Clinical Guide to Cardiology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: Clinical Guides
• Sprache: Englisch

Seitenzahl: 529

Veröffentlichungsjahr: 2016

Beschreibung

Clinical Guide to Cardiology is a quick-reference resource, packed full of bullet points, diagrams, tables and algorithms for the key concepts and facts for important presentations and conditions within cardiology. It provides practical, evidence-based information on interventions, investigations, and the management of clinical cardiology.

Key features include:

• A clear evidence-base providing key guidelines and clinical trials in each chapter
• Coverage of examination techniques, common conditions, imaging modalities (including ECGs, chest X-rays, MRI and CT), interventional therapies, and pharmacology
• A companion website at www.wiley.com/go/camm/cardiology featuring audio clips, developed for differing levels of knowledge, that explain key concepts or an area in greater detail, as well as numerous additional clinical case studies, audio scripts, and self-assessment material

Leseprobe

The Clinical Guides Series

Series Editor: Christian Camm

The Clinical Guides are a brand new resource for junior doctors and medical students.

They provide practical and concise day-to-day information on common conditions, symptoms and problems faced in the clinical environment. They are easy to navigate and allow swift access to information as it is needed, with step-by-step guidance on decision making, investigations and interventions, and how to survive and thrive on clinical rotation and attachment.

This new title is also available as an e-book.For more details, please seewww.wiley.com/buy/9781118755334or scan this QR code:

Clinical Guide to Cardiology

Edited by

Christian F. Camm

John Radcliffe Hospital, Oxford, UK

A. John Camm

St. George’s University of London, London, UK

This edition first published 2016 © 2016 by John Wiley & Sons, Ltd

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Library of Congress Cataloging-in-Publication Data

Clinical guide to cardiology / edited by Christian F. Camm, A. John Camm.       p. ; cm.    Includes bibliographical references and index.    ISBN 978-1-118-75533-4 (pbk.)    I. Camm, Christian F. (Christian Fielder), editor.   II. Camm, A. John, editor.    [DNLM: 1. Heart Diseases–diagnosis.   2. Heart Diseases–therapy.   WG 141]    RC682    616.1′2–dc23                                                                      2015025343

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

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover image: iStockphoto/© Nerthuz

