A primer of anesthesia : for undergraduate 9788184484243, 8184484240

Table of contents :
Cover
Prelims
Chapter-01_Intravenous Anesthetic Agents and Opioids
Chapter-02_Inhalational Anesthetic Agents
Chapter-03_Physiology of Neuromuscular Blockade and Neuromuscular Pharmacology
Chapter-04_The Anesthesia Machine
Chapter-05_Preoperative Evaluation of Patients
Chapter-06_Monitoring the Patient under Anesthesia
Chapter-07_Vascular Cannulation
Chapter-08_Airway Management
Chapter-09_Neuraxial (Spinal and Epidural) Blockade
Chapter-10_Peripheral Nerve Blocks
Chapter-11_Fluid Therapy and Transfusion
Chapter-12_Post-anesthesia Care
Chapter-13_Oxygen Therapy
Chapter-14_Infection and the Anesthesiologist
Chapter-15_Care of the Patient in the ICU
Chapter-16_Cardiopulmonary Resuscitation
Index

Citation preview

A Primer of ANESTHESIA

A Primer of ANESTHESIA (For Undergraduates)

Editor Rajeshwari Subramaniam MD Professor Department of Anesthesiology and Intensive Care All India Institute of Medical Sciences New Delhi, India

®

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad • Kochi • Kolkata Lucknow • Mumbai • Nagpur

Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd Corporate Office 4838/24 Ansari Road, Daryaganj, New Delhi - 110002, India, Phone: +91-11-43574357 Registered Office B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi - 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021 +91-11-23245672, Rel: +91-11-32558559, Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches  2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094 e-mail: [email protected]  202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001, Phones: +91-80-22285971, +91-80-22382956, 91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected]  282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089 Fax: +91-44-28193231 e-mail: [email protected]  4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road, Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929, Fax:+91-40-24758499 e-mail: [email protected]  No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala, Phones: +91-484-4036109, +91-484-2395739 +91-484-2395740 e-mail: [email protected]  1-A Indian Mirror Street, Wellington Square Kolkata 700 013, Phones: +91-33-22651926, +91-33-22276404, +91-33-22276415 Rel: +91-33-32901926, Fax: +91-33-22656075 e-mail: [email protected]  Lekhraj Market III, B-2, Sector-4, Faizabad Road, Indira Nagar Lucknow 226 016 Phones: +91-522-3040553, +91-522-3040554 e-mail: [email protected]  106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel Mumbai 400 012, Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896, Fax: +91-22-24160828 e-mail: [email protected]  “KAMALPUSHPA” 38, Reshimbag, Opp. Mohota Science College, Umred Road Nagpur 440 009 (MS), Phone: Rel: +91-712-3245220, Fax: +91-712-2704275 e-mail: [email protected] USA Office 1745, Pheasant Run Drive, Maryland Heights (Missouri), MO 63043, USA, Ph: 001-636-6279734 e-mail: [email protected], [email protected] A Primer of ANESTHESIA © 2008, Rajeshwari Subramaniam All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the editor and the publisher. This book has been published in good faith that the material provided by editor is original. Every effort is made to ensure accuracy of material, but the publisher, printer and editor will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi jurisdiction only. First Edition:

2008

ISBN 978-81-8448-424-3 Typeset at JPBMP typesetting unit Printed at Ajanta Offset & Packagins Ltd., New Delhi

To the Past, Present and Future Teachers of Anesthesiology

Contributors Anjolie Chhabra MD Assistant Professor, Department of Anesthesiology and Intensive Care All India Institute of Medical Sciences New Delhi, India

Purnima Dhar MD Senior Consultant, Department of Anesthesiology Indraprastha Apollo Hospitals New Delhi, India

Anju R Bhalotra MD Associate Professor, Department of Anesthesia and Intensive Care Maulana Azad Medical College New Delhi, India

Rahul Seewal MD, FRCA Specialist Registrar University College London Hospital NHS Foundation Trust, UK

Ashish Malik MD Clinical Associate, Department of Anesthesiology, Indraprastha Apollo Hospitals New Delhi, India

Rajeshwari Subramaniam MD Professor, Department of Anesthesiology and Intensive Care All India Institute of Medical Sciences New Delhi, India

Chittaranjan Joshi MD, DNB Senior Registrar Intensive and Critical Care Unit Flinders Medical Centre Flinders University, Bedford Park Adelaide, South Australia

Rajesh Tope MD, FRCA Senior Consultant, Department of Anesthesiology Indraprastha Apollo Hospitals New Delhi, India

Indu Kapoor FANZA, FCARCSI, MD Consultant and Pediatric Head Department of Anesthesia and Intensive Care Hutt Valley District Health Board New Zealand Kongbrailatpam Nirmala Devi MD, FRCA Consultant Anesthetist University Hospital, Lewisham London, UK Preethy Mathew MD Assistant Professor Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research Chandigarh, India

Rengarajan Janakiraman MD Fellow in Pain Medicine University of Ottowa Canada Rani Sunder MD Assistant Professor, Department of Anesthesiology and Intensive Care All India Institute of Medical Sciences New Delhi, India Sumesh Arora MD, FJFICM Staff Specialist, Intensive Care Prince of Wales Hospital Randwick, NSW 2031, Australia

Foreword It is not often that a scientific treatise turns out to be a treat to discerning readers’ vision and mind. The editor, Rajeshwari Subramaniam, a former (and still claims to be!) student of mine for some years, has perfected such a piece of work here written so thoughtfully that it eliminates the need for an instructor to explain the contexts any further. The abundance of sensibly selected illustrations, most of them having an aura of originality, reveal the tremendous effort put in to offer a rational presentation of fundamentals. This promises to be an asset to both the postgraduate trainee in anesthesiology and the undergraduate who has an interest to become part of the specialty of anesthesia, pain management and resuscitation. Easy-to-understand sketches and illustrations and facts and vital figures of physiology and pharmacology are most valuable for the new inductee in the specialty. This instructive piece of work is spiced with original drawings and sketches, particularly in sections dealing with monitoring, vascular access, airway management, and the figures on fluid therapy. It is unique in the sense that it does not follow the conventional flow of material down the pages ‘system by system’ or ‘organ by organ’. Rather, the stress is on problems and ways to solve them intelligently, answering questions that all of us want to ask. This book is an asset to the learning process and provides sensible and rational explanations to unravel the issues that are challenges to the trainee, the trainer and the practitioner. I expect this to go far and wide and for a long time to come.

Em Prof VA Punnoose MD, FMCA (Present) Dean of PG Studies, St.Stephen’s Hospital Former Head of Cardiothoracic Anaesthesia All India Institute of Medical Sciences Commonwealth (CFTC) Expert to the University of Ghana Professor of Anaesthesiology University Jos, Cardiac Anaesthesia Fellow at Green Lane Hospital New Zealand

Foreword I have witnessed the growth of anesthesiology as a specialty for more than last four decades and watched its change from an art form to a science based on the known principles of physiology and pharmacology. No other specialty has seen such a transformation in this short time. From an assistant and side-kick to a surgeon, the modern anesthesiologist has become a specialist in his/her own right. This period has also witnessed a widening of the prospects and range of clinical activities of anesthesiologists, covering preoperative evaluation and administration of anesthesia for postoperative pain management, and management of the critically ill surgical and medical patients on various life-support systems. This has prompted some of our colleagues to suggest the new name of “Perioperative Medicine” for the specialty. The present role of anesthesiologists involves a number of functions, unknown to their predecessors. Anesthesiologists have to know and understand the clinical implications of the patient’s disease and its effect on the conduct of anesthesia. In view of this, the knowledge base of an anesthesiologist has widened. Many of our young medical graduates find it difficult to get information of such breadth and ranging topics from a single source. In this context, this book, ‘A Primer of Anesthesia” will fulfill a great need for source material covering a whole lot of different subjects. The authors have compiled a generous source of readily available information in a crisp and concise manner. The subjects covered have been divided into four main sections covering the preoperative period, intraoperative period, postoperative period and critical care which deals with all the major aspects of an anesthesiologist’s day to day work schedule. Each chapter describes briefly, but clearly the essential theoretical details. Addition of a large number of illustrations, both photographs as well as line drawings, ensure that it is easily understandable even to a fresh medical graduate. The MCQs provided can help the reader check his/her grasp of the subject. I would like to give full credit to Prof. Rajeshwari Subramaniam (who has been my student), for accepting this daunting challenge and producing a very readable treatise with support from each of the contributing authors. This book shall be of immense value not only to all those who aspire to become anesthesiologist, but also to fresh medical and surgical residents who find it difficult to get easily accessible information on important day to day patient care functions. It shall also be useful to a busy practitioner as a ready reference volume. I wish the authors well and hope that they shall start right away to prepare the next edition, and include at the end of each chapter a short bibliography for further reading, for those who are interested. Prof HL Kaul MD, FRCA Retired Head Department of Anaesthesiology and Intensive Care All India Institute of Medical Sciences New Delhi, India

Preface Anesthesiology is a rapidly expanding and vital specialty especially in India and other developing countries. There is an ever-increasing need for trained anesthesiologists to provide safe perioperative care to patients at primary health center (PHC) level to tertiary hospitals carrying out cardiac surgery, neurosurgery and organ transplantation. Where do we begin? For a start, it is important to attract more postgraduates to the specialty of anesthesiology. Unfortunately the present scheme of rotation provided to undergraduates is not long enough for the students to get familiar with anesthetic pharmacology, terminology, equipment and skills. Further, the students find themselves at sea in the world of the modern operating theatre and ICU equipped with hitech monitors and gadgets. This book has been written with the primary aim of demystifying anesthesiology and presenting the necessary theory related to pharmacology, equipments and skills in an easy-tounderstand manner. It is hoped that better understanding of this subject at undergraduate level will lead to enhanced appreciation and motivation to pursue it as a career. Rajeshwari Subramaniam

Acknowledgements I gratefully acknowledge all the contributors to this book who devoted time from their busy schedules to write their chapters. I acknowledge with deep gratitude and humility my teachers (Late) Prof. NP Singh, Prof. VA Punnoose, (Late) Prof. GR Gode, Prof. HL Kaul and Prof. TS Jayalakshmi, who inculcated in me not only a sense of obligation to teach and practice evidence-based anesthesia, but also to treat patients with respect and compassion. Their dictum: “It is the enlightened who can enlighten”. I acknowledge the vastness and majesty of this specialty without which no advancements in modern surgical technique would have been possible. My family who encouraged this endeavour cannot be thanked enough. I thank production staff of M/s Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, for their patience for the numerous revisions and modifications I thrust upon them. I would like to add that the photographs of ampoules/vials of drugs displayed in some of the chapters are those in common use and I have no financial gains from the manufacturers. My special thanks to Dr. Sunil Chumber (Additional Professor, Dept. of Surgical Disciplines, AIIMS), who was the one who succeeded in motivating me to write this book. If this book fulfils the expectation of its users I would give all credit to the contributors and I take the responsibility for errors, if any. Last but not the least, I acknowledge my colleagues and students whose faith in me is amazing and humbling.

Contents Section 1 THE PREOPERATIVE PERIOD 1. Intravenous Anesthetic Agents and Opioids Rajesh Tope

3

2. Inhalational Anesthetic Agents Rajesh Tope

18

3. Physiology of Neuromuscular Blockade and Neuromuscular Pharmacology Anju R Bhalotra

32

4. The Anesthesia Machine Rajeshwari Subramaniam, Chittaranjan Joshi

53

5. Preoperative Evaluation of Patients Anjolie Chhabra

64

Section 2 THE INTRAOPERATIVE PERIOD 6. Monitoring the Patient under Anesthesia K Nirmala Devi, Rajeshwari Subramaniam

87

7. Vascular Cannulation Rajeshwari Subramaniam

97

8. Airway Management Indu Kapoor, Rajeshwari Subramaniam

102

9. Neuraxial (Spinal and Epidural) Blockade Rajeshwari Subramaniam, Rani Sunder

121

10. Peripheral Nerve Blocks Rengarajan Janakiraman

143

11. Fluid Therapy and Transfusion Rahul Seewal, Purnima Dhar, Rajeshwari Subramaniam

157

xviii

A PRIMER OF ANESTHESIA

Section 3 THE POSTOPERATIVE PERIOD 12. Post-anesthesia Care Preethy Mathew

191

13. Oxygen Therapy Rajeshwari Subramaniam, K Nirmala Devi

200

14. Infection and the Anesthesiologist Ashish Malik

209

Section 4 CRITICAL CARE 15. Care of the Patient in the ICU Sumesh Arora

219

16. Cardiopulmonary Resuscitation Chittaranjan Joshi, Indu Kapoor

239

Index

255

Introduction  

A Brief History of Anesthesia Scope of Present-day Anesthetic Practice

Numerous path-breaking advances have been responsible for taking the specialty of anesthesia to its pinnacle in today’s practice. Although many are being mentioned here in chronological order. The tremendous progress of the science of anesthesia over the last 150 years can be attributed to the observation, dedication, motivation and perseverance of some extremely committed individuals. These individuals and their labor have resulted in unprecedented developments in the understanding of physiology, safe use of pharmacological agents, monitoring, pain control and provision of perioperative care to even the most compromised patients. The word ‘anesthesia’ can be traced back to the Greek philosopher Dioscorides in the 1st century AD, who used it to describe the narcoticlike effects of the mandragora plant. Ancient civilizations used opium (from poppy), mandrake root, alcohol, coca leaves for phlebotomy, etc. to facilitate surgery. Nerve compression (to produce ischemia, shown in Figure 1) and cryoanalgesia (application of ice parallel to incision) were forms of regional anesthesia. In spite of these obviously meager and inadequate methods, records of trephinations and amputations can be found in medieval texts. However, modern surgery as we know it, was impossible due to poor understanding of disease, lack of asepsis and absence of reliable and safe anesthetic techniques. As early as 1540–1550 Paracelsus noted the soporific effect of ether on chickens. In 1842

Fig. 1: Nerve compression

Crawford W Long and William E Clark, used ether for surgical removal of a sebaceous cyst. However, the first public demonstration of ether anesthesia that convinced the patient, the audience (and the surgeons!) was on 16th October 1846 at the Bullfinch amphitheater of the Massachusetts General Hospital, Boston by WTG Morton (Fig. 2). Ether’s popularity and use spread rapidly through US and Europe. Incidentally, the word ‘anesthesia’, specifically used to denote the sleep-like state that makes painless surgery possible, was coined by Oliver Wendell Holmes, Professor of Anatomy at the Massachusetts General Hospital, soon after the first public demonstration by Morton. John Snow (Fig. 3), a physician, pioneered the use of ether in England. He was fascinated by anesthesia and designed a number of vaporizers for safe and controlled administration of ether, and was one of the most sought-after and famous anesthetists. Chloroform was introduced a year later. It owed its popularity to

xx A PREMIER OF ANESTHESIA

Fig. 2: Public demonstration of ether

Fig. 3: John Snow

Sir James Simpson, an obstetrician, who eventually became a practicing anesthetist. He used it extensively to alleviate pain during labor. The administration of chloroform by Sir John Snow to Queen Victoria for the birth of her eighth child, Prince Leopold (and subsequently, Princess Beatrice) served to heighten the fame of both obstetric analgesia and chloroform.

Joseph Clover (1825-1882) succeeded Snow in London as a practising anesthetist. Due to his impeccable technique he was much sought after by surgeons. He had, to his credit, more than 7000 chloroform anesthetics without a single fatality. It is interesting to note that Clover was the first physician to monitor the pulse (see photograph: Figure 4), color and respiration under anesthesia and the first physician to administer ‘jaw thrust’ and ‘chin-lift’ maneuvers to relieve airway obstruction during anesthesia. Chloroform use rivaled that of ether in the 1850’s-1860’s. The first reported anesthetic death was associated with chloroform anesthesia. The patient was a young girl named Hannah Greener. Its popularity waned gradually due to its tendency to cause arrhythmias, respiratory depression and hepatotoxicity. The report of the Chloroform Commission in 1864 signaled the beginning of the end of chloroform and it was virtually out of use by the Ist World War. Ether was revived in the 1870’s in England and its rival in anesthetic practice at this stage was cyclopropane. Since both were combustible and explosive, the arrival of halothane in the

INTRODUCTION xxi

Fig. 4: Joseph Clover

1960’s (and intravenous anesthesia, mentioned below) was welcomed by all operation theater personnel. Halothane was soon followed by methoxyflurane, enflurane and isoflurane. These agents possessed more useful clinical profiles and were not explosive. Further, precision vaporizers were available by this time, the anesthesia ‘machine’ had evolved, with breathing circuits. Desflurane and sevoflurane are the latest fluorinated anesthetics, introduced in the 1990’s. Intravenous anesthesia gained impetus only after the syringe and needle were invented by Alexander Wood in 1855 (Fig. 5). Chloral hydrate was used as a hypnotic in 1872. Numerous intravenous barbiturates were synthesized and tried in the late 1800’s and early 1900’s. However, only thiopentone sodium, reported simultaneously by Ralph Waters and J.S.Lundy in 1934 has stood the test of time. It is still the most widely used intravenous induction agent and remains the gold standard for any new non-narcotic anesthetic drug. Ketamine, synthesized in 1962 has specific uses and advantages. Di iso propyl phenol (Propofol)

Fig. 5: Alexander Wood and the syringe

synthesized in 1984 is rapidly gaining popularity as a reliable and short acting intravenous agent. The necessity for maintaining an unobstructed airway in war casualties undergoing facio-maxillary procedures was the impetus to the development of tracheal intubation. Sir Ivan Magill (Fig. 6) and Sir Stanley Rowbotham were both proficient in blind nasal intubations before the invention of the laryngoscope. Sir William Macewen, a Scottish neurosurgeon, is credited with the performance of the first endotracheal intubation in 1880. Sir Robert Macintosh (Fig. 7) was the other pioneer in airway management and the most commonly used laryngoscope is named after him. It was by trial and error that a variety of endotracheal equipment was evolved and has perfected to the present day; it is difficult to imagine that sick and injured

xxii A PREMIER OF ANESTHESIA

Fig. 6: Sir Ivan Magill

Fig. 8: August Bier and amputation under spinal anesthesia

Fig. 7: Sir Robert Macintosh

patients underwent surgery and anesthesia without protection of the airway just a century ago, compared to the availability of presentday gadgets like the fiberoptic laryngoscope and other sophisticated airway equipment. The credit for discovering the local anesthetic properties of cocaine and using it for ophthalmic anesthesia goes to Karl Koller in 1884. Subsequently Sir William Halstead, the renowned surgeon, used cocaine for nerve blocks and infiltration. Although August Karl Gustav Bier performed the first spinal anesthetic (Fig. 8) in 1898, it was to be nearly 35 years before lumbar epidural analgesia was demonstrated by Pages and Dogliotti in 1932.The advantages and safety of spinal and epidural anesthesia made these techniques very popular. The use of other regional anesthetic techniques like brachial plexus block and stellate ganglion block also became widespread, due to the development of less toxic drugs, improved knowledge of pharmacokinetics and availability of nerve stimulators and imaging techniques.

The advent of muscle relaxants into the realm of clinical anesthetic practice in 1942 heralded another milestone. Relaxants have not only facilitated tracheal intubation but also tremendously improved surgical access and facilitated prolonged ventilation especially in the ICU. Opiates, which had been out of favor due to their potential to cause respiratory depression, now made a comeback as means of controlled ventilation were available. Lundy’s concept of ‘balanced anesthesia’ introduced in the 1940’s consisted of administration of thiopentone, nitrous oxide, muscle relaxant and an opiate, (usually meperidine) and still finds favor with most anesthesiologists. After the 1970’s, synthetic opiates like fentanyl and sufentanil have become popular. Understanding of opiate receptors and availability of opiate antagonists have increased safety of opioid use. In the 150 years following the clinical demonstration of ether anesthesia, anesthesiology has developed by unprecedented leaps and bounds. The role of the anesthesiologist is not only to provide for pain-free surgery and postoperative recovery, but as a primary care giver in the perioperative period. Thus it is the anesthesiologist’s responsibility to (a) assess and evaluate the patient’s preoperative condition, especially with respect to comorbid illnesses, (b) to optimize the condition whenever possible and

INTRODUCTION

(c) to provide a continuum of intensive monitoring and care till physiological stability is achieved. Anesthesia care is also required beyond the confines of the operating theater in the cardiac catheterization laboratory, the lithotripsy room, CT scan and MRI suites, for electro-conclusive therapy and in the gastrointestinal endoscopy room, to name a few areas. The anesthesiologists’ skill in airway management, instituting invasive monitoring, working familiarity with advanced technology (blood gas analyzers, monitors, ventilators) and thorough knowledge of physiology, pharmacology, and cardio respiratory medicine, makes them a natural choice to manage ICUs. Pain clinics are another example of units serviced by anesthesiologists to evaluate and treat acute and chronic pain. Measures ranging from oral non-steroid anti-inflammatory drugs (NSAIDs) to interventional pain management involving complex procedures like radiofrequency lesioning of the spinal cord and surgical implantation of intrathecal morphine delivery systems are carried out in pain clinics. The teaching of cardiopulmonary resuscitation has also been the prerogative of anesthesiologists due to their constant association with the cardiopulmonary system, skill in intravenous access and airway management. They not only train post-graduates of the specialty but other members of the hospital staff and public. They are an integral part of the casualty (emergency) medical services and maintain check on equipment handled in its environs, and the emergency operation theater. This wide role of the anesthesiologist is unfortunately still not known to the public at large, who perceive them as some kind of evanescent semi skilled technicians who administer a sleeping drug to the patient and disappear. This concept is changing with the wide recognition and necessity of trained anesthesiologists all over the world. It would be no exaggeration to state that advances in surgery would not have been possible in the absence of trained anesthesia personnel familiar with

xxiii

Fig. 9: William Thomas Green Morton and his memorial

hemodynamic monitoring, airway management in routine and difficult situations, vascular access, use of intravenous fluids, respiratory critical care, and provision of analgesia. Quite justifiably, anesthesia has been quoted as “modern medicine’s greatest gift to humanity.” For those of you who have not had an opportunity to visit Morton’s memorial in Boston (Fig. 9) the famous insciption engraved on it is presented below: “Inventor and Revealer of Inhalation Anesthesia: Before Whom, in All Time, Surgery was Agony; By Whom, Pain in Surgery was Averted and Annulled; Since Whom, Science has Control of Pain.” Need we say anything more in praise of this subject? This textbook is designed to take undergraduate students on a ‘guided tour’ of the specialty of anesthesia. Its contents are aimed at teaching the basic principles, pharmacology, physiology, physics involved in anesthetic practice, as well as skills required to manage patients’ airway, knowledge of which will enrich them as future physicians no matter which specialty of medicine they choose to join; it will highlight how anesthesia has woven itself into virtually every specialty. Welcome to the world of anesthesia!

Intravenous Anesthetic Agents and Opioids Rajesh Tope

Properties of an ideal intravenous agent Induction agents  Barbiturates and thiopentone  Propofol  Ketamine Benzodiazepines  Diazepam  Midazolam  Flumazenil Opioid analgesics  Opiate receptors and endogenous opiates  Morphine, pethidine, fentanyl, remifentanil  Naloxone

The intravenous (IV) route is commonly used in adults for induction of anesthesia. It is rapid, comfortable, pleasant and predictable. With the availability of EMLA (eutectic mixture of local anesthetic) the IV route is becoming popular in children as well. IV agents like propofol can also be used to maintain anesthesia. Thiopentone, the first clinically useful intravenous anesthetic, was first used in clinical practice in 1934. This marked the beginning of modern anesthesia and use of the intravenous route for induction of anesthesia. Inhalational agents were generally used for maintenance.

The properties of an ideal intravenous anesthetic agent’s are: i. Should produce rapid, smooth induction within one arm-brain circulation time (< 30 seconds) ii. Should preferably have analgesic properties iii. Should not produce pain on injection; should be possible to use intramuscularly if needed iv. Should not be epileptogenic or raise intracranial pressure v. Should not cause myocardial depression or irritability vi. Should not cumulate on infusion vii. Metabolism should be independent of renal/hepatic function; metabolites should be inactive and non-toxic viii. Should be non-teratogenic. Although no currently used agent fulfils all these criteria, they are useful yardsticks to assess new agents. This chapter will discuss thiopentone, ketamine and propofol which are the most widely used intravenous anesthetic agents, in detail. Passing reference will be made to other agents mainly to highlight the advantages these three have over the others. The second part of this chapter will deal with the commonly used opioids in the perioperative period.

4 A PRIMER OF ANESTHESIA Table 1.1: Effect of substitution at carbon atoms in position 1, 2 and x R1

R2

R3

X

Thiopentone

Ethyl

1-methyl-butyl

H

S

Rapid acting, fairly prompt recovery

Pentobarbitone

Ethyl

1-methyl-butyl

H

O

Prolonged action

Methohexitone

CH2CH=CH2 CH(CH3)C=CC2H5

CH3

O

Rapid action and recovery, excitatory phenomena

Phenobarbitone

Ethyl

H

O

Prolonged action, anticonvulsive properties

Phenyl

Barbiturates Different barbiturates were used as sedatives in the 1920s. Since their actions were unpredictable, research was carried out making substitutions on the barbiturate ring (Fig. 1.2a) leading to compounds with known and/or desirable properties. Of these, sodium thiopentone emerged as the compound with the most acceptable properties. Table 1.1 summarises the effect of substitution. Sodium Thiopentone (Figs 1.1 and 1.2b) It is a yellow colored powder with a faint garliclike smell, available in vials containing 500 mg or 1g. The vial contains six parts of sodium carbonate to 100 parts of barbiturate (by weight) in an atmosphere of nitrogen. Sodium carbonate produces free hydroxyl ions in solution, and is added to prevent the precipitation of insoluble free acid by atmospheric CO2. Thiopentone is dissolved in saline/distilled water to make a 25 mg/ml solution. This is a racemic mixture containing two stereoisomers and has a pH of 10.5–10.8. The solution remains stable in room temperature for up to two weeks, but should be discarded earlier if it appears cloudy. Because of strong alkalinity the solution is bacteriostatic, and also physically incompatible with acidic drugs normally administered as sulphates, chlorides or hydrochlorides. Actions on the Central Nervous System Thiopentone produces anesthesia in less than 30 seconds after IV administration. This is due

Fig. 1.1: Vial of 500 mg thiopentone

Fig. 1.2a: The barbituric acid ring

Fig. 1.2b: Structure of thiopentone

to (i) high vascularity of the brain and (ii) the high lipid solubility of thiopentone. It is a poor analgesic; in fact it has an ‘antanalgesic’ effect, due to which a patient with a painful condition may have an increased perception of pain and may become very restless in the recovery

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

period. It reduces intracranial pressure (ICP) due to cerebral vasoconstriction which leads to a reduction in cerebral blood flow (CBF). Cerebral metabolic rate (CMRO 2 ) is also reduced. Both these properties have made thiopentone the anesthetic agent of choice in patients with elevated ICP (head injury, intracranial tumor) and as an agent for cerebral protection (‘barbiturate coma’). It is a potent anticonvulsant. Consciousness is regained in 5–10 minutes after a single IV dose. Actions on the Cardiovascular System Mean arterial blood pressure falls with administration of thiopentone due to a dosedependent reduction in vascular tone and some myocardial depression especially with high doses. These effects are of concern in all patients with low, fixed cardiac output states. This group includes hypovolemic patients (traumatic shock), patients with valvular stenoses (mitral, aortic), patients on vasodilators or beta-blockers and patients with ischemic heart disease, constrictive pericarditis or cardiac tamponade. Hypotension can be profound, refractory to treatment and can result in mortality. In fact, thiopentone had fallen out of favor in 1934 shortly after its introduction owing to the large number of war casualties resulting after its use on soldiers with hypovolemic shock in World War II. It was then known as ‘the ideal agent for euthanasia’. Effects on the Respiratory System There is often a deep breath or yawn followed by a brief period of apnea. Ventilatory drive is reduced, leading to a fall in both the respiratory rate and tidal volume. Bronchial muscle tone increases and occasionally bronchospasm is induced. Laryngospasm may be induced if food or secretions enter the larynx, or by surgical stimulation under light anesthesia. MISCELLANEOUS EFFECTS Intraocular pressure is reduced. Conjunctival, corneal, and eyelash reflexes are abolished.

5

Abolition of the eyelash reflex is used as a sign of completion of anesthetic induction. Skeletal muscle tone is reduced in high doses; however this is inadequate for surgical purposes. In normal doses it has little effect on the uterine muscle. Although it crosses the placenta, the fetal drug concentration is lower than the maternal blood levels. Both hepatic and renal function are transiently depressed. Thiopentone may induce various cytochrome P-450 isoenzymes; in chronic liver disease the effects are prolonged with delayed recovery. Pharmacokinetics Blood concentration drops rapidly after intravenous injection. 75-85% drug is albumin bound. In malnutrition, chronic renal failure and other conditions with hypoalbuminemia, less drug is protein-bound, hence more free drug is available. Action of the drug is dependent on the free plasma concentration of drug. Thiopentone rapidly diffuses into the CNS because of its lipid solubility and high un-ionised fraction. Consciousness returns when the brain concentration falls as a result of re-distribution in the body. At this time nearly all the drug is still present in the body. Thiopentone is predominantly metabolised in the liver. Metabolism is a linear process when single doses are concerned (10–15% of the remaining drug is metabolised each hour). Hence up to 30% of drug is still in the body after 4–6 hours. The metabolites are thiopental carboxylic acid (inactive), hydroxythiopental (inactive) and pentobarbital (active, with halflife of 20–50 hours). This leads to a hangover effect. With thiopentone infusions the metabolism follows non-linear, or zero-order kinetics and significant amounts are present in the plasma, leading to time prolonged recovery. Dosage and Administration Thiopentone is administered as a 2.5% (25 mg/ml) solution intravenously. 1-2 ml should be injected initially to check that the patient does not have pain at the site of

6 A PRIMER OF ANESTHESIA

injection. The dose in healthy adults is 4–5 mg/ kg administered over 15 seconds. Consciousness will be lost in 30 seconds; if the eyelash reflex is not lost then a further 50–100 mg should be given. Children require about 6 mg/kg, and elderly patients 2.5–3 mg/kg. In patients where the cardiovascular system is depressed (e.g. as in hypovolemic shock) as little as 50 mg may be required. Adverse Effects and Problems with Thiopentone 1. Hypotension: This is more likely to happen if excessive doses are given or if a ‘normal’ dose is given to a hypovolemic patient or one with a low fixed cardiac output. Risk of hypotension is reduced if the drug is injected slowly. Thiopentone should not be injected in the sitting position. 2. Respiratory depression: The risk is increased if opioids have also been administered. Thiopentone should be injected only where facilities for artificial ventilation are available. 3. Tissue necrosis: Perivenous injection may lead to local tissue necrosis. If perivenous injection occurs the needle should be left behind and hyaluronidase injected. 4. Intra-arterial injection: This dreaded complication usually occurs when thiopentone is in advertently injected directly from a syringe into the brachial artery, an aberrant ulnar artery in the cubital fossa, or an aberrant radial artery around the wrist; in each case the artery is mistaken for a vein. The patient usually complains of intense burning pain. This is a strong indication for stopping the injection immediately. The forearm and hand may be blanched and there may be skin blisters. Intense vasoconstriction may lead to ischemia or gangrene in the forearm, hand or fingers. Ischemia results due to (i) physical obstruction of the arteriolar lumen by crystals of thiopentone which precipitate in the

relatively acidic pH and (ii) Vasospasm and thrombosis initiated by intimal damage, local release of noradrenaline and ATP from damaged red cells and platelets. Treatment involves leaving the needle in place, injecting 50 mg lignocaine (5 ml of 1% solution), a vasodilator like papaverine (10–20 ml of 0.4% solution), and performing a stellate ganglion or brachial plexus block. Intravenous heparin should be started and nonurgent surgery postponed. 5. Laryngeal spasm: It is likely to occur if a painful stimulus is administered with in adequate analgesia under the effect of thiopentone, e.g. anal dilatation. 6. Bronchospasm: May occur in asthmatic patients. 7. Allergic reactions: Severe anaphylactic reactions may occur in 1 in 14000 to 20000 administrations. Indications -

For induction of anesthesia. Maintenance of anesthesia for very short procedures. Treatment of status epilepticus. To reduce intracranial pressure.

Absolute Contraindications -

-

Confirmed or suspected upper airway obstruction, e.g. epiglottitis; large oral, pharyngeal or laryngeal tumors. Porphyria—barbiturates may precipitate severe cardiovascular collapse, or lower motor neurone type of paralysis in patients with acute intermittent porphyria by inducing the enzyme ALA synthetase. Previous hypersensitivity to a barbiturate or sulpha drugs.

Precautions -

Cardiovascular disease: Patients with hypovolemia, mitral or aortic valvular stenosis, or constrictive pericarditis are very sensitive to thiopentone. However if thiopentone is

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

-

-

-

injected with extreme caution it is no more hazardous than any other IV anesthetic agent. Severe hepatic or renal disease: Thiopentone may be injected very slowly as the volume of distribution is large, and the protein binding is low. Obstetrics: Excessive dose may lead to respiratory or cardiac depression in the fetus. Outpatient anesthesia: Clear-headed recovery takes time. Slow elimination from the body may result in drowsiness for 24– 36 hours. Thiopentone is therefore not recommended for brief day care procedures where the patient is likely to be discharged in a few hours. Other conditions: Adrenocortical insufficiency, hypothyroidism, asthma: if alternatives like ketamine are available, thiopentone should be avoided.

Propofol (Fig. 1.3) This molecule was invented in 1980 and has been commercially available since 1986. It has achieved great popularity because of its recovery characteristics and its antiemetic effect. In many Western countries and in better funded hospitals in India it has nearly replaced thiopentone as an induction agent. It is currently about four times more expensive than thiopentone in India.

7

hydroxide. The pH of this solution is 6–8.5. The available preparation is a 1% (10 mg/kg) solution in a 20 ml ampoule or vial. Other presentations include 2% solution and 50 ml and 100 ml vials which are suitable for infusion. Pain on injection is a bothersome side effect and can be ameliorated by (i) IV fentanyl 50–100 μg, (ii) premixing the propofol with 1–2 ml of preservative-free lidocaine. Pharmacology

Central Nervous System Anesthesia is induced in 20–40 seconds after intravenous administration. This is slower than with thiopentone. Cerebral blood flow, cerebral metabolic rate, intracranial pressure and intraocular pressure are all reduced. Recovery of consciousness is rapid with minimal ‘hangover’ effect.

Cardiovascular System Propofol reduces arterial pressure to a greater degree than thiopentone. This is mostly due to vasodilatation. However propofol does have a slight negative inotropic effect resulting in a reduction in heart rate which may contribute to fall in cardiac output. In rare cases there may be severe bradycardia and asystole. A vagolytic like atropine or glycopyrrolate must always be drawn up and kept ready for administration.

Physical Properties

Respiratory System

Propofol is extremely lipid soluble, and insoluble in water. The commercially available solution is a 1% milky emulsion made with soyabean oil, purified egg phosphatide, glycerol and sodium

Apnea is common after induction and is of longer duration than thiopentone. There is no effect on the bronchial muscle tone. Laryngeal reflexes are suppressed and laryngospasm is uncommon. The jaw is relaxed. This property is very useful for insertion of a laryngeal mask airway without using muscle relaxants.

Skeletal Muscle, Gastrointestinal System, Uterus and Placenta Fig. 1.3: Structure of propofol

Skeletal muscle tone is reduced.

8 A PRIMER OF ANESTHESIA

Propofol has no effect on gastrointestinal motility. Incidence of postoperative nausea and vomiting is significantly low after use of propofol. Propofol has no effect on the gravid uterine muscle tone. It crosses the placenta. Its safety on the fetus and neonate is not established. Manufacturers do not recommend its use in obstetric practice, in neonates, and during lactation.

Hepatorenal Effects Renal function is transiently depressed but to a lower degree than thiopentone. Hepatic blood flow is reduced in proportion to drop in the arterial blood pressure, however liver function tests are not deranged even after 24 hours of propofol infusion. Pharmacokinetics Propofol is distributed rapidly after an intravenous dose. Blood concentration drops exponentially. It undergoes hepatic glucuronidation and 88% is excreted in the urine. Clearance is much higher than hepatic blood flow, suggesting that the drug is metabolised outside the liver as well. Unlike thiopentone there is no cumulative effect with repeated doses of propofol. Its elimination from the body is unaffected even after a continuous infusion for a few days.

Adverse Effects

Cardiovascular Depression Unless propofol is given very slowly the hypotension produced is far more than with thiopentone.

Pain on Injection About 40% patients complain of pain on injection. The incidence is reduced if a larger vein is used. Injection of 10 mg lignocaine just before propofol or adding lignocaine to propofol reduces this incidence. Accidental extravasation or intra-arterial injection does not cause adverse reactions.

Allergic Reactions The incidence is probably the same as with thiopentone. The incidence was high with earlier preparations (‘Diprivan’) where ‘cremophor EL’ was used as solvent and vehicle. Indications

Induction of Anesthesia At centers where cost is not a major consideration propofol has replaced thiopentone as the routine drug for IV induction. It is however specially indicated for day care anesthesia where recovery is quicker than with thiopentone.

Sedation During Surgery Administration In healthy unpremedicated adults where concomitant narcotic is not given, 1.5–2.5 mg/kg is adequate for anesthetic induction. The elderly are very sensitive to propofol. 1–1.5 mg/kg is usually adequate. In children 3–6 mg/kg is required. Propofol is not recommended in children less than a month of age. For sedation a dose of 1.5–4.5 mg/kg/hour is used. For total intravenous anesthesia doses between 6–10 mg/ kg/hour are used.

Propofol is used for sedation during regional anesthesia and during endoscopy. This must be performed with full monitoring, with facility for ventilation available, and under supervision of an anesthesiologist.

Total Intravenous Anesthesia Propofol is currently the best drug for this technique amongst the available intravenous anesthetics. Cumulation is significantly less than any other anesthetic.

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

Sedation in ICU Propofol is used for prolonged sedation of adult patients in the ICU. Its use in children for sedation in ICU is not recommended because a number of reports with adverse outcomes. Absolute Contraindications 1. Upper airway obstruction 2. Known hypersensitivity to propofol 3. Prolonged sedation in children in ICU. Precautions These are similar to thiopentone. Use in neonates and in obstetric anesthesia is not recommended. However, propofol is safe in porphyrias. Ketamine Hydrochloride Ketamine (Fig. 1.4) is a phencyclidine derivative introduced in 1965. The unique property of this drug is that, unlike other intravenous anesthetics it produces dissociative anesthesia rather than generalised depression of the CNS. Pharmacology

Central Nervous System After intravenous injection it produces anesthesia in 30–60 seconds. The anesthetic effect lasts 15–25 minutes. It is a potent analgesic at subanesthetic doses. Amnesia lasts well into the recovery period after consciousness is regained. Emergence is associated with restlessness, agitation, and disorientation in some patients. Vivid nightmares and hallucinations may occur

Fig. 1.4: Structure of ketamine

9

up to 24 hours after the anesthetic. This emergence delirium is reduced if the patient is not stimulated in the recovery period, and if concomitant narcotics or benzodiazepines are given. EEG changes are unlike those seen with other anesthetics. There is a predominant theta activity. Cerebral metabolic rate, cerebral blood flow, and intracranial pressure are increased. This means that ketamine is to be avoided in patients who have elevated ICP.

Cardiovascular System Arterial pressure, heart rate and pulmonary vascular resistance are increased by 20–40%. The myocardial oxygen consumption is increased. Intrinsically ketamine is a direct myocardial depressant. The increase in blood pressure is because of its sympathetic systemstimulating action.

Respiratory System There may be transient apnea. However after return of respiration the minute ventilation is maintained or increased. Pharyngeal and laryngeal reflexes tend to be better preserved than with other anesthetics. However all precautions must be taken to protect the airway and prevent aspiration. Tracheal intubation should not be attempted under ketamine anesthesia. Bronchodilation is an advantage, but this effect may be offset by bronchorrhea (excessive bronchial secretions).

Other Systems • Skeletal muscle tone is increased. Ketamine cannot be used as sole anesthetic for surgery requiring muscle relaxation. • Ketamine crosses the placenta and is therefore not ideal for obstetric anesthesia. • Intraocular pressure increases. The eyeball is not akinetic and nystagmus may be observed. Ketamine is therefore not ideal for ocular surgery.

10 A PRIMER OF ANESTHESIA

Phar macoki netics Pharmacoki macokinetics

Difficult Locations

The plasma concentration falls as the drug is distributed in the body. This reduction is not as rapid as with other intravenous anesthetic agents. It is metabolised in the liver to norketamine, conjugated and excreted.

To provide analgesia to trauma victims for onsite debridement, fracture reduction or prior to moving. Analgesia for trapped or injured victims at the site of an accident can be provided with IM ketamine.

Administration

Treatment of Postoperative or Intractable Pain

Ketamine is available as 10 mg/ml aqueous solution. The average intravenous induction dose is 2 mg/kg. Additional doses of 1–1.5 mg/kg are required every 5–10 minutes, if anesthesia is being maintained with ketamine. The intramuscular (IM) dose is 8–10 mg/kg.

Adverse Effects • Emergence delirium and hallucinations. • Hypertension and tachycardia. This would be harmful in patients with coronary artery disease. • Delayed recovery. • Increased intracranial pressure. Indications

Patient in Shock for Emergency Surgery (e.g. Splenic/Hepatic/Thoracic Injury) Ketamine is preferred over thiopentone or propofol. However, arterial pressure may still decrease if hypovolemia is present; volume replacement should be continued.

Pediatric Anesthesia The drug is suitable and very useful for children undergoing short procedures like cardiac catheterization, examination under anesthesia and radiotherapy.

Ketamine has been administered through subcutaneous, extradural and intrathecal routes for this purpose.

Change of Wound Dressing Sedation and analgesia are frequently required for burns dressing in the ward. Ketamine is useful for this purpose.

Developing Countries Ketamine is considered safer than other IV anesthetics because of absence of cardiovascular and respiratory depression. It is still extensively used in developing countries due to this safety factor especially where anesthesia sevices are rudimentary. Absolute Contraindications Upper airway obstruction—although the airway is better maintained than other anesthetics, airway control is not guaranteed. - Raised intracranial pressure. - Raised intraocular pressure. Precautions -

The Poor-risk Elderly Patient Ketamine is preferable to other induction agents for this patient sub-group when presenting for surgery.

-

Cardiovascular disease: Ketamine is unsuitable for patients with ischemic heart disease and hypertension. Day care anesthesia: Because of delayed recovery ketamine is not ideal in this situation. Open eye injury: It is prudent to avoid ketamine as there is a risk of increase in IOP leading to ocular damage.

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

-

Psychiatric conditions: Emergence phenomena may be confused with psychiatric illness.

Benzodiazepines Benzodiazepines are primarily used as hypnotics and anxiolytics. The newer, shorter acting analogues are used for sedation and anesthesia. Pharmacology

Mechanism of Action Benzodiazepines act by binding to the benzodiazepine receptor. This receptor is part of the GABA (gamma amino butyric acid) complex on the cell membrane. Binding of the benzodiazepine to the receptor leads to influx of chloride ions into the cell leading to hyper polarisation, which makes the neurone resistant to excitation. The benzodiazepine receptor apart from an agonist also binds inverse agonist. An example of inverse agonist binding to the same GABA site on neurones is R015-4513, which produces anxiety and cerebral excitement. Both agonist and inverse agonist are antagonised by flumazenil, a benzodiazepine antagonist.

Central Nervous System Sedation and anesthesia: dose-dependent depression of cerebral activity occurs. Suppression of neuronal activity between the limbic system and hypothalamus modifies emotional responsiveness and behavior. Reduction in alertness and arousal reactions is seen due to depression of interaction between the limbic and reticular activating systems. As more receptors are blocked the patient progresses from a state of sedation to general anesthesia. Amnesia: Anterograde amnesia is seen with all benzodiazepines. Retrograde amnesia is occasionally seen. Anticonvulsant action: All benzodiazepines have an anticonvulsive action probably due to inhibition of the amygdaloid nuclei.

11

Anxiolysis: In smaller doses these drugs reduce anxiety. They are therefore popular as premedicants.

Muscle Relaxation Benzodiazepines produce mild reduction in muscle tone. This is not due to effect on the neuromuscular tone but due to suppression of polysynaptic reflexes in the spinal cord. Benzodiazepines are also considered as centrally acting muscle relaxants.

Respiratory System Benzodiazepines produce depression of ventilation. Synergistic effect is observed with narcotics. In patients with severe respiratory disease benzodiazepines can precipitate respiratory failure.

Cardiovascular System Benzodiazepines reduce blood pressure by reducing systemic vascular resistance. In patients with hypovolemia, hypotension can be severe.

Pharmacokinetics Benzodiazepines are non-polar and highly lipid soluble, hence well absorbed after oral administration. This makes it very convenient to administer them as premedicant drugs. Most are extensively protein-bound; only the unbound fraction can cross the blood-brain barrier or diffuse across the placenta. They are almost entirely metabolized and small fractions may be excreted unchanged. Diazepam is converted to several active metabolites (Fig. 1.5). Midazolam has a high intrinsic hepatic clearance. After intravenous injection the action of midazolam is terminated by redistribution. It undergoes extensive hepatic metabolism and the water soluble metabolites are excreted by the kidneys. Midazolam (Fig. 1.6) It is a water soluble benzodiazepine with an imidazole ring. On intravenous injection,

12 A PRIMER OF ANESTHESIA

Fig. 1.5: Metabolites of diazepam

Fig. 1.6: Structure of midazolam

sedation or anesthesia, depending on the dose given, starts in 90 seconds, and the peak effect occurs in 2–3 minutes. Its elimination half life is two hours. It is available as 1 or 5 mg/ml solution. Dosage When given on its own the anesthetic dose is 50–150 micrograms/kg. Midazolam has a synergistic effect when given with narcotics or other induction agents like propofol. The oral dose for premedication is 0.5 mg/kg. Midazolam has also been used through the nasal route (0.3 mg/kg) in children, but this route is not popular. Diazepam (Fig. 1.7) This commonly used benzodiazepine is insoluble in water and is solubilized in buffered propylene glycol and ethanol to a pH of 6.4–6.9. This

Fig. 1.7: Diazepam (valium)

makes it very painful for intramuscular injection and there is a high incidence of thrombophlebitis on IV administration. It is available in amber-colored ampoules containing 5 mg/ml. There is another formulation prepared in soya bean oil emulsion (‘Diazemuls’) which is nonirritant to veins and tissues. The main metabolite is the active N-desmethyldiazepam. When diazepam is used chronically in late pregnancy or labor, nordiazepam can accumulate in fetal tissues and produce the ‘floppy’ baby syndrome. The neonate is hypothermic, hypotonic and depressed. Flumazenil It is a benzodiazepine antagonist. Flumazenil has receptor affinity and minimal intrinsic effect. Its half life is 1 hour. It is used to diagnose benzodiazepine over dosage. It is also used to reverse the residual effect of benzodiazepines after use for sedation or anesthesia. The dose for this purpose is 0.1–1 mg. Higher doses up to 3 mg may be given, if needed, as in re-sedation. Side Effects and Contraindications of Flumazenil

Re-sedation Re-sedation could occur because of the short half life of the drug. Thus flumazenil may need to be repeated; patients suspected of midazolam overdose should be kept under observation till recovery is complete.

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

13

Opioids can be classified as (a) naturally occurring-morphine, codeine, and papaverine; or (b) semi synthetic-buprenorphine, hydromorphone; or (c) synthetic-pethidine, fentanyl, sufentanil, alfentanil, and remifentanil.

μ receptors are located in both the brain and spinal cord. The highest concentrations are found in the periaqueductal gray (brain) and substantia gelatinosa (spinal cord). μ1 and k3 are related to supraspinal analgesia. κ receptors are found in the caudate and dorsal nuclei. δ receptors are located mainly at spinal level. Opioid receptors are also found on the nerve terminals of the afferent neurone. When an agonist binds to a receptor the following events occur: • Inhibition of calcium channels at the presynaptic terminal of the afferent nociceptor neurone prevents calcium from entering these cells. Calcium entry in the afferent nociceptor neurones leads to release of excitatory neurotransmitters, and depolarisation. • Opioids increase potassium efflux at the post synaptic terminal, leading to hyperpolarization. In this state a higher voltage change is required to depolarize the cell. • Activation of central descending inhibition. This occurs in the periaqueductal grey matter.

Opiate Receptors

Agonists, Antagonists, and Partial Antagonists

Opioids act on specific receptors. These receptors were discovered in 1973. These were named μ, κ, σ and δ. Since then it has been found that σ is not an opioid receptor. There are subtypes of each of these receptors (i.e. μ1, μ2, μ3 and 3k subtypes). It is suggested that μ1 is an analgesic receptor and μ2 causes respiratory depression. Morphine induced analgesia is a typical example of μ1 stimulation. Another agonist and its receptor, named nociceptin, were discovered in 1995.

When a drug or an endogenous substance (a ligand) binds to a receptor and produces its full physiological effect it is called an agonist (e.g. morphine). When a ligand binds to the receptor and does not produce any physiological effect and blocks the binding of an agonist it is called an antagonist (e.g. naloxone). When a ligand binds to the receptor but increasing doses do not produce maximum physiological effect it is called a partial antagonist (e.g. buprenorphine).

Convulsions In epileptic patients there is a risk of seizures, especially when benzodiazepines have been used as anticonvulsants.

Intracranial Pressure Increase In patients with head injury the intracranial pressure may suddenly increase if flumazenil is given. OPIOID (NARCOTIC) ANALGESICS Opioids are conventionally looked upon as potent pain killers. These drugs depress the central nervous system, reduce the MAC of inhaled anesthetics, and in very high doses (40–60 times the usual dose) may produce complete anesthesia on their own. Classification

Actions

Endogenous Opioid Agonists

Analgesia

Encephalin, β-endorphin, and dynorphin are the agonists that exist in the body for receptors δ, μ, and κ, receptors respectively.

μ receptor agonists are more effective in producing analgesia than κ receptor agonists like pentazocine.

Mechanism and Sites of Action

Respiratory System

The opioid receptor is part of the G-protein inhibitory complex on the cell membrane.

Opioids depress ventilation. The hypoxic drive is reduced, and the sensitivity to carbon dioxide

14 A PRIMER OF ANESTHESIA

is also reduced. Typically the respiratory rate is reduced more than the tidal volume. Opioids depress the tone of the muscles that keep the upper airway patent. As a result of this the airway is likely to get obstructed.

Cardiovascular System If PaCO2 is maintained opioids do not have any direct effect on the cardiovascular system. The vasomotor centre is not depressed. Hypotension seen with morphine use is an indirect effect due to histamine release.

Nausea and Vomiting All opioids cause nausea and vomiting by stimulating the chemoreceptor trigger zone.

Cough Suppression Antitussive action is independent of analgesic effect. Some opioids like codeine have significant antitussive effect but much less analgesic activity.

Gastrointestinal Tract Opioids reduce motility and increase the tone of the gastrointestinal tract. Morphine increases biliary pressure.

The IM dose for premedication is 0.15– 0.3 mg/kg. An antiemetic like promethazine needs to be administered concomitantly to reduce nausea and vomiting. The normal IV analgesic dose is 0.1–0.3 mg/kg. Morphine can be used as infusion for postoperative pain relief in a dose of 10–40 μg/kg/hour, titrated to requirement. Pethidine (Fig. 1.9) This synthetic opioid also has atropine like effects. It has lesser effects on the biliary and renal tract than morphine. It is also shorter acting than morphine. Pethidine is metabolised to norpethidine. Norpethidine has stimulatory effects on the central nervous system. Monoamine oxidase inhibitors (MAOIs) increase the metabolism to norpethidine. As a result of this if pethidine is given to patients on MAOIs it may cause convulsions, hyperthermia, and death. The IM dose of pethidine for premedication is 1–1.5 mg/kg, and like morphine an antiemetic agent like promethazine (0.5 mg/kg) administered concomitantly is useful. The commonly used IV dose is 0.5–1 mg/kg.

Other Effects -

Miosis Suppression of endocrine response to pain. These hormones include adrenaline, noradrenaline, cortisone, and glucagon. Pruritus Hallucinations Dependence and tolerance

Fig. 1.8: Structure of morphine

Morphine (Fig. 1.8) Morphine has all the classic opioid effects mentioned above. It is extensively used as analgesic intraoperatively and in the postoperative period.

Fig. 1.9: Structure of pethidine

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

15

Su fentanil Sufentanil Sufentanil is 10-15 times as potent as fentanyl, and has a slightly shorter duration of action. It is less likely to accumulate in the body than fentanyl. The usual dose is 0.1–0.5 μg/kg. It has recently been licensed for use in India. Fig. 1.10: Structure of fentanyl

Remifentanil Fentanyl (Fig. 1.10) This synthetic opioid is very lipid soluble and has a more rapid onset of action than morphine. Its duration of action is much shorter than morphine while the elimination half life is like morphine. The short effect is entirely due to redistribution. It is about 100 times more potent than morphine. The normal IV dose is 2–4 μg/kg. It has been used as the sole anesthetic in patients where cardiovascular stability is required. The dose required for this use is 40-70 μg/ kg. Fentanyl is used as a transdermal controlled release patch for use in patients with chronic pain. Fentanyl “lollipops” are available for transmucosal (oral) premedication in children. One of the alarming side effects with large doses of IV fentanyl is chest wall rigidity which makes ventilation impossible unless a muscle relaxant is administered. A few patients cough after rapid IV administration. Alfentanil Alfentanil has a rapid onset of action, and a shorter duration of action than fentanyl. It is ten times as potent as morphine and one-fourth to one-tenth as fentanyl. Its elimination half life is 84–90 minutes, which is much lesser than fentanyl. Cumulation is much less of a problem with alfentanil and unlike fentanyl it is safer to use as continuous infusion. Most of its other effects are like fentanyl. The IV dose of alfentanil is 5–10 μg/kg, with supplemental doses of 3–5 μg/kg.

It is an ultra short-acting μ receptor agonist with no cumulative effect. It is given as an infusion during operation. It is metabolised by blood and tissue esterases. Remifentanil is used in a dose of 0.5-1 μg/kg as a bolus before laryngoscopy, and continued as an infusion of 0.25–0.5 μg/ kg/min. Within 3–5 minutes after stopping the infusion the effect of remifentanil is terminated no matter how long the infusion has been running. It is thus well suited for outpatient use. It is not yet licensed for use in India. Tramadol It is a predominantly μ receptor agonist with a weak action. It is less likely to cause respiratory depression than morphine. The side effects include nausea, vomiting, dry mouth, and urinary retention. It interacts like pethidine with MAOIs. Pentazocine It is a σ and κ receptor agonist and has antagonist/partial agonist effect on the μ receptor. It is largely not used in the West but still commonly available and used in India. It has a ceiling analgesic effect of 60 mg in an adult. It can cause hallucinations. Naloxone It is a short acting opioid antagonist. Because of its short duration of action the reversal of respiratory depression induced by naloxone may be short lived. Hence patients must be monitored for some time after naloxone is used. Intense pain may occur as the analgesic effect

16 A PRIMER OF ANESTHESIA

of the originally given opioid is terminated. This may result in tachycardia, hypertension or even myocardial ischemia. In conclusion, Intravenous anesthetic agents, sedatives and narcotics are an essential part of modern anesthetic practice. They have contributed tremendously to patient comfort and safety. STATE WHETHER TRUE (T) OR FALSE (F) 1. An ideal intravenous anesthetic a. Should cause rapid induction of anesthesia b. Should have cumulative effect c. Should not cause pain when injected d. Should not cause muscle relaxation e. Should not cause respiratory depression

e. Methyl paraben is added as a bacteriostatic 5. Thiopentone sodium a. Produces anesthesia within 30 seconds of injection b. Has excellent analgesic property c. Is very lipid soluble d. Reduces the CMRO2 e. Reduces intracranial pressure when ventilation is maintained 6. Thiopentone sodium should be used very carefully in patients with a. Epilepsy b. Constrictive pericarditis c. Significant mitral stenosis d. Significant aortic stenosis e. Shock

2. Regarding intravenous anesthetics a. Upper airway obstruction is an absolute contraindication for their use b. Previous known anaphylactic reaction is a relative contraindication c. All are contraindicated in porphyrias d. Are preferred over inhalation anesthetics for induction e. All can be used as continuous infusion

7. Thiopentone sodium a. Is a respiratory stimulant b. May cause laryngeal spasm if patient stimulated in light planes of anesthesia c. Is a uterine dilator d. Infusions lead to significant cumulation and prolonged recovery e. Un-noticed inadvertent intra-arterial injections may cause or lead to ischemia of the arm or fingers

3. Barbiturates a. Were the most commonly used intravenous anesthetics until the last 15 years b. Methyl barbiturates like methohexidone may cause excitation during induction c. All are antiepileptic d. All have very quick induction and slow recovery properties e. Have been used since 1820s

8. Propofol a. Is available as powder to be dissolved in water b. Usually causes pain on injection c. Causes hangover d. Has anti-emetic property e. Apnea is commoner than with thiopentone

4. Thiopentone sodium a. Is available as white emulsion b. Is packed in glass vials with nitrogen to prevent oxidation c. Sodium carbonate is added to keep solution alkaline at pH 10.5-10.8 d. Is commonly injected in concentration of 2.5%

9. Propofol a. Is suited for infusions b. Has no effect on gravid uterus muscle tone c. Is used extensively in obstetric anesthesia d. Dose in geriatrics is significantly lower than young adults e. May cause significant hypotension

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

10. Ketamine a. May cause hallucinations b. Decreases intracranial pressure c. More likely to maintain respiration than other anesthetics d. Causes severe hypotension e. Less likely to cause cumulation than thiopentone 11. Midazolam a. Causes sedation by chloride ion influx in the cell b. Is a short acting anesthetic c. May cause anterograde amnesia in sedative doses d. Can be used for premedication e. Is hallucinogenic

17

12. Opiates a. Cause μ receptor stimulation that leads to respiratory depression b. Pethidine is extracted from poppy seeds c. Cause nausea and vomiting d. May increase intracranial pressure if ventilation is not controlled e. μ receptor is more effective in causing analgesia than kappa receptor Answers 1. 4. 7. 10.

TFTFT FTTTF FTFTT TFTFT

2. 5. 8. 11.

TFFTF TFTTT FTFTT TFTTF

3. 6. 9. 12.

TTFFF FTTTT TTFTT TFTTT

Inhalational Anesthetic Agents Rajesh Tope

       

Physical principles- MAC, saturated vapor pressure Pharmacokinetics- uptake Pharmacodynamics-Theories of anesthetic action Properties of an ideal anesthetic agent Systemic effects of inhalational agentsCVS, CNS, Induction characteristics Individual Inhalational Agents Diethyl ether-including stages of ether anesthesia Nitrous oxide

The ‘inhalational route’, which refers to the respiratory passages beginning at the nose and mouth, and ending at the alveoli, is nearly exclusively used by anesthetists. Exceptions are respiratory physicians, who may use inhaled steroids and bronchodilators. The identity of the anesthesiologist as the “gas man” originates from the use of this route for administration of anesthesia. Most adults prefer the intravenous route of induction of anesthesia as it is rapid and pleasant. However, inhalational anesthetics are useful for (i) anesthetic induction in children, who dread needles, (ii) patients where controlled anesthetic induction is required, as in airway obstruction, and (iii) maintenance of anesthesia. The main advantages of inhalational agents are ease of administration and titrability.

