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OXFORD MEDICAL PUBLICATIONS

Drugs in
Anaesthesia and
Intensive Care

FIFTH EDITION
Drugs in
Anaesthesia
and Intensive
Care
FIFTH EDITION

Edward Scarth
Consultant in Anaesthesia and Intensive Care Medicine,
Torbay Hospital,
Torquay, Devon, UK

Susan Smith
Formerly Consultant in Anaesthesia and Intensive Care,
Cheltenham Hospital, UK, now practising in Pre- and
In-hospital Trauma Care and Event Medicine

1
1
Great Clarendon Street, Oxford, OX2 6DP,
United Kingdom
Oxford University Press is a department of the University of Oxford.
It furthers the University’s objective of excellence in research, scholarship,
and education by publishing worldwide. Oxford is a registered trade mark of
Oxford University Press in the UK and in certain other countries
© Oxford University Press 2016
The moral rights of the authors have been asserted
First edition published in 1990
Second edition published in 1997
Third edition published in 2003
Fourth edition published in 2011
Impression: 1
All rights reserved. No part of this publication may be reproduced, stored in
a retrieval system, or transmitted, in any form or by any means, without the
prior permission in writing of Oxford University Press, or as expressly permitted
by law, by licence or under terms agreed with the appropriate reprographics
rights organization. Enquiries concerning reproduction outside the scope of the
above should be sent to the Rights Department, Oxford University Press, at the
address above
You must not circulate this work in any other form
and you must impose this same condition on any acquirer
Published in the United States of America by Oxford University Press
198 Madison Avenue, New York, NY 10016, United States of America
British Library Cataloguing in Publication Data
Data available
Library of Congress Control Number: 2015949834
ISBN 978–0–19–876881–4
Printed in China by
C&C Offset Printing Co. Ltd
Oxford University Press makes no representation, express or implied, that the
drug dosages in this book are correct. Readers must therefore always check
the product information and clinical procedures with the most up-to-date
published product information and data sheets provided by the manufacturers
and the most recent codes of conduct and safety regulations. The authors and
the publishers do not accept responsibility or legal liability for any errors in the
text or for the misuse or misapplication of material in this work. Except where
otherwise stated, drug dosages and recommendations are for the non-pregnant
adult who is not breast-feeding
Links to third party websites are provided by Oxford in good faith and
for information only. Oxford disclaims any responsibility for the materials
contained in any third party website referenced in this work.
 v

Preface to the fifth

edition
The aims of this book remain true to those of previous editions. In order to
make changes prior to the publication of this edition, a peer review process
was undertaken. We have tried to accommodate the changes that were
proposed by the reviewers and are grateful for their comments. The book
continues in its original structured format, the major changes being the
removal of agents no longer in use, the addition of new pharmacological
drugs, and the introduction of drug comparison tables and a number of
drug structure diagrams. We hope that this new edition will remain popular
with critical care professionals, operating department personnel, paramed-
ics, pre-hospital care specialists, and anaesthetists of all grades, in addition
to providing sound examination preparation for the FRCA and FFICM. Any
comments will be gratefully received via e-mail to edscarth@me.com and
susan.smith@glos.nhs.uk.
E.J.S.
S.P.S
Cheltenham, January 2015
vi

Preface to the first

edition
The aim of this book is twofold: firstly to summarize concisely the main
pharmacodynamic and pharmacokinetic properties of the drugs with which
the practising anaesthetist might be expected to be familiar. Secondly, it
seeks to introduce the candidate for the FRCAnaes (and, in particular, for
the second part of this examination) to an ordered scheme for the pres-
entation of information, which we have found to be of value in both the
written and oral sections of the examinations. Examiners are more likely to
turn a blind eye to minor errors or omissions of knowledge if they are in
the context of a clear and well-ordered presentation. A further advantage
of this scheme of presentation is that it allows rapid access to specific infor-
mation. It is our hope that this compendium will prove to be a useful rapid
source of reference for clinical anaesthetists in their day-to-day endeavours,
both in the theatre and intensive care unit.
This book is intended to complement, rather than to replace, the stand-
ard texts on pharmacology for anaesthetists, since it includes no discussion
of the principles of pharmacology, an understanding of which is essential for
the clinical use of drugs. We feel that these aspects are very satisfactorily
covered elsewhere.
Although our research has been as comprehensive as possible, there will
obviously remain some information that will have eluded us, or perhaps
remains to be discovered. Many practitioners will disagree with our choice
of 172 drugs. Any comments or suggestions will be most gratefully and
humbly received in order that further editions of this book may hopefully
prove to be more useful.
Finally, we should like to thank the members of the Oxford Regional
Drug Information Unit, the many drug company information departments,
and all our colleagues for their help and support in this venture. In particular,
we should like to thank Professor Roy Spector and Drs John Sear and Tim
Peto for their invaluable advice on the manuscript.
M.P.S
S.P.S.
Oxford, 1990
 vii

How to use this book

The layout of this book requires some explanation in order for the reader
to gain the maximum benefit. The 184 drugs we have included are arranged
in alphabetical order to obviate both reference to an index and the artificial
categorization of some drugs. Each drug is presented in an identical format
and confined to one, two, or three pages under the following headings:
Uses The main clinical uses are listed.
Chemical A brief chemical classification is given.
Presentation The formulations of the commercially available prepara-
tions are described.
Main action The fundamental pharmacological properties are briefly
indicated.
Mode of action The mode of action at a cellular or molecular level
(where known) is described.
Routes of administration/doses The manufacturer’s recommended
dose ranges are listed in this section; alternative clinical uses are also
mentioned.
Effects The pharmacodynamic properties are systematically reviewed.
Where a drug has no specific or known action on a particular physiological
system, the relevant section has been omitted.
The systems described are:
CVS Cardiovascular system.
RS Respiratory system.
CNS Central nervous system.
AS Alimentary system.
GS Genitourinary system.
Metabolic/other Metabolic, endocrine, and miscellaneous.
Toxicity/side effects The major side effects are listed, with particular
reference to the practice of anaesthesia and intensive care.
Kinetics The available pharmacokinetic data are provided. Quantitative
data are not available for all drugs, particularly the long established ones.
Where information on the absorption, distribution, metabolism, or excre-
tion is unavailable for a particular drug, the relevant section has been
omitted.
Absorption Details of the absorption and bioavailability are given.
viii How to use this book

Distribution This section provides information on the volume of distribution

and degree of protein binding of the drug, together with, where appropriate,
details of central nervous penetration, transplacental passage, etc.
Metabolism The site and route of metabolic transformation and the nature
and activity of metabolites are described.
Excretion The excretory pathways, clearance, and elimination half-life are
listed. Although clearances are usually expressed in ml/min/kg, this has not
always been possible due to inadequacies in the original source material.
Special points This section describes points of relevance to the practice
of anaesthesia and intensive care; in particular, significant drug interactions
are reviewed.
This standard format offers great advantages; it enables specific questions
to be answered very rapidly. For example, the question ‘How is fentanyl
metabolized?’ may be answered simply by locating the drug alphabetically
and then consulting the Metabolism section of the text. This principle holds
true for all possible permutations of queries.
 ix

Contents

Glossary of terms used in this book xi

Drugs in anaesthesia and intensive care, A–Z 1

Appendix 417
Index of drug derivation 421
Index of medical uses 425
 xi

Glossary of terms used

in this book
% percent
< less than
≤ less than or equal to
> greater than
≥ greater than or equal to
± plus or minus
°C degree Celsius
®
registered
A2RA angiotensin II receptor antagonist
ACEI angiotensin-converting enzyme inhibitor
ACT activated coagulation time
ACTH adrenocorticotrophic hormone
ADH antidiuretic hormone
ADHD attention-deficit/hyperactivity disorder
ADP adenosine diphosphate
ALT alanine transaminase
AMP adenosine monophosphate
ANC absolute neutrophil count
APTT activated partial thromboplastin time
ARDS acute respiratory distress syndrome
AS abdominal system
AST aspartate transaminase
ATIII antithrombin III
ATP adenosine triphosphate
AUC area under curve
AV atrioventricular
BRCP breast cancer resistance protein
Ca2+ calcium ion
cal calorie
cAMP cyclic adenosine monophosphate
cf. confer (compare with)
cGMP cyclic guanosine monophosphate
cmH2O centimetre of water
CNS central nervous system
CO2 carbon dioxide
COX cyclo-oxygenase
xii Glossary of terms used in this book