CONTENTS

Contributors

Acronyms and Abbreviations

About the Companion Website

PART 1 Examination Techniques

1 Examination Techniques

1.1 Common conditions to be looked for on the examination

1.2 Clinical examination – peripheries

1.3 Clinical examination – the praecordium

1.4 How to present your findings

1.5 Eponymous signs and symptoms

Note

PART 2 Approach to Presenting Complaints

2 Chest Pain

2.1 Definition

2.2 Diagnostic algorithm

2.3 Differentials list

2.4 Key history features

2.5 Key examination features

2.6 Key investigations

2.7 When to call a senior

Key clinical trials

Guidelines

Further reading

3 Shortness of Breath

3.1 Definition

3.2 Diagnostic algorithm

3.3 Differentials list

3.4 Key history features

3.5 Key examination features

3.6 Key investigations

3.7 When to call a senior

Guidelines

Further reading

4 Loss of Consciousness

4.1 Definition

4.2 Classification

4.3 Differentials list

4.4 Key history features

4.5 Key examination features

4.6 Key investigations

4.7 When to call a senior

4.8 Key clinical trials

Guidelines

Further reading

5 Palpitations

5.1 Definition

5.2 Diagnostic algorithm

5.3 Differentials list

5.4 Key history features

5.5 Key examination features

5.6 Key investigations

5.7 When to call a senior

Guidelines

Further reading

6 Cardiac Murmurs

6.1 Definition

6.2 Classification

6.3 Differentials list

6.4 Key history features

6.5 Key examination features

6.6 Key investigations

6.7 When to call a senior

Key clinical trials

Guidelines

Further reading

7 Shock

7.1 Definition

7.2 Diagnostic algorithm

7.3 Differentials list

7.4 Key history features

7.5 Key examination features

7.6 Key investigations

7.7 When to call a senior

Key clinical trials

Guidelines

Further reading

8 Oedema

8.1 Definition

8.2 Diagnostic algorithm

8.3 Differentials list

8.4 Key history features

8.5 Key examination features

8.6 Key investigations

8.7 When to call a senior

Key clinical trials

Guidelines

Further reading

PART 3 Conditions

9 Acute Coronary Syndrome

9.1 Definition

9.2 Underlying concepts

9.3 Key data

9.4 Clinical types

9.5 Presenting features

9.6 Differentials

9.7 Key investigations

9.8 Management options

Key clinical trials

Guidelines

Further reading

10 Stable Angina

10.1 Definition

10.2 Underlying concepts

10.3 Key data

10.4 Clinical types

10.5 Presenting features

10.6 Differentials

10.7 Key investigations

10.8 Management options

Key clinical trials

Guidelines

Further reading

11 Heart Failure

11.1 Definition

11.2 Underlying concepts

11.3 Clinical types

11.4 Heart failure with reduced ejection fraction

11.5 Heart failure with preserved ejection fraction (HF-PEF)

Key clinical trials

Guidelines

Further reading

12 Infective Endocarditis

12.1 Definition

12.2 Underlying concepts

12.3 Key data

12.4 Clinical types

12.5 Presenting features

12.6 Differentials

12.7 Key investigations

12.8 Management options

Key clinical trials

Guidelines

Further reading

13 Arrhythmias

13.1 Definition

13.2 Underlying concepts

13.3 Clinical types

13.4 Atrial fibrillation

13.5 Atrial flutter

13.6 Supraventricular tachycardias

13.7 Ventricular tachycardia

13.8 Other arrhythmias to be aware of

Key clinical trials

Guidelines

Further reading

14 Valvular Heart Disease

14.1 Definition

14.2 Underlying concepts

14.3 Clinical types

14.4 Mitral regurgitation (MR)

14.5 Mitral stenosis (MS)

14.6 Aortic stenosis (AS)

14.7 Aortic regurgitation (AR)

14.8 Other murmurs to be aware of

Key clinical trials

Guidelines

Further reading

15 Cardiomyopathy

15.1 Definition

15.2 Underlying concepts

15.3 Clinical types

15.4 Presentation

15.5 Hypertrophic cardiomyopathy

15.6 Dilated cardiomyopathy

15.7 Restrictive cardiomyopathy

15.8 Other cardiomyopathies

Guidelines

Further reading

16 Hypertension

16.1 Definition

16.2 Underlying concepts

16.3 Key data

16.4 Clinical types

16.5 Presenting features

16.6 Differentials

16.7 Key investigations

16.8 Management options

Key clinical trials

Guidelines

Further reading

17 Pericardial Disease

17.1 Definition

17.2 Underlying concepts

17.3 Clinical types

17.4 Acute pericarditis

17.5 Constrictive pericarditis

17.6 Pericardial effusion

Key clinical trials

Guidelines

Further reading

18 Congenital Heart Disease

18.1 Definition

18.2 Underlying concepts

18.3 Atrial septal defect

18.4 Ventricular septal defect

18.5 Coarctation of the aorta

18.6 Other forms of congenital heart disease

Key clinical trials

Guidelines

Further reading

PART 4 Imaging

19 Electrocardiogram

19.1 Definition

19.2 Outline of procedure

19.3 Indications

19.4 Peri-procedural management

19.5 Key features

19.6 Interpretation

19.7 Potential complications

Guidelines

Further reading

20 Transoesophageal Echocardiogram

20.1 Definition

20.2 Outline of procedure

20.3 Indications

20.4 Peri-procedural management

20.5 Interpretation

20.6 Potential complications

Guidelines

Further reading

21 Trans-Thoracic Echocardiogram

21.1 Definition

21.2 Outline of procedure

21.3 Indications

21.4 Peri-procedural management

21.5 Interpretation

21.6 Potential complications

Guidelines

22 Cardiac MRI

22.1 Definition

22.2 Outline of procedure

22.3 Indications

22.4 Peri-procedural management

22.5 Interpretation

22.6 Potential complications

Key clinical trials

Guidelines

Further reading

23 Cardiac CT

23.1 Definition

23.2 Outline of procedure

23.3 Indications

23.4 Peri-procedural management

23.5 Interpretation

23.6 Potential complications

Key clinical trials

Guidelines

Further reading

24 Cardiac Catheterization

24.1 Definition

24.2 Outline of procedure

24.3 Indications

24.4 Peri-procedural management

24.5 Interpretation

24.6 Potential complications

Guidelines

Further reading

PART 5 Interventional Therapies

25 Pacemakers and Implantable Cardiac Defibrillators

25.1 Definition

25.2 Outline of devices

25.3 Outline of procedure

25.4 Indications

25.5 Peri-procedural management

25.6 Potential complications

Key clinical trials

Guidelines

26 Percutaneous Coronary Intervention and Angioplasty

26.1 Definition

26.2 Basic principles

26.3 Outline of procedure

26.4 Indications

26.5 Peri-procedural management

26.6 Interpretation

26.7 Potential complications

26.8 Thrombolysis

Key clinical trials

Guidelines

Further reading

27 Valvuloplasty

27.1 Definition

27.2 Outline of procedure and devices

27.3 Indications

27.4 Peri-procedural management

27.5 Potential complications

Guidelines

28 Transcatheter Aortic Valve Implantation

28.1 Definition

28.2 Outline of procedure and devices

28.3 Indications

28.4 Peri-procedural management

28.5 Potential complications

Key clinical trials

Guidelines

Further reading

29 Cardiac Ablation

29.1 Definition

29.2 Outline of procedure

29.3 Indications

29.4 Peri-procedural management

29.5 Potential complications

Key clinical trials

Guidelines

Further reading

PART 6 Pharmacology

30 Anti-Arrhythmic Agents

30.1 Adenosine

30.2 Amiodarone

30.3 Flecainide

30.4 Digoxin

30.5 Atropine

Key clinical trials

31 Beta-Blockers

31.1 General notes

31.2 Non-selective

31.3 Cardioselective

Key clinical trials

32 Calcium-Channel Blockers

32.1 General notes

32.2 Cardiac selective

32.3 Action primarily on vascular smooth muscle

Key clinical trials

33 Nitrates

33.1 General notes

33.2 Oral nitrates

33.3 Nitrates used as an infusion

Key clinical trials

34 Drugs Targeting the Angiotensin Axis

34.1 General notes

34.2 ACE inhibitors (ACEi)

34.3 Angiotensin-receptor blockers

35 Diuretics

35.1 Loop diuretics

35.2 Thiazides and thiazide-like diuretics

35.3 Potassium-sparing diuretics

Key trials

36 Anticoagulants

36.1 Heparin

36.2 Low molecular weight heparins (LMWHs)

36.3 Fondaparinux

36.4 Warfarin

36.5 Novel oral anticoagulants

Key trials

37 Antiplatelets

37.1 Aspirin

37.2 Clopidogrel

37.3 Novel antiplatelets

38 Lipid Regulation

38.1 Statins

Index

EULA

List of Tables

Chapter 1

Table 1.1

Table 1.2

Table 1.3

Table 1.4

Table 1.5

Table 1.6

Table 1.7

Table 1.8

Table 1.9

Table 1.10

Table 1.11

Table 1.12

Table 1.13

Table 1.14

Chapter 2

Table 2.1

Table 2.2

Table 2.3

Table 2.4

Chapter 3

Table 3.1

Table 3.2

Table 3.3

Table 3.4

Table 3.5

Table 3.6

Chapter 4

Table 4.1

Table 4.2

Table 4.3

Table 4.4

Chapter 5

Table 5.1

Table 5.2

Table 5.3

Table 5.4

Chapter 6

Table 6.1

Table 6.2

Table 6.3

Table 6.4

Chapter 7

Table 7.1

Table 7.2

Table 7.3

Table 7.4

Table 7.5

Table 7.6

Table 7.7

