from segmental afferent increases the risk of hypoxemia and nociceptive input to the spinal cord. pneumonia. This muscle splinting is a reflex response to acute pain stimuli at The cell body of the second order the level of the spinal cord. It can be neuron lies in the dorsal horn. Axonal prevented or alleviated by appropriate projections of this neuron cross to the analgesic therapy. contralateral hemisphere of the spinal cord and ascend to the level of the The barrage of nociceptive stimuli thalamus. Along the way, this neuron reaching the spinal cord also initiates divides and sends axonal branches that spinally and supra-spinally mediated synapse in the regions of the reticular reflex increases in sympathetic tone. formation, nucleus raphe magnus, peri- This results in hypertension, aqueductal gray, and other areas of the tachycardia, increased contractility and brain stem. In the thalamus, the second an increase in the work demanded of order neuron synapses with a third order the heart. If this occurs in a setting of afferent neuron, which sends axonal decreased oxygen supply, due to blood projections into the sensory cortex. loss and decreased lung efficiency, myocardial ischemia, congestive heart failure and myocardial infarction may result.

Should Know Page 127 Anaesthesia for Medical Smdents

The increased sympathetic tone during Poorly controlled acute pain plays a acute pain also increases intestinal se- significant role in initiating and main- cretions, slows gut motility, and taining the stress-response associated increases smooth muscle tone. These with the trauma of major surgery. This changes may lead to gastric stasis with response includes the development of a nausea, vomiting, ileus and urinary hyper-coagulable state, which can lead retention. to deep vein thrombosis, pulmonary

I Perlaqueductal Gray

1 Reticular Formation

Splnothalamlc Tract

Dorsal Horn Ganglia

Substantla Gelatlnosa

Figure 16.1 Afferent sensory pathways for detectlon and transmission of noclceptlve Impulses. Modifled wlth permission from Lubenow TR, McCarthy RJ, lvankovich AD: Management of acute postoperatlw pain. In Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesla, 2nd ed. Philadelphia: JB Uppincott, 1992. I Page 128 Chapter 16 Acute Pain Management

embolism and myocardial infarction in capable of diffusing across the synapse, the postoperative period. Further binding to the specific synaptic changes associated with the stress receptors and causing depolarization of response to trauma include decreased the secondary neuron. Substance "P" is immunocompetence, hyper-metabolism a neuropeptide that acts as a and mobilization of energy stores. neurotransmitter in this fashion. There These responses explain the tendency are several neurotransmitter substances toward hyperglycemia and large net released by modulatory neurons within protein losses that sometimes delay the substantia gelatinosa that dampen wound healing. transmission either by impairing the release of the neurotransmitter (such as substance "P") or by rendering the neuron's post-junctional membrane more Afferent neurons transmit information difficult to depolarize. from peripheral pain receptors to the CNS. Efferent neurons descend from Examples of such modulatory the brainstem to the dorsal horn to neurotransmitters include: endorphins decrease incoming nociceptive informa- and enkephalins, norepinephrine, tion. serotonin, and gamma amino butyric acid. Pain killers, such as the opioid The peripheral and central components narcotics (morphine,meperidine), mimic of the nervous system that serve to the action of the body's own pain killers detect, transduce and transmit (endorphins, enkephalins) by dampening nociceptive signals are subject to control the afferent pain signals being trans- from higher centres within the CNS. mitted to the CNS. This serves in a negative feed-back fashion to limit the amount of afferent There are also occasions when signals nociceptive stimulation that can be are amplified rather than dampened. perceived as pain. Modulation can Although the mechanisms involved are occur either in the periphery or at any complex, the important principle is that point where synaptic transmission the system is not static. It does not occurs. Anatomically, the most import- function like a hard wired electrical ant site where modulation occurs is in circuit board. The system is dynamic the outer layers of the dorsal horn, and subject to change in how the named the substantia gelatinosa. This is nociceptive signals are handled. Inves- where the synapse between the primary tigators have coined the term neuronal afferent sensory neuron and the second- plasticity, to underscore this principle. ary afferent sensory neuron occurs.

Propagation of a sensory impulse from the primary to the secondary sensory This highly effective class of analgesics neuron depends on the release of an operates at several levels in the nervous adequate amount of neurotransmitter system. They directly dampen the

* * Must Know * Should Know Page 129 Anaesthesia for Medical Students transmission of nociception across the (im.) opioids, every three to four hours, synapse between primary and secondary results in a cyclical pattern of peaks and nociceptive afferent neurons in the troughs in the serum opioid levels. dorsal horn by binding to pre-synaptic, There is a significant time delay post-synaptic or interneuron opioid between the im. administration and the receptors within the substantia attainment of adequate pain relief due to gelatinosa of the dorsal horn. the slow and variable rate of drug absorption from the im. depot. Austin et They activate descending efferent al. found that the average peak serum modulatory pathways, resulting in the level after 100 mg of meperidine release of inhibitory neurotransmitters (~emerol? occurred 44 minutes after such as noradrenaline, serotonin and im. administration (range 15 - 110 min- GABA. These efferent modulatory utes). They also noted a five fold vari- neurons originate in the brain stem (is., ability in the maximum concentration peri-aqueductal grey) and travel down attained and a three fold variability in the spinal cord in the dorsolateral fasci- the minimum effective serum concentra- culus to terminate in the dorsal horn tion for meperidine. This 3 to 4 fold (figure 163). inter-patient variability in the minimum effective drug concentration has also Opioids inhibit the inflammatory been observed for other opioids. Hence response in the periphery and decrease after im. opioid injections, the peak hyperalgesia. Opioids also affect mood concentrations attained are often sub and anxiety by their activity at opioid therapeutic. receptors in the limbic regions of the brain. This helps alleviate the affective Those patients who do have adequate component of the perceived pain. analgesia at peak levels are still subject to sub-therapeutic levels during the Oral analgesics are generally limited for trough portions of the serum opioid use in patients with mild postoperative cycle, which accounts for 30 - 50% of pain. Moderate to severe acute the time. This is especially true in the postoperative pain is poorly controlled early post-operative period when the with oral analgesics alone. This is due pain is the most intense and the drug to their prolonged time to reach peak levels fall quickly due to a rapid redis- effect, lack of flexibility in titration, and tribution within the patient's central dependence on a functional GI tract. compartment.

INTRAMUSCULAROPIOID Hiah incidence of side effects: ADMINISTRATION: When opioids are administered intermit- LIMITATIONSDUE TO tently (every 3 to 4 hours) by im. injec- PHARMACOLOGICPRINCIPLES tion, the therapeutic window during which the effective concentration of the Inadeauate analgesia: The intermit- drug is reached, may last only a fraction tent administration of intramuscular of the time between injections. This Chapter 16 Acute Pain Management

reflects the large variability among quence of having too little drug is pain patients in the maximum drug level with all of its adverse sequelae. The reached in the blood after im. injec- side effects of too much opioid in the tions, and the large variability in the system are sedation, respiratory depress- effective drug concentration among ion, puritis, and an increased incidence patients (see figure 16.4). The conse- of nausea and vomiting.

Perlaquedoctal Gray

Reticular Formation

) Nucleus Raphe Magnus ) ) ) Dorsolateral Fasciculus

) Dorsal Root Ganglia

1 ) i Flgum 16.2 Efferent pathways Invoked in noclcepttve ngulatbn. Modified ) with permission from Lubenow TR, McCarthy RJ, lvankovich AD: Management of acute postoperative pain. in Barash PG, Culien BF, ) Stoeitlng RK (eds): Cllnlcal Anesthesia, 2nd ed. Phlladelphla: JB Upplncott, 1992:1548.

) ** Must Know Should Know Page 131 ) OPIOIDSBY CONTINUOUSINFUSION: of being simple and avoids repeated and painful im. injections. Unfortunately, This approach generally provides post- as with im. opioids, this modality lacks operative analgesia that is superior to sufficient flexibility. The maximum prn im. injections. It has the advantage rate of drug delivery allowable is often

Biofeedback, education Tricyclic antidepressants Relaxation techniques Laughter, psychotherapy Bralndem: (opioid maptors) Rostral spread of epidural, spinal opiolds Oral, I.m., i.v. narcotics via biood brain ba

Antimnvulsants phenytoin, Carbarnazeplne) (Chronic paln disorders see ch 17)

Alpha adrenergic blockers (Cionldine) (periaqueductal g

Epldural and Spinal: Nmtics (spinal opiold receptors) Local anaesthetics Uectrlcal stimulation

Peripheral Nerve: Peripheral Nerve 81

Local: Anaesthetic Infiltration AS& NSAIDs, Physical therapy: (excercise, whirlpool, Accupuncture massage). (Gate theory of Pain) t Figure 16.3: Therapeutic Interventions for Pain Management According to Anatomic Location.

Page 132 Chapter I6 Acute Pain Management

Respiratory Depression

g8 Sedation 8 it 3 Analgesia B

m Pain

123456789 Time (hours) Figure 16.4: Wide fluctuations in serum opioid concentrations are associated with their intermittent intramuscular administration. This results in periods of over-sedation alternating with periods of poor pain control. By contrast, intravenous PCA opioid administration can be rapidly adjusted by the patient. This permits analgesic concentrations of opioids in the serum to be maintained for prolonged periods of time. insufficient, especially early in the acute achieve analgesic levels. A continuous post-operative period when the drug infusion will then maintain stable may redistribute quickly away from the plasma levels. therapeutic site in the CNS to the peripheral compartment. However, after A continuous opioid intravenous infu- several hours, the tissues can become sion is not able to respond to break- saturated and the serum drug levels through pain occurring during periods may begin to rise to dangerous levels. of ambulation, or chest physiotherapy. This means that closer nursing supervi- Adjustment of the infusion rate may sion must be supplied for patients that take hours to reach the effective anal- are on continuous opioid infusions than gesic concentration, (typically 4 - 5 patients on intravenous patient con- times the drugs half life to reach a trolled analgesia (i.v. PCA). Patients in steady state). By contrast, i.v. PCA acute pain starting on a continuous plasma levels can be temporarily infusion of an opioid will require an increased when the patient requests initial bolus loading dose to quickly additional doses, allowing the effective

** Must Know Should Know Page 133 j Anaesthesia for Medical Students 1 concentration to be reached within min- lowing a typical PCA bolus of opioid utes. drug.

In centres without a PCA service, an The rapid onset of analgesia allows the alternative may be a low background i.v. PCA modality to respond quickly to infusion of narcotic (eg. morphine 05 - conditions where breakthrough pain 2 mg i.v. per hour), with added p.rn. may occur (e.g., chest physiotherapy or subcutaneous injections for periods of ambulation). An appropriate bolus dose need (eg. morphine 5 - 75 mg s.q. or of i.v. opioid will be smaller than an im. q 3 hours). This avoids over seda- im. dose, but can be given more fre- tion with high infusion rates, which is quently. An im. injection results in especially important in patients at lower peak serum levels of drug with a night. It is important that infusion rates delay in the peak level when compared are decreased as pain levels decline or with an i.v. injection. An im. injection sedation appears. The time required to also results in a storage depot, which achieve analgesia with this technique continues to release drug after it has will be slower than i.v. PCA due to been administered. time required for: The duration of effect after an i.v. bolus 1. The patient to signal to the nurse of opioid depends upon the rate at that pain control is inadequate. which the drug is cleared away from the 2. The nurse to draw up and administer opioid receptor sites within the CNS. the pain medication. This is determined by the drug's ability 3. The time it takes for the opioid to to diffuse through neural tissues, a char- be absorbed from the s.c. or im. acteristic referred to as lipophilicity. injection site. The duration of effect is also determined by the rate at which the drug is I.V. PCA cleared from the plasma by redistribu- INTRAVENOUSPATIENT CONTROLLED tion, metabolism, and excretion. ANALGESIA Morphine with its low lipophilicity, Pharmacoloaical asvects: The direct i.v. diffuses slowly into and out of neural administration of an opioid results in a tissue. This results in a slower onset rapid peak in the serum drug level. The and a longer duration of action when time to onset of analgesia depends upon compared with other commonly used the rate at which the opioid is able to opioids. The level of analgesia from diffuse from plasma to the CNS, where morphine does not closely parallel mor- binding to specific analgesia opioid phine's serum concentration because of receptors occurs. The major factor a time lag between the concentration at determining the diffusion of the opioid the opioid receptor and in the serum. from the plasma to the CNS is the By contrast, more lipophilic drugs, such drug's lipid solubility. Table 16.1 lists as meperidine and fentanyl, diffuse into the opioid analgesia time profiles fol- and out of the CNS quickly and their

Page 134 Chapter 16 ~c;tePain Management

Table 16.1: Tlme profiles for the cIlnlcal effects of 1.v. PCA oplolds.

Drug Onset (mins.) Peak Effect (mins.) Duration (mins.) Morphine 3-6 20 - 30 40 - 60 Meperidine 2-4 8 - 12 20 - 30 Fentanyl 1-2 4 - 6 6 - 10 Alfentanil < 112 1-2 3-5

plasma levels reflect the opioid receptor PCA PARAMETERS: level concentration and their clinical effect. There are five parameters that define PCA therapy: In summary, i.v. PCA has the following advantages over im. opioid injections The Loading Dose: This is gen- for pain control: erally reserved for patients requiring immediate pain medication. Admin- 1. Rapid onset of analgesia. istration of small bolus doses will 2. Eliminates wide fluctuations in take too long to achieve the required plasma opioid concentrations that plasma concentrations because of follow im. administration (fewer the lockout interval. A typical load- side effects with better pain control). ing dose is 0.1 - 02 mg/kg for mor- 3. Accommodates patient variability in phine, administered over 10 to 20 opioid dose requirements. minutes. Most postoperative 4. Accommodates changes in opioid patients will have received narcotics requirements during the recovery during their procedure and will not period. require a loading dose when PCA is 5. Patients benefit psychologically started after their surgery. when they have control over pain. 6. Avoids painful im. injections. 2. The Bolus Dose: This is the 7. Decreases the risk of accidental amount of opioid delivered to the needle-stick injury to health care patient when the patient presses the providers. PCA demand button requesting pain 8. Improves patient-nurse relations. medication. This should be large (The patient regards the nurse as a enough for patients to perceive an professional who is helping them analgesic effect, but not so large optimize PCA use, rather than that the therapeutic window is someone who is withholding pain exceeded (resulting in side effects). medications). For morphine, a typical bolus dose 9. May decrease morbidity and allow is 1 mg (range 05 - 2 mg); for for earlier discharge from hospital. meperidine 10 mg (range 5 - 20 mg).

** Must Know Should Know Page 135 AnaMhesia for Medical Students

3. The Lockout Interval: The Maximum 4 hour Limit: Like PCA pump is programmed to the infusion parameter, this para- deliver another bolus dose only after meter is also not essential, but may a specified period of time (called the be set at the physician's discretion. lockout interval) has elapsed since It provides an extra safeguard the last bolus dose. If a patient against a programming error, which presses the button before the lockout may occur while setting up the PCA interval has elapsed, a demand delivery system. request will be recorded, however, no drug will be delivered. This By specifying the bolus dose, lockout allows time to elapse for the bolus interval and infusion rate, the physician dose to have an effect (see table has already restricted the patient in the 16.1). Typical lockout intervals are total amount of drug available each 5 to 10 minutes. hour. Example: Morphine bolus 1 mg, lockout interval 5 minutes, and an infu- 4. Continuous Infusion: In addition to sion rate of 0.5 mg per hour, restricts giving the patient a bolus of nar- the patient to a maximum of 12.5 mg cotic when requested, a continuous per hour. Specifying a maximum 4 hour iv infusion can be also be adminis- limit allows the physician to set a lower tered (ordered as PCA + continuous limit that can be delivered to the patient infusion). Typical infusion rates for during this period. If one contrasts this morphine (and for meperidine,) are with typical im. orders of 75 - 12.5 mg 0.5 - 1.0 mg per hour and 5 - 10 mg of morphine every 3 - 4 hours p.r.n., it per hour. There is debate over the is easy to see why patients on i.m. benefits of a continuous infusion narcotics may have inadequate pain with PCA. Proponents of this tech- control. nique argue that it prevents patients from waking in the night with severe pain because they have not received pain medication for several After the first or second postoperative hours. Still, studies show no clear day, the decision to add oral analgesics benefits of a continuous infusion is based on the following consider- over PCA alone. A continuous ations: infusion places these patients at risk of respiratory depression and other 1. The patient is off a continuous PCA complications of excess opioid use. infusion. When used in the early post- 2. The patient is requesting 2 or less operative period, we recommend PCA boluses every 4 hours. that the infusion be discontinued 3. The patient is having no or minimal (PCA mode alone) as soon as the pain at rest, and patient's bolus demands decrease to 4. The patient is able to ambulate and to 2 per four hours. tolerate oral fluids. Chapter I6 Acute Pain Management

Oral analgesics such as acetaminophen brain barrier is bypassed and superior with codeine (Tylenol # 3" 1 - 2 tablets analgesia may be obtained by contrast po. every 3 - 4 hours prn) should be to narcotics administered by the i.v. or started and used as the first line anal- i.m. narcotic routes. The intrathecal gesic, and the PCA used for any addi- administration of 0.2 mg of morphine tional breakthrough pain requirements may provide excellent analgesia for up (Table 163). The PCA can be discon- to 16 hours after a total hip (replace- tinued once the patient is requiring ment) arthroplasty. A similar patient minimal PCA bolus doses and tolerating treated with i.v. PCA morphine may the oral analgesics. The average patient require a total of 60 mg of morphine for having major surgery requires PCA the same initial period, and still have therapy for 2 - 3 days. inferior pain relief as compared to the patient who received spinal narcotics.

Subarachnoid and epidural opioids are Within the superficial layers of the active at both the spinal cord level and substantia gelatinosa, located in the at higher CNS levels. A portion of the dorsal horn of the spinal cord, exists a opioids administered in the intrathecal dense population of opioid receptors. space at the lumbar level will migrate Their activation results in a decrease in along with the CSF circulating back to the release of neurotransmitters, such as the brainstem. As with parentally (i.v., substance P, and a decrease in trans- or i .m .) administered narcotics, high mission of painful stimuli from concentrations of narcotics at the brain- peripheral pain fibers at the level of the stem level can result in respiratory spinal cord. depression, sedation, nausea, vomiting and puritis. The concentration of the The direct administration of opioids into narcotic in the spinal fluid decreases the CSF by a spinal needle is referred to with the distance it migrates. The as an intrathecal opioid injection. The greater the opioid's lipid solubility, the anaesthetist usually adds the opioid to more is taken up at the spinal cord the spinal local anaesthetic administered level. Consequently, less drug migrates prior to surgery. This results in a very to the brainstem. Morphine, for high local concentration of opioid with- example, has a low lipid solubility, and in the CSF. The opioid diffuses readily hence, has a greater tendency to migrate to the opioid receptors located within towards the brainstem as compared with the substantia gelatinosa, to provide meperidine or fentanyl, which have analgesia at the spinal level (figure higher lipid solubilities. 163). Hence, this technique selectively targets opioid receptors responsible for regulating pain transmission at the spinal level. The placement of an epidural catheter, in the epidural space permits a continu- By using the intrathecal route, the blood ous infusion, or repeat administrations,

Must Know Should Know Page 137 ) Anaesthesia for Medical Shrdenrs 1 of analgesics and local anaesthetics for matory drugs may also inhibit several days. Dilute concentrations of prostaglandins that are involved at the local anaesthetic may be combined with spinal cord level in the creating a state epidural opioids in an attempt to exploit known as central h yper-sensitization. In the analgesic properties of both. this case their anti-prostaglandin effect Epidural morphine has been used clini- of NSAIDs mitigate this hypersensitivity cally since 1980 and is now used com- state, thereby decreasing the perception monly to control acute severe pain. of pain.

NON OPIODANALGESICS FOR ACUTE PAIN: Table 16.3 Contraindications to NSAIDs*+ The non steroidal anti-inflammatory b Allergy to ASA, or other drugs (NSAIDs) are the most frequently NSAID. Relative contraindi- used analgesics for acute pain. They cation when there is a history include drugs such as aspirin, ibuprofen, of asthma, nasal polyps, or indomethacin, naproxen, and many angioedema. more. One new drug in this class, b Renal insufficiency recently introduced in North America, is Congestive heart failure ketorolac (Toradol?. Extensive experi- Peptic ulcer disease ence with this drug in Europe and b Active inflammatory bowel Australia for acute postoperative pain disease control, has documented what appears to b Pregnancy or lactation be an acceptable patient safety profile. Bleeding disorders One of the major advantages of ketorolac is its ability to be given both orally, and parentally. This has an obvious advantage in postoperative patients who are unable to take oral When considering using NSAIDs for medications, yet are experiencing nar- acute pain management, physicians cotic side effects despite poor pain should review their contraindications control. and potential side effects (see table 16.3). When indicated, NSAIDs may be When tissues are traumatized they prescribed for short tern therapy (less release peripheral inflammatory media- than 4 - 5 days) as an adjunct to acute tors which sensitize and stimulate perip- pain management. For examples of heral nociceptors. Non steroidal anti- typical regimens using NSAIDs in man- inflammatory drugs inhibit the enzyme, aging acute and chronic pain states see cyclooxygenase, which is involved in Table 16.2. the production of many of these inflammatory mediators, through the arach- In patients for whom NSAIDs are con- nidonic acid pathway (e.g., prosta- traindicated, acetaminophen can be an glandin E2). Non steroidal anti-inflam- effective alternative. Since it has only

Page 138 I Chapter 16 Acute Pain Management

' Indomethacin (Indocid@) 25 - 75 mg po q8hrs Start with 25 mg q8hrs ' 50 - 100 mg pr supp. Max. 200 mglday ) Ibuprofen (~otrin) 400 - 800 mg po q 6-8 hrs Ketorolac (Torado19 10 mg po q 4-6 hrs Max. po 40 mglday j 10 - 30 mg im q 4-6 hrs Max. im 120 mglday )

Trlcycllc Antldepressants (TCA's)

Amitriptyline (~lavil9 25 - 100 mg qhs Use with caution in Irnipramine (Tofranil? 25 - 100 mg qhs patients with glaucoma or Doxepine HCL (~ine~uan?25 - 100 mg qhs urinary retention.

Corn blna tlons

Acetaminophen t Codeinev 1 - 2 tabs po q 4-6 hrs

'+(Tylenol' # 12, and 3 contain 300 mg acetaminophen t 15mg caffeine t 8,15, and 30 mg of codeine per tablet. Tylenol # 4 contains acetaminophen 300 mg, no caffeine, and 60 mg of codeine per tablet.)

Narcotics Agonlst - Antagonlst

Pentazocine HCL (Talwin9 50 - 100 mg po q 4hrs Useful in patients Pentazocine Lactate (Talwin? 30 - 60 mg sc, im, iv q 4hn who cannot tolerate codeine.

Oplolds

Morphine Sulfate 15 - 30 mg po q4hrs Morphine 5 - 15 mg im, sc q4hrs Meperidine HCL @emerol@) 50 - 150 mg po, im, sc q 3 - 4 hrs Codeine 30 - 60 mg po, im q3 - 4 hrs

Table 16.2 Opioid and adjuvant medications commonly used to treat acute or chronic ) pain. Non steroidal anti-inflammatory medications are useful in patients who ,J experience side effects from opioid pain medications. The generic drugs listed are accompanied by examples of common trade names in brackets.

** Must Know * Should Know Page 139 Anaesthesia for Medial Studen~s

weak peripheral inhibiting effects on Cognitive and behaviour interventions prostaglandin synthesis, it lacks the side may influence a patient's pain experi- effects and contraindications listed ence. Useful techniques in managing above for NSAIDs. Still, acetamino- pain include: phen strongly inhibits central prostaglandin synthesis, which accounts for its 1. Education and instruction. analgesic and antipyretic effects. One 2. Relaxation exercises. common postoperative problem is head- 3. Imagery. aches. While a multitude of etiologies 4. Laughter. may be responsible for postoperative 5. Music distraction. headaches (including caffeine with- 6. Biofeedback. drawal), acetaminophen (325 - 650 mg 7. Conversation with family, friends, pa. or par. every 4 - 6 hours) is gen- medical personnel. erally effective, while narcotics are often ineffective. Physical agents useful in alleviating pain include: NONPHARMACOLOGICAL INTERVENTIONS 1. Applying of heat or cold. FORACUTE PAINMANAGEMENT: 2. Massaging, exercising, and stretching. 3. Transcutaneous electrical nerve stim- Anaesthesiologists are physicians who ulation (TENS). specialize in applying their knowledge 4. Acupuncture. of pharmacology and physiology to anaesthesia and analgesia. This chapter has focussed on pharmacological mechanisms and interventions in the management of acute pain. Still, there exist References: other alternative means of pain control that can be employed successfully by 1. Clinical Practice Guideline. Acute themselves or in conjunction with the pain management: Operative or pharmacologic interventions outlined in medical procedures and trauma. U.S. this chapter. Department of health and human services. 1992. Patients have unique responses to pain. This varies according to such factors as 2. White P.F. Use of PCA for man- their emotional and cultural back- agement of acute pain. JAMA grounds, and previous pain experience. 259:(2) 243-7; 1988. Clinicians should anticipate that patients who use opioid analgesics regularly, 3. Austin K.L. et al. Multiple intra- will have increased analgesic require- muscular injections: a major source ments in the perioperative period (nar- of variability in analgesic response to cotic tolerance). meperidine. Pain 8: 47; 1980.

Page 140 Chapter I6 Acute Pain Management

4. Laurito C.E. Recent developments in postoperative pain management. Curr Rev Clin Anesth 12(5) 37-44, 1991.

5. Lubenow T.R. et al. Management of acute postoperative pain. Clin Anesth UPDATES: Vol 3; No.4, 1992.

6. Cousins N. Anatomy of an illness as perceived by the patient. Bantam Books New York, N.Y. 1979.

Notes:

** Must Know Should Know Page 141 \ / Anaesthesia for Medical Students \ / Notes: )tima te dia tients or9:2 Chronic Pain sh del agnos age i 71d .ute p LINDAROBINSON M.D., FRCPC cute F ~ssiblc ~t the: left leg amputated below the hip after a :uralg Chronic pain induces a cascade of combat injury in Korea in 1952. On arcoti changes in the patient involving physi- entering his room, you find a man 'f the cal, emotional and psychosocial distraught, diaphoretic and complaining etter changes. These combine with neural of severe pain in his left lower leg and mporr imprinting in the CNS to greatly influ- foot. Anxious to get some hands on e ris ence the perceived severity and the experience, you proceed to examine the lfiltra consequences of the ongoing pain. affected limb, only to find that you are lesthe more than 40 years late! Is Mr. Ross red s Chronic pain is defined as "an unpleas- faking his pain? How can he be having .chnic ant sensory and emotional experience pain in a leg that he doesn't have? :ian. associated with actual or potential tissue damage, or described in terms of such Corporal Ross has a condition known as

I the ( damage". International Association for "phantom limb pain". Phantom limb :quire the Study of Pain (IASP) 1979. pain, post herpetic neuralgia, and rylenc trigeminal neuralgia are examples of till, This chapter will focus on five common central pain states. Unlike pain which epres: chronic pain syndromes. we have all experienced secondary to iscuss mechanical, chemical or thermal injury, ve. I. Post Herpetic Neuralgia this form of pain arises within the cen- i ndro 11. Causalgia tral nervous system. In these states, litiate 111. Reflex Sympathetic Dystrophy trauma, infection, or other conditions IV. Myofascial Pain Syndromes have damaged nerve tissue, resulting in i tric) V. Low Back Pain abnormal activity in the intermediate sed a! afferent neurons in the CNS (see figure erpeti While similar nociceptive pathways and 16.1 chapter 16). The patient perceives lust stimuli described for acute pain in chap- real pain is occurring even though there ffects ter 16 are also active in chronic pain, is no nociceptive stimulation. Iderlj there are distinct differences between used, acute and chronic pain disorders. To Altered sleep habits, inability to concen- etenti examine these differences, let's look at trate, inability to function (work, recre- ntichc the example of Corporal Robert Ross, ation), as well as depression, and abnor- whom you are asked to see on your mal behavioural coping mechanisms are medical rounds. Corporal Ross had his common sequelae of chronic pain states.

