Medicine_And_Surgery_A_Concise_Textbook.pdf

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See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/222713253 Medicine And Surgery: A Concise Textbook Book · August 2005 CITATIONS READS 3 199,875 2 authors: Giles Simon Kendall Kin Yee Shiu University College London Hospitals NHS Foundation Trust University College London 107 PUBLICATIONS 1,221 CITATIONS 31 PUBLICATIONS 168 CITATIONS SEE PROFILE SEE PROFILE All content following this page was uploaded by Giles Simon Kendall on 16 May 2014. The user has requested enhancement of the downloaded file. P1: FAW BLUK007-FM BLUK007-Kendall June 23, 2005 15:14 Char Count= 0 Medicine and surgery A concise textbook Giles Kendall MBBS, BSc (Hons), MRCPCH Research Fellow Centre for Perinatal Brain Protection and Repair University College London Kin Yee Shiu MBBS, BA Hons (Cantab), MRCP Specialist Registrar in Nephrology Imperial College of Science, Technology and Medicine Hammersmith Hospital London Contributing editor Sebastian L Johnston MBBS, PhD, FRCP Professor of Respiratory Medicine National Heart and Lung Institute & Wright Fleming Institute of Infection and Immunity Imperial College London & St Mary’s NHS Trust i P1: FAW BLUK007-FM BLUK007-Kendall June 23, 2005 15:14 Char Count= 0 Dedication: To our families, our students and our teachers.
C 2005 G. Kendall, K.Y. Shiu and S.L. Johnston Published by Blackwell Publishing Ltd Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia The right of the Author to be identified as the Author of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. First published 2005 Library of Congress Cataloging-in-Publication Data Kendall, Giles. Medicine and surgery : a concise textbook / Giles Kendall, Kin Yee Shiu, with contributing editor Sebastian L Johnston. p. ; cm. Includes index. ISBN-13: 978-0-632-06492-2 (alk. paper) ISBN-10: 0-632-06492-7 (alk. paper) 1. Internal medicine. 2. Surgery. [DNLM: 1. Internal Medicine. 2. Physiological Processes. 3. Surgical Procedures, Operative. WB 115 K51m 2005] I. Shiu, Kin Yee. II. Johnston, Sebastian L. III. Title. RC46.K52 2005 616–dc22 ISBN-13: 978-0-632-06492-2 2005003363 ISBN-10: 0-632-06492-7 A catalogue record for this title is available from the British Library Set in 9.5/12 Minion & Frutiger by TechBooks, New Delhi, India Printed and bound in India by Replika Press Pvt. Ltd Commissioning Editor: Fiona Goodgame, Vicki Noyes and Martin Sugden Development Editor: Geraldine Jeffers Production Controller: Kate Charman For further information on Blackwell Publishing, visit our website: http://www.blackwellpublishing.com The publisher’s policy is to use permanent paper from mills that operate a sustainable forestry policy, and which has been manufactured from pulp processed using acid-free and elementary chlorine-free practices. Furthermore, the publisher ensures that the text paper and cover board used have met acceptable environmental accreditation standards. ii P1: FAW BLUK007-FM BLUK007-Kendall June 23, 2005 15:14 Char Count= 0 Contents Preface and Acknowledgements, iv 1 Principles and practice of medicine and surgery, 1 2 Cardiovascular system, 23 3 Respiratory system, 90 4 Gastrointestinal system, 139 5 Hepatic, biliary and pancreatic systems, 184 6 Genitourinary system, 223 7 Nervous system, 287 8 Musculoskeletal system, 352 9 Dermatology and soft tissues, 384 10 Breast disorders, 409 11 Endocrine system, 420 12 Haematology and clinical immunology, 463 13 Nutritional and metabolic disorders, 507 14 Genetic syndromes, 516 15 Overdose, poisoning and addiction, 521 Index, 533 iii P1: FAW BLUK007-FM BLUK007-Kendall June 23, 2005 15:14 Char Count= 0 Preface The concept of this book arose in part from a frustra- Diseases have been arranged by system and have been tion with traditional textbooks, which address medicine, presented under consistent subheadings to aid under- surgery and pathology as separate disciplines. This sep- standing and revision. This is also the manner in which aration is frequently artificial, as patients often do not students are often expected to present in exams. At the present to the doctor with an isolated medical or surgi- beginning of each chapter the system is considered from cal problem. Medicine and Surgery: A concise textbook is a clinical perspective with a discussion of the symp- a new textbook in which the pathophysiology and epi- toms and signs relevant to that system. Investigations demiology of disease is presented alongside medical and and procedures that are used in multiple conditions are surgical aspects to provide a truly integrated text. This also considered in the clinical sections. Specific topics unique approach allows the book to be used as a com- that have been excluded include diseases of childhood, prehensive undergraduate reference book. orthopaedic, ENT and ophthalmology. These have had Another driving force behind this book was the lack of to be excluded to maintain the book at a manageable a comprehensive text that students could turn to for the size. essential knowledge required to pass their final exams. This book has evolved over the last few years with Medicine and Surgery: A concise textbook is also a book the help of students and specialists who have reviewed that can be used by final year students to enable them and revised individual chapters or sections. We hope you to quickly and efficiently revise their knowledge. Whilst find the final product useful and we encourage you as covering the core syllabus of undergraduate medicine readers to help us revise future editions by sending your and surgery we have kept the information to that which comments and suggestions for improvement. is essential to the undergraduate. Acknowledgements We would like to thank all the anonymous specialists and Dr Téa Johnston for their inspiration, guidance for their review and revision of the individual chapters; and encouragement throughout the project. Finally we without this input the book would have not been as up would like to thank all at Blackwell Publishing, includ- to date and comprehensive as it is. We would also like ing Fiona Goodgame, Martin Sugden and especially to thank our families, friends and colleagues for their Geraldine Jeffers for her tireless work and support. support and encouragement, especially Dr Man Fai Shiu iv P1: JYS BLUK007-01 BLUK007-Kendall May 12, 2005 17:17 Char Count= 0 Principles and practice of medicine and surgery 1 Fluid and electrolyte balance, 1 Perioperative care, 13 Infections, 19 r Intravascular–interstitial fluid balance: The capillary Fluid and electrolyte balance wall is semi-impermeable to plasma proteins, whereas sodium passes freely across the capillary wall. This Water and sodium balance means that proteins (through oncotic pressure), rather than sodium, exert the osmotic effect to keep fluid Approximately 60% of the body weight in men and 55% in the intravascular space. The hydrostatic pressure in women consists of water. Most of this exists within two generated across the capillaries offsets this, driving physiological fluid ‘spaces’ or compartments: about two- intravascular fluid out into the interstitial fluid. If thirds within the intracellular compartment and one- there is a reduction in plasma protein levels (hypoal- third in the extracellular compartment. The extracellular buminaemia), the low oncotic pressure can lead to compartment consists of both intravascular fluid (blood oedema; this is where there is excess interstitial fluid cells and plasma) and interstitial fluid (fluid in tissues, at the expense of intravascular fluid. which surrounds the cells). Additionally a small amount Water is continually lost from the body in urine, stool of fluid is described as in the ‘third space’, e.g. fluid in and through insensible losses (the lungs and skin). This the gastrointestinal tract, pleural space and peritoneal water is replaced through oral fluids, food and some is de- cavity. Pathological third space fluid is seen with gas- rived from oxidative metabolism. Sodium is remarkably trointestinal obstruction or ileus and pleural effusion or conserved by normal kidneys, which can make