Anaesthesia, Intensive Care and Perioperative Medicine: An Encyclopaedia of Principles and Practice A-Z [6 ed.] 9780702071867, 9780702071874

Table of contents :
Front Cover
Inside Front Cover
Half title page
Dedication
Anaesthesia, Intensive Care and Perioperative Medicine A-Z
Copyright Page
Preface
Explanatory notes
Arrangement of text
Cross-referencing
References
Proper names
Drugs
Recommended International Nonproprietary Names (rINNs) and chemical names
Examination revision checklist
Abbreviations
Examination revision checklist
Physiology
Cardiovascular
Cellular/Molecular/Metabolism
Endocrine/Reproductive
Gastrointestinal
Nervous System
Renal
Respiratory and Acid/Base
Clinical Anatomy
Cardiovascular System
Musculoskeletal System
Nervous System
Respiratory System
Special Zones
Pharmacology
Anaesthetic Agents/Sedatives
Analgesics
Anti-infectives
Basic Principles
Cardiovascular
Endocrine/Reproductive
Gastrointestinal
Haematological
Intravenous Fluids
Local Anaesthetics
Neurological/Psychiatric
Neuromuscular Transmission
Respiratory
Other
Physics and Measurement
Applied Physics and Chemistry
Clinical Measurement
Electricity
Statistics
Clinical Anaesthesia
General Topics
Cardiothoracic
ENT/Maxillofacial
Neuroanaesthesia
Obstetrics
Ophthalmic
Orthopaedics
Paediatrics
Pain
Regional
Urology
Vascular
Critical Care
General Topics
Cardiovascular
Gastrointestinal
Neurological
Organisational
Respiratory
Resuscitation
Trauma
Equipment
Airway
Breathing Systems
Gas Supply
Other
Medicine
Cardiology
Dermatology/Musculoskeletal/Rheumatology
Endocrinology
Gastroenterology
General
Haematology/Immunology
Microbiology and Infectious Diseases
Neurology/Psychiatry
Poisoning
Renal
Respiratory
Organisational
Radiology
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Inside Back Cover

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Anaesthesia, Intensive Care and Perioperative Medicine An Encyclopaedia of Principles and Practice Sixth Edition

A-Z

To

Gill, Emma and Abigail to

Alison, Jonathan, Sophie and Alexander and to

Pat, Ethan and Molly

Anaesthesia, Intensive Care and Perioperative Medicine An Encyclopaedia of Principles and Practice Sixth Edition

A-Z Steve M Yentis BSc MBBS FRCA MD MA

Consultant Anaesthetist, Chelsea and Westminster Hospital; Honorary Reader, Imperial College London, UK

Nicholas P Hirsch MBBS FRCA FRCP FFICM Retired Consultant Anaesthetist, The National Hospital for Neurology and Neurosurgery; Honorary Senior Lecturer, The Institute of Neurology, London, UK

James K Ip BSc MBBS FRCA Clinical Fellow in Anaesthesia, Great Ormond Street Hospital, London, UK

Original contributions by Gary B Smith BM FRCA FRCP

EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO

© 2019, Elsevier Limited. All rights reserved. First edition 1993 Second edition 2000 Third edition 2004 Fourth edition 2009 Fifth edition 2013 Sixth edition 2018 The right of Steve Yentis, Nicholas Hirsch and James Ip to be identified as authors of this work has been asserted by them in accordance with the Copyright, Designs and Patents Act 1988. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notices Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

The publisher’s policy is to use paper manufactured from sustainable forests

ISBN: 978-0-7020-7165-2 Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1 Content Strategists: Jeremy Bowes and Laurence Hunter Content Development Specialist: Joshua Mearns Project Manager: Julie Taylor Design: Paula Catalano Illustration Manager: Teresa McBryan Marketing Manager: Deborah Watkins



Preface In the 25 years since the publication of the first edition of our textbook, we have been delighted to find that ‘the A–Z’ has been adopted by both trainees and established practitioners alike. Whilst our original idea was to produce a readily accessible source of information for those sitting the Royal College of Anaesthetists’ Fellowship examinations, it soon became obvious that the book appeals to a far wider readership. We hope that the A–Z will continue to be useful to all staff who help us care for patients on a daily basis, as well as to anaesthetists and intensivists of all grades. As with previous new editions, each entry has been reviewed and, where appropriate, revised, and new ones inserted. We have also developed further the structured ‘revision checklist’ of entries, introduced in the 5th edition, that we hope will be useful to those preparing for examinations. The difference between the list of entries in the first edition and those in the current one continues to increase, with a huge expansion of new entries and revision of existing ones. This change acknowledges the enormous breadth of information needed to satisfy the vast range of activities performed by our anaesthetic, intensive care, nursing and other colleagues, and also reflects the ever-changing field in which we work. With current consolidation of the role of anaesthetists as ‘perioperative physicians’, we have also

developed and/or introduced entries that are particularly relevant to this aspect of our work, and emphasise this in the altered title of the book. The publication of a textbook requires the support of a multitude of people. We are indebted to our colleagues, both junior and senior, who have gently criticised previous editions; their suggestions have been invaluable and have directly resulted in changes found in each new edition over the years. We are particularly grateful to Drs Helen Laycock and Harriet Wordsworth, Chelsea and Westminster Hospital/Imperial College, for advising on entries related to pain and pain management for this edition. We also thank the staff of Elsevier and their predecessors for their support during the life of this project. Finally, this is the second edition of the A–Z on which two of the original authors, SMY and NPH, have worked without the third, Gary Smith, though his contributions exist throughout the book in both the format and content of entries from previous editions. We are both delighted to continue to work with James Ip on this edition, having successfully done so on the previous one. SMY NPH JKI

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Explanatory notes Arrangement of text Entries are arranged alphabetically, with some related subjects grouped together to make coverage of one subject easier. For example, entries relating to tracheal intubation may be found under I as in Intubation, awake; Intubation, blind nasal, etc.

Cross-referencing Bold type indicates a cross-reference. An abbreviation highlighted in bold type refers to an entry in its fully spelled form. For example, ‘ALI may occur …’ refers to the entry Acute lung injury. Further instructions appear in italics.

References Reference to a suitable article is provided at the foot of the entry where appropriate.

Proper names Where possible, a short biographical note is provided at the foot of the entry when a person is mentioned. Dates of birth and death are given, or the date of description if these dates are unknown. No dates are given for contemporary names. Where more than one eponymous entry occurs, e.g., Haldane apparatus and Haldane effect, details are given under the first entry. The term ‘anaesthetist’ is used in the English sense, i.e., a medical practitioner who practises anaesthesia; the terms ‘anesthesiologist’ and ‘anaesthesiologist’ are not used.

Drugs Individual drugs have entries where they have especial relevance to, or may by given by, the anaesthetist or intensivist. Where many different drugs exist within the same group, for example, β-adrenergic receptor antagonists, those which may be given intravenously have their own entry, whilst the others are described under the group description. The reader is referred back to entries describing drug groups and classes where appropriate.

Recommended International Nonproprietary Names (rINNs) and chemical names

national drug nomenclature with rINNs. For most drugs, rINNs are identical to the British Approved Name (BAN). The Medicines Control Agency (UK) has proposed a two-stage process for the introduction of rINNs. For substances where the change is substantial, both names will appear on manufacturers’ labels and leaflets for a number of years, with the rINN preceding the BAN on the drug label. For drugs where the change presents little hazard, the change will be immediate. For some drugs which do not appear in either of the above two categories, the British (or USP) name may still be used. There are over 200 affected drugs, many of them no longer available. Affected drugs that are mentioned in this book (though not all of them have their own entries) are listed below—though please note that, in common with the British Pharmacopoeia, the terms ‘adrenaline’ and ‘noradrenaline’ will be used throughout the text in preference to ‘epinephrine’ and ‘norepinephrine’, respectively, because of their status as natural hormones. Thus (except for adrenaline and noradrenaline), the format for affected drugs is rINN (BAN), e.g., Tetracaine hydrochloride (Amethocaine). Non-BAN, non-rINN names are also provided for certain other drugs (for example, Isoproterenol, see Isoprenaline) to help direct non-UK readers or those unfamiliar with UK terminology. Similarly, the International Union of Pure and Applied Chemistry (IUPAC) nomenclature of inorganic chemistry is used for consistency, even though some of the spelling (outside of drug names) is not widely used in UK English, e.g., sulfur/sulfate instead of sulphur/sulphate.

Examination revision checklist At the front of the book is a checklist based on entries of particular relevance to examination candidates, which have been classified and listed alphabetically in order to support systematic study of examination topics according to the subject area.

continued over page

Following work undertaken by the World Health Organization, European law requires the replacement of existing

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Explanatory notes

BAN

rINN

Adrenaline

Epinephrine

Amethocaine

Tetracaine

Amoxycillin

Amoxicillin

Amphetamine

Amfetamine

Amylobarbitone

Amobarbital

Beclomethasone

Beclometasone

Benzhexol

Trihexyphenidyl

Benztropine

Benzatropine

Busulphan

Busulfan

Cephazolin

Cefazolin

Cephradine

Cefradine

Cephramandole

Ceframandole

Chlormethiazole

Clomethiazole

Chlorpheniramine

Chlorphenamine

Corticotrophin

Corticotropin

Cyclosporin

Ciclosporin

Dicyclomine

Dicycloverine

Dothiepin

Dosulepin

Ethacrynic acid

Etacrynic acid

Ethamsylate

Etamsylate

Frusemide

Furosemide

Indomethacin

Indometacin

Lignocaine

Lidocaine

Methohexitone

Methohexital

Methylene blue

Methylthioninium chloride

Noradrenaline

Norepinephrine

Oxpentifylline

Pentoxifylline

Phenobarbitone

Phenobarbital

Sodium cromoglycate

Sodium cromoglicate

Sulphadiazine

Sulfadiazine

Sulphasalazine

Sulfasalazine

Tetracosactrin

Tetracosactide

Thiopentone

Thiopental

Tribavarin

Ribavarin

Trimeprazine

Alimemazine



Abbreviations ACE inhibitors angiotensin converting enzyme inhibitors ACTH adrenocorticotrophic hormone ADP adenosine diphosphate AF atrial fibrillation AIDS acquired immune deficiency syndrome ALI acute lung injury APACHE acute physiology and chronic health evaluation ASA American Society of Anesthesiologists ASD atrial septal defect ATP adenosine triphosphate AV atrioventricular bd twice daily BP blood pressure cAMP cyclic adenosine monophosphate CMRO2 cerebral metabolic rate for oxygen CNS central nervous system CO2 carbon dioxide COPD chronic obstructive pulmonary disease CPAP continuous positive airway pressure CPR cardiopulmonary resuscitation CSE combined spinal–extradural CSF cerebrospinal fluid CT computed tomography CVP central venous pressure CVS cardiovascular system CXR chest x-ray DIC disseminated intravascular coagulation DNA deoxyribonucleic acid 2,3-DPG 2,3-diphosphoglycerate DVT deep vein thrombosis ECF extracellular fluid ECG electrocardiography EDTA ethylenediaminetetraacetate EEG electroencephalography EMG electromyography ENT ear, nose and throat FEV1 forced expiratory volume in 1 s FIO2 fractional inspired concentration of oxygen FRC functional residual capacity FVC forced vital capacity G gauge GABA γ-aminobutyric acid GFR glomerular filtration rate GIT gastrointestinal tract GTN glyceryl trinitrate HCO3− bicarbonate HDU high dependency unit HIV human immunodeficiency virus HLA human leucocyte antigen 5-HT 5-hydroxytryptamine ICP intracranial pressure ICU intensive care unit IgA, IgG, etc. immunoglobulin A, G, etc. im intramuscular

IMV intermittent mandatory ventilation IPPV intermittent positive pressure ventilation iv intravenous IVRA intravenous regional anaesthesia JVP jugular venous pressure LM laryngeal mask MAC minimal alveolar concentration MAP mean arterial pressure MH malignant hyperthermia MI myocardial infarction MODS multiple organ dysfunction syndrome MRI magnetic resonance imaging mw molecular weight NAD(P) nicotinamide adenine dinucleotide (phosphate) NHS National Health Service NICE National Institute for Health and Care Excellence NMDA N-methyl-D-aspartate N2O nitrous oxide NSAID non-steroidal anti-inflammatory drug O2 oxygen od once daily ODA/P operating department assistant/practitioner PCO2 partial pressure of carbon dioxide PE pulmonary embolus PEEP positive end-expiratory pressure PO2 partial pressure of oxygen PONV postoperative nausea and vomiting pr per rectum qds four times daily RNA ribonucleic acid RS respiratory system SAD supraglottic airway device sc subcutaneous SIRS systemic inflammatory response syndrome SLE systemic lupus erythematosus SVP saturated vapour pressure SVR systemic vascular resistance SVT supraventricular tachycardia TB tuberculosis TBI traumatic brain injury tds three times daily TENS transcutaneous electrical nerve stimulation THRIVE transnasal humidified rapid-insufflation ventilatory exchange TIVA total intravenous anaesthesia TPN total parenteral nutrition TURP transurethral resection of prostate UK United Kingdom US(A) United States (of America) VF ventricular fibrillation V̇/Q̇ ventilation/perfusion VSD ventricular septal defect VT ventricular tachycardia

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Examination revision checklist This checklist has been compiled from entries of particular relevance to examination candidates, classified and listed alphabetically in order to support systematic study of examination topics. This list is not exhaustive, and, for clarity, entries that summarise a topic and incorporate multiple cross-references (e.g. Opioid analgesic drugs) have been included in preference to listing every relevant entry, e.g. Alfentanil, Fentanyl, Remifentanil, etc. The latter should still be referred to where appropriate, to gain relevant detail. Checklist index: Physiology Clinical Anatomy Pharmacology Physics and Measurement Statistics Clinical Anaesthesia Critical Care Equipment Medicine Organisational Radiology PHYSIOLOGY CARDIOVASCULAR

► Afterload. ► Albumin. ► Anaerobic threshold. ► Arterial blood pressure. ► Atrial natriuretic peptide. ► Autoregulation. ► Baroreceptor reflex. ► Baroreceptors. ► Blood. ► Blood flow. ► Blood groups. ► Blood volume. ► Capacitance vessels. ► Capillary refill time. ► Cardiac cycle. ► Cardiac output. ► Cardioinhibitory centre. ► Central venous pressure (CVP). ► Coagulation. ► Coronary blood flow. ► 2,3-Diphosphoglycerate (2,3-DPG). ► Ejection fraction. ► Exercise. ► Fetal haemoglobin. ► Fibrinolysis. ► Fluids, body. ► Haemoglobin (Hb). ► Haemorrhage. ► Heart rate. ► Hüfner constant. ► Hypotension.

p. xi p. xiii p. xiv p. xv p. xvi p. xvi p. xviii p. xix p. xx p. xxii p. xxii

► Insensible water loss. ► Left atrial pressure. ► Left ventricular end-diastolic pressure. ► Mixed venous blood. ► Myocardial contractility. ► Myocardial metabolism. ► Myoglobin. ► Oedema. ► Oncotic pressure ► Osmolality and osmolarity. ► Osmolar gap. ► Osmoreceptors. ► Osmosis. ► Osmotic pressure. ► Pacemaker cells. ► Perfusion pressure. ► Preload. ► Pulmonary artery pressure. ► Pulmonary circulation. ► Pulmonary vascular resistance. ► Pulse pressure. ► Right ventricular function. ► Sinus arrhythmia. ► Sinus bradycardia. ► Sinus rhythm. ► Sinus tachycardia. ► Starling forces. ► Starling’s law (Frank–Starling law). ► Stroke volume. ► Stroke work. ► Systemic vascular resistance. ► Valsalva manoeuvre. ► Vasomotor centre. ► Venous return. ► Venous waveform. ► Vitamin K. CELLULAR/MOLECULAR/METABOLISM

► Action potential. ► Active transport. ► Acute-phase response. ► Adenosine triphosphate and diphosphate. ► Adrenergic receptors. ► Basal metabolic rate. ► Calcium. ► Carbohydrates. ► Carbonic anhydrase. ► Catabolism. ► Catechol-O-methyl transferase (COMT). ► Complement. ► Cyclo-oxygenase (COX). ► Cytochrome oxidase system. ► Cytokines. ► Donnan effect (Gibbs–Donnan effect). ► Energy balance. ► Fats.

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Examination revision checklist

► G protein-coupled receptors. ► Glycolysis. ► Goldman constant-field equation. ► Histamine and histamine receptors. ► Homeostasis. ► 5-Hydroxytryptamine (5-HT, Serotonin). ► Immunoglobulins. ► Ketone bodies. ► Lactate. ► Magnesium. ► Membrane potential. ► Membranes. ► Metabolism. ► Methionine and methionine synthase. ► Monoamine oxidase (MAO). ► Muscle. ► Muscle contraction. ► Nernst equation. ► Nitrogen balance. ► Phosphate. ► Potassium. ► Prostaglandins. ► Second messenger. ► Sodium. ► Sodium/potassium pump. ► Tricarboxylic acid cycle. ► Vitamins. ENDOCRINE/REPRODUCTIVE

► Adrenal gland. ► Calcitonin. ► Corticosteroids. ► Glucagon. ► Growth hormone. ► Insulin. ► Pituitary gland. ► Placenta. ► Pregnancy. ► Thyroid gland. ► Uterus. ► Vasopressin.

GASTROINTESTINAL

► Ammonia. ► Amylase. ► Biliary tract. ► Gastric contents. ► Gastric emptying. ► Liver. ► Lower oesophageal sphincter. ► Nutrition. ► Swallowing. ► Urea. ► Vomiting.

NERVOUS SYSTEM

► Acetylcholine. ► Acetylcholine receptors. ► Acetylcholinesterase. ► γ-Aminobutyric acid (GABA) receptors. ► Autonomic nervous system.

► Blood–brain barrier. ► Catecholamines. ► Cerebral blood flow. ► Cerebral metabolism. ► Cerebral perfusion pressure. ► Cerebrospinal fluid (CSF). ► Chemoreceptor trigger zone. ► Chemoreceptors. ► Dermatomes. ► Dopamine receptors. ► End-plate potentials. ► Evoked potentials. ► Gag reflex. ► Gate control theory of pain. ► Glutamate. ► Intracranial pressure (ICP). ► Memory. ► Monro–Kellie doctrine. ► Motor pathways. ► Motor unit. ► Muscle spindles. ► Myelin. ► N-Methyl-D-aspartate (NMDA) receptors. ► Nerve conduction. ► Neuromuscular junction. ► Neurone. ► Neurotransmitters. ► Nociception. ► Pain pathways. ► Parasympathetic nervous system. ► Pupil. ► Referred pain. ► Reflex arc. ► Refractory period. ► Sensory pathways. ► Sleep. ► Sympathetic nervous system. ► Synaptic transmission. ► ‘Wind-up’. RENAL

► Clearance. ► Clearance, free water. ► Creatinine clearance. ► Filtration fraction. ► Glomerular filtration rate (GFR). ► Juxtaglomerular apparatus. ► Kidney. ► Nephron. ► Renal blood flow. ► Renin/angiotensin system. ► Urine.

RESPIRATORY AND ACID/BASE

► Acid–base balance. ► Acidosis, metabolic. ► Acidosis, respiratory. ► Airway pressure. ► Airway resistance. ► Alkalosis, metabolic. ► Alkalosis, respiratory. ► Alveolar air equation.

Examination revision checklist

► Alveolar–arterial oxygen difference. ► Alveolar gas transfer. ► Alveolar gases. ► Alveolar ventilation. ► Alveolus. ► Anion gap. ► Aortic bodies. ► Apnoea. ► Arteriovenous oxygen difference. ► Base. ► Base excess/deficit. ► Bicarbonate. ► Blood gas analyser. ► Blood gas interpretation. ► Bohr effect. ► Bohr equation. ► Breathing, control of. ► Breathing, work of. ► Buffers. ► Carbon dioxide (CO ). ► Carbon dioxide dissociation curve. ► Carbon dioxide, end-tidal. ► Carbon dioxide transport. ► Carbon monoxide (CO). ► Carotid body. ► Chloride shift (Hamburger shift). ► Closing capacity. ► Compliance. ► Cough. ► Cyanosis. ► Davenport diagram. ► Dead space. ► Diffusing capacity (Transfer factor). ► Elastance. ► Fink effect. ► F O . ► Haldane effect. ► Henderson–Hasselbalch equation. ► Hering–Breuer reflex (Inflation reflex). ► Hydrogen ions (H ). ► Hypoxia. ► Hypoxic pulmonary vasoconstriction. ► Intrapleural pressure. ► Laryngeal reflex. ► Lung. ► Lung volumes. ► Minute ventilation. ► Nitrogen washout. ► Oxygen cascade. ► Oxygen delivery. ► Oxygen extraction ratio. ► Oxygen flux. ► Oxygen saturation. ► Oxygen transport. ► Oxyhaemoglobin dissociation curve. ► Peak expiratory flow rate. ► pH. ► Pulmonary irritant receptors. ► Pulmonary stretch receptors. ► Respiratory muscles. ► Respiratory quotient. ► Respiratory symbols. ► Shunt. ► Shunt equation. 2

I

2

+

► Siggaard-Andersen nomogram. ► Standard bicarbonate. ► Strong ion difference. ► Surfactant. ► Venous admixture. ► Ventilation/perfusion mismatch. CLINICAL ANATOMY CARDIOVASCULAR SYSTEM

► Brachial artery. ► Carotid arteries. ► Coronary circulation. ► Femoral artery. ► Fetal circulation. ► Heart. ► Heart, conducting system. ► Jugular veins. ► Mediastinum. ► Pericardium. ► Venous drainage of arm. ► Venous drainage of leg. ► Vertebral arteries.

MUSCULOSKELETAL SYSTEM

► Cervical spine. ► Ribs. ► Skull. ► Temporomandibular joint. ► Vertebrae.

NERVOUS SYSTEM

► Brachial plexus. ► Brain. ► Cerebral circulation. ► Cranial nerves. ► Hypothalamus. ► Lumbar plexus. ► Meninges. ► Myotomes. ► Sacral plexus. ► Spinal cord. ► Spinal nerves.

RESPIRATORY SYSTEM

► Airway. ► Diaphragm. ► Intercostal spaces. ► Laryngeal nerves. ► Larynx. ► Nose. ► Pharynx. ► Phrenic nerves. ► Pleura. ► Tongue. ► Tracheobronchial tree.

SPECIAL ZONES

► Antecubital fossa. ► Epidural space.

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Examination revision checklist

► Femoral triangle. ► Neck, cross-sectional anatomy. ► Orbital cavity. ► Popliteal fossa. ► Sacral canal. ► Thoracic inlet. PHARMACOLOGY ANAESTHETIC AGENTS/SEDATIVES

► Anaesthesia, mechanism of. ► Concentration effect. ► Fluoride ions. ► Inhalational anaesthetic agents. ► Intravenous anaesthetic agents. ► Meyer–Overton rule. ► Minimal alveolar concentration (MAC). ► Second gas effect.

ANALGESICS

► Analgesic drugs. ► Capsaicin. ► Ethyl chloride. ► Non-steroidal anti-inflammatory drugs. ► Opioid analgesic drugs. ► Opioid receptor antagonists. ► Opioid receptors.

ANTI-INFECTIVES

► Antibacterial drugs. ► Antifungal drugs. ► Antimalarial drugs. ► Antituberculous drugs. ► Antiviral drugs.

BASIC PRINCIPLES

► Adverse drug reactions. ► Affinity. ► Agonist. ► Antagonist. ► Bioavailability. ► Dose–response curves. ► Drug development. ► Drug interactions. ► Efficacy. ► Enzyme induction/inhibition. ► Exponential process. ► Extraction ratio. ► First-pass metabolism. ► Half-life (t ). ► Ionisation of drugs. ► Isomerism. ► Michaelis–Menten kinetics. ► Pharmacodynamics. ► Pharmacogenetics. ► Pharmacokinetics. ► pK. ► Potency. ► Prodrug. ► Protein-binding. 1/2

► Receptor theory. ► Tachyphylaxis. ► Target-controlled infusion (TCI). ► Therapeutic ratio/index. ► Time constant (τ). ► Volume of distribution (V ). ► Washout curves. d

CARDIOVASCULAR

► α-Adrenergic receptor agonists. ► α-Adrenergic receptor antagonists. ► β-Adrenergic receptor agonists. ► β-Adrenergic receptor antagonists. ► Antiarrhythmic drugs. ► Anticholinergic drugs. ► Antihypertensive drugs. ► Calcium channel blocking drugs. ► Calcium sensitisers. ► Cardiac glycosides. ► Diuretics. ► Inotropic drugs. ► Phosphodiesterase inhibitors. ► Statins. ► Sympathomimetic drugs. ► Vasodilator drugs. ► Vasopressor drugs.

ENDOCRINE/REPRODUCTIVE

► Carboprost. ► Contraceptives, oral. ► Corticosteroids. ► Desmopressin (DDAVP). ► Ergometrine maleate. ► Hormone replacement therapy. ► Hypoglycaemic drugs. ► Misoprostol. ► Oxytocin. ► Tocolytic drugs.

GASTROINTESTINAL

► Antacids. ► Antispasmodic drugs. ► Emetic drugs. ► H receptor antagonists. ► Laxatives. ► Octreotide. ► Prokinetic drugs. ► Proton pump inhibitors. 2

HAEMATOLOGICAL

► Anticoagulant drugs. ► Antifibrinolytic drugs. ► Antiplatelet drugs. ► Cytotoxic drugs. ► Factor VIIa, recombinant ► Fibrinolytic drugs. ► Granulocyte colony-stimulating factor. ► Immunoglobulins, intravenous (IVIG). ► Immunosuppressive drugs. ► Protamine sulfate.

Examination revision checklist

► Prothrombin complex concentrate. ► Thrombin inhibitors.

► Magnesium sulfate. ► Propylene glycol.

INTRAVENOUS FLUIDS

► Colloid. ► Colloid/crystalloid controversy. ► Crystalloid. ► Electrolyte. ► Intravenous fluid administration. ► Intravenous fluids. ► Tonicity.

PHYSICS AND MEASUREMENT APPLIED PHYSICS AND CHEMISTRY

LOCAL ANAESTHETICS

► EMLA cream. ► Local anaesthetic agents. ► Minimal blocking concentration (C ). ► Minimal local anaesthetic concentration/dose/ m

volume.

NEUROLOGICAL/PSYCHIATRIC

► Anticonvulsant drugs. ► Antidepressant drugs. ► Antiemetic drugs. ► Antihistamine drugs. ► Antiparkinsonian drugs. ► Antipsychotic drugs. ► Central anticholinergic syndrome. ► Dystonic reaction. ► Flumazenil. ► Nicotine.

NEUROMUSCULAR TRANSMISSION

► Acetylcholinesterase inhibitors. ► Cholinesterase, plasma. ► Denervation hypersensitivity. ► Depolarising neuromuscular blockade. ► Dibucaine number. ► Dual block (Phase II block). ► Hofmann degradation. ► Neuromuscular blocking drugs. ► Non-depolarising neuromuscular blockade. ► Priming principle. ► Recurarisation. ► Sugammadex sodium.

RESPIRATORY

► Bronchodilator drugs. ► Doxapram hydrochloride. ► Mucolytic drugs.

OTHER

► N-Acetylcysteine. ► Alcohols. ► Chemical weapons. ► Dantrolene sodium. ► Herbal medicines. ► Hyaluronidase. ► Lipid emulsion

► Activation energy. ► Adiabatic change. ► Atmosphere. ► Avogadro’s hypothesis. ► Bar. ► Beer–Lambert law. ► Bernoulli effect. ► Boiling point. ► Boyle’s law. ► Calorie. ► Charge, electric. ► Charles’ law. ► Coanda effect. ► Colligative properties of solutions. ► Critical pressure. ► Critical temperature. ► Critical velocity. ► Dalton’s law. ► Density. ► Dew point. ► Diffusion. ► Doppler effect. ► Energy. ► Fick’s law of diffusion. ► Flammability. ► Flow. ► Fluid. ► Force. ► Gas. ► Gas flow. ► Graham’s law. ► Hagen–Poiseuille equation. ► Harmonics. ► Heat. ► Heat capacity. ► Henry’s law. ► Humidity. ► Ideal gas law. ► Isotherms. ► Laplace’s law. ► Laser surgery. ► Latent heat. ► Molarity. ► Normal solution. ► Ohm’s law. ► Partial pressure. ► Partition coefficient. ► Pascal. ► Power (in Physics). ► Poynting effect. ► Pressure. ► Pseudocritical temperature. ► Radiation. ► Radioisotopes. ► Raoult’s law. ► Resonance. ► Reynolds’ number.

xv

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Examination revision checklist

► Saturated vapour pressure (SVP). ► Solubility. ► Solubility coefficients. ► Specific gravity (Relative density). ► Starling resistor. ► Stoichiometric mixture. ► STP/STPD. ► Surface tension. ► Temperature measurement. ► Tension. ► Units, SI. ► Vapour. ► Venturi principle. ► Viscosity (η). ► Work. CLINICAL MEASUREMENT

► Amplifiers. ► Arterial blood pressure measurement. ► Arterial cannulation. ► Arterial waveform. ► Becquerel. ► Bispectral index monitor. ► Body mass index (BMI). ► Calibration. ► Capnography. ► Carbon dioxide measurement. ► Cardiac output measurement. ► Cerebral function monitor. ► cgs system of units. ► Damping. ► Dilution techniques. ► End-tidal gas sampling. ► Fade. ► Fick principle. ► Flame ionisation detector. ► Flowmeters. ► Flow–volume loops. ► Gain, electrical. ► Gas analysis. ► Gas chromatography. ► Haldane apparatus. ► Hygrometer. ► Hysteresis. ► Impedance plethysmography. ► Isosbestic point. ► Korotkoff sounds. ► LiMON. ► Mass spectrometer. ► Monitoring. ► Neuromuscular blockade monitoring. ► Oscillotonometer. ► Oximetry. ► Oxygen measurement. ► Peak flowmeters. ► pH measurement. ► Phase shift. ► Plethysmography. ► Pneumotachograph. ► Pressure measurement. ► Pulse oximeter. ► Respirometer. ► Rotameter.

► Spectroscopy. ► Spirometer. ► Thromboelastography (TEG). ► Transducers. ELECTRICITY

► Antistatic precautions. ► Capacitance. ► Conductance. ► Coulomb. ► Current. ► Current density. ► Defibrillation. ► Electrical symbols. ► Electrocution and electrical burns. ► Impedance, electrical. ► Inductance. ► Resistance. ► Volt.

STATISTICS Absolute risk reduction. Confidence intervals. Data. Degrees of freedom. Errors, statistical. Likelihood ratio. Mean. Median. Meta-analysis (Systematic review). Mode. Null hypothesis. Number needed to treat (NNT). Odds ratio. Percentile. Populations. Power (in Statistics). Predictive value. Probability (P). Randomisation. Receiver operating characteristic curves. Relative risk reduction. Samples, statistical. Sensitivity. Specificity. Standard deviation. Standard error of the mean. Statistical frequency distributions. Statistical significance. Statistical tests. Variance.

► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ► ►

CLINICAL ANAESTHESIA GENERAL TOPICS

► Altitude, high. ► Altitude, low. ► Anaesthesia, depth of. ► Anaesthesia, stages of. ► Anaesthetic morbidity and mortality. ► Anaesthetists’ non-technical skills.

Examination revision checklist

► Anaphylaxis. ► ASA physical status. ► Aspiration of gastric contents. ► Awareness. ► Bariatric surgery. ► Blood loss, perioperative. ► Bronchospasm. ► Carbon dioxide narcosis. ► Cardiac risk indices. ► Cardiopulmonary exercise testing. ► Cell salvage. ► Central venous cannulation. ► Confusion, postoperative. ► Consent for anaesthesia. ► Cricoid pressure (Sellick’s manoeuvre). ► Cricothyroidotomy. ► Day-case surgery. ► Elderly, anaesthesia for. ► Electroconvulsive therapy. ► Emergence phenomena. ► Emergency surgery. ► Environmental impact of anaesthesia. ► Environmental safety of anaesthetists. ► Explosions and fires. ► Extubation, tracheal. ► Eye care. ► Fluid balance. ► Gas embolism. ► Heat loss, during anaesthesia. ► Hypotensive anaesthesia. ► Hypothermia. ► Hypoventilation. ► Hypovolaemia. ► Induction of anaesthesia. ► Induction, rapid sequence. ► Intubation, awake. ► Intubation, blind nasal. ► Intubation, complications of. ► Intubation, difficult. ► Intubation, failed. ► Intubation, fibreoptic. ► Intubation, oesophageal. ► Intubation, tracheal. ► Investigations, preoperative. ► Jehovah’s Witnesses. ► Laparoscopy. ► Laryngoscopy. ► Laryngospasm. ► Liver transplantation. ► Malignant hyperthermia. ► Medicolegal aspects of anaesthesia. ► Nerve injury during anaesthesia. ► Obesity. ► Plastic surgery. ► Positioning of the patient. ► Postoperative analgesia. ► Postoperative cognitive dysfunction. ► Postoperative nausea and vomiting. ► Premedication. ► Preoperative assessment. ► Preoperative optimisation. ► Preoxygenation. ► Radiology, anaesthesia for. ► Recovery, enhanced.

► Recovery from anaesthesia. ► Regurgitation. ► Sedation. ► Seldinger technique. ► Shivering, postoperative. ► Smoking. ► Sore throat, postoperative. ► Stress response to surgery. ► Substance abuse. ► Teeth. ► Temperature regulation. ► Total intravenous anaesthesia (TIVA). ► Tourniquets. ► Transnasal humidified rapid-insufflation ventilator exchange (THRIVE).

CARDIOTHORACIC

► Cardiac surgery. ► Cardiopulmonary bypass. ► Heart transplantation. ► Lung transplantation. ► One-lung anaesthesia. ► Thoracic surgery.

ENT/MAXILLOFACIAL

► Airway obstruction. ► Bronchoscopy. ► Dental surgery. ► Ear, nose and throat surgery. ► Epistaxis. ► Facial trauma. ► Foreign body, inhaled. ► Injector techniques. ► Insufflation techniques. ► Ludwig’s angina. ► Maxillofacial surgery. ► Stridor. ► Tonsil, bleeding. ► Trismus.

NEUROANAESTHESIA

► Head injury. ► Neurosurgery. ► Spinal surgery.

OBSTETRICS

► Amniotic fluid embolism. ► Antepartum haemorrhage. ► Aortocaval compression. ► Caesarean section. ► Confidential Enquiries into Maternal Deaths. ► Fetal monitoring. ► Fetus, effects of anaesthetic drugs on. ► HELLP syndrome. ► Obstetric analgesia and anaesthesia. ► Placenta praevia. ► Placental abruption. ► Postpartum haemorrhage. ► Pre-eclampsia.

xvii

xviii

Examination revision checklist OPHTHALMIC

► Eye, penetrating injury. ► Intraocular pressure. ► Oculocardiac reflex. ► Ophthalmic surgery.

ORTHOPAEDICS

► Bone cement implantation syndrome. ► Bone marrow harvest. ► Fat embolism. ► Fractured neck of femur. ► Kyphoscoliosis. ► Orthopaedic surgery.

PAEDIATRICS

► Apgar scoring system. ► Choanal atresia. ► Croup. ► Diaphragmatic herniae. ► Epiglottitis. ► Facial deformities, congenital. ► Gastroschisis and exomphalos. ► Necrotising enterocolitis. ► Neonate. ► Paediatric anaesthesia. ► Pyloric stenosis. ► Tracheo-oesophageal fistula. ► Transposition of the great arteries.

PAIN

► Acupuncture. ► Central pain. ► Coeliac plexus block. ► Complex regional pain syndrome. ► Gasserian ganglion block. ► Pain. ► Pain evaluation. ► Pain management. ► Pain, neuropathic. ► Patient-controlled analgesia. ► Phantom limb. ► Spinal cord stimulation. ► Stellate ganglion block. ► Sympathetic nerve blocks. ► Transcutaneous electrical nerve stimulation. ► Trigger points.

REGIONAL

► Adductor canal block. ► Ankle, nerve blocks. ► Blood patch, epidural. ► Brachial plexus block. ► Caudal analgesia. ► Cervical plexus block. ► Combined spinal–epidural anaesthesia. ► Dural tap. ► Epidural anaesthesia. ► Fascia iliaca compartment block. ► Femoral nerve block. ► Inguinal hernia field block.

► Intercostal nerve block. ► Interpleural analgesia. ► Intravenous regional anaesthesia. ► Knee, nerve blocks. ► Paravertebral block. ► Pecs block. ► Penile block. ► Peribulbar block. ► Post-dural puncture headache. ► Psoas compartment block. ► Rectus sheath block. ► Regional anaesthesia. ► Retrobulbar block. ► Sciatic nerve block. ► Serratus anterior plane block. ► Spinal anaesthesia. ► Sub-Tenon’s block. ► Transversus abdominis plane block. ► Wrist, nerve blocks. UROLOGY

► Extracorporeal shock wave lithotripsy. ► Renal transplantation. ► Transurethral resection of the prostate. ► TURP syndrome. ► Urinary retention.

VASCULAR

► Aortic aneurysm, abdominal. ► Aortic aneurysm, thoracic. ► Aortic dissection. ► Carotid endarterectomy.

CRITICAL CARE GENERAL TOPICS

► Critical care. ► Imaging in intensive care. ► Lactic acidosis. ► Multiple organ dysfunction syndrome (MODS). ► Organ donation. ► Paediatric intensive care. ► Targeted temperature management. ► Transportation of critically ill patients. ► Withdrawal of treatment in ICU.

CARDIOVASCULAR

► Cardiogenic shock. ► Heparin-induced thrombocytopenia. ► Pulmonary artery catheterisation. ► Pulmonary capillary wedge pressure. ► Septic shock. ► Shock.

GASTROINTESTINAL

► Abdominal compartment syndrome. ► Glycaemic control in the ICU. ► Nutrition, enteral. ► Nutrition, total parenteral (TPN). ► Pancreatitis.

Examination revision checklist

► Refeeding syndrome. ► Selective decontamination of the digestive tract. ► Stress ulcers. NEUROLOGICAL

► ► ► ► ► ► ► ► ► ► ► ► ► ►

Brainstem death. Cerebral hypoxic ischaemic injury. Cerebral protection/resuscitation. Coma. Confusion in the intensive care unit. Coning. Critical illness polyneuropathy. Guillain–Barré syndrome. Intracranial pressure monitoring. Sedation scoring systems. Spinal cord injury. Status epilepticus. Subarachnoid haemorrhage. Vegetative state.

ORGANISATIONAL

► APACHE scoring system. ► Care bundles. ► Intensive care follow-up. ► Intensive care unit. ► Mortality/survival prediction on intensive care unit.

RESPIRATORY

► Acute lung injury. ► Alveolar recruitment manoeuvre. ► Assisted ventilation. ► Barotrauma. ► Continuous positive airway pressure. ► Dynamic hyperinflation. ► Extracorporeal membrane oxygenation. ► High-frequency ventilation. ► Hypercapnia. ► Hypoxaemia. ► Inspiratory: expiratory ratio (I:E ratio). ► Intermittent positive pressure ventilation. ► Lung protection strategies. ► Non-invasive positive pressure ventilation. ► Pleural effusion. ► Pneumothorax. ► Respiratory failure. ► Respiratory muscle fatigue. ► Tracheostomy. ► Transfusion-related acute lung injury (TRALI) ► Ventilator-associated lung injury. ► Ventilator-associated pneumonia. ► Ventilators. ► Weaning from ventilators.

RESUSCITATION

► Advanced life support, adult. ► Basic life support, adult. ► Cardiac arrest. ► Cardiopulmonary resuscitation (CPR). ► Cardiopulmonary resuscitation, neonatal. ► Cardiopulmonary resuscitation, paediatric.

► Choking. ► Intraosseous fluid administration. ► Near-drowning. TRAUMA

► Abdominal trauma. ► Burns. ► Chest trauma. ► Compartment syndromes. ► ‘Golden hour’. ► Pelvic trauma. ► Peritoneal lavage. ► Rib fractures. ► Trauma. ► Traumatic brain injury.

EQUIPMENT AIRWAY

► Airway exchange catheter. ► Airways. ► Cuffs, of tracheal tubes. ► Endobronchial tubes. ► Facemasks. ► Fibreoptic instruments. ► Intubation aids. ► Laryngeal mask (LM). ► Laryngoscope. ► Laryngoscope blades. ► Minitracheotomy. ► Oesophageal obturators and airways. ► Supraglottic airway device (SAD). ► Tracheal tubes.

