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Investigating and

Managing CommonCardiovascularConditions

Juan Carlos KaskiMichael Papadakis

Hariharan RajuEditors

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Investigating and Managing

Common CardiovascularConditions


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Juan Carlos Kaski

Michael PapadakisHariharan RajuEditors

Investigating andManaging CommonCardiovascular

Conditions


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ISBN 978-1-4471-6695-5 ISBN 978-1-4471-6696-2 (eBook)DOI 10.1007/978-1-4471-6696-2

Library of Congress Control Number: 2015949239

Springer London Heidelberg New York Dordrecht© Springer-Verlag London 2015This work is subject to copyright. All rights are reserved by the Publisher,whether the whole or part of the material is concerned, specifically the rights of

translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduc-tion on microfilms or in any other physical way, and transmission or informationstorage and retrieval, electronic adaptation, computer software, or by similar ordissimilar methodology now known or hereafter developed.The use of general descriptive names, registered names, trademarks, servicemarks, etc. in this publication does not imply, even in the absence of a specificstatement, that such names are exempt from the relevant protective laws andregulations and therefore free for general use.The publisher, the authors and the editors are safe to assume that the advice andinformation in this book are believed to be true and accurate at the date of pub-

lication. Neither the publisher nor the authors or the editors give a warranty,express or implied, with respect to the material contained herein or for any errorsor omissions that may have been made.

Printed on acid-free paper

Springer-Verlag London Ltd. is part of Springer Science+Business Media(www.springer.com)

Editors

Juan Carlos KaskiCardiac Research CentreSt George's Universityof LondonLondonUK

Michael PapadakisCardiac Research CentreSt George's University

of LondonLondonUK

Hariharan RajuCardiac Research CentreSt George's Universityof LondonLondonUK

http://www.springer.com/http://www.springer.com/


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Foreword

Junior doctors find the likelihood of being allocated to a postinvolving cardiology a gratifying and thrilling but somewhatfrightening prospect. It is well known that cardiology is adiscipline which deals with acute life-and-death situations,where errors cannot be tolerated. Many young doctors facecardiology posts with “shivers up the spine”. Fortunately this

concern has now been recognised by the editors and authorsof this new handbook. Five potentially terrifying presenta-tions have been identified and their management has beenlaid out in a simple and straightforward fashion. The formatis novel: the section is written primarily by a trainee – closelyaligned to the practical problem – and overviewed by a seniorcardiologist with substantial experience in each of the pre-sentations. This provides a valuable blend of practice and

theory which is crucial to the doctor who is “on the spot”. Thetext is concise and easy to read – it is enormously valuable tothose who have to cope with immediate problems. It is bothpractical and sound from a theoretical perspective – it is goodvalue for the time invested in giving it your attention.

London, UK A. John Camm

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Preface

This clinical handbook aims to serve as a practical guide forgeneral practitioners, cardiology trainees, nurses with aninterest in cardiology, and junior physicians, in general, whoface the challenge of assisting people affected by cardiovas-cular conditions. We envisage our colleagues using this bookas a quick reference in everyday clinical practice but also

when they wish to remind themselves of key diagnosticelements and current management strategies for common –but often problematic – cardiovascular conditions. As such,we have, in the present handbook, focused on thosecardiovascular conditions that clinicians are likely toencounter more frequently in their practice and which posemajor diagnostic and therapeutic challenges.

The chapters in the book, which have all been written by

cardiology trainees under the direct supervision of a seniorauthor with particular expertise in the field, have been struc-tured in a fashion that we believe will provide the reader witha truly practical tool. We have hopefully addressed most ofthe questions commonly asked in relation to the diagnosis,differential diagnoses and management of the cardiovascularconditions presented in the book. Given the practical nature

of the handbook we have incorporated sections such as“Must do’s” and “Red flags” to help the reader in dealingrapidly and efficiently with the most relevant clinical issues.

We have placed emphasis on the pharmacological treat-ment of the conditions mentioned in the handbook, and tothe best of our knowledge all the information contained in

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the chapters is evidence-based. Flowcharts, diagrams andimages have been included to facilitate the reading of the

book.We truly hope that you will enjoy reading the handbook

and find it to be a useful tool to assist you in your clinicalendeavours and will be delighted if our work contributes tobenefit patients accordingly.

London, UK Juan Carlos KaskiMichael Papadakis

Hariharan Raju

Preface


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Acknowledgements

We would like to express our gratitude to all contributingauthors for their hard work and dedication in making thisbook a reality.

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Contents

1 Chest Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Kostas Zacharias and Jayesh Makan

2 Dyspnoea: Focus on Heart Failure . . . . . . . . . . . . . . . 29Lynne Millar and Sanjay Sharma

3 Palpitations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Anthony Li and Magdi M. Saba

4 Syncope . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103Hariharan Raju and Elijah R. Behr

5 Systemic Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . 125Jennifer Roe and Teck K. Khong

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143

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Contributors

Editors

Juan Carlos Kaski Cardiovascular Sciences Research Centre,Cardiovascular and Cell Sciences Research Institute,St George’s University of London, London, UK

Michael Papadakis Cardiovascular Sciences ResearchCentre, Cardiovascular and Cell Sciences Research Institute,St George’s University of London, London, UK

Hariharan Raju Cardiovascular Sciences Research Centre,Cardiovascular and Cell Sciences Research Institute,St George’s University of London, London, UK

Contributors

Elijah R. Behr, MA, MBBS, MD, FRCP CardiovascularSciences Research Centre, Cardiovascular and Cell SciencesResearch Institute, St George’s University of London,London, UK

Teck K. Khong, FRCP, MD, MBA Blood Pressure Unit,St George’s Hospital NHS Trust, London, UK

Institute of Medical & Biomedical Education, St George’sUniversity of London, London, UK

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Anthony Li, MBBS, MRCP Cardiovascular SciencesResearch Centre, Cardiovascular and Cell Sciences Research

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

Jayesh Makan, BSc (Hons), MBBS Department ofCardiology, Shrewsbury and Telford NHS Trust,Shrewsbury, UK

Lynne Millar, MB BCh, BAO, MRCP CardiovascularSciences Research Centre, Cardiovascular and Cell Sciences

Research Institute, St George’s University of London,London, UK

Jennifer Roe, MBBS Blood Pressure Unit, St George’sHospital NHS Trust, London, UK

Magdi M. Saba, MD, FHRS Cardiac Electrophysiology,

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

Sanjay Sharma, BSc(Hons), MBChB, MD, FRCP, FESC

Cardiovascular Sciences Research Centre, Cardiovascularand Cell Sciences Research Institute, St George’s Universityof London, London, UK

Kostas Zacharias Department of Cardiology, Barts HeartCentre, London, UK

Contributors


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1J.C. Kaski et al. (eds.), Investigating and Managing CommonCardiovascular Conditions, DOI 10.1007/978-1-4471-6696-2_1,

© Springer-Verlag London 2015

Introduction

Patients presenting with chest pain account for over 500,000primary care appointments per year and for up to 25 % ofattendances in Emergency Departments in the UK. Thespectrum of diagnoses in patients presenting with chest pain

ranges from acute life threatening conditions such as acutemyocardial infarction, aortic dissection and pulmonaryembolism to benign conditions such as musculoskeletal dis-orders. The timely and accurate diagnosis of such patientstherefore remains a challenge for all physicians. The aim ofthis chapter is to provide guidance regarding the differentialdiagnosis in a patient presenting with chest pain with empha-sis on the diagnosis and management of myocardial

ischaemia.