virtu- ascites. ally sodium-free urine, e.g. in hypovolaemia. Obligatory Water remains in physiological balance between these losses of sodium occur in sweat and faeces, but account compartments because of the concentration of osmoti- for 3 seconds), postural hypotension and/or cellular compartment, but then both the intracellular hypotension, and reduced skin turgor (check over the and extracellular compartments become volume de- anterior chest wall as the limbs are unreliable, partic- pleted, causing symptoms and signs of fluid depletion ularly in the elderly). The jugular venous pressure is (see section Assessing Fluid Balance below). low and urine output reduced (oliguria, see later in r Sodium excess rarely occurs in isolation. It is usually this chapter). found in combination with water excess, causing fluid r Fluid overload is more likely to occur in patients with overload with peripheral oedema, pulmonary oedema cardiac, liver or renal failure, particularly if there has and hypertension. The effect on serum sodium and been over-enthusiastic fluid replacement. Breathless- fluid balance depends on the relative excess of sodium ness is an early symptom. Tachypnoea is common and compared to water. Sodium excess > water excess there may be crackles heard bilaterally at the bases of causes hypernatraemia (see page 3) whereas water ex- the chest because of pulmonary oedema. The jugu- cess > sodium excess causes hyponatraemia. lar venous pressure is raised and sacral and/or an- r Water excess may be due to abnormal excretion e.g. kle oedema may be present (bedbound patients often in syndrome of inappropriate antidiuretic hormone have little ankle oedema, but have sacral oedema). The (SIADH; see page 444) or excessive intake. In normal blood pressure is usually normal (occasionally high), circumstances the kidney excretes any excessive wa- but blood pressure and heart rate are often unreliable ter intake, but in renal disease or in SIADH, water is because of underlying cardiac disease: in heart fail- retained. This invariably causes hyponatraemia (see ure the blood pressure often falls with worsening fluid page 4). Patients often remain euvolaemic, but if there overload. Pleural effusions and ascites suggest fluid is also some degree of sodium excess there may be overload, but in some cases there may be increased symptoms and signs of fluid overload. interstitial or third space fluid with reduced intravas- cular fluid so that the patient has decreased circulating volume with signs of intravascular hypovolaemia. Assessing fluid balance Urine output monitoring and 24-hour fluid balance This is an important part of the clinical evaluation of charts are essential in unwell patients. Daily weights are patients with a variety of illnesses, which may affect the useful in patients with fluid overload particularly those P1: JYS BLUK007-01 BLUK007-Kendall May 12, 2005 17:17 Char Count= 0 Chapter 1: Fluid and electrolyte balance 3 with renal or cardiac failure. Oliguria (urine output cardiac failure, and these patients may require in- below 0.5 mL/kg/h) requires urgent assessment and in- otropic support. tervention. A low urine output may be due to prere- Further investigations and management depend on the nal (decreased renal perfusion due to volume depletion underlying cause. Baseline and serial U&Es to look for or poor cardiac function), renal (acute tubular necrosis renal impairment (see page 230) should be performed. or other causes of renal failure) or postrenal (urinary or Where there is suspected bleeding, the initial FBC may catheter obstruction) failure. be normal, but this will fall after fluid replacement is In fluid depletion, the management is fluid resusci- given due to the dilutional effect of fluids. Chest X- tation. In previously fit patients, particularly if there is ray may show cardiomegaly and pulmonary oedema. hypotension, more than 1 L/h of colloids or crystalloids Arterial blood gases can be helpful in identifying any (usually saline) may be needed and several litres may be acid–base disturbance due to renal failure or degree of required to correct losses. However, the management is hypoxia due to underlying lung disease or pulmonary very different in fluid overload or in oliguria due to other oedema. causes. In most cases, clinical assessment is able to distin- guish between these causes. In cases of doubt (and where Hypernatraemia appropriate following exclusion of urinary obstruction) a fluid challenge of ∼500 mL of normal saline or a colloid Definition (see page 9) over 10–20 minutes may be given. However, A serum sodium concentration >145 mmol/L. care is required in patients at risk of cardiac failure (e.g. Incidence previous history of cardiac disease, elderly or with renal This occurs much less commonly than hyponatraemia. failure), when smaller initial volumes and more invasive monitoring (such as a central line to allow central ve- Age nous pressure monitoring) and frequent assessment is Any. Infants and elderly at greatest risk. needed. Patients should be reassessed regularly (initially usually within 1–2 hours) as to the effect of treatment on Sex fluid status, urine output and particularly for evidence M=F of cardiac failure: r If urine output has improved and there is no evidence Aetiology of cardiac failure, further fluid replacement should be This is usually due to water loss in excess of sodium loss, prescribed as necessary. often in combination with reduced fluid intake. Those r If the urine output does not improve and the patient at most risk of reduced intake include the elderly, infants continues to appear fluid depleted, more fluid should and confused or unconscious patients. be given. However, in patients who are difficult to as- r Causes of water loss include burns, sweat, hyperven- sess, clinically more invasive monitoring such as cen- tilation, vomiting and diarrhoea, diabetes insipidus tral venous pressure (CVP) monitoring may be re- (see page 445) and hyperosmolar non-ketotic coma quired. This is performed via a central line, usually (see page 461). placed in the internal jugular vein. A normal CVP is r Hypernatraemia may be iatrogenic due to osmotic di- 5–10 cm of water above the right atrium. The CVP uretics which cause more water than sodium loss or is either monitored continuously or hourly and fluids excessive administration of sodium, usually in intra- are titrated according to the results. However, CVP venous fluids. measurements should only form part of the clinical r A rarer cause of hypernatraemia is Conn’s syndrome assessment and in practice they can be unreliable. (see page 442) or ectopic ACTH syndrome. r If there is any evidence of cardiac failure, fluid ad- ministration should be restricted and diuretics may Pathophysiology be required. The normal physiological response to a rise in extracel- r If hypotension persists despite adequate fluid replace- lular fluid osmolality is for water to move out of cells. Pa- ment, this indicates poor perfusion due to sepsis or tients become thirsty and there is increased vasopressin P1: JYS BLUK007-01 BLUK007-Kendall May 12, 2005 17:17 Char Count= 0 4 Chapter 1: Principles and practice of medicine and surgery release stimulating water reabsorption by the kidneys. Management Water moving out of cells causes the cells to shrink. r The aim is to gradually reduce the serum sodium con- In response to this, electrolytes are transported across centration by no more than 0.5–1 mmol/L/h in order the cell membrane, changing the membrane potential. to avoid cerebral oedema. Urine output and plasma Changes in the membrane potential in the brain leads to sodium should be monitored frequently. The under- impaired neuronal function and if there is severe shrink- lying cause should also be looked for and treated. age, bridging veins are stretched leading to intracranial r If the patient is alert and conscious he/she should be haemorrhage. Cells also begin to produce organic solutes allowed to drink freely as this is the safest way to correct after about 24 hours to draw fluid back into the cell. hypernatraemia. r If the patient is fluid depleted, intravenous replace- Clinical features