BREATHING SYSTEMS

► Adjustable pressure-limiting valves. ► Anaesthetic breathing systems. ► Carbon dioxide absorption, in anaesthetic breathing systems. ► Circle systems. ► Coaxial anaesthetic breathing systems. ► Demand valves. ► Filters, breathing system. ► Heat–moisture exchanger (HME). ► Humidification. ► Nebulisers. ► Non-rebreathing valves. ► Reservoir bag. ► Scavenging. ► Self-inflating bags. ► Soda lime. ► Triservice apparatus.

GAS SUPPLY

► Air. ► Bodok seal. ► Cylinders. ► Filling ratio. ► Oxygen. ► Oxygen concentrator.

xix

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Examination revision checklist

► Oxygen failure warning device. ► Pin index system. ► Piped gas supply. ► Pressure regulators. ► Vacuum insulated evaporator (VIE). OTHER

► Anaesthetic machines. ► Blood filters. ► Checking of anaesthetic equipment. ► Contamination of anaesthetic equipment. ► Diathermy. ► Gauge. ► Luer connectors. ► Needles. ► Suction equipment. ► Syringes. ► Vaporisers.

MEDICINE CARDIOLOGY

► Acute coronary syndromes. ► Aortic regurgitation. ► Aortic stenosis. ► Arrhythmias. ► Bundle branch block. ► Cardiac catheterisation. ► Cardiac enzymes. ► Cardiac failure. ► Cardiac pacing. ► Cardiac tamponade. ► Cardiomyopathy. ► Cardioversion, electrical. ► Congenital heart disease. ► Cor pulmonale. ► Defibrillators, implantable cardioverter. ► Echocardiography. ► Electrocardiography (ECG). ► Endocarditis, infective. ► Heart block. ► Hypertension. ► Ischaemic heart disease. ► Mitral regurgitation. ► Mitral stenosis. ► Myocardial ischaemia. ► Myocarditis. ► Percutaneous coronary intervention (PCI). ► Pericarditis. ► Prolonged Q–T syndromes. ► Pulmonary hypertension. ► Pulmonary oedema. ► Pulmonary valve lesions. ► Stokes–Adams attack. ► Torsades de pointes. ► Transoesophageal echocardiography. ► Tricuspid valve lesions.

DERMATOLOGY/MUSCULOSKELETAL/RHEUMATOLOGY

► Ankylosing spondylitis. ► Connective tissue diseases. ► Marfan’s syndrome.

► Muscular dystrophies. ► Myotonic syndromes. ► Rheumatoid arthritis. ► Sarcoidosis. ► Stevens–Johnson syndrome. ► Systemic lupus erythematosus. ► Vasculitides. ENDOCRINOLOGY

► Acromegaly. ► Adrenocortical insufficiency. ► Cushing’s syndrome. ► Diabetes mellitus. ► Diabetic coma. ► Hyperaldosteronism. ► Hyperthyroidism ► Hypopituitarism. ► Hypothyroidism. ► Phaeochromocytoma. ► Sick euthyroid syndrome. ► Thyroid crisis.

GASTROENTEROLOGY

► Ascites. ► Carcinoid syndrome. ► Diarrhoea. ► Gastrointestinal haemorrhage. ► Gastro-oesophageal reflux. ► Hepatic failure. ► Hepatitis. ► Hiatus hernia. ► Liver function tests.

GENERAL

► Alcoholism. ► Anaemia. ► Decompression sickness. ► Deep vein thrombosis (DVT). ► Dehydration. ► Down’s syndrome. ► Hypercalcaemia. ► Hyperglycaemia. ► Hyperkalaemia. ► Hypernatraemia. ► Hyperthermia. ► Hypocalcaemia. ► Hypoglycaemia. ► Hypokalaemia. ► Hypomagnesaemia. ► Hyponatraemia. ► Hypophosphataemia. ► Inborn errors of metabolism. ► Malignancy. ► Malnutrition. ► Porphyria. ► Pyrexia. ► Syndrome of inappropriate antidiuretic hormone secretion (SIADH). ► Systemic inflammatory response syndrome. ► Vasovagal syncope.

Examination revision checklist HAEMATOLOGY/IMMUNOLOGY

► Autoimmune disease. ► Blood compatibility testing. ► Blood products. ► Blood storage. ► Blood transfusion. ► Bone marrow transplantation. ► Coagulation disorders. ► Coagulation studies. ► Disseminated intravascular coagulation. ► Glucose-6-phosphate dehydrogenase deficiency. ► Haemoglobinopathies. ► Haemolysis. ► Haemophilia. ► Immunodeficiency. ► Latex allergy. ► Methaemoglobinaemia. ► Rhesus blood groups. ► Thrombocytopenia. ► Thrombotic thrombocytopenic purpura. ► Tumour lysis syndrome. ► von Willebrand’s disease.

MICROBIOLOGY AND INFECTIOUS DISEASES

► Bacteria. ► Blood cultures. ► Catheter-related sepsis. ► Cellulitis. ► Clostridial infections. ► Human immunodeficiency viral (HIV) infection. ► Infection control. ► Influenza. ► Meningococcal disease. ► Necrotising fasciitis. ► Nosocomial infection. ► Notifiable diseases. ► Pseudomonas infections. ► Sepsis. ► Staphylococcal infections. ► Streptococcal infections. ► Tropical diseases. ► Tuberculosis (TB).

NEUROLOGY/PSYCHIATRY

► Amnesia. ► Anorexia nervosa. ► Anterior spinal artery syndrome. ► Autonomic hyperreflexia. ► Autonomic neuropathy. ► Cauda equina syndrome. ► Central pontine myelinolysis. ► Cerebral abscess. ► Cerebral ischaemia. ► Cerebral oedema. ► Cholinergic crisis. ► Coma scales. ► Convulsions. ► Demyelinating diseases. ► Electroencephalography (EEG). ► Electromyography (EMG). ► Encephalopathy.

► Epilepsy. ► Extradural (epidural) haemorrhage. ► Horner’s syndrome. ► Hydrocephalus. ► Lumbar puncture. ► Meningitis. ► Migraine. ► Motor neurone disease. ► Motor neurone, lower. ► Motor neurone, upper. ► Myasthenia gravis. ► Neurofibromatosis. ► Neuroleptic malignant syndrome. ► Paralysis, acute. ► Parkinson’s disease. ► Peripheral neuropathy. ► Post-traumatic stress disorder. ► Stroke. ► Subdural haemorrhage. ► Trigeminal neuralgia. POISONING

► β-Adrenergic receptor antagonist poisoning. ► Alcohol poisoning. ► Barbiturate poisoning. ► Benzodiazepine poisoning. ► Carbon monoxide poisoning. ► Charcoal, activated. ► Chelating agents. ► Cocaine poisoning. ► Cyanide poisoning. ► Heavy metal poisoning. ► Iron poisoning. ► Opioid poisoning. ► Organophosphorus poisoning. ► Paracetamol poisoning. ► Paraquat poisoning. ► Poisoning and overdoses. ► Salicylate poisoning. ► Serotonin syndrome. ► Tricyclic antidepressant drug poisoning.

RENAL

► Acute kidney injury (AKI). ► Crush syndrome. ► Diabetes insipidus. ► Dialysis. ► Glomerulonephritis. ► Hepatorenal syndrome. ► Myoglobinuria. ► Oliguria. ► Renal failure. ► RIFLE criteria.

RESPIRATORY

► Aspiration pneumonitis. ► Asthma. ► Atelectasis. ► Bronchial carcinoma. ► Bronchiectasis. ► Bronchoalveolar lavage.

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Examination revision checklist

► Chest drainage. ► Chest infection. ► Chronic obstructive pulmonary disease. ► Cystic fibrosis. ► Dyspnoea. ► Forced expiration. ► Fowler’s method. ► Helium. ► Hypocapnia. ► Lung function tests. ► Obstructive sleep apnoea. ► Oxygen, hyperbaric. ► Oxygen therapy. ► Oxygen toxicity. ► Pulmonary embolism (PE). ► Pulmonary fibrosis. ORGANISATIONAL Advance decision. Clinical governance. Clinical trials. Coroner.

► ► ► ►

► COSHH regulations (Control of Substances Hazardous to Health). Critical incidents. ► ► Do not attempt resuscitation orders. ► Ethics. ► Incident, major. ► Mental Capacity Act 2005. ► National audit projects. ► Never events. ► Organ donation. ► Pollution. ► Recovery room. RADIOLOGY Chest x-ray. Computed (axial) tomography (CT). Magnetic resonance imaging (MRI). Positron emission tomography (PET). Radioisotope scanning. Radiological contrast media. Ultrasound.

► ► ► ► ► ► ►

A A severity characterisation of trauma (ASCOT). Trauma scale derived from the Glasgow coma scale, systolic BP, revised trauma score, abbreviated injury scale and age. A logistic regression equation provides a probability of mortality. Excludes patients with very poor or very good prognoses. Has been claimed to be superior to the trauma revised injury severity score system, although is more complex. Champion HR, Copes WS, Sacco WJ, et al (1996). J Trauma; 40: 42–8 A–adO2,  see Alveolar–arterial oxygen difference ABA,  see American Board of Anesthesiology Abbott, Edward Gilbert,  see Morton, William Abbreviated injury scale (AIS). Trauma scale first described in 1971 and updated many times since. Comprises a classification of injuries with each given a six-digit code (the last indicating severity, with 1 = minor and 6 = fatal). The codes are linked to International Classification of Diseases codes, thus aiding standardisation of records. The anatomical profile is a refinement in which the locations of injuries are divided into four categories; the AIS scores are added and the square root taken to minimise the contribution of less severe injuries. Gennarelli TA, Wodzin E (2006). Injury; 37: 1083–91 Abciximab.  Monoclonal antibody used as an antiplatelet drug and adjunct to aspirin and heparin in high-risk patients undergoing percutaneous coronary intervention. Consists of Fab fragments of immunoglobulin directed against the glycoprotein IIb/IIIa receptor on the platelet surface. Inhibits platelet aggregation and thrombus formation; effects last 24–48 h after infusion. Careful consideration of risks and benefits should precede use because risk of bleeding is increased. Licensed for single use only. • Dosage: initial loading of 250 µg/kg over 1 min iv, followed by iv infusion of 125 ng/kg/min (max 10 µg/ min) 10–60 min (up to 24 h in unstable angina) before angioplasty with 125 µg/kg/min (up to 10 µg/min for 12 h afterwards). • Side effects: bleeding, hypotension, nausea, bradycardia. Thrombocytopenia occurs rarely. Abdominal compartment syndrome.  Combination of increased intra-abdominal pressure (>12 mmHg [16 cmH2O]) and organ dysfunction (e.g. following abdominal trauma or extensive surgery) resulting from haemorrhage or expansion of the third space fluid compartment. May also follow liver transplantation, sepsis, burns and acute pancreatitis. Intra-abdominal pressures above 15–18 mmHg (20–25 cmH2O) may impair ventilation and be associated with reduced venous return, cardiac output, renal blood flow and urine output. Increased CVP may lead to raised ICP. Diagnosed by clinical features and intra-abdominal

pressure measurement (performed via a bladder catheter or nasogastric tube, in combination with a water column manometer).   Management includes laparotomy ± Silastic material to cover the abdominal contents. Paracentesis may be effective if raised intra-abdominal pressure is due to accumulation of fluid, e.g. ascites. Full resuscitation must be performed before decompression as rapid release of pressure may result in sudden washout of inflammatory mediators from ischaemic tissues, causing acidosis and hypotension. Mortality of the syndrome is 25%–70%. Kirkpatrick AW, Roberts DJ, De Waele J, et al (2013). Int Care Med; 39: 1190–206 See also, Compartment syndromes Abdominal field block. Technique using 100–200 ml local anaesthetic agent, involving infiltration of the skin, subcutaneous tissues, abdominal muscles and fascia. Provides analgesia of the abdominal wall and anterior peritoneum, but not of the viscera. Now rarely used. Rectus sheath block, transversus abdominis plane block, iliac crest block and inguinal hernia field block are more specific blocks. Abdominal sepsis,  see Intra-abdominal sepsis Abdominal trauma. May be blunt (e.g. road traffic accidents) or penetrating (e.g. stabbing, bullet wounds). Often carries a high morbidity and mortality because injuries may go undetected. Massive intra-abdominal blood loss or abdominal compartment syndrome may follow. The abdomen can be divided into three areas: ◗ intrathoracic: protected by the bony thoracic cage. Contains the spleen, liver, stomach and diaphragm. Injury may be associated with rib fractures. The diaphragm may also be injured by blows to the lower abdomen (which impart pressure waves to the diaphragm) or by penetrating injuries of the chest. ◗ true abdomen: contains the small and large bowel, bladder and, in the female, uterus, fallopian tubes and ovaries. ◗ retroperitoneal: contains the kidneys, ureters, pancreas and duodenum. May result in massive blood loss from retroperitoneal venous injury. • Management: ◗ basic resuscitation as for trauma generally. ◗ initial assessment: examination of the anterior abdominal wall, both flanks, back, buttocks, perineum (and in men, the urethral meatus) for bruises, lacerations, entry and exit wounds. Signs may be masked by unconsciousness, spinal cord injury or the effects of alcohol or drugs. Abdominal swelling usually indicates intra-abdominal haemorrhage; abdominal guarding or rigidity usually indicates visceral injury. Absence of bowel sounds may indicate intraperitoneal haemorrhage or peritoneal soiling with bowel contents. Colonic or rectal injuries may cause blood pr. A high

1

2

ABO blood groups

Table 1 Antigens and antibodies in ABO blood groups  

Group A B AB O

Incidence in UK (%) 42 8 3 47

Red cell antigen

Plasma antibody

A B A and B None

Anti-B Anti-A None Anti-A and anti-B

index of suspicion is required for retroperitoneal injuries because examination is difficult. ◗ imaging: abdominal x-ray may reveal free gas under the diaphragm (erect or semi-erect; may also be visible on CXR) or laterally (lateral decubitus x-ray); other investigations include pelvic x-ray and urological radiology if indicated (e.g. iv urogram), CT and MRI scanning and ultrasound. ◗ peritoneal lavage is indicated in blunt abdominal trauma associated with: - altered pain response (TBI, spinal cord injury, drugs, etc.). - unexplained hypovolaemia following multiple trauma. - equivocal diagnostic findings. ◗ insertion of a nasogastric tube and urinary catheter (provided no urethral injury; a suprapubic catheter may be necessary). ◗ indications for laparotomy include penetrating injuries, obvious intra-abdominal haemorrhage, signs of bowel perforation or a positive peritoneal lavage. Al-Mudhaffar M, Hormbrey P (2014). Br Med J; 348: g1140 See also, Pelvic trauma ABO blood groups.  Discovered in 1900 by Landsteiner in Vienna. Antigens may be present on red blood cells, with antibodies in the plasma (Table 1). The antibodies, mostly type-M immunoglobulins, develop within the first few months of life, presumably in response to naturally occurring antigens of similar structure to the blood antigens. Infusion of blood containing an ABO antigen into a patient who already has the corresponding antibody may lead to an adverse reaction; hence the description of group O individuals as universal donors, and of group AB individuals as universal recipients. [Karl Landsteiner (1868–1943), Austrian-born US pathologist] See also, Blood compatibility testing; Blood groups; Blood transfusion ABPI,  see Ankle–Brachial Pressure Index Abruption,  see Antepartum haemorrhage Absolute risk reduction.  Indicator of treatment effect in clinical trials, representing the decrease in risk of a given treatment compared with a control treatment, i.e., the inverse of the number needed to treat. For a reduction in incidence of events from a% to b%, it equals (a − b)%. See also, Meta-analysis; Odds ratio; Relative risk reduction Abuse of anaesthetic agents.  May occur because of easy access to potent drugs by operating theatre or ICU staff.

Anaesthetists are 2.5 times as likely to abuse agents than other physicians. Opioid analgesic drugs (especially fentanyl) are the most commonly abused agents, but others include benzodiazepines, propofol and inhalational anaesthetic agents. Abuse may be suggested by behavioural or mood changes or excessive and inappropriate requests for opioids. Main considerations include the safety of patients, counselling and psychiatric therapy for the abuser and legal aspects of drug abuse. May be associated with alcoholism. Bryson EO, Silverstein JH (2008). Anesthesiology; 109: 905–17 See also, Misuse of Drugs Act; Sick doctor scheme; Substance abuse Acarbose.  Inhibitor of intestinal alpha glucosidases and pancreatic amylase; used in the treatment of diabetes mellitus, usually in combination with a biguanide or sulfonylurea. Delays digestion and absorption of starch and sucrose and has a small blood glucose-lowering effect. See also, Meglitinides; Thiazolidinediones Accessory nerve block.  Performed for spasm of trapezius and sternomastoid muscles (there is no sensory component to the nerve). 5–10 ml local anaesthetic agent is injected 2 cm below the mastoid process into the sternomastoid muscle, through which the nerve runs. Accident, major,  see Incident, major ACD,  Acid–citrate–dextrose solution, see Blood storage ACD-CPR,  Active compression decompression CPR, see Cardiac massage; Cardiopulmonary resuscitation ACE,  Angiotensin angiotensin system

converting

enzyme, see

Renin/

ACE anaesthetic mixture.  Mixture of alcohol, chloroform and diethyl ether, in a ratio of 1:2:3 parts, suggested in 1860 as an alternative to chloroform alone. Popular into the 1900s as a means of reducing total dose and side effects of any one of the three drugs. ACE inhibitors,  see Angiotensin converting enzyme inhibitors Acetaminophen,  see Paracetamol Acetazolamide.  Carbonic anhydrase inhibitor. Reduces renal bicarbonate formation and hydrogen ion excretion at the proximal convoluted tubule, thereby inducing a metabolic acidosis. A weak diuretic, but rarely used as such. Also used to treat glaucoma, metabolic alkalosis, altitude sickness and childhood epilepsy. Useful in the treatment of severe hyperphosphataemia as it promotes urinary excretion of phosphate. May be used to lower ICP (e.g. in benign intracranial hypertension) by reducing CSF production. Has been used to alkalinise the urine in tumour lysis syndrome and to enhance excretion in drug intoxications, e.g. with salicylates. • Dosage: 0.25–0.5 g orally/iv od/bd. Acetylcholine (ACh). Neurotransmitter, the acetyl ester of choline (Fig. 1). Synthesised from acetylcoenzyme A and choline in nerve ending cytoplasm; the reaction is catalysed by choline acetyltransferase. Choline is actively

Acetylcholinesterase

CH3 N+

CH3

(a)

O CH2

CH2

O

C

CH3

Nicotinic

Somatic muscle

CH3

Nicotinic Muscarinic

Parasympathetic Fig. 1 Structure of acetylcholine  

Nicotinic

Adrenergic

To sweat glands

Nicotinic

Muscarinic

To adrenal medulla

Nicotinic

Most nerves

transported into the nerve and acetylcoenzyme A is formed in mitochondria. ACh is stored in vesicles. • ACh is the transmitter at: ◗ autonomic ganglia. ◗ parasympathetic postganglionic nerve endings. ◗ sympathetic postganglionic nerve endings at sweat glands and some muscle blood vessels. ◗ the neuromuscular junction. ◗ many parts of the CNS, where it has a prominent role in CNS plasticity (and therefore learning), attention and memory. Dysfunction of the CNS cholinergic system contributes to the memory disorder in Alzheimer’s disease. Actions may be broadly divided into either muscarinic or nicotinic, depending on the acetylcholine receptors involved. ACh is hydrolysed to choline and acetate by acetylcholinesterase on the postsynaptic membrane. Other esterases also exist, e.g. plasma cholinesterase. [Alois Alzheimer (1864–1915), German neurologist and pathologist] See also, Acetylcholine receptors; Neuromuscular transmission; Parasympathetic nervous system; Sympathetic nervous system; Synaptic transmission

Sympathetic

(b) α

ε δ β

α 10 nm

Lipids

Cytoskeleton Fig. 2 (a) Types of acetylcholine receptors. (b) Structure of nicotinic acetylcholine receptor  

Acetylcholine receptors. Transmembrane receptors activated by acetylcholine (ACh). Classified according to their relative sensitivity to nicotine or muscarine (Fig. 2a). • Nicotinic receptors: ligand-gated ion channels present at numerous sites within the nervous system; notable examples include the neuromuscular junction (NMJ) and autonomic ganglia. Each receptor consists of five glycosylated protein subunits that project into the synaptic cleft. The adult receptor consists of 2 α, β, δ and ε units. The ε subunit is replaced by a γ subunit in the neonate. The subunits span the postsynaptic membrane, forming a cylinder around a central ion channel (Fig. 2b). The two α subunits of each receptor carry the binding sites for ACh. Occupation of these sites opens the ion channel, allowing cations (mainly sodium, potassium and calcium) to flow into the cell down their concentration gradients; this produces an excitatory postsynaptic potential. If these summate and exceed the threshold potential, an action potential is generated. Non-depolarising neuromuscular blocking drugs are reversible competitive antagonists of these receptors at the NMJ. • Muscarinic receptors: G protein-coupled receptors, largely coupled to either adenylate cyclase or phospholipase C, via Gi and Gq proteins, respectively. Mediate postganglionic neurotransmission via parasympathetic neurones, as well as sympathetic outflow to sweat glands (Fig. 2a). Classified according to structural subtype, distribution and function: ◗ M1: Gq-coupled; stomach (stimulates acid secretion) and brain (memory formation). ◗ M2: Gi-coupled; heart; decreases heart rate, contractility and atrioventricular nodal conduction.

◗

M3: Gq-coupled; smooth muscle (increased tone, e.g. bronchiolar, intestinal), exocrine glands (stimulatory), brain (stimulatory at vomiting centre). ◗ M4/5: brain and adrenal medulla. Muscarinic receptor agonists include bethanechol, carbachol and pilocarpine (in the eye); antagonists include hyoscine, atropine and ipratropium bromide.   The activation threshold of muscarinic receptors is lower than that of nicotinic receptors. Injection of ACh or poisoning with anticholinesterases thus causes parasympathetic stimulation and sweating at lower doses, before having effects at autonomic ganglia and the NMJ at higher doses. See also, Neuromuscular transmission; Parasympathetic nervous system; Sympathetic nervous system; Synaptic transmission Acetylcholinesterase.  Enzyme present at the synaptic membranes of cholinergic synapses and neuromuscular junctions. Also found in red blood cells and the placenta. Metabolises acetylcholine (ACh) to acetate and choline, thus terminating its action. Has a high catalytic activity, each molecule of acetylcholinesterase catalysing 25 000 molecules of ACh per second. The N(CH3)3+ moeity of ACh binds to the anionic site of the enzyme, and the acetate end of ACh forms an intermediate bond at the esteratic site. Choline is liberated, and the intermediate substrate/enzyme complex is then hydrolysed to release acetate (Fig. 3). See also, Acetylcholinesterase inhibitors; Neuromuscular transmission; Synaptic transmission

3

4

Acetylcholinesterase inhibitors

Acetylcholine O +

(CH3)3 N

CH2

CH2

O

C H O

CH3

Anionic site

Esteratic site

Choline

O

+

(CH3)3 N

CH2

CH2

OH

C

CH3

Acetylated enzyme

O

O C H O

Acetate CH3

O–

Fig. 3 Action of acetylcholinesterase  

Acetylcholinesterase inhibitors.  Substances that increase acetylcholine (ACh) concentrations by inhibiting acetylcholinesterase (AChE). Used clinically for their action at the neuromuscular junction in myasthenia gravis and in the reversal of non-depolarising neuromuscular blockade. Concurrent administration of an antimuscarinic agent, e.g. atropine or glycopyrronium, reduces unwanted effects of increased ACh concentrations at muscarinic receptors. Effects at ganglia are minimal at normal doses. Central effects may occur if the drug readily crosses the blood–brain barrier, e.g. physostigmine (used to treat the central anticholinergic syndrome).   Have also been used to treat tachyarrhythmias. • Classified according to mechanism of action: ◗ reversible competitive inhibitors: competitive inhibition at the anionic site of AChE prevents binding of ACh, e.g. edrophonium, tetrahydroaminacrine. ◗ oxydiaphoretic (or ‘acid-transferring’) inhibitors: act as an alternative substrate for AChE, producing a more stable carbamylated enzyme complex. Subsequent hydrolysis of the complex and thus reactivation of the enzyme is slow. Examples: - neostigmine, physostigmine (few hours). - pyridostigmine (several hours). - distigmine (up to a day). ◗ organophosphorus compounds: act by irreversibly phosphorylating the esteratic site of AChE; inhibition can last for weeks until new enzyme is synthesised. Examples include: ecothiopate (used for the treatment of glaucoma); parathion (an insecticide); sarin nerve gas (a chemical weapon). Acetylcholinesterase inhibitors augment depolarising neuromuscular blockade and may cause depolarising blockade in overdose. They may also cause bradycardia, hypotension, agitation, miosis, increased GIT activity, sweating and salivation.

  Centrally acting acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine) are used for symptomatic treatment of Alzheimer’s dementia. Of anaesthetic relevance because of their side effects (including nausea, vomiting, fatigue, muscle cramps, increased creatine kinase, convulsions, bradycardia, confusion), enhancement of the actions of suxamethonium, and possible antagonism of non-depolarising neuromuscular blocking drugs. [Alois Alzheimer (1864–1915), German neurologist and pathologist] See also, Neuromuscular transmission; Organophosphorus poisoning N-Acetylcysteine.  Derivative of the naturally occurring amino acid, L-cysteine. A free radical scavenger, licensed as an antidote to paracetamol poisoning. Acts by restoring depleted hepatic stores of glutathione and providing an alternative substrate for a toxic metabolite of paracetamol. Also used as an ocular lubricant and to prevent nephropathy due to radiological contrast media in patients with reduced renal function.   Has been investigated for the treatment of fulminant hepatic failure, MODS, ALI and neuropsychiatric complications of carbon monoxide poisoning, as well as a possible role in protection against myocardial reperfusion injury. Also used as a mucolytic because of its ability to split disulfide bonds in mucus glycoprotein. • Dosage: ◗ paracetamol poisoning: 150 mg/kg (to a maximum of 12 g) in 200 ml 5% dextrose iv over 1 h, followed by 50 mg/kg in 500 ml dextrose over 4 h, then 100 mg/ kg in 1 l dextrose over 16 h (maximum of 110 kg body weight used for obese patients). ◗ to reduce viscosity of airway secretions: 200 mg 8 hourly, orally. May be delivered by nebuliser. • Side effects: rashes, anaphylaxis. Has been associated with bronchospasm in asthmatics. Achalasia.  Disorder of oesophageal motility caused by idiopathic degeneration of nerve cells in the myenteric plexus or vagal nuclei. Results in dysphagia and oesophageal dilatation. A similar condition may result from American trypanosomal infection (Chagas’ disease). Aspiration pneumonitis or repeated chest infections may occur. Treated by mechanical distension of the lower oesophagus or by surgery. Heller’s cardiomyotomy (longitudinal myotomy leaving the mucosa intact) may be undertaken via abdominal or thoracic approaches. Preoperative respiratory assessment is essential. Patients are at high risk of aspirating oesophageal contents, and rapid sequence induction is indicated. [Carlos Chagas (1879–1934), Brazilian physician; Ernst Heller (1877–1964), German surgeon] See also, Aspiration of gastric contents; Induction, rapid sequence Achondroplasia. Skeletal disorder, inherited as an autosomal dominant gene, although most cases arise by spontaneous mutation. Results in dwarfism, with a normal size trunk and shortened limbs. Flat face, bulging skull vault and spinal deformity may make tracheal intubation difficult, and the larynx may be smaller than normal. Obstructive sleep apnoea may occur. Foramen magnum and spinal canal stenoses may be present, the former resulting in cord compression on neck extension, the latter making neuraxial blockade difficult and reducing volume requirements for epidural anaesthesia.

Acidosis, metabolic Aciclovir.  Antiviral drug; an analogue of nucleoside 2′-deoxyguanosine. Inhibits viral DNA polymerase; active against herpes viruses and used in the treatment of encephalitis, varicella zoster (chickenpox/shingles) and postherpetic neuralgia, and for prophylaxis and treatment of herpes infections in immunocompromised patients. Treatment should start at onset of infection; the drug does not eradicate the virus but may markedly attenuate the clinical infection. • Dosage: ◗ as topical cream, 5 times daily. ◗ 200–800 mg orally, 2–5 times daily in adults. ◗ 5–10 mg/kg iv tds, infused over 1 h. • Side effects: rashes, GIT disturbances, hepatic and renal impairment, blood dyscrasias, headache, dizziness, severe local inflammation after iv use, confusion, convulsions, coma. Acid.  Species that acts as a proton (H+) donor when in solution (Brønsted–Lowry definition). [Johannes N Brønsted (1879–1947), Danish chemist; Thomas M Lowry (1874–1936), English chemist] See also, Acid–base balance; Acidosis Acidaemia. Arterial pH 45 nmol/l. See also, Acid–base balance; Acidosis Acid–base balance. Maintenance of stable pH in body fluids is necessary for normal enzyme activity, ion distribution and protein structure. Blood pH is normally maintained at 7.35–7.45 (hydrogen ion [H+] concentration 35–45 nmol/l); intracellular pH changes with extracellular pH. During normal metabolism of neutral substances, organic acids are produced that generate hydrogen ions. • Maintenance of pH depends on: ◗ buffers in tissues and blood, which minimise changes in H+ concentration. ◗ regulation by kidneys and lungs; the kidneys excrete about 60–80 mmol and the lungs about 15 000–20 000  mmol H+ per day. Because of the relationship between CO2, carbonic acid, bicarbonate (HCO3−) and H+, and the ability to excrete CO2 rapidly from the lungs, respiratory function is important in acid–base balance: H 2 O + CO2  H 2 CO3  HCO3 + H −

+

Thus hyper- and hypoventilation cause alkalosis and acidosis, respectively. Similarly, hyper- or hypoventilation may compensate for non-respiratory acidosis or alkalosis, respectively, by returning pH towards normal.   Sources of H+ excreted via the kidneys include lactic acid from blood cells, muscle and brain, sulfuric acid from metabolism of sulfur-containing proteins, and acetoacetic acid from fatty acid metabolism. • The kidney can compensate for acid–base disturbances in three ways: ◗ by regulating the reabsorption of filtered HCO3− at the proximal convoluted tubule (normally 80%– 90%): - filtered Na+ is exchanged for H+ across the tubule cell membrane. - filtered HCO3− and excreted H+ form carbonic acid. - carbonic acid is converted to CO2 and water by carbonic anhydrase on the cell membrane.

- CO2 and water diffuse into the cell and reform carbonic acid (catalysed again by carbonic anhydrase). - carbonic acid dissociates into HCO3− and H+. - HCO3− passes into the blood; H+ is exchanged for Na+, etc. ◗ by forming dihydrogen phosphate from mono­ hydrogen phosphate in the distal tubule (HPO4− + H+ → H2PO4−). The H+ is supplied from carbonic acid, leaving HCO3−, which passes into the blood. ◗ by combination of ammonia, passing out of the cells, with H+, supplied as mentioned earlier. Resultant ammonium ions cannot pass back into the cells and are excreted. In acid–base disorders, the primary change determines whether a disturbance is respiratory or metabolic. The direction of change in H+ concentration determines acidosis or alkalosis. Renal and respiratory compensation act to restore normal pH, not reverse the primary change. For example, in the Henderson–Hasselbalch equation: [HCO3− ] pH = pKa + log [CO2 ] adjustment of the HCO3−/CO2 concentration ratio restores pH towards its normal value, e.g.: ◗ primary change: increased CO2; leads to decreased pH (respiratory acidosis). ◗ compensation: HCO3− retention by kidneys; increased ammonium secretion, etc. An alternative approach, suggested by Stewart in 1983, focuses on the strong ion difference to explain the underlying processes rather than the above ‘traditional approach’, which concentrates more on interpretation of measurements. It is based on the degree of dissociation of ions in solution, in particular the effects of strong ions and weak acids, and the role of bicarbonate as a marker of acid–base imbalance rather than a cause. [Peter Stewart (1921–1993), Canadian physiologist] See also, Acid; Base; Blood gas interpretation; Breathing, control of; Davenport diagram; Siggaard-Andersen nomogram Acid–citrate–dextrose solution,  see Blood storage Acidosis. A process in which arterial pH 45 mmol/l), or would be 94%], pulmonary oedema or ongoing ischaemia), cardiac monitoring, 12-lead ECG, iv access. ◗ aspirin 300 mg orally. ◗ analgesia (e.g. iv morphine in 2 mg increments). ◗ sublingual GTN. ◗ associated pulmonary oedema and arrhythmias should be treated in the usual way. ◗ consideration for immediate reperfusion therapy if: - presentation 0.1 mV in two or more contiguous chest leads or two adjacent limb leads. - new-onset LBBB. - posterior infarction (dominant R wave and S–T depression in V1–V2 chest leads). • Reperfusion strategies include: ◗ pharmacological thrombolytic therapy: agents include streptokinase, alteplase, tenecteplase and reteplase. Survival benefit is reduced with increasing delay, and is negligible from 12 h after onset of symptoms. Administration of thrombolysis within 1 h of the patient calling for professional help is a national audit standard. Contraindications include active bleeding, recent trauma (including surgery and CPR), previous haemorrhagic stroke, uncontrolled hypertension and pregnancy. ◗ primary PCI. ◗ emergency coronary artery bypass surgery. Thrombolysis is generally only preferred if primary PCI is unavailable or there would be delay of >90 min in delivering it and the presentation is within 3 h of symptom onset. Primary PCI is particularly superior if: there is cardiogenic shock; there are contraindications to thrombolysis; or the patient is at high risk of death (e.g. age >75, previous MI, extensive anterior infarct). Emergency surgery

Acute kidney injury is generally reserved for those known to have disease uncorrectable by PCI or in whom primary PCI fails.   Patients not meeting criteria for immediate reperfusion (i.e., those with NSTEACS) are managed either invasively (PCI within 24 h plus abciximab iv) or conservatively (pharmacological management only). High-risk patients are most likely to benefit from invasive therapy. • Pharmacological adjuncts include: ◗ clopidogrel and low-molecular weight heparin (e.g. enoxaparin): should be given to all patients (in the absence of contraindications) with definite or strongly suspected ACS, in addition to aspirin. Prasugrel and ticagrelor are newer alternatives to clopidogrel, but the former is associated with increased risk of lifethreatening bleeding. ◗ GTN sublingually or by iv infusion if pain persists. ◗ glycoprotein IIB/IIIa inhibitors (e.g. abciximab and tirofiban): beneficial in patients undergoing PCI, those at high risk of death, or both. ◗ β-adrenergic receptor antagonists: reduce the rate of reinfarction and VF and should be commenced within 24 h if there are no contraindications, e.g. heart block, pulmonary oedema, hypotension. Those unable to receive β-blockers should receive one of the non-dihydropyridine calcium channel blocking drugs (e.g. verapamil). ◗ ACE inhibitors: improve long-term survival after MI and should be commenced within 24 h, assuming no contraindications. ◗ magnesium and potassium supplementation to maintain normal levels reduces the incidence of arrhythmias. Prophylactic administration of anti­ arrhythmic drugs is no longer recommended. ◗ implantable cardioverter defibrillators should be considered in patients following MI who have an ejection fraction 1.020 >500 2 >20 >40 3.5 g/1.73 m2 body surface area. May be primary due to glomerular disease (classified according to histology) or secondary (e.g. associated with diabetes mellitus, pre-eclampsia, connective tissue disease, post-viral hepatitis or streptococcal infection, drugs such as NSAIDs or captopril). Features include generalised oedema, susceptibility to infection and thromboembolism (especially renal vein thrombosis and DVT) and hyperlipidaemia. Hypo­ albuminaemia may lead to altered drug binding.   Treatment includes a low-sodium diet and diuretic therapy to reduce oedema, and a low-protein diet and angiotensin converting enzyme inhibitors to reduce proteinuria. Other treatment is directed against the cause, e.g. corticosteroids in glomerulonephritis. See also, Renal failure Nernst equation.  Equation for calculating the membrane potential at which an individual ion is at equilibrium across the membrane (assuming complete permeability to that ion). For ion X:

E=

RT [X]o ln [X]i FZ

where E = equilibrium potential R = universal gas constant T = absolute temperature F = Faraday constant (coulombs per mole of charge) Z = valence of the ion [X]o = extracellular concentration of X [X]i = intracellular concentration of X. For chloride, potassium and sodium, E = −70 mV, −94 mV and +60 mV, respectively. Because the normal resting membrane potential is about −70 mV, other factors must affect potassium and especially sodium distribu­ tion (e.g. relative permeability and the sodium/potassium pump). [Hermann W Nernst (1864–1941), German physicist; Michael Faraday (1791–1867), English scientist] See also, Goldman constant-field equation Nerve.  Excitable tissue whose function is the transmission of nerve impulses. Typical peripheral nerves consist of several groups of fascicles. Each fascicle is surrounded by the perineurium and contains a group of neurones, the axons of which are encased in the endoneurium (Fig. 118).   Peripheral nerves originate in the spinal cord, and may be sensory, motor or mixed. Some also carry autonomic nervous system fibres. See also, Motor pathways; Sensory pathways

407

408

Nerve conduction

Perineurium

Artery Vein

Fascicle

Axon surrounded by endoneurium Epineurium

Fig. 118 Cross-section of a typical nerve  

Nerve conduction. Passage of an action potential along neurones; involves waves of depolarisation and repolarisation that move longitudinally across the nerve membrane.   In unmyelinated nerves, impulses spread at up to 2 m/s. Positive charge flows into the depolarised area from the membrane just distally, altering the distal permeability to ions (especially sodium and potassium) as for action potential generation. When the threshold potential is reached, depolarisation occurs. Retrograde conduction is prevented by the refractory period of the membrane proximally.  The myelin sheath of myelinated nerves acts as an insulator that prevents the flow of ions across the nerve membrane. Breaks in the myelin (nodes of Ranvier), approximately 1 mm apart, allow ions to flow freely between the neurone and the ECF at these points. Depolarisation ‘jumps’ from node to node (saltatory conduction), a process that increases conduction velocity (up to 120 m/s) and conserves energy. [Louis A Ranvier (1835–1922), French pathologist and physician] Nerve growth factor  (NGF). Protein produced by many cell types; taken up by small sensory and sympathetic nerve fibres via specific receptors and retrogradely transported to the cell body. Required for growth and survival of neurones in the fetus and neonate; released from connective tissue and inflammatory cells following tissue injury in response to cytokine stimulation. Causes hyperalgesia via both central and peripheral effects; thus thought to be important in acute and chronic pain states. Also involved in immune regulation and other non-neurological system function. Nerve injury during anaesthesia. May occur during general, local or regional anaesthesia. • Causes of neuronal injury include: ◗ general anaesthesia: - poor positioning of the patient; thought to cause local nerve ischaemia. - ischaemia caused by hypotension or use of tourniquets. - hypothermia. - extravasation of drugs into perineural tissue. - toxicity of degradation products of anaesthetic agents, classically trichloroethylene with soda lime.

anaesthesia: positioning/ischaemia/ hypothermia as discussed earlier plus: - direct trauma from a needle or catheter. - intraneural injection of local anaesthetic agent. - cauda equina syndrome following use of spinal catheters for continuous spinal anaesthesia. - infection. - haematoma formation. - chemical contamination of local anaesthetic, or injection of the wrong solution. - poor positioning of the anaesthetised limb with ischaemia as discussed earlier. ◗ other: - central venous cannulation. - tracheal intubation. • Classic division of nerve injuries: ◗ neuropraxia: caused by compression. Typically incomplete, affecting motor more than sensory components (when present, touch and proprioception predominate). Usually recovers within 6 weeks. Damage during general anaesthesia is usually of this nature, and associated with positioning. ◗ axonotmesis: axonal and myelin loss within the intact connective tissue sheath. Typically there is complete motor and sensory loss, with slow recovery due to nerve regeneration from proximal to distal nerve. ◗ neurotmesis: partial or complete severance. Recovery is rare. Electromyographic and nerve conduction studies may aid differentiation between types of injury, and are most useful 1–3 weeks after the event. ‘Baseline’ studies performed immediately after the injury are also useful to identify or exclude pre-existing deficit. • Many specific neuropathies have been described, including lesions of the following: ◗ brachial plexus: usually stretched, typically by shoulder abduction and extension, with supination. Stretch is exacerbated by bilateral abduction. Upper roots are usually affected; weakness lasts up to several months, although recovery usually occurs within 2–3 months. Lower roots may be damaged during sternal retraction in cardiac surgery. Compression may be caused by shoulder rests in the steep head-down position, resulting in temporary palsy. ◗ ulnar nerve: may be compressed between the humeral epicondyle and the operating table or arm supports, or injured by stretcher poles if slid alongside the patient during transfer. ◗ radial nerve: caused by the patient’s arm hanging over the side of the operating table. ◗ median nerve: may be damaged by direct needle trauma, or drug extravasation in the antecubital fossa. ◗ facial nerve: compressed between the anaesthetist’s fingers and the patient’s mandible during mask anaesthesia. ◗ abducens nerve: temporary lesions may follow spinal or epidural anaesthesia. ◗ trigeminal nerve: typically damaged by the trichloroethylene/soda lime interaction. ◗ supraorbital nerve: compressed by the tracheal tube connector, catheter mount, head harness or ventilator tubing. ◗ common peroneal nerve: compressed between lithotomy pole and fibular head. ◗ saphenous nerve: compressed between lithotomy pole and medial tibial condyle. ◗ local/regional