PO TENCY OF INHALATIONAL POTENCY ANESTHETIC AGENTS Just as potency of oral or intravenous drugs is measured in milligrams (or micrograms), potency of volatile anesthetics is associated with the term ‘MAC’ (minimum alveolar concentration). Minimum Alveolar Concentration MAC is the alveolar concentration (in volume%) of an anesthetic at 1 atmospheric pressure that prevents movement in 50% of a population in response to a standard stimulus. Although the partial pressure (in mm Hg or kPa) of the anesthetic appears to be a better way of expressing potency (than volume%), by convention MAC is expressed as volume%. Dose-response Curve By definition, 1 MAC of an anesthetic is equipotent to 1 MAC of another anesthetic. At clinically used concentrations MAC is approximately additive. Hence 0.5 MAC of one anesthetic administered with 0.5 MAC of another will produce an effect approximately equal to 1 MAC. Though MAC only indicates absence of response to surgical stimulus in 50% population, an increase of 10-15% in the concentration

INHALATIONAL ANESTHETIC AGENTS

above MAC (or 1.3 MAC) will ensure absence of response in > 95% of the population (indicating that most patients will be anesthetised). This is because the dose response curve is fairly steep. Unlike most other drugs used in medicine, inhalational anesthetic agents have physical properties that determine their pharmacological properties. We will briefly look at some basic physical principles and definitions to make physical properties more understandable. PHYSICAL PRINCIPLES Gases exist as vapor above their critical temperature. Gases can be liquefied by pressure only below their critical temperature. Gases follow the Universal Gas Law (PV = nRT, where P, V and T are the pressure, volume and temperature respectively and n the number of moles of gas). The pressure at the critical temperature is critical pressure. The critical temperature of nitrous oxide is -37°C, indicating that below this temperature it is possible to store nitrous oxide as a liquid under pressure. Saturated Vapour Pressure In an enclosed system where there is a liquid at equilibrium the number of molecules of liquid that evaporate to turn into vapor are equal to the number that turn back into liquid. The pressure the vapor exerts is termed saturated vapor pressure. It is independent of the atmospheric/ambient pressure and is determined by the particular molecule and the temperature.

19

given by Henry’s Law, which states that the partial pressure exerted by a dissolved gas is proportional to the concentration of gas molecules in solution. PHARMACOKINETICS We will briefly look at factors affecting absorption, distribution, metabolism and excretion of commonly used inhalational anesthetics. Solubility/Partition Coefficient From the inspired gas the anesthetic (in the gaseous phase) dissolves in the blood in the pulmonary capillaries, from where it reaches the brain and other tissues. The passage of the agent from the alveolus through various tissue ‘barriers’ or phases) is governed by certain rules. When an anesthetic agent passes from one phase to another, (e.g. alveolus to blood) the partial pressure across the phases and not the concentration tends to equilibrate. At equilibrium the concentration (in volume percent) in the two phases (or tissues) can be very different and is based on the solubility of the agent in the two phases. If an agent is highly soluble in blood, at equilibrium there will be a higher concentration (partial pressures in blood and alveolus will equilibrate) in blood than in the alveolus. In other words large amounts of anesthetic agent will be needed to be taken up to reach equilibrium. Concurrently, the time taken for equilibration of the blood and brain concentration (brain-blood partition co-efficient) is also delayed. This will prolong induction of anesthesia. Hence agents with higher blood gas coefficients (usually also have higher brainblood coefficients) are slow at inducing anesthesia. On the other hand agents like N2O with a low blood gas coefficient reach equilibration very quickly.

Dalton’s law of partial pressures: This states that in a gas mixture the pressure contributed by each gas is proportional to the number of molecules of that gas. The clinical implication in anesthesia is that since alveolar pressure is constant (760 mm Hg) the increase in partial pressure of any gas (e.g. CO2) will be at the expense of a fall in partial pressure of oxygen.

Uptake of Anesthetic Agents

Concentration and tension (partial pressure): The relationship between these two variables is

The rate of uptake of inhaled anesthetic agents is the ratio of alveolar and inspired (FA/FI)

20 A PRIMER OF ANESTHESIA

concentration seen overtime. As more and more anesthetic is taken up the alveolar concentration (which is zero to begin with) approaches the blood concentration. This is an exponential equation. As the difference between the two phases reduces, less is taken up. Theoretically, at infinity, the alveolar concentration equals inspired concentration, the ratio (FA/FI) becomes unity and uptake ceases. Uptake = solubility × cardiac output × difference in alveolar and venous partial pressures/atmospheric pressure. Factors Affecting Rate of Uptake 1. Increased inhaled concentration speeds induction. 2. Increased alveolar ventilation hastens induction. This will lead to higher alveolar concentration and FA/FI will increase rapidly. 3. Increased cardiac output delays induction because the rate at which the agent is taken away from the alveolus increases and hence FA/FI will increase slowly. 4. A high blood-gas coefficient (increased solubility) delays induction. The higher the coefficient (the more soluble the agent) the higher the uptake, lower the FA/FI rise and slower the induction. 5. Bio-transformation of the agent is not particularly important in the rate of uptake. 6. Elimination of re breathing, use of high fresh gas flows and low anesthetic circuit volume hasten induction and recovery. 7. Mal-distribution of ventilation and perfusion may delay induction. 8. Second gas effect (see N2O) and concentration effect hasten induction. 9. Reduction in pulmonary blood flow (e.g. in right-to-left shunts, as seen in tetralogy of Fallot) delays induction especially with soluble agents. Conversely, a left-to-right shunt is expected to speed up induction as

blood laden with anesthetic re-circulates in the lungs, leading to rapid build-up of anesthetic partial pressure. It can be appreciated that inhaled anesthetics must pass through many barriers between the anesthesia machine and the brain, which is their site of action. Metabolism and Excretion of Inhalational Anesthetics The major portion of most agents is exhaled unchanged from the lungs. The agent most metabolized is halothane (about 20%). PHARMACODYNAMICS We do not know how exactly general anesthetics cause reversible loss of awareness and pain. There is no center in the brain that is specifically depressed by these agents, neither are any specific “anesthetic receptors” present in the brain. However, many theories have been put forward to explain the possible modes of action of inhalational anesthetics. Mayer-Overton Theory It was observed about a hundred years ago that the more lipid- soluble anesthetics (having a high oil-gas coefficient: tends to dissolve more in the lipid phase compared to the gas phase), were more potent. These agents therefore (e.g. Trichloroethylene, ‘Trilene’) had low MAC values. It was then inferred that anesthetics worked on the lipid por tion of the cell membrane. Pressure Reversal and Critical Volume Hypothesis It was observed that when anesthetised mice were kept in a pressure chamber and the pressure of the chamber increased to 50 atmospheres, the mice woke up. It was concluded that anesthetics worked by cellular expansion, and that high ambient pressure led to reversal of anesthesia.

INHALATIONAL ANESTHETIC AGENTS

Mu lti-site Expansion Hypothesis Multi-site Lipids in the cell membrane move and rotate within the bi-layer and cause changes in the protein portion. These changes control ionic and neurotransmitter fluxes across the cell membrane. The movement in the lipid moiety may lead to swelling of the cell membrane. Other Theories 1. Anesthetic action on sodium, potassium or calcium channels. 2. Action mediated through ligand gated channels. Ketamine, which is a non conventional anesthetics inhibits N-methyl-Daspartate (NMDA) which is a selective agonist on glutamate receptors. 3. Depression of postsynaptic response. All inhalational anesthetics and propofol affect GABA receptor channel complex. 4. Protein change. MRI studies have shown that anesthetics affect hydrophobic sites in the cell membrane. This leads to reversible alteration in the non-hydrophobic protein areas. ANESTHETICS IN CLINICAL USE Let’s look at the properties of an ideal inhalational anesthetic: Physical 1. Liquid at room temperature- to facilitate easy storage 2. Low latent heat of vaporization 3. Low specific heat 4. Stability in light and room temperature 5. Nonflammable and non-explosive 6. Environmentally safe (locally and globally) Pharmacological 1. Pleasant odor, nonirritant to respiratory mucosa or airways 2. Low blood gas solubility (high potency, rapid induction)

21

3. High oil-water solubility 4. Potent enough to permit use of high oxygen concentration 5. Minimal depression of the cardiovascular, and respiratory systems. 6. Non-epileptogenic, no effect on ICP 7. Not dependent on intact renal/hepatic function for elimination 8. Least interaction with other drugs or with administering system 9. Minimally metabolized in the body No agent currently available has all these properties. We will now compare the physical properties (Table 2.1) and systemic actions of the commonly used agents system-wise and summarize important features at the end of each comparison. The salient points of the physical characteristics are: 1. Desflurane has the lowest boiling point, so that it exists as saturated vapor at room temperature. It is delivered through a heated, microprocessor-controlled vaporizer. 2. Although desflurane has the lowest bloodgas partition coefficient (it is least soluble) it has the highest MAC value (least potent). The substitution of a fluorine atom (Figs 2.3 and 2.5) for a chlorine atom results in loss of potency. The low blood gas solubility coefficient allows for rapid changes in anesthetic depth and rapid induction and emergence. 3. Halothane has a lower MAC value than isoflurane and enflurane; however, the blood-gas partition coefficient of halothane is the highest and, it has the longest induction time among these three agents. 4. Except for halothane, all other halogenated anesthetics react in some way with sodalime (Table 2.1). When desflurane, isoflurane or enflurane come in contact with dry (used/ exhausted) sodalime, carbon monoxide formation can occur. Sevoflurane is absorbed and degraded by CO2 absorbents.

22 A PRIMER OF ANESTHESIA Table 2.1: Physical properties of inhalational agents Agent

Mac

Color code

B.P.

Sodalime

Blood/gas

Halothane

0.75

Red

50.2°C

No reaction

2.3

Isoflurane

1.15

Purple

48.5°C

CO with dry SL

1.43

Enflurane

1.68

Orange

56.5°C

CO with dry SL

1.9

Sevoflurane

2.00

Yellow

58.6°C

Compound A/B

0.69

Desflurane

6.35

Supplied in bottle with special valve

22.8°C

CO with dry SL

0.42

[CO-carbon monoxide; SL- sodalime] Table 2.2: Induction characteristics and respiratory effects Halothane

Isoflurane

Enflurane

Sevoflurane

Desflurane

Quality of ind.

Good

Not preferred

Not preferred

Best

Worst

Pungency

None

Moderate

Moderate

None

Moderate

Mucosal irritn.

None

Moderate

Mild

None

Maximum

Bronchial dil.

++

+

+

++

Not known

Secretions

No increase

Increase

No increase

No increase

Increase

Tidal volume

↓↓

↓

↓

↓

Not available

Resp. rate

↑↑

↑

↑/↓

↓

Not available

At temperatures of 65°C five breakdown products are formed (Compounds A-E). At clinically encountered temperatures mainly Compounds A and B are formed. Generation of these compounds is more with baralyme as temperatures attained are higher. A new zeolite-coated sodalime is on the pipeline which may absorb these compounds. Properties common to the inhalation agents in current use: • All potentiate neuromuscular blockade. • All can trigger malignant hyperthermia (MH) in susceptible patients. • All produce anesthesia without analgesia (except the historically used agents diethyl ether and trichloro ethylene). • All relax the uterine muscle and may predispose to post partum hemorrhage.

Induction characteristics (Table 2.2): • Since desflurane is most irritant, it reduces the rate at which inspired concentration can be increased during induction. Therefore rapid approximation of inspired and alveolar concentrations (FA/FI) cannot be achieved. Further, concentrations above 6% (1 MAC) cause laryngospasm and breath-holding. Thus, in spite of having the advantage of low blood–gas solubility, it is the least preferred agent for induction. • Because of its pleasant odor halothane is a suitable agent for induction in children, especially where cost is a concern as sevoflurane (see below) is expensive. Isoflurane may precipitate bronchospasm during the initial stages due to irritation of the respiratory mucosa. • Sevoflurane is emerging as an induction agent of choice in children [because of

INHALATIONAL ANESTHETIC AGENTS

23

Table 2.3: Cardiovascular effects Halothane

Isoflurane

Enflurane

Sevoflurane

Desflurane

Myoc. Depr.

Maximum

Min.(1 MAC)

Mild

None

Minimal

Coronary dilat.

V. minimal

+ +, ‘steal’

+

+ +, ‘steal’

+ (>2MAC)

SVR

Minimum↓

↓↓

↓

↓↓

Minimum ↓

Blood press.

Reduced

Reduced

Minimum ↓

Reduced

Not affected

Heart rate

↓↓

↑

Reflex tachy

↓

↑

Arrhythmia pot.

+++

_

+

_

_

speedy induction (low B/G and low oil/gas solubility) and acceptable odor] and also in patients with central airways obstruction (e.g. tracheal/carinal) tumors. Cardiovascular effects (Table 2.3): • Isoflurane is a potent coronary vasodilator and most prone to cause coronary and cerebral ‘steal’. This is a phenomenon whereby healthy vasodilated vessels divert blood away from critically perfused areas supplied by non-compliant vessels. In the heart it can jeopardize ischemic myocardium. • Sevoflurane reduces blood pressure by reducing systemic vascular resistance (SVR); cardiac output remains unchanged. Cardiac output is reduced by reduction in the heart rate, therefore myocardial oxygen supply is enhanced. Sevoflurane causes less coronary dilatation than isoflurane. • Halothane is a potent depressant of the myocardium. Both stroke volume and heart rate are reduced. It has little effect on the peripheral vascular resistance. With reduction in the myocardial contractility the myocardial oxygen consumption decreases unless there is also a marked reduction in blood pressure. Since it has little effect on the peripheral vascular resistance, it does not cause coronary steal. Halothane decreases heart rate by vagal stimulation, reduces phase IV depolarization and slows cardiac conduction velocity. This leads to ventricular escape in the form of premature ventricular contractions (PVCs) and bigeminy.

Halothane maximally sensitizes the heart to exogenously administered catecholamines. Arrhythmias are more likely with hypoxia and hypercarbia. If epinephrine is to be administered, dosage should not exceed 10 ml of a 1:1,00,000 solution (100 μg) in 10 min, and not more than 30 ml per hour. • Desflurane may exhibit coronary vasodilatation and steal upwards of 2.2 MAC. Metabolism and elimination (Table 2.4): • 5% of sevoflurane is metabolized by cytochrome P-450 producing hexafluoroisopropanol and inorganic fluoride. Fluoride levels do not reach toxic threshold described for nephrotoxicity (> 50 μmol/l). Potentially hepatotoxic hexafluoroisopropanol is conjugated before it can cause damage. Compounds A-E formation has been discussed earlier. • 20% of halothane undergoes metabolism and it takes nearly 3 weeks for the metabolites to completely clear. The metabolites Table 2.4: Elimination of inhaled anesthetics Halothane Isoflurane Enflurane Sevoflurane Desflurane

60-80% unchanged via lung, 20% metabolized in liver Primarily exhaled unchanged; 0.2% metabolized in liver Predominantly exhaled via lung; 2.4% metabolized to fluoride 95% exhaled via lung; 5% metabolized by cytochrome P-450 Predominantly exhaled unchanged; 0.02% metabolized in liver

24 A PRIMER OF ANESTHESIA Table 2.5: Central nervous system effects Halothane

Isoflurane

CBF

↑↑

↑

ICP

↑↑

↑

_

_

Epilepsy

are trifluoroacetic acid, chloride and bromide. Nearly 50% patients show a temporary increase in glutathione Stransferase. CNS effects (Table 2.5): All inhalational agents tend to increase the cerebral blood flow (CBF) due to vasodilation and thereby the ICP to a lesser or greater degree. Isoflurane causes the least increase in ICP and may exhibit ‘steal’ which may be par tly responsible for this increase. “Steal” implies that blood may be diverted from areas of vasospasm to those having normal perfusion. SPECIAL FEATURES ABOUT INDIVIDUAL INHALATION AGENTS Halothane (Fig. 2.1) Thymol (0.1%) is added to halothane as preservative. Since it does not readily evaporate but accumulates in the vaporizer, control knobs can stick. These vaporizers require regular

Enflurane

Sevoflurane

Desflurane

_

Minimal ↑

No data

_

Minimal ↑

No data

+++

_

No data

cleaning. Halothane also corrodes aluminium, brass and solder metal. Halothane produces relatively more myocardial depression than fall in SVR (manifest as a fall in blood pressure) and this makes it uniquely useful in patients with obstructive cardiomyopathy, where isoflurane is relatively contraindicated. Halothane is an excellent bronchodilator. A characteristic feature of deep halothane anesthesia is tachypnea and shallow respiration. Halothane induced hepatic dysfunction, though rare (seen more often after repeat halothane anesthetics, in obese middleaged female patients and those with a known history of allergy to halogenated anesthetics) is the most important reason why the drug usage has drastically reduced world over. Clinically hepatic dysfunction presents as mild elevation in liver enzymes which resolves in a few days. Fulminant liver failure is uncommon, and mortality in these cases is between 30–70%. It is interesting to note that hepatic dysfunction is extremely rare in children. It is important to

Fig. 2.1: Halothane bottle; structure of halothane; keyed halothane filler

INHALATIONAL ANESTHETIC AGENTS

25

Fig. 2.2: Structure of enflurane; enflurane vaporizer

Fig. 2.3: Structure of isoflurane; bottle of isoflurane, specific vaporizer for isoflurane

avoid halothane in any patient who gives a history of fever or jaundice on a previous use. The color code for halothane is red. Enflurane (Fig. 2.2) This is the only inhalation agent which is epileptogenic in concentrations more than 3%. Since inorganic fluoride ions are produced consequent to metabolism, it is best to avoid enflurane in patients with chronic renal failure. The color code for enflurane is orange. Isoflurane(Fig. 2.3) Although isoflurane reduces the cardiac output only to a limited extent, it is a potent vasodilator. The drop in blood pressure is due to peripheral

vasodilatation. Severe hypotension may occur with high alveolar concentrations if not adequately monitored. The peripheral vasodilation with minimal myocardial depression and lack of myocardial sensitization to exogenous or endogenous catecholamines makes it an ideal agent for control of intra operative blood pressure in patients with pheochromocytoma. Its advantages are rapid recovery, minimal hepatic or renal toxicity and low risk of arrhythmias. Isoflurane is also the agent of choice for control of intraoperative bronchospasm, considering the fact that these patients would already have received sympathomimetic agents and are at increased risk of arrhythmias. The color code for isoflurane is mauve.

26 A PRIMER OF ANESTHESIA

Fig. 2.4: Structure, bottle and vaporizer of sevoflurane

Sevoflurane (Fig. 2.4) Though the agent was synthesized in 1968, it was introduced in the West for clinical use only in 1994. In the 1990s its reaction with sodalime (used in closed circuit anesthesia leading to production of compounds A-E) and its fluoride ion production were thought to be a major problem. These results were based on animal models which were incorrectly extrapolated to humans. Sevoflurane reacts with soda lime to produce a vinyl ether called compound A. The lower the fresh gas flows in closed circuit, the higher the compound A levels. Compound A is metabolized by cysteine-conjugate β lyase to produce nephrotoxic metabolites in rats. In the last few years it has been shown that in humans there is 10–30 fold absence of this pathway of compound A metabolism. This discovery has popularized the use of sevoflurane since the late 1990s. Its advantages are smooth and fast induction and rapid recovery. For this reason this is the induction agent of choice in pediatric patients. It is however more expensive than isoflurane. Some anesthetists avoid its use in closed circuit using low flows and in patients with hepatic and renal dysfunction. Desflurane (Fig. 2.5) It was first used on humans in 1988 and is the latest anesthetic in contemporary use. Its MAC

is 6% in oxygen in adults. It has however the lowest blood/gas coefficient of any anesthetic (except experimentally used xenon). Because of its low boiling point (23.5°C) its saturated vapor pressure high and it tends to boil at room temperature. This requires the use of a special pressurized vaporizer. This vaporizer is electrically and microprocessor controlled heated by electricity making it more expensive. Desflurane has a biphasic effect on the cardiovascular system. In less than 1 MAC concentration it maintains the heart rate and exhibits a dose related decrease in systemic vascular resistance. In higher concentration it causes a sympathetic response leading to tachycardia, hypertension and myocardial ischemia in some patients. In summary its advantages are rapid recovery, and minimal biodegradation. It is the preferred agent for short duration and outpatient procedures. Its significant disadvantages are irritation to the respiratory mucosa, tachycardia, requirement of a special vaporizer, and a higher cost than sevoflurane. Diethyl Ether (Fig. 2.6) It is a colorless, volatile liquid with a characteristic smell. It forms an explosive mixture with air, oxygen, and nitrous oxide. Ether is still used as a ‘field’ anesthetic in rural primary health centers in India and Africa.

INHALATIONAL ANESTHETIC AGENTS

27

Fig. 2.5: Structure, bottle and vaporizer of desflurane

Fig. 2.6: Structure of ether; copper ether container; Schimmelbusch mask

It has a high blood gas solubility coefficient of 12; as it is irritant to the respiratory mucosa the concentration in the inspired gas can be increased only slowly. These factors make induction slow. It depresses the CNS like other agents. The inhibitory cortex is depressed initially resulting in excitatory phase. Later the entire CNS is depressed. As ether is slow acting, it is possible to see all the classic ‘stages’ of anesthesia described by Guedel (Figs 2.7 A and B). Respiratory centre depression is followed by depression of the vasomotor centre. As ether is irritant to the mucosa, it causes coughing, breath holding, profuse secretions of the respiratory and salivary glands. Premedication with atropine or glycopyrrolate is essential.

Ether stimulates ventilation; hence minute ventilation is maintained till stage three plane three. It is a potent bronchodilator. It also relaxes the skeletal and uterine muscles. It is a direct cardiovascular depressant. However, it is a potent stimulator of the sympathetic system. This results in maintained blood pressure. In deeper planes it causes hypotension. It does not sensitize the myocardium to circulating catecholamines. More than 15% is metabolised to carbon dioxide and water. Other products of metabolism are alcohol and acetaldehyde. Clinical use: Ether has a higher therapeutic ratio than other agents like halothane, and isoflurane. This makes it safer to use in unskilled

28 A PRIMER OF ANESTHESIA

Figs 2.7A and B: Guedel’s stages of anesthesia

hands and with uncalibrated vaporisers than other agents. Inspired concentration of up to 20% is required for induction. Anesthesia can be maintained with 3–6% concentration. In the late 19th century ether was administered by ‘open drop’ method where a mask made of a steel framework, covered with layers of gauze (Schimmelbusch mask) was placed over the patient’s face and ether dropped on it from a bottle (Fig. 2.8). The early anesthesia machines had a mounted ‘ether bottle’ (Fig. 2.9). Subsequently, the EMO (Epstein, Macintosh and Oxford) vaporizer (Figs 2.10 A and B) was designed which is a sturdy and reliable inhaler still in widespread use in field locations and peripheral rural health facilities. The incidence of postoperative nausea and vomiting is high with ether. Nitrous Oxide Amongst inhalational agents, nitrous oxide is the only true ‘gas’ (other agents being vapors). It was also called ‘laughing gas’. It is prepared by heating ammonium nitrate. Various

impurities (including ammonia, nitric acid, nitric oxide, and nitrogen dioxide) can be dangerous if inhaled and are removed. It is stored as liquid in blue cylinders at 5000 kPa pressure. Nitrous oxide is sweet smelling and non irritant. It is a good analgesic but a poor anesthetic because it has a high MAC of 105. A MAC of 105 means it is difficult to measure. In experiments it can be measured at two atmosphere ambient pressure when the MAC is 52.5%. Since it is essential to administer a patient at least 30% oxygen under anesthesia, only close to 70% MAC can be provided by nitrous oxide; the rest has to be provided by some other anesthetic given concurrently. It has a blood/ gas coefficient of 0.47. That makes it a very fast acting anesthetic as only a small amount needs to dissolve in blood to achieve equilibration pressure with the alveolar N 2O. It is not metabolised and exhaled unchanged from the respiratory system. It has little effect on the respiratory system. It is a myocardial depressant but also stimulates the sympathetic system hence blood pressure

INHALATIONAL ANESTHETIC AGENTS

29

Fig. 2.8: The ‘open drop’ technique of ether anesthesia

Fig. 2.10A: The EMO ether vaporizer

Fig. 2.9: The Boyle ether bottle

Fig. 2.10B: Internal structure of EMO vaporizer

is maintained. It has no effect on skeletal or uterine muscles.

Diffusion hypoxia: At the end of an anesthetic when nitrous oxide is switched off and the patient allowed to breathe air, nitrogen starts replacing oxygen in the alveoli and slowly diffuses into the bloodstream. In addition, now there is a gradient for nitrous oxide to move towards the alveolus as the alveolar concentration of N 2 O is low. Because of its low

Advantages and disadvantages of nitrous oxide: Most balanced general anesthetics use nitrous oxide. If it only had a significantly lower MAC it could have been an anesthetic agent coming close to an ideal one. It also has some other significant side effects as listed below.

30 A PRIMER OF ANESTHESIA

solubility, the amount of nitrous oxide (in ml) leaving the blood and entering the alveolus is more than the nitrogen entering the blood from the alveolus. This leads to dilution of the other gases in the alveolus. These are oxygen and carbon dioxide. The low oxygen partial pressure in the alveolus causes hypoxia. It lasts about 10 minutes and can be significant in the sick patient. Thus it is important to administer 100% oxygen at the end of the anesthetic to prevent hypoxemia. Effect on closed gas spaces: There are closed spaces in the body where air exists. These are the bowel lumen and the middle ear cavity. Additionally, in pathological conditions air can exist in the pleural cavity (pneumothorax), the peritoneal cavity or in the blood vessels (air embolus). When nitrous oxide containing blood comes in contact with such cavities nitrous oxide diffuses faster into this cavity than nitrogen into the blood from the cavity. This temporarily leads to higher gas volume in this space. The extra volume in the space stays till the nitrogen is eventually slowly absorbed in the blood. If this closed space in the body has boundaries rigid (like the middle ear cavity) then the extra gas leads to high pressure. This has implications when a graft is placed in the middle ear cavity over the ear ossicles (during modified mastoidectomy), when the graft tends to get lifted off. When air is injected for contrast during a pneumoencephalogram in an anesthetized child inadvertently receiving N2O, Nitrous oxide diffuses into the injected air bolus and may increase ICP to dangerous levels. If N2O is used as part of the anesthetic technique in a patient who is undergoing surgical repair of retinal detachment with intraocular injection of gas (SF6), significant increase in IOP and blindness can result. Avoiding nitrous oxide is a good option in these conditions. Toxicity: Nitrous oxide inhibits the enzyme methionine synthetase. This enzyme affects the

synthesis of vitamin B12. Nitrous oxide also affects folic acid metabolism. The effect on these two vitamin metabolism takes place on exposure longer than 8 hours. Megaloblastic anemia, aplastic anaemia, myeloneuropathy is also very rarely seen after prolonged exposure. To conclude, developments in inhalational agents has resulted in availability of sevoflurane and desflurane, which have favourable pharmaco-kinetic profiles compared to older agents like halothane and isoflurane. Developments in vapourizers and circuits have resulted in accurate delivery of inhalational agents to patients, with maintenance of stable hemodynamics and enhanced recovery. STATE WHETHER TRUE (T) OR FALSE (F) 1. About volatile anesthetics a. Gaseous route for delivery of anesthetic more likely to be used in adults than in children b. Potency is measured in MAC c. MAC is approximately additive d. 1 MAC anesthesia ensures anesthesia in 99% patients e. Inhalational route is safer than intravenous route in patients with upper airway obstruction 2. Physical principles governing volatile anesthetics a. Gases can be liquefied only above their critical temperature b. Critical pressure is the pressure at critical temperature c. Partial pressure and not concentration equilibrates when a gas passes through different tissues d. Induction of anesthetic is quicker when the agent is highly soluble in blood e. Uptake of an anesthetic is more in the initial period after induction

INHALATIONAL ANESTHETIC AGENTS

3. Properties of an ideal inhalational anesthetic are a. High latent heat of vaporisation b. Non-inflammable c. Pleasant odor d. High blood gas solubility e. Completely metabolised in body 4. Physical properties a. Desflurane has the high MAC hence induction is the quickest b. Halothane has a low MAC value hence induction is slowest c. Most anesthetic have no or minimally significant interaction with sodalime except sevoflurane d. Desflurane exists as vapor at room temperature when not under pressure e. Sodalime is used during an anesthetic to absorb carbon dioxide present in atmospheric air 5. Volatile anesthetics a. Can trigger malignant hyperthermia, a highly fatal condition b. Relax the pregnant uterus that can lead to post partum hemorrhage c. Are bronchodilators d. Reduce systemic vascular resistance to variable degree e. Are primarily eliminated from the body by exhalation 6. Halothane a. Halothane hepatitis is a common phenomenon b. Halothane should not be used when repeated anesthesia is given c. Halothane is the most arrhythmogenic of all the modern anesthetics d. Halothane greatly reduces SVR e. Is most likely to cause bradycardia amongst the modern anesthetics

31

7. Amongst modern anesthetics a. Enflurane is epileptogenic b. Enflurane is most likely to cause renal failure c. Desflurane interacts with soda-lime to produce compound A d. Sevoflurane needs special heated vaporizer e. Sevoflurane has the highest MAC 8. Nitrous oxide a. Is available in blue colored cylinders in the liquid form b. Has good analgesic properties c. Has the highest MAC amongst all anesthetics d. Is nearly always administered with some other volatile anesthetic e. Has one of the lowest blood gas solubility coefficients 9. Nitrous oxide a. Is exhaled as nitrogen and oxygen after metabolism b. Causes diffusion hypoxia c. Is a uterine dilator d. Has very little effect on the respiratory system e. During prolonged anesthesia may affect synthesis of vitamin B12 10. Diethyl ether a. Is rarely used nowadays for anesthesia b. Is very inflammable c. Is non-irritant to the mucosa hence used for gas induction d. Has low blood gas solubility hence used for gas induction e. Has a high possibility of causing nausea and vomiting Answers 1. 4. 7. 10.

FTTFT 2. FTTFT 3. FTTFF FFTTF 5. TTTTT 6. FTTFT TTTFF 8. TTTTT 9. FTFTT TTFFT

Physiology of Neuromuscular Blockade and Neuromuscular Pharmacology Anju R Bhalotra

          

Anatomy and physiology of the neuromuscular junction Physiology of neuromuscular transmission Mechanism of action of depolarizers and non-depolarizers Properties of an ideal muscle relaxant Depolarizing relaxants-suxamethonium Non-depolarizing relaxants Side effects of neuromuscular blocking drugs Drug interactions Antagonism of neuromuscular blockade Neuromuscular disease affecting action of relaxants Monitoring of neuromuscular block

Skeletal muscle relaxation facilitates surgical procedures by allowing adequate surgical exposure. It also ensures good conditions for endotracheal intubation, tolerance of the tube by the anesthetized patient and facilitaties mechanical ventilation of the lungs. Reduction in skeletal muscle tone can be achieved by deep levels of inhalation anesthesia, regional nerve block or by the use of neuromuscular blocking agents—commonly

called muscle relaxants. In 1942, Harold Griffith published the results of a study using a refined extract of curare, a South American arrow poison, during anesthesia. Griffith and Johnson suggested that d-tubocurarine was a safe drug to use during surgery to provide surgical relaxation. In 1952, succinylcholine was introduced into clinical practice by Thesleff and Foldes which become popular as a short acting muscle relaxant. It was extensively used to facilitate tracheal intubation. The introduction of vecuronium and atracurium, in the early 1980’s led to extensive use of muscle relaxants in clinical practice for tracheal intubation and in the form of infusions for surgical relaxation; significant development in anticholinesterases also occurred, enhancing the safety margin in the use of these drugs. While muscle relaxants have rapidly become an essential component of the drug arsenal used by the anesthesiologist, it is vital to remember that they merely provide what their name suggests, i.e. only muscle relaxation and not unconsciousness, analgesia or amnesia. They are adjuvants and not substitutes for anesthesia. As an important component of the balanced anesthesia technique they have revolutionized the practice of modern anesthesia.

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

33

ANATOMY AND PHYSIOLOGY OF THE NEUROMUSCULAR JUNCTION The region of approximation between a motor neuron and a muscle cell is called the neuromuscular junction (NMJ; Fig. 3.1). It is specialized on both the nerve and muscle side to transmit and receive chemical messages. Each motor neuron runs from the ventral horn of the spinal cord to the NMJ without interruption as a large unmyelinated axon. As it reaches the muscle, it divides repeatedly to contact many muscle fibers. These muscle fibers and their supplying axon comprise a functional group called a motor unit (Fig. 3.2). The cell membranes of the neuron and muscle fiber are separated by a narrow (20 nm) gap called the synaptic or junctional cleft (Fig. 3.3). The surface of the muscle fiber is heavily corrugated with deep invaginations–the primary and secondary clefts. The shoulders of the clefts are heavily endowed with acetylcholine receptors but these are sparse in the depths of the folds where sodium channels are found. The perijunctional zone is the area of the muscle between and around the receptive area. Since all the muscle cells in a single unit are innervated by a single neuron, stimulation of this neuron causes all the cells in a motor unit to contract

Fig. 3.2: The motor unit

Fig. 3.3: Synaptic cleft, active zone and ACh receptors

synchronously; this synchronous contraction is termed a fasciculation. Most adult human muscles have only one NMJ per cell. The extraocular muscles on the other hand have several NMJs per cell. These muscles contract and relax slowly and maintain a steady contracture when stimulated. This is important physiologically to hold the eyes steadily in position. How does Neuromuscular Transmission Occur? Fig. 3.1: The neuromuscular junction

The portion of the nerve cell towards the junctional side contains vesicles which contain

34 A PRIMER OF ANESTHESIA

the neurotransmitter acetylcholine (ACh). The small thickened electron dense patches where these vesicles are arranged in repetitive clusters is termed the active zone (Fig. 3.3). Between the vesicles are small protein particles which are believed to be special channels, the voltage gated calcium channels. Even when the muscle is not stimulated small spontaneous depolarizing potentials can be seen at the NMJ known as Miniature End Plate Potentials (MEPP’s). These have only 1/100th the amplitude of an evoked End Plate Potential (EPP) which is produced by stimulation of the motor nerve. Although MEPP’s are unitary responses, they are still too big to be accounted for by one molecule of ACh. This finding made way for the Quantal Theory as it was thought that MEPP’s are produced by uniformly sized packages or quanta of transmitter released by the nerve. The EPP produced by nerve stimulation is due to a synchronous discharge of quanta from several hundred vesicles. Once a nerve action potential is propagated, sodium flows across the membrane and the resulting depolarizing voltage opens the calcium channels allowing entry of calcium ions through the voltage gated calcium channels. This change in permeability and movement of ions causes a decrease in the transmembrane potential from –90 to –45 mv (threshold potential). Each nerve impulse causes the release of more than 200 quanta of 5000 molecules of ACh, each causing the activation of about 500,000 ACh receptors. There are 2 pools of vesicles which release ACh; VP2 (vesicle pool 2-readily releasable store) and VP1 (vesicle pool 1 reserve store). The majority of the vesicles belong to the VP2 group. Repeated nerve stimulation requires nerve endings to replenish its stores of transmitter, a process called Mobilization. The simple molecules of choline and acetate are obtained from the vicinity of the nerve ending and are converted to acetylcholine in the presence of the enzyme choline acetyltransferase.

Role of Acetylcholinesterase The ACh released into the junctional cleft reaches specialized receptor proteins in the muscle end plate to initiate a muscle contraction. ACh molecules which do not react with the receptor immediately or are released after binding are almost instantaneously (50 mins)

Steroidal

Pancuronium Pipecuronium

Benzylisoquinolines d-tubocurare, metocurine doxacurium Phenolic ether

Gallamine

Intermediate (20–50 mins)

Short acting (10–20 mins)

Vecuronium, Rocuronium

Rapacuronium

Atracurium, Cisatracurium

Mivacurium

38 A PRIMER OF ANESTHESIA

the drug away from the NMJ and back into the circulation to be metabolized by pseudocholinesterase. The initial metabolite is succinylmonocholine which is metabolized more slowly to succinic acid and choline. What are the reason/s for prolonged neuromuscular block after suxamethonium? A. Low levels of normal pseudocholinesterase: i. Factors that decrease the normal enzyme levels are liver disease, pregnancy, burns, increasing age, malnutrition and neoplasia. Hypothermia decreases the rate of hydrolysis. ii. Anticholinesterase drugs: An example is chronic exposure to organophosphorus compounds like ecothiopate. This group of drugs causes ACh to accumulate, prolonging the block, and also reduce hydrolysis of suxamethonium. B. Antagonism of normal levels of pseudocholinesterase: Drugs competing with pseudocholinesterase: MAO inhibitors, oral contraceptives, cytotoxic drugs, tetrahydroaminacrine, hexafluorenium, metoclopramide, trimethaphan, phenelzine, bambuterol and esmolol. C. Presence of atypical pseudocholinesterase: About 1 in 50 patients has one normal and one abnormal gene for pseudocholinesterase expression and this prolongs the action of suxamethonium by 30–40 minutes. One in 3000 patients are homozygous for the abnormal gene and the atypical pseudocholinesterase results in paralysis lasting up to 6–8 hours. This abnormal gene is diagnosed by the ‘dibucaine number’. Dibucaine is a local anesthetic that inhibits the action of normal pseudocholinesterase up to 80% (normal) and only 20% of the abnormal enzyme. The percentage of inhibition of activity is termed the ‘Dibucaine Number’. Dibucaine number is related to pseudocholinesterase function and not to the quantity of enzyme. The treatment of

prolonged paralysis due to atypical cholinesterase is mechanical ventilation with sedation till the block wears off. Although fresh frozen plasma is another alternative, the infectious risks of transfusion outweigh its benefit. The ‘ Fluoride number’ is useful where an abnormal genotype, associated with a normal dibucaine number, is resistant to fluoride. D. High doses of suxamethonium: At over 6 mg/kg, Phase II block (see above) develops which lasts longer than the depolarizing block produced by normal doses. Clinical Uses of Suxamethonium Despite certain drawbacks with suxamethonium, it remains the drug of choice in situations where it is necessary to intubate the trachea rapidly after induction of anesthesia, as in patients who are termed ‘full stomach’ (refer to chapter on airway management). The potential problems with succinylcholine are diescribed below. Undesirable Effects Associated Specifically with the use Succinylcholine 1. Pediatric patients: Following succinylcholine there may be sudden cardiac arrest in apparently healthy children and adolescents. Hyperkalemia, acidosis and rhabdomyolysis have been demonstrated with the muscle biopsy showing subclinical muscular dystrophy. The highest incidence is seen in males less than 8 years of age. Succinylcholine should perhaps be avoided in this age group, if alternatives are available. 2. Cardiovascular effects: Succinylcholine stimulates cholinergic autonomic receptors, nicotinic receptors on sympathetic and parasympathetic ganglia and muscarinic receptors in the sinus node of the heart. The effect on heart rate is dose-related. In low doses both negative inotropic and chronotropic effects are seen; with higher doses

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

tachycardia is predominant. The incidence of cardiac arrhythmias is significant and may manifest as sinus bradycardia (stimulation of muscarinic receptors in the sinus node), junctional rhythm (suppression of sinus mechanism and emergence of the AV node as the pacemaker) and ventricular arrhythmias. Cardiac arrhythmias are more likely to occur when a second dose is given intravenously about 5 min after the first dose as the hydrolysis products of succinylcholine may sensitise the heart. Bradycardia may be a problem in children who have a high vagal tone. The intravenous administration of atropine 1–3 min before the second dose decreases the chances of bradyarrhythmias. 3. Hyperkalemia: There may be an exaggerated rise of K+ in some patients to an extent as to cause cardiac arrest. This excessive release occurs from extra junctional receptors which develop in denervated or injured muscle. The synthesis of extrajunctional receptors starts within a few hours of inactivity or injury and they cover the entire membrane in a few days. The sensitivity to relaxants starts within 24– 48 hours after the injury; there is an exaggerated hyperkalemic response to depolarizers and resistance to nondepolarisers. Examples of such situations are (a) Burns and Trauma: There may be significant K+ release 24–48 hours after burn injury and at 1 week after massive trauma. As with burns, a patient with massive trauma is susceptible to develop hyperkalemia for at least 60 days after the trauma or until adequate healing of the injured muscle has occurred. To be safe, it is best to avoid this drug in patients with thermal injury from as early as 24–48 hours after injury and up to 1–2 years after healing of the burned skin. (b) Nerve damage or Neuromuscular disease: The vulnerable period is from 72 hours of the onset of hemiplegia or paraplegia up to 2 years and is longer in patients

4.

5.

6. 7.

8.

39

with a progressive disease such as muscle dystrophy. (c) Closed head injury: Marked hyperkalemia has been reported in some patients. (d) Intra-abdominal infection: If this has lasted for more than a week there is a possibility of a hyperkalemic response. (e) Renal failure: The quantum of rise in serum K+ is as usual but lifethreatening hyperkalemia can develop due to high basal levels of K+ and the presence of metabolic acidosis in these patients. (f) Metabolic Acidosis: Such patients may have a high resting serum K + and an exaggerated hyperkalemic response after succinylcholine. The source of K+ is the gastrointestinal tract and not the muscles. Rise in intraocular pressure (IOP): This is postulated to be due to contraction of tonic neurofibrils, transient dilatation of choroidal blood vessels or both. The rise occurs within a minute, peaks at 2–4 minutes and subsides by 6 minutes. Succinylcholine should therefore be used with caution in eye surgery where IOP is already elevated or in ‘open’ eye injuries, where it is best avoided altogether. Rise in intragastric pressure: This effect is due to fasciculations in the abdominal muscles and the acetylcholine- like effect of succinylcholine. Its effect is very variable. Rise in intracranial pressure; its clinical significance and mechanism are unknown. Muscle pains: The incidence is 0.2-89%; is seen especially in the muscles of neck, back and abdomen; more often after minor surgery, in ambulatory patients and in female patients more often than males. For this reason it is not advocated for use in patients undergoing day-care surgery. The pain is due to the unsynchronized contraction of adjacent muscle fibres causing myofibril damage. Masseter spasm: This is one of the dramatic side effects of succinylcholine seen frequently in children due to an exaggerated

40 A PRIMER OF ANESTHESIA

contractile response to succinylcholine at the NMJ. It however does not seem to indicate susceptibility to malignant hyperthermia. 9. Triggering of malignant hyperthermia (MH); succinylcholine is one of the most potent triggers of MH. Onset of MH can be suspected by increased masseter muscle tone immediately after administration. It is soon followed by tachycardia, hyperthermia, hypercarbia, respiratory and metabolic acidosis. MH carries a high mortality. Treatment includes termination of anesthetic agents, active cooling, administration of dantrolene sodium, correction of metabolic acidosis, ventilatory support and observation in ICU. NONDEPOLARIZING RELAXANTS Manufacture and source: The original muscle relaxant extensively studied by Griffith and Johnson, d-Tubocurarine or ‘dTc’ as it became popularly known, was obtained from the Amazonian vine Chondrodendron tomentosum. Unfortunately large-scale exploitation of the rain forest and indiscriminate harvesting of this species has led to its near-extinction and it is no more commercially available. Metocurine and alcuronium are semisynthetic and pancuronium, vecuronium, rocuronium and the rest are synthetic. ‘Quarternisation’ is an essential step in their synthesis which converts lipophilic tertiary amines into hydrophilic compounds. Pharmacodynamics and pharmacokinetics : The action of non-depolarising muscle relaxants is by competitive antagonism of ACh at the postjunctional membrane of the NMJ. After intravenous (IV) administration all relaxants except atracurium and cis atracurium (which undergo elimination in the tissues) demonstrate a rapid decline in plasma concentration (associated with initial distribution in the ECF) followed by a slow terminal elimination phase.

Table 3.2: Doses of nondepolarizing relaxants Drug Pancuronium Doxacurium Vecuronium Rocuronium Atracurium Cisatracurium Mivacurium

ED 95 (mg/kg) Dose for intubation (mg/kg) 0.07 0.025 0.05 0.3 0.23 0.05 0.08

0.08–0.12 0.05–0.08 0.1–0.2 0.6–1.0 0.5–0.6 0.15–0.2 0.2–0.25

Dosage guidelines (Table 3.2): Muscle relaxants are selected on the basis of duration of action and with a view to avoid any possible interaction with therapy, or aggravation of systemic disorder the patient may have. For example, a shortacting agent like succinylcholine or mivacurium may be suitable for esophagoscopy, whereas a longer-acting agent like pancuronium be more suitable for a more prolonged surgical procedure, e.g. Whipple’s procedure. The ED 95 is the estimated dose of a NMB required to produce 95% depression of the height of a single twitch after its administration. For tracheal intubation with nondepolarising relaxants the dose should be 2–3 times the ED 95 to facilitate the manoeuvre in 2–3 minutes. For rapid tracheal intubation 2–4 times ED 95 doses can be used with the consequence of a longer duration of action. Additional doses or ‘top-ups’ should be 10–20% of the initial dose in the case of long acting relaxants and 25–30% of the initial dose for intermediate or short acting relaxants, Maintenance of relaxation can also be provided by a continuous infusion of intermediate/short acting drugs to keep a constant level of relaxation i.e. 90–95% twitch suppression or 1 twitch on train-of-four stimulation. It also permits rapid adjustments in depth of block if required. The dose should be decreased by 30–50% if volatile anesthetics are being used. All these agents can also be administered as infusions.

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

Priming is the use of small doses (20 % of ED 95) of the relaxant given 2–4 minutes before giving a larger dose for intubation. This hastens the onset of the larger dose allowing tracheal intubation within 90 seconds. However, the dose required for intubation following priming is 50-100% higher than the usual dose (which is 2–3 times the ED 95). Preoxygenation, patient preparation and reassurance are important as some patients may experience weakness or lose airway control after the priming dose. If doses more than 5 times ED 95 are to be used, priming may be unnecessary. The rapid onset of action of succinylcholine is unmatched by any other relaxant. However, rocuronium also provides satisfactory intubating conditions at high doses (1.2 mg/kg) in 90 secs and can replace succinylcholine where side effects are of concern, e.g. hyperkalemia or perforating eye injury. Metabolism and elimination: Generally, the hydrophilic nature of the non-depolarizing relaxants implies that they are eliminated primarily by the kidney and their rate of clearance is limited by the glomerular filtration rate (1–2 ml/kg/min). There are a few exceptions to this rule: (i) Vecuronium is more lipid soluble. Therefore, 30–40% is cleared in

41

the bile as a parent compound and 12% undergoes conversion to 3-desacetyl vecuronium. 25% of vecuronium is excreted by the kidney and this combined organ clearance gives it a clearance of about 3–6 ml/ kg/min.(ii) Atracurium is metabolized by Hofmann elimination in the plasma and by Ester hydrolysis in the interstitial fluid. It is cleared 2–3 times more rapidly than the long acting drugs. Hofmann elimination is a chemical process which does not require renal, hepatic or enzymatic function and occurs at a physiological pH and temperature. (iii) Cisatracurium is also metabolized by Hofmann elimination but there is no ester hydrolysis of the parent molecule. It is about 4–5 times more potent than atracurium. (iv) Rocuronium is taken up by the liver and excreted mainly in the bile. Thus, the intermediate acting relaxants have a clearance in the range of 3–6 ml/kg/min due to multiple pathways of degradation which accounts for their intermediate duration of action. (v) Mivacurium is rapidly hydrolyzed by plasma pseudocholinesterase at a rate 70–80% that of succinylcholine, which results in an action duration much shorter than atracurium and vecuronium but about twice that of succinylcholine. The metabolism of muscle relaxants is shown in Table 3.3.

Table 3.3: Metabolism of muscle relaxants Drug

Duration

Metabolism(%)

Kidney (%)

Liver (%)

Metabolites

Pancuronium Rocuronium Vecuronium Cisatracurium

long intermediate intermediate intermediate

85% 70% 50-60% -

3-OH metabolite none 3-OH metabolite Laudanosine,acrylates

Atracurium

intermediate

10-40%

none

Laudanosine, acrylates, alcohols, acids

Mivacurium

short

Liver (10-20%) none Liver (30-40%) Hofmann elimination(77%) Hofmann elimination and nonspecific ester hydrolysis (60-90%) Pseudocholinesterase (95-99%) Pseudocholinesterase (98-99%)

25%. ANTAGONISM OF RESIDUAL NEUROMUSCULAR BLOCKADE The classes of drugs used include: 1. Anticholinesterases: These are drugs which inhibit the enzyme acetylcholinesterase, increase the concentration of acetylcholine at the end plate and thus antagonize competitive neuromuscular block produced by non-depolarisers. They also enhance the release of ACh from motor nerve terminals. The anticholinesterases used include neostigmine, pyridostigmine and edrophonium. As only nicotinic effects of anticholinesterases are desired, the muscarinic effects must be blocked by anticholinergics like atropine and glycopyrrolate. Atropine has a more rapid effect than glycopyrrolate and should be used with edrophonium which also has a more rapid onset of action. Glycopyrrolate is more suited to the longer acting neostigmine and

44 A PRIMER OF ANESTHESIA

pyridostigmine. The doses required are 7-20 μg/kg of atropine with 0.5-1.0 mg/kg of edrophonium and 7-15 μg/kg of glycopyrrolate with neostigmine 40-60 μg/kg. Pharmacokinetics Pyridostigmine has a longer elimination half life and longer duration of action as compared with neostigmine. 50% of neostigmine and 75% pyridostigmine are excreted by the renal route. In patients with renal failure the plasma clearance of these anticholinesterases is reduced to the same extent or even more than the long acting muscle relaxants. Recurarisation (the situation where concentration of NMB rises at the NMJ due to waning action of anticholinesterase) is therefore, not a problem in these patients if NMB’s are used with careful monitoring. Edrophonium is so short acting that it may be unsuitable for clinical use; however with large doses a sustained antagonism of neuromuscular block has been seen. Gamma cyclodextrin derivatives and Potassium channel blockers are the other group of drugs being evaluated for antagonism of neuromuscular blockade. The former can encapsulate and chelate steroidal NMB drugs. It is not enough to know the dose of anticholinesterase to be given- far more important is the timing of the ‘reversal’ (as termination of action of NMB is colloquially known). Unless NMB is adequately ‘reversed’ the patient runs the risk of inadequate breathing, hypoxemia or aspiration in the post operative period. The speed and adequacy of reversal of the block are affected by the following: 1. Depth of block at time of administration of antagonist: A more intense block takes longer to recover and antagonism should not be attempted until some spontaneous recovery of neuromuscular block is seen. Clinically, this is evidenced by a perceptible respiratory effort as seen on the capnograph,

2.

3.

4.

5. 6.

or better still, by movement of the reservoir bag of the breathing circuit or abdomen. If the block has significantly receded, the patient may even open his eyes on command or make attempts to expel the endotracheal tube. Drug used for antagonism: The reversal of block is most rapid with edrophonium, then neostigmine and then with pyridostigmine. However edrophonium becomes less potent with respect to neostigmine as the depth of block becomes more intense. Dose of antagonist: Increasing the dose of anticholinesterase (up to a maximum) increases the antagonism of the block more rapidly and completely than with smaller doses. Beyond this maximal dose any further increase in dose will not improve antagonism of the block. The maximum dose for neostigmine is 60-80 μ g/kg and for edrophonium, 1-1.5 mg/kg. The maximum effect of neostigmine occurs at 10 min. If adequate recovery does not occur by this time, any further recovery is likely to be slow and depends on clearance of the drug from the plasma. Administration of higher doses will have no effect. Rate of spontaneous recovery of the block: This is the natural process of decrease in plasma concentration of the relaxant due to its elimination. Recovery of block is quicker and easier when some spontaneous recovery has occurred. This is why reversal of NMB is easier for short or intermediate acting drugs. Concentration of inhaled anesthetic: Recovery from NMB is delayed by the presence of inhalation anesthetics. Respiratory acidosis: This can ‘hasten’ recovery due to stimulation of the respiratory centre by carbon dioxide. In fact it was standard practice (after introduction of NMB in anesthetic practice) to add CO2 before administering anticholinesterase. This was to overcome the hypocarbia produced

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

by inadvertent hyperventilation when manual ventilation was used. Mild hyperventilation is seen to augment NMB. If maximum doses of anticholinesterases fail to antagonize the neuromuscular block, other factors have to be considered. 7. Acid-base status: Metabolic acidosis and respiratory alkalosis potentiate nondepolarising block. 8. Electrolyte imbalance: Hypokalemia can potentiate neuromuscular block due to an increase in the end plate transmembrane potential resulting from an increase in the ratio of intra to extracellular K+. 9. Others: The use of calcium channel blockers, hypothermia and aminoglycoside antibiotics may delay reversal from NMB. If, for any reason, the reversal of muscle relaxants is judged to be inadequate, the endotracheal tube should be left in situ or reinserted, ventilation should be supported if required and the patient should be reassured and sedated till adequate recovery occurs. Neuromuscular Diseases Altering the Action of Muscle Relaxants 1. Demyelinating diseases: a. Multiple Sclerosis (MS): This condition is associated with upregulation of ‘nAChRs’ (non-Acetylcholine receptors) with risk of hyperkalemia after succinylcholine. There may be also an increased sensitivity to nondepolarisers because of a reduction in muscle mass and a decrease in the safety of neuromuscular transmission. b. Motor neuron diseases: The commonest example is Amyotrophic Lateral Sclerosis. This condition as well as lower motor neuron diseases also exhibit upregulation of the receptors and a presynaptic inhibition of transmission leading to hypersensitivity to nondepolarising relaxants.

45

c. Guillain-Barre syndrome (GBS): There is a functional denervation of muscles and upregulation of the receptors. Succinylcholine is contraindicated and should not be used even after the deficit has recovered. There is enhanced sensitivity to nondepolarisers due to loss of motor units and channel blockade at the NMJ. 2. Muscle diseases: a. Dystrophies: These are genetically determined disorders of the skeletal and cardiac muscles with muscle fibre necrosis and progressive muscle weakness. These patients (usually children) may need anesthesia for strabismus surgery or muscle biopsy. Extrajunctional receptors present due to muscle degeneration make these patients extremely susceptible to the effects of succinylcholine. Hyperkalemia, refractory VF (ventricular fibrillation), rhabdomyolysis and malignant hyperpyrexia can occur with very high mortality. Succinylcholine is therefore contraindicated in these patients. Resistance to nondepolarisers is expected but may be seen due to muscle wasting. b. Mitochondrial myopathies: increased sensitivity to both types of relaxants is seen. 3. Channelopathies are disorders of ion channel function and may be acquired, genetic or transcriptional. a. Myasthenia gravis is an example of an acquired channelopathy. This is an antibody mediated autoimmune disease targeted against the alpha subunit of the postjunctional receptors resulting in muscle weakness and fatiguability. These patients are exquisitely sensitive to nondepolarising relaxants and somewhat resistant to suxamethonium, so neuromuscular junction monitoring is mandatory while anesthetising them.

46 A PRIMER OF ANESTHESIA

b. Myasthenic Syndrome (Eaton Lambert Syndrome) is an acquired channelopathy associated with certain carcinomatous conditions (e.g. oat cell carcinoma). Autoantibodies are directed against the voltage gated calcium channels causing a decrease in release of ACh. It clinically resembles myasthenia gravis but may be differentiated by EMG when high frequency stimulation results in facilitation rather than fade. These patients are sensitive to both depolarizing and nondepolarising relaxants. c. Congenital myasthenic syndromes are diverse disorders characterized by muscle weakness and fatiguability due to congenital defects in different components of the NMJ. d. Ion channel Myotonia is inherited as an autosomal dominant condition and results in wasting of muscles of the face, cervical and proximal limb muscles. The response to nondepolarisers may be normal but these patients may develop generalized contracture following succinylcholine and the use of anticholinesterases may exacerbate the myotonia. Issues with Neuromuscular Blockade in the Intensive Care Unit Role of succinylcholine: Prolonged immobilization may lead to an upregulation of nAChR’s. Succinylcholine, if used after total body immobility for more than 24 hours is associated with a higher incidence of hyperkalemia and cardiac arrest, and is best avoided for intubating ICU patients. Nondepolarizing relaxants: Their prolonged use has a definite association with persistent weakness to various causes which may be: (i) persistent neuromuscular block with circulating levels of the drug or its metabolites, (ii) due to the development of a critical illness,

myopathy or polyneuropathy. This condition is more common with the use of steroidal relaxants. It is therefore important to minimise the dose by maximal use of sedation, using bolus rather than infusion, and allow intermittent recovery. MONITORING OF NEUROMUSCULAR BLOCK Although the degree of neuromuscular block during anesthesia may be evaluated subjectively by clinical signs, objective assessment of the degree of neuromuscular blockade by monitoring the neuromuscular junction is seen to improve the safety margin in the use of these drugs. Neuromuscular blocking drugs have a narrow therapeutic window - whilst there may be no block detectable until 75-85% of the receptors are blocked, paralysis may be complete when 90-95% are occupied. Further, patients may vary in their response to these drugs. Use of NMJ monitoring enables the anesthesiologist to both provide adequate neuromuscular blockade to facilitate surgery and to ensure that the patient has adequate muscle power at the end of surgery. It has been seen that without monitoring of neuromuscular function, up to 40-50% of patients may have inadequate muscle power when they reach the recovery room and this may cause complications like hypoxemia, hypercarbia and pulmonary aspiration. Neuromuscular function is monitored by evaluation of the response of any peripheral nerve to (a) electric or (b) magnetic stimulation. Since the equipment for magnetic stimulation is bulky and not practical for clinical use, electrical stimulation is the modality in use. Equipment required includes a nerve stimulator (Fig. 3.10) with the following features: (1) battery powered, (2) can provide multiple methods of stimulation, i.e. single twitch, train of four, double burst, post tetanic count, (3) ability to calculate and display fade ratio and percent depression of twitch height.

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

Fig. 3.10: Nerve stimulator over ulnar nerve

Terminolog y used in Nerve Stimulation Terminology Threshold current is the lowest current required to depolarize the most sensitive fibres in a given nerve bundle in order to elicit a detectable muscle response, termed Initial threshold for stimulation (ITS). A stimulus should produce a monophasic and rectangular waveform and the length of the impulse should be 0.2-0.3 msecs. A pulse greater than 0.5 msec can stimulate the muscle directly or cause repetitive firing. A supramaximal stimulus is 10-20% higher than the current required to stimulate all the nerve fibres in a particular bundle. It is selected when delivering single twitch stimulus to ensure constant recruitment of all the fibres and is 2-3 times higher than the threshold current for stimulation (about 2.76 times the ITS). Stimulus frequency is the rate at which the stimulus is repeated per second (Hz). Electrodes may be: (1) Surface electrodes which have gel covered surfaces for transmission of impulses to the nerves through the skin. The actual area of contact should be 7-8 mm in diameter. Prior to their application prepare the skin by removing excess hair, light abrasion of skin to reduce thickness of cornified layer and cleaning with alcohol and application of

47

electrolyte solution or a conducting gel. If properly prepared, the ITS should be less than 15 mA. (2) Needle electrodes deliver impulses directly close to the nerve. They are useful in conditions where surface electrodes are unable to deliver supramaximal stimulus as in obese patients or where the skin is thick, edematous or cold. They may cause local irritation, infection, nerve damage, burns, repetitive firing or direct muscle stimulation. Sites of stimulation are of interest due to the differing response of different muscle groups to stimulation. The diaphragm is amongst the most resistant requiring 1.4-2 times the dose of relaxant as the adductor pollicis. The most sensitive are the abdominal muscles, orbicularis oculi, peripheral limb muscles, geniohyoid, masseter and upper airway muscles. The site most commonly used is the wrist where the ulnar nerve is stimulated to elicit response in the adductor pollicis. Two stimulating electrodes are placed on the radial side of the flexor carpi ulnaris. The distal (negative) electrode is placed 1 cm proximal to the proximal palmar crease and the proximal (positive) electrode is placed 2-3 cm more proximally. The recording electrodes are placed over the muscle. Response is seen as finger flexion and thumb adduction. The adductor pollicis remains the gold standard due to (i) its ease of accessibility, (ii) good visual, tactile and mechanographic assessment, and (iii) precision of assessment. The onset and recovery of blockade at both the laryngeal muscles and the diaphragm occur earlier than in this muscle. The other nerve-muscle groups used are: (a) ulnar nerve—first dorsal interosseous muscle, (b) ulnar nerve—abductor digiti quinti, (c) posterior tibial nerve (stimulated behind medial malleolus)—flexors of the great toe and foot, (d) peroneal nerve (stimulated behind the head of the fibula)—dorsiflexors of the foot, (e) facial nerve (stimulated near the tragus)—orbicularis oculi, orbicularis oris and, (f) phrenic nerve (electrically stimulated in the neck)—diaphragm.