1 ** Must Kttow Should Know Page 143 inaerthesia for Medical Students )

described as the worst pain they have ever experienced in their lives and the l"o address the diagnostic and thera- unremitting nature of the pain is very leutic complexity of chronic pain condi- demoralizing and can lead to suicide in :ions, multidisciplinary clinics have extreme cases. Normally the total dur- been established involving individuals ation of the disease is between 7 to 10 with a specific interest in these dis- days, with the skin returning to normal orders. These units commonly staff within 2 to 4 weeks. anaesthesiologists,psy chologists, nurses and occupational or physical therapists. The most debilitating complication of In addition, they have direct access to herpes zoster is the development of post medical and surgical specialists, and herpetic neuralgia. While this complica- various diagnostic services. tion is extremely uncommon in young individuals, it occurs in 50% of patients over the age of 50 with zoster. Typical- ly the patient experiences gradual im- Acute Herpes Zoster (shingles) is a provement over several weeks. How- mononeuropathy caused by the reactiva- ever some patients may be left with a tion of the Varicella-Zoster virus chronic life long neuralgic pain. After (VZV). Varicella is commonly known about 6 - 8 weeks, the pain of herpes as chicken pox. This extremely con- zoster is called Post Herpetic Neuralgia. tagious infection is usually seen as a The chance of a patient developing post benign illness in childhood. The VZV herpetic neuralgia increases steadily may lie dormant in the dorsal root gan- with age. glion for decades. When reactivated it presents as pain followed by a vesicular rash in the dermatomal distribution of the dorsal root ganglia involved. The Various treatments may be considered disease presents as dermatomal pain for herpes zoster, although none is en- which precedes the rash by 2 - 3 days. tirely satisfactory. The acute Herpes The rash is a maculopapular rash which Zoster can be treated with an antiviral evolves into vesicular lesions. The viral agent such as Acyclovir (Zovirax@), but reactivation causes an acute to be of any help this agent must be hemorrhagic inflammation with demye- initiated immediately upon making the lination and axonal degeneration. The diagnosis. Unfortunate1y, Acyclovir damage to the nerve and root is perma- treatment is very expensive; a typical nent and of variable severity. course can run over $1000. Even though it may shorten the acute phase These patients suffer with constant of H.Z. and result in lesions healing severe burning pain. The area is ex- earlier, there is no evidence that it pre- quisitely painful and they cannot bear vents post herpetic neuralgia. even allowing their own clothes to touch them. This is frequently

Page 144 Chapter I8 Chronic Pain

Optimal treatment depends upon accu- (dilantinQ), and carbamazepine (teg- rr~tediagnosis. Frequently, however, retolQ) have also been used with some pi~ticntspresent with pain before the success. Capsaicin (zostrix@) cream is a rr~shdevelops, resulting in an incorrect relatively new treatment designed spe- dingnosis. Common diagnosis at this cifically for this problem. It contains ~lilge include myocardial infarction, capsaicin which depletes the nc.ute prolapsed disc, and kidney stones. neurotransmitter substance P in the Ac.utc pain should be treated as soon as peripheral nerve endings and results in 1)o~sihle.Physicians often use narcotics, a decrease in nociceptive information. lbut these are less effective for treating 1lc.urr11gicpain than other pain disorders. Some patients respond well to Narcotics may, however, 'take the edge' transcutaneous electrical nerve stimula- 01'1'thc pain and make it more tolerable. tion (TENS), which is particularly use- I!c.lt(.r still, nerve blocks can provide ful in elderly patients because it has few I~.III~II)IHIY or permanent relief without side effects. By stimulating the large 1111- risk of the narcotic dependency. diameter nerve fibres, smaller fibres I~~l'iltratingthe area with a dilute local carrying painful stimuli at the level of 1111c.sl11cticand steroid has also been the dorsal horn are inhibited, according IIN~:~.~ucce~sfuIIy, and requires little to the Gate theory of pain. Ie-c'll~lic~Iskill on the part of the phys- i(~ii111. Mexilitene HCL, an oral lb anti arr- hythmic with properties similar to lido- III tllc chronic phase some patients still caine, has also be used to alleviate this rrcl~~ircacetaminophen with codeine form of neuralgic pain. Despite utiliz- ('l'ylcnol No. 39 or a stronger narcotic. ing all these modalities, post herpetic Still, other drugs (tricyclic anti- neuralgia sometimes remains resistant to clrl)rcssants (TCAs) and anticonvulsants, medical treatment. cliscusscd below) are usually moreeffec- livt:. As with the other chronic pain sy~~clromcs,the sooner treatment is i~~ilistcd,the more effective it is. Causalgia is a painful disorder associated with injury of the peripheral A tricyclic antidepressant is frequently nerves. In 1864, Wier Mitchell pres- ~INC~HS a first line drug in treating post ented a treatise entitled, "Gunshot I~c!rpcticneuralgia. Nevertheless care wounds and other injuries of nerves". 111ust be taken to monitor for side In this paper he describes an injured c.l'l'ccts. These patients are frequently unionist soldier as follows: c:ldcrly, and prone to becoming con- I't~scd, dizzy, or developing urinary In our early experience of nerve wounds, we rc.tcntion as a result of the met with a small number of men who were ll~~licholinergicactivity of TCA's. suflering from a pain which they described as 'burning' or as 'mustard red-hot' or as a A~lticonwlsants such as phenytoin 'red hot file rasping the skin' .... it never attacks the trunk, rarely the arm or

" Must Know Should Know Page 145 1naestlresia for Medical Students

'high.... its favoured site is the foot or out treatment most patients progress to band .... the part itself becomes exquisitely develop irreversible trophic changes in hyperaesthstic, so that a touch or a tap of the affected limb. The lower incidence the figer increases the pain. Exposure to of these changes among Vietnam Vet- the air is avoided by the patient with a care erans (1.5%) compared to WW 11 Vet- which seems absurd, and most of the bad erans (5 - 10%) is probably due to the cases keep the hand constantly wet, finding more rapid treatment of injuries with relief from the wet ...As the pain increases the temper changes and grows irritable, and early debridement in Vietnam. the face becomes anxious, and has a look of weariness and suflering. The sleep is rest- Causalgia usually involves the median, less.... and exasperates the hyperaesthetic sciatic or brachial plexus nerves, state so that the rattling of a newspaper, a because they carry the bulk of sensory breath offresh air, the step across the ward, and sympathetic fibres. Nevertheless, or the shock of the feet in walking, gives rise identical syndromes have developed in to increase of pain. patients suffering trigeminal, occipital, and intercostal nerve injuries. Mitchell, provides a classical description of the deep red, glossy, and mottled trophic skin changes that characterize this pain syndrome. He used the term "causalgia" to describe these changes. Most patients develop causalgic pain World wars I and I1 left many soldiers within a week of the injury. They ex- with these traumatic causalgic pain perience a burning superficial pain in disorders. Since then, centres studying the periphery of the extremity, most these peripheral nerve injuries note that intense in the fingers and palm, or toes victims of high velocity missile injuries and sole. The pain is so intense and involving the brachial plexus or sciatic persistent, it overwhelms patients, pro- nerve plexus, are at risk of developing hibiting rest, sleep, and resulting in this chronic pain disorder. profound psychological disturbances.

The pain is aggravated by a variety of One study, using the McGill Pain Ques- physical and emotional factors frequent- tionnaire, found a rating scale of 42 (out ly leading to profound emotional, physi- of 50) in causalgia, as compared to 25 cal and behaviourial disturbances. In for phantom limb pain, 26 for back pain the late stages of the disorder, and cancer pain, and 23 for Post vasomotor (circulatory) and sudomotor Herpetic Neuralgia (see figure 17.1). (sweat gland) changes accompany Two thirds of patients also describe a trophic skin changes. deep, intermittent stabbing, tearing, or crushing pain. If the sympathetic nerves to the affected limb can be interrupted soon after the Initially, the pain is located in the gen- injury, prompt and complete relief of eral territory of the nerve, but as the the pain can be obtained. Occasionally, syndrome progresses it spreads to spontaneous remission occurs, but with- Chapter 18 Chronic Pain ' involve areas well beyond the affected Trophic changes develop and the ) nerve's distribution. affected part becomes red and glossy with denuded skin, tapering digits, and ) Passive movement of the part, light coarse rigid nails. The small interphal- ) touch, loud noises, or emotional out- angeal joints stiffen and become fixed, ) bursts aggravate the pain. Even clothes muscles atrophy and eventually develop or bed sheets are unbearable, and contractions. The trophic changes can ) patients go to any length to avoid mov- be avoided if treatment is instituted ) ing the part. within 1-2 months of the injury.

,) ,) SENSORYAND MOTOR Psychologically, the individual may 1 DISTURBANCES manifest bizarre behaviourial changes, ) with limb guarding, and seclusion. Allodynia (see glossary of terms at the These changes are reversible if the pain ) end of the chapter) to touch and tern- is treated adequately. ) perature develop as does hyperpathia. Vasodilation occurs early followed by Treatment options clinicians utilize for ' vasoconstriction. this disorder include:

EComparison of Pain Scores

Figure 17.1: Comparison of pain scores of common pain conditions using the McGill Pain Questionairre. Modified with permission from Melzack R. Psychological aspects of pain: implications for neural blockade. In Neural blockade. Cousins MJ, Bridenbaugh PO. (eds) 2nd edit. J.B. Lippincott Co. 1988.

Page 1.47 ) ** Must Know * Should Know lnacsthcsia for Medical Students

. Sympathetic blockade with local cal sympathectomy for these anaesthetics or other agents (see la patients, in the hope of effecting a and lb below). This is frequently permanent cure. Unfortunately, useful as a diagnostic tool, how- surgical sympathectomy is not ever, patients who fail to respond always successful, and the pain may have a condition called "Sym- may recur. pathetic Independent Pain". 4. Others modalities that have proved la. Local anesthetic blocks of either useful in treating this condition the stellate ganglion (for the arm), include TENS, dorsal column or the lumbar sympathetic plexus stimulation, physical therapy, and (for the leg). psychotherapy. lb. A "Bier Block" (see chapter 16, figure 16.4) with iv guanethidine or reserpine has also been used to produce a localized sympathectomy. Reflex sympathetic dystrophy (RSD) is a term for a variety of conditions in- These blocks must be repeated to cluding: minor causalgia, post traumatic achieve lasting effect. Guanethidine pain syndrome, Sudeck's atrophy, and displaces norepinephrine from stores in shoulder hand syndrome. the sympathetic nerve endings and also prevents the reuptake of norepinephrine. The precipitating factors include acci- This results in the loss of sympathetic dental or surgical trauma, and a variety adrenergic nerve function for days or of disease states. Pain, vasomotor weeks. changes, autonomic disturbances, delayed recovery of function and trophic 2. Oral alpha 1 adrenergic blockers, changes characterize RSD. Early treat- such as phenoxybenzamine, can be ment with sympathetic interruption used as a means of decreasing the results in pain relief and reverses the excessive sy mpathetic barragepres- pathophysiological abnormalities. ent in causalgic pain disorders. Side effects are nausea and postural Compared to causalgia, a reflex sym- hypotension. pathetic dystrophy is a more common outcome of orthopaedic injuries and 3. Chemical sympathectomy may be industrial accidents. Hence, it must be created by the administration of promptly recognized and treated. local anaesthetics or other agents (see la, lb). If a chemical The most common cause of RSD is sy mpathectomy is effective in pro- trauma (e.g., sprains, dislocations, frac- viding temporary relief, the tures, crush injuries, and lacerations). clinician may recommend a surgi- There is no correlation between the

Page 148 1 Chapter 18 Chronic Pain

) severity of original injury and the devel- TREATMENTOF RSD *: ) opment of RSD. Even a Colles fracture ) resulting in a minor peripheral nerve Original injuries should receive proper injury can result in RSD. and rapid treatment (including removal ) of foreign bodies, immobilization, repair ) Reflex sympathetic dystrophy is one of muscles and tendons, and pain relief) complication of common surgical pro- in the hope of preventing the subsequent ) cedures (e.g., amputations, excision of development of RSD. ) ganglia, tight casts, carpal tunnel , release). It may also be due to an un- Treatment modalities include the early derlying medical condition such as a use of sympathetic blocks, physiother- ) myocardial infarction (shoulder-hand apy, psychotherapy, medical therapy ) syndrome), or diabetes (diabetic (eg. phenoxybenzamine, prednisone), neuropathy). Direct nerve compression and, when these fail, a surgical ) from a herniated disc, tumours of spine, sy mpathectomy. ) or metastases compressing the branchial ) plexus may also result in RSD. IV: MYOFASCIALPAIN SYNDROME *

In contrast with causalgia, where pain This chronic pain syndrome comprises ) develops rapidly, the pain of RSD de- a large group of muscle disorders char- velops over weeks or months after the acterized by the presence of h ypersensi- injury. tive points (called trigger points) producing pain, muscle spasm, tenderness, The criteria for a diagnosis of RSD are: stiffness, and weakness. ) ) 1. There is a history of recent or Various terms such as fibrositis, fibro- , remote accidental or iatrogenic myositis, and muscular rheumatism have trauma or disease. been used to describe the myofascial 1 pain syndrome. The condition is most ) 2. The patient complains of a persist- commonly misdiagnosed as bursitis, ent pain that is burning, aching or arthritis, visceral disease, or a herniated ' throbbing. disc. i One or more of: Trauma to the myofascial structures and ) 3. a. vasomotor/sudomotor changes an acute overload on the affected b. trophic changes, edema, hyper- muscles is the most common cause of ) sensitivity to cold this syndrome. Acute muscle strain c. muscle weakness, or atrophy damages the sarcoplasmic reticulum i releasing excessive amounts of calcium. ) 4. Relief of symptoms is obtained This initiates a complex cascade of 1 after regional sympathetic block- events beginning with local vasocon- ade. striction,sustainedmuscularcontraction, i decreased blood flow, increased metab-

1 " Must Know * Sltould'Know Page 149 ~aesthesiafor Medical Students

ism, and culminating in the release of An acute episode of myofascial pain :rve sensitizing substances. In the often follows overuse of unconditioned Tfected areas, taut muscle bands may muscles (e.g., the weekend athlete), :palpable and are referred to as trigger poor posture during prolonged activities ~ints. Pain from myofascial trigger such as computer work, or automobile oints (TP's) is described as steady, accidents (whiplash). eep, and aching. The pain may be xacerbated by stretch, cold, stress, Patients present with persistent pain, atigue, viral illnesses or direct pressure. tight or aching muscles, limited range of

'able 17.1 Comparison of Causalgia and Reflex Sympathetic Dystrophy. I I I 1 Causalgia I RSD I Onset Within 1 week Over weeks to months 1 I Frequency I Rare ( More common I Etiology Typically involves high Accidental injuries, surgical velocity injuries of the trauma, orthopaedic injuries brachial or sciatic nerve (e.g., sprain, fracture, tight cast, plexus (e.g., gun shot dislocation). wounds). Pain Similar pain characteristics, typically described as a constant Characteristics burning, throbbing, or aching pain. Disturbed sleep, and profound psychological-behavioural changes are more common with causalgia. The affected limb is guarded, and becomes cool, pale or cyanotic, accompanied by decreased hair growth, muscle atrophy, tendon contracture, and joint ankylosis. Causalgia is generally recognized as the most intense form of chronic pain, and has a McGill Pain Score average of 42/50 (see figure 17.1). Prevention Early treatment of the injury with debridement, repair and immobilization of associated fractures.

Treatment Sympathetic blocks: Stellate ganglion block (arm), Lumbar sympathetic block (leg) Guanethidine intravenous Bier block (see figure 15.4) Alpha-1 adrenergic blockers (e.g., phenoxybenzamine) Other: Physical therapy, psychotherapy, TENS, dorsal column stimulation, surgical sympathectomy. Chanter 18 Chronic Pain

I motion and generalized fatigue. They V: Low BACK PAIN* ) may experience continuous or intermit- ) tent muscular pains, aches or a burning Low back pain is one of the most com- sensation in the overloaded muscles. mon problems our society faces. Sixty ) Applying direct pressure on these trig- to eighty percent of all adults will suffer ) ger points exacerbates the pain. Predict- with this at least once during their life- able patterns of pain associated with time. The pain is usually self limited. specific TP's do not follow a derma- Of those who see their doctor, more ) tomal distribution. than 90% will improve and are back to work within 2 months. However, the ) For effective treatment, the pain and remaining 5-10% pose a challenging ) spasm cycle must be interrupted. The problem. ) TP can be injected with local anaesthetic, or the overlying skin Risk Factors for low back pain include: sprayed with a vaporized coolant. Increasing age ) These treatments should be followed by Heavy labour ) stretching of the affected muscle groups. Lower education and income Smoking ) Patients are frequently in poor physical Obesity ) condition and should slowly but meth- Whole body vibration (truck driver) odically undertake a program of pro- Previous back pain ) gressive daily physical fitness. This ) should include aerobic exercises, such A host of clinical entities have been as walking, exercise biking, swimming, described to explain the various types of low impact aerobics and aqua fitness. low back pain, such as muscle strain, ) Physician's may motivate patients by degenerative disc disease, facet syn- ) reminding them that this is the most drome, and myofascial pain syndrome. important aspect of their treatment. However, the signs, symptoms and ) radiological findings of these conditions ) These patients frequently have very overlap, making an accurate diagnosis poor sleep patterns. Tricyclic antide- difficult. For example, a patient who, ' pressants in low doses will improve on clinical examination, appears to have ) sleep and decrease the level of muscular facet joint pain and degenerative disc ) pain (possibly by increasing serotonin disease, may nevertheless have similar levels). Cyclobenzaprine HCL radiological changes to other patients ) (Flexeril? is also commonly used as a who are entirely asymptomatic. ) 'skeletal muscle relaxant'. As this tends to be a chronic condition, narcotics Low back pain is usually not an emer- ) should be avoided due to the risk of gency. Occasionally, conditions* * do i opioid dependence. Plain acetamino- present as low back pain and may have phen can be used instead. dire consequences for a patient should the clinician fail to make the correct diagnosis.

Sliould Know Page 151 naesfhesia for Medical Sludenfs

~ ------Table 17.2: Causes of Low Back Paln

(Nlnety percent of all cases of back paln are due to "medlcal causes") Medlcal Condltlons Musculoskeletal: Inflammatory: Muscle 'strain' Ankylosing spondylitis .Ligament 'sprain' Psoriatic spondylitis Apophyseal joint: 'facet syndrome' Reactive arthritis Discs: 'degenerative disc disease' Inflammatory bowel disease Bone: fractures, spondylolisthesis Metabolic: Neoplastic: Osteoporosis + fractures Benign: osteoid osteoma Osteomalacia Malignant Paget's disease of the bone Primary: Multiple myeloma Secondary: Metastasis Visceral: Pelvic organs Infectious: (endometriosis, prostatitis) Acute: pyogenic discitis, osteomyelitis Renal disease (pyelonephritis) Chronic tuberculosis Gastrointestinal disorder (pancreatitis, peptic ulcer) Aortic aneurysm

Surglcal Emergencies** (see text) Cauda Equina Syndrome (disc herniation, tumor mass, abscess) Aortic aneurysm (leaking, dissecting, ruptured)

Sclatlca wlth Neurologic Signs** Ruptured intervertebral disc Spinal stenosis

For example, the cauda equina syn- ency and rapid decompression of the drome presents as a constellation of spinal cord is needed to avoid perma- symptoms and signs such as a neurolog- nent nerve damage. Causes of cauda ic deficit in the lower extremities (par- equina syndrome include central disc alysis and loss of sensation), loss of herniation, and epidural tumours or bowel or bladder continence, weakness, abscesses. depressed reflexes, and loss of sensation over the buttocks called "saddle An aortic aneurysm may present as anaesthesia". This is a surgical emerg- back pain and may require immediate Cha~ler18 Chronic Pain

) surgical attention. Sciatica is usually Osteo-myelitis may require antibiotics ) caused by a herniated disc or by a nar- and drainage. Arthritis requires specific row spinal canal with compression of treatment for the underlying disease. the nerve roots (spinal stenosis). The ) patient experiences pain that radiates Mechanical low back pain is managed ) below the knee. A herniated disc tends with a several days of rest, oral anal- to be aggravated by prolonged sitting, gesics, NSAID's, and then mobilization. ) or anything that increases intrathecal Chronic low back pain is frequently ) pressure (eg. sneezing, or coughing). difficult to treat and requires a gradual Paresthesia and weakness may be exper- program of aerobic conditioning, ) ienced in the involved nerve root dis- physiotherapy, tricyclic antidepressants, tribution. psychotherapy and education about proper back care. ) Spinal stenosis is more common in ) patients over 60 years of age. Charac- ) teristically, these patients complain of pain in the buttocks, thighs and legs, Allodynla: Pain due to a stimulus ) which develops on standing and walk- that does not normally provide pain. ) ing, and is relieved by 15-20 minutes of ) rest. Patients find that walking with the Analgesla: Absence of pain in trunk flexed is more comfortable. response to stimulation that would normally be painful. ) Other medical causes presenting as sciatica include tumours, infection, and Causalgla: A syndrome of sus- ) arthritis. tained burning pain, allodynia, and ) hyperpathia after a traumatic nerve ) Conservative treatment of sciatica with lesion, often combined with vasomotor rest, analgesics, nonsteroidal anti in- and sudomotor dysfunction and later ) flammatory medications, muscle relax- trophic changes. ) ants, or epidural steroids is usually sufficient, (provided other more serious Dysesthesla: An unpleasant abnor- ) conditions have been excluded - see mal sensation, whether spontaneous or ) Table 17.2). Surgery is indicated if evoked. persistent disabling pain occurs or the ) neurologic deficit increases despite H yperalgesla: An increased response ) conservative measures. to a stimulus that is normally painful. ) The treatment of 'medical back pain' Hyperesthesla: Increased sensitivity to ) should be specific to the medical condi- stimulation, excluding the special ) tion. A tumour with metastasis to the senses. spine may require surgical intervention, chemotherapy or radiotherapy. Hyperpathla: A painful syndrome, i characterized by increased reaction to a

) ** Must Know Should Know Page 153 naesfhesia for Medical Students timulus, especially a repetitive stimu- us, as well as an increased threshold.

-lypoalgesia: Diminished pain .esponse to normally painful stimulus.

Hypoesthesia: Decreased sensitivity to stimulation, excluding the special senses.

Neuralgia: Pain in the distribution of a nerve or nerves.

Neuritis: Inflammation of a nerve or nerves.

Neuropathy: A disturbance of function or pathological change in a nerve; in one nerve, mononeuropathy; in several nerves, mononeuropathy mul- tiplex; if diffuse and bilateral, poly- neuropath y.

Nociceptor: A receptor preferential- ly sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged.

Paln tolerance level: The greatest level of pain that a subject is prepared to tolerate.

Pain threshold: The least experience of pain that a subject can recognize.

Paresthesia: An abnormal sensation, whether spontaneous or evoked.

Page 154 Obstetrical Anaesthesia

ROBERT ELLIOTMD FRCPC

This chapter will focus on the following 11: Suplne Hypotenslve Syndrome**: four topics: The gravid uterus may compress the 1. The physiological changes of preg- inferior vena cava (IVC), and/or the nancy and their clinical signifi- aorta when the parturient lies in the cance. supine position. This occurs in approxi- 2. The importance of the supine mately 15% of patients as early as the hypotensive syndrome and aorto- 20th week, and increases in frequency caval compression. in the third trimester. 3. Available options for providing pain relief during labour and deliv- When IVC compression results from ery, including epidural analgesia. uterine compression, there is a decrease 4. The risks of general anaesthesia in in venous return to the heart. The the parturient. parturient may experience signs and symptoms of shock including I: Physlologlcal Changes*. hypotension, pallor, sweating, nausea, For anaesthetic interventions in the vomiting and changes in mentation. parturient, one must consider both the Venous pressure in the lower extrem- physiological changes that occur during ities and in the uterus increases. Blood pregnancy, as well as the effects of flow to the uterus occurs because of a anaesthetic drugs on the mother and difference between the uterine artery infant. Complications during labour and and venous pressures. Hence an delivery may threaten the life of both increase in uterine venous pressure will the parturient and her infant. The an- decrease the uterine blood flow to the aesthetist must be able to respond placenta and fetus. quickly, working closely with the obstetric, neonatal, and nursing teams. Compression of the aorta by itself, is not associated with maternal hypoten- Profound physiological changes occur sion, but, may result in arterial during pregnancy. Changes in the nerv- hypotension in the uterus. This ous, cardiorespiratory, and gastrointesti- decrease in uterine blood flow may nal systems, and their implications with result in fetal distress or asphyxia. respect to the anaesthetic management, are reviewed in tables 18.1 - 18.3. ) ** Must Know Should Know Page 155 i Anaesthesia for Medical Students

Table 18.1 The physlologlcal changes of pregnancy.

Nervous System

Variable Change Cause Importance General MAC Requirements CNS effect of General anaesthetic Anaesthesia decrease by 25 - 40% progesterone and drug requirements are (or) beta- decreased. endorphin

Regional Local Anaesthef c (LA) Decrease in size Increased epidural Anaesthesia dose requirements of epidural space spread of LA may decrease by about 40% due to engorged occur, esp. if aorto- epidural veins, caval compression is and (or) hormonal not prevented. changes.

Cardlovascular System

Blood Total BV t by 35% Hormonal effect An t of approx. 1000 Volume (BV) Plasma BV t by 45% ml compensates for RBC's BV t by 20% the 400 - 600 ml of blood loss with delivery.

Cardiac t by 40% at 10 weeks Increases in CO Patients with pre- Output (CO) gestation are in response to existing heart disease labour t CO 45% above increased meta- may decompensate. pre-labour values. bolic demands. (eg. Pulm. edema After delivery CO t (Stroke volume may occur duling 60% above pre-labour increases more labour or after deliv- values. than heart rate). ely in the patient with significant mitral stenosis). Peripheral BP normal or 4 SVR decreases to Supine Hypotensive Circulation SVR 4 by 15%. compensate for t Syndrome. (see text) Venous return from legs in CO, leaving decreases. BP normal or 4. Regional Utems increases blood Blood flow in the Placental blood flow Blood Flow now by 500 ml I min. placenta is cannot t but can 4 dependent on with maternal 4 BP blood pressure. due to blood loss, aortocaval compression, or catecholamines.

Page I56 ) 1 Chapter 18 Obstetrical Anaesthesia

Table 18.2 The physlologlcal changes of pregnancy (contlnued). Resplratory System

Varlable Change Cause Importance

Upper Mucosal edema makes Capillary Trauma may occur Airway the parturient prone to engorgement. with suctioning, and bleeding. placing nasal or oral airways. Choose a smaller En. Ventilation Minute Ventilation Increases in O2 Normal resting increases by 50%. consumption maternal PaCO, dmps Tidal volume t 40%. begins in the to appmx. 30 mm Hg Respiratory rate t 10%. Erst trimester. in the Erst trimester. Labour may Pain from labour and increase 0, delivery result in fur- consumption ther hyperventilation. more than 100%.

Lung FRC 4 20%. By Efth month Uptake of inhaled Volumes No change in V.C. the rising uterus anaesthetics occurs begins to force faster due to increased the diaphragm minute ventilation with UP. a smaller FRC. Arterial Increased by 10 mm Hg. Due to Decreased PRC with Oxygenation hyperventilation. increased 0, consump- PaO, tion result in very rapid decreases in PaO, during apnea (eg. induction of general anaesthesia). Pulse oximehy is important

The tenn parturient should never be aorta. Lumbar regional anaesthetics placed in the supine position. Abnor- block the sympathetic nerves and ma1 fetal heart rate patterns indicating decrease vascular tone in the lower insufficient uterine blood flow are fre- body. This may exaggerate the quently observed when patients are hypotensive effects of aortocaval com- placed in the supine position (see figure pression. 18.1). Positioning the parturient on her side, or using a 10 - 15 cm right hip wedge is usually sufficient to move the weight of the uterus off the IVC and 1 ** Murt Know * ShouM Know 1 Anaes~hesiafor Medical Students j

Table 18.3 The physlologlcal changes of pregnancy (continued).

Gastrolntestlnal System

Varlable Change Cause Importance

Gastric Fluid Increased Enlarged uterus N.B. All partudents are con- Volume displaces pylorus. sidered to have a "full stom- Gastric emptying ach". Pain, anxiety and drugs delayed. (esp. namotics) all retard gastric emptying. Mebclopramide may be useful in reducing volume. (see chapter 9: The rapid sequence induction) Gashic Fluid Increased Gastrin secreted Use of HZ-receptor Acidity by placenta. antagonists (anitidine) and Stimulates H+ (or) a non-particulate antacid secretion. (Na citrate) are recommended to increase gastric pH. Gastro- Decreased Enlarging uterus Pulm. aspiration of gashic esophageal competence. distorts the angle contents is the major risk of junction. of the junction. Gen. Anaesthesia. Placement of an E'IT is mandatory in every patturient rendered unconscious by anaesthesia. (see chapter 24: Unusual Anaesthetic Complications: Aspiration Syndrome).

111: Analgesla optlons for transmitted from vlsceral nerve fibres Labour and Delivery**. entering the spinal cord at TlO to L1. During delivery somatic nociceplive How painful is labour? impulses enter the spinal cord at S2 to The pain of labour is generally S4, see figure 18.2. Table 18.4 lists described as being more intense than some of the factors which influence the any other previous pain experience (see degree and intensity of the pain experi- chapter 17 figure 17.1: Comparison of ence during labour. common pain conditions). In women delivering for the first time, the pain of Psychoprophylaxls: The Lamaze labour is described as more intense than method postulates that the parturient's the pain of their subsequent labours. pain which arises from uterine contrac- During labour nociceptive impulses tions and perineal distension can be resulting from labour and delivery are replaced with conditioned "positive"

Page 158 Chapter 18 Obstetrical Anaesthesia reflexes. This method uses a partner or have shown that two-thirds of Lamaze friend who functions as a wach helping mothers will require some kind of anal- the parturient concentrate on breathing gesic aid. Furthermore, it is unfair to techniques and on releasing muscle suggest that, if the method is followed tension. Emphasis is placed on educa- correctly, labour will be painless. This tion about labour and delivery, to give can only lower self-esteem when "fail- the parturient a sense of "control" over ure" occurs. the birth process. Some proponents of the Lamaze method advocate not using In fact, excessive pain may result in any chemical anaesthesia for fear of more harm to the fetus than the judi- placental transfer to the fetus. Psycho- cious use of pharmacologic analgesia. prophylaxis reduces the need for Psychologic stress during labour may "chemical anaesthesian,however studies cause hypoxia and acidosis in the fetus.

/ The Supine Hypotensive Syndrome \

Figure 18.1: The supine hypotensive syndrome. Aortocaval compression occurs in the supine position and is relieved by positioning the parturient in the lateral position. (Adapted with permission from Bonica JJ: Obstetric Analgesia and Anesthesia.

World Federation of Societies of Anaesthesiologists, Amsterdam, 1980.) I

** Must Know Should Know Page 159 ) Anaesthesia for Medical Students ) Table 18.4: Factors lnfluenclng the paln of labour and delivery*.