Neuroleptic malignant syndrome ◗

sciatic nerve: damaged by im injections or compressed against the operating table in emaciated patients. ◗ pudendal nerve: compressed between a poorly padded perineal post and the ischial tuberosity. Nerve injury may also be caused by surgical trauma/ compression.   Similar concerns exist for patients undergoing prolonged treatment on ICU. See also, Cranial nerves; Critical illness polyneuropathy; Eye care Nerve stimulator,  see Neuromuscular blockade monitoring; Regional anaesthesia; Transcutaneous electrical nerve stimulation Netilmicin.  Aminoglycoside and antibacterial drug with similar activity to gentamicin but less active against pseudomonas. Less ototoxic than gentamicin. • Dosage: 4–6 mg/kg im/iv daily or up to 2.5 mg/kg im/ iv bd/tds. Blood concentrations: 1 h post-dose 5 s, open the mouth, protrude the tongue, cough, maintain sustained hand grip, and achieve adequate tidal volume, vital capacity (15 ml/kg) and inspiratory pressure (−20 cm H2O), have all been described. However, these are unreliable as they may all be possible at 50%–80% blockade (TOF ratio 0.5%–0.8%). Naguib M, Brull SJ, Johnson KB (2017). Anaesthesia; 72(Suppl 1): 16–37

Neuromuscular blocking drugs.  Drugs used to impair neuromuscular transmission and provide skeletal muscle relaxation during anaesthesia or critical care. • May be one of two types: ◗ non-depolarising: include tubocurarine (first used as curare in 1912), gallamine (1948), dimethyl tubocurarine (1948), alcuronium (1961), pancuronium (1967), fazadinium (1972), atracurium (1980), vecuronium (1983), pipecuronium (1990), doxacurium (1991), mivacurium (1993), rocuronium (1994), cisatracurium (1995) and rapacuronium (1999). Non-depolarising agents are competitive antagonists at postsynaptic acetylcholine (ACh) receptors of the neuromuscular junction. They are highly ionised at body pH, containing two quaternary ammonium groups (tubocurarine and vecuronium contain one each, but acquire a second following injection). Poorly lipid-soluble with variable protein binding. Following injection, the drugs are rapidly redistributed from blood to the ECF and other tissues, e.g. kidney, liver. The clinical effect depends on individual drug characteristics and drug concentration at the neuromuscular junction, which depends on the drug’s pharmacokinetics. ◗ depolarising: cause depolarisation by mimicking the action of ACh at ACh receptors, but without rapid hydrolysis by acetylcholinesterase. An area of depolarisation around the ACh receptor–drug complex results in local currents that open sodium channels before the continuing current flow inactivates them. Propagation of an action potential is prevented by the area of inexcitability that develops around the ACh receptors. Thus fasciculations occur before paralysis. Examples are suxamethonium (1951) and decamethonium (1948); only the former is available for clinical use in the UK. Apart from the presence or absence of fasciculation, nondepolarising and depolarising neuromuscular blockade may be distinguished by neuromuscular blockade monitoring.   In general, suxamethonium is used for paralysis of rapid onset and short duration, e.g. to allow rapid tracheal intubation. The slower-acting non-depolarising drugs were traditionally used for prolonged paralysis when rapid intubation was not required, although atracurium and vecuronium, and especially rocuronium, have bridged the gap between these drugs and suxamethonium (Table 35). See also, Interonium distance; Nicotine and nicotinic receptors Neuromuscular junction.  Synapse between the presynaptic motor neurone and the postsynaptic muscle membrane. On approaching the junction, the axon divides into terminal buttons that invaginate into the muscle fibre. The synaptic cleft is 50–70 nm wide and filled with ECF and a basement membrane containing high concentrations of acetylcholinesterase. The muscle membrane is folded into longitudinal gutters, whose ridges conceal orifices to secondary clefts. The orifices lie opposite the release points for acetylcholine (ACh) (Fig. 120). • Three types of acetylcholine receptor have been identified at the neuromuscular junction: ◗ postjunctional: involved in traditional neuromuscular transmission. Following activation of both α subunits, sodium and calcium move into the myocyte and potassium exits through specific ion channels (see also Fig. 2b; Acetylcholine receptors). ◗ prejunctional: control an ion channel specific for sodium and respond to released ACh by mobilising

411

412

Neuromuscular transmission

Table 35 Properties of neuromuscular blocking drugs  

Drug

Onset time (min)

Half-life (min)

Vol. of distribution (l/kg)

Clearance (ml/kg/min)

Clinical duration of action (min)

Alcuronium Atracurium

3–5 1.5–2

180–200 20

0.1–0.3 0.16–0.18

1.5 5.5–6.0

20–40 20–30

Cisatracurium Dimethyl tubocurarine (metocurine) Doxacurium Fazadinium

1–1.5 3–5

100 345

0.23 0.5

3.9 1.0

4–5 0.5–1.5

85–100 40–80

0.2 0.2

Gallamine Mivacurium

1–2 1.5–2

160 2–5

Pancuronium

2–3

Pipecuronium Rapacuronium Rocuronium Tubocurarine Vecuronium Suxamethonium

2.5–3 0.5–3.5 2 3–5 1.5–2 0.5–1.5

Route of elimination

Histamine release

Autonomic effects

± +

− −

30–40 90–120

Renal Hofmann degradation + plasma hydrolysis As for atracurium Renal

− +

− Weak ganglion blockade

2.2–2.6 4.0

100–200 40–60

Renal + hepatic Renal

− −

0.25 −

1.2 −

20–30 10–15

− ±

120–140

0.25–0.3

1.8

40–60

Renal Plasma cholinesterase + hepatic Renal + hepatic

− Muscarinic + ganglion blockade Muscarinic blockade −

140 28 22–29 150–190 55–70 2.5

0.3 0.29 0.12–0.16 0.5–0.6 0.27 −

2.5 6–11 4.7–5.7 2–3 5.2 −

90–120 6–30 30 30–50 20–30 2–5

Renal + hepatic Renal + hepatic Hepatic Renal + hepatic Renal + hepatic Plasma cholinesterase

− ++ − ++ − +

−

Weak muscarinic blockade + sympathomimetic action − − ± Ganglion blockade − Muscarinic + ganglionic stimulation

Nerve Myelin Mitochondrion Microtubule

Schwann cell

Nerve terminal Basement membrane containing acetylcholinesterase

Active zone or release site

Synaptic space

Acetylcholine receptors

Primary cleft

Muscle

Secondary cleft

Actin–myosin complex

Fig. 120 Structure of neuromuscular junction  

further ACh storage vesicles to the active zone of the junction, ready for release. Blockade of these receptors is thought to underlie the phenomenon of fade in non-depolarising neuromuscular blockade; activation during tetanic stimulation results in posttetanic potentiation. ◗ extrajunctional: normally present in small numbers, but proliferate over the muscle membrane in

denervation hypersensitivity, burns and certain muscle diseases. See also, Neuromuscular blocking drugs Neuromuscular transmission.  Stages of transmission: ◗ depolarisation of the motor nerve leading to action potential propagation to the nerve endings at the neuromuscular junction.

Neurosurgery of presynaptic voltage-gated calcium channels. Resultant increase in intracellular calcium causes mobilisation of acetylcholine (ACh) vesicles to the active zone and subsequent release into the synapse. ◗ binding of ACh to postsynaptic nicotinic ACh receptors, allowing sodium and calcium ion influx and causing an end-plate potential. If the latter is large enough, depolarisation of the muscle membrane occurs. ◗ resultant action potential causing muscle contraction. ◗ hydrolysis of ACh by acetylcholinesterase within 1 ms. • Transmission may be impaired by: ◗ inhibition of ACh synthesis, storage or release, e.g. by hemicholinium, β-bungarotoxin and botulinum toxins, respectively. Aminoglycosides are also thought to impair ACh release, as does the myasthenic syndrome. ◗ blockade of ACh receptors, e.g. by neuromuscular blocking drugs, α-bungarotoxin, receptor destruction in myasthenia gravis. ◗ acetylcholinesterase inhibitors. See also, Synapse ◗ opening

Neurone.  Basic unit of the nervous system. Consists of: ◗ cell body: contains the nucleus and most of the cytoplasm. Usually at the dendritic end of the neurone. The dendritic zone is the site of integration of incoming impulses via dendrites, and of initiation of the action potential. ◗ axon: may exceed 1 metre in length. May be myelinated or unmyelinated (see Myelin; Nerve conduction). Anterograde and retrograde flow of organelles and proteins occurs along the axon. ◗ terminal buttons (nerve endings): situated near the cell body or dendrites of other neurones and contain neurotransmitters. • Divided into classes in 1924 according to the compound action potential obtained when a mixed nerve is stimulated: ◗ A: 1–20 µm diameter myelinated fibres. Subdivided into: - α: 70–120 m/s conduction; somatic motor and proprioception sensation. - β: 50–70 m/s; touch and pressure sensation. - γ: 30–50 m/s; motor fibres to muscle spindles. - δ: 50 years. ◗ pharyngeal abnormalities (e.g. retrognathia, tonsillar hypertrophy, acromegaly) and other conditions (e.g. hypothyroidism, neuromuscular disorders). ◗ sedative drugs (including alcohol) can precipitate or exacerbate the condition. • Features: ◗ loud snoring, associated with cycles of increasing partial airway obstruction (hypopnoea) leading to total obstruction (apnoea) followed by vigorous respiratory efforts and arousal to lighter planes of sleep and relief of obstruction. These cycles may occur up to 400 times/night. Associated with restlessness, morning headaches and daytime somnolence. ◗ medical consequences of OSA include increased incidence of cognitive disorders, hypertension, stroke, arrhythmias, MI and diabetes mellitus. ◗ severe OSA may result in cor pulmonale (obesity hypoventilation syndrome). Screening questionnaires (e.g. STOP-BANG score) are used to identify those at high risk; formal diagnosis requires sleep studies, with polysomnography (monitoring of respiratory airflow, chest and abdominal movements, EEG and oximetry). OSA severity is classified according to the apnoea–hypopnoea index (number of apnoeas/hypopnoeas divided by the number of hours of sleep): 5–15 = mild; 15–30 = moderate; >30 = severe.   Treatment includes weight loss, nasal CPAP and removal of tonsils if enlarged. Uvulopharyngopalatoplasty (UVPP) is of dubious benefit. Tracheostomy may be indicated in severe cases. • Anaesthetic implications: ◗ of any predisposing cause. ◗ patients may not satisfy criteria for day-case surgery. ◗ sedative premedication may precipitate complete airway obstruction and should be avoided. If feasible, regional anaesthesia should be considered; if not, rapidly cleared anaesthetic agents should be used (e.g. propofol, desflurane).

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Obturator nerve block of the airway during induction of anaesthesia and tracheal intubation may be difficult. Tracheal extubation should only be when fully awake. ◗ patients are particularly sensitive to the depressant effects of sedatives and opioid analgesic drugs; airway obstruction, hypoventilation, hypoxia and carbon dioxide narcosis may readily occur postoperatively. ◗ patients are often nursed in ICU/HDU with nocturnal CPAP and maintenance of a 30-degree head-up tilt. Chung F, Memtsoudis SG, Ramachandran SK, et al (2016). Anesth Analg; 123: 452–73 ◗ maintenance

Obturator nerve block.  Performed to accompany sciatic nerve block or femoral nerve block, or in the diagnosis and treatment of hip pain. The obturator nerve (L2–4), a branch of the lumbar plexus, passes down within the pelvis and through the obturator canal into the thigh, to supply the hip joint, anterior adductor muscles and skin of medial lower thigh/knee.   With the patient supine and the leg slightly abducted, an 8-cm needle is inserted 1–2 cm caudal and lateral to the pubic tubercle, and directed slightly medially to encounter the pubic ramus. It is then withdrawn and redirected laterally to enter the obturator canal, and advanced 2–3 cm. If a nerve stimulator is used, twitches in the adductor muscles are sought. Increasingly performed under ultrasound guidance. After careful aspiration to exclude intravascular placement, 10–15 ml local anaesthetic agent is injected.   In an alternative approach, the leg is externally rotated and abducted and an 8–10-cm needle inserted behind the adductor longus tendon near its pubic insertion, and directed posteriorly and slightly cranially and laterally. 5–10 ml solution is injected at a depth of 2–3 cm. Occipital nerve blocks,  see Scalp, nerve blocks Octreotide. Long-acting somatostatin analogue, used in carcinoid syndrome and related GIT tumours and acromegaly. Also licensed for use in treating complications of pancreatic surgery. Has also been used in bleeding oesophageal varices, to reduce vomiting in palliative care, and in the management of chylothorax. Plasma levels peak within an hour of sc administration, and within a few minutes of iv injection. Half-life is 1–2 h. Lanreotide is a similar agent. • Dosage: ◗ 50  µg sc od/bd, increased to 200 µg tds if required (rarely up to 500 µg tds in carcinoid syndrome). ◗ 50–100  µg iv in carcinoid crisis, diluted to 10%–50% in 0.9% saline. ◗ 50  µg iv followed by 50 µg/h in bleeding varices. • Side effects: GIT upset, glucose intolerance, hepatic impairment. Oculocardiac reflex. Bradycardia following traction on the extraocular muscles, especially medial rectus. Afferent pathways are via the occipital branch of the trigeminal nerve; efferents are via the vagus. The reflex is particularly active in children. Bradycardia may be severe, and may lead to asystole. Other arrhythmias may occur, e.g. ventricular ectopics or junctional rhythm. Bradycardia may also follow pressure on or around the eye, fixation of facial fractures, etc. The reflex has been used to stop SVT with eyeball massage. Reduced by anticholinergic drugs administered as premedication or on induction of anaesthesia. If it occurs,

surgery should stop, and atropine or glycopyrronium should be administered.   Retrobulbar block does not reliably prevent the reflex; peribulbar block may be more effective. Local infiltration of the muscles has also been used. See also, Ophthalmic surgery Oculogyric crises,  see Dystonic reactions Oculorespiratory reflex.  Hypoventilation following traction on the external ocular muscles. Reduced respiratory rate, reduced tidal volume or irregular ventilation may occur. Thought to involve the same afferent pathways as the oculocardiac reflex, but with efferents via the respiratory centres. Heart rate may be unchanged, and the reflex is unaffected by atropine. ODAs/ODPs,  see practitioners

Operating

department

assistants/

Odds ratio.  Ratio of the odds of an event’s occurrence in one group to its odds of occurring in another, used as an indicator of treatment effect in clinical trials. For example, in a trial of PONV with two antiemetic drugs:

PONV No PONV

Drug A a c

Drug B b d

The odds of PONV with Drug A are a/c, and the odds with Drug B are b/d   The odds ratio is therefore a/c ÷ b/d = ad/bc   Harder to understand (but more useful mathematically) than other indices of risk commonly used. See also, Absolute risk reduction; Meta-analysis; Number needed to treat; Relative risk reduction ODIN,  Organ dysfunction and/or infection, see Logistic organ dysfunction system O’Dwyer, Joseph (1841–1898). US physician; regarded as the introducer of the first practical intubation tube in 1885, although the technique had been described previously by others, e.g. Kite. His short metal tube, used as an alternative to tracheostomy in diphtheria, was inserted blindly into the larynx on an introducer; the flanged upper end rested on the vocal cords. He mounted his tube on a handle for use with Fell’s resuscitation bellows in 1888; the Fell–O’Dwyer apparatus could be used for CPR or anaesthesia. Later modifications included addition of a cuff. [George Fell (1850–1918), US ENT surgeon] Baskett TF (2007). Resuscitation; 74: 211–14 Oedema.  Generalised or localised excess ECF. Caused by: ◗ hypoproteinaemia and decreased plasma oncotic pressure. ◗ increased hydrostatic pressure, e.g. cardiac failure, venous or lymphatic obstruction; salt and water retention (e.g. renal impairment, drugs, e.g. NSAIDs, oestrogens, corticosteroids). ◗ leaky capillary endothelium, e.g. inflammation, allergic reactions, toxins. ◗ direct instillation, e.g. extravasated iv fluids, infiltration. Several causes often coexist, e.g. hypoproteinaemia, portal hypertension and fluid retention in hepatic failure.

Oesophageal varices Characterised by pitting when prolonged digital pressure is applied, although fibrosis reduces this in chronic oedema. Generalised oedema occurs in dependent parts of the body, e.g. ankles if ambulant, sacrum if bed-bound. Treatment is directed at the cause. If localised, the affected part is raised above the heart. See also, Cerebral oedema; Hereditary angio-oedema; Pulmonary oedema; Starling’s forces Oesophageal contractility. Used as an indicator of anaesthetic depth and brainstem integrity. • Normal pattern of contractions: ◗ primary: continuation of the swallowing process; propels the food bolus down the oesophagus. ◗ secondary (provoked): caused by presence of food, etc., within the oesophageal lumen. Unrelated to swallowing. ◗ tertiary (spontaneous): non-peristaltic; function is uncertain. Measured by passing a double-ballooned probe into the lower oesophagus. The distal balloon is filled with water and connected to a pressure transducer; the other balloon (just proximal) may be inflated intermittently to study provoked contractions. • Altered by: ◗ anaesthesia: provoked contractions diminish in amplitude as depth increases, and spontaneous contractions become less frequent. Oesophageal contractility index ([70 × spontaneous rate] + provoked amplitude) is used as an overall measure of activity. Thought to be analogous to BP, heart rate, lacrimation and sweating during anaesthesia; i.e., suggestive of anaesthetic depth, but not reliable. Activity may be decreased by atropine and smooth muscle relaxants (e.g. sodium nitroprusside) and increased by neostigmine. ◗ brainstem death: spontaneous contractions disappear, and provoked contractions show a low-amplitude pattern. Has been used to indicate the presence or absence of brainstem activity in ICU, but its role is controversial. Presently not included in UK brainstem death criteria. See also, Anaesthesia, depth of Oesophageal obturators and airways. Devices inserted blindly into the oesophagus of unconscious patients to secure the airway and allow IPPV when tracheal intubation is not possible, e.g. by untrained personnel. They have been used in failed intubation. Consist of a cuffed oesophageal tube, often attached to a facemask for sealing the mouth and nose and preventing air leaks. The cuff reduces gastric insufflation and regurgitation but may not prevent it.   The epiglottis is pushed anteriorly, creating an air passage for ventilation. An ordinary tracheal tube may be used to isolate the stomach and improve the airway in a similar way. • Two main types are described: ◗ blind-ended cuffed tube, perforated level with the hypopharynx for passage of air. Inflation is through the tube and via the perforations to the lungs. ◗ open-ended tube, to allow gastric aspiration. Inflation is through a separate port of the facemask. If accidental tracheal placement occurs, IPPV may be performed through the tube. The above features have been combined in a double-lumen device (Combitube), which may be placed in either the

B

A

C

D Fig. 124 The Combitube (see text)  

oesophagus or trachea (Fig. 124). A distal cuff (15 ml) seals the oesophagus or trachea, whereas a proximal balloon (100 ml) seals the oral and nasal airways. IPPV may be performed through either tube depending on the device’s position; it enters the oesophagus in over 95% of cases initially and ventilation via the longer proximal tube (A) will result in pulmonary ventilation via the proximal openings (C). The shorter distal tube (B) may then be used for gastric suction via the distal opening (D). If the device is tracheal, IPPV may be achieved via tube B and opening D. Has been suggested as a suitable device for non-medical personnel (e.g. for CPR), although trauma is more common than with available alternatives (e.g. SADs). Oesophageal sphincter,  see Lower oesophageal sphincter Oesophageal stethoscope,  see Stethoscope Oesophageal varices. Dilated oesophagogastric veins occurring in portal hypertension, e.g. in hepatic cirrhosis; the veins represent one of the connections between the systemic and portal circulations. Account for up to a third of cases of massive upper GIT haemorrhage. Mortality is up to 30% if bleeding occurs, partly related to the underlying severity of liver disease. • Management: ◗ primary prophylaxis of variceal haemorrhage: treatment with non-selective β-adrenergic receptor antagonists e.g. propranolol or carvedilol is the management of choice. If β-blockade is contraindicated, endoscopic variceal band ligation should be considered. ◗ control of active variceal haemorrhage: - resuscitation and assessment (see GIT haemorrhage) as for acute hypovolaemia. Airway management is complicated by haematemesis and steps

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Oesophagus to avoid aspiration of blood and gastric contents must be taken. - prophylactic antibacterial drugs should be given. - vasoconstrictor therapy should be started as soon as possible and continued until haemostasis is achieved: - vasopressin 20 U over 15 min iv or its analogue terlipressin 2 mg iv followed by 1–2 mg 4–6hourly up to 72 h. Controls bleeding in 60%–70% of cases. - somatostatin 250 µg followed by 250 µg/h or its analogue octreotide 50 µg followed by 50 µg/h. - following successful treatment of the acute bleeding, endoscopic variceal band ligation is the treatment of choice. - if bleeding is uncontrollable, balloon tamponade using a Sengstaken–Blakemore tube should be attempted while awaiting transfer to a specialised centre, where early transjugular intrahepatic portosystemic shunting may be the most appropriate treatment. Tripathi D, Stanley AJ, Hayes PC, et al (2015). Gut; 64: 1680–704 Oesophagus. Tubular organ connecting the pharynx and stomach. Consists of a mucosal lining, surrounded by connective tissue and internal circular and external longitudinal muscle layers (the latter consisting of smooth muscle in the lower third, skeletal muscle in the upper third, both types in the middle third). Approximately 25 cm long in adults, it extends from the level of C6 and descends at the back of the mediastinum, passing through the diaphragm with the vagus and gastric nerves and left gastric vessel branches at the level of T10. Thus lies behind the trachea in the neck, with the recurrent laryngeal nerves alongside, within the pretracheal fascia (see Fig. 116; Neck, cross-sectional anatomy), and behind the trachea and heart in the mediastinum, passing anterior to the thoracic aorta and posterior to the left main bronchus and right pulmonary artery. Has a muscular sphincter at the proximal (upper) end, mostly formed by the cricopharyngeus muscle, and the lower oesophageal sphincter at the distal end.   Afferent and efferent nerve supply is mainly vagal via oesophageal plexuses, but also via sympathetic nerves.   Blood supply is via the inferior thyroid artery (upper part), bronchial arteries (thoracic part) and left gastric/ left inferior phrenic arteries (lower part including sphincter). Venous drainage is via azygos/hemiazygos veins (upper and lower parts) and left gastric vein (middle part).   Propels food from mouth to stomach by peristalsis (see Oesophageal contractility). See also, Achalasia; Cricoid pressure; Gastro-oesophageal reflux; Oesophageal varices; Swallowing; Thoracic inlet; Vagus nerve ‘Off-pump’ coronary artery bypass graft,  see Coronary artery bypass graft Ofloxacin.  Antibacterial drug, one of the 4-quinolones related to ciprofloxacin. Used for respiratory and genitourinary tract infections. • Dosage: 200–400 mg orally or iv (over 30–60 min) od/ bd. • Side effects: as for ciprofloxacin. Hypotension and thrombophlebitis may occur on iv administration.

Ohm’s law.  Current passing through a conductor is proportional to the potential difference across it, at constant temperature. Thus: voltage = current × resistance (i.e., V = IR). An analogous form exists for flow of a fluid: pressure = flow × resistance. [Georg S Ohm (1787–1854), German physicist] Old age,  see Elderly, anaesthesia for Oliguria. Reduced urine output; definition is controversial but usually described as under 0.5 ml/kg/h. Common after major surgery or in ICU. • Caused by: ◗ urinary retention, blocked catheter, etc. ◗ poor renal perfusion, e.g. hypotension, hypovolaemia, low cardiac output. Urine formation usually requires MAP of 60–70 mmHg in normotensive subjects. ◗ drugs, e.g. morphine causes vasopressin secretion. ◗ increased intra-abdominal pressure (e.g. abdominal compartment syndrome): the mechanism is unknown but ureteric stents do not prevent it, suggesting mechanisms other than ureteric compression. ◗ renal failure. • Management: ◗ exclusion of retention or blocked catheter. ◗ urinary and plasma chemical analysis (e.g. sodium, osmolality) is useful in distinguishing renal from prerenal causes (see Renal failure). Management is according to the underlying cause. Omeprazole.  Proton pump inhibitor used to reduce gastric acidity. A prodrug converted to its active form by the acidic conditions of gastric parietal cell canaliculi.   Effects last for up to 24 h after single dosage. • Dosage: 10–40 mg orally od. For reduction of risk from aspiration of gastric contents, 40 mg orally the night before, and 40 mg on the morning of surgery. May also be given iv: 40–80 mg over 40–60 min. • Side effects: uncommon and usually mild: diarrhoea, rash, headache, rarely dizziness, hepatic enzyme and haematological changes. Omphalocele,  see Gastroschisis and exomphalos Oncotic pressure  (Colloid osmotic pressure). Osmotic pressure exerted by plasma proteins, usually about 3.3 kPa (25 mmHg). Important in the balance of Starling forces, and movement of water across capillary walls, e.g. in oedema. Although related to plasma protein concentration, the relationship is thought to be nonlinear because of molecular interactions and effects of charge. See also, Intravenous fluids Ondansetron hydrochloride.  5-HT3 receptor antagonist, introduced in 1990 as an antiemetic drug following anaesthesia and chemotherapy. Does not affect dopamine receptors and unwanted central effects are rare, making it attractive compared with other antiemetics. Evidence suggests greater efficacy for treatment of PONV than for its prophylaxis. Has also been used to treat intractable pruritus following spinal opioids, and to prevent postoperative shivering, although evidence for its effectiveness in both of these is relatively weak. Only 70%–75% protein-bound. Undergoes hepatic metabolism and renal excretion. Halflife is 3 h.

One-lung anaesthesia

- prophylaxis: 4 mg slowly iv/im on induction, or 16 mg orally 1 h preoperatively. In children ≥1 month, 0.1 mg/kg slowly iv up to 4 mg. - treatment: 1–4 mg slowly iv/im (0.1 mg/kg up to 4 mg, in children). ◗ nausea/vomiting due to radiotherapy or chemotherapy: doses of 8–24 mg (5 mg/m2 in children, up to 8 mg) may be used, depending on the actual or anticipated severity of symptoms and the patient’s age. Because of the association with prolonged Q–T syndrome, a single iv dose should not exceed 16 mg (8 mg if >75 years) and should be infused over ≥15 min. Repeat doses should be ≥4 h apart.   An orodispersable film (4 mg) and a ‘melt’ preparation (4 and 8 mg) are also available; when placed on the tongue, they rapidly disintegrate into saliva, which can then be swallowed. • Side effects: headache, constipation, flushing sensation, hiccups, occasionally hepatic impairment, visual disturbances, rarely convulsions. Prolongation of ECG intervals, including heart block, has been reported. May reduce the analgesic efficacy of tramadol. Ondine’s curse.  Hypoventilation caused by reduced ventilatory drive, originally described following CNS surgery (classically to medulla/high cervical spine). Despite being awake, victims may breathe only on command, with apnoea when asleep. The term has also been applied to a congenital form of hypoventilation and to respiratory depression caused by opioid analgesic drugs. [Ondine, German mythological sea nymph; the curse of having to remember when to breathe, and thus being unable to sleep for fear of dying, was inflicted on her unfaithful husband by her father, King of the Sea] See also, Sleep-disordered breathing One-lung anaesthesia. Deliberate perioperative collapse of one lung to allow or facilitate thoracic surgery, while maintaining ventilation and gas exchange on the other side. Requires the use of endobronchial tubes or blockers. Commonly performed for surgery to the lungs, oesophagus, aorta and mediastinum, but most operations are possible without it (sleeve resection of the bronchus being a notable exception). Its main problem is related to hypoxaemia caused by theV̇/Q̇ mismatch produced, exacerbated by the lateral position used for most thoracic surgery. Peri­operative hypoxaemia increases postoperative risk of cognitive dysfunction, atrial fibrillation, renal failure and pulmonary hypertension. • Effects of lateral positioning on gas exchange: ◗ awake: - ventilation: FRC of the upper lung exceeds that of the lower lung, because of mediastinal movement to the dependent side, and pushing up of the lower hemidiaphragm by abdominal viscera. Thus the upper lung lies on a flatter part of the compliance curve (i.e., is less compliant) whereas the lower lung lies on the steep part of curve, i.e., is more compliant (Fig. 125a). In addition, the raised hemidiaphragm on the dependent side contracts more effectively. Thus most ventilation is of the lower lung. - perfusion: mainly of the lower lung because of gravity; i.e., is matched with ventilation.

(a)

(b) Upper lung Lower lung

Pressure

Volume

◗ PONV:

Volume

• Dosage:

Upper lung Lower lung Pressure

Fig. 125 Compliance curve for upper and lower lungs in the lateral position: (a) awake; (b) anaesthetised  

◗ anaesthetised:

- FRC of both lungs is reduced; the upper lung now lies on the steep part of the curve and the lower lung on the flatter part (Fig. 125b). Thus the upper (more compliant) lung is ventilated in preference to the lower (less compliant) lung. - perfusion is still mainly of the lower lung, i.e., V/̇ Q̇ mismatch occurs (usually of minor importance in normal patients, because both blood flow and ventilation usually differ by up to 10% between the two sides). ◗ one-lung anaesthesia: all ventilation is of the lower lung, whereas considerable perfusion is still of the upper lung. Thus significant shunt occurs in the upper lung, with V̇/Q̇ mismatch usual in the lower lung. - CO2 exchange increases via the lower lung; thus CO2 elimination is thought to be maintained if minute ventilation is unchanged. - degree of hypoxaemia is affected by: - side of operation: as the right lung is larger than the left, oxygenation is often better during left thoracotomy. - pre-existing state of the lungs: decrease in oxygenation is greatest in normal lungs, e.g. during non-pulmonary surgery. Conversely, contribution to oxygenation by the diseased, operative lung is usually reduced; thus the drop in arterial PO2 is smaller when it is collapsed. - FIO2: increases above 0.5 may not improve oxygenation, because pure shunt is not corrected by raising FIO2. - cardiac output: hypoxaemia worsens if cardiac output falls because of a decrease in the PO2 of mixed venous blood passing through the shunt. The situation is complicated by altered distribution of pulmonary blood flow caused by changes in cardiac output. - hypoxic pulmonary vasoconstriction: whether it is attenuated by use of anaesthetic agents, or whether it contributes any protection against shunt, is unclear. - ventilation strategy: the optimum tidal volume and level of PEEP are controversial. To prevent atelectasis in the dependent lung, large tidal volumes (e.g. 12 ml/kg) have been used without PEEP (as PEEP may reduce cardiac output or increase shunt through the uppermost lung, exacerbating hypoxaemia). However, an alternative and increasingly common strategy is to use low tidal volumes (e.g. 6–7 ml/kg) with moderate PEEP to prevent atelectasis while reducing the risk of causing volutrauma and ALI.

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Open-drop techniques - content of the collapsed lung: hypoxaemia worsens after about 10 min as contained O2 is absorbed. Arterial PO2 is increased by application of 5–7 cmH2O CPAP using O2, or by intermittent inflation, e.g. every 10–15 min. - surgery: e.g. leaning on mediastinum, reduction of venous return. Tying the uppermost pulmonary artery stops shunt to the uppermost lung. • Practical management: ◗ preoperative assessment as for thoracic surgery; patients particularly at risk during one-lung anaesthesia may be identified. ◗ close monitoring using oximetry and/or arterial blood gas interpretation. ◗ FIO2 is usually set to 0.4–0.5. ◗ surgical ligation of the pulmonary artery is performed early. ◗ management of acute desaturation includes: - increasing FIO2 to 1.0. - use of fibreoptic bronchoscopy to check tube position and clear secretions. - administration of O2 to the uppermost lung, e.g. with CPAP or intermittent inflation. - performing an alveolar recruitment manoeuvre on the dependent lung. - altering the ventilation strategy (i.e., changing tidal volume and/or PEEP). ◗ suction is applied to the collapsed lung before reinflation, to remove accumulated secretions. ◗ slow manual inflation is performed at the end of the procedure, to encourage expansion. The surgeon may request sustained pressures (e.g. 30–40 cmH2O) to test the integrity of the bronchial suturing. Lohser J, Slinger P, (2015). Anesth Analg; 121: 302–18 Open-drop techniques.  Common and convenient techniques for administering inhalational anaesthetic agents in the 1800s/early 1900s. The volatile anaesthetic agent (e.g. chloroform, diethyl ether, ethyl chloride) was dripped on to a cloth (originally a folded handkerchief) on the patient’s face from a dropper bottle. Concentration of agent depended on the rate of drop administration. Specially designed bottles and masks were later developed; the best-known mask is that of Schimmelbusch, although this was adapted from Skinner’s earlier model. Some incorporated channels for O2 insufflation, or gutters around the edge to catch liquid anaesthetic. [Curt Schimmelbusch (1860–1895), German surgeon; Thomas Skinner (1825–1906), Liverpool obstetrician] Operant conditioning. Type of learning in which voluntary behaviour is strengthened or weakened by rewards or punishments, respectively. May be involved in the development of certain behavioural aspects of pain syndromes. Has been used in chronic pain management, concentrating on behaviour secondary to pain instead of pain itself; now largely superseded by other behavioural therapies such as cognitive behavioural therapy. Operating department assistants/practitioners  (ODAs/ODPs). Non-medical anaesthetic support staff; the role arose from the requirements of military surgeons and anaesthetists for specialist non-nursing assistance during World War II, although ‘box carriers’ (so called because they carried the surgeon’s instruments in a box) were in use in the UK in the early 1800s. Specific training

in anaesthesia and surgery for ODAs without passage through the nursing training system was introduced in 1976, while the term ‘ODP’ was introduced in 1989, emphasising that adequately trained staff could equally come from nursing or traditional ODA backgrounds. Current training involves a 2-year diploma or 3-year degree course.   Compulsory registration of all ODPs was established in 2004. The professional body for ODPs is the College (formerly Association) of ODPs, an entity within the union UNISON; it has almost 5000 members and until 2015 published The Journal of Operating Department Practice (formerly Technic).   ODPs have an invaluable role in supporting most anaesthetic activity, e.g. preparing and ordering drugs and equipment, setting up the operating theatre for cases, helping to organise operating lists. They may also assist the surgical staff (including ‘scrubbing’) and the concept of ‘multiskilling’ supports their activity in various roles within the operating theatre suite and beyond, e.g. ICU, trauma teams. More extended practical roles are supported in some units (e.g. assisting at cardiac arrests, placing iv cannulae), although this is controversial. Ophthalmic nerve blocks. Performed for procedures around the eye, nose and forehead, and certain intraoral procedures. • Anatomy (see Fig. 79; Gasserian ganglion block): ◗ ophthalmic division of the trigeminal nerve (V1) is entirely sensory and passes from the Gasserian ganglion, where it divides into branches that pass through the superior orbital fissure: - lacrimal nerve: supplies the lateral upper eyelid and conjunctiva, lacrimal gland and skin of the lateral angle of the mouth. - frontal nerve: supplies the upper eyelid, frontal sinuses and anterior scalp via the supraorbital branch; upper eyelid and medial forehead via the supratrochlear branch. - nasociliary nerve: supplies the anterior dura, anterior ethmoidal air cells, upper anterior nasal cavity and skin of the external nose via the anterior ethmoidal branch; posterior ethmoidal and sphenoid sinuses via the posterior ethmoidal branch; medial upper eyelid, conjunctiva and adjacent nose via the infratrochlear branch; cornea, iris, ciliary body and dilator/sphincter pupillae via the long and short ciliary branches. Sympathetic fibres carried in short ciliary branches synapse in the ciliary ganglion ◗ supraorbital foramen, pupil, infraorbital notch, infraorbital foramen, buccal surface of the second premolar and mental foramen all lie along a straight line. • Blocks: ◗ supraorbital nerve: 1–3 ml local anaesthetic agent is injected at the supraorbital notch. ◗ supratrochlear nerve: 1–3 ml is injected at the superomedial part of the opening of the orbit. ◗ both of these nerves may be blocked by subcutaneous infiltration above the eyebrow. ◗ frontal nerve: 1 ml is injected at the central part of the roof of the orbit. ◗ anterior ethmoidal nerve: 2 ml is injected at the superomedial side of the orbit, at a depth of 3–4 cm. See also, Mandibular nerve blocks; Maxillary nerve blocks

Opioid-induced hyperalgesia Ophthalmic surgery.  Historically, first performed without anaesthesia and then under topical anaesthesia (e.g. by Koller), because of the eye’s accessibility and the disastrous effects of coughing during general anaesthesia. Subsequently, increasingly performed under general anaesthesia because of patients’ expectations and the ability to control intraocular pressure (IOP), and then, with the development of effective and safe eye blocks, local anaesthesia has been favoured again, especially in the elderly. Children (for strabismus repair) and the elderly (for cataract extraction) form the largest groups of patients. • Local anaesthesia: ◗ cornea and conjunctiva: 4% lidocaine (with or without adrenaline) or 2%–4% cocaine is instilled into the conjunctival sac. Cocaine is not used in glaucoma, as it dilates the pupil. ◗ peribulbar block or sub-Tenon’s block (retrobulbar block less commonly performed now because of associated complications). ◗ prevention of blepharospasm: infiltration between the muscles and bone parallel to the lower and lateral orbital margins from a point 1 cm behind the orbit’s lower lateral corner; alternatively, local anaesthetic may be injected above the condyloid process of the mandible. These injections are rarely required with large-volume modern regional techniques. ◗ sedation may be used. Close monitoring is required as the patient’s head is covered by drapes. Supplementary O2 should be delivered. • General anaesthesia: ◗ preoperatively: - preoperative assessment of children with strabismus for muscle disorders and MH susceptibility. Cataracts may occur in dystrophia myotonica, inborn errors of metabolism, chromosomal abnormalities, diabetes mellitus, corticosteroids therapy or following trauma. Lens subluxation may occur in Marfan’s syndrome and inborn errors, e.g. homocystinuria. The elderly should be assessed for other diseases, e.g. diabetes, hypertension (see Elderly, anaesthesia for). - drugs used in eye drops may be absorbed and active systemically, e.g. ecothiopate, timolol. - opioid premedication is usually avoided because of its emetic properties. Benzodiazepines are popular. ◗ perioperatively: - procedures include the above operations, repair of retinal detachment, vitrectomy, repair of eye injuries (see Eye, penetrating injury) and operations on the lacrimal system. - the airway is usually not easily accessible to the anaesthetist. - for children, considerations include those for paediatric anaesthesia, the very active oculocardiac and oculorespiratory reflexes, and the increased incidence of PONV after strabismus repair (thought also to be associated with traction on extraocular muscles). Atropine or glycopyrronium should be available; some advocate routine administration to all patients preoperatively or on induction of anaesthesia. Standard techniques are employed, with tracheal intubation or SAD and spontaneous or controlled ventilation. - for adults, standard agents and techniques are used. Control of IOP is usually achieved by iv induction, IPPV and hyperventilation, and use of a volatile

inhalational anaesthetic agent (for effects of specific drugs, use of sulfur hexafluoride, etc., see Intraocular pressure). Administration of iv acetazolamide may be required. Spontaneous ventilation may be suitable for extraocular procedures. A SAD is often used, because coughing and straining are less pronounced than with tracheal intubation. The oculocardiac reflex may still occur in adults. - systemic absorption of topical solutions, e.g. adrenaline, cocaine, may occur. - coughing, straining and vomiting may increase IOP; especially undesirable if the globe is open. ◗ postoperatively: avoidance of straining and vomiting is desirable. Postoperative pain tends to be mild. Opiates.  Strictly, substances derived from opium. Formerly used to describe agonist drugs at opioid receptors; the terms opioids and opioid analgesic drugs are now preferred. Opioid analgesic drugs.  Opium and morphine have been used for thousands of years; morphine was isolated in 1803 and codeine in 1832. Diamorphine was introduced in 1898, papaveretum in 1909. Other commonly used drugs include: pethidine (1939); methadone (1947); phenoperidine (1957); fentanyl (1960); alfentanil (1976); tramadol (1977); sufentanil (1984) and remifentanil (1997). Drugs with opioid receptor antagonist properties include pentazocine (1962), nalbuphine (1968), meptazinol (1971) and buprenorphine (1968).   May be divided into naturally occurring alkaloids (e.g. morphine, codeine), semisynthetic drugs (slightly modified natural molecules, e.g. diamorphine, dihydrocodeine) and synthetic opioids (e.g. pethidine, fentanyl, alfentanil, remifentanil). May also be classified according to their opioid receptor specificity and actions, or according to their onset and duration of action.   Each drug has slightly different effects on the body’s systems, but their general effects are those of morphine. The ‘purer’ drugs, e.g. fentanyl, alfentanil, sufentanil, do not cause histamine release, and may be used in very high doses with relative cardiostability, e.g. for cardiac surgery. In lower doses, they are used to provide intra- and postoperative analgesia, and to prevent the haemodynamic consequences of tracheal intubation and surgical stimulation. Also used as general analgesic drugs and for premedication, anxiolysis, cough suppression and treatment of chronic diarrhoea. See also, Opioid...; Spinal opioids Opioid detoxification,  see Rapid opioid detoxification Opioid-induced hyperalgesia.  Enhanced pain sensitisation in patients receiving therapy with opioid analgesic drugs. Has been observed in patients on chronic opioid therapy, in postoperative patients and in experimental models of pain. Some clinical studies have reported an increase in postoperative analgesic requirements and pain scores in patients given high-dose opioids at induction of anaesthesia, and small studies of healthy volunteers have implicated remifentanil infusion in the development of mechanical hyperalgesia. The mechanism is unclear but may involve central, descending and peripheral pain pathways, although those involving NMDA receptors in particular have been implicated. Weaning from opioids altogether, and rotation to different drug classes, have been suggested as management options. Fletcher D, Martinez V (2016). Br J Anaesth; 116: 447–9

