Anaesthesia for Medical Students

Pat Sullivan M.D. 1999 Edition

Acknowledgements:

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The author gratefully acknowledges the work of William Sullivan MA., M.D., John 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 writ( ten permission of the author. (

Published by the Department of Anaesthesia, Ottawa Civic Hospital. Address correspondence to: Patrick Sullivan MD, FRCPC Department of Anaesthesia Ottawa Civic Hospital, B310 1053 Carling Avenue Ottawa, Ontario, Canada, K1Y 4E9 T:613 - 761 - 4940 F:613 - 761 -5032 E: [emailprotected]~n.ca

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: Contributing Authors Dr. Gregory Allen Assistant Professor Pennsylvania State University MHAUS Hotline Consultant - Department of Anesthesia - Hershey, Pennsylvania '

- Dr. Wayne Barry - Assistant Professor University of Ottawa Department of Anesthesia - Ottawa Hospital - Civic Campus Dr. Greg Bryson - Assistant Professor - University of Ottawa Department of Anesthesia - Director Preadmission Unit - Ottawa Hospital - Civic Campus Dr. Robert Cirone - Staff Anesthesiologist Department of Anesthesia St. Joseph's Hospital Toronto Dr. Robert Elliot Assistant Professor University of Ottawa Department of Anesthesia Ottawa Hospital General Campus

Dr. John Kitts Associate Professor Anesthesia University of Ottawa Vice President Medical Affairs Ottawa Hospital Dr. Anne Lui Assistant Professor University of Ottawa Department of Anesthesia Ottawa Hospital - Civic Campus Dr. John Penning Assistant Professor University of Ottawa Director of the Acute Pain Service Department of Anesthesia Ottawa Hospital - Civic Campus Dr. Gordon Reid Assistant Prsfessor University of Ottawa Director Malignant Hyperthermia Investigation Unit Department of Anesthesia Ottawa Hospital Civic Campus

Dr. Linda Robinson Assistant Professor University of Ottawa Department of Anesthesia Ottawa Hospital - Civic Campus

Introduction Specialists in the fields of medicine and surgery may ask why medical students should be exposed to the specialty of anesthesia. We believe that there are basic concepts and technical skills that every physician should possess, and that these concepts and skills are best taught by our specialty. Medical school curricula across North America are repeatedly criticized for lacking the teaching of both acute and chronic pain management. In addition, students who pursue a career in surgery, emergency medicine or internal medicine are expected to have the skills to manage a patient's airway. However, they usually have had no formal teaching in these basic skills. Finally, medical school curricula in North America are rapidly changing. Students are now asked to commit themselves to a specialty during the third year of their medical school training. We believe that this process is unfair. We also recognize that a student with no prior exposure to anesthesia is unlikely to choose anesthesia as a career. This manual was written with contributing authors from the Departments of Anesthesia at the Ottawa Civic and General Hospitals for medical students spending two weeks of their clinical rotation in the specialty of anesthesia. Six specific objectives are used to focus the students reading. The text is highlighted by two asterisks (**) for material that is essential and that the student must know, and one asterisks (*) for material which the student

should know. A11 other material is ~ r o v i d e dfor background reading which the student may know. The manual is to be used as a primary reference for lectures on monitoring in anesthesia, and on acute and chronic pain management. The problem-based tutorial question will also be on material covered in this manual. The student who completes the anesthesia rotation should have acquired confidence in airway management skills including mask ventilation and tracheal intubation, as well as securing intravenous access. Important concepts for the student to attain during their rotation include:

1. Preoperative assessment. 2. Basic principles of managing acute and chronic pain disorders. 3. The appropriate use of local anaesthetic agents. 4. Analgesic options for women in labour. 5. Basic neonatal assessment and resuscitation. 6. Intravenous fluid and blood component therapy including the potential complications of a blood product transfusion.

Patrick Sullivan MD, FRCPC Assistant Professor University of Ottawa, Resident Program Director Department of Anesthesia University of Ottawa

Preface The first public demonstration of ether was by W.T.G. Morton in the Etherdome of the Massachusetts General Hospital in 1846. Ether anaesthesia became widely available and would soon be followed by chloroform and nitrous oxide. Surgeons were not particular about who poured the ether or chloroform so long as someone was there to do the job. It was not until the early 1920's that physicians began to show interest in anaesthesia as a specialty. By the end of World War I1 the infant specialty was firmly established and university training programs began. The emphasis has traditionally been on postgraduate teaching. Why has undergraduateanaesthesia teachingbeen neglected or de-emphasized? It was because the medical school curriculum was controlled by older, traditional disciplines that were unwilling to relinquish time for competing specialties. This was complicated by the fact that anaesthetists originally worked only in the operating room, and found it difficult to be freed from that responsibility to undertake teaching outside the operating room. Anaesthesia has expanded to include other services 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 valuable to physicians, regardless of their discipline. They have become specialists in applied physiology, phar-

macology and resuscitation of acutely traumatized patients. The importance of imparting these skills and knowledge to medical students has been realized by those responsible for medical school curricula. Accreditation bodies are demanding that anaesthetists teach medical students. When the new curriculum, founded on problem-based learning, was adopted in the Faculty of Medicine at the University of Ottawa, anaesthesia was given responsibilities in the program. Each student must spend two weeks in an anaesthesia rotation and many anaesthetists participate in small group sessions. Dr. Patrick Sullivan found that an anaesthesia manual, which would meet the needs of medical students submerged in a new curriculum, was not available. The manual he and his co-authors have written covers all of the important material a medical student must and should know. It is best taught by anaesthetists because it falls almost exclusively in their domain. The organization of the manual makes it essential reading for students rotating through anaesthesia who want to optimize their brief exposure to anaesthesia, which has so much to offer.

J. Earl Wynands, M.D. Professor and Chairman Department of Anaesthesia University of Ottawa

Table of Contents

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1. 2 3 4. 5

Rotational Objectives Anaesthesia Overview Preoperative Evaluation and Risk Assessment Premedication Getting Started: A practical approach to the OR Intubation and Anatomy of the Airway 6 7. Intubation Decisions The Laryngeal Mask Airway 8 9 Rapid Sequence Induction 10 Monitoring in Anaesthesia General Intravenous Anaesthetic Agents . . . . . . . . . . . . . . . . . . 11 12 Muscle Relaxants 13 Inhalational Agents Narcotic Agonists and Antagonists 14 Local and Regional Anaesthetics 15 16. Acute Pain Mechanisms and Management 17 Chronic Pain 18 Obstetrical Anaesthesia .............................. 19 Basic Neonatal Resuscitation Intravenous Fluid and Blood Component Therapy 20 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

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Anaesthesia Rotational Objectives There are six speclflc knowledge and sk111s obJect1ves4 for the two week anaesthesia rotation:

The student will demonstrate proper airway and ventilatory management of the unconscious patient by:

1. To become aware of anaesthetic

considerations in the preoperative evaluatlon and preparation of the patient.

This will be accomplished by conducting several preoperative assessments, including: a. b.

c. d.

Taking and recording a pertinent history. Performing an appropriate physical examination, including assessment of the airway, the respiratory and cardiovascular systems, and other systems as indicated. Reviewingrelevantlaboratorydata. Preparing a problem list and assigning appropriate ASA physical status. Prescribing appropriate premedication, including continuing relevant current medications, and demonstrating knowledge of the principles of managing specific medications (eg. insulin,anticoagulants). To learn appropriate airway and ventllatory management.

Must Know

Describing and identifying basic oropharyngeal and laryngotracheal anatomy. Describing the indications, benefits and risks of airway management by mask and endotracheal intubation. Identifying and stating appropriate sizes of masks, oral and nasal airways, laryngoscope blades and endotracheal tubes. Identifying and overcoming upper airway obstruction with mask ventilation using various masks, oral and nasal airways, jaw thrust and or chin lift maneuvers. Successfully preparing appropriate equipment, positioning and intubating several patients with minimal supervisor intervention. Correctly identifying within 30 seconds those patients in whom endotracheal intubation was not successful. Recognizing and discussing the need for controlled ventilation using physical signs, cardiovascular parameters, respiratory measurements, and/or arterial blood gases.

Should Know

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Anaesthesia for Medical Students

Discussing the various methods of monitoring the adequacy of ventilation. Prescribing appropriate parameters for mechanical ventilation. Describing and identifying criteria for extubation. To acqulre skllls necessary to prescribe and conduct approprlate fluld and blood component therapy, lncludlng establlshlng vascular access.

This will be demonstrated by: a. Identifying common sites for venous access. b. Demonstrating skill at establishing venous access by: using sterile technique. - Successfully inserting several peripheral catheters of various calibres. Protecting the venipuncture site and immobilizing the catheter. c. Describing the indications and complications of central venous access. d. Prescribingperioperative fluid and electrolyte replacement, taking into account such factors as NPO status, preoperative bowel prep, NG suction, fever, blood losses, and third space losses. e. Discussing perioperative indications for blood administration, and learning rational use of blood products, and the potential complications of blood product administration. f. Correctly interpreting data from the following monitors of volume status:

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examination of the patient. - pulse and blood pressure. urine output. - invasive monitoring (CVP, PCWP, Arterial pressure waveforms, cardiac output).

To learn local anaesthetlc pharmacology approprlate to general medlclne by: Classifying commonly used agents according to amide and ester linkage. Listing commonly used local anaesthetics for: topical use - local infiltration peripheral nerve blocks iv (Bier's) block epidural anaesthesia spinal anaesthesia Listing acceptable doses of at least two agents used for topical and local infiltration anaesthesia. Describing the diagnostic criteria for, and management of: local anesthetic toxicity. inadvertent intravascular injection of local anaesthetic. - allergic reaction to a local anaesthetic.

To understand the management of pain In the peripartum period and the lnltlatlon of neonatal resuscltatlon. This will be demonstrated by: Discussingindications, contraindia. cations and adverse effects of various modes of obstetrical pain relief.

Rotational Objectives

mask analgesia with nitrous oxide and/or volatile anaesthetic agents. narcotic analgesia (im, or iv). epidural anaesthesia. spinal anaesthesia. The student will develop skills in assessment and management of the healthy newborn by: administeringoxygen by mask. performing oropharyngeal and nasopharyngeal suction. performing an initial physical examination. assigning Apgar Scores. recognizing newborn distress. The student will be able to describe therapeutic steps necessary to begin neonatal resuscitation.

To understand the prlnclples of acute and chronlc paln management.

This will be achieved through the provided reading material in the anaesthesia manual, a pain clinic rotation, and a discussion of modalities for acute pain management including: a. b. c. d.

iv narcotic infusions. non-narcotic analgesics. iv and epidural PCA (patient controlled analgesia). peripheral nerve blocks.

Reading material in the anaesthesia manual and discussion of the diagnosis and management of common chronic pain syndromes will focus on: a. b.

Reflex sympathetic dystrophy. Fibrositis.

c. d. e.

Chronic low back pain. Post herpetic neuralgia. Cancer pain.

ANAESTHESIA CURRICULUM:

KNOW LEDGEfSKILLSIATTITUDE

The following topics will be covered either in the manual, or in seminar format and problem solving sessions during the 12-week surgical - anaesthesia rotation. Preoperative evaluation and preparation. Anaesthetic Surgical risk assessment. Hypoxia Oxygen Therapy. Intubation-indications/complications. Principles of mechanical ventilation. Shock. Fluid Therapy. Blood component therapy. Acute and Chronic Pain management. Obstetrical anaesthesia-analgesia. Basic neonatal resuscitation.

1. 2.

3. 4.

5. 6.

Airway maintenance maneuvers in the unconscious patient. Artificial airway insertion. Mask ventilation. Endotracheal intubation and extubation. Spontaneous, manual, and controlled modes of ventilation. Venous cannulation. Prescription, identificationand administration of blood components, including equipment assembly.w Arterial blood gas sampling.w

Should Know

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4naathaia for Medical Srudenfs

Spinal anaesthesia (Lumbar puncture)." 10. Nasogastric tube insertion." 9.

ti Skills number 1 to 6 must be achieved during the rotation. Students may acquire skills number 7 to 10 depending on clinical opportunity and the students' interest level.

Attitude: We hope that your two-week rotation will stimulate a thirst for knowledge and understandingof the fascinating physiology and pharmacology that occurs in the patient undergoing surgery. Anaesthesia is a somewhat unnatural if not magical state. It is normal to feel technically challenged during your rotation as you acquire vascular access and airway management skills. Each of you can expect to experience (as all doctors have), a humbling but hopefully rewarding, technical learning curve. You should be aware of your difficulties, your response to them, and the response of your patient and other medical personnel to your difficulties. We ask that your eyes and senses not be clouded by technical monitors, but rather be open to the overall care of the patient. We demand a commitment of excellence in your care and concern for the wellbeing of the patient and their family. We expect punctuality and honesty as a basis of good medicine. While students may view anaesthesia as 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

encounters do not have to be devoid of reassurance, kindness or a comforting touch. We expect both positive and negative experiences during your rotation to be discussed openly with us, to ensure the best possible rotation for future students.

Resources: Our University of Ottawa Anaesthesia Manual will be distributed to all students, and will be used as the basic reference text for the rotation. Additional reference material will be available in each hospital's anaesthesia library. Topics covered in this manual have been classified as either must know, should know, or may know material. Material designated as must know will be identified by two asterisks (**), and will have a greater emphasis in content and weighting in the multiple choice, short answer, and OSCE questions at the end of the surgical anaesthesia rotation. Material assigned to the should know portion of each chapter will be identified by one asterisk (*). All other topics covered in the manual provide a general background for the student during their anaesthesia rotation, and are topics which the student may know. A passing grade can be achieved with a good comprehension of the must know material, while an honours mark may be awarded to students correctly answering material covered in the should know and may know sections of the manual.

Rotational Objectives

A computerized anaesthesia simulator will be available as anoption during the students rotation. (The simulator includes models of pharmacology, pharmaco*kinetics, critical incidents, as well as cardiovascular and respiratory physiology).

The hospitals' anaesthesia library and main libraries will be available for reference during the rotation.

Notes:

M w Know

The rotation evaluation will be based on four components.

Participation during problem solving sessions. 11. One or more examinations using a multiple choice format, short answer examination format, or OSCE examination. 111. A clinical profile record. IV. A review of the anaesthesia simulator problems (optional).

Should Know

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Anaesthesia Overview Modem general anaesthesia is based on the ability to provide adequate analgesia and amnesia during surgical procedures. Neuromuscular-blocking drugs may be utilized to facilitatesurgical exposure by providing profound muscle relaxation. The anaesthesiologist attempts to achieve both analgesia and amnesia, with or without muscle relaxation, while maintaining the patient's normal physiological functions. The challenge in anaesthesia is to maintain a balance between the stress of the surgical procedure and the cardiorespiratory depressant effects of deepening levels of anaesthesia (figure 2.1). The anaesthes-

iologist uses both skills in clinical examination and a host of technical monitors to provide ongoing feedback on the patient's physiological status and anaesthetic requirements. Table 2.1 lists options available to the anaesthesiologist for providing analgesia, amnesia and muscle relaxation.

A state of general anaesthesia may be induced with the injection of anaesthetic drugs, or by the inhalation of a mixture of anaesthetic vapours (figure 2.1). With general anaesthesia, muscle relaxants may be used to facilitate both tracheal intubation and muscle relaxation.

Surgery

Anaesthesla Physbbgical Stability End organ homeostasis cardiovascular respiratory - neural renal

S t w - psychological physiologlcal - Blood loss - Cardiovascularstress - Fluid shifts - Respiratorystress - Temperature changes

Figure 2.1: The Anaesthetic - Surgical balance. Page 6

Chapter 2 Anaesthesia Overview

Muscle relaxants are frequently used to facilitate surgical access, and are essential for thoracic and abdominal operations. As muscle relaxants have no effect on the state of consciousness, additional anaesthetic medications must be given to ensure both amnesia and analgesia. The use of muscle relaxants avoids the need for excessive amounts of other anaesthetic agents that would otherwise be required to achieve the same degree of muscle relaxation. Because muscle relaxants also affect the

muscles of respiration, positive pressure ventilation is frequently used to maintain normal minute ventilation when they are given. When muscle relaxants are not used, the patient may be allowed to spontaneously inhale anaesthetic vapours to maintain the anaesthetic state. If efforts at spontaneous ventilation are inadequate, manually assisted or controlled mechanical ventilation may be used by the anaesthetist. Controlled mechanical ventilation is generally used only when the trachea has been intubated.

Table 2.1: Anaesthetic Options*. Anaesthetic Options Local Anaesthesia Alone. Local Anaesthesia with intravenous conscious sedation.

eg. iv Propofol, midazolam, fentanyl and or music for sedation.

Neurolept-analgesia.

Used infrequently. Achieved with high doses of droperidol with a opioid (such as fentanyl) for analgesic supplementation.

Regional Anaesthesia, with or without sedation.

eg. Spinal Anaesthesia Epidural Anaesthesia Brachial Plexus Block Intravenous 'Bier' Block Peripheral Nerve Blocks

General Anaesthesia. (see figure 2.2)

May be combined with regional anaesthesia, peripheral 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

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Anaesthesia for Medical Students

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Intravenous Anaesthetics

Inhaled Anaesthetic Gases

Induction of General Anaesthesia Mask

Endotracheal tube

No muscle relaxants

Assisted Ventilation

Spontaneous ventilation

Controlled y o n Ventilation with muscle relaxants

Figure 2.2: Establishment of General Anaesthesia.

Spontaneous and assisted ventilation may be used in conjunction with a tracheal tube, laryngeal mask airway, or simple face mask (figure 2.2). 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

drugs used during general anaesthesia include antiemetics, neuromuscular blocking agents, and neuromuscular antagonists.

CHAPTER 3

' Preoperative I

: )

Evaluation and Risk Assessment GREGBRYSON M.D., FRCPC AND JOHNB. KITTSM.D., FRCPC -

Preoperative assessment is essential for the safety of anaesthesia. Physicians who have had no exposure to the specialty of anaesthesia are ill-equipped to evaluate, prepare, and institute measures to minimize the patient's risk in the perioperative period. This chapter provides a framework for physicians who need to understand their patients' risk of undergoing a surgical procedure, and the measures that can be used to optimize their patients' condition prior to surgery. Preoperative evaluation serves many purposes. First, it offers the anaesthetist 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 whose condition is not optimal. Finally, the anaesthetist can provide information and reassurance for the patient during this stressful time. An organized approach to the preoperative evaluation will allow the anaesthetist to perform a focused evaluation of the patient's medical and surgical condition, and to address issues relevant to the

Must Know

safe and effective performance of surgery. The preoperative evaluation does not replace the role of the primary care provider, and should not be used to address issues that are not relevant to the performance of anaesthesia and surgery. The preoperative visit should include the following steps: I. 11. 111. IV.

Problem Identification Risk Assessment Preoperative Preparation Plan of Anaesthetic Technique

Identification of the problems a patient brings to the operating room is one of the most vital, yet easily neglected, components of the perioperative management of the surgical patient. A system-oriented approach to the patient is helpful in completing a thorough preoperative assessment. As is the case elsewhere in medicine, the preoperative evaluation should progress through history (including a review of the Should Know

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Anaesthesia for Medical Students

patient's chart), physical examination, and laboratory investigation. Anaesthetic drugs and techniques have profound effects on human physiology. Hence, a focused review of all major organ systems should be completed prior to surgery. The anaesthetist pays special attention to symptoms and disease related to the cardiovascular, respiratory, and neuromuscular systems as they will directly manipulate these systems during surgery. Because one of the goals of the preoperative evaluation is to ensure that the patient is in the best (or optimal) condition, it is important not only to identify symptoms, but also to document their severity and to determine their stability or progress. Patients with unstable symptoms should be postponed for optimization prior to elective surgery. Cardlovascular: Patients with ischemic heart disease are at risk for myocardial ischaemia or infarction in the perioperative period. A thorough history should ascertain whether angina is new or has recently changed from a previously stable pattern. A description of the patient's exercise tolerance must also be included. Patients with a history of a recent myocardial infarction (< 6 months) or unstable angina are poor surgical candidates, with a high risk of significant morbidity or mortality.

Assessment of cardiac risk is discussed later in this chapter. As many anaesthetic agents are also myocardial depressants, a history of congestive heart failure or cardiomyopathy should

be directly sought. Valvular heart disease presents a special set of concerns to the anaesthetist. This includes unfavourable and even dangerous alterations in haemodynamics brought on by the anaesthesia, particularly major regional techniques (see chapter 15: Local and regional anaesthetics). Consider the risk of subacute bacterial endocarditis (SBE) in these patients.

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Although less common with new anaesthetic drugs, arrhythmias are frequently seen in the operating room. In the preoperative visit, identify a past history of arrhythmia or symptoms suggesting the need for a pacemaker. The patient with hypertension will require special attention to perioperative antihypertensive therapy and fluid and electrolyte balance. Respirology: Cigarette smoke has several adverse effects, including alteration of mucus secretion, clearance, and decrease in small airway calibre. It also may alter the immune response. The chronic smoker should be encouraged to abstain from smoking for at least 8 weeks prior to the operation,' but stopping smoking for even 24 hours may produce benefits in cardiovascular physiology2 and carboxyhemoglobin levels.

Patients with chronic obstructive pulmonary disease (COPD) are at increased risk of perioperative respiratory complications. Anaesthesia, surgery and postoperative analgesia all predispose the patient with COPD to respiratory depression, atelectasis, retained secretions, pneumonia and respiratory insuff-

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Chapter

iciency or failure. The patient with asthma is at particular risk as manipulation of the airway and cold dry anaesthetic gases are potent triggers of intraoperative bronchospasm. Determine the presence of cough and the colour and amount of sputum. Ensure that there is no acute upper respiratory infection. The patient's exercise capacity should be evaluated by asking questions such as how they manage around stairs at home, and walking to local stores. Are they able to walk several blocks comfortably at a normal pace? Do they avoid stairs? If they routinely uses stairwells, how many flights are they able to complete? Do they have to rest in the stairwell? Is this the result of fatigue, shortness of breath, or chest pain? lung disease will be worsened by upper abdominal or thoracic surgery, and place the patient at increased risk for perioperative failure. Any disease process which leads to an altered control of breathing (obstructive sleep apnea, CNS disorders, etc.) may lead to profound respiratory depression from the drugs used in the perioperative period, and may require postoperative monitoring in a critical care setting. Potential airway problems are of particular concern to the anaesthetist, and must always be evaluated (see chapter 6: Intubation and Anatomy of the Airway). Restrictive

Neuromuscular: If the patient has an intracranial lesion, seek early signs and symptoms of raised intracranialpressure such as headaches, nausea, vomiting, confusion and

Must Know

3 Preoperative Assessment

papilledema. Pituitary lesions may cause endocrine abnormalities. A history of T M ' s or CVA's suggests significant cerebrovascular disease. The anaesthetist should ask the patient about a history of seizures, and determine the type, frequency and time of last occurrence. Note any anticonvulsant medications the patient is receiving. The patient with a history of spinal cord injury is at risk for a number of perioperative complications including respiratory failure, arrhythmias, autonomic hyperreflexia, hyperkalemia, pathologic fractures and pressure sores. It is important to document the date and level of the neurological injury, as the incidence of many of these complications are dependent on such variables. Patients with lower motor neuron lesions of any kind are at risk for unusual responses to anaesthetic drugs (see chapter 12: Muscle Relaxants Succinylcholine), and regional anaesthesia should be considered only after careful documentation of the patient's nerve deficits.