48 A PRIMER OF ANESTHESIA

Pattern Patternss of Stimulation a. Single twitch: This is the simplest form of stimulation and consists of a single 0.10.2 msec impulse delivered at supramaximal current at a frequency of 1Hz. A control value is recorded before administering the relaxant. During a nondepolarising block there may be no reduction in its height until at least 70-75% of receptors are occupied or blocked. The 1 Hz stimulation results in a faster apparent onset of block as compared to 0.1 Hz stimulation. b. Train of four (TOF) was first described by Dr Hasan Ali, and consists of a sequence of 4 stimuli delivered at a frequency of 2 Hz, i.e. one stimulus every 0.5 sec. At this frequency the immediately available store of ACh is depleted and the amount released by the nerve with each impulse decreases. Normally, even this reduced amount of ACh is enough to elicit normal muscle contraction due to the wide margin of safety in neuromuscular transmission. In the presence of nondepolarizing block this margin of safety is reduced and some end plates will fail to develop propagated end plate potentials. This causes a fade in the TOF responses which is expressed as TOF ratio (TOFR) and is the height of the fourth response expressed as a percent of the first. The disappearance of the fourth response in TOF corresponds to a 70-75% depression in the single twitch height. During depolarising blockade there is no fade seen and the height of all the twitches is uniformly reduced. Fade in TOF after succinylcholine implies the development of a phase II block. When TOF stimulation is used there is no need for a pre relaxant baseline stimulus as it is the relative height of the fourth response to the first response (the ratio) which is taken into account. It is more sensitive than single twitch to detect lesser degrees of block. The degree of fade is similar to that with 50 Hz tetanic stimulation and it is less painful.

c. Tetanic stimulation is high frequency stimulation (30, 50 or 100 Hz) which results in sustained or tetanic contraction of the muscle. During normal neuromuscular transmission or a phase I block the response to tetanus is sustained. During a nondepolarising block and phase II block a fade is seen on tetanic stimulation. During a tetanus large amounts of ACh are released from the immediately available ACh stores. As these stores get progressively depleted this is balanced by an increased synthesis and transfer of transmitter from its mobilization stores and thus, normally, neuromuscular transmission is maintained. The presence of a nondepolarizing block reduces the number of free cholinergic receptors and also impairs the mobilization of ACh within the nerve terminal resulting in a fade in the response to tetanic stimulation. When the TOF ratio is more than 0.7 the response to tetanus at 50 Hz for 5 secs is sustained and no fade is seen. d. Double burst stimulation consists of 2 short tetanic bursts separated by enough time to allow relaxation, i.e. 750 msecs. These ‘minitetani’ fatigue the NMJ to a greater extent than 2 single twitches so that fade is exaggerated allowing a better visual and tactile appreciation of the degree of fade. The most promising pattern seems to be two trains of 3 impulses at 50 Hz separated by an interval of 750 msec. e. Post-tetanic count (PTC) is based on the principle of post tetanic facilitation. It is useful in intense block when there is no response to single twitch, TOF or tetanus. Tetanic stimulation results in an increase in the store of immediately available ACh and a single twitch delivered after the tetanus will be greater than that elicited before the tetanus. A tetanic stimulus is applied at 50 Hz for 5 sec and is followed 3 sec later by single twitch stimulation at 1 Hz. The

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

49

Fig. 3.11: Comparison of responses to various forms of nerve stimulation (The asterix indicates the stimulus applied after tetanus)

number of post tetanic twitches evoked is called the post tetanic count (PTC). This can be repeated not earlier than 6 min. PTC is a prejunctional event and depends on the relaxant used. A PTC of 8-9 implies that the first response to TOF is about to return. The main use of this mode is to: (i) monitor intense degrees of blockade, (ii) when sudden patient movement is undesirable, and (iii) to predict time to reappearance of first response to TOF. The response seen to various kinds of stimuli in the presence of depolarizing, nondepolarizing and Phase-II block is shown in Figure 3.11. Method of clinical use: The nerve stimulator should be set up prior to induction of anesthesia but stimulation should be started only once the patient is asleep. The stimulation should commence with single twitch at 1 Hz to select the supramaximal stimulus. Then TOF stimula-

tion mode can be selected and the relaxant given. Endotracheal intubation can be done once response to TOF disappears or one can wait a further 30-90 secs to ensure better conditions. The onset of neuromuscular block at the larynx is faster and corresponds to the time when response at the adductor pollicis shows palpable weakening. A minimum level of neuromuscular block should be maintained to ensure adequate abdominal muscle relaxation. Intense Block usually occurs 3-6 mins after injection of an intubating dose of relaxant, termed the ‘period of no response’ as there is no response to TOF or single twitch. The time to return of TOF can be estimated by PTC. If intense block is required as patient movement would be detrimental to the patient, as in ophthalmlology or neurosurgery, PTC can be kept at 0 at the thumb. A PTC of or = 0.8

Vital capacity and inspiratory force normal, can bite/clench teeth but may have diplopia and facial weakness.

=0.85

Can bite/clench teeth.

0.85-0.9

But may still be pharyngeal weakness with risk of regurgitation and aspiration. Table 3.6: Tests for adequate reversal from NMB

Parameter

Value

Tidal volume

> or = 5ml/kg

Single twitch

Same as baseline

75-80

TOF

No palpable fade

70-75

Tetanus 50 Hz for 5 secs

No palpable fade

70

Vital capacity

>or = 20 ml/kg

70

DBS

No palpable fade

60-70

Tetanus 100 Hz for 5 secs

No palpable fade

50

whereas a PTC > 9 correlates with a TOF count of 1 and is usually adequate for most surgical procedures. Moderate/surgical blockade begins when the 1st response appears on TOF. With this first response, twitch depression is 90-95%. When the 4th response appears twitch depression is 60-85%. Adequate relaxation for most surgeries is provided up to the appearance of the second twitch. Recovery of the block: The return of the 4th response in TOF heralds the onset of the recovery phase. Response at the adductor pollicis indicates that the laryngeal muscles and diaphragm are recovering. For adequacy of reversal TOF count should be 3-4 prior to attempting reversal of neuromuscular blockade.

Predicted TOFR 80

If TOF count is 1-2, neostigmine is the reversal agent of choice. Reversal should not be attempted if TOF count is 0. Adequate clinical recovery: This implies that it is safe to extubate the trachea and that the patient has adequate protective laryngeal reflexes and adequate respiration. Once all 4 responses appear on TOF and there is no detectable fade, the TOFR may be 40-100%. Correlation between TOFR and recovery is given in Table 3.5. It is wise to use as many tests possible to ensure that no residual block exists. The commonly used tests are tabulated in Table 3.6. Reliable versus unreliable clinical tests are listed in Table 3.7. These are used when neuromuscular monitoring is not available.

PHYSIOLOGY OF NEUROMUSCULAR BLOCKADE AND NEUROMUSCULAR PHARMACOLOGY

51

Table 3.7: Clinical tests of recovery after administration of neuromuscular blockers Unreliable Test

Reliable Test

Sustained eye opening

Sustained head lift for 5 secs

Tongue protrusion

Sustained leg lift for 5 secs

Lift arm to opposite shoulder

Sustained hand grip for 5 secs

Normal tidal volume

Sustained tongue depressor test

Normal vital capacity

Maximum inspiratory pressure >-40-50 cm water

Maximum inspiratory pressure 1 NMJ per cell a. Airway muscles b. Hand muscles c. Diaphragm muscles d. Extraocular muscles 2. ACh at the NMJ is metabolized by a. Acetylcholinesterase b. Pseudocholinesterase c. Butrylcholinesterase d. Anticholinesterase 3. Extrajunctional receptors are synthesized in all conditions but a. Inactivity b. Exercise c. Burns d. Denervation

4. Persistent weakness after succinylcholine indicates a. Reversal of block b. Phase I block c. Phase II block d. Nondepolarizing block 5. All are long acting muscle relaxants except a. Atracurium b. Pancuronium c. D tubocurarine d. Gallamine 6. All are intermediate duration muscle relaxants except a. Atracurium b. Vecuronium c. Mivacurium d. Rocuronium 7. All are short acting muscle relaxants except a. Succinylcholine b. Atracurium c. Mivacurium d. Rapacuronium 8. The normal rise in serum potassium after a dose of succinylcholine is a. 0.5 mEq/l b. 1.0 mEq/l c. 1.5 mEq/l d. 2.0 mEq/l 9. Phase II block is likely to develop after the following dose of succinylcholine a. > 2mg/kg b. > 4 mg/kg c. > 6 mg/kg d. > 8 mg/kg 10. Which muscle relaxant is metabolized by Hofmann elimination a. Pancuronium b. Atracurium c. Vecuronium d. Rocuronium

52 A PRIMER OF ANESTHESIA

11. Succinylcholine causes a rise in all but a. Intragastric pressure b. Intraocular pressure c. Intracardiac pressure d. Intracranial pressure 12. Histamine release is seen with a. Vecuronium b. Atracurium c. Pancuronium d. Rocuronium 13. All are used to antagonize NMB except a. Edrophonium b. Rocuronium c. Neostigmine d. Pyridostigmine 14. NMB can be detected after block of a. 25-35% receptors b. 35-45% receptors

c. 55-65% receptors d. 75-85% receptors 15. TOF consists of sequence of 4 stimuli at a frequency of a. 1 Hz b. 2 Hz c. 3 Hz d. 4 Hz 16. A patient can bite/ clench teeth when TOFR is a. > 0.5 b. > 0.7 c. > 0.85 d. > 1.00 Answers 1. 5. 9. 13.

d a c b

2. 6. 10. 14.

a c b d

3. 7. 11. 15.

b b c b

4. 8. 12. 16.

c a b c

The Anesthesia Machine Rajeshwari Subramaniam, Chittaranjan Joshi

        

Functions of the modern anesthesia machine Components of the anesthesia machine Cylinders, pin index system Pipelines and their connections Flowmeters, oxygen flush Anesthesia breathing systems Mapleson classification Magill circuit, Bain circuit, Ayre’s T-piece Closed circuit and sodalime absorption

It is important for all physicians to have a working knowledge of the anesthesia machine, breathing circuits and various airway devices. Apart from administration of anesthesia, these are useful for emergency airway management, oxygenation and cardiopulmonary resuscitation (CPR). The anesthesia machine in use nowadays is termed a ‘continuous flow’ machine since there is no interruption to gas flow in the respiratory cycle. In earlier times ether or chloroform was dropped on to a wire mask covered with layers of gauze or lint (‘Open-drop anesthesia’ through a Schimmelbusch mask; Fig. 4.1). The concentration of vapor delivered, oxygenation, carbon dioxide elimination and depth of anesthesia were all variable with this technique. The ‘draw-over’ apparatus which was more

Fig. 4. 1: Schimmelbusch mask

superior consisted of inhalers like the EMO apparatus (Fig. 4.2), where gas flow occurred during inspiration and was dependent on patient effort. Oxygen (as gas) and nitrous oxide (as liquid) are stored under high pressure in cylinders which cannot be directly administered to a patient owing to the danger of barotrauma. Further, at high pressures flow rates are difficult to control. The modern anesthesia machine overcomes these problems and serves the following functions: 1. Can deliver compressed gases under physiologically safe pressures. 2. Enables the anesthesiologist to adjust flow and composition of inhaled gases. 3. Is capable of delivering accurate amounts of volatile anesthetic agents.

54

A PRIMER OF ANESTHESIA

Fig. 4.2: EMO vaporizer

4. Has many features preventing delivery of hypoxic mixtures and therefore enhancing patient safety. A typical anesthesia machine can be anatomically divided into two pressure zones: • The high pressure system extending from the cylinder or pipeline inlet up to the flowmeter valve*. A pressure regulating valve reduces the pressure in the oxygen cylinder (2,200 psig) and that in the nitrous oxide cylinder (750 psig) to 45 psig. A conversion factor useful to remember is that 1 kilo Pascal (kPa) = 0.01 bar = 0.1013 atmospheres = 0.145 psig = 10.2 cm H2O =7.5 mm Hg. The pipeline pressure is normally 50-60 psig, kept 10-15 psig above reduced cylinder pressure so that it is preferentially used even if a cylinder is kept open. [Many machines of the ‘Ohmeda’ make also have a second stage pressure regulator in the oxygen supply line downstream of the oxygen failure alarms. This reduces the oxygen pipeline pressure to a fixed value of 14-20 psig before it enters the flowmeter valve]. • The low-pressure system extends from the flowmeter valves to the common gas outlet.

The pressures in this area range from 12-14 psig at the needle valves to 2-4 psig at the machine outlet. In the following text, the structure and function of the components of the anesthesia machine encountered in sequence are described. The safety features of the anesthesia machine are highlighted. The components are: 1. Source of gas supply: pipelines and cylinders 2. Hanger yoke assembly 3. Pressure reducing/regulating valves 4. Oxygen pressure failure safety/warning devices 5. Oxygen ratio control devices 6. Flow meters 7. Vaporizers 8. Common gas outlet.

Source of Gas Supply Anesthetic gases are usually supplied in cylinders made of molybdenum steel, an alloy which allows the cylinders to be made thinner and lighter for comparable working pressures. Medical gas cylinders are color coded (Table 4.1) and the name of the gas is also written on the neck of the cylinder. The Table 4.1: Pressures in, and color of various compressed gases Gases

Pressure when full

Color Coding

Oxygen (gas)

2000 psig

Entonox (gas)

1980 psig

Black body with white shoulder Blue body with white shoulder Gray Orange French blue

Carbon dioxide (liquid) 723 psig Cyclopropane (liquid) 64 psig Nitrous oxide (liquid) 640 psig

(* Some textbooks describe the cylinders, yoke blocks and pressure regulators as ‘high pressure’ area, and the area from the cylinder pressure regulating valves up to the flowmeter valves as ‘intermediate pressure’ and from the flowmeters up to the common gas outlet as ‘low pressure’).

THE ANESTHESIA MACHINE

55

Fig. 4.3: Pin index safety system for medical gas cylinders

cylinders are hydraulically tested every 5 years. These cylinders are provided with a flush type pin index valve (Fig. 4.3). The contents in a cylinder, if a gas, is indicated by the pressure gauge. A formula that is helpful in determining how long an oxygen cylinder can last is given by: Approximate remaining time (hours) = oxygen cylinder pressure (psig)/200 × oxygen flow rate (l/min). If the contents are liquid ( as with nitrous oxide) the cylinder should be weighed and the empty weight subtracted. Reserve gas cylinders are fitted to the rear of the machine.That part of the cylinder which is attached to the anesthesia machine is known as the pin index valve block (Fig. 4.4A). It is a solid cuboid with four faces. One face shows the empty weight (tare), the second the symbol

for nitrous oxide and the third the pressure of the hydraulic test. It is the fourth side which gets attached to the machine which bears the gas outlet and the pin index safety system (Fig. 4.4B). The pin index system (Fig. 4.3) consists of seven holes positioned on the circumference of a circle of 9/16 inch radius centered in the port, with a pair of positions designated for each gas (Table 4.2). The two pins projecting from the inner surface of the yoke get inserted into two corresponding holes in the cylinder valve block when the cylinder is suspended on the machine. The arrangement of these pins is specific for each gas and therefore its cylinder. The pin index system prevents an incorrect cylinder being mounted at the place belonging to another gas.

56

A PRIMER OF ANESTHESIA Table 4.2: Pin index system

Gas Oxygen Nitrous oxide Cyclopropane O2 -CO2 (CO2>7.5%) O2 –He (He>80.5%) Air Nitrogen N2O-O2 (N2O 47.5%-52.5%)

Index Pins 2,5 3,5 3,6 1,6 4,6 1,5 1,4 7

The pipeline inlets: Oxygen, nitrous oxide and, in some hospitals, medical air are supplied from a central manifold (which contains banks of cylinders) through metal pipelines to the operating room and ICUs. These pipes are color coded (white for oxygen, blue for nitrous oxide). On the wall of the operating room, or the ceiling of the operating theatre, the pipeline from the manifold terminates in the form of selfclosing sockets with ‘quick coupling’ attachments (Fig. 4.5). The coupling pairs are specific in size and shape for each gas and vary with the manufacturer. These sockets may be present in modern theatres as ‘gas columns’ and permit only the end of the correct hose to engage in them and open them. At the machine end, the diameter-indexed safety system (DISS, Fig. 4.6) permits the attachment of the correct hose only to be screwed on to the machine so that interchangeability is virtually eliminated.

Yoke Assembly

Fig. 4.4A: Face of pin index block showing tare weight, company and ISI marking

Fig. 4.4B: Face of pin index block of nitrous oxide cylinder showing holes for pins

The hanger yoke assembly (Fig. 4.7) orients and supports the cylinder and connects it to the machine. A gas-tight seal is provided with a Bodok sealing washer, made of rubber with a metal periphery. This should be inspected for integrity every time a cylinder is changed. The pins on the yoke (which are part of the Pin Index system) are 4 mm in diameter and 6 mm long. A one-way check valve present immediately downstream of the hanger yoke has three important functions: i. It prevents a cylinder under higher pressure from emptying into one with lower pressure. ii. It allows change of cylinder on the machine without gas leaking out. iii. It prevents leaking and emptying of a cylinder left open even if one cylinder is absent from a yoke. There is usually a single pressure gauge for two similar cylinders hung on the machine downstream of the check valve and it shows the pressure in the cylinder having the higher

THE ANESTHESIA MACHINE

57

pressure if both are opened at the same time. Therefore, it may not be possible to determine whether, and if any, of the reserve cylinders is empty unless if they are opened one at a time.

Pressure Regulator

Fig. 4.5: ‘Quick coupling’ attachments

The pressure in a cylinder is high and variable as it changes with the contents and temperature. The cylinder pressure regulator is a pressureregulating valve which converts the high variable pressure in the cylinder into a constant working pressure suitable for use in anesthesia machine, usually 45-47 psig. These regulators work on the principle that high pressure exerted by the cylinder contents over a small area is balanced by reduced pressure exerted over a large area.

Oxygen Pressure Failure Warning Devices

Fig. 4.6: The DISS behind the machine

All modern anesthesia machines have an audible whistle with a blinking red light when the inlet gas pressure drops below a preset value (20-35 psig). This alarm cannot be disabled till oxygen supply is restored. Another safety feature is cutting off of all gases (except air) when the pressure after the secondary regulator falls below 20 psig. This feature used to be known as failsafe or nitrous cut-off valve. The third kind of device is a proportioning device (also termed

Fig. 4.7: The hanger yoke assembly:shows retaining screw opened (l) and in place (r). note bodok washer and pins

58

A PRIMER OF ANESTHESIA

Fig. 4.8: The flowmeter assembly (l) and an enlarged view of the Thorpe tube (r)

oxygen failure protection device) which proportionately reduces the pressure of nitrous oxide as oxygen pressure falls.

Flowmeter Assembly All the flow meters have a flow control valve, a graduated stem (which is a glass tube) to measure and see the flow and an outlet. The flow meter used in modern anesthetic machines is of the variable orifice type and is made up of a transparent tapered tube known as Thorpe tube (Fig. 4.8). A float which moves up when the gas is turned on and keeps rotating indicates gas flow. The flow control valve is a needle valve or pin valve used to adjust the amount gas entering the flowmeter block. The knob which rotates the needle valve is color and configuration coded; the oxygen knob is large, fluted and white and always situated towards the gas outlet of the machine (Figs 4.9A to C). This is to prevent escape of oxygen and delivery of a hypoxic mixture in the event of a crack in the flowmeter (Fig. 4.10). Another safety feature of the machine incorporated in the flowmeter assembly is the flow controller mechanism whereby the nitrous oxide is linked to oxygen

flow by a chain-gear system and cannot be independently turned on; this way a minimum of 21-25% oxygen is always present in the gas mixture. Minimal oxygen flow of 150 ml/min which starts as soon as the machine is switched on is another safety mechanism.

Oxygen Analyser The use of an oxygen analyzer with an anesthesia system is the single most foolproof

Fig. 4.9A: Large, fluted oxygen flowmeter knob

THE ANESTHESIA MACHINE

59

Fig. 4.10: Escape of oxygen when oxygen flowmeter is away from outlet (L) Fig. 4.9B: Oxygen flowmeter situated away from gas outlet in older anesthesia machine

Fig. 4.9C: Oxygen flowmeters on the same side as gas outlet in modern machine

measure to prevent delivery of a hypoxic mixture to the patient. This is because it is not dependent on pneumatic or mechanical links, but actually measures the oxygen percentage in the gas mixture either by polarographic method or by using a fuel cell.

Vaporizers A vaporizer is designed to add a controlled amount of an inhalational agent, after changing

it from liquid to vapour, to the fresh gas flow. This is normally expressed as a percentage of saturated vapor added to the gas flow, i.e. a 2% vaporizer setting means that 2 ml of vapor is being carried per 100 ml of total fresh gas flow. Most volatile agents in current use are very potent, and accurate, controlled administration through agent-specific vaporizers is needed to avoid overdose and toxicity. Modern vaporizers compensate for the cooling produced by evaporation and are not affected by ambient temperatures or pressures over a wide range. They are usually mounted on the back bar of the machine (Fig. 4.11). When one vaporizer is in use, restraining rods spring out which prevent another vaporizer from being used simultaneously. This is the ‘Selectatec’ system which can be considered as a safety feature. Most inhalational agents in current use have boiling points well above room temperatures except desflurane (24°C). For this reason a special heated vaporizer (Tec 6) is required for this agent. Characteristics of an ideal vaporizer: 1. Performance should not be affected by changes in: (a) fresh gas flow, (b) volume of the liquid agent, (c) ambient temperature, (d) decrease in temperature or pressure due

60

A PRIMER OF ANESTHESIA

Fig. 4.11: Vaporizers on back bar of anesthesia machine

2. 3. 4. 5. 6.

to vaporization, and (e) pressure fluctuation due to the mode of respiration. Should have low resistance to flow. Should be light weight with small liquid requirement. Economy and safety in use with minimal servicing requirement. Have corrosion and solvent resistant construction. A non return pressure relief safety valve is situated downstream of the vaporizers either on the back bar itself or near the common gas outlet. It opens when the pressure in the back bar exceeds about 35 kPa.

Emergency Oxygen Flush The emergency oxygen flush is usually activated by a non locking button. The flow bypasses the flowmeter and the vaporizer and is derived from an independent pipeline after the pressure regulator. It joins downstream of the high pressure check valve. A flow of about 35-75 l/min at a pressure of about 400 kPa is delivered from this system. Activation of the oxygen flush is frequently required as an emergency, as when one would like to fill the reservoir bag quickly to ventilate a patient. Learn to locate and activate the oxygen flush in the machines in your workspace.

Fig. 4.12: Common gas outlet

Common Gas Outlet All machines have a common gas outlet (Fig. 4.12) where the breathing system (‘circuit’) gets attached. Most machines have an option of selecting the route the gases will take- whether through the sodalime canister and circle system or one of the Mapleson (commonly D or F) systems (termed ‘auxiliary’). Before beginning induction it is vital to check which circuit one is using and whether the selector knob has been appropriately turned. Compressed Oxygen Outlet(s) One or more compressed oxygen outlets may be available to provide oxygen at about 400 kPa. These can be used to drive ventilators or for manually controlled jet injectors. THE ANESTHESIA BREATHING CIRCUITS The breathing circuit is a vital part of anesthesia equipment. This is the interface between the machine and the patient and is the conduit to deliver oxygen, pre-selected gas flows and volatile agents to the patient. The breathing circuit performs another important function of carbon dioxide elimination from the lungs. As we saw earlier, the open drop method is very unreliable both from the point of view of

THE ANESTHESIA MACHINE

61

oxygenation as well as CO2 elimination. A brief description of the circuits used nowadays and their advantages is given below. Properties of an ideal breathing circuit: 1. Should be simple and safe to use 2. Should permit spontaneous and controlled ventilation. 3. Should be suitable and safe for adults as well as children 4. Should be efficient, requiring low fresh gas flow rates. 5. Should have safety features to protect the patient from barotrauma. 6. Should be sturdy, compact and lightweight in design. 7. Should permit easy removal of waste exhaled gases. 8. Easy to maintain and sterilize with minimal running cost.

Fig. 4.13: Magill circuit

The Mapleson Breathing Circuits The common anesthetic breathing circuits in use were described and analyzed by W.W. Mapleson in 1954. All these circuits have common components- a fresh gas flow inlet, a reservoir bag, an expiratory or pop-off valve, and tubing. They are classified into A, B, C, D, E, F type based on the relative positions of the fresh gas flow and expiratory valve. The efficiency of each breathing system is gauged by the fresh gas flow rate required to prevent rebreathing. The Mapleson A or Magill circuit (Fig. 4.13) is still present on many old anesthesia machines in the peripheral areas of the hospital. The importance of the Magill circuit lies in the fact that of all the Mapleson circuits, it is the most efficient for spontaneous ventilation, requiring fresh gas flow equal to the patient’s minute ventilation (MV). However, it is the least efficient for controlled ventilation. We shall discuss the Mapleson D circuit in some detail as its modified version is commonly used as the ‘Bain’ circuit (Fig. 4.14). The bain

Fig. 4.14: Bain circuit showing co-axial arrangement

circuit is a co-axial circuit. The inner tube carrying the fresh gas flow (FGF) enters the outer expiratory tube at the machine end, travels along the length of the expiratory limb (which is a transparent corrugated plastic tube) and terminates at the patient end. The end of the inner tube is attached to the outer tube at the patient end by three spokes (Fig. 4.15). Thus FGF is actually delivered close to the patient. The patient exhales into the outer tube which

62

A PRIMER OF ANESTHESIA

Fig. 4.15: Patient end of Bain circuit. Note inner tube attached to outer by 3 spokes

Fig. 4.16: Jackson-Rees’ modification of Ayre’s ‘T’ piece

ends at the reservoir bag and incorporates an expiratory valve at the reservoir bag end. The Bain circuit has many inherent advantages: 1. It is lightweight and convenient to use. 2. It is re-usable and easily sterilizable. 3. It can be used for both spontaneous and controlled ventilation without making any changes in connection, valves, etc. 4. Exhaled gases in the outer tube warm the inspired FGF. 5. Scavenging of exhaled gases is easy due to the expiratory valve being situated away from the patient. Proper functioning of the Bain circuit should be ascertained by checking the integrity of the inner tube. If broken or kinked it leads to severe hypercarbia. For spontaneous ventilation, FGF needed to prevent rebreathing is 2.5 times the minute ventilation and for controlled ventilation it is 1-2 times the minute ventilation. The Jackson-Rees’ modification of the Mapleson E circuit (Mapleson F, Fig. 4.16) is widely used in pediatric anesthesia. You will notice that it has no valves, which explains the low resistance it offers .It also has advantages of simplicity, allowing spontaneous or controlled ventilation and is lightweight so that there is no

drag on the pediatric endotracheal tube. The FGF required to prevent rebreathing for spontaneous ventilation is 2-3 times the minute ventilation; that for controlled, 2 times the minute ventilation. We discussed semiclosed systems till now where provision of a designated FGF was required to prevent rebreathing. With increasing awareness to reduce theatre and atmospheric pollution by inhaled volatile anesthetics and for purposes of economy a circuit had to be devised which would absorb the exhaled carbon dioxide and so enable recycling of unused oxygen and volatile agent, thereby minimizing spill and wastage. The answer was the closed circuit (Fig. 4.17). The normal FGF used is 1litre. A sterilizable canister packed with ‘high-moisture’ soda lime (80% calcium hydroxide, 15% water, 4% sodium hydroxide and 1% potassium hydroxide) is interposed in the circuit. The reaction that occurs in the sodalime canister is as follows: CO2 + H2O → H2CO3 H2CO3 + 2NaOH → Na2CO3 + 2H2O + Heat Na2CO3 + Ca (OH)2 → CaCO3 + 2NaOH

THE ANESTHESIA MACHINE

63

Fig. 4.17: Schematic representation of closed circuit

Use of the closed circuit results in economy, prevention of theatre pollution and prevention of chronic exposure of personnel to inhalational agents, and conservation of heat and humidity in the inspired gases. A detailed

discussion of the circuit components is out of the purview of this text. Compounds generated due to the interaction of sodalime with inhalational agents is detailed in the section on inhalational agents.

Preoperative Evaluation of Patients Anjolie Chhabra

     

Goals and benefits of preoperative evaluation Steps in preoperative evaluation Guidelines for laboratory testing ASA grading of patients Fasting guidelines and premedication Some specific disease conditions and their anesthetic implications

The anesthesiologist’s involvement in the care of the patient begins before the patient reaches the operating theatre. This interaction in the preoperative phase marks the beginning of anesthetic care. A well performed evaluation leads to accurate estimation of the patient’s physical condition, predicting possible complications and planning appropriate intraoperative and postoperative care. The ultimate goal of assessment is to prevent avoidable morbidity and improve patient outcome.

•

•

•

Goals of Preoperative Evaluation • Obtaining complete information about the patient’s medical history and surgical diagnosis: this will: (a) uncover important medical conditions like hypertension, ischemic heart disease and asthma; and (b) conditions like gastric reflux, snoring and

•

allergies, which have special relevance to anesthesia and peri operative morbidity. The surgical diagnosis is important because procedures can range from minor, e.g. saphenous vein ligation, to a major procedure like pneumonectomy. Establishment of good rapport with the patient and his/her attendants. This is more important (and often better) than pharmacologic premedication. The patient gets an idea of the surgical and anesthetic plan and the options available. He can clarify any doubts or anxieties he may have about the procedure, pain relief, risk, etc. Carrying out a complete physical examination with special emphasis on airway, dentition, cardiorespiratory systems, ease of vascular access and landmarks for regional anesthesia. Decision-making regarding further tests, consultations and/or therapy required to optimize the patient’s condition, especially when the patient has associated medical condition requiring evaluation optimization. Pheochromocytoma is an example of a condition where adequate preoperative preparation is mandatory for enhanced patient safety and improved surgical outcome. Decision of operability (whether the patient can tolerate the surgical procedure) is usually

PREOPERATIVE EVALUATION OF PATIENTS

•

•

• •

taken jointly by the surgeon and anesthesiologist. Obtaining informed consent from the patient after explaining the risks and benefits of the procedure, and the nonsurgical options available. This is especially important where major surgery (for example, in advanced malignancy) is being contemplated, which may involve life-threatening morbidity or disability without significantly prolonging survival. Informed consent is also required for procedures like tracheostomy and colostomy as these can adversely affect the social lifestyle of the patient. Occasionally the patient may be aware of only the anticipated benefits of a procedure and not the risks involved, and these should be explained by the surgeon or anesthesiologist who has the ‘complete’ picture. Planning appropriate anesthetic technique and monitoring keeping in mind the length and nature of surgery, positioning, the patient’s choice and feasibility and benefit of regional anesthetic techniques. Blood and blood products are requisitioned if transfusion is anticipated. Ordering pharmacologic premedication wherever necessary and appropriate. Planning appropriate postoperative care including analgesia and ventilatory support.

What are the Benefits of Preoperative Evaluation? • Morbidity resulting from systemic illness is reduced or avoided by instituting specific measures, e.g. reduction of postoperative pulmonary complications in a patient with chronic bronchitis by chest physiotherapy and breathing exercises. Other examples are cessation of smoking, immunization against pneumococcus and nutritional fortification. • Unnecessary postponement of surgery is avoided, as co-morbid conditions are detected and treated before surgery is

• • •

•

65

scheduled, e.g. control of diabetes and hypertension. Saving of hospital and patient expenditure by shortening stay. Better utilization of hospital beds by faster turnover. Reduces patient’s anxiety regarding the procedure, especially after reassurance and discussion of postoperative pain management. This has been shown to reduce tachycardia and stress in patients with IHD. Enhances patient satisfaction about the quality of hospital care and the fact that his/ her medical conditions have been adequately taken care of.

A Stepwise Approach to Preanesthetic Evaluation

History A. General: • Previous anesthetic exposure and any untoward event: These could be a cardiovascular event, difficulty in intubation, anaphylaxis, reaction to blood or blood products. Check for documentation, similar history in close relative or sibling. • Any known systemic illness; whether on medication; what are the current medications? • Hospitalization in the last 2 years and need for ECG/X-ray in the last year. • Known drug allergies to local anesthetics, non-steroidal anti-inflammatory drugs (NSAIDs) radiological contrast/latex. • History of ‘mild’ chronic medication (including nasal sprays, eye drops, metered dose inhalers) • Possibility of neuromuscular disease, especially muscular dystrophy in children. • Possibility of pregnancy in pre menopausal women • History of smoking and/or tobacco use in any form.

66

A PRIMER OF ANESTHESIA

Sensitive issues: • Drug abuse, alcoholism • Possibility of HIV • Teenage pregnancy B. Cardiovascular Presence of significant cardiovascular disease increases perioperative morbidity and mortality. Symptoms suggestive of congestive failure, arrhythmias, or ischemic heart disease are quite unmistakeable, except for very subtle disease. Poor exercise tolerance (< 4 METs), chest pain or sweating related to exertion (or meals), previous MI (or IHD -related procedures like angioplasty/stenting) and hospitalization, occurrence of palpitations, paroxysmal nocturnal dyspnea and breathlessness on exertion indicate presence of subtle or overt cardiac disease and need a formal evaluation by a cardiologist. Cardiac symptoms can be classified according to the NYHA classification (Table 5.1). Hypertension (blood pressure>140/95 mm Hg) is frequently discovered by chance during pre operative evaluation. Although in some patients it may be part of the ‘white coat syndrome’ (anxiety on being examined by a doctor) it needs to be monitored and charted at 6 or 8 hourly intervals and treated if found to be high. Occasionally the patient may be a diagnosed case of cardiovascular disease and may already be on medication. C. Airway • Snoring (especially in obese adults and children with enlarged tonsils).

• History of airway difficulty in previous anesthetics. An uneventful intubation many years ago is no guarantee that the present one will be easy. • Presence of dentures /other cosmetic dental work • Difficulty/stiffness in neck or jaw movements. Submucous fibrosis (consequent to tobacco chewing) leading to trismus and inability to open the mouth is usually first discovered during the preoperative evaluation. D. Respiratory system: • History of asthma, or seasonal breathing difficulty and its severity. • History of smoking- number of ‘pack years’ of cigarettes/ ‘bidis’ smoked • Emergency hospitalization for breathlessness; treatment administered includes oxygen/ respirator therapy • Use of inhalers or steroids. E. • • • •

Gastrointestinal system: Reflux oesophagitis, peptic ulcer disease. Jaundice, especially in the last 1year. Chronic antacid therapy. Chronic diarrhea.

F. • • • •

Renal or neurological disease: History of renal stones History of muscle weakness Oliguria/polyuria History of dialysis

Table 5.1: New York Heart Association (NYHA) classification

G. History of bleeding: During minor procedures like dental extraction, hemarthrosis after minor injury.

1. Class I – Angina/breathlessness on strenuous physical activity 2. Class II – Angina/breathlessness on moderate activity (climbing more than/2 flight of stairs) 3. Class III – Breathlessness/chest pain on mild activity (level walking, 1 flight of stairs) 4. Class IV –Breathlessness or chest pain at rest or minimal activity

H. Endocrine disease: • History of steroid use, including topical ointment application • History of thyroid medication. • Symptoms suggestive of diabetes mellitus. • Diabetes in family members. • Use of injections/tablets to ‘control sugar’.

PREOPERATIVE EVALUATION OF PATIENTS

Examination This should be unhurried and carried out in a well-lighted area. In patients who cannot be moved (e.g. on traction or on respirator, or patients who are dyspneic or sick, the examination may have to be carried out on the bed itself. It is a good idea to take the patient to the examination room in the ward. Examination complements history; although history points to specific areas requiring examination, facts not elicited in history may be discovered. A. General examination: • Weight of the patient. An accurate weight record is essential for determining drug dosage, fluid therapy, need for blood transfusion, ventilator settings and planning parenteral nutrition. • Resting heart rate and respiratory rate. Especially watch for use of accessory muscles. Asthmatics talk little and breathe quietly using their accessory muscles. Watch for purse-lipped breathing (emphysema). • Presence of fever. • Pulse rate and rhythm. Check whether palms are sweaty/clammy. Check for peripheral cyanosis/clubbing when there is suspicion of cardiac/respiratory disease. If patient has an arteriovenous fistula for dialysis, check for flow and thrill. • Check the blood pressure using Korotkoff sounds. Check supine and erect blood pressures in patients on alpha blockers. Make sure to hold the BP apparatus at heart level when the patient stands. • Check for jaundice in the sclera and anemia in the conjunctiva; check for eye signs of hyperthyroidism, if indicated. B. Airway examination: • Ease or difficulty with mask ventilation: Mask ventilation may be difficult in obese or edentulous patients (details in chapter on Airway Management). • Ease or difficulty with laryngoscopy and intubation can be judged by the following clinical tests:

67

1. Range of neck movements: should be able to flex cervical spine (Fig. 5.1) and extend the head at the atlanto-occipital joint (Fig. 5.2). 2. A mouth opening of three fingers or more suggests ease of laryngoscope placement. 3. A thyroid-to-tip- of-chin (thyromental distance, Fig. 5.3) of more than 6.5 cm indicates ease of glottic visualization. 4. The mandibular space is assessed by attempting to place 3 or 4 fingers between the hyoid bone and mandibular symphysis (Fig. 5.4). If less than 3 fingerbreadths, mandibular hypoplasia with difficult laryngoscopy is anticipated.

Fig. 5.1: Normal neck flexion

Fig. 5.2: Neck extension

68

A PRIMER OF ANESTHESIA

Fig. 5.5: Mallampati grading

Fig. 5.3: Thyromental distance

Fig. 5.6: Mallampati I

Fig. 5.4: Mandibular space

5. Modified Mallampati grading: This is one of the most common assessment procedures to evaluate ease of glottic visualization. The patient is asked to open his/her mouth as wide as possible and to protrude the tongue fully (Fig. 5.5). One of the four following views may be obtained. Mallampati I—faucial pillars, soft palate, uvula visible (Fig. 5.6). Mallampati II—faucial pillars and soft palate visible. Mallampati III—only soft palate visible. Mallampati IV—only hard palate visible. A reduced thyromental distance combined with a Mallampati class III or IV predicts 80% of difficult intubations.

6. The ‘prayer’ sign in diabetics (Fig. 5.7): The patient is typically unable to straighten the interphalangeal joints of the fourth and fifth fingers. Limited joint mobility is commonly seen in longstanding insulin-dependent diabetics because of glycosylation of tissue proteins. This affects the cervical spine, the temporomandibular joint and the larynx. C. Auscultation of the chest for intensity of breath sounds; cardiac ausculation for murmurs, – wheeze/wet sounds/crackles – diminution /absence of breath sounds – heart sounds and murmurs D. Sites and landmarks for regional anesthesia: spine, shoulders, neck. E. Monitoring sites: If radial artery cannulation is planned, the non-dominant hand is selected after adequacy of collateral circulation is checked (refer to chapter on Vascular Cannulation).

PREOPERATIVE EVALUATION OF PATIENTS

69

excessive bleeding during surgery. The practice of discussing the benefit of a particular test before ordering for it in a routine manner is to be encouraged. Guidelines for Laboratory Testing

Fig. 5.7: Prayer sign

F. Biochemical tests Although ‘routine’ tests are being performed on all patients, there is increasing evidence that such testing is not necessary. Routine testing adds expense to the hospital and patient and may result in delay of surgery. Further, the likelihood of an abnormal test is extremely low if history and physical examination are normal. The only point in favor of ‘routine’ testing is that it may detect abnormalities especially if history taking and examination were inadequate and in subclinical, early stages of some diseases like renal failure. Laboratory testing should therefore be directed to patients who have a high likelihood of having an abnormality, the correction of which will have a significant role in reducing morbidity related to anesthetic technique or surgery. A good example is assessment of prothrombin time and its correction in a patient with obstructive jaundice scheduled for laparotomy and possible major surgery. Corrected prothombin time reduces the likelihood of hematoma formation in the epidural space or during central venous cannulation. It also reduces blood loss due to

1. Hemoglobin/Hematocrit: – pallor/anemia on clinical examination – all premenopausal women – patients older than 60 years. – surgical procedures expected to involve significant blood loss. 2. Blood glucose, blood urea and serum creatinine – in all patients older than 40 years, patients undergoing renal procedures or those with a history suggesting renal impairment due to any reason- hypertension, diabetes, polycystic kidney disease, SLE, NSAID use among others. 3. ECG – all patients older than 40 years – all hypertensives (even if younger than 40) – all patients with heart disease (including children) 4. X-ray chest – for patients over 40 years – for patients scheduled to undergo pulmonary resection – patients with history of pulmonary tuberculosis, or pneumonia or chest infection 4-6 weeks prior to surgery. – in patients with hypertension or heart disease (including children) – in patients with chronic obstructive airway disease. ASA Physical Status Grading (Table 5.2) This is a 5 category physical status classification system adopted by the ASA (American Society of Anesthesiologists) in 1961. Later, class 6 was added to include brain dead organ donors. The system is not perfect as underlying disease is only one of the many factors contributing to mortality (for example, does not include intraoperative

70

A PRIMER OF ANESTHESIA

Table 5.2: The ASA scoring system (perioperative mortality in brackets) Class I II III IV V VI

Definition Healthy patient (0.1%) Mild systemic disease, no functional limitation (0.2%) Moderate systemic disease with definite functional limitation (1.8%) Severe systemic disease that is a constant threat to life (7.8%) Moribund patient unlikely to survive 24 hours with or without surgery (9.4%) Brain – dead organ donor

events like hemorrhage, anaphylaxis). However, it is useful in planning anesthesia management (especially monitoring and postoperative care). It is also useful in predicting the morbidity of a scheduled procedure and obtaining informed consent. The suffix ‘E’ when attached to any class denotes that the procedure is emergent, which means even less time is available for optimization; this increases the peri operative mortality risk. FASTING GUIDELINES: PREMEDICATION AND OTHER DRUGS Fasting Guidelines Adult patients for scheduled surgery are generally fasted overnight for solids and for liquids 3-4 hours before the procedure. For those whose surgery is likely to take place after noon, 200 ml of tea or fruit juice can be allowed up to 6 a.m. taking care to reschedule their pre operative medication. Fasting guidelines for small children are less rigorous; an infant or neonate can be breast-fed up to 6 hours before the procedure. Water (if necessary) can be given up to 2 hours before the procedure. However it is safer to withhold milk, formula or any residueproducing food for six hours for older children and instead give clear fluids (sweetened apple juice) up to 2-4 hours before the procedure.

Premedication With the increasing trend of day-care surgery and short hospital stay, narcotic premedication which was routine practice till some years ago has very little place in modern anesthetic management. Availability of short-acting anxiolytics like midazolam which has the added advantage of IV administration is another reason for dispensing with traditional intramuscular(IM) pre medication. A thorough and reassuring pre operative assessment of the patient, providing explanations for any questions or doubts they may have about the procedure, works better than pharmacological premedication in most instances and wins the patient’s confidence. However, there are certain categories of patients where the administration of preoperative sedative and/or narcotic medication has definite benefits and should not be withheld. A discussion of the indications and doses of individual drug groups follows. 1. Oral benzodiazepines: Many anesthesiologists administer a drug from this group the night before surgery (diazepam, nitrazepam, lorazepam, oxazepam). Oral midazolam (0.5 mg/kg) half an hour prior to surgery has proved very effective in non-traumatic separation of small (especially preschool) children from their parents. Oral diazepam is administered in a dose of 0.2 mg/kg 1-2 hours prior to surgery. Contraindications to its use are: – Patients coming for short or day-case procedures – Unattended outpatients for procedures under local anesthesia – Patients with severe liver or renal impairment –receptor antagonists (ranitidine, cimeti2. H2 dine), proton-pump inhibitors (omeprazole, lansoprazole) and prokinetics (metoclopramide) can be given to all adult patients, especially after overnight fasting. Specific indications are: – Patient with history of gastric reflux, peptic ulcer disease.

PREOPERATIVE EVALUATION OF PATIENTS

– Pregnant patients for obstetric/nonobstetric procedures, owing to the increased possibility of regurgitation and aspiration with the use of general anesthesia. – All obese patients, for the same reason. – All patients with a ‘difficult’ airway who are likely to experience multiple attempts at intubation. – Patients for emergency surgery after trauma (e.g. fracture reduction who have had a meal before injury). (Patients with pheochromocytoma should not be prescribed metoclopramide as it can precipitate a hypertensive crisis). 3. Atropine: the routine use of this once ubiquitous drug is now questioned. Some indications for its use still remain, however. They are: – Infants (and most neonates) undergoing routine or emergency procedures under anesthesia, because of the high incidence of bradycardia at induction and laryngoscopy. The intravenous (IV) dose used is 20μg/kg. – Patients undergoing oral surgery and dental procedures, to keep the operative field clear of saliva. Glycopyrrolate (10-20 μg/kg), IV or IM is a better choice for antisialagogue effect owing to the absence of cardiac effects. Side effects: Hyperpyrexia may occur after intramuscular (or even topical application as ophthalmic ointment) administration in children. Glaucoma can worsen or central anticholinergic syndrome may develop in elderly adults. 4. Narcotics are rarely used routinely for premedication. For example, in surgical procedures being performed on day-care basis, nausea and respiratory depression sedation may delay discharge. The availability of potent, short acting narcotics like alfentanil, remifentanil and fentanyl combined with the judicious use of regional

71

anesthesia has obviated the need for long acting drugs like morphine, meperidine (pethidine) and butorphanol. However, there are some situations where narcotic premedication is still indicated: a. Patients with cardiac disease: Morphine administration shifts blood from the central circulation to the periphery, reducing symptoms of pulmonary congestion and dyspnea. It also provides sedation and euphoria, thus reducing tachycardia caused by anxiety. Lastly it reduces the pain caused by pre-induction procedures like intra venous cannulation. The dose of morphine recommended for pre-medication is 150-300 μg/kg administered through the intra-muscular route. Concomitant administration of a phenothiazine like promethazine (‘Phenergan’) in a dose of 0.25-0.5 mg/ kg is useful to counteract nausea induced by morphine. b. Patients with a painful condition like a fracture where moving the patient is made less uncomfortable. Morphine 150130 μg/kg or meperidine (pethidine) in a dose of 1-1.5 mg/kg can be used, along with promethazine. 5. Concurrent medications: patients should take their routine morning dose of all drugs, especially antihypertensives, beta blockers and anti-anginal drugs. Exceptions are: (i) ACE- inhibitors, which may cause profound hypotension with spinal anesthesia and should be discontinued; (ii) Diuretics, which can cause electrolyte imbalance and/ or dehydration; (iii) Insulin and oral hypoglycemic agents; (iv) Tricyclic antidepressants and MAO inhibitors. Systematic assessment is the most important way by which we can detect abnormalities which can adversely affect patient outcome, and this knowledge and preparedness are the strongest weapons which minimize morbidity.

72

A PRIMER OF ANESTHESIA

ANESTHE TIC IMPLICATIONS OF ANESTHETIC CONCURRENT DISEASE Very often the surgical patient has a pre existing medical problem which has come to light for the first time during the present admission. As was mentioned in the section on preoperative evaluation, one of the primary goals of anesthesiologists is to discover concomitant medical problems, grade their severity and optimize the patient with adequate medications to minimize perioperative morbidity and mortality. In this section we will see how a few common cardiac, respiratory, endocrine and hematologic diseases can affect anesthetic management, and the precautions taken preoperatively for optimization. Bronchial Asthma Asthma is a chronic lung disease with episodic manifestations of airway obstruction, airway inflammation and airway hyper responsiveness to a variety of stimuli including exercise, cold air, viral infections, occupational exposure and even emotional stress. Asthma is often termed a “syndrome with myriad presentations” instead of a single disease. The clinical manifestations of asthma are wheezing, shortness of breath, cough and chest tightness. In between two consecutive attacks the patient may be completely asymptomatic.

Preoperative Assessment • History is elicited regarding – – Frequency of attacks – Time and duration of last attack – Treatment that the patient is taking for asthma; steroids? – Whether patient required hospital or ICU admission for treatment of asthmatic attacks in the past – Identification of precipitating factors e.g. weather, cold, dust, medication etc. – Exercise tolerance. Inability to climb at least two flights of stairs indicates poor respiratory and/or cardiac reserve.

• Examination should focus on the patient’s breathing rate, pattern, use of accessory muscles and presence of pulsus paradoxus. Fever may indicate active chest infection and a predilection for bronchospasm intra- and postoperatively. Auscultation should seek out presence of rhonchi or crepitations. • Investigations Investigation would include Hb%, a total blood count, chest X-ray, and pulmonary function tests (PFT) in selected patients. Pulmonary function testing (PFT) is indicated in (a) smokers, (b) obese patients, (c) patients scheduled to undergo thoracic or upper abdominal surgery, (d) to check improvement after bronchodilator therapy. In case the patient is severely symptomatic and shows no improvement with maximal bronchodilator therapy PFTs provide a basis for quantitating the risk of respiratory failure after major surgery. Arterial blood gas analysis is reserved for severely symptomatic patients and those scheduled for pulmonary resection, to determine possibility of respiratory failure and decide operability.

Preoperative Optimization • Cessation of smoking should be enforced. • Treatment with bronchodilators and inhaled steroids is initiated based on severity of the asthma. A chest consultation is obtained for advice regarding optimization of therapy. • Antibiotics and chest physiotherapy if infection is present. • Physical training with deep breathing exercises and incentive spirometry prepares a patient for performing respiratory maneuvers like deep breathing after surgery. Goals of Optimization • Bronchospasm should be relieved. • No evidence of active chest infection: it is prudent to postpone elective surgery by at least 4-6 weeks after respiratory infection in asthmatics as their airways may remain hyper-reactive for this period.

PREOPERATIVE EVALUATION OF PATIENTS

• Patient should be subjectively feelling comfortable and at his best.

Optimal Anesthetic Technique Preanesthetic medication: • Patients should take the morning dose of bronchodilators and inhaled steroids. Even in asymptomatic asthmatics, preoperative use of short acting β2 agonists decreases incidence of intraoperative bronchospasm. • H1 and H2 antihistaminics are beneficial 12 hours prior to and on the morning of surgery. • Benzodiazepines (diazepam 5-10 mg) are useful for anxiolysis in patients unless they are overtly symptomatic. • Adequate hydration is essential; start an IV line if surgery is scheduled 2nd or 3rd on the list.

Choice of Anesthesia and Goals of Anesthetic Management • Asthmatic patients should be ideally taken as the first case in the morning to minimize fasting and dehydration, and waitinginduced anxiety and bronchospasm. • As far as possible anesthetic techniques which minimize airway handling should be used, therefore regional anesthetic techniques (spinal, epidural, nerve blocks) are preferred over GA. • In case general anesthesia (GA) is necessary, agents capable of precipitating bronchospasm by histamine release are avoided, which are thiopentone (induction agent), atracurium, d-tubocurarine, mivacurium (muscle relaxants), morphine (narcotic), desflurane (inhalation agent) and, if possible, neostigmine (anti-cholinesterase). • Agents preferred are propofol, etomidate (induction agents), halothane, isoflurane and sevoflurane (inhalation agents), fentanyl and pethidine (narcotics), succinylcholine and vecuronium (muscle relaxants).

73

• If general anesthesia is to be used, intubation and instrumentation of the airway should be avoided as far as possible. The laryngeal mask airway is an excellent alternative as it permits use of controlled ventilation without the need for laryngoscopy. If intubation is necessary (e.g. as for a thoracotomy), precautions are taken not to perform laryngoscopy in a light plane of anesthesia as this will invariably lead to bronchospasm. • Intraoperative bronchospasm should be treated aggressively by increasing the inspired concentration of inhaled anesthetic, nebulised β2 sympathomimetics, intravenous steroids and ensuring adequate depth of anesthesia. Intravenous or subcutaneous bronchodilators may also be administered (aminophylline 5-6 mg/kg or terbutaline 0.25 mg). • Extubation of the trachea is carried out after administration of intravenous lidocaine 1-1.5 mg/kg and inhaled bronchodilator. • The patient is given adequate analgesia and supplemental oxygen in the post anesthesia care unit. Diabetes Mellitus

Physiological Derangement Diabetes mellitus in an endocrine disease caused by the deficiency of the hormone insulin, resulting in glucose dysregulation and widespread systemic effects. Insulin has important anabolic actions such as facilitation of uptake of glucose by peripheral musculo-skeletal tissue and stimulation of lipid synthesis. In addition it also has equally important catabolic effects such as inhibition of gluconeogenesis or glycogenolysis in the liver along with inhibition of lipolysis, proteolysis and ketogenesis. By these actions insulin helps to maintain blood sugar levels between 120-180 mg/dl. Hyperglycaemia is associated with sluggish phagocyte function, inability of

74

A PRIMER OF ANESTHESIA

immunoglobulins to fix complement and impaired wound healing. Excessive hyperglycaemia may also be associated with osmotic diuresis, dehydration, electrolyte abnormalities and diabetic ketoacidosis. There are four types of diabetes mellitus: 1. Type I: Insulin- dependent or juvenile onset diabetes where insulin is required to prevent hyperglycemia. 2. Type II: Maturity onset or non insulindependent diabetes where there is a relative deficiency of insulin or insulin resistance. This is usually seen in obese individuals and managed with diet control, weight loss and oral hypoglycemic drugs (Table 5.3). 3. Gestational diabetes: Where the diabetes occurs during pregnancy alone. Blood sugar is controlled with diet and insulin. Strict control of blood sugars is essential to prevent fetal and maternal complications. 4. Secondary to pancreatic disease (Pancreatitis) or endocrinopathies (Cushing’s syndrome/ disease, Acromegaly). Long standing diabetes is associated with a number of microvascular and macrovascular complications (Table 5.4). Microvascular complications are commoner in type I diabetics whereas macrovascular complications are commoner in type II diabetics. Effective blood sugar control results in a

Table 5.3: Oral hypoglycemic drugs 1. Sulfonylureas: 1st generation-chlorpropamide: stop 48-72 hours prior to surgery. 2nd generation: glyburide, glipizide, gliclazide, glimepiride; act by stimulating release of insulin from pancreas 2. Thiazolidinediones: Rosiglitazone, pioglitazone troglitazone may be given on morning of surgery; Improve insulin uptake and decrease hepatic gluconeognesis 3. Biguanides: Metformin to be discontinued 24 hours prior to surgery. No action on insulin production or release; lower blood glucose by decreased hepatic glucose output and increased peripheral glucose utilization. 4. Alpha-glucosidase inhibitors: Act by blocking the breakdown and absorption of complex carbohydrates and are only effective when administered with food. Oral sucrose, maltose and starch will not be effective for treatment of hypoglycemia in these patients.

decrease in microvascular but not macrovascular complications. From the anesthesia standpoint, the significant problems faced during management of diabetic patients for surgery are: • Cardiovascular disease: The incidence of coronary artery disease, hypertension and congestive heart failure (CHF) is higher in diabetics. Diabetics are more likely to have silent or asymptomatic myocardial infarction (MI) and death after an MI.

Table 5.4: Microvascular and macrovascular complications Microvascular

Macrovascular

• Eye disease – Retinopathy (non-proliferative/proliferative) – Macular edema – Cataracts – Glaucoma • Neuropathy – Sensory and motor – Autonomic

• Coronary artery disease • Peripheral vascular disease • Cerebrovascular disease

• Nephropathy

• Gastrointestinal – Gastroparesis – Diarrhea • Genitourinary (uropathy/sexual dysfunction) • Dermatological

PREOPERATIVE EVALUATION OF PATIENTS

• Renal: End stage renal disease is commoner in diabetics than non-diabetics. • Peripheral neuropathy: This is common in diabetics. Preoperative neural deficit should be identified and care should be taken to protect the patient from nerve compression intraoperatively. After spinal or epidural analgesia the patient is likely to associate any new neurological deficit with the technique and not the disease and appropriate explanation and consent are important. • Autonomic neuropathy: Manifests as resting tachycardia, absent heart rate variability with respiration (variability is normally 10-15 beats per minute between inspiration and expiration). The other manifestations are orthostatic hypotension, gastrointestinal dysmotility and impotence. Absence of sympathetic nervous system response leads to absence of warning signs of hypoglycaemia, hypovolemia and hypothermia (patients with autonomic neuropathy have a greater decrease in core body temperature than non diabetics). Undetected hypothermia may cause silent MI or sudden cardiac death in the perioperative period. • Airway problems: Abnormal glycosylation of collagen in long- standing diabetes can result in limited joint mobility in the small joints of the hand (Fig. 5.7) as well as the atlantooccipital joint resulting in limited neck extension and difficulty in intubation. • Metabolic derangements: Inadequate blood sugar control can lead to osmotic diuresis, hypovolemia, ketosis or keto acidosis.

Preoperative Assessment • History–regarding – Duration of the disease and drug therapy the patient is receiving, i.e. oral hypoglycemic agents or insulin. – Adequacy of control of blood sugar. – Symptoms suggestive of cardiovascular disease.

75

– Frequency and severity of hyperglycemic and/or hyperglycemic episodes. – Neurological symptoms- stroke, tingling/ numbness, mononeuropathy, glove-andstocking paresthesia, etc. – Diarrhea after meals, reflux esophagitis. • Examination: – Weight, body habitus – Blood pressure in sitting and standing positions – ‘Prayer’ sign (Fig. 5.7) – Airway assessment – Neurological examination to document any deficit – Anatomy of spine for feasibility of spinal anesthesia • Relevant preoperative investigations – The hallmark of diabetes is a fasting blood sugar greater than 126 mg/dl or a random blood sugar of more than 200 mg/dl. – Glycosylated hemoglobin (Hb AIC) levels reflect adequacy of control over the preceding 1-3 months. Levels between 5-7% of total hemoglobin are normal whereas more than 9% indicates poor long term glucose control. – Laboratory investigations include determination of blood sugar, blood urea, serum creatinine, serum electrolytes and urine analysis for glucose, ketones and proteins. • Goals of optimization – To avoid hypoglycaemia as well as hyperglycaemia and maintain blood sugar between 120-180 mg/dL. – Identification of associated end-organ disease and initiation of interventions to limit cardiovascular, renal and metabolic complications.

Optimal Anesthetic Management Pre-anesthetic Instructions: • Ideally a diabetic patient should be scheduled as the first case in the morning to minimize metabolic complications.

76

A PRIMER OF ANESTHESIA

• Type I diabetics: Half the usual dose of shortacting insulin should be administered on the evening before surgery. Withold insulin on the morning of surgery; blood sugar levels, serum electrolytes as well as urine assay for sugar and ketones is carried out on the morning of surgery. A neutralizing drip (containing 8U regular insulin in 500 ml 5% dextrose) at the rate of 100-125 ml/hour is then started. Alternately, separate infusions of dextrose at 100 ml/hour (5 g glucose in an hour) and 1-2U insulin/hour are administered. Blood sugar estimations are done hourly to keep the level between 120-180 mg/100 ml. • Type II diabetics: Patients with blood sugars controlled on diet and oral hypoglycemic drugs should withold the oral hypoglycemic agent with the exception of acarbose on the morning of surgery. For minor procedures where the patient is likely to be allowed oral intake a couple of hours postoperatively, blood sugar is monitored every 2 hours and the patient encouraged to restart oral intake as soon as possible and oral hypoglycemics the next day. • Type II diabetics undergoing major abdominal surgery will required to be admitted at least 48 hours before surgery, started on neutralizing drip with insulin or on separate insulin and glucose infusions as described for type I diabetics.

