A Primer of Anesthesia

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
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A Primer of ANESTHESIA
2008, Rajeshwari Subramaniam
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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
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
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
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.Stephens Hospital
Former Head of Cardiothoracic Anaesthesia
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
patients 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 anesthesiologists 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
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
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
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 todays 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 15401550 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). Ethers 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
1850s-1860s. 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 1870s 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
1960s (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 1990s.
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 1800s and early
1900s. 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. Lundys concept of
balanced anesthesia introduced in the 1940s
consisted of administration of thiopentone,
nitrous oxide, muscle relaxant and an opiate,
(usually meperidine) and still finds favor with
most anesthesiologists. After the 1970s,
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
anesthesiologists responsibility to (a) assess and
evaluate the patients 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 medicines greatest gift to
humanity. For those of you who have not
had an opportunity to visit Mortons 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 agents 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
Thiopentone
Ethyl
1-methyl-butyl
Rapid acting, fairly prompt recovery
Pentobarbitone
Ethyl
1-methyl-butyl
Prolonged action
Methohexitone
CH2CH=CH2 CH(CH3)C=CC2H5
CH3
Rapid action and recovery, excitatory

phenomena
Phenobarbitone
Ethyl
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 10.510.8. 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
510 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.
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 (1015% of the
remaining drug is metabolised each hour).
Hence up to 30% of drug is still in the body
after 46 hours. The metabolites are thiopental
carboxylic acid (inactive), hydroxythiopental
(inactive) and pentobarbital (active, with halflife of 2050 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
injection. The dose in healthy adults is 45 mg/

kg administered over 15 seconds. Consciousness will be lost in 30 seconds; if the eyelash
reflex is not lost then a further 50100 mg should
be given. Children require about 6 mg/kg, and
elderly patients 2.53 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 (1020 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.
Porphyriabarbiturates 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
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.
hydroxide. The pH of this solution is 68.5. 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 50100
g, (ii) premixing the propofol with 12 ml of
preservative-free lidocaine.
Pharmacology
Central Nervous System

Anesthesia is induced in 2040 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.
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, 1.52.5 mg/kg
is adequate for anesthetic induction. The elderly
are very sensitive to propofol. 11.5 mg/kg is
usually adequate. In children 36 mg/kg is
required. Propofol is not recommended in
children less than a month of age. For sedation
a dose of 1.54.5 mg/kg/hour is used. For total
intravenous anesthesia doses between 610 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.
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.
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

After intravenous injection it produces anesthesia in 3060 seconds. The anesthetic effect
lasts 1525 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
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.
Arterial pressure, heart rate and pulmonary
vascular resistance are increased by 2040%.
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.
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
11.5 mg/kg are required every 510 minutes,
if anesthesia is being maintained with ketamine.
The intramuscular (IM) dose is 810 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.
Upper airway obstructionalthough 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.
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.

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.
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,
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 23 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
50150 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 6.46.9. 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 0.11 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.
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.
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). 1 and k3
are related to supraspinal analgesia. receptors
are found in the caudate and dorsal nuclei.
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 , , and . Since then it has been
found that is not an opioid receptor. There
are subtypes of each of these receptors (i.e. 1,
2, 3 and 3k subtypes). It is suggested that 1
is an analgesic receptor and 2 causes respiratory
depression. Morphine induced analgesia is a
typical example of 1 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
(4060 times the usual dose) may produce
complete anesthesia on their own.
Classification
Actions
Endogenous Opioid Agonists
Analgesia
Encephalin, -endorphin, and dynorphin are

the agonists that exist in the body for receptors
, , and , receptors respectively.
receptor agonists are more effective in

producing analgesia than 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
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.
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 0.10.3 mg/kg. Morphine can
be used as infusion for postoperative pain relief
in a dose of 1040 g/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 11.5 mg/kg, and like morphine an antiemetic
agent like promethazine (0.5 mg/kg) administered concomitantly is useful. The commonly
used IV dose is 0.51 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
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 0.10.5 g/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
24 g/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 g/ 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 8490 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 510 g/kg, with supplemental doses of
35 g/kg.
It is an ultra short-acting 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 g/kg as a bolus before laryngoscopy,
and continued as an infusion of 0.250.5 g/
kg/min. Within 35 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 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 and receptor agonist and has antagonist/partial agonist effect on the 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
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
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
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
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 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. 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 -37C, 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 Henrys 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.
Daltons 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)
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.
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
Lets 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.
Table 2.1: Physical properties of inhalational agents
Agent
Mac
Color code
B.P.
Sodalime
Blood/gas
Halothane
0.75
Red
50.2C
No reaction
2.3
Isoflurane
1.15
Purple
48.5C
CO with dry SL
1.43
Enflurane
1.68
Orange
56.5C
CO with dry SL
1.9
Sevoflurane
2.00
Yellow
58.6C
Compound A/B
0.69
Desflurane
6.35
Supplied in bottle
with special valve
22.8C
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 65C 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 bloodgas 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
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 g) 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 mol/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
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 3070%. 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
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.
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 lyase to
produce nephrotoxic metabolites in rats. In the
last few years it has been shown that in humans
there is 1030 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 (23.5C) 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.
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
Figs 2.7A and B: Guedels 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 36% 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
patients 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
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.
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.
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
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 agentscommonly
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
1980s 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 invaginationsthe 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
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 (MEPPs). These have only 1/100th
the amplitude of an evoked End Plate
Potential (EPP) which is produced by
stimulation of the motor nerve. Although
MEPPs 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 MEPPs 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 (<1 msec)
destroyed by the enzyme acetylcholinesterase
in the junctional cleft (Fig. 3.3).
Action of A
Ch on Nicotinic Receptors
AC
Nicotinic receptors are both prejunctional and
postjunctional. Postjunctional receptors are on
the endplate opposite the prejunctional
receptors. The ACh receptors in the innervated
adult NMJ are called adult, mature or junctional
receptors. Another isoform known as extra
junctional, fetal or immature ACh receptor is
seen in certain conditions like inactivity, sepsis,
denervation, burns, other events causing
increased protein catabolism and also in the
fetus. ACh receptors are glycoproteins which
are synthesized in the muscle cell and are
anchored to the end plate by a special 43-Kd
protein. They are formed of 5 subunit proteins
(Fig. 3.4) arranged in a cylindrical shape around
a central cation channel. The pore of this
channel is normally closed by approximation
of the subunits and opens only when both the
Fig. 3.4: The acetylcholine receptor with 5 subunits

(includes 2 subunits)
35
Fig. 3.5: Sodium channel opens when 2 ACh molecules occupy both subunits
alpha subunits are occupied by an agonist (Fig.

3.5). This allows a wave of depolarization which
creates an EPP and stimulates the muscle to
contract.
NEUROMUSCULAR BLOCKING DRUGS
Chemistry: All neuromuscular blockers are
quaternary ammonium compounds. The
positive charge at the ammonium group mimics
the quaternary nitrogen atom of the neurotransmitter ACh and is the principal reason for
the attraction of these drugs to the nicotinic ACh
receptors at the NMJ. In pancuronium and
vecuronium, entire ACh- like structures are
incorporated into the molecule. The depolarizing relaxant succinylcholine consists of two
molecules of ACh linked back to back through
acetate methyl groups.
The quarternary ammonium structure
confers certain specific properties on the NMB
agents. Hepatic uptake is inhibited to a large
extent and urinary excretion facilitated (exceptions will be dealt with while discussing individual
relaxants). These agents are also unable to cross
lipid membranes such as the placenta and the
blood-brain barrier.
Mechanism of Action of Muscle Relaxants
Depolarizing muscle relaxants: Depolarizing
relaxants resemble ACh (Fig. 3.6) and bind to
the ACh receptor, generating a muscle action
potential. Since they are not metabolized by
acetylcholinesterase, they bind repeatedly with
Fig. 3.6: Similarity in the structure of ACh and

succinylcholine
the receptors resulting in a prolonged depolarization of the muscle end plate. Initial binding of
the drug (Fig. 3.7) causes the sodium channels
to open and a wave of depolarization spreads
along the muscle causing muscle contraction.
Soon after, the time dependent inactivation of
the sodium channel ceases and the channel
closes. These sodium channels now cannot
reopen until the end plate repolarises which is
not possible as long as the depolarizer keeps
binding to the receptors. Once the perijunctional channels close, the initial action potential
disappears and the muscle returns to its resting
state. Skeletal muscle paralysis occurs as a
depolarized postjunctional membrane cannot
respond to a subsequent release of ACh. The
depolarizing relaxants are also termed Noncompetitive relaxants and the block induced
is known as a Depolarizing or Phase I block.
Non-depolarizing muscle relaxants: These
relaxants bind to the ACh receptor but are
incapable of inducing conformational changes
for channel opening. ACh is prevented from
Fig. 3.7: Depolarizing block. Red squares (suxamethonium) resemble ACh in structure, block ACh receptors;
Na channels open, depolarization occurs (seen as fasciculations); Na channels close after some time.
Muscle is in resting state (flaccid). Channels cannot re open till receptors are free of suxamethonium and
repolarization occurs
Fig. 3.8: Non-depolarizing block; relaxant molecule occupies non-ACh site but prevents ACh from occupying
its receptor. No depolarization, therefore no fasciculation seen; depolarization can occur only after relaxant
diffuses away and/or is outnumbered by ACh molecules
binding to the receptors (Fig. 3.8) and no EPP

can develop. As they compete with ACh for
binding sites they are also known as Competitive antagonists.
mechanism is unknown and desensitization (see

below) by succinylcholine may be a factor.
Persistent weakness after succinylcholine
indicates a phase II block.
Phase II block: This is a complex event which

occurs if the neuromuscular junction is continuously exposed to depolarizers. The junction
is depolarized initially by the application of the
drug but the membrane potential slowly returns
to normal. It appears to be caused by ionic and
conformational changes that accompany
prolonged muscle depolarization and depends
on duration of exposure to the drug, the drug
used and its concentration. In spite of becoming
repolarised, the postjunctional membrane does
not respond normally to ACh. The exact
Desensitization block: The ACh receptor can

exist in many states. If the receptors do not
undergo the conformational changes required
to open the channel in spite of binding to the
agonist they are said to be desensitized. Drugs
which may cause desensitization and hence
weaken neuromuscular transmission include
volatile anesthetics, antibiotics (polymyxin B),
cocaine, alcohols, barbiturates, decamethonium, anticholinesterases, local anesthetics,
phenothiazines and calcium channel blockers.
37
Properties of an Ideal Muscle Relaxant

Rapid onset of action allowing fast tracheal
intubation.
Prompt reversal with anticholinesterases with
no tendency to for the block to recur.
Cardiovascular stability.
No histamine release.
Complete metabolism to inactive metabolites.
Not dependent on renal or hepatic clearance.
Absence of cumulation even if used for
prolonged periods (e.g. in ICU).
Fig. 3.9A: Structure of succinylcholine
CLASSIFICATION OF MUSCLE RELAXANTS

