Cardiology and Cardiovascular System on the Move

1st Edition by Swati Gupta, Alexandra Marsh,

David Dunleavy ISBN 0429586124 9780429586125
download
https://ebookball.com/product/cardiology-and-cardiovascular-
system-on-the-move-1st-edition-by-swati-gupta-alexandra-marsh-
david-dunleavy-isbn-0429586124-9780429586125-4812/

Download more ebook instantly today - Get yours now at ebookball.com

 Get Your Digital Files Instantly: PDF, ePub, MOBI and More
Quick Digital Downloads: PDF, ePub, MOBI and Other Formats

Cardiology and the Cardiovascular System on the move 1st Edition by

Swati Gupta, Alexandra Marsh, David Dunleavy, Kevin Channer ISBN
9780429586125 0429586124

https://ebookball.com/product/cardiology-and-the-cardiovascular-
system-on-the-move-1st-edition-by-swati-gupta-alexandra-marsh-
david-dunleavy-kevin-channer-isbn-9780429586125-0429586124-4664/

The Cardiovascular System 1st Edition by Kara Rogers ISBN 1615302514

9781615302512

https://ebookball.com/product/the-cardiovascular-system-1st-
edition-by-kara-rogers-isbn-1615302514-9781615302512-2658/

Marsh and Martin's Oral Microbiology 6th Edition by Philip Marsh,

Michael Lewis, Helen Rogers, David Williams, Melanie Wilson ISBN
0702061751 9780702061752

https://ebookball.com/product/marsh-and-martin-s-oral-
microbiology-6th-edition-by-philip-marsh-michael-lewis-helen-
rogers-david-williams-melanie-wilson-
isbn-0702061751-9780702061752-5106/

Surgical Pathology of the Gastrointestinal System 1st edition by

Kaushik Majumda,Siddhartha Datta Gupta 9811663955 9789811663956

https://ebookball.com/product/surgical-pathology-of-the-
gastrointestinal-system-1st-edition-by-kaushik-majumda-
siddhartha-datta-gupta-9811663955-9789811663956-21166/
The Netter Collection of Medical Illustrations Cardiovascular System
Volume 8 2nd Edition by Richard Conti 1455742295 9781455742295

https://ebookball.com/product/the-netter-collection-of-medical-
illustrations-cardiovascular-system-volume-8-2nd-edition-by-
richard-conti-1455742295-9781455742295-2884/

Practical Cardiology Evaluation and Treatment of Common Cardiovascular

Disorders 3rd Edition by Ragavendra Baliga, Kim Eagle ISBN
9783030283285 3030283283

https://ebookball.com/product/practical-cardiology-evaluation-
and-treatment-of-common-cardiovascular-disorders-3rd-edition-by-
ragavendra-baliga-kim-eagle-isbn-9783030283285-3030283283-4680/

Practical Cardiology Evaluation and Treatment of Common Cardiovascular

Disorders 3rd Edition by Ragavendra Baliga, Kim Eagle ISBN
9783030283285 3030283283

https://ebookball.com/product/practical-cardiology-evaluation-
and-treatment-of-common-cardiovascular-disorders-3rd-edition-by-
ragavendra-baliga-kim-eagle-isbn-9783030283285-3030283283-4676/

Interventional Cardiology and Cardiac Catheterisation The Essential

Guide 2nd Edition by John Edward Boland, David Muller ISBN
9781351060332 1351060333

https://ebookball.com/product/interventional-cardiology-and-
cardiac-catheterisation-the-essential-guide-2nd-edition-by-john-
edward-boland-david-muller-isbn-9781351060332-1351060333-4710/

Cardiovascular Physiology 8th Edition by David Mohrman, Lois Heller

ISBN 0071793127 9780071793124

https://ebookball.com/product/cardiovascular-physiology-8th-
edition-by-david-mohrman-lois-heller-
isbn-0071793127-9780071793124-3452/
 Cardiology and the
Cardiovascular System

Authors: Swati Gupta, Alexandra Marsh

and David Dunleavy
Editorial Advisor: Kevin Channer
c lu de d
in
s
es
ook acc
Eb
Medicine on the move
Editor-in-chief: Rory Mackinnon
Series editors: Sally Keat, Thomas Locke, Andrew Walker and Harriet Walker

RECENT AND FORTHCOMING TITLES

Cardiology and the Cardiovascular System on the Move

David Dunleavy, Swati Gupta and Alexandra Marsh, 2015

Clinical Pharmacology and Practical Prescribing on the Move

James Turnbull and Matthew Tate, 2015

Emergency and Acute Medicine on the Move

Naomi Meardon, Shireen Siddiqui, Elena Del Vescovo, Lucy C Peart
and Sherif Hemaya, 2015

Gastroenterology on the Move

Arash Assadsangabi, Lucy Carroll and Andrew Irvine, 2015

Neurology and Clinical Neuroanatomy on the Move

Matthew Tate, Johnathan Cooper-Knock, Zoe Hunter and Elizabeth Wood, 2014

Surgery on the Move

Jenna Morgan, Harriet Walker and Andrew Viggars, 2014

Orthopaedics and Rheumatology on the Move

Terence McLoughlin, Ian Baxter and Nicole Abdul, 2013

Obstetrics, Gynaecology and Women’s Health on the Move

Amie Clifford, Claire Kelly, Chris Yau and Sally Hallam, 2012

Psychiatry on the Move

Molly Douglas, Harriet Walker and Helen Casey, 2012

Anaesthesia on the Move

Sally Keat, Simon Bate, Alexander Bown and Sarah Lanham, 2012

Clinical Investigations on the Move

Andrew Walker, Lina Fazlanie and Rory Mackinnon, 2012

Microbiology and Infectious Diseases on the Move

Thomas Locke, Sally Keat, Andrew Walker and Rory Mackinnon, 2012
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742

© 2016 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business

No claim to original U.S. Government works

Version Date: 20151118

International Standard Book Number-13: 978-1-4441-7600-1 (eBook - PDF)

This book contains information obtained from authentic and highly regarded sources. While all reason-
able efforts have been made to publish reliable data and information, neither the author[s] nor the publisher
can accept any legal responsibility or liability for any errors or omissions that may be made. The publish-
ers wish to make clear that any views or opinions expressed in this book by individual editors, authors or
contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The
information or guidance contained in this book is intended for use by medical, scientific or health-care
professionals and is provided strictly as a supplement to the medical or other professional’s own judgement,
their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate
best practice guidelines. Because of the rapid advances in medical science, any information or advice on
dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to con-
sult the relevant national drug formulary and the drug companies’ and device or material manufacturers’
printed instructions, and their websites, before administering or utilizing any of the drugs, devices or mate-
rials mentioned in this book. This book does not indicate whether a particular treatment is appropriate or
suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to
make his or her own professional judgements, so as to advise and treat patients appropriately. The authors
and publishers have also attempted to trace the copyright holders of all material reproduced in this pub-
lication and apologize to copyright holders if permission to publish in this form has not been obtained. If
any copyright material has not been acknowledged please write and let us know so we may rectify in any
future reprint.

Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, trans-
mitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter
invented, including photocopying, microfilming, and recording, or in any information storage or retrieval
system, without written permission from the publishers.

For permission to photocopy or use material electronically from this work, please access www.copyright.
com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood
Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and
registration for a variety of users. For organizations that have been granted a photocopy license by the CCC,
a separate system of payment has been arranged.

Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used
only for identification and explanation without intent to infringe.
Visit the Taylor & Francis Web site at
http://www.taylorandfrancis.com

and the CRC Press Web site at

http://www.crcpress.com
Contents
Preface ix
List of abbreviations xi
An explanation of the text xv

Part I CARDIOLOGY AND THE CARDIOVASCULAR SYSTEM 1

1. A guide to cardiac history 5

1.1 Presenting complaint 5
1.2 Past medical history 7
1.3 Drug history 8
1.4 Family history 8
1.5 Social history 8
2. A guide to cardiac examination 9
2.1 General inspection 9
2.2 Peripheral signs of cardiovascular disease 9
2.3 Examination of the precordium 11
2.4 Completing the cardiac examination 13
3. Coronary artery disease 15
3.1 Anatomy of the coronary arteries 15
3.2 Pathology of CAD: Atherosclerosis 16
3.3 Primary prevention 21
3.4 Presentations and pathophysiology of CAD 24
3.5 Complications of myocardial infarction 41
3.6 Long-term management 43
4. Acute heart failure 47
4.1 Aetiology 47
4.2 Symptoms and signs 48
4.3 Investigations 50
4.4 Management of acute heart failure 52
4.5 Cardiogenic shock 54
5. Chronic heart failure 59
5.1 Classification 59
5.2 Pathophysiology and presentation of CHF 60
5.3 Investigation of CHF 67
5.4 Management of CHF 69
5.5 Devices 72
5.6 Surgery for heart failure 73
5.7 Additional management 75
vi Contents

6. The myocardium 77
6.1 Structure and function 77
6.2 Myocarditis 77
6.3 Cardiomyopathies 79
7. Pericardial disease 89
7.1 The pericardial SAC 89
7.2 Acute pericarditis 89
7.3 Pericardial effusion and cardiac tamponade 91
7.4 Constrictive pericarditis 95
8. The cardiac valves 99
8.1 Structure of valves 99
8.2 Infective endocarditis 100
8.3 Aetiology of valve disease 105
8.4 Aortic valve 105
8.5 Mitral valve 110
8.6 Tricuspid valve 115
8.7 Pulmonary valve 115
8.8 Valve replacement 116
9. Congenital heart disease 119
9.1 Early circulation 119
9.2 Pathology 121
9.3 Communications 121
9.4 Cyanotic 126
9.5 Obstructive 129
9.6 Complex 131
10. Hypertension 135
10.1 Measuring blood pressure 135
10.2 Classification of hypertension 136
11. Diseases of the aorta 145
11.1 Acute aortic dissection 145
11.2 Aortic aneurysms 150
11.3 Aortic trauma 152
12. A guide to ECG interpretation 155
12.1 ECG interpretation 155
13. Bradycardia 163
13.1 Sinus node-related bradycardia 163
13.2 Heart block 164
13.3 Bundle branch block 167
 Contents vii