Disorders of the neuromuscular junction such as myasthenia gravis, myasthenic syndrome, etc., will cause unpredictable responses to neuromuscular-blocking drugs. Lastly, patients with muscular dystrophies and underlying myopathies are known to have both an increased association withmalignant hyperthermia and an increased risk of postoperative respiratory failure (see chapter 24: Uncommon Anaesthetic Complications Malignant Hyperthermia).

Should Know

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Anaesthesia for Medical Studenis

Endocrlne: Patients with diabetes mellitus require careful management in the perioperative period, as the stress of surgery and perioperative fasting can cause marked swings in blood glucose. Diabetics frequently have widespread end organ damage involving the cardiovascular, nervous and renal systems.

Patients with thyroid disease may experience difficulties under anaesthesia. Profound hypothyroidism is associated with myocardial depression and exaggerated responses to sedative medications. Hyperthyroid patients are at risk for perioperative thyroid storm. Thyroid goitres may compress the airway and involve the recurrent laryngeal nerve leading to vocal cord palsy. These place the patient at risk for airway obstruction. Patients with phaeochromocytoma are particularly challenging for the anaesthetist, surgeon, and internist involved in their care. These patients are at risk for extreme swings in blood pressure and heart rate in the perioperative period, and require intensive preoperative therapy with adrenergic blocking drugs. Patients at risk for adrenal suppression (history of exogenous steroid therapy) may not be able to increase their own corticosteroid production to match the imposed stress of surgery. The incidence of adrenal suppression is not predictable, and depends on the potency and frequency of steroid dose and on the length of steroid therapy. As a general rule, corticosteroid supplementation is provided for patients who have required steroids for more

than one week in the last six months. GI-Hepatic: Patients with hepatic disease frequently present problems with fluid and electrolyte imbalance, coagulopathies and altered drug metabolism. Patients with gastroesophageal reflux (GER), as well as those at risk for GER, are prone to regurgitation of gastric contents and aspiration pneumonitis during the perioperative period (see chapters 9 & 24: Rapid Sequence Induction & Unusual Anaesthetic Complications Aspiration Pneumonitis). These patients should receive anti-reflux prophylaxis preoperatively.

Renal: Disorders of fluid and electrolyte balance are common in the perioperative period, and management of any possible electrolyte deficiency or excess may be part of the anaesthetic management of the patient. Generally all fluid and electrolyte disorders should be corrected prior to elective surgery.

Patients with renal failure, both acute and chronic, frequent the OR. The anaesthetist must be prepared to deal with their fluid and electrolyte disorders, dialysis requirements and altered drug metabolism. Pay careful attention to the patient's dialysis schedule, as important changes in blood volume and serum potassium levels occur pre- and post-dialysis. If possible, plan elective surgery so that the patient receives dialysis either the night before surgery, or on the morning of surgery. Patients with renal insufficiency are at risk for deterioration of their renal function, and

Chapter 3 Preoperative Assessment

careful attention must be paid to their fluid and haemodynamic management in the perioperative period. Haematologic: Anemias of a variety of causes are

common in the patient undergoing surgery. A minimum haemoglobin level of 100 gm/L was traditionally required before a patient could undergo elective surgery. The dogma regarding an adequate haemoglobin level has held less sway in recent years. Now the "transfusion trigger" must be individualized to the patient, bearing in mind the chronicity of the anemia, the likelihood of perioperative blood loss, and the patient's co-existent disease (see chapter 20). Coagulopathles involving clotting factors and platelets, both congenital and acquired, require careful management. Patients with a bleeding tendency are generally poor candidates for major regional anaesthesia and management must be individualized, depending on the nature of the bleeding problem, the proposed surgery, and the patient's medical condition. The Elderly: The elderly have a higher incidence of age-related coexisting disease as well as both diminished organ function and organ reserve. The result is that elderly patients are generally recognized to be in a higher perioperative risk group. Perioperative morbidity and mortality are related to the extent of coexisting disease rather than the patient's age alone. Elderly patients should not be refused elective surgery on the basis of

Must Know

their age alone. However, every attempt must be made in adequately diagnosing and treating coexisting disease preoperatively. The risk of deferring surgery must be balanced against the potential for the patient returning on an emergency basis. Emergency surgery in the elderly patient may lead to a four- to twenty-fold increase in perioperative mortality. Delay in presentation and inadequate time for optimizing coexisting disease place an increased burden on a patient lacking the physiological reserve to tolerate major stress and surgery. Medications and Allergies: A detailed list of the patients' medications and allergies is an essential part of the preoperative assessment. Particular attention should be paid to cardiovascular and respiratory medications, narcotic analgesics, and drugs known to have significant side effects or drug interactions. As a general rule, all cardiac and pul-

monary medications and most other necessary medications should be taken with sips of water at the usual time, up to and including the day of surgery. Possible exceptions to this include coumadin, ASA and NSAID's, insulin (adjustment of the dose is needed on the day of surgery), oral hypogylcemics and antidepressants. Pay special attention to patients receiving monoamine oxidase (MAO) inhibitors and amiodarone. Question patients with allergies to drugs carefully on the nature of the reaction and the circ*mstances under which it Should Know

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Anaesthesia for Medical Students

occurred. Many "allergies" are simply anticipated drug side effects such as nausea and vomiting, or adrenaline absorption from local anaesthetic agents. True allergies to anaesthetics are unusual, but when present, can be fatal.

on evaluation of the airway, the cardiovascular system, the respiratory system, and any other systems identified as having symptoms or disease from the history.

Prlor Anaesthetics: The patient undergoing anaesthesia and surgery should be carefully questioned on their response to previous anaesthetics and a family history of problems with anaesthesia. Investigate any complication or adverse reaction to prior anaesthetics. Document the type of problem, as well as its management and outcome. In the case of serious perioperative events, consult the old chart to complete the history. Seek a family history of adverse anaesthetic experience. Malignant hyperthermia and plasma cholinesterase deficiency are two hereditary disorders that manifest under anaesthesia (see chapter 24: Unusual Anaesthetic Complications).

A general assessment of the patient's

General:

Problems related to Surgery: Information about the patient's general medical condition and anticipated intraoperative problems can be gained from an evaluation of the proposed surgery. Careful consideration of the surgical procedure will reveal the likelihood of significant blood or third space loss, cardiorespiratory compromise, andlor unusual positioning requirements (prone, lateral, lithotomy, etc.). This information will be useful in planning venous access, monitoring, and anaesthetic technique. Physlcal Examinatlon: The physical examination should focus Page 14

physical and mental status is performed. Note whether the patient is alert, calm, and cooperative, or unusually anxious about their scheduled procedure. Is the patient young and physically fit, or elderly incoherent, emaciated and confined to bed? Such obvious differences will dictate the extent and intensity of the examination and the time required to listen to the patient's concerns and provide reassurance. The patient's mental status also influences the type and amount of preoperative medication required (if any), and may influence the type of anaesthetic technique used (eg. general vs. regional). Upper airway: Examination of the upper airway must be performed on all patients. Identify and document any loose teeth, capped teeth, or bridges. The patient should be asked to open their mouth as widely as possible, in order to assess temporal mandibular joint mobility, and allow visualization of the soft palate, uvula, pharyngeal arches and posterior pharynx. The thyromental distance (the distance from the mentum (lower border of the chin) to the thyroid notch, the mobility of the C-spine in both flexion and extension, as well as the position of the trachea should all be assessed, as each of these have implications with respect to the ease of intubation.

Assessment of the upper airway must include evaluation of the range of motion of the neck, as well as mouth opening, dentition, and thryromental distance. The adequacy of visualization of the hypopharyngeal structures is used as an indicator of potential difficulty with direct laryngoscopy. A hypopharyngeal class is assigned in an attempt to quantify the degree of difficulty that will be encountered during direct l a ~ ~ n ~ o s c o (See p y . ~Chapter ~~ 6: Anatomy and Assessment of the Airway).

sites for major regional anaesthetic techniques (eg. spinal, epidural, or brachial plexus blocks). Again, the state of health of the patient will dictate the intensity of the examination required. The healthy 20-year-old male undergoing an arthroscopy, requires a much more abbreviated history, physical examination and chart review when compared to the elderly patient undergoing a major abdominal procedure. Laboratory Testing: Obtain preoperative laboratory testing only if indicated from the preoperative history and physical examination. In September 1993, the Public Hospital's Act in Ontario was amended so that mandatory haemoglobin and urine analysis were no longer required prior to surgery. Perform these tests and all other preoperative tests, however, where indicated by the medical status of the patient, or if the patient is considered in a population at risk for a specific problem. "Routine or standing" re operative tests should be discouraged.

Lower airway: Assess the respiratory rate. Note the shape of the thoracic cage, and whether or not the patient is relying on their accessory muscles (e.g., the barrel shaped bronchitic patient vs. the pink emphysemic puffer). Auscultate the chest for audible rhonchi on quiet and forced expiration, and identify the presence or absence of rales. Note the presence or absence of cyanosis and clubbing. Cardiovascular: Assess the heart rate, rhythm and blood pressure. Identify the location of the apical impulse, and whether it is abnormally displaced. Assess the level of the JVP, and identify the presence or absence of peripheral edema. Identify the first and second heart sounds and listen for the presence of heart murmurs, or a third or fourth heart sound. Anticipate any special invasive procedures, and assess the anatomy for arterial line insertion, central vein cannulation, intravenous access, and

Must Know

Do a CBC for patients in whom there is significant blood loss anticipated, suspected haematological disorder (eg. anaemia, thalassaemia, sickle cell disease), or recent chemotherapy. Patients on antihypertensive medications, including diuretics, chemotherapy, renal disease, adrenal or thyroid disorders, must have electrolytes evaluated preoperatively. Obtain an electrocardiogram (ECG)for patients over 50 years of age, or those who have a history of cardiac disease, hypertension, peripheral

Should Know

Page 15

Anaesthesia for Medical Shtdents

vascular disease, diabetes mellitus, renal, thyroid or metabolic disease. Request chest X-rays prior to cardiothoracic procedures and for patients with debilitating COPD, asthma, or a change in respiratory symptoms in the past six months. Perform urine analysis for patients with diabetes mellitus, renal disease or recent urinary tract infection.

There are three components that must be considered when evaluating perioperative risk: the patient's medical condition preoperatively, the extent of the surgical procedure, and the risk from the anaesthetic. In general, the major contribution to increased risk is that of the patient's health prior to the procedure and the magnitude of the surgery. However, patients presenting for surgery often have more fear about their anaesthetic than the surgery itself. Fortunately, anaesthesia-related morbidity and mortality is rare, but unfortunately, not absent. This does, however, create its own problems. The combination of infrequent but serious events has led one author to state that "Perhaps the most insidious hazard of anaesthesia is its relative safety."' Anaesthetic Mortality:

The wide variety of surgical procedures and anaesthetic techniques, combined with the diversity of a patient's coexisting surgical and medical illnesses, produce a number of risk factors that contribute to overall outcome, and make generalized statements about risk difficult. Specific predictions for a single

patient's outcome is virtually impossible, and the complexity of this issue has made research studies addressing outcome very difficult. Nevertheless, several studies attempting to determine anaesthesia mortality and morbidity have been c ~ m ~ l e t e dIt~is' ~difficult to separate the contributions of anaesthesia and surgery to morbidity and mortality, as patients rarely receive an anaesthetic without undergoing a surgical procedure. Table 3.1 summarizes several studies which have attempted to determine the risk of mortality due solely to anaesthesia. Studies on perioperative mortality have yielded differing results. Differences in the definition of outcome variables, study design, and the duration of follow-up make these results difficult to compare. When reviewed critically, these studies suggest that the often quoted number for overall risk of primary anaesthetic mortality for all patients undergoing all types of surgery is approximately 1:10,000. The question to which anaesthetists and the patient need the answer is: "What is the risk of a particular procedure in a patient with a given medical status receiving a specific anaesthetic technique?" Numerous investigators have attempted to address this very complex question. Most of the work, however, addresses the operative risk according to the patient's preoperative medical status. Perloperatlve Rlsk Assessment: Perhaps the oldest and simplest method for risk assessment is the American

Chapter 3 Preoperative Assessment

Author

Country

Year

No. in study

Incidence of Primary Anaesthetic Mortality

Turnbul16

Canada

1980

195,232

15,138

~ovi-Vivander7

Finland

1980

338,934

1:5,059

Lunn & ~ u s h i n '

United Kingdom

1982

108,000

1:10,000

1985

163,240

1:10,000

Keenan & ~ o ~ e United n ~ States ~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) physical status (table 3.2). The ASA physical status classification system was originally proposed in 1941, and revised by Dripps in 196113 to provide a uniform assessment of a patient's preoperative physical condition. As this system is simple, easy to use, and requires no laboratory investigations, it has now been widely accepted as the standard means of preoperative

Description

Category I I1 I11 IV V

patient classification. Although developed as a tool for classifying a patient's physical condition, the ASA physical status has been used to stratify patient risk. While open to significant criticism because of its vague categories and inconsistencies in its application, the ASA physical status classification has been shown to correlate with perioperative mortality.ld17

Healthy patient. Mild systemic disease - no functional limitation. Severe systemic disease definite functional limitation. Severe systemic disease - a constant threat to life. Moribund patient not expected to survive with or without an operation for 24 hours. A suffix E is added to denote an emergency procedure.

Table 3.2: ASA Physlcal Status Classlflcatlonhc.

Must Know

Should Know

Page I 7

Anaesthesia for Medical Shrdents

Operative Mortality (percent) ASA Class

I I1

nr IV V

Vercantit4

~arx"

&hent6

orr rest "

1970

1973

1986

1990

.07 24 1.43 7.46 938

.06 .40 43 23.4 50.7

.07 .20 1.15 7.66

.OO .04 59 7.95

-----

Table 3.3: ASA Physlcal Status vs. Operative Mortality

Examples of the ASA classification: ASA 1: Healthy patient, no medical problems. ASA 2: Controlled hypertension. ASA 3: Emphysema. ASA 4: Unstable angina. ASA 5E: Ruptured abdominal aortic aneurysm in shock, undergoing emergency surgery.

-----

WO).

tors that predicted life-threatening cardiac complications. A scoring system weighted these factors in their ability to predict adverse cardiac outcome. From these data, Goldman suggested that patients with a score greater than 25 be considered only for life-saving procedures. Patients scoring 13-25were advised to have preoperative medical consultations to lower their morbidity and mortality. Certainly, delaying surgery until the patient is more stable can significantly reduce the cardiac risk index. Waiting for 6 months after a

Cardiac Risk: Several perioperative risk studies have attempted to assess which perioperative cardiac risk factors are important. Ischaemic heart disease has received the most attention because mortality from a Points Risk Factor perioperative myocardial in11 Third heart sound or elevated JVP farction approaches 50%. 10 MI within 6 months of surgery 7 Rhythm other than sinus or PAC's In 1977 Goldman published > 5 PVC's per minute 7 a multifactorial risk index 5 Age > 70 for cardiac patients undergoEmergency procedure 4 ing non-cardiac procedures18 3 Abdominal, thoracic, or aortic surgery (table 3.4). This study, inImportant Aortic stenosis 3 volving 1001 patients, identPoor medical status 3 ified, by multivariate analysis, nine potential risk Table 3.4: Goldman's Cardlac Rlsk Index

i Chapter 3 Preoperative Assessment

Variable

Points

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

10 5 20 10 10 10 5 20 5 5 5 5 10

Table 3.5: Detsky's Multltactorlal Index myocardial infarct, delaying emergency procedures (if feasible) and improving a patient's poor medical status all significantly decrease the risk.

Using likelihood ratios, Detsky was able to construct a nomogram relating the pretest probability of cardiac morbidity for the surgical procedure to the patient's risk score. This generates an overall prediction of the risk of major cardiac morbidity or mortality for a patient of a certain medical status undergoing a specific procedure. Although Detsky's risk index is a better

The Goldman index has high specificity but low sensitivity when predicting risk. Patients with scores of 13 or greater should arouse suspicion. A low score correlates with a low probability of poor outcome. In an attempt to improve the sensitivity of Goldman's index, ~ e t s k y ' ~ % Cardiac Surgery modified Goldman's criteria to Complications include a wider range of carVascular 13.2 diac illness (table 3.5). Detsky Orthopaedic 13.6 also recognized that not all sur8.O Thoracic Abdominal gery carries the same risk, and Head & Neck 2.6 factored in the surgical pro1.6 (TURP, Hernia, ...) Minor cedures for the pretest probability 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 Goldman's, it still has limitations. However, a review of the risk factors described in both these studies alerts the anaesthetist to symptoms or signs of significant disease that may contribute to adverse outcome. Both Goldman and Detsky identified recent myocardial infarction as a risk factor for perioperative cardiac morbidity. The perioperative period is characterized by haemodynamic changes, alterations inventilation, fluid and electrolyte shifts, and changes in coagulation, all of which place the patient with underlying cardiac illness at significant risk of infarction. Several important studies have been conducted over the past 20 years in an attempt to identify the likelihood of perioperative reinfarction in patients with a recent M L ~ " The goal of these studies was to determine the safest time interval following an MI to proceed with elective surgery, and to direct attention to appropriate perioperative monitoring and care (Table 3.7). In Rao's study, patients were managed

with invasive haemodynamicmonitoring and aggressive therapy in an intensive care unit (ICU) setting for 7 2 hours following surgery. Cumulatively, these studies suggest considerable benefit in delaying elective surgery for a period of 6 months following a myocardial infarction. Before six months, invasive monitoring and aggressive postoperative management, appear essential, for those patients in whom surgery must be performed.

Premedicatlon: (see also chapter 4) Anaesthetic indications: The preanaesthetic visit should be designed to alleviate patient anxiety and apprehension about the proposed surgery. However, a benzodiazepine such as diazepam or lorazepam is also frequently administered orally 1 2 hours preoperatively. This may provide sedation, relieve anxiety, and provide a degree of amnesia for the events immediately preceding the operation.

Patients at risk for GE reflux should receive anti-reflux prophylaxis. This is

Time from infarction to Surgery

Tarhan20 (1972)

Steen21 (1978)

Rao22 (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 Page 20

e!).

C h a ~ t e r 3 Preo~erativeAssessment

usually achieved with ranitidine 150 300 mg p ~ 2. hours pre-operatively. Other agents such as metoclopramide may be added to promote gastric emptying. Sodium citrate is an effective nonparticulate antacid that may also be used alone or in conjunction with ranitidine. Surgical indications: According to the American Heart Association Guidelines, appropriate antibiotic prophylaxis must be administered for patients at risk for the development of infective endocarditis.= These include patients for whom a bacteremia is likely to occur as a result of respiratory tract, genitourinary, or gastrointestinal tract interventions. Some patients are at high risk for the development of postoperative deep vein thrombosis (DVT). Prophylactic measures should be used and include low-dose heparin, intermittent calf compression, or wumadin. Patients who are currently receiving steroids and those who have required steroids in the previous six months may require supplemental steroids because of adrenal suppression and a blunted response to stress. Cu-existing Disease Indications: All important medications should be wntinued on the day of surgery. These can be taken orally with sips of water. Some medications, including insulin, prednisone, coumadin, and bronchodilators, require adjustment of dosage and/or alternate routes of administration. Oral hypoglycemics and antidepressants should not be taken on the day of surgery. It is no longer mandatory to discontinue MA0 inhibitors two weeks preoperatively

Must Know

IV: PLANNING TEE ANAESTHETIC* *

Having identified and evaluated our patient's problems we now ask ourselves five questions.

I., Is the patient's optimal? 2.

condition

Are there any problems whlch requlre consultation o r speclal tests?

(For example: In a patient with poorly controlled angina, a cardiology consult would be appropriate. You may write: Consult medicine cardiology. 'Please assess and advise re: optimal perioperative medical management of angina in this patient').

Is there an alternative procedure which may be more approprlate?

This is especially important to consider in the high risk patient. For example: the placement of a suprapubic catheter may be more appropriate than a transurethral prostatectomy (T'URP) in a terminal cancer patient with a recent stroke, congestive heart failure, and obstructive uropathy. Discuss the available options with the staff anaesthetist and the surgeon.

What are the plans for postoperative management of the pa tlent?

Options include: Monitoring in the post-anaesthesia care unit (PACU) for an initial period of observation, then either return to ward or discharge home Should Know

Page 21

Anaesthesia for Medical Students

(e.g., daycare patients). Patients with significant underlying diseases or having major procedures may remain in a critical care setting overnight for closer observation (eg. PACU, ICU, CCU). Consideration should be given to which form of pain management is most appropriate for the patient post. operatively.

What premedication if any is appropriate?

Finally, we plan our anaesthetic technique (see chapter 2: Anaesthesia Overview). This may be: 1. Local anesthesia with 'standby' monitoring with or without sedation. 2. Regional anesthesia with or without intraoperative sedation. 3. General anesthesia with or without intubation. If an intubation is required the anaesthetist may elect to control the patient's ventilation, or allow them to breath spontaneously. If controlled ventilation is used, the anaesthetist may or may not use muscle relaxants. 4. Combined regional anaesthesia with general anaesthesia. Discuss with your staff anaesthetist when and why we would choose each of these techniques. For discussion, let us work through a patient case. We recently gave an anaesthetic to a 50-year-old male for an elective repair of his inguinal hernia. He admitted to smoking one package of cigarettes per day, and has done so for the last 35 years. He has had hyper-

tension for the last six years, and was also found to have NIDDM at the time his hypertension was diagnosed. Our patient's problem list includes: 1. Elective lower abdominal surgery. 2. Controlled hypertension. 3. NIDDM. 4. Smoking history 35 pack years. 5. Identified risk factors for CAD. The anaesthetic history should include: 1. A brief history of present illness. E.g., "Discomfort in groin for 6 months." 2. Current medications (including ASA, alcohol, and illicit drugs if appropriate). Eg., "Enalapril 10 mg and glyburide 10 mg daily." 3. Allergies and type of reaction. E.g., "Penicillin: hives." 4. Significant past medical surgical history. E.g., "Appendectomy". 5. Past anaesthetic history. E.g., "No known problems." 6 . Family history of any anaesthetic problems. E.g., "No known problems." (see chapter 24). 7 . Functional inquiry appropriate to the patient, and concentrating on the cardiorespiratory systems. E.g., "Inactive lifestyle, no symptoms of chest pain or coronary ischemia!' (See also 9 below re: additional appropriate questions. 8. NPO status. E.g., "Nothing to eat or drink since last night." 9. Specific questions directed at the identified problem list, attempting to assess the severity of the problem, its associated disability, and the patient's remaining physiological reserve.

Chapter

Problem: 35 pack year smoker. Do you have a cough on most mornings or a "smoker's cough"? (i.e. Chronic bronchitis). Do you ever wheeze? Have you ever required medications for your breathing? Does your breathing limit your physical activity? What kind of activity would make you short of breath? (A fast walk? One flight of stairs? Two blocks? etc.).

3 Preoperative Assessment

Appropriate questions concerning his cardiovascular risk factors would include: Have you ever had a heart attack? Do you ever get chest pains, or leg cramps with exertion? (Angina, claudication). How often? What relieves them? What are they like? Do you ever wake up at night short of breath? (PND). Are you able to sleep with the head of the bed flat? (Orthopnea)

Problem: Hypertension. When were you first aware that you had high blood pressure? How often is your blood pressure checked? Has it been well controlled with your medications? What is your usual blood pressure when you see your family doctor?

Additional appropriate questions for this patient would include questions regarding gastroesophageal reflux. Do you ever experience acid reflux from your stomach? How often? Next, a physical examination as described previously should be performed. Appropriate laboratory tests for this patient would include a CBC, electrolytes, glucose, and electrocardiogram.