(TABLE 3.1)
i. Depolarizing-suxamethonium, decamethonium.
ii. Nondepolarizing-can be further classified
on the basis of (i) chemical structure or (ii)
duration of action (time taken for recovery
of twitch height to 25% of baseline).
DEPOLARIZING RELAXANTS
Suxamethonium: Succinylcholine, as it is
commonly known (Figs 3.9A and B), is the only
depolarizing relaxant in clinical use. Doses of
0.51.5 mg/kg intravenously produce rapid
(3060 seconds) onset of skeletal muscle
paralysis. The depolarization produced by the
initial administration of the drug is initially
manifested by transient skeletal muscle
contractions known as fasciculations which start
on the face and spread rapidly over the upper
extremities, abdomen and lower limbs. These
fasciculations are associated with a sustained
Fig. 3.9B: Succinylcholine vial
opening of the ion channels and leakage of

potassium ions (K+) from the interior of the cells
enough to cause an increase in the plasma K+
concentration by 0.5 mEq/L. Succinylcholine
has a brief duration of action (5-10 minutes)
due to rapid hydrolysis by plasma pseudocholinesterase which is synthesized in the liver.
Owing to the rapid hydrolysis only a fraction of
the original dose (10%) reaches the NMJ. The
neuromuscular block terminates by diffusion of
Table 3.1: Classification of nondepolarizing muscle relaxants

Chemical structure
Long acting (>50 mins)
Steroidal
Pancuronium Pipecuronium
Benzylisoquinolines d-tubocurare, metocurine

doxacurium
Phenolic ether
Gallamine
Intermediate (2050 mins)
Short acting (1020 mins)
Vecuronium, Rocuronium
Rapacuronium
Atracurium, Cisatracurium
Mivacurium
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 3040
minutes. One in 3000 patients are homozygous for the abnormal gene and the
atypical pseudocholinesterase results in
paralysis lasting up to 68 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
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 13 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 2448 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 2448 hours after injury and up to
12 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 24 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
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
0.080.12
0.050.08
0.10.2
0.61.0
0.50.6
0.150.2
0.20.25
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. Whipples 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 23 times the ED 95 to facilitate
the manoeuvre in 23 minutes. For rapid
tracheal intubation 24 times ED 95 doses can
be used with the consequence of a longer
duration of action. Additional doses or top-ups
should be 1020% of the initial dose in the case
of long acting relaxants and 2530% 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. 9095% 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 3050% if volatile anesthetics are
being used.
All these agents can also be administered as
infusions.
Priming is the use of small doses (20 % of

ED 95) of the relaxant given 24 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 23 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 (12 ml/kg/min). There are a few
exceptions to this rule: (i) Vecuronium is more
lipid soluble. Therefore, 3040% 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 36 ml/
kg/min.(ii) Atracurium is metabolized by
Hofmann elimination in the plasma and by
Ester hydrolysis in the interstitial fluid. It is
cleared 23 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 45 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 36 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 7080%
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%
<10%
40-50%
16% of total
15%
>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%)
<5%
none
<2%
none
Monoester, quaternary
alcohol
Succinylmonocholine,
choline
Succinylcholine ultrashort
Table 3.4: Other effects of muscle relaxants
Drug
Autonomic Ganglia
Cardiac Muscarinic Receptors
Histamine Release
Succinylcholine
Steroidal
Vecuronium
Pancuronium
Rocuronium
Rapacuronium
Benzylisoquinolines
Doxacurium
Atracurium
Cisatracurium
Mivacurium
Others
Gallamine
stimulates
stimulates
slight
blocks moderately
blocks weakly
blocks moderately
? slight
slight
slight
blocks strongly
Side Effects of Neuromuscular Blocking

Drugs
1. Autonomic: Muscle relaxants have effects on
nicotinic and muscarinic receptors in both
the sympathetic and parasympathetic
nervous systems. These effects are dose
related and additive and not attenuated by
slowing the rate of injection and are
displayed in Table 3.4. Gallamine is an
outdated relaxant which was characterized
by a severe vagolytic action.
2. Histamine release: These drugs have only
weak histamine releasing properties.
Histamine release is seen with larger doses
and more commonly with benzylisoquinolines (tubocurarine, atracurium and
cisatracurium). The effect lasts for 5-10 min,
and is dose related. It is reduced by slow
injection of the drug and by prophylaxis with
H1 and H2 blockers. Steroidal compounds
usually do not cause histamine release.
3. Bronchial tone: Due to effects on the
muscarinic receptors in the airway, rapacuronium was associated with a high incidence
of bronchospasm resulting in withdrawal of
the drug from the market. Benzylisoquinolines (except doxacurium) may cause
histamine release leading to increased airway

resistance and bronchospasm in patients
with hyper-reactive airway disease. Vecuronium is less prone to cause bronchospasm.
4. Allergic reactions: Succinylcholine may
trigger anaphylactic or anaphylactoid
reactions. Cross reactivity with a neuromuscular drug is seen in > 60% patients
with a history of anaphylaxis. Rocuronium
has a moderate risk of causing allergic
reactions.
Interactions of Nondepolarizing Muscle
Relaxants
1. Anesthetics: Inhaled anesthetics augment
neuromuscular block in a dose dependent
fashion.
2. Temperature: Hypothermia potentiates
neuromuscular block and also affects the
interpretation of neuromuscular monitoring
3. Drug interactions: (a) Other muscle
relaxants: effects may be additive if
chemically related drugs are co-administered,
or synergistic if the drugs are structurally
dissimilar. (b) Succinylcholine: If a priming
dose of nondepolariser is given before
succinylcholine, its dose needs to be
increased. (c) Antibiotics: Aminoglycoside

antibiotics potentiate neuromuscular
blockade by both a pre and postsynaptic
action. (d) Magnesium sulphate: This is
the current drug used for the perioperative
management
of
eclampsia
and
preeclampsia. MgSO 4 potentiates nondepolarising NMBs probably due to both pre
and post synaptic effects. High concentrations of magnesium ions inhibit calcium
channels at the presynaptic nerve terminals
that trigger the release of ACh. These ions
also have an inhibitory action on the
postjunctional potentials and decrease the
excitability of the muscle fibers. The
interaction of magnesium with succinylcholine is controversial. (e) Calcium: Calcium
triggers release of ACh from the motor nerve
terminal and increases excitation-contraction
coupling. In hypercalcemia there is a
decrease in sensitivity to atracurium and in
the time course of the neuromuscular block.
Use of calcium channel blocking drugs
may be expected to potentiate non-depolarizing NMB but the effects are subclinical.
(f) Lithium: Enters the cells through the
calcium channels and tends to accumulate
intracellularly. By an action on the K +
channels it tends to inhibit neuromuscular
transmission by a presynaptic effect and
muscle contraction postsynaptically. There
is a prolongation of neuromuscular blockade
with the use of both depolarizing and
nodepolarising relaxants. (g) Local Anesthetics and Antidysrhythmics: Local
anesthetics have an action at the presynaptic
membrane, postsynaptic membrane and
muscle membrane. While in smaller doses
they enhance both depolarizing and nondepolarising block, in larger doses they may
block neuromuscular transmission.
(h) Antiepileptic drugs: Depress the
release of ACh at the NMJ. With chronic
therapy patients may demonstrate resistance
to these drugs perhaps due to increased
43
clearance, increased binding to alpha 1

glycoprotein or upregulation of nonacetylcholine receptors. (i) Diuretics:
Furosemide inhibits the production of cAMP
resulting in a decrease in the breakdown of
ATP and decrease in the output of ACh, thus
potentiating non-depolarising neuromuscular block. Mannitol has no such effect.
(j) Miscellaneous: Dantrolene, used for
treating malignant hyperpyrexia potentiates
the effects of nondepolarisers. Azathioprine has an antagonistic action on
neuromuscular block. Steroids may
antagonize a neuromuscular block by acting
presynaptically to enhance release of ACh.
However prolonged treatment can cause
muscle weakness. Antiestrogenic drugs like
Tamoxifen appear to potentiate the effect
of nondepolarisers.
4. Burns: may cause resistance to the effect of
nondepolarisers if the burn surface area is
>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
pyridostigmine. The doses required are

7-20 g/kg of atropine with 0.5-1.0 mg/kg
of edrophonium and 7-15 g/kg of glycopyrrolate with neostigmine 40-60 g/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 NMBs 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 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
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.
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 nAChRs.
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.
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 nervefirst dorsal interosseous muscle,
(b) ulnar nerveabductor 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.
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
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 <1 indicates a deep level of paralysis,
PTC of 2-8 indicates moderately deep block
Table 3.5: Correlation of train-of-four ratio and clinical recovery
Train of four
ratio (TOFR)
Clinical Correlation
< or = 0.4
Cannot lift head/ arm, tidal volume normal, vital capacity and inspiratory force reduced.
= 0.6
Head lift for 3 secs, vital capacity and inspiratory force reduced.
0.7-0.75
Head lift for 5 secs, can open eyes wide, can protrude tongue, adequate cough, grip
strength is still reduced.
> 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.
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<-40-50 cm water
Neuromuscular blocking drugs have

represented one of the most useful adjuncts for
facilitating surgery. They produce a relaxed,
immobile patient. Relaxants also facilitate
intubation and ventilation.
NMJ monitoring has enhanced the safety of
this group of drugs.
NMJ monitoring is ideal in all patients
receiving relaxants to minimise complications
associated with an inadequate reversal of
neuromuscular blockade.
NMJ monitoring is strongly advisable in some
situations-severe liver and renal disease , neuromuscular disorders, severe lung disease, morbid
obesity and use of relaxants as infusion and
during prolonged surgical procedures.
MCQ
MCQss
1. These muscles have > 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
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, Ayres 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
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
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
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
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
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 (24C). 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
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
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 patients
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
Fig. 4.15: Patient end of Bain circuit. Note inner

tube attached to outer by 3 spokes
Fig. 4.16: Jackson-Rees modification of

Ayres 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
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 anesthesiologists 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 patients
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
patients 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 patients 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
patients 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 patients 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
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.
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
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 Ifaucial pillars, soft palate,
uvula visible (Fig. 5.6).
Mallampati IIfaucial pillars and soft
palate visible.
Mallampati IIIonly soft palate visible.
Mallampati IVonly 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).
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
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 patients 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.
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
20g/kg.
Patients undergoing oral surgery and
dental procedures, to keep the operative
field clear of saliva. Glycopyrrolate
(10-20 g/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 g/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 g/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
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 patients

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.
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 2 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 2 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
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 (Cushings
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
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 longstanding 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
Historyregarding
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
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
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 g/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
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 g/kg or morphine 150-300

g/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,
Cushings syndrome, pheochromocytoma, etc.
Initially, to keep up with the increase in systemic

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 (blockers, 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- 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
seconds prior to intubation, (ii) fentanyl