14. Tachycardias 171

14.1 Narrow complex tachycardia 171
14.2 Broad complex tachycardias 184
14.3 Cardiac arrest rhythms 188
15. Cardiac pacemakers 191
15.1 Types of pacemakers 191
15.2 Additional features of a permanent pacemaker 191
15.3 International coding system 192
15.4 Examples of indications 193
15.5 Complications 194
16. Cardiac imaging and investigations 195
16.1 Plain chest radiograph (chest X-ray, CXR) 195
16.2 Echocardiography 196
16.3 Cardiac CT 200
16.4 Cardiac MRI 201
16.5 Nuclear imaging 203
16.6 Angiography 205
16.7 Electrophysiology 207
17. Cardiac pharmacology 209
17.1 Anti-anginal 209
17.2 Anti-hypertensives 214
17.3 Anti-arrhythmics 222
17.4 Anti-coagulants and thrombolytic agents 228
17.5 Anti-platelet agents 233

Part II QUESTIONS AND ANSWERS 239

18. Questions and answers 241

Questions 241
EMQs 241
SBAs 252
Answers 256
EMQs 256
SBAs 264
Preface
Have you ever found cardiology and the physiology of the ­cardiovascular
­system overwhelmingly complicated? Have you struggled to recall the basics
in a clinical situation? Or are you simply short of time and have exams
­looming? If so, this concise, practical guide will help you.
Written by doctors for doctors, this book presents information in a wide
range of formats including flow charts, boxes, summary tables and colourful
diagrams. No matter what your learning style, we hope that you will find the
book appealing and easy to read. We think that the innovative style will help
you, the reader, to connect with this often feared topic, to learn, understand
and even enjoy it, and to apply what you have learned in your clinical practice
and in the pressured run-up to final examinations.
In writing the book, we have drawn on our recent personal experience as
medical students and junior doctors, and hope this book will offer the less-
experienced a portable and practical guide to cardiology that will complement
larger reference texts. We hope you find it helpful!
We would like to thank Dr Pankaj Garg, Cardiac MR Research Fellow,
University of Leeds, Leeds, who provided us several of the images to this book.
AUTHORS
Swati Gupta MBChB (Hons), BMedSci – CT2 Anaesthetic ACCS
Trainee, Cheltenham Hospital, Gloucestershire NHS Foundation Trust,
Gloucestershire, UK
Alexandra Marsh MBChB (Hons), BMedSci – Foundation Year 2 Doctor,
Sheffield Teaching Hospitals, Sheffield, UK
David Dunleavy MBChB, BSc – Ophthalmology Spr, York Teaching
Hospital NHS Foundation Trust, York, UK
EDITORIAL ADVISOR
Kevin Channer BSc (Hons) MBChB (Hons) MD FRCP – Consultant
Cardiologist, Honorary Professor of Cardiovascular Medicine, Sheffield
Hallam University, Sheffield, UK
EDITOR-IN-CHIEF
Rory Mackinnon BSc (Hons) MBChB MRCGP – GP Partner, Dr Cloak &
Partners, Southwick Health Centre, Sunderland, UK
SERIES EDITORS
Sally Keat MBChB BMedSci MRCP – Core Medical Trainee Year 2 in Barts
Health NHS Trust, London, UK
x Preface

Thomas Locke BSc, MBChB, DTM&H, MRCP(UK) – Core Medical

Trainee Year 2, Northwick Park Hospital, London Northwest Healthcare
London, UK
Andrew MN Walker BMedSci MBChB MRCP (London) – British Heart
Foundation Clinical Research Fellow and Honorary Specialist Registrar in
Cardiology, University of Leeds, UK
List of abbreviations
• AA: arachidonic acid
• ABG: arterial blood gas
• ACEi: angiotensin-converting enzyme inhibitor
• ACS: acute coronary syndrome
• AF: atrial fibrillation
• AHF: acute heart failure
• ALS: advanced life support
• APTT: activated partial thromboplastin time
• AR: acute regurgitation
• ARB: angiotensin receptor blocker
• ARDS: acute respiratory distress syndrome
• ARVC: arrhythmogenic right ventricular cardiomyopathy
• ARVD: arrhythmogenic right ventricular dysplasia
• AS: aortic valve stenosis
• ASD: atrial septal defect
• AST: aspartate aminotransferase
• AV: atrioventricular
• AVNRT: AV nodal re-entry tachycardia
• AVRT: AV re-entry tachycardia
• AVSD: atrioventricular septal defect
• BMI: body mass index
• BMS: bare-metal stent
• BNP: brain natriuretic peptide
• BP: blood pressure
• CABG: coronary artery bypass graft
• CAD: coronary artery disease
• CCF: congestive cardiac failure
• CCU: coronary care unit
• CHF: chronic heart failure
• CK: creatine kinase
• COPD: chronic obstructive pulmonary disease
• COX: cyclooxygenase
• CPAP: continuous positive airway pressure
• CPVT: catecholaminergic polymorphic ventricular tachycardia
• CRP: C-reactive protein
• CVD: cardiovascular disease
• CXR: plain chest radiograph
• DAPT: Dual Anti-Platelet Therapy
• DES: drug-eluting stent
xii List of abbreviations

• ESC: European Society of Cardiology

• ESR: erythrocyte sedimentation rate
• FBC: full blood count
• GRACE: Global Registry for Acute Coronary Events
• GTN: glyceryl trinitrate
• HDL: high-density lipoprotein
• HF: heart failure
• HR: heart rate
• HSTn: high sensitivity troponin
• IABP: intra-aortic balloon pump
• ICD: implantable cardioverter defibrillator
• ILR: implantable loop ECG recorder
• INR: international normalized ratio
• ISDN: isosorbide dinitrate
• ISMN: isosorbide mononitrate
• ITU: intensive treatment unit
• IVDU: intravenous drug user
• JVP: jugular venous pressure
• LA: left atrium
• LAD: left anterior descending artery
• LBBB: left bundle branch block
• LDH: lactate dehydrogenase
• LDL: low-density lipoprotein
• LFT: liver function tests
• LMWH: low-molecular-weight heparin
• LV: left ventricle
• LVEF: left ventricular ejection fraction
• LVH: left ventricular hypertrophy
• LVSF: left ventricular systolic function
• MI: myocardial infarction
• NIV: non-invasive ventilation
• NSTEMI: non-ST segment elevation myocardial infarction
• NSVT: non-sustained ventricular tachycardia
• PCI: percutaneous coronary intervention
• PCWP: pulmonary capillary wedge pressure
• PDA: persistent ductus arteriosus
• PE: pulmonary embolus
• PEA: pulseless electrical activity
• PFO: patent foramen ovale
• PND: paroxysmal nocturnal dyspnoea
• PT: prothrombin time
• PVR: peripheral vascular resistance
• RA: right atrium
 List of abbreviations xiii

• RAAS: renin–angiotensin–aldosterone system

• RBBB: right bundle branch block
• RCA: right coronary artery
• RCC: right coronary cusp
• RVH: right ventricular hypertrophy
• RV: right ventricle
• SBP: systolic blood pressure
• SLE: systemic lupus erythematosus
• SPECT: single photon emission computed tomography
• STEMI: ST segment elevation myocardial infarction
• SV: stroke volume
• SVT: supraventricular tachycardia
• TAVI: transcatheter aortic valve implantation
• TC: total cholesterol
• TFT: thyroid function test
• TIA: transient ischaemic attack
• TIMI: Thrombolysis In Myocardial Infarction score
• TOE: trans-oesophageal echocardiography
• tPA: tissue plasminogen activator
• TTE: transthoracic echocardiography
• TTP: Thombotic Thrombocytopenic Purpura
• TXA 2: thromboxane
• U&E: urea and electrolytes
• UA: unstable angina
• UFH: unfractionated heparin
• VF: ventricular fibrillation
• VSD: ventricular septal defects
• VT: ventricular tachycardia
An explanation of the text
The book is divided into two parts covering the clinical aspects of cardiology,
including investigations and prescribing, and a self-assessment section. We have
used bullet points to keep the text concise and supplemented this with a range
of diagrams, pictures and MICRO-boxes (explained below).
Where possible we have endeavoured to include treatment options for the
conditions covered. Nevertheless, drug sensitivities and clinical practices are
constantly under review, so always check your local guidelines for up to date
information.
You will find the following resources useful to find out more about any of
the drugs mentioned in this book:
•• British National Formulary (BNF) (http://www.bnf.org/bnf/index.htm)
•• The electronic Medicines Compendium (eMC) (http://www.medicines.org.
uk/emc/)

MICRO-facts
These boxes expand on the text and contain clinically relevant facts
and memorable summaries of the essential information.

MICRO-print
These boxes contain additional information to the text that may
­interest certain readers but is not essential for everybody to learn.

MICRO-case
These boxes contain clinical cases relevant to the text and include
a number of summary bullet points to highlight the key learning
objectives.