Table 7.8

Chapter 8

Table 8.1

Table 8.2

Table 8.3

Table 8.4

Table 8.5

Chapter 9

Table 9.1

Table 9.2

Table 9.3

Table 9.4

Table 9.5

Table 9.6

Table 9.7

Table 9.8

Table 9.9

Table 9.10

Table 9.11

Table 9.12

Table 9.13

Chapter 10

Table 10.1

Table 10.2

Table 10.3

Table 10.4

Table 10.5

Chapter 11

Table 11.1

Table 11.2

Table 11.3

Table 11.4

Table 11.5

Table 11.6

Table 11.7

Table 11.8

Chapter 12

Table 12.1

Table 12.2

Table 12.3

Table 12.4

Table 12.5

Table 12.6

Table 12.7

Table 12.8

Table 12.9

Table 12.10

Table 12.11

Table 12.12

Chapter 13

Table 13.1

Table 13.2

Table 13.3

Table 13.4

Table 13.5

Table 13.6

Table 13.7

Table 13.8

Table 13.9

Table 13.10

Table 13.11

Table 13.12

Table 13.13

Table 13.14

Table 13.15

Table 13.16

Table 13.17

Table 13.18

Table 13.19

Chapter 14

Table 14.1

Table 14.2

Table 14.3

Table 14.4

Table 14.5

Table 14.6

Table 14.7

Table 14.8

Table 14.9

Table 14.10

Table 14.11

Table 14.12

Table 14.13

Table 14.14

Table 14.15

Table 14.16

Table 14.17

Table 14.18

Table 14.19

Table 14.20

Table 14.21

Table 14.22

Table 14.23

Table 14.24

Table 14.25

Table 14.26

Table 14.27

Table 14.28

Chapter 15

Table 15.1

Table 15.2

Table 15.3

Table 15.4

Table 15.5

Table 15.6

Table 15.7

Table 15.8

Table 15.9

Table 15.10

Table 15.11

Table 15.12

Table 15.13

Table 15.14

Table 15.15

Table 15.16

Chapter 16

Table 16.1

Table 16.2

Table 16.3

Table 16.4

Table 16.5

Table 16.6

Table 16.7

Table 16.8

Table 16.9

Table 16.10

Table 16.11

Table 16.12

Chapter 17

Table 17.1

Table 17.2

Table 17.3

Table 17.4

Table 17.5

Table 17.6

Table 17.7

Table 17.8

Table 17.9

Table 17.10

Table 17.11

Table 17.12

Table 17.13

Table 17.14

Table 17.15

Chapter 18

Table 18.1

Table 18.2

Table 18.3

Table 18.4

Table 18.5

Table 18.6

Table 18.7

Table 18.8

Table 18.9

Table 18.10

Table 18.11

Table 18.12

Table 18.13

Table 18.14

Table 18.15

Table 18.16

Table 18.17

Table 18.18

Chapter 19

Table 19.1

Table 19.2

Table 19.3

Table 19.4

Table 19.5

Table 19.6

Table 19.7

Table 19.8

Table 19.9

Table 19.10

Table 19.11

Table 19.12

Table 19.13

Table 19.14

Table 19.15

Chapter 20

Table 20.1

Chapter 21

Table 21.1

Chapter 22

Table 22.1

Chapter 23

Table 23.1

Table 23.2

Chapter 24

Table 24.1

Table 24.2

Chapter 25

Table 25.1

Table 25.2

Chapter 26

Table 26.1

Chapter 27

Table 27.1

Chapter 28

Table 28.1

Chapter 29

Table 29.1

Chapter 36

Table 36.1

Table 36.2

List of Illustrations

Chapter 1

Figure 1.1

The examination circuit.

Chapter 2

Figure 2.1

Algorithm for the diagnosis of chest pain.

Figure 2.2

Stanford classification.

Figure 2.3

ECG changes of acute anterior ST-Elevation MI.

Chapter 3

Figure 3.1

Diagnostic algorithm for shortness of breath.

Figure 3.2

Examination findings in acute pulmonary oedema.

Figure 3.3

Examination findings in pulmonary embolism.

Figure 3.4

Examination findings in pneumothorax.

Figure 3.5

Examination findings in asthma.

Figure 3.6

Examination findings in pneumonia.

Figure 3.7

Examination findings in pleural effusion.

Figure 3.8

Graphical representation of restrictive and obstructive pulmonary function test results.

Figure 3.9

ECG of a patient with a pulmonary embolism showing the classic S1,Q3,T3 pattern.

Figure 3.10

CXR showing a pleural effusion.

Figure 3.11

CXR showing a right upper-lobe pneumonia.

Figure 3.12

CXR showing a right sided pneumothorax.

Chapter 4

Figure 4.1

Classification of T-LOC aetiology

Figure 4.2

An ECG showing complete dissociation of atrial and ventricular systole. This is consistent with third-degree (complete) heart block. These patients often present with syncope – so-called Stokes Adam's attacks.

Figure 4.3

CT pulmonary angiogram showing a filling defect in the right and left pulmonary arteries consistent with bilateral pulmonary emboli.

Chapter 5

Figure 5.1

Flow chart for evaluation of palpitations.

Figure 5.2

A REVEAL™ device – used for palpitations/syncope of unknown origin.

Chapter 6

Figure 6.1

Flow-chart of potential underlying causes for murmurs based on timing.

Figure 6.2

Heavily calcified aortic valve (AV) in a patient with severe aortic stenosis. There is concentric hypertrophy of the left ventricular (LV) wall and post-stenotic dilatation of the aorta (A). LA, left atrium.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.3

Mitral regurgitation. Doppler shows a jet of blood passing from the left ventricle (LV) into the left atrium (LA). RV, right ventricle; RA, right atrium.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.4

Aortic regurgitation, Doppler imaging shows a jet of blood directed back into the left ventricle (LV) from the aorta. AV, aortic valve; LA, left atrium; RA, right atrium.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.5

Mitral stenosis. The mitral valve (MV) is heavily calcified. The left atrium (LA) is dilated. LV, left ventricle.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.6

Ventricular septal defect (VSD), Doppler imaging shows the movement of blood across the opening. RV, right ventricle; RA, right atrium; vS, ventricular septum; LV, left ventricle; LA, left atrium.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.7

Atrial septal defect (ASD), Doppler imaging shows the movement of blood across the opening. RA, right atrium; LA, left atrium; aS, atrial septum; RV, right ventricle.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.8

  Vegetation (V) on aortic valve in a patient with infective endocarditis. LV, left ventricle; MV, mitral valve; LA, left atrium.Source: Harpreet Kaur Sahemey, Echocardiographer, Hammersmith Hospital.

Figure 6.9

 Work-up of a patient who presents with a murmur.

Chapter 7

Figure 7.1

Diagnostic flow chart for shock.

Figure 7.2

Pneumocystis pneumonia (PCP) – a potential cause of septic shock in immunocompromised patients. Source: Daniel Hughes, FY2 Doctor in Radiology, Queen Elizabeth Hospital, Woolwich.

Figure 7.3

A large right-sided pneumothorax; if this begins to tension it could become a cause of obstructive shock.

Chapter 8

Figure 8.1

Flow chart detailing the pathophysiology of oedema.

Chapter 9

Figure 9.1

The development of acute coronary syndrome.

Figure 9.2

Diagram of coronary occlusion, due to an atherosclerotic plaque and associated thrombus, with downstream infarction.

Figure 9.3

Cardiac markers: approximate levels vs. time of onset post MI.

Figure 9.4

Diagnostic algorithm for differentiating different forms of ACS.

Figure 9.5

Cartoon representation of the pathological features following myocardial infarction.

Figure 9.6

Conditions mimicking non-ST-elevation myocardial infarctions.

Figure 9.7

ECG changes seen over time in ST-elevation myocardial infarction.

Figure 9.8

Management of patients with ACS.

Figure 9.9

Simplified platelet activation pathway.

Chapter 10

Figure 10.1

A partially occluded coronary artery.

Figure 10.2

 Modifiable and non-modifiable risk factors for coronary artery disease.

Figure 10.3

Right hand showing nicotine stains on the index and middle fingers.

Figure 10.4

ECG showing ischaemic changes of someone with stable angina.

Figure 10.5

Investigations for stable angina.

Chapter 11

Figure 11.1

The Frank–Starling curve.

Figure 11.2

Chest radiograph showing pulmonary oedema. Note the presence of cardiomegaly, bilateral pleural effusions and ‘bat's wing’ appearance of the hili.

Figure 11.3

Enlarged chest radiograph showing Kerley B lines. These are short horizontal lines seen at the periphery of the radiograph and are a feature of pulmonary oedema.

Figure 11.4

Diagnostic algorithm for heart failure.

Figure 11.5

Flow chart for the management of heart failure.

Chapter 12

Figure 12.1

Aortic valve vegetation from infective endocarditis. Source: Mr Gopal Soppa, Academic Clinical Lecturer in Cardiothoracic Surgery, St. George's University of London.

Figure 12.2

Hand signs of infective endocarditis.

Figure 12.3

Clubbing. Source: Patrick Jahns, King's College Hospital NHS Foundation Trust.

Figure 12.4

First-degree heart block.

Figure 12.5

Trans-thoracic echocardiogram showing vegetation on the mitral valve.

Chapter 13

Figure 13.1

Normal conduction within the heart.

Figure 13.2

12-lead ECG showing atrial fibrillation.

Figure 13.3

ESC rhythm control flow chart. Source: Camm 2012. reproduced with permission of Oxford University Press. CAD, coronary artery disease; CHF, congestive heart failure; HT, hypertension; LVH, left ventricular hypertrophy.