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Opioid poisoning Opioid poisoning.  Presents with nausea and vomiting, respiratory depression, hypotension, pinpoint pupils and coma. Depressant effects are exacerbated by alcohol ingestion. Hypothermia, hypoglycaemia and, rarely, pulmonary oedema and rhabdomyolysis may occur. Convulsions may occur with pethidine, codeine and dextropropoxyphene. Drug combinations containing opioids include atropine–diphenoxylate for diarrhoea and paracetamol–dextropropoxyphene/ codeine/dihydrocodeine for pain. The former combination may cause convulsions, tachycardia and restlessness (hence it has been withdrawn from US and UK markets); the latter may cause delayed hepatic failure. • Management: ◗ supportive: includes gastric lavage, iv fluids, O2 therapy and IPPV. Activated charcoal may be helpful if oral opioids have been recently ingested. ◗ naloxone 0.4–2.0 mg iv repeated after 2–3 min as required to a total of 10 mg; infusion may be necessary as its duration of action is short. Respiratory depression due to buprenorphine may not be responsive. Boyer EW (2012). N Engl J Med; 367: 146–55 Opioid receptor antagonists.  Different types: ◗ pure antagonists, e.g. naloxone, naltrexone: antagonists at all opioid receptor subtypes. Methylnaltrexone is a peripherally acting mu antagonist, used as a treatment for opioid-induced constipation. ◗ agonist–antagonists: agonists at some receptors but antagonists at others, e.g.: - pentazocine: agonist at kappa and sigma, antagonist at mu receptors. - nalorphine: partial agonist at kappa and sigma, antagonist at mu receptors. - nalbuphine: as for nalorphine, but a less potent sigma agonist. ◗ partial agonists, e.g. buprenorphine, meptazinol (mu receptors); may antagonise mu effects of other opioids (e.g. morphine). Their main clinical use is to reverse effects of opioid analgesic drugs, e.g. in opioid poisoning. Those with agonist properties are also used as analgesic drugs; some have been used to reverse unwanted effects of other opioids (e.g. respiratory depression) while still maintaining analgesia. In practice, this is very difficult to achieve. Also used in diagnosis and treatment of opioid addiction. Receptorspecific compounds have been developed for research and identification of receptor subtypes.   Many result from modification or substitution of the side chain on the nitrogen atom of parent analgesic drugs, e.g. N-allyl group substitution for the N-methyl group (hence the name, nal…). Opioid receptors. Naturally occurring receptors to morphine and related drugs, isolated in the 1970s. Each is the product of a single gene. All are G protein-coupled receptors and activation results in opening of potassium channels and closure of voltage-gated calcium channels; this leads to membrane hyperpolarisation, reduced neuronal excitability and thus reduced nociceptive transmission. This effect is enhanced by reduction of cAMP by inhibition of adenylate cyclase. Found mainly in the CNS but also GIT; thought to be involved in central mechanisms involving pain and emotion. Three primary subgroups are now recognised (each subdivided into two or more putative subtypes), although others have been suggested in the past. More recently, data from transgenic mice lacking a single opioid receptor (e.g. MOP) have

called into question the validity of further subtype classification. • Subgroups: ◗ mu (MOP): - activation causes analgesia, respiratory depression, euphoria, hypothermia, pruritus, reduced GIT motility, miosis, bradycardia, physical dependence; i.e., the classic effects of morphine. - responsible for ‘supraspinal analgesia’; i.e., drugs act at brain level. - the mu1 receptor subtype is thought to be responsible for supraspinal analgesia; the mu2 for most of the other effects; and mu3 receptors have been identified on immune cells. - endogenous ligands: β-endorphins. - agonists: all opioid analgesic drugs. - partial agonists: buprenorphine, meptazinol (thought to be specific at mu1 receptors). - antagonists: nalorphine, nalbuphine, pentazocine. ◗ delta (DOP): - distributed throughout the CNS. Located presynaptically, they inhibit the release of neurotransmitters. - activation has been experimentally shown to produce analgesia and cardioprotection. - endogenous ligands: enkephalins. ◗ kappa (KOP): - activation causes analgesia, miosis, sedation, different sort of dependence. - responsible for ‘spinal analgesia’; i.e., drugs thought to act at spinal level. - endogenous ligand: dynorphin A. - agonists: experimental agents spiradoline and enadoline cause analgesia but adverse effects, including diuresis, sedation and dysphoria, preclude clinical use. Sigma receptors, previously considered opioid receptors, are not considered so now because the effects of their stimulation are not reversed by naloxone. They bind to phencyclidine and its derivatives, e.g. ketamine. All subtypes are antagonised by naloxone and naltrexone (mu and kappa more than delta).   The nociceptin/orphanin FQ peptide (NOP) receptor (previously termed the ‘orphan’ receptor) is related to the above receptors but its lack of sensitivity to naloxone makes it difficult to classify in the original opioid taxonomy. It is found throughout the brain and spinal cord, binds endogenous orphanin FQ, and produces antanalgesia supraspinally and analgesia at spinal level. McDonald J, Lambert DG (2015). BJA Educ; 15: 219–24 Opioids.  Substances that bind to opioid receptors; include naturally occurring and synthetic drugs, and endogenous compounds. Opium.  Dried juice from the unripe seed capsules of the opium poppy Papaver somniferum. Contains many different alkaloids, including morphine (9%–20%), codeine (up to 4%) and papaverine. Used for thousands of years as a recreational drug and for analgesia, especially in the Far East. Use as a therapeutic drug is rare now, purer drugs and extracts being preferred. Oral rehydration therapy.  Method of treating dehydration when mild or where facilities for iv fluid administration are lacking, e.g. in the community or developing countries. Particularly useful in gastroenteritis and in children; it has also been used in less serious

Organ donation burns. Various commercial mixtures exist; all contain glucose, the presence of which in the intestinal lumen facilitates the reabsorption of sodium ions and thus water. A simple version can be made by adding 20 g glucose (or 40 g sucrose because only half becomes available as glucose after ingestion), 3.5 g sodium chloride, 2.5 g sodium bicarbonate and 1.5 g potassium chloride per litre of water. Suitable solutions have been made by taking three 300-ml soft drink bottles of water and adding a level bottle capful of salt and eight capfuls of sugar, or 6 level teaspoons of sugar and 1 2 level teaspoon of salt dissolved in a litre of clean water. Orbeli effect. Increase in strength of contraction of fatigued muscle following sympathetic nerve stimulation. [Leon A Orbeli (1882–1958), Russian physiologist] Orbital cavity.  Cavity containing the eye and extraorbital structures. Roughly pyramidal with the apex posteriorly, its roof is formed by the orbital plate of the frontal bone (and lesser wing of the sphenoid posteriorly); its floor by the maxilla and zygoma; its medial wall by the frontal process of the maxilla and lacrimal bone anteriorly and orbital plate of the ethmoid and body of the sphenoid posteriorly; and its lateral wall by the zygoma and greater wing of the sphenoid (Fig. 126). Has three openings posteriorly: ◗ superior orbital fissure: transmits the third, fourth and fifth (the three branches of the ophthalmic division) cranial nerves. Also transmits branches of the middle meningeal and lacrimal arteries, ophthalmic veins and sympathetic fibres. ◗ inferior orbital fissure: transmits the maxillary nerve. ◗ optic canal: transmits the optic nerve and ophthalmic artery. The extraocular muscles are supplied by the third, fourth and sixth cranial nerves and have the following actions on the pupil: - superior rectus: elevates. - inferior rectus: lowers. - medial and lateral rectus: moves medially and laterally, respectively. - superior oblique: moves downwards and laterally. - inferior oblique: moves upwards and laterally.

Superior orbital fissure

Superior rectus Optic canal Superior oblique

Lateral rectus

Medial rectus Inferior orbital fissure

Inferior oblique

Fig. 126 Frontal view of right orbital cavity  

Inferior rectus

The rectus muscles attach posteriorly to a common tendinous ring surrounding the optic canal and part of the superior orbital fissure; they attach anteriorly to the sclera of the eyeball in front of the equator. The superior oblique muscle attaches posteriorly above the tendinous ring, hooking round the pulley-like trochlea before attaching posterolaterally to the eyeball, behind the equator. The inferior oblique attaches posteriorly to the floor of the orbit and attaches to the posterolateral surface of the eyeball, behind the equator. See also, Peribulbar block; Retrobulbar block; Skull; SubTenon’s block Oré, Pierre-Cyprien (1828–1889). French physician; Professor of Physiology at Bordeaux. Investigated blood transfusion and the effects of iv injection of drugs. Produced general anaesthesia with iv chloral hydrate in 1872, thus becoming the first to employ TIVA. Also treated tetanus with the drug. Orexins  (Hypocretins). Excitatory neuropeptides derived from an amino acid precursor, prepro-orexin, secreted from the lateral and posterior hypothalamus. Involved in arousal, maintenance of the waking state, neural control of food intake and neuroendocrine function, including energy metabolism and reproduction. Deficiency results in a form of narcolepsy. Organ donation.  Demand for organs outstrips supply; in the UK, >7000 people are on the national transplant waiting list, with >3000 transplants per year. In many countries, e.g. the USA, Germany and most of the UK, members of the public identify themselves as potential donors by joining a national registry (an ‘opt-in’ system). In some countries (e.g. Spain, Austria, Belgium), an ‘opt-out’ system operates in which permission is assumed unless specified otherwise; such a scheme results in the availability of more organs for transplantation, and this was introduced in Wales in 2015. • Organ donation may be: ◗ living, e.g. liver, kidney, bone marrow: the main issue concerns the undertaking of anaesthesia and surgery (with their attendant risks) by a healthy patient for altruistic reasons. ◗ dead, e.g. kidney, heart, lung, liver, small bowel, pancreas, skin and cornea: the main issue is around assent and the diagnosis of death: - donation after brainstem death. - donation after circulatory death (DCD): donors are classified according to the Maastricht system of 1995 into patients who: - arrive in hospital dead (I). - suffer a witnessed cardiac arrest outside hospital and in whom CPR is instituted within 10 min but is unsuccessful (II). - are awaiting cardiac arrest after withdrawal of treatment (III). - suffer cardiac arrest after brainstem death (IV). - suffer cardiac arrest as a hospital inpatient (V; added 2000). In the UK, about 40% of all donors are from DCD, mostly in group III. Treatment is withdrawn once the surgical team is ready; death is pronounced 2 min after asystole, and surgery to retrieve organs begins 5–10 min after asystole.

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Organe, Geoffrey Stephen William   Maintenance of tissue oxygenation, organ function and metabolic and cardiovascular stability should be pursued as for critically ill patients, until and during organ removal. Endocrine therapy with methylprednisolone, triiodothyronine and control of blood sugar with insulin may improve donor organ function. Citero G, Cypel M, Dobb GJ, et al (2016). Int Care Med; 42: 305–15 Organe, Geoffrey Stephen William  (1908–1989). English anaesthetist, born in India. A major influence on the development of anaesthesia in the UK and abroad, and involved in much research, particularly into the newly introduced neuromuscular blocking drugs. Professor of Anaesthesia at Westminster Hospital, London, and knighted in 1968. Organophosphorus poisoning.  An important worldwide cause of death due to acute poisoning, organophosphorus compounds are acetylcholinesterase inhibitors, commonly used as insecticides but also manufactured as chemical weapons. One, ecothiopate, is used in glaucoma. Those used in insecticides are usually ester, amide or thiol derivatives of phosphoric or phosphonic acids, or their mixtures. They may be absorbed via the GIT, lungs or skin, and are rapidly distributed to all tissues, especially liver and kidney. Half-lives vary from minutes to hours, with metabolism by oxidation, ester hydrolysis and combination with glutathione, and excretion in faeces or urine. • Toxic effects: ◗ peripheral enzyme inhibition: - phosphorylation of acetylcholinesterase: may be irreversible depending on the compound involved. Features are those of cholinergic crisis and include muscarinic effects (bronchospasm, sweating, increased secretions, abdominal cramps, bradycardia, miosis) and nicotinic effects (muscle twitching, weakness, hypertension and tachycardia). Enzyme ‘reactivation’ may be induced by pralidoxime if administered within 24–36 h. - phosphorylation of other enzymes, e.g. lipases, GIT enzymes. ◗ myopathic effects: weakness may occur within 24 h of poisoning, with recovery taking up to 3 weeks. Muscle paralysis in humans may occur after recovery from the initial cholinergic crisis, 24–96 h after poisoning. Mainly affecting proximal muscles, it is thought to involve postsynaptic dysfunction at the neuromuscular junction. ◗ delayed polyneuropathy: usually follows poisoning with non-insecticide compounds. Develops 2–4 weeks after the cholinergic crisis, with weakness and paraesthesiae. Pyramidal signs may be present. Recovery is variable. ◗ CNS effects: anxiety, tremor, confusion, coma and convulsions may occur, with EEG abnormalities. Respiratory failure may result from peripheral weakness, central depression and increased tracheobronchial secretions.   Diagnosis is based on history, tolerance to atropine therapy, acetylcholine assay and measurement of blood and urine organophosphorus and metabolite levels. • Treatment: ◗ supportive measures as for poisoning and overdoses in general. Care should be taken to avoid selfcontamination.

◗

drug therapy: - atropine 2 mg (20 µg/ml in children) iv each 5–10 min until dry flushed skin, dilated pupils and tachycardia. - pralidoxime 30 mg/kg diluted in 10–15 ml water, iv over 5–10 min. May be repeated up to twice if no improvement is seen within 30 min, up to a usual maximum of 12 g/24 h. Rarely, iv infusion of up to 500 mg/h may be required.

Orphanin FQ  (OFQ; nociceptin), See Opioid receptors Orthopaedic surgery. Anaesthetic considerations may be related to: ◗ indication for surgery: - trauma: presence of other injuries, risks of emergency surgery (e.g. aspiration of gastric contents). Adequate resuscitation is important preoperatively, especially in the elderly, e.g. following fractured neck of femur (NOF). Cases with risk of infection, ischaemia or nerve damage are particularly urgent. - hip/knee joint degeneration requiring replacement: problems are mainly related to co-morbidity associated with age or obesity, or both. - systemic musculoskeletal disease, e.g. rheumatoid arthritis, connective tissue diseases, muscular abnormalities. There may be a higher than normal incidence of MH susceptibility in young patients with musculoskeletal abnormalities. - congenital malformations: may be accompanied by other system involvement, e.g. cardiac lesions. - risk of massive hyperkalaemia following suxamethonium if neurological or muscle lesions are present. ◗ surgical procedure: - may involve repeated anaesthesia. - use of tourniquets. - use of methyl methacrylate cement (see Bone cement implantation syndrome). - problems of specific procedures, e.g. kyphoscoliosis. - increased risk of DVT and PE, especially after hip surgery; prophylactic measures should be taken. Fat embolism may occur after long bone fractures. Oscilloscope.  Device for displaying recorded signals, particularly those of high frequency and when analysis of their shape is required, e.g. ECG or arterial waveform. May also be used without the time-base to plot two signals with respect to each other, e.g. flow– volume loops.   The earliest oscilloscopes utilised a cathode ray tube to generate, accelerate and focus an electron beam on to a fluorescent screen, the beam visible as a bright dot. The signal potential was applied vertically across the beam, causing vertical deflection; a spatial reconstruction of the signal against time was then seen on the screen. The pattern could be made to persist by altering the characteristics of the fluorescent material, or by using a second cathode system. These are now termed analogue oscilloscopes, to distinguish them from the modern digital devices that have replaced them in medical practice. These utilise an analogue-to-digital converter to translate measured voltages (sampled at close, regular time intervals) into digital information that is then displayed

Ovarian hyperstimulation syndrome on liquid crystal or light-emitting diode panels. Digital devices benefit from greater portability and the option to apply processing algorithms to recorded signals (e.g. for S–T segment analysis and detection of arrhythmias). Oscillotonometer.  Obsolete device for indirect arterial BP measurement, using one (upper) cuff for occluding the brachial artery and a second (lower) cuff for detecting pulsations, often incorporated into a double cuff. Both cuffs are inflated by hand to above systolic BP and then allowed to deflate slowly, using a lever to switch the dial to a sensitive ‘indicator’ mode by which increased and then decreased oscillations of the dial needle indicate systolic and then diastolic pressures, respectively. At each of these points, the lever is used to return the indicator dial to a ‘recording’ mode to allow actual cuff pressure to be displayed. Has been replaced by automated devices, which employ similar principles but are more accurate, more reliable and easier to use. Osmolality and osmolarity.  Expressions of concentration of osmotically active particles in solution: ◗ osmolality = the number of osmoles per kilogram solvent. ◗ osmolarity = the number of osmoles per litre solution. ◗ osmoles = the mw of a substance divided by the number of freely moving particles liberated in solution. Thus 1 mmol of a salt that dissociates completely into two ions provides 2 mosmol. In the body, the solvent is water, with density 1 kg/l; thus osmolality and osmolarity are often used interchangeably, although proteins and fats in plasma give rise to a small difference.   Osmolality of plasma is maintained at 280–305 mosmol/ kg. Regulatory mechanisms include stimulation of thirst by osmoreceptors, baroreceptors and the renin/angiotensin system. Osmoreceptors also stimulate vasopressin release. Most contribution to plasma osmolality arises from sodium and its anions, glucose and urea; thus plasma osmolality may be estimated thus: mosmol kg = [glucose] + [urea] + (2 × [Na + ]) (all in mmol l). Alcohols, proteins, triglycerides and mannitol are not accounted for. Proteins usually contribute little because, despite their high concentration, few particles are liberated in solution because of their high mw.   Osmolality/osmolarity is determined by measuring ionic concentration with a flame photometer, measuring osmotic pressure or by employing the colligative properties of solutions (e.g. depression of freezing point, lowering of vapour pressure).   Urinary and plasma osmolality measurement is useful in investigating oliguria and renal failure. See also, Fluid balance; Hyperosmolality; Hypo-osmolality; Osmolar gap; Tonicity Osmolar gap (Osmolality gap). Difference between calculated and measured plasma osmolality. Normally 10–15 mosmol/kg; increased in the presence of lowmolecular-weight substances not included in the formula for calculating plasma osmolality, e.g. alcohols, mannitol, glycine (in the TURP syndrome). May also be applied to urine osmolality, e.g. to indicate the presence of osmotically active substances such as ammonium ions.

Osmoreceptors. Cells in the anterior hypothalamus, outside the blood–brain barrier; respond to changes in plasma osmolality. Control thirst and secretion of vasopressin, possibly via separate groups of osmoreceptors. Osmosis. Movement of solvent molecules across a semipermeable membrane from a dilute solution to a concentrated one, tending to equalise the concentrations on both sides. Thus water moves across cell membranes from the ECF following dextrose infusion, once the dextrose has been metabolised. Similarly, water in very hypotonic iv fluids may move into red blood cells after infusion, causing haemolysis. Osmotic clearance,  see Clearance, osmotic Osmotic diuretics,  see Diuretics Osmotic pressure.  Pressure required to prevent movement of solvent molecules by osmosis across a semipermeable membrane. equals

nRT as for the ideal gas law, V

where n = number of particles   R = universal gas constant   T = absolute temperature   V = volume. Thus proportional to the number of osmotically active particles per unit volume, not mw. Ideal ionic solutions dissociate completely in solution, whereas in the body incomplete dissociation and interactions between ions result in lower osmotic pressure than predicted. Plasma osmotic pressure is approximately 7.3 atmospheres. See also, Oncotic pressure; Osmolality and osmolarity; Tonicity Ouabain. Plant-derived cardiac glycoside, traditionally used as an arrow poison in East Africa. Poorly absorbed from the GIT and administered iv. Faster acting than digoxin; thus was used when rapid action is required. No longer commercially available in the UK. Outreach team.  Similar in role to the medical emergency team: improving the identification and care of acutely ill patients throughout hospitals but especially on general wards. Usually nurse-led, but may also contain experienced medical and physiotherapy staff, often from ICUs, who may provide the following services: rapid response to acutely ill patients in general ward areas; critical care education for ward clinicians; facilitation of early admission to ICU/HDU; early recognition of patients for whom CPR and/or ICU admission is inappropriate; and early post-ICU follow-up. Referral criteria include specific clinical scenarios or the results of early warning scores. Although popular and widely adopted, there is little robust evidence that such teams improve hospital mortality. Goldhill DR (2005). Br J Anaesth; 95: 88–94 See also, Acute life-threatening events—recognition and treatment Ovarian hyperstimulation syndrome. Condition caused by pharmacological stimulation of the ovaries with human chorionic gonadotropin (hCG) in assisted conception programmes. Characterised by ovarian enlargement,

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Overdoses pleural effusion, raised haematocrit and white blood cell count, oliguria, acute kidney injury, hepatic impairment and ascites; the last in particular may be massive and unrelenting. Clinical features range from abdominal discomfort/swelling and nausea/diarrhoea to hypovolaemic shock, renal failure and ALI. DVT may also occur. Mild symptoms occur in up to a quarter of cases of induced ovulation, whereas the severe form occurs in 1%–2%. Prevented by use of gonadotropin-releasing hormone agonists instead of hCG.   Treatment is mainly supportive, with correction of hypovolaemia, careful attention to fluid balance and correction of metabolic disturbances. DVT prophylaxis is recommended. Abdominal paracentesis and pleural drainage are usually performed in severe cases; ultrafiltration and re-infusion of the ascitic fluid iv have been used to replace the protein-rich fluid otherwise lost.

A Absorbance

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B

400

Oxpentifylline,  see Pentoxifylline Oxycodone hydrochloride.  Opioid analgesic drug, described in 1916. Oral preparations are twice as potent as oral morphine due to higher oral bioavailability. Intravenous oxycodone is roughly equivalent to iv morphine. • Dosage: initially 5 mg orally 4–6-hourly, or 10 mg slowrelease 12-hourly, increased to a maximum of 400 mg/ day. May also be given sc/slowly iv: 1–10 mg 4-hourly. Also available as suppositories (as the pectinate) by special order.

600

700

800

900

Wavelength (nm)

Overdoses,  see Poisoning and overdoses Oximetry. Determination of arterial O2 saturation of haemoglobin (SaO2) by measuring absorbance of light by blood. Described in 1934 using open blood vessels, and in 1940 using ear/hand probes, but the technique was cumbersome and difficult to perform. Modern pulse oximeters became widespread from the 1980s following advances in microchip technology, allowing manipulation of the recorded signal. Included in the UK/Ireland minimal monitoring standard for anaesthesia since 1987.   Relies on the principle that absorbance of light energy by haemoglobin varies with its level of oxygenation. Oxygenated and deoxygenated haemoglobin (HbO and Hb, respectively) have different absorbance spectra (Fig. 127). Isosbestic points occur where the lines cross. Thus comparison of absorbance at different wavelengths allows estimation of the relative concentrations of HbO and Hb (i.e., SaO2). Earlier machines used two wavelengths, including one isosbestic point as a reference; modern pulse oximeters may use two or more wavelengths, not necessarily including an isosbestic point.   Blood gas machines estimate SaO2 from arterial samples, whereas pulse oximeters read from ear or finger probes measuring light passing through tissue. Analysis of reflected light has also been used to determine SaO2; surface probes have been developed that may be stuck on to skin at any site, e.g. the head of a fetus. Other applications/derivations include retinal oximetry, in which a digital camera image of the retina is split according to wavelength and analysed for HbO/Hb components, and near infrared spectroscopy.   Oximeters are calibrated using data measured from human volunteers; saturations 5 U and following ephedrine administration. Severe hypotension may occur when oxytocin is given to patients with cardiac disease. ◗ severe hyponatraemia has followed prolonged infusion if diluted in dextrose solutions, exacerbated by a direct antidiuretic effect of the hormone itself. ◗ rashes, nausea, allergic reactions.

P P50,  see Oxyhaemoglobin dissociation curve P value,  see Probability P wave. Component of the ECG representing atrial depolarisation. Normally positive (i.e., upwards) in lead I, and best seen in leads II and V1 (see Fig. 60b; Electrocardiography). Maximal amplitude is normally 2.5 mm in lead II, and its duration 0.12 s (three small squares). In right atrial enlargement, the P wave is tall and peaked (P pulmonale); in left atrial enlargement, it is wide and notched (P mitrale). See also, P–R interval PA(A)s,  see Physicians’ assistants (anaesthesia) Pacemaker cells.  Cardiac muscle cells that undergo slow spontaneous depolarisation to initiate action potentials. Their activity results from a slow decrease in membrane potassium ion permeability, resulting in a gradual increase in intracellular calcium (via T-type calcium channels). Rate of discharge depends on the slope of phase 4 depolarisation, resting membrane potential and threshold potential. Pacemaker cells exist in the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His and ventricular cells. Spontaneous rates of discharge for the different sites: SA node 70–80/min, AV node 60/min, His bundles 50/min and ventricular cells 40/min. Impulses from the faster SA node usually reach and excite the slower pacemaker cells before the latter can discharge spontaneously. See also, Heart, conducting system Pacemakers.  Devices implanted subcutaneously, usually outside the thorax, that provide permanent cardiac pacing (to distinguish them from temporary pacing devices).   Modern devices consist of a titanium casing, containing the pulse generator and lithium iodide battery (the latter lasting >10 years). Electrodes are usually unipolar; i.e., one intracardiac electrode, with current returning to the pacemaker via the body. The heart electrode is usually endocardial, passed via a central vein; epicardial electrodes have been used. Leads may be steroid-eluting to reduce inflammation at the site of contact. Modern pacemakers are checked and adjusted via radiofrequency programming without requiring removal, and recorded data downloaded for analysis of cardiac function.

  Indicated if an arrhythmia is associated with syncope, dizziness and cardiac failure, e.g. in sick sinus syndrome, heart block or post-MI. Prophylactic use is controversial.   A generic pacemaker code identifies function (Table 38), the first three positions indicating basic pacing function. Thus VVI denotes ventricular pacing and sensing, with inhibition of pacing if any spontaneous ventricular complex occurs (e.g. as would apply in temporary transvenous pacing). DDD denotes pacing and sensing of both chambers, with inhibition or triggering to maintain sequential atrial and ventricular contraction, allowing spontaneous activity if it occurs. Rate modulation implies the ability to alter the heart rate in response to the patient’s level of activity; rate-adaptive devices respond to physiological parameters normally associated with changes in heart rate (e.g. body movement, Q–T interval, respiration, temperature, pH, myocardial contractility, haemoglobin saturation) by increasing the pacing rate. The fifth position is allocated to multisite pacing, which refers to stimulation of different sites either within one chamber (e.g. right ventricle) or within two chambers of the same type (e.g. both ventricles). With the development of implantable cardioverter defibrillators, much of the latter functions are covered within the defibrillator codes (see Defibrillators, implantable cardioverter). • Anaesthesia for patients with pacemakers: ◗ preoperatively: - preoperative assessment is particularly directed towards coexisting cardiovascular disease. - pacemaker type and indication are ascertained. Ideally patients should carry a European Pacemaker Patient identification card which provides all necessary details. Pacemakers are usually checked regularly (e.g. every 3 months). - if pacing spikes occur on the ECG before all or most beats, heart rate is pacemaker-dependent. - although traditional advice was to convert older demand pacemakers to fixed rate by placing a magnet over the pulse generator, this is no longer recommended outside specialist cardiac pacing units because the effect on the device’s programming is unpredictable. - CXR: pulse generator and lead position may be identified. ◗ perioperatively: - potential electrical interference or pacemaker damage by diathermy is more likely if the latter

Table 38 North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group generic pacemaker code  

Position 1: chamber paced

Position 2: chamber sensed

Position 3: response

Position 4: rate modulation

Position 5: multisite pacing

0 = None A = Atrium V = Dual D = Dual

0 = None A = Atrium V = Ventricle D = Dual

0 = None T = Triggered I = Inhibited D = Dual

0 = None R = Rate modulation

0 = None A = Atrium V = Ventricle D = Dual

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Packed cell volume is applied near the device. Sensing may be triggered, with resultant chamber inhibition, or arrhythmias induced. Diathermy may also reprogramme the pacemaker to a different mode. - if diathermy must be used, risks are reduced by using bipolar diathermy, or placing the plate distant from the pacemaker if unipolar diathermy is used. Current should not be applied across the chest, and its strength and duration of use should be minimal. - care should be taken with CVP/pulmonary artery catheters because they may dislodge the electrodes. - temporary pacing facilities (or non-invasive transthoracic pacing) and an external defibrillator should be available. - isoprenaline may be required if pacemaker failure occurs. - MRI may be hazardous because the pacemaker may be switched to asynchronous mode, may fail altogether or may move within the chest. ◗ postoperative pacemaker checking may be required. Healey JS, Merchant R, Simpson C, et al (2012). Can J Anaesth; 59: 394–407 Packed cell volume,  see Haematocrit PADP,  Pulmonary artery diastolic pressure, see Pulmonary artery pressure Paediatric Advanced Life Support (PALS). Course set up in the USA by the American Heart Association and the American Academy of Pediatrics. Intended for healthcare professionals caring for acutely ill children (e.g. those working in paediatric, anaesthetic, intensive care and emergency departments). Course objectives include: ◗ recognition of the infant or child at risk of cardiopulmonary arrest and the application of strategies for its prevention. ◗ identification of the cognitive and psychomotor skills necessary for resuscitating and stabilising the neonate, infant or child in respiratory failure, shock or cardiopulmonary arrest (e.g. drug dosages, airway and ventilation techniques, identification of normal and abnormal cardiac rhythms, defibrillation, vascular access). The course is predominantly practical with an emphasis on ‘hands-on’ training. Technical skills and cognitive processes are first taught separately in small group sessions. Practical application of these skills and knowledge in critical situations is then emphasised by using case presentations. See also, Advanced Paediatric Life Support Paediatric anaesthesia.  Main considerations are related to the anatomical and physiological differences between adults and children, especially neonates (defined as 1 year

3.0–3.5 4.0–4.5 (Age in years ÷ 4) + 4.5

Weight in kg + 6 (Weight in kg ÷ 2) + 8 (Age in years ÷ 2) + 12

(Weight in kg + 6) × 1.2 (Weight in kg ÷ 2) + 9 (Age in years ÷ 2) + 15

Neonate (>2 kg) 6 months to 1 year >1 year

2.5–3.0 3.0–4.0 (Age in years ÷ 4) + 3.5

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Paediatric intensive care children older than 3 months. Below this, tracheal intubation and IPPV are traditionally performed, although SADs are preferred by some. ◗ for IPPV using a T-piece, the following fresh gas flows have been suggested, producing slight hypocapnia: - 10–30 kg: 1000 ml + 100 ml/kg per min. - >30 kg: 2000 ml + 50 ml/kg per min. Set minute volume should equal twice fresh gas flow. ◗ routine monitoring, including temperature measurement. ◗ anaesthetic rooms and operating theatres should be warmed. Warming blankets and reflective coverings should also be used, with humidification of inspired gases. ◗ tracheal extubation may be performed with the child awake or anaesthetised, depending on the clinical context. ◗ emergence phenomena such as laryngospasm and agitation/delirium may occur; the latter is particularly common after sevoflurane anaesthesia and in preschool age children. ◗ a multimodal approach to postoperative analgesia is used, where possible combining regional techniques (e.g. caudal analgesia), paracetamol, NSAIDs and opioid analgesic drugs (e.g. morphine or fentanyl). Intravenous opioids may be administered via nursecontrolled analgesia. Ketamine is often useful in severe postoperative pain, and may be added to morphine infusions. Codeine was previously widely used in children, but this has been restricted since 2013 because of the risk of excessive sedation/respiratory depression; it is now contraindicated in children 3 years; prophylactic antiemetic drugs (e.g. ondansetron, dexamethasone) are routinely given. • Other specific problems are related to the procedure performed, e.g.: ◗ repair of congenital defects, e.g. tracheo-oesophageal fistula, pyloric stenosis, gastroschisis, diaphragmatic hernia, congenital heart disease. ◗ related to trauma. ◗ ENT, dental and ophthalmic surgery. Paediatric intensive care.  Classified into levels 1, 2 and 3, primarily on the basis of interventions undertaken. Level 1 is high dependency care; level 3 is almost always provided in tertiary paediatric centres. In general, differs from adult intensive care by virtue of anatomical and physiological differences between adults and children (see Paediatric anaesthesia) and the range of conditions seen. • Main clinical problems encountered include: ◗ acute respiratory failure: - upper airway obstruction: - neonates: choanal atresia, congenital facial deformities, laryngeal/tracheal abnormalities. - infants/children: inhaled foreign body, tonsillar/ adenoidal hypertrophy, croup, epiglottitis and angio-oedema. - lung disorders: - neonates: meconium aspiration, respiratory distress syndrome, diaphragmatic hernia, pneumothorax, chest infection. - infants/children: pneumonia, asthma, bronchiolitis, cystic fibrosis, congenital heart disease, trauma, near-drowning, burns.

- in neonates, respiratory impairment may result in the development of a persistent fetal circulation. ◗ neurological disease: - neonates: birth asphyxia, central apnoea, convulsions. - infants/children: meningitis, encephalitis, status epilepticus, Guillain–Barré syndrome. ◗ trauma: the leading cause of death in children under a year old and the third leading cause in older children (after sudden infant death syndrome and congenital abnormalities). Non-accidental injury must always be considered. - TBI occurs in 50% of cases of blunt trauma. A modified Glasgow coma scale is used for assessment; otherwise, management is along similar lines to that of adults. - spinal cord injury and thoracic/abdominal trauma is usually caused by road traffic accidents. ◗ poisoning and overdoses. • Specific attention must be paid to: ◗ smaller equipment, drug doses and fluid volumes; specialised equipment. ◗ nutrition and electrolyte/fluid balance. ◗ temperature regulation. ◗ sedation and analgesia. ◗ educational and psychological needs. ◗ the risk of retinopathy of prematurity in neonates. In 1997, the Department of Health recommended that level 3 paediatric intensive care should be primarily delivered in lead centres supported by district general hospitals (capable of initiating intensive care), major acute general hospitals (large adult ICUs already managing critically ill children at level 2 or 3) and specialist hospitals (e.g. those caring for children with burns or requiring cardiac or neurosurgery). Each centre must comply with specific standards relating to training, equipment, the experience of medical and nursing staff, access to specialist services and advice, treatment protocols, facilities for families and audit. Regional paediatric retrieval teams have also been established.   Overall mortality ranges from 5% to 10% depending on admission criteria. Scoring systems such as the paediatric trauma score, injury severity score and paediatric risk of mortality score attempt to predict outcome and allow audit of care within and between units. See also, Brainstem death; Cardiopulmonary resuscitation, neonatal; Cardiopulmonary resuscitation, paediatric; Necrotising enterocolitis Paediatric logistic organ dysfunction score (PELOD). Scoring system for the severity of multiple organ dysfunction in paediatric intensive care. Based on 12 variables relating to six organ systems (neurological, cardiovascular, renal, respiratory, haematological and hepatic). Has been used as daily indicator of organ dysfunction. The modified PELOD-2 score takes account of mean arterial pressure and lactaemia while dispensing with hepatic dysfunction. Leteurtre S, Duhamel A, Salleron J, et al (2013). Crit Care Med; 41: 1761–73 Paediatric risk of mortality score (PRISM). Scoring system used in paediatric intensive care to help predict mortality. Originally used weighted scores for 14 variables related to acute physiological status; the latest version (PRISM III) has 17 and includes additional risk factors,

Pain management including acute and chronic diagnosis. Has been validated for most categories of paediatric ICU. Pollack MM, Holbkov R, Funai T, et al (2016). Pediatr Crit Care Med; 17: 2–9 Paediatric trauma score.  Trauma scale designed to allow triage of paediatric patients. Six variables (weight, patency of airway, systolic BP, level of consciousness, presence of skeletal injury and skin injuries) attract scores of 2 (normal), 1 or −1 (severely compromised); scores under 8 indicate increased morbidity and mortality and require referral to a paediatric trauma centre. PAF,  see Platelet-activating factor Pain. Classically defined as an unpleasant sensory and emotional experience resulting from a stimulus causing, or likely to cause, tissue damage, or expressed in terms of that damage. Pain is a subjective experience that can be influenced by various emotional factors, making pain evaluation difficult. Chronic pain is often referred to as pain lasting >3 months (see Pain, chronic). See also, Allodynia; Dysaesthesia; Hyperaesthesia; Hyperalgesia; Hyperpathia; Hypoalgesia; Myofascial pain syndromes; Nociception; Pain, neuropathic; Pain clinic; Pain management; Postoperative analgesia Pain, central.  Neuropathic pain resulting from damage to the central nervous system. May be spontaneous (either continuous or paroxysmal) or evoked by nociceptive stimuli. Usually burning in nature. Most commonly follows a stroke anywhere in the spinothalamic pathway but especially involving the thalamus (hence formerly called thalamic syndrome). Tends to occur within 6 months of the stroke. Proven treatments include amitriptyline, selective serotonin reuptake inhibitors and lamotrigine. Intravenous lidocaine can produce temporary analgesia. Opioid analgesic drugs are largely ineffective. Deep brain stimulation may be effective in drug-resistant patients. Klit H, Finnerup NB, Jensen TS (2009). Lancet Neurol; 8: 857–68 See also, Pain, neuropathic Pain, chronic.  Persistent or recurring pain lasting longer than 3 months. Diagnoses can be classified as chronic: ◗ cancer pain. ◗ postsurgical or post-traumatic pain. ◗ neuropathic pain. ◗ headache or orofacial pain. ◗ visceral pain. ◗ musculoskeletal pain. ◗ primary pain (not fitting into the other categories, e.g. chronic widespread pain). Treede RD, Rief W, Barke A, et al (2015). Pain; 156: 1003–7 See also, Analgesic drugs; Pain evaluation; Pain management; Pain, neuropathic; Pain pathways; Postoperative pain Pain clinic.  Outpatient clinic run by consultants (often anaesthetists) with a special interest in the management of chronic pain. Its role includes diagnosis of the underlying condition and management directed at reducing subjective pain experiences, reducing drug consumption, increasing levels of normal activity and improving quality of life. Requires appropriate facilities for consultation and interventions, which may include drugs, nerve blocks,

surgical procedures, physiotherapy and psychological programmes. Ideally, services are multidisciplinary and include anaesthetists, physicians, psychologists, specialist nurses, occupational therapists, pharmacists and physiotherapists. Primary referrals to the clinic are usually from general practitioners or hospital consultants. See also, Pain, chronic; Pain management Pain evaluation. The gold standard of pain assessment is patient self-reporting because pain is a subjective experience. Should include exploration of the pain’s characteristics, duration, location, intensity, time relations, any modifying factors (e.g. food, exercise) and associated symptoms. • Methods used: ◗ acute pain, e.g. postoperative: - self-reported assessment of pain, e.g. linear analogue scale, discrete rating scales (numerical or verbal rating scale) indicating the degree/severity of pain. Specific image-based scales have been used in children (e.g. Wong-Baker faces scale, consisting of happy/unhappy cartoon faces). - behavioural assessment, used in patients unable to self-report, e.g. behavioural pain scale in sedated critically unwell patients, FLACC (face, legs, activity, cry, consolability scale) in paediatrics, Abbey Pain Scale in patients with dementia and unable to verbalise. ◗ chronic pain: - characterisation of pain plus examination/ investigation as appropriate. - linear analogue/rating scales as above. - more complicated questionnaires that may include evaluation of disability, affect and the pain experience are often used (e.g. Brief Pain Inventory, McGill questionnaire). Functional MRI allows imaging of pain pathways and the processes involved in pain perception. [Donna Lee Wong (1948–2008), US paediatric nurse; Connie Baker, US child life specialist; Jennifer Abbey, Australian nurse] Pain management. Acute pain, e.g. postoperative, is usually treated with systemic analgesics and regional techniques (see Postoperative analgesia). • Chronic pain management may involve the following, after pain evaluation: ◗ simple measures, e.g. exercise, heat and cold treatment, vibration. ◗ systemic drug therapy: - analgesic drugs: different drugs, dosage regimens and routes of administration may be chosen, depending on the severity and temporal pattern of the pain, and efficacy and side effects of the drugs. Drugs used range from paracetamol and mild NSAIDs to opioid analgesic drugs. The latter are usually reserved for severe pain of short duration, or pain associated with malignancy. Implantable devices may be used for intermittent iv, epidural or subarachnoid injection or continuous infusion of opioids. - other drugs used include: - psychoactive drugs, e.g. antidepressant drugs, anticonvulsant drugs (e.g. pregabalin, gabapentin, carbamazepine). Of these, amitriptyline, pregabalin and duloxetine are suitable first-line agents for chronic/neuropathic pain.