Parturient's psychological state Mental preparation Family support Medical support Cultural background Primipara vs. multipara Size and presentation of the fetus Size and anatomy of the pelvis Use of medications to augment labour (eg. oxytocin) Duration of labour

Figure 18.2: Nociceptive pathways in labour and delivery. opioids used in managing pain during labour and delivery.

Meperidine is transferred very quickly across the placenta. However, peak levels in the fetus are not reached until This is believed to result from decreased 2 to 3 hours after administration. uterine blood flow secondary to elevated Therefore, infants born 2 - 3 hours after levels of blood catecholamines and (or) maternal meperidine administration are decreased carbon dioxide tensions at risk of opioid-induced depression. caused by hyperventilation. With Elimination of meperidine from the adequate pain relief, epidural anaes- neonate takes 3 - 6 days. Nor- thesia can minimize the stress of labour, meperidine, an active metabolite, takes and facilitate patient participationduring even longer and may be responsible for labour and delivery. It is important to subtle behavioral changes in the new- recognize differences in pain tolerance born infant. and analgesic requirements in order to promote maternal self-esteem and bond- Fentanyl is transferred to the fetus ex- ing with the newborn. tremely rapidly and redistributes back to the mother, much like thiopental. With Table 18.5 lists some of the options doses of 1 mcglkg, fentanyl does not currently available for pain management produce adverse effects on the neonate, during labour. Table 18.6 lists some of and is eliminated from the fetus much the pharmacokinetic properties of two quicker than meperidine. i Chapter 18 Obstetrical Anaesthesia )

Table 18.5: Options available for pain management durlng labour and delivery8*. Nothing Psychological support (coaches, husband, family members) Behavioral modification (Lamaze technique) Hypnotherapy (relaxation exercises practised in months prior to LBrD). Education (normal expectations for labour and delivery; prenatal classes). Massage, walking. Sedatives. Opioid analgesics (e.g., meperidine p.o., im., i.v., fentanyl i.v.). Opioid - antiemetic combinations (e.g., meperidine 50 - 100 mg with dimenhydrinate [Gravol] 50 mg im.). Epidural analgesia (local anaesthesia alone, or with epidural opioids e.g., bupivacaine 0.125% with fentanyl 2 mcg/ml). Spinal anaesthesia (see text for discussion). General anaesthesia (see text for discussion).

Table 18.7 reviews some of the poten- 15). This results in only a minor motor tial maternal and neonatal advantages of nerve block. As a consequence, the epidural analgesia. The recommended patient maintains her motor strength, doses, complications and contra- permitting her to move during labour. indications to epidural analgesia and During the second stage of labour, the anaesthesia were presented in chapter differential nerve block facilitates her 15: Local and regional anaesthesia. efforts to push, by minimizing the motor block while maintaining an Lidocaine and bupivacaine are the most adequate sensory block. common local anaesthetic agents used for managing epidural analgesia - Epinephrine is frequently added to the anaesthesia. Low concentrations of LA (e.g. 1:200,000 epinephrine or 5 bupivacaine (e.g. 0.125%) can provide mcg/ml). This can increase the duration a differential nerve block (see chapter of nerve blockade by 50%, decrease the

Opioid Agonist Dose Peak Effect Duration Meperidine PO 50 - 150 mg. 1 - 1% hours 2 - 4 hours (~emerol? IM 50 -150 mg. 40 - 50 mins. IV 25 mg. 5 - 10 mins. Fentanyl IM 50 - 100 mcg. IM 7 - 8 mins. 0.5 - 1 (~ublimaze? IV 25 - 50 mcg. IV 3 - 5 mins. hour Table 18.6: Common oplold analgesics for labour and delivery.

** Must Know Should Know Page 161 Anoesthesio for Medico1 Students )

Epldural Analgesia - Anaesthesla. ) Maternal Advantages. Neonatal advantages. ,I 1. Excellent pain rellef, frequently 1. Less drug transfer to the infant, j achieved compared to opioids due to a decrease in maternal alone. sedatives and opioid require- 2. Normal progress of labour ments. once established is not impeded. 2. Improved uterine blood flow 3. General anaesthesla avolded, and fetal well being may result should a Caesarean $ection, or with the relief of the maternal forceps manipulation be required stress response during labour and (epidural level is increased for delivery. C-section). 3. Reduced neonatal trauma dur- 4. Improved maternal partlclpa- ing delivery with improved con- tlon in delivery and during ditions when the use of forceps is bonding with the newborn. required. 4. No neonatal depresslon, when properly managed.

Table 18.7: Epldural anaesthesla In labour and delivery. systemic absorption by 30%, and While general anaesthesia for labour decrease the overall amount of drug and delivery was used in the pioneer required. Epinephrine is believed to days of anaesthesia, our understanding cause vasoconstriction of the epidural of the risks of general anaesthesia to blood vessels, decreasing the drug's both the mother and neonate has made systemic uptake. Potential side effects this mode of analgesia obsolete. of adding epinephrine include a significant increase in motor block, accentu- IV: General Anaesthesla. ation of hypertension in preeclamptic When regional anaesthesia is contraindi- patients, and diminished uterine activity cated, or there is insufficient time to due to the beta-effects of epinephrine. establish regional anaesthesia (eg. severe sustained fetal bradycardia), Spinal anaesthesia is generally not used general anaesthesia for operative deliv- for labour and delivery because of the ery may be required. The anaesthetist intense motor block it creates, making faced with providinggeneral anaesthesia pushing during stage I1 ineffective. As for Caesarean section must consider the spinal anaesthesia is usually provided physiological changes of pregnancy, and by one injection, it lacks the flexibility be ready to provide care for the com- in duration that can be achieved by promised neonate. Immediate concerns using a continuous epidural catheter. include*: Chapter 18 ObstetricalAnaesthesia

1. All parturients must be considered ing the nitrogen with oxygen, we pro- to have a "full stomach" and gas- vide a reserve of oxygen for the period tric precautions including a rapid of apnea that occurs during induction of sequence induction with cricoid anaesthesia. pressure are indicated for general anaesthesia. A small dose of curare is often used in 2. Upper airway edema occurs with a 'rapid sequence induction' to prevent pregnancy and all parturients the intense muscle fasciculations that should be considered to have a may occur following the administration potentially difficult airway to of succinylcholine. In the pregnant intubate. i patient, the muscle fasciculations are 3. General anaesthesia introduces the much less intense, probably due to the risks of a failed intubation, and the effect of progesterone. Many anaesthe- risk of hypoxemia, andlor pulmon- tists omit curare pretreatment in the ary aspiration of gastric acid. obstetrical patient because it prolongs 4. With general anaesthesia we must the onset time of succinylcholine paral- consider the potential of having ysis and reduces the intensity of the matemal drugs transferred to the neurornuscular block. neonate. This may contribute to neonatal depression and the need The difficult Intubatlon: for neonatal resuscitation. On rare occasions, the anaesthetist may be unable to intubate the patient on the The 'rapid sequence induction' was pres- first attempt. Difficult intubations have ented in chapter 9. In the pregnant been associated with pulmonary aspir- patient with a potentially difficult air- ation, and carry a high mortality rate in way, a thorough evaluation of the air- the obstetrical population. Every anaes- way is especially important (see chapter thetist must have a plan for managing a 6). All parturients have a tendency to failed intubation in the parturient. Per- rapid desaturation with induction of sistent attempts without alterations in general anaesthesia. Hence 'pre-oxygen- technique will only result in airway ation' with 100% oxygen prior to induc- edema and trauma, with subsequent tion of general anaesthesia is critically matemal and fetal hypoxemia. Serious important for all parturients. Pre-oxy- hypoxemia can occur after 1 minute of genation is provided with a properly apnea despite pre-oxygenation. sealed mask applied to the patient's face, with the patient breathing 100% Maintaining cricoid pressure at all times oxygen. If the patient breathes 100% is imperative. In the event of a failed oxygen for a 3 minutes, or takes four intubation, gentle ventilation with 100% vital capacity breaths, more than 95% of oxygen using the reservoir bag and the nitrogen in the patients FRC will be mask may be all that is necessary until exchanged with oxygen. The normal the patient awakes. When the parturient resting FRC is approximately 25 litres, has recovered from the effects of the and contains 80% nitrogen. By replac- general anaesthetic agents, a regional

** Must Know Should Know Page 163 Anaesthesia for Medical Students technique or alternatively an 'awake intubation' with topical anaesthesia may Notes: be chosen. If there is fetal distress, the anaesthetist may decide to proceed with the anaesthetic using a volatile agent and ventilating the patient by bag and mask until she begins breathing spontaneously. If hypoxemia persists and attempts to ventilate the parturient are unsuccessful, a cricothyroidotomy with a large-bore needle \and oxygen insufflation may be life-saving. Discuss with the staff anaesthesiologists what other options they would consider for managing this problem.

Induction of anaesthesia in the obstetrical patient may be accomplished by administering a reduced dose of thiopental, propofol, or ketamine (see induction agents, chapter 11). Muscle relaxation for intubation is provided using succinylcholine, while anaesthesia is maintained with 50% nitrous oxide and oxygen, and 05 MAC of a volatile agent such as isoflurane. Once the infant is delivered, narcotics and other agents may be used to deepen the level of anaesthesia.

Intermediate-acting muscle relaxants such as atracurium or vecuronium, when used, are reversed at the end of the procedure with a combination of anticholinesterase and anticholinergic agents (eg. edrophonium-atropine, or neostigrnine-glycopyrrolate). The patient is ventilated with 100% oxygen. Extubation is performed after suctioning the upper airway secretions with the patient positioned on her side, and responding to verbal commands.

Page 164 ) Chapter 18 Obstetrical Anaesthesia ) ) Notes:

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** Must Know Should Know Page 165 I Basic Neonatal Resuscitation ROBERT CRONEMD, AND ROBERT ELLIOTMD, FRCPC

Approximately six percent of newborn doppler ultrasound or phonocardiogram. infants will require resuscitation of It may also be done internally, by some kind in the delivery room. Health attaching an electrode to the fetal scalp care workers providing care during when the head presents at the cervix labour and delivery should ensure that during labour. Unlike intermittent mon- they have the knowledge and skills to itoring, continuous monitoring facilitates resuscitate the newborn infant. Recent- the analysis of FHR trends, and their ly, major efforts have been made to relation to uterine contractions. provide delivery room care-givers with neonatal resuscitationguidelines through What are the broad principles of neo- the Neonatal Resuscitation Program natal resuscitation that I should know*? (NRP). 1. Clear the airway. 2. Keep the infant warm and dry. The purpose of this chapter is to intro- 3. Provide physical Stimulation. duce student's to the basic ABCs of 4. Assess the infants breathing and neonatal resuscitation. We do not expect circulation. students to develop specific skills, such 5. Consider interventions. as intubation of the depressed neonate, (oral suctioning, airway insertion, or to use neonatal resuscitation drugs mask ventilation, intubation, endo- during their clerkship training. Never- tracheal ventilation, external cardiac theless, we hope to stimulate their massage, fluid resuscitation, drug desire to develop neonatal resuscitation administration). skills, and encourage them to attend a Neonatal Resuscitation Workshop and What is the APGAR score**? become a certified NRP provider. The Apgar score is a clinical evaluation of the status of a newborn infant. It Fetal Heart Rate (FHR) Monltorlng: assigns a value of 0, 1, or 2 points to Fetal heart rate monitoring is currently five variables, with the highest possible the most accurate screening technique score being 10. It was devised by an for assessing fetal well being in-utero. American anesthesiologist, Dr. Virginia Fetal heart rate monitoring can be done Apgar. The score is typically recorded intermittently with a stethoscope, or 1 and 5 minutes after birth, however, continuously. Continuous monitoring is one may continue to assess at 5 minute performed externally with either an intervals in depressed infants requiring abdominal electrocardiogram (ECG), resuscitation. The most important vari- Chapter 19 Neonatal Resuscitation

Score 0 1 2

Heart Rate Absent < 100 > 100 Respiration Absent Slow, irregular Good Crying Colour Blue, pale Body pink, hands/feet blue Completely Pink Reflex Irritability Absent Grimace Cough, sneeze Muscle Tone Limp Some Flexion Active Movement Table 19.1: The Apgar Score **

able is the heart rate. An apgar score of What is a normal FHR*? s 6 at five minutes correlates with The normal fetal heart rate in a term increased morbidity and mortality. infant ranges from 120 to 160 beats per Resuscitation should never be postponed minute. It normally varies by 5 to 20 so that a "1-minute Apgar" can be done. beats per minute. A premature infant The five variables measured can be (i.e., less than 37 weeks gestation) has recalled using the individual letters of an average FHR of 130 to 170 beats per Dr. Apgar's surname. minute, which is slightly higher than the term infant. A = Appearance (Colour) P = Pulse (Heart rate) A fetal heart recording with a normal G = Grimace (Reflex irritability) rate, but lacking variability, may be A = Activity (Muscle tone) observed when the fetus is asleep, or R = Respiration premature. It may also occur when the infant has been exposed to drugs What is asphyxia*? through the mother (narcotics, sedatives, Neonatal asphyxia is the combined anaesthetics, etc.), or from chronic fetal result of a reduced oxygen supply, and asphyxia. A completely "flat" baseline, an accumulation of carbon dioxide in (i.e. a FHR without variability) suggests the newborn infant. This may occur either a previous insult that has been before, at the time of, or immediately corrected, or ongoing congenital nerv- following delivery. The need for more ous and cardiac anomalies. The fetal than one minute of positive pressure heart normally increases in rate when ventilation before sustained respirations the baby is active. are established, or an Apgar score < 6 at five minutes, is used in making a How are the fetal heart and lungs clinical diagnosis of asphyxia. The different from the adult? presence of perinatal asphyxia increases In the fetal circulation, blood is able to the infants risk of morbidity and mortal- pass from the right heart to the left ity. heart through two channels which bypass the fetal lungs. The ductus arteriosus acts as a conduit for blood to

** Must Know Should Know Poge 167 Anaesthesia for Medical Students

pass from the pulmonary artery directly residual capacity (FRC) volume of to the aorta. The foramen ovale allows about 30 mlkg. During vaginal deliv- blood from the right atrium to pass ery, most of this fluid is "squeezed" out directly to the left atrium. The amount of the lungs, facilitating initial lung of pulmonary arterial blood flowing expansion and oxygen exchange. through the fetal lungs is small due to Infants born by caesarean section do not their small volume and high vascular have this "squeeze" and may have more resistance. Blood from the right ven- fluid in their lungs, impairing lung tricle bypasses the lungs and eventually expansion, and oxygenation. This con- flows through the low resistance pla- dition is frequently termed transient centa where it picks up maternal oxygen tachypnea of the newborn, and may and excretes waste products of metab- require supplemental oxygen therapy olism (carbon dioxide, urea, etc.) see and observation for the first 24 hours. figure 19.1. Why do infants breathe when they are ?he fetal lungs contain an ultrafiltrate of born? plasma equivalent to their functional When the umbilical cord is clamped, the low resistance placenta is removed from the infants circulation. The result is an increase in the vascular resistance in the aorta, left ventricle, and left atrium associated with a rise in left sided pressures. This creates a functional closure of the foramen ovale and the ductus arteriosus. As these right to left shunt paths are closed, blood is diverted into the lungs. A combination of mild acidosis, hypoxia, touch, noise, pain, and cold all stimulate the infant to take their first breath. The vaginal squeeze referred to above, facilitates lung expansion. Fresh oxygen in the alveoli and Ductus Venosus the expanded lung volume decrease the resistance to blood flowing into the lungs.

Hypoxia, cold, acidosis, hypovolemia, hypoventilation, hypercarbia, and atelectasis will all increase pulmonary vascular resistance, forcing blood through the foramen ovale and ductus arteriosus. These factors tend to cause ( Fig. 19.1 The Fetal Circulation ) a persistent fetal circulation and impede

Page 168 Chapter 19 Neonatal Resuscitation the newborns oxygenationp'dventila- ministered. Consider changing maternal tion. // positions for variable decelerations. Evaluate and correct any maternal What fetal heart rate patterns should I hypotension using an intravenous fluid be concerned about*? bolus and/or ephedrine. Summon help. FHR decelerations may indicate a Ensure accurate FHR monitoring, rule change in the baby's well-being in utero out artifacts and consider more intensive and are most significant if the rate drops fetal monitoring such as a fetal scalp below 100 bpm. Early decelerations clip for continuous internal FHR moni- occurring with contractions and then toring. returning to baseline are probably a reflex response to head compression What is meconium*? during the contraction and are usually Meconium refers to the first discharge benign. Late decelerations are more from the infants intestinal tract. It has ominous, usually occurring with con- a green appearance and consists of tractions and having a delayed return to epithelial cells, mucus, and bile. When the baseline FNR. They often signify meconium is passed by the infant in fetal hypoxia and acidosis. Variable utero, it colours the amniotic fluid and decelerations are not associated with indicates that the infant has been sub- contractions, have a quick onset and jected to a stress at some time. recovery. They are due to transient Meconium excretion in utero is cord compression, and are usually observed more frequently in the term or benign. Sustained bradycardia with a post term infant. A thick "pea-soupn FNR < 100, indicates serious fetal dis- meconium may suggest a recent episode tress, and requires urgent intervention. of hypoxia and prompt more aggressive Sustained tachycardia is often associated fetal monitoring or management of the with fever or sepsis, but may be labour and delivery. observed as a response to maternal drug administration (e.g., atropine or Infants that inhale meconium into their ephedrine). trachea and lungs may have difficulty with oxygenation, ventilation and may If serious FHR decelerations occur, develop complications such as a what can I do*? pneumothorax or pneumonitis. Ensure adequate left uterine displace- Meconium may collect in the pharynx ment to prevent aortocaval compression in the infant and may be inhaled into (see chapter 18: Obstetrical Anaes- the lungs with their first breath. It is thesia). Provide supplemental oxygen to paramount that these infants have thor- the mother. A common way of admin- ough suctioning of their mouth, phar- istering oxygen is by fitting a face mask ynx, and nasopharynx at the time the with rebreathing reservoir bag on the head is delivered and prior to their first mother and setting the oxygen flow rate breath with delivery of the chest. The to 2 6 litres per minute. Discontinue clinician may also decide to intubate the the oxytocin infusion if it is being ad- infant immediately after delivery to

** Must Know * Should Know Page 169 Anaesthesia for Medical Students

Rlsk Factors Anteaartum IntraDsrtum Age > 35 Abnormal presentation. Diabetes Operative delivery. Pregnancy induced hypertension. Premature labour. Chronic hypertension. Premature rupture of No Prenatal Care. membranes. Maternal Substance abuse. Precipitous labour. Rh sensitization. Prolonged labour. Drug therapy (Mg, Li, adrenergic drugs, etc.) FHR abnormalities. Other CVS, Neuro, or Thyroid illness. Maternal narcotics Previous stillbirth. (within 4 hrs. of delivery). 2nd or 3rd trimester bleeding General anaesthesia. Hydramnios Meconium stained fluid. Oligohydrarnnios Prolapsed cord. Multiple gestation. Placental abruption. Post-term. Placenta previa. Small for dates. Uterine tetany. Fetal malformation.

Table 19.2: Rlsk Factors predlctlng the need for neonatal resuscltatlon.

/ , suction as much meconium from the vidual should be capable of perform- trachea as possible. ing a complete resuscitation (i.e., / includingendotracheal intubationand Can I predict which infant may need the use of medications). In many ' resuscitation at delivery? cases, this is the person delivering Infants requiring resuscitation may have the infant. associated pre-existing maternal risk 2. Even for cases when a normal infant factors, complications arising during is expected, a second person who labour and delivery, or underlying fetal will be primarily responsible for the / risk factors. (Risk factors associated infant, must be present in the deliv- , with the need for neonatal resuscitation ery room. This person must be able are presented in table 19.2 for reference to initiate a resuscitation and assist ' purpose only). the fully trained person, should a full , resuscitation become necessary. ' How do I make sure that I am ready to 3. When neonatal asphyxia is antici- provide resuscitation for the newborn pated, two individuals whose sole infant? responsibility is to the infant, should 1. At every delivery, at least one indi- be present in the delivery room and

Page 170 Chapter 19 Neonatal Resuscitation

be prepared to work as a team to preventing excessive heat loss from perform a complete resuscitation. the neonate. The person delivering the infant should not be counted as one of the The Beslcs: two resuscitators. 4. With multiple births, a team is I: Open the Alrwey**. needed for each infant. Position the infant supine or on 5. There should be no delay in initiating their side with the neck either in a resuscitation; waiting a few minutes neutral position or slightly for someone "on-call" to arrive is an extended. Avoid overextension or unacceptable practice and invites flexion, which may produce airway disaster. obstruction. A slight trendelenburg position is also helpful. A 1" folded towel under the infants Radiant heater shoulders may be useful if the Stethoscope infant has a large occiput. Suction and suction catheters If the infant has absent, slow, or Oxygen source and tubing difficult respirations, apply suction Neonatal resuscitation.bag first to the mouth and then nose. Airway pressure manometer If the nose is cleared first, the Face masks, Oral airways. infant may gasp and aspirate secre- Endotracheal tubes (2.5, 3, 3.5) EllStylet tions in the pharynx. If mechanical Laryngoscope suctioning with an 8For IOF cath- Straight blades No. 0 & 1 eter is used, make sure the vacuum Medications (see text) does not exceed -100 rnrn Hg. Umbilical catheters (3.5 and 5 Fr.) Limit suctioning to 5 seconds at a Umbilical catheter tray time and monitor heart rate for Needles and syringes bradycardia, which may occur with ECG monitor deep oropharyngeal stimulation. If meconium is present in the Table 19.3: Baslc Neonatal Re- amniotic fluid, special endotracheal suscltatlon Equlpment. suctioning may be required in the depressed infant. Equipment: (see table 193) (for reference only). 11: Keep the infant warm end dry**. 1. Equipment and medications should be checked daily, and prior to an- Place the infant under an overhead ticipated use. radiant heater. Dry the body and head to remove amniotic fluid and prevent 2. The delivery room should be kept heat loss. The gentle stimulation will relatively warm and the radiant also help initiate and maintain breath- heater should be preheated. Warm ing. blankets can also be helpful in

** Must Know Should Know Page 171 Anaesthesia for Medical Students

111: Physical Stimulation**. should be between 40 - 60 breaths per If drying and suctioning do not minute. Initial lung inflation pressures induce effective breathing, gently may be as high as 30 - 40 cm of 40 to slapping or flicking the soles of the feet or rubbing the infants back r may be useful. Do not waste time continuing tactile stimulation if there is no Method response after 10 - 15 seconds.

IV: Evaluate the infant**. Res~irations:Infants who are apneic or gasping despite brief stimulation attempts should receive positive pressure ventilation. Heart Rate: Monitor either by auscultating the apical beat or by palpating the base of the umbilical cord. If the heart rate is below 100 bpm, begin positive-pressureventilation, even if the infant is making some respiratory efforts. Colour: The presence of central cyanosis indicates that although there is enough oxygen passing through the lungs to maintain the heart rate, the infant is still not well oxygenated. A Fig. 19.2: Adapted with permission face mask with oxygen at 5 Umin. should be held closely to the infants face until the infant becomes pink. ,I987,1990.

Technique of Positive Pressure Venti- lation (PPV): overcome the elastic forces of the lungs Ventilatory support is required when**: if the infant has not taken their first, Apnea or gasping respirations are breath. Subsequent ventilation should present. be achieved with airway pressures of 15 The heart rate is less than 100 bpm. -20 cm H20. Central cyanosis persists despite 100% oxygen. Adequate ventilation is assessed by** observing chest wall motion and hearing Most neonates can be adequately venti- breath sounds bilaterally. If chest ex- lated with a bag and mask (see figure pansion is inadequate: 193). The assisted ventiiatory rate

Page I72 Chaplcr 19 Neonalal Rcsuscilalion

reposition the head; consider extend- accompanied by ventilation with 100% ing the head a bit further and oxygen. Asphyxia in the neonate not repositioning the shoulder towel. only slows the heart rate but decreases suction any secretions. myocardial contractility, resulting in consider an oral airway, and ventilat- diminished blood flow and oxygen ing with the infants mouth slightly delivery to vital organs. open. increase ventilation pressures to 20 - When should I start chest com- 40 cm H20 pressions* *? if unsuccessful, abandon the bag and You should begin chest compressions mask technique, and intubate. when the heart rate remains below 80 bpm despite PPV with 100% 0,. Chest After 15 - 30 seconds of effective venti- compressions can be discontinued when lation, the heart rate of the neonate the heart rate is 80 bpm or greater. should be re-evaluated. The heart rate over a 6 second period is counted and What is the proper technique for admin- multiplied by 10 to give an approxima- istering chest compressions to an tion of the 1-minute heart rate. (e.g., 8 infant*"? beats in 6 seconds = 80 bpm). There are two methods of compressing the chest in infants. Using the thumb Positive pressure ventilation can be method, both hands encircle the torso, gradually withdrawn if the HR > 100 with the fingers supporting the back, and spontaneous breathing efforts are while the thumbs are positioned side by present. The care provider should con- side over the sternum, creating chest tinue to provide physical stimulation compression with downward displace- and supplemental 0, to the infant. ment of the sternum. Using the two- finger approach, the middle and ring If the HR is less than 100, ventilation fingers of one hand are held perpendicu- should continue. Chest compressions lar to the chest as the finger tips apply are initiated if the HR is less than 80 pressure to the sternum. The other hand and decreasing. When the heart rate is is used to support the infants back from less than 60, immediate ventilation with below (see figure 19.2). 100% oxygen is instituted with simulta- The amount of pressure applied with neous chest compressions. compressions is adjusted to achieve 1.5 cm of displacement. A full "cycle Chest Compressions: consists of both a compression and Compression of the sternum results in release phase. This rate is adjusted to compression of the heart and increases achieve 2 cycles per second or I20 intrathoracic pressure. During compres- compressions per minute. sion, blood is pumped into the arterial circulation. Release of the sternum Once the fingers (thumbs) have been results in an increase in venous return to correctly positioned over the sternum, the heart. Chest compressions must be care should be taken to ensure that the

** Must Know Should Know Page 173 Anaesthesia for Medical Students

hands are not moved from this position. Prolonged PPV is required (to mini- Valuable time may be wasted attempt- mize gastric distention). ing to relocate the correct hand position. Ventilation with a bag and mask is Complications of incorrect hand place- ineffective (poor chest expansion, ment and chest compression include persistent low HR). fractured ribs, lacerated spleen, and Tracheal suctioning required (thick or pneumothorax. particulate meconium). Diaphragmatic hernia suspected (to When the infant is intubated and re- prevent bowel distension in the ceiving simultaneous ventilation and chest). chest compressions, ventilation at a rate of 40 - 60 per minute with independent, While endotracheal intubation may play concurrent chest compressions at a rate an essential part of an infants resuscita- of 120 per minute is recommended. tion, it is neither the purpose, nor in the scope of this chapter to discuss the Air may be forced into the infants stom- technique, confirmation, or complica- ach if they are receiving simultaneous tions of this intervention. We hope that PPV (with a bag and mask) and chest this chapter will provide you with a compressions. Hence when the infant is stepping stone for your future courses in being ventilated with a bag and mask, neonatal resuscitation. ventilation should be interposed between compressions. Every three chest com- Which four common drugs used in re- pressions are followed by a pause to suscitation of the depressed neonate interpose an effective breath. The re- should I be familiar with?** sulting 90 compressions with 30 ventilations yield a combined rate of com- 1. Oxygen. pressions and ventilation of 120 per 2. Intravenous Fluids. minute. The variation in recommended 3. Epinephrine. rates of ventilation and chest compres- 4. Naloxone. sions between the intubated and non intubated infant is an attempt to mini- Oxygen: mize the risk of gastric distention and (or) aspiration. For the majority of infants who require resuscitation, the only medication Compressions are interrupted after the needed will be 100%oxygen delivered first 30 seconds, to make a six second with effective ventilation. Some will heart rate count. Compressions are require chest compressions, and a small stopped once the heart rate is above 80, minority of resuscitated infants will and ventilation is stopped when the require other medications, such as epin- heart rate is above 100. ephrine, intravenous fluid resuscitation, or other special drugs. Endotracheal intubation is indicated when*:

Page 174 Chapter 19 Neonafal Resuscitation

Intravenous flulds: What is the normal blood pressure and How will I know whether or not the blood volume in a term infant? infant is hypovolemic? On average, the blood pressure in a Conditions which result in acute term infant is 70144. Hypotension in maternal hypovolemia prior to delivery the neonate has been defined as a sys- of the infant, should make the clinician tolic blood pressure of less than 50 mm suspicious that the infant may also be Hg in a term infant (see table 19.4). suffering from the effects of hypo- The normal blood volume in a term volemia. Maternal hemorrhage prior to neonate is 80 - 100 mllkg. Hence in a delivery is one such condition. A few 3 kg infant with a blood volume of 250 of the causes of maternal hemorrhage ml, a loss of only 50 ml represents 20% prior to delivery include placental ab- of their blood volume. ruption, placenta previa, transection of the placenta during caesarean section, and maternal trauma. Other conditions Weight SBP DBP MAP that may result in neonatal hypovolemia (grams) include multiple gestation pregnancies, umbilical cord tear during delivery, and 1000- 49 26 35 a strangulating umbilical cord requiring 2000 umbilical cord transection for delivery. 2000- 59 32 43 3000 Hypovolemia occurs more frequently in >3000 70 44 53 the newborn than is commonly recognized. Blood loss is often not obvious Table 19.4: Average blood pres- and initial tests of hemoglobin and sures at blrth. hematocrit are usually misleading. The increase in vascular volume secondary to a volume expander should improve What conditions, other than hypovol- tissue perfusion and reduce the develop- emia, may result in hypotension in the ment of metabolic acidosis. neonate ? Other conditions include: Clinical signs of hypovolemia resulting Hypoglycaemia (diabetic mother) from an acute loss of greater than 20% Hypocalcemia (Intrauterine asphyxia) of the blood volume include: Hypermagnesemia (~g-therapy for Pallor persisting after oxygenation. the pre-eclamptic mother) A weak pulse despite a good heart Sepsis (chorioamnionitis or prolonged rate. rupture of membranes) A poor response to resuscitative Pneumothorax (meconium aspiration) efforts. Cardiac pathology A decreased blood pressure (< 55/30). Diaphragmatic hernia

** Must Know Should Know Page 175 Anaesthesia for Medical Students

Assuming we've made a correct diag- ml or 0.1 mg per ml). The intravenous nosis of hypovolemia, how can we cor- dose is 0.01 to 0.03 mg per kg. In a 3 rect it? kg infant, a 114 ml to 314 ml of epin- The most commonly used volume ephrine would be an appropriate starting expanders are normal saline and ringer's dose, as this would be equivalent to 25 lactate. Other volume expanders to 75 mcg (approximately 0.01 to 0.03 include 5% albumen, and 0-negative mag). If an intravenous route is un- blood cross matched with the mother's available, epinephrine can be given blood. The volume of fluid adminis- through the endotracheal tube. Epin- tered should be equivalent to 10 mlkg, ephrine given by endotracheal route and this should be given as an infusion should be diluted with 1-2 ml of saline. over 5 - 10 minutes. In a 3 kg infant When given by the En,plasma con- this would be equivalent to 30 ml. centrations may be lower compared to the intravenous route. If the infant does Eplnephrlne: not respond to the initial E'JT epinephrine dose, the endotracheal epin- When should I consider giving epinephrine dose is increased by a factor of ephrine*? ten (0.1 - 02mgkg). Epinephrine is indicated if no heart rate can be detected or if the heart rate per- Naloxone*: sists below 80 bpm despite adequate What is naloxone and when should I ventilation with 100% oxygen and chest consider giving it? compressions for at least 30 seconds. Naloxone is a pure opioid antagonist without intrinsic respiratory depression Why is epinephrine such an important activity. Naloxone is indicated for the drug in neonatal resuscitation? reversal of respiratory depression when Epinephrine has both a (alpha) and the mother has received opioids within (beta) adrenergic stimulating properties. 4 hours of delivery and the infant is The alpha effect causes vasoconstriction observed to have depressed respirations. which raises the perfusion pressure While naloxone works very rapidly, during chest compressions, augmenting adequate ventilatory assistance should oxygen delivery to both the heart and always be provided first. The duration brain. The beta effect enhances cardiac of naloxone is shorter than that of some contractility, stimulates spontaneous opioids, making respiratory monitoring contractions and increases the heart rate. mandatory for a further 4 to 6 hours.