Chapter 1

Chest PainKostas Zacharias and Jayesh Makan

K. ZachariasDepartment of Cardiology, Barts Heart Centre,London EC1A 7BE, UKe-mail: [email protected]

J. Makan, BSc (Hons), MBBS () Department of Cardiology, Shrewsbury and Telford NHS Trust,Shrewsbury SY3 8XQ, UKe-mail: [email protected]

mailto:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]


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Differential Diagnosis

Chest pain can be the presenting symptom in a range of con-ditions. The most important causes of chest pain are shown inTable 1.1 . Acute Coronary Syndrome (ACS) is the final diag-nosis in only 15–25 % of patients who present with acutechest pain. Nevertheless, the diagnosis of ACS in suchpatients may still be missed, with potentially life-threateningresults. A detailed history and systematic use of basic investi-gations can aid the non-specialist in correctly identifyingpatients with ACS and referring them appropriately for spe-cialist management.

Initial Assessment of the Patient

In the acute setting, initial assessment may take place prior tophysician contact, with paramedics or nurses triaging indi-viduals. A 12-lead electrocardiogram (ECG) should berecorded and assessed at the earliest possible opportunity,preferably within 10 min, in all patients who present withongoing chest pain of suspected cardiac origin. The priority isto address whether the patient is clinically stable or at risk ofa life-threatening condition such as ACS, aortic dissection orpulmonary embolism. If not critically ill, a decision regarding

urgency for further investigation must be made by risk-stratifying patients. Patients who display ST segment eleva-tion on their ECG must be triaged as critical priorities anddirected to specialist cardiology centres with a view to cardiaccatheterisation as an emergency.

The diagnosis and assessment of a patient with suspectedstable angina involves a comprehensive clinical evaluation,including identifying significant dyslipidaemia, hyperglycae-mia or other biochemical risk factors and specific cardiacinvestigations. These investigations may be used to confirmthe diagnosis of ischaemia, to identify or exclude associatedconditions or precipitating factors, assist in risk stratifyingpatients and to evaluate the efficacy of treatment (Fig. 1.1 ).

K. Zacharias and J. Makan


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Table 1.1 Most common causes of chest pain

Category Syndrome Key features

Cardiac Stable angina Precipitated by exertion/relieved by rest

Acute coronarysyndromes

Sudden onset/duration>20 min. Associated withdyspnoea and autonomicsymptoms

Pericarditis Sharp, pleuritic. Relieved

by leaning forwardsRespiratory Pneumothorax Unilateral. Pleuritic.

Sudden onset

Pleuritis/pneumonia

Pleuritic/infectivesymptoms

Vascular Aortic dissection Very severe/radiating to theback

Pulmonaryembolism

Pleuritic/dyspnoea

Gastrointestinal Gastro-oesophageal reflux

Following large meal/relieved by antacid

Peptic ulcer disease Relieved by antacid

Pancreatitis Intense epigastric/

substernal

Gallbladder disease Usually following fattymeal

Musculoskeletal Costochondritis Reproduced on palpation

Trauma History of trauma

Neurological Cervical spine

pathology

Reproduced by neck

movement

Infectious Herpes zoster Burning/dermatomaldistribution

Psychological Panic attack Hyperventilation

Chapter 1. Chest Pain


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History

The classic manifestation of pain that is caused by myocardial

ischaemia is angina. This may be described amongst otherthings as dull discomfort, crushing sensation, restriction,“band-like” sensation or throat tightness. The discomfort isclassically brought on by physical or in some cases emotionalstress and may radiate into the jaw, one or both shoulders orarms (though not to fingertips).

A description of central chest pain that is brought on by

exercise and relieved by rest or by the use of glyceryltrinitrate (GTN) is thought to constitute typical angina.By contrast the following descriptions of pain make thediagnosis of angina less likely:

(a) pain that is primarily pleuritic(b) pain that is entirely in the abdomen

Chest pain

HistoryPhysical examination

12-lead ECG

Stable chest painPossible stable angina

Biomarkers

EchocardiogramCXR in selected patients

LVEF


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(c) pain that can be localized by the patient with the use ofone finger

(d) pain that lasts for a few seconds or pain that persists formany hours or days(e) pain that can be reproduced by movement or palpation

of the chest or of the arms

In general, patients with symptoms of chest discomfort,dyspnoea or dizziness that are clearly related to exertionshould be referred for further assessment with regards to

underlying coronary artery disease (CAD).

Risk Factors

The main risk factors for ischaemic heart disease are welldescribed in various population studies. Non-modifiable risk

factors include increasing age and male gender; malepatients over the age of 70 have over 90 % probability ofunderlying CAD even when presenting with atypical pain(Table 1.2 ).

Amongst the modifiable risk factors, diabetes mellitus,smoking status and hyperlipidaemia confer a higher predic-tive value than hypertension. Familial premature CAD

(below age 55 years in a male non-smoker, below 65 yearsin a female), usually occurs in the context of other risk fac-tors such as familial dyslipidaemia and thus, on its own,does not confer as high a predictive value as previouslythought.

It should be noted that this risk factor profiling applies topatients with no previous diagnosis of CAD, i.e. only at thetime of index presentation. Any patient with a prior myocar-dial infarction (MI), demonstrable CAD on coronary angiog-raphy or prior coronary revascularization has an establisheddiagnosis of CAD. Thus, chest discomfort in such patientsshould be thoroughly evaluated. Risk factor modification insuch patients is important for their prognosis and preventionof recurrent cardiovascular events.



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Physical Examination

A thorough examination of the cardiovascular and respira-tory system should be performed in all patients. Althoughthere are no pathognomonic physical signs of CAD, a physi-

cal examination may reveal signs that point towards alterna-tive diagnoses. These may include signs of:

(i) systemic conditions/illnesses (e.g. sepsis, anaemia, thy-roid disease, generalized malignancy)

(ii) other heart disease (e.g. murmur of aortic stenosis orhypertrophic cardiomyopathy, friction rub of pericarditis)

Table 1.2 Clinical pre-test probability in patients with stable chestpain symptoms

Typical angina Atypical angina Non-anginal painAge (yrs) Male Female Male Female Male Female

30–39 59 28 29 10 18 5

40–49 69 37 38 14 25 8

50–59 77 47 49 20 34 12

60–69 84 58 59 28 44 17

70–79 89 68 69 37 54 24

>80 93 76 78 47 65 32

Adapted from 2013 ESC guidelines on the management of stablecoronary artery disease. Eur Heart J. 2013;34:2949–3003Values are % of people at each mid-decade age with significantcoronary artery disease (CAD)