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Pain, neuropathic - corticosteroids, either by local injection or oral therapy. Often injected with local anaesthetic agents, e.g. epidurally for back pain. - muscle relaxants, e.g. baclofen, dantrolene; may be useful if muscle spasm is problematic. - others, e.g. antimitotic drugs, calcitonin in bony pain, β-adrenergic receptor antagonists, clonidine. ◗ local anaesthetic nerve blocks: may be diagnostic, prognostic (to allow assessment before destructive lesions) or therapeutic. Include: - injection of trigger points in myofascial pain syndromes. - facet joint injection. - caudal analgesia, epidural anaesthesia, spinal anaesthesia. - paravertebral nerve blocks. - sympathetic nerve blocks, e.g. stellate ganglion, coeliac plexus and lumbar sympathetic blocks, iv guanethidine block. ◗ neurolytic procedures: usually reserved for severe pain associated with malignancy, because relief may not be permanent and severe side effects may occur, e.g. anaesthesia dolorosa. X-ray guidance is usually employed to aid percutaneous neurolysis. Methods include: - regional techniques as above, using phenol or absolute alcohol. - extremes of temperature, e.g. cryoprobe, radio­ frequency probe. The latter delivers a highfrequency alternating current, producing up to 80°C heat. It is used at peripheral nerves, facet joints, dorsal root ganglia and trigeminal ganglion, and for percutaneous cordotomy. - surgery: includes peripheral neurectomy, dorsal rhizotomy or lesions in the dorsal root entry zones (DREZ), commissurotomy (sagittal division of the spinal cord), mesencephalotomy and thalamotomy. ◗ electrical stimulation: - TENS and electroacupuncture. - spinal cord stimulation. - stimulation of deep brain structures has also been used, e.g. via electrodes implanted in the periven­ tricular grey matter or thalamus. ◗ acupuncture. ◗ psychological techniques, e.g. psychotherapy, cognitive behavioural therapy, operant conditioning, hypnosis, biofeedback, relaxation techniques. ◗ physiotherapy and graded exercise programmes. ◗ multidisciplinary pain management programmes. The World Health Organization has suggested a ‘pain ladder’ for cancer pain, which is often used as a guide for managing non-cancer pain: mild pain is treated by a nonopioid ± adjuvant; moderate pain by a mild opioid ± non-opioid ± adjuvant; and severe pain with a strong opioid ± non-opoid ± adjuvant. Pain, neuropathic.  Chronic pain arising from a lesion or disease of the somatosensory system. Affects ~8% of the UK population and is more common in women. May be: ◗ peripheral: - diabetic neuralgia. - trigeminal neuralgia. - complex regional pain syndrome. - immune-mediated neuralgia e.g. due to Guillain–Barré syndrome, chronic inflammatory demyelinating neuropathy.

- infection-related eg. postherpetic neuralgia, HIVassociated sensory neuropathy - chemotherapy-induced neuropathy. ◗ central: - post-stroke pain (See also, Pain, central). - multiple sclerosis. - post-spinal cord injury. Signs and symptoms are diverse but often include reduced thermal or mechanical sensation in the area supplied by the affected nerve, or hyperalgesia and dynamic allodynia.   Although notoriously difficult to treat, management usually consists of first-line agents such as anticonvulsant drugs (e.g. gabapentin, carbamazepine) and antidepressant drugs (e.g. amitriptyline, duloxetine). Early referral to specialist multidisciplinary teams should be a priority, for consideration of further assessment and other treatment options, e.g. topical agents (capsaicin or lidocaine patches) or interventional techniques (e.g. spinal cord stimulation). Opioids are usually only a third-line treatment option in neuropathic pain. Finnerup NB, Attal N, Haroutounian S, et al (2015). Lancet Neurology; 14: 162–73 See also, Pain evaluation; Pain management; Pain pathways Pain, paradoxical. Term describing pain that does not respond to opioid analgesic drugs in the usual way. Typically described in patients with cancer pain on large doses of analgesics, especially opioid analgesic drugs. Now thought to represent opioid-induced hyperalgesia rather than a distinct entity itself. Pain pathways. Most pain arises from stimulation of specialised receptors (mechanoreceptors for touch, thermoreceptors for temperature and chemoreceptors for chemical stimulation) on specific primary sensory neurons (nociceptors) that are widely distributed in the skin and musculoskeletal system. Myelinated Aδ fibres convey sharp pain sensation from thermo- or mechanoreceptor stimulation and are responsible for rapid pain transmission and reflex withdrawal. Receptors responding to pressure, heat, chemical substances (e.g. histamine, prostaglandins, acetylcholine) and tissue damage (polymodal receptors) are associated with unmyelinated C-fibre endings, and are responsible for dull pain sensation and immobilisation of the affected part. • Afferent impulses pass centrally thus: ◗ first-order neurones have cell bodies within the dorsal root ganglia of the spinal cord. Aδ fibres synapse with cells in laminae I and V of the cord, while C fibres synapse with cells in laminae II and III (substantia gelatinosa). ◗ most second-order neurones synapse with Aδ fibres in the posterior horn, crossing to the opposite side immediately or within a few segments. They ascend within the anterolateral columns (spinothalamic tract) to the ventroposterior nucleus of the thalamus and periaqueductal grey matter. The substantia gelatinosa does not project directly to higher levels, but contains many interneurones involved in pain modulation (e.g. described by the gate control theory of pain). Some fibres project to deeper layers of the spinal grey matter, giving rise to the spinoreticular tract, which projects to the ascending reticular activating system (ARAS). Fibres are then relayed to the thalamus and hypothalamus

Pancuronium bromide (some fibres reach the thalamus without passing to the ARAS, via the palaeospinothalamic tract). ◗ third-order neurones transmit from the thalamus to the somatosensory cortex. Pain sensation may thus be modified by ascending or descending pathways at many levels. See also, Nerves; Nociception; Sensory pathways Pain, postoperative,  see Postoperative analgesia Palliative care. General approach to care of patients with advanced, progressive illness (often malignancy but also neurological, inflammatory, etc.), aimed at achieving the best quality of life within the time remaining to the patient rather than just prolonging life per se. Recognised as a separate specialty in the UK since 1987. Includes not only symptom control but also psychological, spiritual and social support of the patient and his/her family. Requires a multidisciplinary approach, including the expertise of general physicians, oncologists, surgeons, nursing staff, physiotherapists and religious advisers. Anaesthetists are often involved as they have expertise in controlling symptoms such as pain, anxiety, nausea and vomiting; they also care for patients with terminal disease in the ICU. See also, Ethics; Euthanasia; Withdrawal of treatment in ICU Palonosetron.  5-HT3 receptor antagonist licensed as an antiemetic drug in chemotherapy-induced nausea and vomiting. • Dosage: single dose of 250 µg iv 30 min before, or 500 µg orally 1 h before, chemotherapy treatment. • Side effects include GIT upset, arrhythmias, angina and peripheral neuropathy. PALS,  see Paediatric advanced life support Pancreatitis.  Acute pancreatitis is an autodigestive process caused by unregulated activation of trypsin in pancreatic acinar cells; this in turn leads to release of other enzymes and activation of complement and kinin pathways. Inflammatory processes also occur with the release of other harmful enzymes. Ischaemic changes, together with generation of free radicals, cause ischaemia and haemorrhagic necrosis of the pancreatic parenchyma. Although the condition is mild in 80% of patients, mortality is high in the remainder because of resulting sepsis, respiratory failure, shock and acute kidney injury.   Associated with biliary tract disease or alcoholism in about 80% of cases. May occasionally follow upper abdominal surgery, pancreatic ductal obstruction (e.g. by carcinoma), trauma, mumps, hepatitis, cystic fibrosis, hypothermia, hypercalcaemia, hyperlipidaemia, diuretics or corticosteroids. More common in smokers and those with type 2 diabetes mellitus. • Features: ◗ severe epigastric pain (typically radiating through to the back), nausea and vomiting, fever, occasionally mild jaundice. ◗ epigastric tenderness, progressing to features of peritonitis. ◗ discoloration in flanks caused by tracking of blood from the retroperitoneal space (Grey Turner’s sign) or via the falciform ligament to the umbilicus (Cullen’s sign). ◗ hypotension, oliguria, respiratory failure.

Investigations reveal raised serum and urinary amylase (secondary to leakage from the pancreas), leucocytosis, hyperglycaemia, hypocalcaemia (secondary to calcium sequestration in areas of fat necrosis), hypoproteinaemia and hyperlipidaemia. Because many other disorders also result in increased amylase levels, measurement of the more specific marker serum lipase is increasingly used for diagnosis. Abdominal x-ray may reveal a ‘sentinel loop’ of small bowel overlying the pancreas. CXR may show a raised hemidiaphragm, pleural effusion, atelectasis or ALI. CT scanning may be helpful in confirming the diagnosis and assessing the severity of pancreatic damage.   Poor prognosis may be indicated by: age >55 years; systolic BP 15 × 109/l; temperature >39°C; blood glucose >10 mmol/l; arterial PO2 15 mmol/l; serum calcium 500/ml) or red cells (>100 000/ml), or bacteria, indicates the need for diagnostic laparoscopy or laparotomy. Introduction of blood during the procedure itself may lead to a falsepositive result. Abdominal ultrasound is used as a less invasive diagnostic method.   Continuous peritoneal lavage has been used in acute pancreatitis, peritonitis and postoperatively in intra-

abdominal sepsis in an attempt to wash away bacteria and toxins. See also, Paracentesis Peritonitis.  Inflammation or infection of the peritoneum. Infection is usually with bacteria, most commonly involving mixed anaerobic and aerobic organisms, although ‘spontaneous’ (primary) peritonitis is caused by a single species (usually streptococci, pneumococci or haemophilus). • Caused by: ◗ perforation of part of the GIT. ◗ penetrating trauma (including postoperative infection from drains). ◗ direct spread from an infected organ, e.g. appendicitis, cholecystitis. ◗ haematogenous spread in bacteraemia. Clinical features include fever (or hypothermia in severe sepsis), tachycardia, pain (worse on movement and breathing), guarding and rigidity. Bowel sounds may be sparse or absent, with abdominal distension. Untreated, shock may occur. Diagnosis may be aided by paracentesis; imaging may reveal an underlying cause. If the diagnosis remains in doubt, exploratory laparotomy may be indicated as for intra-abdominal sepsis. • Treatment: ◗ general resuscitative measures: iv fluids, inotropes, respiratory support. ◗ nasogastric tube. ◗ broad-spectrum antibacterial drug therapy, e.g. a cephalosporin, metronidazole and aminoglycoside. ◗ surgical correction of the underlying cause. ◗ peritoneal lavage with or without antibiotics has been used, especially postoperatively. Complications include MODS, GIT obstruction caused by adhesions and persistent ileus. TPN may be required. Overall mortality is approximately 10%, although rates of 50%–70% may occur in faecal peritonitis in high-risk patients (e.g. elderly). Permissive hypercapnia. Acceptance of hypercapnia in patients undergoing IPPV, e.g. for respiratory failure especially asthma and ALI. Used as part of a lung protective strategy, when ventilation to a normal PCO2 may result in excessive airway pressure, barotrauma and volutrauma. Permissive hypotension,  see Damage control resuscitation Peroneal nerve block,  see Ankle, nerve blocks; Knee, nerve blocks Persistent vegetative state,  see Vegetative state PET,  Pre-eclamptic toxaemia, see Pre-eclampsia PET scanning,  see Positron emission tomography Pethick’s test,  see Checking of anaesthetic equipment Pethidine hydrochloride. Synthetic opioid analgesic drug, developed in Germany in 1939. One-tenth as potent as morphine, with duration of action of 2–4 h and half-life of about 3–4 h. Approximately 60% protein-bound in plasma. 5%–10% is excreted unchanged in urine, more if the urine is acidic. 90% undergoes hepatic metabolism to norpethidine, an active substance (half-life 20–40 h) that may cause hallucinations and convulsions.

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PFA-100

Table 42 Corresponding values for pH and hydrogen ion concentration  

pH units 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 8.0

[H+] (nmol/l) 158 126 100 79 63 50 40 32 25 20 16 13 10

  Has similar effects to morphine, but also has local anaesthetic and anticholinergic actions. May cause bronchodilatation, but may also cause histamine release. May relax contracted GIT and urinary smooth muscle. High doses may cause convulsions and myocardial depression.   Indications for use are as for morphine. • Dosage: 50–150 mg orally or 25–50 mg iv 4-hourly. Also used in obstetric analgesia and anaesthesia (50–150 mg im, max 400 mg/day), and has been given by subarachnoid injection (50–100 mg). Has been used as a component of the lytic cocktail.   Should be avoided in patients taking monoamine oxidase inhibitors. PFA-100,  see Coagulation studies pH. Negative logarithm to base 10 of hydrogen ion concentration (lower case ‘p’ being the symbol for −log10); i.e., pH = −log [H+]. Used as an indication of acidity; the more acid a solution, the lower the pH (Table 42). pH of normal arterial blood is 7.34–7.46, corresponding to [H+] of 34–46 nmol/l. See also, Acid–base balance pH measurement. Relies on the principle that, when two electrolyte solutions are separated by a semipermeable membrane, an electrical potential difference is generated across the membrane that is proportional to the hydrogen ion concentration gradient across it.  The pH electrode uses H+-sensitive glass as the membrane; this separates the sample solution (e.g. blood), from the silver/silver chloride measuring electrode immersed in an internal buffer solution of constant pH. Thus, the potential difference across the glass is dependent on the [H+] of the sample. A mercury/mercurous chloride/potassium chloride electrode system also makes contact with the blood (via a membrane to prevent contamination), acting as a reference electrode. The potential difference between the reference and measuring electrodes is amplified and displayed.   The system is maintained at 37°C; potential output is linear at approximately 60 mV per pH unit. See also, Blood gas interpretation Phaeochromocytoma.  Rare tumour secreting catecholamines, originating from chromaffin tissue. 90% occur in the

adrenal gland, 10% at other sites within the sympathetic nervous system. 10% are bilateral and 10% malignant. May occur as part of multiple endocrine adenomatosis 2A or 2B or in association with neurofibromatosis.   Usually presents with headache, psychosis, palpitations, sweating and hypertension (episodic or sustained). Tumours secreting mainly adrenaline cause tachyarrhythmias; those secreting noradrenaline cause vasoconstriction, ischaemia and hypertension. Some tumours secrete both these catecholamines and also dopamine. Glucose intolerance and cardiomyopathy may occur. • Diagnosis is confirmed by: ◗ measuring plasma catecholamines or urinary catecholamine metabolites (e.g. metanephrine, normetanephrine, hydroxymethylmandelic acid; HMMA). ◗ suppression tests (e.g. using clonidine) with measurement of plasma catecholamines. ◗ provocation tests (e.g. using histamine, tyramine or glucagon). Rarely used now, because dangerous hypertension may occur. Tumours may be located using selective venous catheterisation and catecholamine assays, arteriography (may provoke hypertensive crises), CT scanning, MRI and radioactive meta-iodobenzyl guanidine (MIBG) scintigraphy. Positron emission tomography has also been used.   Definitive treatment is with surgical excision, traditionally by open laparotomy but increasingly by laparoscopy. Anaesthetic considerations: ◗ preoperatively: - chronic hypertension may lead to hypertrophic or dilated cardiomyopathy, the latter associated with cardiac failure. Preparation includes several weeks’ oral therapy with α-adrenergic receptor antagonists (e.g. traditionally phentolamine or phenoxybenzamine but more recently with α1-selective antagonists, e.g. prazosin or doxazosin). With the older non-selective α-receptor antagonists, β-adrenergic receptor antagonists are administered when α-receptor blockade is complete, but doxazosin may be used without β-receptor antagonists because it does not block presynaptic α2-receptors and thus is not associated with increased cardiac sympathetic activity (unless tumours are predominantly adrenaline-secreting). Initiation of β-receptor blockade before α-receptor blockade is contraindicated as it may exacerbate hypertension because of antagonism of β2-mediated vasodilatation in muscle. Labetalol and atenolol are often used. α-Methyl-p-tyrosine and calcium channel blocking drugs have also been used. - fluid therapy may be required; this may be aided by central venous cannulation. ◗ perioperatively: - drugs causing minimal cardiovascular disturbance are used for anaesthesia. - direct arterial BP measurement and CVP with or without pulmonary capillary wedge pressure monitoring are required. - catecholamines may be released in response to surgical stress, anaesthetic drugs and handling of the tumour. Sodium nitroprusside, phentolamine, GTN, prazosin, calcium channel blocking drugs and magnesium sulfate have been used to control perioperative hypertension. β-Receptor antagonists or other antiarrhythmic drugs may be used to control tachycardia.

Pharmacokinetics - following the tumour’s removal, iv fluids and occasionally phenylephrine or dopamine may be required to maintain BP. ◗ postoperatively: - ICU care is required. - hypoglycaemia, cardiovascular instability and fluid imbalance may occur. - bilateral adrenalectomy will require replacement of corticosteroids. Rarely, phaeochromocytoma may present for the first time during incidental surgery, pregnancy or labour; morbidity and mortality are higher in this context. Connor D, Boumphrey S (2016). BJA Educ; 16: 153–8 Phantom limb.  Sensation of the continued presence of an amputated limb, occurring in around 65% of amputees after six months and commonly described as throbbing, aching or burning. The ‘limb’ may also be felt to be in an abnormal position. Risk factors include upper limb amputation, pain before amputation and female gender. Putative mechanisms include the peripheral afferent theory (ectopic firing and lowered stimulation thresholds in the neuroma or damaged afferent) and the central nervous theory (neuroplastic changes in the dorsal horn as a result of prolonged stimulation, causing decreased sensitivity to descending inhibitory pathways and reorganisation of the somatosensory cortex). Treatment includes anticonvulsant drugs, ketamine, opioid analgesic drugs, local somatic and sympathetic nerve blocks, spinal cord stimulation, mirror therapy (in which the remaining limb is placed into a mirror box that gives the illusion that two limbs are present) and biofeedback therapy.   Epidural anaesthesia has been claimed to prevent the development of phantom limb pain when instituted before surgical amputation, but the evidence for this is weak. Pharmacodynamics.  Describes the effects of drugs on the body. Drugs may act by physical interactions (e.g. antacids, general anaesthetics), or by interacting with receptors (receptor theory) or enzymes. See also, Dose–response curves; Gender differences and anaesthesia; Pharmacogenetics; Pharmacokinetics Pharmacogenetics (Pharmacogenomics). Describes variations in the pharmacodynamics and/or pharmacokinetics of a drug that are attributable to the genetic make-up of the individual. Examples include a prolonged action of suxamethonium due to variations of plasma cholinesterase, and variation in metabolism of opioid drugs, benzodiazepines, paracetamol and other NSAIDs due to genetic variation in the cytochrome P450 enzyme system. Easiest to characterise if single nucleotide polymorphism (SNP) is involved, in which variation in a single nucleotide of the genome leads to different responses; a number of SNPs may be relevant to differences in response to a particular drug or drug group. Potential applications include the ‘tailoring’ of drug therapy to individual patients based on their genotype, which could be analysed from a single blood sample. Current obstacles include the incomplete understanding of many drugs’ mechanism of action, the involvement of multiple genes in a given response to a drug, and the difficulty in predicting actual patients’ responses from genotype alone. Landau R, Bollag LA, Kraft JC (2012). Anaesthesia; 67: 165–79 See also, Gender differences and anaesthesia

Pharmacokinetics.  Describes the absorption, distribution, metabolism and elimination of drugs, i.e., effects of the body on drugs. These factors determine how the effector site concentration of a drug varies over time. Population differences in pharmacokinetic characteristics may arise from general individual variations and genetic factors (see Pharmacogenetics). • Absorption: ◗ may be via oral, sublingual, buccal, inhalational, iv, im, sc, rectal or topical routes. ◗ rate of absorption affects the maximum concentration and duration of drug action. Most drugs are absorbed by simple diffusion; i.e., rate depends on drug solubility, tissue permeability, surface area and vascularity of the absorption site. Lipid solubility depends on the degree of ionisation of the drug, which depends on the pK of the drug in solution and body pH. Some drugs are absorbed by active transport, e.g. L-dopa, α-methyldopa. ◗ absorption from the GIT also depends on drug characteristics, gut motility, vomiting, destruction of drug by digestive enzymes, interaction with food or other drugs, GIT disease and intestinal microflora. First-pass metabolism reduces the bioavailability of many orally administered drugs, e.g. opioid analgesic drugs. Other routes of administration avoid this. ◗ absorption occurs via the lungs for inhalational anaesthetic agents. • Distribution: ◗ related to lipid solubility, pK, body fluid pH, proteinbinding, regional blood flow, and specific properties of the drug (e.g. iodine taken up by thyroid tissue). ◗ protein-binding limits both the amount of free drug and redistribution of drugs from the blood. Volume of distribution and clearance of a drug are inversely proportional to its protein-binding. ◗ initial redistribution may reduce blood levels of a drug with recovery from its effects, although the total amount in the body has hardly changed, e.g. thiopental and other iv anaesthetic agents. ◗ compartment models have been described to explain the distribution of drugs in the body: - one-compartment model: plasma concentration declines as a simple negative exponential process after a bolus injection (first-order kinetics; Fig. 130a), i.e.: Ct = C0 e − kt where Ct = concentration at time t C0 = concentration at time zero k = rate constant e ≈ 2.718 A straight line is obtained when it is plotted using a semi-logarithmic scale (Fig. 130b). The slope of the line =

k 0.693 , and half -life = 2.303 k

Clearance = k × volume of distribution D = AUC where AUC = area under the plasma concentration/ time curve D = dose of drug at time zero

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(a)

(b)

(c)

Log10 concentration

Log10 concentration

Pharynx

Concentration

464

Time

Time

α phase

β phase

Time

Fig. 130 Drug concentration against time: (a) and (b) one-compartment model; (c) two-compartment model  

- two-compartment model: bi-exponential decline in plasma level; an initial rapid α distribution phase is followed by a slower β elimination phase (Fig. 130c). Each component of the curve may be analysed separately. Drug is distributed from a central compartment (i.e., blood, brain, lungs) to a peripheral one (e.g. ECF, tissues). The central compartment does not necessarily correspond to an anatomical volume, but is defined in terms of its apparent volume. Elimination occurs from the central compartment. - three-compartment distribution: one central and two peripheral compartments are assumed. • Metabolism: ◗ drug activity may be enhanced (e.g. morphine metabolised to morphine-6-glucuronide), decreased (most drugs) or unaltered (e.g. certain benzodiazepines). ◗ usually occurs in two phases in the liver. Phase I involves oxidation, reduction or hydrolysis, often involving the cytochrome P450 enzyme system. Phase II reactions involve conjugation with glucuronic acid, glycine, glutamine and sulfate, increasing water solubility. Rate of metabolism may be altered by enzyme induction/inhibition. ◗ other sites may be involved, e.g. plasma cholinesterase (suxamethonium), kidney (e.g. dopamine). • Elimination: ◗ may occur via lungs, bile, urine, GIT, saliva or breast milk. Renal excretion depends on GFR, water solubility and extent of active tubular secretion and reabsorption. ◗ most drugs are eliminated by first-order kinetics, whereby rate of elimination is proportional to the amount of drug in the body (i.e., simple exponential decay). ◗ in zero-order kinetics, a constant amount of drug is eliminated per unit time (e.g. alcohol, phenytoin). Zero-order kinetics may replace first-order kinetics when elimination pathways are saturated, i.e., at high drug concentrations. These analyses allow prediction of drug kinetics for calculation of appropriate dosage regimens or incorporation into the software of computer-controlled infusion pumps. For a continuous drug infusion, 50% of steady-state levels are reached after one half-life, 75% after two half-lives, 87.5% after three, 93.75% after four, 96.875% after five, etc. A loading dose achieves steady-state levels more quickly, but is limited by adverse effects if a large dose is given, depending on the drug’s therapeutic ratio/index. At steady

state, the infusion rate equals the rate of elimination of drug for a one-compartment model, or the rate of transfer to a peripheral compartment for a multi-compartment model. Rigby-Jones AE, Sneyd JR (2012). Anaesthesia; 67: 5–11 See also, Drug interactions; Gender differences and anaesthesia; Pharmacogenetics; Michaelis–Menten kinetics; Target-controlled infusions Pharynx. Common upper end of the respiratory and alimentary tracts, extending from the base of the skull to the level of C6. • Divided into: ◗ nasopharynx: lies behind the nasal cavities, above the soft palate. Contains the adenoids, and a Eustachian tube orifice on each lateral wall. ◗ oropharynx: lies behind the mouth and tongue, below the soft palate. Bounded anteriorly by the anterior pillars of the fauces (with buccal cavity anteriorly), superiorly by the palate and inferiorly by the tip of the epiglottis. Contains the tonsils, lying between the anterior and posterior pillars (containing palatoglossus and palatopharyngeus muscles, respectively). ◗ laryngopharynx: lies behind and around the larynx, extending from the level of the epiglottic tip to the C6 level. The larynx projects into the laryngopharynx, leaving a deep recess (piriform fossa) on each side. Composed of mucosa (ciliated columnar type in the nasopharynx; stratified or squamous elsewhere), submucosa, muscle layer and loose areolar sheath. The muscles (superior, middle and inferior constrictors) are arranged so that the upper parts of each overlap the lower fibres of the muscle above. They arise thus: ◗ superior: from the pterygomandibular raphe, and bony points at either end. ◗ middle: from the hyoid bone and stylohyoid ligament. ◗ inferior: from the thyroid and cricoid cartilages. Their anterior borders are open to form the nasal, buccal and laryngeal cavities. Their posterior borders insert into a median raphe along the length of the pharynx. • Blood supply: ◗ arterial: via superior thyroid and ascending pharyngeal branches of the external carotid artery. ◗ venous: via pharyngeal plexus to the internal jugular vein.

Phentolamine mesylate

• Nerve

supply: ninth and 10th cranial nerves, with additional nasal innervation via the fifth nerve. [Bartolomeo Eustachio (1513–1574), Italian physician] See also, Nose Phase II block,  see Dual block

Phase shift.  Delay between the arrival of a signal at a monitoring device (e.g. transducer) and the latter’s output. Distortion of the signal is minimised by applying the same delay to all components of the waveform, thus maintaining the phase relationship between harmonics. This is achieved by adjusting the damping of the system to about two-thirds critical damping, at which there is a linear relationship between phase lag and the frequency of the wave. Phenobarbital/Phenobarbital sodium (Phenobarbitone). Long-acting barbiturate and anticonvulsant drug, introduced in 1912. Used as a secondary agent in all types of epilepsy except absence attacks. Also used in the treatment of status epilepticus. Although absorbed slowly after oral administration, it has an oral bioavailability of 90% with duration of action up to 16 h. Elimination half-life is about 90 h. 20%–45% protein-bound, and 75% metabolised by hepatic microsomal enzymes; 25% is normally excreted unchanged in urine. • Dosage: ◗ 60–180 mg orally od (5–8 mg/kg/day in children). ◗ for status epilepticus: 15–18 mg/kg. • Side effects include sedation and ataxia. Paradoxical excitation may occur in children. Hepatic enzyme induction may reduce the effectiveness of other drugs, e.g. warfarin, oral contraceptives, corticosteroids. Phenol (Carbolic acid). Organic compound with the chemical formula C6H5OH. Widely used in manufacturing, including drug production. Medically, used as a neurolytic agent in chronic pain management. Thought to spare large myelinated fibres while damaging unmyelinated C pain fibres by protein denaturation. Hyperbaric 5% solution in glycerine is used for subarachnoid neurolysis of posterior nerve roots; 0.5–2.0 ml has an effect lasting up to 14 weeks. 6%–7% solution in water is used for sympathetic nerve blocks.   Also used for sclerotherapy of haemorrhoids, and as a throat gargle. 1%–5% solution (carbolic acid) is also used for disinfection of equipment. Irritant to the skin. Used for surgical antisepsis by Lister in Glasgow in 1865. [Joseph Lister (1827–1912), English surgeon] Phenoperidine hydrochloride.  Obsolete synthetic opioid analgesic drug related to pethidine; discontinued in the UK in 1997. Phenothiazines. Group of sedative and antipsychotic drugs. Also have antimuscarinic, antiemetic, antihistamine, antidopaminergic and α-adrenergic receptor antagonist properties. Some may potentiate the effects of opioid analgesic drugs. Different drugs have varying degrees of these properties, depending on the side chains of the molecule. Act mainly on the ascending reticular activating system, limbic system, basal ganglia, hypothalamus and chemoreceptor trigger zone. Cause sedation, with reduced muscular, GIT and cardiovascular activity. Effect on respiration is variable. Central temperature regulatory mechanisms, shivering, and peripheral vasoconstriction are impaired,

but metabolic rate is unaffected. Highly lipid-soluble and extensively protein-bound. Metabolised in the liver to mostly inactive metabolites. • Side effects: ◗ extrapyramidal symptoms, e.g. tardive dyskinesia, dystonia, tremor, facial grimacing. ◗ drowsiness, insomnia, depression, hypothermia, prevention of shivering. ◗ anticholinergic effects, e.g. tachycardia, arrhythmias, dry mouth, urinary retention, blurring of vision. ◗ galactorrhoea, menstrual irregularity, gynaecomastia, weight gain. ◗ blood dyscrasias, haemolysis. ◗ photosensitivity, contact dermatitis, rash. ◗ obstructive jaundice. ◗ hypotension. ◗ neuroleptic malignant syndrome. ◗ potentiation of other depressant drugs. Chlorpromazine is the standard phenothiazine; others include alimemazine (trimeprazine), promethazine, perphenazine, promazine, thioridazine, fluphenazine and trifluoperazine. Phenoxybenzamine hydrochloride. Irreversible nonselective α-adrenergic receptor antagonist, chemically related to the nitrogen mustards; forms covalent bonds with α-adrenergic receptors. Used mainly to control hypertension caused by phaeochromocytoma. Has also been used in complex regional pain syndrome type 1. More active at α1-receptors than at α2-receptors. Onset of action may be up to 1 h after iv injection, due to conversion to an active form. Effects last for several days, although its elimination half-life is about 24 h. • Dosage: ◗ 10 mg orally od, increased by 10 mg/day as required. ◗ 1 mg/kg in 200 ml saline over 2 h od (profound hypotension may occur). • Side effects: postural hypotension, tachycardia, inhibition of ejaculation, nasal congestion, miosis, rarely GIT disturbances. See also, Vasodilator drugs Phenoxymethylpenicillin  (Penicillin V). Natural penicillin used especially in streptococcal infections and in rheumatic fever prophylaxis. Also used for pneumococcal prophylaxis after splenectomy or in sickle cell anaemia. Similar to benzylpenicillin but less active and more acid-stable; thus suitable for oral administration, following which peak serum levels occur in about 60 min (although somewhat variably, hence the recommendation that it not be used for severe infections). 80% of the drug is protein-bound. Excreted in urine (the dose should be reduced in renal impairment) and faeces. Elimination half-life is 40 min. • Dosage: ◗ 500–1000 mg orally bd/qds. ◗ for prophylaxis, 250 mg (rheumatic fever) or 500 mg (splenectomy, sickle cell) bd. • Side effects: as for benzylpenicillin. Phentolamine mesylate. Non-selective α-adrenergic receptor antagonist, with an additional direct relaxant action on vascular smooth muscle. Used in hypotensive anaesthesia and to control hypertensive crisis, e.g. caused by phaeochromocytoma, monoamine oxidase inhibitor interactions and clonidine withdrawal. An oral preparation is used for the treatment of erectile dysfunction. Previously used for diagnosing phaeochromocytoma and in the

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Phenylephrine hydrochloride assessment of complex regional pain syndromes. Acts within 2 min of iv injection, with duration of action 10–15 min. • Dosage: 2–5 mg iv repeated as required; 0.1–2.0 mg/ min by infusion. • Side effects: postural hypotension, tachycardia, abdominal pain, diarrhoea, nasal congestion. See also, Vasodilator drugs Phenylephrine hydrochloride. Synthetic selective α1adrenergic receptor agonist, used as a vasopressor drug, e.g. in spinal anaesthesia. Causes intense vasoconstriction and compensatory bradycardia. Popular in obstetric regional anaesthesia, because it appears more effective than ephedrine, and fetal acid–base profile is better than if large doses of ephedrine are used. Has been administered topically to the nasal mucosa and eye to cause vasoconstriction and mydriasis, respectively, and as a vasoconstrictor agent for local anaesthesia. Has also been used to treat SVT. Of similar structure to adrenaline, lacking only the 4-hydroxyl group. • Dosage: ◗ 2–5 mg im or sc. ◗ 100–500  µg iv (5–10 µg/kg in children); 30–180 µg/min by infusion. Boluses of 25–100 µg (or increasingly, 25–50 µg/min infusion) are used to treat hypotension in obstetric regional anaesthesia. ◗ 2.5–5 mg added to 100 ml local anaesthetic solution. • Side effects: hypertension, bradycardia, vomiting. Phenytoin/phenytoin sodium. Hydantoin anticonvulsant drug, introduced in the late 1930s. Used to treat all types of epilepsy except petit mal, in chronic pain management, and previously as a class Ib antiarrhythmic drug (especially for digoxin-induced arrhythmias). Has membrane-stabilising effects on all neuronal cells, including peripheral nerves and cardiac muscle; acts by blocking voltage-gated sodium channels.   A poorly water-soluble weak acid, with pKa ~ 8.3. Variably absorbed from the GIT, it may cause gastric irritation. Erratically absorbed after im injection, probably due to local precipitation. About 90% protein-bound, and metabolised in the liver to inactive metabolites that are excreted renally. Elimination follows first-order kinetics at plasma levels below 10 mg/l; zero-order kinetics occur above 10 mg/l, due to saturation of enzyme systems (see Pharmacokinetics). Elimination half-life is about 24 h but varies. Susceptible to hepatic enzyme induction, and is itself an enzyme inducer. • Dosage: ◗ 3–4 mg/kg daily as one or two oral doses, increased up to 600 mg/day. ◗ for status epilepticus: 20 mg/kg (up to 2 g) iv slowly, with ECG monitoring, followed by 100 mg tds/qds. ◗ to prevent/treat seizures after neurosurgery or head injury: 2.5 mg/kg orally bd up to 4–8 mg/kg/day. Plasma levels should be monitored; therapeutic range is 10–20 mg/l (40–80 µmol/l). IV administration should be via a large vein at no more than 1 mg/kg/min (up to 50 mg/ min). Flushing with saline should follow as the solution is strongly alkaline and irritant. Arrhythmias and hypotension may occur. • Side effects: ◗ headache, vomiting, confusion, tremor. Ataxia, nystagmus and blurred vision may indicate overdosage. ◗ skin eruptions, lymphadenopathy, hirsutism, fever, hepatitis, gingival hyperplasia. The purple glove

syndrome (blue/purple discoloration followed by oedema and necrosis) may occur around the site of iv administration. ◗ osteomalacia. ◗ rarely, megaloblastic anaemia (due to impaired folate absorption and storage), other blood dyscrasias. ◗ fetal neural tube defects and neonatal bleeding may follow its use in pregnancy. Chronic usage may cause resistance to non-depolarising neuromuscular blocking drugs.   Available as a prodrug, fosphenytoin. PHI,  see Prehospital index Phlogiston.  Imaginary substance proposed in the 1720s, thought to separate from combustible material during burning. Following experiments in the 1770s, Priestley concluded that ‘dephlogisticated air’ (O2) and ‘dephlogisticated nitrous air’ (N2O) were deficient in phlogiston and could thus support combustion, whereas ‘nitrous air’ (NO2) was saturated with it and was unable to do so. The phlogiston theory was subsequently disproved by Lavoisier. Phonocardiography.  Technique employing contact microphones placed on the chest, for amplification and recording of heart sounds. Used to obtain an objective record of heart sounds and heart murmurs. May be performed simultaneously with ECG and arterial waveform recording, allowing calculation of systolic time intervals. A similar technique is employed in fetal monitoring. See also, Cardiac cycle Phosphate.  Total body content is about 25 000 mmol, most of which is intracellular. 80% is in bone, 15% is in soft tissues and only 0.1% is in ECF. Most intracellular phosphate is in the organic form. Normal plasma inorganic phosphate levels: 0.8–1.45 mmol/l. Dietary phosphate is absorbed mainly in the duodenum and jejunum via active and passive transport mechanisms.   Involved in cell membranes (phospholipids), enzyme regulation, energy storage (ATP), O2 transport (2,3-DPG) and acid–base buffering.   Levels are controlled by renal excretion; most of the filtered phosphate is reabsorbed in the proximal tubule of the nephron. Excretion is increased by parathyroid hormone, calcitonin, adrenaline and increased phosphate intake. Decreased excretion occurs when intake is low or in response to thyroxine or growth hormone. Hyperphosphataemia causes no specific clinical sequelae but may disturb calcium metabolism. Hypophosphataemia is common in ICU patients, especially associated with TPN and ketoacidosis. Phosphodiesterase inhibitors.  Substances that prevent conversion of 3′,5′-adenosine monophosphate (cAMP) to 5′-adenosine monophosphate, or 3′,5′-guanosine monophosphate (cGMP) to 5′-guanosine monophosphate by the enzyme phosphodiesterase (PDE; see Fig. 5; Adenosine monophosphate, cyclic). Both cAMP and cGMP are important intracellular messengers. Many isoenzymes of PDE exist; PDE3 inhibitors include amrinone, milrinone, enoximone, piroximone and pimobendan; PDE4 inhibitors include ibudilast (asthma), apremilast (psoriasis) and roflumilast (COPD); and PDE5 inhibitors include sildenafil and dipyridamole.   Aminophylline, papaverine and caffeine are nonselective PDE inhibitors.