How can I give epinephrine? Naloxone can be given either intra- Epinephrine can be given either intravenously or by an endotracheal tube. venously or by the endotracheal tube Subcutaneous or intramuscular routes every 3 to 5 minutes as required. The can also be used if the infants perfusion epinephrine concentration used in neo- is adequate, however, the onset of natal resuscitation is supplied as a action may be slower with these routes. 1:10,000 dilution (i.e. 1 gram in 10,000 If maternal opioid addiction is suspect-

Page 176 3 / Place under radiant heater (Suction trachea - if meconium stained fluid) Dry thoroughly Remove wet linen Position Suction mouth then nose Provide tactile stimulation

Chest Compressions

HR c 80 after 30 secsdespite Figure 19.3: An overview of Resuscitation in the Delivery Room. PPVwitt~1000b 02and Reproduced with permission. Textbook of Neonatal Resuscitation. chest Compressions @ 1994 American Heart Association. Anaesthesia for Medical Students ed, it is probably prudent not to give References: naloxone. Rather, simply support 1. Bloom RS, Cropley C. Textbook ventilation until respiratory drive is of Neonatal Resuscitation. ed. adequate. Administrating naloxone to Chameides L and the AHAIAHP infants of opioid dependent mothers Neonatal Resuscitation Steering may result is a withdrawal reaction and Committee. American Heart Asso- severe seizures in the infant. Naloxone ciation, 1990. is supplied in a 0.4 mg/ml concentration for neonatal resuscitation. The dose is 2. Emergency CardiacCare Committee 0.1 mg/kg for infant resuscitation, and and Subcommittees, American hence a typical 3 kg infant would Heart Association. Guidelines for require 314 of a ml (iv, Em,im, or sc) cardiopulmonary resuscitation and of naloxone (0.4 mg/ml) as an initial emergency cardiac care, VII: neona- dose. tal resuscitation. JAMA 1992; 268:2276-2281. Notes: 3. Christenson JM, Solimano AJ, Williams J, et al. The new American Heart Association guidelines for cardiopulmonary resuscitation and emergency care: presented by the Emergency Cardiac Care Subcommittee of the Heart and Stoke Foundation of Canada. Can Med Assoc J 1993;149:585-590.

Page 178 i 1 Chapter 19 Neonatal Resuscitation

" Must Know Should Know Page I79 Intravenous Fluid and Blood Component Therapy WAYNEBARRY MD., FRCPC

Optimal perioperative fluid therapy Body Fluid Compartments: requires an understanding of the Total body water (TBW) constitutes changes that occur in the volume and 60% of the body weight, or approxi- composition of the body fluid compart- mately 42 liters in a 70 kg adult. Two ments. Intravenous fluids are used to thirds of the TBW is contained within replenish fluid losses while maintaining cells as intracellular fluid (ICF). The the blood volume, coagulation status, ICF represents 40% of the body weight, and oxygen delivery. Inadequate fluid which is approximately 28 liters in a 70 therapy risks organ hypoperfusion, kg adult. The remaining 113 of the coagulopathy, and electrolyte imbal- TBW exists outside the cells as extra- ances. Excessive fluid therapy risks cellular fluid (ECF). It represents 20% circulatory overload as well as organ of the body weight or 14 liters of water and tissue edema. To avoid inadequate in a 70 kg adult (see table 20.1). or excessive fluid therapy, the clinician must makes serial evaluations of the Sodium (140 meqA) and potassium (150 patients fluid requirements in terms of meqA) are the principle cations in the their maintenance fluids, fluid deficit, ECF and ICF respectively. Albumen third space losses, and ongoing blood (40 gd) is the primary molecule res- losses. ponsible for the oncotic pressure generated by the ECF. Aldosterone and With this in mind, this chapter shall antidiuretichormone (ADH) increase the enable the reader to calculate: extracellular fluid volume by increasing salt (aldosterone) and water (ADH) 1. Maintenance fluid requirements reabsorption. Atrial natriuretic protein 2. Fluid deficit estimation decreases the ECF volume by promoting 3. Ongoing fluid 3rd space losses, and salt and water excretion. 4. Fluids required to replace blood lost. I. MalntenanceFluidRequirements*: We shall also review the indications and Intravenous fluid requirements for complications of transfusing blood prod- periods of less than one week can be ucts. provided for with water, sodium, and

Page 180 Chopfer 20 Infrovenous Fluid ond Blood Component Theropy

Compartment % Body Welght Volume In llters 1 70 kg Total Male (70 kg) 60 42 Female (70 kg) 50 35

ECF' 20 14 Plasma 4 2.8 Interstitial Fluid 16 11.2 I CF 40 28

Table 20.1: Distribution of body water. *Ihe ECF represents approximately 113 (range 27 - 45%) of the total body mass, while the ICF occupies approximately 213 of the total body mass. potassium; Chloride, magnesium, cal- of 112 normal saline with 15 - 20 meq cium, and other trace mineral of potassium per liter. At maintenance supplementation is required for patients infusion rates, this will meet the patients needing chronic intravenous mainten- daily water, sodium and potassium ance therapy. As hyperglycemia is a requirements. notmal response to surgery, dextrose is recommended only for those patients at Intravenous fluids for surgery scheduled risk of hypoglycemia (e.g., infants and to be performed within 24 hours: diabetic patients). Noml saline, or ringer's lactate are the preoperative intravenous fluids of choice A normal 70 kg adult requires approxi- for surgery scheduled within 24 hours. mately 25liters of water a day with 75 The rationale for this recommendation meq of sodium, and 40 meq of potas- includes: sium. Water and salt administration in 1. Potassium replacement is not excess of this, will result in their excre- required for brief periods of time. tion in the urine (provided cardiac and 2. Intravenous fluids containing potas- renal function are normal). sium pose a potential hazard should the patient receive an inadvertent Intravenous fluids for a period of > 24 fluid bolus (e.g., rapid i.v. adminis- hours and < 1 week: Preoperative fluid tration for hypotension associated requirements during this period of time with the induction of anaesthesia). can usually be met with a solution of 3. Normal saline and ringer's lactate are 213 of 5% dextrose with 113 normal the most common fluids administered saline (referred to as 2/3rds, 1/3rd) with intraoperatively, as they are used to 15 - 20 meq of potassium per liter. replenish the sodium rich plasma and Alternatively, we could use a solution interstitial fluid compartments.

" Must Know Should Know Page 181 Anaesthesia for Medical Students

Table 20.2: Maintenance water requirements Per hour* * Per Dav * * 1st to 10th kg 4 mlkg 100 mlkg 11th to 20th kg 2 mlkg 50 mlkg 21st to nth kg 1mlkg 20 mlkg

Exercise caution when administering ments by the number of hours fasted. crystalloids such as NS or RL to (Fluid Deficit = Maintenance require- patients with congestive heart failure, ments per hour x number of hours renal failure, or advanced age. In these fasted). A fluid deficit resulting from a patients, a preoperative intravenous pathological process is much more solution of 2L3rds and 1/3rd may be difficult to quantify accurately. Table more appropriate. 20.3 lists clinical conditions frequently associated with fluid deficits, with asso- Maintenance fluid requirements for any ciated physical and laboratory findings. body weight can be calculated using the For example, a patient with a fractured "4-2-1hle for hourly fluid require- hip may have 1 - 2 liters of blood se- ments or the "100-50-20"mle for daily questered in their thigh tissues. When fluid requirements (see table 20.2). For such significant fluid deficits are not example, a 75 kg adult will require: appreciated and corrected prior to anaesthesia, profound cardiovascular collapse Per hour: may occur with induction of anaes- 10 kg x 4 mlhr = 40 mlhr thesia. 10 kg x 2 mlhr = 20 mlhr 55 x 1mlhr = 55 mlhr 111. Third Space Losses*: Total: 75 kg 115 mlhr A reduction in ECF volume during surgery results from evaporative losses, Per day: exudative losses, tissue edema second- 10 kg x 100 mllday = 1000 ml ary to surgical manipulation, and fluid 10 kg x 50 mllday = 500 ml sequestration in organs, such as the 55 x 20 mllday = 1100 ml bowel and lung. These fluid losses can Total: 75 kg 2600 mllday be surprisingly extensive. The simplest guideline for replacing third space fluid losses is a 4 - 6 - 8 mllkglhr rule. Four 11: Fluld Deficit Estimation*: for minor, 6 for moderate, and 8 A fluid deficit may develop as a result mlkg/hr for major surgical trauma. For of a period of fasting or a pathologic example, we can anticipate that a bowel process. The fluid deficit from fasting resection will have 6 mlkg/hr of 3rd can be calculated by multiplying the space fluid losses during the operation. patient's hourly maintenance require- This fluid is usually administered as

Page 182 Chapter 20 Intravenous Fluid and Blood Component Therapy

Table 203: Common conditions associated with preoperative fluid deficits. Fractured hip, femur, pelvis Protracted vomiting and diarrhea Bowel obstruction Bums Preoperative bowel preparation Sepsis Trauma Pancreatitis Common physical findings supporting a preoperative fluid deficit. Tachycardia Tachypnea Orthostatic hypotension Decreased jugular venous pressure (JVP) Supine hypotension Dry mucous membranes Oliguria (c 05 ml/kg/hr) Decreased tissue turgor Common laboratory findings associated with a fluid deficit. Elevated urea Elevated urine osmolarity Elevated creatinine Elevated hematocrit Low urinary sodium concentration (U, c 20 mM) either normal saline or ringer's lactate, solutions may be synthetic (e.g., penta- and must be given in addition to the span, hetaspan, dextran), or collected patient's maintenance requirements, from the donor blood pool (eg. albu- calculated fluid deficit, and ongoing men, plasma, whole blood). blood losses. Mobilization of third space fluid occurs approximately 72 If 1000 ml of NS is infused intra- hours after surgery, and may result in venously, only 113 (approx. 300 ml) will circulatory overload in the patient with remain in the intravascular compart- compromised cardiac or renal function. ment. The remaining 213 (- 700 ml) will move into the interstitial and intra- IV. Blood Loss Replacement*: cellular compartments. As a conseq- Intravenous crystalloid or colloid sol- uence, 3 to 5 times the volume of utions may be administered to replenish blood lost must be infused when crys- the intravascular volume. Crystalloid talloids such as NS or RL are used to solutions are salt containing solutions maintain the intravascular volume. that are semipermeable to cellular mem- With colloid solutions, however, blood branes. Examples of crystalloid sol- losses can be replaced on a 1:l volume utions include NS, RL, and 213, 113 basis. intravenous solutions. By contrast, colloid intravenous solutions contain D5W: aggregates of molecules that resist diffu- Similarly,the intravenous administration sion across cellular membranes. Colloid of 1000 ml of D5W (5% dextrose in

** Must Know Should Know Page 183 Anaeslhesia for Medical Students )

Table 20.4: Common intravenous solutions and their cornponenls. SoluCon Dextrose Na CI K pH Osm Other &dl meqA Plasma 140 103 4 7.4 290 Ca 5 meqA D5W 5 5.0 253 u3 D5W,l/3 NS 3.3 51 51 4.8 270 2/3,1/3 + 20 meq KCL 3.3 51 51 20 4.8 290 0.9% Saline (NS) 154 154 5.7 308 Ringer's lactate 130 109 4 6.7 273 Ca l.SmeqA, lactate 20 meq A 0.45% Saline (SNS) 77 77 5.3 154 Pentaspan 154 154 5.0 326 10gmIdl pentastach

water), results in minimal intravascular Sallne: volume expansion, because most of the The infusion of large amounts of intra- fluid moves into the interstitial and venous NS (e.g., trauma resuscitation) intracellular compartments. Hyponat- may be accompanied with a hyper- remia, hyperglycemia and a decrease in chloremic, hypematremic non anion gap serum osmolarity will result when large metabolic acidosis. In trauma patients, volumes of D5W are infused. For these this source of acidosis is commonly reasons, D5W is a poor choice for cor- overlooked by clinicians. An increase in recting a blood volume deficit. More- minute ventilation, produces a respira- over, large amounts of D5W should be tory alkalosis, which is the normal com- avoided in patients receiving oxytocin, pensation for an acute metabolic acido- because oxytocin's inherent ADH effect sis. This additional respiratory work, in may result in hyponatremia and water a spontaneously breathing patient, may intoxication. be detrimental in a patient with other coexisting disease. The severity of an ischemic cerebral event may be increased if iatrogenic Chronic gastric losses may produce a hyperglycemia is induced with the ad- hypochloremic metabolic alkalosis. The ministration of dextrose containing administration of NS can be used to fluids. This has special relevance for correct this abnormality. neurosurgical procedures, and patients with cerebrovascular pathology.

Page 184 .avenous Fluid and Blood Component Therapy

Ringer's lactate: dilution of platelets and coagulation Ringer's lactate solution contains 4 factors4. A maximum volume of 2000 meqfl of potassium, and should be used ml per 24 hours is recommended. with caution in patients with pre-existing hyperkalemia or renal failure. Side effects of pentaspan include circu- Patients with chronic diarrhea may latory overload (pulmonary edema, develop a h yperchloremic metabolic congestive heart failure), altered coagu- acidosis. This will respond to treatment lation (prolonged clotting times, pro- with a bicarbonate (lactate) containing longed INR and P'fi), and hypersensi- solution, such as ringer's lactate. tivity reactions such as wheezing and urticaria. It is contraindicated in The administration of hypotonic sol- patients with bleeding disorders, renal utions to patients with brain injury may disease, and circulatory overload. It is contribute to brain cell swelling. As supplied in 100, 250, and 500 ml infu- saline is relatively more hypertonic than sion bags. Hetaspan and dextran are RL, it is generally the preferred two other synthetic intravenous colloids. crystalloid for these patients (see table We use them less frequently at our 20.4). centre because there is an increased incidence of anaphylactoid reactions Pentaspan: associated with them. Pentaspan has the same sodium and chloride concentration as NS. Each 100 Albumen: ml contains an additional 10 grams of Albumen is available as a 5% and 25% pentastarch, of which 70% is eliminated solution. It is heat treated at 60°C for by the kidneys within 24 hours. The 10 hours to eliminate bacterial and viral plasma volume expansion achieved is contamination. Administration of the equal to the volume of pentaspan ad- 5% solution will produce an equal ministered (1:l ratio). Pentaspan is increase in intravascular volume expan- more expensive than crystalloid so- sion. Administration of the 25% sol- lutions, but less expensive than other ution will draw interstitial fluid into the blood substitutes such as albumen. intravascular space and increase the intravascular volume by a factor of 4 Note, however, that pentaspan is not a times the albumen volume. Albumen RBC substitute and has no oxygen can be used as a plasma volume carrying capacity. The hemodynamic expander in patients with adequate effects of pentaspan are equal or oxygen carrying capacity, however it is superior to those of albumen. Both not recommended as a method of cor- result in expansion of the plasma vol- recting nutritional deficiencies. ume, with increases in preload, cardiac output, and oxygen delivery. Increases Autologous blood: in bleeding and clotting times resulting Autologous blood involves the preoper- from an infusion of albumen or penta- ative collection of blood from a patient starch are believed to be secondary to a who is scheduled to have surgery, and

** Must Know Should Know Page 185 Anaest/tesia for Medical Students for whom one anticipates the need for a 30 to 50 gm1L. Such an acute decrease perioperative blood transfusion. Con- in hemoglobin is only tolerated when trary to popular belief, autologous blood normovolemia is maintained, and mech- is discarded if it is not administered to anisms to increase oxygen transport by the donor. As it is not placed in the increasing cardiac output and 2,3 DPG general donor homologous blood pool, levels are intact. Patients with cardiac patients should not be encouraged to disease or atherosclerotic lesions that donate autologous blood on the basis restrict blood flow to vital organs are that it could benefit someone else. limited in their ability to adapt to acute Patients with bacterial or viral infections anemia. A balance between the risk of are not suitable donors, as there is a risk transmitting an infectious disease, and of exposing other patients to the con- the need for administering blood prod- taminated blood (e.g., clerical error). ucts for their oxygen carrying capacity Suitable candidates are able to donate a and coagulation properties, must be maximum of 1 unit of blood every 4 to reached in each patient undergoing 7 days, and should stop donating three surgery. or more days prior to the planned procedure. Unsuitable candidates include Postoperative hemoglobins in the range patients with a hemoglobin level less of 60 to 80 gm/L are now considered than 110 gmL, and patients with acceptable in patients who do not have unstable angina or critical aortic cardiovascular disease. Transfusion stenosis. As the maximum shelf life of should be used only to replace losses stored blood is 35 days, a donor could beyond this level. Nevertheless, even a donate up to 4 units prior to surgery. modest anemia with hemoglobin levels Oral iron andlor recombinant erythro- of 80 to 100 g& requires an increase poietin therapy may be used to increase in heart rate and stroke volume to meet the number of units that can be coll- the body's oxygen requirements. This ected preoperative1 y. Autologous blood introduces an additional cardiac stress. is not separated into components like Physicians must consider the con- homologous blood, but rather is stored sequences of this imposed cardiac stress as whole blood. when deciding to transfuse patients with moderate anemia and coexisting Acceptable blood loss*: atherosclerosisorcardiovasculardisease. We do not have a universal answer to In the end, each patient must be evalu- the question "What is the minimal ac- ated individually. ceptable hemoglobin?" Evidence suggests that a r~ormalcirculating blood Questions that may be helpful in formu- volume can be reduced by as much as lating a decision to administer blood 25% with little stress being placed on products to a particular patient include: the patient, provided that the intravascular blood volume is maintained. 1. Does the patient accept the possibil- Animals are able to tolerate acute reduc- ity of receiving blood products? tions in hemoglobin to levels between 2. If anemic, is this an acute anemia or Chopfer 20 I~~frave~rousFluid artd Blood Compo~ie~trTl~erapy

a chronic anemia to which the fusing blood products, we can calculate patient has adapted? the acceptable blood loss (ABL). 3. Is the patient likely to lose more blood in the immediate future? ABL = Hb(i) - Hb(Q x EBV 4. Does the patient have risk factors for Hb(i .) atherosclerosis, coronary artery dis- Hb(i) = Initial hernoglobill ease, or cerebrovascular disease? = 150 gm/L (e.g., Smoking history, hypertension, Hb(Q = Final hemoglobin diabetes, hypercholesterolemia, per- = 90 gm/L sonal or family history of heart disease). Therefore: 5. Is their evidence of a coagulopathy ABL = 150 - 90 x 4900 = 1960 ml , in which additional blood loss is 150 1 anticipated (prolonged INR, PIT, or decreased platelets)? The most common blood products ad- 6. Does the blood loss exceed what was ministered are whole blood (autologous calculated as the acceptable blood blood donors), packed red blood cells 1 loss for this patient? (see text below). (RBCs), platelets, and fresh frozen 7. Is the patient hemodynamically plasma. One unit of whole blood has a ) unstable despite other fluid resuscita- volume of 500 ml, while a unit of tion? packed RBCs has a volume of epproxi- i mately 300 ml (including their ------anticoagulant volume). One unit of i Table 20. 5 Blood Volume packed RBCs will raise the hemoglobin rnllkg by 10 gm/L in the average adult. Alter- natively, 3 mlkg of RBCs will raise the Premature infant 90 ) hemoglobin by 10 gm/L. This later 80 Term infant formula is useful for calculating the 75 Slim male volume of blood required for transfusion 70 Obese male in neonates and infants. Packed RBCs 65 Slim female are indicated when there is a deficiency 60 Obese female in the patients oxygen carryingcapacity.

Fresh Frozen Plasma: Calculation of tire acceptable blood Fresh frozen plasma contains all coagu- loss: lation factors at levels close to normal Since, an adult male has a blood vol- plasma levels. It is indicated to replace ume of 70 ml/kg (see table 20.5), the deficiencies of factors 11, V, VII, IX, X, estimated blood volume (EBV) is 70 kg XI and antithrombin 111. All coagu- x 70 ml/kg = 4900 ml. If the initial lation factors, with the exception of hemoglobin is 150 gm/dl and we have factors V and VIII, are stable in whole decided that we will allow the hemo- blood. Factors V and VIII decrease to globin to drop to 90 gm/L before trans- 15 and 50% respectively by 21 days of

** Must Know SItould KI~OIV Page 187 i Pnaesthesia for Medical Shtdents

\ / Potential Cornplicatlons of Blood Tramfuslonsn

3. Cold ---+ Hypothennia 4. RBC1s +MajorIMinor reactions 5. WBC's -Febrile reaction Dilutional coagulopathy

9. Microaggreg+Dyspnea

Figure 20.1: The components of whole blood all have potential side effects. By recalling the components of whole blood, one can readily recall their potential complications with their administration.

storage. However, only 20 percent of A dilutional coagulopathy may result factor V, and 30% of factor VIII are when coagulation factor levels decrease. needed for adequate hemostasis. This occurs with a RBC transfusion equivalent to one blood volume (z 10 Packed RBCs, however, do not have units of PRBCs in adults). When the adequate amounts of coagulationfactors, blood loss approaches one blood vol- and fresh frozen plasma is frequently ume, in a patient with a previously useful in correcting deficiencies in normal coagulation status, fresh frozen factors V and VIII when transfusing plasma should be considered. Once multiple unitsts of packed RBCs. Fresh fresh frozen plasma is required, one unit frozen plasma is also indicated in will be required for every two units of patients with liver disease who are PRBCs. bleeding and have multiple coagulation defects. Patients taking coumadin re- Platelets: quiring emergency surgery may benefit Platelet transfusions are indicated after from vitamin K, and FFP to correct massive transfusion (> 1blood volume their coagulation defect. transfused), associated with abnormal

Page 188 Chapter 20 Intravenous Fluid and Blood Component Therapy

bleeding and dilutional thrombo- step becomes especially important when cytopenia. Acute thrombocytopenia administering multiple units of blood. (platelet count 50,000 - 100,000 x 109/1) Figures 20.2 and 203 illustrate a simple accompanied by microvascular bleeding method of checking the ABO com- is an indication for platelet transfusion. patability when type specific blood is Platelets may be indicated prophylactic- not available and another ABO group ally in the severely thrombocytopenic must be used for blood product adminis- patient (e.g., thrombocytopenia second- tration. ary to chemotherapy). Patients with disorden resulting inplatelet destruction 1. Aic During operative procedures or sequestration (e.g., hypersplenism) do when blood loss is brisk, the blood not usually require platelet transfusions. products may be pressurized to The administration of one unit of facilitate rapid administration. platelets to an adult will raise the Whenever blood is administered platelet count by approximately 5,000 - under pressure, the risk of air em- 10,000 x lo9A. Once platelet products bolism exists. Blood units that are are required, 1 - 2 units of platelets for now used to warm blood during every two units of PRBCs, are needed rapid administration incorporate an to maintain hemostasis. air trap to minimize this risk.

Potentlal Compllcatlons of blood 2. Volume: Excessive administration transfusions**: of blood products may result in The most common cause of an ABO circulatory overload with pulmon- incompatible transfusion results from a ary edema, and congestive heart clerical error in patient and blood identi- failure. fication. Each unit must be checked prior to transfusion, preferably by two 3. Cold: The rapid administration of individuals. The patient's name and cold blood (massive transfusion) identification number must be identical can result in a precipitous drop in to that on the unit of blood. The ABO the core body temperature. and Rh type, blood product number, Ventricular dysrhythmias are more requisition number, expiry date, and any likely if the temperature drops special precautions should also be below 30°C. 7he risk of checked. ventricular fibrillation peaks at 28OC. Figure 20.1 lists the potential complications of blood transfusions. As ABO 4. RBCs: Immediate hemolytic errors are the most common and serious transfusion reactions are caused by errors made in the administration of the recipient's red cell antibodies blood products, it is prudent to know (e.g., anti-A or anti-B) binding the patients ABO blood group and compliment and lysing the ensure this is correct before checking transfused RBCs. They are usually and administering blood. This simple the result of an ABO incom- 1 ** Must Know Should Know Page 189 / 4naesrhesia for Medical Shtdenrs ) patibility. The destruction occurs lets, FIT, or cyroprecipitate as indi- immediately, and as little as 20 ml cated. may initiate a reaction. The reaction is characterized by severe RBCs: Delayed hemolytic transfu- signs and symptoms which may sion reactions occur 2 - 21 days include: chills, fever, dyspnea, after the transfusion. Unlike the nausea, and chest or flank pain. immediate ABO transfusion reac- Under anaesthesia, other signs such tion, these reactions are often not as hypotension, wheezing, hypox- preventable. They are usually due emia, abnormal bleeding, and to trace antibodies formed after a hemoglobinuria may be noted. previous transfusion or pregnancy. Free hemoglobin is released from The concentration of these antibod- the lysed RBCs and is present in ies is so low they go undetected at the urine and plasma (red urine and the time of compatibility testing. plasma). The most serious compli- The antibodies in the recipient's cations are acute renal failure (from blood coat the transfused blood the hemoglobin obstructing the cells but do not result in immediate tubules), and coagulopathy . Treat- lysis. Later, the reticulo-endothelial ment includes: system (RES) removes the cells from the circulation. The usual A. Stop the blood immediately. course is benign and often only B. Notify the blood bank of the prob- detected because of the drop in lem. hemoglobin and rise in bilirubin. C. Send the remaining blood, as well as blood samples from the patient 5. WBCs: White blood cells cause to the lab. febrile reactions. These reactions D. Send a urine sample for analysis may be accompanied by nausea, (hemoglobinuria). chills, headaches and myalgias. E. Administer oxygen. Less commonly, chest pain, F. Support the circulation (ephedrine, hypotension, and vomiting may epinephrine, dopamine). occur. Other causes of a fever G. Promote a diuresis and renal excre- during a transfusion includes major tion of hemoglobin by administer- transfusion reactions (see above), ing fluids, mannitol, furosemide, reactions to platelets, and fever and/or dopamine. Consider alkalin- arisingfrom bacterial contamination izing the urine with intravenous of the blood. Acetaminophen may sodium bicarbonate administration. be helpful in minor reactions. Maintain a minimal urine output of Occasionally, WBC filters, or WBC 1 - 2 ml/kg/hr. reduced blood products may be H. Monitor for disseminated intravas- required if repeated febrile reactions cular coagulopathy (DIC). Follow occur. the platelet count, fibrinogen level, INR, and P'IT, and treat with plate-

Page 190 Chapter 20 Intravenous Fluid and Blood Component Therapy

' Packed RBC donation Plasma donation

Figure 20.2: Donors with ABO Figure 20.3: Donors with ABO blood pup0 may donate packed blood group 0 may receive plasma RBC's to patients with blood group from donors with blood group 0, A, 0, A, B, or AB, and are referred to B, or AB. However, patients with 0 as universal donors. Donors with blood, can only donate their plasma the ABO blood pupAB are only to patients with 0 type blood. able to donate packed RBCs to AB \ recipients.