2 g/kg or esmolol 150-300 g/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 g/kg/min
30-60 sec
1-5 min
Nitroglycerin
0.5-10 g/kg/min
1 min
3-5 min
Esmolol
0.5 mg/kg over 1 min
1 min
12-20 min
50-300 g/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 g/kg/min
5 min
5 min
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, Whipples 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
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. Mothers milk administered 4 hours
prior to surgery.
c. Formula feed administered 2 hours
prior to surgery.
d. Mothers 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 2 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.
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:
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
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.
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.
Figs 6.5A to C: Appropriate cuff size
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
Beers 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
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 m) by CO2.
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
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.
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
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 Recklinghausens 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
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
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
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 Allens
test is performed to ensure good collateral
100
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
BB
101
Fig. 7.7A to E: Steps in cannulation of radial artery
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).
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.
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 patients 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
Guedels 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 patients 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
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
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 childs 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 1980s 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
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
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 (Sellicks 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 patients 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 Sellicks
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
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 patients 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
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
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
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
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 Whipples 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 patients 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
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:
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
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,
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
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 (Ringers 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 g) 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
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 Ringers 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
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 (Tuffiers 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 patients 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
131
Fig. 9.10: Skin preparation
Fig. 9.8: Tuffiers 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
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 patients 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
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
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
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 patients umbilicus. With
136
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
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 patients
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 mg2 mg increments can
be used.
138
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
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
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
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
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
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25.
b
d
a
c
a
d
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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.
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16.
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24.
a
c
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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
Hiltons law.
Hiltons 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
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 sec 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
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
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 Horners
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 legs 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
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
24 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
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
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.
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 patients 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
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
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
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
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 11.5 mA, 100300

sec 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 0.30.5 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 6065%.
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
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
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
<1
40
209
Anions
Cl
HCO3
Protiens
Others
Total
112.0
25.8
15.1
8.2
161.1
117.0
27.1
<0.1
8.4
152.5
3
7
45
154
209
40% of TBW is extracellular = 17L termed

ECF.
Interstitial fluid is 75% of ECF and equals
13 L. Plasma constitutes 20% of ECF (3L) and
transcellular fluid accounts for 5% of ECF(1 L).
Transcellular fluid is defined as fluid outside the
cells but separated from plasma and interstitial
fluid by membrane barriers, e.g. cerebrospinal
fluid, synovial fluid, mucus, pleural and
peritoneal fluid. Table 11.1 depicts the composition of these fluid compartments.
Interstitial fluid
Intracellular fluid
Definitions of Some Commonly used Terms

in Fluid Physics and Physiology
1. Osmolarity: Number of solute particles
per litre of solution. As volume of solvent
can change with temperature (Boyles law),
temperature needs to be specified for
measurements.
2. Osmolality: Number of solute particles
per kg solvent. It is a better measure than
osmolarity as mass, unlike volume, is
unaffected by changes in temperature.
FLUID THERAPY AND TRANSFUSION
However, in practice, there is little difference

between osmolarity and osmolality.
3. Osmole: Amount (in Moles) of solute that
exerts an osmotic pressure of 1 atmosphere
when placed in 22.4 litres of solution at 0
degrees centigrade. For a substance that does
not dissociate in solution, e.g. glucose, 1
mole = 1 Osmole. For a substance that
dissociates into two osmotically active
particles, e.g. NaCl (Na+ + Cl-), 1 mole = 2
osmoles. Therefore if 58 g of NaCl
(1g mol.wt) were dissolved in one litre of
water, it will be a 2 osmolar solution. If
58 mg of NaCl were dissolved in one litre
water, the concentration is 2 mOsm/l. If mean
plasma osmolality were taken as 300 mOsm/
l, [582] 300 = 8,700 mg or 8.7 g NaCl
needs to be dissolved in one litre water. That
makes a concentration of 0.87% or roughly
0.9%. Since dextrose does not dissociate, 1
mOsm/l is generated when 180 mg is
dissolved in one litre water. Therefore to
generate 300 mOsmoles 180 300 =
54,000 mg or 54 g/l or 5.4 g% of dextrose is
needed. Thus 5% dextrose is isotonic with
plasma.* It can be seen that it is not the kind
of particle but the number of osmotically
active particles that is important when one
considers osmolality.
4. Tonicity: Molecules restricted to ECF by
selective permeability and charge of the cell
membrane (Na+ , Cl, HCO3) are important
in determining ECF volume and are said to
provide effective osmoles. The concentration of these effective osmoles is
referred to as tonicity. Tonicity can also
be understood as relative osmolality. A
solution which is isotonic (for example
0.9% or normal saline, 5% dextrose) will not
result in net movement of molecules in and
out of the cell when given intravenously as it
does not result in a change in plasma
osmolality. Hypertonic saline (3-5%) will
159
result in movement of fluid out of cell, while

a hypotonic fluid (distilled water) will result
in diluting the plasma and cellular swelling.
5. Osmosis: Movement of solvent particles
across a semipermiable membrane which
separates solutions of different solute
concentrations (tonicity).
6. Osmotic pressure: If two solutions are
separated by a semipermeable membrane,
solvent particles will tend to move in the
direction of higher solute concentration. If
an arbitrary pressure is applied to the
compartment of higher solute concentration,
which opposes this movement, that pressure
equals osmotic pressure of the solution
(Fig. 11.2).
7. Colloid osmotic pressure: Colloids are large
gelatinous molecules with molecular weight
greater than 10,000 Da. Examples include
plasma proteins like albumin and other
synthetic colloids like gelofusine. These
molecules are unable to cross biological cell
membranes due to their size, and hence exert
their own pressure on the membrane called
colloid osmotic pressure. Though this is
significantly less that osmotic pressure exerted
on membrane by ions, it does become
important in conditions like liver failure and
Fig. 11.2: Concept of osmotic pressure
*What happens after infusion of 5% dextrose is explained on page 161.
160
Figs 11.3A to C: Concept of electroneutrality: The Gibbs-Donnan equilibrium
burns, when plasma protein concentration

deceases significantly, resulting in edema.
8. Oncotic pressure: this is the net osmotic
pressure developed at a biologic membrane
by molecules which are restricted to one side
of the membrane, not just by virtue of size,
but also charge (See Gibbs Donnan effect
below).
9. Gibbs-Donnan effect: This refers to the effect
of distribution of a large charged ion (like
albumin, which is negatively charged) which
cannot diffuse across a biological membrane,
on the distribution of smaller ions (like Na+
and Cl) which would otherwise diffuse much
more freely across the membrane and have
different concentrations across membrane in
the absence of this larger ion (Figs 11.3A to
C).
According to the law of mass action, the product of ions on one side of the membrane should
equal the product of ions on the other side.
(Cation)A (anion) A = (cation) B
(anion) B
(Na+)A (Cl) A = (Na+) B (Cl) B =>

9Na+ 4Cl = 6 Na+ 6Cl
Hence, diffusion of ions down their chemical
concentration gradient is balanced by the
electrostatic attraction of protein molecules
trapped in one compartment.
Intravenous fluids can be divided into
crystalloids and colloids.
WHAT ARE CRYSTALLOIDS?
These are solutions of ions (Na+, Cl-, HCO3,
K+, etc.) and/or small sugars (eg. glucose) in
water. Crystalloids can be further classified into
(a) maintenance type and (b) replacement
type. Maintenance fluids are essentially lowsodium or sodium-free fluids used to replace
fluid loss due to fasting, urinary losses and
evaporation. Examples are 5% glucose in water,
0.45% saline in dextrose, 0.33% saline in dextrose, etc. Replacement fluids resemble plasma
with respect to electrolyte composition (mainly
sodium), i.e. contain 0.9% NaCl along with
273
28
1.5
4
130
Lactated
Ringers (US)
109
278
2
5
131
Hartmanns
solution
111
5% dextrose
29
(as Lactate)
278
5
308
154
154
0.1
26
2.5
0.9
4.5
HCO3
(mmol/L)
Gluconate
(mmol/L)
Ca2+
(mmol/L)
Mg2+
(mmol/L)
K+
(mmol/L)
Cl
(mmol/L)
103
0.9% sodium
chloride
This is essentially water. The glucose added

renders it iso-osmotic and capable of providing
calories through metabolism. The solution
contains the -isomer of glucose. Although
initially 5% dextrose contributes to the tonicity
of plasma, this effect is short lived in the
presence of insulin when it is rapidly taken up
by cells. The residual water is then distributed
throughout total body water (intracellular and
extracellular) and produces negligible plasma
volume expansion in moderate amounts.
Na+
(mmol/L)
1. 5% Dextrose
Table 11.2: Electrolyte concentration of normal serum and common crystalloid solutions
Relatively cheap (compared to colloids).

Most crystalloids are iso-osmotic with plasma
and of a small molecular size. Hence the
molecules are able to pass freely through
microvascular endothelium and do not by
themselves, contribute to oncotic pressure.
- When used to replace plasma loss for
example in trauma or burns, the volume
needed for replacement is three times plasma
volume lost. Therefore, if 500 ml of blood
loss is to be replaced with lactated Ringers
solution or normal saline, 3 times 500 or
1500 ml would be needed. This is because
1530 minutes after intravenous administration crystalloids start to move out of the
intravascular compartment under the
influence of Starling forces and get distributed
to the entire extracellular compartment,
which is approximately twice the volume of
the intravascular compartment. Thus the
replaced volume has to be adequate enough
to simultaneously fill the intravascular and
interstitial compartments. This notion is now
being challenged in recent studies.
The electrolyte composition of most commonly used crystalloids has been compared in
Table 11.2. A few individual fluids are discussed
below.
Glucose
(mmol/L)
142
Salient Features
161
Serum values
Calculated
Osmolality
other electrolytes like potassium and calcium.

Examples are Ringers lactate and normal saline.
290
162
It is mainly used as
- Maintenance during the peri operative
period, in combination with 0.9% saline.
- Correction of hypernatremia
- Dilution for various drugs given as intravenous infusion, as it is non electrolyte
based.
- Correction of hypoglycaemia (though 20%
or 50% is preferred for rapid correction) as
it can be given through peripheral veins
compared with more concentrated solutions
which require to be given via central veins.
- Along with insulin for maintenance of
normal blood sugar in diabetics during
perioperative period (sliding scale) and
correction of hyperkalemia.
Disadvantage
Severe hyponatremia will result if 5% dextrose
is infused rapidly and in large volumes as
glucose gets rapidly metabolised and free water
dilutes extracellular sodium. This potentially
hazardous situation (also termed as water
intoxication) can occur when women in labor
receive oxytocics dissolved in dextrose for
prolonged periods without other electrolyte
supplementation. Oxytocin (vasopressin)
contributes to water retention due to its ADH
like action. For similar reasons, this should not
be the sole solution to treat hypovolemia or
post operative fluid deficit.
2. 0.9% Sodium Chloride (Normal Saline)
As was shown above, this solution contains 154
mmol/L each of sodium and chloride in distilled
water and is isotonic with serum (as normal
serum Osmolality is also 298308 mmol/L).
Uses
- As volume expander to treat hypovolemia
along with balanced salt solutions (see
below).
- Correction of hyponatremia.
- Dilution fluid for various drugs given through
intravenous infusion in diabetics and other
patients in ICU.
Disa
dvantages
Disadvantages
-
Potential to cause hypernatremia and

volume overload if given in large volumes
to replace blood/fluid loss. This is of special
concern in patients with renal dysfunction
or congestive cardiac failure.
- It can also cause hyperchloremic acidosis.
After infusion of large volumes, the body tries
to get rid of the sodium load with concomitant excretion of HCO3 by the kidneys.
In return, kidneys conserve H+ and Cl- which
results in hyperchloraemic acidosis. Hence
it is worthwhile checking the chloride when
evaluating metabolic acidosis in a patient
who has been receiving saline infusion.
- It can theoretically cause microshock when
used with electronic infusion pumps
Coming back to osmolality of normal saline
(0.9% solution):
9,000 = [582] osmolality
osmolality= 9,000 29 = 300. Thus,
although in the strict sense normal saline is not
normal but slightly hypertonic, its osmolality
stays less than 300 mOsm/l since all of NaCl
does not dissociate in solution.
3. Balanced Salt Solutions
These are isotonic crystalloid solutions containing potassium and calcium in addition to
sodium and chloride and are therefore physiologically more balanced or close to plasma
electrolyte concentrations in comparison to
simple electrolyte solutions like saline. The
purpose of these solutions is to maintain the
composition of extracellular environment when
large volumes are infused over a short period of
time.
They form the basis of volume resuscitation
in ATLS protocol.
Main examples are Hartmanns solution
(USA), Ringers Lactate (UK) and Plasmalyte M.
These solutions are excellent for maintenance
as well as replacement, and have less sodium
compared to normal saline.
Disadv
antages
Disadvantages
-
As they contain calcium, these fluids are

incompatible with stored blood (the citrate
anticoagulant gets chelated and blood clots)
Due to the same reason, they are not ideal
drug diluents.
Lactate present in these solutions gets
metabolised by liver to bicarbonate; in
patients with significant hepatic dysfunction,
it can accumulate and cause lactic acidosis.
PERIOPERATIVE FLUID REPLACEMENT