CRP C-reactive protein

CSF cerebrospinal fluid
CVS cardiovascular system
CYP cytochrome
DIC disseminated intravascular coagulation
DNA deoxyribonucleic acid
DVT deep vein thrombosis
ECG electrocardiogram
EEG electroencephalogram
e.g. exempli gratia (for example)
EMLA® Eutectic Mixture of Local Anaesthetics
ESBL extended-spectrum beta-lactamase
ESR erythrocyte sedimentation rate
FEV1 forced expiratory volume in first second
FiO2 partial pressure of oxygen in inspired air
FVC forced vital capacity
g gram
GABA gamma-amino-butyric acid
GU genitourinary
HAFOE high airflow oxygen enrichment
HAS human albumin solution
HDL high-density lipoprotein
HepBsAg hepatitis B surface antigen
HFIP hexafluoroisopropanol
HIT heparin-induced thrombocytopenia
HITT heparin-induced thrombocytopenia and thrombosis
HIV human immunodeficiency virus
HMGCoA 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase
5HT 5-hydroxytryptamine
Hz hertz
i.e. id est (that is)
IgG immunoglobulin G
IL-1 interleukin-1
IL-6 interleukin-6
IL-8 interleukin-8
INR international normalized ratio
ITU intensive treatment unit
IU international unit
K+ potassium ion
kcal kilocalorie
 Glossary of terms used in this book xiii

kg kilogram
KIU kallikrein inhibitory unit
kPa kilopascal
l litre
LMA laryngeal mask airway
LMWH low-molecular-weight heparin
MAC minimal alveolar concentration
MAOI monoamine oxidase inhibitor
mb millibar
MDMA 3,4-methylenedioxymethamphetamine
mEq milliequivalent
mg milligram
MIC minimal alveolar concentration
min minute
ml millilitre
mmHg millimetre of mercury
mmol millimole
MOP mu-opioid
mOsm milliosmole
MRI magnetic resonance imaging
mRNA messenger ribonucleic acid
MRSA meticillin-resistant Staphylococcus aureus
Na+ sodium ion
NAC N-acetylcysteine
NAPQI N-acetyl-p-benzo-quinoneimine
ng nanogram
nm nanometre
NMB neuromuscular-blocking
NMDA N-methyl-D-aspartate
NO nitric oxide
N2O nitrous oxide
NSAID non-steroidal anti-inflammatory drug
PaCO2 partial pressure of carbon dioxide in arterial blood
PaO2 partial pressure of oxygen in arterial blood
PBP penicillin-binding protein
PCO2 partial pressure of carbon dioxide in arterial blood
PEFR peak expiratory flow rate
PIFE pentafluoroisopropenyl fluoromethyl ether
PMFE pentafluoromethoxy isopropyl fluoromethyl ether
PONV post-operative nausea and vomiting
xiv Glossary of terms used in this book

ppm part per million

PVR pulmonary vascular resistance
RDS respiratory distress syndrome
REM rapid eye movement
RNA ribonucleic acid
RS respiratory system
rtPA recombinant tissue plasminogen activator
spp. species
SSRI selective serotonin reuptake inhibitor
STP standard temperature and pressure
TCI target-controlled infusion
TNF tumour necrosis factor
TPN total parenteral nutrition
tRNA transfer ribonucleic acid
UK United Kingdom
USA United States of America
VD volume of distribution
VDSS volume of distribution at steady state
VIE vacuum-insulated evaporator
VMA vanillylmandelic acid
vpm volume per million
VRE vancomycin-resistant Enterococcus
vWF von Willebrand factor
w/v weight per volume
w/w weight per weight
 1

Drugs in anaesthesia and

intensive care, A–Z
2 A2RAs

A2RAs
Uses Angiotensin II receptor antagonists (A2RAs) are used in the
treatment of:
1. essential and renovascular hypertension
2. diabetic nephropathy
3. congestive cardiac failure, and
4. in patients intolerant of angiotensin-converting enzyme inhibitors
(ACEIs).
Chemical A2RAs belong to the tetrazoles group.
Presentation A2RAs are available in tablet, capsule, liquid, and a pow-
der form as an oral suspension. A number of commercially available types
are available, including losartan, irbesartan, candesartan, and valsartan. The
drug may also be combined with a thiazide diuretic.
Main actions Antihypertensive.
Mode of action A2RAs selectively block the G-protein-coupled angio-
tensin II receptor AT1, therefore preventing the physiological effects of
angiotensin II via the renin–angiotensin–aldosterone system. The drug does
not affect bradykinin-induced vasodilatation.
Routes of administration/doses A2RAs are available for oral admin-
istration. The specific dose and frequency of an agent administered are
dependent on the clinical indication, age of the patient, and particular agent
being used.
Effects
CVS A reduction in the systemic vascular resistance occurs, leading to a fall
in the systolic and diastolic blood pressures.
GU A2RAs cause a significant increase in the renal blood flow.
Toxicity/side effects A2RAs are generally well tolerated. Dizziness
secondary to hypotension may occur. Angio-oedema occurs rarely. The
development of a dry cough (cf. ACE inhibitors) is not associated with
A2RAs. Hyperkalaemia can occur.
Kinetics Data are incomplete.
Absorption A2RAs are generally well absorbed from the gastrointestinal
tract. Bioavailability for some A2RAs are as follows: losartan (33%), irbe-
sartan (60–80%), candesartan (15%), and valsartan (23%).
Distribution The percentage of drug bound to plasma proteins (predomi-
nantly albumin) is high: losartan (99.7%), irbesartan (90%), candesartan
(>99%), and valsartan (94–97%). The volume of distribution (VD) of A2RAs
is highly variable: losartan (34 l), irbesartan (53–93 l), candesartan (9.1 l),
and valsartan (17 l).
 A2RAs 3

Metabolism A2RA metabolism varies widely. Losartan undergoes extensive

hepatic metabolism, generating an active metabolite. Irbesartan undergoes
hepatic glucuronide conjugation and oxidation to inactive metabolites.
Candesartan is a pro-drug presented as candesartan cilexetil, which under-
goes rapid ester hydrolysis in the intestinal wall to the active drug candesar-
tan. Valsartan undergoes minimal hepatic metabolism.
Excretion Losartan is excreted 35% in the urine, and 60% in faeces. It has a
half-life of 2 hours for the parent drug, and 6–9 hours for its active metabo-
lite. Irbesartan has a half-life of 11–15 hours. Candesartan is excreted 75%
unchanged in the urine and faeces, with a half-life of 9 hours. Valsartan is
excreted 80% unchanged (83% in faeces and 13% in the urine), with a half-
life of 5–9 hours.
4 ACE inhibitors

ACE inhibitors
Uses ACEIs are used in the treatment of:
1. essential and renovascular hypertension
2. congestive cardiac failure, and
3. diabetic nephropathy.
Chemical ACEIs are derived from peptides originally isolated from the
venom of the pit viper Bothrops jararaca.
Presentation ACEIs are available in tablet or capsule form, and a num-
ber of commercially available types are available, including captopril, enal-
april, perindopril, lisinopril, and ramipril.
Main action Antihypertensive.
Mode of action ACEIs inhibit angiotensin-converting enzyme (with
an affinity many times greater than that of angiotensin I), so prevent-
ing the formation of angiotensin I from angiotensin II. Part of their action
may also be exerted through the modulation of sympathetic tone or the
kallikrein–kinin–prostaglandin system.
Routes of administration/doses ACEIs are only currently available
for oral administration. The specific dose and frequency of an agent admin-
istered are dependent on the clinical indication, age of the patient, and par-
ticular agent being used.
Effects
CVS The systemic vascular resistance decreases, leading to a decrease in
the systolic and diastolic blood pressures; the cardiac output may increase
by up to 25%, especially in the presence of cardiac failure.
GU ACEIs cause an increase in the renal blood flow, although the glomeru-
lar filtration rate remains unchanged. Natriuresis may ensue, but there is
little overall effect on the plasma volume.
Toxicity/side effects ACEIs are generally well tolerated; hypotension,
dizziness, fatigue, dry cough (due to an accumulation of bradykinin), gastro-
intestinal upsets, and rashes may occur. Renal function may deteriorate in
patients with renovascular hypertension.
Kinetics Data are incomplete.
Absorption ACEIs are reasonably well absorbed from the gastrointesti-
nal tract. Bioavailability for individual drugs is as follows: captopril (75%),
enalapril (40%), perindopril (75%), lisinopril (25%), ramipril (50–60%).
Distribution The percentage of drug bound to plasma proteins is vari-
able: captopril (30%), enalapril (50%), perindopril (76%), ramipril (73%).
Metabolism Captopril undergoes metabolism to a disulfide dimer and
cysteine disulfide. Enalapril and perindopril are pro-drugs that are metabo-
lized to their respective active forms. ACEIs undergo minimal metabolism
in man.
 ACE inhibitors 5