Anesthetic Technique Regional anesthesia should be used whenever feasible. Advantages 1. The patient can alert the anesthesiologist if he feels uneasy, and complications such as hypoglycemia or myocardial ischemia may be diagnosed in time. 2. The use of spinal epidural or regional blockade decreases the stress response to surgery by modulating secretion of catabolic

hormones and thus protects against severe rise in blood sugar. Precautions 1. In the presence of pre-existing peripheral neuropathy local anesthetic requirement can be significantly reduced and pre-existing neurological loss should be recorded to avoid medicolegal claims. 2. In patients with autonomic neuropathy profound hypotension can occur after spinal or epidural block. General Anesthesia: • The airway should be secured with an endotracheal tube as there is risk of regurgitation and aspiration because of gastroparesis. • Premedication should include anti aspiration prophylaxis with metoclopramide and H2 receptor blocker. • Choice of anesthetic agents is not very important as long as maximal stress suppression achieved with good analgesia to prevent counter- regulatory hormone- induced hyperglycemia. • Precautions should be taken for cardiovascular stability and protection of peripheral nerves from injury. Careful perioperative hemodynamic and blood sugar monitoring is important. Valvular Heart Disease Why should the anesthesiologist be concerned about valvular heart disease? All types of valvular disease cause a burden to be imposed on the right ventricle, the left ventricle, the pulmonary or systemic circulation, singly or in combination. All anesthetic agents as well as regional anesthetic techniques affect cardiac performance, pulmonary and systemic vascular resistance. Further, the stress of surgery or pregnancy adds additional burden on the already precarious circulatory homeostasis in a patient with valvular disease. Thus, it is imperative that the anesthesiologist has a

PREOPERATIVE EVALUATION OF PATIENTS

thorough understanding of the pathophysiology of each condition so that appropriate measures can be taken (i) for intraoperative monitoring, (ii) to compensate for intraoperative hemodynamic events, and (iii) to prevent peri operative hemodynamic compromise. Patients coming for non-cardiac surgery after valve replacement need careful assessment of prosthetic valve function. Antibiotic prophylaxis for procedures associated with bacteremia and evaluation and careful management of anti coagulation is also essential.

– –

–

General Evaluation Goals of history-taking, examination and laboratory evaluation are: 1. To determine the severity of the lesion 2. To determine existing cardiac function 3. To assess the effect on pulmonary vascular resistance, hepatic and renal function 4. To confirm/exclude the presence of concomitant coronary artery disease. History: Breathlessness (NYHA scale, Table 5.1) and its severity, presence of chest pain and peripheral edema are noted. History of easy fatiguability and medications used are important. Physical examination – Features of congestive heart failure (tachycardia, jugular venous distension, pedal edema, pulmonary rales, S3 gallop and hepatic engorgement) – Pulse characteristics – Blood pressure in both upper and lower limbs – Auscultation in the valvular areas can help to confirm the diagnosis of valvular abnormality. Lab investigations – In addition to routine hematology (Hb%, hematocrit), renal function tests, liver function tests (to evaluate effect of passive

–

77

congestion) and serum electrolyte estimation (especially for patients on diuretics and digoxin) should be done. EKG can reveal arrhythmias, axis deviation, chamber hypertrophy as well as non-specific ST-T segment changes. A chest X-ray is invaluable to assess cardiomegaly, specific chamber enlargement, pulmonary vascular congestion, kerley-B lines, pulmonary edema and presence of chest infection. Echocardiography helps to assess the nature and severity of the valvular abnormality, the degree of ventricular impairment, any coexisting abnormality (e.g. a patent foramen ovale). In patients with severe valvular abnormality and high suspicion of concurrent coronary artery disease coronary angiography can also be done. Radionuclide angiography and cardiac catheterization are usually reserved for patients scheduled to undergo valve replacement.

Premedication -

-

Patients are instructed to continue with their usual medications on the morning of surgery. Diuretics are usually omitted. Sedation has to be individualized. Patients with poor ventricular function tend to be very sensitive to ‘normal’ doses of sedatives. Oral diazepam (0.2 mg/kg at bedtime and on the morning of surgery) may provide good anxiolysis with minimal sedation. Morphine in small doses (100-150 μg/kg intra muscularly) may be desirable in patients with pulmonary congestion. Infective endocarditis prophylaxis is to be administered to all patients with valvular abnormalities (including prosthetic valves) 30 minutes to 1 hour prior to dental, oral, nasal, pharyngeal or upper airway surgery and to be repeated 6 hours after the procedure.

78

A PRIMER OF ANESTHESIA

Anticoagulant Therapy Patients with prosthetic heart valves or known thrombo-embolic events on oral warfarin should have warfarin stopped 3-4 days prior to the procedure and started on subcutaneous or intravenous heparin. Heparin is usually stopped 4-6 hours prior to surgery. A coagulation profile including PT and APTT (activated partial thromboplastin time) should be determined and adequate FFP (fresh frozen plasma) arranged prior to surgery. Antibiotic prophylaxis against infective endocarditis (IE) is adminstered as per AHA guidelines which can be found in all standard textbooks or accessed on the internet. Monitoring and anesthetic agents 1. Hemodynamic monitoring: Apart from continuous ECG monitoring and noninvasive blood pressure, direct arterial blood pressure and pulmonary capillary wedge pressure (PCWP) is indicated in major surgery. PCWP indicates the LA-LV pressure gradient and may not reflect true LV enddiastolic pressures especially in mitral stenosis. There may be a tendency to overrestrict fluids if high LA pressures are misinterpreted as true ventricular filling pressures. CVP monitoring may not be very useful especially if tricuspid regurgitation is present, and the high right-sided pressures again do not reflect left ventricular filling pressures. However, both CVP and PCWP are very useful as a trend to guide fluid loss monitoring and replacement. 2. Ketamine and pancuronium should be avoided in lesions where tachycardia is detrimental. Thiopentone and propofol are acceptable alternatives, but require careful titration as a ‘normal’ dose can cause disastrous hypotension. Etomidate, if available, is the most cardio-stable induction agent. Vecuronium is acceptable as a muscle relaxant as it is cardiostable and does not cause tachycardia. High-dose opioids

(fentanyl 3-4 μg/kg or morphine 150-300 μg/kg) can be used as alternatives for induction; they provide added advantage of blunting tachycardia in response to intubation and skin incision. Inhalation agents can be avoided or used in very low concentrations (halothane 0.3-0.5% is suitable as it decreases the heart rate and is least vasodilating). High concentrations of volatile agent can lead to junctional rhythm, and hypotension. Severe hypotension needs to be treated with phenylephrine rather than ephedrine. Hemodynamic deterioration due to AF needs cardioversion. Intraoperative tachycardia may be controlled by increasing anesthetic depth with a bolus of fentanyl, or esmolol, diltiazem or digoxin. Heart rates between 70-90 bpm are targeted in regurgitant lesions (MR, AR). In these lesions a mild reduction in SVR reduces the regurgitant fraction and enhances forward flow. 3. Postoperative care includes continuous monitoring of the cardiovascular system for signs of decompensation, oxygen therapy, normalization of electrolyte and hematocrit, and adequate analgesia. Morphine is an excellent analgesic for the cardiac patient and can be given as IV boluses, continuous IV infusion or as PCA, or through an epidural catheter. Hypertension Physiological derangement in hypertension: Hypertension is defined as a blood pressure (BP) of greater than 140/90 mm Hg. Long standing hypertension is associated with arteriosclerosis and hypertensive vascular changes leading to cardiac, cerebral, renal and vascular damage. Hypertension can either be idiopathic (or essential) or secondary to renal disease, Cushing’s syndrome, pheochromocytoma, etc. Initially, to keep up with the increase in systemic

PREOPERATIVE EVALUATION OF PATIENTS Table 5.5: Classification of hypertension Stages

Systolic arterial Diastolic arterial pressure pressure (mm Hg) (mm Hg)

Stage 1 (mild)

140-159

90-99

Stage 2 (moderate)

160-179

100-109

> 180

> 110

Stage 3 (severe)

vascular resistance (SVR), cardiac output increases. With a persistent increase in afterload, concentric left ventricular hypertrophy (LVH) develops to maintain cardiac output at normal levels. Auto-regulatory limits of perfusion of vital organs such as brain, heart, kidneys are reset to higher levels. Classification of hypertension is shown in Table 5.5. Accelerated hypertension is defined as a recent progressive increase in BP above 180/110 mmHg which may be associated with renal dysfunction. Malignant hypertension is defined as a BP reading greater than 220/114 mmHg associated with papilledema and encephalopathy. This is a medical emergency.

Preoperative Optimization Ideally hypertensive patients scheduled for elective surgery should have their BP controlled with antihypertensive drugs. Mild hypertension is usually controlled with a single drug (βblockers, calcium channel blockers, ACE inhibitors or diuretics). For moderate to severe hypertension two or more drugs may be required. • The blood pressure should be measured in both supine and standing position. It may be necessary to keep a 6 or 8 hourly record to see adequacy of control throughout the day in severe hypertensives or when modifying treatment. The anesthesiologist may want to see this chart.

Preoperative Evaluation History to be elicited from a hypertensive patient include duration of hypertension,

79

compliance with drug therapy and symptoms of IHD.

Investigations • An EKG, a chest X-ray and an echocardiogram are desirable to evaluate the presence and extent of myocardial ischemia, cardiomegaly, left ventricular hypertrophy, to estimate left ventricular function including the presence of regional wall motion abnormalities. • Ophthalmoscopy can be done to ascertain hypertensive retinal changes • Renal function can be evaluated by serum creatinine, blood urea nitrogen levels and serum electrolytes.

Premedication • Antihypertensive medications should be taken on the morning of surgery with a sip of water. Diuretics may be omitted unless the patient is in congestive failure or fluid overload. • Anxiolysis with diazepam 0.2 mg/kg on the night before and 2 hours prior to surgery or intravenous midazolam prior to surgery is helpful in reducing preoperative anxietyinduced increase in blood pressure and is highly desirable in hypertensive patients. Anesthetic Management The overall anesthetic plan for hypertensive patients is to maintain the pressures between 10-20% of the pre-induction pressures. Any anesthetic drug is suitable for induction except ketamine because of its propensity to cause tachycardia and hypertension. A balanced anesthesia technique using opioid, inhalational agents and muscle relaxant can be routinely used intraoperatively. In-β blocked patients, concomitant use of fentanyl and vecuronium may exaggerate bradycardic response. • To blunt the intubation response (i) intravenous lignocaine 1.5 mg/kg IV 60-90

80

A PRIMER OF ANESTHESIA

seconds prior to intubation, (ii) fentanyl 2 μg/kg or esmolol 150-300 μg/kg/min can be used. • Intraoperatively, patients with poor antihypertensive control can have swings in blood pressure. A wide range of agents are available for intraoperative control of blood pressure (Table 5.6). • Regional anesthesia, especially graded epidural or combined spinal epidural block are the anesthetic techniques of choice in hypertensives if feasible for the surgery under consideration. These techniques not only provide good intraoperative and postoperative analgesia but also avoid the hypertensive response to intubation/extubation. • Postoperative monitoring of blood pressure should be continued. Anemia Anemia continues to be a common problem in developing countries. From the anesthesia point of view, reduction in hemoglobin reduces the oxygen carrying capacity of the blood. Oxygen flux

(the oxygen delivered to tissues per minute) is derived by the following formula: 1. Oxygen content = [(0.003 ml O2/100 ml blood/mmHg) × PO2] + [SaO2 × Hb% × 1.31 ml/100 ml blood] = [0.003 × 100] + (0.975 × 15 × 1.31) = 19.5 ml/100 ml blood 2. 20 ml O2/100 ml blood × 5000 ml/min (cardiac output) =1000 ml/min That is, the normal oxygen content of arterial blood is 20 ml/100 ml only if the Hb is 15 g%. Since arterio-venous oxygen difference is 4.7 ml/100 ml, the body normally consumes only 25% of the oxygen carried in blood. If the hemoglobin is reduced by 50% (7.5 g%), the content drops to 10 ml/100 ml, but the extraction increases at tissue level to maintain normal arterio-venous difference. Three more changes help oxygen delivery in the anemic patient: (i) reduced hemoglobin reduces viscosity and improves microcirculation; (ii) levels of 2,3 diphospho glycerate DPG increase in the reticulocytes which reduce affinity of hemoglobin for oxygen and help to

Table 5.6: Antihypertensive drugs which can be used for intraoperative blood pressure control Agent

Dosage range

Onset

Duration

Nitroprusside

0.5-10 μg/kg/min

30-60 sec

1-5 min

Nitroglycerin

0.5-10 μg/kg/min

1 min

3-5 min

Esmolol

0.5 mg/kg over 1 min →

1 min

12-20 min

50-300 μg/kg/min

1-2 min

4-8 h

Labetalol

5-20 mg

Propranolol

1-3 mg

1-2 min

4-6 h

Phentolamine

1-5 mg

1-10 min

20-40 min

Diazoxide

1-3 mg slowly

2-10 min

4-6 h

Hydralazine

5-20 mg

5-20 min

4-8 h

Nifedipine (S/L)

10 mg

5-10 min

4h

Nicardipine

0.25-0.5 mg

1-5 min

3-4 h

Enalapril

0.625-1 mg

6-15 min

4-6 h

Fenoldopam

0.1-1.6 μg/kg/min

5 min

5 min

PREOPERATIVE EVALUATION OF PATIENTS

offload it in the tissues. This causes a rightward shift of the oxygen dissociation curve; (iii) cardiac output increases due to increase in plasma volume and stroke output. Important points regarding clinical management and optimization: – Adequate replacement of fluid or blood lost during surgery. – Stored RBCs take up to 24 hours to regenerate 2,3 DPG; hence preoperative transfusion for an anemic patient should be given at least 24 hours prior to surgery. – Cyanosis is detectable clinically only when deoxyhemoglobin level is 5 g%. Hence in severely anemic patients cyanosis is rarely seen. Anesthetic Technique, Monitoring and Precautions in the Anemic Patient 1. Although 10 g% is the international norm for minimum acceptable Hb levels for elective procedures, many authorities now accept a value of 8 g% in those who have no cardiac disease. 2. Packed red cells should be cross-matched and kept ready. 3. Maximum allowable losses are kept at 10% of estimated blood volume for the anemic patient when considering replacement for surgical losses. Tachycardia is a sensitive guide and signals an attempt by the body to increase cardiac output and maintain oxygen delivery. 4. Standard monitoring suffices for minor (cataract, surface biopsies) and moderate (hernia repair, hysterectomy, gastrojejunostomy) procedures where minimal blood loss is anticipated. 5. For major procedures involving fluid shifts and blood loss (abdomino-perineal resection, Whipple’s procedure, major limb disarticulation) CVP and invasive arterial pressure monitoring along with urine output help to keep close track of volume status. Careful patient observation and interpre-

81

tation of parameters like heart rate, blood pressure, CVP and urine output are important clinical guides for good patient outcome. 6. Regional anesthesia is well tolerated by the anemic patient who is not in failure. Supplemental oxygen should be given even during minor procedures, to fully saturate the circulating hemoglobin. 7. For general anesthesia, all induction and inhalational agents are tolerated. The hyperdynamic circulation may hasten intravenous and inhalational induction. Minimum alveolar concentration (MAC) of inhalational agents therefore patients are induced at lower inspired concentrations of inhalational agents has been seen to reduce when the hematocrit reduces to < 10%. Agents causing tachycardia (pancuronium, ketamine, atropine) can be avoided; if congestive cardiac failure is/was present, an opioid-based technique (with morphine or fentanyl) is more suitable. Patients who have had massive transfusion or major fluid shifts pulmonary edema or are hypothermic may benefit with postoperative ventilation till fluid compartments normalize. 8. Postoperative care should include mandatory oxygen therapy, checking and normalizing the hematocrit and avoiding tachycardia and pulmonary complications by judicious analgesia. Morphine is an excellent analgesic in this setting and may be given as IV bolus, IV infusion, PCA or through the neuraxial route. Many other conditions notably ischemic heart disease, neuromuscular disease and hepatic and renal impairment affect anesthetic management and require the anesthesiologist to be well versed in their diagnosis, presentation and interpretation of investigations to judge their severity and to plan an appropriate anesthetic technique. Thorough preoperative evaluation reduces or eliminates avoidable perioperative morbidity, aids in perioperative planning and improves outcome.

82

A PRIMER OF ANESTHESIA

MCQ MCQss 1. The most important aim of preoperative evaluation of a patient prior to surgery is: a. To reassure the patient and his relatives. b. To evaluate and optimize the co-existing medical disorders the patient may be suffering from. c. To record vital signs and order sedation/ anxiolytics. d. To ascertain the indication for the surgery. 2. A 25 years old student, a juvenile diabetic since the age of 12 years who is not eating regularly and also not taking insulin as prescribed due to examination stress is brought to the hospital casualty with acute pain abdomen. The following should be done: a. The patient should be rushed first for ultrasound abdomen. b. Dextrose containing intravenous fluids should be administered. c. Estimate the blood sugar and urine for sugar and ketones. d. Take up the patient for an emergency laparotomy. 3. The following fasting guidelines are acceptable for a 3 month old baby scheduled for a herniotomy under general anesthesia. a. Formula milk feed administered 4 hours prior to surgery. b. Mother’s milk administered 4 hours prior to surgery. c. Formula feed administered 2 hours prior to surgery. d. Mother’s milk administered 6 hours prior to surgery.

4. A 55 years old male patient a known asthmatic for the last 10 years is scheduled for a laparoscopic cholecystectomy. On preoperative evaluation the patient is found to have bilateral rhonchi. The following should be immediately administered to the patient: a. Steam inhalation and antibiotics. b. Nebulized β2 agonists and anticholinergic medications. c. Intravenous aminophylline infusion. d. Chest physiotherapy and incentive spirometry. 5. A 35 years old male is brought to the casualty following a road traffic accident. The patient is conscious but disoriented with a feeble pulse and unrecordable blood pressure. Blunt trauma to the abdomen is suspected. The following should be done first: a. A large bore I/V lines secured and blood sent for cross match b. Patient rushed to the OT for an emergency laparotomy. c. The trachea should be immediately secured with an endotracheal tube (ETT). d. Large bore I/V lines secured and crystalloids rushed into the patient. 6. A 28 years old primigravida with an anticipated difficult intubation is scheduled to undergo an elective LSCS. The anesthetic technique of choice would be: a. General anesthesia with an awake intubation. b. Spinal anesthesia c. Epidural anesthesia d. General anesthesia combined with spinal anaesthesia.

PREOPERATIVE EVALUATION OF PATIENTS

7. An 80 kg, 55 years old female patient with a height of 5 ft is posted for hemicolectomy under GA. The most preferred airway device to secure the airway would be: a. Proseal LMA (laryngeal mask airway) b. Classic LMA c. LMA unique d. Endotracheal tube 8. The following condition is associated with a difficult intubation in a diabetic patient: a. Poorly controlled blood sugars b. Orthostatic hypotension c. Inability to approximate the interphalangeal joints of the fingers of the 2 hands held in apposition with the palm facing inwards d. Presence of diabetic retinopathy, nephropathy. 9. During preoperative evaluation in a patient of insulin dependent diabetes mellitus, history of which of the following complaints is most significant: a. History of blood sugars going upto 200 mg % occasionally. b. History of orthostatic hypotension and dizziness. c. History of getting up several times at night to empty bladder. d. History of low blood sugar during which the patient feels dizzy. 10. A 65 years old male patient, a chronic smoker for the last 30 years with atrial fibrillation on oral anticoagulant is scheduled for left toe amputation due to gangrene. The least indicated anaesthesia technique is: a. General anaesthesia b. Femoral and sciatic nerve block. c. Combined spinal epidural anaesthesia. d. Ankle block

83

11. All the following are features of difficult intubation except: a. Mallampatti grade III, IV oropharyngeal view. b. Mento-hyoid distance of 1.5 cm c. Thyromental distance of 6.5 cm d. Restricted mouth opening with an interincision gap of 1.5 cm. 12. Which of the following medicines is discontinued on the morning of surgery even if the patient is otherwise taking them regularly? a. Metoprolol b. Insulin c. Nifedipine d. Pioglitazone 13. A patient with history of unstable angina would be classified as: a. ASA grade I b. ASA grade II c. ASA grade IV d. ASA grade V 14. Which of the following drugs is not administered to a day care surgery patient who is driving from home on the morning of surgery? a. Diazepam b. Ranitidine c. Metoclopromide d. Metoprolol 15. The minimum acceptable hemoglobin concentration for a 21 year old scheduled for herniorrhaphy is: a. 10 g% b. 9 g% c. 5 g% d. 7 g% Answers 1. 5. 9. 13.

b d d c

2. 6. 10. 14.

c b c a

3. 7. 11. 15.

b d c d

4. b 8. c 12. b

Monitoring the Patient Under Anesthesia K Nirmala Devi, Rajeshwari Subramaniam

 

   

Importance of monitoring Noninvasive monitoring • ECG • Non-invasive blood pressure (NIBP) • Pulse oximetry • Capnography Invasive arterial pressure monitoring Temperature monitoring Neuromuscular monitoring Selection of appropriate monitor

What is a M onitor? Monitor? A monitor is a device, which cautions, reminds, advises or admonishes. In anesthesia practice we refer to devices which record or follow a process/processes as monitors. Monitors serve to act as extensions of our senses because the physical principles they are based on enables them to detect physical quantities which are outside of the normal physiological range for humans. A simple example is the estimation of arterial desaturation- the human eye can detect a fall in SpO2 only when cyanosis occurs (PaO2 < 80 mm Hg) whereas a monitor detects even a 1% fall. Thus they enhance our vigilance. Monitors are also used to collect specific data which are important for morbidity profiling and formulating treatment protocols.

Wh y is Monitoring Necessary? Why Strange as it may sound, although anesthesia is integral to any surgical procedure, it is still considered as “incidental”. Harvey Cushing, the famous neurosurgeon realized that anesthesia techniques were associated with labile hemodynamics, and advocated monitoring of heart rate and respiration by a precordial stethoscope. A risk management committee set up at Harvard to examine insurance claims for intraoperative deaths from 1976-1985 found that nearly 31% of these deaths were preventable, and occurred due to multiple reasons (unfamiliar equipment, lack of knowledge and supervision, esophageal intubation, circuit disconnect, kinked endotracheal tube, etc). Most of them occurred not in old or sick patients but previously healthy individuals. The common denominator was failure to detect low oxygen levels or failure to detect absence of ventilation. This committee found that pulse oximetry and capnography could have probably prevented more than 90% of the mishaps. It also recognized the fact that physicians were responsible for the patients’ safety and well being. Thus, monitoring in ASA-I-II (‘normal’) patients is necessary to:

88 A PRIMER OF ANESTHESIA

1. Prevent unnecessary morbidity or mortality (“safety monitoring”) 2. Meet ‘high-level goals’ of anesthesia: – preventing awareness – preventing pain In ASA III, IV or V patients monitoring further helps to: 3. Accurately manage co-existing disease and keep hemodynamic and other variables in physiological range 4. For ‘goal-directed’ therapy in very sick patients, e.g. pulmonary capillary wedge pressure (PCWP) for planning inotropic therapy for low cardiac output. The number of elderly patients with significant co-existing disease (IHD, diabetes) presenting for major procedures is on the increase. This has been made possible by the increase in lifespan consequent to better awareness, development of medical facilities and economic growth. Anesthesia can increase morbidity in these patients if their cardiovascular and respiratory variables are not kept within physiological limits safe for their age, especially when combined with surgical stress. The Harvard standard of monitoring set up in 1985 recommended that: 1. An anesthesiologist should be continuously present in the OT. 2. Blood pressure and heart rate be recorded every 5 minutes. 3. Continuous recording of ECG. 4. Continuous monitoring of ventilation (capnography, blood gas analysis). 5. Continuous monitoring of circulation (ECG, pulse, capillary fill, pulse oximetry, heart sounds). 6. Breathing system disconnect monitoring. 7. Oxygen analyser. 8. Temperature monitoring. These guidelines were adapted and modified to form the current ASA standards. The above monitoring is known as “mandatory monitoring” which is applicable for any ASA class patient, for any anesthesia technique and

Fig. 6.1: ECG electrode placement for modified V5 lead

any surgery. The term “minimum mandatory monitoring” includes SpO2, ECG, NIBP and ETCO2 and indicates that this level of monitoring should be provided to all patients undergoing surgery under local or general anesthesia. It signifies that if the patient appears to require more intensive monitoring, it should be provided. COMMON MONITORING TECHNIQUES ECG Monitoring: Indications and Contraindications All patients must have continuous ECG monitoring during anesthesia. There are no contraindications. The electrodes should be placed after cleaning the skin with alcohol to improve conductance and ensuring that conducting gel is generously applied. To detect leads I , II, III, aVL, aVR and aVF the electrodes are placed as shown in Figure 6.1. Selection of lead depends on specific need; for example since the axis of lead II is parallel to the electrical axis of the atria, it is best for P wave morphology and arrhythmia detection. The

MONITORING THE PATIENT UNDER ANESTHESIA

Chest leads V5 and V4 are useful for ischemia detection. However, it is recommended to monitor both II and V as each provides unique information. A modified V5 can be monitored by re-arranging the limb leads. If the LA lead is placed at V5 and lead I is selected, a modified V5 lead is displayed. Esophageal leads are sensitive for arrhythmia detection. Needle electrodes can be used in the extensively burnt patient.

89

Blood pressure monitoring is mandatory no matter how ‘short’ or ‘trivial’ an anesthetic is. Any of the techniques (see below) can be used; it is important to avoid placing cuffs on arms that have hemodialysis shunts, intra arterial or intravenous lines.

The non-invasive methods that can be used are as follows: - Palpation and auscultation: This is the least expensive method; however systolic pressure may be underestimated. Mean arterial pressure values are not obtainable. Observer variability tends to be high. Auscultatory gap has to be kept in mind in hypertensive patients. Korotkoff sounds may be difficult to hear in the presence of electrocautery, in hypotension or vasoconstriction. Position of the BP apparatus (Figs 6.2A and B) induces change in reading- e.g. a difference of height of 20 cm =14.7 mm Hg in pressure. Too small a cuff gives erroneously high readings because more pressure has to be applied on a small area to occlude the artery. Cuff width should be 120-150% of the width of the upper arm (Fig. 6.3). - Doppler probe: A Doppler probe emits an ultrasonic signal that is reflected by the flowing blood. The probe has to be directly over the artery and a coupling gel is applied between the probe and skin. This technique is sensitive for systolic pressures only. - Oscillometric technique: This is the most commonly used automated blood pressure measurement technique. The principle is based on the fact that when blood flow

Figs 6.2A and B: Change in BP reading with position

Fig. 6.3: Width of open BP cuff compared to arm width

Non-invasive Blood Pressure (NIBP) Monitoring

90 A PRIMER OF ANESTHESIA

Fig. 6.4: Oscillometric blood pressure recorder

resumes as obstruction is released from a cuff, oscillations produced by arterial pulsations are recorded as systolic pressure (Fig. 6.4). The maximum oscillations are recorded at the mean pressure and the lowest at diastolic. Microprocessors derive the various pressure using algorithms. These cuffs should not be used in patients on cardiopulmonary bypass. The cuff size used in any of these techniques should be appropriate (Figs 6.5A to C). A cuff 20% too narrow will significantly over read the systolic pressure. • Arterial tonometry provides beat-to-beat arterial pressure, but requires frequent calibration and is susceptible to movement artifact.

A

Invasive (direct) arterial pressure monitoring: This involves placing a cannula directly in an artery and connecting it to a pressure transducer. Indications for invasive arterial pressure monitoring are: 1. When deliberate hypotension with potent vasodilators is planned. 2. When massive blood loss and/or transfusion is anticipated e.g. liver transplant. 3. When large blood pressure swings are expected and need to be treated aggressively, as in pheochromocytoma. 4. When tight regulation of blood pressure is required to enhance patient outcome, e.g. in a patient with IHD or undergoing microvascular aneurysm surgery. 5. When frequent blood gas analysis is required. 6. In patients with hypotension due to any cause where non-invasive techniques may be inaccurate or fail. The technique of arterial cannulation is described in the chapter on Vascular Cannulation. Central Venous Pressure monitoring and indications of central venous cannulation: 1. To record central venous pressure during major surgery, especially in procedures that are prolonged and/or involve significant blood loss.

B

Figs 6.5A to C: Appropriate cuff size

C

MONITORING THE PATIENT UNDER ANESTHESIA

2. Critically ill patients in ICU and in all patients with hemodynamic instability, to plan volume and inotrope management. 3. To administer parenteral nutrition to patients unable to tolerate oral or enteral nutrition. 4. Patients with poor peripheral venous access who need periodic sampling and/or drug administration, as patients receiving chemotherapy, patients with burns or polytrauma, patients in ICU, neonates. 5. For administration of sclerosant/irritant solutions over a prolonged period, e.g. 10%/ 25% dextrose, calcium gluconate and noradrenaline. 6. To aspirate air emboli. 7. To insert pacing leads.

91

Fig. 6.6: The pulse oximeter

Pulse Oximetry (Fig. 6.6) Pulse oximetry is mandatory for any anesthetic procedure and even when moderate sedation is planned. It gives a continuous, non-invasive evaluation of oxygenation in routine as well as specialized sugical procedures. Principles (Fig. 6.7) 1. Pulse oximetry is based on Lambert and Beer’s laws of absorbance. Oxyhemoglobin absorbs more infrared light (960 nm) whereas deoxyhemoglobin absorbs more red light (660 nm) and thus appears cyanotic. 2. Two diodes-red and infra-red are present on the fingertip sensor. 3. A Photocell detects transmitted radiation. 4. The Diodes are switched on and off at high frequency to eliminate effect of other light sources. 5. A microprocessor analyses changes of absorption at pulsatile flow, discards nonpulsatile component due to tissues and venous component and analyzes ratio of absorption at the red and infrared wavelengths.

Fig. 6.7: Principles of working of the pulse oximeter

6. SpO2 provides an idea of tissue perfusion and heart rate. 7. SpO2 is normally close to 100%; because of this fact and the shape of the oxygenhemoglobin dissociation curve, SpO2 of 90% may indicate PaO2 < 65 mm Hg. 8. In CO poisoning falsely high readings are obtained (as COHb and HbO2 absorb light at 660 nm identically). 9. In methemoglobinemia, SpO2 over estimates actual fractional oxygen saturation (SaO2) proportional to the concentration of methemoglobin. SpO2 plateaus at 8486% when methemoglobin concentration

92 A PRIMER OF ANESTHESIA

Fig. 6.8A: Infra-red analyzer

Fig. 6.8B: CO2 sampling path

reaches 35%. At constant methemoglobin levels if additional desaturation is induced, SpO2 falls less than SaO2. This is because methemoglobin has the same absorption coefficient at both wavelengths- this causes a 1:1 absorption ratio corresponding to an SpO2 of 85%. 10. Venous pulsations, low perfusion states, methylene blue dye and excessive ambient light can also cause artifacts. Capnography This is recommended as mandatory for all anesthetics. It has numerous uses in all patients undergoing surgery:

1. Confirms correct placement of endotracheal tube. 2. Helps to diagnose endobronchial intubation. 3. Sensitive indicator of decline in, or cessation of pulmonary blood flow as in: a. Cardiac arrest b. Pulmonary embolism due to air/tumor c. Hypovolemia, severe hypotension 4. Sensitive indicator of circuit disconnection. 5. Partial /total airway occlusion(endotracheal tube kinking) 6. Difficult CO2 exhalation (bronchospasm). Principles of Capnography (Figs 6.8A and B) a. It is based on absorption of specific infrared wavelength (4.28 μm) by CO2.

MONITORING THE PATIENT UNDER ANESTHESIA

93

b. Infra-red waves are emitted by a hot wire and passed through a filter. c. The waves then enter the sampling chamber, are absorbed by CO2 and exit. d. Exiting radiation directed at a photodetector. e. Amount of radiation detected is inversely proportional to amount of absorption and therefore the amount of carbon dioxide. Figure 6.8B traces the path of sampled CO2. Temperature monitoring: This is indicated when a patient is to undergo prolonged surgery, especially involving a body cavity like the thorax or abdomen. It is especially indicated in extremes of age where heat loss is rapid due to large surface area (neonates, infants and children) or where subcutaneous tissue is poorly in evidence, as in old age (Fig. 6.9). Hypothermia has grave implications in the patient with coronary artery disease, where the increased oxygen demand due to shivering can precipitate myocardial ischemia. In the preterm child or newborn hypothermia can cause bradycardia, reduced cardiac output, hypoxemia and apnea. Neuromuscular monitoring (Fig. 6.10): This has been extensively discussed in the chapter on neuromuscular blocking agents. This is indicated in operations where complete immobility is mandatory, as in microvascular neurosurgery, or corneal transplants. In patients with disordered hepatic/renal function or neuromuscular disorders like myasthenia gravis it is vital to titrate the dose of relaxants so that minimum required dose is used and the need for postoperative ventilation avoided. How is Appropriate Monitoring for a Patient Selected? Depending on the gravity of the surgical procedure and the preoperative condition of the patient, monitoring is selected and implemented. Patient ASA status and intensity

Fig. 6.9: Temperature probe in right naris in an elderly patient

Fig. 6.10: Neuromuscular transmission monitoring

of monitoring are directly related, i.e. a sicker patient does better if monitored more closely. Thus a 40-year old ASA I patient scheduled for knee replacement surgery may not require anything beyond minimum monitoring and may be managed with spinal or epidural anesthesia. On the other hand if he has coronary artery disease (CAD), he will need invasive arterial monitoring for control of hemodynamic changes which accompany anesthesia and surgery. Similarly minimally invasive surgery, for example, laparoscopic nephrectomy may be carried out with routine monitoring in an ASA I-II patient; however if same the patient has

94 A PRIMER OF ANESTHESIA

CAD, the hemodynamic changes induced by pneumoperitoneum and access devices (trocars, ports) can be accurately monitored and treated by invasive monitoring. Thus a thorough knowledge of the surgical procedure is integral to the institution of appropriate monitoring and good anesthesia care. Apart from displaying variables, the other important function of monitors is to warn the anesthesiologist about any deviation from the set normal range of physiological variables. • To draw attention • Transfer information about machine/ breathing system/patient • Enhance vigilance, especially in fatigued personnel • Warn of impending/existing adverse condition

In spite of the array of monitors (Figs 6.11 and 6.12) available it is vital to maintain physical contact with the patient, e.g. palpation of a pulse. Monitors should be used with appropriate alarm limits. For example, HR monitor with limits 80-100/min for an adult has to be

Fig. 6.11: Modern OT monitor

Fig. 6.12: Respiratory monitor

reset to 100-180/min for a neonate; otherwise bradycardia will be missed. Any alarm generated by a monitor needs to be genuinely analysed before it is silenced. STATE WHETHER TRUE (T) OR FALSE (F) 1. The basic principles of monitoring during anesthesia suggest that a. The monitor warns b. It measures physiological variables and indicate trends of change c. The device can replace conscientious observer d. Human error is absolutely prevented with monitoring equipments 2. The evolution of guidelines of monitoring standards in the world reveals the a. The 1986 guidelines of the anesthesia department of Harvard Medical School b. Standards of monitoring during anesthesia and recovery in 1988 in Great Britain and Ireland c. Minimal monitoring standards in Australia in later 1998 d. International standards for a safe practice of anesthesia by The World Federation of Societies of Anesthesiologists in June, 1992

MONITORING THE PATIENT UNDER ANESTHESIA

3. The importance of monitoring is supported by the following facts a. One third of intraoperative deaths was preventable b. Sensitive devices complement humane vigilance c. Previously healthy patients were not at risk d. Intra-operative deaths are due solely to existing systemic diseases 4. The following parameters should be continuously checked during anesthesia a. Inspired oxygen concentration b. Displaying ECG c. Measurement of expired gas analysis or observation of ventilation d. Circulation, i.e. pulse oximetry 5. Noninvasive monitoring of cardiovascular system can be performed with a. Capillary refill time b. Central and peripheral body temperature difference c. Central venous pressure measurement d. Electrocardiogram with chest leads V5 and V4 6. Blood pressure is directly measured by the following techniques a. Von Recklinghausen’s oscillotonometer b. An automated oscillometer c. Pressure transducer and arterial cannulation d. Finger on a peripheral pulse 7. Common complications associated with arterial cannulation a. Accidental disconnection and hemorrhage b. Pulmonary embolism c. Damage to the vessel wall and subsequent thrombosis d. Erroneous blood pressure reading from variable position of transducer or patient

95

8. Placement of a central venous pressure catheter provides the following uses a. Avoidance of infection from common organisms found in the skin b. Parenteral or enteral nutrition c. Monitoring blood volume by direct central venous pressure reading d. It is easier to do because the central veins (internal or external jugular)are larger 9. The following drugs or fluids are safe to give via a central vein a. Norepinephrine b. 50% Dextrose solution c. 0.25% Bupivacaine d. Bleomycin 10. Principles of pulse oximetry is as follows a. The finger probe contains two light emitting diodes and two light detectors b. Oxyhemoglobin absorbs infrared light (660 nm) and deoxyhemoglobin absorbs more red light (960 nm) c. At the isobestic point, absorption is identical and it is different at other wavelengths d. Saturation of hemoglobin is calculated by measuring the absorption at two different wavelengths 11. Shortcomings of pulse oximeter may be due to presence of the following a. Carboxyhemoglobin b. Methemoglobin c. Deoxyhemoglobin d. Bilirubin 12. The following diagnosis are helpful by the shape and magnitude of capnograph a. Chronic obstructive airway disease b. Massive pulmonary embolism c. Misplacement of endotracheal tube in the esophagus d. Aspiration of blood in the lungs during tonsillectomy

96 A PRIMER OF ANESTHESIA

13. Temperature monitoring is mandatory in the management of a. Six months old baby with inguinal hernia b. Two years old with brain stem injury c. Eighty years old for hip replacement under GA d. Young man for liver transplant 14. You are asked to choose only one equipment under anesthesia and the most useful one would be a. ECG monitor b. Automated blood pressure monitor c. A portable pulse oximeter d. A compact EEG monitor to guide the level of anesthesia

15. The stethoscope may be used to monitor the following observations a. Position of the tracheal tube placement b. Cardiovascular status by measuring blood pressure c. It may warn presence of irregular heart beat d. Ventilator disconnection by auscultation over the chest Answers 1. 4. 7. 10. 13.

T T F F 2. TTFT 3. T T F F FTTT 5. TTFT 6. F F T F TFTT 8. F F T F 9. TTFT F F T T 11. TTFT 12. TTTF FTTT 14. F F T F 15. TTTT

Vascular Cannulation Rajeshwari Subramaniam

Indications of peripheral venous cannulation  Technique of peripheral venous cannulation  Technique of central venous cannulation  Technique of arterial cannulation 

The skill of vascular cannulation is as integral to the practice of anesthesia as airway management. Although with practice one can become good at inserting vascular cannulas the chances of success increase if certain simple rules are followed and a patient will not be subjected to an (often) unnecessary extra prick. Indications of peripheral venous cannulation: 1. In the operating theatre, provides route for administration of intravenous(IV) drugs, both anesthetic and emergency. 2. Route for hydrating the patient in ICU, emergency and operating theatre. 3. Necessary if blood or blood products need to be transfused. 4. In the radiology department for injection of contrast prior to CT scan/MRI. 5. In the outpatient setup, provides route for administration of sedation and/or emergency drugs.

Fig. 7.1: Veins over the dorsum of the hand

The common peripheral veins are found on the dorsum of the hand (Fig. 7.1), at the wrist (the cephalic), at the elbow (cephalic or basilic; (Fig. 7.2) and the ankle (saphenous). Sizes and parts of an IV cannula: The IV cannula (Fig. 7.3) is made of Teflon or suitable non-toxic, inert material (polytetrafluoroethylene). The soft and pliable cannula is mounted over a steel stylet which gives it rigidity and enables sharp and atraumatic penetration of the skin. The beveled stylet projects for 1-2 mm beyond the cannula (Fig. 7.3). Thus after entering the vein it is important to insert the stylet-cannula combination well into the vein to prevent the blunt cannula being left outside the vein as the stylet is withdrawn.

98

A PRIMER OF ANESTHESIA

Fig. 7.2: Veins at the elbow

Fig. 7.3: The tip of the cannula shows the protruding stylet

The color coding for IV cannulae is: 14 G, orange; 16 G, grey; 18 G, green; 20 G, pink; 22G, blue and 24 G, yellow. The smaller the gauge number, the thicker the cannula. STEPS IN INSERTING AN IV CANNULA The vein chosen should be well visible and made prominent (Fig. 7.4A) by light tapping on it by the fingertips. A patient who is not anxious may be asked to open and close his fingers and make a tight fist. You can confirm a patent vein by rolling it under your fingers. Gently ‘ballot’ it to make sure it is not thrombosed. It is a good idea to infiltrate local anesthetic at the site. Clean the skin gently by wiping with an antiseptic swab. Never rub with alcohol as it stings when the cannula is inserted. Tie an elastic tourniquet or a piece of rubber tubing around the wrist to make the vein fill up. Take care not to occlude the arterial circulation with too tight a tourniquet or manual pressure! This is espe-

cially likely to occur in children. Insert the cannula at a 30° angle in three steps: (i) enter the skin, (ii) travel between the skin and vein for 2-3 mm, (iii) enter the vein by dimpling its superior surface. Blood enters the ‘flash back chamber’ when the vein is entered (Fig. 7.4B). As the blood appears, advance the cannulastylet set for 2-3 mm to ensure the cannula is completely inside the vein. Then stabilize the stylet with the left hand and slide off the cannula over it into the vein (Fig. 7.4C). Locate and press down on the tip of the cannula to prevent blood from trickling out and completely withdraw the stylet (Fig. 7.4D). You can now either screw on the white disposable cap or connect an IV fluid set to the cannula. A transparent dressing is applied to secure the cannula in place (Fig. 7.4E). Precautions to be observed: 1. Wear gloves and make sure to clean up any spilt blood. 2. Remember to take away the sharp stylet and put it in the needle destroyer. 3. Do not pick up things like your pen, the phone or forms wearing gloves that have been soiled. 4. Mark the tip of the cannula on the skin with a pen. 5. Make sure the IV tubing is de-aired (that is, all air bubbles are scrupulously tapped out). This is especially important in children with intra-cardiac shunts. TECHNIQUE OF CENTRAL VENOUS CANNULATION Central venous cannulation is most commonly performed through the right internal jugular vein as it is in straight line with the right atrium. The other routes are the subclavian, the femoral and the basilic veins. Figure 7.5 shows the location of some veins chosen for central cannulation. Figures 7.6 A to E give a simplified list of steps in cannulating the internal jugular vein. Each approach has unique advantages and disadvantages.

VASCULAR CANNULATION

99

Fig. 7.4A: The vein is made prominent

Fig. 7.4D: Tip of cannula occluded

Fig. 7.4B: Blood enters the flash back chamber

Fig. 7.4E: Dressing applied and IV fluid connected

TECHNIQUE OF ARTERIAL CANNULATION

Fig. 7.4C: Cannula slid over stylet

Arterial cannulation is performed (commonly in either of the radial arteries) when continuous monitoring of the blood pressure (BP) is vital for a good outcome. Examples are mentioned in Chapter 6. Arterial pressure is measured by an electronic transducer and displayed on the monitor. The radial artery is normally chosen because of its superficial location and ease of access, and also the fact that the ulnar artery provides good collateral flow to the hand. The modified Allen’s test is performed to ensure good collateral

100

A PRIMER OF ANESTHESIA

Fig. 7.6C: Locating the IJV Fig. 7.5: Veins chosen for central cannulation

Fig. 7.6D: Insertion of guide wire Fig. 7.6A: Landmarks for IJV cannulation

Fig. 7.6B: Palpating the carotid artery

Fig. 7.6E: Triple lumen catheter sutured in place

VASCULAR CANNULATION

AA

D

BB

E

101

Fig. 7.7A to E: Steps in cannulation of radial artery

C

C

circulation from the ulnar artery. The patient is asked to make a tight fist. The examiner occludes the radial artery with one hand and the ulnar with the other. The patient releases the fist,

which would be blanched. The examiner then releases occlusion of the ulnar artery, and the palm should flush pink for a positive test. The other arteries that can be chosen are brachial (may get kinked) or the dorsalis pedis and posterior tibial (may produce distorted waveforms). The area is swabbed clean and a small wheal of local anesthetic raised. The wrist is extended and stabilized on a small rolled towel. The left hand palpates and ‘tracks’ the course of the artery; the cannula is inserted at an angle of 30° to the skin. As soon as it enters the artery, bright red blood can be aspirated. The cannula is slid off the stylet and secured in place (Figs 7.7A to E).

D

E

Airway Management Indu Kapoor, Rajeshwari Subramaniam

Definition of ‘airway management’ Mask ventilation Recognizing airway obstruction Technique of endotracheal intubation The LMA-indications, contraindications, technique of insertion  Airway obstruction and failed intubation  Airway equipment     

Airway management is such an integral part of the knowledge and skill of anesthesia that anesthesiologists are usually identified with the act of laryngoscopy and intubation. Even in remote corners of the hospital, when a patient is in respiratory distress it is the anesthesiologist who is summoned to ‘manage’ the airway as his/her skill in this area is unquestioned. It is in the specialty of anesthesia that training in airway management is imparted in an elective and safe manner. What is Meant by ‘Airway Management ? Airway management essentially encompasses use of suitable anesthetic technique/s, appropriate patient positioning and use of airway devices with an end point of achieving, and maintaining, an unobstructed airway. The patient can then be allowed to breathe

spontaneously or receive assisted ventilation, as required. Most patients undergoing major abdominal, thoracic, head and neck, orthopaedic or neurosurgical procedures require general anesthesia. As you have seen in the preceding chapters, all anesthetic agents and narcotics depress ventilation. Endotracheal intubation and protection of the airway allows the use of muscle relaxants, adequate depth of anesthesia and provides good surgical conditions. Oxygenation and carbon dioxide homeostasis can be maintained with controlled ventilation for prolonged periods. Other supraglottic airway devices can also be used in place of the endotracheal tube and are described with their indications and contraindications. This chapter outlines steps on: 1. How to maintain a patent airway after induction of anesthesia; 2. How to manage mask ventilation; 3. How to recognize upper airway obstruction and overcome it; 4. Step-by-step guide to endotracheal intubation; 5. Checking proper endotracheal tube placement; 6. Advantages, contraindications and steps of insertion of an LMA; 7. Management of failed intubation; 8. Management of the obstructed airway;

AIRWAY MANAGEMENT

103

9. ‘Rapid Sequence’ induction and intubation; 10. How to use a combitube; 11. Some other supraglottic devices. (You can refer back to this chapter when you read about CPR). Initial Airway Management Airway management in anesthesia begins at induction itself. It is VITAL that all airway equipment, the anesthesia machine and availability of suction is routinely checked before every anesthetic. Drugs prepared would include an induction agent, a narcotic, a muscle relaxant, atropine and lignocaine 2% or other appropriate drug to attenuate the intubation response, if needed. It is useful to preoxygenate all patients with deep breaths of 100% oxygen for 3 minutes (or four breaths at total lung capacity) especially if (i) the patient may be difficult to mask ventilate (discussed later), (ii) has reduced oxygen reserve (is obese, pregnant or anemic), (iii) has a ‘difficult’ airway or (iv) requires ‘rapid sequence’ induction (explained later). Preoxygenation increases the margin of safety in the apneic period during intubation. As anesthesia induction is completed, the eyelash reflex is abolished and there is loss of upper airway muscle tone. Loss of tone in the genioglossus causes the tongue and epiglottis to fall against the posterior pharyngeal wall (Fig. 8.1). The ‘head tilt’ (Fig. 8.2) and ‘jaw thrust’ (Fig. 8.3) are the appropriate maneuvers to displace the tongue and epiglottis away from the posterior pharyngeal wall and restore airway patency. Head tilt is performed by a simultaneous act of lifting the chin up with one hand and pushing the head downward with the other. Without allowing the head to slump forward, jaw thrust is applied. The four fingers of the hand grasp the angle of the mandible on both sides with the thumbs on the chin and attempt to bring the mandible forward (Fig. 8.3). We can judge

Fig. 8.1: Tongue falling back on posterior pharyngeal wall

Fig. 8.2: The “head tilt” maneuver

Fig. 8.3: The ‘Jaw thrust’ maneuver

the adequacy of jaw thrust by bringing the lower incisors in line with, or in front of, the upper incisors. The facemask is then placed on the patient, and mask ventilation commenced.

104 A PRIMER OF ANESTHESIA

facemask, the movements of the reservoir bag can be observed. If the patient is not breathing, positive-pressure ventilation can be administered by intermittently squeezing the reservoir bag of the anesthesia circuit. A two-handed technique is required for beginners and in difficult patients (discussed below).

Fig. 8.4: Single handed mask ventilation

With the correct technique of adequate mask ventilation one you can observe the following: 1. Rise and fall of the chest wall. Remember that expiration should also be adequate. 2. Appearance of respiratory moisture on a transparent mask. 3. Absence of inflation of the stomach. 4. Maintenance of oxyhemoglobin saturation. 5. Appearance of a good capnograph trace on the monitor. Mask ventilation can be difficult in: a. Presence of a Beard b. An Obese patient c. No teeth (edentulous) d. Elderly individuals e. Snorers. You can remember these factors by the mnemonic ‘BONES’.

Fig. 8.5: Two handed mask ventilation

Mask Ventilation This is one of the most important aspects of airway management. Ability to ventilate well with a mask even if one fails to accomplish intubation ensures that the patient is safe and well oxygenated till help arrives or until other alternative techniques are being considered. On the other hand if mask ventilation is not easy or improperly performed it jeopardizes the patient’s safety if there is a delay in intubation or a failed intubation. Mask ventilation can be performed with one hand (Fig. 8.4) or both (Fig. 8.5). If the patient is breathing spontaneously through the

PROBLEMS WITH MASK VENTILATION 1. Airway obstruction: In spite of the headtilt and jaw thrust maneuvers, the airway may still be obstructed due to a large tongue or obesity. How do you diagnose airway obstruction if the patient is (i) making respiratory efforts (Table 8.1)? ‘Paradoxical’ respiration is so termed because the chest moves inward during inspiration instead of the common outward movement, so that a ‘rocking’ pattern is seen. This is because the patient making an effort to breathe generates a high negative intrathoracic pressure while trying to inspire through an obstructed airway; this causes the chest wall to get ‘sucked’ inwards. (ii) If

AIRWAY MANAGEMENT

105

Table 8.1: Comparing the unobstructed and obstructed airway Parameter observed

Patent airway

Movement of chest and abdomen

Normal

‘Paradoxical’

Movement of reservoir bag

Present

Absent

Presence of respiratory moisture

Present

Absent

Oxyhemoglobin saturation

Maintained

May start falling

Capnograph trace

Satisfactory

Absent; apnea alarm

the patient is not breathing, airway obstruction is diagnosed by inability to expand the chest by squeezing the reservoir bag of the anesthesia breathing circuit. If obstruction remains uncorrected, the SpO2 falls and exhaled CO2 cannot be detected. The stomach may get distended. Once airway obstruction is diagnosed, it has to be treated speedily to prevent hypoxemia. The simplest solution is to insert a Guedel’s airway or a nasopharyngeal airway (Figs 8.15 and 8.16). Mask ventilation is immediately made easier and more effective. Paradoxical movements disappear in spontaneously breathing patients. 2. Expiratory obstruction: If the chest is inflating well but not deflating freely the cause is usually a very tightly applied jaw thrust in combination with the tongue acting like a one-way ‘ball valve’. This problem is relieved by reducing the jaw thrust or inserting an oropharyngeal airway which keeps the tongue away and permits exhalation. 3. Leaks: A significant leak results in failure of the reservoir bag to fill and therefore, inability to ventilate. Leaks usually occur due to poor mask fit, whose causes can be many-ranging from inappropriate size, damaged air cushion, edentulous patient (Fig. 8.6) and presence of a beard. The concave regions of the face, e.g. the cheeks and eye sockets, can be ‘sealed’ with gauze. For intubation, muscle relaxant is administered after ascertaining adequate mask ventilation and the patient’s chest ventilated for

Obstructed airway

Fig. 8.6: Difficult mask fit in edentulous patient

3-4 minutes to achieve satisfactory conditions for intubation. Apart from selecting appropriate airway equipment the other important conditions to be fulfilled for successful and atraumatic laryngoscopy and intubation are: 1. The patient should be adequately anesthetized to prevent awareness, tachycardia and hypertension during intubation. 2. There should be no motor response, i.e. coughing, gagging in response to laryngoscopy and intubation. This is achieved by adequate neuromuscular blockade. 3. The patient should be appropriately positioned. When the head is in the neutral position, (Fig. 8.7) it can be seen that the oral axis (which is an imaginary line), the pharyngeal axis and the laryngeal axis are all in different directions. Flexion of the cervical spine (by

106 A PRIMER OF ANESTHESIA

Fig. 8.7: The neutral position

Fig. 8.8C: Larynx visualized

Laryngoscopy (Figs 8.10 A to D)

Fig. 8.8A: Flexion of the cervical spine

Fig. 8.8B: Extension of atlanto-occipital joint

placing a 10 cm pillow beneath the occiput) and extension at the atlanto-occipital joint maximally aligns these three axes (Figs 8.8 A and B), so that it becomes easy to visualize the larynx using a laryngoscope (Fig. 8.8C). This is also termed the ‘sniffing’ position.

The laryngoscope is held in the left hand. The fingers of the right hand open the mouth using a ‘no-touch’ technique by depressing the chin slightly. The laryngoscope is gently introduced from the right angle of the mouth. The laryngoscope travels all the way down the tongue. The laryngoscopist takes care that no part of the tongue is protruding from behind the right side of the blade. At the end of the tongue the edge of the leaf-like epiglottis is visible. The tip of the laryngoscope blade is engaged in the vallecula, which is a groove at the junction of the tongue and epiglottis, also known as the glosso-epiglottic fold. The laryngoscope is lifted upwards and outwards (Fig. 8.9A) and NOT towards the laryngoscopist (Fig. 8.9B); that is a rotating movement which will injure or break teeth. The glottic chink bordered by the pearly white vocal cords then comes into view (Fig. 8.10C). Intubation

Selection of Appropriate Tube Size Endotracheal tube size is conventionally stated in terms of the internal diameter (ID) in mm.

AIRWAY MANAGEMENT

107

Fig. 8.10B: Introducing the laryngoscope from the right corner of the mouth Fig. 8.9A: Correct exertion of force

Fig. 8.10C: The larynx exposed Fig. 8.9B: Incorrect direction of applying force during laryngoscopy

Fig. 8.10A: Opening the mouth by depressing the jaw

Fig. 8.10.D: Introducing the endotracheal tube

108 A PRIMER OF ANESTHESIA

Adult males can be intubated with size 8.0 or 8.5 mm ID cuffed PVC endotracheal tubes. (A description of various endotracheal tubes is given in the section on Anesthesia Equipment). Cuffed endotracheal tubes of size 7.0 or 7.5 mm ID are suitable for adult female patients. In children it is important to be aware of the size of the appropriate tube which is usually calculated by age. The width of the small finger of the hand is often used as a rough guide. Table 8.2 lists the appropriate tube size for children. The endotracheal tube is held with the tips of the thumb, index and middle fingers of the right hand and brought in an inclined manner towards the mouth so that the vision of the glottis is not obscured (Fig. 8.10D). It is always inserted under vision. The tube should be seen actually entering the larynx and the cuff positioned immediately below the vocal cords. The black ring marked just above the cuff should be positioned at the level of the vocal cords. Occasionally in an anteriorly placed larynx we may have to shape the endotracheal tube with a malleable stylet (Figs 8.27 A and B). Inflating the Cuff with Air The blood supply to the tracheal mucosa and cartilage is derived from the submucosa, which has a rich capillary network. If the intra-cuff pressure exceeds capillary pressure (19-25 mm Hg), mucosal ischemia and ulceration results. Table 8.2: Approximate ETT size in children Age Neonate

Weight (kg)

Size

2-4

2.5-3.5

1-6 months

4-6

4.0-3.5

6-12 months

6-10

4.0-4.5

1-3 years

10-15

4.5-5

4-6 years

15-20

5-6

7-10 years

25-30

6.5-7.0

10-14 years

40-50

7.0-7.5

In prolonged intubations (as in ICU patients) if cuff pressure is consistently above capillary pressure, deep ulcerations occur involving the cartilage. Ultimately this heals by stricture formation. The majority of patients of tracheal stenosis have a history of prolonged intubation. The amount of air in the cuff is thus a matter of concern. To regulate the amount injected into the cuff, a hand is kept over the sternal notch where a ‘gurgle’ is felt and heard as air leaks with every inspiration. Air is injected through the one-way valve of the pilot balloon in increments till the leak is not felt or heard. In children up to 8 years of age non-cuffed tracheal tubes (Fig. 8.11) are preferred so that there is no compromise on the maximal external diameter possible that can be used. The resistance offered to breathing through a tube is inversely proportional to the fourth power of the radius of cross section of the tube. Further, selection of the largest size that comfortably passes through at the level of the cricoid provides a circular ‘seal’ as this is the narrowest portion of a child’s airway. The correct size in a child should allow a gas leak at 15-20 cm H2O pressure for a non-cuffed tube. The tube is now checked for correct position. Even before one auscultates the chest, respiratory moisture is visible with every inspiration in the tube. While ventilating manually, the chest is visually inspected for bilaterally equal expansion, following which the apices and bases of both lungs are auscultated sequentially to check whether the intensity of breath sounds is

Fig. 8.11: A non-cuffed PVC endotracheal tube

AIRWAY MANAGEMENT

equal on both sides. The epigastrium is auscultated to confirm absence of air entry. Obtaining a trace of exhaled carbon dioxide (capnography) is the gold standard that confirms endotracheal placement of the tube. The tube is then firmly secured in place with a length of sticking tape. In infants and children it is prudent to make a note of the tube marking (in cm) at the angle of the mouth which can be used as a reference if tube position needs to be re checked. It is also common practice to cut off extra length of the tube in infants and small children to prevent drag on the circuit. In head and neck, ophthalmic and neurosurgical procedures, the importance of fixing the tube correctly and securely cannot be over emphasized; dislodgement or displacement of the tube in a patient where access to it is not possible spells disaster.

109

The Laryngeal Mask Airway (LMA) The laryngeal mask airway (LMA) is being frequently used as an alternative to either the facemask or tracheal tube during anesthesia. This supraglottic airway device was designed by Dr. Archie Brain of UK. Since the 1980’s it has been replacing the endotracheal tube for most routine procedures. It has proved to be extremely useful in managing failed intubation situations. It can be described as a device intermediate to the facemask and endotracheal tube. There are now five versions of the LMA available (Figs 8.12A to D): the classic, the flexible, the intubating LMA ( ILMA or LMAFastrach), the Proseal LMA and the LMA-C Trach which has a camera at the observer end which helps to visualize the laryngeal inlet in ‘difficult’ airways. The LMA can be used in all

Fig. 8.12A: The LMA ‘classic’

Fig. 8.12B: The flexible LMA

Fig. 8.12C: The intubating (Fastrach) LMA

Fig. 8.12D: The ‘Proseal’ LMA

110 A PRIMER OF ANESTHESIA

situations except those where it is contraindicated (see below). The advantages of the LMA over the endotracheal tube are: 1. Can be inserted without the use of muscle relaxants 2. Does not need laryngoscopy 3. High success rate after 10 insertions; can be taught to paramedics and students 4. Does not elicit tachycardia and hypertension during/after insertion 5. Permits the use of light planes of anesthesia especially when a regional block is used concomitantly 6. Does not produce cough/breath-holding during emergence. This smooth emergence is of great value after ophthalmic procedures and tonsillectomy 7. Can be retained in small children and elderly till they are fully awake, thus increasing airway safety 8. Useful in ‘cannot intubate, cannot ventilate’ situations as a rescue airway device 9. Can be used as a conduit for the fibreoptic bronchoscope to guide an endotracheal tube into the trachea in patients with difficult intubation. Disadvantages of the LMA: – may get displaced (usually in very small children, edentulous adults) – gastric insufflation always a possibility – does not guarantee against aspiration – positive pressure ventilation may be difficult if high airway pressures are required – the large epiglottis of a child may get folded and result in obstruction to expiration – may provoke regurgitation. Technique of insertion (Figs 8.13A to C): It is important to ensure that the jaw is adequately relaxed. Propofol is an ideal agent for LMA placement due to its depressant effect on the respiration and airway reflexes. The LMA can also be placed under inhalational anesthesia (with halothane or sevoflurane), or after thiopentone-relaxant sequence.