MICRO-references
These boxes contain references to important clinical research and
national guidance.
   Part
I
Cardiology and the
cardiovascular system
1. A guide to cardiac history 5
1.1 Presenting complaint 5
1.2 Past medical history 7
1.3 Drug history 8
1.4 Family history 8
1.5 Social history 8

2. A guide to cardiac examination 9

2.1 General inspection 9
2.2 Peripheral signs of cardiovascular disease 9
2.3 Examination of the precordium 11
2.4 Completing the cardiac examination 13

3. Coronary artery disease 15

3.1 Anatomy of the coronary arteries 15
3.2 Pathology of CAD: Atherosclerosis 16
3.3 Primary prevention 21
3.4 Presentations and pathophysiology of CAD 24
3.5 Complications of myocardial infarction 41
3.6 Long-term management 43
2 Cardiology and the cardiovascular system

4. Acute heart failure 47

4.1 Aetiology 47
4.2 Symptoms and signs 48
4.3 Investigations 50
4.4 Management of acute heart failure 52
4.5 Cardiogenic shock 54

5. Chronic heart failure 59

5.1 Classification 59
5.2 Pathophysiology and presentation of CHF 60
5.3 Investigation of CHF 67
5.4 Management of CHF 69
5.5 Devices 72
5.6 Surgery for heart failure 73
5.7 Additional management 75

6. The myocardium 77
6.1 Structure and function 77
6.2 Myocarditis 77
6.3 Cardiomyopathies 79

7. Pericardial disease 89
7.1 The pericardial SAC 89
7.2 Acute pericarditis 89
7.3 Pericardial effusion and cardiac tamponade 91
7.4 Constrictive pericarditis 95
8. The cardiac valves 99
8.1 Structure of valves 99
8.2 Infective endocarditis 100
8.3 Aetiology of valve disease 105
8.4 Aortic valve 105
8.5 Mitral valve 110
8.6 Tricuspid valve 115
8.7 Pulmonary valve 115
8.8 Valve replacement 116

9. Congenital heart disease 119

9.1 Early circulation 119
9.2 Pathology 121
9.3 Communications 121
9.4 Cyanotic 126
9.5 Obstructive 129
9.6 Complex 131
 Cardiology and the cardiovascular system 3

10. Hypertension 135

10.1 Measuring blood pressure 135
10.2 Classification of hypertension 136

11. Diseases of the aorta 145

11.1 Acute aortic dissection 145
11.2 Aortic aneurysms 150
11.3 Aortic trauma 152

12. A guide to ECG interpretation 155

12.1 ECG interpretation 155

13. Bradycardia 163

13.1 Sinus node-related bradycardia 163
13.2 Heart block 164
13.3 Bundle branch block 167

14. Tachycardias 171

14.1 Narrow complex tachycardia 171
14.2 Broad complex tachycardias 184
14.3 Cardiac arrest rhythms 188

15. Cardiac pacemakers 191

15.1 Types of pacemakers 191
15.2 Additional features of a permanent pacemaker 191
15.3 International coding system 192
15.4 Examples of indications 193
15.5 Complications 194

16. Cardiac imaging and investigations 195

16.1 Plain chest radiograph (chest X-ray, CXR) 195
16.2 Echocardiography 196
16.3 Cardiac CT 200
16.4 Cardiac MRI 201
16.5 Nuclear imaging 203
16.6 Angiography 205
16.7 Electrophysiology 207

17. Cardiac pharmacology 209

17.1 Anti-anginal 209
17.2 Anti-hypertensives 214
17.3 Anti-arrhythmics 222
17.4 Anti-coagulants and thrombolytic agents 228
17.5 Anti-platelet agents 233
 1 A guide to
cardiac history
1.1 PRESENTING COMPLAINT
CHEST PAIN
Site
•• Cardiac pain is most commonly central in the chest, retro-sternal or
epigastric.
•• Pain that is felt in the sides of the chest or well-localized pain is more likely
to be mechanical.
Onset
•• Sudden (usual) or gradual.
•• What was the patient doing when the pain started?
Character
•• Crushing, squeezing or a sensation of pressure may represent cardiac
ischaemia.
•• Severe or ‘tearing’ pain may be associated with aortic dissection.
•• Stabbing pain may be associated with pericarditis or pleurisy.

MICRO-facts
Levine’s sign (a clenched fist held over the sternum to describe pain
character) is associated with ischaemic pain but has a low positive
predictive value. The strongest predictive features of cardiac pain are
an association with exercise and radiation to the shoulders or arms.
Tenderness in the chest wall does not preclude cardiac chest pain but
may be a useful negative predictor.

Radiation
•• Radiation to the jaw, arm and hand may occur in ischaemic pain.
 6 A guide to cardiac history

Associated features
•• Autonomic symptoms: sweating, clamminess, anxiety, nausea and
breathlessness.
•• Other cardiac symptoms (see below).
Timing
•• Risk of Acute coronary syndrome (ACS) is threefold higher in the 3 hours
after waking.
•• Continuous pain over several days is unlikely to be cardiac.
Exacerbating and alleviating factors
•• Relationship to activity, cold temperatures or large meals.
•• Relationship to specific movements suggests musculoskeletal pain.
•• Alleviating factors: cardiac pain may respond to glyceryl trinitrate (GTN)
within minutes; note that oesophageal spasm may also respond to GTN
spray but does so much more slowly.
•• Pericardial pain is exacerbated by inspiration (like pleuritic chest pain) and
may be relieved by sitting upright or leaning forward.

MICRO-facts
An atypical presentation of myocardial infarction (MI) without pain
can occur in elderly patients or those with conditions such as diabetes
­mellitus and rheumatoid arthritis. Sometimes termed a ‘silent’ MI.
Cardiology and the cardiovascular system

BREATHLESSNESS
•• Onset, timing and exacerbating factors.
•• Associated cough, sputum production or wheeze may suggest a respiratory cause.
•• Assess for orthopnoea by asking about the number of pillows the patients
needs to sleep and whether they are breathless on lying flat.
•• Paroxysmal nocturnal dyspnoea (PND).
•• If exercise tolerance is limited by breathlessness, record the current exercise
capability and grade it by NYHA class (see Section 5.2, Chronic heart failure).

MICRO-facts
The absence of both PND and orthopnoea has a strong negative pre-
dictive value for the presence of heart failure in those not taking heart
failure medication.

•• Also record the trend in symptoms, i.e. a rapid deterioration is more

­concerning than chronically poor exercise tolerance.
 1.2 Past medical history 7

PALPITATIONS
•• Onset: gradual or sudden.
•• Timing and frequency of episodes: ask about precipitating factors (exercise,
stress, caffeine intake, smoking and alcohol) or any techniques used to
terminate palpitations.
•• Ask the patient to tap out the rhythm to determine regularity.
•• Ask about associated pre-syncopal and syncopal symptoms.
•• Associated chest pain or breathlessness implies decompensation.
SYNCOPE
•• Describe pre-syncopal symptoms.
•• Describe the situation in which syncope occurred, e.g. syncope occurring
upon standing up from a recumbent or sitting position implies a postural
hypotension.
•• Association with palpitations, exercise or recent alterations in drug prescription.
•• Association with neck position, e.g. due to vertebrobasilar insufficiency.
•• Syncopal symptoms while in the supine position are a worrying feature.
OTHER SYMPTOMS
•• Leg swelling and leg pain:
•• Peripheral oedema may be a result of heart failure.
•• Oedema and pain may be due to deep vein thrombosis related to
­pulmonary embolism causing non-cardiac chest pain.

Cardiology and the cardiovascular system

•• Pain in the calves on walking that eases with rest is called intermittent
claudication and is usually caused by peripheral arterial obstruction.
•• Malaise and fatigue may be caused by low cardiac output in heart failure.
•• Nausea and anorexia may be caused by hepatic congestion in heart failure.
1.2 PAST MEDICAL HISTORY
•• Previous occurrence of angina, and if so the frequency and precipitators.
•• Previous myocardial infarctions and treatments.
•• Previous cardiac investigations such as echocardiograms, perfusion scans
and angiograms.
•• Previous cardiac intervention such as angioplasty or pacing devices.
•• Previous cardiac surgery including coronary bypass surgery and valvular surgery.
•• Congenital cardiac conditions.
•• History of conditions that are risk factors for ischaemic heart disease such as
diabetes, hypertension and hypercholesterolaemia.
•• History of conditions that are risk factors for infective endocarditis
(e.g. recent dental work, invasive procedures such as colonoscopy, and
­intravenous drug use).
•• History of previous rheumatic fever (may result in valvular disease).
 8 A guide to cardiac history

•• Recent viral illness if pericarditis or myocarditis is suspected.

•• Enquire about conditions such as Marfan’s syndrome which may cause
aortic root dilatation or aortic dissection.
•• A history of stomach ulcers or severe gastritis may require caution in the use
of anti-platelet medications, particularly aspirin.

1.3 DRUG HISTORY

•• Ask about any recent changes to prescriptions, particularly in association
with syncopal symptoms or myocarditis as these may be drug induced.
•• Ask in particular about current cardiac medications.
•• Ask about warfarin use and the latest INR.
•• Consider the possible cardio-toxic profile of certain medications:
•• Anti-neoplastic agents, e.g. doxorubicin, cyclophosphamide, paclitaxel
•• Tachycardia-inducing drugs such as salbutamol
•• QTc prolonging medications (see Chapter 12, QTc section)
•• Ask about drug allergies and clarify the reaction type.
1.4 FAMILY HISTORY
•• Enquire about risk factors for ischaemic heart disease: first-degree female
relative with a heart attack at less than 65 years of age or a first-degree male
relative with a heart attack at less than 55 years of age.
•• Enquire about a family history of sudden cardiac death, unexplained death
or cardiac defibrillator insertions that may suggest inherited channelopathies
Cardiology and the cardiovascular system

such as Brugada syndrome or hypertrophic obstructive cardiomyopathy.

•• Enquire about conditions such as familial hypercholesterolaemia or
Marfan’s syndrome.

1.5 SOCIAL HISTORY

•• Smoking in pack years (number of cigarettes smoked daily × years
smoked/20; e.g. 20 cigarettes per day for 20 years is 20 pack-years).
•• Excessive alcohol consumption can cause dilated cardiomyopathy.
•• Illicit drug use can cause arrhythmias or cardiomyopathy.
•• There is specific guidance relating to driving for patients who have had an
ischaemic cardiac event, transient loss of consciousness or cardiac device
insertion; this can be found on the UK Driver and Vehicle Licensing
Agency (DVLA) website.

MICRO-reference
The DVLA website has condition-specific guidelines (https://www.gov.uk/
health-conditions-and-driving).
 2 A guide to cardiac
examination
2.1 GENERAL INSPECTION
•• Does the patient appear unwell?
•• Does the patient appear breathless or cyanosed: check use of oxygen (type of
mask; percentage oxygen), is the patient propped up on pillows?