ment should be with 0.9% saline to restore intravascu- The symptoms of hypernatraemia include thirst, nausea lar volume. In severe hypernatraemia even 0.9% saline and vomiting. Patients may be irritable or tired, pro- is less hypertonic than the plasma so this will help to correct the high sodium. gressing to confusion and finally coma. On examination r If the patient is not fluid depleted but is unable to there may be features of fluid depletion including re- drink, 5% dextrose is given slowly. duced skin turgor, hypotension, tachycardia, peripheral r In hyperosmolar non-ketotic coma saline or half- shutdown and reduced urine output. Signs of fluid over- load suggest excessive administration of salt or Conn’s normal saline (0.45% saline) should be used until glu- syndrome. Polyuria and polydipsia suggest diabetes in- cose concentrations are near normal. This is to prevent sipidus or hyperglycaemia. There may be neurological worsening hyperglycaemia which can alter the osmo- signs such as tremor, hyperreflexia or seizures. lality further. Complications Prognosis Hypernatraemic encephalopathy and intracranial haem- The mortality rate of severe hypernatraemia is as high as orrhage (may be cerebral, subdural or subarachnoid) 60% often due to coexistent disease, and there is a high may occur in severe cases. Too rapid rehydration can risk of permanent neurological deficit. cause cerebral oedema as the cells cannot clear the or- ganic solutes rapidly. Hyponatraemia Investigations Definition r The diagnosis is confirmed by the finding of high A serum sodium concentration 6.0 mmol/L can cause risk of arrhythmia. An arterial blood gas to look for aci- cardiac arrhythmias and sudden death without warning. dosis may be indicated and diabetics should have their glucose checked. Incidence An ECG should be performed immediately in all cases. This is a common problem, affecting as many as 1 in 10 Abnormalities occur in the following order: tall, tented inpatients. T-waves, small P-wave and a widened, abnormal QRS complex. Patients may develop bradycardia or complete Aetiology heart block, and if left untreated may die from ventricular The causes are given in Table 1.2. standstill or fibrillation. Continuous ECG monitoring should occur until the hyperkalaemia is treated and ECG Pathophysiology abnormalities resolve. Hyperkalaemia lowers the resting potential, shortens the cardiac action potential and speeds up repolarisation, Management therefore predisposing to cardiac arrhythmias. The ra- Ideally hyperkalaemia should be prevented in at-risk pa- pidity of onset of hyperkalaemia often influences the risk tients by regular monitoring of serum levels and care with of cardiac arrhythmias, such that patients with a chron- medication and intravenous supplements. Once hyper- ically high potassium level are asymptomatic at much kalaemia is diagnosed, withdraw any potassium supple- greater levels. ments or causative drugs. If the hyperkalaemia is mild (7 mmol/L, potassium include bananas, citrus fruits, tomatoes and it is a medical emergency: salt substitutes. The first indication of hyperkalaemia r Calcium gluconate is given intravenously. The calcium provides some immediate cardio-protection by reduc- Table 1.2 Causes of hyperkalaemia* ing myocardial excitability, even in a patient with nor- mal serum calcium levels. It can be repeated after a Increased Transcellular Decreased few minutes if the abnormalities on ECG persist. intake movement output r Until treatment of the underlying cause can take place, Excess K+ therapy: Acidosis Renal failure a glucose and insulin infusion promotes intracellular (oral or i.v.) Insulin deficiency Drugs e.g. K+ Diet β-blockers sparing K+ uptake. Salbutamol nebulisers have a similar effect Massive Haemolysis diuretics, ACE through β receptor stimulation. These can be repeated transfusion of Rhabdomyolysis inhibitors whilst the underlying cause is addressed, but have only stored blood Digoxin toxicity Addison’s disease a temporary effect. *Artefactual hyperkalaemia may occur in old or haemolysed blood r Diuretics, e.g. loop diuretics can be used to increase samples. renal excretion. Oral ion-exchange resins or enemas P1: JYS BLUK007-01 BLUK007-Kendall May 12, 2005 17:17 Char Count= 0 8 Chapter 1: Principles and practice of medicine and surgery may be used to increase gastrointestinal elimination of repolarisation. This causes muscle weakness including potassium. Oral resins can cause severe constipation, the respiratory muscles and ECG changes (see below) so these should be given with laxatives and are not a predisposing to atrial and ventricular arrhythmias. In long-term solution. severe hypokalaemia sudden cardiac or respiratory ar- r Any acidosis should be corrected. rest may occur. Other effects include the following: r Refer to a renal physician or intensive care unit for r Metabolic alkalosis: In hypokalaemia there is reduced haemofiltration or haemodialysis if the hyperkalaemia potassium secretion into the renal tubules and in- is refractory to treatment or if there is severe renal creased reabsorption at the H+ /K+ ATPase pump failure. so more H+ ions are lost. Hypokalaemia can both cause and maintain a metabolic alkalosis. Alkalosis Hypokalaemia also tends to promote the movement of K+ into cells, worsening the effective hypokalaemia. Definition r Increased digoxin toxicity: Digoxin acts by inhibition A serum potassium level of 10% age, immunodeficiency, liver damage and malignancy. immature (band) forms. Specific causes include Organ hypoperfusion may manifest as altered mental r direct introduction of bacteria into the blood stream state, lactic acidosis or oliguria. Systemic hypotension via peripheral or central intravenous line (Staph. epi- is defined as a systolic blood pressure below 90 mmHg dermidis), or a reduction of more than 40 mmHg from baseline. r gastrointestinal perforation, rupture or ischaemia Patients may go on to develop multiorgan dysfunction leading to bacterial translocation (E. coli, Streptococcus including acute respiratory distress syndrome, dissem- faecalis, anaerobic organisms), inated intravascular coagulation, hepatic failure, renal r bacteraemia arising from the urinary tract including failure and confusion or coma. pyelonephritis, renal abscess, acute prostatitis (E. coli, Klebsiella aerogenes, Proteus mirabilis), Investigations r overwhelming pneumococcal infection in patients Blood and where appropriate, urine, stool, pus and CSF with impaired or absent splenic function (Streptococ- should be sent for culture prior to starting treatment cus pneumoniae), whenever possible. Full blood count, glucose, urea and r meningococcaemia from a respiratory source may also electrolytes, liver function tests, arterial blood gases and result in sepsis with or without associated meningitis coagulation screen should be sent and repeated regularly (Neisseria meningitidis), until the patient is stable. r patients with surgical site infections (Staph. aureus, E. coli, anaerobes) and Management r burns (Staph. aureus, Streptococci, Pseudomonas). r Aggressive resuscitation is essential. Airway patency and oxygenation must be maintained and may require Pathophysiology the use of an oropharyngeal airway or endotracheal in- The normal mechanisms involved in overcoming in- tubation. Blood pressure support involves aggressive fection become detrimental when the infection is fluid replacement via wide bore canulae with care- generalised. Bacteria cell wall components such as ful monitoring. CVP measurement allows assessment lipopolysaccharide (gram-negative bacteria), peptido- of fluid resuscitation, and the response of the CVP glycan (gram-positive and gram-negative bacteria) and to fluid challenge helps guide further resuscitation. P1: JYS BLUK007-01 BLUK007-Kendall May 12, 2005 17:17 Char Count= 0 22 Chapter 1: Principles and practice of medicine and surgery Refractory hypotension despite adequate volume re- be treated with cefuroxime, gentamicin and metron- placement requires the use of inotropic agents such as idazole. Septicaemia from the urinary tract should adrenaline, noradrenaline, dopamine or dobutamine be treated