`
`41ST EDITION
`
`ME DICAL
`DICTIONARY
`
`
`
`Edited by
`Dr Harvey Marcovitch
`
`APPLE 1047
`
`1
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`APPLE 1047
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`BLACK’S
`MEDICAL
`DICTIONARY
`
`41 S T EDITION
`
`Edited by
`Dr Har vey Marcovitch
`
`A & C Bl ack • London
`
`2
`
`
`
`41st edition published 2005
`A & C Black Publishers Limited
`37 Soho Square, London W1D 3QZ
`www.acblack.com
`
`ISBN 0–7136–6146–1
`eISBN-13: 978-1-4081-0419-4
`
`© 2005 A & C Black Publishers Limited
`
`A CIP catalogue record for this book is available from the British Library
`
`All rights reserved. No part of this publication may be reproduced in any
`form or by any means – graphic, electronic or mechanical, including
`photocopying, recording, taping or information storage and retrieval
`systems – without the prior permission in writing of the publishers.
`
`In its earlier editions Black’s Medical Dictionary was edited by:
`J. D. Comrie, MD—first to seventeenth editions, 1906–1942
`H. A. Clegg, FRCP—eighteenth edition, 1944
`W. A. R. Thomson, MD—nineteenth to thirty-fourth editions,
`1948–1984
`C. W. H. Havard, FRCP—thirty-fifth and thirty-sixth editions, 1987
`and 1990
`G. Macpherson, MB, BS—thirty-seventh to fortieth editions, 1992–2002
`
`A & C Black uses paper produced with elemental chlorine-free pulp,
`harvested from managed sustainable forests.
`
`Typeset in Adobe Garamond by RefineCatch Limited, Bungay, Suffolk
`Printed and bound by William Clowes Ltd, Beccles, Suffolk
`
`3
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`H
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`320 Heart, Artificial
`
`membrane is known as epicardium; the muscu-
`lar substance as myocardium; and the smooth
`lining membrane as endocardium.
`Important nerves regulate the heart’s action,
`especially via the vagus nerve and with the sym-
`pathetic system (see NERVOUS SYSTEM). In the
`near part of the atria lies a collection of nerve
`cells and connecting fibres, known as the sinu-
`atrial node or pacemaker, which forms the
`starting-point for the impulses that initiate
`the beats of the heart. In the groove between the
`ventricles and the atria lies another collection of
`similar nerve tissue, known as the atrioventricu-
`lar node. Running down from there into the
`septum between the two ventricles is a band of
`special muscle fibres, known as the atrioven-
`tricular bundle, or the bundle of His. This splits
`up into a right and a left branch for the two
`ventricles, and the fibres of these distribute
`themselves throughout the muscular wall of the
`ventricles and control their contraction.
`
`Openings There is no direct communica-
`tion between the cavities on the right side and
`those on the left; but the right atrium opens
`into the right ventricle by a large circular open-
`ing, and similarly the left atrium into the left
`ventricle. Into the right atrium open two large
`veins, the superior and inferior venae cavae,
`with some smaller veins from the wall of the
`heart itself, and into the left atrium open two
`pulmonary veins from each lung. One opening
`leads out of each ventricle – to the aorta in the
`case of the left ventricle, to the pulmonary
`artery from the right.
`Before birth, the FETUS’s heart has an open-
`ing (foramen ovale) from the right into the left
`atrium through which the blood passes; but
`when the child first draws air into his or her
`lungs this opening closes and is represented in
`the adult only by a depression (fossa ovalis).
`
`Valves The heart contains four valves. The
`mitral valve consists of two triangular cusps; the
`tricuspid valve of three smaller cusps. The aor-
`tic and pulmonary valves each consist of three
`semilunar-shaped segments. Two valves are
`placed at the openings leading from atrium into
`ventricle, the tricuspid valve on the right side,
`the mitral valve on the left, so as completely to
`prevent blood from running back into the
`atrium when the ventricle contracts. Two more,
`the pulmonary valve and the aortic valve, are at
`the entrance to these arteries, and prevent
`regurgitation into the ventricles of blood which
`has been driven from them into the arteries.