Problem: NIDDM How long have you been aware of your diabetes? How has it affected you? (end organs involved include: eyes, heart, kidneys, peripheral circulation, autonomic and peripheral nerves). How do you monitor your blood sugar? Have you ever had to come to the emergency because of your diabetes? Identified risk factors for CAD include hypertension, smoking history, male gender, age and diabetes.

Must Know

After discussion with the patient and surgeon, a spinal anaesthetic was chosen for this patient. While a general anaesthetic would also be an option, we chose a spinal anaesthetic because we would be able to avoid intubation and its associated sympathetic stimulation (increased heart rate and blood pressure), as well as its potential to trigger airway reflexes resulting in bronchospasm.

Should Know

Anaeslhesia for Medical Students

References: Wamer MA, Offord KP, Wamer ME et al. Role of preoperative cessation of smoking and other factors in postoperative pulmonary complications: a blinded prospective study of coronary artery bypass patients. Mayo Clin Proc 64:609, 1989 Pierce AC, Jones RM: Smoking and anesthesia: preoperative abstinence and perioperative mortality. Anesthesiology 6 1576, 1984 Mallampati SR, Gatt SP, Gugino LD,et al: A clinical sign to predict difficult tracheal intubation: A prospective study. Can J Anaesth 32429, 1985. Samsoon GLT, Young JRB: Difficult tracheal intubation: A retrospective study. Anaesthesia 42487, 1987. Cooper JB, Newbower RS, Kitz RJ: An analysis of major errors and equipment failures in anaesthesia management: Considerations for prevention and detection. Anesthesiology 60:34, 1984. Tumbull KW, Fancourt-Smith PF, Banting GC: Death within 48 hours of Anaesthesia at the Vancouver General Hospital. Can Anaesth Soc J 27:159, 1980. Hovi-Viander M: Death associated with anaesthesia in Finland. Br J Anaesth 52:483, 1980. Lunn JN,Mushin WW: Mortality associated with anaesthesia. Nuffield Provincial Hospitals Trust, London. 1982. Keenan RL, Boyan CP. Cardiac arrest due to anesthesia: A study

of incidence and causes. JAMA 253:2372, 1985. Tiret L, Desmonts JM, Hatton F, et al: Complications associated with anaesthesia a prospective study in France. Can J Anaesth 33:336, 1986. Holland R. Anaesthetic mortality in New South Wales. Br J Anaesth 59:834, 1987. Buck N, Devlin HB, Lunn JL: Report on the confidential enquiry into perioperative deaths. The Nuffield Provincial Hospitals Trust, London. The King's Fund Publishing House, London. 1987. Dripps RD, Lamont A, Eckenoff JE: The role of anaesthesia in surgical mortality. JAMA 178:261, 1961. Vancanti CJ, VanHouten RJ, Hill RC: A statistical analysis of the relationship of physical status to postoperative mortality in 68,388 cases. Anesth Analg 49564,1970. Marx GF, Mateo CV, Orkin LR: Computer analysis of post anaesthetic deaths. Anesthesiology 3954, 1973. Cohen MM, Duncan PG, Pope WDB, et al: A survey of 112,000 anaesthetics at one teaching hospital (1975-83). Can J Anaesth 33:22, 1986. Forrest JB, et al: Multicenter study of general anesthesia. 11. Results. Anesthesiology 72262, 1990. Goldman L, Caldera DL, Nussbaum SR, et al: Multi-factoria1 index of cardiac risk in non cardiac surgical procedures. N 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. J A M 264:2919,1990. Notes:

Must Know

Should Know

Page 25

)

Anaesthesia for Medical Students

)

Notes:

Page 26

i Prernedication Most patients scheduled for surgery will experience some degree of apprehension. The psychological stress a patient experiences prior to surgery can be more detrimental than the actual physical insult of the surgical procedure. Preoperative anxiety may be caused by many factors. Some of the more common causes include*: 1. The fear of relinquishing control to someone else while under general anaesthesia. 2. The fear of dying during the operation. 3. The fear of experiencing pain postoperatively. 4. The inability to preserve their modesty and dignity during the operation. 5. The fear of separation from family, and loved ones. 6. The fear of discovering a serious problem such as cancer. 7. The fear of surgical mutilation and an altered body image.

It is important that time is taken to answer each patient's questions. If you are unable to answer their questions honestly, then reassure them that their questions are important to you and that, while you may not know the answer, you will speak to the attending staff physician and provide them with an answer. Perhaps the most important

Must K n o w

part of our preoperative visit is to convey a reassuring, honest and caring attitude. The patient's desire for sedation prior to a planned surgical procedure is the most common reason for prescribing a preoperative medication. We also prescribe medications preoperatively to avoid potential complications associated with the procedure (eg., antibiotics to prevent the development of endocarditis in a patient with valvular heart disease), or to continue the patient's current medications for coexisting medical conditions. Reasons* for prescribing a preoperative medication include:

I. Patient-related reasons: 1. Sedation 2. Amnesia 3. Analgesia 4. Antisialogogue effect (to dry oral secretions) 5. Medications to decrease gastric acidity and gastric volume. 6. To facilitate induction of anaesthesia. 11. Procedure-related reasons:

1. Antibiotic prophylaxis to prevent infective endocarditis in susceptible patients.

Should K n o w

Page 27

Anaesthesia for Medical Students

2. Gastric prophylaxis (to minimize the

risk of gastric aspiration during anaesthesia). 3. Corticosteroid coverage in patients who are immunosuppressed (see chapter 3). 4. To avoid undesired reflexes arising during a procedure (e.g., vagal reflex during eye surgery). 5. Anticholinergic agents to decrease oral secretions and facilitate a planned awake intubation with a fiberoptic bronchoscope. 111. Coexisting Diseases:

1. To continue the patient's own medications for coexisting diseases. (e.g., beta blockers, antihypertensive medications, nitrates, antiparkinsonian medications etc.) 2. To optimize the patients status prior to the procedure. (e.g., bronchodilators, nitroglycerine, beta blockers, antibiotics etc.) Patients with significant coexisting diseases should be given a reduced amount of preoperativesedative medication. The obese patient does not necessarily require more preoperative medication. It is safer to underestimate the required amount of preoperative medication. Additional medications can be given intravenously as needed when the patient arrives in the operating room. Patients older than 65 years of age should have a reduced drug dosage. Caution should be exercised in prescribing sedatives to patients 75 years of age or older, as they may experience excessive depressant effects from these medications.

Benzodiazepines are the most frequently used class of drugs to achieve sedation, relief of anxiety, and amnesia preoperatively. Diazepam (5 to 15 mg pa.) may be given with sips of water 1% to 2 hours preoperatively. Lorazepam (1to 3 mg) may be given either by the sublingual or oral route. Lorazepam provides excellent amnesia and sedation, but occasionally, patients remain excessively drowsy after the surgery. Alternatively, lorazepam can be reserved for the very anxious patient who is scheduled for afternoon surgery. The rationale of an early morning premedication with lorazepam is to allow the patient to remain calm and relaxed throughout the morning without prolonging the postoperative recovery time. Midazolam (0.07 mglkg im., approximately 5 mg in a young healthy 70 kg adult) provides excellent amnesia, sedation, and anxiolysis when given 112 hour preoperatively. Midazolam (as a premedication) is not available at all hospitals. The discomfort of an intramuscular injection and midazolam's associated higher costs have generally made it the third choice of the benzodiazepine class. Opioids such as morphine and meperidine provide both sedation and analgesia. They are appropriate for patients experiencing pain prior to their surgery, (e.g., fractured extremity awaiting surgery). Morphine has a better sedative effect than meperidine. Troublesome side effects of intramuscular (im.) opioids may occur. These include nausea, vomiting, respiratory depression, bradycardia, hypotension, and true allergic reactions. In addition,

Chapter

I )

Table

4.1:

4 Premedicalion

Premedlcatlon

Drug I Dose I Route

Class

Comments

Diazepam* (Valium) 5 15 m g p o .

Benzodiazepine

1% to 2 hours preop. with sips of water. Sedation, amnesia, and anxiolysis. Anticonvulsant (regional anaesthesia). Respiratory depression with high doses.

Lorazepam* (Ativan) 1 - 3 m g p o . or 6.1.

Benzodiazepine

Good amnestic and sedative. Best given early for late case. Occasionally excessive postoperative sedation.

Midazolam (Versed)

Benzodiazepine

112 to 1 hour preop. Excellent arnnestic, sedative, and anxiolytic. Not available in all hospitals.

Morphine* 5 15 mg im.

Opioid

1 hour preop. Occasional side 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 as morphine. Perhaps more nausea, and less biliary spasm.

Atropine* 0.4 0.6 mg im.

Anticholinergic

1 hour preop. Fair drying agent, often significant tachycardia (HR > 100). Avoid in patients with CAD.

Hyoscine (Scopolamine)

Anticholinergic

1hour preop. Excellent drying agent, confusion in elderly, occas. delirium in young. Good amnestic and antiemetic.

GIycopyrrolate (Robinal) 0.2 - 0.4 mg im.

Anticholinergic

Good drying agent for oral secretions, less tachycardia than atropine, no confusion.

Promethazine (Phenergan) 12.5 - 50 mg im.

Antihistamine

1 hour preop. Good sedative and

0.07 mg/kg im.

(appmx. 5 md70 kg)

50 100 mg im.

0.2 0.4 mg im.

antiemetic. Occasional postoperative delirium.

Must Know

Should Know

Page 29

Anacs~hesiafor Medical Students

morphine, and to a lesser extent all other opioids, may cause biliary spasm. Opioids should be used with caution in patients with known cholelithiasis. Drugs with both antiemetic and sedative qualities, are often used in combination with an opioid to avoid nausea and to enhance the sedative effects of the opioid. Promethazine is one such drug (antihistamine - phenothiazine class), and is given in a dose of 125 to 50 mg im. together with the opioid. Dimenhydrinate ( ~ r a v o l 9also possesses sedative and antiemetic qualities. It is given in a dose of 12.5 to SO mg im. with the opioid (e.g., 'Demerol 75 mg with gravol 50 mg ism. in one syringe one hour preoperatively 9. Anticholinergics may be given with morphine or meperidine to avoid the potential opioid-induced bradycardia. An anticholinergic agent may also be used if an awake fiberoptic intubation is planned. The use of an anticholinergic in these patients causes decreased secretions from oral salivary glands, thereby facilitating both absorption of topical anaesthetics and visualization of the 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

does not cross the blood brain barrier and causes less tachycardia than atropine. Other special premeditations include: oxygen, antibiotics, steroids, antihistamines, H-2 blockers, beta blockers, calcium channel blockers, nitroglycerine, bronchodilators, antacids, desmopressin, insulin, etc. Ask your staff anaesthesiologist when and why they would prescribe these medications. General contraindications* to the use of a prernedication include:

1. Allergy or hypersensitivity to the drug. 2. Upper airway compromise, or respiratory failure. 3. Hemodynamic instability or shock. 4. Decreased level of consciousness or increased intracranial pressure. 5. Severe liver, renal, or thyroid disease. 6. Obstetrical patients. 7. Elderly or debilitated patients. Notes:

Getting Started (A Practical Approach to the OR) Medical students, beginning their rotation in anaesthesia, will undoubtedly feel unsure of their role and what they ought to do to assist the anaesthesiologist. As anaesthesiologists we observe many operations, however, we recognize that passively watching a procedure does not give us the understanding or skills required to perform it. Accordingly, the more active a role you take in the anaesthetic management of the patient, the more you will get out of the rotation, in terms of understanding, sense of accomplishment, and development of technical skills. Naturally, you should not attempt to perform tasks for which you have little knowledge or supervision. Of all the specialties, anaesthesia is one of the few which can offer intensive one-on-one teaching, and you should try to take as much advantage of this as possible. What can I do when the patient arrives to the operating room? Every patient undergoing general, regional, or monitored anaesthesia care requires*:

1. A safe transfer from their bed to the operating room table. 2. An anaesthetic record removed from the chart and placed on the anaesthesia clipboard. Check to

Must Know

make sure that any information that was missing (eg. Hb, ECG, etc.) at the time of the preoperative visit is now available and on the anaesthetic record. 3. Monitors attached including an ECG, blood pressure cuff, and pulse oximeter to start with. (See chapter 10: Monitoring in Anaesthesia). 4. Establish an intravenous. Prepare your intravenous equipment before the patient arrives. 5. Record the patients initial vital signs on the anaesthesia record. The above tasks will occupy the first 5 to 10 minutes of your time following the patients arrival in the OR. A preanaesthetic check list can be used to ensure that YOU are ready when the patient arrives to the operating room. There are many ways anaesthetists ensure that everything is checked and ready to proceed safely with anaesthesia. Whatever system that is used, it should be simple yet comprehensive, and one that will be followed wnsistently. One such method can be recalled by using the abbreviation 'SAM'. If you check with SAM before you give an anaesthetic, things should proceed smoothly. What does SAM stand for? Should Know

Page 31

Anaeslhesia for Medical Sluden/s

SAM* (really SAMMM') stands for:

B. Anaesthesla Machlne:

S Suctlon checked and functioning. A Airway equipment checked and prepared. (This includes checking that you have a functioning and backup laryngoscope, an appropriate sized endotracheal tube and stylet, oropharyngeal airways, as well as an oxygen source and manual resuscitation bag). M Machine checked. (see anaesthesia machine checkout procedure and make sure you know how to check your machine. You can go to the operating room before or after scheduled procedures to explore the machine. Ask your staff anaesthetist to go through this procedure with you). M Monltors available and functioning. M Medications prepared and labelled. You should know where the emergency drugs are kept and location of the difficult intubation cart.

1. Oxygen and nitrous oxide pipeline pressures should be at 40-60 psi. 2. Check that an adequate amount of oxygen is present in the reserve cylinder on the back of the machine. By turning the cylinder on, the pressure can be read from the pressure gauge on the front of the machine. An oxygen reserve cylinder (E tank) has a full pressure of 2200 psi. The amount in the oxygen tank varies directly with its pressure. Hence, a reading of 1100 psi indicates the tank is half full. A full E tank contains approximately 660 liters of oxygen. 3. Turn the reserve cylinder on the back of the machine off after checking it, to prevent a possible leak from draining the oxygen from the tank. 4. Test that the flowmeters for 0 2 and N20 are functioning by increasing and decreasing the oxygen and nitrous oxide flows. Ensure that the flowmeter bobbins move freely and do not stick. Turn the nitrous oxide off. 5. The vaporizer should be filled, turned off, and the filling port closed. 6. The oxygen bypass flush valve should release a flush of oxygen when it is activated by pressing the flush button on the front left-hand side of the machine. 7. The oxygen fail-safe device should be functioning, and will produce a shrill Ritchie whistle if the oxygen pipeline is temporarily disconnected from the wall or ceiling source.

You will notice that the last thing that SAM has you do is check your medications. If you follow this routine, in this order, you will never put a patient to sleep and then discover, for instance, that their ECG is abnormal, or that a laryngoscope is unavailable. Anaesthesla Machine Checkout Procedure (Modified from CAS 1989; 36, 6 suppl. 82-7.) A. Gas Plpeilnes: Secure connections between terminal units (medical gas outlet) and machine.

Chapter

8. Check for the oxygen analyzer

which will be located on the respiratory gas monitor or mounted on the machine as a separate unit. It should be turned on and calibrated, if this has not been done recently. 9. The 0 2 and N20 proportioning device prevents the delivery of less than 30% oxygen, and greater than 70% N20, and can be tested by varying the 0 2 and N20 flows through the flowmeter. 10. The common fresh gas outlet located on the front left-hand side of the machine releases anaesthetic gases from the flowmeters, vaporizer and flush valve. C. Breathing Clrcult: 1. The two most common anaesthesia circuits used for adult anaesthesia are the circle circuit and the Bain circuit. An anaesthesia circuit functions to take the anaesthetic gases from the machine to and from the patient. The circle circuit contains a soda lime canister to absorb the exhaled carbon dioxide, an inspiratory and expiratory valve to direct the flow of gases, and light weight corrugated tubing to transport the gases. A sample port near the patient end of the circuit is used for analysis of the respiratory gases. These include inspired and expired oxygen, carbon dioxide, nitrous oxide and volatile anaesthetic gas tensions. 2. Connect the anaesthesia circuit to common fresh gas outlet. 3. Turn the oxygen flowmeter on. 4. Check for fresh gas exiting at the face mask.

Must Know

5 Getting Started

5. Pressurize the circuit and check for leaks. (Fill the circuit with fresh gas, occluding the outlet while pressurizing the circuit to 30 cm H20. The circuit should maintain a pressure of 30 cm H20 with a fresh-gas. inflow of less than one liter per minute). 6. Ensure the high pressure relief valve is functioning. (The circuit should develop a leak when the pressure is sustained above 75 cm H20. By occluding the end of the circuit and squeezing the reservoir bag, a pressure of greater than 75 cm H 2 0 can be created. When this is done, the high pressure release valve will open preventing any further increase in pressure in the circuit). 7. Unidirectional valves are functioning. (Watch the valves open and close smoothly as you take a test breath through the mask and anaesthetic circuit) 8. Check that the soda lime is fresh and that the canister is full, D. Vacuum system: Suction is connected and working.

E. Scavenging System: Correctly connected to patient circuit.

F. Ventllator functioning. (Test the ventilator using the 2 Litre reservoir bag as a set of test lungs. Once the system has been filled with fresh gas, turn the ventilator on. With the fresh gas flows at < 1 Umin, the bellows should continue to refill as the ventilator cyles. The maximal accepted leak is 1 Umin). Should Know

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Anaesthesia for Medical Students

" SAMMM"

Preanaesthetlc Check Llst

Suction

Tonsillar tip connected to suction tubing and suction functioning.

Airway's

Laryngoscope, blades, Em,syringe, stylet, oral and nasal airways, tape, mask and manual resuscitation bag.

Machine

Wall-source DHSS medical gas pipelines connected, 4 N20 & 0 2 cylinder and pipeline pressures OK, Machine tumed on, flowmeters functioning, 0 2 flush functioning, N20 and 0 2 proportioning device functioning, Oxygen pipeline disconnect (Ritchie) whistle functioning.

- Vaporizer - Circuit - Ventilator Monitors

Full and turned off.

Assembled, valves functioning, and circuit leak less than 1L / min at 30 cm H20 pressure.

Disconnect alarm functioning, and test ventilation leak of less than 1 L / min.

Capnograph connected to circuit and functioning.

ECG,BP cuff, oximeter, peripheral nerve stimulator, and temperature probe monitors available and working. Meds

Intravenous fluids and equipment for starting i.v. 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 airways* preoperatively is to attempt to identify potential problems with maintaining, protecting, and providing a patent airway during anaesthesia. The assessment is performed with the aid of a physical examination and a review of the patients history and anaesthetic records. The '1-2-3' test** is used to assess several factors that may affect decisions concerning the patient's airway management. The first component of the test is used to identify any restricted mobility of the temporomandibular joint (TMJ). Ask the patient to sit up with their head in the neutral position and open their mouth as wide as possible. Note the mobility of the mandibular condyle at the TM joint. The condyle should

Fig.6.1:

1 = TMJ mobillty. ++

Must Know

rotate forward freely such that the space created between the tragus of the ear and the mandibular condyle is approximately one fingerbreadth in width. The opening aperture of the patient's mouth should admit at least 2 fingers between their teeth. Note any loose, capped, or missing teeth as well as any bridge work on the teeth. If the opening is less than 2 fingerbreadths, it will be difficult to insert the laryngoscope blade, let alone visualize the larynx. With the patient's tongue maximally protruded, the structures visualized should include: the pharyngeal arches, uvula, soft palate, hard palate, tonsillar beds, and posterior pharyngeal wall. Technical difficulties with intubation should be anticipated when only the

Fig. 6.2: 2 +

Should Know

= Mouth opening. Page 35

Anaesthesia for Medical Students

Adults who have less than 3 fingerbreadths (or < 6 5 cm) between their mentum and thyroid notch may have either an anterior larynx or a small mandible, which will make intubation difficult.

Flg.6.3: 3 = Thyromentai distance. tongue and soft palate are visualized in a patient during this above maneuver'. The third component of this test assesses the patient's thyromental distance. 'Ihe thyromental distance is measured from the thyroid notch to the mentum (lower border of the chin).

Next, evaluate the mobility of the cervical spine. This is performed by asking the patient t o 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, which may create difficulties during attempts to intubate. This is certainly true if the atlanto-occipital joint is involved, as restriction of this joints mobility may impair one's ability to visualize the larynx. With the patient sitting upright with their head in the neutral position, mouth 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

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

tongue maximally protruded, the airway can be classified according to the stmctures visualized in the hypopharynx2 (figure 6.4, table 6.1). In those patients who have a class I hypopharyngeal view, adequate exposure of the glottis during direct laryngoscopy should be easily achieved. A s the hypopharyngeal class number increases, so does the difficulty one anticipates in performing intubation using direct laryngoscopy. We can predict that a patient with a class IV hypopharynx, a full set of teeth, a restricted thyromental distance and restricted atlanto-occipitalextension will be difficult to intubate using direct laryngoscopy. Patients who have a restricted airway may require techniques other than direct laryngoscopy to secure an airway. Choosing regional or local anaesthesia, rather than general anaesthesia, is one way to avoid the need for intubation. Other airway management options include "awake" intubation with topical anaesthesia and intravenous

** I

Must Know

conscious sedation, or the use of a laryngeal mask rather than an endotracheal tube. Finally one should try to ascertain whether there could be any difficulty with the lower airway (glottis, larynx, and trachea). This is particularly important in patients who have had a previous airway injury, or surgery on their airway such as a tracheostomy. Observe the patient for hoarseness, stridor, or a previous tracheostomy scar suggesting a potential underlying tracheal stenosis. Figure 6 5 illustrates the visualization of the laryngeal structures at the time of laryngoscopy. Just as the visualization of the hypopharyngeal structures has been classified, the extent to which laryngeal structures may be visualized has also been graded from I t o IV. While there is not a perfect correlation between the hypopharyngeal class and Should Know

P a g e 37

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. Anesthesia 39:1105 11,1984.

the laryngeal grade, we anticipate that a patient with a class one hypopharyngeal view and no other identified airway abnormalities will have a grade I laryngeal view. Similarly a class IV hypopharyngeal view is a predictor of difficulty visualizing laryngeal anatomy. The technique of tracheal intubation involves five steps* *. Positioning the patient. Opening the patients mouth. Performing laryngoscopy. Insertion of the ElT through the vocal cords and removing the laryngoscope. V. Confirmation of correct placement, and securing the E?T tube. I. 11. 111. IV.

I. Posltlonlng the patlent When preparing to intubate a patient, their head and neck should be positioned using a combination of both cervical flexion and atlanto-occipital

(AO) extension. We describe this as the sniffing position. This enables one to align the axes of the patient's mouth, pharynx, and larynx permitting direct visualization of the larynx during laryngoscopy (figures 6.6, 6.7, 6.8). Atlanto-occipital extension alone increases the angle between the axes of the pharynx and the larynx. By con-

(

Axis

Axis of the Mouth

Figure 6.6: Poor alignment of the axes of the mouth, pharynx, and larynx in the neutral position.

Chapter 6 Intubation and Anatomy of the Airway

Figure 6.7: Alignment of the axes of the pharynx and larynx produced with cervical flexion. trast, the combination of cervical flexion of the neck with A 0 extension results in the alignment of the axes of the pharynx and larynx. Optimizing the position of the patients head and neck before attempting laryngoscopy is an important initial step

Flg. 6.9: Inadequate (suplne) posltlonlng for Intubatlon.