with a cephalosporin and gentamicin. If in an intensive care setting. Pseudomonas infection is suspected piperacillin or r Identification and management of underlying causes ciprofloxacin are effective. may require surgical intervention or the removal of r Other treatments such as immunoglobulin, anticy- indwelling catheters or lines. tokine antibodies, recombinant protein C and nitric r Antibiotic therapy should be based on local guidelines oxide synthetase inhibitors are under investigation. and chosen on the basis of presumed infection source Steroids and nonsteroidal anti-inflammatory agents until the results of microbiological investigations are have not been shown to be of benefit. known. Septicaemia originating in skin and soft tis- sue infections requires flucloxacillin and benzylpeni- Prognosis cillin. If methicillin resistant Staph. aureus (MRSA) is The reported mortality from septicaemia ranges from suspected vancomycin or teicoplanin should be used. 15 to 50% depending on the severity of sepsis and the Septicaemia following intestinal perforation should general status of the patient prior to the illness. P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Cardiovascular system 2 Clinical, 23 Cardiac failure, 61 Hypertension and vascular Ischaemic heart disease, 32 Disorders of pericardium, diseases, 73 Rheumatic fever and valve myocardium and Congenital heart disease, 84 disease, 40 endocardium, 65 Cardiovascular oncology, 88 Cardiac arrhythmias, 48 r The pain of chronic stable angina is brought on by Clinical exercise or emotion, and it is usually relieved within 2–3 minutes by rest and relaxation. It tends to be worse in cold weather or after meals. It may be associated Symptoms with shortness of breath. Sublingual glyceryl trinitrate (GTN), which dilates the coronary arteries, should Cardiovascular chest pain also rapidly relieve it. Chest pain can arise from the cardiovascular system, the r Angina that occurs at rest or is provoked more easily respiratory system, the oesophagus or the musculoskele- than usual for the patient is due to acute coronary syn- tal system. The major causes of chest pain in the car- drome (see page 36). It often persists for longer and diovascular system include ischaemia, pericarditis and although it may respond to GTN, it tends to recur. aortic dissection. In acute coronary syndrome it is not possible to dif- Enquire about chest pain ask about the site, nature ferentiate angina from myocardial infarction without (constricting, sharp, burning, tearing), radiation, pre- further investigations. cipitating/relieving factors and any associated symp- r In myocardial infarction the pain bears no relationship toms. Ask also about the time course, i.e. onset, duration, to exertion. Typically the pain has the same character, constant or episodic. SOCRATES may be used as a but it is more severe and unrelieved except by opiate mnemonic: analgesia. Features suggestive of myocardial infarction r Site rather than angina include pain, which lasts longer r Onset than 30 minutes, associated symptoms due to the re- r Character lease of catecholamines including sweating, dizziness, r Radiation nausea and vomiting. Some patients describe a feeling r Alleviating factors of impending doom (angor animi). r Time course Pericarditis causes a sharp or aching pain. It is a ret- r Exacerbating factors rosternal or epigastric pain that radiates to the neck, r Symptoms associated with the pain back or upper abdomen. The pain is usually altered in Ischaemic heart pain is classically a central aching chest severity in relation to posture, typically exacerbated by pain, often described as a tightness or heaviness, con- deep inspiration or lying flat and relieved by leaning for- stricting or crushing in nature, radiating into the arms wards. The pain of pericarditis may last days or even 2–3 (particularly the left) and jaw. However, this varies be- weeks. tween individuals and therefore the pattern of pain is Aortic dissection causes a very severe central tearing very significant. chest or abdominal pain that radiates through to the 23 P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 24 Chapter 2: Cardiovascular system back. Its onset is abrupt and of greatest intensity at the and may hang their legs over the side of the bed or go time of onset. to the window to relieve the dyspnoea. Chest pain associated with tenderness is suggestive of r Cheyne–Stokes respiration is alternate cyclical hy- musculoskeletal pain. Pleuritic pain (e.g. pneumonia, perventilation and hypoventilation (or even apnoea). pulmonary embolism) is usually sharp and made worse This occurs in patients with very severe left ventricular by inspiration and coughing. Oesophageal pain is a ret- failure, in some normal individuals (often elderly), in rosternal sensation often related to eating and may be patients with cerebrovascular disease and patients re- associated with dysphagia. Oesophageal reflux causes a ceiving opiate analgesia. It is thought that this pattern retrosternal burning pain, often exacerbated by bending of breathing results from depression of the respiratory forwards. Pain from the gallbladder or stomach can often drive centre within the brain. mimic cardiac pain. Equally, pain arising from structures r Patients with severe acute left ventricular failure often in the chest may present as abdominal pain, e.g. myocar- have a cough productive of frothy sputum, which may dial infarction, pneumonia. be blood stained. Frank haemoptysis may occur in mitral stenosis or following a pulmonary embolus. Dyspnoea However, the major causes of frank haemoptysis are from the respiratory system. Dyspnoea is defined as difficulty in breathing. In general dyspnoea arises from either the respiratory or cardio- vascular system and it is often difficult to distinguish Palpitations between them. A palpitation is an increased awareness of the heartbeat. r Cardiac dyspnoea is generally the result of left ventric- It may be a fluttering, rapid sensation or a slow, some- ular failure when fluid accumulates in the interstitium times heavy thumping sensation. The patient may feel of the lungs. The patient may notice it on strenuous ‘a missed beat’, or their heart beating irregularly. exertion initially, with gradually reducing ‘exercise tol- It is important to try to elicit from the patient when erance’ (the distance a patient can walk before having the palpitations occur, precipitating factors, duration, to stop for a rest). In severe failure, patients are breath- rate and rhythm (ask the patient to tap out the beat with less at rest. In any acute exacerbation of cardiac dys- their hand). Associated symptoms may include breath- pnoea an underlying cause should be sought, such as lessness, dizziness, syncope and/or chest pain. ischaemia, arrhythmias or a worsening heart valve le- r Palpitations during or just after exercise, or caused by sion. anxiety are often simply awareness of a normal heart r Orthopnoea is defined as breathlessness on lying flat. rate. This symptom normally arises when a patient’s exer- r Palpitations lasting just a few seconds are often due cise tolerance is already reduced. It is thought that two to premature beats. The patient becomes aware of the mechanisms are responsible for this phenomenon: a pause that occurs in the normal rhythm after a prema- redistribution of fluid through gravity in the lungs ture beat and may sense the following stronger beat. and a pressing of the abdominal contents on the di- r Post-palpitation polyuria is a feature of supraventric- aphragm, which reduces the vital capacity of the lungs. ular tachycardia due to the release of atrial natriuretic Many patients avoid the sensation of breathlessness by peptide. Some patients may know how to terminate propping themselves up on pillows at night, or, in se- their rapid palpitations with manoeuvres such as vere cases, sleeping in a chair. Orthopnoea is highly squatting, straining or splashing ice-cold water on the suggestive of a cardiac cause of dyspnoea, although it face. These features are very suggestive of a distinct may also occur in severe respiratory disease due to the tachyarrhythmia