Excretion ACEIs have markedly variable half-lives and clearance data. The
half-life of captopril is 1.9 hours, whereas that of lisinopril is 12 hours, enal-
april 35 hours, perindopril 30–120 hours, and ramipril >50 hours. Captopril
has a low clearance, compared to enalapril and perindopril which have
plasma clearance values of approximately 300 ml/min.
Special points The hypotensive effects of ACEIs are additive with that
of anaesthetic agents. However, they do not necessarily protect against the
cardiovascular responses to laryngoscopy.
There is an increased risk of renal failure with the co-administration of
ACEIs and non-steroidal anti-inflammatory drugs (NSAIDs) in the presence
of hypovolaemia.
6 Acetazolamide

Acetazolamide
Uses Acetazolamide is used in the treatment of:
1. glaucoma
2. petit mal epilepsy
3. Ménière’s disease
4. familial periodic paralysis and
5. the prophylaxis and treatment of altitude sickness.
Chemical A sulfonamide.
Presentation As 250 mg tablets of acetazolamide and in vials containing
500 mg of the sodium salt of acetazolamide for reconstitution with water
prior to injection.
Main action Diuresis and a decrease in the intraocular pressure.
Mode of action Acetazolamide is a reversible, non-competitive inhibitor
of carbonic anhydrase situated within the cell cytosol and on the brush bor-
der of the proximal convoluted tubule. This enzyme catalyses the conver-
sion of bicarbonate and hydrogen ions into carbonic acid and then carbonic
acid to carbon dioxide (CO2) and water. Under normal circumstances,
sodium ions (Na+) are reabsorbed in exchange for hydrogen ions in the
proximal and distal renal tubules; acetazolamide decreases the availability of
hydrogen ions, and therefore Na+ and bicarbonate ions remain in the renal
tubule, leading to a diuresis.
Routes of administration/doses The adult oral and intravenous
dose is 250–1000 mg daily.
Effects
RS Acetazolamide produces a compensatory increase in ventilation in
response to the metabolic acidosis and increased tissue CO2 that the drug
causes.
CNS Acetazolamide has demonstrable anticonvulsant properties, possi-
bly related to an elevated CO2 tension within the central nervous system
(CNS). The drug decreases the pressure of both the cerebrospinal fluid
(CSF) and the intraocular compartment by decreasing the rate of formation
of the CSF and aqueous humour (by 50–60%).
AS The drug inhibits gastric and pancreatic secretion.
GU Acetazolamide produces a mild diuresis, with retention of Na+ and a
subsequent increase in plasma Na+ concentration. The drug also decreases
renal excretion of uric acid.
Metabolic/other The excretion of an alkaline urine results in the develop-
ment of a hyperchloraemic metabolic acidosis in response to the admin-
istration of acetazolamide. The drug also interferes with iodide uptake by
the thyroid.
Toxicity/side effects Occur rarely and include gastrointestinal and hae-
mopoietic disturbances, rashes, renal stones, and hypokalaemia.
 Acetazolamide 7

Kinetics
Absorption Acetazolamide is rapidly and well absorbed when administered
orally; the bioavailability by this route is virtually 100%.
Distribution The drug is 70–90% protein-bound in the plasma.
Metabolism Acetazolamide is not metabolized in man.
Excretion The drug is excreted unchanged in the urine; the clearance is
2.7 l/hour, and the elimination-half-life is 1.7–5.8 hours.
Special points The use of acetazolamide is contraindicated in the pres-
ence of hepatic or renal failure, as the drug will worsen any metabolic
acidosis and may also cause urolithiasis. Pre-treatment with the drug will
obtund the increase in intraocular pressure produced by the administration
of suxamethonium; however, the use of acetazolamide is of dubious value
during eye surgery, as it simultaneously increases the intrachoroidal vascu-
lar volume. Acetazolamide has been used effectively for the correction of
metabolic alkalosis in the critically ill.
Acetazolamide is removed by haemodialysis.
8 Aciclovir

Aciclovir
Uses Aciclovir is used in the treatment of:
1. Herpes simplex infections of the skin and eye
2. Herpes simplex encephalitis
3. recurrent varicella-zoster virus infections, and
4. for the prophylaxis of herpes simplex infections
in immunocompromised patients.
Chemical An analogue of the nucleoside 2′-deoxyguanosine.
Presentation As 200/400/800 mg tablets, a suspension containing
40 mg/ml, a white lyophilized powder in vials containing 250 mg of aciclovir
sodium which is reconstituted prior to injection in water, and as a 3% oph-
thalmic ointment and 5% w/w cream for topical application.
Main action Aciclovir is an antiviral agent, active against herpes simplex
(I and II) and varicella-zoster virus.
Mode of action Aciclovir is activated within the viral cell via phosphoryl-
ation by a virus-coded thymidine kinase and thus has a low toxicity for nor-
mal cells. Aciclovir triphosphate inhibits viral deoxyribonucleic acid (DNA)
polymerase by becoming incorporated into the DNA primer template,
effectively preventing further elongation of the viral DNA chain.
Routes of administration/doses The adult oral dose is 200–400 mg
2–5 times daily, initially for a period of 5 days. The corresponding intra-
venous dose is 5–10 mg/kg 8-hourly, infused over a period of 1 hour.
A higher dose is used for zoster than for simplex infections. Topical applica-
tion should be performed 5 times daily, again for an initial period of 5 days.
Effects
Metabolic/other Increases in plasma levels of urea and creatinine may occur
if the drug is administered intravenously too rapidly.
Toxicity/side effects Aciclovir is generally well tolerated. CNS dis-
turbances (including tremors, confusion, and seizures) and gastrointestinal
upset may occur. Precipitation of the drug in the renal tubules leading to
renal impairment may occur if the drug is administered too rapidly or if
an adequate state of hydration is not maintained. The drug is an irritant to
veins and tissues.
Kinetics
Absorption Oral absorption of the drug is erratic; the bioavailability by this
route is 15–30%.
Distribution The drug is 9–33% protein-bound in the plasma; the VD is
0.32–1.48 l/kg.
Metabolism The major metabolite is 9-carboxymethoxymethyl guanine
which is inactive.
 Aciclovir 9

Excretion The drug is excreted by active tubular secretion in the urine,

45–80% unchanged. The elimination half-life is 2–3 hours.
Special points A reduced dose should be used in the presence of renal
impairment; haemodialysis removes 60% of the drug.
10 Adenosine

Adenosine
Uses Adenosine is used in the diagnosis and treatment of paroxysmal
supraventricular tachycardia.
Chemical A naturally occurring nucleoside that is composed of adenine
and d-ribose. Adenosine or adenosine derivatives play many important bio-
logical roles, in addition to being components of DNA and ribonucleic acid
(RNA).
Presentation As a clear, colourless solution containing 3 mg/ml adeno-
sine in saline.
Main action Depression of sinoatrial and atrioventricular (AV) nodal
activity and slowing of conduction. The drug also antagonizes cyclic adeno-
sine monophosphate (cAMP)-mediated catechol stimulation of ventricular
muscle. Both actions result in negative chronotropic and inotropic effects.
Mode of action Adenosine acts as a direct agonist at specific cell
membrane receptors, classified into A1 and A2 subsets. A1 receptors are
coupled to potassium channels by a guanine nucleotide-binding protein in
supraventricular tissue.
Routes of administration/doses Adenosine is administered as a
rapid intravenous bolus, followed by a saline flush. The initial adult dose
is 3 mg, followed, if necessary, by a 6 mg and then a 12 mg bolus at
1- to 2-minute intervals until an effect is observed. The paediatric dose is
0.0375–0.25 mg/kg. The drug acts within 10 seconds and has a duration of
action of 10–20 seconds.
Effects
CVS Depression of sinoatrial and AV nodal activity leads to the termina-
tion of paroxysmal supraventricular tachycardia. Atrial dysrhythmias are
revealed by AV nodal block, leading to a transient slowing of the ventricu-
lar response. Adenosine has no clinically important effects on the blood
pressure when administered as a bolus. A continuous high-dose infusion
may result in a decrease in the systemic vascular resistance and decreased
blood pressure. When administered as an infusion, adenosine causes a
dose-dependent reflex tachycardia and an increase in the cardiac output.
The drug also causes a dose-dependent increase in myocardial blood flow,
secondary to coronary vasodilation mediated via endothelial A2 receptors.
Adenosine decreases the pulmonary vascular resistance (PVR) in patients
with pulmonary hypertension.
RS Bolus administration of adenosine leads to an increase in both the
depth and rate of respiration, probably mediated by A2 receptor stimu-
lation in the carotid body. Infusion of the drug results in a fall in PaCO2.
Bronchospasm may occur.
CNS Infusion of adenosine results in increased cerebral blood flow.
Low-dose adenosine induces neuropathic pain, hyperalgesia, and ischaemic
pain. Adenosine itself is a neurotransmitter.
 Adenosine 11