The head is extended at the atlanto-occipital joint and the mouth opened with the left hand. The cuff should be fully deflated and not have any folds. The LMA is held like a pencil with the concavity (bowl) facing the tongue. The right index finger is insinuated into the groove between the stem and the cuff and the LMA inserted into the mouth. It is advanced by pressing against the hard palate; the index finger travels down all the way in a smooth, single, fluid movement behind the tongue till the LMA encounters resistance below the hypopharynx. The left hand then steadies the LMA and the right index finger withdrawn. The requisite amount of air is then injected into the cuff; the LMA is seen to ‘rise’ and occupy its position in the hypopharynx. An ideally placed LMA is bordered superiorly by the base of the tongue, laterally by the pyriform sinuses and inferiorly by the upper esophageal sphincter. If the esophagus lies within the cuff the stomach will be insufflated. Correct placement of an LMA is confirmed by the presence of all of the following findings: a. expansion of the chest b. absence of gastric inflation c. a square wave capnogram which touches the baseline d. maintenance of normal saturation e. airway pressures below 20 cm H2O f. in the case of LMA ‘Proseal’ (Fig. 8.11D), the gastric drainage tube should be easily inserted in the stomach. The recommended sizes and cuff inflation volumes for laryngeal mask are shown in Table 8.3. Contraindications to the use of the LMA These relate to patient factors or surgical conditions. Patient factors: – Morbid obesity: the LMA may not withstand the high airway pressures needed to ventilate these patients.

AIRWAY MANAGEMENT

111

Figs 8.13A to C: Steps in insertion of LMA Table 8.3: LMA sizes and volume of air to inflate cuff Size

Size of patient

Cuff inflation volume

1 11/2 2 21/2 3 4 5 6

Neonates, infants upto 5 kg Infants 5-10 kg Infants/Children 10-20 kg Children 20-30 kg Paediatric 30-50 kg Adult50-70 kg Adult70-100 kg Large adult >100 kg

Up Up Up Up Up Up Up Up

to to to to to to to to

4 ml 7 ml 10 ml 14 ml 20 ml 30 ml 40 ml 50 ml

– ‘Full stomach’(see below) patients: the LMA does not guarantee against aspiration. – Difficult airway: although the LMA may be used as an interim device to oxygenate the

patient, it is important to secure a definitive airway by fibreoptic intubation or tracheostomy before proceeding with surgery. – Gastroesophageal reflux disorders. – Neonates and small infants for major procedures: the LMA might get dislodged or malpositioned and it is very difficult to access these small patients under the surgical drapes. Surgical factors: – Oral surgery; major head and neck procedures – Microlaryngeal surgery – Surgery in prone position – Procedures where the patient is likely to require postoperative intubation/ventilatory support

112 A PRIMER OF ANESTHESIA

‘RAPID SEQUENCE INDUCTION AND INTUBATION (FIG. 8.14) Patients in whom intra-gastric/proximal bowel contents are likely to be increased due to mechanical conditions such as bowel obstruction or physiological conditions such as pregnancy/obesity are termed as being ‘full stomach’. These patients are at high risk of regurgitating and aspirating their bowel contents. Therefore, it is vital that minimum time elapses between onset of unconsciousness and endotracheal intubation. The normal sequence of induction and intubation is modified in these patients. The sequence is as follows: – Ability to tilt the operating table and availability of suction is ensured. – All airway equipment is checked. The endotracheal tube cuff is deflated and a syringe with 5 ml air connected to the pilot balloon. – The patient is preoxygenated for three minutes. – A precalculated amount of induction agent (usually thiopentone) is injected. – The assistant applies backward pressure on the cricoid (Sellick’s maneuvre) as soon as induction starts. This is to compress the upper esophagus between the cricoid and

Fig. 8.14: Rapid sequence intubation

–

– – • •

the vertebral column to prevent any regurgitation of gastric contents. A short-acting muscle relaxant (succinylcholine 1.5-2 mg/kg) is administered. If there is any contraindication for Suxamethonium, Rocuronium, 1.2 mg/kg can be given. The patient’s chest is NOT ventilated. Exactly after 45 seconds, the trachea is intubated, maintaining cricoid pressure. The cuff is immediately inflated; cricoid pressure is released after confirming correct tube position. After confirming endotracheal tube placement, ventilation is resumed.

Management of Airway Obstruction and Failed Intubation A significant number of patients have problems which prevent access to the airway by the means mentioned above. Examples are patients with burn contractures, ankylosing spondylitis and cervical spine fractures where neck movements may be restricted or prohibited; large growths in the oral cavity which preclude insertion of a laryngoscope; facio-maxillary injuries and temporomandibular joint ankylosis which prevent mouth opening. The difficult airway is thus ‘anticipated’. These patients require good planning and sophisticated airway management techniques like fibreoptic intubation, retrograde intubation and submental intubation. Occasionally, unanticipated difficulty occurs with laryngoscopy and it may not be possible to intubate or ventilate a patient even after multiple attempts. The management of this situation involves consideration of multiple factors: the urgency of the surgery, the expertise available to manage a difficult intubation, ease or difficulty of mask ventilation, availability of alternative devices and most important, the condition of the patient. The safest option, if surgery is not a dire emergency, is to place the patient in the lateral position, apply Sellick’s

AIRWAY MANAGEMENT

maneuver and continue to mask ventilate till the return of spontaneous ventilation, wake up the patient and reschedule the procedure. The importance of timely recognition of airway obstruction in an anesthetized patient cannot be over emphasized. There is every chance of severe morbidity or mortality once hypoxemia sets in. Most deaths under anesthesia have been a consequence of failure to oxygenate. Corrective action must be initiated ideally well before onset of hypoxemia. Signs of airway obstruction include noisy, poor or absent ventilation, paradoxical chest and/or abdominal movements and inability to cause chest expansion with a bag in an apneic patient. This condition is an emergency and needs to be managed by a planned sequence of actions or an ‘algorithm’ to maximize success and minimize morbidity/mortality. DIFFICULT AIRWAY ALGORITHM 1. Attempt to ventilate using only 100% oxygen. Desaturation occurs in 65% cases and hypoxemia is the cause of death. 2. Try chin lift and jaw thrust 3. Call for help immediately. Four people will be required: – Person I holds mask and jaw with both hands and intubates as soon as conditions permit. – Person II holds emergency oxygen flush valve and squeezes reservoir bag. – Person III ensures adequate anesthesia and IV access. – Person IV finds and passes equipment and helps others. 4. It should be strongly considered to wake up the patient 5. If not so, try to visualize and clear pharyngeal airway 6. Insert oral/nasal airway 7. ‘Team’ mask IPPV/CPAP 8. If still cannot ventilate – Someone to feel pulse and call out SPO2

113

– Assistant to have scalpel + tube ready – Consider paralysis if not already paralysed – Make one attempt at intubation under vision 9. If you cannot intubate – Consider LMA 10. If this fails, emergency cricothyrotomy is indicated. Needle cricothyrotomy can be performed through a 12 or 14G cannula inserted through the cricothyroid membrane (Fig.8.15). Oxygenation can be maintained for 10 minutes. However ventilation to remove CO 2 is not achieved and spontaneous ventilation is impossible through a cricothyrotomy. It is therefore important to convert to a surgical cricothyrotomy or tracheostomy without further delay. – Ventilate with 100% oxygen The patient is then reviewed to exclude pulmonary aspiration and post obstructive pulmonary edema. The patient should be later

Fig. 8.15: Landmarks for cricothyrotomy

114 A PRIMER OF ANESTHESIA

explained about what happened, reassured and advised to warn future anesthesiologists.

3. A bite block which lies between the upper and lower incisors.

AIRWAY EQUIPMENT

Features 1. Anatomically shaped. 2. Inserted through the mouth above the tongue in to the oropharynx. 3. Maintains patency of the upper airway. 4. Can cause trauma and injury to oral structures. 5. Risk of stimulation of gag reflex and vomiting.

This small section will make you familiar with the common equipment used to maintain an open airway in an unconscious patient. The Oropharyngeal (Guedel s) Airway This anatomically shaped airway (Fig. 8.16A) is inserted through the mouth into the oropharynx above the tongue (Fig. 8.16B) to maintain the patency of the upper airway. It is important to select the right size so that the tongue is not pushed back against the posterior pharyngeal wall. Components 1. A curved body 2. A flange which lies outside the mouth

The Nasopharyngeal Airway (Figs 8.17A and B) 1. Inserted through the nose into the nasopharynx by rotating so that concavity faces

Fig. 8.17A: The nasopharyngeal airway Fig. 8.16A: Oropharyngeal airways

Fig. 8.16B: Oropharyngeal airway inserted appropriately

Fig. 8.17 B: Correct insertion of nasopharyngeal airway

AIRWAY MANAGEMENT

the patient’s lips. With correct placement tip lies immediately posterior to the tongue. 2. A useful alternative to the oropharyngeal airway especially in combative patients, who may gag with an oropharyngeal airway. 3. It softens after contact with mucosa at body temperature and is well tolerated. 4. Not recommended in coagulopathy, fractures of skull base and nose, nasal sepsis and deformities. Components 1. Rounded curved body. 2. Left facing bevel. 3. Flange.

Fig. 8.18A: The face mask

The Face Mask (Fig. 8.18A) The face mask is designed to fit the face anatomically and is available in different sizes. It can be made of black rubber or transparent plastic or silicone. Components 1. The body with an air filled cuff 2. 22 mm connector 3. Steel hooks to attach harness Features 1. Usually made of silicone rubber or plastic 2. The body may be opaque or transparent 3. The design ensures a snug fit over the face of the patient 4. Can produce an increase in dead space (upto 200 ml in adults) 5. Specially designed masks known as ‘Rendell Baker Soucek’ masks with very low dead space are available for neonates and infants, and fit their facial contour well. These masks lack an air cushion (Fig. 8.18B).

Fig. 8.18 B: Rendell-Baker pediatric mask

Fig. 8.19: A cuffed PVC endotracheal tube

The Endotracheal Tube Endotracheal tubes are commonly used for airway management during general anesthesia. These can be made of either polyvinyl chloride (PVC, Fig. 8.19) or rubber. They may be cuffed or non-cuffed. The older red rubber (Fig. 8.20) endotracheal tubes had low-volume, high

Fig. 8.20: The now obsolete red rubber endotracheal tubes

115

116 A PRIMER OF ANESTHESIA

pressure cuffs. In these cuffs the intra cuff pressure is distributed over a smaller area, which means that a given volume of air will exert more pressure on the tracheal mucosa in a red rubber tube compared to a PVC tube. These tubes are almost obsolete now.

Parts Bevel – Left facing and oval in shape – Murphy eye- hole just above and opposite the bevel Cuff – When inflated, provides an airtight seal between the tube and the tracheal wall. – Cuffs can either be high pressure, low volume or low pressure, high volume type.

accepts 100 ml of air and the smaller distal cuff, 15 ml. In between the two cuffs the blue tube has many perforations. The blue end of the tube after blind placement enters the esophagus in 95% of instances. After gentle, blind placement connecting the self-inflating bag or anesthesia circuit end to the blue end results in oxygen escaping from perforations in the pharyngeal part and entering the trachea (Fig. 8.22). If this end has inadvertently entered the trachea, the circuit is connected to the clear adaptor and the distal cuff used as an endotracheal tube cuff (Fig. 8.23). Other supraglottic devices are the COPA (Fig. 8.24) and the Laryngeal Tube (Fig. 8.25) which enjoy limited use as they are not widely available.

Connectors – Connect the tracheal tubes to the breathing system. – Also known as “universal” connectors; all sizes have 15 mm internal diameter.

Possible Problems with Endotracheal Tubes – May get obstructed due to kinking, herniation of the cuff, occlusion by secretions, foreign body or the bevel lying against the wall of the trachea. – Oesophageal or bronchial intubation can result in hypoxemia. – Trauma and injury to the various tissues and structures during and after intubation.

Fig. 8.21: The combitube

The Combitube The combitube is a rescue airway device mainly used during CPR in the field situation; however, it can come in handy when handling a difficult airway. The combitube (Fig. 8.21) is made up of two fused tubes, each with a 15 mm connector at the proximal end. The blue tube is slightly longer and ends in a closed, blunt tip. The shorter clear tube has an opening at its end. There are two cuffs. The larger proximal one

Fig. 8.22: Normal route of combitube-Blue end enters oesophagus

AIRWAY MANAGEMENT

117

Fig. 8.26: The Magill forceps

Fig. 8.23: The combitube entering the trachea

the endotracheal tube into the trachea during nasal intubation, for oro-pharyngeal packing and retrieving objects, e.g. dislodged teeth, blood clots etc from the oral cavity. Its angulation ensures that visibility is unimpaired when the object is being held. The Laryngoscope (Figs 8.27 A and B) This device is familiar to everyone associated with the operating room. It consists of a flanged

Fig. 8.24: The cuffed oropharyngeal airway (COPA)

Fig. 8.27A: The Macintosh blade

Fig. 8.25: The laryngeal tube-airway (LTA)

Magill Intubating Forceps (Fig. 8.26) This angulated forceps is an essential part of the airway trolley (or ‘cart’). It is one of the numerous contributions of Sir Ivan Magill towards airway management. It is used to guide

Fig. 8.27B: The Miller blade

118 A PRIMER OF ANESTHESIA

Figs 8.28A and B: (A) The malleable stylet (B) In a tube and shaping it

blade hinged on a handle, which houses two batteries. The blade has a bulb midway along its length. When the blade is opened out on the handle to 90 o, electrical connection is established and the bulb glows. The laryngoscope illuminates the oropharynx and enables visualization of the trachea. Many varieties of blade have been designed, each with its unique use or advantage. The one most commonly used is the curved Macintosh blade (named after Sir Robert Macintosh) available in 4 sizes. The straight blade, useful in infants to directly lift up a large epiglottis, is the Miller blade. Other special blades are the McCoy and Polio blades. The Malleable Stylet (Figs 8.28A and B) This long, flexible length of copper or steel wire encased in a plastic sheath is useful for bending the endotracheal tube to the desired shape if

the larynx is difficult to reach by normal methods. The precaution to be observed while using this device is that it should not protrude beyond the endotracheal tube tip as tracheal perforation can result. In summary, protection of the airway and prevention of hypoxemia start right from induction of anesthesia. Elective endotracheal intubation is an atraumatic, safe and smooth procedure. Every attempt must be made to identify the patient likely to have difficult mask ventilation or intubation (refer to Chapter 5). A difficult airway can be managed by a variety of techniques in the elective situation. The difficult airway algorithm should be followed in case of failure to mask ventilate or intubate any patient. Emergency surgical airway may be required in the ‘Cannot intubate, cannot ventilate’ (CICV) situation where preventing hypoxemia and mortality becomes the priority. MCQ MCQss 1. Which of the following is a contraindication for using a laryngeal mask airway? a. When inhalational anaesthesia is required b. Large obstructive lesion in the upper airway c. Maintaining airway during difficult intubation d. Emergency management of airway during resuscitation 2. In children: a. The larynx is at a lower level than in an adult b. The epiglottis is relatively large and floppy when compared to that of an adult c. The narrowest part of the airway is at the cords d. The larynx is less susceptible to oedema

AIRWAY MANAGEMENT

3. The following are signs of inadvertent oesophageal intubation: a. Lack of fogging of the endotracheal tube with ventilation b. Absence of waveform on capnograph c. Absence of breath sounds on auscultation of lung apices d. All of the above 4. The best way for sizing the correct length of an oropharyngeal airway is: a. Vertical distance from the tragus of the ear to the angle of the mouth b. Vertical distance from the tragus of the ear to the medial incisor c. Vertical distance from the angle of the jaw to the medial incisor d. Vertical distance from the angle of the jaw to the angle of the mouth 5. In adults: a. The larynx is at the level of 2nd and 3rd cervical vertebrae b. The length of the trachea is approximately 15 cm c. The narrowest part of the airway is at the cords d. All of the above 6. The nasopharyngeal airway: a. Is sized from the tragus of the ear to the ala of the nose of the same side b. Can be used to relieve partial airway obstruction c. Should be soft, flexible and should be secured at the nostril d. All of the above 7. The third component of the triple maneuvre for maintaining a clear airway in an unconscious patient is: a. Head tilt b. Jaw thrust c. Left lateral position d. Pulling the tongue

119

8. Internal diameter of the endotracheal tube most commonly used for males and females respectively, are: a. 7mm and 6mm b. 8mm and 7mm c. 9mm and 8mm d. 10mm and 9mm 9. Recommended times for fasting to prevent aspiration during anaesthesia are: a. 4 hrs for clear fluids and 8 hrs for solids b. 2 hrs for clear fluids and 6 hrs for solids c. 6 hrs for all types of fluids and solids d. Overnight fasting for fluids and solids 10. In case of choking on a solid object the following might be helpful: a. Placing the person upside down b. Sharp blows in the middle of the back with Heimlich Manoeuvre c. Putting a spoon in the mouth to pull out the solid substance d. Giving the person a drink of water to wash down the solid 11. The adequacy of bag mask ventilation can be assessed by: a. 3-5 cm rise in chest during inspiration b. Hearing of breath sounds on both sides of chest c. Maintenance of good oxygenation d. Absence of expansion of stomach in the left hypocondrium e. All of the above 12. Difficult intubation is associated with: a. Short thick neck b. Limited mouth opening c. Prominent front incisors d. Limited neck movements e. All of the above 13. Problems with airway management is common in patients: a. Having caesarean section b. With rheumatoid arthritis c. With downs syndrome d. With acromegaly e. All of the above

120 A PRIMER OF ANESTHESIA

14. In case of laryngospasm: a. It is easy to ventilate the patient with a bag and mask b. It is easy to maintain oxygenation c. There is paradoxical respiratory effort with no air movement d. There is no need for senior doctor help

Answers 1. 5. 9. 13.

b d b e

2. 6. 10. 14.

b d b c

3. d 7. b 11. e

4. c 8. b 12. e

Neuraxial (Spinal and Epidural) Blockade Rajeshwari Subramaniam, Rani Sunder

         

Advantages of neuraxial block Indications for neuraxial blockade Anatomy of the vertebral column and spinal cord Pharmacology, mode of action and toxicity of local anesthetic agents Physiological effects of neuraxial blockade Patient preparation and monitoring Technique and complications of epidural anesthesia Subarachnoid block Caudal block: technique, drug dosage, complications Combined spinal-epidural technique

-

-

-

Spinal, epidural and caudal block are also termed ‘neuraxial’ blocks. Each can be performed as a single injection or through an indwelling catheter to allow intermittent boluses or continuous infusion not only for the duration of surgery but up to many days postoperatively.

-

ADVANTAGES OF NEURAXIAL BLOCK FOR SURGERY

-

-

Suppresses the neuroendocrine response to surgery resulting in a stable hemodynamic state. The pain afferents are blocked at the spinal level.

-

Avoids intubation and its associated hazards, when used as sole anesthetic Provides excellent intra-operative and postoperative analgesia without sedation or respiratory depression. The need for intravenous or intramuscular opiates is almost eliminated. Reduces blood loss due to pooling of blood in capacitance vessels and reduction in systemic vascular resistance. Reduces incidence of pulmonar y complications (especially in high-risk patients with chronic lung disease). This is due to multiple factors like ability to avoid narcotic induced sedation and respiratory depression, good pain relief and early resumption of deep breathing and ambulation. Reduces incidence of venous thrombosis and pulmonary thromboembolism due to amelioration of the hypercoagulable state associated with surgery. This also reduces the incidence of vascular graft occlusion. Significant reduction in maternal morbidity and mortality has resulted from routine use of spinal anesthesia in Caesarean section. Permits earlier retur n of bowel function.

122

A PRIMER OF ANESTHESIA

IND ICATIONS FOR SPINAL/EPIDURAL INDICATIONS ANESTHESIA Spinal or epidural anesthesia can be used as primary anesthetic (that is, as sole anesthetic technique) for almost all kinds of lower abdominal, perineal, urethral, rectal and lower limb orthopedic procedures. Epidural analgesia can be continued to provide postoperative pain relief (for 3 days to a week), during labor, to relieve pain of pancreatitis and pain of ischemic origin. Implanted epidural and spinal catheter systems are very effective in the treatment of benign chronic pain and cancer pain. WHY IS EPIDURAL ANESTHESIA COMBINED WITH GENERAL ANESTHESIA SOMETIMES? Major surgery like Whipple’s procedure, gastrectomy and hepatic resections involve large incisions, are prolonged, associated with blood loss and hypothermia and will not be feasible under neuraxial block alone. Similarly, thoracic surgery cannot be performed using neuraxial block alone in an awake, spontaneously breathing patient because the lung on the operated side will collapse when the chest wall is opened, resulting in hypoxemia. General anesthesia (GA) for these procedures protects the patient’s airway, permits lengthy procedures, ensures oxygenation and CO2 homeostasis at all times and obviates the need for patient cooperation. When epidural anesthesia (EA) is concomitantly administered we can have all the advantages listed above combined with the comforts of GA. Postoperatively epidural morphine (in doses of 3-5 mg diluted in 10 ml saline) confers analgesia of superior quality which ensures patient comfort and increases cooperation and willingness to perform respiratory maneuvers. This significantly reduces incidence of postoperative atelectasis after major surgery. It is important to understand the structure of the vertebrae, the spinal canal, local anesthetic

Fig. 9.1: The spinal nerves and corresponding dermatomes

pharmacology and physiology of neuraxial blockade to appreciate the technique of neuraxial block, the different approaches and why complications occur. ANATOMY OF THE VERTEBRAL COLUMN AND THE SPINAL CORD We have 7 cervical, 12 thoracic, 5 lumbar, 5 sacral and 4 coccygeal vertebrae (Fig. 9.1). In the cervical region the nerves exit above the vertebrae, but starting from T1, they exit from below; there are 8 pairs of cervical, 12 thoracic, 5 lumbar and 5 sacral nerves, and 1 coccygeal spinal nerve. The cervical and upper thoracic nerves emerge at the same level as the corresponding vertebra. From the lower thoracic vertebrae the spinal nerves take more and more of an oblique

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

course through the spinal canal, as the spinal cord ends at L1 in adults (known as the ‘conus medullaris’). After L1, the leash of nerves comprising T10-S5 float as the ‘cauda equina’ in the CSF. The cord ends at L3 in the newborn and slowly recedes to L1 by adulthood with growth in height. The dural sac enclosing the subarachnoid, CSF and the cauda equina ends at S2 in adults and at S3 in children. Therefore children are more prone to accidental dural puncture during a caudal block as compared to adults. The extension of pia mater starting from the tip of the cord known as ‘filum terminale’ pierces the dural sac and is tethered to the coccyx. The vertebral body is solid and disc-like (Fig. 9.2). It forms the anterior border of the spinal canal. From either side projects a pedicle which forms the lateral border of the spinal canal; a transverse process is given off from the pedicle, and the pedicle continues as the lamina, which forms the posterior border of the spinal canal. The laminae (from either side) fuse in the midline to form the spinous process. The pedicles have notches on their superior and inferior borders; in adjacent vertebrae, the superior and inferior notch form the intervertebral foramen, through which exit the spinal nerves.

Fig. 9.2: The vertebral body: Note the relationship between the cord, epidural and subarachnoid spaces

123

Fig. 9.3: Sagittal view depicting layers between skin and epidural space

Many ligaments stabilize and support the spinal canal and cord. The vertebral bodies and discs are supported anteriorly by the anterior longitudinal ligament and posteriorly by the posterior longitudinal ligament. From the dorsal aspect (that is, looking at the back of the patient) we cross the following layers in our approach to the epidural and subarachnoid space (Fig. 9.3): - Skin - Subcutaneous tissue - Supraspinous ligament - Interspinous ligament - Ligamentum flavum - Dura. The epidural space is the potential space between the ligamentum flavum and the dura. Although the spinal and the cranial subarachnoid space (and the CSF) are in continuity, the same is not true of the epidural space. The spinal dura is attached to the foramen magnum. The spinal epidural ‘space’ begins from the foramen magnum and ends at S2. The epidural space contains the spinal nerves, the valveless vertebral venous plexus of Batson, fat and fibrous tissue. Adiposity increases with age. When the spinal nerves exit the spinal

124

A PRIMER OF ANESTHESIA

Local anesthetic (LA) molecules consist of a hydrophilic group (a tertiary amine) and a lipophilic group (a benzene ring) connected by an intermediate chain which has an ester or an amide linkage. Physicochemical Properties of LA Agents

Fig. 9.4: Investment of the spinal nerves with the dural sheath

canal, they are covered (‘invested’) with a layer of dura and arachnoid as they exit from the intervertebral foramina (Fig. 9.4). PHARMACOLOGY OF LOCAL ANESTHETIC AGENTS Nerve cells maintain a resting membrane potential of –70 mV across the membrane due to the action of the sodium-potassium pump, which actively extrudes sodium and transports potassium into the cell. This creates a transcellular gradient favoring sodium to move in and potassium to move out. Since the cell membrane is much more permeable to potassium, anions accumulate inside the cell, causing the negative resting potential. When an impulse is conducted along the fiber due to electrical, mechanical or chemical stimulation, depolarization occurs along the membrane; when the resting potential reaches –55 mV (threshold depolarization) there is a sudden mass influx of sodium into the cell, raising the potential to +35 mV. This is followed by inactivation of the sodium channels and increased potassium conductance outwards, returning the membrane to its original state. Most local anesthetics bind to inactivated sodium channels and prevent subsequent depolarization. Some agents penetrate the membrane, causing membrane expansion.

• Potency: Potency is directly proportional to lipid solubility, which indicates the ease with which the LA molecule penetrates a hydrophobic environment. Potency and hydrophobicity increase by: – Increase in the total number of carbon atoms – Addition of a halide to the aromatic ring (2-chloroprocaine is more potent than procaine) – An ester linkage (procaine versus procainamide) – Large alkyl groups on the tertiary amide nitrogen (etidocaine versus lidocaine) • Cm (the minimum concentration of LA that will block nerve impulse conduction) is affected by: – pH : acidic pH antagonizes block. – Frequency of nerve stimulation enhances block. – Hypokalemia, hypercalcemia antagonize block. – Myelinated, thin diameter fibers are blocked easily. • Onset of action: This is determined by the amount of LA available in the unionized form to penetrate the epineurium. LA agents exist in both nonionized and ionized forms in solution, and the proportion of each form is determined by the pH of the solution. The pH of the solution at which both forms are in equilibrium is the pKa. Since it is the nonionized form which is required for entering the neuron, any measure that makes the milieu more acidic ionizes the LA further, so that less non-ionized form is available. Mepivacaine is the LA whose pKa approaches body pH (7.6). There are four important clinical implications of pKa:

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

– When injected into infected tissue (which is acidic) more LA is ionized, explaining lack of efficacy. – Commercially available LA solutions have a pH of 6-7. Since epinephrine is unstable in alkaline environments, LA preparations containing epinephrine are made even more acidic (pH 4-5). It is therefore recommended to add epinephrine to LA solution immediately before use. Commercial epinephrinecontaining solutions have a prolonged onset of action. – Tachyphylaxis: Decreasing efficacy of repeated doses-can also be explained by the fact that the acidic LA solution consumes the available extracellular buffering capacity. – Addition of 8.4% sodium bicarbonate solution (1 ml/10 ml of 1% lidocaine): Also known as ‘carbonation’, hastens onset of block, prolongs action (the CO2 released from sodium bicarbonate diffuses into the cell, causes acidosis and ionization of the LA molecule, ‘trapping’ it inside the cell. Intracellularly, it is the ionized cation which is responsible for blocking the sodium channels). Carbonation also reduces pain on subcutaneous infiltration. • Absorption After topical application: Most LA agents can cross conjunctiva or buccal mucous membrane and provide topical anesthesia (2%lidocaine for the eye, benzocaine lozenges for painful oral ulcers). EMLA [Eutectic (easily melted) Mixture of Local Anesthetic] is an oil-in-water emulsion of 5% lidocaine and 5% prilocaine mixed in a 1:1 ratio. This provides adequate topical analgesia for IV line insertion, laser removal of port-wine stains, skin graft harvesting and circumcision. The depth of penetration is reported as 3-5 mm. The contact time should be at least an hour under an occlusive

125

dressing (Tegaderm). The dose recommended is 1-2 g/10 cm2 of skin area with a maximum application area of 2000 cm2 in the adult and not to exceed 100 cm2 in children weighing less than 10 kg. Contraindications to use of EMLA include infants less than 1 month old, broken skin, mucous membranes and in patients with a predilection to methemoglobinemia. After injection: The rate of absorption is proportional to firstly, the vascularity of the site. If we count out intravenous injection, the order of decreasing absorption is tracheal> intercostal> caudal> paracervical> epidural> brachial> sciatic> subcutaneous. Secondly, addition of epinephrine causes vasoconstriction and delays absorption. This effect is most apparent with shorter acting LA agents. • Metabolism of LA agents Esters: These are predominantly metabolized by plasma cholinesterase (pseudocholinesterase). One of the by products of ester metabolism is p-aminobenzoic acid (PABA) which may be responsible for allergic manifestations to esters. Pseudocholinesterase deficiency can lead to prolonged action and vulnerability to toxic effects. As the CSF lacks cholinesterase enzyme, termination of intrathecally administered esters depends on absorption by the bloodstream. In contrast to other esters, cocaine undergoes partial metabolism in the liver and is partly excreted unchanged. Amides: All amide anesthetics are metabolized by hepatic microsomes. Prilocaine undergoes the most rapid metabolism followed by lidocaine and bupivacaine. Patients with reduced hepatic blood flow (congestive cardiac failure) or reduced hepatic function (cirrhotics) are very susceptible to amide overdose toxicity. Otoluidene derivatives are metabolites of prilocaine which accumulate if prilocaine

126

A PRIMER OF ANESTHESIA

dose has exceeded 10 mg/kg. These can convert hemoglobin to methemoglobin. Neonates born of mothers who have received prilocaine for epidural anesthesia are prone to develop methemoglobinemia and may be adversely affected by a reduction in oxygen transport. Benzocaine use can also result in methemoglobinemia. Treatment of significant methemoglobinemia is by administration of 1-2 mg/kg of a 1% methylene blue solution (1ml of 1% solution contains 10 mg/ml), which reduces Fe3+ to Fe2+. • Effect on the cardiovascular system – All LA agents depress phase IV depolarization. – Reduce duration of refractory period. – At higher concentrations, reduce myocardial contractility and conduction velocity. – All above effects are due to sodium channel blockade and the clinical manifestation is one of bradycardia, heart block and hypotension which may culminate in cardiac arrest. Sodium channels take longer to recover after bupivacaine cardiotoxicity because it alters mitochondrial function and has a high degree of protein binding. Resuscitation is usually difficult or unsuccessful. Bretylium is the agent of choice for treatment of bupivacaine cardiotoxicity. Pregnancy, respiratory acidosis and hypoxemia are risk factors. – Ropivacaine is a structural isomer of bupivacaine and 50% as lipid soluble as bupivacaine. The low lipid solubility or its availability as a pure (S-) enantiomer may be responsible for its low toxicity profile. – Cocaine inhibits the reuptake of norepinephrine at the adrenergic nerve terminals, leading to hypertension and ventricular ectopy. Cocaine is also the only LA agent with vasoconstricting

property. Cocaine-induced dysrhythmias may be treated with calcium channel or adrenergic antagonists. – Cardiac dysrhythmias or circulatory collapse is the most common presenting sign of LA overdose in the anesthetised patient. • Neurological effects – Premonitory symptoms of LA toxicity in the awake patient occur in the CNS. – Early symptoms are circumoral numbness, paresthesiae and dizziness. – Excitatory symptoms (restlessness, paranoia, agitation, ner vousness) precede CNS depression (drowsiness and coma). – Muscular twitching may signal the onset of tonic-clonic convulsions. Thiopentone 1-2 mg/kg is the ideal agent to terminate seizures; adequate ventilation and oxygenation must be maintained. – Toxic effects of cocaine are manifested by restlessness, tremors, convulsions, emesis and respiratory failure. – The maximum safe dose for lidocaine without epinephrine is 4 mg/kg; if epinephrine is added, it is 7 mg/kg. Maximum dose permissible for bupivacaine is 2 mg/kg. – Midazolam and diazepam increase the seizure threshold. Hyperventilation, (by reducing cerebral blood flow and further drug exposure) is also protective. – IV lidocaine 1.5 mg/kg decreases cerebral blood flow and attenuates the raise in intracranial pressure that accompanies the hemodynamic intubation response. • Neurological side effects unrelated to dose: – Prolonged neurological sequelae have been reported after accidental subarachnoid administration of a large dose of chloroprocaine. This has been attributed to the preservative sodium bisulfate,

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

which has since been replaced with a derivative of EDTA. – Severe back pain after epidural has also been reported after chloroprocaine; the possible causes could be (i) large volumes of chloroprocaine, (ii) low pH, (iii)EDTA preservative and (iv) local infiltration with chloroprocaine. Recently a preservativefree formulation of chloroprocaine has been prepared. – Cauda equina syndrome refers to permanent damage to the fibres of the cauda equina reported with the repeated injection of 5% lidocaine and 0.5% tetracaine through spinal microcatheters. – Transient neurologic symptoms (TNS) consist of dysesthesia, burning pain, and aching in the buttocks and lower extremities after apparently uneventful spinal anesthesia with a variety of agents. Risk factors appear to be lidocaine, obesity, lithotomy position and outpatient status. • Drug interactions – Since succinylcholine and ester LA are both metabolized by pseudocholinesterase, concomitant administration potentiates the effects of both agents. – Nondepolarizing neuromuscular block is potentiated by LA agents. – Dibucaine, an amide anesthetic, inhibits pseudocholinesterase and can be used to detect genetically abnormal enzyme in suspected pseudocholinesterase deficiency. – Fentanyl, morphine, epinephrine and clonidine potentiate analgesia produced by LA agents. PHYSIOLOGICAL EFFECTS OF NEURAXIAL BLOCKADE The site of action of local anesthetic solution in the epidural or subarachnoid space is the nerve root. As the nerve root carries somatic, visceral

127

and autonomic fibers, physiological effects observed are related to block of conduction in these fibers. Somatic Blockade 1. Epidural and spinal blocks interrupt transmission of impulses both in the dorsal root (which carries somatic and visceral afferents) and the ventral root (which carries motor and autonomic efferents). 2. Spinal roots contain fibers which vary in size and myelination; as a rule, thinner, myelinated fibers get blocked earlier. 3. There is complete absence of pain perception and profound skeletal relaxation, which produces excellent operating conditions. 4. The phenomenon of ‘differential blockade’ is seen with respect to somatic blockade whereby sympathetic blockade is two to six segments higher than sensory block, which in turn is two segments higher than motor block. 5. Motor and proprioceptive fibres are blocked the last and need high concentration of LA; sympathetic and nociceptive fibres (Pain, temperature) are the most vulnerable. Autonomic Blockade 1. Cardiovascular signs: Spinal and epidural blocks produce hypotension in proportion to the number of segments blocked (height of block). Vasomotor tone is determined by the sympathetic outflow from T5-L1. Sympathetic blockade results in dilatation of the capacitance vessels(the large veins in the pelvis and IVC), pooling of blood and reduced venous return to the heart, resulting in reduced cardiac output. Some arteriolar dilatation may also occur. If the block extends up to and above T4, block of cardiac accelerator fibres leads to severe bradycardia and also compromises compensatory vasoconstriction which usually occurs above the block. The drastic reduction in cardiac

128

A PRIMER OF ANESTHESIA

output may lead to cardiac arrest. All these effects are exaggerated in the pregnant or grossly obese patient or patients with large intra-abdominal tumors or tense ascites, which further reduce venous return by compressing the inferior vena cava. Hypotension can be prevented by preloading the patient with 10-20 ml/kg of a crystalloid solution (Ringer’s lactate) before administering the block and left uterine displacement in the pregnant patient. Hypotension should be treated aggressively with 5-10 mg boluses of ephedrine or mephentermine. Oxygen should be given through facemask. If bradycardia is also present, atropine 0.30.6 mg should be given. Phenylephrine bolus (25-50 μg) is another option. If hypotension persists in spite of these vasopressors, epinephrine should be administered. 2. Pulmonary manifestations: Properly performed spinal and epidural blocks do not affect the respiratory system. Normally attained levels up to T6 which paralyze the external oblique are not seen to produce any distress in patients who do not have respiratory disease. Even with accidental injections of large volumes of LA into the subarachnoid space, phrenic nerve (C3-C5) block rarely occurs probably because the LA gets diluted by CSF and is unable to block the large fibers of the phrenic nerve. However, clinical implications of respiratory muscle involvement with spinal blockade are seen in patients with significant respiratory disease like emphysema, who rely on active expiration for carbon dioxide elimination. A block involving the accessory muscles of expiration can prevent effective breathing, coughing and clearing of secretions and can cause significant distress and panic to the patient and may even lead to respiratory failure. Thus, spinal anesthesia is not without its dangers in a patient with severe lung disease.

3. Gastrointestinal effects: Since a major part of the thoracolumbar sympathetic outflow is blocked, there is parasympathetic predominance evidenced by a contracted, ribbon-like small bowel. This greatly facilitates abdominal and pelvic surgery and also results in earlier return of bowel function. Neuraxial block does not block the vagus. 4. Urinary tract: Neuraxial block interrupts both sympathetic and parasympathetic control of bladder function and results in urinary retention till the block wears off. This is especially seen in elderly patients with prostatic enlargement. The shortest acting agent commensurate with the procedure must be used. Other factors promoting retention are use of neuraxial opiates and surgery on the urethra or bladder. Contraindications to Neuraxial Blockade Absolute contraindications are: - Patient refusal - Coagulopathy - Infection at proposed site of injection - Severe hypovolemia - Raised intracranial pressure - Severe aortic or mitral stenosis. Relative contraindications are: - Sepsis - Pre-existing neurologic deficit - Progressive neurological disease (demyelinating disorders) - Deformity of spine at proposed site of injection. PREOPERATIVE PREPARATION OF THE PATIENT PRIOR TO NEURAXIAL BLOCK Preoperative preparation should fulfill all criteria as for GA and neither the patient, surgeon or physician should regard it as a short cut to safety, especially in high-risk patients. Psychological Preparation -

The patient will have many doubts and questions regarding the plan of neuraxial

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

-

-

-

-

block and the preoperative period is the time to clarify them. After completing the preanesthetic assessment and ensuring that major contraindications are absent, the patient is provided with full explanation covering the conduct of the block and management of his comfort during surgery. It is important to let the patient understand that he/she will be kept comfortable at all costs. The patient should be given the choice of whether to remain fully awake or receive intravenous sedation during the procedure. The patient should be explained that he/she may be able to appreciate deep pressure or position changes, specially if an epidural is being planned (as the large diameter proprioceptive fibers may not be blocked). The advantages neuraxial blockade has over GA can be explained to the patient to increase acceptance. In spite of all explanations there may be a patient who refuses to accept neuraxial block. In that case, the refusal should be documented in the case sheet.

Physical Preparation -

-

-

Making the patient assume the position to be used the next day for the block (sitting up or lateral decubitus position) is very helpful. In obese patients the sitting position helps to identify the midline more accurately than the lateral decubitus position. The full term pregnant patient scheduled for labor epidural would probably be more comfortable sitting. This has the advantage of checking out any difficulty (e.g. patient may be unable to lie on the side planned) and also letting the patient know that this is the position expected from him prior to the block. There should be no infection at the planned site and the space should be well felt. If there is a lot of hair instructions may be given to apply epilator cream at night.

129

Shaving may produce scratches or cuts which can harbor infection. OPERATION THEATER MANAGEMENTPREPARATION AND MONITORING -

-

-

-

Check the anesthesia machine and connect a simple tube attached to a facemask at the common gas outlet. Check the Bain circuit and keep it handy. Check laryngoscope, endotracheal tube. Check functioning suction. Check table tilt and the anesthesia monitor connections. Staff in the operating theatre should be made aware of the impact their conversation and noise are likely to have on the patient. The area where the block is being given should be well lighted. Prepare (i) Atropine 0.1 mg/ml, (ii) Ephedrine 5 mg/ml, (iii) Mephentermine 6 mg/ml, and (iv) Midazolam 1 mg/ml. Check that thiopentone and succinylcholine are readily available. Ability to administer GA rapidly if need arises, should be checked. Attach the desired monitors. For straightforward procedures in ASA-I-II patients, EKG, pulse oximetry and non-invasive blood pressure (NIBP) suffice. For patients who are sick (ASA-III and above) the level of monitoring will be decided by the gravity of the procedure. For patients undergoing major surgery under combined epidural anesthesia and GA, monitoring will be planned according to the needs of the procedure (CVP, invasive arterial pressure, urine output, etc.). Set up an IV infusion of Ringer’s lactate or normal saline. Give the patient 500ml-1l while the block is being given. Position the patient as previously planned. If the patient is unduly anxious, midazolam 1-1.5 mg may be administered. (Children and adolescents may require GA for placement of the block). The patient in the

130

A PRIMER OF ANESTHESIA

sitting position can place the feet on a stool and rest the arms on a trolley placed across the operating table. Remember not to sedate the patient heavily if the patient has to sit for the procedure. Stabilizing the patient from the front is another option (Fig. 9.5). The patient in the lateral position has to be told to ‘curl up as in winter’ with the knees drawn up as high as possible, and the chin flexed on the chest (Fig. 9.6). This maximally opens the vertebral space (Fig. 9.7). The assistant can help to maintain this position till the block is given (Figs 9.5 and 9.6). - Verbal contact shoud be maintained with the patient, offering reassurance and explaining the progress. - Anatomic landmarks are identified. Normally a line drawn joining the highest points of the iliac crest passes through the body of L4 or the L4 - L5 interspace (Tuffier’s line, Fig. 9.8). A line joining the two posterior superior iliac spines passes through the S2 posterior foramina. It is usual to count the spaces upwards or downward from these reference points. Ensure that the patient’s back is kept vertical with respect to the trolley surface. - In adult males the spine tilts caudad and in females cephalad (Fig. 9.9), due to the breadth of the shoulders in the male. The table should be appropriately tilted to keep the spine level. - The skin is prepared in an aseptic manner (Fig. 9.10) by cleaning the proposed site of injection first and moving outwards in a circular manner using a detergent, povidone iodine and finally alcohol. (The solution used will vary with institutional protocol). Make sure all traces of iodine are removed and that the alcohol has dried; otherwise chemical meningitis may result due to introduction of these agents into the CSF. Also ensure that cleaning solutions do not fall or splash on your needles and/ or catheter. - After informing the patient, a wheal of local anesthetic is raised using a 25G or 26G

Fig. 9.5: The patient can be steadied by an assistant or allowed to lean on a trolley

Fig. 9.6: The assistant grasps the head and the undersurface of the knees and helps maintain the flexed position

Fig. 9.7: (L) neutral spine; (R) Opening up of the interspinous space

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

131

Fig. 9.10: Skin preparation

Fig. 9.8: Tuffier’s line between L4 and L5

Fig. 9.11: Injection of local anesthetic

EPIDURAL ANESTHESIA

Fig. 9.9: Tendency of LA to track in different directions

needle in the center of the desired interspace (Fig. 9.11). The needle is withdrawn and the point of entry marked with the hub of the same needle. This simple maneuver ensures that the point of insertion of the spinal or epidural is exactly at the same site as the LA.

Epidural anesthesia offers a wide range of applications and can be performed at the lumbar, thoracic or cervical levels. Sacral epidural block is also known as caudal block. Epidural block is slower in onset than and not as dense as spinal anesthesia. This characteristic confers several advantages on epidural analgesia: (i) differential block is pronounced, so dilute LA solutions combined with an opiate can be used to block pain and sympathetic fibers, and avoiding motor blockade in patients receiving labor analgesia; (ii) it is possible to produce segmental analgesia which is a well defined band-like area of analgesia by placing the catheter in the appropriate spinal interspace. (iii) If the catheter is only to be used for

132

A PRIMER OF ANESTHESIA

postoperative neuraxial opiate delivery, a lumbar catheter is satisfactory for both thoracic and abdominal incisions. (iv) It is possible to titrate the amount of LA by giving incremental doses. - The needle chosen for epidural block is a wide bore (18G or 16G) needle known as the ‘Tuohy’ needle (Fig. 9.12). It has a blunt, upward-curving tip termed the Huber point. It is graduated in centimeters and the first mark is 2 cm from the tip. - This tip reduces the likelihood of dural puncture and allows caudad or cephalad orientation of the catheter (Fig. 9.13). - The lumbar interspaces are the most common insertion site for epidural anesthesia and analgesia. The spinous processes are nearly horizontal and the direction of introduction of the needle is with a slight cephalad tilt. Theoretically likelihood of injury to the cord is unlikely for levels below L3. - Flush the catheter and filter with saline to eliminate air. - The Tuohy needle with its stylet is introduced up to the interspinous ligament (after LA infiltration described above). - The subcutaneous tissue does not offer any special resistance. As the supraspinous and interspinous ligaments are crossed, the needle can be left and does not sag downward (Fig. 9.14). - The stylet is removed and a 2 ml or 5 ml glass syringe with a smoothly moving plunger and containing 2-4 ml air (the ‘loss of resistance’ or LOR syringe) is attached firmly to the Tuohy needle. - The needle-syringe combination is gradually introduced deeper with the left thumb checking resistance to injection of air with short, sharp ‘jabs’ or a sustained pressure. As the ligamentum flavum is encountered, the right hand experiences increased resistance and exerts force needed to traverse it, and simultaneously is steadied against the patient’s back to prevent a

Fig. 9.12: Enlarged view of the ‘Huber’ point of an epidural needle

Fig. 9.13: The direction of the Tuohy needle tip will guide the catheter

-

‘lunging’ entry into the epidural space (Fig. 9.15), with possible accidental dural puncture. As the ligamentum flavum is crossed, there is a sudden loss of resistance and injection of the air in the syringe is easy. Saline can also be used in place of air; each has its advantages and disadvantages (Table 9.1). Only 3 ml air should be injected to avoid patchy block. If a ‘single shot’ technique is being used, 3 ml 2% lidocaine plus epinephrine 1:200,000 is injected. If the test dose is negative, the dose of LA agent is injected in 3-5 ml aliquots, maintaining

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

133

Fig. 9.14: (L) Epidural needle in subcutaneous tissue; (R) engaged in ligamentous layer

Fig. 9.15: Entering the epidural space

conversation with the patient (see complications), till the appropriate effect is achieved. In adults depending on the position of the catheter, volumes from 6-15 ml may be needed (Table 9.2). -

If a catheter is to be inserted, the needle is rotated so that the bevel faces cephalad or caudad to insert the catheter. The notch on

the hub of the needle tells us the direction. Normally, 5-7 cm of the catheter is inserted in the epidural space. The catheter left externally is taped to the back by adhesive (Fig. 9.16). This can be easily calculated by adding this length to the depth of the epidural space. The test dose and subsequent complete dose may be given through the catheter.

134

A PRIMER OF ANESTHESIA

Table 9.1: Loss of resistance (LOR) to air or saline Air

Saline

• Requires LOR syringe • • Easy to learn • • Needle control with • both hands • Air bubbles may expand with N2O • • Danger of air embolism in patients with R → L shunts

Ordinary syringe More difficult Single handed control; other hand on syringe plunger Saline may be confused with CSF

COMPLICATIONS SPECIFIC TO EPIDURAL TECHNIQUE -

Accidental dural puncture: this commonly occurs in learners; however even in trained hands it remains a possibility. Risk factors include pregnancy, obesity and spinal deformities. In the first two conditions, increased intra-abdominal pressure causes engorgement of the epidural venous plexus, and increased CSF pressure. It results in mild to debilitating occipital and bi frontal

Table 9.2: Drug doses in epidural anesthesia (injection at l3-l4) Drug Chloroprocaine Lidocaine Mepivacaine Prilocaine Bupivacaine Ropivacaine

Concentration 2%,3% 1% 2% 2% 3% < 0.25% 0.5% < 0.2% 0.5%-0.75%

Onset

Sensory

Motor

Rapid Intermediate Intermediate Intermediate Fast Slow Slow Slow Slow

Dense Analgesic Dense Dense Dense Analgesic Dense Analgesic Dense

Mild Minimal Dense Dense Dense Minimal Moderate Minimal Mod-dense

Fig. 9.16: Fixing the epidural catheter

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

-

-

headache. Treatment for mild symptoms is conservative (fluids, analgesics, bed rest and sometimes an abdominal binder). If unresponsive to these measures, an epidural blood patch should be administered after 24-48 h which is immediately effective in >95% patients. Total spinal: This term refers to a situation where inadvertently the entire volume of LA meant for epidural administration is injected into the subarachnoid space. This mishap can occur (i) when the tip of the epidural needle is partly in the subarachnoid space, so that CSF was not aspirated freely but injection of LA was possible, and (ii) if the epidural catheter tip had accidentally migrated into the subarachnoid space, and aspiration was not performed or was negative. The symptoms are dramatic and frightening- the patient loses consciousness, has severe bradycardia, hypotension and respiratory arrest. If verbal contact is maintained with the patient during injection of large volumes of LA, lack of response or the beginning of a slurred response is sufficient for a diagnosis. The patient is rapidly turned supine and both legs elevated to augment venous return. IV fluids are rushed, atropine 0.6 mg and ephedrine, phenylephrine or epinephrine administered. Simultaneous management of the airway with assisted ventilation through face mask or endotracheal tube, with 100% oxygen is necessary. Although so precipitous, uneventful recovery occurs as the LA diffuses away from the respiratory center. Epidural hematoma: Although rare, this can occur in patients with significant coagulopathy or those on anticoagulants. The following guidelines are recommended for use of neuraxial block in patients with disordered coagulation: – INR< 1.5 – Platelets > 90,000/mm3 – Bleeding time < 16 min

-

135

– PTT not prolonged – PT not more than 2 seconds over control. The clinical implication is that if there is a patient with, for example, alcoholic cirrhosis scheduled for laparotomy and would need and benefit from postoperative epidural analgesia, his PT needs to be checked and corrected with fresh frozen plasma prior to surgery if it is prolonged. Epidural abscess: This is also a rare but devastating complication, because unless diagnosed and decompressed within 12 hours of onset of symptoms, neurological damage (paraplegia) is permanent. The cause is usually lack of observing asepsis, bacteremia or sepsis at the time of injection. The patient complains of recent onset backache, weakness in the lower limbs and urinary incontinence. Treatment includes removal of the catheter, broadspectrum antibiotics, MRI imaging to confirm diagnosis and, if necessary, laminectomy and evacuation of the abscess.

SUBARACHNOID (SPINAL) ANESTHESIA (FIG. 9.17) Selection of the right needle is vital to the successful performance of spinal block. 22G and 23G needles are robust and suitable for use in patients where the ligaments may be calcified and the CSF pressure low, as in elderly patients; the incidence of post dural puncture headache (PDPH) is minimal in this group. In younger patients, 26-29G short bevel Quincke needles (Fig. 9.18) or 24G pencil point Whitacre needles are preferred as they have the lowest incidence of PDPH. After infiltration of local anesthetic as described, the thumb or index finger of the nondominant hand covers the upper spinous process; the needle is introduced immediately caudad to the thumb exactly in the midline and and advanced with a slight cephalad tilt, pointing toward the patient’s umbilicus. With

136

A PRIMER OF ANESTHESIA

CSF flow, the drug injected at a rate of 0.1ml/ sec to prevent a patchy effect. Hyperbaric solutions (most commonly used) tend to gravitate and produce a dense block on the dependent side if this position is maintained for 5-6 min. This effect is used to produce unilateral effect for a lower limb procedure or hernioplasty. Major factors influencing the level of block are (i) Baricity, (ii) Patient position during and immediately after injection, (iii) Drug dosage and (iv) Site of injection. Others include age, CSF volume, drug volume, intra-abdominal pressure, patient height and pregnancy. DIFFERENCES BETWEEN EPIDURAL AND SPINAL BLOCKADE Fig. 9.17: Needle entering the subarachnoid space

Fig. 9.18: The ‘spinal’ needle

the fine needles in use nowadays, it is a good idea to use a 21G or 18G hypodermic needle as an ‘introducer’ up to the interspinous ligament (approximately 2-2.5 cm). The fine 26G needle can be introduced through this needle; it will then not get bent or deviate from its path. Although the difference in feel of the various layers is difficult to appreciate with fine needles initially, the ‘pop’ or ‘give’ of dural puncture is unmistakeable. The stylet should now gradually be withdrawn and the CSF should appear at the hub. After ensuring free

The difference in the modes of action of subarachnoid versus epidural injection of drugs is as below (Table 9.3): The clinical implications of these differences are as follows: - Subarachnoid block is always administered in the lower lumbar region, i.e. L2-3, L3-4 or L4-5 and the CSF acts as a vehicle for spread of the drug. By positioning we can increase the height or restrict it to the perineum by making the patient sit for 5 minutes. On the other hand, for epidural anesthesia the catheter should be sited at the segments where effect is required; for example, for analgesia for thoracotomy, at T5 or T6. - The height of block with subarachnoid injection is more or less predictable for a given volume in adult patients of normal build. On the other hand, the epidural drug has to be given in a large volume to ensure spread in a space filled with other structures. Since there is no CSF to ensure cephalad spread the catheter or injection has to be sited as near the spinal nerves as possible. - Since the drug directly bathes the nerve roots in subarachnoid block, dense motor blockade is invariably present. This is

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

137

Table 9.3: Comparison of spinal and epidural blocks

-

-

Parameter

Subarachnoid

Epidural

1. Drug volume

Small

Large

2. Spread

Via CSF

Relies on mass and volume

3. Onset

Rapid (3-5 min)

Slower (15-30 min)

4. Motor block

Invariable, dense

May be weak or absent

5. Height of block

Not dependent on level of injection

Effect maximal on dermatomes nearest to site of injection

beneficial for surgery as the field is quiet and intense relaxation facilitates surgery, especially lower intra-abdominal procedures. The patient has to be specially informed that no ambulation will be possible for at least 4-6 hours. With epidural blockade, presence of motor blockade depends on the concentration and volume of local anesthetic. Motor blockade can be achieved using full concentrations (2% lignocaine, 0.5% bupivacaine) of LA. Dilute LA solutions (0.125% bupivacaine, 0.5% lignocaine) can be provided to patients without hampering motor activity, which is important in, for example patients receiving neuraxial analgesia for cancer pain and obstetric patients for labor analgesia(‘walking epidural’). Possibility of toxic effects of dose is more with epidural because of the large volume of drug used. Onset of cardiovascular effects like bradycardia and hypotension is rapid and sometimes precipitous in subarachnoid block. On the other hand, these are more gradual with epidural and usually not severe, and allow for some time for correction.

ASSESSMENT OF EFFECTIVENESS OF SPINAL/EPIDURAL BLOCK -

Asking the patient – The patient can be asked for heaviness in the legs

-

-

– Tingling, pins and needles – For motor block, see if the patient can flex the ankle joint or the knees Observe – Vasodilatation and engorgement of the veins over the penis. – Even an elderly, arthritic patient can be easily placed in lithotomy position with the thighs abducted. – In very thin patients, pulsations of the femoral artery, abdominal aorta and bowel peristalsis may be observed. Testing the level and effectiveness – With an alcohol swab start from the area which is blocked and go up dermatome by dermatome till the patient can appreciate the cold swab. – Ask the surgeon to gently hold the proposed site of skin incision with a nontoothed forceps and shake it from side to side. Keep your eyes on the patient’s face to observe any grimacing or reaction.

SEDATION – Sedation should be individualized – The elderly already have reduced input to the reticular formation (due to ageing of the sensory organs) and start sleeping as soon as afferent input falls further. – Excessive sedation will defeat the purpose of sparing GA in patients with pulmonary disease – Midazolam in 0.5 mg–2 mg increments can be used.

138

A PRIMER OF ANESTHESIA

PRECAUTION S PRECAUTIONS – Hypothermia-especially in the elderly. Shivering should be prevented and aggressively treated with radiant heat, blankets, small doses of pethidine (10-15 mg) – Keep verbal contact with the patient – Occasionally sudden severe bradycardia may occur due to unopposed vagal action and visceral manipulation (especially elderly on beta blockers): Atropine is given in doses of 0.3-0.6 mg. CAUDAL ANESTHESIA (TABLE 9.4) There is less effect on cardiovascular, respiratory and bowel function as caudal block is limited to the sacral and lumbar nerves. Motor blockade is limited to the legs. Autonomic dysfunction is limited to bladder and anorectal sphincter. Indications of caudal anesthesia are outlined in Table 9.4. Technique There is a tendency to treat the caudal approach with less respect than lumbar epidural technique as it appears to be very easy and quick. It must be remembered that the sacral hiatus is also a portal of entry to the epidural space and thus

can carry infection if aseptic technique is not followed. This is especially important considering the proximity of the sacral hiatus to the peri anal region. The pediatric patient is placed in the lateral decubitus position. The ‘jack-knife’ position is preferred for adults. A small child can be ‘tucked’ into position by an assistant (Fig. 9.19) after anesthesia is induced and the airway maintained by a facemask or LMA. After cleaning and draping the area the sacral hiatus is palpated. The two posterior superior iliac spines and the sacral hiatus form the vertices of an equilateral triangle (Fig. 9.20). The hiatus is felt as a depression between the two sacral cornua and usually admits the pulp of the index finger. The skin over the center of the hiatus is infiltrated with 1% lidocaine injected through a 26-G needle after informing the patient. In adults 20 ml volume is sufficient for perineal and urethral procedures. For groin and other sub-umbilical procedures (supra pubic cystostomy), a volume of 25-30 ml is required. In pre-adolescent children the Armitage formula given in the Table 9.5 is useful to calculate the volume of local anesthetic needed. Needle size: In children 23-G needles and in adults 22-G serve the purpose.

Table 9.4: Indications of caudal anesthesia Adult

Pediatric

1. Surgery • Anorectal • Gynecological • Orthopedic

1. 2. 3. 4.

•

Urethral

2. Obstetric • Episiotomy suturing • Manual removal of placenta 3. Chronic pain • Coccydynia • Spinal manipulation

Surgery on genitalia Inguinal hernia repair Orchidopexy To deliver neuraxial opioid for major abdominal and thoracic surgery 5. To thread an epidural catheter to provide for prolonged postoperative analgesia especially after major vascular/orthopedic lower limb procedures

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

139

Table 9.5: The Armitage formula

Fig. 9.19: Positioning for caudal block

Block level

Volume of LA in ml/ segment

1. Lumbosacral

0.5

2. Thoracolumbar

1.0

3. Mid thoracic

1.5

Technique of insertion: The needle is inserted at a 60° angle into the skin (Fig. 9.21) and through the sacrococcygeal ligament. As soon as the ‘give’ of the ligament is felt, the needle is lowered to 20-30° or nearly parallel to the skin and gradually advanced into the sacral ‘canal’ up to 3-5 mm before injecting the drug. It should be remembered that the dura ends at S3 in infants and S2 in adults and use of long needles can lead to dural puncture. Caudal catheters are becoming popular in children to provide continuous postoperative analgesia for 2-3 days after major procedures like hip surgery, limb salvage procedures and major abdominal procedures. Complications of Caudal Block

Fig. 9.20: The sacral hiatus and posterior superior iliac spines

Fig. 9.21: Technique of insertion of needle in caudal space

• Wrong needle placement : Needles can get directed into the subcutaneous tissue (when the injected drug will produce a visible swelling), or more seriously, through the coccyx into the pelvis. This way misdirected needles have been known to perforate hollow viscera or even the fetal head in the birth canal. Injection into the periosteum is diagnosed by high resistance and pain if the patient is awake. • Accidental intravascular injection/injection into the marrow of one of the sacral vertebrae produces symptoms of systemic toxicity. • Accidental dural injection is always a possibility considering the proximity of the dural sac to the sacral hiatus. • Infection is a constant risk if poor technique is employed.