2.2 
PERIPHERAL SIGNS OF
CARDIOVASCULAR DISEASE
HANDS
•• Colour and temperature.
•• Capillary refill time: raise hand to the level of the heart, press for 5 seconds,
release and count time to refill.
•• Tar staining (from cigarettes).
•• Nail clubbing.
•• Digital infarcts or nail fold splinters.
•• Rare signs of infective endocarditis on the palmar aspect: Janeway lesions
and Osler’s nodes.

MICRO-facts
Cardiac causes of nail clubbing:
• Cyanotic congenital heart disease
• Infective endocarditis
• Atrial myxoma

FACE
•• Cyanosis or pallor under the tongue.
•• Poor dentition may provide a source of bacteraemia for infective
endocarditis.
•• Malar flush may be present in mitral stenosis or pulmonary hypertension.
 10 A guide to cardiac examination

MICRO-facts
Hyperlipidaemia: Xanthelasma, xanthomata (on Achilles tendon) and
corneal arcus
Marfan’s syndrome: Arachnodactyly, tall stature, high arched palate,
increased flexibility
Infective endocarditis: Osler’s nodes, Janeway lesions, splinter haem-
orrhages, Roth’s spots

PULSES AND BLOOD PRESSURE

Radial
•• Assess rate and rhythm and check for radio-radial and radio-femoral delay.
Brachial or carotid pulse
Volume
•• Variation in pulse volume and blood pressure is seen with respiration
(increases in expiration and decreases in inspiration due to a rise and fall in
intrathoracic pressure, respectively).
•• When exaggerated (>10 mmHg change in systolic BP in inspiration), this is
known as pulsus paradoxus and occurs if intrathoracic pressure decreases
in COPD or asthma or when pericardial pathology alters the heart’s ability
to expand (see Section 7.3).
Cardiology and the cardiovascular system

•• Low volume pulse is caused by hypovolaemia, peripheral vascular

­disease or a decreased pulse pressure as happens in mitral and aortic
stenosis.
•• High volume pulse is caused by hypertension, age, exercise, anaemia,
CO2 retention or pregnancy.
Character
•• Hyperdynamic pulse is a large-volume bounding pulse seen in anaemia,
sepsis, thyrotoxicosis and pregnancy.
•• Slow-rising pulse (pulsus parvus et tardus) is a pulse increasing gradually
in volume that occurs with aortic stenosis.
•• Bisferiens pulse is a slow-rising pulse with two systolic peaks, felt in aortic
stenosis combined with aortic regurgitation.
•• Pulsus alternans alternates between normal and low volume and occurs in
conditions such as mitral or aortic valve stenosis, severe ventricular failure or
effusive pericarditis.
•• Collapsing pulse (water hammer) has an early peak with a rapid decrease
in volume that can be exaggerated by raising the arm above the level of the
heart (occurs in severe aortic regurgitation).
 2.3 Examination of the precordium 11

a
c v

x y

Figure 2.1 JVP waveform. ‘a’ wave – right atrial contraction, ‘c’ wave – tricuspid
­closure with ventricular contraction, ‘x’ descent – right atrial relaxation, ‘v’ wave –
right atrial venous filling, ‘y’ descent – atrial emptying with tricuspid opening.

Jugular Venous Pressure (JVP)

•• If visible, the JVP should appear as a diffuse two-peaked pulsation between
the two heads of the sternocleidomastoid (see Figure 2.1).
•• It alters with inspiration and can be occluded with gentle pressure.
•• The height of the JVP above the level of the sternal angle should be
­measured with the patient reclining at 45 degrees, the usual upper
limit of normal height is 3 cm.
•• Increased JVP height may reflect increased right atrial pressure:
•• Cor pulmonale
•• Right heart failure as part of congestive cardiac failure
•• Fluid overload

MICRO-print

Cardiology and the cardiovascular system

Kussmaul’s sign – JVP rises in inspiration (seen in impaired right
­ventricular filling with constrictive pericarditis and pericardial
effusion)
Cannon waves – contraction of right atrium against a closed tricuspid
valve (seen in complete heart block)
Large ‘a’ waves – delayed or restricted right ventricular filling (seen in
tricuspid stenosis)
Large ‘v’ waves – tricuspid regurgitation

2.3 EXAMINATION OF THE PRECORDIUM

INSPECTION
•• Central sternotomy scar
•• Lateral surgical scars due to mitral valvotomy
•• Evidence of pacing (pacemaker box usually below left clavicle)
•• Chest deformity: pectus excavatum, pectus carinatum
 12 A guide to cardiac examination

PALPATION
•• Assess for deviation of the apex beat, which is usually located at the fifth
intercostal space in the mid-clavicular line.
•• Palpate the chest for heaves parasternally (right ventricular hypertrophy),
heaves at the apex (left ventricular hypertrophy) and thrills (palpable
murmurs).
AUSCULTATION
•• First heart sound (S1): closure of the mitral and tricuspid valves
•• Second heart sound (S2): closure of the aortic and pulmonary valves (this is
physiologically split on inspiration)
Additional sounds
•• A third heart sound (S3) is heard early in diastole – it is pathological in
patients above 40 years of age when it is most likely to be associated with
reduced left ventricular function or mitral regurgitation.
•• A fourth heart sound (S4) precedes S1 – it is always pathological and caused
by atrial contraction against the non-complaint left ventricle.
•• Pericardial rub is a harsh sound heard in pericarditis – characteristically
scratchy and heard both in systole and diastole.

MICRO-facts
An onomatopoeic memory aid for recognizing the third heart sound
Cardiology and the cardiovascular system

is to remember the word ‘kentucky’ where S1 = ken, S2 = tuck, S3 = y.

Similarly, the word ‘tennessee’ may help to remember that the S4
sound appears before S1, where S4 = ten, S1 = nes, S2 = see.

Volume change
•• Systemic and pulmonary hypertension increase the volume of the aortic
and pulmonary heart S2 sounds, respectively (often termed a loud A2 and
a loud P2, respectively).
•• A calcific or immobile valve may shut quietly or silently, while a click
may be heard with a mobile valve leaflet.
•• Quiet heart sounds may occur in the presence of a reduced cardiac output,
pericardial effusion or emphysema.
Splitting of heart sounds
•• Delay in right ventricular emptying causes exaggerated S2 splitting.
•• Delay in left ventricular emptying reverses the splitting of S2 so splitting
occurs in expiration.
•• Reverse splitting (A2 after P2) occurs in left bundle branch block.
•• Fixed splitting is seen with atrial septal defect.
 2.4 Completing the cardiac examination 13

MICRO-print
Left-sided murmurs are accentuated on expiration, as increased
­thoracic pressure increases cardiac output from the left ventricle.
Right-sided murmurs are accentuated on inspiration as a negative
thoracic pressure increases the blood flow through the right-sided
cardiac chambers.

Murmurs
•• A murmur is caused by turbulent blood flow, usually through an abnormal
valve.
•• A flow murmur can develop across a normal valve when the blood flow
velocity is abnormally increased as in high cardiac output states, e.g. thyro-
toxicosis, anaemia, sepsis and pregnancy.
•• Describe a murmur according to:
•• Timing: systolic, diastolic or continuous (note that a systolic murmur
is simultaneous with the carotid pulsation)
•• Location on the precordium
•• Volume (1–6) may not be related to valve disease severity as murmurs
may become quieter with increasing severity
•• Quality: high pitched, blowing
•• Radiation
•• Any additional sounds

Cardiology and the cardiovascular system

2.4 
COMPLETING THE CARDIAC
EXAMINATION
•• Auscultate the lung bases and palpate the sacrum and ankles for signs of
dependent pitting oedema.
•• Palpate the liver to assess for congestion or pulsatility.
•• Assess for splenomegaly that may be present in infective endocarditis.
•• Perform fundoscopy for signs of hypertensive retinopathy or Roth’s spots
that may be seen in infective endocarditis.
•• Perform a urine dipstick test for haematuria that may be present in infective
endocarditis.
 3 Coronary artery
disease
Symptoms characterized by reduced blood flow to the myocardium

MICRO-print
The latest national public statistics for coronary artery disease (CAD)
(British Heart Foundation, UK, and Centers for Disease Control and
Prevention, USA) indicate that:
• CAD is the leading single cause of death in the UK and the USA.
• CAD causes approximately 25% of deaths in the USA (2009), and
12–17% of deaths in the UK (2010).
• 124,000 heart attacks occur annually in the UK.
• 1998–2008 saw a 49% decrease in deaths in males aged 55–64
in the UK.
• £3.2 billion was spent on CAD in the UK in 2006.

3.1 ANATOMY OF THE CORONARY ARTERIES

The coronary arteries run in the subepicardial connective tissue (see Figure 3.1).
•• Right coronary artery (RCA) arises from the anterior sinus behind the
aortic cusp and:
•• Runs between the pulmonary trunk and the right atrium
•• Continues posteriorly along the atrioventricular groove to give off branches:
– Marginal branch runs along the lower costal surface to reach the apex.
– Posterior descending interventricular branch runs towards the
apex of the heart in the posterior interventricular groove.
•• Left coronary artery arises from the posterior sinus behind the aortic
cusp and:
•• As the left main stem between the pulmonary trunk and the left atrium
•• Enters the atrioventricular groove and divides into:
– Anterior descending interventricular branch runs towards the
apex in the anterior interventricular groove and gives off diagonal
and septal branches.
– Circumflex branch winds around to the back of the heart in the
atrioventricular groove and gives off the left marginal branch(es).
 16 Coronary artery disease

Left coronary artery arises

Right coronary artery from the posterior sinus
arises from the anterior behind the aortic cusp
sinus behind the Left main stem runs
aortic cusp between the pulmonary
Runs down the right trunk and left auricle
atrioventricular groove Enters the atrioventricular
groove and divides
Posterior Circumflex artery’s left
interventricular branch marginal branch
runs down towards
the apex of the heart Circumflex winds around
the back in the AV groove
Marginal branch runs
along the lower margin Anterior interventricular
of the costal surface branch
towards the apex

RCA Left marginal Circumflex

LAD RAD LMS

Figure 3.1 Anatomy of the coronary arteries.