GU Hypotensive doses of adenosine stimulate A2 receptors, resulting in

renal and hepatic arterial vasoconstriction, although low doses have no
effect on the glomerular filtration rate or sodium excretion.
Metabolic/other Adenosine inhibits lipolysis and stimulates glycolysis.
Toxicity/side effects The commonest side effects are transient facial
flushing, dyspnoea, and chest discomfort. Bronchospasm has also been
reported. The induced bradycardia predisposes to ventricular excitability
and may result in ventricular fibrillation. Profound bradycardia requiring pac-
ing may occur.
Kinetics
Absorption Adenosine is inactive when administered orally.
Metabolism Exogenous adenosine is absorbed from the plasma into red
blood cells and the vascular endothelium where it is phosphorylated to
adenosine monophosphate (AMP) or deaminated to inosine and hypoxan-
thine. The plasma half-life is <10 seconds.
Special points No dose adjustment is necessary in the presence of renal
or hepatic impairment. Adenosine has been used to induce hypotension
perioperatively.
Intraoperative use of adenosine decreases the minimal alveolar con-
centration (MAC) of isoflurane and decreases post-operative analgesic
requirements.
12 Adrenaline

Adrenaline
Uses Adrenaline is used in the treatment of:
1. anaphylactic and anaphylactoid shock
2. asystole
3. low cardiac output states
4. glaucoma and
5. as a local vasoconstrictor, and
6. is added to local anaesthetic solutions to prolong their duration
of action.
Chemical A catecholamine.
Presentation As a clear solution for injection containing 0.1/1 mg/ml
of adrenaline hydrochloride, a 1% ophthalmic solution, and as an aerosol
spray delivering 280 micrograms metered doses of adrenaline acid tartrate.
Main action Sympathomimetic.
Mode of action Adrenaline is a directly acting sympathomimetic amine
that is an agonist of alpha- and beta-adrenoreceptors; it has approximately
equal activity at both alpha- and beta-receptors.
Routes of administration/doses The drug may be administered
intravenously either as an intravenous bolus in doses of 0.1–1 mg for the
treatment of asystole or as an infusion at the rate of 0.01–0.1 micrograms/
kg/min, titrated according to response; low doses tend to produce pre-
dominantly beta-effects, whilst higher doses tend to produce predomi-
nantly alpha-effects. The dose by the subcutaneous route is 0.1–0.5 mg.
Adrenaline may be administered by inhalation; a maximum daily dose of
10–20 metered doses is recommended.
Effects
CVS Adrenaline is both a positive inotrope and a positive chronotrope, and
therefore causes an increase in the cardiac output and myocardial oxygen
consumption. The drug causes an increase in the coronary blood flow.
When administered as an intravenous bolus, adrenaline markedly increases
the peripheral vascular resistance, producing an increase in the systolic
blood pressure with a less marked increase in the diastolic blood pressure.
When administered as an intravenous infusion, the peripheral vascular
resistance (a direct beta-2 effect) and diastolic blood pressure both tend
to decrease. The heart rate initially increases and subsequently decreases
due to a vagal reflex. The plasma volume decreases as a result of the loss
of protein-free fluid into the extracellular fluid. Adrenaline increases platelet
adhesiveness and blood coagulability (by increasing the activity of factor V).
RS Adrenaline is a mild respiratory stimulant and causes an increase in both
the tidal volume and respiratory rate. The drug is a potent bronchodilator
but tends to increase the viscosity of bronchial secretions.
 Adrenaline 13

CNS Adrenaline only penetrates the CNS to a limited extent but does have
excitatory effects. The drug increases the cutaneous pain threshold and
enhances neuromuscular transmission. Adrenaline has little overall effect
on the cerebral blood flow. It has weak mydriatic effects when applied topi-
cally to the eye.
AS The drug decreases the intestinal tone and secretions; the splanchnic
blood flow is increased.
GU Adrenaline decreases the renal blood flow by up to 40%, although
the glomerular filtration rate remains little altered. The bladder tone is
decreased and the sphincteric tone increased by the drug, which may lead
to difficulty with micturition. Adrenaline inhibits the contractions of the
pregnant uterus.
Metabolic/other The drug has profound metabolic effects; it decreases
insulin secretion whilst increasing both glucagon secretion and the rate
of glycogenolysis, resulting in elevation of the blood sugar concentration.
The plasma renin activity is increased by the drug (a beta-1 effect), and the
plasma concentration of free fatty acids is increased by the activation of tri-
glyceride lipase. The serum potassium concentration transiently rises (due
to release from the liver), following the administration of adrenaline; a more
prolonged decrease in potassium concentration follows. Adrenaline admin-
istration increases the basal metabolic rate by 20–30%; in combination with
the cutaneous vasoconstriction that the drug produces, pyrexia may result.
Toxicity/side effects Symptoms of CNS excitation, cerebral haemor-
rhage, tachycardia, dysrhythmias, and myocardial ischaemia may result from
the use of adrenaline.
Kinetics Data are incomplete.
Absorption The drug is inactivated when administered orally. Absorption is
slower after subcutaneous than intramuscular administration. The drug is
well absorbed from the tracheal mucosa.
Metabolism Exogenous adrenaline is predominantly first metabolized by
catechol-O-methyl transferase, predominantly in the liver, to metadrena-
line and normetadrenaline (uptake-2); some is metabolized by monoamine
oxidase within adrenergic neurones (uptake-1). The final common products
of adrenaline metabolism are 3-methoxy 4-hydroxyphenylethylene and
3-methoxy 4-hydroxymandelic acid (which are inactive).
Excretion The inactive products appear predominantly in the urine.
Special points The dose of adrenaline should be limited to 1 microgram/
kg/30 min in the presence of halothane and to 3 micrograms/kg/
30 min in the presence of enflurane or isoflurane, in an attempt to pre-
vent the appearance of serious ventricular dysrhythmias. Infiltration of
adrenaline-containing solutions should be avoided in regions of the body
supplied by end arteries.
14 Alfentanil