rather than general anxiety or pre- second mechanism. mature beats. r Paroxysmal nocturnal dyspnoea is waking from sleep suddenly breathless. It is thought to occur by a simi- Syncope lar mechanism to orthopnoea coupled to a decreased sensory response whilst asleep. Patients awake breath- Syncope is defined as a transient loss of conscious- less and anxious, they often describe having to sit up ness due to inadequate cerebral blood flow. Cerebral P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Chapter 2: Clinical 25 perfusion is dependent on the heart rate, the arterial cases the pain causes the patient to limp, hence the term blood pressure as well as the resistance of the whole vas- claudication and the pain characteristically disappears culature. Changes in any of these may result in syncope. when exertion is stopped, hence the term intermittent. There may be no warning, or patients may describe feel- The distance a patient can usually walk on the flat be- ing faint, cold and clammy prior to the onset. They may fore onset of pain is termed the claudication distance. have blurred vision, tinnitus and appear very pale prior Intermittent claudication is caused by peripheral vascu- to the loss of consciousness. Whilst unconscious they lar insufficiency to the muscles of the legs. The disease is are hypotonic with a very slow or difficult to feel pulse. in proximal large and medium-sized arteries to the lower Within a few seconds they spontaneously recover, they limbs, i.e. the iliac and femoral arteries. As the narrowing tend to be flushed and sweaty but not confused (unless of the arteries becomes more significant, the claudication prolonged hypoxia leads to a tonic-clonic seizure). distance decreases. Eventually rest pain may occur, this r Vasovagal syncope is very common and occurs in the often precedes ischaemia and gangrene of the affected absence of cardiac pathology. Predisposing factors in- limb. clude prolonged standing, fear, venesection, micturi- tion or pain. There is peripheral vasodilation causing a reduced ventricular filling. The heart contracts force- Signs fully, which may lead to a reflex bradycardia via vagal stimulation and hence a loss of consciousness. Oedema r Postural syncope (fainting on standing) is seen in pa- Oedema is defined as an abnormal accumulation of fluid tients with autonomic disorders, salt and water deple- within the interstitial spaces. A number of mechanisms tion, hypovolaemia or due to certain drugs especially are thought to be involved in the development of oedema. antianginal and antihypertensive medication. Normally tissue fluid is formed by a balance of hydro- r Cardiac arrhythmias may result in syncope if there is a static and osmotic pressure. sudden reduction of the cardiac output. This may oc- Hydrostatic pressure is the pressure within the blood cur in bradycardias or tachycardias (inadequate ven- vessel (high in arteries, low in veins). Oncotic pressure is tricular filling time). The loss of consciousness occurs produced by the large molecules within the blood (albu- irrespective of the patient’s posture. A Stokes–Adams min, haemoglobin) and draws water osmotically back attack is a loss of consciousness related to a sudden into the vessel. The hydrostatic pressure is high at the loss of ventricular contraction particularly seen dur- arterial end of a capillary bed hence fluid is forced out of ing the progression from second to third degree heart the vasculature (see Fig. 2.1). block. The colloid osmotic pressure then draws fluid back in r Carotid sinus syncope is a rare condition mainly seen at the venous end of the capillary bed as the hydrostatic in the elderly. As a result of hypersensitivity of the carotid sinus, light pressure, such as that exerted by a tight collar, causes a severe reflex bradycardia and hence syncope. r Exertional syncope occurs in aortic valve or subvalve Net fluid Net fluid movement movement stenosis. The syncope results from an inability of the heart to increase cardiac output in response to in- Hydrostatic Oncotic 0ncotic Hydrostatic creased demand. pressure pressure The immediate management of syncope or impending Capillary syncope is to lie the patient down and raise their legs increasing cerebral blood flow. Intermittent claudication Artery Vein Claudication describes a cramp-like pain felt in one or both calves, thighs or buttocks on exertion. In severe Figure 2.1 Mechanism of oedema. P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 26 Chapter 2: Cardiovascular system pressure of the venules is low. Any remaining interstitial oxygenation. This may be a result of blood bypassing fluid is then returned to the circulation via the lymphatic the lungs (right to left shunting) or due to severe lung system. disease. Mechanisms of cardiovascular oedema include the fol- lowing: r Raised venous pressure raising the hydrostatic pres- The arterial pulse sure at the venous end of the capillary bed (right ven- The pulse should be palpated at the radial and carotid tricular failure, pericardial constriction, vena caval ob- artery looking for the following features: struction). r The rate is normally counted over 15 seconds and mul- r Salt and water retention occurring in heart failure, tiplied by 4. The normal pulse is defined as a rate be- which increases the circulating blood volume with tween 60 and 100 beats per minute. Outside this range pooling on the venous side again raising the hydro- it is described as either a bradycardia or a tachycardia. static pressure. r The rhythm is either regular, regularly irregular, i.e. r The liver congestion that occurs in right-sided heart irregular but with a pattern, or irregularly irregular, failure may reduce hepatic function, including albu- which is suggestive of atrial fibrillation. min production. Albumin is the major factor respon- r The character and volume of the pulse are normally sible for the generation of the colloid osmotic pressure assessed at the brachial or carotid artery. Character and that returns the tissue fluid to the vasculature. A drop volume felt at the carotid may be described according in albumin therefore results in an accumulation of to the waveform palpated (see Fig. 2.2). oedema. r Pulse delay is a delay in the pulsation felt between two Oedema is described as pitting (an indentation or pit pulses. Radio-femoral delay is suggestive of coarcta- is left after pressing with a thumb for several seconds) tion of the aorta, the lesion being just distal to the or nonpitting. Cardiac oedema is pitting unless long origin of the subclavian artery (at the point where the standing when secondary changes in the lymphatics may ductus arteriosus joined the aorta). Radio-radial de- cause a nonpitting oedema. Distribution is dependent lay suggests arterial occlusion due to an aneurysm or on the patient. Patients who are confined to bed develop atherosclerotic plaque. oedema around the sacral area rather than the classical ankle and lower leg distribution. Pleural effusions and Jugular venous pressure ascites may develop in severe failure. The internal jugular vein is most easily seen with the pa- tient reclining (usually at 45˚), with the head supported Cyanosis and the neck muscles relaxed and in good lighting con- Cyanosis is a blue discolouration of the skin and mu- ditions. The jugular vein runs medial to the sternomas- cous membranes. It is due to the presence of desaturated toid muscle in the upper third of the neck, behind it haemoglobin and becomes visible when levels rise above in the middle third and between the two heads of ster- 5 g/dL. Cyanosis is not present in very anaemic patients nocleidomastoid in the lower third. It is differentiated due to the low haemoglobin levels. Cyanosis is divided from the carotid pulse by its double waveform, it is non- into two categories: palpable, it is occluded by pressure and pressure on the r Peripheral cyanosis, which is seen in the fingertips and liver causes a rise in the level of the pulsation (hepato- peripheries. When occurring without central cyanosis jugular reflex). The jugular waveform and pressure give it is due to poor perfusion, as the sluggish circulation