`The noises made by these valves in closing con-
`stitute the greater part of what are known as the
`
`heart sounds, and can be heard by anyone who
`applies his or her ear to the front of a person’s
`chest. Murmurs heard accompanying these
`sounds indicate defects in the valves, and may
`be a sign of heart disease (although many mur-
`murs, especially in children, are ‘innocent’).
`
`Action At each heartbeat the two atria con-
`tract and expel their contents into the vent-
`ricles, which at the same time they stimulate to
`contract together, so that the blood is driven
`into the arteries, to be returned again to the
`atria after having completed a circuit in about
`15 seconds through the body or lungs as the
`case may be. The heart beats from 60 to 90
`times a minute, the rate in any given healthy
`person being about four times that of the res-
`pirations. The heart is to some extent regulated
`by a nerve centre in the MEDULLA, closely con-
`nected with those centres which govern the
`lungs and stomach, and nerve fibres pass to it in
`the vagus nerve. The heart rate and force can be
`diminished by some of these fibres, by others
`increased, according to the needs of the various
`organs of the body. If this nerve centre is injured
`or poisoned – for example, by lack of oxygen –
`the heart stops beating in human beings;
`although in some of the lower animals (e.g.
`frogs, fishes and reptiles) the heart may under
`favourable conditions go on beating for hours
`even after its entire removal from the body.
`
`Heart, Artificial
`A mechanical device in the chest that enhances
`or takes over the pumping action of the HEART,
`thus maintaining the necessary level of circula-
`tion of blood through the lungs and other body
`structures. An artificial heart was first used in
`humans in 1985 and the three types in use are:
`an intra-aortic balloon pump, driven by com-
`pressed air, which inflates a balloon in the
`AORTA with every heartbeat, increasing the vol-
`ume of circulating blood; an electrical device
`that assists the left VENTRICLE by pumping
`blood into the abdominal aorta; and a mechan-
`ical artificial heart that replaces a diseased heart
`that has been removed. As yet there is no arti-
`ficial heart suitable for long-term use. Existing
`devices are intended to tide over a patient who
`is extremely ill until a live heart can be trans-
`planted from a donor. The results from artificial
`hearts have been disappointing because of
`complications and also because the patients
`have usually been already dangerously ill.
`Heart, Diseases of
`Heart disease can affect any of the structures of
`the HEART and may affect more than one at a
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`
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`time. Heart attack is an imprecise term and may
`refer to ANGINA PECTORIS (a symptom of pain
`originating in the heart) or to coronary artery
`thrombosis, also called myocardial infarction.
`
`Arrhythmias An abnormal rate or rhythm
`of the heartbeat. The reason is a disturbance in
`the electrical impulses within the heart. Some-
`times a person may have an occasional irregular
`heartbeat: this is called an ECTOPIC beat (or an
`extrasystole) and does not necessarily mean that
`an abnormality exists. There are two main types
`of arrhythmia: bradycardias, where the rate is
`slow – fewer than 60 beats a minute and some-
`times so slow and unpredictable (heartblock) as
`to cause blackouts or heart failure; and tachy-
`cardia, where the rate is fast – more than 100
`beats a minute. A common cause of arrhythmia
`is coronary artery disease, when vessels carrying
`blood to the heart are narrowed by fatty
`deposits (ATHEROMA), thus reducing the blood
`supply and damaging the heart tissue. This
`condition often causes myocardial infarction
`after which arrhythmias are quite common and
`may need correcting by DEFIBRILLATION (appli-
`cation of a short electric shock to the heart).
`Some tachycardias result from a defect in the
`electrical conduction system of the heart that is
`commonly congenital. Various drugs can be
`used to treat arrhythmias (see ANTIARRHYTHMIC
`DRUGS). If attacks constantly recur,
`the
`arrhythmia may be corrected by electrical
`removal of dead or diseased tissue that is the
`cause of the disorder. Heartblock is most effect-
`ively treated with an artificial CARDIAC PACE-
`MAKER, a battery-activated control unit
`implanted in the chest.
`
`Cardiomyopathy Any disease of the heart
`muscle that results in weakening of its contrac-
`tions. The consequence is a fall in the efficiency
`of the circulation of blood through the lungs
`and remainder of the body structures. The
`myopathy may be due to infection, disordered
`metabolism, nutritional excess or deficiency,
`toxic agents, autoimmune processes, degener-
`ation, or inheritance. Often, however, the cause
`is not identified. Cardiomyopathies are less
`common than other types of heart diseases, and
`the incidence of different types of myopathy
`(see below) is not known because patients or
`doctors are sometimes unaware of the presence
`of the condition.