140

A PRIMER OF ANESTHESIA

MCQ MCQss 1. In ‘low subarachnoid block’ the level of the block is limited to: b. T10 a. L1 c. L2 d. T12 2. Contraindications for spinal anaesthesia would include: a. COAD b. Epilepsy c. Rheumatoid arthritis d. Intracranial hypertension

Fig. 9.22: The combined spinal epidural (CSE) technique

Co mbined Spinal-Epidural Anesthesia (CSE) Combined Technique (Fig. 9.22) This technique of neuraxial blockade combines the advantages of both spinal and epidural techniques. The technique consists of first locating the epidural space with a (usually) 16 G Tuohy needle. Then a very fine gauge (usually 26/27G) spinal needle is inserted through it to pierce the dura and enter the subarachnoid space. The stylet of the spinal needle is withdrawn gradually and CSF tracks down the needle. The calculated subarachnoid drug is injected slowly. The spinal needle is then withdrawn and an epidural catheter threaded through the Tuohy needle, and the needle removed. The initial part of the surgery is managed by subarachnoid block, with its advantages of rapid onset and dense motor blockade. As the signs of regression of the block appear, it is augmented with epidural local anesthetic and opioids. This elegant technique is now the most commonly employed neuraxial block for prolonged orthopedic, urologic and peripheral vascular procedures of the lower limb.

3. Subdural space is the space between: a. Dura mater and arachnoid mater b. Dura mater and pia mater c. Pia mater and arachnoid mater d. Ligamentum flavum and dura mater 4. The epidural space extends from the: a. Foramen magnum to sacral hiatus b. C1 vertebral level to L5 vertebral level c. C1 vertebral level to S1 vertebral level d. C1 vertebral level to S2 vertebral level 5. The sacral hiatus results due to failure of fusion of lamina b. S2-S5 a. S1-S5 c. S3-S5 d. S4-S5 6. Dura- cutting needles include a. Whitacre needle b. Quincke needle c. Sprotte needle d. Tuohy needle 7. Incidence of post dural puncture headache can be reduced by a. Use of smaller gauge needles b. Use of dura cutting needles c. Use of adjuvants to local anesthetics d. Using smaller doses of local anesthetic 8. The long acting local anesthetic dispersed in crystal form is a. Mepivacaine b. Levobupivacaine c. Tetracaine d. Cocaine

NEURAXIAL (SPINAL AND EPIDURAL) BLOCKADE

9. Hypobaric local anaesthetics have a baricity less than a. 1.000 b. 1.0069 c. 0.0069 d. 0.0089 10. The following factor will affect the height of subarachoid block a. Coughing b. Direction of needle level c. Gender d. Intra-abdominal pressure 11. The fact not true about ‘Ropiva caine’ is a. Shorter acting than bupivacaine b. Has vasoconstrictive property in clinically used concentrations c. Less cardiotoxic than bupivacaine d. Better quality of motor block as compared to bupivacaine 12. Carbonation of local anesthetics a. Increases the speed of onset of block b. Delays the speed of onset but gives better quality of block c. Delays the onset but prolongs the duration of block d. Has no effect on onset of block 13. In patients receiving LMWH (low molecular weight heparin) neuraxial blocks should a. Never be performed b. Should be delayed by 2 hours after administration of drug c. Should be delayed by 12 hours after administration of drug d. Can be performed any time depending on the dose of LMWH 14. Side effects associated with subarachnoid block do not include a. Hypotension b. Tinnitus c. Tremors d. Nausea

141

15. The LA whose pKa is closest to body pH is: a. Bupivacaine b. Mepivacaine c. Ropivacainea d. Etidocaine 16. ‘EMLA’ cream consists of a. 1:1 mixture of 2% prilocaine and lidocaine b. 1:1 mixture of 4% prilocaine and 4% lidocaine c. 2:1 mixture of 5% prilocaine and 5% lidocaine d. 1:1 mixture of 5% prilocaine and 5% lidocaine 17. The normal dose of EMLA recommended is: a. 1-2 g/10 cm2 of skin b. 3-4 g/10 cm2 of skin c. 5-6 g/10 cm2 of skin d. 7-8 g/10 cm2 of skin 18. Fastest absorption of local anesthetic after injection occurs from: a. Caudal epidural b. Intercostal c. Tracheal d. Subcutaneous 19. Allergic manifestation of ester local anesthetics are due to: a. EDTA preservative b. Large volumes c. Sodium bisulphate d. Para-amino benzoic acid 20. The amide anesthetic undergoing most rapid metabolism is: a. Lidocaine b. Prilocaine c. Etidocaine d. Benzocaine 21. Neonates born of mothers receiving prilocaine for epidural anesthesia are more prone to develop: a. Hyperbilirubinemia b. Hemolytic crisis c. Myoglobinemia d. Methemoglobinemia

142

A PRIMER OF ANESTHESIA

22. Methemoglobinemia after prilocaine use can be due to all except: a. Prilocaine dose > 10 mg/kg b. Accumulation of ortho-toluidene derivatives c. Patients with cirrhosis d. Patients with chronic renal failure

25. The agent of choice for treating bupivacaine cardiotoxicity is: a. Lidocaine b. Adenosine c. Bretylium d. Amiodarone

23. The only LA with intrinsic vasoconstrictive property is: a. Bupivacaine b. Procaine c. Cocaine d. Mepivacaine

Answers

24. The LA associated with hypertension and ventricular dysrhythemia is: a. Etidocaine b. Cocaine c. Procaine d. Ropivacaine

1. 5. 9. 13. 17. 21. 25.

b d a c a d c

2. 6. 10. 14. 18. 22.

d b d c c d

3. 7. 11. 15. 19. 23.

a a d b d c

4. 8. 12. 16. 20. 24.

a c a d b b

Peripheral Nerve Blocks Rengarajan Janakiraman



      

Indications, advantages, contraindications of peripheral nerve blockade Upper Limb Blocks Brachial plexus anatomy Various techniques of brachial plexus block Digital nerve block Lower Limb Blocks Lower limb anatomy Femoral nerve block Sciatic nerve block Ankle block Blocks for hernia surgery Penile block

INTRO DUCTION INTRODUCTION Peripheral nerve blockade is an important component of regional anesthesia (RA). This chapter will deal with the anatomy, indications and technique of some common blocks. Peripheral nerve blockade involves the injection of local anesthetic into the area around a single or group of sensory or motor nerves that supply a particular region of the body. The main purpose is to block the afferent pain impulses carried to the brain and efferent motor impulses from the brain to the muscles. By virtue of this unique characteristic peripheral nerve

blockade is very useful in providing ideal surgical conditions as well as postoperative analgesia. TECHNIQUE The golden rule that “logic and a little hardship leads to success” applies to peripheral nerve blocks. As simple as they may seem, they can be hazardous when a shotgun approach is executed. A thorough knowledge of anatomy with precise focus on dermatome, osteotome and myotome is mandatory. Before stepping into actual techniques it is prudent to consider Hilton’s law. Hilton’s Law The nerve supplying a joint also supplies both the muscles that move the joint and the skin covering the articular insertion of those muscles.

There are various methods to localize the nerve. They are i. Electrical nerve stimulation ii. Eliciting paresthesia iii. Ultrasound (described at the end) Electrical Nerve Stimulators (Fig. 10.1) The old rule of “No paresthesia –No anesthesia” is obsolete. We are now in the ‘Golden era’ of nerve stimulators. The main advantages over paresthesia technique are objective localization

144

A PRIMER OF ANESTHESIA

Fig. 10.1: An electrical nerve stimulator

of the nerve, better reliability and less nerve damage. The principle of nerve stimulation consists of triggering depolarisations in the nerve with the help of electrical pulses generated from the nerve stimulator. This may cause muscle contractions at the efferent muscle group or paresthesia in the sensory distribution area. Nerve Localization The following technique is to be followed as described for all peripheral blocks unless otherwise specified. Aseptic precautions are mandatory. After marking the puncture point, the skin is infiltrated with 1% lignocaine. A short bevel unipolar insulated needle with conductive tip set at 1.2 mA current intensity, and 100 – 300 μsec pulse width is used for approximate localization of the nerve. The nerve is identified by the contraction of the desired group of muscles or paresthesia. The second step involves fine movement of the needle to get more closer to the nerve at a lower threshold current (0.2– 0.4 mA).

The lower the threshold current, the more accurately the nerve is localized, resulting in a more reliable blockade with a shorter onset. After accurate localization of the nerve, local anesthetic (LA) is injected. The volume and dose vary depending on the: Indication (e.g. Anesthesia vs. Analgesia) Thickness of the nerve (e.g. Sciatic vs. Median) Maximum dose (e.g. Lignocaine vs. Bupivacaine) Presence of Additives (e.g. Lignocaine vs. Lignocaine + Adrenaline) Concentration of Local anesthetic (e.g. Lignocaine 1% vs. Lignocaine 2%) A detailed discussion on local anesthetics may be found in the chapter on epidural and spinal anesthesia. ADVANTAGES Regional Anesthesia offers several advantages over General Anesthesia. They are - Suitable for day-care (ambulatory surgery) - Provision of ideal surgical conditions - Avoidance of airway manipulation (intubation) - Reduced need for narcotics and sedatives - Extended postoperative pain relief - Hospital cost savings due to reduced length of stay and faster patient turnover. INDICATIONS The dictum of Peripheral nerve blockade is selection of Right Patient Right Surgery Right Technique Right Equipment This means that appropriate choice of the block should provide satisfactory condition for

PERIPHERAL NERVE BLOCKS

surgery and not result in patient discomfort or risk. Thus it is important to know, for example, which approach to choose for an upper limb peripheral block for shoulder surgery. It is mandatory to assess the patient from the point of view of general anesthesia (GA), keeping in mind that the block may fail or be partial, or may not last long enough for the surgery, so that supplementation by GA becomes necessary.

145

CONTRAINDICATIONS Absolute Patient refusal Local infection Relative Coagulopathy Preexisting progressive neurological deficit. COMPLICATIONS (TABLE 10.1)

Table 10.1: Complications related to peripheral nerve/plexus blocks Complication

How can it be avoided?

Hematoma

i. Avoid multiple needle insertion ii. Evaluate all patients for coagulopathy

Systemic toxicity CNS – Seizures CVS - Arrhythmias

i. Rule out intravascular injection byTest dose – inject 3 ml of Saline in 1:200,000 Adrenaline. Increase in HR 20% above the base line signifies intravascular placement of the needle tip. ii. Slow injection of Local anesthetic. iii. Repeated aspiration of blood after every 5 ml of injection. iv. Careful attention to volume and dose of local anesthetic.

Nerve injury

i. Always use nerve stimulator to confirm the needle position. ii. Always use short bevel needle. iii. Raj test – After obtaining the desired muscle twitch at low threshold current (0.3 – 0.4 mA) inject 0.5 ml – 1 ml of local anesthetic. Positive Raj test – No resistance to injection, No pain and the twitch disappears immediately.

Pneumothorax Interscalene, Supraclavicular and Infraclavicular block Neuraxial injection (Interscalene and All paravertebral blocks) Spinal cord – Quadriplegia, Paraplegia. Subrachnoid – Headache, Total spinal Opposite side affected Epidural – Opposite side affected Phrenic nerve block Supraclavicular, Infraclavicular block

i. Use nerve stimulator or Ultrasound.

i. Thorough knowledge of anatomy. ii. All paravertebral blocks should be considered as potential epidural blocks. iii. Use 18 G Tuohy needle for paravertebral blocks. iv. Restricting the needle depth to 2.5 cm in Interscalene block. v. Watchful expectancy for Spinal fluid. Avoid these blocks in COPD patients.

146

A PRIMER OF ANESTHESIA

UPPER LIMB BLOCKS Anatomy (Fig. 10.2A) The anatomy of the Brachial plexus can be better understood when the Brachial plexus is visualized like a Banyan tree. Like a Banyan tree the Brachial plexus has ROOTS – C5, C6, C7, C8, T1 TRUNKS (Between Scalenus Anterior and Scalenus Medius) UPPER – C5 + C6 MIDDLE – C7 LOWER – C8 + T1 DIVISION Behind the Clavicle each trunk divides into Anterior and Posterior division. UPPER MIDDLE LOWER

Fig. 10.2A: Anatomy of the brachial plexus

Anterior Posterior Anterior Posterior Anterior Fig. 10.2B: Cords of brachial plexus

Posterior

CORDS (accompany (Fig. 10.2B)

axillary

artery);

LATERAL – Upper anterior + Middle anterior MEDIAL – Lower anterior POSTERIOR – Upper posterior + Middle posterior + Lower posterior BRANCHES (Beyond Pectoralis Minor) LATERAL — Lateral pectoral nerve Musculocutaneous nerve Lateral root of Median nerve MEDIAL — Medial pectoral nerve Medial root of Median nerve Ulnar nerve Medial cutaneous nerve of arm Medial cutaneous nerve of forearm

POSTERIOR — Subscapular (Upper) nerve Thoracodorsal nerve Axillary nerve Radial nerve Subscapular (Lower) nerve INTERSCALENE BLOCK Interscalene block involves blocking the roots of Brachial plexus in the interscalene groove between the Anterior Scalene and Middle Scalene muscles (Fig. 10.3). The patient is placed in the supine position and the head is turned 45o towards the contralateral side. A line is drawn over the clavicle on the ipsilateral side. Another line parallel to the clavicular line at the level of ipsilateral cricoid cartilage is also drawn (Fig. 10.4). The interscalene groove is identified at the cricoid line

PERIPHERAL NERVE BLOCKS

147

beyond 3.0 cm. It is important to remember that interscalene block has its own unique complications in addition to the list described above (Table 10.1). They are Horner’s syndrome and Ipsilateral Phrenic nerve block. Maneuvers to Accentuate the Landmarks

Fig. 10.3: Anatomy of interscalene block

The groove between SCM and the Anterior Scalene muscle is the most deceiving false landmark. Following maneuvers help in accurate localization of the interscalene groove. a. The external jugular view (EJV) crosses the needle insertion point. b. Ask the patient to - Sniff - Take deep breaths - Lift the head – posterior border of SCM prominent. SUPRACLAVICULAR BLOCK

Fig. 10.4: Technique of interscalene block

by rolling the finger posterior to the clavicular head of Sternocleidomastoid (SCM) muscle. With middle and index fingers in the interscalene groove the stimulating needle is introduced 45o to the skin with the tip pointing towards the opposite leg’s great toe (Fig. 10.4). The brachial plexus is usually identified by contraction of the Pectoralis Major or Biceps. A volume of 40 ml provides excellent analgesia for shoulder surgeries. This block usually spares the ulnar nerve. Utmost caution should be exercised regarding the depth of needle insertion. The needle should never be inserted

Supraclavicular block involves blocking the trunk of the Brachial plexus (refer to Fig. 10.2). Place the patient in supine position with the head turned towards the opposite side and mark the following landmarks (Fig. 10.5). - 1 cm above the mid point of the clavicle or - 1 cm above and posterior to Subclavian artery pulsation.

Fig. 10.5: Technique of supraclavicular block

148

A PRIMER OF ANESTHESIA

-

Parasagittal plane – Draw a line parallel to midline at this point and extend it 1 inch above and below the clavicle. The brachial plexus is usually identified by flexion or extension of fingers at a depth of 2–4 cm. Incidence of pneumothorax is very high with this block. The direct needle should never deviate from the parasagittal plane. This block should be used only in circumstances where other approaches are absolutely contraindicated or not possible. INFRACLAVICULAR BLOCK (SUPERIOR CORD BLOCK)

Fig. 10.7A: Technique of axillary block

Infraclavicular block involves blocking the Cords of the Brachial plexus. This is the most common block performed for upper limb surgeries below the shoulder because of a wide safety margin. The cords are blocked as they lie in the coraco-clavicular trough. The Coracoclavicular trough is one of the easiest landmarks to identify. It is bounded by Concavity of the lateral clavicle superiorly. Coracoid process laterally. The technique is shown in Fig. 10.6. AXILLARY BLOCK This is a useful block for all surgeries on the upper limb. When a tourniquet is used, the intercostobrachial nerve is blocked using a ring block around the upper arm.

Fig. 10.6: Infraclavicular block-insertion of needle in coracoclavicular trough

Fig. 10.7B: Cross sectional view indicating disposition of nerves around the axillary artery

Axillary block involves blocking the branches of the brachial plexus. The Axillary artery is palpated high in the axilla in the groove between the Pectoralis Major and Coracobrachialis.The artery is fixed firmly between the index and middle finger by firmly pressing against the humerus. The needle is inserted perpendicular to the skin at the superior border of the axillary artery (Fig. 10.7A). The median nerve is identified in quadrant 1 and the musculocutaneous nerve in quadrant 2. Each nerve is injected with 10 ml of Local anesthetic. After completing the injection the needle is redirected towards the lower pole of the axillary artery. The Ulnar nerve is identified in quadrant 3 and the Radial nerve in quadrant 4 (Fig. 10.7B). The axillary sheath contains multiple septae, which

PERIPHERAL NERVE BLOCKS

prevent the spread of local anesthetic from one quadrant to another. So it is important to block all the nerves separately. Axillary and infraclavicular block are not useful for shoulder surgeries.

149

epinephrine should not be used for digital block to avoid gangrene of the digits. Digital blocks are useful for draining abscesses/suturing of fingers, removing foreign bodies (glass), etc. LOWER LIMB ANATOMY

DIGITAL NERVE BLOCK Digital nerve block is the technique of blocking the nerves of the digits to achieve anesthesia of the fingers. Each digit is supplied by a Palmar and a Dorsal digital nerve. The Palmar digital nerves are derived from Median and Ulnar nerves. They run on the ventro lateral aspect of the finger. The Dorsal digital nerves are derived from Radial and Ulnar nerves and run on the dorso lateral aspect of the fingers (Fig. 10.8). Technique The hand is pronated and rested on a flat surface. Skin wheals are raised at the dorsolateral borders of the proximal phalanx and the needle is introduced at the dorsal surface of the lateral border of the phalanx. Needle is advanced until it contacts bone.1 ml of Local anesthetic is injected after withdrawing the needle 1 mm from the bone. An additional 1 ml is injected continuously as the needle is withdrawn. The same procedure is repeated on the other side of the base of the finger. Solutions containing

Gross Anatomy The nerve supply of the lower limb is derived from the lumbar and sacral plexuses. The lumbar plexus is formed from roots of L1L4, while the sacral plexus is formed from L4, L5, S1, S2 and S3. Arising from these plexuses are the five main nerves that innervate the lower limb. These five nerves are the femoral, sciatic, and obturator nerves, as well as the lateral and posterior cutaneous nerves of the thigh. The dominant nerve above the knee anteriorly is the femoral nerve. The dominant nerve on the posterior aspect of the leg above and below the knee is the sciatic nerve.

The Lumbar Plexus This gives rise to the femoral nerve, obturator nerve and lateral cutaneous nerve of the thigh. The femoral nerve stems from the anterior rami of L2-L4 and runs in the groove between the psoas major and iliacus muscles, and is covered by the fascia of these muscles. It enters the thigh after passing deep to the inguinal ligament, where it is lateral to the femoral artery. The femoral nerve block is performed distal to this point. The lateral cutaneous nerve of the thigh and the obturator nerve both have important sensory distributions to the lateral thigh and medial side of the knee respectively.

The Sacral Plexus

Fig. 10.8: Technique of digital nerve block

This gives rise to the Sciatic nerve and the posterior cutaneous nerve of the thigh. Although these nerves are formed separately within the plexus, they pass through the pelvis together. The sciatic nerve leaves the pelvis and enters the buttock area through the greater sciatic

150

A PRIMER OF ANESTHESIA

foramen, and then passes along the midpoint between the greater trochanter (GT) and the ischial tuberosity (IT), lying just posterior to the hip joint. It can be blocked at several points along this course; parasacral, transgluteal, subgluteal or popliteal. On leaving the buttock area the sciatic nerve runs distally down the thigh to the popliteal fossa between the biceps femoris and semimembranosus and semitendinosus muscles. At the apex of the popliteal area, approximately 7-9 cm above the crease behind the knee, the sciatic nerve splits into the tibial nerve medially and the common peroneal nerve laterally. From its divergence from the sciatic nerve, the common peroneal nerve continues its path downward and descends along the head and neck of the fibula. Its terminal branches are superficial and deep peroneal nerves. The tibial nerve is the larger of the two divisions of the sciatic nerve. The tibial nerve continues its path vertically through the popliteal fossa. Its terminal branches are the medial and lateral plantar nerves. Its collateral branches give rise to the cutaneous sural nerves, muscular branches to the muscles to the calf, and articular branches to the ankle joint. Surface Anatomy When performing the nerve blocks, it is essential to be able to locate the surface landmarks accurately, since these form the reference points we use for determining the correct site for needle insertion.

Anterior Superior Iliac Spine (ASIS) If we follow the iliac crest (ridge of the pelvic bones) from the flank forwards, it ends in an obvious bony prominence at the side of the lower abdomen. This is the anterior superior iliac spine.

Pubic Tubercle This is the bony prominence that can be felt at the inner (medial) end of the groin crease. It is

about 2-4 cm from the midline, at the top of the genital area.

Posterior Superior Iliac Spine (PSIS) The PSIS is the bony prominence at the posterior end of the iliac crest. It is directly caudal to the “sacral dimple” and is visible as a depression in the skin just above (superior to) the buttocks close to the midline.

Greater Trochanter This bony landmark is part of the lateral femur, just below the hip joint. It is the most lateral bony point, and can be identified by internally and externally rotating the hip.

The Ischial Tuberosity This is the part of the pelvic bone structure that can be felt on the medial side of the base of the buttock. It is the bony structure that we sit on. FEMORAL NERVE BLOCK At the inguinal crease, the nerve is deep to the fascia lata and covered by the fascia iliaca. It is separated from the femoral artery and vein by the femoral fascia sheath, a portion of the psoas muscle and the ligamentum ileopectineum. It may be useful to think of the mnemonic “VAN” (vein, artery, nerve) going from medial to lateral in the femoral triangle (Fig. 10.9). After numbing the skin, the block needle, usually a 22 an insulated stimulating needle, is introduced 1 cm lateral to the femoral artery and 1 cm below the femoral crease (Fig. 10.10). It is advanced at 45o, and two distinct pops can usually be felt as the needle penetrates the fascia lata and fascia iliaca. Clear quadriceps contractions can be observed if the femoral nerve is encountered with the stimulating needle. This should not be confused with sartorius muscle motor response, which does not cause the patella to move as seen with femoral nerve stimulation. 20-40 ml of local anesthetic is injected through the needle.

PERIPHERAL NERVE BLOCKS

151

Fig. 10.9: Disposition of femoral view, artery and nerve

Fig. 10.10: Landmarks for femoral nerve block

Before injecting the local anesthetic agent through the needle, a larger bore needle such as an 18-guage Tuohy needle may be used to thread a catheter through the needle for continuous nerve block and treatment of postoperative pain. This can be done by placing the catheter blindly through the needle, placing a nerve stimulator on the proximal end of a stimulating catheter, or with the aid of ultrasound. Femoral nerve block is useful for providing analgesia to a patient with fracture neck or shaft of femur, especially to shift from the site of injury to the trolley or bed.

trochanter (GT) is palpated on the outside of the leg, and the ischial tuberosity (IT) is located, as the main prominence at the base of the buttock. A line is drawn joining these two points (Fig. 10.11). 2 cm below the midpoint between these two landmarks is the injection point (Fig. 10.12). A definite groove will be palpable along the course of sciatic nerve at this point. Insert the needle perpendicular to the skin. As the needle is advanced, twitches of the gluteal muscles are observed first. These twitches merely indicate that the needle position is still too shallow. Once the gluteal twitches disappear, brisk response of the sciatic nerve to stimulation is observed (plantar flexion or eversion of the ankle). This typically occurs at a depth of 5-8 cm. After negative aspiration for blood, 15-20 mL of local anesthetic is slowly injected.

SCIATIC NERVE BLOCK Infragluteal Approach To perform this block, the patient lies on the side with the side to be blocked uppermost. The operator stands by the patient’s bed, on the side to be blocked. The hip is then flexed as much as possible with the knee bent. The greater

ANKLE BLOCK The ankle block is a safe and effective method for obtaining anesthesia and analgesia of the foot.

152

A PRIMER OF ANESTHESIA

Fig. 10.11: Locating the sciatic nerve

Fig. 10.12: Technique of sciatic nerve block

This block is very useful for short procedures like excision of bunions, drainage of abscesses, removal of foreign bodies (glass, thorns) from the foot. Anatomy Five nerve branches supply sensation to the foot (Fig. 10.13). All are branches of the sciatic nerve,

Fig. 10.13: Nerves supplying the foot

except the saphenous nerve, which is the terminal branch of the femoral nerve. The tibial nerve divides into the posterior tibial and sural nerves, and the common peroneal nerve into the deep and superficial peroneal nerves. The posterior tibial nerve finally divides into the medial and lateral plantar nerves. The deep peroneal nerve innervates the first web-space and so must be blocked for anesthesia of the great toe. The posterior tibial nerve lies immediately posterior to the posterior tibial artery, behind the medial malleolus. The superficial peroneal nerve divides into terminal branches anterior to the ankle, necessitating a wide fan of infiltration for blockade. Technique All five nerves can be blocked with the patient supine and the foot on a padded support. The aim is sensory block alone and so low concentrations of local anesthetic (LA) are

PERIPHERAL NERVE BLOCKS

Fig. 10.14: Landmarks for posterior tibial nerve block

153

Fig. 10.15: Blocking the sural nerve

sufficient (e.g. 0.25% bupivacaine) in most cases. It is best to avoid adrenaline in the LA because of concerns of theoretical risks to the foot from the vasoconstrictor effect. The five nerves are blocked by injections that form a ring of infiltration around the ankle at the level of the malleoli. Posterior Tibial Nerve Insert the needle at the mid point between the medial malleolus and tendo achilles at its insertion into the calcaneum (Fig. 10.14). If paresthesia is felt, inject 3-5 ml LA. If not, advance to contact the tibia, withdraw 0.5 cm and then inject 5-7 ml local anesthetic. Sural Nerve Introduce the needle along the lateral border of the Achilles tendon at the level of the cephalic border of the lateral malleolus (Fig. 10.15). Advance anteriorly towards the fibula. If paresthesia is felt inject 3-5 ml LA. If not, inject 5-7 ml LA as the needle is withdrawn. This gives subcutaneous infiltration from the Achilles tendon to the fibula. Deep Peroneal Nerve The needle is inserted just lateral to the tendon of extensor hallucis longis , between the superior

Fig. 10.16: Blocking the deep peroneal nerve

margin of the two malleoli (Fig. 10.16). This tendon is prominent on the dorsum of the foot, during extension of the big toe. From the position described above, advance the needle posterior (i.e. at 90° to the skin). Inject 3-5 ml LA deep to the fascia. Superficial Peroneal Nerve After blocking the deep peroneal nerve, withdraw the needle to just stay in the skin. Turn the needle towards the lateral malleolus and inject 5 ml LA in a subcutaneous band between the lateral malleolus and the anterior border of the tibia. This should reach all the branches of this nerve.

154

A PRIMER OF ANESTHESIA

Saphenous Nerve Again withdraw the needle to just stay in the skin and turn the needle to point towards the medial malleolus. Infiltrate 5 ml LA subcutaneously as the needle is advanced towards the medial malleolus. BLOCKS FOR HERNIA SURGERY Inguinal canal anatomy (Fig. 10.17): The Inguinal canal is approximately 4 cm long and is directed infero medially through the inferior part of the anterior abdominal wall. The canal is parallel and 2-4 cm superior to the medial half of the inguinal ligament. The Inguinal area receives sensory innervations from Ilioinguinal, Iliohypogastric and Genitofemoral nerve. There is great variation in the sensory innervation in the inguinal region with free communication between the branches of these nerves. Traction discomfort of the sac is minimized by Genitofemoral block. Some fibers cross the midline from the contralateral side and supply the inguinal region. So the Inguinal field block is a combination of blocks of:

-

Inguinal nerve Iliohypogastric Genital branch of Genitofemoral nerve Midline infiltration and Local infiltration of the skin (T12 distribution)

Ilioinguinal Nerve Block A regional anesthesia short bevel needle is passed 1 inch inferior and medial to the Anterior Superior Iliac Spine (ASIS). First ‘pop’ indicates penetration of External oblique aponeurosis. 10 ml of local anesthetic is injected between External oblique aponeurosis and Internal oblique muscle. Iliohypogastric Block Advance the needle till the second ‘pop’ is felt. This signifies the penetration of Internal oblique muscle. 10 ml of local anesthetic is injected between Internal oblique and Transverse abdominis muscle. A further 10 ml of local anesthetic is injected slowly while withdrawing needle through various layers. Genitofemoral Nerve The genital branch of the Genitofemoral nerve is blocked by infiltrating 10 ml of Local anesthetic just lateral to the pubic tubercle below the inguinal ligament. Traction pain is relieved by injecting an additional 10 ml of local anesthetic into the sac by the surgeon. Inguinal field block is a ‘high volume’ block. So the potential complication of local anesthetic toxicity should always kept in mind. Infiltration anesthesia for hernia repair is very useful in patients who are poor candidates for general anesthesia. This group includes patients with severe pulmonary disease or neurologic disease. PENILE BLOCK Anatomy (Fig. 10.18)

Fig. 10.17: Anatomy of the inguinal canal

The penis is innervated by the left and right dorsal nerves, which are branches of the

PERIPHERAL NERVE BLOCKS

155

block is being used. It is advisable to inject 1-2 mls of anesthetic at the base of the ventral aspect of the penis Local anesthetics containing adrenaline should never be used because they cause arterial vasoconstriction, which may lead to ischemia or necrosis of the penis. RECENT ADVANCES IN PERIPHERAL NERVE BLOCKADE The Stimulating Catheter Technique Fig. 10.18: Anatomy and technique of penile block

pudendal nerve. The dorsal nerve on each side passes under the inferior ramus of the pubis and penetrates the layer of superficial fascia to supply the skin and a branch to the corpus cavernosus. The nerves on either side are separated by the suspensory ligament of the penis. Technique of Dorsal Penile Nerve Block With the patient supine, a 27 gauge needle is inserted over the middle of the pubic arch at the base of the penis until it contacts the pubic symphysis, it is then withdrawn slightly and redirected to pass below the symphysis to left or right of midline to a depth of 3-5 mm deeper than the depth to the pubic symphysis to feel a pop. After aspiration to confirm no flash back, 5-7 ml local anesthetic solution is injected. Without taking the needle out of the skin the procedure is repeated on the other side. The needle may then be withdrawn completely or withdrawn to skin and the dorsal part of a ring block performed. Ring Block is the circumferential subcutaneous injection of 10 ml of local anesthetic at the base of the penile shaft using a 26 or 27 gauge needle.

Pitfalls and Complications Dorsal penile nerve block can miss the nerves to the frenulum if a penile block without a ring

A nerve stimulator, set to 1–1.5 mA, 100–300 μsec pulse width, and a frequency of 1-2 Hz is attached to an insulated Tuohy needle and the nerve or plexus appropriate to the surgery is approached. When correct motor response is elicited, the needle is advanced until a brisk motor response is elicited with a current output of 0.3–0.5 mA. The needle is then held steady without injecting any fluid through the needle, the nerve stimulator is attached to the proximal end of the catheter, and the catheter is advanced through the needle. The elicited motor response should now be similar to that elicited by stimulating via the needle. The catheter is advanced beyond the tip of the needle with the motor response remaining unchanged. The main advantage of this technique is the 100% success secondary block rate, whereas for the other techniques it is 60–65%. Ultrasound Guided Blocks Ultrasound guided placement of blocks is making rapid progress and is likely to replace nerve stimulation in many blocks. Advantages afforded are prevention of vascular injection and injury to other structures, and a very high success rate with reduced volumes of local anesthetic agent. A problem with ultrasound is that, although it works well for superficial nerves (where it is not really needed), the depth of penetration of most readily available and affordable ultrasound probes is not sufficient to identify deeper nerves, especially in obese

156

A PRIMER OF ANESTHESIA

patients (where it is most needed). Just as the ultrasound does not replace x-rays in orthopedics, it is ultimately not likely to replace nerve stimulation for continuous nerve block. It is most likely to be a valuable addition to nerve stimulation. CONCLUSION Interest in Regional anesthesia has waxed and waned since its introduction into clinical practice over a century ago. The elegance, safety, and comfort of a successful peripheral nerve blockade are undeniable. However, a high success rates depends on flawless understanding of intricate anatomy. Technological advancements do not replace the basic anatomy knowledge required for Regional anesthesia. Throughout this chapter the golden rule of

“Right patient, Right surgery, Right technique and Right equipment is emphasized”. The technique should be custom made for the surgery and not vice versa. It should always kept in mind that – “A determined fool with a long needle can cause all complications.” ACKNOWLEDGEMENT I sincerely thank Dr Andre Boezaart (who invented the Stimulating Catheters) and Dr. Robert Raw (who pioneered the Infraclavicular ‘Superior’ approach technique) for their valuable guidance in crafting this chapter. I extend my gratitude to Arunkumar J., V Amulya Ankanapalli and Corey Stotts for finetuning my chapter. I also appreciate Dr. Admir Hadzic (nysora.com) for helping me with trouble shooting tabular columns.

Fluid Therapy and Transfusion Rahul Seewal, Purnima Dhar, Rajeshwari Subramaniam

         

Distribution of body fluids and physical principles of equilibrium Crystalloids-definition and examples Colloids-definition and examples Indications of blood transfusion Blood components Complications and hazards of transfusion Fluid infusion and effect on body fluid compartments Hyponatremia and hypernatremia-clinical features, diagnosis, treatment Hypokalemia and hyperkalemia-clinical features and management Hypocalcemia and hypercalcemia- clinical features and management

Why do we Need Intravenous Fluids during the Perioperative Period? The perioperative period can be divided into preoperative, intraoperative and postoperative periods. Fluid loss in these periods results from a combination of existing fluid derangements, preoperative fasting, volume derangement caused by surgery, blood loss and inability of the patient to resume oral intake immediately after surgery. Postoperative vomiting may add to the problem of volume loss. Different fluids in different volumes are needed to balance

nutrition and fluid requirements of the patient in each period. Appropriate Perioperative Fluid Therapy Serves the Following Functions: a. Replaces deficit caused by fasting and supplies the basal fluid requirement b. Replaces surgical losses –this includes blood transfusion, non-blood colloids when indicated c. Corrects osmotic losses and acid-base imbalance d. Delivers potent drugs in dilute forms: for example, inotropes like adrenaline and dopamine; hormones like insulin e. Replaces additional losses, e.g. soakage from the wound and nasogastric drainage in the postoperative period. How is Body Fluid Distributed? In a normal adult, 60% of body weight is water, termed Total Body Water or TBW. Hence in a 70 kg adult man, 60/100 × 70 = 42 kg or 42 L is the total body water, the rest being mainly bone and fat. This 42 L is divided into various compartments as shown in Figure 11.1. 60% of TBW is intracellular = 25L termed ICF.

158

A PRIMER OF ANESTHESIA

Fig.11.1. Distribution of body water Table 11.1: Composition of fluid compartments Composition of plasma, interstitial and intracellular fluid (mmol/L) Substance

Plasma

Cations Na+ K+ Ca2+ Mg2+ Total

153.0 4.3 2.7 1.1 161.1

145.0 4.1 2.4 1 152.5

10 159 40

Pulse/minute

>100

>100

>120

140 or higher

Blood pressure (mmHg)

Normal

Normal

Decreased

Deceased

Pulse pressure (mmHg)

Normal/ Increased

Decreased

Decreased

Decreased

Capillary refill time (sec)

< 2 sec

> 2 sec

> 2 sec

> 2 sec

Respiratory rate per minute

14 – 20

20–30

30–40

> 35

Urine output (mL/hr)

> 30

20–30

< 15

Negligible

Mental status

Slightly anxious

Mildly anxious

Confused

Lethargic

Fluid replacement (3:1 rule for colloid : Crystalloids)

Crystalloid

Crystalloid

Crystalloid + Blood

Crystalloid + Blood

FLUID THERAPY AND TRANSFUSION

167

Fig. 11.4: Fractionation of whole blood into components

or acquired, usually drug induced) exists. One pool of platelets usually increases the platelet count by 10,000 per ml. Platelets should never be refrigerated and need a special filter set for transfusion as they would filter out if a normal blood giving set (with a filter size 200 μm) is used. 3. Fresh Frozen Plasma (FFP) – It is rich in factor V(labile factor), factor VIII and plasma proteins. It is used to correct bleeding associated with clotting factor deficiency and to reverse the effects of anticoagulant drugs

like warfarin immediately. The volume transfused is usually 15–20 ml/kg.The duration of action of these clotting factors is usually 4 hours. 4. Cryoprecipitate – contains factor VIII, von Willebrand factor and fibrinogen and is therefore indicated in bleeding specifically associated with the deficiencies of these factors. This is a frequent finding in disseminated intravascular coagulation (DIC). Cryoprecipitate can be given without ABO compatibility as the concentration of antibodies is very low.

Table 11.6: Blood group classification Blood Group

Antigens

Antibodies

Can give blood to

Can receive blood from

AB A B O

A and B A B None

None B A A and B

AB A and AB B and AB AB, A, B, O

AB, A, B, O A and O B and O O

168

A PRIMER OF ANESTHESIA

Table 11.7: Estimated blood volume in various groups Age

Blood volume

Premature Neonates Full Term Neonates Infants Adult Men Adult Women

95 mL/kg 85 mL/kg 80 mL/kg 75 mL/kg 65 mL/kg

Which are the donor blood groups that a patient can receive and donate to? Table 11.6 provides the answer to this question.

How do we calculate the “Transfusion Trigger” or the amount of blood loss that can be allowed before ordering for a transfusion during surgery? Parameters needed: patient’s weight, hemoglobin (g%), acceptable hemoglobin before commencing transfusion (‘transfusion trigger’) and estimated blood volume (EBV). The estimated blood volume (EBV) for various age groups is given in Table 11.7. The formula used is – Allowable blood loss = [EBV × wt (Initial Hb – transfusion trigger)] ÷ Initial Hb For example, if a patient undergoing major orthopedic surgery has an initial Hb of 14 g/dl and a transfusion trigger of 10 g/ dl is considered appropriate, assuming a weight of 70 kg, his allowable blood loss will be [75 × 70(14–10)] ÷ 14 = 1500 ml. Hence blood loss up to 1500 ml in this patient can (and should) be safely replaced by either crystalloids (3 × 1500 = 4500 ml) or colloids (1 × 1500 = 1500 ml) or both. The patient’s hemoglobin is expected to be approximately 10 g/dl after losing 1500 ml. If this loss is replaced by non blood containing fluids, he should remain hemodynamically stable as long as intravascular volume is maintained. Blood loss during surgery can be judged by taking into account –

1. Blood collected in suction drains 2. Blood in swabs, which can either be weighed before and after use or a rough estimate, can be judged by the size of the swab. A standard 4” × 4” sponge holds ~ 10–20 ml blood. ‘Lap sponges’ (large sponges) ~ 30– 100 ml blood These are only estimates, and ideally patient’s hemoglobin and hematocrit should be checked before commencing blood transfusion. The management schema of a patient who is actively bleeding is given in Figure 11.5. What are the Complications of Blood Transfusion? 1. Changes in oxygen transport (Valtis Kennedy Effect). This refers to the leftward shift of the oxyhemoglobin dissociation curve of stored blood and is mainly due to lowered levels of 2, 3 DPG in stored blood. This implies that hemoglobin of stored blood has a much higher affinity for oxygen than normal blood and would offload oxygen with difficulty.Thus transfused blood becomes ‘functional’ only after 24 hours. 2. Coagulopathy. This is mainly seen after massive transfusion, which is defined as transfusion of one blood volume in 24 hours or less. The main contributing factors to coagulation abnormality seen after blood transfusion are: a. Volume of blood given and duration of hypotension: It has been shown that patients who have been hypotensive for less than one hour have a better chance of not developing coagulopathy after multiple transfusions. b. Thrombocytopenia: At 4ºC, which is the temperature of stored blood, platelet activity decreases very rapidly and is only 5–10% after 24 hours of storage. Transfusion of large volumes of banked blood can result in thrombocytopenia.

FLUID THERAPY AND TRANSFUSION

169

Fig. 11.5: Management scheme in a patient who is bleeding

c. Low factors V and VIII: most factors are stable in stored blood except factors V and VIII which decrease to 15 and 50% of normal after 1–3 days of storage. d. Disseminated intravascular coagulation (DIC): the specific reason for DIC seen after massive transfusion is not clear. However, it seems that hypoxic, acidotic tissues with stagnant blood flow probably release tissue thomboplastin

directly or indirectly through some toxins and activate the extrinsic pathway of coagulation. The rapid coagulation in the microcirculation leads to microthrombi, further hypoxic damage and consumption of fibrin and platelets which leads to activation of fibrinolysis (secondary fibrinolysis) and further loss of fibrin. The drugs useful in this scenario have been enumerated in Figure 11.6.

170

A PRIMER OF ANESTHESIA

Fig. 11.6: Mechanism of primary and secondary fibrinolysis

e. Hypothermia and citrate intoxication: the main reason for hypothermia is the rapid transfusion of large volumes of blood stored at 4ºC. Coagulation factors (which are proteins and enzymes) do not function optimally at temperatures lower than body temperature, and hence coagulopathy develops. Citrate intoxication can result because the citrate load (the anticoagulant component of CPDA1)* chelates calcium, resulting in hypocalcemia. This affects coagulation as calcium is one of the major co factors in the coagulation cascade. 3. Transfusion reactions: the response of body to allogenic blood is known as a

transfusion reaction. These can be further classified as: a. Hemolytic transfusion reactions: These occur mainly due to ABO incompatibility. The incidence is 1/300,000 to 1/700,000 RBC transfusions and is invariably attributed to clinical error. Classical signs are fever, chills, chest pains and nausea, all of which can be masked by anesthesia. The main sign under anesthesia is hypotension. The management of hemolytic transfusion reaction is summarized in Table 11.8. b. Delayed hemolytic transfusion reaction (immune vascular reaction): Initially the transfused RBCs

* CPD-A1 is Citrate-Phosphate-Dextrose with Adenine, the solution used to preserve banked blood.

FLUID THERAPY AND TRANSFUSION

171

Table 11.8: Treatment of hemolytic transfusion reaction STOP THE TRANSFUSION. Maintain urine output @ 75–100 ml/hr by intravenous colloid/crystalloid, mannitol (10–20 gm) or furosemide (20–40 mg). Alkalinize the urine with 1 mEq/kg of NaHCO3 I/V. Check for urine and plasma hemoglobin concentration. Determine platelet count, PT, APTT and fibrinogen levels. Return unused blood to blood bank for crossmatch. Send patient’s blood and urine sample to blood bank for analysis. Prevent hypotension with use of intravenous fluids or inotropes or both.

survive for 2–21 days before being hemolysed. The level of antibody at the time of transfusion is presumably too low to elicit a reaction, but as the levels gradually increase after secondary stimulus (anamnestic response) the cells get lysed. This mainly presents as jaundice and hemoglobinuria. Management is symptomatic. c. Nonhemolytic transfusion reactions: These reactions are usually not serious and are either febrile or allergic in nature. The main reason is bacterial contamination and hence these are most commonly seen in relation to transfusion of platelets which need to be stored at room temperature. 4. Infection: Infections commonly associated with blood transfusion are hepatitis B, hepatitis C, HIV, HTLV, Cytomegalovirus, Yersinia enterocolitica, syphilis and malaria. Others repor ted are Leishmaniasis, Brucellosis, Salmonellosis, measles, Filariasis and typhus. 5. Transfusion associated Graft-versus – Host Disease: Donor lymphocytes from transfused blood products engraft in the recipient initiating an immune reaction. This can be prevented by using appropriate filters and irradiating blood components. 6. Transfusion related acute lung injury (TRALI): This manifests as noncardiogenic

pulmonary edema after transfusion. Though the clinical picture is similar to ARDS and warrants similar management, the mortality rate is much lower ( 145 mEq/L, calculate the pure water deficit and replace fluid losses with oral fluid if the patient can tolerate it or is not NPO; or D5W can be given IV. 5. Correct only half of estimated volume deficit in initial 24 hours 6. Do not forget to provide for ongoing losses. Insensible losses = {0.6 ml/(kg/hour)} × kg wt × 24 hours 7. Continue to replace fluid losses with oral fluids, D5W or half normal saline. 8. Monitor the serum Na+ hourly. 9. Calculate body water deficit as shown in the example below.

Example A 70 kg adult male presents with a serum sodium level of 170 mEq/L after suffering from heat stroke. Calculate his water deficit.

Fig. 11.7: Management of hypernatremia

174

A PRIMER OF ANESTHESIA

Assuming that hypernatremia is due to water loss mainly, Normal TBW (60% × body weight) × normal plasma sodium = current TBW × current plasma sodium 60/100 × 70 × 140 = Current TBW × 170 5880 kg = Current TBW × 170 Current TBW = 34.5 kg Hence, deficit = 42–34.5 = 7.5 kg Thus, 7,500 ml of 5% dextrose has to be given. Half of this should be given in 12–24 hours and the rest in the next 24–36 hours. Plasma sodium should be checked hourly, and not allowed to fall by > 2 mEq/L/hr. In case of hypervolemic hypernatremia: 1. Discontinue offending agents (IV infusion). 2. Use loop diuretics to promote sodium and water excretion, i.e. furosemide. 3. If the patient’s serum Na+ level returns to normal just provide fluids for renal losses and insensible losses using the minimum fluid requirement regime, with half normal saline. 4. If the serum Na+ still remains > 145 mEq/L, calculate the pure water deficit and proceed as with isovolemic hypernatremia. 5. If the patient is receiving D5W monitor glucose levels for hyperglycemia. 6. In diabetic patients with hypernatremia, when the blood glucose has fallen below 300 mg/dl, 5% dextrose in half-normal saline should be used as replacement fluid. Further, diabetics need a correction factor for calculating the actual [Na+] as follows: Corrected serum Na+ = Measured Na+ + [1.6 × (glucose-150)/100] 7. Replace renal and insensible losses with half normal saline. HYPONATREMIA AND ITS MANAGEMENT In contrast to hypernatremia which always results in hyperosmolality, hyponatremia can exist with normal or even elevated plasma osmolality; these conditions are known as ‘pseudohyponatremia’. These are:

Normal plasma osmolality: 1. Marked hyperlipidemia 2. Marked hyperproteinemia 3. Excessive glycine absorption during trans urethral prostate surgery Elevated plasma osmolality: 1. Hyperglycemia 2. Mannitol administration Causes of the more common hypo-osmolal hyponatremia are: a. associated with decreased total body sodium content - diuretics - mineralocorticoid deficiency - renal tubular acidosis, salt-losing nephropathies - vomiting, diarrhea - ‘third-space’ losses (ascites) - burns, sweating b. associated with normal body sodium content - hypothyroidism - drug-induced - syndrome of inappropriate ADH secretion c. associated with increased sodium content - congestive cardiac failure - cirrhosis - nephrotic syndrome There are a few high-risk patients where development of hyponatremia may lead to major neurological complications (Table 11.9). Prevention of hyponatremia should be the clinical goal while managing these patients. While treating hyponatremia the following principles are observed: - It is important to assess the volume status and urine osmolality. These will give a clue to the etiology (Fig. 11.8). - The underlying condition needs to be treated simultaneously, e.g. demeclocycline therapy for SIADH.

FLUID THERAPY AND TRANSFUSION

175

Table 11.9: Hyponatremic patients at risk for neurological complications Complication

Patients at risk

Acute cerebral edema

Postoperative, premenopausal women Elderly women on thiazides Children Psychiatric polydipsic patients Hypoxemic patients

Osmotic demyelination syndrome

Alcoholics Malnourished patients Hypokalemic patients Burn victims Elderly women on thiazides

Fig. 11.8: Assessment algorithm in hyponatremia

Acute symptomatic hyponatremia requires prompt therapy (Fig. 11.9). - It is important to remember that correction up to 125 mEq/L is sufficient. The formula used for determining the Na+ deficit is: Na+ deficit = TBW × (desired [Na+ ] – present [Na+]) -

Example: Sodium deficit in a 60 kg female with plasma sodium of 120 mEq/L = 60 × 0.5 (130– 120) = 300 mEq; hence roughly 300÷154 = 2 liters of normal saline will be needed. [The

0.5 is because in women TBW is 50% of body weight]. Also, co-existing fluid deficits should be corrected. Addition of a loop diuretic can hasten correction. - Very rapid correction of hyponatremia can result in central pontine myelinolysis, symptoms of which are listed in Table 11.10. Therefore the recommended rate of correction is 0.5 mEq/L/hr for mild symptoms, 1 mEq/L/hr for moderate symptoms and not more than 1.5 mEq/L/hr for severe symptoms.

176

A PRIMER OF ANESTHESIA

Fig. 11.9: Treatment plan for severe hyponatremia

Table 11.10: Central pontine myelinolysis Symptoms of Central Pontine Myelinolysis Initial Symptoms Mutism, Dysarthria, Lethargy and affective changes Classic symptoms Spastic quadriparesis Pseudobulbar palsy Lesions in the midbrain, medulla oblongata and pontine tegmentum Pupillary and oculomotor abnormalities: • Altered sensorium • Cranial neuropathies Extrapontine myelinolysis • Ataxia, dystonia • Behavioral abnormalities • Parkinsonism

-

Hypertonic saline is indicated in markedly symptomatic patients with sodium levels less than 110 mEq/L. - Hypertonic saline can cause pulmonary edema, hyperchloremic metabolic acidosis and hypotension. The urgency of management of severe hyponatremia is determined by the patient’s symptomatic status. If symptomatic, and of acute onset, it indicates severe hyponatremia which may cause death if not treated aggressively. On the other hand, an asymptomatic patient with serum sodium < 120 mEq/L needs to have sodium levels brought up gradually to prevent pontine myelinolysis. Treatment plan in severe hyponatremia is shown in Figure 11.9.

FLUID THERAPY AND TRANSFUSION

DISORDERS OF POTASSIUM HOMEOSTASIS Major causes of hypokalemia are 1. Inadequate intake/replacement of potassium 2. Excess loss a. Gastrointestinal- vomiting, diarrhea b. Renal- Conn’s syndrome • Hyperaldosteronism • Diuresis • Chronic metabolic alkalosis • Antibiotics: Amphotericin B, Carbenicillin, Gentamicin • Bartter’s syndrome • Renal tubular acidosis 3. ECF → ICF shifts – Acute alkalosis – B-2 adrenergic agonist therapy (bronchodilators) – Insulin therapy – Hypokalemic periodic paralysis Clinical Features of Hypokalemia Hypokalemia is defined as a potassium level below 3.5 mEq/L. Most patients are asymptomatic till levels fall below 3 mEq/L. Potassium values at 3 mEq/L and below indicate a deficit of 200–400 mEq. Neuromuscular weakness (especially quadriceps), cramps and tetany are

177

characteristic. Cardiovascular effects include an abnormal ECG (T wave flattening and inversion, appearance of a ‘U’ wave, P-R prolongation and S-T depression; Figure 11.10) and labile blood pressure. Hypokalemia induced by diuretics is associated with alkalosis, as the kidneys reabsorb bicarbonate to compensate for chloride loss. Intracellular acidosis occurs due to inward movement of H+ to compensate for low K + . Intracellular acidosis leads to ammonia production and this, coupled with metabolic alkalosis, can precipitate encephalopathy in patients with serious liver disease. Treatment of Hypokalemia (Fig. 11.11) The points to be remembered are - The goal of treatment is to prevent imminent danger like arrhythmias or respiratory failure, and NOT complete replacement at one go. - Peripheral administration should be avoided as potassium solutions are very irritating and produce severe pain. If used, rate should not exceed 0.2 mEq/kg/hr. Faster replacements (0.4–0.5 mEq/kg/hr) can be given through a central or femoral catheter. - Central line administration of potassium should be monitored as high localised concentrations in the heart can result. The best route is through the femoral vein.

Fig. 11.10: ECG changes in hypokalemia

178

A PRIMER OF ANESTHESIA

Fig. 11.11: Plan for treatment of hypokalemia

FLUID THERAPY AND TRANSFUSION

-

-

Dextrose solutions are to be avoided as vehicles as they can result in insulin secretion which favours intracellular migration of potassium and the extracellular values fall further. Potassium chloride is preferred as it corrects chloride deficiency (as discussed above); however potassium bicarbonate can be used if there is metabolic acidosis.

Anesthe tic Implications of Hypokalemia and Anesthetic Precautions during Anesthesia -

1. 2. 3. 4. 5. 6. 7.

Chronic mild hypokalemia without ECG changes does not need aggressive correction before surgery; however if the patient is on digoxin it should be corrected to 4 mEq/L. Vigilant ECG monitoring and IV potassium if arrhythmias develop. Glucose-free solutions to be used Hyperventilation to be avoided. Dose of neuromuscular blocking drugs to be reduced by 25-50%. Desirable to use NMJ monitoring to guide neuromuscular blocking drug dosing. Patients may experience ‘re-curarisation’ in the immediate post operative period. Debilitated patients may require ventilatory support due to reduced respiratory muscle strength.

HYPERKALEMIA—CAUSES, DIAGNOSIS AND TREATMENT Hyperkalemia is defined as potassium levels above 5.5 mEq/L. It can result from impaired excretion of potassium as occurs in renal failure, due to translocation from the ICF as is seen after succinylcholine administration or acidosis or increased intake. These are listed in Table 11.11. The main clinical effects of concern are on the cardiac muscle and skeletal muscle. ECG changes (Fig. 11.12) characteristic of delayed depolarisation appear at levels of 7 mEq/L and above. Changes progress from tall, peaked T waves, usually with a shortened Q-T interval,

179

to widening of the QRS complex, prolongation of P-R interval, S-T segment depression or elevation, VF and asystole. Skeletal muscle weakness occurs due to sustained spontaneous depolarisation and inactivation of the Na channels. It occurs above 8 mEq/L and results in ascending paralysis. At serum levels of 11–12 mEq/L before the onset of VF the ECG may resemble a ‘sine wave’. Anesth etic Considerations and Precautions Anesthetic 1. Elective surgery should not be undertaken with hyperkalemia. 2. Succinylcholine and Ringer’s lactate are contra indicated. 3. Avoid respiratory or metabolic acidosis; mild hyperventilation is desirable. 4. ECG monitoring is mandatory; neuromuscular function monitoring is desirable. 5. Use calcium gluconate, sodium bicarbonate and glucose-insulin if emergency surgery cannot wait (e.g. limb ischemia). Principles of Treatment (Fig. 11.13) -

Potassium levels above 6.5 mEq/L can be rapidly lethal and should be corrected aggressively. Underlying cause (e.g. hypoaldosteronism) should be treated (mineralocorticoid replacement).

Fig. 11.12: ECG changes of hyperkalemia

180

A PRIMER OF ANESTHESIA Table 11.11: Causes of Hyperkalemia

Spurious • Leakage from RBCs if separation of serum from clot is delayed • Thrombocytosis, with release of K from platelets • Marked elevation of white blood cells • Repeateed fist clenching during phlebotomy with release of K from forearm muscles • Blood drawn from K infusion Decreased excretion • Renal failure, acute or chronic • Severe oliguria (decreased urine output) from shock or dehydration • Renal secretory defects: SLE, renal transplant, sickle cell disease, obstructive uropathy, amyloidosis, interstitial nephritis • Hyporeninemic hypoaldosteronism or selective hypoaldosteronism (seen in AIDS) • Drugs inhibiting potassium excretion (triamterene, spironolactone, ACE inhibitors, etc.) Shift of potassium from tissues • Massive release of intracellular potassium (burns, crush inujury, hemolysis, internal bleeding, vigorous exercise, rhabdomyolysis • Metabolic acidosis • Hyperosmolality insulin deficiency • Hyperkalemic periodic paralysis • Drugs: digitalis toxicity, B-adrenergic antagonists, arginine, succinylcholine Excessive intake of potassium • Excessive K, orally or parenterally

-

-

-

-

Potassium intake should be stopped. Calcium supplementation (calcium gluconate 10%, preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias. Nebulised or intravenous salbutamol is a “rapidly acting catecholamine”. Catecholamines promote movement of K into cells, lowering the blood levels. β-agonists may be useful in acute hyperkalemia associated with massive transfusion, and will also provide inotropic support. Low dose epinephrine (0.5–2 mg/min) is used for this purpose. Insulin and dextrose (e.g. 20 Units of insulin and 50 ml 50% dextrose) act similarly, leading to a shift of potassium ions into the intracellular compartment. Some of the glucose transport mechanisms bring a K ion

-

-

into the cell with each glucose molecule transported. This mechanism takes 1 hour for peak effect. When metabolic acidosis is present, IV sodium bicarbonate (1-2 mEq/kg) can decrease plasma K+ in 15 min. Polystyrene sulfonate (Calcium Resonium, Kayexalate) is a binding resin that binds K within the gut and removes it from the body in feces. Calcium Resonium (15 g three times a day in water) can be given by mouth. Kayexelate can be given by mouth or as an enema. In both cases, the resin absorbs K within the gut and carries it out of the body. Refractory or very severe cases may need dialysis to remove the potassium from the circulation. When mineralocorticoid deficiency is responsible, high dose hydrocortisone and intravenous saline solution may be all that is necessary.

FLUID THERAPY AND TRANSFUSION

Fig. 11.13: Management of hyperkalemia

181

182

A PRIMER OF ANESTHESIA

HYPERCALCEMIA AN D HYPOCALCEMIA AND Hypercalcemia- causes, Treatment and Anesthetic Implications Normal plasma calcium is 8.5–10.5 mg/dl (2.1– 2.8 mmol/L). Ionised calcium is normally 4.75– 5.3 mg/dl (1-1.3 mmol/L). Levels of ionised calcium is affected by plasma albumin (each increase or decrease of albumin by 1g/dl increases or decreases total calcium by 0.8–1 mg/dl), or by pH (each decrease of 0.1 unit pH increases ionised calcium by 0.36 mmol/L). Ionised calcium fraction is the physiologically active calcium. Causes of Hypercalcemia (Table 11.12) The commonest cause is hyperparathyroidism which may be primary or secondary to renal failure. Patients are usually extremely debilitated and bedridden. They may have multiple fractures or renal stones (which is how the condition is usually diagnosed). They may have poor intravenous access (due to fractures and casts) and may not be able to sit up on account of debility or vertebral fractures. These factors increase their perioperative morbidity and mortality. Clinical Manifestations The common symptoms are fatigue, anorexia, nausea, vomiting, weakness and polyuria. Irritability, ataxia, lethargy or confusion precede Table 11.12: Causes of hypercalcemia Common causes of hypercalcemia Hyperparathyroidism Renal failure Thyrotoxicosis Granulomatous diseases Milk-alkali syndrome disease Vitamin D or A intoxication Familial hypocalciuric hypercalcemia

Immobilization Thiazide diuretics Lithium Malignancy Granulomatous Rhabdomyolysis

Fig. 11.14: Short Q-T interval in hypercalcemia

coma. Patient may have concomitant pancreatitis, peptic ulcer disease or renal stones/ renal failure. Terminal hypotension is preceded by hypertension. A short ST segment and shortened QT (Fig. 11.14) interval are the salient ECG findings. Hypercalcemia sensitises the myocardium to digoxin. Treatment Symptomatic hypercalcemia requires aggressive treatment. The most important initial treatment is rapid hydration with normal saline and administration of a loop diuretic to ensure brisk diuresis. The management plan can be followed on the flow chart (Fig. 11.15). Rarely emergency parathyroidectomy may be indicated if conservative measures fail to reduce serum calcium levels. Anesthetic Considerations for Hypercalcemia 1. Hypercalcemia is a medical emergency and should be treated before elective procedures. 2. Hypercalcemic patients require careful volume monitoring as they are on diuretics. 3. Concomitant monitoring of K+ and Mg+ should be done. 4. Acidosis should be avoided as it can increase hypercalcemia. HYPOCALCEMIA The causes of hypocalcemia are outlined in Figure 11.16. Clinically, the commonest observed cause of hypocalcemia is citrate intoxication consequent to massive blood transfusion and following total thyroidectomy, where removal of parathyroids results in fall in

FLUID THERAPY AND TRANSFUSION

Fig. 11.15: Management of hypercalcemia

183

184

A PRIMER OF ANESTHESIA

Fig. 11.16: Causes of hypocalcemia

serum calcium usually 12–24 hours after surgery. Clinical symptoms 1. The clinical symptoms arise primarily due to increased neuromuscular irritability secondary to a decrease in ionized calcium. 2. Patients usually complain of numbness and tingling sensations in the perioral area or in the fingers and toes. 3. Muscle cramps are common in the back and lower extremities and may progress to carpopedal spasm (ie, tetany). 4. Neurological symptoms, including irritability, impaired intellectual capacity, depression, and personality changes, may be present. 5. Seizures of all types can occur in patients with hypocalcemia. 6. Respiratory disturbances may develop from laryngospasm and bronchospasm. 7. Other complaints may include hypotension and symptoms of heart failure. ECG reveals a prolongation of QT interval and ST-T changes mimicking myocardial ischemia in severe hypocalcemia (Fig. 11.17); these changes revert after calcium replacement. Figure 11.18 shows you all the clinical signs elicited in a patient with hypocalcemia.