Figure 13.4

12-lead ECG showing atrial flutter.

Figure 13.5

Supraventricular tachycardia starting in a patient.

Figure 13.6

12-lead ECG showing ventricular tachycardia.

Figure 13.7

12-lead ECG of multifocal atrial tachycardia.

Chapter 14

Figure 14.1

Diagrammatic representation of heart chamber and valves. Note the mitral valve is the only valve with two leaflets.

Figure 14.2

Auscultation locations for cardiac valves.

Figure 14.3

Auscultatory findings in mitral regurgitation.

Figure 14.4

Auscultatory findings in mitral stenosis. Note the presence of presystolic potentiation due to atrial systole (increased amplitude of murmur in figure), which is only seen in sinus rhythm.

Figure 14.5

Auscultatory findings in aortic stenosis.

Figure 14.6

Auscultatory findings in aortic regurgitation.

Chapter 15

Figure 15.1

Clinical types of cardiomyopathy. (a) Normal heart. (b) HCM with the characteristically enlarged ventricular walls. (c) DCM characterized by enlarged ventricles which attempt to compensate for ventricular dysfunction. (d) RCM characterized by infiltration which stiffens the ventricular walls and causes diastolic dysfunction.

Figure 15.2

Pathophysiology of HCM.

Figure 15.3

12-lead sinus rhythm ECG in HCM patient showing prominent left ventricular hypertrophy (Sokolow criteria). Source: TP Mast, MD, and MJM Cramer, MD, University Medical Center Utrecht, the Netherlands.

Figure 15.4

TTE in HCM. Parasternal long-axis TTE in HCM patient showing prominent septal hypertrophy (A and B), as well as septal anterior motion (anterior leaflet of mitral valve touching the septum in systole, B). Source: TP Mast, MD, and MJM Cramer, MD, University Medical Center Utrecht, the Netherlands.

Figure 15.5

Pathophysiology of DCM.

Figure 15.6

Chest X-ray in DCM patient showing enlarged heart with cardiothoracic ratio (CTR) >0.5. Source: BK Velthuis, MD, University Medical Center Utrecht, the Netherlands.

Figure 15.7

MRI IN DCM. Cardiac magnetic resonance imaging in DCM patient in the four-chamber (A) and short-axis (B) view showing an enlarged LV (end-diastolic volume 330 mL) with reduced wall thickness and reduced function (ejection fraction 28%).Source: BK Velthuis, MD, University Medical Center Utrecht, the Netherlands.

Figure 15.8

Pathophysiology of RCM.

Chapter 16

Figure 16.1

Autoregulation. Blood flow in an organ is maintained constant despite fluctuations in blood pressure through means of myogenic and metabolic mechanisms. In chronic hypertension there is a rightward shift in this relationship making them more vulnerable to hypoperfusion with lowering of blood pressure.

Figure 16.2

Management of hypertension. Source: NICE 2011. Reproduced with permission of NICE.

Chapter 17

Figure 17.1

12-lead electrocardiogram from a patient with acute pericarditis showing widespread ST-segment elevation and PR-segment depression.

Figure 17.2

Flowchart of acute pericarditis management.

Figure 17.3

CT chest showing pericardial effusion.

Figure 17.4

Chest X-ray showing a large pericardial effusion.

Figure 17.5

Trans-thoracic echocardiogram of a pericardial effusion.

Chapter 18

Figure 18.1

Atrial septal defect.

Figure 18.2

Ventricular septal defect.

Figure 18.3

Diagram of Fallot's tetralogy.

Figure 18.4

Diagram of transposition of the great arteries.

Chapter 19

Figure 19.1

Image of lead placement both within the limbs and on the chest.

Figure 19.2

Direction of ECG limb leads.

Figure 19.3

The view each lead provides of the heart. Note the two separate axes (coronal and axial).

Figure 19.4

 ECG waves and segments.

Figure 19.5

ECG graph paper detailing the technical aspects of an ECG.

Figure 19.6

Axis of overall ventricular depolarization.

Figure 19.7

Standard information found on most ECG print outs. Axis of the atrial (P) and ventricular (QRS) depolarization are displayed as the fourth item on the list.

Figure 19.8

P-wave morphology. (A) Normal morphology. (B) ‘Pulmonale’ P-wave due to right atrial enlargement. (C) ‘Mitrale’ P-wave due to left atrial enlargement.

Figure 19.9

ECG – sinus rhythm.

Figure 19.10

ECG – sinus arrhythmia.

Figure 19.11

ECG – supraventricular tachycardia.

Figure 19.12

ECG – left bundle branch block.

Figure 19.13

ECG – right bundle branch block.

Figure 19.14

ECG – polymorphic ventricular tachycardia (torsades de pointes).

Chapter 20

Figure 20.1

TOE probe.

Figure 20.2

Positioning of TOE probe.

Figure 20.3

TOE image of an aortic dissection.

Figure 20.4

Copy of a TOE report.

Chapter 21

Figure 21.1

Echocardiogram machine.

Figure 21.2

Parasternal long-axis view (TTE) showing the left ventricle (LV), left atrium (LA), and right ventricle (RV). The mitral and aortic valves are also seen.

Figure 21.3

Parasternal short-axis view (TTE) showing typical mitral valve ‘fish mouth view’.

Figure 21.4

Sub-costal view. Showing the left (LA) and right (RA) atria and the left (LV) and right (RV) ventricles.

Figure 21.5

Sample TTE report.

Chapter 22

Figure 22.1

Line drawing of a typical MRI scanner.

Figure 22.2

Normal cardiac MRI.

Figure 22.3

Delayed gadolinium hyper-enhancement.

Chapter 23

Figure 23.1

Multi-detector CT uses multiple rows (often ≥ 64) of detectors opposite the X-ray beams. The more detectors present the faster the speed of image acquisition. The ring is known as the gantry. This rotates around the patient as the patient passes through the ring at a set speed.

Figure 23.2

Axial slice of a cardiac CT for calcium scoring demonstrating a calcified plaque in the right mid stem of the RCA. The Agastson score was 115 for this vessel.

Figure 23.3

Axial slice of a CT contrast coronary angiogram demonstrating the left main stem which is unobstructed.

Figure 23.4

CT contrast coronary angiogram is used to create a 3D reconstruction of the coronary arteries to allow detailed views of the anatomy.

Chapter 24

Figure 24.1

Cardiac catheterization suite.

Figure 24.2

Sample cardiac catheters.

Figure 24.3

Fluoroscopic imaging: left ventriculogram.

Figure 24.4

Fluoroscopic imaging: aortogram.

Chapter 25

Figure 25.1

Line drawing of a single-chamber pacemaker

in situ

.

Figure 25.2

Line drawing of a dual-chamber pacemaker

in situ

.

Figure 25.3

Line drawing of a bi-ventricular pacemaker

in situ

.

Figure 25.4

Line drawing of an implantable cardiac defibrillator. The LV and RA leads are optional.

Figure 25.5

Selection of pacemaker systems for patients with atrioventricular block. Source: Adapted from Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. J Am Coll Cardiol. 2008;51(21):2085–2105.