`The three recognised groups of cardio-
`myopathies are hypertrophic, dilated and
`restrictive.
`•Hypertrophic myopathy, a familial condi-
`tion, is characterised by great enlargement of
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`H
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`Heart, Diseases of 321
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`the muscle of the heart ventricles. This
`reduces the muscle’s efficiency, the ventricles
`fail to relax properly and do not fill suf-
`ficiently during DIASTOLE.
`•In the dilated type of cardiomyopathy, both
`ventricles overdilate, impairing the efficiency
`of contraction and causing congestion of the
`lungs.
`•In the restrictive variety, proper filling of the
`ventricles does not occur because the muscle
`walls are less elastic than normal. The result
`is raised pressure in the two atria (upper
`cavities) of the heart: these dilate and develop
`FIBRILLATION. Diagnosis can be difficult and
`treatment is symptomatic, with a poor prog-
`nosis. In suitable patients, heart TRANSPLAN-
`TATION may be considered.
`Disorders of the heart muscle may also be
`caused by poisoning – for example, heavy con-
`sumption of alcohol. Symptoms include tired-
`ness, palpitations (quicker and sometimes
`irregular heartbeat), chest pain, difficulty in
`breathing, and swelling of the legs and hands
`due to accumulation of fluid (OEDEMA). The
`heart is enlarged (as shown on chest X-ray) and
`ECHOCARDIOGRAPHY shows thickening of the
`heart muscle. A BIOPSY of heart muscle will
`show abnormalities in the cells of the heart
`muscle.
`is
`Where the cause of cardiomyopathy
`unknown, as is the case with most patients,
`treatment is symptomatic using DIURETICS to
`control heart failure and drugs such as DIGOXIN
`to return the heart rhythm to normal. Patients
`should stop drinking alcohol. If, as often
`happens,
`the patient’s
`condition
`slowly
`deteriorates, heart transplantation should be
`considered.
`
`Congenital heart disease accounts for
`1–2 per cent of all cases of organic heart disease.
`It may be genetically determined and so
`inherited; present at birth for no obvious rea-
`son; or, in rare cases, related to RUBELLA in the
`mother. The most common forms are holes in
`the heart (atrial septal defect, ventricular septal
`defect – see SEPTAL DEFECT), a patent DUCTUS
`ARTERIOSUS, and COARCTATION OF THE
`AORTA. Many complex forms also exist and can
`be diagnosed in the womb by fetal echocardi-
`ography which can lead to elective termination
`of pregnancy. Surgery to correct many of these
`abnormalities is feasible, even for the most
`severe abnormalities, but may only be palliative
`giving rise to major difficulties of management
`as the children become older. Heart transplan-
`tation is now increasingly employed for the
`uncorrectable lesions.
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`H
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`322 Heart, Diseases of
`
`Coronary artery disease Also known as
`ischaemic heart disease, this is a common cause
`of symptoms and death in the adult population.
`It may present for the first time as sudden
`death, but more usually causes ANGINA PEC-
`TORIS, myocardial infarction (heart attack) or
`heart failure. It can also lead to a disturbance of
`heart rhythm. Factors associated with an
`increased risk of developing coronary artery
`disease include diabetes, cigarette smoking,
`high blood pressure, obesity, and a raised con-
`centration of cholesterol in the blood. Older
`males are most affected.
`
`Coronary thrombosis or acute myo-
`cardial
`infarction
`is
`the acute, dramatic
`manifestation of coronary-artery
`ischaemic
`heart disease – one of the major killing diseases
`of western civilisation. In 1999, ischaemic heart
`disease was responsible for about 115,000
`deaths in England and Wales, compared with
`153,000 deaths in 1988. In 1999 more than
`55,600 people died of coronary thrombosis.
`The underlying cause is disease of the coronary
`arteries which carry the blood supply to the
`heart muscle (or myocardium). This results in
`narrowing of the arteries until finally they are
`unable to transport sufficient blood for the
`myocardium to function efficiently. One of
`three things may happen. If the narrowing of
`the coronary arteries occurs gradually, then the
`individual concerned will develop either angina
`pectoris or signs of a failing heart: irregular
`rhythm, breathlessness, CYANOSIS and oedema.