GUIDELINES
How do we calculate the amount of intravenous
fluid needed to compensate for the duration
patients are fasting (Basal fluid requirement)?
- Parameters needed body weight and
duration of fasting
- For the 1st 10 Kg of body weight 4 ml/kg/
hr is needed
- For the next 10 Kg of body weight 2 ml/
kg/hr
- Thereafter 1 ml/Kg/hr
For example Intravenous fluid required to
correct fluid deficit due to fasting for a child
weighing 8 kg, who has been kept nil per mouth
for surgery for 10 hours is 4 ml 8 kg 10 hrs
= 320 ml.
The same needed for a 15 kg child would
be 4 ml/kg for the first 10 Kg body weight = 40
ml and 2 ml/kg for the next 5 kg or 10 ml. Hence
40 + 10 = 50 ml/h for 10 hrs, which would be
500 ml.
Similarly, the requirement for a 50 Kg adult
would be (10 4 +10 2+30 1) =
90 ml/ hr for 10 hrs or 900 ml.
How is the volume of crystalloid needed to
replace ongoing plasma volume loss (replacement) calculated?
Crystalloids solutions start moving out of the
intravascular space and get equally distributed
throughout the extracellular compartment after
intravenous infusion. As the extracellular
compartment is approximately three times the
163
volume of intravascular compartment, crystalloids in the volume of three times the volume of
plasma lost have to be given to maintain
intravascular volume. That is, for a 500 ml
plasma loss, 3 500 = 1500 ml of crystalloid
(for example saline or Hartmanns solution) will
be needed.
Approximate guidelines are provided to
estimate fluid losses in various types of surgery
according to the severity of trauma. Surface/
peripheral procedures like ocular/dental/
cystoscopy require maintenance + 2 ml/kg/hr.
Procedures like inguinal hernia repair or
appendicectomy, most orthopedic limb procedures require maintenance + 4-6 ml/
kg/hr. Major body cavity procedures, surgery on
the spine, hepatic resection etc require 10-15
ml/kg/hr and fluid replacement is guided by urine
output and central venous pressure.
REPLACEMENT FLUIDS COLLOIDS
Definition: colloids are solutions of molecules
with molecular weight greater than 10,000
daltons (Da), which contribute to the oncotic
pressure at the microvascular endothelium.
Use: Colloids are generally used for replacing
plasma loss on an equal volume basis. For
example if a patient has lost 500 ml of blood
which is to be replaced with a colloid, then 500
ml of colloid would be needed. Also colloids by
virtue of their size are restricted to intravascular
compartment for a significantly longer time than
crystalloids (duration of action 2-12 hrs,
compared with 30-60 minutes for crystalloids).
Colloids cannot pass through vascular endothelium due to a combination of greater size and
molecular weight and also the negative charge
which is repelled by vascular endothelium.
Hence their elimination is slow and dependent
on kidneys or reticulo-endothelial system (see
below). If colloids are given rapidly or in large
volumes without close monitoring of patients
volume status they can result in fluid overload,
especially in patients with congestive cardiac
164
Table 11.3: Classification of colloids
Natural colloids
Synthetic colloids
derived from blood
derived from animal and

plant collagen
Examples Albumin,
Plasma, Fresh Frozen
plasma, Cryoprecipitate,
Packed Red Blood Cells.
Examples- Haemaccel,
Gelofusine, Hetastarch.
failure or renal failure. Colloids may be natural

or synthetic (Table 11.3).
Synthetic Colloids
These are solutions of molecules, greater than
10,000 Da atomic weight, synthesised from
animal and plant collagen molecules, which
have been linked together or modified in other
ways (e.g. by adding side chains) to increase
their size, enough for them to stay intravascularly
in order to exert oncotic pressure at the vascular
endothelium.
The molecular weight in these solutions can
vary by a 1000 times (10001000,000 Da).
Mean molecular weight and median molecular
weight are used to further subclassify colloids.
For example Dextran 60 would mean a solution
of Dextran molecules with mean molecular
weight of 60 kDa. The classification is physiologically important since very small or very large
molecules do not contribute to oncotic pressure,

and it is the average (mean) or size of middle
molecules (median) molecular weight which is
more representative rather than a maximum or
a range.
1. Gelatins
Gelatins are products of degradation of animal
collagen, which are then modified by linking the
molecules to each other by either urea linkage
(forming polygelines, e.g. Haemaccel) or
succinyl linkage (forming modified fluid gelatins
like Gelofusine).
These two types of gelatins are compared
with normal saline in Table 11.4
Side effects and precautions during use
a. Fluid overload: This can result owing to the
slow removal from the intravascular
compartment, especially in patients with
poor myocardial/renal function.
b. Anaphylaxis: This complication can occur as
gelatins are derived from animal products.
c. Interference with clotting: Gelatins can cause
coagulopathy by (i) diluting clotting factors,
and (ii) interfering with fibrin polymerization
and platelet aggregation. Hence the volume
infused over 12 hours should be limited to
20 ml/kg.
Table 11.4: Composition of commonly used colloids and comparison with saline
Colloid
Modified fluid
gelatin (Gelofusine)
Polygelines
(Haemaccel)
(0.9%)
Saline
MW in Da (Average)
Concentration of Solution
Bonding of Gelatin molecules
Colloid osmotic pressure
Negative charge
Ca2+ (mmol/L)
K+ (mmol/L)
Na (mmol/L)
Cl (mmol/L)
30,000
4.0%
Succinyl linkage
4045 mmHg
34
<0.4
<0.4
154
120
35,000
3.5%
Urea linkage
25 mmHg
17
6.25
5.1
145
145
58
0.9%
Not applicable
Not applicable
Not applicable
0
0
154
154
2. Dextrans
Dextran is a naturally occurring glucose polymer, which unlike other synthetic colloids is not
modified during the manufacturing process.
It is produced from sucrose by the action of
the bacterium Leuconostoc mesenteroides and
is available as Dextran 70 [mean molecular
weight (MWw) 70,000 Da, as a 6% solution],
and Dextran 40 (MWw 40,000) as a 10%
solution.
Molecules< 50,000 Da are mainly eliminated by the kidneys, whereas larger molecules are
broken down by dextranases or taken up by the
reticulo-endothelial system.
After intravenous administration, Dextran 70
has a t of 6 hours. Dextran 40 has a t of
1-2 hours as kidneys rapidly eliminate its smaller
molecules. However as it is a more concentrated
solution (10%) than Dextran 70 (which is a 6 %
solution), it is hyperoncotic. This leads to
movement of fluid from the interstitium to the
intravascular space.
Dextrans interfere with clotting (see
mechanism above) and have been used to
prevent thromboembolism after surgery and
improve blood flow in muscle and skin grafts.
In the past they were associated with a high
incidence of anaphylaxis; this was related to the
length of side chain. Shortening the length of
the side chain has reduced this problem.
3. Starches: Hydroxy Ethyl Starch (HES)
These are solutions of starch molecules
(synthesized from amylopectin which itself is
derived from corn wax starch) linked together
by hydroxyl ethyl side chains to form a polymer.
Synthesis: Corn wax starch amylopectin
starch many molecules linked together by
hydroxyl-ethyl beads hydroxyl ethyl starch.
Degradation:
i. Hydroxy ethyl starch (slowly by
amylase) glucose
ii. Starch molecules (if not linked by hydroxyl
ethyl molecules) rapid degradation by
amylase glucose.
165
The starches are classified by degree of

substitution which indicates the number of
Hydroxyethyl molecules, per 10 molecules of
glucose. For example if there are 6 Hydroxyethyl
molecules per 10 molecules of glucose, the
degree of substitution is 0.6 and the solution is
called Hexastarch. (Hexa = 6). A solution with
a degree of substitution of 0.5 is called
Pentastarch; a degree of substitution of 0.7,
Hetastarch and 0.4, Tetrastarch.
Elimination: Kidneys eliminate molecules less
than 60 kDa, while larger molecules are slowly
hydrolysed by a amylase or degraded in the
reticuloendothelial system.
Starches interfere with clotting by mechanisms similar to other colloids and the volume
given should be limited to 20 ml/kg body weight
over a 1224 hours period.
BLOOD TRANSFUSION
What are the indications of blood transfusion?
The main purpose of blood transfusion is to
increase or normalise the oxygen carrying
capacity.
Guidelines were issued in 1989 by the food
and drug administration (FDA) of the United
States of America which stated that adequate
oxygen carrying capacity can be met by
hemoglobin of 7 g/dl or less as long as
intravascular volume is adequate for
perfusion. The maintenance of intravascular
volume can be aided by the use of colloids and
crystalloids as discussed in the previous section.
This was later followed by recommendations
of the American Society of Anesthesiology
practise guidelines which stated:
1. Transfusion is rarely indicated when hemoglobin concentration is greater than
10 g/dl and is almost always indicated when
it is less than 6 g/dl, especially when the
anemia is acute.
2. The determination of whether intermediate
hemoglobin concentration (6 to 10 g/dl)
justify or require red blood cell (RBC)
166
transfusion should be based on the

individual patients risk for complications of
inadequate oxygenation. Hence patients
who can possibly have a higher demand to
supply ratio of oxygenated blood to end
organs (for example patients with coronary
artery disease or peripheral vascular disease)
should have a higher transfusion trigger
(explained on page 168) compared to
normal healthy individuals.
Other factors to be considered are the speed
of blood loss and ability of patient to
compensate effectively. Hence very rapid blood
loss, for example secondary to polytrauma or
injury to a major vessel is more likely to require
rapid blood transfusion, especially in the elderly
or in a small child, who have limited capacity to
compensate for such rapid blood loss, than in
a healthy athlete.
The following guideline for transfusion is
based on the assumption that one unit of
packed RBC (PRBC) will increase the hematocrit value by 35% (increasing hemoglobin by
1-2 g/dl), and should be transfused if:
1. Blood loss is more than 20% of blood
volume (normally 5 Liters in adults), i.e.
>1000 ml.
2. Hemoglobin < 8 g/dl.
3. Hemoglobin < 10 g/dl with major cardiorespirator y disease (e.g. emphysema,

ischemic heart disease).
4. Hemoglobin <10 g/dl after autologous blood
transfusion.
5. Hemoglobin< 12 g/dl in ventilated patients.
The American College of Surgeons classified
acute haemorrhage depending on clinical signs
and symptoms and indicated the type of fluid
replacement justified in a given scenario
(Table 11.5).
Whole blood is rarely used nowadays for
transfusion. Whole blood is separated into
various components (Fig. 11.4) to direct the
therapy towards individual deficiency.
1. Packed Red Blood Cells (PRBC) are
used for correction of anemia. The blood is
leukocyte depleted (irradiated) and transfused through a filter to minimize febrile non
hemolytic reactions. Indications for use
depend on the transfusion trigger as
explained.
2. Platelets for correction of bleeding
associated with inadequate platelet number
(thrombocytopenia: when platelet count
is less than 80,000 per ml, or platelet
dysfunction (thrombasthenia) congenital
Table 11.5: Classification of acute hemorrhage