Alfentanil
Uses Alfentanil is used:
1. to provide the analgesic component in general anaesthesia
2. in sedation regimens for intensive care, and
3. to obtund the cardiovascular responses to laryngoscopy.
Chemical A synthetic phenylpiperidine derivative.
Presentation As a clear, colourless solution for injection containing
0.5/5 mg/ml of alfentanil hydrochloride. The pKa of alfentanil is 6.5; alfen-
tanil is 89% unionized at a pH of 7.4 and has a relatively low lipid solubility.
Despite the low lipid solubility of the drug (octanol:water partition coef-
ficient of 128.1), it has a faster onset of action, compared to fentanyl which
has a much higher lipid solubility due to its low pKa and consequently large
amount of unionized drug available to cross lipid membranes.
Main actions Analgesia and respiratory depression.
Mode of action Alfentanil is a highly selective mu-opioid (MOP) ago-
nist; the MOP receptor appears to be specifically involved in the media-
tion of analgesia. Opioids appear to exert their effects by interacting with
pre-synaptic Gi protein receptors, leading to a hyperpolarization of the cell
membrane by increasing potassium conductance. Inhibition of adenylate
cyclase, leading to a reduced production of cAMP and closure of voltage-
sensitive calcium channels, also occurs. The decrease in membrane excit-
ability that results may decrease both pre- and post-synaptic responses.
Routes of administration/doses Alfentanil is administered intrave-
nously in boluses of 5–50 micrograms/kg. The drug may be administered
by intravenous infusion at a rate of 0.5–1 micrograms/kg/min. Alfentanil
acts rapidly, with the peak effect occurring within 90 seconds of intrave-
nous administration, and the duration of effect is 5–10 min. Administration
of alfentanil reduces the amount of hypnotic/volatile agents required to
maintain anaesthesia.
Effects
CVS The most significant cardiovascular effect that alfentanil demon-
strates is bradycardia of vagal origin; cardiac output, mean arterial pres-
sure, pulmonary and systemic vascular resistance, and pulmonary capillary
wedge pressure are unaffected by the administration of the drug. Doses of
5 micrograms/kg increase left ventricular contractility and cardiac output in
animal models. Alfentanil obtunds the cardiovascular responses to laryngo-
scopy and intubation.
RS Alfentanil is a potent respiratory depressant, causing a decrease in both
the respiratory rate and tidal volume; it also diminishes the ventilatory
response to hypoxia and hypercarbia. The drug is a potent antitussive agent.
Chest wall rigidity (the ‘wooden chest’ phenomenon) may occur after the
administration of alfentanil—this may be an effect of the drug on MOP
receptors located on GABA-ergic interneurones. Alfentanil causes minimal
histamine release; bronchospasm is thus rarely produced by the drug.
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rescue, and had not the Horse Guards opportunely fell in upon them, as they lay
battering before my house, it had not been in my power to have prevented a further
mischief.” (Letter from Humphrey Weld to the Earl of Craven in Calendar of State
Papers, Domestic, 1671, pp. 241–2).
478. Historical MSS. Commission, Duke of Portland’s MSS., Report XIII.,
App. 1, 683.
479. He was certainly there in April of that year. “Letter for the French
Ambassador brought by a sea captain enclosed to Humphrey Wield, at his house in
Wield Street, London.” (Calendar of State Papers, Domestic, 1673, p. 166).
480. For example: (i) 10 March 1676–7. Information of William Herriot that
“at Nieuport he met Captains Douglas and Ennys, who desired him to make his
address to the Spanish Ambassador at London, who lived at Wild House.”
(Calendar of State Papers, Domestic, 1677–8, p. 14); (ii.) 29 March, 1679. Lord
Clarendon reports that “in Mr. Weld’s garden in a grotto are 27 chests of goods....
Mr. Bedloe present said they belonged to Don Pedro de Ronquillio who was
present at the search and would not admit to have the letters perused.” (Historical
MSS. Commission, House of Lords MSS., App. to 11th Report, Part II., pp. 126–7);
(iii.) 26 April, 1681. Evelyn records his visit to “Don Pietro Ronquillio’s, the
Spanish Ambassador, at Wild House”; (iv.) 9th September, 1686. “The Spanish
Ambassador made a bonfire at Wild House last night and brought out wine for the
mob, but the rabble overthrew the bonfires, broke the cask of wine and broke the
windows, and pulled down some of the brick wall.” (Historical MSS. Commission,
Duke of Portland’s MSS., III., p. 397).
481. See Petition and Appeal of Ralph Lister, MSS. of House of Lords, New
Series, IV., pp. 274–5.
482. 21st December, 1693. “The Spanish Ambassador has taken a house in the
Old Spring Garden, where the Duke of Norfolk lately lived, and has, in a manner,
fitted up his chapel. Notice was sent to his Excellency that for some reasons a
Romish chapel could not be permitted within the verge of the Court, so he is
removing back to Weld House.” (Calendar of State Papers, Domestic, 1693, p.
433).
“Weld House is to be Lett, containing 33 Rooms, Garrets and Cellars, with
other suitable conveniences, in Weld Street near L.I. Fields. Enquire at Weld
House, or at Marybone House.” (London Gazette, Sep. 13–17, 1694).
483. Reproduced here.
484. Indenture between Isaac Foxcroft and others and Hugh Jones (in
possession of the London County Council).
485. Reproduced here.
486. Close Roll, 5 Chas. I. (2800)—Indenture between Richard Holford and
Sir Edward Stradling, reciting the earlier indenture.
 487. See p. 93.
488. Chancery Proceedings, Bridges, 465–184. Plea of John Corrance.
489. Reproduced here.
490. Middlesex Feet of Fines, 32 Eliz., Hilary.
491. Ibid., 21 Jas. I., Easter.
492. Recited in Indenture between Matthew Francis and Symond Harborne,
in the possession of the London County Council.
493. Lease by the Rt. Hon. Lord Cary to William Loringe, in the possession of
the London County Council.
494. See p. 112.
495. Katherine Clifton, only daughter and heiress of Gervase, Lord Clifton of
Leighton Bromswold.
496. Calendar State Papers, Domestic, 1623–5, p. 488; 1627–8, p. 10; 1628–
9, p. 359; 1629–31, p. 38.
497. Ibid., 1628–9, p. 369.
498. Somerset House Wills, Harvey, 6 (Proved 15th January, 1638–9).
499. Lady Elizabeth Cust’s The Brownlows of Belton (Records of the Cust
Family Series), II., p. 61.
500. This is not quite certain, but there does not seem much doubt that the
entry refers to Lennox House.
501. The two portions were subsequently assessed for the Hearth Tax at 26
and 11 hearths respectively. The whole house was therefore comparable in size with
Bristol House, assessed at 40 hearths.
502. The Countess of Dysart writes from “Lady Allington’s house, Drury
Lane,” on 22nd August, 1667 (Calendar State Papers, Domestic, 1667, p. 409), and
in November, 1668 or 1669, Lord Allington refers to his mother’s house in Drury
Lane (Ibid., 1668–9, p. 55). Lady Allington was succeeded in this house by Lady
Ivey (Hearth Tax Roll for 1675).
503. Somerset House Wills, Batt, 136. (Proved, with 39 codicils, 28th June,
1680).
504. Middlesex Registry Memorials, 1716, III., 24.
505. Parton states that Brownlow Street appears in the parish books in 1685.
506. Indenture of 28th April, 1722, between Gilbert Umfreville and Chas.
Umfreville and Ric. Baker (Middlesex Registry Memorials, 1722, VI., 85).
507. See p. 105.
508. Grey’s St. Giles’s of the Lepers, pp. 114–5.
 509. Reproduced here.
510. See p. 103.
511. Parton’s Hospital and Parish of St. Giles, p. 125.
512. The ratebooks from 1730 (earliest extant) to 1746 show “Daniel Hahn,”
possibly a more correct form of the name, at this house.
513. Indenture dated 27th May, 1728, between Peter Walter and Nicholas
Lovell (Middlesex Registry Memorials, 1728, VI., 15).
514. Grey’s St. Giles’s of the Lepers, p. 116.
515. Reproduced here.
516. Close Roll, 12 William III. (4863)—Indenture between (1) Mary
Rawlinson, (2) Giles Powell and (3) Jeremiah Ridge.
517. See p. 109.
518. See p. 112.
519. Privy Council Register, Vol. 29, p. 424.
520. Calendar State Papers, Domestic, 1611–18, p. 551.
521. Ibid., p. 555.
522. Privy Council Register, Vol. 29, p. 484.
523. Privy Council Register, Vol. 46, p. 274.
524. It is just possible that a later reference to the spring is to be found in the
petition dated 7th July, 1637, of the inhabitants of the Old Town of St. Giles,
“complayning of ye stopping up of a fair large and open well in ye said towne; being
of great use and comfort to ye peters who now find ye want thereof in these times of
contagion, ye same being continued to bee stopped up as aforesaid, by ye now
landlord Frauncis Garrett.” (Privy Council Register, Vol. 48, p. 105).
525. Parton’s Hospital and Parish of St. Giles, p. 114.
526. Close Roll, 9 Eliz. (742).
527. Close Roll, 24 Eliz. (1129)—Indenture between Jas. Briscowe, Joan his
wife and John Wise and Jas. Mascall.
528. Close Roll, 11 Chas. I. (3057).—Indenture between Thos. and Olive
Godman and Francis and Frances Gerard.
529. Property on the east side of Drury Lane and on the north side of Broad
Street is mixed up with this, and it is not possible entirely to separate them.
530. “... abutting east on a court called Ragged Staffe Court (which court was
heretofore in the possession of John Vavasour.” (Close Roll, 12 William III. (4863)
—Indenture between Mary Rawlinson, etc., cited above).
 531. Parton’s statement that the two were identical (Hospital and Parish of St.
Giles, p. 127) is incorrect. The Hearth Tax Rolls mention both, and both are clearly
shown in the map accompanying Strype’s edition of Stow (Plate 5).
532. He died in 1585 (Inquisitiones Post Mortem, Series II., Vol. 208 (173).)
533. John Vavasour’s will (Somerset House Wills, Winderbanck, 65), was
proved on 18th June, 1608.
534. Close Roll, 9 Eliz., (749).
535. Middlesex Registry Memorials, 1723, V., 181–2.
536. On 16th January, 1717–8, Edward Theedham leased to Chas. Hall and
Ant. Elmes The Bear Brewhouse, in St. Giles (Middlesex Registry Memorials, 1717,
IV., 263).
537. Ancient tavern signs were nearly always “on the hoop,” which seems to
have originated “in the highly ornamented bush or crown, which latterly was made
of hoops covered with evergreens.” (Larwood and Hotton, History of Signboards,
p. 504.)
538. Hospital and Parish of St. Giles, p. 237.
539. Close Roll, 31 Chas. II. (4527).
540. Sewer Rate Book for that year.
541. Parton’s Hospital and Parish of St. Giles, p. 320.
542. Close Roll, 9 Eliz. (742).
543. On 27th March, 1573, Henry Amptill and Roger Mascall, brewers, were
convicted of having set at large certain suspected persons, whom William Westone,