RIGHT CORONARY ARTERY LEFT CORONARY ARTERY

Cardiology and the cardiovascular system

SUPPLIES SUPPLIES
RV and RA LV and LA
Part of LA and diaphragmatic surface
of LV
Posterior 1/3 of the ventricular septum Anterior 2/3 of the ventricular septum
Sinoatrial node in 65% of the Sinoatrial node in 35% of the
population population
Atrioventricular node in 90% of the Atrioventricular node in 10% of the
population population
Some of the left bundle branch Right bundle branch and left bundle
branch

3.2 PATHOLOGY OF CAD: ATHEROSCLEROSIS

Coronary arteries:
•• Tunica adventitia: outermost layer
•• Tunica media: muscular middle layer
•• Tunica intima: endothelial inner lining
 3.2 Pathology of CAD: Atherosclerosis 17

ATHEROSCLEROSIS
Early lesion: fatty streak
•• Early precursor of the atherosclerotic plaque.
•• Present from childhood in the aorta, from adolescence in the coronary arteries.
•• Deposition of foam cells in the intima of muscular artery walls:
•• Foam cells are macrophages that migrate into the intima in response
to inflammation caused by harmful oxidized low-density lipoprotein
(LDL) molecules in the arterial wall.
•• Macrophages ingest lipids through special scavenger receptors.
•• Macrophages may undergo necrosis and rupture, depositing lipids.
•• Not all fatty streaks will progress to become atherosclerotic plaques.
Advanced lesion: atherosclerotic plaque
•• Two components (see Figure 3.2):
•• Atheroma: soft inner core composed of lipids and a periphery of necrotic
foam cells and cholesterol crystals – highly thrombogenic in nature.
•• Fibrous capsule: outer layer composed of smooth muscle cells that have
migrated from the media into the intima sequestering the lipid core –
may start to calcify.
•• Plaques become problematic:
•• In angina, increased luminal obstruction will result in a mismatch
between O2 delivery in situations of increased demand such as during
exercise (usually the stenosis has to be >50% of the arterial lumen
diameter [75% cross-sectional area] for symptoms to appear).

Cardiology and the cardiovascular system

•• In acute myocardial infarction, the fibrous capsule erodes or ruptures,
exposing the lipid core to the blood and resulting in thrombus forma-
tion and distal embolization.
Vulnerable atherosclerotic plaques
•• These features make plaques prone to rupture or erosion:
•• Large-volume, necrotic lipid core

Adventitia
Intima
Media

Myocytes migrating into

intimal abnormality
Cholesterol
Lipid core
Foam cells
Monocytes attracting
to abnormal intima
Fibrous cap

Figure 3.2 Atherosclerotic plaque components.

 18 Coronary artery disease

••Thin fibrous cap

••Angiogenesis with haemorrhage within the plaque
••Release of extracellular proteases by macrophages
••Inflammation within a thin fibrous cap
•• Vulnerable plaque rupture or erosion may be precipitated by high blood
pressure and tachycardia due to the changes in shear stress over the
plaque.

MICRO-facts
Plaque rupture or erosion may be independent of plaque size and
­luminal stenosis, hence may not be preceded by stable angina.

RISK FACTORS FOR CAD

Risk factors predisposing to coronary artery disease may:
•• Be modifiable or non-modifiable
•• Encourage formation of unstable atherosclerotic plaques
•• Precipitate plaque rupture or erosion and subsequent thrombosis

MICRO-print
Acute myocardial infarctions occur most commonly in the morning.
This may be due to a morning increase in blood pressure and vasocon-
striction secondary to a heightened sympathetic drive (precipitants of
Cardiology and the cardiovascular system

plaque rupture or erosion) and also due to increased platelet aggrega-

tion in the morning (propagation of thrombus formation).

NON-MODIFIABLE RISK FACTORS

Age Atherosclerotic lesions mature with age
Declining testosterone levels and oestrogen levels in
ageing men and women, respectively, result in a loss
of their cardioprotective effect
Male gender Oestrogens have a protective effect in pre-­menopausal
women
Effects of individual risk factors also differ between
gender and may confer protection to women
Family history First-degree relative with stroke or CAD <65 years (♀)
or <55 years (♂)
Continued
 3.2 Pathology of CAD: Atherosclerosis 19

MODIFIABLE RISK FACTORS AND RELATIVE RISK RATIOS

RR (♂–♀)a
Diabetes mellitus 1.69–2.74 Risk of a patient with diabetes having
a first myocardial infarction is
approximately that of a non-diabetic
patient who has already had
a myocardial infarction
Hypertension 1.46–1.42 Enhances the atherosclerotic process
Contributes to plaque instability and
rupture
Causes left ventricular hypertrophy
increasing myocardial O2 demand and
decreasing coronary artery reserve
Smoking 1.41–1.42 Smoking increases inflammation in
atherosclerosis
Smoking affects high-density lipoprotein
(HDL) levels and fibrinogen levels
A single cigarette increases platelet
aggregation and the risk of plaque
rupture and thrombus formation
Risk returns to that of a non-smoker
after 10 years of cessation at any age

Cardiology and the cardiovascular system

Physical inactivity 1.28–1.36 Inactivity increases the risk of obesity
Exercise decreases the basal heart
rate (basal rate >70 beats per ­minute
is associated with a higher risk of CAD)
Hypercholesterolaemia 1.22–1.23 Plaques with a large lipid core are
unstable
Elevated LDL and low HDL levels
increase risk
Total cholesterol to HDL ratio is
a useful clinical measure
Obesity 1.20–1.19 Waist circumference may be a b­ etter
indicator than body mass index
Triglycerides 1.06–1.33 Risk factor independent of total
cholesterol levels
Increases risk of CAD more
­significantly in women
Continued
 20 Coronary artery disease

NOVEL RISK FACTORS

Chronic inflammation Rheumatoid arthritis may lead to at
least a twofold increase in risk of
myocardial infarction and stroke
Type A personality
High C-reactive protein
High fibrinogen levels
High homocysteine levels
Abnormal ankle brachial index
Low income
Ethnic group, e.g. South Asians
Small and dense LDL particle
a Interheart study: Schnohr P, Jensen JS, Scharling H, et al. Coronary heart disease
risk factors ranked by importance for the individual and community. European
Heart Journal 2002; 23: 620–626.
Definition of relative risk (RR): chance of an event occurring in a population
exposed to a factor compared to the chance of the event occurring in an
unexposed population.

Metabolic syndrome
•• A collection of factors closely linked with obesity that increase the risk of
Cardiology and the cardiovascular system

CAD, certain cancers, hypotestosteronemia in men and non-alcoholic fatty

liver disease.
•• It is diagnosed when at least three of the five criteria are met (International
Diabetes Federation and American Heart Association Criteria):

Abdominal obesity (waist circumference)

Men >102 cm (>40 in)
Women >88 cm (>35 in)
Asian men >90 cm (>35 in)
Asian women >80 cm (>32 in)
Triglycerides ≥1.7 mmol/L or on therapy
HDL cholesterol
Men <1.03 mmol/L or on therapy
Women <1.29 mmol/L or on therapy
Blood pressure ≥130/≥85 mmHg or on therapy
Fasting plasma glucose ≥5.6 mmol/L or on therapy
 3.3 Primary prevention 21

MICRO-reference
International Diabetes Federation website on the metabolic syndrome:
http://www.idf.org/metabolic-syndrome

3.3 PRIMARY PREVENTION

•• Mortality from coronary heart disease has almost halved in the last three
decades:
•• Half of this decrease is attributed to better treatment measures, such
as the use of anti-hypertensives, statins, aspirin and interventions like
primary angioplasty.
•• The remainder of the decrease is attributable to modification of risk
factors.
•• Primary prevention modifies risk factors in individuals with no clinical
evidence of CAD, e.g. anti-hypertensives, diabetes management, smoking
cessation.
•• Secondary prevention aims to reduce recurrence of events and improves
survival in those who have had a cardiovascular event, e.g. aspirin use
in patients with angina, angiotensin-converting enzyme inhibitors
post-MI.

Cardiology and the cardiovascular system

MICRO-facts
‘Good cholesterol versus bad cholesterol’
Apolipoproteins are proteins that bind lipids.
Apolipoprotein B makes up low-density lipoprotein (LDL,
‘bad cholesterol’)
• LDL invades the arterial wall, is oxidized and results in inflammation
attracting macrophages that engulf the LDL and become foam cells.
• Familial hypercholesterolaemia is autosomal dominant and associ-
ated with high levels of LDL and CAD risk.
 polipoprotein A1 makes up high-density lipoprotein (HDL,
A
‘good cholesterol’)
• HDL composed of apolipoprotein A1 undertakes reverse cholesterol
transport from foam macrophages in the arteries to the liver and
faeces.