Figure 25.6

Selection of pacemaker systems for patients with sinus node dysfunction. Source: Adapted from Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. J Am Coll Cardiol. 2008;51(21):2085–2105.

Figure 25.7

Chest radiograph of a permanent pacemaker with leads in the right atrium and right ventricle.

Chapter 26

Figure 26.1

Coronary artery anatomy.

Figure 26.2

Origins of the right and left coronary artery (from above the aortic valve).

Figure 26.3

Stenosis of the proximal left circumflex artery.

Figure 26.4

Left circumflex artery post stent insertion.

Chapter 27

Figure 27.1

Fluoroscopy image of guide wire inserted across the aortic valve.

Figure 27.2

Fluoroscopy image of catheter balloon opening the aortic valve.

Chapter 28

Figure 28.1

Insertion of a TAVI valve into place (line drawing).

Figure 28.2

A TAVI valve (Edwards Sapien®). Source: Image kindly provided by Edwards Lifesciences LLC, Irvine, CA. Edwards SAPIEN is a trademark of Edwards Lifesciences Corporation.

Figure 28.3

TAVI valve being inserted and expanded using a transfemoral approach.

Figure 28.4

TAVI valve being inserted and expanded using a transapical approach.

Figure 28.5

TAVI complications.

Chapter 29

Figure 29.1

Pulmonary vein isolation.

Figure 29.2

Ablation of accessory pathway conduction ECG; note disappearance of δ-wave (last two beats).

Figure 29.3

Chest CT showing left-sided pulmonary vein obliteration following pulmonary vein isolation ablation.

Chapter 30

Figure 30.1

Structure of adenosine.

Figure 30.2

Structure of amiodarone.

Figure 30.3

Structure of flecainide.

Figure 30.4

Structure of digoxin.

Figure 30.5

Structure of atropine.

Chapter 31

Figure 31.1

Chemical structure of propranolol.

Figure 31.2

Chemical structure of bisoprolol.

Chapter 32

Figure 32.1

Chemical structure of verapamil.

Figure 32.2

Chemical structure of amlodipine.

Chapter 33

Figure 33.1

Chemical structure of isosorbide mononitrate.

Figure 33.2

Chemical structure of glyceryl trinitrate.

Chapter 34

Figure 34.1

Structure of ramipril.

Figure 34.2

Structure of losartan.

Chapter 35

Figure 35.1

Structure of furosemide.

Figure 35.2

Structure of bendroflumethiazide.

Figure 35.3

Structure of spironolactone.

Chapter 36

Figure 36.1

Structure of fondaparinux.

Figure 36.2

Structure of warfarin.

Figure 36.3

Structure of rivaroxaban.

Chapter 37

Figure 37.1

Structure of aspirin.

Figure 37.2

Structure of clopidogrel.

Figure 37.3

Structure of ticagrelor.

Chapter 38

Figure 38.1

Structure of simvastatin.

Guide

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Contributors

Laura Ah-Kye

King's College Hospital, London, UK

Kristopher Bennett

Whipps Cross Hospital, London, UK

Lucy Carpenter

Barts Health NHS Trust, London, UK

Yang Chen

Imperial College Healthcare NHS Trust, London, UK

Ji-Jian Chow

Queen Elizabeth Hospital, Woolwich, UK

James Cranley

Royal Brompton & Harefield NHS Foundation Trust, London, UK

George Davies

Oxford University Hospitals NHS Trust, Oxford, UK

Akshay Garg

King's College Hospital, London, UK

Harminder S. Gill

King's College Hospital, London, UK

Katie Glover

Conquest Hospital, Hastings, UK

Stephanie Hicks

King's College Hospital, London, UK

Fritz-Patrick Jahns

King's College Hospital, London, UK

Sophie Maxwell

Walsall Manor Hospital, Walsall, UK

Blair Merrick

Hammersmith Hospital, London, UK

Madeline Moore

King's College Hospital, London, UK

Sarah Morrow

Hammersmith Hospital, London, UK

Rahul K. Mukherjee

King's College Hospital, London, UK

Anna Robinson

King's College Hospital, London, UK

Arvind Singhal

Imperial College Healthcare NHS Trust, London, UK

Nicholas Sunderland

King's College Hospital, London, UK

Anneline te Riele

University Medical Centre, Utrecht, The Netherlands

Maria Tsakok

Hammersmith Hospital, London, UK

Robert A. Watson

North West London Hospitals NHS Trust, London, UK

Acronyms and Abbreviations

2D

two-dimensional

3D

three-dimensional

A2

aortic valve component of heart sound 2

AAA

abdominal aortic aneurysm

ABG

arterial blood gas

ABPM

ambulatory blood pressure monitoring

ACC

American College of Cardiology

ACE

angiotensin-converting enzyme

ACEi

angiotensin-converting enzyme inhibitor

ACR

albumin:creatinine ratio

ACS

acute coronary syndrome

ACTH

adrenocorticotropic hormone

ADP-P2Y

adenosine diphosphate-P2Y receptor

AF

atrial fibrillation

AHA

American Heart Association

AI

angiotensin I

AII

angiotensin II

AKI 

acute kidney injury

ALD

alcoholic liver disease

ALP

alkaline phosphatase

ALS

advanced life support

AMA

American Medical Association

AMB

acute marginal branch

AMTS

Abbreviated Mental Test score

APS

antiphospholipid syndrome

aPTT

activated partial thromboplastin time

AR

aortic regurgitation

ARB

angiotensin-II receptor blocker

ARDS

acute respiratory distress syndrome

AS

aortic stenosis

ASD

atrial septal defect

AST

aspartate aminotransferase

ATP

adenosine triphosphate

AV

atrioventricular

AVN

atrioventricular node

AVNRT

AV-nodal re-entrant tachycardia

AVPU

alert/responsive to voice/responsive to pain/unresponsive

AVRT

atrioventricular re-entrant tachycardia

AVSD

atrioventricular septal defect

BAH

bilateral adrenocortical hyperplasia

BAV

balloon aortic valvuloplasty

BCS

British Cardiovascular Society

BD

twice a day

BE

base excess

beta-hCG

beta human chorionic gonadotrophin

BM

Boheringer-Mannheim – capillary glucose test

BMI

body mass index

BNP

brain natriuretic peptide

BP

blood pressure

BPH

benign prostatic hyperplasia

bpm

beats per minute

CABG

coronary artery bypass graft

CAC

coronary artery calcium

CAD

coronary artery disease

Cath Lab

(coronary) catheterization laboratory

CCB

calcium-channel blocker

CCF

congestive cardiac failure

CCP

cyclic citrullinated peptide

CCU

cardiac care unit

CK-MB

creatine kinase – MB isoform

CKD

chronic kidney disease

CMV

cytomegalovirus

CN

coagulase negative

CNS

central nervous system

CO

cardiac output

CoA

coarctation of the aorta

COPD

chronic obstructive pulmonary disease

COX

cyclo-oxygenase

CPAP

continuous positive airway pressure

CPR

cardiopulmonary resuscitation

CRP

C-reactive protein

CRT

cardiac resynchronization therapy

CRT-D

cardiac resynchronization therapy + cardiac defibrillator

CT

computed tomography

CTPA

computed tomography pulmonary angiogram

CTR

cardiothoracic ratio

CV(S)

cardiovascular (system)