Factors
Class 1
Class 2
Class 3
Class 4
Blood loss in mL
< 750
7501500
15002000
> 2000
Blood loss % of Blood Volume
> 15
1530
3040
> 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
2030
3040
> 35
Urine output (mL/hr)
> 30
2030
< 15
Negligible
Mental status
Slightly anxious
Mildly anxious
Confused
Lethargic
Fluid replacement
(3:1 rule for colloid : Crystalloids)
Crystalloid
Crystalloid
Crystalloid
+ Blood
Crystalloid
+ Blood
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 m) 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 1520 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
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: patients 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(1410)]
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
patients 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 ~ 1020
ml blood. Lap sponges (large sponges) ~ 30
100 ml blood
These are only estimates, and ideally
patients 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 4C, which is
the temperature of stored blood, platelet
activity decreases very rapidly and is only
510% after 24 hours of storage. Transfusion of large volumes of banked blood
can result in thrombocytopenia.
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 13 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
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 4C. 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.
171
Table 11.8: Treatment of hemolytic transfusion reaction

STOP THE TRANSFUSION.
Maintain urine output @ 75100 ml/hr by intravenous colloid/crystalloid, mannitol (1020 gm) or furosemide
(2040 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 patients blood and urine sample to blood bank for analysis.
Prevent hypotension with use of intravenous fluids or inotropes or both.
survive for 221 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 (<10%) compared to that
seen in ARDS.
7. Immunosuppression: Blood transfusion
has been associated with non-specific
immune suppression. This has been associated with tumour recurrence or reduced
survival in cancer patients. It is therefore,
recommended that cancer patients should
be given packed RBCs instead of whole
blood. The mechanism has been related to
increased synthesis of PGE and Interleukin2 in stored blood.
DIAGNOSIS AND CORRECTION OF SOME
COMMON ELECTROLYTE ABNORMALITIES
Use of large amounts of crystalloids in the peri
operative period can occasionally cause
disturbances in the extra- and intra cellular
electrolyte balance and also with total body
water and its distribution. These imbalances can
profoundly affect cardiovascular, neurological
and neuromuscular function and can even cause
mortality. In this section we will discuss about:
- Effect of different fluid loads on extra-cellular
and intra-cellular water content
- Causes and management of disorders of
sodium homeostasis
- Management of potassium disorders
- Management of calcium disorders.
172
As you saw earlier in this chapter, the

intracellular and extracellular solutes maintain
equal osmolality on either side of the cell
membrane, which separates the ICF from the
ECF. The normal ECF and ICF osmolar load is
calculated as follows:
- Total body solute (280 mOsm/kg
TBW) = 280 42 = 11,760 mOsm
- Intracellular solute = 280 mOsm/kg
28 kg = 7840 mOsm
- Extracellular solute = 280 mOsm/kg
14 kg = 3920 mOsm
- Extracellular sodium concentration =
280 2 = 140 mEq/L
Effect of Infusion of 2 L Crystalloid Load on
TBW and its Distribution in a 70 kg Adult
A. When 2 L of normal saline is infused
(isotonic load): Isotonic saline stays mainly
extracellularly and its osmolality is nearly
equal to that of plasma.Therefore the
changes that are expected are as follows:
- Total body solute = 280 mOsm/kg
44 kg = 12,320 mOsm
- Intracellular solute = 280 mOsm/kg
28 kg = 7840 mOsm
- Extracellular solute = 280 mOsm/kg
16 = 4480 mOsm
- No change in osmolality; water gain of 2
kg in ECF space
B. When 2 L of water or 5% dextrose is
infused: (dextrose is metabolised quickly,
leaving behind a water load).
- New TBW = 42 + 2 =44 kg
- New body osmolality = 11,760 44 =
267 mOsm/kg
- New intracellular volume = 7,840 267
= 29 L
- New extracellular sodium concentration
= 267 2 = 133 mEq/L
Thus the osmolality is reduced and the fluid
has distributed itself into both ECF and ICF.
C. When a hypertonic load of e.g. 600 mEq

NaCl is administered (no water):
- Total body solute = 11,760 + 600 =
12,360 mOsm/kg
- New body osmolality = 12,360 42 =
294 mOsm/kg
- New extracellular solute = 600 + 3920
= 4520 mOsm
- New extracellular volume = 4520 294
= 15.4 L (Gain of 1.4 L)
- New intracellular volume = 42-15.4 =
26.6 L (Loss of 1.4L)
- New extracellular sodium = 294 2 =
147 mEq/L
Thus, there is a net movement of 1.4 L water
from the ICF to the ECF and the [Na+] increases.
HYPERNATREMIA AND ITS MANAGEMENT
Hypernatremia occurs either due to hypotonic
losses (i.e. more water lost than sodium) or due
to sodium retention. Thirst and water intake
usually prevent hypernatremia secondary to
sodium retention, but this mechanism cannot
operate in the debilitated or unconscious patient.
Hyperosmolality is an inevitable consequence
of hypernatremia.
The major causes of hypernatremia are:
I. Impaired thirst perception:
- Coma
- Essential hypernatremia
II. Excessive water loss:
- Sweating
- Neurogenic diabetes insipidus
- Nephrogenic diabetes insipidus
III. Solute diuresis:
- Osmotic diuresis as seen in diabetic
ketoacidosis, mannitol administration
IV. Combined causes:
- Coma and hypertonic enteral feeding
Signs and symptoms of hypernatremia
depend on whether the patient is conscious,
when the overpowering symptom is intense
thirst, progressing to unconsciousness and
death. Small children are especially prone to
intracerebral and subarachnoid hemorrhage that can result from rapid shrinking of
the brain. The symptoms in order of severity
are listed below.
Clinical Manifestations of Hypernatremia
-
Common manifestations of hypernatremia

are non-specific, and include restlessness, irritability, muscular twitching,
hyperreflexia, spasticity, and seizures
- Patients with hypotonic losses may
present with signs of volume loss tachycardia, hypotension, decreased jugular
venous pressure, dry mucosa, reduced skin
turgor and thick doughy skin
- common symptoms in infants include
hyperpnea, muscle weakness, restlessness,
characteristic high-pitched cry, insomnia and
lethargy
- the level of consciousness correlates
with the level of hypernatremia;
however, muscle weakness, confusion and
coma can be due to the underlying coexisting condition
Principles of treatment are outlined in
Figure 11.7. Rapid correction of any form of
chronic hypernatremia can lead to brain edema,
seizures and permanent neurological damage.
With the loss of fluid from the extracellular
compartment, fluid shifts from the intracellular
compartment to the extracellular compartment.
173
Brain cells respond by accumulating intracellular

solutes (potassium and amino acids). With rapid
correction of hypernatremia fluid will enter the
intracellular compartment, and brain swelling
may develop resulting in deterioration of central
nervous function.
1. It is important to determine the volume
status of the patient with CVP and urine
output.
2. Plasma sodium should not be reduced by
more than 0.5 mEq/L/hr.
3. Underlying problem needs to be treated.
4. If the serum Na+ > 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
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 = 4234.5 = 7.5 kg
Thus, 7,500 ml of 5% dextrose has to be
given. Half of this should be given in 1224
hours and the rest in the next 2436 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 patients 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.
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 300154 =
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
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 patients
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.
DISORDERS OF POTASSIUM
HOMEOSTASIS
Major causes of hypokalemia are
1. Inadequate intake/replacement of potassium
2. Excess loss
a. Gastrointestinal- vomiting, diarrhea
b. Renal- Conns syndrome
Hyperaldosteronism
Diuresis
Chronic metabolic alkalosis
Antibiotics: Amphotericin B, Carbenicillin, Gentamicin
Bartters 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 200400 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
(0.40.5 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
Fig. 11.11: Plan for treatment of hypokalemia
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.
HYPERKALEMIACAUSES, 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 1112 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 Ringers 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
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.
-agonists may be useful in acute hyperkalemia associated with massive transfusion,
and will also provide inotropic support. Low
dose epinephrine (0.52 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.
Fig. 11.13: Management of hyperkalemia
181
182
HYPERCALCEMIA AN
D HYPOCALCEMIA
AND
Hypercalcemia- causes, Treatment and
Anesthetic Implications
Normal plasma calcium is 8.510.5 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 0.81
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
Fig. 11.15: Management of hypercalcemia
183
184
Fig. 11.16: Causes of hypocalcemia
serum calcium usually 1224 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. Trousseaus sign (carpopedal spasm) on
inflating blood pressure cuff, 2) Chvosteks
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.
Fig. 11.18: Clinical signs in hypocalcemia
185
186
Fig. 11.19: Management strategy for hypocalcemia (serum Ca2+< 88.5 mg/dl or 2 mmol/l)
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 patients 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 Iwhere monitoring should be
equivalent to an intensive care unit, and Phase
IIwhere 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
patients 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
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 patients 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
300500% and contributes to hypoxemia.
194
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
patients condition. A 1020% 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-
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.
-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
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 <35C),
hypoglycemia, hyperglycemia and hypothyroidism are other causes. If diagnosis is still not
clear, emergency computed axial tomographic
scanning helps in evaluating neurological causes
like cerebral edema or subarachnoid bleed.
197
Nausea and Vomiting
MISCELLANEOUS
Most general anesthetics induce or facilitate

nausea and vomiting. The type of surgical
procedure has an important influence on the
occurrence of nausea and vomiting: the
incidence is higher following laparoscopic
surgery and strabismus surgery. Apart from
causing patient discomfort, vomiting following
anesthesia can result in aspiration of the vomitus.
The patient should be turned to the side in
the Trendelenburg position, allowing the material
to drain out of the mouth rather than into the
larynx. The airway can then be cleared with
suction. In the event of aspiration, most patients
can be treated conservatively, but an occasional
patient may develop acute respiratory failure
warranting ventilatory management.
Metoclopramide is an effective and safe
antiemetic. Recently, serotonin anatagonists
(ondansetron, granisetron) also being widely
used for postoperative vomiting.
Seizures in the postoperative period are rare

and the management includes securing the
airway and administering oxygen along with the
use of anticonvulsants-benzodiazepines,
thiopentone sodium.
Emergence delirium is described as a side
effect of ketamine anesthesia. Recently, post
emergence restlessness is noted when using
agents with rapid recovery like sevoflurane. This
restlessness can be attenuated with small doses
of opioids or benzodiazepines.
Hypothermia and Shivering