•• Tertiary prevention aims to prevent complications, e.g. closure of post-

infarction ventricular septal defects.
 22 Coronary artery disease

CARDIOVASCULAR RISK PREDICTION CHARTS

•• To implement primary prevention, primary care providers can use the
World Health Organization cardiovascular disease risk prediction charts;
these are tailored to geographical subregions.
•• These predict the risk of developing a cardiovascular event in the next
10 years (includes cardiovascular death, new-onset angina, myocardial
infarction, transient ischaemic attacks and stroke) (see Figure 3.3).
•• Risk factors taken into account:
•• Gender
•• Age (useful for individuals up to 70 years of age)
•• Smoking status (cessation in the past 5 years is still classified as ‘smoker’)
•• Systolic blood pressure
•• Serum total cholesterol: HDL ratio
Charts can help physicians make decisions on the provision of treatment for:
•• Hypertension (treatment recommended at CAD risk >20% if ambulatory
blood pressure or home blood pressure >135/85 mmHg) (see Section 10.5).
•• Hyperlipidaemia (CAD risk >10% over the next 10 years warrants the use of
statins).
•• In some cases, these will be elevated enough in themselves to warrant treatment.
•• Implement lifestyle changes and medications.
•• Do not use the chart for treatment decisions in:
CLINICALLY ESTABLISHED CVD SECONDARY PREVENTION
IMPLEMENTED
Cardiology and the cardiovascular system

Diabetes mellitus type 1 or 2 Treat appropriately and implement

primary prevention
Renal dysfunction Treat appropriately and implement
primary prevention
Familial hyperlipidaemia Statin therapy
Total cholesterol: HDL >6
Persistently raised BP >160/100 mmHg Treat blood pressure using
Hypertension with end-organ damage guidelines
 3.3 Primary prevention 23

Risk Level <10% 10% to <20% 20% to <30% 30% to <40% ≥40%
EUR A People with Diabetes Mellitus
Age Male Female SBP
(years) Non-smoker Smoker Non-smoker Smoker (mmHg)
180
160
70 140
120

180
160
60
140
120

180
160
50
140
120

180
40 160
140
120
4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8
Cholesterol (mmol/L)
EUR A People without Diabetes Mellitus
Age Male Female SBP
(years) Non-smoker Smoker Non-smoker Smoker (mmHg)
180
160
70
140
120

Cardiology and the cardiovascular system

180
160
60
140
120

180
160
50
140
120

180
160
40
140
120
4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8
Cholesterol (mmol/L)

Figure 3.3 World Health Organization CAD risk prediction charts for Europe
­subregion A including the United Kingdom.
 24 Coronary artery disease

MICRO-facts
In addition to decreasing plasma LDL and plaque lipid content and
thrombogenicity, statins have an anti-inflammatory action and increase
collagen:inflammatory cell ratio in plaques, making them less vulner-
able. Some indications for the use of statins include the following:
• Primary prevention of CAD if 10-year risk is >10% or TC:HDL >6
• Secondary prevention of CAD
• Familial hyperlipidaemia
• Diabetes mellitus in patients >40 years or younger if target end-
organ damage or multiple risk factors are present

3.4 
PRESENTATIONS AND
PATHOPHYSIOLOGY OF CAD
•• Mismatch between myocardial O2 requirement and supply manifests as
ischaemic chest pain:
•• Stable chronic angina
•• Acute coronary syndrome (ACS): acute myocardial ischaemia
– Unstable angina (UA)
– Non-ST segment elevation myocardial infarction (NSTEMI)
– ST segment elevation myocardial infarction (STEMI)
•• The diagnostic triad in ACS consists of history, ECG changes and cardiac
Cardiology and the cardiovascular system

enzymes.
•• Chest pain at rest or minimal exertion suggests ACS rather than chronic
stable angina.
•• Elevated cardiac markers will differentiate between UA and NSTEMI/STEMI.
•• ST segment elevation will differentiate between NSTEMI and STEMI.
•• The table below outlines the pathophysiology underlying stable angina
and ACS.

Myocardial O2 Requirement Pathology: Mismatch Myocardial Supply

O2 requirement Difference between Presence of a fixed

Stable Angina

heart rate Coronary

basal blood flow atherosclerotic
contractility vasodilatation
and maximal blood stenosis or thrombus
afterload to match this
flow is coronary decreases the CFR
preload requirement
flow reserve (CFR) and so blood supply

Acute pathology with thrombus:

Normal basal Plaque rupture (most common) Obstruction to blood
requirement Plaque erosion
ACS

flow or reduced
OR Coronary artery embolism
requirement blood supply
Coronary artery spasm
Coronary artery dissection
 Differences between the various CAD presentations

PRESENTATION PATHOPHYSIOLOGICAL DIAGNOSTIC

HISTORY ECG CHANGES CARDIAC
MARKERS
Chronic stable Fixed stenosis >50% and decreased Chest pain on Normal at Rest ↔
angina coronary reserve flow exertion ST depression or
<10 minutes T inversion on exertion
Unstable angina Acute thrombus formation and Chest pain ST depression or ↔
resolution at rest or T inversion at rest
OR minimal May be normal
Severe stenoses >90% interfering exertion
with basal coronary blood supply
NSTEMI Acute thrombus Chest pain ST depression or ↑
Partial occlusion >20 minutes T inversion at rest
May be normal
STEMI Acute thrombus Chest pain ST elevation at rest ↑
Complete occlusion >20 minutes
3.4 Presentations and pathophysiology of CAD
25

Cardiology and the cardiovascular system

 26 Coronary artery disease

CHRONIC STABLE ANGINA

MICRO-facts
The leading cause of angina is CAD but any factor decreasing
­myocardial O2 supply will result in angina.
• Coronary vasospasm → Prinzmetal’s angina
• Short diastole decreasing coronary filling:
• Tachyarrhythmias
• Aortic stenosis
• Hypertrophic obstructive cardiomyopathy
• Decreased O2 provision → severe anaemia or hypoxia

•• Stable angina is a result of inadequate myocardial O2 provision in states of

increased O2 utilization within the context of a fixed reduction in coronary
reserve flow.
•• It precipitates chest pain on physical exertion, with severe emotion or in
cold air.
•• Typical anginal pain has all the following features:
•• Central chest pain, constricting in nature
•• Precipitated by exertion
•• Relieved by rest or glyceryl trinitrate (GTN) in about 5 minutes
– Two of the above features: atypical angina
Cardiology and the cardiovascular system

– One or no features: non-anginal chest pain

Investigations
Laboratory FBC Severe anaemia may cause angina
tests U&E Look for renal dysfunction
Fasting lipids Dyslipidaemia as a risk factor for CAD
Glucose Diabetes as a risk factor for CAD
Thyroid Thyrotoxicosis and hypothyroidism may present
function with angina
ECG Resting Look for resting changes indicative of ischaemia,
tachyarrhythmias or previous MI
Exercise Look for changes of ischaemia (see Chapter 12)

Further tests: guidelines for the diagnosis of CAD in suspected stable angina
(see NICE guidelines 2010; see Chapter 16 for details of these investigations).
Risk stratify patients according to typicality of chest pain, risk factors, age and
gender:
•• <10% probability of CAD: seek other possible causes for the chest pain.
•• 10–29% probability of CAD: should be offered CT calcium scoring.
 3.4 Presentations and pathophysiology of CAD 27

•• 30–60% probability of CAD: should be offered non-invasive functional

testing, e.g. myocardial perfusion scan or stress echocardiogram.
•• 61–90% probability of CAD: should be offered invasive angiography.
•• >90% probability of CAD: should be started on treatment for stable angina.

MICRO-print
Cardiac syndrome X is the combination of chest pain and cardiac
ischaemia suggested by stress tests and ECG findings. However, these
patients have a normal coronary angiography. Prinzmetal’s angina
should be excluded. Symptomatic treatment may be continued.

MICRO-reference
National Institute for Health and Care Excellence. Chest pain of recent
onset: assessment and diagnosis of recent onset chest pain or dis-
comfort of suspected cardiac origin. NICE guidelines [CG95]. London:
National Institute for Health and Care Excellence, 2010. http://www.
nice.org.uk/guidance/cg95/chapter/guidance

ECG changes in acute MI

ECG changes in ischaemia are:
• T wave inversion, ST segment depression (seen co-incident with

Cardiology and the cardiovascular system

chest pain)
ECG changes in an acute STEMI classically appear in the following
chronological order:
• Giant, peaked, hyperacute T waves
• ST segment elevation (>2 mm in chest leads or >1 mm in
limb leads)
• Pathological Q waves (>25% height of R wave, >0.04 seconds wide,
inverted T waves)
• Return of ST segment to normal and inversion of T wave with
­persisting ischaemia over about 48 hours
STEMI can present with left bundle branch block (LBBB) indicating
wide anterior wall necrosis.
In an acute posterior STEMI, ST segment depression is seen in the
V1–V3, diagnosis assisted by the use of posterior chest ECG leads.
Note that ST segment elevation does not always indicate STEMI,
­differentials include:
• Myocarditis
• Acute myo-pericarditis (saddle-shaped ST segment elevation)
• Ventricular aneurysm (persistent ST segment elevation)
Other documents randomly have
different content
 ro BAIL DON AND The small croft and other lands
hereabouts belonging to the Chapel were, as will appear in due
course, inclosures from the moor made at various times for the
augmentation of the stipend of the Incumbent. Whether Baildon Hill
was ever used as a beacon in early times I cannot say ; its situation
makes it not improbable, but I have not found any list ot Yorkshire
Beacons. At the time of Queen Victoria's two Jubilees, in 1887 and
1897, when beacons were lit in many places, Baildon Hill had its
bonfire. There does not appear to be any record of the fires visible
from this spot. From Rawdon Billing, those at Queensbury, Pudsey,
Bramley, Otley Chevin, Almes Cliff, Beamsley Beacon, Brimham Crag,
Skipton and Ingleborough were noted in 1887; and from the heights
above Bingley, those at Eldwick Crag, Otley Chevin, Hope Hill
(Baildon), Wrose Hill, Horton, Queensbury, Haworth and Keighley
were noted in 1897. ' From Baildon most of these would also be
visible. From the highest point of the hill the view in every direction
is well worth noting, reaching, as it does, far over the Haworth
Moors into Lancashire, eastwards over the thick woods of Esholt and
Calverley towards Leeds, where the dome of the Town Hall is seen,
and north and west are wide stretches of heath, and hidden valleys,
bounded by the Craven and Wharfedale hills. " From the Shooting
House, which stands on Rumbold's Moor, some 1200 feet above sea-
level, Ingleborough can be distinctly seen,"1 some 26 miles or more
to the north-west. This spot, however, is not in Baildon. In 1899, the
Corporation of Bradford purchased from Colonel Maude all his rights,
powers, privileges and authorities, as Lord of the Manor of Baildon, "
in, under and over Baildon Moor, Bracken Hall Green (otherwise
Shipley Glen), Baildon Green, Baildon Bank, and all other common
lands and open spaces in the township or parish ot Baildon, forming
part ot the Manor of Baildon ; " the necessary authority was
contained in the Bradford Tramways and Improvement Act, 1899,
(62 G? 63 Vict., cap. 270, part 4). The total area thus acquired was
770 acres, 1 Bradford Observer, June 23, 1887; June 24, 1S97. -'
Speight. Airedale, p. 151. 3 Ibid., p. I56.
The text on this page is estimated to be only 24.54%
accurate