CVA

cerebrovascular accident

CVD

cerebrovascular disease

CVP

central venous pressure

CXA

X-ray coronary angiography

CXR

chest X-ray

DAPT

dual anti-platelet therapy

DC

direct current

DCM

dilated cardiomyopathy

DH

drug history

DHP

dihydropyridine

DKA

diabetic ketoacidosis

DM

diabetes mellitus

DVLA

Driver and Vehicle Licensing Agency

DVT

deep vein thrombosis

EBV

Epstein–Barr virus

ECG

electrocardiogram

echo

echocardiogram

ED

emergency department

EDV

end-diastolic volume

EEG

electroencephalogram

EF

ejection fraction

EGDT

early goal-directed therapy

eGFR

estimated glomerular filtration rate

ELR

external loop recorder

EPS

electrophysiological study

ESC

European Society of Cardiology

ESM

ejection systolic murmur

ESR

erythrocyte sedimentation rate

ESV

end-systolic volume

EVAR

endovascular aneurysm repair

FAST

focused assessment with sonography for trauma

FBC

full blood count

FFP

fresh frozen plasma

FFR

fractional flow reserve

FH

family history

FY2

foundation year 2 doctor

G6PD

glucose-6-phosphate dehydrogenase

GCS

Glasgow coma scale

GFR

glomerular filtration rate

GI

gastrointestinal

GMP

guanosine monophosphate

GORD

gastro-oesophageal reflux disease

GP

general practitioner

GRA

glucorticoid-remediable aldosteronism

GRACE

Global Registry of Acute Coronary Events

GTN

glyceryl trinitrate

GZA

glycyrrhizic acid

HACEK

organisms associated with culture-negative infective endocarditis

Hb

haemoglobin

HbA1c

glycated haemoglobin

HBPM

home blood pressure monitoring

HCG

human chorionic gonadotrophin

HCM

hypertrophic cardiomyopathy

HDL

high density lipoprotein

HDU

high dependency unit

HF

heart failure

HF-PEF

heart failure with preserved ejection fraction

HF-REF

heart failure with reduced ejection fraction

HIT

heparin-induced thrombocytopenia

HIV

human immunodeficiency virus

HOCM

hypertrophic obstructive cardiomyopathy

HPC

history of the presenting complaint

HR

heart rate

HTN

hypertension

IABP

intra-aortic balloon pump

IC

intercostal

ICD

implantable cardioverting defibrillator

ICH

intracerebral haemorrhage

IE

infective endocarditis

IGG

immunoglobulin G

IHD

ischaemic heart disease

ILR

internal loop recorder

IM

intramuscular

INR

international normalized ratio

ISMN

isosorbide mononitrate

ITU

intensive therapy unit

IV

intravenous

IVCD

intraventricular conduction delay

IVDU

intravenous drug user

IVUS

intravascular ultrasound

JVP

jugular venous pulse/pressure

LA

left atrium

Lac

lactate

LAD

left anterior descending coronary artery

LBBB

left bundle branch block

LCx

left circumflex artery

LDH

lactate dehydrogenase

LDL cholesterol

low density lipoprotein cholesterol

LFT

liver function test

LGV

large goods vehicle

LL

left leg

LMA

laryngeal mask airway

LMCA

left main coronary artery

LMWH

low molecular weight heparin

LQTS

long QT syndrome

LV

left ventricular/left ventricle

LVEDP

left ventricular end-diastolic pressure

LVEDV

left ventricular end-diastolic volume

LVEF

left ventricular ejection fraction

LVESD

left ventricular end-systolic diameter

LVH

left ventricular hypertrophy

LVOT

left ventricular outflow tract

LVOTO

left ventricular outflow tract obstruction

MAHA

microangiopathic haemolytic anaemia

MAOI

monoamine oxidase inhibitor

MAP

mean arterial pressure

MAU

medical assessment unit

MCA

middle cerebral artery

MCV

mean corpuscular volume

MDCT

multi-detector row computed tomography

MDM

multidisciplinary meeting

MDT

multidisciplinary team

MEN

multiple endocrine neoplasia

MI

myocardial infarction

MIBG

meta-iodobenzylguanidine

MR

mitral regurgitation

MRA

mineralocorticoid receptor antagonist

MRI

magnetic resonance imaging

MS

mitral stenosis

MVP

mitral valve prolapse

NAC

N-acetylcysteine

NBM

nil by mouth

NICE

National Institute for Health and Care Excellence

NOAC

novel oral anticoagulant

NPA

nasopharyngeal mask airway

NSAID

non-steroidal anti-inflammatory drug

NSTE ACS

non-ST-elevation acute coronary syndrome

NSTEMI

non-ST-elevation myocardial infarction

NYHA

New York Heart Association

OCT

optical coherence tomography

OD

once a day

OMB

obtuse marginal artery

OMT

optimal medical therapy

OR

odds ratio

OSCE

objective structured clinical examination

P2

pulmonary valve constituent of the second heart sound

PAD

peripheral arterial disease

P

a

O

2

partial pressure of arterial oxygen

PCA

patient-controlled analgesia

PCC

prothrombin complex concentrate

PCI

percutaneous coronary intervention

PCR

protein:creatinine ratio

PCV

passenger-carrying vehicle

PDA

patent ductus arteriosus

PDE-5

phosphodiesterase-5

PE

pulmonary embolism

PEF

peak expiratory flow

PET

positron emission tomography

PFO

patent foramen ovale

PG

prostaglandin

PICC

peripherally inserted central catheter

PLV

posterior left ventricular branch

PMC

percutaneous mitral commisurotomy

PMH

past medical history

PND

paroxysmal nocturnal dyspnoea

PO

per os

- taken orally

PP

pulse pressure

PPI

proton-pump inhibitor

PR

per rectum

PRN

pro re nata

– as needed

PT

prothrombin time

PUO

pyrexia of unknown origin

PVI

pulmonary vein isolation

QDS

four times a day

QTc

corrected QT interval

RA

right atrium

RAA

renin–angiotensin–aldosterone

RBBB

right bundle branch block

RCA

right coronary artery

RCM

restrictive cardiomyopathy

RCT

randomized controlled trial

RF

risk factor

ROSC

return of spontaneous circulation

RR

respiratory rate

RRR

relative risk reduction

RV

right ventricular

RVOT

right ventricular outflow tract

RVST

right ventricular systolic pressure

S1

heart sound 1

S2

heart sound 2

S3

heart sound 3

S4

heart sound 4

SAN

sinoatrial node

S

a

O

2

saturation of arterial oxygen

SAVR

surgical aortic valve replacement

SBAR

situation/background/assessment/recommendation

SC

subcutaneously

SG

specific gravity

SHO

senior house officer

SIRS

systemic inflammatory response syndrome

SLE

systemic lupus erythematosus

SOB

shortness of breath

SOBOE

shortness of breath on exertion

SPECT

single-photon emission computed tomography

SpO

2

oxygen saturation

SpR

specialist registrar

SSRI

selective serotonin reuptake inhibitor

STE ACS

ST-elevation acute coronary syndrome

STEMI

ST-elevation myocardial infarction

SV

stroke volume

SVC

superior vena cava

SVR

systemic vascular resistance

SVT

supraventricular tachycardia

T-LOC

transient loss of consciousness

TA

transapical

TAVI

transaortic valve implantation

TB

tuberculosis

TDS

three times a day

TF

transfemoral

TFT

thyroid function test

TGA

transposition of the great arteries

TIA

transient ischaemic attack

TIMI

Thrombolysis In Myocardial Infarction (study)