Physostigmine salicylate/sulfate Phrenic nerve pacing.  Intermittent electrical stimulation of the phrenic nerves (usually bilaterally), to pace the diaphragm in chronic hypoventilation due to brainstem, medulla or upper cervical cord lesions. Has also been used in COPD. Described in the 1960s, it requires intact phrenic nerves and diaphragm function, thus excluding its use in lower motor neurone lesions and myopathies.   Platinum electrodes are implanted around the nerves in the neck or thorax and connected to a subcutaneous radio receiver, which is triggered by an external power source. Respiratory rate, inspiratory time and sighs may be adjusted. Neck electrodes risk inadvertent stimulation of the brachial plexus. Nerve trauma at surgery, infection and poor contacts may cause failure. Diaphragmatic fatigue may also occur. Obstructive apnoea may be precipitated in some cases of central alveolar hypoventilation.   Implantation of electrodes directly into the diaphragm has also been used, thus not requiring intact phrenic nerves. Pimpec-Barthes F, Legras A, Arame A, et al (2016). J Thorac Dis; 8 (suppl 4): S376–86 Phrenic nerves.  Originate from the ventral rami of C3–5 on each side, supplying the motor innervation of the diaphragm. Also convey sensory fibres from the diaphragm; hence the shoulder-tip referred pain caused by diaphragmatic irritation. Sensory fibres from the mediastinal pleura, fibrous pericardium and parietal serous pericardium are also conveyed.   Descend vertically on the scalenus anterior muscles, which they cross from lateral to medial sides. Each nerve passes to the root of the neck beneath the sternomastoid muscle, inferior belly of omohyoid, internal jugular vein and (on the left) the thoracic duct. The right phrenic nerve enters the thorax behind the subclavian/internal jugular venous junction, descending subpleurally next to the right brachiocephalic vein, superior and inferior venae cavae and pericardium. Some of its branches pass through the caval foramen of the diaphragm, spreading over its peritoneal surface. The remainder pierce the diaphragm just lateral to the caval orifice. The left nerve enters the thorax between the subclavian artery and vein. It passes superficially to the aortic arch, to pierce the diaphragm anteriorly and to the left of the caval opening. Some of the divisions of each nerve cross to the other side.   Local anaesthetic block has been advocated as a treatment for chronic hiccups. 10 ml local anaesthetic agent is injected 1–2 cm deep at a point 2 cm above the sternoclavicular joint and for 5 cm laterally.   Phrenic paralysis may complicate brachial plexus block, trauma, tumour, neurological disease and cardiac surgery. Clinically, paradoxical inward abdominal movement is seen on inspiration, with a raised hemidiaphragm on CXR. See also, Phrenic nerve pacing Physicians’ assistants (anaesthesia). Non-medically qualified personnel able to deliver anaesthesia under supervision by a qualified anaesthetist. In the UK, the term is specific to graduates of 2-year programmes (plus 3 months’ supervised practice) approved by the Royal College of Anaesthetists, set up as pilots initially in 2003, in response to predicted shortfalls in manpower. The scheme mirrors those introducing other support roles within the NHS, taking on some of the activities and duties traditionally exclusive to qualified doctors. The original term ‘Anaesthesia Practitioners’ was replaced by the new title in 2008 to bring it into line with Physicians’ Assistants

(now ‘Physician Associates’) in other areas/specialties within the NHS, and to aid understanding of the role. Physiological and operative severity score for the enumeration of mortality and morbidity (POSSUM). Scoring system described in 1991 as a method of predicting outcome (morbidity and mortality) for surgical patients. Patients are scored before operation (using measures of physiological derangement) and at operation (using an operative severity score) to give predictions of morbidity and hospital mortality. The original POSSUM model has been modified for specific subspecialties to provide greater accuracy (e.g. P-POSSUM for general surgery, CRPOSSUM for colorectal cancer surgery, V-POSSUM for vascular surgery). Moonesinghe SR, Mythen MG, Das P, et al (2013). Anesthesiology; 119: 959–81 Physiotherapy.  Treatment and prevention of disease using passive and active movement, vibration, massage and application of heat. Used for neurological, musculoskeletal and respiratory disorders. Has an important role in the ICU in preventing stiffness of limbs and joints during prolonged immobility, and in helping the patient mobilise during recovery.   Chest physiotherapy aims to maintain clear airways, increase lung expansion and thus reduce atelectasis and sputum retention. Often beneficial pre- and postoperatively in patients with respiratory disease, helping to optimise respiratory function. It is also valuable in the ICU management of patients with respiratory failure, before, during and after IPPV. It is thought to be most useful when excessive sputum is present; its place in uncomplicated COPD, chest infection without sputum production, and routine postoperative management is unclear. Thought to be of little benefit if disease is mainly peripheral; thus it is most effective if secretions are within the bronchi. • Techniques include: ◗ postural drainage: positioning according to the anatomy of the tracheobronchial tree, with or without breathing exercises. ◗ breathing exercises, e.g. incentive spirometry, coughing. Forced expirations may be more effective than cough alone, especially if combined with postural drainage. ◗ intermittent lung inflations using ventilators, to increase lung expansion. ◗ chest wall percussion and vibration: their efficacy has also been questioned. ◗ upper airway suction: usually combined with the above. Administration of nebulised bronchodilator drugs before physiotherapy may produce a better sputum yield. Nebulised saline, humidified O2 and mucolytics are also commonly used.   May be painful, especially postoperatively, and adequate analgesia is essential. Physostigmine salicylate/sulfate.  Acetylcholinesterase inhibitor, derived from the West African Calabar bean. Causes reversible inhibition of acetylcholinesterase by binding to its esteratic site, lasting 1–2 h. Readily crosses the blood–brain barrier because of its tertiary amine structure. Used to treat the central anticholinergic syndrome, and topically in glaucoma. Has also been used in γ-hydroxybutyric acid poisoning. Formerly used as a general CNS stimulant, e.g. in tricyclic antidepressant drug

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PiCCO poisoning and to reverse opioid-induced respiratory depression. No longer available in the UK. • Dosage: 0.04 mg/kg slowly iv. • Side effects: nausea, hypertension, tachycardia. Large doses may result in cholinergic crisis. PiCCO.  Commercial non-invasive cardiac output measurement system made available in 1997, combining the principles of transpulmonary thermodilution, in which the ‘cold’ transverses the lungs after injection, and arterial pulse contour analysis. Requires injection of a single bolus injection of cold saline through a central venous catheter and its detection by a specially modified cannula placed in a large artery (e.g. femoral/brachial). Permits continuous estimation of cardiac output, intrathoracic blood volume, left ventricular afterload, extravascular lung water and stroke volume variation. Provides cardiac output measurements with similar accuracy to that obtained from pulmonary artery catheterisation, although frequent calibration may be required in unstable patients (e.g. in sepsis or haemorrhage).   PiCCO 2 uses a more refined algorithm and was released in 2008. Litton E, Morgan M (2012). Anaesth Intensive Care; 40: 393–409 Pickwickian syndrome,  see Obesity hypoventilation syndrome Pierre Robin congenital

syndrome,  see

Facial

deformities,

Pin index system. International system introduced in 1952, preventing accidental connection of a gas cylinder to the wrong anaesthetic machine yoke. The cylinder valve block bears holes into which fit pins protruding from the yoke. A flush connection is only achieved if the holes and pins align correctly. The positions of the holes on the valve block (and corresponding pins on the yoke) are specified by an international standard (Fig. 131): ◗ O2: positions 2 and 5. ◗ N2O: positions 3 and 5.

1

2 3 4 5 7

6

Fig. 131 Position of holes (1–7) in pin index system  

air: positions 1 and 5. CO2: positions 1 and 6. Entonox: position 7. The system may be circumvented, e.g. by removing pins or using several Bodok seals. When piped gas supplies were first introduced, pin-indexed fittings were attached to the pipelines; these could be inserted upside-down into the cylinder yokes, allowing incorrect gas connection. The positions for cyclopropane were 3 and 6. ◗ ◗ ◗

Pipecuronium bromide. Non-depolarising neuromuscular blocking drug, related to pancuronium, synthesised in Hungary in the late 1970s and made available in the USA in 1990 (and withdrawn in 1999). Piped gas supply.  Networks of pipes and socket outlets that distribute medical gases from a central source to points of use. In the UK, only O2, N2O, Entonox, CO2 (rarely) and compressed air may be distributed by such systems. All are supplied at 4 bar except air, which may be required at 7 bar for surgical instruments. Medical vacuum is also supplied by a pipeline system. • Essential features include: ◗ indexing system to prevent cross-connection. ◗ prevention of contamination of gases. ◗ automatic function, especially when switching over supplies. ◗ anti-combustion and anti-explosion controls. • Systems consist of: ◗ central gas source: either a large primary source and small reserve supply, or large primary and secondary sources used alternately with a small reserve supply. The primary source may be a manifold of cylinders, vacuum insulated evaporator, air compressor or O2 concentrator. ◗ pipeline distribution network: made of phosphorus deoxidised non-arsenical copper, greased and specially cleaned with steam, shot and medical air. Joints are usually made with a silver alloy, although some are threaded. They should be colour-coded and marked with the name of the gas contained. Isolation valves should be supplied. ◗ terminal distribution system: includes self-closing sockets, probes, flowmeters, and hoses and their connections with anaesthetic machines. The probes and sockets should be specific for the service supplied, the probe of one gas fitting only the socket for the same gas. Some probes (e.g. for ward use) may incorporate flowmeters. Connecting hoses to probes should only be possible if specialised equipment is used, reducing the risk of misconnection. Hose connections to anaesthetic machines are made specific for each service by non-interchangeable screw-thread connectors. UK colour coding of hoses: - N2O: French blue. - O2: white. - air: black/white. - Entonox: French blue/white. - vacuum: yellow. ◗ system failure alarms: predominantly low-pressure alarms, they sound when secondary and reserve systems are in use. Usually situated at hospital telephone switchboards. Howell RS (1980). Anaesthesia; 35: 676–98 See also, Suction equipment

Placenta Piperacillin. Semisynthetic penicillin derivative with broad-spectrum antibacterial activity; has greater activity against gram-negative organisms than narrow-spectrum penicillins, with slightly reduced effectiveness against certain gram-positive organisms (e.g. Streptococcus pneumoniae). Especially effective against pseudomonas infections, although bacterial resistance is a growing problem. Often given with an aminoglycoside in severe pseudomonas infections because the combination is synergistic (but the two drugs should not be mixed in the same syringe). Only available combined with the β-lactamase inhibitor tazobactam. Piperacillin is 20% protein-bound with volume of distribution 15–20 l. Excreted via urine and faeces. Elimination half-life is approximately 1 h. • Dosage: 4.5 g iv tds (qds in neutropenic patients). • Side effects: as for benzylpenicillin. The high sodium content of the preparation may result in hypernatraemia. Pirbuterol.  β-Adrenergic receptor agonist, developed for the treatment of asthma but has been investigated as an orally active inotropic drug. Active at β1-adrenergic receptors, with some activity at β2-receptors. Thus increases cardiac output and causes vasodilatation; BP may fall. Tachycardia is uncommon. Piritramide.  Opioid analgesic drug, developed in 1960. Of faster onset than morphine, with similar duration of action and ~75% as potent. Not available in the UK. Pirogoff, Nicholai Ivanovich  (1810–1881). Russian surgeon at St Petersburg, a pioneer of battlefield trauma surgery, also known for introducing rectal diethyl ether for surgery in 1847. Also studied the effects of ether, designed apparatus for its rectal and inhalational administration, and published the first book on the subject in 1847. Secher O (1986). Anaesthesia; 41: 829–37 Piroxicam. Oxicam NSAID. Rapidly absorbed after oral administration, it is 99% protein-bound and has a long (50 h) half-life; thus can be given once daily. Due to a high incidence of cutaneous and GIT adverse reactions, its use is now restricted to analgesia in chronic inflammatory or rheumatoid conditions. • Dosage: 10–20 mg orally, od/bd. • Side effects: as for NSAIDs (though see above). Pituitary gland.  Lies in the pituitary fossa of the sphenoid bone, above the sphenoid air sinuses and below the optic chiasm. Composed of anterior and posterior lobes, connected to the hypothalamus by the infundibular stalk, which contains nerve fibres and the hypophyseal portal blood system. The infundibulum pierces the diaphragma sellae, a dural sheet that covers the gland. • Function: ◗ anterior lobe: - contains cells formerly classified by their staining properties (chromophobe, eosinophil and acidophil cells); now identified on an immunocytochemical basis into five cell types: - somatotrophs: secrete growth hormone. - lactotrophs: secrete prolactin. - corticotrophs: secrete ACTH. - thyrotrophs: secrete thyrotropin. - gonadotrophs: secrete luteinising and folliclestimulating hormones.

- secretion is controlled by hypothalamic inhibitory or releasing factors, carried to the anterior pituitary by the portal blood system and by negative feedback control by circulating end-organ hormones. ◗ posterior lobe: secretes vasopressin and oxytocin. Pituitary gland disease may be associated with over- or under-secretion of hormones (usually the latter). Enlargement may cause visual field defects, optic atrophy and raised ICP. See also, Acromegaly; Cushing’s disease; Diabetes insipidus; Hypopituitarism pK.  Negative logarithm (to base 10) of the dissociation constant for a weak acid or base in aqueous solution. The law of mass action states that for a weak acid (HA) dissociating in solution, HA ⇌ H+ + A−: dissociation constant Ka =

[H + ][A − ] [HA]

Thus − log [H + ] = − log Ka + log

[A − ] [HA]

Substituting pH for −log [H+], and pKa for −log Ka: pH = pKa + log

[A − ] [HA]

For a weak base (B): pH = pK b + log

[B] [BH + ]

The pK represents the pH value at which the solute is 50% dissociated; i.e., [A−] = [HA] or [B] = [BH+].   While pKa strictly refers to an acidic substance and pKb to a basic one, by convention pKa is used to refer to both acids and bases.   The stronger an acid, the lower its pKa, and the stronger a base, the higher its pKa. Thus important when considering ionisation of drugs and passage of drugs or other substances across membranes. Placenta. Structure dividing the fetal and maternal circulations. Approximately 5–6 days after conception the fertilised egg (now a mass of uniform cells) attaches to the endometrium. The endometrium is invaded by the outer layer of the trophoblast of the egg, the syncytiotrophoblast. Further proliferation of the trophoblast forms finger-shaped masses of tissue, the chorionic villi, between which spaces (lacunae) appear. The tips of the villi erode the walls of the endometrial spiral arteries so that the lacunae expand to form large spaces filled with maternal blood within which float the villi. Primitive blood vessels appear in the villi from about 18 days after fertilisation, eventually joining the fetal umbilical vessels. Densely packed masses of fetal villi (fetal cotyledons) are supplied by branches of the umbilical arteries, distributed radially as end-arteries. Several cotyledons form a single placental lobe. Thus the barrier between fetal and maternal circulations is two cells thick, consisting of the fetal capillary endothelium and its covering of syncytial trophoblast. • Blood supply: ◗ fetal: blood arrives via two umbilical arteries and leaves by a single umbilical vein. Umbilical blood flow is up to 100 ml/min at 22 weeks and 300 ml/min

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Placenta praevia at term, of which about 20% does not participate in exchange with maternal blood. ◗ maternal: delivered via the uterine arteries. Uterine blood flow (UBF) at term is 500–700 ml/min, 80% of which passes to the placenta. There is no autoregulation in the placental circulation and therefore flow is directly related to mean uterine perfusion pressure and inversely related to uterine vascular resistance. UBF may be reduced by maternal hypotension, hyperventilation and stress, and by vasopressor drugs. Placental function is related to its total surface area (~15 m2) and UBF. Impaired function causes fetal hypoxaemia and acidosis if acute, and may lead to delayed fetal growth if chronic. • Functions: ◗ gas exchange: O2 and CO2 exchange is favoured by fetal haemoglobin and the double Bohr effect, respectively. ◗ nutrient exchange: all energy substrates, water, minerals and electrolytes enter the fetus via the placenta by facilitated or active transport. ◗ hormone synthesis and release: hormones include chorionic gonadotrophin, human placental lactogen, oestrogens, progesterone, prolactin, somatomammotrophin and renin. Several corticosteroid hormones are synthesised by the fetoplacental unit, e.g. placental pregnenolone is metabolised by the fetus before further placental metabolism to form oestrogens. ◗ drug transfer across the placenta depends on placental surface area, metabolism, UBF and the pH of maternal and fetal blood; drug characteristics influencing transfer include molecular weight (drugs 55 years and immunodeficiency (especially associated with HIV infection and leukaemia).   Most commonly affects the T5 and T6 dermatomes. Pain usually precedes the appearance of cutaneous vesicles, although no rash may appear (zoster sine herpete). In 10% of cases, scarring and pain persist; the latter may be severe and intractable, triggered by contact, draughts and stress.   Treatment may be disappointing, but includes tricyclic antidepressant drugs, anticonvulsant drugs and topical lidocaine and capsaicin. Use of aciclovir during acute infection may reduce pain duration. Less evidence exists for the use of TENS, acupuncture, repeated epidural anaesthesia and peripheral or sympathetic nerve block. Johnson RW, Rice ASC (2014). N Engl J Med; 371: 1526–33

Postoperative analgesia.  Increasingly managed by acute pain teams; duties include education of medical and nursing staff, audit, research, and visiting postoperative patients specifically to monitor and adjust analgesia regimens.

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Postoperative care team.  Proposed system of comprehensive postoperative care that includes regular rounds and a team of specialist ‘postoperative care’ nurses to support ward nursing and medical staff by providing additional expertise and equipment. An extension of the role of acute pain teams and incorporated into the concept of perioperative medicine. Aims include better maintenance of vital organ function, decreased postoperative complications, reduced postoperative mortality, greater comfort and satisfaction and a shorter hospital stay. Goldhill DR (1997). Br Med J; 314: 389 See also, Care of the critically ill surgical patient; Medical emergency team; Outreach team; Safe transport and retrieval team

of aspiration of gastric contents. May lead to electrolyte imbalance and dehydration if prolonged. • In the absence of prophylaxis, PONV occurs after up to 90% of surgical procedures, the following increasing the risk: ◗ patient factors: - young age. - female gender. Incidence increases during menstruation and decreases after the menopause, i.e., is presumably hormonally mediated. - anxiety, especially in patients who ‘always vomit’. Increases in circulating catecholamine levels may be important. - previous history of PONV or motion sickness. - non-smoking. - early postoperative mobilisation, eating and drinking. ◗ surgical factors: - gynaecological/abdominal/ENT/squint surgery. - laparoscopic procedures. - severe pain. ◗ anaesthetic factors: - use of opioid analgesic drugs, including premedication. - use of certain anaesthetic drugs, e.g. diethyl ether, trichloroethylene, cyclopropane, etomidate, N2O (the last via a direct central effect, GIT distension and/or expansion of middle ear cavities). - possibly prolonged anaesthesia and the use of neostigmine (though these are disputed). - physical factors, e.g. gastric insufflation, pharyngeal stimulation. ◗ other factors: - hypoxaemia/hypotension. - dehydration. Various scores have been devised for predicting the likelihood of PONV in a particular case, based on the presence or absence of the following factors: female gender; history of PONV/travel sickness; non-smoker; postoperative opioids; ± prolonged procedure. • Reduced by: ◗ avoidance of triggers where possible, e.g. anxiety, opioids, N2O, vigorous pharyngeal suction, and possibly general anaesthesia altogether. ◗ use of specific antiemetic drugs and procedures (e.g. acupuncture at the wrist), especially in combination. ◗ use of drugs, techniques and procedures associated with low incidence of nausea and vomiting, e.g. propofol. ◗ administration of iv fluids. With prophylaxis the incidence is usually under 30% in high-risk cases. The most effective approach for preventing PONV is thought to be the use of multiple strategies and different drugs. See also, Vomiting

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IV infusions of lidocaine (1–3 mg/kg/h) have been shown to reduce pain/opioid requirements after major surgery; however, this is not widely used because of the low therapeutic ratio of lidocaine and the risk of toxicity. ◗ inhalational anaesthetic agents: some postoperative benefit is derived from the agents used perioperatively. Entonox is the only agent used postoperatively, e.g. for physiotherapy or changes of dressings, and is limited by its adverse effects on the haematological system. ◗ nerve destruction (e.g. cryoanalgesia) has been used in thoracic surgery, but has limited application elsewhere. ◗ other methods less widely used include TENS, acupuncture and hypnosis. See also, Analgesic drugs; Pain; Pain evaluation; Pain management

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Postoperative cognitive dysfunction  (POCD). Reduced cognitive function following anaesthesia and surgery, without altered level of consciousness, as distinct from florid postoperative delirium/confusion. Requires neurocognitive testing for diagnosis. Occurs in up to 25% of elderly patients in the first week after non-cardiac surgery, and in 10%–15% at 3 months. Patients with pre-existing cognitive problems and those undergoing cardiac surgery are especially at risk. The contribution of perioperative factors such as sedative drugs, intraoperative hypotension/ hypoxaemia/hypocapnia and sleep disturbance is unclear, although all have been implicated. Possible pathophysiological factors include: ◗ poor control of postoperative delirium. ◗ neuronal and synaptic loss due to sedative/anaesthetic agents or hypoxic/ischaemic injury. ◗ cytokine release triggered by tumour necrosis factor alpha. ◗ deposition of neurotoxic proteins (similar to those found in Alzheimer’s disease) in brain cells following anaesthesia. ◗ neuroinflammatory changes due to surgical trauma. It has been suggested that preoperative cognitive function testing may identify those patients at risk. [Alois Alzheimer (1864–1915), German neurologist and pathologist] Steinmetz J, Rasmussen LS (2016), Anaesthesia; 71: 58–63

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Postoperative nausea and vomiting (PONV). Consistently rated by patients as one of the most feared/ unpleasant aspects of undergoing surgery. Apart from its unpleasantness, it may also increase pain, disturb dressings/ surgical repairs, increase bleeding and increase the risk

Postpartum haemorrhage  (PPH). Divided by the Royal College of Obstetricians and Gynaecologists into minor (blood loss 30 mg/mmol or 24-hour urine >300 mg protein. Represents a multisystem disease with many other manifestations; hence the move in definition away from the classic ‘triad of PET’ (hypertension, oedema and proteinuria), towards the definition of gestational hypertension as above, with or without other features. Gestational hypertension occurs in 10%–12% of pregnancies whereas PET itself has an incidence of 2%–3%. Commoner in: first pregnancies with a particular partner (typically the features are less severe or present later in subsequent pregnancies); older age; family or previous history; preexisting hypertension, kidney disease or diabetes mellitus; polyhydramnios; obesity; black race; and multiple pregnancy. Perinatal mortality is increased. Usually improves rapidly following delivery of the fetus, although the clinical picture may first worsen before recovery.   Pathogenesis is unclear but is thought to involve impaired trophoblastic invasion of myometrial arteries, with reduced placental perfusion and increased placental oxidative stress. This leads to release of inflammatory mediators from the placenta, resulting in a generalised inflammatory response with systemic endothelial dysfunction. • Maternal features: ◗ cardiovascular: thought to involve increased sensitivity to angiotensin II (sensitivity is normally decreased

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Pre-ejection period,  see Systolic time intervals

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Ejection systolic heart murmurs are common, and third or fourth heart sounds may occur. - decreased SVR as a result of the smooth muscle relaxation caused by progesterone. Engorgement of cutaneous and epidural veins, the latter presumed to affect height of block in epidural anaesthesia. - reduced MAP, being lowest at the time of maximal cardiac output. - aortocaval compression in the supine position. - ECG changes caused by cephalad displacement of the diaphragm by the uterus include left axis deviation and inverted T waves in leads V2 and V3. ◗ respiratory: - increased minute ventilation (by 50% in the first trimester), mainly caused by increased tidal volume (thought to be a central effect of progesterone). - reduced arterial PCO2 to about 4 kPa (30 mmHg) with resulting respiratory alkalosis by the 12th week of pregnancy; arterial PO2 increases by about 1.3 kPa (10 mmHg). Arterial pH remains normal due to renal excretion of bicarbonate. - reduced FRC (both expiratory reserve volume and residual volume decrease) from the 20th week onwards, caused by the upward displacement of the diaphragm by the uterus. - increased O2 consumption throughout pregnancy, but especially in the third trimester (up to 20%). - increased risk of hypoxaemia during anaesthesia results from reduced FRC and increased O2 demand. - venous engorgement of the upper airway, predisposing to spontaneous epistaxis or haemorrhage on instrumentation. ◗ gastrointestinal: gastric emptying is probably normal apart from during labour, when it may be reduced (markedly if opioids are given). Gastric acidity is probably normal. Gastro-oesophageal reflux occurs in at least 80% of women, caused by the effects of progesterone on the lower oesophageal sphincter, and the uterus pushing the stomach into a horizontal position. The time after conception at which the GIT effects occur, and the time after delivery at which they revert to normal, are unknown. 16–20 weeks has been suggested as the time of onset; progesterone levels fall to non-pregnant levels by 24 h of delivery, and reflux usually resolves by 36 h. ◗ coagulation: increased levels of fibrinogen and all clotting factors except XI and XIII, predisposing towards thromboembolism. Platelet count falls slightly. Systemic fibrinolytic activity is depressed, but localised activity (i.e., ability to lyse clots from within) is maintained. Thus the level of fibrin degradation products increases as pregnancy progresses. However, in normal pregnancy neither bleeding nor clotting times are increased. ◗ renal: dilatation of the renal pelvises and ureters from the end of the first trimester. Renal blood flow and GFR increase by 40%. Increased renin/ angiotensin system activity increases sodium and water retention, with falls in serum creatinine and urea; glycosuria may occur. ◗ endocrine: peripheral insulin resistance due to antagonism by hormones (e.g. human placental lactogen) may aggravate or precipitate gestational diabetes.

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- contraindicated if there is a coagulopathy or low platelet count (95% nitrogen washout is determined by the alveolar minute ventilation and size of the FRC (see Exponential process); in an adult undertaking normal tidal breathing,

Pressure-regulated volume control ventilation. Ventilatory mode combining the benefits of pressure-controlled IPPV with a decelerating inspiratory flow pattern and a guaranteed tidal volume. The ventilator automatically monitors the lung’s properties and modifies the inspiratory pressure level to deliver a predetermined volume. Maximum inspiratory pressure permitted is just below the preset upper pressure limit and, if the tidal volume cannot be delivered with this pressure, the ventilator alarms, indicating that the breath has been pressure-limited. Useful mode where lung/chest compliance alters during inspiration, e.g. atelectasis, bronchospasm. Achieves a set tidal/minute volume with the lowest possible inspiratory pressure. The maximum pressure change between two breaths is preset by the ventilator (approximately 3 cmH2O). Pressure regulators. Formerly called reducing valves, devices for reducing the high pressures delivered by cylinders to anaesthetic machines, and maintaining the reduced pressure at a constant level that is easier to use. Also reduce the requirement for high-pressure tubing. • May be: ◗ direct (Fig. 132a): cylinder pressure P tends to open the valve. ◗ indirect (Fig. 132b): cylinder pressure P tends to close the valve. The diaphragm moves according to p and the tension in the springs. As p falls, the diaphragm bulges into the regulator, allowing more gas flow into the upper half and thus maintaining p. If p increases, the diaphragm is pushed upwards, decreasing gas flow and again maintaining p. Thus pressure is maintained despite changes in demand. If cylinder pressure P falls, p is likewise maintained.

Probability limits central sensitisation and long-term postoperative pain, rather than just surgical incision, and that the nature and duration of therapy are more important than the timing per se. Clarke H, Poon M, Weinrib A, et al (2015). Drugs; 75: 339–51

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Main spring Diaphragm

Priestley, Joseph (1733–1804). English scientist and theologian, best known for his work on various gases. A major proponent of the phlogiston theory, he isolated ammonia (as ‘alkaline air’), sulfur dioxide (‘vitriolic acid air’), O2 (‘dephlogisticated air’), N2O (‘dephlogisticated nitrous air’), nitrogen dioxide (‘nitrous acid air’) and methane. Also investigated electrical conduction. Emigrated to the USA in 1794.

Reduced pressure p

Cylinder pressure P Sealing spring

Prilocaine hydrochloride. Amide local anaesthetic agent, introduced in 1959. Slower in onset than lidocaine, but lasts about 1.5 times as long and less toxic. pKa is 7.9. 55% protein-bound. Undergoes hepatic and renal metabolism. Maximal safe dose: 5 mg/kg alone, 8 mg/kg with adrenaline. Used as 0.5%–1.0% solutions for infiltration, 1%–2% for nerve blocks and 0.5% for IVRA. Also available as a 4% plain or 3% solution with felypressin for dental infiltration, and in EMLA cream. May cause methaemoglobinaemia in doses above about 600 mg in adults, due to its metabolite ortho-toluidine.   A preservative-free hyperbaric 2% solution (with 6% glucose) for spinal anaesthesia was introduced in the UK in 2011.

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Sealing spring

Pressure sores,  see Decubitus ulcers

PRISM,  see Paediatric risk of mortality score

Pressure support,  see Inspiratory pressure support

Proarrhythmias.  Arrhythmias caused or exacerbated by antiarrhythmic drugs. May occur even with standard dosage and normally therapeutic plasma drug levels. Common examples include VT and torsade de pointes.

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ry   The regulators are specific to each gas, and should be labelled accordingly. Pressure relief valves are incorporated in case of excessive pressures. Pressure gauges may also be incorporated.   Two-stage regulators are often used, to reduce wear and tear on the diaphragm and reduce pressure fluctuations, especially if high gas flows are required. The output of one stage is the input of the second. Demand valves may be based on this principle.   Slave regulators are those whose output depends on the output of another regulator. For example, the output of an O2 regulator may be applied above the diaphragm of an N2O regulator, keeping the latter’s valve open. If the O2 pressure fails, the N2O valve closes.

Priming principle. Shortening of the time of onset of non-depolarising neuromuscular blockade by administration of a non-depolarising neuromuscular blocking drug in divided aliquots. The priming dose (15%–20% of the usual intubating dose) is followed by the remainder of the intubating dose 4–8 min later, depending on the drug used. • Suggested explanatory theories: ◗ the priming dose occupies a proportion of post­ synaptic receptors at the neuromuscular junction; the main dose can thus occupy more rapidly the critical mass of receptors for neuromuscular blockade. ◗ the priming dose occupies presynaptic receptors, reducing mobilisation and release of acetylcholine; the main dose thus acts faster. Initially thought to answer the need for rapid tracheal intubation without using suxamethonium. However, the priming dose itself may cause unpleasant symptoms (e.g. diplopia and weakness) and serious complications, e.g. hypoventilation and aspiration of gastric contents. Jones RM (1989). Br J Anaesth; 63: 1–3

Fig. 132 Diagram of pressure regulators: (a) direct; (b) indirect. See text

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Preventive analgesia.  Intervention during the perioperative period with the aim of reducing postoperative pain and/or analgesic consumption. Distinct from the concept of ‘pre-emptive analgesia’, which refers solely to an intervention given before surgical incision with the intention to provide greater analgesia than if it were given post-incision. ‘Preventive analgesia’ incorporates all perioperative methods used to reduce postoperative pain and arose as a result of an appreciation that several mechanisms (such as premorbid psychological factors, perioperative immobilisation and postoperative inflammation) can contribute to

Probability (P). In statistics, the likelihood that the observed result is a chance occurrence. Analogous to, but distinct from, the chance of a type I error. Statistical significance is usually denoted by a P value 4 mg/ kg/h) for prolonged periods (>2 days), but it has also been reported after lower infusion rates and total doses. Thought to be related to exacerbation of poor tissue oxygenation and impaired cellular utilisation of glucose, due to impairment of mitochondrial oxidative phosphorylation. Inhibition of fatty acid oxidation may also be involved. Treatment is supportive and includes withdrawal of propofol; haemodialysis has been used successfully. Mortality is around 50% overall. Krajčová A, Waldauf P, Anděl M, Duška F (2015). Crit Care; 19: 398

• Dosage:

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and target plasma propofol concentration (in healthy patients, 4–8 µg/ml for induction of anaesthesia and 3–6 µg/ml for maintenance). ◗ 1.0–4.0 mg/kg/h for sedation. Contamination during preparation for infusion has led to iatrogenic bacteraemia; hence the development of the EDTA preparation.   Contains the same energy content as 10% fat emulsion (900 Cal/l). Plasma lipid levels should be monitored in all patients receiving propofol infusions for longer than 3 days.   The 1% solution is licensed for induction/maintenance of anaesthesia and sedation for short procedures in children over 1 month (the 2% solution should not be used in children PA > Pv; thus flow depends on the difference between Pa and PA, and not on Pv. ◗ zone 3: Pa > Pv > PA; i.e., flow depends on the difference between Pa and Pv, as usually occurs in other tissues. ◗ zone 4: suggested as existing at lung bases; pulmonary interstitial pressure exceeds Pa, thus impairing blood flow. The vessels are supplied by sympathetic vasoconstrictor (α-receptors) and vasodilator (β2-receptors) fibres, and by parasympathetic vasodilator fibres. However, resting vascular tone is minimal, with vessels almost maximally dilated in the resting state. Other factors affecting vessel calibre include vascular responses to local changes, e.g. hypoxic pulmonary vasoconstriction and other factors affecting pulmonary vascular resistance.   The pulmonary circulation contains about 10%–20% of the total blood volume (i.e., 0.5–1.0 l). It changes during respiration (especially IPPV) and may increase by 25%–40% in moving from the erect to the supine position. [John B West, Australian-born Californian physiologist] See also, Starling resistor; Ventilation/perfusion mismatch

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Pulmonary embolism  (PE). Mechanical obstruction of a pulmonary artery/arteriole; usually refers to blood-borne thrombus. The most common cause of death within the first 10 postoperative days. Thrombus usually arises from a DVT in the legs/pelvis, although the venae cavae and right side of the heart are sometimes sources. The effects depend on the size and distribution of the PE; release of vasoactive mediators (e.g. prostaglandins) may contribute to resultant vasospasm. Massive PEs cause rapid respiratory and cardiovascular collapse, and death. Smaller PEs may cause few haemodynamic effects, but may result in infarction of a section of lung tissue if collateral blood flow is inadequate. Multiple PEs may cause widespread pulmonary vascular obstruction and lead to pulmonary hypertension.   Risk factors are as for DVT. • Features: ◗ pleuritic chest pain, haemoptysis, dyspnoea and mild pyrexia in small PEs.

Pulmonary fibrosis.  Thickening and infiltration of alveolar walls and perialveolar tissue. • May result from: ◗ localised loss of lung parenchyma, e.g. following infection, infarction or aspiration of irritant substances (e.g. aspiration of gastric contents). May also follow treatment with cytotoxic drugs, e.g. bleomycin. Causes decreased movement and breath sounds, dullness to percussion and increased vocal resonance. Neighbouring structures (e.g. trachea) may be pulled towards the affected portion. ◗ generalised alveolitis: a degree of fibrosis may remain following ALI. ◗ idiopathic interstitial pneumonitis: progressive, irreversible and usually lethal. Loss of the pulmonary vascular bed may lead to pulmonary hypertension and cor pulmonale. Typically, there is hypoxaemia with hypocapnia due to hyperventilation. V/̇ Q̇ mismatch is now thought to be responsible for the hypoxaemia, rather than alveolar membrane thickening, as previously suspected. Diffusing capacity, compliance and lung volumes are reduced, with normal FEV1/FVC ratio.

Pulmonary oedema

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Pulmonary hypertension  (PH). Defined as mean pulmonary artery pressure (PAP) >25 mmHg at rest, measured by cardiac catheterisation. Prevalence is ~100 per million in the UK. Prognosis varies widely according to clinical subtype, patient characteristics and response to treatment. Absolute PAP values are not usually of prognostic value; clinical features are more useful for assessing severity. High-risk features (implying a 1-year mortality of >10%) include rapid progression of symptoms, signs of right ventricular (RV) failure and repeated syncope.   Anaesthesia presents significant risk to patients with PH, who should ideally be managed in specialist centres. Patients with PH requiring intensive care support have a mortality of ~40%. PH also carries a very high maternal mortality (~40%–50%) and pregnancy is actively discouraged. • Previously described as either ‘primary’ or ‘secondary’, now classified by the World Health Organization into 5 groups according to pathology, clinical features and treatment strategies (although individual patients may overlap multiple groups): ◗ group 1: pulmonary arterial hypertension (PAH). Characterised by PH with pulmonary capillary wedge pressure (PCWP) 3 Wood units. Causes include: idiopathic (previously termed ‘primary’); heritable; drug-induced (e.g. by amfetamines); connective tissue diseases (e.g. systemic sclerosis); portal hypertension; schistosomiasis; and congenital heart disease (commonly left-to-right shunt lesions, e.g. ASD, VSD, patent ductus arteriosus). Also includes pulmonary veno-occlusive disease and persistent pulmonary hypertension of the newborn (PPHN). ◗ group 2: PH due to left heart disease resulting in pulmonary venous/capillary hypertension, e.g. in left ventricular failure, left heart inflow/outflow tract obstruction (e.g. mitral stenosis). ◗ group 3: PH due to lung diseases that result in chronic hypoxaemia, e.g. COPD, pulmonary fibrosis, sleepdisordered breathing. ◗ group 4: PH due to chronic PE or other pulmonary artery obstruction. ◗ group 5: PH with unclear/multifactorial mechanisms. Pathological mechanisms are complex and variable, but include: vascular remodelling of the pulmonary arteries with medial hypertrophy and intimal thickening; impaired production of nitric oxide and prostacyclin; localised inflammation and fibrosis; and hypoxic pulmonary vasoconstriction. The increased RV afterload causes progressive hypertrophy and dilatation as ventricular failure supervenes; biventricular failure may then ensue, owing to ventricular interdependence. • Features: ◗ fatigue, dyspnoea, angina, syncope, haemoptysis. ◗ low cardiac output, cyanosis, features of right ventricular enlargement/failure, e.g. sternal heave, peripheral oedema.

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Pulmonary function tests,  see Lung function tests

ECG findings: right axis deviation, right bundle branch block, prolonged Q–T syndromes, right atrial and ventricular hypertrophy. ◗ CXR: right atrial and ventricular enlargement, large pulmonary arteries with peripheral pruning. • Diagnosis and assessment: ◗ echocardiography is used initially to assess the probability of PH; suggestive features include peak tricuspid regurgitation velocity of >3.4 m/s, RV/ RA enlargement and significant diastolic pulmonary valve regurgitation. If PH is suspected, high resolution chest CT, lung function tests ± V/̇ Q̇ scans are then performed, and cardiac catheterisation considered. ◗ definitive diagnosis requires right heart catheterisation, which is always performed before commencing specific treatment for PH. • Treatment: ◗ supportive treatment includes oral anticoagulant drugs, diuretics, and oxygen therapy. ◗ specific drug therapy includes calcium channel blocking drugs, prostacyclin analogues, endothelin receptor antagonists and type 5 phosphodiesterase inhibitors, alone or in combination. ◗ treatment of the underlying cause where possible. ◗ lung-transplantation (or rarely, heart-lung transplantation). • Anaesthetic management: ◗ centres around supporting right ventricular output by optimising preload and contractility and avoiding factors that increase PVR (e.g. hypoxia, acidosis). ◗ SVR should be proactively maintained and tachycardia avoided to protect coronary blood flow to the right heart. ◗ combinations of midazolam, fentanyl, and etomidate may be used for induction. A balanced technique with volatile agent and opioids may be used for maintenance. N2O is often avoided as it may increase PVR. ◗ direct arterial blood pressure measurement is usual. ◗ transoesophageal echocardiography may be used to direct intraoperative management. ◗ an acute rise in PVR (‘PVR crisis’) is managed with 100% oxygen, adequate anaesthesia/neuromuscular blockade, hyperventilation (to achieve respiratory alkalosis) and pulmonary vasodilators (e.g. inhaled nitric oxide). Galie N, Humbert M, Vachiery JL, et al (2016). Eur Heart J; 37: 67–119 See also, Cor pulmonale ◗

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Work of breathing is increased; rapid, shallow breathing is common. CXR may reveal diffuse nodular/reticular shadowing, with local contraction in focal disease.   Treatment is of the underlying cause; corticosteroids are often used. • Anaesthesia: although the pulmonary defect is restrictive instead of obstructive, principles are as for COPD.

Pulmonary irritant receptors. Receptors situated between airway epithelial cells, responsible for initiating bronchospasm and hyperpnoea in response to inhaled noxious gases, smoke, dust and cold air. Afferent impulses pass via the vagi to the medulla. May be involved in initiating asthma attacks. Pulmonary oedema.  Increased pulmonary ECF (normally minimal). Small amounts of fluid normally pass through the capillary wall into the interstitial space of the lung. The junctions between alveolar epithelial cells are relatively resistant to fluid, which is removed by the lymphatic system at about 10 ml/h. Lymphatic removal may increase dramatically if transudation into the interstitial space increases. Net flux into the interstitial space is governed by Starling forces.

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Pulmonary stretch receptors ◗

venesection may be performed for pulmonary oedema due to volume overload, with removal of 200–500 ml blood.

Pulmonary stretch receptors.  Mechanoreceptors within the smooth muscle of the lower airways; transmit impulses via the vagi to the dorsal medulla. Excitation limits inspiration during pulmonary overinflation (Hering–Breuer reflex). Sensitivity is increased by decreased arterial PCO2 and increased pulmonary venous pressure. May also be involved in other pulmonary reflexes, e.g. gasp and deflation reflexes.

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Pulmonary valve lesions. Include: ◗ pulmonary stenosis (PS): may occur at the valve (90%), infundibulum or within the artery. Almost always congenital, accounting for 5%–10% of congenital heart disease. Other causes include rheumatic fever and carcinoid syndrome. Usually asymptomatic; if severe, PS may cause fatigue, dyspnoea and angina secondary to decreased cardiac output. Right ventricular (and later atrial) hypertrophy may occur, with associated diastolic dysfunction. May be associated with right-to-left shunt and cyanosis, e.g. Fallot’s tetralogy. Features: ejection systolic murmur at the upper left sternal edge, heard best during inspiration. Splitting of the second heart sound is increased, with a quiet pulmonary component in severe PS. Right ventricular and atrial enlargement may be suggested by the ECG and CXR; a prominent pulmonary artery and pulmonary oligaemia may appear on the latter. During anaesthesia, increased right ventricular O2 consumption (e.g. caused by tachycardia and increased contractility) should be avoided. ◗ pulmonary regurgitation (PR): usually a feature of pulmonary hypertension, and results from dilatation of the valve ring. Other causes include congenital absence of the valve, endocarditis (usually in iv drug abusers) and surgical valvotomy. Causes right ventricular hypertrophy with subsequent dilatation if persistent and severe. Features: high-pitched blowing diastolic murmur at the upper left sternal edge.