Probability < 15 % can be managed without further testing

Probability of 15–65 % should have a non-invasive imaging basedtest for ischaemia, allowing for local expertise and availability. Inyoung patients radiation issues should be considered. An exerciseECG is an alternative as the initial test

Probability between 66 and 85 % should have a non-invasiveimaging functional test for making a diagnosis of CAD

Probability of >85 % one can assume that CAD is present. They

need risk stratification only



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(iii) vascular disease (e.g. difference in arm blood pressuresindicating aortic dissection, signs of pulmonary hyper-

tension in pulmonary embolism)(iv) respiratory disease (e.g. signs of pneumonia, pleural rub,signs of pneumothorax)

Investigations

ECG

A 12-lead ECG should be obtained and interpreted at pre-sentation. The following criteria constitute acute transmuralischaemia, consistent with the diagnosis of ST elevation myo-cardial infarction (STEMI) in a patient presenting withsymptoms of chest pain and should prompt urgent specialistreferral:

ST elevation of ≥2 mm in at least two contiguous precor-dial leads (V1-V6)

ST elevation of ≥1 mm in at least two limb leads of sameterritory (lateral: I, aVL; inferior: II, III, aVF)

Left bundle branch block (LBBB) that is not known to beold

ST-depression in leads V1-V3 with associated dominantR-wave (suggestive of isolated posterior STEMI)(Fig. 1.2 )

ST-segment elevation in lead aVR, particularly when asso-ciated with precordial lead ST depression is suggestiveof left main stem ischaemia (Fig. 1.3 )

The presence of a ventricular paced rhythm and LBBBmake interpretation of the ECG for evidence of acute isch-aemia challenging. In such cases, patients with ongoing symp-toms suggestive of myocardial ischaemia, such as persistentchest pain, autonomic symptoms (sweating and nausea), signsof acute heart failure or impending shock also deserve promptspecialist assessment. It’s also important to remember that anormal ECG does not rule out an acute coronary event!



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a

b

Figure 1.2 (a) ECG demonstrating an infero-postero-lateralSTEMI in a patient with acute chest pain. Note the presence ofST-depression in leads V1-V3 with associated dominant R-wave. (b)

Placing leads V4-V6 posteriorly (V7-V9) unmasks the posteriorST-elevation

Figure 1.3 ECG demonstrating ST-segment elevation in lead aVR,with associated ST depression in the precordial leads, suggestive ofleft main stem ischaemia



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Patients with ECG abnormalities that do not fall into anyof the categories detailed above are not thought to benefit

from early reperfusion therapy. However patients with clearlydynamic ECG changes (dynamic ST depression that occursduring episodes of chest pain or progressive T-wave inversionand deepening) may be considered for early coronaryangiography.

ECG rhythm monitoring should be initiated as soon aspossible in all patients with suspected STEMI and continuefor at least 24 h after successful reperfusion therapy due to

the risk of acute ischaemic or early post-MI ventriculararrhythmia.

Myocardial Biomarkers

The use of biomarkers in the diagnosis of myocardial isch-

aemia has changed considerably over recent years. The diag-nosis of myocardial infarction was initially reliant on assays ofcreatine kinase (CK), its iso-enzyme (CK-MB) and myoglo-bin. Although useful, they were limited by low sensitivity andspecificity. The advent of troponin assays allowed for greaterdiagnostic accuracy and thus troponin is now the biomarker ofchoice for detecting myocardial damage. In patients with a

myocardial infarction, levels may be elevated as early as 4 hafter the event and can remain elevated for up to 2 weeks. Atroponin assay may therefore also be of value in the assess-ment of patients who present late. High sensitivity troponinassays provide even greater sensitivity and by using serialsamples, for example 3 h apart, the sensitivity for diagnosingMI approaches 100 %. Current guidance advocates a troponinsampling at admission and repeat measurement between 10and 12 h after the onset of symptoms. This provides the oppor-tunity to assess the pattern of change. The progression fromthe first to second sample is important as it may help to dif-ferentiate acute infarction from chronic myocardial necrosis.

It is important to note that troponin should not be used asthe sole investigation to diagnose or exclude ACS. The history,



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clinical findings and ECG remain the cornerstone of the diag-nostic process. Troponin levels may be elevated in response toother pathologies (Table 1.3 ) and one must be prepared toconsider an alternative diagnosis as suggested by the historyand clinical examination findings.

Other biomarker assays have been evaluated. Theseinclude myeloperoxidase and ischaemia modified albumin.Their value in clinical practice over high-sensitivity troponinhas not yet been established. Measurement of B-typeNatriuretic Peptide (BNP) levels provides useful prognosticinformation but should not be used to determine initialtherapeutic strategies in ACS. Similarly, high sensitivity CRPcan predict long-term mortality but is of limited use in acutecardiac presentations.

Functional Imaging

There are various testing modalities that try to look forobjective evidence of functional ischaemia in patients whopresent with stable symptoms.

Table 1.3 Causes of raised troponin levels (apart from ACS)

1. Pulmonary embolism

2. Congestive heart failure

3. Arrhythmias

4. Septicaemia

5. Myocarditis

6. Neurological conditions e.g. subarachnoid haemorrhage

7. Aortic dissection8. Iatrogenic e.g. pacing, electrophysiological studies

9. Chronic or acute kidney injury

10. Infiltrative disease e.g. sarcoidosis, haemochromatosis

11. Drugs e.g. chemotherapy



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The exercise ECG (ExECG), also referred to as an exer-cise tolerance test, has been used for a number of years as the

investigation of choice in most of these patients. Although, itretains its Class I recommendation in guidelines from theUSA, it is no longer recommended as the first-line screeningtest for functional ischaemia in the UK and the rest ofEurope. Its main advantage of widespread availability hasbeen overshadowed by the high number of inconclusive tests,approximately 30 % in most studies. Its role is now limited tothe assessment of exercise capacity in patients with estab-

lished CAD. Allowing for availability of local expertise andresources, alternative stress imaging modalities such asechocardiogram, cardiac magnetic resonance imaging (CMR),single photon emission computed tomography (SPECT) orpositron emission tomography (PET) are recommended inpatients with suspected but stable CAD with intermediatepre-test probability, as first line investigation. Clinician and

patient preference also dictate the choice of test.Stress echocardiography is a well-established functionalassessment modality. It provides real-time information oncardiac structure and function, coupled with a high degree ofsensitivity and specificity for CAD. Patients who are unableto exercise can undergo assessment with a pharmacologicalstressor such as dobutamine. The introduction of echocardio-graphic contrast media has improved endocardial definition

to the point where a diagnostic-standard test can be per-formed in all but a very small minority of patients.

Nuclear myocardial perfusion study (MPS), includingSPECT and PET, is another well-established functional imag-ing technique. It has a comparable sensitivity and specificityto stress echocardiography. Its main disadvantages includethe need for specialized equipment and the involvement of

ionizing radiation. It can also underestimate the severity ofCAD in the context of balanced ischaemia, such as seen inthree-vessel disease.

Cardiac magnetic resonance (CMR) imaging is developinginto a viable alternative assessment for functional ischaemia.However, this imaging modality is not yet widely availableand its cost may limit its widespread use in the future. Its



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main benefit is the additional anatomical information pro-vided, which is accepted as surpassing that of

echocardiography.