6. Plasma: A dilutions1coagulopathy cytopenia with a platelet count of may result when coagulation factor less than 100,000 x 109/1 occurs in levels decrease (see text above). over 90% of patients receiving 10 Allergic reactions are due to foreign or more units of packed RBCs. proteins in the blood. The most This is the most common cause of common manifestation of an aller- a coagulopathy in a massively gic reaction is urticaria, which transfused patient. usually responds to antihistamines such as diphenhydramine 8. Biochemical abnormalities: (benadryl@). More severe reactions Rapid administration of packed may result in an anaphylactic trans- RBCs (> 100 mllminute) may result fusion reaction with hypotension, in citrate toxicity. Citrate is used and require the administration of as an anticoagulant in packed corticosteroids, epinephrine, and RBCs. Citrate binds calcium, pro- fluids (see chapter 24: Unusual ducing hypocalcemia, decreased Anaesthetic Complications; myocardial contractility, hypo- Anaphylaxis). These patients may tension, and a widened QRS be found to be deficient in IgA and complex with a prolonged QT to have formed anti-IgA antibodies. interval. Administration of calcium Subsequent transfusions may chloride 10 - 15 mg/kg, infused in require specific RBCs that are slowly iv over 2 - 3 minutes, is washed free of IgA. indicated with documented hypocalcemia, or ECG changes accom- 7. Platelets: Dilutional thrombo- panying hypotension.

** Must Know * Should Know Page 291 dnaesthesia for Medical Shtdents

Potassium concentrations of > 25 screened for hepatitis B and syph- ) meqA, with pH values of < 6.7 are ilis. Testing the blood for malaria, normal values in stored packed cytomegalovirus, Epstein-Bar virus 1 RBCs. As the blood is transfused (infectious mononucleosis) and 1 and the pH normalizes, the potas- many other potentially transmissible i sium rapidly shifts back into the diseases, is not done unless RBC. Hence either hyperkalemia, specifically requested. j or occasionally hypokalemia may be observed after a blood transfu- Immune: There is a non-specific sion. suppression of the immune system that occurs after transfusing blood 9. Microaggregates: Standard blood products. This property has been administration sets are equipped exploited to improve renal allograft with 170 pm filters. They prevent survival. Adverse effects of the small clots present in the donor immuno-suppression may be associ- units from being transfused and ated with an increased risk of lodging in the pulmonary circula- postoperative infections and recur- tion. These filters should be used rence of cancer. on RBC products, platelets, FFP, and cyroprecipitate. Micro- References: aggregates consist of platelets, WBCs, and fibrin which aggregate 1. Transfusion Practices. Second edi- to form clumps in RBC products. tion 1992. American Society of Standard 170 pm blood filters, Anesthesiologists Committee on however, do not filter out micro- Transfusion Medicine. aggregates. Microaggregate filters (20 - 40 pm) are not recommended 2. McIntyre, BG. Blood conservation as their use has never been shown and transfusion practices. Contemp to reduce the incidence of respira- Anaesth 1994; 4: 4-7. tory distress syndrome following multiple transfusions. 3. Barash PG, Cullen BF, Stoelting RK. (ed.) In: Clinical anesthesia. 10. Infections: The most common type Second edition. JB Lippincott Co. of infection following a transfusion 1993. is viral. Screening tests for hepatitis C, HIV and HTLV-I 4. Doyle DJ. Complications of blood depend upon detection of the transfusion. Contemp Anaesth antibody to the virus, which may 1994; 3:18 - 19. not have formed, despite the presence of a viremia. Antibodies 5. Waxrnan K., et al. Hemodynamic ' can take up to 1 year to reach de- and oxygen transport effects of tectable levels in the case of an pentastarch in bum resuscitation. HIV infection. Blood is also Annals of surgery 1989; 29: 3.

Page 192 Chapter 20 Intravenous Fluid and Blood Component Therapy

Notes:

** Must Know Should Know Page 193 Common Perioperative Problems

This chapter provides a general For any resuscitation problem, a approach to common perioperative stepped XBC' (airway, breathing, problems. Abnormalities in heart rate circulation) approach is used. and blood pressure are common problems for which an organized approach in their initial management is essential. 1. Evaluate and ensure the patient Tables 21.1 - 21.5 present the classifica- has an adequate and unobstructed tion and differential diagnosis (Ddx.) of airway. common hemodynamic problems. These tables may be used for reference, Maneuvers to resolve a partial or com- and are not to be memorized. plete airway obstructiontake precedence over any other interventions. The I A common approach to clinician must be able both to recognize emergency problems an airway obstruction and utilize man- I1 Ddx. of Bradycardia euvers to resolve it. I11 Ddx. of Tachycardia IV Ddx. of Hypertension If the patient is not intubated: V Ddx. of Hypotension and shock states. Quickly assess whether the patient has M Nausea, emesis an airway obstruction preventing them MI Confusion, agitation from breathing. In the unconscious and delirium patient maneuvets such as a chin lift, jaw thrust, removal of foreign bodies, I. A Common Approach to and insertion of oral or nasal airways Emergency Problems. may be used to overcome an airway obstruction. Signs of an obstructed Over the next few years of your medical airway include lack of air movement training, you will undoubtedly be faced despite respiratory efforts, noisy or with emergency situations requiring stridorous respirations, intercostal in- your intervention. The following dis- drawing, tracheal tugging, accessory cussion of common problems aims to muscle use, and lack of air entry on prepare you for this situation. This may auscultation of the chest. occur on the ward, in the emergency department, or in a critical care setting such as the operating room. Chapter 21 Common Perioperarive Problems

If the patient is intubated: ministered with this device when the patient is not breathing (see figure If the patient is intubated it is important 23.4). quickly to ensure that the endotracheal tube is in fact in the trachea. Indirect Examine the patient. Is there evidence confirmation includes listening for equal of cyanosis? Quickly scan any monitors air entry to both lung fields and observ- attached to the patient. Ask for assisting chest excursion during positive ance in applying monitors such as a pressure ventilation. You should be blood pressure cuff, ECG monitor, and able to pass a suction catheter through pulse oximeter. Ensure that oxygen is the tracheal tube without meeting any being delivered from the source to the obstruction. Final1y, epigastric patient. auscultation should be negative for air entry to the stomach during positive 3. Evaluate and ensure the patients pressure ventilation. A portable chest ventllation Is adequate. X-ray can be used to confirm that the tip of the tube is in the mid-trachea. There are many conditions that can result in respiratory insufficiency. Ven- Direct confirmation that the tracheal tilation must be provided when a patient tube is in the trachea can be immediate- is not breathing. Auscultation, palpa- ly obtained by visualizing the tube tion, and percussion of the chest, in passing through the glottis during direct combination with the vital signs and laryngoscopy. When doubt exists con- pulse oximetry, are used in the immedi- cerning the positioning of the tracheal ate evaluation of the patient. Arterial tube or its patency, a fiberoptic blood gas analysis, chest X-ray, and bronchoscope can be passed through the pulmonary function tests may also be tube into the trachea. Observing carbon required to formulate a working diag- dioxide returning with each exhaled nosis of the etiology of the respiratory breath (end-tidal C02 monitoring) pro- insufficiency. vides immediate confirmation of tracheal intubation. 4. Assess the heart rate and rhythm.

2. Evaluate and ensure that the Quickly confirm or rule out an arrest patient Is receiving adequate oxy- situation. gen. Severe bradycardia must be assumed to be secondary to hypoxemia until proven In any emergency situation, it is always otherwise**. wise to apply oxygen. The Arnbu bag and mask provide a rapid method of 5. Assess the blood pressure and providing 100% oxygen. It allows the perfusion. patient to breathe 100% oxygen with the option of assisting their spontaneous Hypotension may result in decreased efforts. Manual ventilation can be ad- organ perfusion. Clinical findings that

** Must Know Should Know Page 195 Anaesthesia for Medical Students are associated with decreased organ temperature losses. Temperature losses perfusion include: result from evaporative, conductive, radiant and convective loss of body CNS: anxiety heat. Patients undergoing surgery are confusion exposed to a cold operating room with unconsciousness cold instruments, intravenous fluids and CVS: dysrhythmias or ECG an open wound through which heat loss evidence of ischemia occurs. The resulting hypothermia may Renal: decreased urine output. result in postoperative shivering, with a rise in heart rate, blood pressure and 5 The blood pressure should be confirmed to 6-fold increase in oxygen consump- by a manual cuff if there is any question. Increases in temperature peri- tion concerning its validity. Arterial operatively may result from drugs such lines, automated blood pressure cuffs, as atropine, or from the administration and human error can all be responsible of blood products. Other causes of an for factitious blood pressures. increased temperature include fever, sepsis, active intraoperative warming 6. Assess the patients volume status. efforts, and underlying disease states such as thyrotoxicosis or malignant Important changes in a patient's blood hyperthermia. volume status may be clinically subtle. Significant alterations in vital signs and 8. Scan for obvious causes of the mental status may result. Assess the abnormality. jugular venous pressure and the patients recent urine output. In the operating Correct any obvious underlying abnor- room, it would be appropriate to review mality. Hypotension and tachycardia the patient's duration of fasting, examine with inadequate fluid replacement, and the surgical wound, sponges, suction hypertension and tachycardia with inad- apparatus, and nasogastic drainage. An equate analgesia are common examples. overall assessment of the blood losses, Scan any monitors that are attached to and third space losses as well as the the patient, and consider establishing a adequacy of fluid replacement should be large bore intravenous. made (see chapter 20: Intravenous and Blood Component Therapy). 9. Establish addltional monitors where appropriate. 7. Check the patients temperature. Examples of additional monitors that Alterations in temperature associated may be appropriate include an ECG with anaesthesia and surgery may result monitor, blood pressure cuff, pulse in important cardiorespintory abnor- oximeter, and temperature probe. Invas- malities. Both hypothermia and ive monitors may include a foley cath- hyperthermia may occur. Hypothermia eter, arterial line, central venous pres- is frequently the result of intraoperative sure line or pulmonary artery catheter. Chapter 21 Common Perioperotive Problems

cardiac output is determined by the heart rate, preload, contractility and Common investigations that may aid in afterload (SVR). confirming the diagnosis include a CBC, INR, PlT, ABG, CXR, ECG, In a normal adult, hypotension is gen- glucose, electrolytes, and creatinine. erally defined as a systolic blood pressure of less than 90 mm Hg, or a mean 11. Formulate a plan, and recruit arterial pressure of less than 60 mm Hg. additional help if necessary. The most common cause of a hypotensive state is a decrease in intra- In an emergency situation, you may not vascular volume. This may result from have the luxury of having an extensive an acute hemorrhage or from a loss of history before you are required to act. fluids and electrolytes (see table 203: Nevertheless, you can proceed with Common conditions associated with assessing the status of the patient's fluid deficits). Acute hypovolemia airway, oxygenation, ventilation, heart reduces the venous return to the heart rate, rhythm, and blood pressure. Once (preload) resulting in a decrease in the patient is hemodynamically stable cardiac output and systemic blood pres- and receiving adequate oxygen and sure. Carotid and aortic baroreceptors ventilation, review the patient's history, sense the decrease in arterial pressure, recent lab data, perioperative course (in and initiate a series of events resulting the case of recent surgery), and formu- in an increase in sympathetic output late a provisional diagnosis so that you from the central nervous system and may initiate treatment. Remember to adrenal gland. The resulting release of recruit help in any emergency. norepinephrine and epinephrine increase the heart rate, contractility and SVR in I1 - IV: Tables 21.1 to 213 list the an effort to redirect and maintain blood causes of alterations in heart rate and flow to vital organs. increases in blood pressure perioperatively. Hypovolemic shock is the most common type of shock. A low central V: Hypotenslon venous pressure and low pulmonary The purpose of the cardiopulmonary capillary wedge pressure (PCWP) is circulation is to deliver oxygen and diagnostic of hypovolemia. Other forms nutrients to body tissues. When tissue of circulatory shock include distributive needs are not met, a state of shock is shock, obstructive shock and cardio- said to exist. The blood pressure is genic shock. Table 21.4 characterizes used as a gross indirect measurement of the hemodynamic features of the differ- organ perfusion and assessment of the ent forms of shock. adequacy of the circulation. It represents a complex interaction between cardiac output, blood volume and systemic vascular resistance (SVR). The

** Must Know Should Know ) 4naesthcsia for Medical Students

Table 21.1: Differential Diagnosis of a Decreased Heart Rate RESP Hypoxemia Hypercarbia Acidosis CVS Congenital Heart Block Decreased Sympathetlc Increased Parasympathetic tone: Tone: - Vagal reflexes (see CNS) - Beta Blockers - Drugs - High spinal or epidural - Paediatric patients anaesthesia (> T1 - T4) - Neurogenic shock Decreased Conductlon: - Atrial Fibrillation with a - Sinus bradycardia slow ventricular response - Junctional bradycardia - Type I1 Second degree AV - Idioventricular escape rhythm block - Sick Sinus Syndrome - Complete Heart Block - - Ventricular Asy stole CNS Baroreceptor reflex secondary to increased blood pressure or increased ICP Vagal Reflexes: Drugs: - Vasovagal reflex - Anaesthetic overdose - oculocardiac reflex - Succinylcholine - carotid sinus reflex - Opioids - airway manipulation (especially - Edrophonium, neostigmine important in paediatric patients) - Halothane - Digoxin - Beta blockers Other Hypothermia Hypothyroidism Athlete 8 Treatment options might include: - atropine - oxygen - ephedrine - fluids - isuprel - Trendelenburg position - epinephrine - remove offending cause - transcutaneous or - treat underlying drug toxicity transvenous pacemaker (eg. Digibind for digoxin toxicity) - cardiopulmonary resuscitation

Distributive shock is characterized by tributive shock is septic shock. systemic vasodilation, relative hypo- Arteriovenous shunting at the tissue volemia and an increase in cardiac out- level results in an accumulationof lactic put. The most common form of dis- acid and tissue anoxia. Table 21.4 lists

Page 198 Chapter 21 Common Ptrioperative Problems

Table 21.2: Dlfferentlal Dlagnosls of an Increased Heart Rate RESP Hypoxia Hypercarbia Acidosis CVS Slnus Tachycardla: A reflex sinus tachycardia may occur in shock states (see Table 21.5: Classification of Shock States). Sinus tachycardia may arise due to decreases in preload, afterload or contractility. Increased sympathetic stimulation arising from anxiety, pain, drugs and surgical stress is a common cause of sinus tachycardia. Other rhythms: - paroxysmal atrial tachycardia (PAT) - accelerated junctional rhythm - multifocal atrial tachycardia (eg. COPD patient) - atrial flutter with or without heart block - atrial fibrillation - pre-excitation syndromes with accessory pathways - ventricular tachycardia CNS Awareness under anaesthesia Anxiety Pain GU Full bladder HEME Anemia Transfusion reaction END0 Hypermetabollc states: Other: - fever - Addisonian crisis - sepsis - porphyria - pheochromocytoma - hypoglycemia - thyrotoxicosis - hypercalcemia - malignant hyperthermia - malignant neuroleptic syndrome IMMUNE Anaphylaxis DRUGS Atropine Ephedrine Cocaine (used for local anaesthesia) Isoflurane Dopamine Isoproterenol Epinephrine Pancuronium Treatment is directed at the underlying cause of the increased heart rate. examples of the four classes of shock. heart fails to perform its pumping function. This occurs as a result of a Cardiogenic shock results when the myocardial, valvular, or electrical

" Must Know Should Know Page 199 .i Anaesthesia for Medical Students j

Table 21.3: Differential Diagnosis of an Increased Blood Pressure Perloperatlvely RESP Hypoxia Hypercarbia CVS Essential hypertension Coarctation Post-carotid endarterectomy (acute denervation of carotid baroreceptors) CNS Pain Full bladder Autonomic mass reflex Shivering Light Anaesthetic level (quadraparetic or Hypothermia Emergence delirium paraplegic patients) Anxiety Increased ICP GU Renal artery stenosis Parenchymal Disease Pregnancy induced hypertension Toxemia END0 Hyperthyroidism Carcinoid Cushings disease or syndrome Hyperparathyroidism Pheochromocytoma - hypercalcemia Conn's syndrome (hyperaldosteronism) MSK Malignant hyperthemia Malignant neuroleptic syndrome DRUGS Ephedrine Rebound from stopping Epinephrine antihypertensive drugs: Cocaine - clonidine Phenylephrine - beta blockers Ketamine Acute narcotic reversal with naloxone Drug interactions: - Monoamine oxidase inhibitors (MAOI's) with meperidine - MAOI's with indirect acting vasopressors (eg. ephedrine) Treatment is directed at the underlying cause of the increased blood pressure.

problem. Amyocardial infarctionis the with a cardiac index of less than 1.8 most common cause of cardiogenic Umin/m2 and a systolic BP less than 80 shock. Characteristic findings include mm Hg (see table 10.1 and 10.2 for an increase in CVP, PCWP, and SVR, derivations and normal values). Chapter 21 Common Perioperalive Problems

Obstructive shock occurs when there is maintained, but digital capillary refill is an obstruction preventing cardiac filling slightly retarded. Urinary output is only or emptying. Two immediately treat- mildly depressed. Postural hypotension able causes of obstructive shock include may be associated with class I1 a tension pneumothorax and cardiac hemorrhage, as may subtle central nerv- tamponade. ous system changes such as fright and hostility. Hemorrhagic Shock Classification: The normal response to increasing Class 111 hemorrhage: hemorrhage produces characteristic Defined as a 30 - 40% loss of blood physiological signs. These signs have volume. Patients with class I11 been used to classify hemorrhagic shock hemorrhage present with tachycardia, according to the quantity of blood loss. systolic and diastolic hypotension, Table 21.6 defines 4 classes of hemor- delayed capillary refill (>2 seconds), rhagic shock based on the patient's vital reduced urinary output, and an appre- signs, and predicts the percent blood hensive, slightly clouded sensorium. loss and appropriate initial therapy. Class IV hemorrhage: Class I hemorrhage: Defined as a blood loss of 40% or more Defined as the loss of as much as 15% of the blood volume. The patient mani- of blood volume. It is associated with fests signs of frank shock with cool, minimal physiologic changes. diaphoretic, ashen skin, tachycardia, hypotension or unobtainable blood pres- Class I1 hemorrhage: sure, anuria, and a reduced level of Defined as a 15 - 30% loss of blood consciousness. volume. Class 11 hemorrhage is associated with modest elevations in heart rate Patients with class Ill and IV and decreases in pulse pressure as dia- hemorrhages will require immediate stolic pressures rise with smaller stroke intravenous fluid administration to sur- volumes. Systolic pressures tend to be vive. Patients with class IV hemorrhage

** Musf Know Should Know Page 201 Anaes~hesiafor Medical Students )

Table 21.5: Classification and Etlology of Shock States Hypovolemic Shock - most common cause of shock - occult blood or fluid losses Cardlogenic Shock Myocardial: Myocardial (continued): - relative drug overdose - arrhythmias (anaesthetic drugs) - cardiomyopathy (congestive, - other drug effects hypertrophic, restrictive, or (p-blocker, ca2+channel blocker) obliterative) - ischemia Valvular Disease: - infarction (esp. NB when stress is - rupture superimposed) (papillary muscle, ventricular Aortic regurgitation septum, chordae tendonae) Mitral regurgitation

Distributive Shock Anaphylaxis, Anaphylactoid reaction Addisonian crisis Sepsis Transfusion reaction Drugs (Vasodilators) Severe liver disease Neurogenic shock A - V fistulas High regional sympathectomy Thyrotoxicosis (eg. high spinal anaesthesia) Hypothyroidism Obstructive Shock Tension pneumothorax Aortic dissection Pericardial tamponade Aortic cross-clamping Pulmonary embolism Atrial myxoma (blood clot, fat, air, tumor, etc) IHSS Supine hypotension during Valvular heart disease with stress pregnancy (aortocaval compression (eg. Aortic or mitral stenosis with gravid uterus) pregnancy or trauma). IVC, or heart compression by surgical instruments will require blood transfusion to sur- Hematocrits as low as 20 to 25% may vive, but class 111 hemorrhage patients be well tolerated if total blood volume may tolerate post-resuscitation anemia if is adequate. The use of clinical signs to fluid resuscitation is accompanied with estimate traumatic blood loss is very immediate control of the hemorrhage. important because soft tissues and body Chapter 21 Common Perioperative Problems

Table 21.6: Classlflcatlon of Hemorrhagic Shock Hemorrhage 46 Blood Physlologlcal changes. Treatment Volume loss

Class I s 15 HR < 1001min. Rapidly infuse 1 - 2 SBP normal liters of balanced salt PP:normal or increased solution (BSS), then CR: normal maintenance fluids. RR: 14 - 201min. CNS: Anxious Class 11 15 - 30 HR > 1001min. Rapidly infuse 2 liters SBP normal of BSS, re-evalua te DBP increased continued needs Postural hypotension PP: decreased CR: delayed RR: 20 - 30Imin. CNS: more anxious Class 111 30 - 40 HR > 120lmin. Rapidly infuse 2 liters SBP decreased of BSS; re-evaluate; PP: decreased replace blood losses CR: delayed or absent with 1:3 BSS or 1:l RR: 30 - 401min. with blood (PRBC's, CNS: Confused colloid, other blood products). Maintain Class IV r 40 HR > 140jmin. urine output > 0.5 SBP decreased ml/kg/hr. PP: decreased CR: absent RR > 35lmin. CNS: Lethargic i HR = heart rate (bpm); SBP = systolic blood pressure; DBP = diastolic blood ' pressure; PP = pulse pressure; CR = capillary refill; RR = respiratory rate; j CNS = central nervous system

) cavities frequently conceal large quan- VI: Nausea and vomltlng. ) tities of blood with minimal external ) body changes. Nausea and vomiting, have a profound effect on the patients perception of their ) i ** Must Know Should Know Page 203 Anaesthesia for Medical Students perioperative care. It has been shown to Nausea and vomiting perioperatively significantly increase the time the must be assumed to be secondary to patient spends in the post anaesthetic bradycardia and hypotension until care unit (PACU), and places the patient proven otherwise**. who is recovering from anaesthesia at risk of gastric aspiration. When assessing a patient with perioperative nausea and vomiting, quickly Preoperative patient risk factors include: evaluate the patients vital signs. Vagal reflexes, with a decrease in blood pres- 1. Previous history of anaesthetic asso- sure and heart rate, may present as ciated nausea and vomiting (review nausea and vomiting. old chart if possible). 2. Young age. A differential diagnosis for nausea and 3.. Female gender. (The probability of vomiting includes: postoperative nausea and vomiting Hypotension has been linked to a woman's men- Bradycardia strual cycle.) Drug induced nausea 4. Operative procedure. (Increased - opioids incidence with eye, middle ear, and - anaesthetic agents female pelvic surgery). Surgical manipulation 5. Obesity. Pain - surgical Many anaesthetic agents have been - biliary or renal colic associated with nausea and vomiting. - migraine The mechanisms are multiple and com- Drug toxicity: plex. Opioids are perhaps the most - digoxin potent emetics. They have been shown - theophylline to directly stimulate the chemoreceptor - ASA trigger zone of the fourth ventricle, - alcohol stimulate the vestibular apparatus, delay Hyponatremia gastric emptying, and increase gastric - postoperative TCIRP patients secretions. Hypercalcemia - cancer patients Nitrous oxide may have a direct action Diabetic ketoacidosis on the chemoreceptor trigger zone, as Pregnancy well as acting on the middle ear, and Coexisting gastroenteritis cause both gastric and bowel distension. Acute hepatitis Other common agents associated with Other: perioperative nausea include sodium - renal failure thiopental, inhalational agents, and - hepatic failure cholinesterase inhibitors. - adrenal failure - hypothyroidism - raised ICP

Page 204 Chapter 21 Common Perioperative Problems

There is no one treatment for this prob- tered- one hour prior to anaesthesia in lem. Frequently a number of factors patients with a ,history of resistant contribute to the patient's nausea. nausea and vomiting associated with Switching the opioid used for, anaesthesia. This is followed by 2 postoperative analgesia, or adding a non additional doses of 8 mg each at 8 hour steroidal anti-inflammatory agent may intervals. Alternatively, established resolve the problem. nausea and vomiting may respond to a single injection of 4 mg intravenously. Common agents used to treat perioperative nausea and vomiting include: A combination of antiemetic drugs may be more effective in preventing roperi idol^ postoperative nausea and vomitting. 0.25 - 0.5 mg iv pm The combination of ondansetron and ~imenh~drinate(Gravel@) dexamethasone has been shown to be 10 - 50 mg iv/im/po effective in reducing the incidence of (maximum 50 mg q 3 - 4 hours). nausea and vomitting in cisplatin Metochlorpropamidet chemotherapy. Ondasetron (4mg) and 10 - 20 mg iv every 6 hours pm. dexamethasone (8 mg) has recently (contraindicated in bowel obstruction) shown promising results in preventing Prochlorperazine (Stemetil@)t nausea and vomitting postoperatively4. 10 mg im every 6 hours prn. VII: Postoperative Agitation and Dopamine re~e~tor'antagonists.The delirium. potential for extrapyramidal reactions increases as dosage and number of The agitated, delirious, or aggressive agents used increase. Dysphoric patient is rarely seen in the PACU reactions and disturbed sleep patterns today. This is due perhaps to a combi- have been reported with moderate nation of our improved understanding of doses of droperidol (2.5 mg iv). pain management, the availability of shorter-acting anaesthetic agents, and Less common agents used include: improvements in our monitoring equip- Propofol 10 mg iv. ment (oximetry, peripheral nerve One mglkgfhr infusions have been used stimulator, and end-tidal carbon dioxide successfully to prevent nausea and monitoring). vomiting in patients receiving chemotherapy, who have a past history of An initial ABC approach is used, with nausea and vomiting. the use of physical restraints if needed to protect both the patient and the medi- Ondansetron is a new selective cal team. The physical restraints are serotonin antagonist. It is more com- removed as soon as the offending cause monly used to treat radiation or chemo- is removed or chemical restraints substi- therapy-related nausea and vomiting. tuted. An oral dose of 8 mg may be adminis-

** Must Know Should Know Page 205 Anaesthesia for Medical Studen& .

Upper airway obstruction, residualpar- Following clinical evaluation, appropri- alysis, hypercarbia, and hypoxemia are .ate investigations may include a all potent stimulants which can produce measurement of the patient's glucose, an agitated state**. electrolytes, calcium, arterial blood gas, and tests of neuromuscular strength. A gross neurological examination should be performed quickly (e.g., If a thorough search fails to identify any pupillary assessment, movement of arms of the above causes of postoperative and legs, Glascow coma scale (GCS) agitation, small doses of a benzo- score), while communicating reassur- diazepine such as midazolam (0.5 - 1.0 ingly with the patient. mg iv), or an antipsychotic such as haldol (2.5 - 5.0 mg ivlim) may be Elderly patients are particularly prone to warranted. postoperative confusion and agitation. Common causes of agitation include Consider small doses of: pain and bladder or bowel distension. Naloxone (0.04 - 0.08 mg increments) Patients recovering from anaesthesia Flumazenil '(0.2 - 0.6 mg iv), or may appear able to communicate Physostigmine (0.5 - 2 mg iv) verbally, but unable to recognize that respectively, if excessive sedation is felt the cause of their distress is pain or a to be secondary to opioids, benzo- full bladder. diazepines, or anticholinergic agents.

Less common causes of an agitated References: postoperative state include: Drug effect 1. Review Article: Anaesthesia and - ketamine emesis. I, 11. Palazzo MGA, - anticholinergics: Strunin L. Can Anaesth. Soc. J. - atropine 1984; 31: 178-87, 407-15. - scopolamine - tricyclic antidepressants 2. Review Article: Postoperative TURP syndrome nausea and vomiting: Its etiology, - hyponatremia treatment and prevention. Watcha - glycine toxicity MF, White PF. Anesthesiology Hypercalcemia 1992; 77: 162-84. - cancer patients Hypoglycemia 3. Larijani GE, GratzI, Afsar M, Acute Stroke Minassian S. Anesth Analg 1991; Raised ICP 73; 246-9. Anxiety Fear 4. Rajeeva V, Bhardwaj N, Batra YK, Separation from caregivers Dhaliwal LK. Can J Anesth 1999; Acute drug withdrawal 46: 40 - 44. Acute drug intoxication Chapter 21 Common Perioperative Problems

Notes:

j ** Must Know * Should Know Managing the Circulation

Hemodynamic abnormalities of the a factor of 10 during extreme exercise circulation may necessitate interventions in normal adults. The three determi- to maintain normal oxygen transport and nants of the stroke volume are the pre- organ perfusion. This may occur in the 10~4afterload, and contractility. perioperative period as a result of pain, anxiety, hypoxia, hypercarbia, and The preload is defined as the end-dia- abnormalities of temperature or intra- stolic stretch of the left ventricle. As vascular volume (see chapter 21). preload increases so does the left Correcting these abnormalities should ventricular work, cardiac output, blood precede the administration of any pressure, and stroke volume (recall the vasoactive agents. Frank-Starling curves). Excessive increases in end-diastole stretch results Pharmacologicmanipulation of both the in a decline in cardiac performance parasympathetic and sympathetic when the left ventricle becomes over- nervous systems may be required to distended. The left ventricular end-dia- correct hypotensive, ischemic or stolic volume (LVEDV) is our best hypertensive emergencies. Table 22.1 measurement of preload. Since the lists the different classes of medications LVEDV is difficult to measure clinical- that may be used to restore circulatory ly, the filling pressures of the left ven- homeostasis. tricle at end-diastole (LVEDP) may be estimated by the measuring the pulmon- Central to our understanding of the ary capillary wedge pressure (PCWP) circulation and oxygen transport is the with a pulmonary artery catheter. Gen- concept of cardiac output. The cardiac erally, an increase in the LVEDP corre- output (CO) is defined as the amount of sponds with an increase in LVEDV. In blood pumped to the peripheral circula- patients with normal a right and left tion per minute. It is expressed as the ventricle, mitral valve, pulmonary product of the heart rate multiplied by vasculature, and airway pressures, the the stroke volume. assessment of the central venous pressure (CVP)may be used to estimate the LVEDV and preload.