Must Know

Figure 6.8: Alignment of the axes of the airway with cervical flexion and A 0 extension, permitting visualization of the larynx with direct laryngoscopy. in ensuring a successful intubation (figures 6.9, 6.10). This is especially true in obese or pregnant patients, or those patients in whom you anticipate a difficult intubation. It is good practice to make sure that your first attempt at intubation is your best.

Flg. 6.10: Optlmlzed posltlonlng for lntubatlon wlth cervlcal flexlon. Should Know

Page 39

Anaesfhesia for Medical Shtdenfs

Fig. 8.11: Scissors technlque. Repeat attempts at intubation should be avoided unless there is something that can be done differently to improve one's chance of success. Persistent repeat attempts at intubation traumatize the patients airway, interrupt and delay both oxygenation and ventilation, and place the patient at risk of significant morbidity and mortality. If you are having difficulty, retreat, regroup, and resume manual mask ventilation and oxygenation. Call for help and allow the patient to recover from any sedative relaxant medications that have been given. No more than three attempts should be made at intubation. Discuss with your staff anaesthetist what other options are available for patients whom you anticipate will be difficult to intubate, or the patient in whom attempts at intubation have failed.

Flg. 6.12: Modlfled sclssors technique. 11. Opening the patlent's mouth The next step in performing intubation is to open the mouth. Take the laryngoscope in your left hand as you stand directly behind the patient's head. The right hand is used to open the patient's mouth and, later, to advance the Em. Mouth opening can be accomplished by using the right hand to open the patients teeth (e.g., the scissors technique, as illustrated in figures 6.11 and 6.12), or by placing the operators right hand on the patient's occiput to rotate the occiput backward and create A 0 extension (see figures 6.13 and 6.14). Using the scissors maneuver the index finger pulls the upper right incisors towards the operator, and serves to open the mouth, extend the atlanto-occipital (AO) joint, and protect the teeth and lips. At the same time, the thumb depresses the lower mandible, further opening the mouth. One can modify this technique by opening the patient's

Chapter

6 Infubafionand Anatomy of the Airway

)

) )

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 depress the lower teeth (figure 6.12). If the clinician chooses the extraoral technique of mouth opening, their right hand is placed on the patient's occiput and the patient's head is rotated into the sniffing position. With this movement, the mandible drops and the mouth opens. This method of mouth opening is more suitable for the edentulous patient than the scissors technique. 111: Laryngoscopy The third step involves insertion of the laryngoscope into the mouth (figure 6.15). The tip of the laryngoscope blade is advanced to the base of the tongue -by rotating its tip around the tongue (figure 6.17). The laryngoscope blade should follow the natural curve of the oropharynx and tongue. The blade should be inserted to the right of the tongue's midline, so that the tongue moves toward the left and out of the line of vision. Avoid pushing the

tongue into the back of the oropharynx, as this will also obscure your vision. Once the tip of the blade lies at the base of the tongue (just above the epiglottis), apply firm, steady upward and forward traction to the laryngoscope. The direction of force should be at 45' from the horizontal. Once the laryngoscope is properly positioned at the base of the tongue, avoid rotating it, as this action might exert pressure on the upper teeth and damage them. Damage to the immobile upper maxillary teeth is more common than to the lower mandibular teeth, which are free to move forward with the jaw during laryngoscopy. Figures 6.15 and 6.17 illustrate how the larynx is more visible if the blade of the laryngoscope moves the tongue to the left of the mouth and out of the line of vision. Students learning the technique of laryngoscopy have a common tendency to adopt a stooped posture, which posi-

GlossoEplglottlc 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 patient's. This posture limits the power that can be used by the arms, making laryngoscopy technically more difficult to perform. Try to maintain a good posture during laryngoscopy. This allows the arms to exert traction on the laryngoscope, rather than attempting to lift the laryngoscope with the wrists. The larynx is located at the level of the 4& to 6& cewical vertebrae in adults. It consists of numerous muscles, cartilages and ligaments. The large thyroid cartilage shields the larynx and articulates inferiorly with the cricoid cartilage. 'lbo pyramidal shaped arytenoid cartilages sit on the upper lateral borders of the cricoid cartilage. The aryepiglottic fold is a mucosal fold ruming from the epiglottis posteriorly to the arytenoid cartilages. The cuneiform cartilages appear as small flakes within the margin of the aryepiglottic folds (fig. 6.16). The adult epiglottis resembles the shape of a leaf, and functions like a trap door for the glottis. In figure 6.16, the trap door' is shown in both its open and closed positions. The epiglottis is attached to the back of the thyroid cartilage by the thyroepiglottic ligament and to the base of the tongue by the glossoepiglottic ligament. The covering membrane is termed the glossoepiglottic fold, and the valleys on either side of this fold are called valleculae. The valleculae are a common site for the impaction of sharp swallowed objects, such as fish bones. When performing laryngoscopy, one should advance the tip of the curved laryngoscope's blade to the base of the tongue at it's union with

Must Know

the epiglottis. Try to visualize this anatomy as well as possible when you perform laryngoscopy. IV: Insertlon of the ETT Intubation is performed with the iefC hand controlling the laryngoscope blade, while the right hand opens the mouth and then passes the ElT tip through the laryngeal inlet. When a limited laryngeal view is encountered (grade 111 IV larynx), the epiglottis can be used as a landmark for guiding the E?T through the hidden vocal cords. The tip of the E'LT is passed underneath the epiglottis and anterior to the esophageal inlet. Recall that the glottis lies anterior to the esophagus (or above the esophagus during laryngoscopy). When the epiglottis partially obscures the view of the glottis, an assistant may be used to apply cricoid pressure. This maneuver moves the larynx posteriorly and helps to bring the vocal cords into view. A malleable stylet, shaped so that it forms a distal anterior J curve, can also be helpful in guiding the E?T tip through the laryngeal inlet. When you have had a limited view of the E m passing through the vocal cords, the Ford Maneuver can help you to visually confirm its correct placement in the glottis. One performs this maneuver by displacing the glottis posteriorly using downward pressure on the ETT prior to withdrawing the laryngoscope. This maneuver is useful in the patient with a grade 111 or IV larynx for whom difficulty was encountered visualizing the glottic structures.

The cuff of the ETT should be observed passing through the vocal cords and

Should Know

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Anaesthesia for Medical Sludenb

a. Introduction of the larygoscope blade using left wrist rotation.

c. The tip of larygoscope blade is

properly positioned at the base of tongue. The blade is lifted forward

e. Laryngeal blade inserted to the left of midline, with tongue obscuring visualization of the larynx.

b. The tongue obscun the laryngeal view due to inadequate advancement of the larygoscope blade .

. d. Laryngeal blade inserted too deep, .

pushing epiglottis over laryngeal inlet.

f. Laryngoscope blade inserted too far, with visualization of the esophageal inlet.

Figure 6.17: Laryngoscopy. Adapted with permission from Lui PL. inciples and Procedures in Anesthesiology. J.B. Lippincott Co. 1992 Page 44

Chapter

should lie just inferior (2 to 3 cm) to the cords. As soon as you withdraw the laryngoscope blade from the mouth, note the length of the ETT at the lips using the centimetre markers on the ElT. This may prove to be useful if the endotracheal tube moves from its original position. The usual distance from the tip of the ETT to the mouth is approximately 21 to 24 cm in adult males, and 18 to 22 cm in adult females. The usual distance for a nasally intubated adult male (from the tip of the E n to the naris) is 25 cm. The E l T cuff is inflated with enough air to create a seal around the ETT during positive pressure ventilation. A cuff leak may be detected by listening at the patient's mouth, or over their larynx. Confirmation of correct ETT placement. Immediate absolute proof that the E l T is in the tracheal lumen may be obtained by observing the ETT passing through the vocal cords, observing carbon dioxide (ETCOJ returning with each respiration, or by visualizing the tracheal lumen through the ETT using a fiberoptic scope. Indirect confirmation that the trachea is intubated with a tracheal tube includes: listening over the epigastrium for the absence of breath sounds with ventilation, observing the chest to rise and fall with positive pressure ventilation, and listening to the apex of each lung field for breath sounds with ventilation. There are, however, numerous reports of physicians auscultating "distant breath sounds" in each lung field, when the ETT was, in fact, incorrectly placed in the esophagus. Hence, listening to the V:

Must Know

6 Intubation and Anatomy of the Airway

lung fields may reveal bronchospasm or evidence of an endobronchial intubation, but cannot be relied on as absolute proof that the tube is correctly positioned in the trachea. If the tube is positioned in the tracheal lumen and the patient is breathing spontaneously, the reservoir bag will fill and empty with respiration. If the patient is awake they will not be able to vocalize with an ETT positioned in the tracheal CXR the tip of the lumen. On an 'A-P' E'IT should be located between the midpoint of the thoracic inlet and the carina. Decreased air entry to one lung field may indicate that the E l T is in a mainstem bronchus (usually the right mainstem bronchus). In this situation, the patient may become increasingly hypoxic, or continue to cough. You may suspect an endobronchialintubation when you observe one side of the chest moving more than the other with ventilation. In this situation, the airway pressures will be higher than normal (greater than 25 cm H20), and an abnormally distant tube position at the patient's lips will be noted. "IF IN DOUBT TAKE IT OUT:"** This is prudent advice for anyone who has just intubated a patient and is unsure and unable to confirm the tube's placement. It is better to be safe by removing the ElT, resuming mask ventilation with 100%oxygen, stabilizing the patient, and calling for help, than to risk hypoxic injury and gastric aspiration.

Should Know

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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. Upper elrwey obstruction**: The most common cause of an upper airway obstruction in an unconscious supine patient is from the tongue falling back into the hypopharynx (figures 6.18 and 6.19). In the unconscious state there is a decrease in the tone of muscles attaching the tongue to the mandible, hyoid bone and epiglottis. The respiratory efforts of the unconscious patient tend to pull the tongue backward causing further airway obstruction. Finally in the unconscious patient the epiglottis tends to fall downward, also increasing upper airway obstruction.

Figure 6.19: 0topharGgeal airway restoring airway patency. Excluding intubation, simple maneuvers** to overcome upper airway obstruction in the unconscious supine patient, include: 1. Clearing the airway of any foreign material. 2. Using a chin lift maneuver. 3. Using a jaw thrust maneuver. 4 Inserting an oral andlor nasal airway. 5. Positioning the patient on their side in the semi-prone recovery position.

)

1 )

1 i

, ,

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.

Figure 6.18: Obstructed airway in the unconscious supine patient.

Page 46

Samsoon GLT, Young JRB: Difficult tracheal intubation: A retrospective study. Anaesthesia 42:487,1987.

Intubation Decisions In chapter 6, we reviewed the technical skills required for tracheal intubation in adults. In this chapter we present four clinical cases as an illustration of the process used when deciding to intubate. A clinician will readily recognize that the comatose patient with a severe head injury will need tracheal intubation for airway protection, maintenance, and hyperventilation. However, the need to intubate a dyspneic patient with chronic obstructive lung disease and a recent respiratory infection is not so readily apparent. Tables 7.1 and 7.2 list common criteria anaesthesiologists use to evaluate a patient's need for intubation. The individual criteria are not absolute indications. They are to be used together, in the context of the patient's clinical presentation, in formulating a decision concerning the patients need for intubation. Case Studies on intubation decisions: Case 1: On the first day of your rotation, you are scheduled to assist with anaesthesia in the general surgical room. The first patient is a moderately obese forty year old female who is scheduled for an open cholecystectomy. What kind of anaesthesia should we provide for this patient? You ponder whether you

Musf Know

should prepare equipment and medications for tracheal intubation. Most open cholecystectomies today are performed under general anaesthesia with tracheal intubation. While it may be possible to provide regional anaesthesia (e.g., epidural anaesthesia) for this procedure most anaesthetists today will opt to provide general anaesthesia. The rationale for this decision includes: 1. A high abdominal incision with the need for muscle relaxation. 2. Surgical retractors which may impair spontaneous ventilation. 3. A moderately obese patient who will have difficulty breathing spontaneously when lying supine, due to the surgical retractors restricting the muscles of respiration. 4. Epidural anaesthesia used by itself would require a high level of block to provide adequate anaesthesia. This could impair the patients intercostal and abdominal muscles of respiration, resulting in respiratory insufficiency. In the early days of anaesthesia, ether or chloroform was administered through a face mask during spontaneous respiration for this procedure. Ether produced marked muscle relaxation when used with minimal doses of muscle relaxants 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

P a 0 2 < 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 depression was accepted. When the ether was discontinued the patient recovered their muscle strength and increased their ventilation to match metabolic needs. Pulse oximeten, end tidal carbon dioxide monitors, nerve stimulators,mechanical ventilators, and antagonists for

muscle relaxants were not available to the anaesthetist during these early years. Today, by contrast, we routinely plan general anaesthesia with intubation, muscle relaxation, and controlled mechanical ventilation for patients undergoing an open cholecystectomy. This allows the anaesthetist to produce pro-

)

Chapter

Table 7.2

7 Intubation Decisions

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

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.

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 procedure, protect the airway from aspiration of gastric contents, and provide good ventilation and oxygenation. The anaesthetist can also administer potent anaesthetic drugs, such as opioids and volatile anaesthetic agents (e.g., isoflurane) to minimize the stress of the surgical procedure. Accordingly, you should plan to assist by preparing the

Must Know

endotracheal tube, checking the anaesthesia machine, and preparing the anaesthetic medications. Case 2: Having recently completed your anaesthesia rotation, you are working in the emergency department, when a pale diaphoretic 50 year old man stumbles through the door and collapses in front Should Know

Page 49

Anaesthesia for Medical Students

of the receptionist. The patient is quickly placed on a bed and taken to the resuscitation room. Unable to find a pulse, the emergency physician immediately applies chest paddles, identifies a chaotic rhythm on the monitor, and defibrillates at 200, then 300 and finally 360 joules, in rapid succession. Unfortunately, the patient fails to respond. You are at the head of the bed and have initiated manual ventilation with an Ambu bag and mask. Chest compressions are initiated, while a nurse attempts, unsuccessfully, to insert an intravenous catheter. Should you proceed to intubate the patient? The emergency physician appreciates your help and asks you to proceed with tracheal intubation. After placing the E m , you confirm its position, secure it, and continue with controlled ventilation. At your suggestion, 10 mls of 1:10,000 epinephrine is injected down the E m and propelled to the lungs and central circulation with subsequent ventilation. The cardiac rhythm changes to a coarser form of ventricular fibrillation. Repeat defibrillation at 360 joules converts the man's rhythm to a sinus tachycardia with a systolic pressure of 110 mm Hg. Frequent ventricular premature beats (VPB's) are noted, and lidocaine 100 mg is given through the now secure intravenous. An infusion of lidocaine is started and arrangements are made for the patient's transfer to the CCU. The resuscitation of this patient could have proceeded with mask ventilation and chest compressions. By choosing to intubate this patient, we were able to protected the patient's lungs from the Page 50

risks of aspirating gastric contents. The E'IT also provided a route for administrating epinephrine, which played an important role in this man's resuscitation. Later, a classmate asks why you didn't give any medications to intubate the patient. You explain that patients with profound cardiovascularcollapse requiring emergent intubation, do not need any anaesthetic medications such as thiopental or succinylcholine to perform tracheal intubation. In fact the administration of thiopental could have a detrimental result by further depressing his already compromised myocardium. If your colleague asks what other medications can be given through the EIT,tell him to remember the word NAVEL'. This stands for the drugs: Naloxone, Atropine, Ventolin, Epinephrine, and Lidocaine, all of which can be given through an E'IT. Case 3:

Later, another clinical clerk asks for your opinion regarding a 68 year old man with known COPD. He is evaluating this patient in the emergency room because he is feeling more short of breath than usual. Your colleague was ready to send him home on antibiotics but hesitated after seeing his arterial blood gases (ABGs). He is concerned that this man may need to be intubated because his PaCO, is so high. On room air his ABGs were pH = 734, PaCO, = 65, PaO, = 54, HCO, = 34. How would you assess and treat this patient. The patients ABGs demonstrate hypoxemia and an acute on chronic

Chapter

respiratory acidosis with metabolic compensation. You review his old chart and note that his HCO, was 33 and his PaO, was 59 mrn Hg at the time of discharge 4 months previously. This, you suggest, probably represents his optimal blood gas values. You complete your evaluation by examining the patient noting a RR = 22 per minute, HR = 90 bpm, BP = 160185, and diffuse mild rhonchi throughout the chest with no significant (i.e. < 10 mm Hg) pulsus paradoxus. You also note that the patient is able to talk without stopping frequently to catch his breath, and that he is not vigorously using his accessory muscles of respiration. Reviewing his other lab tests you note a Hb = 170, WBC = 12,000, and an ECG which is unchanged from his former cardiogram. The CXR demonstrates hyperinflation with basal bullae, but gives no evidence of cardiac failure or pulmonary infection. The patient admits to having stopped his bronchodilators in the last week. After clinical and subjective improvement w i t h salbutamol (ventolinQ) and ipratropium bromide (atrovent@), the patient is discharged home with a prescription for his inhalers and a follow-up visit with his family practitioner. Case 4

Four weeks later you are completing your emergency rotation when the patient in the case 3 returns. You are alarmed at his ill appearance. His wife accompanies him and relates that he 'caught a cold' a week ago and has been getting progressively worse. He has been unable to eat or sleep for the last day because of his shortness of breath.

Must Know

7 Iniubation Decisions

When you examine him you find that his breathing is laboured at 28 breaths per minute with a prolonged expiratory phase and a surprisingly quiet chest. He is diaphoretic, clammy, and has difficulty catching his breath to talk. His vital signs reveal a HR of 130 bpm, BP = 1801100, with a pulsus paradoxus of 35 mm Hg, and maximal use of his accessory muscles. The emergency physician orders salbutamol with ipratropium bromide by nebulization. An intravenous is established, ABGs are drawn, ECG, oximetry, and BP monitoring is initiated, and a portable CXR is ordered. Your classmate thinks you better intubate him now. Do you agree?

ABGs and CXR return, the patient is noted to have become increasing drowsy, while little clinical improvement has occurred. The ABGs on face mask oxygen at 8Umin reveal pH = 7.10, PaO, = 66, PaCO, = 120, and a HCO, = 36. The emergency physician orally intubates the patient using topical aerosol lidocaine anaesthesia to the hypopharnyx and glottis, and initiates hyperventilation at 20lmin in order to 'blow off the carbon dioxide. The nurse reports that the patients systolic pressure is now 65 mm Hg, and his cardiac monitor is showing sinus tachycardia at 120lmin with multiple ventricular premature beats (VPB's). Your classmate reviews the CXR and states that he believes the patient has a pneumothorax on the left side. How are you going to manage the patient? As the

Before rushing to insert a needle thoracotomy and chest tube for a possible tension pneumothorax, you review Should Know

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Anaesthesia for Medical Students

the patient's status. Although he has become unresponsive to verbal stimulation, his trachea is in the midline, and you are able to manually ventilate him without excessive airway pressures. The emergency physician orders 100 mg lidocaine i.v., and asks you to take over ventilation while h e reviews the chest radiograph. A repeat CXR is ordered to verify the E l T position. A fluid bolus of 1000 mL of ringer's lactate increases the patient's blood pressure to 100 rnm Hg systolic. The VPB's remain but are now unifocal and less frequent. A mechanical ventilator is set up to provide ventilation, with an inspired 0, concentration of SO%, a tidal volume of 850 mL, an intermittent mandatory ventilatory (IMV) rate of 12, and 5 cm of positive end expiratory pressure (PEEP). Arrangements are made to transfer the patient to the ICU. Review of the initial CXR shows the previous basilar bullae, but no evidence of a pneumothorax. The second CXR shows the E l T tip to be correctly positioned in the mid trachea. Your classmate was correct about the patient requiring intubation. Clinical examination, and ABG analysis confirmed that the patient was indeed in acute respiratory failure. Analysis of the ABGs revealed a severe acute on chronic respiratory acidosis. Often we have no background information regarding the patient's usual PaCO, and HCO, levels. In patients with COPD who may retain carbon dioxide, we rely on the pH more than the CO, to guide our management (as in case 3). A primary Page 52

respiratory acidosis, with a pH of 7.20 or less, indicates that the patient is no longer able to compensate. His condition was likely precipitated by his recent chest infection superimposed on his former severe COPD. PaCO, levels of greater than 95 mm Hg become increasingly anesthetic, (MAC CO, = 245, see chapter 14 re: MAC definition). The decreased level of consciousness may be accounted for by the low blood pressure and the high arterial carbon dioxide tension. This case illustrates several common problems. The patient presented in an extreme condition, following an illness which likely resulted in significant dehydration. Upon his arrival in the emergency department, his cardiorespiratory system was being maximally stressed. Following intubation, his blood pressure fell precipitously. Patients with cardiorespiratory decompensation who require urgent intubation will often demonstrate a fall in blood pressure following intubation. This occurs irrespective of whether sedative drugs are given prior to intubation. The fall in blood pressure may be due to: 1. The sedative drugs given. 2. The removal of endogenous catecholamines by treating the condition that caused the patient to decompensate (i.e., removing the work of breathing from patient). 3. Decreasing venous return to the heart due to positive pressure ventilation. 4. All of the above, plus the unmasking of a significant underlying hypovolemia or concurrent illness (e.g., myocardial infarction).

Chapter 7 Intubation Decisions

The occurrence of multiple ventricular premature beats may reflect an irritable myocardium secondary to hypercapnia, hypotension, and hypoxemia. Another explanation for the appearance of the VPB's may be the result of an acutely induced hypokalemia. Mechanical hyperventilation may result in a precipitous drop in the PaCO, level. The sudden lowering of PaCO, will rapidly increase the patients pH and shift Kt into the cells, creating an acute extracellular hypokalemia. The differential diagnosis of this patient's acute hypotension, dysrhythmias, and abnormal CXR includes a tension pneumothorax. In this case, the emergency physician correctly interpreted the lucency on the CXR as chronic basilar bullae, and avoided the potential disastrous consequences of a needle thoracostomy and chest tube insertion in this patient (i.e., risk of a bronchopleural-cutaneous fistula).