THE BAILDONS n and the price paid was £7,000. Subject to

certain provisions, this land was to be "at all times kept open,
unenclosed and unbuilt on, and (subject to the exercise of all
pasture gates and existing common rights thereon) as open spaces
for the recreation and enjoyment of the public, " and the Corporation
was to preserve BO far as possible " the natural aspect and state of
the moor. " Certain new roads have been made and others
improved, but this is all that has been done. The City of Bradford
may justly boast of having one of the finest open spaces in the
kingdom. The township of Baildon contains several outlving hamlets.
Thus, in addition to the main village, sometimes called High Baildon,
we have Low Baildon, Baildon Green, Baildon Bridge, Baildon Wood
Bottom, Tong Park, Moorside and Charlestown. I shall have
something to sav of most of these in the alphabetical section which
follows. But before leaving the township as a whole we must
consider the highways.
 CHAPTER TWO BRIDGES, STREETS, AND ROADS BRIDGES
Until half a century ago, Baildon had only one bridge over the Aire,
namely, Baildon Bridge, leading direct to Shipley. Though Shipley has
for some considerable time been a larger and much more important
place than Baildon, yet the fact that the bridge is, with one or two
exceptions, always called Baildon Bridge, points clearly to Baildon
being the more ancient settlement. Some notes on the history of the
old bridge will be found in Book II; the present uninteresting iron
structure was built in 1894. I am not aware of any view of the old
stone bridge ; it was of the type of the existing Ilkley and Otley
Bridges. There are now several other bridges crossing the river into
Baildon, in addition to railway bridges. The most westerley of these
is Saltaire Bridge. This was built by Sir (then Mr.) Titus Salt to
provide access to Saltaire Park. There were formerly stepping stones
at this point, and it was in crossing these that John Nicholson, the
Airedale Poet, fell into the river and died of exposure, on April 13,
1843. There is a foot-bridge joining Baildon and Thackley, at Buck
Mill, or, to give it its ancient name, Idle Mill, where there were
formerly stepping-stones and a ford. The bridge, which is 80 yards
long, was built at the joint cost (about £jyo) of the Idle and Baildon
Local Boards, and was formally opened in April, 1889. l ROADS,
STREETS AND LANES " At the beginning of the eighteenth century,
the only roads about Leeds and the other manufacturing towns of
the West Riding were pack-horse roads, with a narrow strip of
pavement, 1 Speight, Walks round Bradford, p. 35 ; inscription on
the Bridge.
 i4"°X BAILDON AND called a calsey, in the middle or at one
side only, along which strings of pack-horses travelled, and
occasionally heavy wagons, with very broad wheels, made their way
very slowly in the summer months and when the ground was
hardened by frost in the winter. " ' This description exactly fits with
the condition of things at Baildon until near the close of the
eighteenth century, when the improvement of old roads and the
making of new ones became very general all over the country.
Portions of these old paved tracks may still be seen on the moor. In
the following pages the roads, &c, of any historical interest, are
briefly dealt with, in alphabetical order : Baildon Road. — This is a
comparatively modern road, made about 1780, 2 on the site of an
old lane, and leads from Baildon Bridge to Lane Ends, where it joins
Green Lane, and turns into Browgate. It passes under the beautiful
grounds of Ferniehurst, built by the late Mr Edward Salt, a son of Sir
Titus Salt, Baronet. The Otley Road branches out on the right, and at
the junction a considerable hamlet, called Baildon Wood Bottom, has
sprung up. Temple Rhydding lies on the north side of the road, and
the road to Low Baildon on the right. Baildon Hall is on the right just
before reaching Lane Ends, opposite the Bay Horse Inn. This was
the main road between Shipley and Otley until the construction of
the new Otley Road in 1824-5. ^ts steep gradients must have been
very inconvenient, so that we are not surprised to find that the new
road avoided the village of Baildon altogether. Browgate. — This is
Baildon's most picturesque street, for I must explain for the benefit
of those readers who are not familiar with north-country speech,
that "gate" frequently means street or road. Browgate is a steep hill,
climbing, as it does, this portion of the Bank. The houses are built at
all sorts of elevations, steps have frequently to be used instead of
lanes or passages, and the general effect is one of picturesque
confusion. At the lower end on the right is the Primitive Methodist
Chapel. Further up, on the left, is the Moravian Church, perched high
1 Baines, Yorkshire Past and Present, vol. ii, p. 137. " Round about
Bradford, p. 321.
The text on this page is estimated to be only 5.73%
accurate

■>'"' /'■ '4 See />. L a n

The text on this page is estimated to be only 1.00%
accurate

& : ; ; '; ^ i
The text on this page is estimated to be only 7.88%
accurate

Sirf. .5 ?4 \ Itfe 1 1 IjSllkiaailfe! . tj K e 1 1 c I i ft Moravian

Church, Browi;at< Photograph by J. Hodgson
 THE BAILDONS '5 above the level of the road, and
approached by a flight of steps. Opposite to this may be seen the
curious little ravine known to Baildoners as " Kefflicks, " but more
properlv KelclifF. At the top, on the right, is the Mechanics' Institute,
having one front in Towngate, which was built in 1862 and enlarged
in 1870. There are no very old houses in Browgate, they look mostly
of the eighteenth or early nineteenth century. One has a date and
initials, partlv defaced, probably of some member of the Ambler
family and his wife. Wesley once preached from a window of a
house here, which is still pointed out. Butler Lane. — So called from
the Butler family, atone time prominent in Baildon. It is a
continuation of the old bridle road known as Green Lane, and runs
from the lower end of Browgate, past the back of Butler House, into
Chapel Hill bevond the east end of the Church and Church Schools.
Before the opening of the new Otley Road, Butler Lane would be the
easiest road for anyone travelling between Otley and Shiplev without
going into Baildon village. It still presents much of fif: its ancient
appearance. It crosses KelclifF bv a bridge. At the end, just below
the Chapel, is a house with the date 1726 and the initials T.B. ; it
was probably built by Thomas Butler. Chapel Hill. — Chapel Hill is a
continuation of Hall Cliffe, beyond the Church and Schools. It was
anciently called Idel Gate, as the road leading to Idle across the ford
at Idle or Buck Mill : this name occurs in a deed of 1265, but I have
not found it elsewhere. Cliff Lane. — This is an ancient bridle-road,
now widened and improved, leading straight up from the bridge to
the foot of Baildon Bank, a pretty stiff climb. An old causeway was
found here in 1874, several feet below the level of the present
road.1 On reaching nearly to the foot of the cliff, the lane divides,
one branch leading towards Trench and Brackenhall, where remains '
Round about Bradford, p. 321.
 i6 BAILDONAND of the paved track have been noted by Mr
Speight. ' The other branch, known as Green Lane, turns to the
right, and runs to the lower end of Browgate. Glovershaw Lane. —
The road from Eldwick when past Lobley Gate is known as either
Glovershaw Lane or Lobley Lane; it was widened and improved in
the year 1777. In 1778, the old pack-horse bridge over Hawksworth
Beck was replaced by a new and substantial carriage bridge. At the
West Riding Sessions held at Leeds, on October 8th in that year, it
was represented that the inhabitants of the several townships of
Bingley, Hawksworth and Baildon were expending large sums of
money in the erection of this bridge, and, on July 15th, 1779, the
townships named received £25 as a gratuity out of the Riding stock ;
an additional £25 was allowed at the Sessions held at Pontefract,
April 3rd, 1780. s Green Lane: — so called from its leading to and
along Baildon Green. From Lane Ends it goes under Baildon Bank,
past the new Board School and Sandles Pond, to the hamlet of
Baildon Green, and then turns south-west to the Bridge. It has
recently been re-christened Green Road, which seems a pity. Hall
Cliffe. — This is a short street leading eastwards from Town Gate,
past the Church. It contains nothing of interest, except a much-
altered house of seventeenth-century date. Hey gates Lane. — Some
fields here were known as Heygates, and they probably gave the
name to the lane. I doubt if the name has anything to do with hay,
but it is possible ; one would expect the hay land to be down in the
valley. The lane leads from four lane ends at the top of H olden Lane
to the hamlet of Baildon Moorside, and on by a foot-path to
Hawksworth. Hold en Lane : — so called from the Holden family,
which once held considerable property in this part of Baildon. The
new Vicarage is at the north end, and there are some modern
residences, which do not call for any special remark. A " boggart " or
ghost was at one time supposed to haunt this road, hence it is still
sometimes called Boggart Lane by the older inhabitants. 1 Through
Airedale, p. 150. " Speight, Old Bingley, p. 84.
The text on this page is estimated to be only 1.71%
accurate