TOE

transoesophageal echocardiogram

TR

tricuspid regurgitation

TSH

thyroid-stimulating hormone

TTE

trans-thoracic echocardiogram

TXA2

thomboxane A2

U&E

urea and electrolytes

UA

unstable angina

UFH

unfractionated heparin

USS

ultrasound scan

UTI

urinary tract infection

VBG

venous blood gas

VF

ventricular fibrillation

VKA

vitamin K antagonist

VSD

ventricular septal defect

VT

ventricular tachycardia

VTE

venous thromboembolism

WCC

white cell count

WHO

World Health Organization

WPW

Wolff–Parkinson–White syndrome

About the Companion Website

This book is accompanied by a companion website:

www.wiley.com/go/camm/cardiology

The website includes:

MCQs

EMQs

SAQs

Clinical cases

Audio

Audio scripts

PART 1Examination Techniques

1Examination Techniques

Christian F. Camm

John Radcliffe Hospital, Oxford, UK

1.1 Common conditions to be looked for on the examination

Arrhythmias                                   

Valvular pathology                        

Endocarditis                                   

Heart failure                                   

Ischaemic heart disease               

Inherited cardiac conditions       

Poor perfusion/shock                   

Anaemia                                          

1.2 Clinical examination – peripheries

Table 1.1 Elements to be undertaken prior to examining the patient

Item

Detail

1. Appropriate hand hygiene

Wash hands with soap and water or alcohol hand rub

2. Introduce yourself

Full name and job title

3. Confirm patient identity

Check full name and date of birth, verify against wrist band

4. Gain permission for the examination

Explain your role and what the examination will involve

5. Enquire about pain

Particularly chest and shoulder pain

6. Position the patient

45° on examination couch or bed

7. Expose the patient appropriately

Entire chest (women can leave bras on) Remember to cover patient when not examining the chest itself

Table 1.2 Examination features from the end of the bed

Item

Detail

1. Does the patient look well?

Sitting up and talking, or reduced consciousness?

Difficulty breathing?

Severe cyanosis?

Pallor?

Sweating?

2. Are there any obvious scars?

Midline sternotomy

Lateral thoracotomy

Saphenous vein harvest scar

Pacemaker/ICD device or scar

3. Lines in and out of patient

IV infusions

Catheters

Oxygen

4. Patient monitoring

Continuous ECG

Pulse oximetry

Haemodynamic monitoring (e.g. blood pressure)

5. Any medications around the patient

Glyceryl trinitrate (GTN) spray or inhalers

Drug infusions

Warfarin (or anticoagulation cards/booklets)

Table 1.3 Examination findings in the nails

Item

Conditions

1. Clubbing

/

2. Splinter haemorrhages

3. Capillary refill time >2 seconds

4. Peripheral cyanosis

/

5. Nicotine stains

Box 1.1 Stages of clubbing

Fluctuation and softening of the nail bed

Loss of normal nail bed angle (Lovibond's angle)

Increased convexity of the nail fold

Thickening of the whole distal finger

Striations and increased shine on nails and surrounding skin

Table 1.4 Examination findings in the hand

Item

Conditions

1. Tendon xanthomata

/

2. Osler nodes

3. Janeway lesions

4. Palmar crease pallor

5. Temperature

6. Bruising (anticoagulation or antiplatelet agents)

Table 1.5 Examination findings in the wrist

Item

Conditions

1. Pulse rate

/

2. Pulse rhythm

3. Radio-radial delay

4. Radio-femoral delay

5. Collapsing pulse

6. Blood pressure

/ / /

Table 1.6 Examination findings in the eyes

Item

Conditions

1. Corneal arcus

/age

2. Conjunctival pallor

3. Petechial haemorrhages

4. Xanthelasma over eyelids

5. Roth spots

6. Lens dislocation

Table 1.7 Examination findings in the mouth

Item

Conditions

1. Hydration status

general

2. Dentition

3. Central cyanosis

/

4. High arched palate (Marfan's)

Table 1.8 Examination findings in the neck

Item

Conditions

1. Carotid pulse – character

/

2. JVP

Box 1.2 How to examine the JVP

Located between heads of sternocleidomastoid

JVP has double pulse (rather than single found in carotid)

JVP can be occluded

JVP may be made more visible by lowering angle of the bed

Hepato-jugular reflux

Height measured from the sternal angle (angle of Louis)

Box 1.3 Central pulse character

Slow rising:

aortic stenosis

Small volume:

tachycardia, volume depletion, cardiogenic shock, aortic stenosis

Bounding:

CO

2

retention, Paget's disease, aortic regurgitation

Collapsing:

aortic regurgitation

Pulsus bisferiens:

combined aortic stenosis and regurgitation

Table 1.9 Examination findings in the legs. This is often undertaken after examining the praecordium

Item

Conditions

Pitting oedema

Saphenous vein harvest scars

1.3 Clinical examination – the praecordium

Table 1.10 Inspection features of the praecordium

Item

Conditions

1. Scars

/ /

2. Pacemaker/ICD

/

3. Visible apex beat

/

Table 1.11 Palpation features of the praecordium

Item

Conditions

1. Apex beat

2. Thrills

(aortic and pulmonary valve pathology)

3. Right ventricular heave

/

Box 1.4 The apex beat

Most lateral and inferior precordial cardiac pulsation

Normal position – fifth intercostal space, inside mid-clavicular line

Lateral and inferior displacement represents LV dilation

Diffuse apex beat represents LV dilation

Tapping of the apex beat is seen in mitral stenosis

Double impulse is a sign of hypertrophic obstructive cardiomyopathy

Table 1.12 Auscultation of the praecordium

Location

Valve auscultated

1. Apex

Mitral valve

2. Fourth intercostal (IC) space, left sternal edge

Tricuspid valve + aortic (regurgitation)

3. Second IC space, left sternal edge

Pulmonary valve

4. Second IC space, right sternal edge

Aortic (stenosis)

5. Axilla

Mitral (reguritation)

6. Carotids

Aortic (stenosis) + carotid bruits

Box 1.5 Auscultatory elements

To be successful at auscultation, it is important to actively listen (ask yourself what you can hear)

The auscultatory elements that make up each cardiac cycle must be identified

When identified, each component should then be characterized:

First heart sound:

mitral and tricuspid valve closure

Second heart sound:

aortic and pulmonary valve closure

Additional sounds:

S3, S4

Murmurs

Non-valvular sounds:

e.g. pericardial rub

Mechanical heart valve sounds

Box 1.6 Reinforcement manoeuvres

Rolled to left side:

for mitral valve murmurs

Hold breath in expiration:

left-sided murmurs

Hold breath in inspiration:

right-sided murmurs

Sit patient forward:

aortic regurgitation

Box 1.7 The first heart sound

Caused by blood hitting the closed mitral and tricuspid valves

Represents the start of ventricular systole

Usually a single sound

Heard best at the cardiac apex

Split sound:

bundle branch block

Soft S1:

first-degree AV block, aortic regurgitation

Loud S1:

mitral stenosis

Variable intensity:

ventricular arrhythmias, variable AV block

Box 1.8 The second heart sound

Caused by blood hitting the closed aortic and pulmonary valves

Represents the end of ventricular systole

Heard well over the entire praecordium

Usually a split sound on inspiration

Pulmonary component follows aortic

Widely split:

right bundle branch block

Fixed splitting:

atrial septal defects

Soft aortic component:

aortic stenosis

Table 1.13 Examination findings on the back

Item

Conditions

Lung bases

Sacral oedema

Figure 1.1 The examination circuit.