In retrospect, this patient fulfilled several criteria for intubation (Tables 7.1 and 7.2). This emergency was best met by first supporting his ventilation. As this patient's condition is likely to require prolonged ventilatory support, this is most easily accomplished by endotracheal intubation. Typlcal Endotracheal tube slzes* Adult male 8.0, 8 5 , and 9.0 mm Adult female 7.0, 7.5, and 8.0 rnrn ETT slze calculation for children: Size (mm) = age14 + 4. The presence of a soft distal cuff on the FIT is equivalent to having a 112 size

Must Know

larger E n . Endotracheal tubes less than 6 mm do not have distal inflatable cuffs. This decreases the risk of post intubation swelling and stridor, as a result of trauma from the E n . Example: A 10 year old child would generally use a 6.0 mm cuffed E n , uncuffed tubes are generally used for patients age 8 and less. 6 yr. old child = 5 5 or 6 uncuffed ETT Term newborn = 3 5 E l T Premature infant = 2 5 3.0 E I T

P o t e n t i a l C o m p l i c a t i o n s of Intubation*: Direct injury can be caused by either the laryngoscope, or the ETT. The lips, tongue, pharynx, larynx and trachea are all susceptible to injury. Damage to the teeth may be caused by the laryngoscope, or by biting on the E I T or tonsillar suction tip. Damage to the teeth, though rare, is still the most frequent problem resulting in litigation against anaesthetists. Damaged teeth can fragment and may be aspirated by the patient. The patient who experiences a sore throat following their operation (with tracheal intubation), may obtain some relief with throat lozenges. This discomfort rarely persists for more than 24 hours. Beware of the patient who recalls a severely sore throat on previous operations. They may have a restricted airway, and their larynx may have been traumatized because they were difficult to intubate. Inserting the ETT through the larynx can injure the vocal cords or even dislocate the arytenoid cartilages. Patients with Should Know

P a g e 33

Anaesthesia for Medical Students

arthropathies, such as rheumatoid arthritis, may have an arthritic involvement of the arytenoids, creating a 'functional laryngeal stenosis'. If symptomatic, they may note hoarseness or pain on speaking. Always consider these patients to be at an increased risk for vocal cord and arytenoid injury, use a smaller E n ,and take extra care during intubation. If the E'IT is too short it may result in accidental extubation. Excessive advancement of the EIT into the trachea may result in an endobronchial intubation. Prolonged E'IT placement may lead to vocal cord granulomas or tracheal stenosis. Although a cuffed ETT will protect against gastric aspiration, they do bypass the bodies natural humidifying and warming mechanisms, and afford a potential conduit for pathogens to enter the lung. Upon inserting the ElT, a patient is subjected to a significant sympathetic stress, which may precipitate tachycardia, dysrhythmias, and myocardial ischemia. Pediatric patients have a relatively higher parasympathetic tone than adults. Hence tracheal intubation of infants and children may result in a significant bradycardia. In both adult and paediatric patients, medications are commonly given prior to intubation in an attempt to minimize these reflexes. The most serious complication of tracheal intubation is an unrecognized esophageal intubation. The resulting gastric distension with ventilation, subjects the patient to hypoxia, hypercarbia,

impairment of chest excursion, and increases the chance of regurgitation and pulmonary aspiration. Criteria for extubation*: The criteria for extubation are generally the reverse of those for intubation. The patient should not require an E'IT for airway provision, protection, maintenance or tracheobronchial toilet, and should meet criteria for adequate oxygenation, ventilation, and lung mechanics. The condition that initially required intubation should b e corrected prior to extubation. The patient should be able to protect their airway, i.e., they must be awake with a gag and cough reflex. They should be hemodynamically stable, and their RR should be greater than 8/min, and less than 35lmin. Respiratory muscles will fatigue with prolonged rates greater than 35 breaths per minute. Oxygenation should be adequate, which means a PaO, of at least 60 mm Hg on an inspired oxygen concentration of 50% or less. This should be at accompanied with evidence of adequate ventilation with a PaCO, of less than 50 mm Hg. Vital capacity should be greater than 1 5 mUkg (- 1 litre in a 70 kg patient), with a tidal volume of greater than 5 mUkg and the negative inspiratory force (NIF) should be more negative than -25 cm H,O. The vital capacity, tidal volume, and NIF can be measured at the bedside with simple spirometry equipment.

The Laryngeal Mask Airway (LMA) IV11at is the differecrtce between a LMA and a traclteal tube*? The laryl~gealmask airway is a specialized airway device made of wide bore PVC tubing, which incorporates a distal inflatable non-latex laryngeal cuff (figure 8.1). The LMA is inserted without special equipment, in the back of the patient's pharynx with the soft laryngeal cuff resting above the vocal cords at the junction of the larynx and esophagus. An endotracheal tube ( E n ) generally requires a laryl~goscopefor its il~sertionillto the trachea. Unlike a LMA, the E l T passes through the vocal cords with its tip positioned in the mid trachea.

A foreign body in the trachea, such as an endotracheal tube, evokes an inteuse reflex. This results in an increase in heart rate, blood pressure a l ~ da cough reflex. The anaesthetist routinely administers poteut anaesthetic agents such as opioids a l ~ dmuscle relaxants to blunt or abolish this reflex. The tracheal "foreign body" reflex does not result from the il~sertiol~ of a LMA because it does not enter the trachea. Therefore, the LMA can be positioned with minimal amounts of anaesthetic agents (e.g., propofol alone). Mailltellance of anaesthesia can be easily achieved by spontaneous respiration of a mixture of anaesthetic gases such as nitrous oxide and

Must KIIOW

isoflurane because the il~ternaldiameter of the L M A is relatively large compared to an ETT. Does the LMA protect the patient against gastric aspiration*? No. Should gastroesophageal reflux occur, the LMA will 1101 prevent gastric contel~tsfrom entering the trachea. (see chapter 24: Ul~usualAnaesthetic Complications: Aspiration Pneumonitis, and chapter 9: Perioperative Aspiration Risk: The Rapid Sequence Induction). Wltich patients woi~ldbe si~itablefor general annesthesia wit11 a LMA? Patients who have no identified risk factors for aspiration (see chapter 9), and who d o not require intubation and col~trolledventilation, are suitable candidates for the LMA. It may be difficult to obtain an adequate seal using a face mask in patiel~tswith no teeth or with a full beard. The LMA is particularly useful in these patients, providing a good seal and an unobstructed ainvay. i"lticlt patients are not suitable for a LMA? 1. Patients with risk factors for gastric aspiration. The comatose patient in the emergency department with a presumed drug overdose and intermittent airway obstruction, would not be a Should Kno\v

Page 55

Anaesthesia for Medical Students

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

ETT

LMA

~ e ~ u ~ ~ ~ a e s t h hands, etid's when compared to a face mask alone. Provides a better airway in the unconscious patient than a face mask alone. Can often be positioned with minimal anaesthetic drugs (e.g., Propofol alone, i.e., no "Foreign body in trachea reflex")

Provides airway protection against gastric aspiration. Allows for tracheal suctioning. Allows positive pressure ventilation without increasing the risk of gastric distension and aspiration.

DISAD ETT

LMA

Doesn't protect against gastric aspiration. Positive pressure ventilation with airway pressures of > 20 cm H20 results in increasing gastric insufflation and risks pulmonary aspiration of gastric contents. Laryngospasm can occur with the LMA in place. This may result in complete airway obstruction.

good candidate for the LMA, as they are at high risk for gastric aspiration. 2. Patients with oropharyngeal or retropharyngeal pathology, or foreign bodies in the hypopharynx. Examples include peritonsillar abscess, Ludwig's angina, epiglottitis, and trauma to the mouth.

Muscle relaxants are usually require for intubation. Technically more difficult to insert and position compared to LMA. * Trauma and positioning complications e.g., endobronchial intubation. (see chapter 8). "Foreign body in trachea reflex": resulting in an undesired reflex sym pathetic stimulation (see text). Laryngospasm can occur when the E'IT is removed.

3. Patients with limited mouth opening. (e.g., wired jaw, TMJ disease) 4. Patients with a cervical vertebrae or laryngeal cartilage fracture. 5. Patients requiring positive pressure ventilation with airway pressures of greater than 20 cm H20 (e.g., patients with significant restrictive or obstructive airway disease, trendelenburg position, laparoscopy).

Chapter 8 The Laryngeal Mask Airway

upwards againet the hard palate as it is advanced into

C. A wrzectly positioned LMA. The cuff should be inflated without holding on to the LMA.

B. With the neck flexed and head extended, the mask is advanced dong the posterior pharyngeal w

D. When m e d y positioned the LMA cuff does not push the epiglottis 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 M e d i c a l Sfude~tts

Figure 8.2: A number 4 (top) and number 3 (bottom) laryngeal mask airway. How do you position a LMA? The laryngeal mask is positioned after the induction of general anaesthesia. The laryngeal mask should be lubricated, and the cuff valve checked. It is recommended that the cuff is fully deflated prior to insertion. Our experience, however, has been that a small amount of air in the cuff (6 - 10 m L in an adult cuff) facilitates its insertion. The patient is placed in the supine position with their head and neck oriented in the usual 'sniffing position' used for intubation.

Anaesthesia is typically induced with the use of propofol. Other agents such as thiopental, ketamine or halothane can

be used to induce anaesthesia. Propofol is the preferred induction agent as it is superior to thiopental for reducing laryngeal irritability and laryngospasm during LMA insertion. If thiopental is used for LMA insertion, the use of succinylcholine will facilitate its insertion and prevent laryngospasm. After general anaesthesia is induced, the patient's mouth is opened by creating atlanto-occipital extension of the neck in combination with forward displacement of the jaw. The tip of the LMA i s inserted into the mouth, and pressed u p against the hard palate as it is advanced into the pharynx with the right hand. The cuff of the tube is guided along the

C k a ~ l e r 8 Tlte Larvneeal Mask Airwav

)

posterior pharyngeal wall, and inserted

j as far as possible into the pharynx.

)

As an aid to advancing the laryngeal

) cuff past the tongue, it is recommended )

)

) )

) ) )

) )

)

that the right index finger be positioned at the tube-cuff interface guiding the cuff into the pharynx, while the palm of the right hand pushes the proximal end of the LMA into the pharynx. Resistance 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) ever, if left inflated, the cuff removes ) any upper airway secretions as it is ) taken out. Deflating the cuff risks having secretions stimulate the vocal cords ) with the potential for laryngospasm. ) Deflation of the LMA cuff in the lightly anaesthetized patient may result in ) laryngospasm because of stimulation of the vocal cords by secretions. Laryngospasm** is an involuntary reflex closure of the glottis by adduction of the vocal j cords. It may result in the inability to

Must Know

oxygenate or ventilate the patient, with secondary hypercarbia and hypoxemia. Stridor, a high pitched inspiratory sound produced by an upper airway obstruction, may be noted during laryngospasm. Occasionally a muscle relaxant, such as a small dose of succinylcholine, is needed to break the laryngospasm and permit positive pressure ventilation and oxygenation.

Figure 8.3: LMA Sizes and weights. # 1: for wt. c 6.5 kg. # 2: for wt. 6.5 - 25 kg. # 3: for wt: 25 kg. up to adult females # 4: for adult males References: 1. Brain AIJ. The laryngeal mask - a new concept in airway management. Br J Anaesth 1983; 55:801-5. 2. Fischer JA, Ananthanarayan C, Edelist G. Role of the laryngeal mask in airway management. Can J Anaesth 39:l-3; 1992. Sltould K I I O W

Page 59

Rapid Sequence Induction A 'rapid sequence induction'* is used when a patient requires general anaesthesia who has been identified as having risk factors for gastric aspiration (see table 9.1). All patients are at risk of aspirating gastric contents when general anaesthesia is induced, because it impedes the patient's protective airway reflexes. For this reason, all patients requiring elective surgery are asked to abstain from eating solid foods for at least 8 hours, and clear liquids, for at least 4 hours prior to their procedure. Should gastric contents reflux into the hypopharynx during the general anaesthetic, the use of a cuffed endotracheal tube prevents it from entering the lungs.

ness, and tracheal intubation with a cuffed E m . Without a cuffed tracheal tube, the patient is at risk of pulmonary aspiration of gastric contents. Cricoid pressure is applied by an assistant with the induction of anaesthesia. It's purpose is to reduce the risk of passive regurgitation and aspiration before an endotracheal tube can be placed. Cricoid pressure is only released when the tracheal tube cuff has been inflated, and the tube position confirmed by auscultation of both lung fields and measurement of carbon dioxide in the exhaled gases (ETCOJ. Technique for Rapid Sequence*

The predisposing factors for gastric aspiration include a depressed level of consciousness(4 LOC),impaired airway reflexes, abnormal anatomical factors, decreased gastroesophageal (GE) sphincter competence, increased intragastric pressure, and delayed gastric emptying. Patients who have any of these predisposing risks for gastric aspiration, and who require a general anaesthetic, should have measures taken to prevent aspiration during the perioperative period. The three key components of a rapid sequence induction are: preoxygenation, the application of cricoid pressure with loss of consciousPage 60

1. Prepare for CeneralAnesthesia. The suction is checked, on and under the patient's pillow. Airway equipment is checked. An appropriately sized E m with a stylet is prepared. A laryngoscope and laryngoscope blade is checked. The machine is checked, the monitors applied, and the medications are prepared and labelled.

2. If a nasogastric tube is in place, suction and remove it, or leave it open to drainage.

Anaestlaesia for Medic&/Students

Table 9.1:

Aspiration : Predisposing Factors and Preventative Measures**

& LOC

- Drug overdose (e.g., ETOH)

- Head injury - CNS Pathology - Trauma or shock

- Anaesthesia

Impaired Airway Reflexes

states .

- Prolonged Tracheal intubation - Myopathies - Local anaesthesia to the airway - CVA - & LOC

Abnormal Anatomy

- Zenkers Diverticulum

- Esophageal stricture

& GE Competence

- NG tube - Elderly patient - Pregnancy

- Hiatus Hernia - Obesity - Curare

t Intragastric Pressure

- Pregnancy - Obesity - Bowel Obstruction

- Large abdominal - Ascites

Delayed Gastric Emptying

- Narcotics

- Pregnancy

- Fear, Pain, Labour - Trauma

- Diabetes

Prevention

- Preoperative Fasting - H2 Antagonists (&acidity)

tumours

- Anticholinergics

1 Antacids

(4 acidity)

- Renal Failure

- Metoclorpropamide ( t motility) - Antiemetics - Regional or Local anaesthesia rather than General Anesthesia (GA) about the role of ketamine or propofol as alternatives to thiopental when anaesthesia is induced. Why is succinylcholine the most commonly used muscle Page 62

- NG tube to empty stomach prior to induction - Cricoid Pressure on induction of general anaesthesia - Extubation awake on side

relaxant for a rapid sequence induction? When would a muscle relaxant other than succinylcholine be chosen for a rapid sequence induction?

Chapter 9 Rapid Sequence Induction 1

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

Notes:

Must Know

Should Know

Page 63

Monitoring in Anaesthesia Inspection, palpation, percussion and auscultation are the cornerstones of monitoring in anaesthesia. In addition, numerous technical monitors are used to improve our understanding of the patients physiological status and minimize the patients anaesthetic risk.

ANAESTHETIC DEPTH*: Patients undergoing surgery with local or regional anaesthesia are able to provide verbal feedback regarding their well being. When we induce a state of general anaesthesia, the onset of anaesthesia is signalled by the lack of response to verbal commands and the loss of a 'blink' reflex when the eyelash is lightly touched. Inadequate anaesthesia may be signalled by facial grimacing to a painful stimulus or by movement of an arm or leg. In the case of full paralysis with muscle relaxants, inadequate anaesthesia is suggested by hypertension, tachycardia, tearing or sweating. Excessive anaesthetic depth may be signalled by cardiac depression manifesting as bradycardia and hypotension. In the patient who has not been given muscle relaxants and is breathing spontaneously, excessive anaesthetic depth may result in hypoventilation with hypercapnia (increasing PaCOJ and hypoxemia

Monltorlng Current Canadian guidelines to the Practice of Anaesthesia and patient monitoring are: 1. An anaesthetist present. "The only indispensable monitor is the presence at all times, of an appropriately trained and experienced physician." 2. A completed preanaesthetic checklist. (Current history and physical documented, appropriate laboratory investigations reviewed, pre-anaesthesia evaluation completed, ASA classification recorded, and npo policy observed if it is an elective procedure). 3. An anaesthetic record. Every patient receiving general anaesthesia, major regional anaesthesia, or monitored intravenous conscious sedation, should have their HR and BP measured at least every 5 minutes, unless impractical. The time, dose, and route of all drugs and fluids should be charted. 4. Oxygenation, ventilation, circulation, and temperature are continually evaluated both clinically and quantitatively. (Continual is defined as 'repeated regularly').

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 m m

158/82 (114)

Arterial Pressure

4 Central Venous Pressure

32lO Right Ventricular Pressure

27/14 (19) Pulmonary Artery Pressure

12 Pulmonary Capillary 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

Chapter

10 Monitoring in Anaesthesia

I. OXYGENATION: Oxygenation is monitored clinically by providing adequate illumination of the patient's colour and by pulse oximetry. The inspired oxygen concentration (FiOJ is quantitatively monitored during all general anaesthetics using an oxygen analyzer. Each analyzer is equipped with an audible low oxygen concentration alarm. 11. VENTILATION: Ventilation is monitored clinically by verification of a correctly positioned endotracheal tube as well as by observing chest excursions, reservoir bag displacement, and breath sounds over both lung fields. Ventilation is quantitatively monitored using end tidal carbon dioxide @?'KO3 analysis as well as an audible disconnection alarm on all mechanically ventilated patients. The measurement of expired gas volumes and the ability to perform arterial blood gas analysis are useful adjuncts in assessing the adequacy of both oxygenation and ventilation. 111. CIRCULATION: The circulation is monitored clinically by using one or more of: palpation of the pulse, auscultation of heart sounds, a - a r t e r i a l pressure monitoring, doppler pulse monitoring, or oximetry. Quantitative evaluation of the circulation includes an audible electrocardiogram (ECG) signal, and arterial blood pressure measurements at least every 5 minutes.

system has electrodes positioned on the right arm, left arm, and chest position. Lead I1 is usually monitored with a three lead system, as the axis of this vector is similar to the P-wave axis. Identification of P waves in lead I1 and it's association with the QRS complex is useful in distinguishing a sinus rhythm from other rhythms. The chest electrode is usually placed in the left anterior axillary line at the fifth interspace and is referred to as the V5 precordial lead. A five lead electrode system adds a right leg and left leg electrode and allows monitoring of vectors I, 11, 111, AVR, AVL, AVF and V5 (see figure 10.1) Today's anaesthesia monitors are capable of analysis of the ST segment as an indicator of myocardial ischemia. Depression or elevation of the ST segment may be indicative of myocardial ischemia or infarction respectively. Over 85% of ischemic events occurring in the left ventricle during surgery can be detected by monitoring the S T segments of leads I1 and V5.

BP Measurement: The simplest method of blood pressure (BP) determination estimates the systolic blood pressure by palpating the return of the arterial pulse as an occluding BP cuff is deflated. Other methods include auscultation of the Kortokoff sounds with cuff deflation. This allows both systolic (SBP) and diastolic (DBP) pressure measurements. The mean arterial pressure (MAP) can be estimated 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 M e d i c a l Students

rable 10.1: Normal values for a healthy adult undergoing general anaesthesia*. ---

Systolic Blood Pressure Diastolic Blood Pressure Heart Rate Respiratory Rate Oxygen saturation by pulse oximetry End tidal carbon dioxide tension Skin appearance Colour Temperature Urine production

SBP DBP

Central Venous Pressure Pulmonary Artery Pressure Pulmonary Capillary Wedge Pressure Mixed venous oxygen saturation Cardiac Output

CVP PAP (mean) PCWP Sv02 CO

HR RR Sp02 ETCO,

85 - 160 50 - 95 50 - 100 8 20 95 100 33 - 45 warm, dry pink 36 37.5 2 0.5

mmHg mmHg bpm rpm

1 - 10

mmHg mmHg mmHg % 1- mid'.

10 - 20 5-15 75 4.5 - 6

mmHg

O C ml. kg-'. min"

Table 10.2: Derived Cardio~ulmonarvValues:

1, Mean Body Surface Area (BSA) Arterial Pressure

MAP = DBP + 113 Pulse pressure Cardiac Index (CI) = COIBSA Systemic Vascular Resistance SVR = MAP - CVP x 79.9

Normal Values: MAP = 80 - 120 mmHg CI = 2.5 - 4.0 L. min". mq2 SVR = 1200 - 1500 dynes-cm-secSs

Pulmonary Vascular Resistance PVR = PAP(mean) - PCWP x 79.9

PVR = 100 - 300 dynes-cm-sec"

Stroke Volume = CO x 1000 HR

SV = 60 - 90 ml. bear1

Alveolar Oxygen Tension PAO, = (P, P,,)Fi02- PaC0dR.Q.

PAO, = 110 mmHg (Fi02= 0.21) (where P, = 760, Pm= 47, R.Q. = 0.8)

' Alveolar-arterial oxygen gradient -

A-a02 gradient < 10 mmHg (FiO, = 0.21

A-a02 = P A O ~Pao, CaO, = 21 mI.100ml" Arterial Oxygen Content (Ca02) = (SaOJ(Hb x 134) + PaO, x 0.0031

Chapter

10 Monitoring in Anaesthesia

Automated non-invasive BP measurements are routinely performed intra-

operatively using a microprocessorcontrolled oscillotonometer such as a Dinamape. These units have replaced routine BP measurements by auscultation or palpation techniques. They automatically inflate the BP cuff to occlude the arterial pulse at preset time intervals. The cuff pressure is sensed by a pressure transducer. Repeated step deflations provide oscillation measurements which are digitalized and processed as the cuff is deflated. Rapid, accurate (+ 9 mmHg) measurements of SBP, DBP, MAP and HR can be obtained several times a minute. Artifacts can occur with patient movement, arrhythmias, or blood pressure fluctuations due to respiration. When automated non-invasive BP measurements are unsuccessful, simple auscultation or palpation techniques can be used with a manual cuff. Automated BP measurements are routinely performed every 3 to 5 minutes during general anaesthesia. Repeated rapid measurements for prolonged periods of time are not recommended due to a small risk of a compressive peripheral nerve injury.

Procedures frequently requiring direct arterial pressure monitoring include major cardiac, thoracic, vascular and neurosurgical procedures. Arterial line placement is also indicated in procedures requiring induced hypotension or induced hypothermia. Patients with co-existing diseases, including significant cardiopulmonary disease, severe metabolic abnormalities, morbid obesity, and major trauma, may also require perioperative arterial line placement. A central venous pressure (CVP) catheter provides an estimate of the right atrial and right ventricular pressures. The CVP reflects the patients blood volume, venous tone, and right ventricular performance. Serial measurements are much more useful than a single value. The HR, BP, and CVP response to a volume infusion (100 500 ml of fluid) is a very useful test of right ventricular performance. CVP monitoring is useful in patients undergoing procedures associated with large fluid volume shifts. Shock states, massive trauma, significant cardiopulmonary disease or the need for vasoactive medications are other indications for using a CVP catheter.

lnvasive monitoring of the circulation

may include the use of an arterial, central venous, or pulmonary artery catheter. An arterial line is established with a small (20 22 gauge) catheter in a peripheral artery. The radial artery at the wrist is the most common site for an arterial catheter insertion. The femoral, brachial, and dorsalis pedis arteries are alternative sites for arterial line inset-

Must Know

Unlike a CVP catheter that lies in the superior vena cava, the pulmonary artery catheter (PAC) passes through the right atrium and right ventricle and rests in a branch of one of the pulmonary arteries (see figure 10.1). Inflation of a plastic cuff at the tipof the catheter allows occlusion of the proximal pulmonary artery and measurement of the Should Know

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distal pressure. This distal (back) pressure is referred to as the pulmonary artery wedge pressure (PCWP) and reflects the left atrial filling pressure. Thermodilution calculations of cardiac output are performed by injecting a fixed volume of cool fluid into the right atrial port and measuring the temperature change over time from a thermistor probe at the distal tip of the PA catheter. A sample of blood taken from the distal tip of the PA catheter can be analyzed to determine the mixed venous Detailed oxygen saturation (SvO,). analysis of the patient's blood and fluid requirements, as well as the adequacy of oxygen transport can be made with the measurements obtained from a PA catheter. The results of manipulating the patient's hemodynamic parameters with ionotropic agents, vasopressors, vasodilators, diuretics, fluids or blood products, can then be followed. Figures 10.2 and 1 0 3 illustrate typical cardiorespiratory variables monitored during general anaesthesia. Tables 10.1 lists normal cardiorespiratory values during general anaesthesia for a healthy adult. Table 10.2 lists formulas used in calculating common cardiorespiratory values. IV. TEMPERATURE: A temperature monitor must be readily available to continuously measure temperature. Temperature monitoring is mandatory if changes in temperature are anticipated or suspected.