`If the narrowing occurs suddenly or leads to
`complete blockage (occlusion) of a major
`branch of one of the coronary arteries, then the
`victim collapses with acute pain and distress.
`This is the condition commonly referred to
`as a coronary thrombosis because it is usually
`due to the affected artery suddenly becoming
`completely blocked by THROMBOSIS. More
`correctly, it should be described as coronary
`occlusion, because the final occluding factor
`need not necessarily be thrombosis.
`
`Causes The precise cause is not known, but a
`wide range of factors play a part in inducing
`coronary artery disease. Heredity is an import-
`ant factor. The condition is more common in
`men than in women; it is also more common in
`those in sedentary occupations than in those
`who lead a more physically active life, and more
`likely to occur in those with high blood pressure
`than in those with normal blood pressure (see
`HYPERTENSION). Obesity is a contributory fac-
`tor. The disease is more common among
`smokers than non-smokers; it is also often
`
`associated with a high level of CHOLESTEROL in
`the blood, which in turn has been linked with
`an excessive consumption of animal, as opposed
`to vegetable, fats. In this connection the
`important factors seem to be the saturated fatty
`acids (low-density and very low-density lipo-
`proteins [LDLs and VLDLs] – see CHOLES-
`TEROL) of animal fats which would appear to
`be more likely to lead to a high level of choles-
`terol in the blood than the unsaturated fatty
`acids of vegetable fats. As more research on the
`subject is carried out, the arguments continue
`about the relative influence of the different fac-
`tors. (For advice on prevention of the disease,
`see APPENDIX 2: ADDRESSES: SOURCES OF
`INFORMATION, ADVICE, SUPPORT AND SELF-
`HELP.)
`
`Symptoms The presenting symptom is the
`sudden onset, often at rest, of acute, agonising
`pain in the front of the chest. This rapidly radi-
`ates all over the front of the chest and often
`down over the abdomen. The pain is frequently
`accompanied by nausea and vomiting, so that
`suspicion may be aroused of some acute abdom-
`inal condition such as biliary colic (see GALL-
`BLADDER, DISEASES OF) or a perforated PEPTIC
`ULCER. The victim soon goes into SHOCK, with
`a pale, cold, sweating skin, rapid pulse and dif-
`ficulty in breathing. There is usually some rise
`in temperature.
`
`Treatment is immediate relief of the pain by
`injections of diamorphine. Thrombolytic drugs
`should be given as soon as possible (‘rapid door
`to needle time’) and ARRHYTHMIA corrected.
`OXYGEN is essential and oral ASPIRIN is valuable.
`Treatment within the first hour makes a great
`difference to recovery. Subsequent treatment
`includes the continued administration of drugs
`to relieve the pain; the administration of
`ANTIARRHYTHMIC DRUGS that may be necessary
`to deal with the heart failure that commonly
`develops, and the irregular action of the heart
`that quite often develops; and the continued
`administration of oxygen. Patients are usually
`admitted to coronary care units, where they
`receive constant supervision. Such units main-
`tain an emergency, skilled, round-the-clock
`staff of doctors and nurses, as well as all the
`necessary resuscitation facilities that may be
`required.
`The outcome varies considerably. The first
`(golden) hour is when the patient is at greatest
`risk of death: if he or she is treated, then there is
`a 50 per cent reduction in mortality compared
`with waiting until hospital admission. As each
`day passes the prognosis improves with a first
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`6
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`coronary thrombosis, provided that the patient
`does not have a high blood pressure and is not
`overweight. Following recovery, there should be
`a gradual return to work, care being taken to
`avoid any increase in weight, unnecessary stress
`and strain, and to observe moderation in all
`things. Smoking must stop. In uncomplicated
`cases patients get up and about as soon as pos-
`sible, most being in hospital for a week to ten
`days and back at work in three months or
`sooner.
`
`Valvular heart disease primarily affects
`the mitral and aortic valves which can become
`narrowed (stenosis) or leaking (incompetence).
`Pulmonary valve problems are usually con-
`genital (stenosis) and the tricuspid valve is
`sometimes involved when rheumatic heart dis-
`ease primarily affects the mitral or aortic valves.