A normal CO value for an adult is 25 Afterload is defined as the myocardial to 35 Umin/m2, or 45 to 6.0 Umin in wall stress of the left ventricle during a 70 kg adult. The CO can increase by ejection. It is a measure of the work

Page 208 Chapter 22 Managing the Circulation the left ventricle performs with each Patients presenting to, or leaving the contraction. In the absence of aortic operating room with vasoactive medica- stenosis, afterload depends on the elas- tions infusing, must be considered to be ticity of the large arteries and on the serious1y ill. All vasoactive agents have systemic vascular resistance (SVR). serious potential side effects that must The SVR can be estimated using a be considered whenever they are used. calculation incorporatingthe mean arter- Indiscriminate infusions of vasopressors ial blood pressure, cardiac output, and may produce the desired increase in CVP (see table 10.1 and 10.2). blood pressure, but may also severely restrict blood flow to vital organs such Contractility is the myocardium's intrin- as the bowel, liver and kidney. Marked sic ability to perform work at any given increases in peripheral vascular resis- level of end-diastolic fiber length tance produced by vasopressors may (preload). It is primarily determined by precipitate cardiac failure. the availability of intracellular calcium. All agents that increase myocardial The principle goal of circulatory support contractility produce an increase in is to optimize tissue perfusion with intracellular calcium. Contractility oxygenated blood. To achieve this, one increases with sympathetic stimulation must assess and optimize the preload, and inotropic drugs, such as digoxin. afterload, heart rate, contractility, oxy- Hypoxia, acidosis, beta blockers, cal- gen transport and organ perfusion (see cium channel blockers, and myocardial table below). ischemia or infarction are common conditions that depress contractility. Increases in preload, heart rate, contrac- Optimize Assessed by: tility or decreases in afterload, all promote forward flow and an increase in Preload PCWP: 10 - 15 mmHg CW: 8 12 mmHg cardiac output. - Aftedoad SVR = 900 - 1500 Vasoactive drugs may be classified as dynes.sec.cm4 acting by either a catecholamine or a CI > 2.5 L./inin/mz non-catecholamine mechanism. Drugs ContracClity acting through a catecholamine mechan- Heart Rate 60 - 90 bpm ism may have either agonist or antagonist receptor activity. Most Oxygen Arterial blood gas catecholamine vasoactive drugs have a Transport Mixed venous oxygen saturnlion (MvOJ combination of alpha and beta Hemoglobin adrenergic receptor activity (see tables 223 - 22.5). When choosing to use a Organ MvO, saturation vasoactive medication, one ought to Pefision Serum lactate consider the risks of using the drug, the ABG hemodynamic goals one seeks, and the Urine output pharmacologic properties of the drug. CNS sensorium

** Must Know Should Know Page 209 j Anaesfhesia for Medical Students

Table 22.1: Cardiorespiratory effects of receptor stimulation. 1

) Receptors Agonlst Antagonlst 1 Adrenergic: ) Peripheral vasodilation, Alpha-1 Vasoconstriction of the skin, ) gut, kidney, liver, and heart reflex tachycardia, (e.g., phenylephrine). hypotension (e.g., prazosin) j Alpha-2 Reduces sympathetic outflow CNS stimulation, increased ) from the CNS inhibiting sympathetic outflow. J norepinephrine release increased HR, contractility, j (e.g., clonidine, and cardiac output. dexametomidine). Beta-1 Increased heart rate, myocardial Decreased HR, contractility, J conduction, and contractility and conduction, ) (e.g., isoproterenol) (e.g., esmolol).

Beta3 Bronchodilation, peripheral Bronchospasm, peripheral ) vascular smooth muscle vasoconstricton. relaxation, (e.g., salbutamol). 1 1 Dopamine-1 Peripheral vasodilation of the renal and splanchnic vasculature, (e.g., dopamine). 1 Cholinergic Decreases heart rate, conduct- Anticholinergics increase (Muscarinic) ion, and cardiac output. heart rate, conduction, and Increases bronchial secretions, contractility. They also (e.g., edrophonium). decrease bronchial secretions, (e.g., atropine). Calcium Increases contractility, vaso- Decreases contractility, channel constriction (e.g., calcium). increases vasodilation, (e.g., nifedipine). Other Phosphodiesterase inhibitors: Produce a concentration dependant increase in contractility with arterial and venous dilation (e.g ., amrinone).

Cardiac glycosides: (e.g., digoxin)

Page 210 Chauter 22 Mananina the Circulation

Table 22.2: Manipulating the determinants of cardiac output to correct hemodynamic disturbances in the circulation. Tables 21.1 - 21.6 are presented for reference only.

Determlnants Hemodynamlc Disturbance of Cardiac (accompanied by lists of vasoactlve agents and Output lnterventlons used to treat the disturbance) Preload Increased Preload Decreased Preload Venous vasodilators Crystalloid, colloid infusion - nitroglycerine (see chapter 20) - nitroprusside Diuretics - furosemide Phlebotomy Heart Rate Increased Heart Rate Decreased Heart Rate Beta blockers Anticholinergics - propranolol - atropine - metoprolol Beta Agonists - esmolol - isoproterenol Calcium channel blockers - ephedrine - verapamil Pacemaker Contractlllty Increased contractlllty Decreased Contractlllty General anaesthetics Digoxin Norepinephrine - halothane Amrinone Epinephrine Beta blockers Dopamine Surgery Calcium channel blockers Ephedrine Intra-aortic Dobutamine balloon pump

Afterload Increased afterload Decreased afterload Arterial vasodilators Alpha agonists - sodium nitroprusside - phenylephrine - hydralazine - norepinephrine Labetalol Amrinone Crystalloid or colloid fluid ACE inhibitors therapy - captopril - enalapril - lisinopril Dobutamine

** Must Know * Should Know Page211 Anacslhesia for Medical Students i In October 1992, the National Confer- 3. Merin RG. Autonomic nervous ence on Cardiopulmonary Resuscitation system pharmacology, Anesthesia (CPR) published the current recommen- third ed. Edited by Miller RD. dations for adult cardiac life support Churchill Livingstone 1990, pp 471 (ACLS). A summary of the algorithms - 504. are presented (for reference) in figures 22.1 to 225. 4. American heart association: Text- book of advanced cardiac life sup- The Guidelines for Cardiopulmonary port. 1992. Resuscitation published in JAMA in 1992 classified therapeutic interventions 5. Emergency Cardiac Care Committee as: and Subcommittees, American Heart Association. Guidelines for Class I: Recommendation is cardiopulmonary resuscitation and definitely helpful. emergency cardiac care, 111: Adult Class IIa: Recommendation Advanced Cardiac Life Support. acceptable, and probably JAMA 1992; 268: 2199-241. helpful. Class Ilb: Recommendation acceptable and possibly helpful. Class 111: Recommendation is not Footnotes for figure 22.1, page 213: indicated, and may be harmful. a. Unstable condition must be related to the tachycardia. Signs and symptoms The properties of vasoactive medica- may include chest pain, shortness of tions used in manipulating circulatory breath, decreased level of conscious- abnormalities are presented (for refer- ness, low blood pressure (BP), shock, ence) in tables 223 to 22.7. pulmonary congestion, congestive heart failure, acute myocardial References: infarction. I 1. Hug CC, Kaplan JA: Pharmacology b. Carotid sinus pressure is contraindi- - cardiac drugs, Cardiac Anesthesia, cated in patients with carotid bruits; ' Edited by Kaplan JA. Grune and avoid ice water immersion inpatients ; Straton, 1979, pp 39 - 69. with ischemic heart disease.

2. Thys DM, Kaplan JA. Cardiovas- c. If the wide-complex tachycardia is ; cular physiology, Anesthesia, third known with certainty to be PSVT and ed. Edited by Miller RD. Churchill BP is normallelevated, sequence can I Livingstone 1990, pp 551 - 583. include verapamil.

Page 212 Chapter 22 Managing the Circulation

/ Egure22.1,Tachycardia Algorithm > 150 bpm, prepare Assess vital signs for immediate Review history cardioversion Administer oxygen Perform physical exam. May give trial of I Attach Monltor, pulse oxtmeter, Order 12 lead EGG medications based on and automatic blood pressure Order portable CXR arrhythmia. I Immediate cardioverslon Is seldom needed for Unstable, wlh serlous signs or ~~m~toms?~l- yes*~HR<150bpmm J I I I

~tria~flutter b supraventrlcular tachycardia of 3 3 pGGGq I Lldocaine 1 - 1.5 1 ( tidocaine 1 - 1.5 1 Oiltiazem Imgkg lv push ) ( mgkg iv push ] Beta blockers 3 evew 6 - 10 mlns every 6 - 10 mlm Verapamil

Digoxin rapid iv push ' ~docal&0.5475 mgkg Iv push, mgkg iv push, Qulnldine maxjmum 3 mgkg maximum 3 mglkg I \ JI Anticoagulants (~denosine12 rng;) 5. rapid iv push ( Adenosine 6 mg , \ over 1 - 3 secs rapid iv push (may repeat once

(may repeat once

Procalnarnide 20 - 30 mglmin Normal maximum total 17 mgkg or elevated or unstable

** Must Know Should Know Page 21 3 Anaesthesia for Medical Students

R1uw22.2: Bradycardia algorithm (Patient is not in cardiac arrest)

Assess ABCs Assess vital signs Secure airway Review history Administer oxygen Perform physical examination Start iv Order 12 lead ECG Attach monitor, pulse Order portable CXR oximeter, and automatic I blood pressure Too slow (< 60 beatslmln) 1

( Serious signs or symptoms? I

NO I Yes

CI CI '~~~e11 second-degree' 'intervention sequence: AV heart block? Atropine 0.5 - 1.O mg" (I & Ila) or TCP, if available (I) Third-degree Dopamine 5 - 20 ug/kg/min (Ilb) \ AV heart block? , Epinephrine 2 - 10 ug/min NO I yes Isoproterenol .1 d [observe I Prepare for transvenous pacer Use TCP as a bridge device

Footnotes for bmdycardia algorithm: a. Serious slgns or symptoms must be related to the slow rate. Cllnlcal manlfestatkms Include chest pain, shortness of hth,decreased level of consciousness, bw BP, shock, pulmonary congestion, CHF; acute myocardial Infarcfion. b. Do not delay TCP u3rlle awaiting lvaccess or for atropine to take effect If patient Is symptomeb. c Denervated fmsplanted hearts wfll not respond to atmpine. Qo at once to pacing, catechohine Infusion, or both. d. Airoplne should be given In repeat doses In 3 - 5 mln krtervels up to 0.04 mg.Gmdder shorter daslng Intervals In severe conditions. e. Never treat thid-degreeheart block plus ventricular escape beats wlth Ildocalne. f. lsopmterenol should be used, if at all, with extreme cautlon. At low doses It Is Class Ilb (possibly helpfuu; at hlgher doses it kr Class 111 (hamfull. \ g. VenW patient tolerance and mechanical capture. Use analgesia and sedation as needed.

Page 214 Chapter 22 Managing the Circulation

/ ngureP.3: Asystoe treatment algorithm (* Continue CPR 1 lntubate at once I Obtaine iv access 1 Confirm asystole in more than one lead

1 Class I: definitely helpful f~onsiderpossible Class Ila: acceptable, probably helpful Hypoxia Class Ilb: acceptable, possibly helpful Hyperkalemia Hypokalemia Preexisting acidosis Drug overdose \. Hypothermia I I Consider immediate

Atropine 1 mg iv repeat every 3 - 5 mlns up to 0.04 mghg. + [ Consider termination of effortsf 1 Foolnotes lbr asyslde algoijttun: a TCP Is a class Ilb Intervenlion. Lack of success may be due to delays In pacing. To be effectl~,TCP must be pdmnd ear& eimuhaneously wkh drugs. Eddencs does not support rwtlne use of TW for asystole. b. The rewmmended dose of eplnephifne Is 1 mg Ivpush every 3 - 5 mlns. If thls approach MIS, sewd Class IIb dosing regimens can be considered: lntermedlate eplnephme 2 - 5 mg Ivpush, evew 3 - 5 mln; Escalating epinephifne 1 mg - 3 mg - 5 mg Ivpush, 3 dnaper;, Hlgh ephephifne 0.1 n@g Iv push, every 3 - 5 mln. c. Sodium bicarbonate 1 mE& Is Cless 1Ifthe patient has known perexldlng hyperkalmla. d. Shorter atropine blngIntervals are Class Ilb In asystollc errest. e. Sodium bicarbonate 1 mE&: Class Ila: if known preexlstlng bkatbonate-responsive addosls; if overdose wkh tifcydlc entldepresaants; to alkalinlze the urine In drug overdoses. Class Ilb: if lnhrbated end oonlbued long arrest Interval; upon return of spontaneous clrculetion seer bng arrest Interval. Class 111: hypoxk lactic acMosls f. If patlenl remalns In asyetole or other agonal rhythms after successful lntubetbn and InillaI medkations and no reversible causes en, Identified, oonslder tennlnetion of resuscitative efforts bye physlclen. Conslder time interval shce arrest.

" Must Know Should Know Page 225 Anaesthesia for Medical Students

rng~r.221: Ventricular Fibrillation - Pulseless Ventricular Tachycardia Algorithm (VF I VT)

ABCs Perform CPR until defibrillator attached a

Provide medications appropriate for BP,

'continue CPR lntubate at once FOOE~~IBSfor M/ ~7dgotithm: Obtain IVaccess a. PrecordLl thump is a Class Ilb action In witnessed arrest, no pulse. and no defibrillator Immediately 4 avalble. Epinephrine 1 mg iv pushG b. ~ypolhermiccardlac arrest lo treated diiferently repeat every 3 - 5 mins. aner lhls point. See ACLS sedlon on hypothemla. 4 c. The recommended dose of epinephrine Is 1 mg iv J push every 3 - 5 mlns. If fhls approad fells, Defibrillate 360 within sewel Class Ilb ddngreghens can be .30 - 60 sea consMered (see footnotes figure 22.3 b). # d. Sodlum bhrbonate (I mErykgI Is Class I Ifpatlent Administer medications of probable' haknown~reexlsti& h~p&!+mla. a MUII~~I~SBQUW~~S~O~ (2~J. rn 300 J, benefit (Class Ila) in persistent or - 360 4 are acceptable hen, (ass I), eespeclal& Lrecurrent VF / VT g / when medlcatbns are delayed. 4 f. Medicatbns: '~efibrillate360 J, 30 - 60 secs after- Udmlne l.5mMgivpush. Re~mlln3 - 5 mins each dose of medication to total loading dose of 3 mglkg; lhen use Eretyllum 5 mgkg ivpush. Repeat In 5 mlns at 10 Pattern should be mag ,drug-shock, drug-shock , Magnesium sulfete I - 2gm iv dn tomade de polnfes or suspected hypomagnesemlc state or severe retkachvy M PmcahmMe 30 m&mln h rehadory VF (mlmum total 17 m&g). g. Sodium blaubonate (I mEWg iv): (see footnotes figure 22.3 e)

C $ Table 223: Properties of cardiovascular drugs. (n invasive pressure monitoring manditory) s?i Drug Receptor Activity Single Bolus Infusion Rate and Comments a-1 a-2 p-1 82 Dose Preparation Epinephrinen 2+ 3+ 1+ 2+ Anaphylaxis: 0.01 - 0.2 Inotropic beta effects at 0.02 - 0.09 mcgkghnin, (Adrenalin) 3 - 5 mcgkg mcgkgbin; pressor alpha effects at > 0.09 mcg/kg/min. Used Arrest 1 mg 4 mg in 500 ml for hypotension with myocardial depression. (8 mcghnl) Amri none Phosphodiesterase 0.75 mgkg 2 - 10 mcgkghnin CO increased, HR unchanged, BP may decrease. (Inocor) inhibitor with positive over 2 - 3 PAP, PCWP, SVR all decrease. Used as an inotropic action mins. inotrope in patients with end stage heart disease. independent of Produces arterial and venous vasodilation and may adrenergic receptors. decrease BP. Dopamine 1-4+ 0 1+ 2-4+ 1 - 10 mcg/kg/min Renal effects via dopaminergic DA-1 receptor at 1 (Inotropin) plus 400 mg in 500 ml - 4 mcgkghnin. At 5 - 10 mcgkghnin beta effects Dopamine receptor (800 mcghnl) predominate with an increase in HR, and CO. agonist Above 10 mcgkghnin alpha effects predominate and renal blood flow may decrease. Commonly used in lower doses to increase CO while preserving renal perfusion.

Dobutaminen 0-1+ 0 1+ 3+ 1 - 20 mcgkg/min CO increases, SVR and PCWP decrease. At lower (Dobutrex) 500 mg in 500 rnl doses CO increases without severe tachycardia or (1 mg/ml) hypotension. At 10 - 15 mcg/kg/min, HR and vasodilation become more prominent BP may not change. Used to increase CO. L\ .-%-LL,LbLLLbLLLLbbbbLbLLLb--- -

Table 22.4: Properties of cardiovascular drugs. (%vasive pressure monitoring manditory)

DNg Receptor Activity Single Bolus Infusion Rate Comments a-1 a-2 fk1 82 Dose and Preparation Norepinephrine 4+ 4+ 2+ 0 0.05 - 0.5 Direct alpha and beta receptor agonist Decreases in (Levophed) mcg/lr&infi renal blood flow occur with even low doses. At 4 mg in 500 ml low doses the alpha effects increase blood pressure, (8 mcghnl) causing vasoconstriction, and reflex bradycardia. At higher doses, beta receptor stimulation increases contractility. - Phenylephrine 4+ 0 1+ 0 SO - 100 0.1 - 0.5 Phenylephrine represents an almost pure alpha-1 (Neosy nephriae) mcg mcg,kghninfi agonist Beta stimulation only occurs at very high 10 mg in 500 doses. Phenylephrine may be used temporarily to ml provide profound vasoconstriction while the (20 mcgEml) underlying cause of hypotension is corrected. Reflex bradycardia may occur. May be useful in patients with hypotension associated with a decreased SVR and tachycardia. Ephedrine 3+ 0 2+ 1+ 5 - 10 mg iv Onset within 1 Ephedrine is an indirect acting alpha and beta 25 - 50 mg minute with a agonist It causes vasoconstriction and an increase im duration of in heart rate, blood pressure and cardiac output It 5 - 10 minutes. is useful in patients with hypotension without Genetally not tachycardia. It is the drug of choice for hypotension used as an due to regional anaesthesia during labour and ibsion due to delivery as its combined adrenergic effects result in tachyphylaxis. an increase in blood pressure without uterine (50 mghnl amp) vasoconstriction. Anaesthesia for Medical Students

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fr, 9a = 'E - 0 h 'i , 8 .;. & AS 8 2 2 4 23 B 1 4.3 g 1 8 a J 1 a z6 'i: Z PIG A& Table 22.6: Properties of cardiovasc Iar drugs. 1 Single Bolus Dose 1 Comments Action - - - - Calcium No beta adrenergic Used to treat hypocalcemia, ECG changes of Chloride activity. Rapid hypocalcemia in the presence of hypotension, and direct acting calcium channel blocker overdose. May also be useful inotrope with a in the treatment of hypermagnesemia, and to protect duration of 5 - 10 the myocardium from the effects of hyperkalemia. minutes. - - Metoprolol Selective beta-1 1 - 5 mg iv every 2 - 5 mins pm., Useful in controlling hypertension, tachycardia, and (Betabloc) antagonist may require up to 15 mg for full reducing myocardial ischemia. Potential side effects beta blockade. include bradycardia, heart block, pulmonary edema, bronchospasm, and impaired insulin release resulting in hypoglycemia.

Esmolol Selective beta-1 Single bolus: 0.5 mgkg iv Rapid onset of less than 2 minutes with a duration of (Brevibloc) antagonist less than 30 minutes. Lndicated in the treabnent of Iafusion: 1 mghl solution hypertension and tachycardia in patients at risk of 50 - 300 mcgkghnin hernodynamically induced myocardial ischemia. Also indicated in the control of the ventricular rate in acute atrial fibrillation and atrial flutter. ------verapamil Calcium channel Single bolus: 2.5 - 5 mg iv Useful in terminating a supraventricular dysrhythmia. (Isoptin) antagonist maximum 10 mg iv. Also used in controlling the ventricular rate in patients with atrial fibrillation and atrial flutter. Contraindicated in preexcitation syndromes (e.&, Wolff-Parkinson-White syndrome) as it may increase conduction in the accessory pathway. 3 Table 22.7: Properties of cardiovascular drugs. 2 h h DN~ Mechanism of Single Bolus Dose Comments Action

Atropine Anticholinergic 0.3 - 0.6 mg iv increments Most commonly used to treat bradycardia (heart rate c max. 3 mg 45 bpm). Also useful as an antisialogogue to dry oral secretions and aid oropharyngeal topical anaesthesia for an awake fiberoptic intubation.

Adenosine Antidysrhythmic 6 mg iv Useful in pamyma1 supraventricular tachycardia's. (Adenocard) May be associated with significant hypotension, facial flushing, and shortness of breath. Does not convert atrial fibrillation, atrial flutter, or ventricular tachycardia to a sinus rhythm, but may be useful in distinquishing an SVT hmother tachydysrhythmias.

Enalapril Angiotensin 1.25 mg iv Useful in treating hypertension and heaFailure. Onset (Vasotec) converting enzyme within 15 minutes, with maximum effect between 1 - 4 inhi bitor maintenance 1.25 mg iv q6hrs. hours. Use with caution in patients with renal insufficiency. Decrease in BP is exagerated in patients on diuretics. Hypotension responds to volume expansion.

Nifedipine Calcium cha~el 10 mg sublingual Used in treating hypertension, coronary vasospasm, and (Adala t) blocker angina. Especially useful in treating hypertension in Usual dose is 10 - 20 mg po tid the npo patient Vasodilation is accompanied with a Maximum dose is 120 mg per day. decrease in BP, SVR and an increase in HR. Negative inotropic action of nifedipine with beta blockers may precipitate heart failure. Nifedipine displaces digoxin and increases it's plasma level. Oxygen Therapy and Hypoxia

Oxygen is an essential and vital feet, the barometric pressure is only 270 substrate used for many metabolic func- mm Hg. Hence the partial pressure of tions. Over 200 oxidase enzyme sys- oxygen is only 47 mm Hg (270 mm Hg tems participate in our body's metabolic x 21% = 47 mm Hg). processes. The cytochrome c oxidase enzyme system in the mitochondria is The oxygen cascade refers to the pro- responsible for over 90 percent of the gressive decrease in the partial pressure bodies oxygen consumption. This of oxygen from the ambient air to the enzyme system provides energy as tissue level (see figure 23.1). At sea adenosine triphosphate (ATP) for bodily level, the inspired partial pressure of functions through the oxidative phosphorylation of food products.

Under normal resting conditions, circulatory arrest with anoxia will result in brain cell injury within 1 minute and irreparable damage by 5 minutes. The heart, liver, kidney, and skeletal muscle have decreasing sensitivities to the effects of anoxia. Skeletal muscle is able to tolerate anoxic periods of up to two hours without suffering irreversible damage.

The Oxygen Cascade:

The partial pressure of oxygen is the concentration of oxygen multiplied by the barometric pressure. At one atmos- 1 Tssue Level ----+ phere of pressure, the partial pressure of Figure 23.1: The oxygen cascade, oxygen is 160 mm Hg (760 mm Hg x illustrating the decreasing levels of 21% = 160 mm Hg). While the oxygen PO2 from the ambient air to the concentration on top of Mount Everest mitochondria. remains at 21% at an altitude of 26,000 I 1 ** Must Know Should Know Page 223 Anaesthesia for Medical Students

Table 23.1: Factors influencing oxygenation at various levels in the oxygen cascade.

Partial Pressure Affected by: I: Inspired Oxygen Barometric Pressure Oxygen Concentration PiO, pa FiO, 11: Alveolar Gas Oxygen Consumption Alveolar Ventilation PAO, vo2 VA 111: Arterial Blood Dead Space Ventilation Shunt Pa 0, t V/Q 4 VIQ IV: Cellular Cardiac Output Hemoglobin PO, CO Hb

oxygen is 160 mm Hg. At the tissue 111: Arterial hypoxemia may occur as a level, the partial pressure of oxygen in result of ventilation perfusion ab- the mitochondria varies from 4 to 23 normalities. These mismatches mm Hg. Hence, there is a progressive occur with an increase in either decrease in the partial pressure of oxy- dead space ventilation or shunted gen from the alveolar and arterial level, blood. to the cellular level. Table 23.1 lists various factors that influence theoxygen IV: Tissue hypoxia will result when- partial pressures at each level of the ever any of the above factors cause cascade. a decrease in the PiO,, PAO,, or PaO,. In addition, tissue hypoxia I: A decrease in either the inspired results from either inadequate car- oxygen concentration or the baro- diac output (with poor tissue metric pressure (e.g., in a high alti- perfusion), or from an insufficient tude environment) will lower the amount of hemoglobin to carry inspired oxygen partial pressure oxygen to the tissues. (FiOJ. Hypoxia is defined as a low level of 11: An increase in either oxygen con- oxygen in the air, blood, or tissues. sumption (e.g., as a consequence of Hypoxemia is a low level of oxygen in sepsis or shivering) or a decrease in the blood. Cyanosis is a descriptive alveolar ventilation will decrease the term used to describe the dark bluish or alveolar oxygen partial pressure purplish coloration of the skin and (PAOJ. mucous membranes accompanying hypoxemia. Cyanosis becomes evident when the reduced hemoglobin (deoxy-

Page 224 Chapter 23 Oxygen Therapy and Hypoxia

Table 23.2: Oxygen delivery systems for spontaneously breathing patients.

0, Dellvery Devlce Flow Rate Percent Oxygen (Limln.) Nasal prongs 1-6 24 - 44% FiO, increases by approximately 4% for every 1Vmin. increase in 0, flow. Simple face mask 5 - 6 40% (Hudson mask) 6-7 50% 7-8 60% Venturi mask 4 - 12 24,28,31, 35,40% Non-rebreathing 6 60% mask with reservoir 7 70% bag. 8 80% 9 - 10 80% + Puritan mask with: Single bottle setup > 10 Umin. 35 - 50% Double bottle setup 50 - 80% + hemoglobin) exceeds 5 grams per 100 postoperative atelectasis are common ml of blood. It may be detected at an candidates for supplemental oxygen oxygen saturation as high as 85%. pro- therapy. These patients do not necessar- vided there is a normal hemoglobin ily require mechanical ventilatory sup- level, good lighting conditions, and no port (see criteria for ventilation; table excessive pigmentation. At an oxygen 7.1). A general goal of oxygen therapy saturation of 75%, which corresponds to is to achieve an oxygen saturation of at a PaO, of approximately 40 mm Hg, least 90%. At our institution, the mini- cyanosis is generally easily detected mal acceptable saturation for post-surgi- (see figure 10.4 oxygen dissociation cal patients who are cared for in a non curve). Anemia, poor lighting condi- critical care setting, such as a hospital tions, and dark pigmentation may mask ward, is 92%. cyanosis and the presence of hypoxemia. There are a number of oxygen delivery systems available for providing supple- Oxygen Therapy: mental oxygen to patients who are Postoperative surgical patients, patients breathing spontaneously (table 23.2). with pneumonia, and patients with Oxygen delivered by nasal prongs is

** Must Know Should Know Page 225 Nasal prongs Simple face mask oxygen (Hudson face mask)

Venturi face mask Non-rebreathing face mask with reservoir bag.

Figure 23.2: Oxygen delivery systems for spontaneously breathing patients. Figure. 23.3: The puritan face mask provides a high level humidity and predicatable concentrations of oxygen. Shown here with a single bottle set up for delivering inspired concentrations of up to 50%.

Figure 23.4: The Ambu manual resuscitation bag and mask unit. Used for providing primary airway management in patients requiring positive pressure ventilation and oxygenation. Note the hand and finger positioning on the mask. The fingers are used to displace the mandible forward and create a seal ( between the mask and the patient's face. Anoesfhesio for Medical Sfudenfs generally well tolerated, provided the The puritan mask delivers the highest flow rate is limited to less than 5 or 6 level of humidified oxygen of all these liters per minute. Flow rates above systems. When two outlet sources are these levels cause an uncomfortable connected to the puritan mask, oxygen drying of the nasal mucosa. Common flow rates of greater than 30 liters per masks used to provide supplemental minute can be achieved, ensuring a oxygen include the simple (Hudson) consistent inspired oxyen concentration face mask, the venturi mask, and the by minimizing room air entrainment. non-rebreathing mask with reservoir One ought to use a double flow setup or bag. The type of mask utilized depends a non-rebreathing face mask with reser- on the patient's tolerance, the desired voir bag, when greater than 50% inspired concentration of oxygen, the inspired oxygen concentration is desired level of humidification, and required. economic considerations. A manual resuscitation unit, such as the Entrainment of room air will result in a Ambu bag and mask is used to provide decrease in the inspired oxygen concen- positive pressure ventilation and oxy- tration. In general, the higher the genation (figure 23.4). This can be patient's minute ventilation the greater used as the primary system for airway will be the reduction in the inspired management in the patient requiring oxygen concentration. A simple face ventilatory support. Adequate oxygen- mask and nasal prongs are two ation and ventilation can be maintained examples of low flow oxygen delivery for prolonged periods of time while systems. These devices have a limited other supportive therapy is initiated. If reservoir to store oxygen and are unable tracheal intubation is required, mask to deliver consistent inspired oxygen ventilation should be maintained until concentrations in the setting of varying all the equipment is available and respiratory rates and tidal volumes. properly checked. The mask should fit over ihe bridge of the nose, producing The venturi, non-rebreathing, and puri- an air tight seal around the nose, tan face masks are high flow oxygen cheeks, and chin. Change the size of delivery systems. They are suitable for mask, or insert an oral or nasal airway delivering consistent and predictable if you encounter difficulty maintaining concentrations of oxygen (see figures airway patency or positive pressure 23.2 and 233). The venturi mask is ventilation. designed to deliver specific percentages of oxygen by varying the size of the air Note the hand and finger positions used entrainment port and the oxygen flow when providing positive pressure venti- rate. A non-rebreathing mask with a lation with an Ambu bag and mask unit reservoir bag allows high concentrations (figure 23.4). The thumb is positioned of oxygen to be delivered to a sponta- over the nasal bridge of the mask. The neously breathing patient. index finger exerts downward pressure on the base of the mask over the chin.