An EKG with defibrillator, as well resuscitation and emergency drugs must be immediately available. In addition a

peripheral nerve stimulator must be immediately available.

Cyanosb: Cyanosis has been defined historically as the presence of 5 grn/dL of deoxygenated hemoglobin (deoxy Hb). When the hemoglobin level is 15 gm/dL and 5 gm/dL of this Hb releases oxygen to the tissues, the oxygenated hemoglobin portion (OxyHb) is 10 gm/dL. Hence the oxygen saturation is: SaO, = OxyHb 1 (OxyHb + DeoxyHb) SaO, = 10 1 (10 + 5) = 66% An oxygen saturation of 66% corresponds to an arterial oxygen tension of approximately 35 mmHg (see oxygen dissociation curve figure 10.4). Should the patient become anemic, however, the oxygen tension (PaO,) at which cyanosis is detected will be even lower. Assume for example that the patient's Hb is now 10 gm/dL. The saturation at which we will detect cyanosis (ie., when the DeoxyHb = 5 gm/dL) will be: SaO, = OxyHb / (OxyHb + DeoxyHb) SaO, = 5 / (5 + 5) = 50% An oxygen saturation of 50% corresponds to an oxygen tension (PaOJ of only 27 mmHg!

We now recognize that under optimal lighting conditions with no excessive skin pigmentation and a normal hemoglobin level, the earliest that cyanosis can be appreciated is at an oxygen saturation of approximately 85%. This corresponds to a PaO, of 55 rnmHg. At a SaO, of 70% most clinicians will be able to detect cyanosis (PaO, of apptoximately 40 mmHg).

Chapter

10 Monitoring in Anaesthesia

p ght Shift in curve: Hb

27 40

Uremia Ci tthosis Hypoxemia Anemia

Hypophosphatemia Banked blood Aadosis

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

Pulse Oximetry*: Pulse oximetry allows beat to beat analysis of the patient's oxygenation status. Oximetry is based on the differences in light absorption by hemoglobin as it binds and releases oxygen. Red and infra-red light frequencies are transmitted through a translucent portion of tissue, such as the finger tip or earlobe. The signal is filtered to isolate pulsatile changes in light absorption. Microprocessors are then used to analyze the amount of light absorbed by the two wave lengths of light, and this is compared with an empiric table of measured values to determine the concentration of oxygenated and deoxygenated forms of hemoglobin. Once the concentrations of oxyHb and deoxyHb have been determined, the oxygen saturation can be calculated. Current pulse oximeters have numeric LED displays for the heart rate and percent saturation. A pulse plethysmograph allows visual analysis of the pulse waveform, while

Must Know

an audible tone, which varies with the percent saturation, allows an auditory assessment of the patients oxygenation status. Pulse oximetry (SpOJ includes measurements of oxyHb, deoxyHb, metHb, and carboxyHb. An over estimation of the true measured oxygen saturation (SaOJ may occur in the presence of significant carbon monoxide poisoning (e.g., a bum victim). Oximeters may become inaccurate or unable to determine the oxygen saturation when the tissue perfusion is poor (e.g., shock. states o r cold extremities), when movement occurs, when dysrhythmias are present, or when there is electrical interference (e.g., electrosurgical cautery unit). The oxyhemoglobin dissociation curve describes a sigmoidal shape (see figure 10.4). A decrease in PaO, of less than 60 mrnHg (corresponding to a SpO, of Should Know

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voestkesio for Medico1 Students

Real time capnograpgh with recarder speed at 12.5 mm/sec.

Trend speed recording at 25 mm/sec.

Expiratory phase occurs from 1 3. Inspiratory phase occurs from 3 - 1. 1 - 2: Alveolar C 0 2 increases in concentration during expiration. 2 - 3: Alveolar plateau. C 0 2 level peaks at 3 and is recorded as the ETC02. 3 - 4: Inspiratory phase begins, and C 0 2 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. P a g e 72

Chapter

90%) results in a rapid fall in the oxygen saturation. The lower limit of acceptable oxygen saturation is 90% as this represents an arterial oxygen tension just above hypoxic values. End-Tidal CO, Monltorlng Definitions: Capnometry: Is the measurement of the carbon dioxide (COJ concentration during inspiration and expiration. Capnogram: Refers to the continuous display of the CO, concentration waveform sampled from the patient's airway during ventilation. Ca pnogra phy : Is the continuous monitoring of a patient's capnogram.

End-tidal C0,monitoring is standard for all patients undergoing general anaesthesia with mechanical ventilation. It is an important safety monitor and a valuable monitor of the patient's physiologic status. Examples of some of the useful information that capnography is able to provide include*: 1. Confirmation of tracheal intubation. 2. Recognition of an inadvertent esophageal intubation. 3. Recognition of an inadvertent extubation or disconnection. 4. Assessment of the adequacy of ventilation and an indirect estimate of Pa CO,. 5. Aids the diagnosis of a pulmonary embolism (e.g., air or clot). 6. Aids the recognition of a partial airway obstruction (e.g., kinked Em. 7. Indirect measurement of airway reactivity (eg., bronchospasm). 8. Assessment of the effect of cardiopulmonary resuscitation efforts.

Must Know

I 0 Monitoring in Anaeslhesia

Measurement of ETCO, involves sampling the patient's respiratory gases near the patients airway. A value is produced using either an infrared gas analysis, mass spectrometry, or raman scattering technique (see figure 10.2 and 105). Provided the inspired CO, value is near zero (no rebreathing of COJ, the ETCO, value is a function of the CO, production, alveolar ventilation and pulmonary circulation. During general anaesthesia the PaCO, to ETCO, gradient is typically about 5 mmHg. In the absence of significant ventilation perfusion abnormalities and gas sampling errors, an ETCO, value of 35 mmHg will correspond to a PaCO, value of approximately 40 mmHg. Increases or decreases in ETCO, values may be the result of either increased CO, production or decreased C0, elimination (see table 103). Monltorlng Neuromuscular function: In order to quantify the depth of neuromuscular blockade, electomyography is commonly employed during anaesthesia. This involves the application of two electrodes over an easily accessed peripheral nerve. The ulnar nerve is the most common nerve used for monitoring neuromuscular function during general anaesthesia. Other nerves that may be used include the facial nerve and the common peroneal nerve. The electrodes are attached to a nerve stimulator, which applies an electrical impulse to the nerve. By attaching a strain gauge to the muscle being stimulated, the muscle response to stimulation may be observed or measured. Ulnar nerve stimulation Should Know

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/ Lnaesfhesia for Medical Sfudenfs

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,

Changes in CO, Production I

Hypothermia Hypometabolism

Hyperthermia Sepsis, Thyroid storm Malignant Hyperthermia Muscular Activity

I I

Changes in CO, Elimination I

Hypoventilation Rebreathing

results in the contraction of the abductor pollicis muscle and a twitch in the thumb. Up to 70% of the neuromuscular receptors may be blocked by a neuromuscular blocking drug before a change in the twitch height can be observed. When 90% of the receptors are blocked, all observable twitches are eliminated. Common methods of stimulation of the nerve include a single twitch stimulus, four twitch stimuli, (each separated by 112 second) referred to as a train-of-four stimulus (TOF), or a continuous stimulus referred to as a tetanus stimulation. The intensity of neuromuscularblockade and type of blockade (i.e., depolarizing versus a non-depolarizing blockade) can be characterized by the response to these different type of stimuli. Clinical relaxation will occur when a single twitch or first twitch of a TOF stimulus, is reduced by 75% to 95% of its original height (see figure 10.6).

Hyperventilation Hypoperfusion Embolism A pure depolarizing block produces a uniform reduction in the height of a single twitch, TOF stimulus, and tetanus stimulation. If excessive amounts of succinylcholine are given (> 5-6 mgkg), the block may begin to resemble a non-depolarizing block and is said to be a phase I1 block (see succinylcholine). Tetanus stimulation of a nerve will demonstrate a continued weak contraction in the presence of a depolarizing block, but will progressively fade with a non-depolarizing block. In the case of a non-depolarizing blockade, there is an increasing reduction in each of the four TOF twitches. The ratio of height of the fourth to first twitch (i.e., the TOF ratio) is less than 0.7 in a non-depolarizing block. Also both the single twitch and the TOF stimulus, will be increased following a tetanus stimulation. This is referred to as post-tetanic facilitation, and only occurs with a non depolarizing block.

Chapter

10 Monitoring in Anaesthesia

The intensity of non-depolarizing neuromuscular blockade can be estimated by the height and number of twitches that are present following a TOF stimulus. When the first twitch is reduced in height by 75%, the fourth twitch disappears. With an 80% reduction in height of the first twitch both the third and fourth twitches are lost, and with a 90% reduction in the first twitch the remaining three twitches disappear.

Single %itch Stimulus

(

When all twitches disappear r 90% of all receptors are occupied. For procedures requiring muscle relaxation attempts are made to maintain one twitch present with a TOF stimulus. Reversal of a neuromuscular block will be easily accomplished if all four twitches of the TOF are present, and will be difficult or impossible if one or no twitches are observed.

11l1

Train of Four Stimulus (TOF)

Train of Four Ratio (T4lTI) = 0.4

Tetanus Stimulation

I -.

Tetanus Fade

Post tetaNc facilitation

Depolarizing neummuscular block. (eg. Succinylcholine 2 mgfltg) 1 minute

S 8 minutca

1. Block established within 1 minute. 2. No fade with tetanus stimulation. 3. No post tetanic facilitation. 4. Block cannot be reversed. 5. TOF ratio > 0.4

Non Depolarizing neummuscular block. (eg. Atncurium 0.4 mgflt)

2-25mlnutcs 4

40minutes

1. Blockestablished over 2 2.5 mlnutes. 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

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) Anaesthesia for Medical Students

Notes:

Intravenous Anaesthetic Agents For over forty years, the ultra short acting thiobarbiturate, sodium thiopental, has been the intravenous induction agent of choice. Thiopental's popularity is currently being challenged by a new akylphenol class of drug called propofol. Propofol's rapid metabolism and elimination, as well as its anti-emetic properties, are welcome features to the specialty of anaesthesia. Ketamine is infrequently used as an intravenous induction agent due to its unpopular psychological side effects. Despite this, it continues to play an important role in anaesthesia due to its unique cardiorespiratory pharmacodynamics.

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, pharmaco*kinetics, pharmacodynamics, dosage, indications and contraindications. Other adjuvant intravenous anaesthetic agents such as midazolam and droperidol are also presented. Opioid analgesics and neuromuscular blocking agents are presented in the following chapters. A. Sodium Thiopental (Pentothala)

Definition: Ultra short acting barbiturate

M Y EKnow ~

Classification: Intravenous anaesthetic hypnotic

Physical Chemical Properties: Thiopental is a highly lipid soluble compound, that is supplied as a yellow powder with a sulphuric smell and a bitter taste. When combined with sodium carbonate, it becomes water soluble. It is bacteriostatic in water and has a pH of 10.6 to 10.8. When injected, sodiumcarbonate is neutralized and the thiopental is converted to its lipid soluble non ionized form (pKa = 7.6, i.e. 40% ionized at pH = 7.4). Thiopental is highly protein bound by albumen (75%), which prevents its precipitation out of solution in vivo.

Figure 11.1: Sodium thiopentothd.

Supplied: Thiopental is supplied in the form of a yellow powder, dissolved in water and sodium carbonate to make a Should Know

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j Lnacsthcsia for Medical Sludents

2 5 % solution (25 mg/ml). It is stable as a solution at room temperature for a period of 2 weeks. Structure Activity Relationship:

CH3 at N-1: shortens the duration (eg. methohexital) S substitution at C-2: markedly shortens the duration of narcosis C-5 substitution with branched chains: increases potency and toxicity Pharmaco*kinetics: (i.e., What happens to the drug with respect to uptake, distribution, metabolism, and excretion.)

An intravenous dose of 3

5 mgkg results in loss of consciousness. The time required to render the patient unconscious 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 after this period of time not because the drug has been metabolized ('I% = 5 12 hours), but rather because the thiopental has moved away from the brain and is entering the more slowly perfused organs. Hence, the termination of action of the drug is due to its 'redistribution' from the brain to other tissues and organs.

glands comprise the vessel rich group*. They receive 75% of the cardiac output, even though they constitute only 10% of body mass. After reaching its peak serum level within these vessel rich organs, thiopental is then distributed to the muscles, fat and the vessel poor group of organs (see figure 11.2). 'Ihe muscle group receives just less than 20% of the cardiac output (second only to the vessel rich group), and constitutes approximately 50% of the body mass. While peak serum concentrations of thiopental are reached within seconds of the injection, the fat group and vessel poor group (e.g., bone, and cartilage) may require hours before peak levels are achieved. The longer time for thiopental to reach peak levels in these compartments is due to the lower perfusion rates of the vessel poor organs.

The brain, liver, kidney's, and adrenal

1 4

64 256

Logarithmic Time Scale (minutes)

Figure 11.2 Distribution of thiopentothal in the vessel rich and vessel poor groups over time, following a rapid intravenous injection. (Modified with permission from Miller RD., Anesthesia 3rd Ed. Churchill Livingstone 1990). \

Chapter 11 Intravenous Anaesthetic Agents

Sulphur containing drugs, acidosis, and non steroidal anti-inflammatory drugs (NSAIDS) may displace thiopental from albumen. This results in an increase in free thiopental which increases the anaesthetic potency and toxicity. Liver and renal disease may be associated with lower albumen levels, also raising free serum thiopental concentrations. Metabolism occurs primarily in the liver with approximately 10 to 15% of the remaining drug level being metabolized per hour. A desulfuration reaction occurring in the liver produces pentobarbital, which then undergoes oxidative metabolism yielding two compounds with no anaesthetic activity. Less than one per cent of the administered thiopental is excreted unchanged in the urine. Pharmacodynamics: (i.e., What the drug does in the body.) CNS: Barbiturates, including thiopental, interact with chloride ion channels by altering the duration they spend in an 'open state'. This facilitates inhibitory neurotransmitters such as gama amino butyric acid (GABA), as well as blocking excitatory neurotransmitter actions such as glutamic acid.

) )

3 ) )

)

Thiopental will decrease both cerebral electrical and metabolic activity. Hence, it can be used to stop seizure activity in an emergency situation. To maintain depression of cerebral electrical activity, very high doses of thiopental are required. To maintain seizure control and avoid significant Must Know

cardiovascular depression from high doses of thiopental, other antiepileptic drugs are used (e.g., a benzodiazepine class of drug). Elevated intracranial pressure (ICP) can be quickly reduced by administering thiopental. The improvement in ICP is transitory and would require excessive amounts of thiopental to maintain. The use of high doses of barbiturates in patients with persistently elevated ICP, has not been shown to improve their overall outcome. The reduction of ICP from thiopental is a result of cerebral vasoconstriction, reduced cerebral metabolism and oxygen requirements. This is associated with a decrease in cerebral blood volume. The overall effect is an improvement in cerebral perfusion pressure (CPP), as the decrease in ICP is generally greater than the decrease in mean arterial pressure (MAP).

Thiopental has an anti-analgesic effect, since low doses may decrease a patients pain threshold. Intraocular pressure (IOP) decreases up to 25% with 3 5 m a g of thiopental. The decrease in IOP persists for 3 to 5 minutes.

CVS: Thiopental causes a dose related depression of myocardial function as measured by cardiac output (CO), stroke volume (SV), and blood pressure. Coronary blood flow, heart rate, and myocardial oxygen uptake all increase Should Know

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lnaesthesia for Mcdical Shtdcnts

following administration of thiopental. Venous tone decreases (decreased preload) and contributes to the increase in HR, and decrease in BP. Little change in the total peripheral resistance occurs following thiopental administration.

RESP: Induction of anaesthesia with thiopental may be associated with 2 or 3 large breaths followed by apnea. The duration of apnea following a 'sleep' dose of thiopental is usually less than one minute. There is a dose related depression of the respiratory response to hypercarbia and hypoxia. Laryngospasm may occur with induction, especially at light levels of anaesthesia and with airway manipulation. Bronchoconstriction may be associated with thiopental, but is much more commonly seen following the combination of a small dose of thiopental with airway manipulation or intubation. As with any general anaesthetic agent, the functional residual capacity (FRC) is reduced with the induction of anaesthesia by up to 20%. GI: Enzyme induction may occur with prolonged high dose therapy, as in barbiturate induced comas. Hypoalbuminemia will result in an increase in unbound (free) thiopental and an increase in the potency of thiopental. GUPregnancyIFetus: Thiopental has little or no effect on the kidney's or gravid uterus. Although thiopental rapidly crosses the placenta to reach the fetus, it has no significant effect on the fetus when used for cesarean section provided the dose used is

limited to 4 m&. Dose and Administration: Thiopental must be used with caution in patients suffering from a shock state. This was quickly appreciated by the anaesthetists caring for the casualties of pearl harbour. They presented to the operating room in shock states secondarily to massive blood loss. The administration of the usual sleep dose of thiopental of 3 to 6 m a g for induction of anaesthesia resulted in their rapid demise. For a frail elderly lady who has fractured her hip, a dose of 25 to 50 mg (05 1 m a g ) may be all that is required for the induction of anaesthesia. For short procedures (eg. cardioversion) a dose of 2 mglkg is generally sufficient.

Indications: 1. Sole anaesthetic agent for brief surgical procedures (less than 15 minutes). 2. For induction of anaesthesia, prior to administration of other anaesthetic agents. 3. For control of convulsive states. 4. For the supplementation of regional anaesthesia, or low potency anaesthetic agents such as N20. Contraindications to Thiopental*: I. ABSOLUTE: 1. Lack of knowledge of the drug. 2. Lack of resuscitative equipment. 3. Inability to maintain a patent airway. 4. Complete absence of suitable veins. 5. Allergy or hypersensitivity to barbiturates. 6. Status asthmaticus. 7. Porphyria (Varigate Porphyria, or 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 2 5 % 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 the injured area.

Figure 11.3: Propofol.

Time (minutes) Figure 11.4: Simulated time course of whole-blood levels of propofol following an induction dose of 2.0 mglkg. (With permission from Miller RD., Anesthesia 3rd Ed. Churchill Livingtone, 1990.)

Other side effects not mentioned above include allergic reactions, which may manifest as a skin rash, pain on injection, urticaria, angioedema, bronchospasm, laryngospasm, and cardiovascular collapse.

B. Propofol (DiprivanB) Definition: Intravenous anaesthetic - hypnotic Classification: Akylphenol Phvsical Chemical Properties:

Must Know

1% propofol (10mg/mL) 10% soyabean oil 2.25% glycerol 1.2% purified egg phosphatide Propofol is a highly lipid soluble oil that is combined with glycerol, egg, and soyabean oil for intravenousadministra-

Should Know

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Lnaesthesia for Medical Shcdena

:ion. It's appearance is similar to that of 2% milk, as the solution that is used to dissolve it is similar to total parenteral nutrition (TPN) solutions. It has a pH of 7 and is supplied in 20 mL ampules with a concentration of 10 mg/ml.

blood vessels remain responsive to C 0 2 during a propofol infusion. Cerebral metabolic rate is decreased up to 36%. Propofol appears to have neither epileptic nor anticonwlsant properties.

Pharmaco*kinetica: TIA initial distribution = 2 8 minutes. 'l?4 redistribution = 30 - 60 minutes. 'l?4 elimination = 4 7 hours.

The respiratory rate is decreased with the induction of anaesthesia, and approximately one quarter of patients become apneic at induction. The period of apnea depends on the dose given, the speed of injection, and concomitant use of an opioid. The frequency of apnea is greater than that seen following thiopental. Maintenance anaesthesia (100 mcg/kg/min iv) with propofol results in a decreased tidal volume and increased respiratory rate. At this same infusion rate the ventilatory response to C 0 2 is depressed similar to that caused by administration of 1 MAC (0.76%) halothane. Unlike halothane, however, doubling the infusion rate of propofol does not result in a marked increase in depression of the C02 response curve.

RESP:

Following a single bolus injection, peak serum concentrations are reached rapidly. Propofol's high lipid solubility results in a quick transfer to the brain and rapid onset (one 'arm-brain' circulation time). Recovery from a single bolus injection results from both redistribution and elimination. Propofol is metabolized in the liver, yielding water soluble inactive conjugated compounds which are excreted by the kidney. Less than 2% of propofol is excreted unchanged in the urine and feces. Propofol is cleared from the blood faster than hepatic blood flow, which suggests that extrahepaticmetabolismandelimination may be occurring in the lungs. Pharmacodvnamics:

CNS: Unlike barbiturates, propofol is not antanalgesic. At low (subhypnotic) concentrations, propofol can provide both sedation and amnesia. Patients report a general sense of well being on awakening from propofol anaesthesia. lntracranial and intraocular pressure are both decreased by propofol. Cerebral perfusion pressure undergoes a small decrease with propofol. The cerebral Page 82

cvs: Systolic, mean and diastolic blood pressure are reduced 25-40% with an induction dose of 2-2.5 mg/kg. Cardiac output, stroke volume and systemic vascular resistance are all decreased with induction by 15-20%. The decrease in blood pressure is believed to be secondary to both myocardial depression and vasodilation. Heart rate may increase, remain the same, or decrease following propofol. Concomitant administration of an opioid tends to result in a greater reduction in heart rate, cardiac output, and arterial pressure.

Chapter

OTHERS: Propof01 neither precipitates histamine release, nor triggers malignant hyperthermia. Propofol has no effect on muscle relaxants and is associated with a low incidence of nausea and vomiting. Pain on injection is more common than with thiopental, especially if given in a small vein in the hand. The discomfort at injection can be decreased by the administration of a small dose of lidocaine with propofol, or by administering propofol through a fast flowing more proximal intravenous catheter. Intravenous Induction Dose: An induction dose of 2.5 - 3.0 mglkg is used for healthy unpremedicated patients. When an opioid, or a 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. Intravenous conscious sedation for operative procedures with local anaesthesia can be facilitated with propofol infusions of 25 75 mcgkglmin.

Contraindications to Pro~ofol*: 1. Allergy (egg allergy). 2. Lack of resuscitation equipment or knowledge of the drug. 3. Inability to maintain a patent airway. 4. Conditions in which precipitous reductions in blood pressure would not be tolerated; in patients with a fixed

Must Know

11 Intravenous Anaesthetic Agents

cardiac output (severe aortic or mitral stenosis, IHSS, pericardial tamponade) and those in shock states. C.

Ketamine (KetalarB)

DefinitionIClassification: Dissociative Anaesthetic Agent Physical Chemical Properties: Ketamine is chemically related to the psychotropic drug phencyclidine (PCP), and cyclohexamine. It is water soluble and is 10 times more lipid soluble than thiopental. It exists as two enantiomers s (+) and r (-) ketamine, and is supplied as a 50:50 mixture. It has a pH of 35 5 5 and is supplied as a clear colourless solution of 10 and 50 mg/mL.

(

Figure 11.5: Ketamine.