`RHEUMATIC FEVER, usually
`in childhood,
`remains a common cause of chronic valvular
`heart disease causing stenosis, incompetence or
`both of the aortic and mitral valves, but each
`valve has other separate causes for malfunction.
`
`Aortic valve disease is more common
`with increasing age. When the valve is nar-
`rowed, the heart hypertrophies and may later
`fail. Symptoms of angina or breathlessness are
`common and dizziness or blackouts (syncope)
`also occur. Replacing the valve is a very effective
`treatment, even with advancing age. Aortic
`stenosis may be caused by degeneration (senile
`calcific), by the inheritance of two valvular leaf-
`lets instead of the usual three (bicuspid valve), or
`by rheumatic fever. Aortic incompetence again
`leads to hypertrophy, but dilatation is more
`common as blood leaks back into the ventricle.
`Breathlessness is the more common complaint.
`The causes are the same as stenosis but also
`include inflammatory conditions such as SYPH-
`ILIS or ANKYLOSING SPONDYLITIS and other
`disorders of connective tissue. The valve may
`also leak if the aorta dilates, stretching the valve
`ring as with HYPERTENSION, aortic ANEURYSM
`and MARFAN’S SYNDROME – an inherited dis-
`order of connective tissue that causes heart
`defects. Infection (endocarditis) can worsen
`acutely or chronically destroy the valve and
`sometimes lead to abnormal outgrowths on the
`valve (vegetations) which may break free and
`cause devastating damage such as a stroke or
`blocked circulation to the bowel or leg.
`
`Mitral valve disease leading to stenosis is
`rheumatic in origin. Mitral incompetence may
`be rheumatic but in the absence of stenosis can
`be due to ISCHAEMIA, INFARCTION, inflamma-
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`H
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`Heart-Lung Machine 323
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`tion, infection and a congenital weakness (pro-
`lapse). The valve may also leak if stretched by a
`dilating ventricle (functional incompetence).
`Infection (endocarditis) may affect the valve in
`a similar way to aortic disease. Mitral symptoms
`are predominantly breathlessness which may
`lead to wheezing or waking at night breathless
`and needing to sit up or stand for relief. They
`are made worse when the heart rhythm changes
`(atrial fibrillation) which is frequent as the dis-
`ease becomes more severe. This leads to a loss of
`efficiency of up to 25 per cent and a predis-
`position to clot formation as blood stagnates
`rather than leaves the heart efficiently. Mitral
`incompetence may remain mild and be of no
`trouble for many years, but infection must be
`guarded against (endocarditis prophylaxis).
`
`Endocarditis is an infection of the heart
`which may acutely destroy a valve or may lead
`to chronic destruction. Bacteria settle usually
`on a mild lesion. Antibiotics taken at vulnerable
`times can prevent this (antibiotic prophylaxis) –
`for example, before tooth extraction. If estab-
`lished, lengthy intravenous antibiotic therapy is
`needed and surgery is often necessary. The mor-
`tality is 30 per cent but may be higher if the
`infection settles on a replaced valve (prosthetic
`endocarditis). Complications
`include heart
`failure, shock, embolisation (generation of
`small clots in the blood), and cerebral (mental)
`confusion.
`PERICARDITIS is an inflammation of the sac
`covering the outside of the heart. The sac
`becomes roughened and pain occurs as the
`heart and sac rub together. This is heard by
`stethoscope as a scratching noise (pericardial
`rub). Fever is often present and a virus the main
`cause. It may also occur with rheumatic fever,
`kidney failure, TUBERCULOSIS or from an
`adjacent lung problem such as PNEUMONIA or
`cancer. The inflammation may cause fluid to
`accumulate between the sac and the heart (effu-
`sion) which may compress the heart causing a
`fall in blood pressure, a weak pulse and circula-
`tory failure (tamponade). This can be relieved
`by aspirating the fluid. The treatment is then
`directed at the underlying cause.
`
`Heart-Lung Machine
`A device that temporarily takes over the func-
`tion of the heart and lungs. It is used in certain
`operations in the chest, giving the surgeon more
`time for operations such as open-heart surgery,
`heart transplants and heart-lung transplants.
`The machine also ensures an operating area
`largely free of blood, which helps the surgeon to
`work more quickly. A pump replaces the heart
`
`7
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`