Anatomical Imaging

Invasive coronary angiography is considered the gold-standard for investigation of epicardial coronary artery dis-ease. At present, it is considered as a first-line investigation

for stable angina in individuals with a high pre-test probabilityof CAD (>85 %) where revascularisation is being considered.It is also appropriate for further evaluation of functional isch-aemia on non-invasive investigations as a prelude to revascu-larisation, which may take place at the same time. The risks ofinvasive coronary angiography should be taken into account,which include vascular damage and systemic thromboem-

bolic phenomena.Computed tomography coronary angiography (CTCA) isnow available as a non-invasive anatomical test. Its main useat present is in patients with low or low-intermediate pre-testprobability (10–50 %) of CAD as a rule-out test. The advanceof technology has significantly limited the amount of radia-tion involved. A CTCA can also be performed to delineatethe course of anomalous coronary vessels or grafted vessels

in patients with a previous history of coronary bypasssurgery.

Management

NSTEMI and Unstable Angina

Patients who present with cardiac chest pain occurring at rest,or minimal exertion and that is not responsive to a short act-ing nitrate should be treated as unstable. Patients with anginaof recent onset that occurs at decreasing levels of exertion(crescendo angina) should also be considered unstable.



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As with any critically ill patient, respiratory and haemody-namic assessment should triage direction and urgency offurther assessment. The patient should have cardiac monitor-ing instituted with intravenous access obtained. Often, localinstitutions have departmental policies for management of

ACS. However, the priority is to establish a hierarchy of dif-ferential diagnoses prior to initiation of any treatment, sincetreatments targeted at ACS, such as aggressive antiplateletagents, may be deleterious in other conditions.

The overall mortality and morbidity risk of patients withsuspected ACS should be calculated early on and taken intoconsideration when further therapy is decided. Current clinicalguidelines recommend quantitative assessment with the use of a

scoring system such as the GRACE or TIMI scores. An onlinecalculator for the GRACE score is accessible at www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html . TheGRACE score provides an estimation for the probability ofdeath or myocardial infarction both in-hospital and at 6 months.This calculation can help the clinician to tailor treatment accord-ingly. Patients can be categorized on the basis of their GRACE

score (Table 1.4 ) to low, intermediate or high risk. It is worthnoting that a patient with dynamic ECG changes and a negativetroponin has an equal or greater risk than a patient of similarcharacteristics with no ECG changes and a positive troponin.This further illustrates the pitfall of basing ACS diagnosis andmanagement on the troponin value alone.

Table 1.4 Risk assessment of ACS patients (GRACE Score,adapted from NICE Clinical guideline 94)

Predicted 6 monthmortality Risk of future adverse cardiovascularevents

1.5–3 % Low risk

>3–6 % Intermediate risk

>6–9 % High risk

>9 % Highest risk


http://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.htmlhttp://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.htmlhttp://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.htmlhttp://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html


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The overall risk/benefit ratio with regards to potentialbleeding complications in an individual patient should also be

assessed. Online tools such as the Crusade bleeding score( www.crusadebleedingscore.org ) are easily accessible and canbe used to calculate the risk of in-hospital major bleeding.

Symptomatic Treatments

Appropriate analgesia will render the patient more comfort-

able and should therefore be initiated early. Systemic nitrates,such as glyceryl trinitrate (GTN), are rapidly absorbed sublin-gually or bucally. Alternatively, they also come in intravenouspreparations for continuous infusion for ongoing pain. Theyact by coronary vasodilation, thereby improving subendocar-dial ischaemia. Opioids such as morphine or diamorphine maybe required and administration is usually combined with that

of an antiemetic such as metoclopramide. Resultant vasodila-tion from these treatments may rarely precipitate hypoten-sion, though cardiogenic shock must be considered in thiscontext. Universal use of high flow oxygen is not warrantedunless the oxygen saturations are low (less than 94 %).

Antiplatelet/Antithrombin Therapy

A wide variety of drugs are available in this category oftherapeutic agent and local guidance, if available, should beconsulted. We have presented here an overview of availableoptions and factors that may favour one agent over another.

A loading dose of 150–300 mg aspirin (acetylsalicylic acid)should be given in suspected ACS, unless there is a clear his-

tory of significant aspirin allergy. It is important to note thatpatients may state that they are allergic to aspirin on the basisof a mild gastric upset or asthma. In such cases, aspirin shouldstill be offered. In definite systemic, respiratory or cutaneoussensitivity reactions to prior aspirin use, however, monother-apy with another antiplatelet agent such as an adenosinediphosphate (ADP) receptor inhibitor should be considered.


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An ADP receptor inhibitor such as clopidogrel (300–600 mgloading dose, 75 mg daily maintenance dose), ticagrelor

(180 mg loading dose, 90 mg twice-daily maintenance dose) orprasugrel (60 mg loading dose, 10 mg daily maintenance dose)should be co-administered with aspirin. The latter two neweragents, are now recommended as first choice as they carry abetter ischaemic prognosis, albeit at somewhat higher risk ofbleeding events. Additionally, the newer agents have morepredictable antiplatelet effects. Based on the ESC guidelines,ticagrelor, is recommended for all patients at moderate to high

risk of ischaemic events including those pre-treated with clopi-dogrel, which should be discontinued when ticagrelor is com-menced. Prasugrel on the other hand should be considered inADP-inhibitor naïve patients, particularly diabetics, in whomthe coronary anatomy is known and who are proceeding tocoronary intervention (PCI).

Anticoagulation is recommended for all patients in addi-

tion to anti-platelet therapy. It should be selected accordingto both ischaemic and bleeding risks and according to theefficacy and safety profile of individual agents. Unfractionatedheparin, low molecular weight heparins (such as enoxaparinor dalteparin), and fondaparinux (a more selective anti-factorXa agent) reduce recurrent ischaemic events and overallmortality. Fondaparinux 2.5 mg subcutaneously is recom-mended as first choice as it has the most favourable efficacy-

safety profile with the most favourable bleeding profile.Unfractionated heparin may be preferred in those with end-stage kidney disease; dose reduction and/or adjustment maybe necessary if low molecular weight drugs or fondaparinuxare used in those with renal impairment or when used overprolonged periods.

In very high-risk patients, the addition of other anti-platelet

agents such as glycoprotein IIb/IIIa inhibitor (GPI –egTirofiban, Eptifibatide) should be considered, with combina-tion of GPI. The combination of GPI and heparin analogueor GPI with bivalirudin if the benefit of giving these agentsis thought to outweigh the potential extra bleeding risk. Thelatter has a better bleeding profile and is considered appropri-ate for those at high ischaemic and high bleeding risk.



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Patients at low risk can be managed conservatively in thefirst instance but should still be offered a non-invasive

functional test for ischaemia prior to discharge from hospital.It is important to remember that when considering absolutenumbers, the majority of subsequent coronary events occur inpatients deemed at low risk. This is because, numerically,these patients represent the overwhelmingingly largest groupof presentations. It is therefore important to accurately fur-ther risk stratify these patients by means of a functional testprior to discharge. Invasive investigation with angiography

should be reserved for those with demonstrable inducibleischaemia on functional testing.