Pharmaco*kinetics: Ketamine may be given iv, im, po, or pr. Extensive first pass metabolism and decreased absorption necessitates the administration of higher doses when given by the oral or rectal routes. Ketamine undergoes biotransformationin the liver, yielding eight metabolites. The most significant metabolite is norketamine (also known as Metabolite I), which has 113 the potency of ketamine, *

Should Know

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lnaesfheria for

Medical Studenfs

and subsequently undergoes hydoxylation, conjugation, and excretion in the liver. Following administration, there is rapid absorption and distribution to the vessel rich group (see thiopental), with recovery of consciousness probably secondary to its redistribution to other tissues. Over 90% of an im. injection is bioavailable. Hepatic metabolism is required for elimination, with less than 5% of the administered drug recovered in the urine unchanged. There is a three phase exponential decline in ketamine levels with a 'I% distribution of 24 seconds, a l% redistribution of 4.7 minutes, and 'I% elimination of 2 2 hours. Mechanism of Action: Three current theories about ketamines mechanism of action are: 1. N. Methvl Aspartate receptor theory. NMA receptors may represent a subgroup of the sigma (a) opiate receptors (the PCP site),' that block spinal pain reflexes. 2. Opiate receptor theory. Ketamine may have some affinity for opiate receptors but its effects cannot be reversed with naloxone. 3. ~iscellaneousreceptor theory. Ketamine interacts with muscarinic, cholinergic, and serotonergic receptors. Ketamine was originally thought to cause a 'functional and electrophysiological dissociation between the thalamoneocortical and limbic systems'. Ketamine is a potent analgesic at subanaesthetic plasma concentrations. Its analgesic and anaesthetic effects may be

due to different mechanisms, with the analgesic effects resulting from an interaction between ketamine and central or spinal opiate receptors.

CNS: Ketamine anaesthesia produces a cataleptic state during which nystagmus as well as intact corneal and pupillary light reflexes may be observed. There is a generalized increase in muscle tone and purposeful movements, and vocalization may occur. Unpleasant dreams, hallucinations, or frank delirium may occur with ketamine, especially if the patient is young, female, and large doses of ketamine are given rapidly. The incidence of delirium is decreased with the concomitant administration of a benzodiazepine (eg. diazepam or midazolam), and by giving small doses slowly. The overall incidence of delirium in the 15 to 35 year old population is approximately 20%. Intracranial pressure is not increased with ketamine provided ventilation is adequate. Intraocular pressure may or may not increase with ketamine.

RESP: Ketamine provides general anaesthesia while preserving laryngeal and pharyngeal airway reflexes. Despite this, there are reports of pulmonary aspiration of gastric contents during ketamine anaesthesia when an artificial airway is not used. Ketamine is associated with mild respiratory depression in healthy patients following 2 m a g intravenously. The C 0 2 response curve is shifted to the left with its slope unchanged (similar to opiates). Func-

Chapter

tional residual capacity (FRC), minute ventilation (VA,and tidal volume (V,), are preserved as is hypoxic pulmonary vasoconstriction (HPV). In dogs, ketamine is as effective as halothane or enflurane in preventing bronchospasm. Changes in the respiratory pattern may be observed with periods of prolonged apnea, resulting in hypoxic episodes. Increased secretions occur with ketamine, and can be limited with the prior administration of an anticholinergic, such as atropine or glycopyrrolate.

cvs: Ketamine produces both a central sympathetic stimulation and a direct negative ionotropic effect on the heart. The central sympathetic stimulation results in an increase in HR, BP, SVR, pulmonary artery pressures (PAP), coronary blood flow (CBF) and myocardial oxygen uptake (MV02). Pulmonary vascular resistance (PVR) is unchanged if ventilation is controlled. If the normal sympathetic nervous system is blocked or exhausted, ketamine may cause direct myocardial depression. GI: Anorexia, nausea, and vomiting are minimal. GU/Placenta/Fetus: Placental transfer does occur, but neonatal depression has not been observed if the ketamine dose is limited to s 1 mgfltg. MSK: At the neuromuscular junction, there is an increase in skeletal muscle tone, and the effects of muscle relaxants, such as

Must Know

I 2 Intravenous Anaesthetic Agents

succinylcholine and enhanced by ketamine.

curare,

are

ENDO: Ketamine's sympathetic stimulation will result in an increase in blood glucose, plasma cortisol, and heart rate. Dosage: im: 5 10 m a g iv: 1 2 mgfltg (To limit the risk of delirium following ketamine, it should be injected at a rate of s 40 mdminute).

Intramuscular injections in children of 9 13 m g k g produce surgical anaesthesia within 3 - 4 minutes with a duration of 20 25 minutes. Peak plasma levels are reached approximately 15 minutes following an im injection. With iv administration a dissociated state is noted in 15 seconds, and intense analgesia, amnesia and unconsciousness occur within 45 - 60 seconds. A dose of 1 2 m g k g will produce unconsciousness for 10 15 minutes, analgesia for 40 minutes, and amnesia for 1 2 hours. Subsequent iv doses of 113 to 112 the initial dose may be required.

Indications for ketamine*: 1. Sole anaesthetic for diagnostic and surgical procedures. 2. For induction of anaesthesia prior to the use of other anaesthetic agents. 3. To supplement regional anaesthetic or local anaesthetic techniques. 4. For anaesthetic induction in the severe asthmatic patient or the patient with cardiovascular collapse requiring emergency surgery.

Should Know

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Lnaesthesia for Medical Students

Contraindications to ketamine: 1. Lack of knowledge of the drug. 2. Lack of resuscitative equipment. 3. Inability to maintain a patent air-

way. 4. Allergy or hypersensitivity to ketamine. 5. History of psychosis. 6. Cerebrovascular disease. 7. Patients for whom hypertension is hazardous. (eg. severe hypertension, aneurysms, heart failure, etc.) Other side effects and toxicity: Respiratory depression may occur and should be managed with ventilatory support. Ketamine has a wide margin of safety, and in cases of relative overdoses (up to 10 times the usual dose) there has been a protracted though complete recovery. Other adJuvant anaesthetic agents:

intravenous

Benzodiazepines: Features which result in the popularity of benzodiazepines as adjuvant intravenous anaesthetic agents include:

1. Ability to produce amnesia. 2. Minimal cardiorespiratory depressant effects. 3. Anticonvulsant activity. 4. Low incidence of tolerance and dependence. Benzodiazepines inhibit the actions of glycine and facilitate the actions of the inhibitory neurotransmitter gamma aminobutyric acid (GABA). Benzodiazepines antianxiety and skeletal Page 86

muscle relaxant effects are due to an increase in the concentration of a glycine inhibitory neurotransmitter. Facilitation of the effects of GABA results in the sedative and anticonvulsant effects of benzodiazepines. Benzodiazepines are highly lipid soluble and highly protein bound. In patients with reduced albumen levels (e.g., cirrhosis, renal insufficiency,malnutrition), the decreased plasma binding may result in an increase in free drug concentration, and an increase in drug related toxicity. Benzodiazepines are metabolized in the liver by hepatic microsomal enzymes. The metabolites are conjugated with glucuronic acid and excreted by the kidneys. Elimination half times range from 1 - 4 hours for midazolam (Versed@), to 10 20 hours for lorazepam (Ativana), and 21 37 hours for diazepam (Valium@). Midazolam and diazepam are the two most commonly used benzodiazepines during operative procedures.

Midazolam (Versed@): Midazolam's most common use intraoperatively is to provide intravenous sedation, amnesia, and to reduce anxiety. A dose of 0.5 to 3 mg intravenously (up to 0.1 mglkg) is effective for intravenous conscious sedation. Higher doses of 0.2 0.4 m g k g may be used to induce anaesthesia. Midazolam has a more rapid onset, greater amnestic effect and less postoperative sedative effects than diazepam. Pain on injection and subsequent thrombophlebitis is less likely with midazolam than with diazepam. Midazolam's duration of action is less than diazepam's, but

C h a ~ t e r 11 Intravenous Anaesthetic Aeenfs

almost 3 times that of thiopental. It is supplied for intravenous use as a clear liquid in concentrations of 1 to 5 mglml. Diazepam: Diazepam has 1/2to 1/3the potency of midazolam. A dose of 1 10 mg is effective for intravenous conscious sedation. Higher doses of 0.15 to 15 m a g are used to induce anaesthesia. Diazepam has a high incidence of pain on intravenous injection, as well as a high incidence of subsequent phlebitis. An emulsion of diazepam (DiazemulsCO) is available and has a lower incidence of venous irritation and phlebitis. DiazemulsB contains a diazepam emulsoid of soybean oil, egg lecithin, and a glycerol solution (similar to propofol), however, it is more costly than plain diazepam.

Benzodiazepine Antagonists: Flumazenil (Anexate@) is an imidazobenzodiazepine that specifically antagonizesbenzodiazepine'scentraleffects by competitive inhibition. The mean elimination half life of flumazenil is approximately one hour, considerably shorter than most benzodiazepines. Hence, repeat administration or infusions may be required when benzodiazepines with a longer T% elimination are being antagonized. Flumazenil is supplied as a colourless liquid in a concentration of 0.1 mg per mL. The usual initial dose is 0.2 mg iv over 15 seconds. If the desired level of consciousness is not obtained within 60 seconds of administration, repeated doses of 0.1 mg can be given every minute up to a maximum of 2 mg. If

Must Know

sedation recurs, infusions of 0.1 to 0.4 mglhour may be used. Flumazenil is generally well tolerated. The most common side effect is nausea, and this is seen in only 4 % of patients. Droperidol: Butyrophenones such as droperidol and haldol are classified as major tranquilizers. Droperidol is more commonly used in the perioperative period than is haldol, because it has a shorter duration of action, and has less significant alpha adrenergic antagonist effects so marked reductions in blood pressure are unlikely. Droperidol acts at the postsynaptic receptor sites to decrease the neurotransmitter function of dopamine. It is used in the operating suite as an antiemetic and as an adjuvant to opioid analgesia (neuroleptanalgesia). Droperidol is a powerful antiemetic, inhibiting dopa m i n e r g i c r e c e p t o r s i n the chemoreceptor trigger zone of the medulla. The usual dose of droperidol as an antiemetic is 0.25 to 2.5 mg iv. Adverse side effects are dose related. Extrapyramidal reactions are seen in approximately 1% of patients and are due to its antagonism of dopamine. For this reason, droperidol is contraindicated in patients with known Parkinson's disease. Other adverse reactions include orthostatic hypotension, and dysphoric reactions resulting in increased anxiety and an agitated state. Abnormal sleep patterns in the first 24 hours following the administrationof 1.25 mg of droperidol have been reported in healthy patients undergoing minor surgical procedures. Droperidol may be adminShould Know

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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*:

The neuromuscular junction consists of:

1. A motor nerve ending with mitochondria and acetylcholine vesicles (prejunctional). 2. A synaptic cleft of 20 30 nm in width containing extracellular fluid. 3. A highly folded skeletal muscle membrane (postjunctional). 4. Nicotinic cholinergic receptors located on both the presynaptic (nerve) and postsynaptic (muscle) membranes.

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 sodium and potassium flux across the muscle membrane. This flux of ions decreases the muscles transmembrane electrical potential. When the resting transmembrane potential decreases from -90 mV to -45 mV, an action potential spreads over the surface of the skeletal

Must Know

muscle resulting in a muscular contraction. Acetylcholine's action is rapidly (< 15 milliseconds) terminated as it diffuses away from the muscles end plate, and is hydrolysed by acetylcholinesterase. Muscle relaxants produce skeletal muscle paralysis by interfering with acetylcholine at the neuromuscular junction. Fortunately, involuntary muscles such as the heart are not affected by neuromuscular blocking drugs.

Figure 12.1: The neuromuscular junction. Ach = Acetylcholine; AChE = acetylcholinesterase; JF = junctional folds; M = mitochondria; V = Vesicle. (With permission from Drachman DB; Myasthenia gravis. \N Engl J Med 298:136-142,1978).

Should Know

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)

Classlflcation*:

Non Depolarizing Muscle Relaxants:

Muscle relaxants may be classified according to their duration of action (short, intermediate, or long), and on the basis of the type of neuromuscular block they produce. A non-competitive depolarizing muscle relaxant such as succinylcholine cannot be antagonized. The termination of succinylcholine's activity is dependent on hydrolysis by plasma cholinesterase. All other currently used muscle relaxants are competitive non-depolarizing agents. Their activity does not result in depolarization of the motor end-plate or muscle fibre, and their action can be reversed by the administration of an anticholinesterase agent such as neostigmine or edrophonium.

Non-depolarizing neuromuscular blocking drugs compete with acetylcholine for the cholinergic nicotinic receptor. As the concentration of muscle relaxant increases at the NMJ, the intensity of muscle paralysis increases. Anticholinesterase agents inhibit the break down of acetylcholine. This results in an increase in the concentration of acetylcholine at the NMJ. Anaesthesiologists exploit this pharmacological action by administering ~ t p l c h o l i n esterase agents such as neostigmine and --.. . ----.. edrophonium to competitively 'reverse' the effects of a non-depolarizing neuromuscular blockade.

Cholce of muscle relaxant:

Considerations for choosing a muscle relaxant include*: 1. Duration of action of relaxant, and duration of required muscle relaxation. 2. Route of excretion. 3. Tendency to release histamine. 4. Cardiopulmonary side effects resulting from administration. Potential adverse reactions include bradycardia, tachycardia, bronchospasrn and hypotension. 5. The ability to reverse the neuromuscular block. 6. Cost. 7. Contraindications to any specific muscle relaxant. Table 12.1 summarizes the duration of action of some commonly used muscle relaxants, and the extent to which they depend on renal excretion.

Mlvacurlum: Mivacurium is a new short-acting non-depolarizing neuromuscular blocking drug which, like succinylcholine undergoes hydrolysis by plasma cholinesterase. Patients who have deficiencies in the quality or quantity of plasma cholinesterase will have a prolonged duration of action with both mivacurium and succinylcholine (see succinylcholine, p.93). The effective dose to produce a 95% reduction in the twitch height (ED,) is 0.08 m&g (see chapter 10: Monitoring Neuromuscular Function). Intubation with a non-depolarizing muscle relaxant is typically accomplished by the administration of 2 to 3 times the EDQ5. Intubation with mivacurium can be performed approximately 2 2.5 minutes after administering twice the EDB. With rapid injection of an intubating dose of mivacurium, a transient fall in blood pressure may be observed secondary to the release of histamine. Special infusion pumps are

Chapter

12 Muscle Relarants

)

Brand Name (Trade Name) Concentration Succinylcholine (Anectine) 20 mg/ml Mivacurium (Mivacron) 2mgiml

Duration (mins.)

Block

Non Competitive (Depolarizing) Competitive Non Depolarizing

Time to intubation (90%block) at 2 x ED,

Intubating Dose (mgkg)

< 60 sec

1-2

Short 5

- 10

- 30

Intermediate

Vecuronium (Norcuron) 10 mgtvial

dependent on renal excietion

% ,

- 3 min

0.16 .30

10 25

2.5 - 3 min

.07 0.10

- 80 secs

0.6

3.3 min

0.1

45 60

Rocumnium (Zemuron) 10 mglml Cisatracurium (Nimbex) 10 mg/ml

- 45

- 60

Long

Pancuronium (Pavulon) 1 2 mg/ml

Doxacurium (Nuromax) 1 mg/ml

- 75

- 130

60 80

- 8 min

.06 - , l o

- 80

- 10 min

0.05

)

Table 12.1: Properties of neuromuscular blocking agents. ) frequently utilized in the operating room )

) )

to deliver opioid analgesics, sedatives, or muscle relaxants. These pumps allow for both continuous infusions and bolus doses to be administered. Continuous infusions of 5 10 mcgkglmin of mivacurium may be used to maintain a stable neuromuscular blockade during the procedure. Cisatracurium: Cisatracurium is classified as an intermediate-acting neuromuscular blocking drug, and is

Muslfiow

one of 1 0 isolated isomer of it's predescesor atracurium. It undergoes hydroiysis in the plasma by a nonenzymatic process referred to as Hoffman elimination, and by an ester hydrolysis reaction. Significant histamine release resulting in hypotension, tachycardia, and bronchospasm, that may occur after rapid administration of atracurium i s not seen with cisatracurium. This lack of histamine release, is the main advantage of Should Know

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:isatracurium over it's parent compound atracurium. The EDg5of cisatracurium is 0.05 mglkg. A stable neuromuscular block can be achieved using an infusion of cisatracurium' at a rate of 1 - 5 mcg/kg/min. Cisatracurium is an ideal agent for patients with renal or hepatic insufficiency requiring muscle relaxation.

Vecuronium: Vecuronium is an intermediate-acting neuromusc~larblocking agent. It is a popular agent because it does not' produce any undesirable cardiovascular side effects even when administered rapidly in large doses. Its ED, is 0.05 mg/kg. The onset time for neuromuscular relaxation following 2 x the ED, is 150 - 200 seconds. This can be shortened by the administration of a small 'priming' dose (0.01 m a g ) of vecuronium, followed by 2 4 times the ED,. This can achieve conditions suitable for intubation in approximately 90 seconds from the time of administration. The duration of neuromuscular block'will be increased to more than 1 hour if a larger dose is used for intubation. Continuous infusions of 0.5 - 1.5 mcglkglmin have been used to maintain a stable neuromuscular block during the procedure.

Racuronium: This new intermediate acting non-depolarizing neuromuscular relaxant may replace atracurium, vecuronium, and mivacurium as the relaxant of choice for short and intermediate procedures. It has just recently been released, and has a duration of action, route of metabolism, and lack of hemodynamic side-effects similar to that of vecuronium. Rocuronium's major adPage 92

vantage is it's ability to quickly induce a neuromuscular block, making it suitable for a rapid induction and intubation sequence. It has an ED, of approximately 0.3 m&g. The onset time (i.e. time to 90% depression of TI twitch height) for an intubating dose of rocuronium (i.e. 2 x EDgs) is 60 80 seconds. By contrast, vecuronium has a much slower onset time of 150 200 seconds. Rocuronium's onset time is comparable to the onset time following 1.5 mglkg of s~ccinylcholine(50 - 70 seconds). Hence, rocuronium matches succinylcholine's onset time, and avoids its potential side effects. Nevertheless, it must be remembered that the duration of action of this dose of succinylcholine is only 8 - 12 minutes, compared to 35 - 45 minutes for rocuronium. Continuous infusions in the range of 4 - 16 mcglkglmin. can be used to maintain a stable neuromuscular block. This should be reduced by 30 50% when administered in the presence of 1% isoflurane (similar to all other neuromuscular relaxants).

Paneoronium: Pancuronium is a longacting neuromuscular blocking drug. Administration of pancuronium is frequently associated with a modest (< 15%) increase in heart rate, blood pressure, and cardiac output. The increase in heart rate is due to its blockade of the cardiac muscarinic receptors, as well as an inhibition of catecholamine reuptake by sympathetic nerves. Pancuronium administration does not result in histamine release. The ED, of pancuronium is 0.06 m&g. Pancuronium is much more dependent on renal excretion than the other clinically used

Chapter 12 Muscle Relaxants

muscle relaxants. A prolonged neuromuscular block will result when pancuronium is administered to patients with renal failure or insufficiency.

)

I )

' )

)

) )

)

) ) ) ) )

)

Tebocurare: The muscle paralyzing properties of curare were well know to South American natives who used this drug to immobilize and kill animals with blowgun darts. In 1942 Griffith and Johnson in Montreal introduced the medical world to the paralyzing properties of curare. Since the early 1990's curare has been unavailable in Canada, and is now only of historical interest. In the 1980's curare was most frequently used to attenuate the muscle fasciculations and postoperative myalgias associated with the administration of succinylcholine. A small 'pretreatment' dose of curare (3 mg per 70kg) was administered approxi. mately 3 minutes prior to the administration of succinylcholine, and was appreciated f o r it's excellent 'defasciculating' properties. Today, anesthesiologists who wish to attenuate the muscle fasculations and postop myalgia's seen with succinylcholine administer a small (- 1/10 intubating dose) of a non-depolarizing muscle relaxant 3 minutes prior t o succinylchole (eg., rocuronium 5 m g per 70 kg). d

1 1

Depolarizing Muscle Relaxants: Succinylcholine is the most frequently ) used muscle relaxant that is administered outside the operating room by a i non-anaesthetist physician. Hence a detailed discussion of its properties is included in this chapter. Succinylcholine is the only depolarizing

, i 1

M u t Know

neuromuscular blocking agent that is clinically used. Depolarizing muscle relaxants bind and depolarize the endplate cholinergic receptors. By contrast, non-depolarizing muscle relaxants competitively block the action of acetylcholine. The initial depolarization can be observed as irregular, generalized fasciculations occurring in the skeletal muscles.

Succinylcholine (AnectineB) Classification: Non-competitive depolarizing neuromuscular blocking agent.

_Phvsical-Chemical: Succinylcholine physically resembles two acetylcholine molecules linked end to end. It has two quaternary ammonium cations which interact with the anionic sites on the muscle end plate receptors. Ninety percent of succinylcholine undergoes hydrolysis by plasma cholinesterase (psuedocholinesterase) before it reaches the neuromuscular junction. After binding to the end plate muscle receptors and causing skeletal muscle relaxation, it diffuses out of the NMJ. Outside the NMJ, succinylcholine is again exposed to plasma cholinesterase and the remaining 10% is hydrolysed. The metabolites of succinylcholine are excreted in the urine. Peak effect is reached within 60 seconds of administration, and the neuro-muscular blocking effects of succinyl-choline typically dissipate over the next 5 to 10 minutes.

Slrould Know

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naesthesia for Medical Students

'hase I and Phase I1 Blocks: ;uccinylcholine produces a 'prolonged rcetylcholine (Ach) effect'. It combines with the Ach receptor to depolarize the :nd plate, resulting in a generalized iepolarization (seen as succinylcholine induced fasciculations). The membrane remains depolarized and unresponsive until succinylcholine diffuses away from the endplate (due to a concentration gyadient). This initial neuromuscular block is referred to as a phase I block. If large amounts of succinylcholine are given (eg. 4 6 mg/kg), a different neuro-muscular block may occur. This block is referred to as a phase I1 block. Clinically this may occur when repeated doses of succinylcholine are given, or when succinylcholine infusions are used. A phase I1 block has features which resemble a neuromuscular block that is produced by non-depolarizing muscle relaxants. The actual mechanism of a phase I1 block is unknown.

5. ~ e s ~ o nto s ea tetanus stimulus fades during the stimulus 6. The neuromuscular block can be reversed with anticholinesterase agents

The presence of a normal amount of active plasma cholinesterase is essential to terminate the effects of succinylcholine. In certain conditions, the levels of plasma cholinesterase may be low, and this is referred to as a quantitative decrease in cholinesterase levels. The consequences of a low plasma cholinesterase level are generally of little significance. In patients with severe liver disease with plasma cholinesterase levels as low as 20% of normal, the duration of a neuromuscular block resulting from the administration of succinylcholine increases threefold (eg. 5 to 15 minutes). Liver disease, cancer, pregnancy, and certain drugs such as cyclophosphamide, phenylzine, and monoamine oxidase inhibitors have all been associated with low p : cholinesterase levels. 1. Similar response to a single twitch 2. No post-tetanic facilitation Abnormalities in plasma cholinesterase 3. Train of four (TOF) ratio > 0.7 activity are inherited. Patients may 4. Muscle fasciculations prior to paralhave normal plasma levels of ysis cholinesterase, with a severely impaired 5. Decreased amplitude, but sustained enzyme activity. This is referred to as response to tetanic stimulus a qualitative decrease in plasma 6. The neurornuscular block is increased cholinesterase. Plasma cholinesterase ,when cholinesterase inhibitors are enzyme activity is genetically deteradministered mined by four alleles identified as the silent or absent allele (s), the usual Characteristics of Phase I1 Blocks: allele (u), the dibucaine allele (d), and 1. Decreased response to a single twitch the fluoride allele (f). The normal 2. Post-tetanic facilitation present plasma cholinesterase genotype is EuEu. 3. Train of four (TOF) ratio < 0.7 Patients with abnormal cholinesterase 4. No fasciculations with onset of paralysis activity are otherwise healthy and can

Clzapter 12 Muscle Relarants

)

) be identified only by a specific blood

)

) )

)

test that identifies the genotype and enzyme activity. The sixteen possible genotypes are expressed as ten possible phenotypes. Six of these ten phenotypes are associated with a marked reduction in the hydrolysis of succinylcholine. Patients with the genotype EaEa have a marked reduction in the hydrolysis of succinylcholine. These patients will have a prolonged neuromuscular block that can be increased from ten minutes to several hours following a normal intubating dose of 1 - 2 mg/kg of succinylcholine. The EaEa genotype has a frequency of approximately 1:3200.