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alteration of Starling forces: - increased hydrostatic pressure, e.g. hypervolaemia, left ventricular failure, mitral stenosis. - decreased plasma oncotic pressure, e.g. hypoproteinaemia. - acute severe subatmospheric airway pressure, e.g. upper airway obstruction. ◗ damage to the alveolar–capillary membrane, e.g. ALI. ◗ impairment of lymphatic drainage, e.g. lymphangitis carcinomatosis, silicosis. ◗ causes of uncertain aetiology: - neurogenic: thought to involve sudden catecholamine release following TBI, with vasoconstriction increasing lung capillary pressures and capillary permeability. - following naloxone administration: also thought to involve catecholamine release. - in opioid poisoning, possibly related to decreased vascular permeability. - following pulmonary surgery or re-expansion of a pneumothorax: probably involves local changes in capillary pressures and permeability. - after exposure to high altitude, possibly via pulmonary vasoconstriction. As fluid clearance mechanisms are overwhelmed, interstitial oedema increases, until alveolar oedema occurs. Eventually, frothy oedema fluid fills the airways, impairing gas exchange. Airways and pulmonary vessels become narrowed by interstitial oedema, and FRC and compliance decrease. • Features: ◗ dyspnoea, tachypnoea, cough with pink frothy sputum, and tachycardia. Respiratory distress is worse lying flat (orthopnoea). ◗ wheeze and basal crepitations on auscultation. ◗ features of respiratory failure. ◗ arterial blood gas interpretation usually reveals hypoxaemia, with hypocapnia secondary to hyperventilation. Metabolic acidosis may be present in severe cases. ◗ CXR features include those of the underlying condition. Lung oedema itself appears as fluffy shadowing, typically perihilar (‘bat’s wing’) in left ventricular failure and patchy (‘cotton-wool’) and peripheral in ALI. Bronchial and vascular markings may appear thickened due to interstitial oedema. Kerley’s (B) lines and fluid in the transverse fissure may be present. Differentiation between hydrostatic and other causes may be aided by measurement of pulmonary capillary wedge pressure. Alveolar fluid protein content may also be measured. Total lung water content has been measured using radioactive or dye dilution techniques. • Treatment of severe acute pulmonary oedema: ◗ of the underlying condition. ◗ O2 therapy. CPAP may be useful. ◗ sitting the patient, with the legs over the edge of the bed. ◗ diuretics, e.g. furosemide 20–120 mg iv (causes vasodilatation and diuresis). ◗ opioids, e.g. morphine, diamorphine 1–5 mg iv (for anxiolysis and vasodilatation). ◗ inotropic and vasodilator drugs. ◗ IPPV may be required. Gas exchange is usually improved by PEEP.

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• Mechanisms of formation of pulmonary oedema:

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Pulmonary vascular resistance (PVR). Resistance in the pulmonary circulation, analogous to SVR. May be calculated using the principle of Ohm’s law: mean pulmonary artery pressure − left atrial pressure (mmHg) × 80 PVR = (dyne s cm 5 ) cardiac output (l min) where 80 is a correction factor. Normally 20–120 dyne s/cm5 (N.B. 1 dyne s/cm5 = 100 N s/m5). May also be expressed as Wood units.   Resistance is distributed more evenly than in the systemic circulation, with approximately 50% residing in the arteries and arterioles, 30% in the capillaries and 20% in the veins. The pulmonary arteries are thin-walled, large in diameter and easily distensible. The pulmonary circulation is therefore more dependent on gravity, posture and the relationship between alveolar and intravascular pressures than on vascular muscular tone. • PVR is affected by: ◗ passive factors: - lung expansion: at lung volumes below FRC, the radial forces holding the extra-alveolar vessels

Pulse pressure

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Pulse oximeter.  Device used to determine arterial O2 saturation using oximetry. Consists of the following components: ◗ two light-emitting diodes (LEDs) within the probe emit monochromatic light at red (660 nm) and infrared (940 nm) wavelengths. ◗ a photodiode on the opposite side of the probe detects the transmitted light; because it is unable to differentiate between the wavelengths, each LED is alternately switched on and off, the timing of which allows identification of red and infrared pulses. The periods when both LEDs are off allow compensation for ambient light conditions. ◗ the signal is converted to a DC component representing tissue background, venous blood and the constant part of arterial blood flow, and an AC component representing pulsatile arterial blood flow. The former is discarded, the latter amplified and averaged over a few seconds. ◗ the ratio of pulsatile transmitted red to infrared light is calculated and compared with stored calibration curves (derived from healthy human volunteers) to give an estimated SpO2 (suggested as appropriate notation of SaO2 measured by a pulse oximeter). ◗ the signal is displayed ideally as a continuous trace, showing quality of signal and a numerical value of SpO2. Most modern machines automatically adjust gain to maintain a constant size of trace. An important part of routine monitoring during anaesthesia/sedation and on intensive care. Oximetry is also used to monitor sleep apnoea during sleep studies, in cardiac and respiratory function testing, CPR and assessment of peripheral circulation. It has been shown to detect desaturation in patients when clinical assessment reveals no abnormality, e.g. during anaesthesia, recovery and transport of patients. • Inaccuracy may result from excessive ambient light, movement artefact, poor peripheral perfusion, electrical interference, venous congestion, and when SaO2 is less than 80% (as calibration data below this level are extrapolated). Response time to detecting desaturation varies with probe location (e.g. up to 30–60 s with a finger probe). Coloured nail polish may produce inaccuracies (tends to increase readings). Effects of other pigments: ◗ carboxyhaemoglobin: most is counted as HbO; thus SpO2 is falsely high. ◗ methaemoglobin and bilirubin: counted as Hb; thus SpO2 is falsely low (but may be falsely high if true saturation is very low, i.e., 2–4 mm, or more than a quarter of the height of the R wave in the same lead). In the absence of left bundle branch block they suggest MI, which may be old or of new onset; in acute S–T elevation MI, Q waves are associated with poorer outcomes.

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qSOFA,  see Sepsis-related organ failure assessment

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Q–T interval. Represents the duration of ventricular systole; varies with age, sex and heart rate. Measured from the beginning of the QRS complex to the end of the T wave of the ECG (see Fig. 60b; Electrocardiography). Corrected for heart rate by dividing by the square root of the preceding R–R interval in seconds (Bazett’s formula). Normal range is 0.35–0.43.   Shortened in hypercalcaemia, hyperkalaemia and digoxin therapy. Prolonged Q–T syndromes may be caused by hypocalcaemia, hypothyroidism and hypothermia, and are associated with recurrent syncope or sudden death due to ventricular arrhythmias, including VT and torsade de pointes. [H Cuthbert Bazett (1885–1950), English-born US physiologist] Q–Tc dispersion. Difference between the longest and shortest measurable corrected Q–T interval on the 12-lead ECG. Originally described using manual calculation, although automatic measuring methods have been described. Has been shown to be a powerful predictor of arrhythmias and sudden cardiac death in several cardiac conditions.   Suggested explanations for Q–Tc dispersion include patchy myocardial fibrosis and left ventricular dilatation, although the exact mechanism is unclear. Sahu P, Lim PO, Rana BS, Struthers AD (2000). Q J Med; 93: 425–31 Quadratus lumborum block,  see Transversus abdominis plane block

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Quinupristin/dalfopristin. Synergistic combination of antibacterial drugs that inhibits the 50S bacterial ribosomal unit. Used for serious skin infections (e.g. severe cellulitis) caused by Staphylococcus aureus or Streptococcus pyogenes. Has short half-life (0.8 h) and excreted mainly through faeces. • Dosage: 7.5 mg/kg iv by infusion over 1 h, 12-hourly. • Side effects: pain and inflammation over infusion site, hyperbilirubinaemia, GIT upset, rash.

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Quinidine.  Class Ia antiarrhythmic drug. An isomer of quinine. Used to treat SVT and VT, but rarely used now because of side effects including include ventricular arrhythmias (e.g. torsade de pointes), anticholinergic effects; CNS effects (cinchonism) including tinnitus and visual changes, and hypersensitivity reactions. Unavailable in the UK although still licensed in a number of other countries. May possibly have a role in reducing the frequency and severity of arrhythmias in Brugada syndrome, as a far

4-Quinolones.  Class of broad-spectrum antibacterial drugs, which include ciprofloxacin, levofloxacin, moxifloxacin, ofloxacin and norfloxacin. More effective against gramnegative than gram-positive bacteria, they have limited activity against anaerobes. Side effects include prolonged Q–T syndromes, spontaneous tendon rupture and muscle weakness. May also induce convulsions in susceptible individuals, especially if NSAIDs are taken concurrently. They should be used with caution in hepatic or renal impairment.

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Quincke, Heinrich Irenaeus  (1842–1922). German physician; described and standardised lumbar puncture in 1891, originally as a treatment for hydrocephalus. Used the paramedian approach and suggested 24 hours’ bed rest afterwards. His bevelled needle design is still used for lumbar puncture and spinal anaesthesia. Quincke’s sign is pulsation in the nail capillary bed and is seen in aortic regurgitation. Also first to describe angio-oedema. Minagar A, Lowis GW (2001). J Med Biogr; 9: 12–15

Quinine sulfate/dihydrochloride.  Antimalarial drug, reserved for treatment (but not prophylaxis) of falciparum malaria. Also used to treat nocturnal leg cramps. • Dosage ◗ malaria: - 600 mg orally tds for 5–7 days. - 20 mg/kg over 4 h iv as initial dose (unless a related drug has been given within 24 h), then 10 mg/kg over 4 h tds until able to complete the 7-day course with oral therapy. ◗ leg cramps: 200–300 mg orally at night. • Side effects: tinnitus, headache, visual disturbances (cinchonism), GIT disturbances, hypersensitivity (including thrombocytopenia and DIC), arrhythmias, renal failure, hypoglycaemia, convulsions.

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Quantiflex apparatus. Continuous-flow anaesthetic machines that can deliver preset mixtures of O2 and N2O, adjusted by a percentage control (minimum of 30% O2). A single dial adjusts total gas flow delivered. Individual flowmeters indicate flow of O2 and N2O; the O2 flowmeter is usually on the right, and N2O flowmeter on the left. They are sometimes used in dental surgery.

cheaper alternative to implantable cardioverter-defibrillators, especially in resource-poor countries. [Pedro and Josep Brugada, Spanish-born cardiologists]

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Quantal theory.  Widely accepted theory proposed in the 1950s to explain miniature end-plate potentials recorded from the neuromuscular junction postsynaptic membrane, at approximately 2 Hz. Postulates that small ‘quanta’ (packets) of acetylcholine are released randomly from the nerve cell membrane, even in the absence of motor nerve activity. Each quantum is thought to be one vesicle’s content, about 10 000 acetylcholine molecules. During single motor nerve activation about 200 quanta are released into the synaptic cleft.

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Rabeprazole sodium.  Proton pump inhibitor; actions and effects are similar to those of omeprazole. • Dosage: 20 mg orally od. • Side effects: as for omeprazole.

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Radial nerve  (C5–T1). Terminal branch of the posterior cord of the brachial plexus. Descends in the posterior upper arm, passing laterally behind the middle of the humerus in the radial groove. Crosses the antecubital fossa anterior to the elbow joint, between brachialis and brachioradialis. Descends under brachioradialis lateral to the radial artery in the forearm, passing posteriorly proximal to the wrist to end on the dorsum of the hand as digital branches. • Branches: ◗ axillary: to deltoid, teres minor and skin of the posteromedial upper arm. ◗ upper arm: - to triceps, brachioradialis and extensor carpi radialis longus. - skin of the lower posterolateral arm. ◗ forearm: - to the elbow joint. - posterior interosseous nerve arising at the elbow joint: passes posteriorly round the radial neck to supply the elbow, wrist and intercarpal joints, and all extensor muscles of the forearm apart from extensor carpi radialis longus. - via digital branches to the lateral side of the dorsum of the hand and posterior aspects of the lateral 2.5 digits up to the distal phalanx. May be blocked at the elbow, wrist, and at mid-humerus with the elbow flexed (the nerve is palpable in the radial groove). See also, Brachial plexus block; Elbow, nerve blocks; Wrist, nerve blocks

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Rabies.  Infection caused by a lyssavirus of the rhabdovirus family, eradicated from Britain in 1902; however, occasional cases thought to have originated outside the UK have occurred in animals, e.g. dogs and bats. Fewer than five cases occur annually in Europe and the USA. Dogs are the source of infection in 99% of cases but bats and other wildlife are occasionally responsible. Transmitted via infected saliva penetrating broken skin or intact mucosa; it has also been reported following organ transplantation from a person who has died of the disease. The virus replicates in local muscle then migrates proximally along peripheral nerves to dorsal root ganglia and the CNS, eventually causing lethal encephalitis. Incubation period is usually 20–90 days in humans, but may be 4 days to several years.   Malaise, fever, depression and psychosis may be followed by laryngeal spasm, and extreme anxiety on drinking fluids. Respiratory and autonomic failure occurs early and cardiac involvement, including myocarditis, is common.   Treatment of established rabies includes injection of human antirabies immunoglobulin, early IPPV, sedation and paralysis, with careful maintenance of acid–base and fluid balance. Almost inevitably fatal once established (death typically occurs 7–10 days after symptoms appear), it may be prevented by wound cleaning and active and passive immunisation. Crowcroft NS, Thampi N (2015). Br Med J; 350: g7827

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R wave. First upward deflection of the QRS complex of the ECG (see Fig. 60b; Electrocardiography). Tends to increase in size from V1 to V6, with an accompanying reduction in size of S wave across these leads. Loss of this ‘R wave progression’, with a sudden increase in R wave size in V5 or V6, may indicate old anterior MI. In V1–6, at least one normally exceeds 8 mm, but none exceeds 27 mm.

and runs distally on the tendons and muscles attached to the radius (biceps tendon, supinator, pronator teres, flexor digitorum superficialis, flexor pollicis longus, pronator quadratus). Lies deep to brachioradialis muscle in the upper forearm, but subcutaneous in the lower forearm and easily palpable, especially over the distal quarter of the radius. Runs deep to abductor pollicis longus and extensor pollicis brevis tendons at the radial styloid, entering the anatomical snuffbox. Then enters the palm between the first and second metacarpals, forming the deep palmar arch. Branches include a superficial palmar branch (enters the palm superficial to the flexor retinaculum), which supplies the muscles of the thenar eminence before anastomosing with the superficial palmar arch. At the wrist, it is a common site for palpation of the pulse and for arterial cannulation. See also, Ulnar artery

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R on T phenomenon. Arises when the R wave of a ventricular ectopic beat falls on the T wave of the preceding beat. At the middle of the T wave, the myocardium is partly depolarised and partly repolarised, and thus vulnerable to establishment of re-entrant and circulatory conduction, leading to VF or VT.

Radford nomogram.  Diagram showing the relationship between tidal volume, patient’s weight and respiratory frequency. Used to aid appropriate selection of ventilator settings for children and adults. Now rarely used. [Edward P Radford (1922–2001), US physiologist] Radial artery. Terminal branch of the brachial artery. Arises in the antecubital fossa, level with the radial neck,

Radiation.  Emission of energy in the form of waves or particles. Includes emission of electromagnetic waves (e.g. light), most of which is non-ionising (does not have sufficient energy to overcome electron binding energy). Ionising radiation may result in displacement of electrons in organic material with the potential for tissue damage, and includes:

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Radiography in intensive care

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Radiological contrast media.  Contain large molecules that absorb x-rays (e.g. barium [enteral] or iodine [enteral or iv]) or have paramagnetic properties (e.g. gadolinium) for MRI scanning. Adverse reactions may follow iv injection: ◗ related to high osmolality (up to 7× that of plasma): - initial hypervolaemia followed by osmotic diuresis and hypovolaemia. - damage to red blood cells and vascular endothelium. ◗ immunological: - reactions range from mild symptoms to cardiovascular collapse and death. - adverse reactions are most likely to be due to direct histamine release or complement activation. ‘True’ anaphylaxis (involving previous exposure to the antigen) is not thought to occur. ◗ direct toxicity: myocardial depression and systemic vasodilatation. Thus initial hypertension may be followed by prolonged hypotension. Renal failure may result from cardiovascular changes plus direct toxicity.   Incidence of reactions and renal failure is decreased by using low osmolar, non-ionic media. Other measures to prevent renal injury include adequate hydration and administration of N-acetylcysteine. Resuscitation equipment and drugs must always be available. Pasternak JJ, Williamson EE (2012). Mayo Clin Proc; 87: 390–402 See also, Adverse drug reactions

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Radiography in intensive care.  Increasingly used as the range and quality of techniques and equipment available increase. Consultation with radiologists aids the proper selection and interpretation of many imaging techniques. In most cases, the use of mobile equipment results in less than optimal results but may be acceptable given the difficulty of transporting critically ill patients from the ICU; subtle changes between sequential films may be misleading if this is not taken into account. Investigations include CXR, ultrasound (including echocardiography) and CT and MRI scanning; bedside CT scanners are now available but not widespread; therefore CT and MRI require transport to the imaging department. MRI scanning times are often long and therefore CT imaging is favoured in critically ill patients. Radioisotope scanning requires transfer from the ICU, often to a specialist centre.   Practical considerations include the requirement for sedation and adequate monitoring during transport or the procedure itself, the interference of the procedure with background therapy including the requirement for moving the patient (e.g. to place films underneath), and the potentially adverse effects of radiological contrast media. See also, Imaging in intensive care

by certain tissues, allowing imaging of the tissue concerned, e.g. fibrinogen labelled with iodine-123 accumulates in a clot and may be used to detect DVT. Therapeutic use includes radiotherapy. See also, Radioisotope scanning

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α particles: helium nuclei consisting of two protons and two neutrons. Have high energy but penetrate matter poorly. ◗ β particles: electrons or positrons with variable energy and velocity. Those with high energies are more penetrating than α particles but much less than γ-rays and x-rays. ◗ γ-rays and x-rays: electromagnetic waves emitted from (γ-rays) or outside (x-rays) the nuclei of excited atoms. Have extremely high penetration of matter and thus pose a health hazard requiring radiation safety precautions. γ-Rays are used in radiotherapy and imaging, and x-rays in imaging. Exposure to ionising radiation is kept to a minimum with appropriate storage and handling of radioisotopes, minimal use of x-rays and appropriate use of shielding. Formal training is required for those performing or directing radiology procedures. See also, Environmental safety of anaesthetists ◗

Radioisotope scanning. Use of radioisotopes to label certain parts of the body in order to investigate organ function, either directly or attached to circulating cells. Includes the following: ◗ assessment of blood flow: cerebral blood flow, renal blood flow, lung perfusion scans (e.g. combined with ventilation scans in suspected PE). ◗ nuclear cardiology. ◗ localisation of lesions: PE, bone metastases/infection/ fracture, intra-abdominal sepsis. The radiation contained within the body after scanning is negligible, posing no risk to staff.

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Radioisotopes.  Isotopes of elements that undergo disintegration; i.e., the nucleus emits α, β or γ radiation either spontaneously or following a collision. Used clinically as labels to determine fluid compartments, blood flow, pulmonary V/̇ Q̇ distribution and sites of infection. Technetium99m and xenon-133 are often suitable because they are easy to use and their half-lives are short. Also used to label metabolically active substances that are taken up

Radiology, anaesthesia for.  Most radiological procedures require neither general anaesthesia nor sedation. Anaesthesia may be required for the very young, confused or agitated patients and those with movement disorders. Procedures include CT scanning, MRI, angiography and invasive procedures, e.g. embolisation of vascular lesions in neuroradiology. • Main anaesthetic considerations: ◗ underlying disease process. ◗ remote location, often cramped conditions, with poor lighting. ◗ old or incomplete anaesthetic/monitoring equipment. ◗ poor access to the patient. ◗ adverse effects of radiological contrast media. ◗ specific problems of MRI. Preoperative assessment and preparation should be as for any anaesthetic procedure. Radiotherapy.  Use of ionising radiation to treat neoplasms. May involve: ◗ external radiation. ◗ implantation of internal sources (brachytherapy), e.g. in gynaecological or CNS tumours. ◗ administration of radioactive radioisotopes, e.g. iodine-131 in hyperthyroidism, phosphorus-32 in polycythaemia. • General anaesthesia is rarely required, except when patients are unco-operative, i.e., mainly children and patients with movement disorders. Anaesthetic considerations:

Rate–pressure product

Ranking,  see Statistical tests

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Ranolazine. Antianginal drug, licensed as adjunctive therapy. Inhibits the late inward sodium current in cardiac muscle, reducing intracellular calcium concentration and thus wall tension and oxygen demand. • Dosage: 375–750 mg orally bd. • Side effects: GIT upset, headache, dizziness, hypotension, prolonged Q–T interval, oedema, confusion. Raoult’s law.  The addition of a solute to an ideal solution reduces the vapour pressure of the solvent in proportion to the molar concentration of the solute. [François M Raoult (1830–1901), French scientist] See also, Colligative properties of solutions RAP, Right atrial pressure, see Cardiac catheterisation; Central venous pressure

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Randomisation. Technique for allocating subjects (e.g. patients to treatment groups in clinical trials) that reduces allocation bias when samples are compared. Ensures that both known and unknown factors affecting the outcome (e.g. baseline characteristics, environmental exposure) are randomly distributed among the groups; i.e., any difference in these factors is due to chance alone. • Randomisation may be: ◗ simple: no restriction on allocation. Groups may be unequally sized. ◗ block: allocation is performed in blocks, so that groups are equally sized within each block. ◗ stratified: factors such as age and sex are randomised separately, so that they are equally distributed among the groups. A more sophisticated method, minimisation, involves the distribution of successive subjects to the groups by taking into account the number of subjects already allocated who have these various factors, using a scoring system. For example, if age, weight and female sex are felt to be important prognostic factors in a particular study, an obese subject may still be allocated to a group that already has several obese subjects in it, if there are fewer older subjects and females than in the other groups. Computer-generated random numbers are usually employed. Use of coins or dice is tedious and presents the temptation to repeat an allocation if the result is not liked. Other methods have also been used, e.g. allocation of alternate patients, or according to patients’ birthdays or record numbers. However, these methods cannot always be guaranteed free of hidden bias.

is excreted via urine; hence the dose is reduced in renal failure. • Dosage: ◗ 50 mg iv/im tds. Effective if given 45–60 min preoperatively. If administered iv, 50 mg should be diluted into 20 ml and injected over at least 2 min, because severe bradycardia may occur. May also be given by continuous infusion: 125–250 µg/kg/h. ◗ 150–300 mg orally bd. For prophylaxis against aspiration pneumonitis, 150 mg orally qds (e.g. in labour), or 2 h preoperatively (preferably preceded by 150 mg the night before). • Side effects: blood dyscrasias, impaired liver function and confusion; all are rare.

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general condition of the patient: features of malignancy, site and nature of the neoplasm and drug therapy. Haematological abnormalities are common. ◗ repeated anaesthetics: multiple treatments are required, e.g. daily for several weeks. Considerations include fear of injections and repeated periods of starvation (especially important in children). IV cannulation may be difficult, although long-term catheters are often sited. ◗ immobilisation of the head may be required, e.g. for CNS tumours; clear plastic casts that cover the whole face are often used, with risks of airway obstruction. Head-down positioning may be required. ◗ treatments usually consist of short periods of radiation (e.g. a few minutes), during which the anaesthetist cannot be present. Monitoring is usually visible via remote-control cameras, but may be restricted. Techniques used include sedation or general anaesthesia using TIVA with propofol, or intermittent boluses of ketamine (especially in children).   Patients formerly treated by radiotherapy may have inflammatory or fibrotic changes in the irradiated area. Pulmonary, cardiac, neuroendocrine, renal and hepatic involvement may be present. Tissue fibrosis around the airway may make tracheal intubation difficult. Kolker A, Mascarenhas J (2015). Curr Opin Anaesthesiol; 28: 464–8 ◗

Ranitidine hydrochloride.  H2 receptor antagonist; better absorbed and more potent than cimetidine, with fewer side effects. Does not inhibit hepatic enzymes or interfere with metabolism of other drugs. Oral bioavailability is about 50%. Plasma levels peak within 15 min of im injection and 2–3 h after oral administration; effect lasts about 8 h. Half-life is about 2 h. Undergoes hepatic metabolism and

Rapacuronium bromide. Non-depolarising neuromuscular blocking drug, introduced in the USA in 1999 and withdrawn in 2001 just before its introduction in the UK, because of reports of fatal bronchospasm. Chemically related to vecuronium, it causes rapid onset of neuromuscular blockade (tracheal intubation possible within 60 s) with fast recovery (6–30 min depending on dosage) and was thus suggested as an alternative to suxamethonium. Rapid opioid detoxification.  Technique for treating opioid addiction by precipitating withdrawal using opioid receptor antagonists, e.g. naloxone or naltrexone, supposedly reducing relapse rates compared with conventional management. Ultrarapid opioid detoxification refers to administration of general anaesthesia or heavy sedation for prolonged periods to reduce awareness or recall of unpleasant withdrawal symptoms while the opioid antagonists are given. The technique is controversial (especially the ultra­ rapid form) because deaths have occurred and supportive evidence for its efficacy is poor, leading many authorities to abandon its use. Rapid sequence induction,  see Induction, rapid sequence

Rate–pressure product  (RPP). Product of heart rate and systolic BP, used as a rough indicator of myocardial workload and O2 consumption. It has been suggested that RPP should be maintained below 15 000 in patients with ischaemic heart disease during anaesthesia. Its usefulness has been questioned, because a proportional increase in rate may increase myocardial O2 demand more than the same increase in BP. A pressure–rate quotient (MAP/rate)

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RBBB

Rebreathing techniques,  see Carbon dioxide measurement

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Receiver operating characteristic (ROC) curves. Curves drawn to indicate the usefulness of a predictive test, originally derived from analysis of radar signals between the World Wars (i.e., did a deflection represent a real signal or just random noise; and if the former, with what degree of certainty?). For the test to be analysed (e.g. the usefulness of ASA physical status to predict mortality after anaesthesia), each cut-off level is examined in turn, and sensitivity and specificity calculated for it. Thus, for example, an ASA grade of 1 has high sensitivity (all deaths have an ASA grade of 1 or above) but low specificity (most patients with a grade of 1 or above do not die). For an ASA grade of 2, sensitivity is a little lower (some patients who die have a grade of 1, and will not be predicted by a grade of 2) while specificity is higher, although still poor (a grade of 2 is better at predicting death than a grade of 1, although most patients achieving 2 or above still do not die). The process continues until grade 5, which has low sensitivity (few of the deaths have a grade of 5) but high specificity (most patients who are graded 5 do, by definition, die). Sensitivity is plotted against (1 − specificity) and a curve obtained (Fig. 136); the area under the curve (AUC) represents the usefulness of the test: a perfect test includes 100% of the available area and one where prediction is no better than chance, 50%.

Receptor theory. States that receptors are specific proteins or lipoproteins located on cell membranes or within cells that interact selectively with extracellular compounds (agonists) to initiate biochemical events within cells. The structures of the agonist and receptor determine the selectivity and quantitative response. Drugs that interact with the receptor and inhibit the effect of an agonist are antagonists. Degree of binding to receptors is affinity; ability to produce a response is intrinsic activity.   Initial assumptions that the degree of response is proportional to the number of receptors occupied are not universally accepted. Other suggestions include: ◗ reduced occupancy is required for a potent agonist compared with a less potent agonist, to produce the same response. ◗ degree of response is proportional to the rate of receptor–agonist interaction and dissociation. Interaction of drug and receptor may resemble Michaelis– Menten kinetics. Covalent, ionic and hydrogen bonding, and van der Waals forces may be involved. • Different types of receptor: ◗ ligand-gated ion channels: direct opening of membrane pores allowing passage of ions (e.g. Na+, K+, Ca2+, Cl−) across the membrane, e.g. nicotinic acetyl­ choline receptor. Typically fast responses (90%

Residual volume

Table 43 Peptides of the renin/angiotensin system  

Substance

Converted to

By the action of

Site

Angiotensinogen Angiotensin I

Angiotensin I Angiotensin II

Plasma Mainly in lungs

Angiotensin II

Angiotensin III

Renin Angiotensin converting enzyme Aminopeptidase

Many tissues

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subsequent production of the peptides angiotensin I, II and III, involved in arterial BP control and fluid balance (Table 43). Angiotensin I is a precursor for angiotensin II, a powerful vasoconstrictor with a half-life of a few minutes. It causes aldosterone release from the adrenal cortex, and noradrenaline release from sympathetic nerve endings. It also stimulates thirst and release of vasopressin, and acts directly on renal tubules, resulting in sodium and water retention. Some may also be produced in the tissues. Angiotensin III also causes aldosterone release and some vasoconstriction.   Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists are used to treat hypertension. Aliskiren, a direct renin inhibitor, has recently been introduced for the treatment of essential hypertension; it has been associated with renal impairment, stroke, hypotension and hyperkalaemia, and avoidance of its combination with the above inhibitors/antagonists has been recommended.   Angiotensin II or its analogues have been used as vasopressor drugs when α-agonists are unable to correct severe hypotension, e.g. during surgery for hepatic tumours secreting vasodilator substances.

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for live donors. Indicated for patients with stage 4 or 5 renal failure. Previously considered an emergency and performed on unprepared patients, but the importance of proper preoperative assessment and preparation is now generally accepted. Major contraindications include active malignancy and infection. Most patients are already on dialysis although transplantation may be done before this is needed (pre-emptive transplant). If on dialysis, this is usually performed within 24 h of surgery. • Anaesthetic problems and techniques are as for chronic renal failure and transplantation. Additional points: ◗ general anaesthesia is preferred, although epidural and spinal anaesthesia have been successfully used. ◗ direct arterial blood pressure measurement is not necessarily required (although ischaemic heart disease and cardiac failure are common in these patients); CVP monitoring is routinely used to guide perioperative fluid therapy. ◗ adequate perioperative hydration is vital to optimise intravascular volume and BP in order to avoid acute tubular necrosis in the transplanted kidney. ◗ the patient should be kept normothermic. ◗ mannitol, furosemide and dopamine are sometimes given before the vessels to the new kidney are unclamped, in order to increase BP, stimulate urine production and improve graft function. ◗ transient hypertension may follow unclamping of the renal vessels. ◗ postoperatively, PCA may be used with care. NSAIDs are avoided. ◗ there is an increased incidence of kidney rejection in patients who have received blood transfusion during transplantation; preoperative correction of anaemia with erythropoietin should be considered. ◗ donors should be well hydrated to optimise perfusion of the kidney before harvesting. Ricaurte L, Vargas J, Lozano E, Díaz L (2013). Transplant Proc; 45: 1386–91 See also, Organ donation

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Renal tubular acidosis.  Group of conditions characterised by decreased ability of each nephron to excrete hydrogen ions (cf. renal failure, where the overall number of functioning nephrons is reduced, but those that remain excrete more hydrogen ions than normal). Characterised by normal GFR, metabolic acidosis, hyperchloraemia and a normal anion gap. May be associated with distal tubule dysfunction (type 1), proximal tubule dysfunction (type 2; usually associated with other abnormalities of proximal tubule function, e.g. Fanconi’s syndrome), or aldosterone deficiency or resistance (type 4). Type 3 is now considered a combination of types 1 and 2 and not a separate entity. Acidosis may be severe, and accompanied by marked hypokalaemia (hyperkalaemia in type 4). Treatment includes alkali (e.g. oral sodium bicarbonate) in types 1 and 2, thiazides in type 2 and mineralocorticoid therapy in type 4. [Guido Fanconi (1892–1979), Swiss paediatrician] Renin/angiotensin system.  Renin, a proteolytic enzyme (mw 37 kDa), is synthesised and secreted by the juxtacapillary apparatus of the renal tubule. Formed from two precursors, prorenin and preprorenin, its half-life is about 80 min. Secretion is increased in hypovolaemia, cardiac failure, cirrhosis and renal artery stenosis. Secretion is decreased by angiotensin II and vasopressin. Renin cleaves the circulating glycoprotein angiotensinogen with

Reperfusion injury.  Tissue injury resulting from restoration of blood flow after a period of ischaemia. Mechanisms include intracellular calcium excess, cellular oedema and free radicals. Although any tissue may be affected, most work has focused on cardiac function following hypoxic insult or hypoperfusion. Arrhythmias and myocardial stunning (reversible impairment of cardiac function) may also follow reperfusion. See also, Isoprostanes, No reflow phenomenon Reptilase time,  see Coagulation studies Reserpine.  Antihypertensive drug, no longer available in the UK. Depletes central and peripheral post-ganglionic adrenergic neurones of noradrenaline by irreversibly preventing its reuptake from axoplasm into storage vesicles. Side effects include bradycardia and postural hypotension, depression, sedation and extrapyramidal signs. Reservoir bag.  Usually 2 l capacity in most adult anaesthetic breathing systems and 0.5–1.0 l for paediatric use; its volume must exceed tidal volume. Movement indicates ventilation, but estimation of tidal volume from the degree of movement is inaccurate. Made of rubber (usually latexfree), distending when under pressure; maximal pressure is thus prevented from rising above about 60 cmH2O (Laplace’s law). Residual volume  (RV). Volume of gas remaining in the lungs after maximal expiration. About 1.5 l in the average

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Resistance

Resonance. Situation in which an oscillating system responds with maximal amplitude to an alternating external driving force. Occurs when the driving force frequency coincides with the natural oscillatory frequency (resonant frequency) of the system. May occur in pressure transducer systems if long, compliant tubing is used. May give rise to artefacts in the arterial waveform during direct arterial BP measurement. See also, Damping

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Resistance vessels. Term given to those blood vessels involved in regulation of SVR. 50% of resistance to blood flow occurs in the arterioles, which are thus the main regulators of SVR and therefore distribution of cardiac output.

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Resistance.  In electrical terms, the ratio of the potential difference across a conductor to the current flowing through it (Ohm’s law). Measured in ohms (Ω). Resistance to flow of a fluid through a circular tube is analogous to this; it equals the ratio of the pressure gradient along the tube to the flow through it.

therapy improves hypoxaemia due to V/̇ Q̇ mismatch but not shunt; the response to breathing 100% O2 may indicate the degree of shunt. PCO2 is often low because of hyperventilation in response to hypoxaemia. ◗ type II failure (ventilatory failure): hypoxaemia accompanied by arterial PCO2 >6.5 kPa (49 mmHg). Causes are as for hypoventilation. Acute exacerbation of COPD is a common cause. Diagnosis is made by arterial blood gas interpretation, but may be suspected clinically by signs of hypoxaemia and hypercapnia, with tachypnoea and use of accessory respiratory muscles. • Treatment: ◗ of underlying cause. ◗ sitting the patient up increases FRC and often improves oxygenation. ◗ oxygen therapy: should be titrated cautiously in type II failure if chronic hypercapnia is suspected. ◗ respiratory stimulant drugs (e.g. doxapram) have been used to avoid IPPV, e.g. in COPD, but are rarely used now. ◗ CPAP or non-invasive positive pressure ventilation may improve oxygenation and ventilation, avoiding the need for tracheal intubation. ◗ IPPV may be required if PCO2 is rising or the patient is exhausted. Criteria similar to those used in weaning from ventilators have been suggested for institution of IPPV. Tracheostomy may be necessary to aid weaning from mechanical ventilation. ◗ intravenous oxygenator, extracorporeal oxygenation and extracorporeal CO2 removal have been used.

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70-kg male; measured as for FRC. Increased RV accounts for most cases of increased FRC. See also, Lung volumes

Respiratory depression,  see Hypoventilation

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Respiratory distress syndrome  (RDS; Hyaline membrane disease). Occurs in approximately 1% of all live births, almost exclusively in premature babies. Caused by deficiency of surfactant, normally detectable in the fetal lung at 24 weeks’ gestation, although reversal of amniotic fluid lecithin/sphingomyelin ratio (related to fetal lung maturity) only occurs at 30 weeks. Decreased lung compliance, increased work of breathing and alveolar collapse may lead to respiratory failure, with characteristic granular appearance of the CXR.   Treatment is directed towards preventing hypoxaemia with CPAP initially, although IPPV is usually necessary, while trying to avoid O2 toxicity, barotrauma and retino­ pathy of prematurity. Exogenous surfactant given immediately after birth decreases mortality. Extracorporeal membrane oxygenation has been used.

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Respiratory exchange ratio.  Estimation of respiratory quotient derived from expired CO2/inspired O2 measurements; thus dependent on ventilation. Respiratory failure.  Defined as an arterial PO2 1.5 × baseline or GFR >25% decrease

2 × baseline or GFR >50% decrease

3 × baseline or >355 µmol/l (with a rise of >44) or GFR >75% decrease

4 weeks

End-stage renal disease

Complete loss of function for >3 months

Head

Rifabutin.  Antituberculous drug used for prophylaxis against Mycobacterium avium in immunocompromised patients. • Dosage: prophylaxis: 300 mg orally od; treatment: 150–450 mg od. • Side effects: blood dyscrasias, nausea, vomiting, hepatic impairment, orange discoloration of body secretions.

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Rifampicin.  Antibacterial drug, used primarily as an antituberculous drug but also in brucellosis, Legionnaires’ disease, severe staphylococcal infection, leprosy and as prophylaxis against meningococcal disease (thus may be given to ICU staff after caring for an infected patient or to household contacts). Causes hepatic enzyme induction and thus decreases the efficacy of oral contraceptives, anticoagulants and phenytoin. • Dosage: 300 mg orally (iv in severe infections) bd–qds. • Side effects: GIT upset, haemolytic anaemia, dyspnoea, renal and hepatic impairment, rashes, myopathy. Colours body secretions orange.

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Groove for subclavian a and brachial plexus

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Fig. 138 Anatomy of (a) a typical rib, seen from undersurface; (b) the first rib, seen from above

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posteriorly with the transverse process of the corresponding vertebra. ◗ shaft: flattened in the vertical plane. Curves forwards and inwards from the angle, lying lateral to the tubercle. The intercostal neurovascular bundle runs in the subcostal groove at the inferior border. • The first rib is of particular anaesthetic importance because of its relationship to the brachial plexus and other structures (Fig. 138b). Features: ◗ short, wide and flattened in the horizontal plane. ◗ lower surface is smooth and lies on pleura. ◗ upper surface is grooved for the subclavian vessels and brachial plexus. ◗ sympathetic chain, superior intercostal artery and upper branch of the first intercostal nerve lie anterior to its neck, between it and the pleura. ◗ scalenus anterior and medius attach to the scalene tubercle and body of the rib, respectively. See also, Intercostal nerve block; Intercostal space

RIFLE criteria.  Consensus staging classification of acute kidney injury described in 2004, consisting of five stages of increasingly severe impairment graded according to plasma creatinine level, GFR and/or urine output (Table 45):   Limitations of the classification include: frequent disparity between creatinine and urine output criteria; requirement for knowledge of baseline creatinine/GFR; poor sensitivity of the ‘Risk’ criteria, i.e., less severe renal impairment is also associated with worse outcome.   A modified version, the AKIN (Acute Kidney Injury Network) classification, includes the following changes: ◗ stages 1–3 corresponding to RIF categories; removal of ‘Loss’ and ‘End-stage’ categories. ◗ addition of an absolute increase in creatinine of 26.5 µmol/l to stage 1. ◗ 48-h timeframe specified for period of deterioration. ◗ patients receiving renal replacement therapy automatically classed as stage 3. ◗ diagnostic criteria to be applied only after fluid optimisation. Lopes JA, Jorge S (2012). Clin Kidney J; 6: 8–14 Right atrial pressure,  see Cardiac catheterisation; Central venous pressure

Rocuronium bromide

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of alterations to the operating list caused by cancellations due to lack of beds, a patient arrives in the anaesthetic room without the diseased limb marked and has the wrong leg amputated. ◗ prevention of risks associated with routine activities (e.g. proper training and supervision, provision of trained anaesthetic assistants, implementing the World Health Organization Surgical Safety Checklist). ◗ avoidance of particularly high-risk activities (e.g. wider use of regional anaesthesia for caesarean section). ◗ minimising the severity of adverse events should they occur (e.g. training in defibrillation, maintenance of emergency drugs and equipment). ◗ risk financing (e.g. indemnity). ◗ having a system for dealing with disasters and complaints, to reduce both psychological and legal sequelae. Audit is an integral part of a risk management programme, the costs of which may be considerable, although the avoidance of litigation is a strong incentive. Protocols may contribute to risk management by standardising care. See also, Clinical governance; Quality assurance/ improvement

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Ritodrine hydrochloride.  β-Adrenergic receptor agonist, used as a tocolytic drug in premature labour but discontinued because of its side effect profile including arrhythmias, pulmonary oedema, and blood dyscrasias after prolonged use. Rivaroxaban. Orally active direct factor Xa inhibitor, licensed in adults for DVT prophylaxis after elective hip or knee replacement surgery, stroke prophylaxis in nonvalvular AF, and prevention of thrombotic events after acute coronary syndromes. More effective than enoxaparin at preventing DVT and PE, with comparable risks of haemorrhagic side effects. Also used off-license for treatment of DVT/PE and acute coronary syndromes.   Rapidly absorbed via the oral route (peak plasma concentration within 2–4 h) with 80%–100% oral bioavailability. 70% undergoes hepatic metabolism (by the cytochrome P450 system) to inactive products; 30% is excreted unchanged in urine. Thus, caution is required in patients with renal failure, and those taking drugs that cause hepatic enzyme induction/inhibition. • Dosage: ◗ prevention of DVT after knee or hip replacement surgery: 10 mg orally od, starting 6–10 h after surgery and continued for 2 or 5 weeks, respectively. ◗ treatment of DVT/PE: 15 mg orally bd for 21 days, then 20 mg od. ◗ prevention of stroke: 20 mg orally od. ◗ following acute coronary syndromes: 2.5 mg orally bd, with aspirin ± clopidogrel. • Side effects: nausea, haemorrhage.