Urgent discussion and referral to a specialist should takeplace in the cases of patients who suffer from haemodynamicinstability, acute left ventricular dysfunction with pulmonaryoedema, or display on-going ischaemia evidenced bysymptoms or ECG changes. Decisions regarding the exact

management strategy in ACS can be complex and a specialistshould be involved as early as possible after the first steps inthe management of the patient have taken place. The timingof investigations and involvement of the specialist team maybe dictated by local protocol. An example of a pathway forthe management of suspected ACS is shown in Fig. 1.4 .

ST Elevation Myocardial Infarction (STEMI)

The management strategy in STEMI differs from that ofNSTEMI and unstable angina in that urgent coronary reper-fusion is the treatment of choice. This should be primaryPercutaneous Coronary Intervention (PCI) at a designatedheart attack centre with round-the-clock cardiaccatheterization facilities. In situations when a PCI strategy isnot available, primary thrombolysis may be considered(Fig. 1.5 ).

Eligibility for urgent coronary reperfusion is establishedby assessing the patient’s symptoms and ECG changes asdescribed earlier on (Fig. 1.1 ). The greatest benefit fromreperfusion results if symptoms have been present for lessthan 12 h although treatment can be initiated if symptoms



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have continued beyond this period if there is ongoing evi-dence of ischaemia or the pain and ECG changes are stutter-ing. If primary PCI can be delivered within 120 min of thetime when thrombolysis could be administered, the patientshould be transferred to a heart attack center for treatment(Fig. 1.5 ). An initial assessment with regards to the generalstate of the patient, appropriate analgesia and monitoringshould take place in the same way as described earlier forNSTEMI patients. A loading dose of Aspirin 300 mg shouldbe given in all patients but those with a significant allergy. Aloading dose of an additional antiplatelet, ticagrelor or prasu-grel (the latter if no history of stroke/TIA and age 70 bpm & no contra-indicationsSerial ECGs and interval serum Troponin

Serial ECGsand

interval serum Troponin

Figure 1.4 Local chest pain pathway (Adapted from RoyalShrewsbury and Telford NHS Trust ACS Protocol). 1 Consider defer-ring if the patient’s bleeding risk is unfavourable (e.g. advancing age,female, significant renal impairment or pre-existing anaemia). Referto crusadebleedingscore.org for more detail. 2 Reduce regime ofenoxaparin to OD if age >75 years or eGFR


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If primary PCI is unavailable or cannot be delivered within120 min, thrombolysis using an agent such as alteplase,

reteplase or tenecteplase may be considered in consultationwith a specialist. The potential risks of thrombolysis, in particu-lar that of major haemorrhage or haemorrhagic stroke, shouldbe explained to the patient prior to the drug administrationalthough formal informed consent is not thought to be neces-sary. The absolute and relative contraindications of thromboly-sis are well established and are summarised in Table 1.5 .

A patient who has undergone thrombolysis should bemonitored continuously for reperfusion arrhythmias. Serial12 lead ECGs should be performed. Successful thrombolysisis suggested by resolution of symptoms and resolution of theST segment elevation on the ECG within 60–90 min. In casesof ongoing symptoms and no resolution of the ST segments,a rescue PCI strategy should be contemplated. There is no

STEMI diagnosis

Consider co-morbidities and quality of life. Do they make re-vascularisation unlikely? → Medical therapy

Primary PCI capable centre Non-primary PCI capable centre

PCI possible within 120 min

Primary PCIImmediate transfer to PCI centre

(Preferably within 90 mins)

Immediate rescue PCI

Successful

fibrinolysis?Immediate transfer to PCI centre

Immediate fibrinolysis

(preferably within 30 mins)

Invasive coronary

angiography

(ideally within 24 h)

NO

YES

NOYES

Figure 1.5 Reperfusion strategies in patients presenting withSTEMI (Adapted from ESC Guidelines for the management ofacute myocardial infarction in patients presenting with ST-segmentelevation. Eur Heart J. 2012:33;2569–619)



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evidence to support the use of further thrombolysis in suchcases and this should not be considered, as the risk of majorbleeding is significant.

Secondary Prevention

A number of pharmacological agents have been shown to con-fer significant prognostic benefit in patients who are diagnosedwith coronary artery disease. In addition to the antiplatelet

Table 1.5 Contraindications to thrombolysis

Absolute

Intracranial haemorrhage or stroke with unknown cause

Ischaemic stroke within the last 6 months

Brain tumour or AV malformations

Recent major trauma/surgery/head injury in the last 3 weeks

Known bleeding disorder e.g. haemophilia

Gastrointestinal bleeding within the last monthAortic dissection

Procedures not amenable to manual haemostasis e.g. liverbiopsy within 24 h

Relative

Oral anticoagulant therapy e.g. warfarin

Transient ischaemic attack in the last 6 months

Pregnancy or 1 week post partum

Elevated blood pressure (>180/110 mmHg)

Advanced liver disease

Infective endocarditis

Active peptic ulcer

Prolonged cardiopulmonary resuscitation



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therapies described above, patients with ACS should be initi-ated on ACE inhibitors such as Ramipril as soon as they are

haemodynamically stable with the dose titrated to the maxi-mum tolerated in a gradual fashion and with monitoring of thepatient’s renal function.

The long-term use of beta-blockers such as Bisoprolol isnow recommended only in patients with left ventricularimpairment as guidelines suggest that beta-blockers may bestopped after a year if the LV function is preserved. In prac-tice however, most specialists advocate the long-term use of

a beta-blocker in all patients with a history of ACS given theirantiarrhythmic properties. In patients with symptoms andsigns of left ventricular impairment, the addition the aldoste-rone antagonist Epleronone is also recommended.

Statin therapy post myocardial infarction is of undoubtedbenefit and must be considered in all such patients irrespectiveof the serum cholesterol. Atorvastatin 80 mg is currently rec-

ommended but different agents or doses may be considereddepending on patient’s tolerance and response to therapy.In addition to pharmacological agents, measures which

have been shown to confer profound prognostic benefit inpatients treated for ACS include lifestyle changes such assmoking cessation and weight reduction, optimization ofblood pressure and diabetic control and exercise based reha-bilitation programmes as delivered by multidisciplinary teams.

Stable Angina

Symptom Control

Patients with stable angina will typically describe symptoms

on exertion or during periods of emotional stress. A usefulclassification system is the Canadian Cardiovascular Society(CCS) grading:

Class I: Angina during strenuous or prolonged physicalactivity

Class II: Slight limitation, with angina only during vigorousphysical activity



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Class III: Symptoms with everyday living activities, i.e.,moderate limitation

Class IV: Inability to perform any activity without anginaor angina at rest, i.e., severe limitation

Currently available anti-anginal medications are shown inTable 1.6 . These can be effective at relieving symptoms but,with the exception of beta-blockers, there is limited data withregards to any potential prognostic benefit.