information about the pressures within the right atrium leads to increased desaturation of haemoglobin. This as there are no valves separating the atrium and the in- may be as a result of normal vasoconstriction in the ternal jugular vein (see Fig. 2.3). cold, poor peripheral circulation or a poor cardiac The height of the jugular venous pressure (JVP) is as- output. sessed as the vertical height from the sternal angle to the r Central cyanosis also affects the warm mucous mem- point at which the JVP is seen. A height of greater than branes such as the tongue. It is a result of failure of 3 cm represents an abnormal increase in filling pressure P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Chapter 2: Clinical 27 Normal The normal pulsation has a rapid rise in pressure followed by a slower phase or reduction in pressure. Slow rising The slow rising pulse is seen in aortic stenosis due to obstruction of outflow. The pressure in the pulse rises slowly. Collapsing The collapsing pulse of aortic regurgitation is characterised by a large upstroke followed by a rapid fall in pressure. This is best appreciated with the arm held up above the head and the pulse felt with the flat of the fingers. Alternans Pulsus alternans describes a pulse with alternating strong and weak beats. It is a sign of severe left ventricular failure indicating a poor prognosis. Bisferiens This is the waveform that reults from mixed aortic stenosis and regurgitation. The percussive wave P T (P) is due to ventricular systole, the tidal wave (T) is due to vascular recoil causing a palpable double pulse i.e. an exaggerated dicrotic notch. Paradoxus This is an accentuation of the normal situation with an excessive and palpable fall of the pulse Inspiration pressure during inspiration. When severe the pulse disappears briefly with early inspiration. Occurs in cardiac tamponade, pericardial constriction and severe acute asthma. Figure 2.2 Arterial pulse waveforms. Once the atrium is filled with blood it contracts to give the ‘a’ wave a The ‘a’ wave is lost in atrial fibrillation. The ‘a’ wave is increased in pulmonary stenosis, pulmonary hypertension and tricuspid stenosis (as a consequence of right atrial or right ventricular hypertrophy). The atrium relaxes to give the ‘x’ descent; however, the start of a ventricular contraction causes ballooning of the tricuspid valve as c it closes, resulting in the ‘c’ wave. The further ‘x’ descent is due to descent of the closed valve towards the cardiac apex. x a cv wave With the tricuspid valve closed the return of venous blood fills the v c atrium giving the ‘v’ wave. Tricuspid regurgitation gives a ‘cv’ wave. x a c v The tricuspid valve opens at the end of ventricular systole giving the ‘y’ descent. y x Figure 2.3 The jugular venous pressure Diastole Systole Diastole waveform. P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 28 Chapter 2: Cardiovascular system of the right atrium. This may occur in right-sided heart Timing to systole or diastole is achieved by palpation failure, congestive cardiac failure and pulmonary em- of the carotid pulse whilst auscultating. A systolic mur- bolism. mur occurs at the same time as the carotid pulse, whereas a diastolic murmur occurs in the pause between carotid pulses. Murmurs are further described according to their Precordial heaves, thrills and pulsation relationship to the cardiac cycle. r A parasternal heave is a cardiac impulse palpated by r A systolic murmur may be pansystolic when the first placing the flat of the hand on the costal cartilages, to and second heart sounds cannot be heard separate the left of the patient’s sternum. It may be due to right from the murmur. This occurs in mitral regurgitation, ventricular hypertrophy when the impulse is at the tricuspid regurgitation and with a ventricular septal same time as the apex beat and carotid pulsation. Less defect. commonly it is due to left atrial enlargement when r An ejection systolic murmur is a crescendo–decres- the pulsation occurs before the apex beat or carotid cendo murmur and the second heart sound can be pulsation. heard distinct from the end of the murmur. It is heard r A thrill is a palpable murmur and is due to turbulent with aortic stenosis, pulmonary stenosis and with an blood flow. A thrill is indicative of a loud murmur. atrial septal defect (the sound being produced by in- The flat of the hand should be placed at the base and creased flow across the pulmonary valve). apex of the heart. For example, a diastolic thrill at r A late systolic murmur is heard in mitral valve pro- the apex is suggestive of severe mitral stenosis (aortic lapse. regurgitation rarely produces a thrill). r An early diastolic murmur is heard with aortic re- r The apex beat is defined as the most inferior and lateral gurgitation, and a mid-late diastolic murmur is heard cardiac pulsation. It should be identified and its po- with mitral stenosis. sition defined according the intercostal space (count The area in which the murmur is heard at the greatest down from the sternal angle which is at the second in- intensity and any radiation should be noted. This is most tercostal space) and the relationship to the chest (mid- helpful when the flow of blood is considered according clavicular line, anterior axillary line, etc). The normal to the lesion, for example aortic stenosis radiates to the position is the fourth or fifth intercostal space in the neck, mitral regurgitation radiates to the axilla. The in- left midclavicular line. The character of the pulsation tensity of the murmur may be graded (see Table 2.2) and should also be palpated, but these may be subtle (see the pitch also noted. Table 2.1). Investigations and procedures Heart murmurs Coronary angioplasty Heart murmurs are the result of turbulent blood flow. Certain features of any murmur should be noted. Coronary angioplasty is a technique used to dilate stenosed coronary arteries in patients with ischaemic heart disease. The indications for use of angioplasty have Table 2.1 Character of an abnormal apex beat changed over the years with the technique now used for Typical underlying Description Character lesion Table 2.2 Simple grading of the intensity of a Tapping Sudden but brief Mitral stenosis heart murmur pulsation Thrusting Vigorous, Mitral or aortic Grade Description nonsustained regurgitation 1/4 Just audible with concentration Heaving Vigorous and Aortic stenosis, 2/4 Easily audible, but not loud sustained systemic 3/4 Loud hypertension 4/4 Loud and audible over a wide area P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Chapter 2: Clinical 29 many stenoses previously thought to be treatable only reduce this to approximately 15–20% and this has been by bypass grafting. Current practice is for left main stem further reduced with drug-eluting stents. These slowly disease or triple vessel disease to be treated by bypass release a drug (e.g. sirolimus) over 2–4 weeks to modify grafting for prognostic reasons with almost all other the healing response. lesions being considered for angioplasty for symptom control. In addition, patients with concomitant condi- Coronary artery bypass surgery tions precluding bypass surgery, e.g. lung disease, may be considered for angioplasty even for left main stem or Surgery for coronary artery disease is useful in patients advanced multivessel disease. with severe symptoms despite medical treatment. It has Early angiography and angioplasty is now being in- also been shown to improve outcome in patients with creasingly used immediately following a myocardial triple vessel disease or left main stem coronary artery infarction, in order to reduce the risk of further infarc- disease. tion. This is especially where the acute event is a limited or non-ST elevation myocardial infarction. Cardiopulmonary bypass PTCA (percutaneous transluminal coronary angio- In order to operate safely in a bloodless, immobile field plasty) is performed under local anaesthetic. A small whilst maintaining an adequate circulation to the rest balloon is passed up the aorta via peripheral arterial ac- of the body cardiopulmonary bypass is most commonly cess under radiographic