Fig. 11.17: Prolonged Q-T in hypocalcemia

Starting from above left, clockwise: 1. Trousseau’s sign (carpopedal spasm) on inflating blood pressure cuff, 2) Chvostek’s sign (spasm of facial muscles and masseter spasm on tapping the facial nerve), 3) Vocal cord adduction (stridor), 4) Neonatal tetany or seizures, 5) Retinal and ECG changes (prolonged Q-T interval) and 6) hyper reflexia. Treatment of hypocalcemia is outlined in the Fig. 11.19.

FLUID THERAPY AND TRANSFUSION

Fig. 11.18: Clinical signs in hypocalcemia

185

186

A PRIMER OF ANESTHESIA

Fig. 11.19: Management strategy for hypocalcemia (serum Ca2+< 8–8.5 mg/dl or 2 mmol/l)

FLUID THERAPY AND TRANSFUSION

Anesthetic Considerations 1. Hypocalcemia should be corrected preoperatively. 2. Alkalosis and hypothermia should be avoided to prevent further fall in ionised calcium. 3. Calcium replacement should be judiciously done after rapid and/or massive blood or albumin transfusion. 4. Neuromuscular block monitoring is essential as these patients are very sensitive; dose modification may be required.

187

5. Tracheal extubation should be done with care; post-operative intubation may be necessary till calcium levels stabilize. 6. Negative inotropic effect of intra venous and inhalational anesthetics may be exaggerated. Thus, the wide-ranging and clinically significant impact of electrolyte abnormalities has to be understood by the anesthesiologist in order to provide optimum anesthesia care and post operative recovery. Phosphate, bicarbonate and acid-base disorders are also important but are outside the purview of this text. Standard physiology textbooks may be consulted for these disorders.

Post-anesthesia Care Preethy Mathew

      

General design of PACU Outline of patient management Complications in the postoperative period Respiratory problems Circulatory problems Nausea and vomiting Hypothermia and shivering

INTRODUCTION The residual effects of either general or regional anesthesia, wear off over a period of time (few minutes to few hours) after surgery. During this period, the body homeostatic mechanisms restore the alterations in physiology induced by anesthesia and surgery: essentially a period of physiologic stabilization. This duration is one of potential, yet considerable danger to the patient and is therefore a mandatory period of highintensity care when the patient is observed closely and continuously until fully conscious, the vital parameters are stable and can be preserved without assistance. The anesthesiologist supervises this period of patient care. Where is the Patient Observed during Postoperative Period? The observation room, often called post anesthesia care unit (PACU) is close to the operating room and part of the ‘clean’ area,

permitting surgeons and anesthetists to be nearby and allowing rapid return of the patient to the operating room if necessary. Patient monitoring equipment includes continuous electrocardiography, sphygmomanometer and pulse oximeter at each bed. An adequate and accessible supply of emergency drugs, equipment for airway management (oral and nasal airways, endotracheal tubes and tracheostomy tubes, laryngoscopes, AMBU bags) and defibrillator is essential. Each bed has its dedicated oxygen supply point to which a face mask, or if needed a ventilator can be attached; suction facility should be available. General Management The patient’s prior health status, nature of surgical procedure and intraoperative events guide the duration as well as nature of postoperative care: sicker patients and extensive surgery require higher level of care. Based on this, postoperative care can be divided into two phases: Phase I—where monitoring should be equivalent to an intensive care unit, and Phase II—where transition is made from intensive observation to stabilization for care in a surgical ward or at home. At the end of the surgical procedure, the patient’s trachea is extubated and the patient is transported to the post anesthesia care unit on a stretcher (gurney) accompanied by the attending anesthesiologist. During transfer, the

192

A PRIMER OF ANESTHESIA

patient is ideally transported in the lateral position with head extended (‘safe’ position: Fig. 12.1) to minimize the risk of airway obstruction or aspiration of gastric contents from vomiting. The patient undergoes continuous evaluation in the PACU by monitoring of consciousness, oxygenation, ventilation, circulation and temperature. In addition to monitoring vital parameters, surgical aspects like bleeding, drain output, wound soakage are assessed and any relevant complications of specific procedures (e.g. gut perforation or bladder perforation after endoscopy) are looked for. The awake patient is usually nursed in the supine propped-up position to improve lung mechanics. Exceptions to this position are patients with risk of bleeding into the airway, excessively drowsy patients and patients who have received subarachnoid block. Care should be taken to avoid flexion of the neck as it may cause airway obstruction. The lateral position with head-down tilt is the safest for the airway, with one or the other knee drawn up to prevent rolling (Fig. 12.1). Oxygen administration is indicated in all patients after major surgical procedure, and also in situations of known or suspected decrease in PaO2 or SaO2. A patent airway should be ensured until patient recovers full consciousness wherein

Fig. 12.1: The lateral (Safe) position during recovery from anesthesia

ability to maintain airway spontaneously is present and the pharyngeal and laryngeal protective reflexes are active. A ‘patent airway’ means that there is unobstructed air movement into the patient’s chest. This can be clinically assessed by feeling for the normal movement of air at the nostril or the mouth during expiration. Breathing through a patent airway is smooth, devoid of abnormal sounds and accompanied by regular and good chest excursions. On the other hand, an obstructed airway is indicated by absence of such air movement, snoring or noisy breathing, absent or abnormal chest excursions. If simple maneuvers like extending the head or tilting the chin do not improve the situation, the patient has to be carefully observed for signs of worsening airway obstruction and managed accordingly. Patency of intravenous access should be maintained by running the fluid drip continuously. The blood and extracellular fluid loss during surgery and the adequacy of replacement in the intraoperative period guide the amount of fluid to be administered. In addition, maintenance volume for the postoperative period as well as replacement for postoperative losses is infused. Urine output is a useful guide, as well as CVP, if central venous access is in place. Onset of tachycardia, altering sensorium, cold and pale extremities also indicate significant blood loss which may be visible or concealed. Pain remains the most common and most important issue in the postoperative period. Ineffective and inadequate analgesia delays recovery and affects the quality of life in the postoperative period. The site of surgery influences the severity of pain: thoracotomy and upper abdominal surgery tend to be more painful than limb surgery. Opioids are the first line of analgesics in the postoperative period. They may be administered as intermittent intramuscular or intravenous boluses or continuous intravenous infusion. Patient controlled analgesia is an excellent option that allows the patient to determine the timing of

POST-ANESTHESIA CARE

analgesic doses and thus improves titration of analgesia. NSAIDs, though not as potent as narcotics, are useful adjuncts to opioids. Narcotics administered in the epidural space have the advantages of effective and prolonged analgesia. The patients are observed until they are fit to be discharged to the surgical ward. The recovering patient is fit for the ward when awake and extubated, is arousable and can respond appropriately, can lift the head on command, is breathing quietly and comfortably, is not hypoxic and has satisfactory pulse and blood pressure. Complications related to the procedure should be ruled out, ensuring that tubes, drains and catheters are functioning properly. Patients who receive regional anesthesia should be able to move and perceive touch in the blocked extremities. The steps of management of a patient recovering from general anesthesia are summarized in Table 12.1. COMPLICATIONS 24-30% of the patients observed may develop a complication in the postoperative phase. Greater ASA physical status tends to have a higher incidence of complications. The complications may be grouped as: respiratory, circulatory, failure to regain consciousness, nausea and vomiting, hypothermia and shivering, and miscellaneous issues. Table 12.1: Steps in management of patient after general anesthesia 1. Administration of oxygen 2. Position-Propped-up, if awake Head down and lateral, if drowsy 3. Record of vital parameters- heart rate, blood pressure, respiratory rate and pattern, oxygen saturation 4. Intravenous fluid administration 5. Ensure adequate pain relief 6. Look for surgical bleeding, drain output, etc.

193

What are the Possible Respiratory Complications? The majority of complications in PACU are related to the respiratory system and include airway obstruction, hypoxemia and hypoventilation. The risk factors for these complications following general anesthesia are age older than 60 years, obesity, emergency surgery, prolonged surgical procedures and heavy opioid or sedative medications. i. Airway obstruction: The most common cause of postoperative airway obstruction is pharyngeal obstruction caused by the tongue falling back on the posterior pharyngeal wall. Laryngeal obstruction may occur due to laryngospasm, direct airway injury or vocal cord paralysis. L aryngospasm is more common in children, in light planes of anesthesia and in the presence of blood or secretions in the pharynx. Direct airway injury results from multiple intubation attempts or prolonged intubation and is more common in children. Edema of the upper airways may present as sore throat and hoarseness progressing to respiratory stridor and dyspnea. Intrinsic compression, as from a rapidly expanding wound hematoma after thryoid surgery gives rise to life threatening airway obstruction. ii. Hypoxemia: Measurement of arterial oxygen saturation with the pulse oximeter provides early and reliable detection of hypoxemia and is now the standard of care in postoperative period. The common causes of hypoxemia can be severe airway obstruction, atelectasis (i.e. collapse of entire lung or lobe or segment), bronchial obstruction with secretions, or pneumothorax. Other important causes of hypoxemia are pulmonary edema and pulmonary embolism. Postoperative shivering increases oxygen consumption by 300–500% and contributes to hypoxemia.

194

A PRIMER OF ANESTHESIA

Table 12.2: Causes of postoperative hypoventilation 1. Inadequate central respiratory drive Inhalational induced Narcotic induced 2. Inadequate function of respiratory muscles Inadequate reversal of neuromuscular blocking agents Inadequate analgesia resulting in respiratory splinting Obesity Tight dressings/ Body casts 3. Intrinsic lung disease 4. Increased CO2 production Hyperthermia, Thyrotoxic crisis.

iii. Hypoventilation: Hypoventilation is defined as reduced alveolar ventilation resulting in an increase in arterial CO2 tension (Pa CO2). The causes are listed in Table 12.2. How do you Manage a Patient with Respiratory Compromise? Prompt recognition and management of these life-threatening situations are crucial. All patients with any form of respiratory complication should receive oxygen by facemask. Prop-up the patient to alter the ventilation-perfusion ratio favorably. Airway obstruction is initially managed with a combination of backward tilt of the head (head extension) and anterior displacement of the mandible (jaw thrust). If the obstruction is not immediately reversible, a nasal or oral airway should be inserted. If the airway cannot be opened by simple maneuvres, positive-pressure ventilation with a bag, mask, and 100% oxygen is indicated. During management of airway obstruction using any maneuvre, one must target for regular and good chest excursions. If a bag and mask are used to supplement oxygen, then bag movement is a good indicator of airway patency. Orotracheal intubation is necessary if these measures fail. Airway edema secondary to trauma responds to aerosolized racemic adrenaline

(2.25%). Some experts recommend the use of corticosteroids. Laryngeal spasm may be relieved by continuous positive airway pressure (CPAP) or a small dose (0.2 mg/kg) of suxamethonium and assisted ventilation till spontaneous ventilation results. Management of airway obstruction secondary to external compression of larynx or trachea by a tense hematoma (e.g. following thyroidectomy, cervical dissection) is a surgical emergency and demands urgent evacuation of the hematoma under local infiltration anesthesia. In the event of hypoxemia and hypoventilation without airway obstruction, evaluate and treat the cause. Chest auscultation, a portable chest roentgenogram (X-ray) and arterial blood gases are valuable tools. Hypoxemia due to atelectasis may be managed by humidifying inspired gases and encouraging the patient to cough with the help of chest physiotherapy, deep breathing and incentive spirometry. If hypoxemia persists (PaO2 < 60 mmHg) despite maximal oxygen therapy (FiO2=1.0), tracheal intubation and assisted ventilation may be required. The treatment of pneumothorax depends on the size of the pneumothorax and the patient’s condition. A 10–20% pneumothorax in a spontaneously breathing patient can be observed for any increase or clinical deterioration. A pneumothorax of >20% in a spontaneously breathing patient or any pneumothorax in a mechanically ventilated patient should be treated by insertion of an intercostal drainage. Tension pneumothorax with circulatory compromise should be relieved immediately using a large gauge needle until a chest tube is inserted. Narcotic induced respiratory depression can be reversed with naloxone. Pain management with nerve block or epidural analgesia prevents respiratory embarrassment due to surgical pain. Inadequate reversal of neuromuscular blockade can be prevented by ensuring adequate neuro-

POST-ANESTHESIA CARE

195

Table 12.3: Management of specific respiratory complications Complication

Intervention

Pharyngeal obstruction

Head extension + Jaw thrust Oral/ Nasal airway Continuous positive airway pressure Suxamethonium 0.2 mg/kg Aerosolized racemic adrenaline Humidified oxygen Chest physiotherapy Encourage coughing, and deep breathing Intercostal drainage Morphine + diuretics Naloxone Administer additional neostigmine + glycopyrrolate Additional narcotics: IV, IM, epidural Consider adding NSAIDs

Laryngospasm Airway edema Atelectasis Pneumothorax Pulmonary edema Narcotic induced respiratory depression Inadequate reversal of neuromuscular blockade Inadequate analgesia

muscular recovery using bedside clinical testssustained head lift, eye opening, hand grasping/ tongue protrusion for several seconds. Table 12.3 lists the common respiratory complications that one may encounter and the recommended specific interventions. Circulatory Complications Patient and surgical risk factors are more contributory than anesthetic factors in the development of cardiovascular problems in the postoperative period. Hypotension Low blood pressure is a common problem. Ensure that the low blood pressure is not an artifact of an improperly placed or incorrectsize blood pressure cuff or an error of blood pressure measurement. Hypovolemia is the most common cause and is often accompanied by rapid and thready pulse, cold clammy skin, pale or grey color, disorientation, restlessness or anxiety resulting from cerebral ischemia and possibly rapid and shallow respiration. How do you Manage a Patient with Hypotension? The algorithm depicted in Figure 12.2 may be useful.

Hypertension Hypertension is frequent in patients with previous history of hypertension. The causes in a previously normotensive patient are pain, hypercapnia, hypoxemia and bladder distension. Significant hypertension should be treated to prevent further cardiac complications and should be directed at finding the cause and correcting it. If no correctable cause is found, initiate drug therapy. Systolic pressures over 180 mmHg and diastolic pressures exceeding 120 mmHg in previously normal patients are accepted as levels requiring treatment. β-blockers-(metoprolol, esmolol), vasodilators(sodium nitroprusside, nitroglycerine), labetalol and diltiazem are some of the drugs that may be employed. Dysrhythmias The common dysrhythmias during the post-op period are sinus tachycardia, sinus bradycardia and ventricular premature beats. Ventricular tachycardia and supraventricular tachyarrhythmias are rare, but life threatening. Obvious causes such as hypokalemia, hypoxemia, hypercapnia, metabolic acidosis or pre-existing heart disease should be looked for and treatable conditions corrected. The management has to

196

A PRIMER OF ANESTHESIA

Fig. 12.2: Approach to hypotension

be two-fold: (1) Treatment of the arrhythmia and (2) Treatment of the underlying cause. Electrocardiographic Changes Nonspecific T wave flattening or inversion, ST segment depression may be encountered in a postoperative patient. These should be compared with the pre-operative ECG, if available. These changes are not always due to myocardial ischemia but may result from cold, stress, electrolyte abnormalities and drug effects. However, one must rule out a myocardial event with the help of enzyme studies (Trop-T, CPKMB) and serial electrocardiograms.

Failur e to Regain Consciousness Failure The residual effect of anesthetics, sedatives and preoperative medications is the common cause for persistent somnolence in the postoperative period. Management includes pharmacologic reversal aimed at the most likely sedative drug: naloxone for narcotics and flumazenil for benzodiazepines. Once pharmacologic etiology is ruled out, metabolic and structural causes must be sought. Hypothermia (temperature 20% in a spontaneously breathing patient is to be drained. 7. Hypovolemia is not accompanied by a. Rapid and thready pulse b. Cold, clammy skin c. Rapid and shallow respiration d. Capillary refilling time < 2 seconds.

8. A 42-year-old female patient underwent laparoscopic cholecystectomy under general anesthesia. In the postoperative period, the recovery staff observed a pulse rate of 106/min and blood pressure of 156/110 mmHg. The following reasons are to be ruled out except: a. Pain b. Hypercapnia c. hypervolemia d. Bladder distension. 9. If a patient develops ST segment depression on continuous electrocardiography monitor, which of the following is not warranted immediately: a. Order for 12 lead electrocardiography b. Compare with pre-op electrocardiography c. Rule out electrolyte abnormalities d. Order CPK-MB enzyme levels. 10. Which of the surgical procedures has a high incidence of postoperative nausea and vomiting? a. Fixation of fracture femur b. Breast surgery c. Strabismus surgery d. Inguinal hernia repair. 11. In the event of vomiting after general anesthesia, the following steps are to be done except: a. Put the patient in Trendelenburg position b. Turn the patient lateral c. Apply suction to the oropharynx d. Turn the patient prone. 12. Which of the following is not true about shivering? a. Is commonly caused by hyperthermia b. Is commonly caused by hypothermia c. Increases oxygen demand of the body d. Increases carbon dioxide production.

POST-ANESTHESIA CARE

199

13. Which of the following physiological alterations is present in hypothermia? a. Generalized vasodilatation b. Systemic vasoconstriction c. Hypotension d. Metabolic alkalosis.

15. Propped up position is not advised in the following situations except: a. Risk of bleeding into the airway b. Obese patient c. Excessively drowsy patient d. After subarachnoid block.

14. Oxygen administration to the patient is not indicated after: a. Inguinal hernia repair in a 30-year-old b. Inguinal hernia repair in a 3-year-old c. Laparoscopic cholecystectomy d. Mastoidectomy.

Answers 1. 5. 9. 13.

a b d b

2. 6. 10. 14.

b b c a

3. 7. 11. 15.

d d d b

4. c 8. c 12. a

Oxygen Therapy Rajeshwari Subramaniam, K Nirmala Devi

     

Objectives of oxygen therapy Assessment of patient requiring oxygen therapy Classification of oxygen delivery systems Low flow systems High flow systems Calculation of FiO2 in entrainment systems

A patient on an oxygen mask or receiving oxygen through a nasal cannula is a common sight in hospital wards. This chapter aims at enumerating goals of oxygen therapy, various devices to provide it with their function, advantages and limitations. Further, it can guide selection of appropriate mode of therapy. Objectives of Oxygen Therapy • To correct acute hypoxemia (due to any cause) • To provide symptom relief in chronic hypoxemia by – reduction of dyspnea – improving mental alertness – reducing angina – reducing fatigue • To reduce cardiopulmonary workload by – reduction in work of breathing – reduction in myocardial work – reduction in pulmonary vasoconstriction – reduction in right ventricular strain.

How does One D etermine whether a Determine Patient Needs Oxygen? This is decided by evaluating clinical signs of hypoxemia, assessing the severity of the clinical situation, and by laboratory testing of arterial blood gas values. Clinical signs of hypoxemia are shown in Table 13.1. Clinical Situations which may be Associated with Hypoxemia • • • • • •

Postoperative patient CO poisoning Shock Trauma Sepsis Acute myocardial infarction (AMI).

Laboratory and Bedside Measurements to Diagnose Hypoxemia a. Adults, children and infants>28 days of age: PaO2 5 μm) can occur in H- influenza type B, Mycoplasma pneumonii and Rubella infections. 3. Contact precautions apply to direct skin to skin or mucous membrane to skin contact, e.g. Conjunctivitis, large abscesses, herpes simplex. Decision for postexposure prophylaxis (PEP) is taken based on the flow chart shown (Fig. 14.9). Determination of the Exposure Code (EC) (Fig. 14.9)

Post-exposure Management Contact can occur due to: • Percutaneous inoculation • Contamination of an open wound

INFECTION AND THE ANESTHESIOLOGIST

213

Fig. 14.9: Determination of exposure code (EC)

• Contamination of breached skin • Contamination of mucous membrane including conjunctiva. First Aid • Allow to bleed in case of needle stick injury. Wash with water and apply antiseptic. Splashes to the nose, mouth, eyes and skin should be flushed with saline, water or sterile irrigants. • Do not put pricked finger in mouth reflexly. • Report all spills/accidents to supervisor. • Keep medical records of all such events.

• Easy access to medical advice and counseling should be available. • Laboratory testing after consent and counselling, within 2 weeks, 6 weeks, 12 weeks, 24 weeks and 1 year. For ECI category, with low chance of seroconversion (SC), PEP is not recommended. For EC1 with high SC and EC2 basic regime is recommended. For EC2 and EC3, expanded PEP regime should be administered. Anti-retroviral therapy: To be started in case of suspected injury from HIV patient.

214

A PRIMER OF ANESTHESIA

Basic regime: Zidovudine 600 mg/day in 2 to 3 divided doses with Lamivudine 150 mg twice daily. In cases with drug resistance/EC2/EC3, expanded regime with Indinavir 800 mg thrice daily for 4 weeks is to be taken. What Measures should be taken when Exposure to a HBV-positive Patient s Blood Occurs? For non-vaccinated persons sustaining a percutaneous inoculation to HBSAg positive blood, a single intramuscular (IM) dose of HBIG, 0.06 ml/kg is administered within 24 hours followed by a complete course of hepatitis B vaccine within the first week of exposure. Pre-exposure prophylaxis of hepatitis B vaccine is recommended at 0, 1, and 6 months (intramuscularly). Anti-HBs titre of > 10 mIu/ ml (micro international unit) confers long-term protection. For hepatitis C no effective measure is recommended. (Standard serum globulin may be valuable in the dose of 0.12 ml/kg I/m up to 10 ml. CONCLUSION Anesthesiologists and intensivists have constant contact with broad range of patients many of whom may be HIV, HBV or HCV seropositive. Hence, rigorous infection control is imperative for self protection as well as to prevent accidental transmission of infection from one patient to another. If exposure does occur PEP should be followed. MCQ MCQss 1. Which procedure has the highest risk of causing infection to the anesthesiologists. a. 3 in 1 block b. Ankle block c. Subarachnoid block d. Epidural block

2. Risk of transmission of HIV through needle stick injury is: a. 0.03% b. 0.003% c. 0.3% d. 3% 3. Risk of transmission of Hepatitis B via needle stick injury a. 0.3% b. 3% c. 30% d. 300% 4. Risk of transmission of Hepatitis C is: a. 0.02% b. 0.3% c. 30% d. 3% 5. Most commonest cause of transmission of blood borne infections in anesthesiologist a. Needle stick injury b. Intubation c. Mouth to Mouth resuscitation d. Tears of patients 6. Double gloving reduces risk of transmission by a. 10 times b. 5 times c. 20 times d. 50 times 7. Type of needle causing maximum transmission of infection is: a. Solid bore needle b. Hypodermic needle c. Cannula stillete d. Phelebotomy needle 8. First measure to be taken following needle stick injury is: a. Allow it to bleed b. Wash with saline c. Put finger in the mouth d. Wash with spirit

INFECTION AND THE ANESTHESIOLOGIST

9. What are the precautions taken to prevent needle stick injuries called: a. Transmission based precaution b. Universal Precaution c. Double standard precautions d. Prevention 10. Transmission based precautions are used in which of the following disease: a. Herpes simplex b. HIV c. Hepatitis d. Conjunctivitis 11. Infected sharps should be kept in: a. 0.02% bleach b. 0.1 % bleach c. 10 % bleach d. 5% bleach 12. If large volume contact occurs through compromised skin it is referred to as a. EC1 b. EC2 c. EC3 d. EC4

215

13. PEP for HIV infection includes : a. Zidovudine b. Zidovudine + Lamivudline c. Lamivudine d. Zidovudine + Lamivudine + indinavir 14. Anti-Hbs titre for long term protection should be more than a. > 10 mIu/ml b. 1-9 mIu/ml c. 0.1-1 mIu/ml d. 1 mIu/ml 15. Dose of HBIG following exposure to hepatitis B is a. 0.08 ml/kg b. 0.06 ml/kg c. 0.05 ml/kg d. 1 ml/kg Answers 1. 5. 9. 13.

c a b d

2. 6. 10. 14.

c b a a

3. 7. 11. 15.

c b b b

4. d 8. a 12. b

Care of the Patient in the ICU Sumesh Arora

 

       

Design and staffing of ICU Monitoring in the ICU: Cardiovascular, respiratory and neuromonitoring Infection control Respiratory care: ventilatory modes Cardiovascular care: uses of PAC Classification of shock states Septic shock-diagnosis and management Renal failure and replacement therapies Nutrition in the ICU Ethical issues and care of the dying patient

DESIGN OF THE INTENSIVE CARE UNIT [ICU] Most intensive care units have 10–12 beds. The beds are a combination of (i) open ward beds and (ii) isolation rooms for patients who have contagious infections (e.g. meningococcus), infections due to multi-drug resistant bacteria (e.g. Methicillin resistant Staph. aureus), or those more prone to infections (e.g. immunosuppressed patients). Each bed area in the open ward should be at least 21 m2. In single rooms, in addition to the bed area, additional space is required for hand washing, gowning, and seating of the staff.

Each bedside is equipped with a monitor and facilities to connect and operate a ventilator. Oxygen, air, suction and electrical power outlets are provided at all bedsides. At least some bed areas should be equipped with water supply for dialysis. Monitoring and drug charts are kept near the foot end of the bed. There are separate areas for viewing imaging studies and for storing clean and dirty equipment. A separate room/ area is desirable for holding discussions with the family. STAFFING IN THE ICU Intensive care is a team approach. Broadly, the intensive care team consists of doctors, nurses, administrative staff, technicians and ancillary staff. In an open ICU, any physician/surgeon with admission rights in the hospital may direct the care of patient and bears the overall responsibility of the patient management in the ICU. In a closed ICU, the intensivist, who is a physician (or anesthesiologist) bears the overall responsibility of management of the patient. The intensivist does the ward round every day, and the primary team provides specialist support. This allows for easier implementation of management protocols, improves efficiency and possibly improves outcome. In a transitional unit, both intensivist and patient’s admitting physician share patient care and responsibility.

220

A PRIMER OF ANESTHESIA

MONITORIN G IN THE INTENSIVE CARE MONITORING UNIT

Fig. 15.1: A hemofiltration unit

Critically ill patients generally have limited mobility, require multiple drugs and undergo multiple procedures (Fig. 15.1). The need for adequate number of trained nursing staff cannot be overemphasized. Ideally, one nurse should care for one patient, but this generally depends upon the available nursing resources. An ICU with technical staff like respiratory technicians who look after ventilator management, weaning protocols etc. may improve outcome. The administrative staff looks after the records, research work and other administrative needs of the unit. The ancillary staff consists of social workers, equipment in- charge, cleaners, wards persons etc. They are also important components of the ICU team. ADMISSION TO INTENSIVE CARE UNIT Patients may be admitted to Intensive care unit from the emergency department, operation suite, any hospital ward or from another hospital. Appropriate patient selection is important to derive maximum benefit out of the available (and usually limited) resources. Patients who only need monitoring may be managed in a high dependency unit (HDU). Critically ill patients for whom intensive care is likely to be futile [e.g. with advanced metastatic malignancy] should not be admitted to ICU.

Respiratory system monitoring: Most of the patients in the ICU will be on ventilatory support. Adequacy of oxygenation is monitored continuously by pulse oximetry; while adequacy of ventilation is monitored by end tidal CO2. The shape of the end tidal CO2 curve may provide additional information about position of the endotracheal tube after intubation, disconnection, expiratory airway obstruction and breathing efforts made by a paralyzed patient. Modern ventilators are equipped with a monitor that displays information about airway pressure, flow rate, tidal volumes and dynamic relations like flow-volume curve and pressure-volume curves. These curves give information about airway resistance and compliance of the respiratory system. Cardiovascular monitoring: Lead II and a chest lead are generally monitored continuously. Lead II is generally most helpful for the diagnosis of arrhythmia. The ST segment may be monitored for diagnosis of ischemia. Measurement of blood pressure may be done non-invasively or invasively using intra-arterial catheter. Beat to beat intra-arterial blood pressure is measured for patients who are hemodynamically unstable, are on vasopressors, or if non-invasive blood pressure measurement is likely to be inaccurate [e.g. in the very obese, or at very low blood pressure]. Pulse pressure variation with respiration on intra-arterial blood pressure trace may give additional information about the intravascular volume status. Central Venous Pressure [CVP] is the intravascular pressure in the great thoracic veins. It is the equivalent of right atrial pressure and in the absence of tricuspid valve disease is a measure of right ventricular preload. It is measured at the level of fifth intercostal space in the mid-axillary line [Phlebostatic axis; Fig. 15.2]. Most of the patients in the ICU have

CARE OF THE PATIENT IN THE ICU

221

Fig. 15.2: The phlebostatic axis

Fig. 15.4: CVP trace with, a, c and v waves

Fig. 15.3: A triple lumen central venous catheter (CVC)

central venous catheters (CVC; Fig. 15.3), which may be connected to a transducer to measure CVP (Fig. 15.4). Positive pressure ventilation affects CVP by changes in intrathoracic pressure. CVP increases in inspiration because of increase in intrathoracic pressure. To minimize the effect of mechanical ventilation, CVP should be recorded at end expiration. Because of multiple factors affecting the absolute CVP value [Intrathoracic volume, venous tone, right ventricular function, cardiac rhythm and tricuspid valve disease] trends of CVP are more useful than a single value for assessment of intravascular volume status.

Fig. 15.5: A pulmonary artery catheter (PAC)

Pulmonary artery catheter [PAC; Fig. 15.5] is a balloon tipped, flow directed multi-lumen catheter. The PAC gives direct information about three important parameters: • Pulmonary artery wedge pressure [PAWP; Fig. 15.6]. • Cardiac output • Mixed venous oxygen saturation. The catheter has a balloon at the tip. The initial part of the insertion procedure is like that

222

A PRIMER OF ANESTHESIA

Fig. 15.6: The PAC with balloon deflated (left half trace) and balloon inflated (right half trace)

of a central venous catheter in one of the central veins [Commonly right internal jugular vein or left subclavian vein]. When the tip of the catheter reaches the right atrium [this is made out by the pressure tracing and waveform on the monitor Fig. 15.6], the balloon is inflated with air. This makes the tip of the catheter very light so that it can be floated by the flow of blood. It follows a path through the right side of the heart to the pulmonary artery until the balloon wedges in one of the branches. In this position, the lumen that opens at the tip of the catheter is now in contact with an uninterrupted blood column up to the left atrium (there are no valves in the pulmonary venous system). This pressure is called pulmonary artery wedge pressure [PAWP]. It gives an assessment of left atrial pressure, which is approximately equal to the left ventricular end-diastolic pressure (LVEDP) in the absence of mitral valve disease. The LVEDP gives an estimate of how well filled the left ventricle is, and also its compliance. Cardiac output is measured by thermodilution technique. Blood in the pulmonary artery is called mixed venous blood. It represents mixed deoxygenated blood from entire body. Mixed venous oxygenation is directly proportional to cardiac output. If the cardiac output is low, mixed venous saturation drops. Mixed venous oxygen saturation less than 65% may indicate low cardiac output. Trends of mixed venous oxygen saturation can be used to follow response to therapy in patients with shock. However the use of the PAC is not without risk. In addition to all

complications associated with CVC, the risks specific to pulmonary artery catheter are balloon rupture, air embolism, catheter knotting, pulmonary infarction [1.3%], pulmonary artery rupture [0.1-0.2%] and a high incidence of arrhythmias including transient right bundle branch block. Hemoptysis in a patient with PAC may indicate pulmonary artery rupture. Despite numerous studies, monitoring with PAC has not shown to improve patient outcome and the benefits should be balanced against risks in individual patients. Other common methods of monitoring cardiac output are using pulse contour analysis, Transpulmonary thermodilution (PiCCO) and Lithium dilution technique (LiDCO)], esophageal doppler, and electrical impedance cardiography. Echocardiography is useful to assess intravascular volume status, ventricular function, regional wall motion abnormalities, valvular function and for diagnosis of infective endocarditis. It is not strictly a monitoring tool, but its use in ICU is increasing. Many intensivists are now trained to do echocardiography. Neuromonitoring: Glasgow Coma Score [GCS] is a simple and objective clinical method to monitor the level of consciousness. Patients with status epilepticus require continuous monitoring of the EEG to monitor seizure frequency, which may occur without any motor manifestations. EEG is also used to monitor patients with severe head injury who are treated with barbiturate coma for high intracranial pressure [ICP]. For patients with high intracranial pressure [e.g. with head injury], the ICP needs to be monitored. The most reliable method to monitor ICP is by an intraventricular catheter inserted in one of the lateral ventricles through a small burr hole in the cranium (Fig. 15.7). It also allows drainage of CSF if ICP is very high. Normal ICP is less than 10 mm Hg. Cerebral perfusion pressure [CPP] is the difference between the mean arterial pressure and intracranial pressure.

CARE OF THE PATIENT IN THE ICU

223

susceptible to ischemia. The catheter can measure regional glucose, lactate, glutamate and pyruvate concentrations in brain interstitium and diagnose early brain ischemia. Unlike ICP and SjvO2, microdialysis is a regional monitor of the brain and can diagnose ischemia when global indicators of ischemia are still normal.

Infection Control in ICU

Fig. 15.7: Measurement of ICP

It is a global indicator of cerebral perfusion. Above CPP 60 mm Hg, cerebral autoregulation maintains cerebral blood flow independent of blood pressure. At CPP less than 60 mm Hg, cerebral autoregulation fails and the cerebral blood flow decreases with decrease in pressure. Ventriculitis and intracranial hemorrhage are most common complications of monitoring ICP with intraventricular drains. Jugular venous oxygen saturation [SjvO2] is measured by retrograde insertion of a catheter in the jugular vein [i.e. towards the brain] so that the tip of the catheter lies in the jugular bulb. Normal SjvO2 is 55-71%. SjvO2 below 50% is considered critical and indicates decreased blood flow to brain.

Nosocomial infection [NI] refers to infection that was neither present nor incubating at the time of hospital admission. ICU patients are at high risk of acquiring NI. Taking precautions to prevent NI should be an obsession for all the health care workers in the ICU. The importance of this point cannot be overemphasized as much of ICU morbidity is due to NI. Many NI are preventable. Poor infection control practices leads to increase in number of NI and therefore higher morbidity and mortality. Hand wash is a simple and most effective measure of preventing NI (Fig. 15.8). Hands should be washed before and after every patient contact, before and after removal of gloves, after contact with blood or body fluids or contaminated items. It the hands are visibly soiled, they should be thoroughly washed with soap and

Transcranial Doppler ultrasonography measures blood velocity in one of the major arteries supplying brain. Increase in velocity of blood in cerebral arteries indicates vasospasm after subarachnoid hemorrhage. The ratio of blood flow in middle cerebral artery to an extra-cranial part of the internal carotid artery (Lindegaard ratio) can be calculated to differentiate between hyperemia and vasospasm. A ratio > 2 indicates vasospasm. Microdialysis catheters are very small caliber catheters that can be inserted into the brain parenchyma. A microdialysis catheter is inserted in those parts of the brain that are most

Fig. 15.8: Hand washing

224

A PRIMER OF ANESTHESIA

water. It hands are not visibly soiled, alcohol based hand rubs may be used. Provision of alcoholic hand rubs at the bedside ensures better compliance with hand hygiene compared to hand washing. Gloves should be worn for anticipated contact with blood, mucus membrane or contaminated items. The use of gloves does not obviate the need for hand wash, and hands should be washed before wearing and after removing gloves. Sterile precautions should be used for ICU procedures like CVC insertion. Urinary tract infection is the most common nosocomial infection in ICU. Indwelling catheters should be removed at the earliest possible. Patients on ventilator are at risk of development of ventilator associated pneumonia [VAP]. The risk increases with increased duration of mechanical ventilation. Risk of VAP can be reduced by raising the head end of the bed by 15-30°, minimizing the number of disconnections of ventilator circuit, avoiding routine change of ventilator circuit, use of heat and moisture exchange [HME] filter between ET tube - circuit connection and compliance with hand wash guidelines. Infection control in ICU requires compliance of all the members of the health care team. Even one noncompliant staff member may spread infection. Inadequate staffing particularly at night-time and overcrowding in ICU are associated with poor compliance with infection control practices in ICU. Regular teaching of the ICU staff and audit of infection control practices helps to evaluate and improve the ICU performance. RESPIRATORY ISSUES IN ICU Most of the patients admitted to ICU require intubation and mechanical ventilation. Airway: Indications of intubation are: (i) protection of airway from collapse or aspiration and (ii) positive pressure ventilation. Most

critically ill patients are considered to be ‘full stomach’. Rapid sequence intubation with cricoid pressure is usually performed. Facilities for suction, hemodynamic resuscitation and a ‘difficult airway’ cart should be available at the time of intubation. The position of the endotracheal tube should be confirmed by capnography. Patients are often hemodynamically unstable at the time of intubation. If conventional dose of anesthetic drugs are used severe hypotension may result. Positive pressure ventilation in hypovolemic patients decreases venous return to the heart and can cause severe hypotension. Large volume of fluids or vasopressors may be required for resuscitation soon after intubation. An experienced intensivist should be present at the time of intubation. POSITIVE PRESSURE VENTILATION [PPV] PPV may be delivered through an endotracheal tube or a tight fitting mask. The latter is known as non-invasive ventilation [NIV]. The best way to learn the working of a mechanical ventilator is to stand at the bedside and watch the monitor of the ventilator and the breathing pattern of the patient. The following section discusses the basic components of mechanical ventilation. Initiation of the mechanical breath: The ventilator, or patient, may initiate the breath. For patients who cannot initiate a breath, the ventilator is set to deliver timed breaths. Such a mode of ventilation is called control mode ventilation. In control mode ventilation, the ventilator controls the rate and rhythm of breathing. When the spontaneously breathing patient makes a breathing effort, the ventilator circuit senses a decrease in pressure in the circuit. The ventilator then delivers a positive pressure breath. Such a mode of ventilation is called support mode. Pressure support ventilation [PSV] is an example of this mode of ventilation. In support mode ventilation, the patient controls the rate and rhythm of breathing.

CARE OF THE PATIENT IN THE ICU

In synchronized modes of ventilation, the ventilator synchronizes with the patient effort. If the patient fails to initiate a breath, the ventilator delivers a timed breath. This mode combines the characteristics of control mode and support mode ventilation. Depth of breathing: The depth of breathing [Limit of breath] can be set in different ways. In the volume control or volume support modes, the tidal volume is set. Generally, tidal volume of 6–8 ml/kg body weight is used. In these modes, the ventilator will deliver each breath to a preset volume, regardless of the pressure required to reach the volumes. The other way to set the depth of ventilation is to deliver a breath to preset peak inspiratory pressure. Pressure control ventilation [PCV] and pressure support ventilation [PSV] are such modes. The tidal volume delivered in these modes varies from breath to breath but the peak inspiratory pressure remains constant. End of inspiration: Cycling from inspiration to expiration can be set in different ways. At the end of inspiration, the inspiratory valve of ventilator closes and the expiratory valve open, allowing the patient to exhale passively. Ventilator modes may be time or flow cycled. In the time-cycled modes, inspiratory time is set. At the end of inspiratory time, the inspiratory valve closes and the expiratory valve open. In the flow-cycled modes, [e.g. PSV] after the inspiratory flow reaches a particular fraction of the peak inspiratory flow [10–30%], the ventilator changes from inspiration to expiration. In obstructive air way disease [asthma, emphysema] adequate time should be given for expiration because of predominantly expiratory airflow obstruction. Positive end expiratory pressure (PEEP): During expiration, the alveoli have a tendency to collapse. Collapsed alveoli do not participate in gas exchange. To keep the alveoli open, positive pressure is applied to the airways during

225

expiration. This pressure is called positive end expiratory pressure [PEEP]. PEEP improves oxygenation by keeping alveoli open during expiration. In healthy lungs, 5 cm H 2O is generally sufficient to prevent alveolar collapse. In acute respiratory distress syndrome [ARDS], high PEEP is generally required. Respiratory rate and minute ventilation: Minute ventilation is the product of tidal volume and respiratory rate. CO2 removal is a function of the minute ventilation. Respiratory rate is set to achieve adequate minute ventilation and CO2 removal. Alarm settings: The following alarms are commonly set on ventilator: 1. High airway pressure: To avoid injury to alveoli form high pressure [Barotrauma]. It is generally set at 30–35 mm H2O. It is particularly important when ventilating with a volume limited ventilation mode. 2. Low airway pressure: To detect accidental disconnection or leak from circuit and hypoventilation because of leak. It is generally set at just below PEEP. 3. High minute ventilation. 4. Low minute ventilation: It is particularly important when ventilating with pressure limited mode. 5. High and low respiratory rate. Side effects of PPV: Mechanical ventilation is uncomfor table. Patients on PPV need sedation. It reduces mobility and makes patients dependent for their most basic needs. It increases nursing requirements. PPV may cause injury to the lung by excess pressure in the alveoli [Barotrauma] or excess stretching of the alveoli [Volutrauma]. Barotrauma may present suddenly as tension pneumothorax. Repeated opening and closure of alveoli may also injure the alveoli [Atelectrauma] which manifests as acute lung injury and worsening of oxygenation. PPV leads to release of inflammatory mediators from the lung that may cause systemic

226

A PRIMER OF ANESTHESIA

inflammatory response syndrome [Biotrauma]. By increasing intrathoracic pressure, PPV may reduce venous return to the heart. In hypovolemic patients, it may lead to hypotension. The endotracheal tube bypasses the defense of the upper respiratory tract and makes the patient more prone to respiratory tract infection [Ventilator Associated Pneumonia or VAP]. Weaning from mechanical ventilation: ‘Weaning’ refers to transition from ventilator support to spontaneous breathing without support. Weaning is started when the reasons for initiation of mechanical ventilation have stabilized, oxygenation and hemodynamics are stable and spontaneous breathing efforts are present. Patients on PPV should be assessed for weaning every day. There is no single method of weaning. Trials of spontaneous breathing without ventilator support or gradual reduction of PSV are established methods of weaning. Many patients are difficult to wean. Poor gas exchange, poor respiratory muscle strength or inability to clear respiratory secretions are the most obvious causes of weaning failure. Cardiac failure, malnutrition, excessive sedation, fluid overload and sepsis are other common causes of failure to wean. In ‘difficult to wean’ patients, the potential causes should be looked for and treated. For patients who have been on ventilator for a long time [>2 weeks] or who are likely to require mechanical ventilation for a prolonged period, tracheostomy may reduce the duration of mechanical ventilation and possibly improve outcome. Protocol based weaning and daily interruption of sedation may help in early weaning. Non-invasive ventilation [NIV]: NIV refers to delivery of PPV using a tight fitting mask. The mask may fit over the whole face or over the nose or over nose and mouth. It avoids intubation and the risks associated with it. NIV offers many advantages over invasive ventilation. It

may be delivered outside the ICU in ward or high dependence unit. It is discontinuous and allows patient periodic breaks from ventilation. The patient retains the ability to speak and cough. Risk of infection is less compared to invasive ventilation. NIV instituted in time may avoid intubation and invasive ventilation. For patients who have refused intubation, NIV may be used as a ceiling of therapy. Contraindications to NIV: Patients who are unable to protect their airway from aspiration or maintain a patent airway are inappropriate candidates for NIV. Similarly patients who are profoundly hypoxic, who require high PEEP to maintain oxygenation cannot be managed on NIV. Recent esophageal or upper GI surgery are contraindications for NIV. CARDIOVASCULAR ISSUES IN ICU Critically ill patients are frequently in a state of shock and require fluid resuscitation, vasopressors and invasive hemodynamic monitoring. Choice of vascular access site: For resuscitation, peripheral IV catheter [PIVC] is quick and easy to insert. The resistance to flow through a catheter is directly proportional to the length of catheter. Therefore, for the same caliber of the catheter, faster fluids can be given through the PIVC. Attempts to insert CVC during resuscitation wastes precious time without any benefit. The PIVC should be changed every 48–72 hours to reduce infectious complications. PIVCs inserted in pre-hospital care or emergency department are associated with higher risk of infectious complications and should be removed as soon as possible, preferably within the first 24 hours. A CVC generally has 3–4 lumens to allow multiple infusions. A CVC is inserted when the patient is more stable. The common sites for CVC insertion are the internal jugular, subclavian or femoral veins. CVCs in the subclavian vein

CARE OF THE PATIENT IN THE ICU

are the most comfortable, easy to nurse and have the least incidence of infectious complications. However, it is associated with maximum rate of serious complications at the time of insertion [pneumothorax and hemothorax from subclavian artery puncture]. The risk of complication is inversely related to the experience of the physician. Nowadays CVCs are inserted using ultrasound guidance which minimises or prevents complication like arterial puncture. CVCs can be kept in situ for longer duration than PIVCs.

Assessment and Management of Shock State Patients admitted to ICU are frequently hypotensive or in a state of shock. Shock results from failure to deliver adequate oxygen to the tissues. The causes are circulatory failure, severe hypoxia from pulmonary disease or failure to utilize oxygen.

Classification of shock I. Hypovolemic shock: It occurs because of reduced circulating blood volume. Loss of volume may occur from hemorrhage, third space loss of intravascular volume, diarrhea, vomiting, excessive sweating or reduced fluid intake. Shifting of fluid from one compartment to other may also manifest as hypovolemia; for example in peritonitis, fluid shifts to peritoneal space and the patient manifests signs of hypovolemia. II. Cardiogenic shock: It occurs because of impaired cardiac pump function. The causes include myocardial infarction, valvular heart disease as aortic stenosis, acute aortic regurgitation, cardiac arrhythmias, cardiomyopathy, etc. III. Obstructive shock: It results from mechanical obstruction to the cardiac output. Tension pneumothorax, cardiac tamponade and air embolism are examples of obstructive shock.

227

IV. Distributive shock: It occurs because of maldistribution of the cardiac output. Cardiac output is frequently normal or even elevated in distributive shock but the blood is shunted away from vital organs as brain and kidneys. Septic shock is the most common form of distributive shock seen in intensive care setting, but it also occurs in neurogenic shock [loss of sympathetic vascular tone] and anaphylaxis [Release of vasodilator mediators e.g. histamine and platelet activating factor].

Septic Shock Septic shock affects 10% to 15% of ICU patients and has a high mortality [50–60%]. Invasion of blood stream by microorganisms or their products triggers a complex host response characterized by activation of inflammatory and anti-inflammatory pathways, coagulation and anticoagulation pathways and initiation of endothelial dysfunction. Systemic inflammatory response syndrome [SIRS] is a term used to describe systemic response to a variety of insults. The presence of two or more of the following clinical features defines SIRS: I. Temperature > 38° C or < 36° C. II. Heart rate > 90 beats per minute. III. Tachypnea > 20 breaths/min. IV. Leucocytosis > 12000/mm3 or leucopenia < 4000/mm3 or more than 10% immature neutrophils. Sepsis is defined as SIRS due to proven or suspected infection. Severe sepsis is sepsis with end organ dysfunction [e.g. respiratory failure]. Septic shock is severe sepsis with hypotension despite adequate fluid resuscitation. Pathophysiology of septic shock: Both proinflammatory and anti-inflammatory pathways are activated in sepsis leading to vasodilatation and increased vascular permeability leading to reduced blood pressure. Activation of both

228

A PRIMER OF ANESTHESIA

procoagulant and anticoagulant pathways leads to microvascular thrombosis and a disseminated intravascular coagulation (DIC)-like picture. Endothelial dysfunction leads to release of nitric oxide which causes vasodilatation and hypotension. Relative adrenal and vasopressin insufficiency may also contribute to hypotension. Vasodilatation reduces the systemic vascular resistance and patient may have raised cardiac output despite shock. Increased capillary permeability leads to loss of intravascular volume into the third space and therefore intravascular hypovolemia. Treatment of septic shock: The treatment of severe sepsis and septic shock is based on following principles. 1. Early source control: Without early control of the source of sepsis, any therapy is unlikely to be effective. For example drainage of abscess, laparotomy for resection of gangrenous gut are essential for treatment of sepsis. 2. Early antibiotic therapy: Early antibiotic therapy reduces mortality in sepsis. If possible, appropriate specimens should be collected for culture before antibiotics are administered. However, this should not cause undue delay in the administration of antibiotics. Initial antibiotic therapy is empirical and broad spectrum based on local flora and sensitivity patterns. Later, antibiotic therapy is modified depending upon the results of culture. 3. Fluid resuscitation: Most patients with septic shock are hypovolemic and require large amount of fluid for resuscitation. Fluid requirements are frequently underestimated and patients often under-resuscitated. The importance of adequate fluid resuscitation cannot be overemphasized. Vasopressors may transiently improve blood pressure but that does not cure shock. Cardiac output remains low and organs remain hypoperfused without adequate fluid resuscitation.

The choice of ideal fluid is controversial. If the patient is significantly anemic, [Hemoglobin < 7 g/dl], packed red blood cells should be transfused both to treat anemia and as part of fluid resuscitation. Crystalloids [e.g. 0.9% saline, Ringer’s Lactate] are solutions of small molecules in water. Crystalloids freely cross the endothelium. They distribute in both the intravascular and ‘extravascular extracellular’ (interstitial) space. Colloids [e.g. dextran, starch, and albumin] are solutions of large molecules that do not freely cross the semipermeable membrane. Theoretically, colloids remain in the intravascular space whereas crystalloids distribute in both intravascular and extravascular space. Colloids seem to be an attractive choice because less fluid may be required to correct intravascular hypovolemia. However, because of increased capillary permeability in septic shock, colloids also diffuse out of the intravascular space. Colloids have not been shown to reduce mortality in sepsis. They are also significantly more expensive than crystalloids and may cause anaphylactic reaction. The choice of resuscitation fluid is influenced by individual physician’s understanding of literature, existing practice in the ICU and availability or resources. At present crystalloids may represent cheaper and equally effective fluids for resuscitation compared to colloids. 4. Vasopressors: Patients may need vasopressors to maintain blood pressure while fluid resuscitation is under way or if hypotension persists even after adequate fluid resuscitation. The choice of vasopressor agent is controversial. Recently several studies have shown that noradrenaline may be the vasopressor of choice in sepsis. Dopamine is no longer considered to be vasopressor of choice in septic shock. There is some evidence that its use may actually be associated with increase in mortality. Low dose dopamine [1–3 μg/kg/min] has been

CARE OF THE PATIENT IN THE ICU

used for many years to preserve renal function in septic patients but is no longer recommended. Vasopressin [or anti-diuretic hormone] is secreted by the pituitary gland. It acts on V-1 receptors in the vasculature and cause vasoconstriction. Vasopressin increases vascular responsiveness to catecholamines. Septic patients may become deficient in vasopressin. Low dose vasopressin [0.01 – 0.04 units/min] increases in mean arterial pressure and reduces catecholamine requirements. It is not recommended as initial vasopressor. High dose of vasopressin can cause intense vasoconstriction and ischemia of intestine, digits or other organs. 5. Mechanical ventilation: Mechanical ventilation in sepsis should follow the principles as outlined in the previous section on respiratory support. 6. Steroids: Patients in septic shock may have relative adrenal insufficiency. Low dose hydrocortisone [200–300 mg/day] may reduce the duration of shock and may reduce mortality in septic shock. Steroids should not be used in sepsis in the absence of shock. High dose steroids are not recommended. 7. Normoglycemia: Hyperglycemia is common even in non-diabetic ICU patients. Hyperglycemia causes osmotic diuresis, increases risk of infection, slows wound healing and increases mortality. Hyperglycemia should be prevented or treated with insulin. Oral hypoglycemic agents may have unpredictable pharmacokinetics and drug interactions. Metformin may cause lactic acidosis in patients with severe hepatic or renal impairment. Short acting plain insulin as an intravenous infusion is the most predictable way of insulin delivery. The target blood sugar level is controversial. Blood sugar level of 80–110 mg/dl has been shown to reduce

229

mortality in ICU patients. Hypoglycemia may occur in an attempt to maintain blood sugar level with in target range. The benefits of tight glycemic control should be weighed against risks of hypoglycemia. Tight blood sugar control should be attempted only if nursing resources are available to monitor for hypoglycemia. 8. Activated Protein C [APC]: Protein C is a natural anticoagulant. In sepsis, the procoagulant pathways are activated, which leads to disseminated intravascular coagulation [DIC] that causes organ dysfunction. APC prevents this DIC like picture and has been shown to reduce mortality in severe sepsis. It is associated with risk of bleeding and the benefits should be weighed against risks. At present, APC is an extremely expensive drug. Considering that the reduction in mortality is only modest, its high cost has limited its widespread use in severe sepsis.

Acute Heart Failure in ICU Pulmonary edema is common in the ICU. It may be cardiogenic or non-cardiogenic [e.g. ARDS] in origin. Ischemic heart disease is the most common cardiogenic cause of pulmonary edema. The diagnosis of pulmonary edema is not always straightforward. It may be confused with acute severe asthma or exacerbation of chronic obstructive pulmonary disease or pneumonia. Non-cardiogenic pulmonary edema may occur in acute lung injury and ARDS. The distinction between cardiogenic and noncardiogenic pulmonary edema may be difficult. In a patient with respiratory failure, when the cause of respiratory failure is not apparent, assessment of Brain Natriuretic Peptide [BNP] may be useful. BNP is secreted by the ventricular myocardium and the levels increase when myocardium is stretched. BNP levels below 100 pg/ml rule out cardiogenic pulmonary edema. If BNP is above 500 pg/ml, cardiogenic pulmonary edema is very likely. The usefulness

230

A PRIMER OF ANESTHESIA

of BNP measurement in critically ill patients in ICU is however limited because levels may be elevated even in the absence of heart failure. Severe sepsis, pulmonary hypertension and pulmonary thrombo-embolism are other conditions where the BNP levels may be very high and BNP cannot be used to differentiate these conditions from congestive cardiac failure. Cardiogenic pulmonary edema may be distinguished from non-cardiogenic pulmonary edema on chest X-ray by the presence of an enlarged heart, redistribution of pulmonary blood flow to upper lung zones, peribronchial cuffing, Kerley B lines, pleural effusion and central distribution of pulmonary edema. Treatment of acute cardiogenic pulmonary edema: 1. Sit the patient upright. 2. Provide supplemental oxygen to maintain SpO2 above 95%. 3. Diuretics: Generally loop diuretics, e.g. frusemide 40 mg IV in the average adult. Patients previously on diuretics may require a higher dose. There is a risk of dehydration and pre-renal azotemia with high doses or repeated doses of diuretics. 4. Nitroglycerine infusion: At a dose range 5-100 μg/min, it reduces cardiac preload and reduces pulmonary edema. Tachyphylaxis occurs after prolonged administration [beyond 24 hours]. 5. Nesiritide: It is a BNP analogue. It causes vasodilatation and reduces cardiac preload. It is given as IV bolus [2 μg/kg] followed by infusion 0.01–0.03 μg/kg/min]. It may be as efficacious as nitroglycerine for acute pulmonary edema. It is a new drug and its role in management of acute heart failure is yet to be firmly established. 6. Inotropes may be necessary in hypotensive patients. 7. Mechanical ventilation: Non-invasive ventilation may be used. CPAP improves oxygenation and may reduce the need for

intubation. Intubation may be necessary for patients who cannot be managed with noninvasive ventilation. PPV may cause hypotension necessitating the use of inotropes. 8. Intra-aortic balloon pump may be used particularly in the setting of acute MI. 9. Revascularization/surgery may be necessary, e.g. after acute MI or acute valvular regurgitation. Other cardiovascular problems in ICU: Both supraventricular and ventricular arrhythmias are common in ICU. ICU medical and nursing staff should be experienced in arrhythmia recognition and treatment. After acute MI, coronary angioplasty or coronary artery bypass, many patients may be on mechanical cardiac support. Intra aortic balloon pump [IABP] is a catheter with an inflatable balloon that is inserted into the aorta from the femoral artery. The balloon inflates in diastole and deflates in systole. When it inflates in diastole, it increases the diastolic blood pressure and increases coronary perfusion. When the balloon deflates in systole, it leaves the aorta relatively empty and thus reduces cardiac afterload. Balloon inflation may be synchronized with the R wave on ECG or the dicrotic notch on the arterial pressure trace, or the ventricular spike of pacemaker. If the position of the balloon is too high in the aorta, it may cause ischemia of the left arm by occluding the left subclavian artery. The position of the tip should be checked on daily chest X-ray. It should be in descending thoracic aorta below the origin of left subclavian artery. A Ventricular Assist Device [VAD] is used in patients with severe ventricular dysfunction. The VAD may be used in the waiting period prior to heart transplant or as a permanent measure. ICU patients may have implanted permanent pacemakers or Automated Implanted Cardioverter Defibrillator [AICD]. Electrocautery or MRI may cause pacemaker malfunction and ICU personnel should be aware of such devices

CARE OF THE PATIENT IN THE ICU

in the patient. Most of the modern pacemakers/ AICDs are not affected by mobile phones. Pacemakers may be changed from the demand mode (Pacemaker senses the heart rhythm and paces if required) to asynchronous mode (Pacemaker paces at a fixed rate) by application of external magnet if electrocautery is to be used. Temporary pacing may be done in the ICU transvenously (By inserting pacemaker wires into the right ventricle) or transcutaneously. Most modern defibrillators are equipped with capability for transcutaneous pacing using the same pads as are used for defibrillation. RENAL PROBLEMS IN ICU Acute renal failure [ARF] affects approximately 5% of hospitalized patients and 15% of ICU patients. ARF in patients with multiorgan failure approximately doubles the mortality. Hypertension, diabetes mellitus and chronic compensated renal insufficiency are risk factors for development of ARF in ICU. The most common causes of ARF in ICU are prolonged hypotension, sepsis, drug toxicity, and radiocontrast dye. Acute tubular necrosis is the most common pathological finding. The pathogenesis of ARF in sepsis still remains to be elucidated. Intra renal vasoconstriction may occur because of inflammatory mediators and down regulation of nitric oxide synthesis within the kidney. Formation of micro thrombi may cause renal ischemia. Oxidative damage may occur from free radicals. Some recent data suggest that apoptosis [Programmed cell death] may be the predominant pathogenic mechanism responsible for ARF in sepsis. The physiologic consequences of acute renal failure are because of following. • Accumulation of uremic toxins. • Disorders of water balance [Fluid overload], and electrolyte balance [Hyponatremia or hypernatremia, hyperkalemia, hypermagnesemia, hyperphosphatemia and hypocalcemia].