a “hedborowe” of St. Giles, had taken in a certain tenement of the said Henry
Amptill and had imprisoned. (Middlesex County Records, Sessions Rolls, I., p. 82).
544. In 1621, John Ampthill was granted leave to alienate 5 messuages, 11
cottages and 4 gardens to Anne, Robert, James and Thomas Foote (Patent Roll, 19
Jas. I. (2263)); in 1614 he sold 3 houses to Richard Windell (Middlesex Feet of
Fines, 12 Jas I., Mich.), whose grandson in 1630 parted with them to Abraham
Hawkins (Close Roll, 6 Chas. I. (2823)); and in 1625 he obtained leave to alienate
14 messauges to John and Abraham Hawkins. On the death of Abraham in 1645,
he was still in possession of 14 messuages in St. Giles (Inquisitiones Post Mortem,
2nd Series, 707 (41).)
545. The Hawkins property seems to have descended to Sir William Dawes,
Archbishop of York, whose mother was Jane Hawkins. By a deed of 1726
(Middlesex Registry Memorials, 1726, IV., 389) Jane Lewis sold the remainder of
a lease granted by Sir William, and comprising inter alia a house which by
reference to the ratebooks can be shown to be the second westwards from Lamb
Alley.
 546. Close Roll, 7 Chas. I. (2895).
547. Close Roll, 1655 (3866).
548. On 3rd December, 1603, William Barber, of St. Giles, gardener, was
convicted, with others, of throwing filth and dung near the highway in a certain
close called “Blumsberrie fieldes.” (Middlesex County Records, Sessions Rolls, II.,
p. 4).
549. Middlesex Feet of Fines, 32 Eliz., Easter.
550. Hospital and Parish of St. Giles, p. 319.
551. Sale by Arthur Blythe to William Wigg and Thomas Whitfield, in trust for
John Smallbone, dated 1680, and quoted by Parton (op. cit.) p. 126.
552. See p. 106.
553. Hospital and Parish of St. Giles, p. 125.
554. Hospital and Parish of St. Giles, p. 113. Newlands was actually in the
parish of St. Marylebone (see p. 125).
555. Blemundsbury, p. 308.
556. “Maslyn’s Pond” and “Maslyn Fields” are mentioned in the parish books
in 1644 and 1656 (Parton’s Hospital and Parish of St. Giles, pp. 270–1).
557. See p. 101.
558. See Sale by Arthur Blythe to Wigg and Whitfield, quoted by Parton
(Hospital and Parish of St. Giles, p. 126).
559. Kingsford’s edition, II., p. 91.
560. Reproduced here.
561. See p. 123. The Close had a reputed area of 10 acres (See e.g., Rents of
Henry VIII. in London and the Suburbs, 35 Henry VIII. (Rentals and Surveys,
General Series), Roll 452).
562. Parliamentary Survey (Augmentation Office), Middlesex, 24.
563. I.e., the field called Long Acre or Elm Field, lying between Castle Street
and the street called Long Acre.
564. Obviously a mistake for “south”; Castle Street is the thoroughfare meant.
565. Monmouth Street, now Shaftesbury Avenue, and West Street.
566. I.e., The Bowl property, see p. 110.
567. Sir John Brownlow. The same variation occurs in the Hearth Tax Rolls.
568. Close Roll, 2 Geo. II. (5363).
569. Endowed Charities, County of London, Vol. V., p. 946.
 570. Patent Roll, 24 Charles II. (3137).
571. The existence of a “Tower Street” between King Street and White Lion
Street is impossible. A portion of the close was in 1690 used as a laystall (Calendar
of State Papers, Domestic, 1689–90, p. 389).
572. Chancery Proceedings, Bridges, 36–47. Suit of Jas. Kendricke.
573. Chancery Proceedings, Bridges, 614–105. Suit of William Jennens.
574. There are records inter alia of (a) four houses built in Great St. Andrew
Street, between Michaelmas, 1693, and August, 1694 (Middlesex Registry
Memorials, 1734, V., 266), and (b) houses built in Monmouth Street and Little Earl
Street in July, 1693, and October, 1694 (Chancery Decree Roll, 1933. Suit of
William Lloyd).
575. The leases of many of the houses erected on the south-west of the close do
not seem to have been granted before 1708–9.
576. Notes and Queries, 11th Series, VIII., pp. 182–3.
577. The plan is probably a little later than 1691 (the date assigned to it), for,
as has been shown, Neale did not obtain his lease until 1693.
578. Wheatley and Cunningham’s London Past and Present, III., p. 234.
579. Reproduced here.
580. Recited in Indenture of 25th October, 1728, between Jas. Joye (1), Oliver
Martin and Thos. Russell (2) and Rev. Thos. Blackwell (3) (Close Roll, 2 Geo. II.
(5364)).
581. Much of the above information is taken from Emily Dibdin’s Seven Dials
Mission: the story of the old Huguenot Church of All Saints, West Street.
582. Reproduced here.
583. It should be mentioned, however, that in a petition, probably belonging
to the year 1354, the Mayor and Commonalty of London claimed that the Hospital
had been founded by a citizen of London suffering from leprosy. (Calendar of
Letterbooks of the City of London, Letterbook G., p. 27).
584. Parton (History of the Hospital and Parish of St. Giles-in-the-Fields, p.
1) and, following him, Dugdale (Monasticon VII., p. 635) give the date of the
Hospital’s foundation as 1101. This is certainly wrong. Parton’s authority was an
entry in Leland’s Collectanea, I., p. 418 (2nd edn.), which under the date 1101
mentions several events, (i.) Henry’s marriage with Maud, (ii.) his appointment of
a military guard for his brother Robert who was in prison, (iii.) Maud’s foundation
of the Hospital of St. Giles. The next entry is dated 1109. The date 1101 is obviously
only intended to cover (i.) (which took place strictly speaking in 1100), for Robert
was not taken prisoner until the battle of Tinchebray in 1106. The passage
therefore would seem to suggest a date between 1106 and 1109 for the foundation
of St. Giles.
 585. Survey of London (Kingsford’s edn.), II., p. 90.
586. Historia Anglicana, p. 176b.
587. Parton in his transcription of the document reads “forty” throughout, and
has been copied by everybody. It is, however, clearly “quatuordecim” in all cases.
588. Ancient Petitions, E. 617.
589. Ancient Petitions, E. 617; 2448.
590. Calendar of Letterbooks of the City of London, Letterbook G., p. 28.
591. Ibid., p. 29.
592. I.e., 27 Edw. I. (Calendar of Patent Rolls, p. 404). It has been generally
assumed that the date was 1354, i.e., 27 Edw. III., no doubt because Parton
(Hospital and Parish of St. Giles, pp. 23, 26) when translating the document
relating to the suit between the Abbot of St. Mary Graces and the Master of Burton
Lazars gave the name of the King as Edward the son of Edward, whereas the
reading is clearly “Edward the son of Henry.”
593. It really extended somewhat to the west of the eastern side of the modern
road, which has been formed by widening the ancient Hog Lane.
594. Close Roll, 16 James I. (2384).—Indenture, dated 19 March, 1617–8,
between Robert Lloyd and Isaac Bringhurst.
595. See p. 124.
596. Inquisitiones Post Mortem, 3 Edward VI. (89).
597. Close Roll, 8 Elizabeth (722).
598. Close Roll, 8 James I. (2066)—Indenture, dated 20th February, 1610–11,
between John Graunge and Robert Lloyd.
599. A sixth was sold in 1622 by John and William Flood to Zachery Bethel,
lying to the south of Sir Edward Fisher’s house, but this seems to have only
recently been built on land taken out of the four acres (see p. 122).
600. Close Roll, 16 James I. (2384).
601. The reversion was then sold to Francis Ashburnham (Close Roll, 5
Charles I. (2800)—Indenture, dated 1st March, 1628–9, between John Stafey and
Isaac Bringhurst and The Worshipful Francis Ashburnham).
602. Endowed Charities (County of London), Vol. III. (1900), p. 348.
603. Close Roll, 10 James I. (2123)—Indenture between Robert Floyd and
William Holt and John Harman.
604. Close Roll, 1652 (3683)—Indenture between John Hooker and Walter
Bigg.
 605. Letter dated 5th May, 1677, from Philip, Lord Wharton to Sir R. Verney
(Historical MSS. Commission, Verney MSS., App. to VII. Report, p. 469).
606. Parton’s Hospital and Parish of St. Giles-in-the-Fields, p. 117.
607. Middlesex Registry Memorials, 1727, VI., 138.
608. Close Roll, 16 James I. (2384)—Indenture between Robert Lloyd and
Isaac Bringhurst.
609. Close Roll, 16 James I. (2384).
610. Close Roll, 7 Charles I. (2895)—Indenture between Anne Bringhurst and
John Stafey and the Lady Alice Dudley.
611. Close Roll, 10 Charles I. (3017).
612. Chancery Proceedings, Bridges, 455–66.—Suit of John Boswell.
613. The boundaries are given as (E) tenement now in occupation of Nicholas
Holden; (W) churchyard; (N) Kilburn to Holborn Highway; (S) orchard of Nicholas
Holden (Close Roll, 9 Elizabeth (742)—Indenture between Lord Mountjoy and
Percival Rowland).
614. The boundaries are given as: (S) highway from St. Giles to Knightsbridge;
(W) a tenement late of Rowland Percival, and a close of John Graunge; (N)
highway through St. Giles to Uxbridge (Close Roll, 11 Elizabeth (797)—Indenture
between Lord Mountjoy and Edward Kyngston).
615. See p. 125.
616. Inquisitiones Post Mortem, II. Series, Vol. 139 (134).
617. Inquisitiones Post Mortem, II. Series, Vol. 384 (139).
618. Recovery Roll, 21 James I. Trinity.—Indenture between John and
William Flood, and Zachery Bethel.
619. Somerset House Wills, Gee, 159.
620. Patent Roll, 23 Charles II. (3125).
621. Augmentation Office, Deed of Sale, E. 19. The Master of Burton Lazars
apparently lost by the transaction, but from a letter, dated 1st April, 1535, written
by Richard Layton to Cromwell, it would seem that at one time there was a distinct
prospect of his faring still worse. “I sent for the Master of Burton Lazer as you
desired, advertising him of the King’s pleasure commanding him to be here by
Easter eve, and desire you to intercede for him with the King that he might obtain
other lands for his lands of St. Giles’s. He came, and I have been with him divers
times. I have persuaded him to put his sole trust in you and that he shall not go to
the King in anywise before you bring him to His Grace. He is content to do so.
When you wish that I should bring him unto you to make further declaration to
him of the King’s pleasure, let me know.” (Calendar of Letters of Henry VIII., 26
H. VIII., p. 168).
 622. These were in St. Anne’s, Soho.
623. After the Duke of Norfolk had heard that Legh was scheming to get the
mastership, he wrote that Legh was married, adding, “Alas! what pity it were that
such a vicious man should have the governance of that honest house!” (Letters and
Papers of Henry VIII., XII., i., p. 282).
624. Patent Roll, 28 Henry VIII. (671).
625. The whole of the above information is obtained from Chancery Decree
Roll (1).
626. Abstracts of Inquisitiones Post Mortem relating to the City of London,
ed. Geo. S. Fry, Part I., p. 62. Legh was buried in the old church of St. Leonard,
Shoreditch, and an illustration of his effigy is given in Ellis’s Antiquities of
Shoreditch. The following inscription was underneath (Hatton’s New View of
London, 1908):—