Poge 228 Chapter 23 Oxygen Therapy and Hypoxia

The middle finger lifts the mandible Causes of Hypoxemla: forward into the base of the mask. The little finger is hooked around the angle Hypoxemia may result from a decrease of the mandible and displaces the man- in the inspired oxygen concentration, a dible forward to create an open airway. decrease in the minute ventilation, an increase in shunted blood, or a decrease

Table 23.3: Causes of Hypoxemla Decreased Fi 0, Decreased inspired oxygen concentration Decreased barometric pressure (high altitude) Decreased alveolar Hypoventilation ventilation - hypoventilation secondary to sedative drugs or pain are common causes. Increased dead space venti- Unlike hypoxemia from shunted blood, lation hypoxemia from V/Q inequalities responds to (ventilation - perfusion supplemental oxygen therapy. inequality) - conditions which increase zone I in the lung will result in an increase in dead space ventilation. Examples include hypovolemia, and high airway pressures with positive pressure ventilation. Other examples of dead space ventilation include pulmonary embolism, emphysema, and bronchitis. Increased4 shunt Perfusion of alveoli without ventilation results in an intrapulmonary shunting of blood. Examples include atelectasis, aspiration, congestive heart failure, pneumonia, and endobronchial intubation with lobar collapse. Shunting of blood may also occur outside the lung as a result of intracardiac shunts, or peri- &+ pheral arteriovenous shunts. Decreased diffusion Problems with oxygen diffusing across the alveolar capillary membrane are rare, but may occur with high altitude, anemia, or severe exercise in normal individuals. Pulmonary fibrosis, emphysema, and interstitial pulmonary pathology such as sarcoidosis, may also result in a decrease in diffusion of oxygen and hypoxemia.

** Must Know Should Know Page 229 Anaesthesia for Medical Students

Table 23.4: Causes of Tlssue Hypoxla Decreased functional hemoglobin Anemia, hemoglobinopathies Decreased PaO, Hypoxemia (see table 233)

Decreased tissue perfusion Shock states (see table 215) - hypovolemic - cardiogenic - distributive - obstructive Cellular hypoxia Histotoxic hypoxia - cyanide poisoning in the diffusion of oxygen across the 4. Nunn JF. Oxygen. Applied respira- alveolar capillary membrane (see Table tory physiology. Third edit. 233). Butterworth and Co. 1987;pp. 235 - 383. Tissue hypoxia will result from a decrease in circulating hemoglobin, a decrease in the arterial oxygen tension (PaOz), a decrease in tissue perfusion, or from a cellular toxin such as cyanide (see Table 23.4).

References:

1. Shapiro BA., et.al: Oxygen therapy. Clinical application of respiratory care, 4th ed. Mosby year book. 1991; pp. 123 - 150.

2. Finucane BT, Santora AH. Airway management equipment. Principles of airway management. FA Davis Co. Philadelphia. 1988; pp. 34 - 68.

3. Barash PG, Cullen BF, Stoelting RK. Monitoring the anesthetized patient. Clinical anesthesia. Second edit. JB Lippincott Co. Philadelphia, 1993.

Page 230 Chapter 23 Oxygen Therapy and Hypoxh

Notes:

) ** Must Know Should Know Page 231 Unusual Anaesthetic Complications GREGORYALLEN M.D., FRCPC AND GORDONREID M.D., FRCPC

In this chapter we shall present three increases in oxygen consumption, carbon life threatening anaesthetic related com- dioxide production and heat result in plications. desaturation or cyanosis, elevated end- tidal C02 values and rapid increases in I. Malignant Hyperthermia (MH) temperature (up to 1°C / 5 min), as well as a host of other abnormalities (see What is MH*? table 24.1). Malignant hyperthermia is a rare clinical syndrome that has been observed during How serious is it? general anaesthesia. Patients may ex- The mortality of MH has decreased from perience an acute fulminant form, which over 80% in the 1960's to less than 10%. can be triggered by certain anaesthetic Only about 10% of MH episodes are drugs, and result in a hypermetabolic fulminant, with a rapid onset and severe state because of acute uncontrolled physiological derangements and compli- skeletal muscle metabolism. Rapid cations.

, , Table 24.1: Cllnlcal features of mallgnant hyperthermia.

Hypermetabolism: Muscle Rigidity: Increased oxygen consumption Masseter muscle spasm Dark blood in surgical wound (unable to open mouth) Cyanosis Chest wall rigidity Increased C02 production (difficulty ventilating) Increased end-tidal C02 Abdominal rigidity Respiratory acidosis Limb rigidity Elevated temperature Sweating Rhabdomyolysis: Metabolic acidosis Hyperkalemia Increased lactate levels Painful, tender, swollen muscles Tachycardia Elevated creatinine kinase (CPK) Tachypnea Myoglobinemia, myoglobinuria Arrhythmias Unstable BP

Page 232 Chapter 24 Unusual Anaesthetic Complications

Can you predict who is susceptible? What anaesthetic agents trigger MH*? MH is an inherited disorder of skeletal The triggers of MH include the depolar- muscle. History and physical examin- izing muscle relaxant succinylcholine, ation are usually not helpful in the pre- and any of the volatile anaesthetic agents operative diagnosis of MH-susceptibil- (isoflurane, halothane, enflurane, and ity. A history of uneventful anaesth- sevoflurane). etics in the past is no guarantee that the patient does not have the disorder. A What anaesthetic agents are safe? history of intraoperative cardiac arrest, Intravenous agents including any barbitu- muscle rigidity or stiffness under anaes- rate (eg. pentothal), benzodiazepine (eg. thesia, high fever under anaesthesia, midazolam, diazepam), as well as pro- dark urine after anaesthesia, or family pofol or ketamine may be used safely to member who died unexpectedly under induce andlor maintain anaesthesia. anaesthesia warrant further investiga- Nitrous oxide and any narcotic may be tions and a review of any available used. Muscle relaxants such as pan- medical records. Patients with muscular curonium, vecuronium or atracurium can dystrophy or myopathy have been all be used, and their action reversed observed to have an increased associ- with a combination of an anticholin- ation with MH. esterase and anticholinergic agents such as neostigmine and glycopyrrolate, or The pattern of inheritance is autosomal edropl~oniumand atropine. Local anaes- dominant. Molecular geneticists have thetic agents including the amide class identified an abnormal locus on chromo- (e.g., bupivicaine, lidocaine), and ester some 19q in the area of the skeletal class (e.g., tetracaine, chlorprocaine), muscle ryanodine receptor (RYR 1). with or without epinephrine, have been The ryanodine receptor is associated used safely in MH patients. with the calcium influx channel in the skeletal muscle sarcoplasmic reticulum, How do you treat an MH crisis? and is thought to be the site of the MH Early diagnosis and administration of defect. Unfortunately a simple screen- dantrolene are the primary focus of ing blood test is not likely to be avail- treatingand reversing the hypermetabolic able in the near future because of the abnormalities of MH. Measures such as complicated genetics. The only test cooling, treating hyperkalemia, currently used to make the diagnosis arrhythmias, etc., focus on dealing with reliably and accurately involves taking the consequences of the MH reaction. a muscle biopsy from the patient's Dantrolene is classified as a skeletal quadriceps muscle. Muscle from a muscle relaxant, and is used occasionally patient with MH is noted to develop an in patients with disorders of skeletal abnormally strong response when muscle spasticity. It may result in exposed to caffeine or halothane. The skeletal muscle weakness, but typically test is only done at certain special test- does not result in muscle paralysis. It is ing centres, and is not used for screen- supplied as a yellow powder in vials ing patients. containing 20 mg of dantrolene and 3

** Must Know Should Know Page 233 Anaesthesia for Medical Students grams of mannitol. Each vial of dan- anaesthetic services is required to keep a trolene is mixed with 60 mL of water, current stock (minimum 36 vials) of dan- which can be a time consuming task trolene available in their pharmacy because dantrolene is so insoluble. department. Every hospital that provides general

Table 24.2: Treatment of a suspected MH crlsls. Malignant Hyperthermla Assoclatlon guldellnes (Revlsed 1993).

1. Immediately discontinue volatile anaesthetic agent and succinylcholine. Hyperventilate with 100% oxygen at high flow rates (> 10 Umin). 2. Administer dantrolene sodium 2 - 3 mgkg initial bolus, up to 10 mgikg. 3. Administer bicarbonate to correct metabolic acidosis as guided by blood gas analysis. In the absence of blood gas analysis, 1 - 2 mgflcg should be administered. 4. At the same time institute cooling measures for the hyperthermic patient, (goal = 38'C). Administer iced saline 15 mUkg iv q 15 minutes x 3. a. Lavage stomach, bladder, rectum and open cavities with iced saline as appropriate. b. Surface cool with ice and hypothermia blanket. c. Monitor closely since over-vigorous treatment may lead to hypothermia. 5. Dysrhythmias will usually respond to treatment of acidosis and hyperkalemia. Persistent dysrhythmias may be treated as per ACLS protocol, with the exception of calcium channel blockers (calcium channel blockers in these patients may result in hyperkalemia and cardiovascular collapse). 6. Determine and monitor end-tidal C02, arterial, central or femoral venous blood gases, serum potassium, calcium, clotting studies and urine output. 7. Hyperkalemia is common and should be treated with hyperventilation, bicarbonate, intravenous glucose and insulin (10 units regular insulin in 50 mL 50% glucose titrated to potassium level). Life-threatening hyperkalemia may also be treated with calcium administration (eg. 2 - 5 mglkg of CaClJ. 8. Ensure urine output of greater than 2 mUkg/hr. Consider central venous or PA monitoring because of fluid shifts and hemodynamic instability that may occur. 9. Boys less than 9 years of age who experience sudden cardiac arrest after succinylcholine in the absence of hypoxemia should be treated for acute hyperkalemia first. In this situation, calcium chloride should be administered along with other means to reduce serum potassium. They should be presumed to have subclinical muscular dystrophy.

Source: Malignant Hyperthermia Association of the United States, Westport, CT, USA Chapter 24 Unusual Anaesthetic Complications

Potential complications of MH include: MH related issues:

Acute hyperkalemia (from cell lysis) Postoperative fever: Acute renal failure (myoglobinuria) An increase in body temperature above Arrhythmias 38S°C in the perioperative period is the Pulmonary edema result of either (1) an increase in body ARDS heat production, (2) a decrease in body Severe muscle pains, weakness heat elimination, or (3) the result of Hepatic dysfunction active warming measures. Postoperative Hemolysis fevers are very rarely due to MH. More Disseminatedintravascularcoagulation common causes of an elevated tempera- Cerebral injury - seizures, coma ture in the perioperative period include:

Following the initial treatment of an coexisting infections MH suspected crisis: anticholinergic medications (e.g., atropine resulting in decreased A. The patient should be observed in sweating) an ICU setting for at least 24 hours, transfusion reaction since recrudescence of MH may dehydration occur, particularly following a excessive coverings on the patient fulminant case. elevated room temperature active warming measures B. Administer dantrolene 1 mglkg iv (blankets, fluids) every 6 hours for 24 - 48 hours after thyrotoxicosis the episode. Heat stroke: C. Follow ABG, CPK, potassium, cal- MH patients may be more susceptible to cium, urine and serum myoglobin, heat stroke compared to the normal clotting studies and core body tem- population. However, most patients perature until such time as they suffering from heat stroke are not MH return to normal values (eg. 6 susceptible. Patients who have suffered hours). Central temperature (eg. from heat stroke and also have an abnor- rectal, esophageal) should be con- mal family history of anaesthesia prob- tinuously monitored until stable. lems suggestive of MH, should be in- vestigated for MH. D. Counsel the patient and family regarding MH and further precautions. Refer the patient to the MH North American registry, and biopsy centre.

i ** Must Know + Should Know Page 235 Anaesthesia for Medical Students

11: Asplratlon Syndrome. any antacid if aspirated. Gastric emptying by nasogastric tube is im- Chapter nine introduced the concept of portant in patients with a bowel ob- a rapid sequence induction and ident- struction. ified factors that placed a patient at risk for gastric aspiration. The severity of 3. In patients with an anticipated diffi- gastric aspiration is related to the vol- cult intubation, topicalization and ume and acidity of the aspirate, the local anaesthetic blocks of the upper presence of contaminated particulate airway will permit the trachea to be matter (e.g., bowel contents) and the intubated with the patient awake. former health of the patient. This reduces the chance of a failed intubation, difficult mask ventila- Strategies useful in reducing the peri- tion, and subsequent gastric aspir- operative risk of gastric aspiration ation. include*: 4. Patients with identified risk factors 1. Avoid impairing airway reflexes. for gastric aspiration who require The risk of gastric aspiration is general anaesthesia (see Table 9.1), reduced in the awake patient. Sur- must have a rapid sequence induc- gery that can be accomplished with tion. This involves a period of pre- local or regional anaesthesia should oxygenation, the application of be considered in the patient at risk cricoid pressure, and tracheal of aspiration. intubation with a cuffed E'lT (see chapter 9; Rapid Sequence Induc- 2. Reduce gastric volume and acidity. tion). Extubation should only be A period of fasting (minimal 8 performed when the following cri- hours for solid foods and 4 hours teria are met: for clear liquids) is mandatory in a patient undergoing non-emergency a. the patient is responding to verbal surgery. A planned regional or local commands anaesthetic does not negate the need b. the patient has regained an to fast as unforseen events may arise oropharyngeal gag reflex necessitating a general anaesthetic. c. the patient is positioned on their Metochlorpropamide and domper- side, and idone have been used to stimulate d. the need for tracheal intubation is no gastric motility and promote gastric longer present. emptying. H-2 antagonists and antacids are useful when given pre- The consequences of gastrlc operatively to reduce both gastric asplratlon: secretion and acidity. Sodium citrate is the antacid of choice in an- Apiration of a liquid causes a vigorous aesthesia as it is non-particulate cough, accompanied by a transient and produces the least damage of period of hypoxemia in the normal

Page 236 t Chapter 24 Unusual Anaesthetic Complications ) awake adult. Significant cellular dam- be the only indication of aspiration. age occurs in a dog model when the pH Gastric contents in the upper airway and is less than 2.5 and the volume is mouth, may or may not, accompany greater than 0.4 mlkg. If the liquid has gastric aspiration. a pH of 2.5 or more, it will generally not cause cellular damage. When gas- Treatment of asplratlon: tric acid is aspirated, surfactant is destroyed, the alveoli collapse, and The first few minutes following an aspir- hemorrhage and exudation into the ation are critical, and attempts must be alveoli and interstitium occurs. Severe made to remove as much material as bronchospasm usually accompanies a possible from the mouth, pharynx and significant aspiration. Lung compliance trachea. As the most common site for decreases as alveoli collapse, and areas aspiration is the apical posterior segment of shunt occur, resulting in severe of the right lung, the patient should be hypoxemia. positioned head down in the right lateral position to limit spread to the left lung, Aspiration of particulate (food or fecal) and aid drainage by gravity. Immediate matter may result in blockage of distal bronchoscopy is used to remove any bronchi, resulting in large areas of col- particulate matter that has been aspirated. lapse, edema formation and shunting. Within the first few days a mononuclear With a significant aspiration, severe foreign body response occurs. The lung hypoxemia with decreased lung compli- distal to the obstructed bronchi collapses ance and difficulty providing positive and fills with secretions. Without resol- pressure ventilation are expected to ution, lung infection or abscess forma- occur within the first 30 to 60 minutes. tion are inevitable. Positive pressure ventilation with continuous positive airway pressure (CPAP) Dlagnosls of asplratlon: or positive end expiratory pressure (PEEP) are used to prevent alveolar Early diagnosis and treatment may collapse, limit the reduction in residual reduce the severity of the aspiration volume, and prevent further atelectasis syndrome. During mask anaesthesia and shunting. Crystalloid solutions are with either a face or laryngeal mask, the preferable to colloid solutions (see chap- detection of aspiration may be difficult. ter 20), because the pulmonary capillary Sudden laryngospasm, coughing or membrane is injured, and may allow stridor may be the first indication that colloid solutions to cross into the alveoli, aspiration has occurred. Bronchospasm increasing the degree of pulmonary may also occur, and the compliance of edema. the chest may decrease resulting in increased airway pressures during mech- Steroids are not generally indicated, and anical ventilation. Alternatively, de- may promote granuloma formation in saturation with hypoxemia and the need cases of aspirated food particles. Anti- for higher concentrations of oxygen may biotics are also not indicated, unless

** MUSI Know Should Know Page 237 Anaesthesia for Medical Students there is evidence of gross aspiration exposure to the drug. This form of from bowel contents. Bronchodilators reaction can be diagnosed with skin tests are used in treating bronchospasm. and specific antibody assays. Prolonged positive pressure ventilation and critical management of intravascular An anaphylactoid reaction occurs when volume status, oxygenation, and ventila- the allergen causes direct release of tion are the principles of treating a histamine. This reaction is not immune significant aspiration. Invasivemonitor- mediated and IgE antibodies are not ing and frequent blood gas analysis may involved. be required. Mortality and morbidity usually results from the initial severe hypoxemia that occurs at the time of Table 243: Clinical Features* aspiration. This emphasizes the need Anxiety, headache, nausea for initial aggressive treatment. Impending sense of doom Dyspnea, tachypnea 111: Allergic reactions Tachycardia Flushing, hives, urticaria (70%) Muscle relaxants and exposure to latex Facial, orbital, mucous materials are the two most common membrane edema, sneezing causes of an allergic reaction occurring Hoarseness, laryngeal edema during anaesthesia. The frequency of Hypotension (85%) anaphylactic shock is 1 in 3500 anaes- Bronchospasm (35%) thetics. The allergic response manifests Hypoxemia within minutes of an intravenous injec- Desaturation tion of the offending agent. By con- Increased airway pressures trast, signs of an allergic response resulting from latex are delayed.

Definitions: Table 243 lists the clinical manifesta- tions of an allergic reaction. Exposure ' Anaphylactoid is a general term used to to the allergen results in the release of , describe the clinical features of an aller- histamine, tryptase, leukotrienes and , gic reaction. The term anaphylactoid cytokines from mast cells and basophils. shock is used to designate an allergic These act on both histamine (HI and reaction in which the mechanism may H2) receptors throughout the body pro- ; be either the result of a direct release of ducing the clinical features. An immedi- histamine, or from an immune mediated ate brief surge in plasma histamine ' mechanism. levels occurs followed by a gradual rise in tryptase levels which are specific to , Anaphylactic or anaphylaxis is used anaphylactic reactions and can be when an allergic reaction is immune measured in the serum (see figure 24.1). mediated, and implicates IgE antibodies Analysis of the urine can be used to , and prior sensitization from previous detect a metabolite of histamine, urinary

Page 238 Chapter 24 Unusual Anaeslhe~icComplications

the antigenic site. As this is common to many muscle relaxants, cross reactivity between different relaxants is common. I Histamine Prior exposure to a muscle relaxant is not required, as previous sensitization may have occurred following exposure to household products containing substances with ammonium structures (e.g., disinfectants, cosmetics). Latex allergy accounts for approximately 12% of allergic reactions. Patients with repeat exposure to latex products have an increased risk of a latex allergy. These include patients requiring repeat urinary catheterization (paraplegia, spina bifida), Figure 24.1: Schematic time profile and health care workers who frequently of the release of histamine, tryptase, work with latex gloves. Less than 15% and urinary methylhistamine of allergic reactions are the result of exposure to blood products, opioids, benzodiazepines, and antibiotics. methylhistamine, and aid in the diag- Treatment of anaphylaxis:++ nosis. Elevated levels of urinary methylhistamine and serum tryptase A useful memory tool in recalling the support the diagnosis of an anaphylactic emergency treatment steps for reaction, but do not identify the anaphylaxis is to recall the "Anaphylaxis allergen. Serum IgE antibodies can be ABCsW: used to perform radioimmunoassays (RIAs) to identify the responsible A Airway, and adrenaline allergen. Specific antibodies to B Breathing and benadryl thiopental, propofol, muscle relaxants C Crystalloids and cimetidine and latex are now available. Blood and s steroids urine samples should be taken at 1 to 3 hours, and 24 hours after the reaction to Tachycardia with an allergic reaction measure these mediators. The patient results from the chronotropic effects of should be referred for skin testing with H2 receptor stimulation. Epinephrine is cutaneous skin prick tests within two the principle initial drug treatment. In months of the reaction. cases of severe hypotension or laryngospasm, 0.1 ml of 1:1000 epinephrine Muscle relaxants account for 70% of the may be given intravenously, and cases of anaphylaxis during anaesthesia. repeated as needed. A single bolus dose The tertiary or quaternary ammonium of epinephrine should generally not group on muscle relaxants is frequently exceed 05 ml (05 mg). Excessive

** Must Know * Should Know Pogc 239 Anaesthesia for Medical Students

epinephrine administration risks References: malignant arrhythmias (ventricular tachycardia, and ventricular fibrillation) 1. Allen GC. Malignant Hyperthermia. severe hypertension, pulmonary edema, Aether 1994; 1: 3 - 6. myocardial infarction and stroke. Nevertheless, patients taking beta- 2. Gibbs CP, Model1 JH. Management blockers may be resistant to the effects of Aspiration Pneumonitis, of epinephrine, and may require higher Anesthesia 3rd edition. Edited by doses of epinephrine. The Miller RD. Churchill Livingstone administration of beta- blockers, to Inc. 1990. pp. 1293 - 1319. control the heart rate response, is contraindicated in patients experiencing 3. Laxenaire MC, Moneret-Vautrin DA. an anaphylactoid reaction. Allergy and Anaesthesia. Aether 1994: 2: 14 - 17.

Table 24.4: Management of Notes: Anaphylaxis during Anaesthesia Stop drug or allergen administration Provide 100% oxygen Discontinue surgery and anaesthesia as soon as feasible. Give epinephrine 50 - 100 mcg iv with hypotension, 05 - 1.0 mg iv with cardiovascular collapse. Epinephrine infusion 0.05 - 0.2 mcglkglmin (see chapter 22). Crystalloids (e.g., NS, RL) iv, may require 2 - 4 liters for a 70 kg adult, i.e., 25 - 50 ml/kg. Diphenhydramine 50 mg iv (~enadryl"- 1 mag) Cimetidine 300 mg iv, or ranitidine 50 mg iv Hydrocortisone 100 mg iv (Solucorte~- 1.5 mgtkg), or methy lpredniso lone (Solumedrol@) 1mag iv q6hn x 24 hours. Inhaled salbutamol (ventolin? for bronchospasm. Avoid beta blockers. ) Appendix: ) )

J Intravenous Access

/ Intravenous (iv) cannulation provides The Hagen-Poiseuille equation explains direct access to the venous circulation. why a 5 inch long 16 gauge central ) This discussion will focus on practical venous catheter will achieve less than aspects of securing venous access to the half the maximum flow rate of a 2 inch ) peripheral circulation. Students are not long 16 gauge peripheral catheter. ) expected to acquire skills for insertion Alternatively, by halving the radius of of catheters into the central circulation, the catheter, the maximum flow rate or for performing a venous cutdown will decrease to 1/16. Warming the during this rotation. Intravenous intravenous fluids will cause ) catheterization is most commonly venodilation, decrease fluid viscosity, indicated for administering medications and increase the maximum flow rate. ' or fluids, or to sample blood for analy- Similarly, pressurizing the fluid in the ) sis. intravenous bag will increase the pressure differential between the fluid A plastic catheter, which is inserted and venous system and permit more ) over a hollow needle, is the most rapid fluid administration. ) common intravenous catheter system used for peripheral venous cannulation. Venous Anatomy: ) The length of the catheter, and it's ) internal diameter, the viscosity of the The upper extremities venous anatomy intravenous fluid, and the pressure dif- is relatively consistent. Digital veins ferential between the vein and the fluid run proximally from the digits to the ) being administered all determine the dorsal arch of veins on the dorsal sur- ) maximum flow rate, as specified by the face of the hands. A vein can usually Hagen-Poiseuille equation: be located just above the head of the 1 3rd and 4th metacarpals. The dorsal ) Hagen-Poiseuille equation: arch turns radially to the anatomical snuff box, where a large superficial vein can be located at the level of the distal radial tubercle. This vein continues along the lateral forearm to the anticubital fossa where it joins other veins ) P = pressure across the catheter to form the cephalic vein. The cephalic ) r = radius of the callteter vein can sometimes be followed up the n = viscosity of the fluid arm over the biceps muscle, crossing the ' 1 = length of the cadeter deltoid muscle anteriorly, and disappear-

) ** Must Know * Sl~ouldKnow Page 241 Anaesthesia for Medical Studertts

ing between the heads of the deltoid and the knee, passing behind the femoral pectoralis muscles to enter the axillary condyle. It continues proximally along vein. Other superficial veins travel up the medial thigh entering the thigh the forearm to form the basilic vein muscles approximately 1.5" below the located just medial to the insertion of inguinal ligament, where it joins the the biceps muscle in the anticubital femoral vein. The anatomy of the fossa. The basilic vein continues prox- femoral vessels (lateral to medial) can imally (becoming obscured in the lower be recalled using the pneumonic 113 of the arm as it enters the muscles NAVEL* where: of the ann) to join the axillary vein in the axilla. Identification of superficial N = Nerve veins may be difficult in obese patients. A = Artery Fortunately, the volar aspect of the wrist V = Vein generally lacks adipose tissue. Examin- E = Empty space ation of this area may reveal small veins L = Lymphatics that can be used for access when attempts at other sites have failed. (*recall that the NAVELpneumonic was also used for drugs which can be given The upper extremity is used for venous through a tracheal tube. See pg. 50). cannulation in the vast majority of patients. Patient anxiety (increased The femoral artery is located at the catecholamines), a cold environment midpoint between the anterior superior (venoconstriction), adipose tissue, or a iliac spine and the pubic symphysis. pre-existing fluid deficit, may make the The femoral vein lies approximately 1 identification of suitable veins for cm medial to the artery. Cannulationof venous cannulation difficult. To the femoral vein is less popular than improve the chance of successful other veins because of the restriction in cannulation, keep the extremity below patient mobility, and the risks of infec- the level of the heart, use a tourniquet tion or thrombosis. Peripheral intra- around the biceps muscle to distend the venous catheters are generally too short vein, avoid cooling the patient, and to be used for the femoral vein, and a consider using warm blankets or heating longer central venous catheter (approxi- pads on the extremity to dilate the mately 5 inches in length) is more suit- veins. When venous cannulation of the able. upper extremity fails, one can use the lower extremity. The foot has a dorsal Cholce of site for intravenous venous arch that can be used for venous cannulatlon: access. The saphenous vein is the equivalent to the superficial radial vein in The most common sites used for iv the forearm. It continues from the cannulation are the dorsum of the hand, dorsal arch of the foot to pass over the medial aspect of the forearm, and the anterior aspect of the medial malleolus. anticubital fossa. Of these, the dorsum It then travels up to the medial aspect of of the hand is perhaps the most com- Appendix: Intrt've~~ousAccess

Figure 1: Peripheral venous anatomy.

** Must Know Should Know Page 243 Anaestl~esiafor Medical Students

mon choice. It allows one easy.access 24, and 26 gauge catheters. The 24 and to the vein, and, should the intravenous 26 gauge catheters are generally only fail, one may still use a more proximal used in the neonatal or paediatric popu- site. For patients who will require their lation. Sixteen to 20 gauge catheters intravenous for a period of time greater are the most common sizes used in than 24 hours, the forearm may be a adults. Catheter lengths for peripheral better choice. It restricts their activities veins vary from 1" to 2". less, and remains relatively inimobile' when they move their arms. They are Patients who may require blood prod- also less likely to catch their intra- ucts and large amounts of intravenous venous on other objects. fluids should have several large boie intravenous catheters (i.e., 14 or 16 The anticubital fossa is a good choice gauge). We routinely manage patients when a large vein is required, and the undergoing minor ~rocedures,in which anticipated period in which the catheter the need for rapid fluid administration is will be used is a short one. As a gen- remote, with a single 18 or 20 gauge eral rule, however, it is best to chose a intravenous catheter. site for the intravenous that does not lie over a joint. When a patient flexes and Intravenous catheters of 18 gauge or extends their joint, the intravenous site larger may cause moderate discomfort will be uncomfortable, and this motion when inserted in the awake patient. By may dislodge the catheter from the vein using local anaesthesia, you may be making it interstitial. One also risks able to decrease this discomfort. A 25 injuring the median nerve or or 27 gauge needle can be used to catheterizing the brachial artery when administer approximately 114 ml of 2% attempting anticubital vein cannulation. lidocaine into the dermis either directly over the vein or immediately lateral to The lower extremity and femoral veins the vein. Aspiration before injection is . are less commonly chosen for iv access not necessary. Insert the intravenous because they restrict patient's mobility cannula through the local anaesthetic and increase the risk of complications wheal. including infection, phlebitis, and thromboembolism. Technique of Intravenous Choice of Intraveno~~sSize: Cannalation:

Intravenous catheters are supplied in Assemble your required equipment in- various sizes and lengths. The size of cluding: iv bag and tubing, iv cathe- catheter increases as the gauge number ters, tourniquet, alcohol swab, gloves, of the catheter decreases. In adult an- tape, (+/- povidone-iodine swab, 114 ml aesthesia, we consider a 20 gauge cathe- 2% lidocaine local anaesthetic in a 3 ter to be small. The catheters come in ml syringe with a 25 or 27 gauge even numbers i.e., 14, 16, 18, 20, 22, needle, and gauze to clean spilt blood).