)

' )

)

/ )

) )

The treatment of postoperative paralysis secondary to deficiencies in plasma . cholinesterase activity includes controlled ventilation, reassurance, and sedation. Blood samples should be taken to confirm the diagnosis and identify the enzyme genotype. Immediate family members should be tested to determine their genotypes and susceptibility. Medical alert bracelets should be worn by any patient with a significant reduction in their plasma cholinesterase activity. harmacodvnamics:

) Succinylcholine has no known effect on

consciousness, pain threshold or cerebral function. An increase in intraocular pressure (IOP) begins within 1 min of administration of succinylcholine. A peak rise in IOP of 6-10 mmHg occurs at 2-4 minutes, and subsides by 6 minI utes. Factors that may increase IOP include: an increase in central venous

Mud Know

pressure, changes in pH, PaCO,, mean arterial pressure, and a direct effect from the extraocular muscles. A normal IOP is 10 - 20 mmHg. An increase in IOP under anaesthesia is undesirable in patients with an injury that disrupts the globe's integrity. These patients are at risk of vitreous extrusion and damage to the eye if the IOP increases. While succinylcholine increases IOP, crying, straining, or coughing can result in much greater increases of up to 50 mmHg. Increases in intracranial pressure (ICP) of up to 10 mmHg may occur following succinylcholine administration. The mechanism of the increase in ICP is thought to be due to the central mobilization of blood that results from succinylcholine's generalized muscle contractions.

REP: . A progressive paralysis from eyelids to the jaw, limbs, abdominal, intercostal and diaphragmatic muscles follows the administration of succinylcholine.

cvs: Succinylcholine stimulates both the nicotinic and muscarinic cholinergic autonomic receptors. As a consequence of muscarinic cholinergic stimulation, bradycardia, dysrhythmias, and sinus arrest may be observed. This vagal response is prominent among children and, after repeated doses, in adults. It may be inhibited with anticholinergics such as atropine. GI: Succinylcholine iincreases the intragastric in proportion to the intensity of the muscle fasciculations in the abdo-

Should Know

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inaesthesia for Medical Students

nen. It can be limited with prior use of on-depolarizing muscle relaxant. GZf: Succinylcholine does not rely on renal excretion. It's metabolites, succinic acid and choline, however, are excreted by the kidney. Patients with renal failure may have pre-existing hyperkalemia, and ma,y be susceptible to succinylcholine-induced hyperkalemia.

The usual serum potassium response following succinylcholine is a transient and brief increase in the extracellular K t concentration of 0.5 meq/L. Generally patients with K+ concentrations of r 5.5 meq/L should not receive succinylcholine, and all but emergency procedures should be delayed. Succinylcholine does not cross the placenta because of its low fat solubility and its ionized state.

MSK: Succinylcholine has no direct effect on the uterus or other smooth muscles. Myalgias following the administration of succinylcholine are infrequent in children, the geriatric population, and pregnant patients. The incidence of succinylcholine myalgias can be decreased with prior administration of a non-depolarizing muscle relaxant such as curare (3 mgl70kg). Fasciculations result in the release of myoglobin into the serum (myoglobinemia). The excretion 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

patients may respond with an abnormally high tone in masseter muscle following succinylcholine. These patients are said to have developed a masseter muscle spasm, and may represent a subgroup of patients susceptible to malignant hyperthermia.

Hyperkalemia following succinylcholine**: A few cholinergic receptors are located along skeletal muscle membranes outside of the NMJ. The receptors are called extrajunctional cholinergic receptors. The numbers of these receptors increase dramatically over a period of 24 hours whenever nerve impulse activity to the muscle is interrupted. Acute disruption of nerve activity to skeletal muscle occurs in patients who have sustained third degree burns or traumatic paralysis (paraplegia, quadriplegia). Administration of succinylcholine to these patients will result in an abnormally high flux of potassium out of the muscle cells because of the increased number of receptors. An acute rise in the serum potassium to levels as high as 13 meq/L following succinylcholine may result in sudden cardiac arrest. Succinylcholine is absolutely contraindicated in these patients. The administration of a non-depolarizing muscle relaxant in these patients does not result in a hyperkalemic response because the receptors are simply blocked and not depolarized.

Chapter 12 Muscle Relavnnts

) Patients who are at risk of a hyper-

kalemic response following the adminis) tration of succinylcholine include:

) ) )

) )

) ) ) )

)

1. Patients with extensive third degree burns. Succinylcholine should be avoided if the injury is more than.24 hours old, and for 6 months following the healing of the bum injury. 2. Patients with nerve damage or neuromuscular diseases such as muscular dystrophy are susceptible to hyperkalemia and cardiac standstill with succinylcholine. The degree of hyperkalemia appears to be related to the degree and extent of muscle affected. 3. Severe intra-abdominal infections. 4. Severe closed head injury. 5. Upper motor neuron lesions.

3. Myotonia:

Patients with myotonia congenita, myotonia dystrophica, and paramyotonia congenita may all develop a severe, generalized contracture if given succinylcholine. The use of a depolarizing muscle relaxant such as succinylcholine in these patients may result in a secondary generalized contracture of the skeletal muscles, and prevent airway maintenance and ventilation.

4. Familial Periodic Paralysis: ~uccin~lcholine can precipitate a generalized contracture and should be avoided in these patients.

Dosage & Administration: Intubating dose: With curare pretreatment: 1.5 - 2 mg/kg intravenously:

) Specific Diseases:

) 1. Myasthenia Gravis - All muscle re) laxants are best avoided, if possible, in patients with myasthenia gravis. ) These patients behave as if partially ) curarized. They are very sensitive to non-depolarizing muscle relaxants, ) and may be sensitive or resistant to ) depolarizing muscle relaxants.

Myasthenic Syndrome: The EatonLambert Syndrome is a proximal muscle myopathy associated with a carcinoma of the bronchus. Unlike myasthenia gravis, muscle fatigue decreases with exercise, and the eyelids are less affected. These patients are unusually sensitive to both depolarizing and non-depolarizing muscle relaxants.

Must Know

Without curare pretreatment: 1 - 1.5 mglkg iv. Infusion: An infusion may be used for short procedures to maintain a stable neuromuscular block. Recommended rates for infusion are 50 - 150 mcg/kg/min.

Indications: 1. Skeletal muscle relaxation during endotracheal intubation 2. Abdominal operations of short duration 3. Prior to electroconvulsive therapy (ECT), to prevent the possibility of seizure induced injury (e.g., vertebral fracture) 4. Emergency treatment for laryngospasm Should Know

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naesfhesiafor Medical Students

ibsolufe .. Inability to maintain an airway !. Lack of resuscitative equipment b. Known hypersensitivity or allergy I. Positive history of Malignant Hyperthermia 5. Myotonia (M.Congenita, M. Dystrophica or Paramyotonia congenita) 6. Patients identified as being at risk of a hyperkalemic response to succinylcholine (see above).

Relative: 1. Known history of plasma cholinesterase deficiency 2. Myasthenia Gravis 3. Myasthenic Syndrome 4. Familial Periodic Paralysis 5. Open eye injury Reversal of neuromuscular blockade: Muscle relaxation produced by nondepolarizing neuromuscular agents may be "reversed" by anticholinesterase agents such as edrophonium and neostigmine. These agents prevent the .breakdown of acetylcholine in the NMJ. The increased concentration of acetylcholine at the NMJ competes with the muscle relaxant allowing the receptor once again to become responsive to the release of acetylcholine from the nerves. The increased concentrations of acetylcholine also stimulate the muscarinic cholinergic receptors, resulting in bradycardia, salivation, and increased bowel peristalsis. Anticholinergic agents such as atropine and glycopyrrolate are administered prior to Page 98

reversal, to block these unwanted muscarinic effects. Common combinations of anticholinergic and anticholinesterase agents used to reverse a neuromuscular block are atropine 0.01 mg/kg with edrophonium (TensilonB) 0.5 - 1.0 mg/kg, or glycopyrrolate 0:01 rnglkg with neostigmine (ProstigminB) 0.05 0.07 mg/kg intravenously.

Timing of reversal: There are numerous methods of assessing the depth of neuromuscular blockade. The most common of these' include the train of four (TOF) stimulus, tetanus stimulus, and the train of four (TOF) ratio. The train of four stimulus (TOF) applies four brief electrical stimuli of 2 Hz each over a period of 2 seconds. The train of four ratio, (T4/Tl), is the ratio of the twitch response of the fourth stimulus (T4) to the first stimulus (TI). In most circ*mstances, adequate muscle relaxation for surgery occurs when only one of the four twitches is observed. This corresponds to a r 90% blockade of the NMJ receptors. One must consider the intensity and anticipated duration of neuromuscular block before attempting to antagonize it. Reversal may be unsuccessful if only one of the four twitches is present. With inadequate reversal of muscle relaxation, the patient will have a weak hand grip, be unable t o ' cough effectively, and unable to sustain lifting their head from their pillow for 5 seconds. Treatment of inadequate reversal includes supportive ventilation, sedation, analgesia, and adequate time for the neuromuscular block to dissipate.

Inhalational Anaesthetic Agents The intravenous anaesthetic agents introduced in chapter 11 (propofol, ketamine, and thiopentothal) are frequently used to induce the anaesthetic state. To maintain the anaesthetic state, volatile anaesthetic agents are commonly vaporized and delivered to the patient through the anaesthetic machine and anaesthetic circuit. This volatile vapour is then delivered to the lungs where it diffuses across the alveolar capillary membrane and is dissolved in the blood. The blood then carries it to the brain and other organs in the body. Intravenous drugs are typically delivered according to a specific number of milligrams or micrograms per kilogram of body tissue. Inhalational agents on the other hand are administered according to a specific concentration. The concen-' tration of a gas is expressed as a percentage of the volume of anaesthetic gas to the total volume of the gas mixture. For example if we deliver 2 literslmin. of oxygen and 4 literslmin. of nitrous oxide (N20) to a patient, the concentration of N20 is 4/(2 + 4) = 66%. If we want to add a 1% concentration of isoflurane to this mixture we would have to add approximately 60 ml of a saturated isoflurane vapour to the 6 liters of fresh gas flow (0.01 x 6000 ml = 60 ml). Modem anaesthetic vaporizers are able to vaporize liquid

** Must Know

inhalational anaesthetic agents such that very accurate concentrations can be delivered to the patient by simply setting the vaporizer dial at the desired concentration. The role of inhalational anaesthetic drugs in current anaesthetic practice is changing. The introduction of potent intravenous agents, including muscle relaxants, opioids, benzodiazepines, propofol, and intravenous infusion techniques have decreased the need for high doses of inhalational agents. In anaesthesia, a number of different agents representing different classes of drugs are chosen to minimize the side effects of any one agent and capitalize on each agent's benefits. Inhalational agents are compared to one another according to their minimal alveolar concentration** or "MAC" values. The MAC value of an ihhalational agent is the alveolar concentration in oxygen at one atmosphere of pressure that will prevent 50% of the subjects from making a purposeful movement in response to a painful stimulus such as a surgical incision. The MAC value can be considered the effective dose in 50% of the subjects or the ED,. Knowledge of the MAC value allows one to compare the potencies of different inhalational agents. The MAC values of dif-

Should Know

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rrnesflresia for Y e d i c a l Sfuderr~s

Cable 13.1: Factors whlch alter anaesthetic re' ulren~ents(MAC). 1

Increased MAC

No change In M A C

Decreased M A C

Hyperthermia Chronic drug abuse: Ethanol Acute use of amphetamines

Gender Duration of anaesthesia Carbon dioxide tensions: PaC0,21 - 9 5 mmHg Metabolic acid-base status

ferent anaesthetic agents are additive. Nitrous oxide is the only inhalational agent that is routi~lelycombined with another inhalational agent such as isoflurane, enflurane, or halothane. It is necessary to establish a n anaesthetic depth equivalent t o 1.2 to 1.3 of the MACvalue. The added 20 - 30% M A C depth of anaesthesia will prevent movement in 95% of patients. The M A C value of N20is 105%, which is approximately one-hundred-fold greater than the other inhalational agents. Because the recommellded millimum concentration of oxygen delivered during general anaesthesia is 30%, the maximum concentration on N 2 0 is 70% (approximately 0.7 MAC). Hence, nitrous oxide alone is unable to provide adequate anaesthesia. Opioid a~lalgesics,benzodiazepines, or other inhalational agents may be added to supplement the nitrous oxide. Table 13.1 lists factors that increase or decrease the M A C values. Table 13.2 lists differences in inhalational agents a s well as their M A C values, with and without nitrous oxide.

Increasing age Hypothermia Severe hypotension Other anaesthetic agents: opioids, benzodiazepines Acute drug intoxication: Ethanol Pregnancy Hypothyroidism Other drugs: clonidine, reserpine

The rapidity with which the anaesthetic state is reached depends o n how quickly the anaesthetic inhalational agent reaches the brain to exert its partial pressure effects. Factors determining how quickly the inhalational agent reaches the alveoli include: 1. The inspired concentration of anaesthetic gas being delivered by the anaesthetic machine (concentration effect). 2. The gas flow rate through the anaesthetic machine. 3. The amount o f alveolar ventilation (V, = Respiratory Rate x Tidal Volume). I~lcreasing any of these factors will result in a faster rise in the alveolar concentratio~lof the inhalational agent. Factors determining how quickly the inhalational agent reaches the brain from the alveoli in order to establish anaesthesia include: 1. The rate of blood flow to the brain. 2. The solubility of the inhalational agent in the brain.

Chapter 13 Inhalational Anaesthetic Agents

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

,---c---------Delivered Concentration

Nvmlar Brain

Fresh gas flow rate = 4 Umin. I

10 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 venous concentrations of the inhalational agent. Increasing any of these factors will hasten the onset of anaesthesia. Patients with low cardiac output states (eg. shock states) may have a rapid rise in the alveolar partial pressure of an inhalational anaesthetic agent. This will result in a more rapid onset in anaesthesia, with possible exaggerated cardiorespiratory depressant effects.

Must Know

The cascade of anaesthetic partial pressures starts at the vaporizer. The gas from the vaporizer is diluted by exhaled gas to form the inspired gas. With a circle system, a fresh gas flow of 4 - 5 liters per minute will raise the inspired anaesthetic tension close to the vaporizer's delivered concentration. As the body continues to take up the inhaled anaesthetic gas, the alveolar anaesthetic tension will remain below the inspired anaesthetic tension for Should Know

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L~~aes/lresia for Medical Slude~lls

many hours. The brain can be co~lsidered the final step in the anaesthetic cascade. The brain tension will approach the alveolar tension within 8 to 10 minutes of any change. Monitoring the alveolar end-tidal concentration of the inhaled anaesthetic agent provides a reasonable estimate of the brain anaesthetic tension (see figure 13.1 and 13.2). Nitrous Oxide: Nitrous oxide is an inert, inorganic, colourless, tasteless, and odourless gas. It has a rapid onset and a quick recovery of 3 to 10 minutes due to its low solubility in blood. Its low potency (MAC = 105%) limits the amount that can be administered, and its usefulness when high concentrations of oxygen are required. Myocardial depression is usually minimal in healthy patients, however significant cardiovascular depression may occur in patients with coexisting myocardial dysfunction or in patients in a shock state. Nitrous oxide is 34 times more soluble than nitrogen. This property results in three special anaesthetic phenomena. At the begirlrling of anaesthesia, N 2 0 leaves the alveoli much faster than nitrogen can leave the body tissues to fill the space left by N20. The result is an increase in the concentratio~lof other gases in the alveoli (oxygen, and other inhalational agents). This increase in concentratio~lspeeds the onset in inhalational anaesthetic effect, and is referred to as the sccond gns cffcct. Diffusion hypoxin may result at the end of the anaesthetic. As nitrous oxide is discontinued, the body stores of nitrous

oxide are released and flood the alveoli, diluting the oxygen present in the alveoli. When only room air is administered at the end of the anaesthetic, the dilution of oxygen may be sufficient to create a hypoxic mixture, and result in hypoxemia. Other factors contributing to hypoxemia at the end of anaesthesia include respiratory depression due to anaesthetic agents, residual neuromuscular blockade, and pain with splinted respirations. The administration of 100% oxygen at the end of an anaesthetic may avoid hypoxemia resulting from any of these causes. Finally, closed air spaces will expand in the presence of nitrous oxide due to the differences in solubility of nitrogen and nitrous oxide. With the administration of 66% N20, a closed air space will expand 2 times in volume over a period of approximately 15 minutes. For this reason N 2 0 is contraindicated in patients with a pneumothorax, closed loop bowel obstruction, air embolism, or any other closed air space in the body. Nitrous oxide undergoes very little metabolism and is excreted uncha~lged by the lu~lgs. The most conlrno~llyused inhalational agents today are nitrous oxide, isoflurane, enflurane, and halothane. The latter three are synthetic, colourless liquids that are non flammable and administered as a vapour from a vaporizer on the anaesthesia machine. A dose-related depression of cardiorespiratory function is common to each of these inhalational agents. All three produce smooth muscle relaxation, and

this property has been exploited to produce bronchodilation in patients with status asthmaticus, and uterine relaxation in patients with a retained placenta. Halothane, enflurane, and isoflurane are all contraindicated in patients with malignant hyperthermia. Isoflurnne:

Isoflurane is the most common inhalational agent used for adult anaesthesia in North America. It has a MAC value of 1.16%, and has the fastest uptake and washout times of these three inhalational agents. It is not as well tolerated as halothane for an inhalational anaesthetic illdu

Anaesthesia for Medical Students - PDF Free Download (2024)

FAQs

What are the 4 stages of anesthesia? ›

There are four stages of general anesthesia, namely: analgesia - stage 1, delirium - stage 2, surgical anesthesia - stage 3 and respiratory arrest - stage 4. As the patient is increasingly affected by the anesthetic his anesthesia is said to become 'deeper'.

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How to learn Anaesthesia? ›

Earn an MBBS degree

You must complete the MBBS course to become an anaesthetist. It is a five-and-a-half-year course, including one year of internship. During your MBBS programme, you will learn the basics of anaesthesia, including anaesthesia technology and anaesthesia techniques in an operation theatre.

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What is anesthesia pdf? ›

Anesthesia is the use of medicine to prevent the feeling of pain or another sensation during surgery or other procedures that might be painful.

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How do I prepare for anesthesiology? ›

A pre-med bachelor's degree is the first step, followed by four years of medical school, anesthesiology residency, and licensure. Securing a fellowship and earning certification are often optional, although these additional steps can increase marketability and earning power.

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What are the 5 levels of sedation? ›

Procedural Sedation - Levels of Sedation

Minimal Sedation. A drug-induced state during which patients respond normally to verbal commands, and respiratory and cardiovascular function is unaffected. ...
Moderate Sedation/ Conscious Sedation. ...
Deep Sedation. ...
General Anesthesia.

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What are the 5 types of general anesthesia? ›

The primary goal of general anesthesia is to render a patient unconscious and unable to feel painful stimuli while controlling autonomic reflexes. There are five main classes of anesthetic agents: intravenous (IV) anesthetics, inhalational anesthetics, IV sedatives, synthetic opioids, and neuromuscular blocking drugs.

Is it hard to study anesthesiology? ›

Anesthesiology is an intensive field, and becoming an anesthesiologist requires a great deal of education and training. It's not for everyone; it can take 12 to 15 years after high school before you are fully certified and licensed to practice.

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How to study for basic anesthesia? ›

How To Study For The Anesthesia BASIC Exam

Understand the exam content. ...
Formulate a study schedule. ...
Choose quality resources. ...
Consider study groups. ...
Take practice exams. ...
Simulate exam conditions. ...
Manage exam-related stress. ...
What Happens If You Fail the ABA BASIC Exam?

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Jan 18, 2024

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How many years to study anesthesiology? ›

To ensure they can provide optimal and safe care to patients, aspiring anesthesiologists undergo extensive education and training. Anesthesiologists spend 12 to 14 years in school and training after high school.

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What are the 6 A's of anesthesia? ›

Contemporary general anesthesia focusses on what may be referred to as the 6 A's. These are, in random order, anxiolysis, areflexia, autonomic areflexia, analgesia, amnesia and anesthesia.

What is the basic knowledge of anesthesia? ›

Anesthesia uses drugs called anesthetics to keep you from feeling pain during medical procedures. Local and regional anesthesia numbs a specific area of your body. General anesthesia makes you temporarily unconscious (fall asleep) so you can have more invasive surgeries.

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What drugs do anesthesiologists use? ›

Propofol, etomidate, and ketamine are the intravenous (IV) sedative-hypnotic agents commonly used to induce general anesthesia (table 1), while adjuvant agents (eg, opioids, lidocaine, midazolam, and volatile anesthetics) are often used to supplement the effects of the primary sedative-hypnotic induction agent (table 2 ...

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What is the best way to study anaesthesia? ›

Practice, practice, practice. The best way to learn anaesthesia is to practice. The more you practice, the more confident you will be. Practice questions and cases pertaining to anaesthesia scenarios.

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Why are anesthesiologists paid so much? ›

Rigorous Training and Education

This intensive training ensures that anesthesiologists are well-prepared for their demanding role. The long years of study and training partly explain the high salary, as the road to becoming an anesthesiologist is not for the faint-hearted.

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What makes anesthesiology difficult? ›

The most challenging and rewarding aspects of anesthesiology: A difficult part of our profession is that you do not know if a patient is genuinely healthy and will proceed with their surgery uneventfully until they leave the hospital. An anesthesiologist must maintain a constant state of hypervigilance.

What stage of sleep are you in under anesthesia? ›

Anesthesia is nothing like that. During sleep, the brain moves between the slow waves of non-REM sleep and the fast waves of REM sleep. Under general anesthesia, brain waves are held hostage in the same state and remain there for the length of the operation. Then we turn the anesthetics off and allow you to come to.

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How long does it take for anesthesia to wear off after major surgery? ›

After your surgery, you'll go to a recovery room to wake up. Nurses will monitor your heart rate, breathing, and other vital signs for about 30 minutes. As you come out of the anesthesia, you might feel groggy and confused. The drugs' effects can take a few hours to fully wear off.

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How many times is it safe to go under anesthesia? ›

In general, anesthesia is considered safe, and most people can undergo multiple procedures with anesthesia without any long-term adverse effects. However, each time you undergo anesthesia, there is a small risk of side effects or complications such as nausea, vomiting, sore throat, headache, or confusion.

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Anaesthesia for Medical Students - PDF Free Download (2024)

FAQs

What are the 4 stages of anesthesia? ›

What is the basic knowledge of anesthesia? ›

References