“Here under lye the Ashes and the Bones

Of Sir Tho. Leigh, that good and learned Knight,
Whose hasty Death, alas, the Godly still bemoan,
Tho his Soul always rejoice in God’s sight,
Great was his Wisdom, and greater was his Wit,
His Visage comely, with no sad Change dismay’d,
A Man in all Affairs a King to serve most fit,
Had not Death so soon his mortal Life betray’d.”

627. Chancery Decree Roll, No. 3.

628. Close Roll, 37 Henry VIII. (444).
629. This was in the parish of Edmonton, now Southgate.
630. On the north side of Broad Street, now in the parish of St. George,
Bloomsbury.
631. The Great Close of Bloomsbury and Wilkinson’s Close.
632. I.e., Middle Row (see Close Roll, 12 Elizabeth (832).—Indenture between
Lord and Lady Mountjoy and William Perye), formerly standing just outside
Holborn Bars.
633. These were in St. Marylebone. The Inquisition on the death of Sir John
Grange (1611) refers to “a close of land commonly known by the name of
Newlondes containing 24 acres, and ... all that parcel of land or lane (“venelle”)
near adjoining the aforesaid close ... situated within the parish of Marylebone.”
(Inquisitiones Post Mortem, II. Series, Vol. 686 (113)).
634. Licence to alienate granted 6th July, 1546.
635. Inquisitiones Post Mortem, II. Series, 3 Edward VI. (89).
636. Inquisitiones Post Mortem, 15 Elizabeth, Vol. 165, on Thomas Carew.
 637. Ibid., 6 Elizabeth, Vol. 139.
638. Ibid., Series II. (49), Vol. 109.
639. Her second husband was Sir Thomas Chaloner.
640. According to the Dictionary of National Biography, he “spent the
fortune of his family in the pursuit of alchemy.”
641. The “Lorde Mountjoye and the Lady Katherine” are mentioned in a
mortgage by the former to John Mery, dated 1st February, 1556–7. (Close Roll, 4
and 5, Philip and Mary (547)).
642. Close Roll, 7 Eliz. (695).
643. Considerable doubt seems to have existed on this point. Side by side with
assertions to the contrary, there are plain statements that the mortgage was
redeemed (see e.g., Chancery Decree Roll, 54, concerning a complaint by Jas.
Mascall against Thomas Harrys and others). Nevertheless it is quite certain that
the statement in the text is true, for (1) the recognisance accompanying the
mortgage is not cancelled; (2) Blount’s son Charles (afterwards Earl of Devonshire)
definitely stated that the manor was not redeemed (Chancery Proceedings,
Elizabeth B. 15–52), suit of Charles Blount; (3) the steps by which the manor
descended from the Brownes are known.
644. Close Roll, 21 Eliz. (1059); Common Plea Roll, 25 Eliz., Hilary, 4010;
Close Roll, 34 Eliz. (1425). Parton (Hospital and Parish of St. Giles-in-the-Fields,
p. 331) bridges over the gap between Blount and Cope by the supposition that the
manor came into the hands of the last-named in consequence of a mortgage to one
“Master Cope, citizen of London.” But (1) the mortgage is not of the manor of St.
Giles, and (2) the proper reading is not “Cope” but “Rope.”
645. He was knighted on 20th April, 1603.
646. Close Roll, 14 Jas. I. (2308)—Indenture between Sir Henry Rich, Dame
Isabella, and Dame Dorothy Cope and Gifford and Risley.
647. Vestry Minutes, 1624–1719.
648. See p. 1.
649. Newcourt, op. cit., p. 612.
650. The sketch given by Parton, Hospital and Parish of St. Giles-in-the-
Fields, p. 54, is quite untrustworthy, and is in conflict with the little that is known
of the church. He gives no authority for the sketch save that it was as “preserved in
rude delineations of it, made near the time.”
651. Parton’s Hospital and Parish of St. Giles-in-the-Fields, p. 56.
652. Ibid., pp. 191–2.
653. Vestry Minutes, 1624–1719, f. 4.
 654. A Mirrour of Christianity and a Miracle of Charity, etc., by R. B. [i.e.,
Robert Boreman], p. 121.
655. A New View of London (1708), I., p. 259.
656. Strype’s edition of Stow, 1720, II., pp. 77ff. The greater portion of what
follows is taken from Strype’s description.
657. See illustrations on map in Strype’s edition of Stow (Plate 5).
658. A list of Lady Dudley’s benefactions comprises the following: “She gave to
the Church of St. Giles, the greatest bell in the steeple; and divers great pieces of
massive plate; paved the chancel with marble, built the fair blue gate at the
entrance to the churchyard, and purchased a fair house of £30 a year value for the
perpetual incumbent. She also gave the hangings for the choir, which cost £80
10s., 2 service books, embroidered in gold, £5; velvet altar cloth with gold fringe
£60; a cambric cloth to lay over it with a deep bone lace £4 10s.; another fine
damask cloth £3; 2 cushions for the altar, richly embroidered with gold, £10; a
Turkey carpet to lay before the altar £6; a long screen to sever the chancel from the
church, richly carved and gilt, £200; a fair organ £100; the organ loft richly
wrought and gilt, and a tablet of the Ten Commandments, the Creed and Lord’s
Prayer, richly adorned, £80; the rails before the altar curiously carved and gilt,
£40.” (Calendar of State Papers, Domestic, 1668–9, p. 176).
659. Parton’s Hospital and Parish of St. Giles-in-the-Fields, pp. 200–1.
660. 4 Geo. I., cap. 14.
661. 3 Geo. II., cap. 19.
662. Parton’s Hospital and Parish of St. Giles, p. 213.
663. Hatton’s New View of London (1708), p. 262.
664. Parton’s Hospital and Parish of St. Giles, p. 224
665. Parton’s Hospital and Parish of St. Giles-in-the-Fields, pp. 216–7.
666. Novum Repertorium Ecclesiasticum Parochiale Londinense, p. 173.
667. Reproduced here.
668. See p. 123.
669. Reproduced here.
670. Parton’s Hospital and Parish of St. Giles-in-the-Fields, p. 117.
671. Reproduced here.
672. See p. 1.
673. Close Roll, 30 Henry VI.—Grant, dated 2nd April, 1452, by Jo. Crouton
and W. Horn to Jo. and Katherine Nayler.
674. To the east of Church Close.
 675. Close Roll, 13 James I. (2275).
676. History of London, p. 1363.
677. Tyburn Gallows (published by the London County Council), p. 16.
678. The gallows in St. Giles Fields erected for the execution of Lord Cobham
were obviously put up for that special purpose. There may, of course, have been a
manorial gallows, but no mention of such for St. Giles occurs in the Quo Warranto
Rolls.
679. Endowed Charities, County of London, III., p. 350.
680. Parton’s Hospital and Parish of St. Giles, p. 228.
681. Chancery Decree Roll, No. 3.
682. Inquisitiones Post Mortem, II. Series, Middlesex, Vol. 200 (5).
683. Formerly on the east side of Dyott Street, just outside the parish
boundary.
 684. Close Roll, 9 Elizabeth (742).
685. Close Roll, 8 Charles I. (2946).
686. Close Roll, 1649 (31). Indenture, dated 20th March, 1648–9, between
John Barber als Grigg and Henry Baynbrigge.
687. Hospital and Parish of St. Giles-in-the-Fields, p. 152.
688. Edmund Buckeridge and Henry Loveday querentes: and Jane