Page 244 Appendix: InIravenous Access

3 cc syringe, 2% lidocaine, 27 gauge needle, intravenous catheter, tape, tourniquet, and gauze.

Intravenous bag, tubing and tape.

Intravenous catheter and needle. 1 Common intravenous cannulas. Note that the needle is longer Small bore = 22 and 20 gauge, 1 than the catheter. Large bore = 16 and 14 gauge.

Figure 2: Equipment for peripheral intravenous access. I )

) ** Must Know Should Know Page 245 1. Apply a tourniquet to the extremity. 11. Advance the catheter and needle 2. Identify a suitable vein. Gently tap (maintaining skin traction and vein over the vein to facilitate veno- immobilization) visualizing where dilation. the tip of the needle is in relation to 3. Cleanse the area with an alcohol the vein, watching for a flash of swab (or povidone-iodine swab blood in the hub of the catheter. followed by an alcohol swab). 12. When blood comes back into the 4. Wear disposable gloves hub, advance the needle and cathe- (recommended). ter another 2 mm to ensure the 5. Optional: Inject local anaesthesia catheter is in the vein (and not still with a 25 or 27 gauge needle into outside the wall of the vein). the dermis either directly over the 13. Without moving the catheter, with- vein or 2 - 3 mm lateral to it using draw the needle approximately 1 114 ml of 2% lidocaine. cm. (Alternatively, without moving 6. Optional: Break the seal between the needle, the catheter can be the catheter and the needle (this advanced over the tip of the needle may make it easier to advance the by approximately 1 cm). catheter off the needle once you 14. With the needle back from the tip enter the vein). of the catheter, advance both the 7. Immobilize the vein by applying needle and catheter together until traction to the skin distal to the you feel resistance or the catheter is insertion site with the hand that is fully inserted. not holding the intravenous catheter. 15. Release the tourniquet. Maintain immobilization of the vein 16. Using the hand that was maintaining during iv insertion. Avoid putting skin traction, occlude the vein by your hand immediately below the pressing with your finger proximal vein as this will prevent you from to the tip of the catheter (lying in lowering the intravenous catheter the vein). This prevents blood from into the same plane as the vein. coming back out of the catheter 8. Hold the hub of the needle between when the needle is removed. your thumb and forefinger with the 17. Remove the needle, leaving the bevel facing up. Watch for the catheter in the vein. blood to flash back into the plastic 18. Secure the intravenous tubing to the hub when you enter the vein. catheter (a luer lock connecting end 9. Puncture the skin through the an- accompanies certain iv tubing sys- aesthetic skin wheal holding the tems). needle at a 30 - 45 degree angle to 19. Open the intravenous roller clamp, the vein. Advance the needle until and adjust the flow to the desired the catheter is beneath the skin. rate. 10. Lower the angle of the intravenous 20. Secure the intravenous to the patient catheter to approximate that of the with tape. vein you are attempting to enter.

Page 246 Appendix: Intravenous Access

Figure 3: Venous anatomy, immobilization and cannulation.

j Superficial radial vein. Basilic vein. I - I

Immobilization of the dorsal Immobilization of the veins of the hand. superficial radial vein.

I Local anaesthetic skin wheal. using the catheter hub. )

Forearm vein cannulation: Angulating the catheter prior to insertion I permits insertion of the cannula in the same plane as the vein. )

) ** Must Know Should Know Page 247 Anaesthesia /or Medical Students

Fig. 4: Note that vein immobilization is maintained throughout iv insertion.

I Puncture skin at 30 - 45' Decrease angle of insertion. I

Blood flashes back into cannula Advance another 2 - 3 mm to hub as the vein is entered. ensure catheter is in the vein.

Catheter is left in the vein while With the needle back 1 cm, the the needle is withdrawn 1 cm. catheter is advanced to the hub. I

Once the vein is occluded (to prevent back-bleeding), the needle is removed and the iv tubing is connected. The iv is then secured with tape.

Page 248 ) Appendix: Inrravenous Access

) i 1 ) 1 Puncture the skin holding the needle at a 30 - 45 degree ) angle and advance the needle ) until the catheter tip is beneath the skin. ) )

1 Decrease the angle of the ) intravenous catheter in 1 relation to the vein. Watch for blood in the iv hub as the vein 1 is entered. ) i Advance the needle and ) catheter another 2 mm to 1 ensure the catheter is in the vein. 1

) Without moving the catheter, withdraw the needle approximately 1cm back from 1 the tip of the catheter. Now i advance both the catheter and needle into the vein. i i Release the tourniquet. i Occlude the vein proximal to ) the catheter tip. Remove the needle, and secure the intravenous tubing to the 1 catheter. i Figure 5: Establishing peripheral intravenous access.

) ** Must Know Should Know Page 249 Anaestl~esiafor Medical Students

Problems with Intravenous 3. You advance the catheter easily into cannulatlon: the vein but then encounter resistance before it is completely 1. Resistance is felt when attempts are inserted. made to advance the catheter over the needle. The catheter tip is likely lying next to a valve or junction in the vein. Do not The most likely problem is the catheter force the catheter, you may be able to is outside or only partially through the connect the catheter to the intravenous wall of the vein. Make sure that the tubing and advance the catheter once needle and catheter are advanced ap- fluid is flowing through the tubing. If proximately 2 mm into the vein after not, you may still be able to achieve the flash back occurs so that the cathe- adequate administration of fluids and ter will be in the vein before attempts medications without having the catheter are made to advance the catheter over advanced all the way into the vein. the needle. If the catheter is at a sharp angle to the vein you will only have a 4. The patient experiences excessive short distance before the tip of the pain when inserting the intravenous. needle is through the vein when it is advanced. To avoid this, try to lower The intravenous needle and catheter the angle of the catheter to keep it in may be dissecting along the vein wall. the same plane as the vein. The vessel walls have sensory fibres and if the needle scrapes along the wall 2. A large hematoma develops when rather than entering it cleanly, the attempting to insert the intravenous. patient may experience significant pain with even a small intravenous. Other A hematoma may develop whenever the possibilities include nerve injury with vein is entered. This may occur when needle insertion (e.g., median nerve in injecting local anaesthetic if the local is the anticubital fossa, radial nerve in the injected beneath the skin and into the anatomical snuff box). Remove the vein. By injecting local anaesthetic intravenous and use an alternative site immediately lateral to the vein, the with local anaesthesia. chance of causing a hematoma is less. If a hematoma results while you are 5. Unable to enter the vein with the attempting to insert the intravenous, and intravenous catheter. your ability to visualize the vein is lost, you should remove the catheter and Inadequate stabilization of the vein is apply pressure with a gauze to prevent the most common mistake made when further bleeding. Release the tourni- learning to insert an intravenous. quet, and hold the site for a couple of Immobilize the vein by applying skin minutes before trying again at another traction distal to the vein. Try to site. visualize where the tip of the needle is in relation to the vein. Lift the tip of

Page 2J0 Appendix: Intravenous Access

the needle up so that you can see its \ relation to the vein. Line up the needle / The iv catheter is direction and plane with that of the angulated prior to vein. If you have advanced the needle and cannot enter the vein, withdraw the needle and catheter such that the catheter tip is just below the skin, and start again, adjusting to a different angle and depth. With time, the needle may become obstructed by clotted blood IV catheter preventing a flash back from occuring when the needle is in the vein. Con- sider changing the intravenous needle during cannulation. and catheter after attempting catheterization for several minutes. I ) Other helpful hints: Figure 6: ) To approximate the plane of the intra- Cannulation of forearm veins: ) venous catheter with the plane of the Angulating the iv catheter prior to vein being cannulated, it is often useful insertion may decrease the chance ' to create a slight (10 - 15 degree) of passing through the back wall angulation in the iv catheter before of the vein during cannulation. ) inserting it. This is particularly useful in cannulation of veins of the forearm, ) where it is difficult to hold the catheter at a low enough angle to approximate the plane of the iv catheter with the vein (figure 6).

The plastic iv housing unit which is supplied with the iv catheter can be used to create this angle just distal to ) the catheter hub. Angulate the catheter such that the bevel is facing up. The ' angulation allows the catheter hub to be ) held at a comfortable angle, and matches the plane of the iv catheter with the vein. )

** Must Know Should Know Page 2111 Review Questions

Chapter 3: Chapter 6: Preoperative assessment. Intubation and anatomy of the airway.

1. Define the ASA physical status 1. What is the "1-2-3" test? classification. 2. What does a class I hypopharyngeal 2. How long should elective surgery view mean? What structures are be postponed following a visualized in a class I hypo- myocardial infarction? What is the pharyngeal view? basis of this recommendation? 3. What structures are visualized in a 3. What information should be grade 111 laryngeal view? obtained in the anaesthetic history? 4. What is the optimal position of the 4. What common anaesthetic tech- head and neck for intubation using niques can be used to provide an- direct laryngoscopy? aesthesia for lower abdominal sur- 5. How is tracheal intubation con- gery? firmed? 5. What anaesthetic risks might be 6. Name 4 simple maneuvers that can associated in a patient who smokes be used to overcome an upper air- regularly? What information way obstruction. obtained from history, physical, or laboratory examination might be Chapter 7: useful in assessing this risk? Are Intubation decisions. there any means of decreasing the risks of perioperative complications 1. What laboratory criteria should you related to smoking? use to assess the objective need for intubation and ventilation? Chapter 4: 2. What are some important historical Premedication. and clinical factors that suggest the need to intubate and ventilate a 1. Why are patients premedicated prior patient? to surgery? 2. What are the general contra- Chapter 8: indications to the use of Laryngeal mask airway. benzodiazepine or opioid pre- medications? 1. What is the difference between a LMA and an endotracheal tube?

Page 252 Review Questions

2. Why would a laryngeal mask air- 2. Why would one choose propofol way be used rather than a endo- over thiopental as an intravenous tracheal tube? induction agent? 3. When would one choose ketamine Chapter 9: over either thiopental or propofol as Rapid sequence induction. the intravenous induction drug? 4. What are the concentrations and 1. What is the purpose of a rapid induction doses of thiopental and sequence induction? propofol? 2. Describe the sequence of maneuvers used in a rapid sequence induction. Chapter 12: 3. What is the purpose of pre- Muscle relaxants. oxygenation? 4. Which patients should be regarded 1. What is the difference between a as being at risk of pulmonary aspir- depolarizing and non-depolarizing ation of gastric contents? muscle relaxant? Give examples of 5. What measures can be taken to each. decrease the risk of aspiration? 2. What are the absolute contraindications to the use of succinyl- Chapter 10: choline? Monitoring in anaesthesia. 3. Which patients are susceptible to hyperkalemia following succinyl- 1. What information does the anaes- choline? thetist use to assess the depth of 4. What is the concentration that succ- anaesthesia? inylcholine is supplied? What is the 2. What information can be obtained dose for intubation? by monitoring the capnograph? 5. Which drugs can be used to 3. What relationship does the ETCO2 antagonize a neuromuscular block? value have to the PaC02? What conditions might result in a ETCO2 Chapter 13: measurement of 20 mm Hg with a Inhalational anaesthetic agents. PaC02 measurement of 40 mm Hg? 1. What is MAC? Chapter 11: 2. What is the relationship between the Intravenous anaesthetic agents. anaesthetic concentration that is set on the anaesthetic vaporizer and the 1. Why do patients awaken from a anaesthetic concentration in the sleep dose of thiopental within 5 to patient's brain? 10 minutes of its administration 3. What is diffusion hypoxia? when the elimination half life is of 4. What are the MAC values of iso- the order of 5 - 12 hours? flurane, enflurane, and halothane in oxygen?

Page 253 Anaesthesia for Medical Students

Chapter 14: 10. What is the difference between a Narcotic agonists and antagonists. spinal and an epidural anaesthetic? 11. How many milligrams of lidocaine 1. What undesirable effects do opioids are in 20 mls of a 2% solution? have? 2. Name an opioid antagonist. What Chapter 16: dose of this drug would be appropri- Acute pain management. ate to reverse opioid induced respiratory depression. What, if any, 1. List the physiological effects of are there any potential problems of acute pain. giving too much of this antagonist? 2. Contrast intramuscular and PCA opioid administration. 3. What are the adverse effects result- Chapter 15: ing from the administration of ex- Local and regional anaesthesia. cessive opioid analgesics? 4. What non-opioid analgesic agents 1. Name two classes of local anaes- are available for the control of thetic agents, and give examples of acute pain? each. 5. What are the contraindications to 2. What is PABA, and what role does administering a non-steroidal anti- it have in local anaesthesia? inflammatory drug? 3. Name 4 techniques of administering 6. List an appropriate dose and sched- a local anaesthetic drug. ule for two common NSAID's used 4. Why is a vasoconstrictor often used to control of acute pain. with a local anaesthetic? Give an example of a LA vasoconstrictor and Chapter 17: its concentration. When would the Chronic pain. use of a vasoconstrictor be contraindicated? 1. What is the difference between 5. Which regional block results in the acute and chronic pain? highest concentration of local an- 2. What is RSD? What conditions aesthetic in the blood? may lead to the development of 6 What is the maximum recommended RSD? dose of plain lidocaine, and of lido- 3. What modalities are commonly caine with a vasoconstrictor? used to treat RSD? 7. Why might a regional anaesthetic be 4. How is a diagnosis of RSD made? given as well as a general anaesthe- 5. What are trigger points? tic? 6. Name two surgical conditions that 8. Describe some of the signs and may present with back pain and symptoms of local anaesthetic toxic- require emergency surgical inter- ity. vention ? 9. Describe the steps in treating an acute local anaesthetic toxicity.

Page 254 Review Questions

Chapter 18: 2. List conditions that may be associ- Obstetrical anaesthesia. ated with a significant preoperative fluid deficit. 1. What is the supine hypotensive 3. What is the difference between a ) syndrome? How can it be pre- crystalloid and a colloid? Give ) vented? examples of each. 2. What factors may influence a 4. Which patients should consider ) patient's experience of pain during autologous blood donation? For ) labour and delivery? which patients is this not suitable? What options are available for deal- 5. Calculate the acceptable amount of ) 3. ing with the pain of labour and blood that can be lost in a 70 kg ) delivery? male if his initial hemoglobin is ) 4. What are the major risks of general 140 gmldl, and the accepted anaesthesia in the parturient under- minimal hemoglobin after surgery is ' going a cesarian section? 80 gmldl. ) 6. What is the most common cause of ) Chapter 19: an ABO incompatible blood trans- Basic neonatal resuscitation. fusion? 7. Name three different blood compo- What is the Apgar score of a baby nents that may be transfused. that is limp, blue, has no response to oropharyngeal suctioning, a heart Chapter 21: rate of 60 bpm, and irregular gasp- Common perioperative problems. ing respiratory efforts? Describe the basic steps in neonatal 1. Define shock? Classify the differ- resuscitation. ent types of shock and give When is positive pressure ventila- examples of each. tion (PPV)indicated in the newborn 2. What are some treatable causes of infant? Describe the technique of an agitated postoperative state? PPV. Assuming a newborn infant weighs Chapter 22: 3 kg, what is the concentration and Managing the circulation. dose of epinephrine, and how ought it be administered? 1. What are the broad goals in controlling the circulation? Chapter 20: 2. What are the differences between an ) Intravenous fluid and blood component alpha-1 and beta-1 adrenergic therapy. agonist? Give examples of each. ) 3. What are the factors which deter- ) 1. How are the hourly and daily main- mine cardiac output? ) tenance fluid requirements calculated? I

Page 255 ~aestltesiafor Medical Students

hapter 23: Xygen therapy and hypoxia.

. List some devices that are commonly used to deliver oxygen to spontaneously breathing patients. . When should a puritan face mask be used? When should one use a manual resuscitation device, such as an Arnbu bag and mask unit? i. List the five categories of conditions causing hypoxemia. I. List the four categories of conditions causing hypoxia.

Bapter 24: Unusual anaesthetic complications.

1. What is MH? 2. List two anaesthetic agents that may trigger an MH reaction. 3. Which drug is used specifically to treat an MH reaction? 4. What strategies are useful in reducing the perioperative risk of pulmonary aspiration of gastric contents? 5. Describe the steps used to treat an anaphylactic reaction.

Page 256 j Index

J ) Acceptable blood loss, 187 Anemia, 13 Acetaminophen with codeine, 137,139, Angina, 10 140,145 Anoxia, 223 ) Acupuncture, 7, 140 Anti-cholinesterase agent, 164 ) Acute pain pathophysiology, 127 Aorto caval compression, 155 Acyclovir, 144 Apgar score, 166 ) Adenosine, 222 Arm-brain circulation time, 78 ) Adrenal suppression, 12, 28 Arrhythmias, 10 Adrenergic receptors, 209 - 210, Arterial oxygen content, 68 I 218 - 222 Arterial oxygen partial pressure (PaOJ, ) Afterload, 207, 211 157, 223, 224 Airway assessment, 35 ASA classification, 17 ) Airway obstruction, 45, 204 Asphyxia, 167 Albumen, 184, 185 Aspiration syndrome, 158, 236 - 238 Alfentanil, 107 - 109, 135 Asthma, 10 Allergies, 13, 14 Atelectasis, 10 ) Alveolar arterial oxygen gradient, 68 Atlanto-occipital extension, 36, 40 ) Alveolar oxygen partial pressure Atracurium, 94, 164 (PAOJ, 223,224 Atropine, 29, 98, 164, 222 Alveolar oxygen tension, 68 Autologous blood, 185 ) Ambu resuscitation bag, 228 Bier block, 7, 119, 148 ) hidelocal anaesthetic, 112 Biofeedback techniques, 7, 140, 158, Amitriptyline, 139 161 ) Amrinone, 223 Blood pressure, 67 Anaesthesia machine check, 32 Blood replacement fluids, 180, 182 Anaesthesia monitors, 64 - 75 Blood transfusion complications, ) Anaesthetic depth, 6, 64 188 - 193 ) Anaesthetic family history, 14 Body fluid compartments, 180 Anaesthetic morbidity, 16 Brachial plexus block, 7 ) Anaesthetic mortality, 16,17,18 Bradycardia, 194, 198 ) Anaesthetic record, 31, 35, 64 Breathing circuit, 32 ) Anaesthetic tension cascade, 102 Bupivicaine, 112, 114, 161 Anaphylactic shock, 238 - 240 Calcium chloride, 221 Anaphylaxis, 238 - 240 Capnogram, 73

Page 257 Anaesthesia for Medical Students

Capnography, 73 Diabetes mellitus, 11, 23 1 Capnometry, 73' Diazepam, 20,28,29, 87 Capsaicin, 145 Differential nerve blockade, 114 . ) Carbamazepine, 145 Diffusion hypoxia, 103 Cardiac index, 68, 209 Dimenhydrinate, 205 ) Cardiac output, 68, 156, 208 Diphenhyramine, 191 ) Cardiac risk, 10, 18 Distributive shock, 198, 201, 202 Cardioaccelerator fibers, 122 Dobutamine, 218 1 Cardiogenic shock, 199, 200, 202 Dopamine, 199, 218 ) Cardiopulmonary values, 68 Dopamine-1 receptor, 210, 218 1 Cauda equina syndrome, 151 Doxacurium, 91 Causalgia, 143, 145 - 148 Doxepine, 139 ) Cellular oxygen partial pressure (POJ, Droperidol, 87, .205 ) 223, 224 Dural puncture headache, 122, 123 Central disc herniation, 151 Edrophonium, 98, 164 1 Central neural blockade, 120 Effective dose in 50% (ED,& 100 1 Central venous catheter, 69 Electrocardiogram, 67 Central venous pressure, 68, 208, 209 Emergency surgery, 18, 19 I Cerebrovascular disease, 11 Enalapril, 222 ) Chest compressions, 173 End-tidal concentration, 102, 103 Chlorprocaine, 112 Endotracheal tube sizes, 52 Cholinergic muscarinic receptor, 210 Enflurane, 103, 105 ) Chronic obstructive resp. disease, 10,16 Entonox, 7 ) Chronic pain clinics, 144 Ephedrine, 219 Chronic pain definition, 143 Epidural anaesthesia, 7 ) Cisatracurium, 91 Epidural anaesthesia complications, 122 ) Closed air spaces, 103 Epidural anaesthesia contraindications, Coagulopathy, 13 122 ) Codeine, 107 Epidural blood patch, 123 I Colloids, 182 Epidural opioids, 126, 137, 138 I Congestive heart failure, 10 Epinephrine, 161, 176, 218, 240 Contractility, 208, 209 Esmolol, 221 Coronary Steal, 104 Ester local anaesthetic, 112 Cricoid pressure, 6 1 Estimated blood volume, 187 Crystalloids, 182 Extubation criteria, 54 Cyanosis, 224 Familial periodic paralysis, 97 d-tubocurare, 92 Fentanyl, 107 - 109, 135, 137,160, 161 Dantrolene, 233, 234 Fetal circulation, 167, 168 Depolarizing neuromuscular block, 74, Fetal heart rate monitoring, 166 90, 92 Fiberoptic intubation, 28 Desflurane, 106 Fluid deficit estimation, 180, 183 Detsky's multifactorial risk index, 19 Flumazenil, 87, 206 Dextrose 5% in water (DSW), 183 Fresh frozen plasma, 188

Page 258 Index

Gastric aspiration, 60, 163 Local anaesthetic duration, 113 Gastroesophageal reflux, 12,20, 23,56 Local anaesthetic lipid solubility, 113 .General anaesthesia, 7 Geriatric, 13 Local anaesthetic maximum dose, 114, Glycopyrrolate, 29, 98, 164 115 Goldman risk index, 18 Local anaesthetic onset, 113 Halothane, 103, 104 Local anaesthetic pKa, 113 Halothane hepatitis, 104 Local anaesthetic potency, 113 Hemorrhagic shock'classification, 201 Local anaesthetic protein binding, 113 Hyoscine, 29 Local anaesthetictoxicity, 115,116,117 Hypertension, 10, 23, 100, 127, 194, Local anaesthetic vasoconstrictor, 114, 200 115,161 Hyperthyroidism, 12, 74, 100 Lorazepam, 20,28, 29 Hypopharyngeal classification, 15, 36 Low back pain, 143, 151 - 153 Hypotension, 100, 195 - 197 Maintenance fluid requirements, 180 Hypothyroidism, 12, 100 Malignant hyperthermia (MH), 11, 14, Hypovolemic shock, 197 74, 232 - 2350 Hypoxemia, 127, 163,195,205,224, Masseter muscle spasm , 232 229,230, 238 McGill Pain Questionnaire, 146, 147 Hypoxia, 224 Mean arterial pressure, 68 Ibuprofen, 139 Meconium, 169 Imipramine, 139 Meperidine, 28,29, 107 - 109, 126, Indomethacin, 139 129, 135, 137, 160, 161 Infiltrative anaesthesia, 119 Metochlorpropamide, 20,158,205,236 Inhibitory neurotransmitters, 130 Metoprolol, 211, 221 Intramuscular opioids, 130, 137 Mexilitine, 145 Intrathecal, 137 Midazolam, 28, 86 Intubation criteria, 48, 49 Minimal alveolar concentration (MAC), Intubation, complications of, 53 100, 156, 164 Intubation, difficult, 163 Mivacurium, 90,91 Ischemic heart disease, 10 Mixed venous oxygen saturation, Isoflurane, 103, 104 68, 209 Ketamine, 77, 83, 100 Monitoring neuromuscular function, Ketamine contraindications, 86 73, 74 Ketorolac, 139, 168 Monitoring oxygenation, 67 Labetalol, 211, 220 Monitoring the circulation, 67 Lamaze technique, 7, 158 Monitoring the temperature, 70, 196 Laryngeal classification, 37, 38 Monitoring ventilation, 67 Laryngeal mask airway, 55 - 59 Morphine, 28, 29, 107 - 109, 126, 129, Laryngoscopy, 38, 42, 43 135, 137 Larynx, 43 Muscular dystrophy's, 11, 233 . Lidocaine, 112, 114, 161 Myasthenia gravis, 11, 96 Local anaesthesia, 7, 112 Myasthenic syndrome, 11, 96

Page 259 4naesthesia for Medical Students

Myocardial infarction, 10 134 Myocardial ischemia, 128 PCA bolus dose, 135 PCA continuous infusion, 135 Myofascial pain syndromes, 143, 150, PCA loading dose, 135 151 PCA lockout interval, 135 Myotonia, 97 PCA maximum limit, 135 Naloxone, 107, 110, 176, 206 Pentaspan, 184, 185 Narcotic tolerance, 140 Pentazocine, 139 Nausea and emesis, 193,203 - 205 Perioperativemyocardialreinfarction,20 Neonatal depression, 163, 164 Peripheral nerve blockade, 120 Neonatal resuscitation equipment, 171 Phaeochromocytoma, 12 Neonatal resuscitation overview, 177 Phase I and I1 block, 93 Neonatal resuscitation program, 166 Phenylephrine, 211, 219 Neonatal resuscitation risk factors, 170' Phenytoin, 145 Neostigmine, 98, 164 Physostigrnine, 206 Neuroleptanalgesia, 7, 87 Plasma cholinesterase, 112 Neuromuscular antagonists, 98 Plasma cholinesterase deficiency, 14,94 Neuromuscular junction, 89 Platelets, 187 Neuromuscular physiology, 89 Positive pressure ventilation, 172 Nifedipine, 222 Post herpetic neuralgia, 143 - 145 Nitroglycerine, 220 Post traumatic pain syndrome, 148 'Nitroprusside, 220 Postoperative agitation and delirium, Nitrous oxide (N20), 100, 101, 103 205 - 206 Nociception, 127 Pregnancy, physiologic changes of, 155 Non Depolarizing neuromuscular block, Pregnancy, risks of general anaesthesia, 74, 75, 90 155, 162, 163 Non steroidal anti-inflammatory drugs Preload, 208, 209 (NSAID'S), 138 - 140, 153 Premedication, 20 Norepinephrine, 219 Preoperative anxiety, 27 Normal saline, 184 Preoperative testing, 15 Obstructive shock, 201, 202 Prochlorperazine, 205 Ondansetron, 205 Propofol, 77, 81, 100, 164, 205 Opioid infusions, 133 Propofol contraindications, 83 Opioid receptors, 107 Propranolol, 220 Osteomyelitis, 153 Psychologic stress, 6, 27, 159 Oxygen cascade, 223 Pulmonary artery catheter, 69 Oxygen concentration, 223 Pulmonary artery pressure, 68 Oxygen delivery systems, 225 Pulmonary capillary wedge pressure, 68, Oxygen partial pressure, 223 208, 209 Packed red blood cells, 188 Pulmonary vascular resistance, 68 Pancuronium, 92 Pulse oximetry, 71 Paraaminobenzoic acid, 112 Raised intracranial pressure, 11 Patient controlled analgesia (PCA), 126, Ranitidine, 20, 158

Page 260 Index

Rapid sequence induction, 60 - 62, 158, Systemic vascular resistance, 68 163, 236 Tachycardia, 127, 194, 199 Temporomandibular joint, 35 Reflex sympathetic dystrophy, Tetanus stimulus, 74, 98 143, 148,150 Regional anaesthesia, 7, 107, 116, 117 Thiopental, sodium, 77, 100, 164 Remifentanil, 111 contraindications, 80 Renal failure, 12 Third space fluid losses, 180, 182 Respiratory failure, 10 Thyromental distance, 14, 36 Rha bdomyolysis, 232 Tissue hypoxia, 230 Ringer's lactate, 184 Topical anaesthesia, 119 Risk assessment, 16 Train of four ratio, 98 Sciatica, 152 Train of four stimulus, 75, 98 Second gas effect, 103 Transcutaneous electrical nerve Sevoflurane, 106 stimulation (TENS), 140, 145, 148 Shock states, 194, 201 Tricyclic antidepressants (TCA's), 139, Shoulder hand syndrome, 148 145, 153 Shunted blood, 229 Trigger points, 150 Smoking, 10, 22 Valvular heart disease, 10 Sniffing position, 38 Vecuronium, 92, 164 Sodium channel, 113 Ventilation perfusion inequalities, 229 Sodium citrate, 21, 158, 236 Verapamil, 221 Spinal anaesthesia, 7 Vessel rich group, 78 Spinal anaesthesia complications, 122 Whole blood, 188 Spinal anaesthesia contraindications, 122 Spinal cord injury, 11 Spinal opioids, 126, 137 Spinal stenosis, 152, 153 ST segment, 67 Stroke volume, 68 Subacute bacterial endocarditis, 10, 21, 27 Substance P, 129, 137 Substantia gelatinosa, 129, 130 Succinylcholine, 93 Succinylcholine contraindications, 97 Succinylcholine hyperkalemia, 95 Sudeck's atrophy, 148 Sufentanil, 107 - 109 Supine hypotensive syndrome, 155 Surgical stress response, 6, 129 Sympathetic blockade, 122, 148

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