Anesthesia and surgery prevent normal
physiological heat conservation and aggravate
heat loss. The most important factor in
producing postoperative hypothermia is the
duration of time spent inside the operating room.
Hypothermia impairs peripheral perfusion by
intense vasoconstriction and results in metabolic
acidosis; hypovolemia may be masked. The
most effective method to re-warm the patient is
forced air rewarming system (Bair Hugger).
Postoperative shivering is usually caused by
hypothermia. Shivering increases oxygen
consumption and carbon dioxide production.
Re-warm the patient, along with oxygen
supplementation. Certain drugs are found to be
useful: chlorpromazine, droperidol, pethidine (in
subnarcotic doses of 1015 mg IV).
Hyperthermia may occur in the presence of
sepsis or rarely in thyrotoxic crisis.
CONCLUSION
This chapter describes a concise and direct approach to managing patients recovering from surgery and anesthesia. The basic motto of eternal
vigilance during anesthesia holds good during
postoperative period as well. Apart from being
vigilant to prevent complications, one must also
ensure a comfortable recovery by judicious use
of analgesics, anti-emetics and a caring attitude.
MCQ
MCQss
1. The most common cause of airway
obstruction in a postoperative patient
is:
a. Pharyngeal obstruction due to tongue
falling back
b. Pharyngeal obstruction due to foreign
body
c. Laryngeal obstruction due to foreign
body
d. Laryngeal obstruction due to laryngospasm.
2. Which of the following is not true
about laryngospasm?
a. It is more common in children
b. It is more common in elderly
c. Is found in light planes of anesthesia
d. Is exacerbated by blood or secretions
in the pharynx.
198
3. The following therapeutic interventions are recommended for

laryngospasm except:
a. Continuous positive airway pressure
b. Suxamethonium
c. Maneouvres to maintain airway patency
d. Aerosolized racemic epinephrine.
4. Which of the following statements
about positioning in the postoperative
phase is not correct?
a. Propped up position is desirable in an
awake patient
b. Avoid flexion of the neck
c. Avoid extension of head in a drowsy
patient
d. Head should be extended in a drowsy
patient.
5. Tracheal intubation to assist ventilation is indicated if PaO2 is less than
_____ mmHg despite maximal oxygen
therapy.
a. 50
b. 60
c. 80
d. 90
about pneumothorax?
a. Tension pneumothorax should be
drained immediately
b. Pneumothorax < 20% in a mechanically ventilated patient can be managed
conservatively
c. Pneumothorax < 20% in a spontaneously breathing patient can be managed
conservatively
d. Pneumothorax > 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.
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.
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<60 mm Hg or SpO2<90%
b. Neonates: PaO2< 50 mm Hg, SpO2<85%
Oxygen Delivery Systems
These are classified based on the basic design:
I. Low- flow systems
II. Reservoir systems (This category also
includes hoods and tents)
III. High-flow systems
OXYGEN THERAPY
201
Table 13.1: Clinical signs of hypoxemia

System
Mild/ moderate
Severe
Respiratory
Tachypnea
Tachypnea/Bradypnea
Dyspnea
Dyspnea/ Gasping
Cardiovascular
Pallor
Cyanosis
Tachycardia
Tachycadia, arrhythmia
Hypertension
Bradycardia
Hypertension Hypotension
Neurologic
Restlessness
Confusion, blurred vision
Disorientation
Slow reaction, reduced responsiveness
Headache
Combative behavior, thrashing
Lassitude
Coma
Or, on the basis of FiO2 range:

A. Low FiO2 devices (<35%)
B. Moderate FiO2 devices (3560%)
C. High FiO2 devices (> 60%). Some devices
can deliver from 21100%.
Or, whether the system is fixed output or
variable output:
1. Fixed: The system can provide the patients
entire inspired gas needs and the FiO 2
remains stable.
2. Variable: The device provides some of the
inspired gas and the patient draws the rest
from surrounding air. The more the patients
respiratory effort and need, the more is the
dilution, and the less the resultant FiO2.
Here we shall discuss them according to the
first classification (i.e. basic design).
LOW FLOW SYSTEMS
These provide supplemental oxygen at flows
up to 8l/min. Since inspiratory flow of an adult
is always more than this value, these devices
also perform as low FiO2/variable FiO2 devices.
A. Nasal Cannula (Nasal Prongs)

Functioning- This is a disposable plastic device
made up of 2 tips or prongs 1 cm long,
Fig. 13.1: Nasal prongs
connected to several meters of oxygen supply

tubing (Fig. 13.1). It is secured on the head by
an elastic strap. Flows are not recommended to
exceed 8l/min; in infants should not exceed
2l/min. Prongs can provide an FiO2 of 2235%.
Advantages: Inexpensive, easy to use, disposable. Can be kept on while eating.
Disadvantages: High flows are uncomfortable.
Mouth breathing dilutes FiO2. Nasal dryness and
bleeding may result with high flows.
B. Nasal Catheter
This is a soft plastic catheter with several terminal
holes (Fig. 13.2) and is inserted up to the uvula.
Although flows up to 8l may be used, it is best
not to exceed 4l/min. FiO2 range delivered is
the same as prongs (2245%).
202
Disadvantages: Catheter frequently gets

displaced or blocked; high cost and risk of
infection are concerns.
How ccan
an you Estimate the FiO2 Provided by
Low Flow Systems?
Each litre of supplemental oxygen increases FiO2
by 4% in a patient with normal tidal volume
and respiratory rate; therefore a patient receiving
3l/min through a nasal cannula is receiving
(21+12) = 33% oxygen.
RESERVOIR SYSTEMS
Fig. 13.2: Nasal catheter
Disadvantage: It can cause gagging or aspiration

if high flows are used. Frequent change is
required (68 hourly) as it promotes production
of secretions and gets blocked.
These systems collect and store oxygen between

breaths. During the next breath the patient draws
upon this reservoir when the inspiratory flow
exceeds oxygen inflow. Thus dilution with air is
reduced and the FiO2 provided is higher than
low flow systems. They are of two varieties:
reservoir cannula and reservoir mask.
A. The Reservoir Cannula (Fig. 13.3)
C. Transtracheal Catheter
This is a thin Teflon catheter inserted surgically
into the trachea between the 2nd and 3rd
tracheal rings, and secured on the neck with a
thin chain.
Advantages: Flows required are 4060% less
than nasal cannula or prongs; useful in patients
who cannot tolerate prongs.
This is available as a nasal reservoir or as a

pendant reservoir. The nasal reservoir holds
20 ml oxygen. As the patient exhales into it with
every breath the reservoir volume increases.
Although comfor table to wear it is not
aesthetically acceptable to many patients. These
cannulae reduce oxygen use by 50-75% (i.e. if
2l is required through prongs, only 0.5l is
Fig. 13.3: Nasal reservoir and pendant reservoir
OXYGEN THERAPY
203
required through reservoir cannula. The device

functions only if the patient exhales into it every
time as it resets the reservoir membrane. The
cannula requires to be replaced every 3 weeks.
B. Reservoir Masks
These are the most commonly used reservoir
systems. The simple mask is an important item
of postoperative recovery room equipment.
The simple face mask (Fig. 13.4) is a
disposable plastic device which covers the nose
and mouth and has a securing elastic strap.
There are multiple holes through which the
patient can exhale and also draw air during
inspiration. FiO2 is variable. Flows of 5-12l can
be used. Flows less than 5l/min may result in
CO2 retention.
To improve the performance of this mask, a
flexible reservoir bag of 11 can be attached to
the mask at the oxygen inlet. This partial
rebreathing mask (Fig. 13.5) has expiratory
ports but no unidirectional valves. The patient
partly exhales the anatomical dead space gas
into the bag. The last 2/3rds of the exhaled gas
high in CO2 escapes through the ports. As long
as enough O2 flows to prevent the bag from
collapsing during inspiration, re breathing is
negligible. A leak-free non-rebreathing mask
fitted with competent unidirectional valves
Fig. 13.5: A partial rebreathing mask
Fig. 13.6: A non-rebreathing mask with

reservoir bag
(inspiratory valves open and facilitate breathing

in from bag during inspiration and expiratory
valves prevent exhalation into reservoir bag)
can ideally provide 100% oxygen (Fig. 13.6).
C. Oxygen Tent
Fig. 13.4: A simple face mask
This consists of a canopy into which cooled and

oxygen-enriched air is circulated. It can provide
a maximum of 4050% O2. Frequent opening
causes large swings in FiO2 even with flows of
12-15l/min.
204
D. Oxygen Hood
This is a very useful method of oxygen therapy
for infants as it allows nursing without interrupting oxygenation. Oxygen is delivered
through a heated air-entrainment nebuliser or
blending system. A minimum flow of 7 l/min is
required to prevent rebreathing. However flows
above 15 l/min can generate noise stress for
the infant and are not recommended. Care is
to be taken to maintain temperature and
humidity levels. The air-oxygen mixture should
not be directed at the infants face.
HIGH FLOW SYSTEMS
These systems provide (i) flows exceeding
patients peak inspiratory flow or (ii) use
entrainment systems whose final flow exceeds
the patients peak inspiratory flow. In either case,
it is possible to provide the patient with the
desired FiO2. A high-flow system is also defined
as one which can provide > 60 l/min of total
flow. This calculation is based on the fact that
the peak inspiratory flow of an adult is 3 times
the minute ventilation (MV). 20 l/min is the
upper limit of normal MV for an adult. The high
flow systems can be either entrainment
devices which draw atmospheric air to
generate the high flow, or blenders where
separate pressurized sources of air and oxygen

are used to obtain the desired FiO2 by blending
manually or mechanically.
A. Entrainment Devices
The ventimask (Fig. 13.7) a commonly used
entrainment devices is erroneously named
because (i) the original venturi tube is not used
in this device. Instead, a simple orifice or jet is
present through which oxygen flows at high
velocity; (ii) air is entrained due to shear forces
and NOT due to low lateral pressures. The
amount of entrainment and therefore the total
flow output depends upon the port size and
the velocity of oxygen flow.
Since all high-flow systems mix air and
oxygen it is important to know how to calculate
the FiO2 the patient is receiving, the flow rate
the device is able to generate, the air-to-oxygen
ratio needed for a particular FiO 2 and the
volume of oxygen that has to be added in order
to get a given FiO2. The basic equation is based
on dilution equation for solutions:
VfCf =V1C1 + V2C2 , where V1 and V2 are
the volumes of two gases being mixed and C1
and C2 the concentration of oxygen in these
two volumes; Vf the final volume and Cf the
final concentration. The equations used for computing oxygen percentage, ratio and flow are:
Fig. 13.7: Ventimask with array of connections
OXYGEN THERAPY
1. To calculate oxygen percentage in a mixture

of air and oxygen:
% O2 =
(Air flow 21) + (Oxygen flow 100)

Total flow
2. To calculate the air: oxygen ratio needed to

obtain a desired O2 percentage:
Litres of air = (100-desired %O2)
Litres of O2 = (desired %O221)
3. To compute total flow from an entrainment
device,
a. Calculate air: O2 ratio
b. Add the ratio parts
c. Multiply the sum by the oxygen input.
Numerical Examples
1. An air entrainment device mixes at a fixed
ratio of 4 volumes of air to one volume of
oxygen. What is the FiO2 delivered by this
device?
Using the first equation:
%O2 = [(Air flow 21) + (O2 flow 100)]
total flow
= [(4 21) + (1 100)] (4+1)
=184 5 = 36.8% O2.
2. A patient is receiving oxygen through an air
entrainment device set to deliver 40%
oxygen. The input oxygen (from the wall
outlet) is at 10 l/min. What is the total output
flow of the system?
205
We first find the air-to-oxygen ratio:

Litres of air = 100- set % O2 = 60
Litres of O2 = set % O2 - 21 = 19
Air: O2 = 60:19 = 3:1
Then we add the ratio parts: 3+1 = 4
Then we multiply this sum by the O2 flow:
4 10 = 40 l/min
Thus an entrainment device which delivers
40% oxygen generates a flow of 40 l at 10 l
oxygen flow.
The air-to-oxygen ratio can also be
computed by the magic box.
Make a square and enter 20 on the top left
hand corner and 100 on the lower left hand
corner. Write the desired O2% in the center.
Subtract from lower left to upper right and
from upper left to lower right = 60 and 20
=60:20 =3 :1
The commonly used nebulisers are also
entrainment devices. A nebuliser functioning
also as entrainment device at times may not be
able to provide the FiO2 that is mentioned on
itthe extremely small jet needed to produce
an aerosol limits the nebuliser inflow to 12-15 l/
min. The total flow generated may be insufficient
for those with high inspiratory flow or minute
volume.
Example
Your consultant has advised 60% oxygen
through a nebuliser for the patient on bed no.20
who is recovering from pneumonia. Your patient
has a tidal volume of 400 ml and a respiratory
rate of 40/min. If the maximal nebuliser flow is
15 l/min, will he be able to get 60% oxygen?
Patients MV= 400 40 =16 l/min
Patients peak inspiratory flow =3 16
= 48l/min
Total flow from nebuliser = sum of ratio
parts* (1+1) 15= 30 l/min
Thus, the nebulizer output falls short of the
peak flow and the patient will be entraining air
*[air oxygen=(100 60)(60 21), = 4039 = 1:1; ratio parts=1+1]
206
to make up, thus reducing the calculated FiO2.

The total flow has to be at least 60 l/min if the
FiO2 has to remain stable.
However, if a nebuliser entrainment device
is set to deliver 40% for the above patient, the
total flow would be = sum of ratio parts (3+1)
15 = 60 l/min which would provide a
consistent FiO2 of 40%. In the first scenario,
extra oxygen can be bled into the patients
mask through a cannula to increase FiO2. Thus
air entrainment devices behave as high flow and
fixed output devices at lower FiO2 values.
Practically, to determine whether the total
flow from a nebuliser is sufficient, the mist
escaping from the orifices of the mask is
observed. If it is seen throughout inspiration it
indicates that the flow is sufficient and that the
set FiO2 is being delivered.
B. Blenders
When air entrainment devices cannot provide
high enough oxygen concentration or flow,
blending systems are the next step. Here
pressurized oxygen and air are separately
delivered into a mixing chamber where
blending is done by manual adjustment or
mechanically by a proportioning device.
Special, calibrated high-flow flow meters are
used. Blenders can be used to fill non
rebreathing reservoir bag circuits to provide a
full range (21100%) oxygen.
How to select the ideal oxygen delivery
system?
One examines (i) the objectives, (ii) patient
factors and (iii) equipment performance and
limitations.
I. The primary objective/purpose is to correct
arterial hypoxemia. Secondary benefits
follow.
II. Patient factors to be considered:
a. Severity and cause of hypoxemia: An
FiO2 of 100% should be provided in cases
of cardiac arrest, severe trauma, shock,
CO or cyanide poisoning (the latter may
need hyperbaric oxygen therapy). Those

patients are usually intubated and on
assisted ventilation. The ventilators are
capable of providing 100% oxygen. High
FiO2 levels can be achieved with blending
systems which provide high flows thus
preventing dilution. For a critically ill adult
patient with moderate to severe
hypoxemia, who is able to breathe
spontaneously, a reservoir or a high-flow
system capable of providing at least 60%
oxygen should be used. These patients
are carefully monitored and if hypoxemia
remains uncorrected, they should be
intubated and receive mechanical
ventilation with FiO2 > 0.6, and possibly,
PEEP. For adult patients in more stable
condition (acute MI, postoperative
hypoxemia) a system capable of low to
moderate oxygen concentration can be
used, e.g. a nasal cannula or air entrainment device. Adult patients with COPD
and acute-on-chronic hypoxemia need
careful oxygen augmentation so that their
hypoxic drive is not suppressed. In these
patients, low flow nasal oxygen or a
2428% entrainment device can be
used.
b. Presence of adequate respiratory effort:
If a patient is generating a good tidal
volume (evident by chest excursions) and
has a resonable respiratory rate, oxygen
can be supplemented by any of the
means listed in Table 13.2.
c. Degree of consciousness and alertness:
An unconsious patient who is also
hypoxemic needs to the intubated and
then given appropriate FiO2 to correct the
hypoxemia. If respiration and sensorium
do not improve, mechanical ventilation
is required. Similarly even if an alert
patient is unable to maintain PaO2 of 60
mm Hg while breathing 60% oxygen,
needs respiratory support.
OXYGEN THERAPY
207
Table 13.2: Choice of oxygen therapy equipment

Desired FiO2
Fixed Stability
Variable Stability
Low (<35%)
AE Nebuliser
Blending system
Incubator for infant
AE Nebuliser
Blending system
Oxyhood (infant)
Blending system
Oxyhood (infant)
Non rebreathing reservoir
Nasal catheter
Nasal cannula
Transtracheal catheter
Simple mask
AE Nebuliser
Tent (child)
Partial rebreathing reservoir
Moderate (35-60%)
High (>60%)
III. Equipment factors

This pertains to the performance characteristics, maximum output and other limitations to
use, as shown in Table 13.2 so that the
appropriate device can be selected for a patient,
who is capable of breathing spontaneously.
Once a patient is intubated and connected
to a mechanical ventilator, continuous monitoring of respiratory parameters and other organ
systems is required. This is best carried out in
an intensive care unit (ICU). Efficiency of oxygen
delivery can be improved with sedation,
paralysis, and positive end expiratory pressure
(PEEP).
This is explained in the Section on Critical
Care.
3. The following devices are normally

used to administer oxygen in a patient
with spontaneous breathing
a. Simple face mask
b. Nasal speculae
c. Oxygen hood
d. Transthoracic catheters
4. Many factors influence percentage of
oxygen in the inspired air in low flow
system
a. Normal tidal breathing
b. Regular respiratory rate
c. Each litre of oxygen supplemented
increases oxygen concentration to 40%
d. A patient is receiving 29% oxygen if we
give 2l/min with nasal cannulae
1. The following are not clinical features

of hypoxemia
a. Restlessness
b. Cyanosis
c. Tachypnea
d. Warm peripheries
5. Oxygen therapy is useful in the

following patients
a. Cystic fibrosis
b. Chronic lung disease
c. Full term babies
d. Motion sickeness
2. The following bedside tests are useful

in monitoring hypoxia
a. Colour of lips
b. Saturation of fingers or toes
c. Respiratory rate
d. Arterial blood gases
6. Unwanted effects of oxygen commonly

seen are
a. Dryness of mouth and nose
b. Fire hazards
c. Formation of new retinal blood vessels
d. Respiratory distress syndrome
208
7. The following facts are correct in

oxygen therapy with high flow systems
a. Entrainment of air from surrounding
atmosphere
b. Flows higher than peak expiratory flow
is delivered
c. Blenders provide accurate FiO 2 by
mixing pressurized oxygen and nitrogen
d. Ventimask is a common example
8. Optimising oxygen therapy may
include
a. Controlling fever
b. Good nutrition
c. Treating heart failure
d. Appropriate antibiotics for chest
infection
9. Useful parameters to monitor in a
patient who is given oxygen
a. Respiratiory rate
b. Temperature and humidity of the
inspired air
c. Blood pressure
d. Glasgow coma scale
10. Oxygen reaches the tissues from the
heart in the following ways
a. Carried by normal haemoglobin
b. Dissolved in the plasma
c. As carboxyhemoglobin
d. By diffusion from higher towards lower
partial pressure
11. Common sources of oxygen supply in
large hospitals are
a. Liquid oxygen tanks
b. Cylinders
c. Green oxygen tubings
d. Oxygen concentrators
12. Dramatic hypoxia may be features of

a. Tension pneumothorax
b. Flail chest
c. Amniotic fluid embolism
d. Marathon race
13. Choose the correct statements
a. Oxygen is an anesthetic gas
b. Commercial preparation of oxygen is
by fractional distillation of liquid air
c. No harm would come to the patient
from receiving oxygen
d. Molecular weight of oxygen is 16
14. Perioperative patients are given
oxygen for the following reasons
a. At the start of GA 100% oxygen is given
to replace air from the FRC
b. After prolonged GA with N2O, oxygen
must be given to avoid diffusion hypoxia
c. Pain causes increase respiratory rate and
hence better oxygenation
d. Massive blood transfusion of bank blood
interferes with oxygen delivery
15. The following maneuvres would
complement oxygen therapy
a. Sitting position rather than supine
b. CPAP (Continuous Positive Airway
Pressure)
c. Bronchodilators in asthmatics
d. Tracheostomy
Answers
1.
4.
7.
10.
13.
FFFT
TTFT
TFFT
TTFT
TTFF
2.
5.
8.
11.
14.
TTTF
TTFF
TFTT
TTFT
TTFT
3.
6.
9.
12.
15.
TTTF
TTTT
TTTT
TTTF
TTTF
Infection and the Anesthesiologist

Ashish Malik
Antigenic structure of HIV, HCV and HBV

Causes of injury at workplace
Universal safety precautions
Determination of exposure code
Post exposure prophylaxis
While managing patients, anesthesiologists are

exposed to numerous communicable diseases.
Exposure to needles in their clinical activities
places them at increased risk of acquiring needle
stick injury which may lead to serious or fatal
infections with blood borne pathogens such as
Hepatitis B virus (HBV), hepatitis C virus (HCV)
or human immunodeficiency virus (HIV). The
activities associated with majority of needle stick
injuries are administering injections, withdrawing
blood, performing invasive procedures like
central venous and arterial cannulation and
recapping of needles. Incorrect disposal of
needles, handling trash and dirty linen are
responsible for downstream injuries.
is cytopathic, has a long latent period and runs

a chronic course.
The HIV virus (Fig. 14.1) is a 120 nm,
icosahedral, RNA virus. The virus has an outer
envelope consisting of a lipid bilayer enclosing
a protein matrix containing a nucleoid core. The
nucleoid core contains two copies of RNA and
the enzyme reverse transcriptase. HIV is a very
fragile virus. It is susceptible to heat.
A temperature of 56 C for 30 minutes or
boiling for a few seconds will kill the virus. Risk
factors for HIV transmission include multiple
homosexual or heterosexual partners,
transfusion of contaminated blood, infections
with contaminated needles and/or syringes, and
feto- maternal transmission.
ANTIGENIC STRUCTURE AND