(See Audio Podcast 1.1 at www.wiley.com/go/camm/cardiology)

1.4 How to present your findings

Safety first approach

Details

An approach that works well when not sure of your findings

Useful for objective structured clinical examinations (OSCEs) to ensure that information is not missed

Discuss the positive findings (and key negatives) in the order that you examined

Give a potential diagnosis after presenting findings

Example

I examined this 52-year-old patient. He presented with shortness of breath and leg swelling. On inspection he was clearly dyspnoeic but otherwise appeared well. He was alert. There was a well healed midline sternotomy scar. His pulse was regular at 80 bpm. His blood pressure was 110/80 mmHg. The patient was well hydrated. The JVP was raised by 8 cm. There were no additional peripheral signs elucidated. On the praecordium he had no additional scars. His apex beat was not inappropriately located. On auscultation S1 and S2 were both heard. Additionally a third heart sound was heard across the praecordium. There were no additional sounds. There were inspiratory crackles at the lung bases and some sacral oedema. A clear scar along the course of the long saphenous vein was seen on the left leg, this was combined with bilateral pitting oedema reaching the mid-calf.

In conclusion, this patient presents with shortness of breath and signs suggestive of heart failure.

Ward-round based

Details

An approach to be used when you are confident or pressed for time

Give your suspected diagnosis first

Discuss the examination findings that support the diagnosis and help to exclude others

Discuss findings in the order of most supportive to least supportive of your diagnosis

Example

I examined this 52-year-old patient. He presented with shortness of breath and leg swelling. Examination revealed a patient with a clinical picture of congestive heart failure. This was supported by findings of inspiratory crackles at the lung bases, pitting oedema in the sacral region and bilaterally in the legs up to the mid-calf level. In addition, the JVP was raised to 8 cm above the angle of Louis. On auscultation S1 and S2 were clearly heard with the addition of a third heart sound. The patient has a history of coronary artery bypass surgery as supported by the midline sternotomy scar and long saphenous vein graft scar on the left leg. Given these findings, this suggests a history of heart failure potentially secondary to ischaemic heart disease.

1.5 Eponymous signs and symptoms

Table 1.14 Eponymous signs in cardiology

Eponym

Details

Austin Flint murmur

Low-pitched rumbling murmur in mid-diastole due to aortic regurgitation causing mitral stenosis

Beck's triad

Three signs associated with cardiac tamponade:

Low arterial blood pressure

Distended neck veins

Muffled heart sounds

Corrigan's pulse

A large-volume pulse which collapses away due to aortic regurgitation – observed at the carotid

De Musset's sign

Rhythmic nodding of the head due to increased pulse pressure in aortic regurgitation

Duroziez's sign

Compression of the femoral artery with the bell of the stethoscope leads to an audible diastolic murmur – aortic regurgitation

Ewart's sign

Collection of signs at the left lung base due to pericardial effusion:

‘Woody’ dullness to percussion

Increased vocal resonance

Bronchial breath sounds

Friedreich's sign

Significant drop in JVP during the diastolic phase due to constrictive pericarditis

Graham Steell murmur

Pulmonary regurgitant murmur heard in the left 2

nd

intercostal space

Janeway lesions

Non-tender, small erythematous nodular lesions on the palms/soles indicative of endocarditis

Kussmaul's sign

Paradoxical rise in JVP on inspiration, indicative of reduced right ventricular filling (e.g. right heart failure or constrictive pericarditis)

Mayne's sign

A drop >15 mmHg in diastolic blood pressure when the arm is raised – aortic regurgitation

Müller's sign

Bobbing of the uvula due to wide pulse pressure of aortic regurgitation

Oliver's sign

Downward tug of the trachea during systole – aneurysm of the aortic arch

Osler nodes

Painful, raised lesions on the hands/feet caused by immune complex deposition and suggestive of infective endocarditis

Osler's sign

Falsely elevated blood pressure due to calcification of the vessels

Quinke's pulse

Alternating blushing and blanching of the fingernails – aortic regurgitation

Roth spots

Retinal haemorrhages with a pale fibrin centre caused by immune complex deposition and suggestive of infective endocarditis

Still's murmur

Innocent flow murmur

Watson's waterhammer pulse

As with Corrigan's pulse, but observed over the radial artery

For additional resources and to test your knowledge, visit the companion website at:

Note

1. Arrhythmias 2. Valvular pathology 3. Endocarditis 4. Heart failure 5. Ischaemic heart disease 6. Inherited cardiac conditions 7. Poor perfusion/shock 8. Anaemia

PART 2Approach to Presenting Complaints

2Chest Pain

Maria Tsakok

Hammersmith Hospital, London, UK

2.1 Definition

Any pain or discomfort that is felt to originate in and around the thorax.

2.2 Diagnostic algorithm

Figure 2.1 Algorithm for the diagnosis of chest pain.

2.3 Differentials list

Dangerous diagnoses

Acute coronary syndrome

Aortic dissection

Pulmonary embolism

Tension pneumothorax

Boerhaave's syndrome (oesophageal rupture)

Common diagnoses

Cardiac causes

Stable angina

Pericarditis

Pulmonary causes

Pneumonia

Pneumothorax

Gastrointestinal causes

Gastro-oesophageal reflux disease

Oesophageal spasm

Musculoskeletal causes

Rib contusions/fractures

Intercostal muscle strains

Costochondritis (including Tietze and Bornholm syndromes)

Diagnoses to consider

Psychiatric causes

Herpes zoster

2.4 Key history features

(See Audio Podcast 2.1 at www.wiley.com/go/camm/cardiology)

Dangerous diagnosis 1

Diagnosis: Acute coronary syndrome

Questions

a. Is the pain crushing or heavy in nature?

These are the typical descriptions, but the pain may also be described as tight, gripping or pressing.

b. Does the pain radiate to the left arm or jaw?

These distinctive sites of radiation are highly suggestive of myocardial pain.

c. Are there associated autonomic symptoms?

Commonly nausea/vomiting and sweating.

d. Are there any cardiac risk factors?

See Box 2.1.

Box 2.1 Cardiac risk factors

Non-modifiable:

Increasing age

Male gender

Family history

Previous cardiovascular events

Diabetes

Modifiable:

Smoking

Hypertension

Obesity

Low physical activity

Dangerous diagnosis 2

Diagnosis: Aortic dissection

Questions

a.