231

• Reduced metabolic function of kidneys [e.g. anemia from reduced erythropoietin, reduced vitamin D synthesis]. • Reduced drug clearance. • Side effects of renal replacement therapy. • Reduced immune response. Prevention of ARF in ICU: The various strategies for prevention of ARF in ICU are as follows: 1. Adequate hydration: Maintaining intravascular fluid volume will provide adequate blood flow to the kidneys. In certain situations like trauma and rhabdomyolysis, aggressive fluid resuscitation may have salutary effect on preserving renal function. Diuretics should not be given to hypovolemic, oliguric patients. 2. Adequate mean arterial pressure: At very low mean arterial pressures, renal blood flow decreases and ischemic Acute Tubular Necrosis (ATN) can occur. Hypertensive patients require higher mean arterial pressures to maintain adequate renal perfusion. 3. Avoid nephrotoxin exposure: Many drugs used in ICU are nephrotoxic. Therapeutic plasma level monitoring may prevent toxic levels. Drug level is commonly monitored for aminoglycosides and vancomycin. In patients with renal dysfunction, drug dose or dose interval should be adjusted. Aminoglycosides are taken up actively by the renal tubular epithelium. They are released slowly as the plasma levels fall, to very low levels. Dosing aminoglycosides once daily allows adequate time for excretion of the drug from renal tubular epithelium and is therefore more effective and less nephrotoxic than divided dose regimes. 4. Prevention of Contrast nephropathy: ICU patients frequently require imaging studies with intravenous contrast. Intravenous contrast can cause renal dysfunction by direct toxic damage to renal tubules and ischemia due to renal vasoconstriction. Patients with

232

A PRIMER OF ANESTHESIA

preexisting renal dysfunction and diabetes are at high risk of developing contrast nephropathy. Maintenance of adequate hydration before and after contrast exposure may limit contrast nephropathy. Use of N acetyl cysteine has also been shown to reduce contrast induced nephropathy. 5. Renal dose dopamine: Low dose dopamine, at 1–3 μg/kg/min, has been used for many years as selective renal vasodilator. Renal dose dopamine is not useful to reduce the incidence of renal failure in ICU and is not recommended. Treatment of ARF in ICU: ARF in ICU is generally transient but 10–30% of survivors will require long-term dialysis. Most patients will require transient support of renal function. The general principles for management of ARF in ICU are as follows: 1. Fluid balance: Daily weight is a simple way of assessing fluid balance in ward patients but is often not practical in the ICU. Fluid intake and output should be monitored. For euvolemic patients fluid intake should be restricted to output plus some additional fluid to account for insensible losses. Restriction is not recommended in patients who require fluid resuscitation, e.g. for septic shock or hemorrhage. Despite renal dysfunction and oliguria [or anuria], these patients may require large volume of fluids for resuscitation. When ARF is resolving, patients often develop polyuria due to tubular dysfunction. These patients are at risk of prerenal azotemia if urinary fluid loss is not replaced. 2. Electrolyte and acid base balance: Hyperkalemia is a common electrolyte abnormality in renal failure. Calcium antagonizes the cardiac conduction effects of hyperkalemia. Beta 2 agonists [salbutamol], alkalosis [NaHCO3] and insulin-glucose cause potassium to shift from extracellular to intracellular space. Potassium binding

3.

4. 5.

6.

7.

resins [Calcium resonium], diuretics [particularly loop diuretics] and dialysis remove potassium from the body. Kidneys excrete 1 mmol/kg H+ ions per day. Bicarbonate is useful in chronic renal failure, but the benefits in ARF are not clearly established. Severe hypocalcemia may require Ca 2+ supplementation. Hyponatremia is generally a manifestation of fluid overload. Free water intake should be restricted as discussed above. Nutrition: Urea is a product of protein metabolism. Proteins are often erroneously restricted to prevent increase in urea. Patients should continue to receive approximately 1 g protein/kg body weight/day. Calorie-dense formulas are used to reduce volume of feeds. Some patients may develop diarrhea because of high osmolality of such feeds. Prevention of infection: Urinary catheter, if present should be removed in anuric or oliguric non-obstructed patients. Prevention of further renal insult: Most ARF in ICU is reversible. Further insult to the kidney should be prevented by avoiding nephrotoxic drugs and adjusting the dose of drugs excreted by kidney. Diuretics: Diuretics make the fluid management easier in ARF and may allow adequate volume of feeds in patients who are not on dialysis. However, diuretics do not alter the course of ARF or alter mortality in patients with ARF. Intravascular volume status should be carefully assessed before diuretics are administered. Diuretics in hypovolemic patient may worsen renal injury. Renal replacement therapy: This is discussed in the following section.

Renal Replacement Therapy Renal replacement therapy is required for patients with persistent and/or severe ARF. Common indications for dialysis in ICU include uremia, fluid overload, severe electrolyte

CARE OF THE PATIENT IN THE ICU

Fig. 15.9: Apparatus for continuous renal replacement therapy (CRRT)

imbalance and severe acidosis. Hemodialysis is effective in the treatment of barbiturate, ethanol, salicylate and theophylline poisoning. Continuous Renal Replacement Therapy (CRRT; Fig. 15.9) has been used for severe sepsis and liver failure but the role for these indications is not yet clearly established. Peritoneal dialysis is rarely used in the ICU for acute renal failure unless the patient is previously on peritoneal dialysis before admission to ICU. It provides insufficient solute clearance and carries the risk of peritonitis. In hemodialysis, blood is separated from the dialysis fluid [dialysate] by a semi-permeable membrane. Solutes [e.g. Potassium, creatinine] are removed by diffusion and convection. Ultrafiltration refers to removal of fluid [H2O] across the membrane by pressure differential on both sides. The higher pressure on the blood side of dialysis membrane will remove H2O from circulation and waste products like urea move along concentration gradient by convection. Intermittent hemodialysis (IHD) is done three to six times per week. Each session lasts for three to four hours. The blood flow and dialysate flow rate are high. It allows rapid solute clearance and high ultrafiltration rate. Anticoagulation is required only during the period of dialysis, to

233

prevent clotting of the blood in the filter during therapy. The main disadvantage is hypotension because of rapid fluid removal by ultrafiltration. CRRT is different form IHD in that it is done continuously. It employs lower blood flow and lower dialysate flow rate. Because it is less efficient than IHD, it requires longer treatment times [to achieve same amount of solute clearance] and the same amount of fluid is removed over a longer period. CRRT is useful for management of hemodynamically unstable patients with ARF or CRF. Because of slow fluid removal, there is less hypotension during therapy. The disadvantages of CRRT are immobilization during prolonged therapy, prolonged anticoagulation, and discontinuation of therapy due to procedures that require moving out of the ICU [e.g. CT scan], high nursing requirements and high cost. NUTRITION IN THE ICU Providing nutritional support is a routine part of the care of the critically ill. Adequate nutrition prevents development of malnutrition, preserves muscle mass and improves immune response. The general principles of nutritional support in ICU are as follows. 1. When to start nutrition: The earlier, the better! Most patients should start receiving nutrition within the first 24 hours of admission to ICU. Delay in start of feeding beyond 96 hours in the critically ill is associated with poor outcome. 2. Route of administration: Enteral nutrition [EN] is delivery of feed into the gut. Parenteral nutrition [PN] refers to intravenous administration of nutrients. EN is generally delivered through a nasogastric tube. Patients who cannot tolerate nasogastric feeds can be given feeds through naso-duodenal or naso-jejunal tube which may improve tolerance. Jejunostomy is performed routinely at the time of some gastrointestinal surgeries [e.g. Whipple’s procedure, esophagectomy] to provide EN when the upper

234

A PRIMER OF ANESTHESIA

gastro-intestinal tract (GIT) cannot be used for prolonged periods. The parenteral feed formulas have high osmolality and can cause thrombophlebitis if given through a peripheral vein. PN is generally given through dedicated lumen of a CVC. The number of disconnections of PN lines should be kept to minimum. The PN solution bag should be changed every 24 hours and any unused solution should be discarded. Advantages of EN: Whenever possible EN should be used in preference to PN. EN preserves integrity of intestinal mucosa and may prevent translocation of bacteria from gut to blood stream. EN is relatively cheap, easily available and does not require central line for administration. The incidence of hyperglycemia and infections is less with EN compared to PN. 3. Type of feed: Most patients will tolerate standard formula feeds. Patients with renal failure may be given high calorie feeds to reduce the fluid intake. Feeds with high fat content and low carbohydrate content may be useful for patients with poor respiratory function. A low carbohydrate load decreases CO2 production, reduces the workload of the respiratory system and may facilitate weaning. A diet enriched with branched chain amino acids may be useful in hepatic failure. It should be noted that all the above feeds are significantly costlier than standard feeds and the benefits are not clearly established. 4. Immunonutrition: Immunonutrients are glutamine, arginine, nucleotides, omega- 3 polyunsaturated fatty acids, vitamin E and selenium. They may improve the immune response. There are no definitive recommendations at this stage, but immunonutrition does seem to reduce the rate of infection without having an impact on mortality.

5. Control of hyperglycemia: It is well established that hyperglycemia is associated with a poor outcome. Blood sugar levels should be controlled aggressively as discussed in the section on septic shock.

Stress Ulcer Prophylaxis in ICU Critically ill patients are susceptible to development of stress related ulceration in the esophagus, stomach or duodenum. Mucosal ischemia is the most likely mechanism for stress ulcers. Mechanical ventilation, coagulopathy, steroids and previous history of upper GI ulcers are risk factors for stress ulcers. Sucralfate, H2 blockers [e.g. ranitidine] and proton pump inhibitors [e.g. omeprazole] are useful for prophylaxis. Reducing the acidity in the stomach by inhibiting gastric acid secretion can promote gastric colonization with bacteria. Gastric colonization may increase the risk of pneumonia from aspiration. Therefore, only patients at high risk of stress ulcers should receive prophylaxis.

Sedation and Analgesia in ICU ICU patients need sedation and analgesia to reduce anxiety and pain, prevent asynchrony with ventilator, for transport, during painful procedures and for amnesia. Benzodiazepines [commonly midazolam, diazepam and lorazepam], propofol and alpha 2 adrenergic agonists [clonidine and dexmedetomidine] are the most common sedatives used in ICU. Opioids [generally morphine or fentanyl or remifentanil], paracetamol and alpha 2 adrenergic agonists are commonly used analgesics. Postoperative patients may have subarachnoid or epidural catheters in situ. Non-steroidal anti-inflammatory drugs NSAIDs are uncommonly used because of the potential to cause renal dysfunction and displacement of various drugs from protein binding sites. The sedation and analgesic requirements of all patients are different. There is no single dose applicable to all patients.

CARE OF THE PATIENT IN THE ICU

Most of the times a benzodiazepine or propofol is used in combination with an opioid. Clonidine is useful for its sedative, analgesic and antihypertensive properties. Administration of protocol-based sedation with a well-defined target is associated with reduced sedation requirements and reduced ICU length of stay. Daily interruption of sedation reduces the duration of mechanical ventilation, ICU length of stay and number of investigations done for altered mental status. Thromboprophylaxis in ICU: Patients in ICU are at high risk for development of deep venous thrombosis [DVT] and pulmonary thromboembolism [PTE]. All patients admitted to ICU should receive thromboprophylaxis. Mechanical methods include pressure stockings and pneumatic calf compressors. The pneumatic calf compressors is tied around the calf and thigh. It inflates at periodic intervals to pump blood in the deep veins of lower limbs. Pharmacological methods are subcutaneous heparin or low molecular weight heparin. Low molecular weight heparin [e.g. enoxaparin] has a long half-life and more predictable pharmacokinetics. Unlike heparin, low molecular weight heparins do not increase APTT. Their effect can be monitored by measuring activated factor Xa level. The half life of low molecular weight heparin may be prolonged in renal failure. Because of these reasons, heparin may be better in ICU patients. Warfarin also prevents DVT or PTE. Warfarin is not a practical drug to use in ICU patients because its effect cannot be reversed at short notice, e.g. in an ICU patient urgently requiring CVC insertion. ETHICAL ISSUES IN ICU Many ICU patients will die. Patients, family and ICU physicians view death from different perspectives. The approach towards end of life is influenced by cultural and social background. Not infrequently, the opinions of the patient and family differ from that of the treating physician.

235

When a patient is critically ill and likely to die, decisions may have to be taken for several end-of-life issues. For example, if the patient suffers a cardiac arrest, should CPR be done or not; or, if the patient has respiratory failure, should mechanical ventilation be offered or not. Patient autonomy is liberty to follow one’s will, and implies personal freedom. It means that the patient should be able to choose the course of his/her therapy and the physician, who shares this knowledge with the patient, acts as a guide. Medical paternalism refers to the practice that allows the physician to make the decision for the patient. Neither of the two approaches is perfect. In most circumstances, decision-making is shared between the patient or his surrogate and the physician. Mentally competent patients may participate in decision making themselves. Many patients may have advance directives that guide the physician to make decisions when they fall ill. A living will is the most common form of advance directive by which a person may express his desire to receive or refuse treatment should he become critically ill and incapable of making a decision. Patients may also nominate a surrogate decision maker who will make decisions on their behalf when they are unable to make decisions themselves. If no such individual has been designated, an appropriate family member is sought. The common hierarchy is from spouse to elder adult child to parent to adult sibling, in that order. Limiting therapy in ICU may take the form of a)withholding treatment [e.g. not offering mechanical ventilation to a patient who is in respiratory failure] to b)withdrawal of treatment [ e.g. extubating a patient who needs mechanical ventilation for respiratory failure] to c) ‘Do Not resuscitate’ order [i.e. not to do CPR in the event of cardio-respiratory arrest]. Before making a decision to limit therapy, the physician should have a clear understanding of the patient’s diagnosis, physiologic and functional status. The other members of the health care team should agree to the decision.

236

A PRIMER OF ANESTHESIA

Informed consent should then be sought from the legally competent patients or their surrogate. The primary referring physician should be involved in the decision making as well.

Care of the Dying Patient As the decision to forgo further life prolonging therapy is made, the patient, family and the clinical team should be prepared for further management. The clinical team may be familiar with such a situation, but for the patient, this is a singular event in his/her life. It may also be the first such experience for the family. Decision to withhold life prolonging treatment does not mean withdrawal of care. Patients are still cared for. All patients have the right to be treated with respect and die with dignity. This decision only means that the focus of therapy has changed from intended cure to palliation. If possible, the patient should be transferred to a separate room. (Transferring the patient out of the ICU to a ward may give an impression that the care is withdrawn; the family should be reassured that this is not the reason). There is often a pressure to admit more patients in ICU. Often the family may itself desire to transfer the patient to a quieter environment. The family should be allowed unrestricted time to be with the patient. The monitors should be turned off and the cables should be disconnected. Catheters may be removed if they are interfering with comfort. Control of pain is one of the most important aspects of care of the dying. Generous doses of analgesics should be prescribed as dictated by the severity of pain. Nausea and vomiting should be controlled using anti-emetics. Hydration and feeding are controversial issues in management of dying patients. Traditional view is that feeding and hydration contribute to patient comfort and it should be continued until death. The current thinking is that loss of hunger and thirst are normal to dying process. Feed and hydration prolong the dying

process and do not contribute to patient comfort. They should be provided only if a positive contribution to patient comfort is obvious. The decision is also influenced by the beliefs of the patient, family and physician and should be taken as a shared decision. Other drugs may or may not be given depending upon the situation. For example, fever may be uncomfortable and antipyretics may be indicated. Patients should know that their cultural beliefs are understood and cultural and religious expectations should be met [e.g. a visit by a priest]. The needs of the family should not be overlooked. Unrestricted visiting time should be allowed. Regular updates about the changing condition of the dying patient should be provided. They should be assured of the patient’s comfort and that their decisions were right. Many family members would have reached a level of exhaustion by this time and need to be comforted, rested and fed. In addition to medical knowledge, the importance of communication skills to put these principles before the patients and their family cannot be overemphasized. When discussing end of life issues, simple words should be used that are easily understood by the patient or the family. Unfamiliar words [e.g. CPR, ventricular fibrillation, etc.] should be avoided. Whenever possible, the news of death should be delivered in person. When delivering the news of death, ambiguous words as ‘passed away’ etc. should be avoided, and the physician should not hesitate to use the word ‘death’.

Predicting the Outcome Intensivists are frequently questioned about prognosis. Unfortunately, there is no definitive answer to this question. Various scoring systems have been devised to predict outcome of critically ill patients. They may be useful when predicting the outcome of a group of patients, but cannot be used for the individual patient.

CARE OF THE PATIENT IN THE ICU

Examples of such scoring systems include ‘Acute Physiology and Chronic Health Evaluation’ [APACHE II and III] scores, Trauma Severity score [TSS], Simplified Acute Physiology Score [SAPS], etc. These scoring systems take into account the patient data [e.g. age, sex], physiological parameters [e.g. blood pressure], principal diagnosis and comorbidities to calculate the score. It may be emphasized that scoring systems are generally not helpful in guiding therapy in individual patient. The major applications of severity of illness scores are for performance assessment [e.g. comparing different ICUs], predicting and planning resource utilization, and research. Critical care offers hope of life to many critically ill patients and to those after major surgery, who, a few decades ago would not have survived, ICUs are integral to most tertiary medical centers. MCQ MCQss 1. Which of the following statements is not true about ICU? a. In open ICU, there are no isolation beds for patients infected with multiresistant organisms b. Ideally, one nurse should look after one patient c. There should be designated areas for holding family discussions d. Closed intensive care units may lead to better implementation of protocols and may improve efficiency and outcome. 2. Which of the following monitoring technique can provide information about accidental disconnection of a ventilator from patient? a. Pulse oxymeter b. End tidal CO2 c. Lithium dilution technique d. Mixed venous oxygen saturation

237

3. Which of the following is not an indication for invasive [intra-arterial] monitoring of blood pressure? a. Need for vasopressors b. Need to take repeated arterial blood gas samples c. Difficult measurement, e.g. obese patients d. Pregnant patients in ICU. 4. All of the following can be used to measure cardiac output except: a. Pulmonary artery catheter b. Microdialysis catheter c. Transpulmonary thermodilution d. Esophageal Doppler. 5. Which of the following is the most effective in preventing spread of nosocomial infections? a. Hand wash b. Use of gloves c. Gowning before invasive procedures d. Avoiding use of Foley’s urinary drainage catheters 6. Which of the following statements is not true? a. Positive end expiratory pressure [PEEP] is applied to prevent collapse of alveoli during expiration b. Tidal volume of 6-8 ml/kg body weight is usually sufficient while on mechanical ventilator c. Ventilator can sense breathing effort made by the patient and synchronize mechanical breath with patient effort d. Ventilators help in expiration by applying negative pressure during expiration. 7. Which of the following is not a side effect of positive pressure ventilation? a. Ventilator associated pneumonia b. Barotrauma c. Esophagitis d. Atelectrauma

238

A PRIMER OF ANESTHESIA

8. Which of the following is not usually started in ICU to prevent deep venous thromboprophylaxis? a. Heparin b. Warfarin c. Low molecular weight heparin d. Pneumatic calf compressors. 9. Which intravascular device should usually be inserted during resuscitation from hypovolemic shock? a. Peripheral intravenous cannula [PIVC] b. Central venous catheter c. Intraosseous catheter d. Saphenous venous cut down. 10. Which of the following statement is true? a. Sepsis is defined as systemic inflammatory response syndrome as a result of proven blood stream infection b. Severe sepsis is sepsis with organ system dysfunction c. Septic shock is defined as severe sepsis with hypotension before fluid resuscitation is started d. Septic shock may have a mortality rate of up to 10%. 11. Which of the following statements regarding septic shock is correct? a. Control of source of infection should be deferred until blood pressure has been stabilized to reduce risk of anaesthesia b. Antibiotics should be delayed until the results of blood cultures are back c. Blood sugar should be maintained between 300-400 mg% to provide nutrition d. Crystalloids like Ringer’s Lactate are good choice to resuscitate patients with septic shock. 12. BNP is useful in the diagnosis of a. Ischemia of the intestine b. Heart failure

c. Renal failure d. Subarachnoid hemorrhage 13. Which of the following is not a useful strategy to prevent renal failure in ICU? a. Maintain adequate mean arterial pressure b. Avoid hypovolemia c. Use of renal dose dopamine d. Avoid use of intravenous contrast media as much as possible. 14. Which of the following statements is true regarding nutrition in ICU? a. Patients in ICU do not require nutrition because body cannot metabolize glucose in critical illness b. Total parenteral nutrition is better than enteral nutrition for mechanically ventilated patients c. Insulin should be used to treat hyperglycemia d. Patients with respiratory failure may benefit from feeds rich in carbohydrates 15. In the care of the dying patients, the following principles are true except: a. Control of pain is one of the most important goals of good care of the dying b. Artificial feeding and hydration may be discontinued c. It is unethical to not do CPR on a patient who had cardiac arrest in ICU d. Unrestricted visiting time should be allowed for the family of the dying patient Answers 1. 5. 9. 13.

a a a c

2. 6. 10. 14.

b d a c

3. 7. 11. 15.

d c d c

4. b 8. b 12. b

Cardiopulmonary Resuscitation Chittaranjan Joshi, Indu Kapoor

BLS: – algorithm – mouth to mouth ventilation – external cardiac compression  ACLS: – defibrillation – vascular access – definitive airway – foreign body obstruction – drugs  CPR in infants and children  Complications of BLS 

Providing emergency cardiac care (ECC) at any time and place, especially in the hospital setting is a core skill that every practicing doctor must acquire. The survival rate of in-hospital cardiac arrest patients is nearly 35-39%, which underscores the importance of knowing exactly what to do and how to do it, so that patient salvage rate is maximal with minimal neurologic deficit. This chapter is designed to provide the necessary knowledge to handle a cardiac arrest in a stepwise, logical sequence. Although the history of resuscitation dates back to biblical times, contemporary approaches to cardiopulmonary resuscitation (CPR) began in 1966, when a National Research Council Conference generated consensus standard for the performance of CPR.

Subsequently, the International Liaison Committee on Resuscitation (ILCOR), an international consortium of representatives from many of the world’s resuscitation councils, was formed. ILCOR and the American Heart Association (AHA) produced the emergency cardiac care (ECC) guidelines in 2000. These recommendations have been recently modified in 2005. This chapter presents the 2005 AHA guidelines for CPR. Cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC) should be considered for any patient who is unable to breathe and/or maintain circulation, and not just for patients who have had a cardiac arrest. Effective CPR is based on the artificial delivery of oxygenated blood to systemic circulatory beds at rates that are sufficient to preserve vital organ function and at the same time providing the physiologic substrate for the rapid return of spontaneous circulation. The causes of cardiac arrest are many, and may be related solely to an acute insult (for example, hypothermia) or be due to a preexisting systemic disease or metabolic disorder. Regardless of the cause of arrest, it is of paramount importance to RECOGNIZE IT and INSTITUTE TREATMENT. The AHA 2005 guidelines differ in certain important aspects from the previous ones. These are:

240 A PRIMER OF ANESTHESIA

1. The lay rescuer does not check for the pulse in an unresponsive victim but straightaway provides two rescue breaths to an unresponsive victim. 2. All breaths (whether given mouth-tomouth or mouth-to-device) are to be given over 1 second with sufficient volume to achieve visible chest expansion. 3. A universal compression-to-ventilation ratio of 30:2 is to be provided by single rescuers for victims of all ages except newborn infants. 4. Definition of pediatric victim in the case of a health care provider (HCP) includes up to the pre-adolescent age; in the case of a lay person it remains 1–8 years. 5. Emphasis on quality of chest compressions: ‘Push hard, push fast (100 compressions / min), allow complete chest recoil, and minimize interruptions in chest compressions’. 6. EMS (Emergency Medical Service) providers should provide 5 cycles or 2 minutes of CPR pending arrival of a defibrillator especially when the interval from the call to arrival is expected to be more than 4–5 minutes. 7. In pulseless arrest, CPR should be resumed immediately after shock delivery and check for return of pulse made after 5 cycles (or 2 minutes) of CPR. 8. All rescue interventions (e.g. insertion of airway devices, administration of medications and re-assessment of patient) should be done in a way as to minimize interruptions in chest compressions. 9. Only 1 shock is recommended followed immediately by CPR (beginning with chest compressions) instead of 3 stacked shocks. This recommendation is based on the high first-shock success rate of new defibrillators and the fact that immediate resumption of

chest compressions improves oxygen delivery to the myocardium, making success of subsequent shocks more likely. 10. Emphasis on importance of ventilation and de-emphasis on the use of high concentrations of oxygen for resuscitation of the newborn. 11. Administration of intravenous fibrinolytics to patients with acute ischemic stroke by a knowledgeable team and institutional commitment to stroke care. Components of Adult BLS Sequence (Fig. 16.1) Make sure it is safe to approach the patient. Move patient only if absolutely necessary, e.g. burning building, middle of busy road.

Check for Response (Box 1) Assess responsiveness by tapping on the shoulder and calling. If injured but responsive and needs assistance, leave to phone, return quickly to check condition.

Activate EMS (Box 2) • Lone lay rescuer finds unresponsive adult-activate EMS, get AED (automatic electrical defibrillator) (if available), return to provide CPR and defibrillation if needed. • If 2 rescuers available, one activates EMS and other starts CPR. • If occurs in hospital, notify emergency system. • Lone healthcare provider (HCP) witnesses sudden collapse-phone EMS, ask for AED, returns to provide CPR. • Lone HCP aids asphyxial arrest (drowning): 5 cycles/2 minutes of CPR before activating EMS.

Open the Airway and Check Breathing (Box 3) • Lay rescuer should open airway using head tilt – chin lift manoeuvres (Fig. 16.2) for both injured and non-injured personnel. The jaw-thrust is no more recommended as it is (a) difficult to learn, (b) often not effective and (c) may result in spinal movement.

CARDIOPULMONARY RESUSCITATION

241

Fig. 16.1: BLS algorithm • HCP provider also uses head-tilt and chin-lift techniques; however if c-spine injury is suspected (2% victims of blunt trauma, 6% blunt trauma with craniofacial injuries or with GCS < 8 or both), uses jaw thrust Priority is patent airway, ventilation and oxygenation and if jaw thrust does not open the airway should use head tiltchin lift. • Check breathing: while maintaining an open airway look, listen and feel for a breath (Fig. 16.3). Gasping, agonal movements should be differentiated from breaths and the patient given rescue breaths and CPR.

Give Rescue Breathing (Box 4) The following points are emphasized: • Rescue breaths are not as important as chest compressions in the first few minute of Ventricular Fibrillation (VF) or Sudden Cardiac Arrest (SCA), as the oxygen level in the blood is still high an myocardial and cerebral oxygen delivery is limited more by an impairment of blood flow. • Both ventilation and compressions become important in prolonged arrest where hypoxemia is invariable, e.g. asphyxial arrest due to drowning.

242 A PRIMER OF ANESTHESIA

Fig. 16.2: Head tilt-chin lift

Fig. 16.3: Listening and feeling for breathing

(A)

(B) Figs 16.4A and B: Mouth-to-mouth breathing

• Since blood flow to the lungs is substantially reduced during CPR, use of lower tidal volumes (500–700 ml; 6–7 ml/kg) is recommended to maintain ventilation-perfusion ratio. • Excessive ventilations are not only unnecessary, but (i) increase intrathoracic pressure and impair venous return; reduced venous return causes a fall in cardiac output and coronary and cerebral perfusion; (ii) may cause gastric inflation which might result in regurgitation and aspiration and (iii) reduce respiratory compliance by elevating the diaphragm.

• The delivered volume should produce a visible chest rise. • Avoid rapid and forceful breaths. • Mouth-to-mouth breathing: Open the airway, pinch the victim’s nose and create an airtight mouth-to-mouth seal (Fig. 16.4A). Give one breath over 1 second, take a regular (NOT a ‘deep’) breath and give a second breath over 1 second. If the chest does not rise with the first breath, perform the head tilt-chin lift and give the second rescue breath (Fig. 16.4B).

CARDIOPULMONARY RESUSCITATION

243

Fig. 16.5: Bag-mask ventilation with one person (L) and 2 persons (R) • When oxygen is available, HCP should provide it at a minimum flow rate of 10–12 l/min. • Bag-mask ventilation requires training and practice for competence. It is most effective when provided by 2 experienced and trained rescuers (Fig. 16.5). Ideally the bag should be attached to a source providing 100% oxygen. Both rescuers should watch for visible chest rise. • If an advanced airway (LMA, endotracheal tube) has been inserted, one rescuer delivers 8–10 breaths per minute and the other provides continuous chest compressions at 100 per minute. The breaths and compressions should be synchronized. The rescuers should switch roles every two minutes to avoid compressor fatigue and deterioration in quality of compressions.

Pulse Check (for Health Care Providers) (Box 5) Lay rescuers should assume that cardiac arrest is present if an unresponsive victim is not breathing. Pulse check has been deleted for lay rescuers and de-emphasised for HCPs. The HCP should take no more than 10 seconds to check for a pulse (brachial, femoral or carotid). If a pulse is not definitely felt within 10 seconds, the HCP should proceed with chest compressions. If a definite pulse is felt the HCP (Only) should continue to give rescue breaths at 10–12 breaths per minute. The circulation is checked every 2 minutes.

Chest compressions (Box 6) • Effective compressions produce a systolic blood pressure of 60-80 mm Hg and a mean arterial pressure of 40 mm Hg. • Blood flow generated by compressions delivers a small but critical amount of oxygen and substrate to the brain and myocardium. • In victims of Ventricular Fibrillation and Sudden Cardiac Arrest (VF SCA), effective compressions increase the likelihood of a successful shock. • To provide ‘effective’ compressions, the rescuer should ‘push hard and push fast’. The adult chest is compressed at 100/min with a compression depth of 4–5 cm. The chest should be allowed to recoil between compressions. Approximately equal time should be given to compression and relaxation. Interruptions in chest compressions should be minimal. • The victim should be positioned on a hard surface and the rescuer should kneel beside the thorax (unless if there are space constraints). The heel of one hand should be kept over the lower half of the sternum (between the nipples) in the centre of the chest. The heel of the second hand is then placed on the first so that the hands are overlapped and parallel (Figs 16.6A to C and 16.7). • Chest compressions should continue till the victim begins to move, an AED arrives or EMS personnel take over. Compressors must switch after 2 minutes and within 5 seconds.

244 A PRIMER OF ANESTHESIA • A compression-ventilation ratio of 30:2 is recommended as it increases the number of compressions, minimizes hyperventilation and interruptions in compression. • If lay persons are unwilling to provide mouth-tomouth ventilation they should be encouraged to provide cardiac compressions which is better than doing nothing at all.

Defib rillation Defibrillation (A)

This is described in the following section on advanced cardiac life support. ADVANCED CARDIAC LIFE SUPPORT (ACLS) Defibrillation

(B)

(C) Figs 16.6A to C: External cardiac compression– note weight of shoulders provides the force

Although AEDs are part of BLS, manual defibrillation forms the first step of ACLS. A sequence of a single shock followed by CPR is presently recommended. The rationale is explained at the beginning of this chapter. If the first shock is not delivered within 3 minutes of cardiac arrest survival declines by 10% every minute without defibrillation. The defibrillator is connected to the patient, not interrupting cardiac compressions. Defibrillators may deliver energy in two directions (biphasic truncated exponential, BTE) or one direction (monophasic damped sine, MDS). The former is preferred as it gives more effective shocks with less energy and thereby causes less myocardial injury]. Everyone is warned to stay clear and the shock (320 J for a monophasic model; 175– 200 J for a biphasic model) is delivered. CPR is immediately resumed and after 5 cycles or 2 minutes the rhythm is assessed. A second shock of 200/320 J is delivered if the rhythm is ‘shockable’. Details of pulseless arrest algorithm and treatment of pulseless electrical activity (PEA) will be found in the issue of Circulation (2005) Nov, Vol 113 Supplement, freely available on the Internet. Placement of paddles: The sternal paddle is placed in the right infraclavicular area and apical

CARDIOPULMONARY RESUSCITATION

paddle at the infero-lateral left chest lateral to the left breast. Other acceptable positions are the bi-axillary position and the standard left paddle position along with the sternal paddle placed on the back. The paddles should not be placed on any medication patch as they may cause a burn. Access for Medications • Central line access is NOT required in most resuscitation attempts. A large peripheral line is desirable. Drugs take 1–2 minutes to reach the central circulation; each drug should be followed by a bolus of 20 ml saline and elevation of the limb. Peripheral intravenous (IV) line placement does not interrupt CPR while placement of a central line certainly will. A femoral central venous access is perfectly acceptable and can be performed without interrupting cardiac compressions. The advantages of having central venous access include rapid onset of drug action and a route for pacemaker wire insertion. • Intraosseous (IO) route (Fig. 16.7) can provide emergency vascular access in children. A rigid 18-G cannula with a stylet is inserted into the distal femur or proximal

245

tibia; in the latter situation the needle is inserted at a 45 degree angle, 2–3 cm below the tibial tuberosity and directed away from the epiphyseal plate. The advantages of this route are ease, rapid rates of infusion (including colloids and blood) and an alternative route for antibiotics, inotropes and other agents. Displacement of the cannula, osteomyelitis and compartment syndrome are important considerations in using this route. Intraosseous cannulation is accepted in children and adults. If spontaneous circulation does not return after defibrillation and peripheral/IO drug administration, central cannulation may be indicated. • If IV/IO access cannot be established some drugs can be administered through the endotracheal route. These include lidocaine, epinephrine, atropine, naloxone and vasopressin. Sodium bicarbonate should not be administered through this route. The main disadvantage is that drug concentrations achieved are lower than with IV/IO routes. The drug dose required is usually 2.5–3 times the IV dose. It should be diluted in 5–10 ml of saline or water (latter preferred) and directly injected into the endotracheal tube.

Securing the Airway (Fig. 16.8)

Fig. 16.7: Intraosseous infusion

Although endotracheal intubation remains the gold standard for securing the airway, it is by no means compulsory. As soon as practical during the resuscitative process, trained personnel should intubate the trachea. Currently the tracheal tube is considered the ventilation adjunct of choice because it: • Keeps the airway patent. • Permits suctioning of airway secretions. • Ensures delivery of a high concentration of oxygen. • Provides a route for the administration of certain drugs • Prevents aspiration of blood or gastric contents.

246 A PRIMER OF ANESTHESIA

(A) Oropharyngeal (Guedel) airway

Fig. 16.8: Endotracheal intubation

It is important to remember that it is oxygenation which is vital, NOT intubation. So if one Fails To Intubate but can manage a patent airway, ventilations should continue through a facemask held tightly over the patient’s face and connected to a self-inflating (Ambu) bag at a rate of 12–15 breaths per minute. Look for chest movement to assess ventilation. Make sure that oxygen is flowing at 10–12 litres per minute into the bag and that you have attached a non-rebreathing valve to the mask. It is far more sensible to oxygenate a patient this way till expert help arrives rather than succumb to the temptation of multiple attempts at laryngoscopy, which not only cause trauma and edema, making ventilation progressively difficult, and the patient irretrievably hypoxic. If you find that the patient’s chest expansion is not satisfactory, you can insert an oropharyngeal airway, an LMA or a Combitube (Figs 16.9 A to C) which may assist in opening the airway and facilitating ventilation. Care, familiarity and practice are required in placement of these airway adjuncts because incorrect insertion can displace the tongue into the hypopharynx and result in airway obstruction. Nasopharyngeal airways are especially

(B) Laryngeal mask airway

(C) Combitube

Figs 16.9A to C: Alternatives to endotracheal intubation

CARDIOPULMONARY RESUSCITATION

useful in patients with trismus, biting or with clenched jaws which prevent placement of an oral airway. Bleeding into the airway during placement however is a real risk. The LMA in particular enjoys a good track record for providing an effective and safe conduit during resuscitation. It facilitates airway management by one person and leaves the other free to manage intravenous access, thereby expediting ACLS. If none of the devices is helpful in achieving adequate chest expansion or ventilation and the patient’s saturation is falling, the possibility of serious airway obstruction needs to be considered (which may have led to the cardiorespiratory arrest). If the symptoms are highly suggestive, attempts should be made to clear the airway (Figs 16.10A to C) using back-blows, Heimlich maneuvre or a combination or abdominal thrust. Unrelieved airway obstruction indicates the need for a surgical airway, either a cricothyrotomy with a wide-bore intravenous cannula or a tracheostomy. Emergency cricothyrotomy is frequently a difficult proposition. Morbidity and even mortality can result due to trapping of gas at high pressure or inadequate ventilation. It should ideally be performed by someone who is familiar with the technique and equipment Attending airway workshops and practicing on cadavers enhances confidence and success rate. When an endotracheal tube or other airway device is in place, it must be secured with adhesive tape. Adequacy of ventilation and oxygenation is judged by arterial blood gas analysis. Appearance of end-tidal CO2 signals resumption of pulmonary perfusion. Once a tracheal tube is in place ventilation need not be synchronised with chest compressions. The respiration rate during cardiac or respiratory arrest when the patient has been intubated should be 8 to 10 breaths per minute. As soon as feasible, an arterial cannula may be inserted which will allow accurate hemo-

247

(A)

(B)

(C)

Figs 16.10A to C: Back blows, Heimlich maneuver and abdominal thrust to clear airway

248 A PRIMER OF ANESTHESIA

dynamic monitoring as well as tracking and correcting acid-base abnormalities. Arrhythmia recognition: This is the cornerstone of ACLS as further treatment actions and specific maneuvres depend on the rhythm, or dysrhythmia that is noted. These can be ‘shockable’ like VF or VT; or ‘unshockable’, like pulseless electrical activity (PEA) or asystole. The various treatment algorithms can be accessed on the AHA website, or you can access the Circulation 2005 issue (supplement), vol.112, p 25–54. DRUGS The indications, doses and mode of action of drugs commonly used in CPR are listed at the end of the chapter. Newer the guidelines regarding use of some drugs, which, till recently, were administered ‘routinely’ during CPR, should be followed. For instance, calcium salts are indicated only with documented hypocalcemia or hyperkalemia. Examples are massive transfusion, calcium channel blocker overdose or hypomagnesemia. Sodium bicarbonate reacts with metabolic acids forming carbonic acid and raises plasma pH; however carbonic acid dissociates to form carbon dioxide which readily crosses the blood-brain barrier leading to intracellular acidosis. Increased intramyocardial carbon dioxide may reduce the possibility of successful resuscitation. Further, sodium bicarbonate may shift the oxygen dissociation curve to the left, reducing oxygen delivery to the tissues. Sodium bicarbonate is thus indicated only in established metabolic acidosis, hyperkalemia, tricyclic antidepressant or barbiturate overdose. Dysrhythmia recognition, institution of appropriate antiarrhythmic therapy, insertion of transvenous pacemaker and overdrive pacing are some of the other important aspects of ACLS. Post-resuscitation Care The immediate goals of post-resuscitation care are to:

• Transport the prehospital cardiac arrest patient to the hospital emergency department and then to an appropriately equipped critical care unit. • Provide cardiorespiratory support to optimize tissue perfusion especially to the brain and maximize neurological recovery. • Attempt to identify the precipitating causes of the arrest. • Institute measures such as antiarrhythmic therapy to prevent recurrence. A good way to acquire familiarity with CPR is to familiarize oneself with the contents of the emergency trolley: Airway equipment (Fig. 16.11), and vascular equipment (Fig. 16.12), and the location and working of the defibrillators in each ward. Airway equipment should be kept on the trolley in a tray. Syringes and emergency drugs should also be on the same cart so that only a single trolley is needed in an emergency. In addition, the wall oxygen outlets and vacuum points should be regularly checked and serviced. This gives every one a sense of security and highlights the importance of equipment maintenance and preparedness in ancillary hospital staff. Practicing CPR in a simulator or in a course environment (specifically designed ACLS Provider Course with mannequins) helps in familiarizing oneself with all the equipment, drugs and algorithms required for resuscitation. Practicing and training in CPR in a controlled environment has been shown to improve response time and patient outcome. Every effort should be made by all medical caregivers to enroll for these courses as CPR is a core skill. CPR FOR INFANTS AND CHILDREN The grouping of children for purposes of CPR remains 1–8 years and above 8 years for the lay rescuer. It has been changed to pre-pubertal and post-pubertal groups for the health care provider (HCP). This makes it easy for the lay person to get involved immediately instead of worrying about the age.

CARDIOPULMONARY RESUSCITATION

249

Oropharyngeal airway

Nasopharyngeal airway

Rubber facemask

Ambu self inflating bag

Malleable stylet

Cuffed and plain endotracheal tubes

Laryngeal mask airway

Suction catheter

Laryngoscope kit with batteries and assortment of blades

Combitube

Fig. 16.11: Emergency airway equipment

250 A PRIMER OF ANESTHESIA

IV Cannulae

Infusion set

Syringes

IV fluids

Pressure infusor bag

Three-way stopcock

Fig. 16.12: Vascular equipment

CARDIOPULMONARY RESUSCITATION

Fig. 16.13: ‘Safe’ position for a child

Small children may not respond to call or stimulation if hypoxic. If the child has breathing activity, allow the child to assume the most comfortable position or move it gently into the ‘safe’ position (Fig. 16.13). The most recent guidelines for pediatric CPR have been laid down in 2005 by the European Resuscitation Council (ERC) and the American Heart Association (AHA). They have a few differences from the 2000 guidelines. 1. Shout for help; ask someone to phone and get AED. 2. If you are alone with the child give one minute of CPR before going to call for help. 3. Open the airway and check for breathing. Give 2 slow breaths (recommended by AHA) and watch the chest rise. The ERC recommends 5 initial breaths which may be a better option as most cardiac arrests in children are due to hypoxia. Both the nose and mouth are covered by the rescuer’s mouth for giving the breath. 4. Compression:ventilation ratio is 30:2. If there are two rescuers a 15:2 ratio is used. The depth of compression should be at least one-third to half the anteroposterior diameter of the chest. The chest should be allowed to recoil completely after every compression. In infants, two fingers (index, middle) of one hand compress the sternum 2 finger breadths below a line joining the nipples (Fig. 16.14); alternatively both

251

hands can encircle the chest and the thumbs used for compression at the same point (Fig. 16.15). For older children one or both hands are placed at the lower half of the sternum. 5. Check for signs of circulation-breathing, coughing, movement. This has now been given greater emphasis than palpating the pulse both for lay persons and health care providers. Traditionally the brachial artery has been recommended as the standard in infants and the carotid in older children by the ERC. However now the AHA recommends palpation of the femoral artery in children above one year of age as it is easily felt even when the brachial is difficult

Fig. 16.14: External cardiac compression in infant

Fig. 16.15: Chest encircling technique of cardiac compression

252 A PRIMER OF ANESTHESIA

6.

7.

8.

9.

to palpate in hypotensive children. When the pulse is felt, auscultation at the precordium is carried out to determine the rate, as ECC will have to continue if the rate is 60/min or below, with signs of poor perfusion. If foreign body obstruction is suspected, it is recommended to look into the mouth before starting CPR and also to perform sharper compressions. Back blows and chest thrusts are still recommended for infants while abdominal thrusts can be performed in older children. In ACLS, bag-mask ventilation is considered as effective as ventilation through a tracheal tube for a short period (10-15 minutes). However effective mask ventilation in infants needs to be taught and learnt in the operating theatre. Although the ERC recommends use of LMA where ‘providers experienced in its use’ are available, the AHA guidelines to use the LMA in difficult intubations appears more appropriate. A cuffed endotracheal tube should be used for older children. Uncuffed tubes are appropriate up to size 5.5 mm ID. Intraosseous and tracheal routes can be used for drug administration when the intravenous route is not available. The tracheal doses recommended by ERC are 0.1 mg kg–1 for adrenaline, 2–3 mg kg–1 for lidocaine and 0.03 mg kg–1 for atropine. Fluid boluses of normal saline or lactated Ringer’s solution are recommended. Infant paddles (4.5 cm) are recommended for infants 32° C with stable circulation. 12. It is beneficial for the parent/s to stay during CPR as they will know that all efforts were made to revive their child, and also helps in the grieving process. Details of pediatric and neonatal resuscitation are not covered in this text and will be taught during paediatric rotation.You can refer to Circulation (2005,Supplement 13), vol.112, for details on paediatric BLS and ACLS. COMPLICATIONS OF BLS Potential complications of rescue breathing: • Gastric distension • Regurgitation • Reduction in lung volumes by elevation of diaphragm Potential complications of cardiac compression: • Fracture of ribs • Fracture of sternum • Separation of ribs from sternum • Hemothorax • Pneumothorax • Lung contusions • Laceration of liver and spleen • Fat embolism. Drugs Used in CPR and their Doses Adenosine: 6 mg over 1–3 sec IV; flush with saline; 12 mg after 1–2 min, twice; total dose 30 mg. Amiodarone (VF/VT): 300 mg IV push (diluted in 20 cc D5W) • Consider repeat 150 mg IV once in 3–5 min. • Max dose: 2.2g in 24 hours

CARDIOPULMONARY RESUSCITATION

Atropine: 0.5–1 mg every 3–5 min, up to 0.04 mg/kg Epinephrine: 1 mg every 3-5 min IV. Diltiazem: load 0.25 mg/kg IV over 2 min, then 0.35 mg/kg over 2 min in 15 min, infuse 5-15 mg/hour. Dopamine: 5–10 μg/kg/min; add 400 mg in 250 ml D5W Lidocaine: 1–1.5 mg/kg bolus • Additional 0.5–1.5 mg/kg every 5–10 min, up to total 3 mg/kg. • Then infuse 1–4 mg/min Magnesium sulfate: 1–2 g in 10 ml D5 W over 1–2 min Procainamide: load 20 mg/min up to 17 mg/ kg (1000 mg) • then infuse 1–4 mg/min • Side effects: HTN, torsade de pointes Vasopressin: 40 IU × 1 dose only (for pulseless VT/VF) Verapamil: 2.5–5–10 mg bolus Sodium bicarbonate: 1 mEq/kg for cardiac arrest of uncertain origin; repeat, if required, 0.5–1 mEq/kg. MCQ MCQss 1. All patient in cardiac arrest receive resuscitation unless: a. The patient has a valid DNAR order b. The patient has signs of irreversible death c. No physiological benefit can be expected because the vital function have deteriorated despite maximal therapy d. The patient has hypovolemic shock 2. Which of the following is not true about bag mask ventilation during CPR?

253

a. Without O2 supplement: tidal volume approx 10 ml/kg over 2 seconds should be given b. With O2 supplement (> 40%): a smaller tidal volume of 6–7 ml/kg should be delivered over 2 second c. Intubation of trachea must be done before starting of bag and ask ventilation d. Alternative airway devices may be acceptable when rescuer are trained in their use. 3. All of the following are signs of circulation except: a. Swallowing b. Normal breathing c. Coughing d. Movement. 4. Which of the following is true about adult CPR: a. The compression rate is approximately 100 per minute b. The compression-ventilation ratio for 1 and 2 rescuer CPR is 15 compressions to 2 ventilations when the victim’s airway is unprotected c. Depression of sternum should be approximately 7–8 cm d. Chest compression can produce systolic arterial blood pressure peaks of 100 to 120 mmHg. 5. Which of the following is not a recommended maneuver to open the airway during CPR: a. Head tilt-chin lift maneuver b. Jaw thrust maneuver c. Mandibular retraction maneuver d. Jaw thrust without head tilt. 6. Which of the following is not a technique to provide rescue breathing: a. Mouth-to-mouth breathing b. Nose-to-mouse breathing c. Mouth-to-stoma breathing d. Mouth-to-face shield breathing

254 A PRIMER OF ANESTHESIA

7. Which of the following is a false statement for bag-mask ventilation? a. It consists of a self inflating bag and a non-breathing valve attached to a face mask b. Most commercially available adult bagmask units have a volume of approximately 1600 ml c. Self inflating bag-mask units are most effective when 2 trained and experienced rescuers work together d. If supplementary oxygen is available, bag mask ventilation should be attempted to deliver 10–12 ml/kg of tidal volume.

12. Which of the following is true about epinephrine? a. Produces beneficial effects in patients during cardiac arrest primarily because of its b-adrenergic receptor-stimulating properties b. Dose of epinephrine for tracheal delivery is atleast 10–15 times the peripheral IV dose c. The recommended dose of epinephrine is 1.0 mg administered IV every 3-5 minutes during resuscitation d. Intracardiac administration of epinephrine should be done routinely.

8. All of the following are complications of chest compression except: a. Gas embolism b. Fracture of the sternum c. Hemothorax d. Fat embolism.

13. All of the following are potentially reversible causes of adult cardiac arrest except: a. Hypothermia b. Metabolic acidosis c. Tension pneumothorax d. Hypocalcemia.

9. ACLS includes all of the following except: a. Basic life support b. Blood transfusion c. Establishment and maintenance of intravenous access d. Treatment of patients with suspected acute coronary syndrome. 10. The percentage inspired oxygen concentration delivered to the patient through ventilation using exhaled air: a. 16-17% b. 20-22% c. 22-24% d. 24-26% 11. Alternative airways recommended for the maintenance of airway during CPR are all except: a. Laryngeal mask airway (LMA) b. Esophageal-tracheal combiture (ETC) c. Pharyngotracheal lumen airway (PTC) d. Cuffed oropharyngeal airway (COPA).

14. All of the following steps are included in the ACLS algorithm except: a. Administration of calcium gluconate b. BLS c. Defibrillation d. Administration of vasopressors. 15. The dose of vasopressin administered during the management of adult cardiac arrest is: a. 20 U IV b. 30 U IV c. 40 U IV d. 50 U IV. Answers 1. 5. 9. 13.

d c b d

2. 6. 10. 14.

c b a a

3. 7. 11. 15.

a d d c

4. b 8. a 12. c

Index A Acetylcholine (ACh) 34 role of acetylcholinesterase 34 action of ACh on nicotinic receptors 34 Acute heart failure 229 Acute renal failure 231 Airway management 102 airway equipment 114 difficult airway algorithm 113 initial airway management 103 problems with mask ventilation 104 rapid sequence induction and intubation 112 Airway obstruction 104, 193 Anemia 80 Anesthesia breathing circuits 60 Anesthesia monitoring 87 appropriate monitoring 93 common monitoring techniques 88 central venous pressure monitoring 90 ECG monitoring 88 invasive (direct) arterial pressure monitoring 90 neuromuscular monitoring 93 non-invasive blood pressure monitoring 89 temperature monitoring 93 Anticholinesterase drugs 38 Anticoagulant therapy 78 Antihypertensive drugs 80

Arterial blood gas analysis 72 Arterial tonometry 90 Atracurium 32

B Bag-mask-ventilation 243 “Balanced” salt solutions 162 Basal fluid requirement 163 Blenders 206 Blood transfusion 165 complications 168 components 166 cryoprecipitate 167 fresh frozen plasma 167 packed red blood cells 166 platelets 166 Bronchial asthma 72

C Capnography 92 Cardiogenic shock 227 Cardiopulmonary resuscitation 239 advanced cardiac life support 244 access for medications 245 defibrillation 244 BLS algorithm 241 Complications of BLS 252 CPR for infants and children 248 drugs 248 post-resuscitation care 248 Caudal anesthesia 138 Central pontine myelinolysis 176 Channelopathies 45 Chest compressions 244 Citrate intoxication 170 Coagulopathy 168

Colloid osmotic pressure 159 Colloids 163 dextrans 165 gelatins 164 hydroxy ethyl starch 165 Combitube 116 Common gas outlet 60 Compressed oxygen outlet 60 Congenital myasthenic syndromes 46 Cricothyrotomy 113 Crystalloids 160 “balanced” salt solutions 162 dextrose 161 sodium chloride 162

D Dalton’s law of partial pressures 19 Defibrillation 244 Demyelinating diseases 45 Depolarizing block 36 Depolarizing relaxants 37 Desensitization block 36 Determination of exposure code 213 Diabetes mellitus 73 Dibucaine number 38 Differential blockade 127 Disseminated intravascular coagulation 169 Distributive shock 227 Double burst stimulation 48 Draw-over apparatus 53 Dysrhythmias 195 Dystrophies 45

E Eaton Lambert syndrome 46 Electrical nerve stimulators 143, 144

256 A PRIMER OF ANESTHESIA Electrolyte abnormalities 171 Emergency cardiac care 239 Emergency oxygen flush 60 EMO vaporiser 54 Endotracheal intubation 246 Endotracheal tube 115 Entrainment devices 204 Epidural anesthesia 131 Ester hydrolysis 41 Expiratory obstruction 105

F Face mask 115 Fasciculation 33 Fluoride number 38

G Gibbs-Donnan effect 160 Glasgow coma score 222 Guedel’s stages of anesthesia 28 Guillain-Barre syndrome 45

H Henry’s law 19 Hepatitis B virus 210 Hepatitis C virus 210 High pressure system 54 Hilton’s law 143 Hofmann elimination 41 Hypercalcemia and hypocalcemia 182 causes of hypercalcemia 182 causes of hypocalcemia 184 clinical sings in hypocalcemia 185 management of hypercalcemia 183 management strategy for hypocalcemia 186 prolonged Q-T in hypocalcemia 184 Hyperkalemia 179 anesthetic considerations 179 causes 180

ECG changes 179 management 181 principles of treatment 179 Hyperkalemia 232 Hypernatremia 172 Hypertension 78, 195 Hypokalemia 177 ECG changes 177 plan for treatment 178 Hyponatremia 174 Hypotension 195 Hypothermia 170 Hypotonic fluid 159 Hypoventilation 194 Hypovolemic shock 227 Hypoxemia 193

I Immunosuppression 171 Infrared light 91 Inhalational anesthetics 18 anesthetics in clinical use 21 individual inhalation agents 24 desflurane 26 diethyl ether 26 enflurane 25 halothane 24 isoflurane 25 nitrous oxide 28 sevoflurane 26 induction characteristics and respiratory effects 22 metabolism and excretion 20 pharmacodynamics 20 pharmacokinetics 19 factors affecting rate of uptake 20 solubility/partition coefficient 19 uptake of anesthetic agents 19 physical principles 19 physical properties 22 potency 18 dose-response curve 18

minimum alveolar concentration 18 Intensive care unit 219 admission 220 cardiovascular issues 226 design 219 ethical issues in ICU 235 care of the dying patient 236 predicting the outcome 236 infection control 223 monitoring 220 cardiovascular monitoring 220 neuromonitoring 222 respiratory system monitoring 220 nutrition in the ICU 233 renal problems 231 respiratory issues 224 positive pressure ventilation 224 staffing 219 Intraosseous infusion 245 Intravenous anesthetic agents and opioids 3 barbiturates 4 benzodiazepines 11 pharmacokinetics 11 pharmacology 11 diazepam 12 flumazenil 12 side effects and contraindications 12 ketamine hydrochloride 9 absolute contraindications 10 administration 10 adverse effects 10 cardiovascular system effects 9 central nervous system effects 9 indications 10 other systems effects 9 pharmacokinetics 10 precautions 10 respiratory system effects 9

INDEX midazolam 11 dosage 12 propofol 7 administration 8 adverse effects 8 cardiovascular system effects 7 central nervous system effects 7 hepatorenal effects 8 pharmacokinetics 8 physical properties 7 respiratory system effects 7 sodium thiopentone 4 absolute contraindications 6 actions on the cardiovascular system actions on the central nervous system 4 adverse effects and problems 6 dosage and administration 5 effects on the respiratory system 5 indications 6 pharmacokinetics 5 precautions 6 Intubation 106 Ion channel myotonia 46

J Jugular venous oxygen saturation 223

L Laryngeal mask airway 109, 246 Laryngoscope 117 Laryngoscopy 106 Low-pressure system 54

M Macintosh blade 118 Magill intubating forceps 117

Malleable stylet 118 Mapleson breathing circuits 61 Jackson-Rees’ modification 62 Mask ventilation 104 Masseter spasm 39 Mayer-Overton theory 20 Medical paternalism 235 Microdialysis 223 Miller blade 118 Minimum alveolar concentration 18 Motor neuron diseases 45 Mouth-to-mouth breathing 242 Multiple sclerosis 45 Muscle diseases 45 Muscle relaxant 37 Muscle relaxants 32 Myasthenia gravis 45 Myasthenic syndrome 46

N Nasal catheter 201, 202 Nasopharyngeal airway 114 Needle stick injuries 212 Neoromuscular blocking agents 32 Nerve localization 144 Nerve stimulation 47 Neuraxial block for surgery 121 advantages 121 assessment of effectiveness of spinal/epidural block 137 caudal anesthesia 138 combined spinalepidural anesthesia technique 140 complications 139 technique 138 The Armitage formula 139 contraindications 128 epidural and spinal blockade 136 epidural anesthesia 131 complications 134

257

indications for spinal/ epidural anesthesia 122 pharmacology of local anesthetic agents 124 absorption 125 drug interactions 127 effect on the cardiovascular system 126 metabolism of LA agents 125 neurological effects 126 neurological side effects 126 onset of action 124 potency 124 physiological effects 127 autonomic blockade 127 somatic blockade 127 preoperative preparation 128 physical preparation 129 psychological preparation 128 operation theater management-preparation and monitoring 129 sedation 137 subarachnoid (spinal) anesthesia 135 Neuromuscular blockade 43 issues in the intensive care unit 46 monitoring 46 pharmacokinetics 44 Neuromuscular blocking drugs 35 mechanism of action of muscle relaxants 35 depolarizing 35 non-depolarizing 35 Neuromuscular junction 33 Non-depolarizing block 36 Non-depolarizing relaxants 40 doses 40

258 A PRIMER OF ANESTHESIA objectives 200 oxygen delivery systems 200 high flow systems 204 low flow systems 201 reservoir systems 202

interactions 42 metabolism of muscle relaxants 41 pharmacodynamics 40 pharmacokinetics 40 side effects 42 Non-invasive ventilation 226

P O Obstructive shock 227 Oncotic pressure 160 Open-drop anesthesia 53 Opioid (narcotic) analgesics 13 classification 13 agonists, antagonists, and partial antagonists 13 alfentanil 15 endogenous opioid agonists 13 fentanyl 15 morphine 14 naloxone 15 opiate receptors 13 pentazocine 15 pethidine 14 remifentanil 15 sufentanil 15 tramadol 15 Oral hypoglycemic drugs 74 Oropharyngeal (Guedel’s) airway 114, 246 Osmolality 158 Osmolarity 158 Osmole 159 Osmotic pressure 159 Oxygen analyser 58 Oxygen failure protection device 58 Oxygen hood 204 Oxygen pressure failure warning devices 57 Oxygen tent 203 Oxygen therapy 200 clinical situations 200 laboratory and bedside measurements to diagnose hypoxemia 200

Paradoxical respiration 104 Patterns of stimulation 48 Peripheral nerve blockade 143 advantages 144 ankle block 151 blocks for hernia surgery 154 complications 145 contraindications 145 digital nerve block 149 femoral nerve block 150 indications 144 lower limb anatomy 149 greater trochanter 150 ischial tuberosity 150 lumbar plexus 149 posterior superior iliac spine 150 pubic tubercle 150 sacral plexus 149 penile block 154 recent advances in peripheral nerve blockade 155 stimulating catheter technique 155 ultrasound guided blocks 155 sciatic nerve block 151 technique 143 upper limb blocks 146 axillary block 148 infraclavicular block 148 interscalene block 146 supraclavicular block 147 Phase II block 36 Pin index safety system 55 Pipeline inlets 56

Positive end expiratory pressure 225 Positive pressure ventilation 224 Post-anesthesia care 191 complications 193 circulatory 195 electrocardiographic changes 196 hypothermia and shivering 197 nausea and vomiting 197 respiratory 193 general management 191 Preoperative evaluation 64 anesthetic implications of concurrent disease 72 ASA physical status grading 69 benefits 65 Fasting guidelines 70 premedication 70 goals 64 guidelines for laboratory testing 69 stepwise approach 65 examination 67 history 65 Pressure regulator 57 Priming 41 Pseudo-hyponatremia 174 Pulmonary artery wedge pressure 222 Pulmonary function testing 72 Pulse oximetry 91

R Renal replacement therapy 232 Reservoir cannula 202 Reservoir masks 203

S Saturated vapour pressure 19 Schimmelbusch mask 53 Sedation 137 Selectatec system 59

INDEX Sepsis 227 Septic shock 227 Stimulus 47 Structure of the HIV virus 209 Supramaximal stimulus 47 Suxamethonium 37 clinical uses 38 undesirable effects 38

Transcranial Doppler ultrasonography 223 Transfusion reactions 170 Transtracheal catheter 202

U Universal safety precautions 211

T

V

Tetanic stimulation 48 Threshold current 47 Thrombasthenia 166 Thrombocytopenia 168 Tonicity 159

Valtis Kennedy effect 168 Valvular heart disease 76 Vaporizers 59 Vascular cannulation 97 indications of peripheral 97

259

sizes and parts of an IV cannula 97 steps in inserting an IV cannula 98 technique of arterial cannulation 99 technique of central venous cannulation 98 Vecuronium 32 Ventimask 204 Ventricular end-diastolic pressure 222 Vertebral column and the spinal cord 122

Y Yoke assembly 56