A short acting nitrate such as GTN sublingual spray can be

used to provide symptomatic relief on an as-required basis.Patients should be given clear instructions with regards to itsuse during an angina attack and be advised to seek furthermedical attention if symptoms don’t resolve in a timely fash-ion, usually within 5–10 min. Patients should also be giveninformation with regards to the storage and replenishment ofGTN containing formulations over time to ensure easy accessto the medication especially when used very infrequently.

Regular anti-anginal medications currently recommendedas first line include beta-blockers and calcium channel antag-onists which can be combined together for symptom controlif necessary. Caution is advised when combining a beta-blocker with a calcium channel blocker given the potentialfor bradycardias and the use of a dihydropyridine calciumblocker such as Amlodipine is preferred in this instance. If

either of these classes of drug cannot be tolerated, otheragents that can be used as monotherapy include Nicorandil,Ivabradine, Ranolazine or a long acting oral nitrate. Theseagents can also be added to a beta-blocker or calcium chan-nel antagonist when symptoms are difficult to control ascombination therapy. A third agent may be added if patientsremain symptomatic and are not considered suitable for arevascularization strategy (Table 1.6 ).

Revascularization

The treatment of stable angina by way of coronary arterybypass surgery and PCI may be necessary should medicaltherapy fail to control symptoms or if there are high riskfeatures on ischaemia testing and risk stratification. Decisions



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with regards to revascularization in stable patients shouldideally be made in a multidisciplinary forum involving spe-cialist cardiologists and cardiothoracic surgeons.

Also Worth Knowing

Echocardiography

Echocardiography is recommended for all patients withACS. It is important to assess ventricular function, so thatappropriate therapy can be initiated and to look for the pres-ence or absence of significant valve disease. Patients may beadvised to stop driving if the left ventricular function is sig-

nificantly impaired.

Anaemia

Patients with chronic anaemia are more likely to experienceangina symptoms even in the absence of flow limiting coronaryartery disease in the epicardial coronary vessels. This is due to

the decreased oxygen delivery to the myocardium at a cellular

Table 1.6 Anti anginal therapy

Class of drug Example Use

Beta blockers Bisoprolol, metoprolol 1st lineDihydropyridine calciumchannel antagonists

Amlodipine, felodipine 1st line

Non – dihydropyridine calciumchannel antagonists

Diltiazem, verapamil 1st line

Nitrates Isosorbide mononitrate,dinitrate

2nd line

Potassium channel activators Nicorandil 2nd line

IF channel inhibitors Ivabradine 2nd line

Late sodium current inhibitors Ranolozine 2nd line

2nd line agents may used as initial therapy if 1st line agents are nottolerated. If using combination therapy of beta blockers and calciumchannel antagonists, avoid non-dihyrdropyridine preparations



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level. Patients with unexplained anaemia should be thoroughlyinvestigated to ensure there is no underlying sinister pathology

such as a gastro-intestinal malignancy. Patients with a pre-existing anaemia with a known aetiology should be managedin consultation with a specialist to ensure that their haemoglo-bin levels remain in the normal range as much as feasible.

Renal Function

Drugs used in the treatment of ischaemic heart disease suchas ACE inhibitors and aldosterone antagonists can impairrenal function, which should be closely monitored. Contrastinduced nephropathy (CIN) following coronary angiographyis more likely in patients with pre-existing chronic kidneydisease and the risk increases significantly in patients with alow Glomerular Filtration Rate (GFR). Such patients should

be managed in consultation with a nephrologist and anyplanned angiographic procedures are best performed in cen-ters with combined cardiac and renal specialist facilities.

Diabetes

Tight blood glucose control is important in patients with

ACS. The aim should be to keep the levels below 11 mmol/l,and this is best achieved with a dose adjusted insulin infusion.Patients who are treated with Metformin should have thisdiscontinued for a period of time around ACS presentationand especially if coronary angiograph is planned as itincreases the risk of CIN.

Other Cardiac Conditions Presentingwith Chest Pain

Pericarditis

Pericarditis presents as pleuritic central pain, worse on inspi-

ration and lying flat. The patient may have had a recent upper



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respiratory tract infection. They may be pyrexial and haveraised inflammatory markers.

Clinical examination can be unremarkable but on occasionthe patient may have a pericardial friction rub. The ECGshows saddle shaped ST elevation (Fig. 1.6 ). The echocardio-gram is often normal unless there is an associated effusion.There may be an increase in serum troponin levels.

The aetiology may be difficult to diagnose but the com-

monest causes are: 1. Neoplasia2. Tuberculosis3. Autoimmune4. Viral5. Purulent (bacterial/fungal)6. Post myocardial infarction

7. Uraemia8. Traumatic

Treatment is most effective with non-steroidal anti-inflammatory drugs (ibuprofen, indomethacin, aspirin) orcolchicine. Steroids may be indicated in patients with connec-tive tissue disease or refractory pericarditis.

Figure 1.6 ECG demonstrating widespread saddle shaped ST seg-ment elevation in a young patient with pericarditis



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Aortic Dissection

Patients with aortic dissection usually present with severe,tearing anterior or posterior chest pain. Aortic dissectionhowever can present as associated myocardial infarction,stroke, heart failure, cardiac tamponade, paraplegia or otherneurological sequelae such as Horner’s syndrome.

A history of risk factors such as hypertension, vasculitis,collagen disorders like Marfan’s syndrome or a history ofcongenital heart diseases such as bicuspid aortic valve orcoarctation of the aorta should raise the clinical index ofsuspicion in patients who present with shearing chest pain.The finding of a diastolic murmur of aortic regurgitation ordifference in systolic blood pressure of more than 20 mmHgbetween the two arms in such patients should prompt furtherinvestigations. The finding of mediastinal widening on a chestX-ray is not pathognomonic of dissection. A CT aortogram is

the investigation of choice in most centers with echocardiog-raphy being of some value in unstable patients when dissec-tion of the aortic root is suspected. Patients with aorticdissection should be referred to a cardiothoracic center as anemergency.

Frequently Asked Questions

Q. My patient has had a heart attack, what should I tellthem about driving?

A. For group 1 license holders, driving may recommenceafter 1 week if successfully treated with PCI and noother urgent revascularisation is planned in 4 weeks. TheLV ejection fraction must be above 40 %.

If not successfully treated by PCI, driving shouldcease for 4 weeks. You do not have to inform theDVLA. Further information can be found at www.gov.uk/government/publications/at-a-glance

Q. The patient is on warfarin and is admitted with anNSTEMI, what should I do?


http://www.gov.uk/government/publications/at-a-glancehttp://www.gov.uk/government/publications/at-a-glancehttp://www.gov.uk/government/publications/at-a-glancehttp://www.gov.uk/government/publications/at-a-glance


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A. This is always challenging, but the importance of anti-platelet therapy should not be underestimated. Aspirin

and a P2Y12 inhibitor should be given as advised earlierin the chapter and the warfarin stopped. If the INR isbelow 2.0, LMWH/fondaparinux should be adminis-tered as per guideline/protocol.

Q. I am concerned about prescribing triple therapy (aspi-rin/P2Y

12 inhibitor/warfarin) long term after ACS.