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Right ventricular function. The right ventricle (RV) receives blood from systemic and coronary veins, and pumps it into the left ventricle (LV) across the pulmonary vascular bed. The pulmonary bed is of low resistance, therefore RV pressures (15–25/8–12 mmHg) are lower than systemic. The low intraventricular pressure permits right coronary blood flow to be continuous throughout the cardiac cycle. The output of the right heart is influenced by its preload, contractility and afterload.   The RV is very compliant and, when afterload increases (e.g. because of pulmonary vascular resistance secondary to lung injury), the RV dilates. The end-diastolic volume may increase to a greater extent than the preload; consequently, the RV ejection fraction will decrease markedly with increasing afterload. Changes in the geometry of the RV affect the function of the LV, and vice versa (ventricular interdependence), e.g. impaired RV function (whether acute or chronic) may hinder LV function via RV distension and deviation of the interventricular septum.   Although the RV is analogous to the LV in terms of control mechanisms, it is more difficult to assess; e.g. the relationship between RV preload, RV volume and RV filling pressures is not always constant. In addition, attempts to study RV function are hindered by the greater effect of respiratory excursions on the RV because the pressures involved are less than those on the left side of the heart.   RV function may be altered in acute respiratory failure, sepsis, chest trauma, ischaemic heart disease, and after cardiac surgery. The possibility of RV ischaemia or infarction in critically ill patients as a cause of RV dysfunction is increasingly recognised. During IPPV, decreased venous return due to the increased intrathoracic pressure results in decreased RV end-diastolic volume and thus cardiac output. RV impairment may result in the classic features of right-sided cardiac failure, but may present as a general poor perfusion state. Vandenheuval MA, Bouchez S, Wouters PF, DeHert SG (2013). Eur J Anaesthesiol; 30: 386–94

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Ringer’s solution.  Developed as an in vitro medium for tissues and organisms, emphasising the importance of inorganic ions in maintaining cellular integrity. Exact constitution varies between laboratories, but approximates to sodium 137 mmol/l, potassium 4 mmol/l, calcium 3 mmol/l and chloride 142 mmol/l. Modifications include Ringer’s lactate (Hartmann’s solution) and Ringer’s acetate (similar to Hartmann’s solution but with acetate instead of lactate). [Sydney Ringer (1834–1910), English physician] Lee JA (1981). Anaesthesia; 36: 1115–21 rINNs, Recommended International Non-proprietary Names, see Explanatory notes Risk management.  Process for reducing the frequency and overall cost of adverse events, e.g. complications of anaesthesia. Consists of: ◗ analysis of risks (e.g. morbidity/mortality meetings, critical incident reporting schemes). Risks are often categorised into: - individual-based (e.g. arising from human error), e.g. wrong drug given. - environment-based (e.g. arising from the interaction between anaesthetists and the operating theatre), e.g. disconnection of breathing system. - system-based (human actions superimposed on inherent flaws in a system or process), e.g. because

Rivastigmine,  see Acetylcholinesterase inhibitors ROC curves,  see Receiver operating characteristic curves Rocuronium bromide. Non-depolarising neuromuscular blocking drug, introduced in 1994. Chemically related to vecuronium, with similar lack of cardiovascular effects, although tachycardia may accompany very large doses. Has been suggested as an alternative to suxamethonium in rapid sequence induction. Good intubating conditions

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Rotational therapy  (Kinetic therapy). Technique in which critically ill patients are turned laterally from the horizontal to an angle of about 40 degrees, often several times per hour on a programmable bed. Shown to reduce the incidence of nosocomial pneumonia and possibly decubitus ulcers, DVT and PE. Also reported to shorten duration of both IPPV and ICU stay. May share mechanisms of action with prone ventilation techniques. Compared with the prone position, it has less chance of accidental displacement of tubes and catheters/cannulae, damage to eyes/face/limbs, stimulation of coughing and cardiovascular instability. Accessibility to the patient remains good. Staudinger T, Bojic A, Holzinger U, et al (2010). Crit Care Med; 38: 486–90

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Rotameter.  The trade name of a type of flowmeter commonly used on anaesthetic machines; first used in the 1930s and still in common use. • Features include: ◗ constant pressure, variable orifice. ◗ consists of a needle valve, below a bobbin within a tapered tube. Gas flow rates are marked along the tube’s length. Readings are taken from the top of the bobbin. Tubes are arranged in banks at the back of the anaesthetic machine, traditionally for O2, CO2 and cyclopropane (the last two on older machines only), N2O, and air, from left to right in the UK (see later). ◗ accurate to within 2%. ◗ bobbins are made of light metal alloy; each is individually matched to its particular tube, and is specific for a certain gas. ◗ the tube’s taper is narrower at the bottom to allow accurate measurement of low flow rates, and wider above to measure higher flows. ◗ the space between the bobbin and walls of the tube is narrow at the bottom of the tube; gas flow behaves as through a tube, i.e., is largely laminar. Thus gas viscosity is important at low flow rates. Higher up the tube, the space between the bobbin and tube is wide compared with the length of the bobbin, because of the tube’s taper. Gas flow behaves as through an orifice, i.e., is turbulent. Thus gas density is important at high flow rates. ◗ inaccuracies may result from sticking of the bobbin against the sides of the tube. This is reduced by: - keeping the tube vertical to reduce friction between bobbin and tube. - angular notches in the bobbin, causing it to rotate when gas flows. - regular cleaning to prevent dirt accumulating within the tube.

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Ropivacaine hydrochloride. Amide local anaesthetic agent, introduced in 1997. Chemically related to bupi­ vacaine (a propyl group replacing a butyl group) but less lipid-soluble and less toxic, being associated with less severe CNS and CVS adverse effects. pKa is 8.1. Presented as the (S)-enantiomer (see Isomerism). Used in 0.2%–1.0% concentrations; initially reported to be approximately equipotent to bupivacaine in terms of analgesia while producing less motor block, e.g. for epidural anaesthesia. However, this is disputed, the reduced motor block seen with ropivacaine being related to its lower potency and thus selection of non-comparable solutions in comparative studies. In addition, comparable concentrations contain slightly less ropivacaine than bupivacaine.   Has vasoconstrictor properties; thus relatively unaffected by addition of vasoconstrictor drugs. About 94% proteinbound; undergoes hepatic metabolism with 1% excreted unchanged in the urine. Has about 40% greater clearance than bupivacaine. Maximal safe dose is estimated at 3.5 mg/ kg.

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- reduction of static charge building up within the tube. Many are internally coated with a thin layer of gold. Alternatively, regular spraying with antistatic solution may be performed. the O2 control knob is larger than the others and differently shaped to aid recognition. All are colourcoded as for cylinders. on some older machines, the CO2 bobbin could be hidden at the top of the tube if the CO2 valve was accidentally left fully open. with the traditional arrangement of rotameters, i.e., O2 upstream, O2 may be lost if there is a leak from a tube downstream. This may be prevented by placing the O2 inlet downstream from the others, e.g. by fitting a baffle across the top of the rotameter tubes so that N2O enters first, and O2 last. in modern machines, N2O and O2 rotameters are mechanically linked such that less than 25% O2 cannot be delivered.

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occur 60 s after an initial dose of 0.6 mg/kg; relaxation lasts for about 30–40 min (about 20 min after 0.45 mg/ kg). During a rapid sequence induction, an intubating dose of 1–1.2 mg/kg is advocated by some; it produces better intubating conditions in a shorter time. Supplementary dose: 0.15 mg/kg; effects last for about 15 min. May be infused iv at 0.3–0.6 mg/kg/h after a loading dose. Primarily excreted by the liver. Cumulation is unlikely at recommended doses. Reversed by sugammadex.

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Rowbotham, Edgar Stanley  (1890–1979). English pioneer of anaesthesia. With Magill, developed tracheal intubation, including blind nasal intubation, and endotracheal anaesthesia. Also pioneered basal narcosis with rectal paraldehyde, and local and intravenous techniques. The first anaesthetist in the UK to use cyclopropane. Designed several pieces of apparatus, including a vaporiser, airway, local anaesthetic needles and other equipment. Condon HA, Gilchrist E (1986). Anaesthesia; 41: 46–52 Royal College of Anaesthetists.  Arose from the granting of a Charter to the College of Anaesthetists by Queen Elizabeth II in March 1992. Regulates and promotes research, training, education and maintenance of standards in anaesthesia. Administers the FRCA examination. Has around 17 000 members in various categories, of whom ~14  000 are UK-based (~5000 of whom are trainees without the Final FRCA). Created the Faculty of Pain Medicine in 2007 and the Faculty of Intensive Care Medicine in 2010. The British Journal of Anaesthesia has been its official journal since 1990. Spence AA (1992). Br J Anaesth; 68: 457–8 R–R interval.  Time between successive R waves on the ECG. Thus heart rate = 60 R−R interval(s) Normally varies by less than 0.16 s at rest (sinus arrhythmia). Useful in the diagnosis of autonomic neuropathy.

Rule of nines ◗ ◗ ◗

RT,  Reptilase time, see Coagulation studies RTS,  see Revised trauma score

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Rule of nines.  Guide to the percentage of body surface area represented by various parts of the body; used in assessment and treatment of burns: ◗ head: 9%. ◗ arms: 9% each.

trunk: 18% front; 18% back. legs: 18% each. perineum: 1%. For small areas, the patient’s palmar surface of the hand and fingers represents about 1% of surface area. For children, proportions of body parts vary with age, with the head comprising up to 18% in infants (and the lower limbs contributing proportionally less); for accurate assessment specialised charts should be used.

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S S-100β protein.  Calcium-binding protein present in glial cells, studied as an early marker of damage to the blood– brain barrier, e.g. after stroke, TBI, cardiac surgery and neurosurgery. A normal level reliably excludes significant CNS injury. After moderate or severe TBI, raised levels reliably predict poor short- and long-term prognosis. Metabolised in the kidney with a half-life of ~25 min, the serum concentration is usually negligible but increases after brain injury, although it is thought that S-100β may also be produced from other tissues and its relationship with functional impairment is uncertain. Cata JP, Abdelmalak B, Farag E (2011). Br J Anaesth; 107: 844–58

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Sacral hiatus

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Sacral foramen

Fig. 139 Anatomy of the sacrum (posterior view)

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S wave.  Downward deflection following the R wave of the ECG (see Fig. 60b; Electrocardiography). Its size usually decreases from V2 to V6; the deepest wave is normally less than 30 mm. Prominence in standard leads I, II and III (S1S2S3 pattern) may be normal in young people but may be associated with right ventricular hypertrophy. May also be seen in MI along with other changes. See also, QRS complex

Articular process

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SA node, Sinoatrial node, see Heart, conducting system

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Sacral nerve block,  see Caudal analgesia Sacral plexus.  Supplies the pelvic and hip muscles, and the skin of the buttock and posterior thigh. Lies on piriformis muscle on the posterior wall of the pelvis, deep to the pelvic fascia, and is formed from the anterior primary rami of L4–S4 (Fig. 140). Its major branches are the sciatic, pudendal and gluteal nerves. See also, Sciatic nerve block SAD,  see Supraglottic airway device

Superior gluteal n

S2

Inferior gluteal n S3 S4

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Sacral canal. Cavity, 10–15 cm long and triangular in section, running the length of the sacrum, itself formed from five fused sacral vertebrae (Fig. 139). Continuous cranially with the lumbar vertebral canal. The anterior wall is formed by the fused bodies of the sacral vertebrae, and the posterior walls by the fused sacral laminae. Due to failure of fusion of the fifth laminar arch, the posterior wall is deficient between the cornua, forming the sacral hiatus, which is covered by the sacrococcygeal membrane (punctured during caudal analgesia). Congenital variants of fusion are common, e.g. deficient fusion of several laminae; this is thought to be a contributing cause of unreliability of caudal analgesia. The canal contains the termination of the dural sac at S2, the sacral nerves and coccygeal nerve, the internal vertebral venous plexus and fat. Its average volume in adults is 32 ml in females and 34 ml in males. Crighton IM, Barry BP, Hobbs GJ (1997). Br J Anaesth; 78: 391–5

S1

Posterior cutaneous n of thigh

Sciatic n

Perforating cutaneous n Pudendal n Fig. 140 Plan of the sacral plexus  

Saddle block,  see Spinal anaesthesia Safe transport and retrieval  (STaR). Course conceived by the Advanced Life Support Group and first run in 1998. Teaches a systematic approach to the safe transfer and retrieval of critically ill and injured patients. Aimed at doctors, nurses and paramedics. See also, Transportation of critically ill patients Salbutamol.  β-Adrenergic receptor agonist, used mainly as a bronchodilator drug. Relatively selective for β2receptors, although it does cause β1-receptor stimulation. Undergoes extensive first-pass metabolism if given orally; thus usually administered by inhalation or iv. Produces bronchodilatation within 15 min; effects last 3–4 h. May also reduce the release of histamine and inflammatory

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Saline solutions.  Intravenous fluids containing sodium chloride, used extensively to replace sodium and ECF losses, e.g. in dehydration, and perioperatively. A 0.9% solution is most commonly used (‘physiological saline’; often erroneously called ‘normal saline’); other salinecontaining solutions include Hartmann’s solution, Ringer’s solution and dextrose/saline mixtures. Hypertonic saline (e.g. 3%) is used in the treatment of symptomatic hyponatraemia and raised intracranial pressure.   Administration of large volumes of saline may result in hyperchloraemic acidosis, the clinical significance of which is unclear. See also, Hypertonic intravenous solutions; Normal solution

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Salicylate poisoning.  Usually acute but may be chronic, especially in children. • Features: ◗ nausea, vomiting, haematemesis, sweating, tinnitus, deafness, confusion, hallucinations. Loss of consciousness is uncommon unless poisoning is severe. ◗ hyperventilation results from direct respiratory centre stimulation, possibly via central uncoupling of oxidative phosphorylation. Respiratory alkalosis results. Compensatory renal excretion of bicarbonate results in urinary water and potassium loss with dehydration and hypokalaemia. ◗ metabolic acidosis is caused by the salicylic acid, and its metabolic effects (increased production of ketone bodies, lactic acid and pyruvic acid, hyperglycaemia or hypoglycaemia). Thus the urine, initially alkaline, becomes acid. ◗ arrhythmias, hypotension. ◗ convulsions, pulmonary oedema, hyperthermia and acute kidney injury may occur. ◗ impaired coagulation is rarely significant. • Treatment: ◗ general measures as for poisoning and overdose, e.g. O2 therapy, iv fluid administration. Activated charcoal (1 mg/kg up to 50 mg) should be given within an hour of ingesting >125 mg/kg. ◗ increased elimination may be indicated if plasma levels exceed 500 mg/l (3.6 mmol/l) in adults or 300 g/l (2.2 mmol/l) in children. Techniques include dialysis (preferred if plasma levels exceed 700  mg/l [5.1 mmol/l]), haemoperfusion and forced alkaline diuresis (monitoring potassium levels closely to avoid hypokalaemia). Mortality of acute overdose is approximately 2%; mortality of chronic overdose about 25%. Pearlman BL, Gambhir R (2009). Postgrad Med; 121: 162–8 See also, Forced diuresis

inhibit both central and peripheral synthesis of prostaglandins. Inhibit platelet and vascular endothelial cyclooxygenase; at low dosage, they selectively inhibit platelet cyclo-oxygenase. They are thus used as antiplatelet drugs. Effects on platelets are irreversible, lasting until new platelets are synthesised (7–10 days).   Used for mild-to-moderate pain, pyrexia, rheumatic fever, rheumatoid arthritis, and peripheral and coronary artery disease. Contraindicated in gout as they may impair excretion of uric acid.   Absorbed rapidly from the upper GIT after therapeutic dosage, with peak plasma levels within 2 h of ingestion. Absorption is determined by the composition of tablets, intestinal pH and gastric emptying. About 90% proteinbound, they compete with other substances for protein binding sites, e.g. thyroxine, penicillin, phenytoin. Metabolised in the liver and excreted mainly in the urine, especially if the latter is alkaline. Half-life is about 15 min, but is very dependent on the dose taken. • Side effects: as for NSAIDs and salicylate poisoning. Implicated in causing Reye’s syndrome in children. Contraindicated in children 48 h, and oral administration not used at all as the evidence for benefit is small.

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Salicylates.  Group of NSAIDs derived from salicylic acid. Aspirin (acetylsalicylic acid) is the most commonly used; others are available but are less potent, e.g. sodium salicylate. Have anti-inflammatory and antipyretic effects; they

Samples, statistical. Parts of populations, selected for statistical tests or analysis. In order to represent the true population, samples should be as large as possible to ensure appropriate power, and free of bias; i.e., should be random. Matched samples refer to groups matched for possible confounding variables, allowing better comparison of the desired measurements. Optimum matching occurs when subjects act as their own controls (i.e., measurements are paired). See also, Clinical trials; Randomisation; Statistics Sanders oxygen injector,  see Injector techniques Saphenous nerve block,  see Ankle, nerve blocks; Knee, nerve blocks SAPS,  see Simplified acute physiology score Sarcoidosis.  Systemic disease, possibly caused by immunological derangement secondary to an infective agent, characterised by non-necrotising granuloma formation. The lungs or hilar lymph nodes are affected in 90%–95% of patients, but the disease may involve the eyes, skin, musculoskeletal system, abdominal organs, heart or nervous system. Often acute in onset and self-limiting, with ∼85% undergoing spontaneous remission within 2 years. Most common in women, with peak incidence at 20–30 years.

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SCCM,  see Society of Critical Care Medicine Schimmelbusch mask,  see Open-drop techniques Sciatic nerve block.  Used for surgery to the lower leg, often combined with femoral nerve block, obturator nerve block and lateral cutaneous nerve of the thigh block (see Fig. 69; Femoral nerve block). May also be performed to provide analgesia after fractures, or sympathetic nerve block of the foot.   The sciatic nerve (L4–S3) arises from the sacral plexus, leaving the pelvis through the greater sciatic foramen beneath the piriformis muscle, and between the ischial tuberosity and the greater trochanter of the femur. It becomes superficial at the lower border of gluteus maximus, and runs down the posterior aspect of the thigh to the popliteal fossa, where it divides into tibial and common peroneal nerves. It supplies the hip and knee joints, posterior muscles of the leg and skin of the leg and foot below the knee, except for the medial calf. The posterior cutaneous nerve of the thigh runs close to it and is usually blocked by it. • Four different approaches are commonly used: ◗ posterior: with the patient lying with the side to be blocked uppermost, and the uppermost hip and knee flexed, a line is drawn between the greater trochanter and posterior superior iliac spine. At the line’s midpoint, a perpendicular is dropped 3 cm, and a 12-cm needle introduced at this point, at right angles to the skin. The nerve lies on the ischial spine and is identified using a nerve stimulator (seeking contraction of the hamstrings and muscles of the back of the lower leg and foot). 15–30 ml local anaesthetic agent is injected. Onset of blockade may take 30 min. ◗ anterior: with the patient lying supine, a line is drawn between the pubic tubercle and anterior superior iliac spine, and divided into thirds. A perpendicular line is dropped from the junction of the medial and middle thirds. Another line, parallel with the original line, is drawn from the greater trochanter; its intersection with the perpendicular marks the site of needle

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Scalp, nerve blocks.  Local anaesthetic infiltration is usually performed with added adrenaline, because of the rich vascular supply of the scalp. Injection is performed first in the subcutaneous tissue above the aponeurosis (where nerves and vessels lie), then below. Infiltration in a band around the head, above the ears and eyebrows, provides anaesthesia of the scalp. Individual branches of the maxillary nerve may also be blocked. The occipital nerves supplying the posterior scalp may be blocked by infiltrating between the mastoid process and occipital protuberance on each side.

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Saturated vapour pressure  (SVP). Pressure exerted by the vapour phase of a substance, when in equilibrium with the liquid phase. Indicates the degree of volatility; e.g. for inhalational anaesthetic agents, diethyl ether (SVP 59 kPa [425 mmHg]) is more volatile and easier to vaporise than halothane (SVP 32 kPa [243 mmHg]). SVP increases with temperature, therefore SVPs of volatile agents are quoted at a specified temperature (usually 20°C). At boiling point, SVP equals atmospheric pressure. See also, Vapour pressure

disposal system: may be: - passive: no external energy supply; the gases pass through wide-bore tubing to the roof of the building, terminating in a ventile. Maximal resistance should be 0.5 cmH2O at 30 l/min. The least efficient system, because it depends on wind direction. Requires a water trap to remove condensed water vapour. - assisted passive: employs the air-conditioning system’s extractor ducts. - active: uses a dedicated fan system or ejector flowmeter. Requires a low-pressure, high-volume system (able to remove 75 l/min with a peak flow of 130 l/min); thus, hospital suction equipment is unsuitable. Workplace exposure limits set out in COSHH regulations for Great Britain and Northern Ireland are 100 ppm N2O, 50 ppm enflurane/isoflurane and 10 ppm halothane (each over an 8-h period). Maximum permitted levels vary between countries; e.g. in the USA, the National Institute for Occupational Safety and Health has recommended an 8-h time-weighted average limit of 2 ppm for halogenated anaesthetic agents in general (0.5 ppm together with exposure to N2O). See also, Environmental safety of anaesthetists; Pollution

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  Diagnosed on clinical grounds, supported by tissue biopsy, CXR, hypercalcaemia (due to derangement of vitamin D metabolism), raised angiotensin converting enzyme levels; the Kveim test (granuloma formation following intradermal injection of sarcoid tissue suspension) is no longer used in the UK.   Anaesthetic and ICU considerations include the possibility of pulmonary fibrosis, cardiac failure, heart block, laryngeal fibrosis, renal failure and hypercalcaemia. Corticosteroids are often prescribed. [Morten A Kveim (1892–1967), Norwegian pathologist] Valeyre D, Prasse A, Nunes H, et al (2014). Lancet; 383: 1155–67

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Scavenging.  Removal of waste gases from the expiratory port of anaesthetic breathing systems; desirable because of the possible adverse effects of exposure to inhalational anaesthetic agents. Adsorption of volatile agents using activated charcoal (Aldasorber device) has been used but does not remove N2O. • Scavenging systems consist of: ◗ collecting system: usually a shroud enclosing the adjustable pressure limiting valve. For paediatric breathing systems, several attachments have been described, including various connectors and funnels. ◗ tubing: standard plastic tubing is usual; all connections should be 30 mm to avoid improper connection to the breathing system. ◗ receiving system: incorporates a reservoir to enable adequate removal of gases, even if the volume cleared per minute is less than peak expiratory flow rate. May use rubber bags or rigid bottles. If the system is closed, a dumping valve and pressure-relief valve are required to prevent excess negative or positive pressure, respectively, being applied to the patient’s airway. Vents are often present in rigid reservoirs. Requirements: - negative pressure: maximum 0.5 cmH2O at 30 l/ min gas flow. - positive pressure: maximum 5 cmH2O at 30 l/min gas flow, and 10 cmH2O at 90 l/min. Ideally, the relief valve should be as near to the expiratory valve as possible.

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  On ICU, there has been a shift towards light sedation following the recognition that early deep sedation is consistently associated with increased morbidity and mortality, prolonged hospital and ICU stay, haemodynamic instability, long-term cognitive decline and psychological problems including confusion in the intensive care unit. Although deep sedation is necessary for some patients (e.g. those with severe ALI, TBI, status epilepticus), most can be managed with low levels, especially as new ventilatory modes can reduce patient-ventilator asynchrony. Most modern minimal sedation guidelines aim to allow patients to be comfortable, calm and able to co-operate with staff and interact with family. • Achieving adequate comfort involves consideration of the following: ◗ pre-existing conditions, e.g. continuing treatment of chronic neuropathic pain with gabapentin. ◗ acute pain, e.g. opioid analgesic drugs for trauma/ surgery. ◗ ICU intervention-related discomfort, e.g. tracheal intubation/IPPV, physiotherapy, chest drains. • Drugs used include: ◗ morphine 2.5–5-mg boluses (20–60 µg/kg/h infusion). Accumulation of metabolites may occur after prolonged infusion, especially in renal failure. Increased susceptibility to infection has been shown in experimental animals receiving very large doses. ◗ fentanyl 1–5 µg/kg/h; accumulation readily occurs after prolonged infusion, because its short duration of action initially is due to redistribution, and clearance is slower than that of morphine. ◗ alfentanil 30–60 µg/kg/h; accumulation is less likely than with fentanyl. ◗ remifentanil 0.025–0.1 mg/kg/min. ◗ NSAIDs and regional techniques may also be used. Light sedation equates to a Richmond Agitation Sedation Scale of -1/0 (see Sedation scoring systems). There is a move away from benzodiazepines, which are associated with increased duration of IPPV and length of ICU stay. Propofol, clonidine or dexmedetomidine are considered the drugs of choice in adults. A continuous low-level infusion of sedation appears to be as effective as intermittent daily sedation interruptions. Daily sedation checks should be carried out to ensure the minimal sedation necessary is employed. Reade MC, Finfer S (2014). N Engl J Med; 370: 444–54

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insertion. A 12-cm needle is directed slightly laterally to encounter the femur, then withdrawn and directed medial to the femur to a depth of 5 cm from the femur’s anterior edge. 15–30 ml solution is injected. This approach is particularly useful if movement is painful, e.g. fractured femur. ◗ lithotomy: with the hip and knee on the side to be blocked flexed to 90 degrees, a needle is inserted perpendicular to the skin at the midpoint of a line between the greater trochanter and the ischial tuberosity. 15–20 ml solution is injected at a depth of 4–8 cm. The posterior cutaneous branch (supplying the posterior thigh) may be missed. ◗ lateral: with the patient lying supine, a needle is inserted horizontally at a point 2–3 cm below and 4–5 cm distal to the greater trochanter. When the femur is encountered the needle is withdrawn and redirected posteriorly ~30 degrees and cranially ~30–45 degrees to reach the nerve at 8–10 cm. 20–30 ml solution is injected. See also, Regional anaesthesia Scleroderma,  see Systemic sclerosis

Scopolamine,  see Hyoscine Scribner shunt,  see Shunt procedures

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Second. SI unit of time; defined according to the frequency of radiation emitted by caesium-133 in its lowest energy (ground) state.

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Second gas effect.  Increased alveolar concentration of one inhalational anaesthetic agent caused by uptake of a second inhalational agent. Most marked when the second gas occupies a large volume, e.g. N2O. Analogous but opposite to the Fink effect at the end of anaesthesia. Second messenger.  Intracellular substance (e.g. cAMP, calcium ions) linking extracellular chemical messengers (first messengers) with the physiological response. G protein-coupled receptors are often involved in second messenger systems.

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Sedation.  State of reduced consciousness in which verbal contact with the patient may be maintained. Used to reduce discomfort during unpleasant procedures, e.g. regional anaesthesia, dental surgery, endoscopy, cardiac catheterisation, and on ICU. For short procedures, drugs of short duration of action causing minimal cardiorespiratory depression are preferable. Best control is usually achieved with iv administration, although other routes may be used, e.g. oral premedication. Routine monitoring should be employed during procedures as for general anaesthesia. Drugs may be given by intermittent bolus, or by continuous infusion; the latter is easier to titrate. The level of sedation required depends on the individual patient and the procedure performed. Patient-controlled sedation has been used during procedures performed under local or regional anaesthesia; the patient uses a PCA device containing, e.g. propofol as required.

Sedation scoring systems. Used in intensive care to assess the level of sedation of patients in order to balance its beneficial (reduced stress, cardiovascular stability, ventilator synchrony) and adverse effects (increased risk of ventilator-associated pneumonia, deep vein thrombosis). Facilitates titration of sedation against predefined endpoints (e.g. assessments of consciousness, agitation and/ or ventilator synchrony). Other parameters assessed include pain, anxiety, muscle tone and response to tracheal suction. Most systems use single numerical scores: ◗ Ramsay scale: described in 1974. Has three levels of ‘awake’ states (1–3) and three of ‘asleep’ states (4–6). Although widely used in the UK, it lacks discrimination between sedation levels. A score of 2 represents an ideal sedation level. ◗ Sedation–Agitation Scale (SAS): described in 1999. Ranges from +3 (agitated) to −3 (unrousable) with an optimal score of 0. Has good reliability and is well validated against other systems.

Sengstaken–Blakemore tube

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Self-inflating bags.  Rubber or silicone bags used for IPPV that reinflate when released after compression. Thus may be used for IPPV without requiring an external gas supply, e.g. during draw-over anaesthesia, transfer of ventilated patients or CPR. May be thick-walled or lined with foam rubber. Usually assembled with a non-rebreathing valve at the outlet and a one-way valve at the inlet; thus fresh air is drawn in during refilling. O2 may be added through a port at the inlet; a reservoir bag may also be added to the inlet to increase FIO2. Available in adult and paediatric sizes. Bellows may be used in a similar way, but are less convenient to use.

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Seldinger technique.  Method for percutaneous cannulation of a blood vessel (e.g. central venous cannulation), described in 1953. A needle is inserted into the vessel, and a guide-wire passed through it. After removal of the needle, the cannula is introduced into the vessel over the wire, which is then removed. Refinements include the use of a dilator passed over the wire to enlarge the hole made by the needle, before the cannula is inserted.   Also used to cannulate other body cavities, e.g. the trachea in percutaneous tracheostomy formation, the chest for insertion of a chest drain or the abdominal cavity in paracentesis. [Sven-Ivar Seldinger (1921–1998), Swedish radiologist]

Selenium.  Trace element found in meat, chicken and fish; normal intake ~60–75 µg/day. Selenoproteins are antioxidants and are involved in certain biological reactions, e.g. conversion of thyroxine to triiodothyronine. Low blood selenium levels have been recorded in ICU patients, especially those with septic shock, and are associated with a high ICU mortality; however, the evidence that supplementation with selenium decreases nosocomial infection and mortality is disputed.

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Seebeck effect,  see Temperature measurement

  May cause hepatic enzyme inhibition (by competing with other drugs for the same metabolic pathways), thus increasing the action of certain tricyclics, type Ic antiarrhythmic drugs (especially lipid-soluble β-adrenergic receptor antagonists), phenytoin and benzodiazepines. Increased bleeding may occur in warfarin therapy. Concurrent administration of drugs that have 5-HT reuptake blocking effects (e.g. pethidine) may provoke the serotonin syndrome.

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Motor Activity Assessment Scale (MAAS): system based on observed levels of motor activity developed in surgical patients in 1999. Ranges from 0 (unresponsive) to 6 (dangerously agitated and unco-operative). Optimum sedation level is 3. Not widely used. ◗ Richmond Agitation Sedation Score (RASS): reliable and well validated system increasing in popularity. A 10-point scoring system ranging from +4 (agitated and combative) to -5 (unrousable). Optimum level is 0. ◗ Adaptation to the Intensive Care Environment (ATICE): more complex system that scores level of consciousness, comprehension and tolerance (assessing calmness, ventilator synchrony and facial relaxation). [Michael AE Ramsay, US anaesthetist; Richmond, Virginia, city where the scale was developed]

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Sellick’s manoeuvre,  see Cricoid pressure Semon’s law,  see Laryngeal nerves

Sengstaken–Blakemore tube.  Double-cuffed gastric tube designed to compress gastro-oesophageal varices, thereby controlling bleeding. Passed via the mouth into the stomach; the distal balloon is then inflated with 150–250 ml air, preventing accidental removal. The proximal balloon is then inflated to 30–40 mmHg (4–5 kPa), compressing the varices. Traction has been advocated but is rarely used. Newer versions include channels for aspiration of gastric and oesophageal contents (Fig. 141); the latter may be

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Selective decontamination of the digestive tract (SDD; Selective parenteral and enteral antisepsis regimen, SPEAR). Selective oropharyngeal decontamination (SOD) and SDD are prophylactic antibiotic regimens aimed at preventing nosocomial infection in ICU patients. During SOD, antibiotics are exclusively applied to the oropharynx throughout the ICU stay. In SDD, antibiotics are not only applied to the oropharynx but also to the GIT throughout the stay, in combination with iv cefotaxime for the first 4 days. Non-absorbable antibacterial drugs (e.g. tobramycin, colistin, amphotericin, neomycin) are administered to the pharynx/mouth/upper GIT. Although studies show SDD and SOD reduce rates of ventilator-associated pneumonia, mortality and ICU length of stay appear to be unaffected. The technique has not been widely adopted due to concerns about bacterial resistance. Plantinga NL, Bonten MJ (2015). Crit Care; 19: 259 Selective serotonin reuptake inhibitors (SSRIs). Antidepressant drugs introduced in 1987 and largely replacing tricyclic antidepressant drugs. Inhibit the presynaptic reuptake of 5-HT in the CNS, leading to an increase in 5-HT activity. Include citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine and sertraline; they have similar actions and are metabolised in the liver with half-lives of about a day (4–6 days for fluoxetine).   Have fewer side effects than tricyclic antidepressants because muscarinic, dopamine, histamine and noradrenergic receptors are unaffected. However, GIT upset, insomnia and agitation may occur; the syndrome of inappropriate antidiuretic hormone secretion and impaired platelet function have been reported. In overdose, severe adverse effects are uncommon, although the serotonin syndrome may occur if tricyclics or monoamine oxidase inhibitors are also taken.

For aspiration

Oesophageal cuff

Gastric cuff

For aspiration Fig. 141 Distal end of Sengstaken–Blakemore tube  

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Sensitivity aspirated continuously to reduce pulmonary soiling. Thus four lumens may be present: ◗ for aspiration above the oesophageal balloon. ◗ for aspiration from the stomach. ◗ for inflation of each balloon. Usually kept inflated for 12–24 h; the oesophageal balloon is deflated first. Careful placement is essential to avoid airway obstruction, pulmonary aspiration, ischaemic necrosis of gastric mucosa or oesophageal rupture. The tubes are very uncomfortable. [Robert W Sengstaken (1923–1978) and Arthur H Blakemore (1879–1970), US surgeons] Sensitivity. In statistics, the ability of a test to exclude false negatives. Equals:

- third-order neurones project to the somatosensory cortex. The primary somatosensory area of the cerebral cortex is in the postcentral gyrus, although there is a large distribution of sensory fibres in other areas. Regions of greatest importance (e.g. face, mouth, hands) have a disproportionately greater representation than other areas. • Signs of sensory pathway loss: ◗ peripheral nerve lesion: complete loss of sensation in the nerve’s distribution (although the zone of loss may be limited because of overlap between nerves). ◗ posterior root lesion: pain and paraesthesia are experienced in the dermatomal distribution. If the root involves a reflex arc, the reflex will be diminished or lost. ◗ posterior column lesion: ipsilateral loss of position and vibration sense with preservation of pain, touch and temperature sensation. ◗ spinothalamic tract lesion: contralateral loss of pain and temperature sensation. ◗ brainstem and thalamus lesions: upper brainstem or thalamic lesions may cause complete hemisensory disturbance with loss of postural sense, light touch and pain sensation. ‘Pure’ thalamic lesions may result in central pain. ◗ sensory cortex lesions: paraesthesia may be felt, with or without impaired sensation, e.g. inability to distinguish between heat and pain, or inability to identify objects by touch. [Georg Meissner (1829–1905), German anatomist; Filippo Pacini (1812–1883), Italian anatomist; Angelo Ruffini (1864–1929), Italian histologist] See also, Dermatomes; Spinal cord injury

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Sensory pathways.  The sensory system includes the special senses, visceral sensation and general somatic sensation. The latter is divided into: ◗ exteroreceptive sensation: provides information about the external environment and includes modalities such as touch, pressure, temperature and pain. ◗ proprioceptive sensation: provides information about body position and movement. Free nerve endings may be associated with nociception. Some nerve endings are ‘specialised’, e.g. Meissner’s corpuscles (touch), Pacinian corpuscles (vibration and joint position) and Ruffini corpuscles (joint position). The last two may be involved with muscle spindles.   The sensory fibres enter the spinal cord through the dorsal root, their cell bodies lying in the dorsal root ganglia. Subsequent pathways (Fig. 142): ◗ dorsal columns: carry impulses concerned with proprioception (movement and joint position sense), vibration and discriminative touch: - first-order neurones turn medially and ascend in the ipsilateral posterior columns (the fasciculus gracilis and cuneatus) to the lower medulla, where they synapse with cells in the cuneate or gracile nuclei. - second-order neurones cross (decussate) to the contralateral side of the medulla and ascend in the medial lemniscus to the ventral posterior nucleus of the thalamus. - third-order neurones project to the somatosensory cortex. ◗ spinothalamic tract: carries impulses concerned with pain, temperature, non-discriminative touch and pressure: - first-order neurones synapse in the dorsal horn of the spinal cord (most nociceptive Aδ- and C-fibres terminate in laminae I–II whereas Aβ fibres terminate in laminae III–IV). - second-order neurones carrying pain and temperature cross within one segment of their origin, whereas those carrying touch and pressure may ascend for several segments before crossing. They ascend in the spinothalamic tract; in the medulla, this forms the spinal lemniscus, which ascends to the ventral posterior nucleus of the thalamus.

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Sensory evoked potentials,  see Evoked potentials

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the number correctly identified as positive total with the condition See also, Errors; Predictive value; Specificity

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Sepsis.  Life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3 2016 definition); characterised by an acute increase in the sepsis-related organ failure assessment (SOFA) score of 2 or more. The latest definition eliminates the term systemic inflammatory response syndrome, the features of which are inadequate and non-specific for the accurate diagnosis of sepsis. Similarly, the terms ‘severe sepsis’ and septicaemia are now considered redundant, the former being replaced by the term septic shock. Although the definitions are supported by evidence from large databases, these data apply to adults in high-income countries and may be less able to predict morbidity and mortality in other populations. In addition, data used to provide the definitions are derived from groups of patients with highly heterogeneous conditions and therefore may be limited when applied to individual patients.   Sepsis is a major cause of organ failure in ICU, being directly or indirectly responsible for 75% of all ICU deaths.   Most ICU infections are endogenous, caused by colonisation of the patient’s GIT by pathogenic organisms that gain access to the systemic circulation through bacterial translocation. Gram-negative bacteria (e.g. Escherichia coli, klebsiella, pseudomonas, acinetobacter and proteus species) have traditionally been most commonly responsible, because of their widespread presence, their tendency to acquire resistance to antibacterial drugs and their resistance to drying and disinfecting agents. Gram-positive bacteria (e.g. streptococci, staphylococci) are increasingly common, especially associated with invasive cannulation;

Sepsis

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Ventral posterolateral nucleus of thalamus

Putamen Globus pallidus

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Medial lemniscus

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Dorsal columns: vibration, proprioception, discriminative touch

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Spinothalamic tract: pain, temperature, non-discriminative touch, pressure  

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Fig. 142 Anatomy of sensory pathways

other organisms (e.g. fungi) may also be responsible. The inflammatory response involves cytokines, nitric oxide, thromboxanes, leukotrienes, platelet activating factor, prostaglandins and complement. Endothelial and neutrophil adhesion molecule expression increases, resulting in cellular infiltration into the tissues. • Critically ill patients are susceptible to sepsis because of: ◗ impaired local defences, e.g. anatomical barriers, ciliary activity, coughing, gastric pH. Tracheal tubes, indwelling catheters and cannulae provide routes for infection. ◗ impaired immunity. Contributory factors include drugs, malnutrition, diabetes mellitus, old age, malignancy, organ failure and infection itself. Patients receiving systemic cancer treatment or immunological therapy are susceptible to neutropenic sepsis (i.e., sepsis in the presence of a white cell count