guidance. Once within the af- used. A cannula is placed in the right atrium in order fected coronary artery, the balloon is inflated to dilate to divert blood away from the heart. The blood is then the stenosis, compressing the atheromatous plaque and oxygenated by one of two methods: stretching the layers of the vessel wall to the sides. A stent r Bubble oxygenators work by bubbling 95% oxygen is often used to reduce recurrence. Some stenoses cannot through a column of blood. be dilated due to calcification of the vessel, small vessel or r Membrane oxygenators work by bringing the blood the position or length of stenosis. During the procedure and oxygen together via a gas permeable membrane. there is a risk of thrombosis, so patients are given intra- Bubbles are then removed by passing the blood through venous heparin and aspirin. If stents are used, another a sponge. The blood is then heated or cooled as required. antiplatelet agent (clopidogrel) is also used to prevent A roller pump compresses the tubing driving the blood in-stent thrombosis in the first few days/weeks and the back into the systemic side of the circulation at an arte- patient remains on lifelong aspirin. rial perfusion pressure of between 50 and 100 mmHg. If the myocardium is to be opened, cross-clamping the Complications aorta gives a bloodless field; the heart is protected from The main immediate complication of balloon angio- ischaemia by cooling to between 20 and 30˚C. Systemic plasty is intimal/medial dissection leading to abrupt ves- cooling also lowers metabolic requirements of other or- sel occlusion. This, and the problem of late restenosis, gans during surgery. Beating heart bypass grafting is now has been largely resolved with the routine implantation possible using a mechanical device to stabilise the target of a stent. There is a risk of complications, including surface area of the heart, but access to the posterior sur- emergency coronary artery bypass surgery, myocardial face of the heart can be difficult. infarction and stroke (due to thrombosis and plaque, or haemorrhage) but these tend to be lower than for Coronary artery surgery coronary artery bypass surgery. More commonly, local The internal mammary artery is the graft of choice haematoma at the site of arterial puncture may occur. as 50% of saphenous grafts become occluded within Overall mortality is approximately 0.5%. 10 years. The coronary arteries are opened distal to the obstruction and the grafts are placed. If the saphenous Prognosis vein is used, its proximal end is sewn to the ascend- Depending on the anatomy of the lesion, significant ing aorta. The surgery takes approximately 1–2 hours. restenosis occurs between 30 and 60% after balloon Once the heart is reperfused, it rapidly regains activ- angioplasty without stenting. Stent implants generally ity. Ventricular fibrillation is deliberately induced during P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 30 Chapter 2: Cardiovascular system cardiopulmonary bypass to reduce heart movement and r Open valvotomy and valve repair is performed under avoid additional ischaemia and internal defibrillating cardiopulmonary bypass. The valve leaflets are sepa- paddles are used to restore sinus rhythm. rated under direct vision. This is used for patients with coexisting mitral regurgitation. Complications Valvular regurgitation when due to dilation of the valve Aspirin is usually continued for the procedure, but other ring may be treated by sewing a rigid or semi-rigid antiplatelet drugs such as clopidogrel are stopped up to ring around the valve annulus to maintain size (annulo- 5 days in advance. During the procedure patients are plasty). If regurgitation is due to areas of flail leaflets, e.g. heparinised to prevent thrombosis. Antibiotic cover is due to infective endocarditis or chordal rupture, part of provided using a broad spectrum antibiotic to prevent the leaflet may be resected or even repaired with a piece bacteraemia. Operative mortality depends on many fac- of pericardium to restore valve competence. tors including age and concomitant disease, it usually Valve replacement: Using cardiopulmonary bypass the varies from 1 to 5%. There is a similar, age-related risk diseased valve is excised and a replacement is sutured of stroke. into place. Valves may be divided into mechanical and biological types: r Early mechanical valves were ball and cage type such Prognosis as the Starr–Edwards valve. Current designs all have Approximately 90% of patients have no angina postop- some form of tilting disc such as the single disc Björk– eratively, with almost all patients experiencing a signifi- Shiley valve or the double disc St Jude valve. They are cant improvement. Over time symptoms may gradually durable, but require lifelong anticoagulation therapy return due to progression of atheroma in the arteries or to prevent thrombosis of the valve and risk of em- occlusion of vein grafts. Less than half are symptom-free bolism. at 10 years. Outcome is improved by risk factor modifi- r Biological valves may be xenografts (from animals) cation (stopping smoking, lowering high blood pressure, or homografts (cadaveric). Xenografts are made from treating hyperlipidaemia and diabetes effectively, etc). porcine valves or from pericardium mounted on a sup- Angioplasty or re-do coronary artery surgery may be portive frame. They are treated with glutaraldehyde to possible if medication is insufficient to control symp- prevent rejection and are used to replace aortic or mi- toms; however, repeat surgery has a higher mortality. tral valves. They do not require anticoagulation unless Angioplasty using stent implantation is suitable for grafts the patient is in atrial fibrillation but have a durabil- or native vessels. ity of approximately 10 years. Valve failure may result from leaflet shrinkage or weakening of the valve com- petence causing regurgitation, or calcification causing Valve surgery valve stenosis. Valve surgery is used to treat stenosed or regurgitant Valve replacements are prone to infective endocarditis, valves, which cause compromise of cardiac function. which is difficult to treat (and may require removal of a Conservative surgery is performed whenever possible. mechanical valve). The aortic valve is not usually amenable to conservative Valve replacement provides marked symptomatic re- surgery and usually requires replacement if significantly lief and improvement in survival. Operative mortality diseased. A stenosed mitral valve may be treated by fol- is approximately 2%, but this is increased in patients lowing procedures: with ischaemic heart disease (when it is usually com- r Percutaneous mitral balloon valvuloplasty in which a bined with coronary artery bypass grafting), lung dis- balloon is used to separate the mitral valve leaflets. ease and the elderly. Perioperative complications include This is now the preferred technique unless there is haemorrhage and infection. Late complications include coexisting mitral regurgitation. haemolysis and valve failure. Arrhythmias also occur. All r Closed valvotomy uses a dilator that is passed through prosthetic valves require antibiotic prophylaxis against a left sub-mammary incision into the left atrial ap- infective endocarditis during non-sterile procedures, e.g. pendage. dental treatment, lower gastrointestinal or urogenital P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Chapter 2: Clinical 31 procedures and they may also become infected from any suitable interval by a ventricular beat if the atrium source of bacteraemia. does not contract spontaneously. Procedure Permanent pacemakers The pacemaker is inserted under local anaesthetic nor- mally taking 45 minutes to 1 hour. A small diagonal Cardiac pacemakers are used to maintain a regular incision is made a few centimetres below the clavicle and rhythm, by providing an electrical stimulus to the heart the electrodes are passed transvenously to the heart. The through one or more electrodes that are passed to the pacemaker box is then attached to the leads and im- right atrium and/or ventricle. planted subcutaneously. The procedure is covered with Common