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Pharmacology for Anaesthesia
and Intensive Care
THIRD EDITION

Tom Peck, Sue Hill and Mark Williams

CAMBRIDGE UNIVERSITY PRESS
Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo, Delhi

Cambridge University Press

The Edinburgh Building, Cambridge CB2 8RU, UK
Published in the United States of America by Cambridge University Press, New York

www.cambridge.org
Information on this title: www.cambridge.org/9780521704632

C Tom Peck Sue Hill and Mark Williams 2008

This publication is in copyright. Subject to statutory exception

and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without
the written permission of Cambridge University Press.

First published 2000

Printed in the United Kingdom at the University Press, Cambridge

A catalogue record for this publication is available from the British Library.

Library of Congress Cataloging-in-Publication Data

Peck, T. E.
Pharmacology for anaesthesia and intensive care / Tom Peck, S. Hill, Mark Williams. – 3rd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-0-521-70463-2 (pbk.)
1. Pharmacology. 2. Anesthetics. 3. Anesthesia. 4. Critical care medicine.
I. Hill, S. A. (Sue A.) II. Williams, Mark (Mark Andrew) 1965- III. Title.
[DNLM: 1. Anesthetics–pharmacology. 2. Cardiovascular Agents–pharmacology.
3. Intensive Care. QV 81 P367p 2007]

RM300.P396 2007
615 .1–dc22 2007029048

ISBN 978-0-521-70463-2 paperback

Cambridge University Press has no responsibility for the persistence or accuracy of URLs for
external or third-party internet websites referred to in this publication, and does not guarantee
that any content on such websites is, or will remain, accurate or appropriate.
CO N T E N TS

Preface page ix
Foreword xi

SECTION I Basic principles 1

1 Drug passage across the cell membrane 1
2 Absorption, distribution, metabolism and excretion 8
3 Drug action 24
4 Drug interaction 40
5 Isomerism 45
6 Mathematics and pharmacokinetics 50
7 Medicinal chemistry 85

SECTION II Core drugs in anaesthetic practice 99

8 General anaesthetic agents 99
9 Analgesics 135
10 Local anaesthetics 163
11 Muscle relaxants and anticholinesterases 175

SECTION III Cardiovascular drugs 197

12 Sympathomimetics 197
13 Adrenoceptor antagonists 217
14 Anti-arrhythmics 228
15 Vasodilators 246
16 Antihypertensives 258

SECTION IV Other important drugs 270

17 Central nervous system 270
18 Antiemetics and related drugs 282
19 Drugs acting on the gut 292
20 Intravenous fluids 298
21 Diuretics 305
22 Antimicrobials 311
23 Drugs affecting coagulation 335

v
vi Contents

24 Drugs used in Diabetes 347

25 Corticosteroids and other
hormone preparations 353

Index 360
CO N T R I B U TO R

Dr. A.S. Grice, BSc, DCH, FRCA, Consultant Anaesthetist, Exeter

vii
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P R E FAC E

The third edition has seen further changes. The mathematics section has been over-
hauled and expanded to give a better base for the kinetics. An additional chapter
has been added on intravenous fluids, and the chapters on intravenous and volatile
anaesthetics have been combined with an expanded section on the molecular mech-
anism of anaesthesia.
We have tried to maintain the style of the previous two editions with an emphasis
on clarity both in terms of presentation and content. In addition we have tried very
hard to eliminate those small errors that are disproportionately irritating. We hope
that this book will continue to be a helpful aid to the wide range of readers it appears
to have attracted.

Tom Peck
Sue Hill
Mark Williams

ix
FO R E WO R D

I can remember my first day as an anaesthetic senior house officer, back in August
1985, and the advice that I received on that first day is still relevant for the twenty
first century anaesthetist. “Anaesthesia is based on three basic sciences, physiology,
physics and pharmacology,” said my first college tutor. The following weekend I took
a trip to Lewis’s book shop in Gower Street to buy the recommended texts of the day.
None of those I bought are still in print, but the pharmacology text has certainly been
replaced by “Pharmacology for Anaesthesia and Intensive Care.”
The first two editions established themselves as the core pharmacology text for
aspiring anaesthetists. It has evolved with each edition and the third edition has
continued this trend, with some interesting new features. The mathematics and
pharmacokinetics chapter is particularly well presented, and explains the concepts
concisely and clearly. This is core knowledge that appears in the examinations of the
Royal College of Anaesthetists but should be retained for all clinical anaesthetists
and intensive care specialists.
Perhaps the title of the book should be changed for future editions as there has
been a large change in medical education in the UK since the second edition, namely
Modernising Medical Careers. This book is relevant to all foundation trainees who
rotate through anaesthesia, intensive care and acute medical specialties. The new
chapter on fluids is especially relevant to those at the start of their careers. The
core knowledge presented should help to encourage good prescribing practice on
all acute medical and surgical wards and avoid fluid management errors.
In summary the new edition is essential reading for those embarking on an anaes-
thetic career and is a core text for the FRCA. The authors come from district gen-
eral and teaching hospital backgrounds but this book offers concise common sense
pharmacology knowledge to all grades, even those who started anaesthesia before
propofol was introduced!!