SV, /■ I n North sjati ' w n

The text on this page is estimated to be only 29.80%
accurate

THE BAILDONS 17 Jenny Lane. — This leads from near the

top or Northgate into Heygates Lane. It is said to derive its name
from a certain Jenny Milner, horn 1742, who lived in a cottage there.
Ladderbanks Lane. — This lane, the name of which is now-a-days
more generally spelled as pronounced, " Latherbanks, " is doubtless
so called from its steepness. Some fields here are known as Upper
and Lower Latherbanks, and show traces of terrace cultivation. It
leads from near the Church to Hawksworth, and has a deep descent
to Baildon Gill. Langley Lane. — I am inclined to think that some
part of Baildon adjoining this lane must at one time have been called
" Langley, " though I have not found any positive evidence of it. A
William de Baildon of Langley occurs in 1390, and I cannot identify
his place of abode unless it were in Baildon. The only Langley
mentioned in Langdale's Topographical Dictionary of Yorkshire is
near Sheffield. Langley Lane leads to Tong Park and Esholt. Lobley
Lane. — See Glovershaw Lane, [ante, p. 16]. Milne Gate. — I have
only found this name once, in a deed of 126$, post. It was obviously
the road leading to the mill, and it was most probably the lane now
represented by Baildon Road [see ante, p. 14]. Northgate. —
Northgate leads due north out of Towngate. None of the houses are
of much antiquity, though there are few quite modern. In Northgate
is a mill, built by the late F. W. Kolmes ; in 1876 it was the property
of Messrs T. and W. W. Holmes. ' Otley Road. — Mr Cudworth states
that this road was begun in 1824 and opened in 1825.* I cannot
help thinking that he is a vear too early in each case. So far as I can
make out, it was made under one of the numerous Turnpike Road
Acts, namely, 6 George IV, cap. cxlix, which received the royal assent
on June 10th, 1825. It appears to have been in the main a new
road, and not merelv the widening of one already existing. Its object
was to afford better communication between Shipley and Otley.
Running roughly parallel with the river through Baildon, 1 Round
about Bradford, p. 1^2. ' Ibid, p. 33S.
 i8 BAILDONAND it crosses Baildon Gill Beck at Esholt Mill,
and turns north-west, just skirting Menston and the west end of
Otley Chevin. It escapes the steep gradients of the former road by
avoiding the village of Baildon altogether. The hamlet of Charlestown
has sprung up in part of it, about a mile and a half from Baildon
Bridge. The Airedale Cemetery, opened in 1863, and St. James's
Mission Church are close by. Prod Lane. — I cannot even make a
guess, however wild, at the derivation of this extraordinary name ; I
have not found it in any document. The lane leads from Baildon
Green to Bracken Hall Green. Slaughter Lane. — This lane, which
has lately been rechristened " Kirklands Road, " runs from Low
Baildon to the Otley Road. The old name was not euphonious, but it
seems a pity to have changed it ; for it undoubtedly records an
episode as to which history is silent. That the lane was called from
some forgotten battle or skirmish, I have no doubt ; the difficulty is
to guess when it took place. It was prior to the Parliamentary Civil
War, as is shown by the fact that the lane is mentioned by name in
the Survey of 1645. I am not aware of any righting in the
neighbourhood during the Wars of the Roses, and am inclined to
ascribe it to an earlier date. When we come to deal with the history
of the Chapel, we shall see that there is some reason to believe that
the Scots penetrated as far south as Baildon in their savage raid into
Yorkshire in 13 18-9. I cannot help thinking that the " slaughter "
recorded in the name of the lane took place then. Town gate. —
Towngate is the name given to the wide triangular space at the
south end of Northgate, where the four main streets cross,
Browgate, Westgate, Hall Cliffe and Northgate. Its size and shape
lend some little colour to the local tradition that Baildon once had a
market, though I have not found any documentary evidence that
such was the case. But old Baildoners will tell you with pride that
Baildon was a market town before Otley, and they point to the cross
as a confirmation of the statement. Most villages, however, had
crosses in medieval times, many of which still exist ; so that the
presence of a cross at Baildon is no evidence of a market. Indeed,
where a market
The text on this page is estimated to be only 4.11%
accurate

The Cress & Stocks, L 1 nfcroangate, Uaildon. j

 THE BAILDONS *9 town has a market cross, the cross may
well be the older of the two ; for markets are franchises, and the
creation of a royal charter. Nevertheless, this Baildon legend, if
incorrect in detail, probably records the substantial fact that the
Celtic settlement is older than the Anglian, and must at some early
date have been the more important. The cross, as we see it to-day,
is not an interesting object. The square platform of two stages, with
its well worn stones, looks as though it might be medieval, and part
of the original work. In the centre of this is a large square block of
stone, from which rises a tall cylindrical shaft. The base is square,
with chamfered corners, and a plain roll moulding at the upper edge
; the cap is a plain square block, without any attempt at ornament.
It was at one time surmounted by a gas-lamp, the gift of the late
Thomas Butler ; this has now been removed, but the forlorn
remnants oi the iron scrolls supporting it and the two arms for the
lamplighter's ladder still remain. Cudworth states that the cross was
erected by some oi the Butler family, ' but this can only be partially
true. The connection of this family of Butlers with Baildon only dates
from the seventeenth century, which was not a time for building
crosses. My own view is that there was probably a cross here in
medieval times ; that it was destroyed, either after the Reformation
(as so many were), or by the Puritan soldiery during the Civil War;
that the steps and perhaps the base remained ; and that in the
eighteenth century, when the Butlers were one of the leading
families in the place, one of them may have erected a new shaft on
the old site. At the north side of the cross are the stocks. They were
removed prior to 1 876, 2 but fortunately not destroyed. They had
been built into a wall surrounding the new reservoirs on the moor,
where they were found intact in 1904, and put back in their former
place. The beck formerly ran down the middle of Northgate and
Towngatc, a as one did until lately down Brook Street at llkley. It is
now covered in, but there appears to be no record of when this was
done. The drinking fountain was givren by the late Lord Justice 1
Round about Bra J for J, p. 330. ' Ibid. '" Ibid.
The text on this page is estimated to be only 27.54%
accurate

20 BAILDON AND Amphlett of Wychbold Hall, Somerset,

and Mrs Amphlett in 1 862. It bears the following inscriptions : —
THIS FOUNTAIN WAS ERECTED AND PRESENTED TO THE
INHABITANTS OF BAILDON BY RICH : PAUL AMPHLETT, ESQ., AND
HIS WIFE FRANCES, IN MEMORY OF HER MOTHER, I 862. TO THE
MEMORY OF FRANCES, WIDOW OF EDWARD FERRAND, ESQ., OF S.
IVES AND DAUGHTER OF WILLIAM HOLDEN, ESQ., OF THIS PLACE.
Jesus stood and cried, saying, If any man thirst let him come unto
me and drink. S.John, jth yjth. Worship him that made Heaven and
Earth and the Sea and the Fountains of Waters. Rev., \^th Jth.
Trench Lane. — This lane derives its name from the circle of stones
known as " the Soldiers' Trench. " It has now been partly widened
and diverted, but I am sorry to see that the name has disappeared
from the 1908 edition of the Ordnance Survey Map. It led from
Trench Gate at the south end of Brackenhall Green to the ford and
stepping stones at Dixon Mill. We st gate. — This street runs
westwards from Towngate, and has no special features, except the
house now generally known as " the Old Hall. " After clearing the
older part of the village, it becomes West Lane. An open brook
formerly ran down the street ; I have not been able to ascertain
when it was covered in. Some of the yards, or " folds, " as they are
called on the south side of Westgate are quite picturesque. The
Wesleyan Chapel is a conspicuous object on the north side. West
Lane. — This is a continuation of Westgate, along the top of Baildon
Bank, to Clarke's House and Lucy Hall. A good many modern villas
have been recently erected here, and in new roads adjoining.
The text on this page is estimated to be only 7.83%
accurate

S,r p. 2 , West and South elevations of the Old Chapel

The text on this page is estimated to be only 4.22%
accurate

Set /■ i . Ltntf of present buHdi n$ ;-f 0rotLniJ PI Art Plan

of tlu- OKI Chape
 CHAPTER THREE THE OLD CHAPEL AND THE NEW
CHURCH; OTHER PLACES OF WORSHIP BAILDON CHURCH Eaildon
was formed into a separate ecclesiastical parish and vicarage in 1869
; ' prior to that time it was a Parochial Chapelry in the parish of
Otley. The old chapel was dedicated to St. fohn the Evangelist, as is
the present church. A statement will be found in a considerable
number ot books that the dedication was formerly to St. Giles. This
statement, which is absolutely incorrect, I have traced to John
Ecton's Thesaurus Return Ecc/esiasticarum, first published in 1754.
Whether Ecton originated the error, or whether he copied it from
some earlier source, I have not been able to ascertain. It has been
repeated in Bacon's Liber Regis, Langdale's Topographical Dictionary
of Yorkshire, and other works ; one ingenious author, anxious at all
costs to square his facts with one another, says that the dedication
was altered at the rebuilding in 1848, a statement which does more
credit to his imagination than to his accuracy. There is no record of
the foundation of the old chapel, and what there is to be recorded of
its history will be found in Book II, where the statements on the
board in the vestry are also considered. Its appearance prior to its
demolition in 1847 maY ^e gathered from the accompanying
illustrations. The plan, elevations and the sketch of the old font,
were made by Messrs. Mallinson and Healey of Bradford, the
Architects of the present church, and their successors, Messrs. F. and
R. Healey, have very kindly supplied me with tracings of them. The
extraordinary sketch of the chapel and the old vicarage was
unearthed at Baildon by Mr. Scruton, and the block has been
produced from a copy he made for me. The drawing is a weird
production, but it shows the east 1 London Gazette, October 8,
1869.
Welcome to Our Bookstore - The Ultimate Destination for Book Lovers
Are you passionate about books and eager to explore new worlds of
knowledge? At our website, we offer a vast collection of books that
cater to every interest and age group. From classic literature to
specialized publications, self-help books, and children’s stories, we
have it all! Each book is a gateway to new adventures, helping you
expand your knowledge and nourish your soul
Experience Convenient and Enjoyable Book Shopping Our website is more
than just an online bookstore—it’s a bridge connecting readers to the
timeless values of culture and wisdom. With a sleek and user-friendly
interface and a smart search system, you can find your favorite books
quickly and easily. Enjoy special promotions, fast home delivery, and
a seamless shopping experience that saves you time and enhances your
love for reading.
Let us accompany you on the journey of exploring knowledge and
personal growth!

ebookball.com