A. Always discuss this scenario with a cardiologist. Factors

to take into consideration include indication for antico-agulation, type of stent used and bleeding risk.

Q. A surgeon wishes to stop the P2Y12

inhibitor for anoperation. Is it safe to do so?

A. It may not be and this will depend on whether the patienthas had PCI recently and the type of stent used. Do notstop the medication until it has been discussed with a

cardiologist.Q. A patient presents to me 72 h after a suspected ACS. How

should I manage them?A. If the patient has signs of complications such as pulmo-

nary oedema, an urgent assessment in hospital should beorganized. If they are completely asymptomatic, take anECG and troponin level and then make a clinical judg-

ment as to whether the patient should be seen urgentlyor not.

Q. I sometimes find it difficult to decide whether a patient’ssymptoms are consistent with ACS or aortic dissection.

A. This can be challenging. The clinical history is vital andusually provides you with the information to make adiagnosis. Severe, tearing pain of sudden onset, radiating

to the back tends to favor a diagnosis of dissectionwhereas severe anterior pain of a crescendo naturepoints more towards an ACS. Use the chest X-ray andblood pressure differentials to help and consult a spe-cialist if still in doubt. Occasionally, imaging the aortamay be the only option.



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Red Flags

ST-depression in leads V1-V3 with associated dominantR-wave should raise suspicion suggestive of isolated pos-terior STEMI.

ST-segment elevation in lead aVR, particularly when associ-ated with precordial lead ST depression is suggestive ofleft main stem ischaemia.

In STEMI, if primary PCI can be delivered within 120 min ofthe time when thrombolysis could be administered, thepatient should be transferred to a heart attack centre fortreatment.

Caution is advised when combining a beta-blocker with acalcium channel blocker given the potential for bradycar-dias and the use of a dihydropyridine calcium blocker suchas Amlodipine is preferred in this instance.



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© Springer-Verlag London 2015

Background

The American Thoracic Society defines dyspnoea as ‘a termused to characterize a subjective experience of breathingdiscomfort that is comprised of qualitatively distinct sensa-tions that vary in intensity. The experience derives from inter-actions among multiple physiological, psychological, social,

and environmental factors, and may induce secondary physi-ological and behavioural responses’. This in-depth definitioninfers that breathlessness is a complex entity, which can becaused by many conditions. The majority of conditions pre-senting with breathlessness are respiratory or cardiac in ori-gin (Fig. 2.1 ). Comprehensive discussion of all of theseconditions is beyond the scope of this chapter, which

Chapter 2

Dyspnoea: Focus on HeartFailureLynne Millar and Sanjay Sharma

L. Millar, MB BCh, BAO, MRCP

S. Sharma, BSc(Hons), MBChB, MD, FRCP, FESC (

) Cardiovascular Sciences Research Centre,Cardiovascular and Cell Sciences Research Institute,St George’s University of London, London SW17 0RE, UKe-mail: [email protected]; [email protected]

mailto:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]


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negotiates the clinical approach to a patient presenting withbreathlessness with a primary focus on the management ofchronic heart failure.

Definition of Heart Failure

Heart failure (HF) is a common clinical syndrome wherebythe heart fails to meet the metabolic demands of the body.Heart failure represents the end-stage of a number of struc-tural and functional cardiac disorders that impair the ability

of the ventricle to fill with (diastolic dysfunction) or eject(systolic dysfunction) blood. The clinical diagnosis of heartfailure is based on the presence of a triad of typicalsymptoms, signs and objective evidence of a structural orfunctional cardiac abnormality (as assessed by an imagingmodality or serum natriuretic peptides). The clinical

SOB

Respiratory

causeCardiac Other

Obstructive airways

disease e.g.asthma, COPD

Interstitial lung disease

Malignancy

Pulmonary embolism

Pulmonary hypertension

Pleural effusion

Obesity hypoventilation

Diaphragmatic weakness

Congestive cardiac failure

Ischaemic heart disease

Arrhythmias

Valvular heart disease

Pericardial disease

Deconditioning

Obesity

Anaemia

Anxiety/panic disorders

Pregnancy

Thyroid disease

Figure 2.1 Differential diagnosis of dyspnoea. SOB shortness ofbreath

L. Millar and S. Sharma


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features of heart failure are attributed predominantly to areduction in cardiac output (fatigue, weakness) and to

increased pulmonary or systemic venous congestion andfluid accumulation (dyspnoea, oedema, hepatic congestionand ascites).

Epidemiology

Heart failure has reached epidemic proportions worldwide,

affecting approximately 2–3 % of the world’s population.Despite treatment advances within the past few decadespatient outcome is still poor, with a 5 year survival


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Table 2.1 Causes of heart failure

Ischaemic heart disease Accounting for 70 % of patients with

heart failure in the developed worldIdiopathic Sporadic

Familial in up to 50 % of cases

Valve disease Accounting for 10 % of patients withheart failure

Hypertension The primary cause of heart failure inpatients of African/Caribbean descent

Alcoholiccardiomyopathy

Tachycardia-inducedcardiomyopathy

Often atrial fibrillation or flutter butany long-standing supraventriculartachycardiaHigh burden of ventricular ectopy/arrhythmias

Other acquired causes Myocarditis (usually viral, otherinfectious causes include HIV, Chaga’sdisease, Lyme disease)Peripartum cardiomyopathyInfiltrative disease (amyloidosis,sarcoidosis, haemochromatosis)With other systemic conditions: thyroiddisease, connective tissue diseaseStress-induced or TakotsubocardiomyopathyIatrogenic (chemotherapy, radiotherapy)Nutritional (Beri-Beri)

Other inheritedcardiomyopathies

Arrhythmogenic right ventricularcardiomyopathyLeft ventricular non-compaction

Burnt out stage of hypertrophiccardiomyopathy



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Heart Failure with Preserved Ejection Fraction

Heart failure with preserved ejection fraction, also known asdiastolic heart failure refers to abnormal cardiac relaxationor filling. It is characterised by a normal or near normal ejec-tion fraction (usually >50 %) and normal left ventricularend-diastolic volume, with echocardiographic evidence ofdiastolic dysfunction. It is important to note that impaireddiastolic function and diastolic heart failure are not synony-mous. As part of the ageing process a number of individualsdevelop a degree of diastolic dysfunction, but not every onewith diastolic dysfunction has diastolic heart failure. Thediagnosis of heart failure with preserved ejection fraction orHFpEF requires the presence of symptoms and signs of heartfailure. Management of diastolic heart failure primarilyrequires identifying and treating the underlying cause, how-ever a strong evidence-base is lacking for most of the treat-

ments used currently. General management principles includemeticulous blood pressure control, control of ventricular ratein arrhythmias such as atrial fibrillation and use of diureticsfor symptomatic relief of fluid overload. Despite the systolicfunction being preserved, diastolic heart failure is not abenign condition, with diastolic heart failure having a similarprognosis to that of systolic heart failure.