indications for a permanent pacemaker: antibiotics to reduce the risk of infection. r Complete heart block. r Sick sinus syndrome with symptomatic bradycar- Complications dia. The procedure is generally low-risk. The most impor- tant complications are pneumothorax due to the venous access and surgical site infection. As long as aspirin and Types of permanent pacemaker anti-coagulants are stopped prior to the procedure, sig- There are several types of pacemaker, most pacemak- nificant haematoma or bleeding is unusual. ers are programmable through the skin by radio trans- The pacemaker function is checked within 24 hours mission. Pacemakers may be single chamber, i.e. single of implantation. Annual follow-up is required to ensure electrode usually to the right ventricle, or dual cham- that the battery life is adequate and that there has not ber, i.e. one electrode to the right ventricle and one to been lead displacement. Patients are allowed to drive the right atrium. The descriptive code for the most com- after 1 month (current DVLA rules), i.e. after the 4-week monly used pacemakers consists of up to four letters (see pacemaker check. Most pacemakers last 5–10 years. Table 2.3). In electromagnetic fields such as in airport security Common types of pacemakers are as follows: most pacemakers are now programmed to go into a de- r VVI is a single chamber pacemaker that senses and fault pacing mode so as not to fail. Even so patients are paces the ventricle. If it senses a beat, the paced beat advised to avoid close proximity to strong electromag- is Inhibited. It is often used in patients with atrial netic fields. MRI scanning is contraindicated and pace- fibrillation with AV block. makers must be removed postmortem, if the patient is r DDD is a dual chamber pacemaker that is capable to be cremated. of sensing and pacing both the atrium and ventricle. It is used in complete heart block in the absence of Echocardiography atrial fibrillation. It can sense if an atrial beat is not followed by a ventricular beat (due to lack of AV node Echocardiography essentially means ultrasonography of conduction), in which case it will trigger a ventricular the heart. It is a very useful, non-invasive method by beat. It can also trigger an atrial beat followed at a which the heart and surrounding structures can be Table 2.3 Descriptive codes for pacemakers Code position 1 2 3 4 Category Paced chamber Sensed chamber Pacemaker response Program functions V (Ventricle) V (Ventricle) T (Triggered) P (Programmable) A (Atrium) A (Atrium) I (Inhibited) M (Multi-programmable) D (Dual) D (Dual) D (Dual) 0 (none) 0 (none) R (Reverse) R (Rate responsive) P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 32 Chapter 2: Cardiovascular system imaged. It requires technical expertise to obtain images Two dimensional is useful for evaluating the anatomical and clinical expertise to interpret the results appropri- features. Standard views are obtained. ately. The following features are typically assessed: r Left parasternal: With the transducer rotated appro- r Anatomical features such as cardiac chamber size, my- priately through a window in the third or fourth inter- ocardial wall thickness and valve structure or lesions. costal space, long and short axis views can be obtained. Ventricular aneurysms or defects such as atrial or ven- r Apical: This is a view upwards from the position of tricular septal defects can be seen. the apex beat and gives a long axis view of the heart, r Functional features including wall motion (any lo- where all four chambers can be seen simultaneously. calised wall motion abnormality as well as a general M-mode is a way by which the motion of individual assessment of the overall contractility of the ventri- structures along a narrow path can be carefully studied. cles, often measured as fractional shortening or ejec- It is a one-dimensional view (depth) with time as the tion fraction) and valve motion. Doppler ultrasound second dimension on the image produced. Structures is used to measure the velocity of jets of blood, e.g. to that do not move appear as a horizontal line, whereas assess severity in valve stenosis. structures that move, e.g. valves, are seen as zigzag lines, r The aortic root may be examined for dilatation or which move in time with the cardiac cycle. The distances dissection. between structures, or the thickness of structures, can r Pericardial fluid appears as an echo-free space between therefore be carefully measured at different times of the the myocardium and the parietal pericardium. cardiac cycle. r Mass lesions such as thrombus or tumour may be seen Doppler allows the analysis of the direction and velocity within the heart. of blood flow, and therefore is particularly useful in the The principles of echocardiography are the same as evaluation of valve lesions. It is used to calculate pressure those of ultrasound. A transducer is used to generate gradients, e.g. in aortic stenosis. It can also be used to ultrasound waves that are directed at the heart. When generate 2-D images with simultaneous imaging of flow a wave encounters an interface of differing echogenic- direction and velocity. ity, some of it is reflected and some absorbed. Any Common indications for echocardiography: reflected waves (echoes) that reach the transducer are r Suspected valvular heart disease, including infective sensed and processed into an image. The time taken endocarditis. for the wave to bounce back measures the distance of r Heart failure, to assess left ventricular function and the interface. Tissues or interfaces that reflect the waves look for any valve lesions or regurgitation, and any strongly such as bone/tissue or air/tissue will appear evidence of a cardiomyopathy. very white (echogenic) and also prevent any tissues un- r Postmyocardial infarction for suspected complica- derneath from being imaged well. Fluid is anechoic, so tions, such as ventricular septal rupture or papillary appears black. The ribs and lungs limit the ability to visu- muscle rupture. It will also identify areas of ischaemic alise the heart because they cast acoustic shadows. Tran- myocardium or previous myocardial infarction as ar- soesophageal echocardiography (TOE) is a more invasive eas of hypokinetic or akinetic myocardium, as well as method used when poor views are obtained on transtho- an overall assessment of left ventricular function. racic echocardiography, or when more detailed views are required particularly of structures near the oesophagus such as the atria and great vessels, the mitral valve or prosthetic valves. A transducer probe is mounted on the Ischaemic heart disease tip of a flexible tube that is passed into the oesophagus. The patient needs to be nil by mouth prior to the proce- Ischaemic heart disease dure, local anaesthetic spray is used on the pharynx, and intravenous sedation may be required for the procedure Definition to be tolerated. In the normal heart there is a balance between the oxy- There are three types of echocardiography: two di- gen supply and demand of the myocardium. A supply of mensional, M-mode and Doppler. oxygen insufficient for the myocardial demand results P1: JYS BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0 Chapter 2: Ischaemic heart disease 33 in ischaemia of the myocardial tissue. The predomi- Chronic stable angina nant cause of cardiac ischaemia is reduction or inter- Definition ruption of coronary blood flow, which in turn is due to atherosclerosis +/− thrombosis causing coronary artery Chest pain occurring during periods of increased my- narrowing. ocardial work because of reduced coronary perfusion. Incidence Incidence Ischaemic heart disease results in 30% of all male deaths Angina is common reflecting the incidence of ischaemic and 23% of all female deaths in the Western world. heart disease. Age Age Increases with age. Incidence increases with age. Sex Sex M>F M > F. Premenopausal women are relatively protected. Geography Geography More common in the Western world where it is the com- Predominantly a disease of the Western world, but this monest cause of death. pattern is changing with the increasing affluence of the