TRANSMISSION
HIV belongs to the family Retroviridae and
genus lentivirus. Two distinct forms of HIV exist,
HIV-1 and HIV-2. The most common cause of
HIV disease throughout the world is HIV-1. HIV
Fig. 14.1: Structure of the HIV virus
210
Fig. 14.2: The hepatitis B virus
Fig. 14.3: The hepatitis C virus
The efficacy of transmission is determined

by the amount of virus in body fluids and the
extent of contact. Urine, sweat, milk, bronchoalveolar lavage fluid, synovial fluid, feces and
tears have reported to yield zero or few HIV
particles. Cerebrospinal fluid (CSF) on the other
hand has the highest content of disease and
poses an increased risk to anesthesiologists
during subarachnoid block.
Hepatitis B is a blood-borne or sexually
transmitted virus. It is 42 nm in diameter and
has an outer lipid envelope containing hepatitis
B surface antigen (HBSAg) and an inner protein
core made of hepatitis B core antigen (HBcAg),
a genome of double stranded DNA and a DNA
polymerase (Fig. 14.2). HBV is found in blood
and blood by-products, tears, saliva, semen,
urine, feces, breast milk, synovial fluid and CSF.
Hepatitis C (HCV) however, is the greatest
risk to an anesthesiologist. HCV belongs to the
Flavivirus family. It is an enveloped virus (Fig.
14.3) measuring 3550 nm in diameter. It
contains a single stranded, linear, positive sense
RNA surrounded by a protein capsid. HCV is
transmitted among intravenous drug abusers
and shares similar epidemiological characteristics
with HBV. The risk of sexual and maternalneonatal transmission appears to be low.
There will be an increase in the number

of patients undergoing surgery who are going
to be seropositive or have AIDS, hepatitis B or
C. The possibility of nosocomial transmission
of HIV highlights the need for anesthesiologists
to enforce vigorous infection control policies to
protect themselves, other health workers and
their patients.
Transmission from Patient to
Anesthesiologist
Exposure of infected body fluids
Sharp injury, splashing of mucous membrane
Risk of Transmission of Bloodborne Viruses
to Health Care Workers
Human immunodeficiency virus (HIV)
Percutaneous exposure 0.05 0.4%
Mucocutaneous exposure 0.006 0.05%
Hepatitis B virus (HBV)
Percutaneous exposure
930%
Hepatitis C virus (HCV)
Percutaneous exposure
310%
Needle stick injury is the commonest cause
of transmission of the above diseases. The
highest risk of injury is from blood filled hollow
INFECTION AND THE ANESTHESIOLOGIST
Fig. 14.4: Causes of injury at the workplace
211
Fig. 14.5: Effective hand washing
bore needles. The pie chart (Fig. 14.4) below

depicts the various causes of injuries and total
percutaneous injuries by hollow bore needles.
Infection with solid needles is 10 fold less
than hollow needles.
Patient to Patient Transmission
Use of common syringe with anesthetic drugs
for multiple patients.
Contaminated equipment used for more
than one patient (endotracheal tubes,
intravenous giving sets).
Anesthesiologist to Patient Transmission
Very minimal 2.4 to 24 per million procedures.
Precautions: Although screening of all patients
for HIV infections before routine surgery would
identify a substantial proportion of patients who
might be infected, this is not acceptable due to
political, ethical and social constraints. The risk
of contamination can be reduced by following
the universal safety precautions which
include:
1. Effective hand washing: It is necessary to
wash hands in between tasks and procedures
(Fig. 14.5). Hand washing should be strictly
followed before and after removal of gloves
even if no contact with infected blood or
fluid has occurred.
Fig. 14.6: Prepacked sterile gloves
2. Double gloving: (Risk decreases by 5 fold

by wearing two gloves). Gloves (Fig. 14.6)
should be removed immediately after use,
before touching noncontaminated items and
environmental surfaces.
3. Using eye glasses, eye protection shield,
disposable gowns, boots and masks to
protect mucous membrane of the eyes, nose
and mouth during procedures and patient
care activities that are likely to generate
splashes or sprays of blood, or other body
fluids (e.g. amniotic fluid).
4. Gowns: A clean (even if nonsterile) gown is
adequate to protect skin and to prevent
soiling of clothing.
212
Fig. 14.8: Sharps placed in puncture resistant

containers
Fig. 14.7: Any needle stick injury should be
attended to and reported
5. Needle stick injuries should be reported

(Fig. 14.7).
6. Resuscitation: Minimise emergency mouth
to mouth resuscitation; mouthpieces, masks,
bags and other ventilation devices should
be used.
7. If the health care professional has open skin
lesions he/she should refrain from direct
patient contact.
8. All procedures should be done in an orderly
manner with minimum movement.
9. All sharps instruments, e.g. needles, cannulas
and blades should be placed in a dish and
not handed directly to the person receiving
them.
Even the briefest of violations of these
standard precautions are not to be condoned.
Rigid infection control measures must be
exercised for all interventional equipment used
by anesthesiologists including bronchoscopes
and laryngoscopes.
Infected sharp wastes (needles, IV cannulas)
should be placed in puncture resistant containers
(Fig. 14.8) containing 0.1 to 0.5% bleach.
Needles should not be recapped, bent or
broken. Swabs should be chemically disinfected
followed by incineration. Proper packing,
storage and transport of waste should be
rigorously practiced in the hospital.
Transmission-based Precautions
Transmission-based Precautions should be
followed when patients are known to be or
suspected or being infected with highly
transmissible pathogens. They are based on the
properties of specific pathogens and can be used
in addition to standard (universal) precautions.
1. Airborne precautions are used when
transmission of small particles or droplets
(< 5 m) is likely. Special filters and air
handling is necessary when handling patients
with open tuberculosis or measles.
2. Droplet transmission by larger particles
(> 5 m) 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
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
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
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 1012 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 patients admitting physician
share patient care and responsibility.
220
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
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.
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
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.
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 68 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 [1030%], 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 3035 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
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 4872 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 34 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
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 [5060%]. 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
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, Ringers
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
physicians 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 [13 g/kg/min] has been
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 [200300 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
80110 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
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 g/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 g/kg] followed by
infusion 0.010.03 g/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
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
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 13 g/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 1030% 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
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. Whipples procedure, esophagectomy] to provide EN when the upper
234
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.
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 ones
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 patients diagnosis, physiologic and
functional status. The other members of the
health care team should agree to the decision.
236
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
patients 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.
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 Foleys urinary drainage
catheters
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
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 Ringers 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.
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 worlds 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:
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 18 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 45 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.
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
(500700 ml; 67 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 victims 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).
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 1012 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 810
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 1012 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 45 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.

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
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 12 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, 23 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
2.53 times the IV dose. It should be diluted
in 510 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.
(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
patients face and connected to a self-inflating
(Ambu) bag at a rate of 1215 breaths per
minute. Look for chest movement to assess
ventilation. Make sure that oxygen is flowing at
1012 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 patients 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
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
patients 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
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 2554.
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 18 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.
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
IV Cannulae
Infusion set
Syringes
IV fluids
Pressure infusor bag
Three-way stopcock
Fig. 16.12: Vascular equipment
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
rescuers 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
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 kg1 for adrenaline, 23 mg kg1
for lidocaine and 0.03 mg kg1 for atropine.
Fluid boluses of normal saline or lactated
Ringers solution are recommended.
Infant paddles (4.5 cm) are recommended
for infants <10 kg in weight. ERC
recommends a 4J/kg single shock for
shockable rhythms. In case required to
be repeated, ERC recommends 2 minutes
of CPR in between shocks. AHA recommends 2 J/kg initial shock; subsequent
are 4 J/kg. 5 cycles of CPR should be interposed in between two shocks.
10. Epinephrine should be used for shockable

and unshockable arrhythmia (e.g. asystole)
every 35 minutes.
11. Fever should be immediately treated after
CPR. Core hypothermia may be beneficial.
Active warming should not be performed
on a child with temperature>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 13 sec IV; flush with
saline; 12 mg after 12 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 35 min.
Max dose: 2.2g in 24 hours
Atropine: 0.51 mg every 35 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: 510 g/kg/min; add 400 mg in
250 ml D5W
Lidocaine: 11.5 mg/kg bolus
Additional 0.51.5 mg/kg every 510 min,
up to total 3 mg/kg.
Then infuse 14 mg/min
Magnesium sulfate: 12 g in 10 ml D5 W over
12 min
Procainamide: load 20 mg/min up to 17 mg/
kg (1000 mg)
then infuse 14 mg/min
Side effects: HTN, torsade de pointes
Vasopressin: 40 IU 1 dose only (for pulseless
VT/VF)
Verapamil: 2.5510 mg bolus
Sodium bicarbonate: 1 mEq/kg for cardiac
arrest of uncertain origin; repeat, if required,
0.51 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
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 67 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 victims
airway is unprotected
c. Depression of sternum should be approximately 78 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
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 1012 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 1015 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
Daltons 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

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
Guedels stages of anesthesia
28
Guillain-Barre syndrome 45
H
Henrys law 19
Hepatitis B virus 210
Hepatitis C virus 210
High pressure system 54
Hiltons 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
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

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 (Guedels)
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
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
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

A Primer of Anesthesia

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What is the book about?

What is the book about?

What topics are covered in the book?

What topics are covered in the book?

A Primer of

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Rahul Seewal MD, FRCA

Chittaranjan Joshi MD, DNB

Rajesh Tope MD, FRCA

Indu Kapoor FANZA, FCARCSI, MD

Em Prof VA Punnoose MD, FMCA

2. Inhalational Anesthetic Agents

3. Physiology of Neuromuscular Blockade and Neuromuscular Pharmacology

4. The Anesthesia Machine

5. Preoperative Evaluation of Patients

9. Neuraxial (Spinal and Epidural) Blockade

10. Peripheral Nerve Blocks

11. Fluid Therapy and Transfusion

13. Oxygen Therapy

14. Infection and the Anesthesiologist

16. Cardiopulmonary Resuscitation

A Brief History of Anesthesia

Numerous path-breaking advances have been

Fig. 1: Nerve compression

Crawford W Long and William E Clark,

Fig. 2: Public demonstration of ether

Fig. 3: John Snow

Sir James Simpson, an obstetrician, who

Joseph Clover (1825-1882) succeeded

Fig. 4: Joseph Clover

1960s (and intravenous anesthesia, mentioned

Fig. 5: Alexander Wood and the syringe

synthesized in 1984 is rapidly gaining popularity

xxii A PREMIER OF ANESTHESIA

Fig. 6: Sir Ivan Magill

Fig. 8: August Bier and amputation under

Fig. 7: Sir Robert Macintosh

patients underwent surgery and anesthesia

The advent of muscle relaxants into the realm

(c) to provide a continuum of intensive

Fig. 9: William Thomas Green Morton and his

hemodynamic monitoring, airway management

Properties of an ideal intravenous agent

The intravenous (IV) route is commonly used

The properties of an ideal intravenous

Rapid acting, fairly prompt recovery

Rapid action and recovery, excitatory

Prolonged action, anticonvulsive

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

INTRAVENOUS ANESTHETIC AGENTS AND OPIOIDS

period. It reduces intracranial pressure (ICP)

Abolition of the eyelash reflex is used as a sign

injection. The dose in healthy adults is 45 mg/

relatively acidic pH and (ii) Vasospasm and

For induction of anesthesia.

Confirmed or suspected upper airway

Cardiovascular disease: Patients with hypovolemia, mitral or aortic valvular stenosis,