Baynbrigge, widow; William Maynard and Mary, his wife; Nicholas Buckeridge,
and Sara, his wife; and Simon Dyott and Jane, his wife, deforciantes; of 100
messuages, 200 cottages, 40 gardens and 10 acres of land in St. Giles, Mary, Sara
and Jane renounce for their heirs. It will be seen that the property had grown, and
it is known that Bainbridge had purchased more (see e.g., purchase from Sir John
Bramston and others, Middlesex Feet of Fines, 1665, Trinity).
689. “The Rookery,” was a triangular space bounded by Bainbridge, George,
and High Streets; it was one dense mass of houses, through which curved narrow
tortuous lanes, from which again diverged close courts—one great mass, as if the
houses had originally been one block of stone, eaten by slugs into numberless
small chambers and connecting passages. The lanes were thronged with loiterers;
and stagnant gutters, and piles of garbage and filth infested the air. In the
windows, wisps of straw, old hats, and lumps of bed-tick or brown paper,
alternated with shivered panes of broken glass, the walls were the colour of
bleached soot, and doors fell from their hinges and worm-eaten posts. Many of the
windows announced, “Lodgings at 3d. a night,” where the wild wanderers from
town to town held their nightly revels.” (Timbs’ Curiosities of London (1867), p.
378.)
690. Opened in 1847.
691. Except perhaps the extreme east.
692. Wheatley and Cunningham (London, Past and Present) give the date of
the street’s formation as approximately 1670.
693. Memoirs of the Life and Works of Sir Christopher Wren (1823), p. 522.
694. Collins’s Peerage of England, 5th Edition, III., p. 328.
695. Memoirs of the Life and Works of Sir Christopher Wren, p. 522.
696. Burke’s Peerage.
697. Hospital and Parish of St. Giles, p. 372.
698. Dictionary of National Biography.
699. Walpole’s Letters (Toynbee Edn.) XI., p. 52.
700. Survey of London, Vol. III., pp. 88–89.
701. Parish ratebooks.
 702. Reproduced here.
703. Information kindly supplied by His Grace the Duke of Bedford.
704. Richardson and Gill’s London Houses from 1660 to 1820, p. 67.
705. A. E. Richardson’s Monumental Classic Architecture in Great Britain
and Ireland.
706. Survey of London, Vol. III. (St. Giles-in-the-Fields, Part I.), p. 108.
707. Beresford Chancellor’s History of the Squares of London, pp. 202–10.
708. Information kindly supplied by His Grace the Duke of Bedford.
709. Middlesex Registry Memorials, 1778, II., 409.
710. Reproduced here.
711. In the Parish of St. George, Bloomsbury.
712. Painted Decoration—the Georgian Period, by Ingleson C. Goodison
(Architectural Review, January, 1913).
713. Information kindly supplied by the Rev. Lewis Gilbertson, M.A., F.S.A.
714. Reproduced here.
715. In the Parish of St. George, Bloomsbury.
716. Middlesex Registry Memorials, 1778, II., 409.
717. Survey of London, Vol. III. (St. Giles-in-the-Fields, Part I.), p. 67.
718. Reproduced here.
719. In the Parish of St. George, Bloomsbury.
720. Middlesex Registry Memorials, 1778, IV., 505.
721. Reproduced here.
722. In the Parish of St. George, Bloomsbury.
723. Middlesex Registry Memorials, 1778, IV., 505.
724. See p. 153.
725. Boyle’s Court Guide, however, shows him at the house from 1796 to 1799.
726. The Dictionary of National Biography says that it was at No. 11, Bedford
Square.
727. Reproduced here.
728. Partly in the Parish of St. Giles-in-the-Fields and partly in that of St.
George, Bloomsbury.
729. Reproduced here.
730. Information kindly supplied by His Grace the Duke of Bedford.
731. See p. 151.
732. See pp. 84–5.
733. Reproduced here.
734. Reproduced here.
735. Reproduced here.
736. Reproduced here.
737. See p. 168.
738. Reproduced here.
739. Middlesex Registry Memorials, 1777, VII., 263.
740. Reproduced here.
741. Middlesex Registry Memorials, 1776, VI., 487.
742. Reproduced here.
743. Middlesex Registry Memorials, 1776, VI., 630.
744. Reproduced here.
745. Middlesex Registry Memorials, VI., 631.
746. Survey of London, Vol. III. (St. Giles-in-the-Fields, Part I.), p. 102.
747. Reproduced here.
748. Middlesex Registry Memorials, 1778, II., 314.
749. Dictionary of National Biography.
750. Reproduced here.
751. Middlesex Registry Memorials, 1777, VII., 351.
752. Reproduced here.
753. Middlesex Registry Memorials, 1777, VII., 353.
754. Reproduced here.
755. Middlesex Registry Memorials, 1777, VII., 254.
756. Reproduced here.
757. Middlesex Registry Memorials, 1777, VII., 252.
758. Reproduced here.
759. Middlesex Registry Memorials, 1777, VII., 257.
760. Reproduced here.
761. Middlesex Registry Memorials, 1777, I., 637.
 762. Reproduced here.
763. Middlesex Registry Memorials, 1777, II., 526.
764. Reproduced here.
765. In the Parish of St. George, Bloomsbury.
766. Middlesex Registry Memorials, 1777, I., 631.
767. Reproduced here.
768. Reproduced here.
769. See licence to alienate granted in Patent Roll, 9 Elizabeth (1038).
770. See p. 125.
771. See pardon for alienation granted in Patent Roll, 30 Elizabeth (1321).
772. Information kindly supplied by the City of London Corporation.
773. A. E. Richardson’s Monumental Classic Architecture.
774. A copy is in the County Hall collection.
775. It was the last of several designs prepared for a Select Committee of the
House of Commons who engaged in deliberating on the improvements to the Port,
including a new London Bridge. The view shows two bridges of six arches each,
with a drawbridge in the centre intended for the passage of ships. Between the
bridges flights of steps lead down to the river. The two large areas beyond the
bridges are terminated by crescents. The Monument stands in the chord of the
northern crescent, and a large obelisk in that of the southern.
776. Inquisitiones Post Mortem, Chas. I. (765), 37.
777. John Holles, first Earl of Clare (1564?–1637).
778. It seems probable that the land in question (which, being partly in St.
Giles and partly in St. Pancras, was described sometimes as in one parish,
sometimes in the other) is identical with the land in St. Pancras sold, together with
Clement’s Inn, by Sir William Hawte to William (afterwards Sir William) Holles,
ancestor of the Earls of Clare, in 1532 (Middlesex Feet of Fines, 23 Henry VIII.,
Hil.).
779. The boundary between St. Giles and St. Pancras used to run through the
middle of the close.
780. Middlesex Registry Memorials, 1772, VI., 111.
781. The Old Farm House in Tottenham Court Road, by Ambrose Heal.
782. Reproduced here.
 TRANSCRIBER’S NOTES
1. Silently corrected obvious typographical errors and
variations in spelling.
2. Retained archaic, non-standard, and uncertain spellings
as printed.
3. Linked larger images of maps as indicated by [Click
image for larger version.]
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