Richard Griffiths MD FRCA

Consultant in Anaesthesia & Intensive Care Medicine
Peterborough & Stamford Hospitals NHS Trust.
Chairman of Structured Oral Examination I for the FRCA Pt I

xi
SECTION I Basic principles
1
Drug passage across the cell membrane

Many drugs need to pass through one or more cell membranes to reach their site
of action. A common feature of all cell membranes is a phospholipid bilayer, about
10 nm thick, arranged with the hydrophilic heads on the outside and the lipophilic
chains facing inwards. This gives a sandwich effect, with two hydrophilic layers sur-
rounding the central hydrophobic one. Spanning this bilayer or attached to the outer
or inner leaflets are glycoproteins, which may act as ion channels, receptors, interme-
diate messengers (G-proteins) or enzymes. The cell membrane has been described as
a ‘fluid mosaic’ as the positions of individual phosphoglycerides and glycoproteins
are by no means fixed (Figure 1.1). An exception to this is a specialized membrane
area such as the neuromuscular junction, where the array of post-synaptic receptors
is found opposite a motor nerve ending.
The general cell membrane structure is modified in certain tissues to allow
more specialized functions. Capillary endothelial cells have fenestrae, which are
regions of the endothelial cell where the outer and inner membranes are fused
together, with no intervening cytosol. These make the endothelium of the capil-
lary relatively permeable; fluid in particular can pass rapidly through the cell by
this route. In the case of the renal glomerular endothelium, gaps or clefts exist
between cells to allow the passage of larger molecules as part of filtration. Tight
junctions exist between endothelial cells of brain blood vessels, forming the blood–
brain barrier (BBB), intestinal mucosa and renal tubules. These limit the passage
of polar molecules and also prevent the lateral movement of glycoproteins within
the cell membrane, which may help to keep specialized glycoproteins at their site
of action (e.g. transport glycoproteins on the luminal surface of intestinal mucosa)
(Figure 1.2).

Methods of crossing the cell membrane

Passive diffusion
This is the commonest method for crossing the cell membrane. Drug molecules
move down a concentration gradient, from an area of high concentration to one
of low concentration, and the process requires no energy to proceed. Many drugs
are weak acids or weak bases and can exist in either the unionized or ionized form,
depending on the pH. The unionized form of a drug is lipid-soluble and diffuses easily
by dissolution in the lipid bilayer. Thus the rate at which transfer occurs depends on

1
Section I Basic principles

Extracellular

K+

β
γ α
Na+

Na+
ATP ADP
Intracellular
Figure 1.1. Representation of the cell membrane structure. The integral proteins embedded in
this phospholipid bilayer are G-protein, G-protein-coupled receptors, transport proteins and
ligand-gated ion channels. Additionally, enzymes or voltage-gated ion channels may also be
present.

the pKa of the drug in question. Factors influencing the rate of diffusion are discussed
below.
In addition, there are specialized ion channels in the membrane that allow inter-
mittent passive movement of selected ions down a concentration gradient. When
opened, ion channels allow rapid ion flux for a short time (a few milliseconds) down
relatively large concentration and electrical gradients, which makes them suitable
to propagate either ligand- or voltage-gated action potentials in nerve and muscle
membranes.
The acetylcholine (ACh) receptor has five subunits (pentameric) arranged to form
a central ion channel that spans the membrane (Figure 1.3). Of the five subunits,
two (the α subunits) are identical. The receptor requires the binding of two ACh
molecules to open the ion channel, allowing ions to pass at about 107 s−1 . If a thresh-
old flux is achieved, depolarization occurs, which is responsible for impulse trans-
mission. The ACh receptor demonstrates selectivity for small cations, but it is by
no means specific for Na+ . The GABAA receptor is also a pentameric, ligand-gated

Tight Cleft Fenestra

junction

Figure 1.2. Modifications of the general cell membrane structure.

2
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