How to Assess Individuals with Dyspnoea

History

A detailed history is important in investigating the cause ofbreathlessness, as in many cases the diagnosis or a good dif-

ferential can be gained (Table 2.2 ). In those with establishedheart failure it is important to document their New YorkHeart Association (NYHA) class (Table 2.3 ), as it provides ameasure of their functional capacity and forms the basis for a

Chapter 2. Dyspnoea: Focus on Heart Failure


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Table 2.2 Questions you must ask patients presenting with dys-pnoea and the potential differential diagnosis

Question InterpretationDuration/patternof breathlessness

This helps determine the chronicity of thecondition.

Exercise tolerance Quantify degree of breathlessness withregards to exercise tolerance using NYHAclass.

Symptoms related

to reduced cardiacoutput

Fatigue

Symptoms relatedto fluid overload

Orthopnoea, breathlessness that is worse onlying flat.Paroxysmal nocturnal dyspnoeaPeripheral oedema and ascitesPolyphonic wheeze: usually in keeping withobstructive airways disease such as COPD

and asthma although can occur in heartfailure, so-called ‘cardiac asthma’.Sputum: white in keeping with COPD,white-pink usually in keeping withpulmonary oedema, yellow-green usually inkeeping with infection or suppurative lungdisease.

Gastrointestinalsymptoms

Abdominal distension and pain, anorexia,bloating, nausea, constipation and jaundicesecondary to congestive hepatomegaly,ascites, reduced bowel perfusion andoedema

Genitourinarysymptoms

Oliguria/anuria, urinary frequency, nocturiasecondary to impaired renal perfusion

Cerebrovascularsymptoms

Confusion, memory impairment, anxiety,headaches, insomnia, bad dreams ornightmares, psychosis with disorientation,delirium, or hallucinations secondary tocerebral hypoperfusion and associatedelectrolyte abnormalities



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Table 2.2 (continued)

Question Interpretation

Musculoskeletalsymptoms

Gout, carpal tunnel syndrome, musclecramps

Past cardiac history Ischaemic heart disease, hypertension orvalvular heart disease are risk factors forheart failure.Cardiac arrhythmias especially atrialfibrillation with a fast ventricular response,can present with breathlessness

Past respiratoryhistory

Do they have established pulmonarypathology such as obstructive airwaysdisease, previous pulmonary embolism,bronchiectasis or pulmonary fibrosis.

Other past medicalhistory

Do they have a known history of diabetes,thyroid disease or HIV? These can be riskfactors for heart failure.Do they have a history of allergic rhinitisor atopic eczema? These may predispose toasthma.Any history of bleeding disorders oranaemia?Anaemia itself may cause shortness ofbreath.Are they deconditioned or obese? Being

overweight itself can lead to a subjectivefeeling of shortness of breathDo they have a history of autoimmunedisease or a rheumatological condition? Thismay predispose them to pulmonary fibrosis.Any history of neuromuscular disorderse.g. motor neurone disease which canlead to respiratory muscle weakness and

breathlessness.Any past psychiatric history? As theremay be a psychogenic component to thebreathlessness.

(continued)



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number of therapeutic interventions. It is also important toremember that heart failure is a multi-system disorder sopatients may present with gastrointestinal, genitourinary andcerebrovascular symptoms.

Table 2.2 (continued)

Question Interpretation

Social history There may be several environmental factorswhich could predispose or exacerbatesymptoms.Smoking history: this could predisposeto COPD or ischaemic heart disease orexacerbate asthma.Does the patient have any pets? Pets maypredispose to extrinsic allergic alveolitis or

asthma.What is the patient’s occupation? Incertain jobs the patient may be exposedto chemicals or toxins which can cause oraggravate certain conditions. Exposure tocarcinogens could lead to lung cancer orasbestos exposure could lead to asbestosisor predispose to lung cancer. Asthma

can be exacerbated by several chemicalsand therefore is not uncommon amongpainters, hairdressers and domestic staff. Acharacteristic feature of this type of asthmais amelioration of the symptoms when awayfrom work or on holiday.

Drug history Have they started any new medicationswhich could induce breathlessness?

Are they on any long term drugs e.g.amiodarone or methotrexate whichpredispose to lung fibrosis?Have they had previous chemotherapy?Certain chemotherapeutic agents can causea dilated cardiomyopathy.If they are on long-term pharmacologicaltherapy do they comply with their

medications?



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Clinical Examination

General Inspection

• It is important to establish the patient’s vital signs includ-ing blood pressure (to ensure haemodynamic stability andexclude hypertension), oxygen saturations, pulse (rate and

whether regular or irregular).• Is there pallor suggestive of anaemia or cyanosis suggestive

of hypoxia?• Is there nicotine staining on the fingers, suggestive of

smoking history?• Assess for finger clubbing which can occur in lung cancer,

suppurative lung disease, congenital cyanotic heart disease

and endocarditis.

Cardiovascular System

• Begin by assessing the radial and carotid pulse. Documentthe rate, rhythm and character.

• Measure the jugular venous pressure (JVP), to check forfluid overload.

• Palpate the apex beat. Is it displaced? Lateral displacementcan occur in patients with left ventricular enlargement.

• Are the heart sounds normal and regular? Are there anyadded sounds for example, a third heart sound (S3) in leftventricular failure or a fourth heart sound (S4) suggestiveof a stiffened left ventricle, or murmurs to suggest valvularheart disease.

Table 2.3 NYHA Classification of heart failure

Class I No limitation of physical activity

Class II Slight limitation of physical activity. Comfortable atrest, but normal daily activities cause breathlessness

Class III Marked limitation of physical activity. Comfortableat rest, but less than normal activity results inbreathlessness

Class IV Severe limitation. Breathless may be present at rest



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• Listen for pericardial rub which could be a sign of pericar-dial inflammation.

• Is there peripheral oedema (pitting), if so how high does itextend? (this may be indicative of right or biventricular failure).

Respiratory System

• Are there abnormalities of the chest wall e.g. a barrelshaped chest which may be in-keeping with longstandingchronic obstructive pulmonary disease (COPD).

• Is chest expansion equal? If it is unequal this could be asign of pneumonia, pleural effusion or pneumothorax.

• What is the character of the percussion note? A dull per-cussion note can be suggestive of pneumonia/collapse but astony dull percussion note is in keeping with a pleural effusion.

• Polyphonic wheeze is usually in keeping with obstructiveairway disease such as asthma or COPD but can also be

due left ventricular failure (so called ‘cardiac asthma’).• Is there bronchial breathing? The presence of bronchial

breathing is suggestive of pneumonia but can rarely becaused by localised pulmonary fibrosis or at the air-fluidinterface of a pleural effusion.

• Are there any crackles and if so are they coarse or fine?Early inspiratory coarse crackles suggest pneumonia or bronchi-ectasis whereas both pulmonary fibrosis and pulmonary oedemacause fine inspiratory crackles. Classically pulmonary fibrosiscauses late inspiratory crackles whereas pulmonary oedemacauses early to mid coarse inspiratory crackles (Table 2.4 ).

Investigation of Dyspnoea

Bloods Tests

A full blood picture is recommended to check the white cellcount (and neutrophil count) which might suggest infectionand haemoglobin to exclude anaemia. Anaemia in itself cancause breathlessness, and patients with heart failure and



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anaemia (Hb


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failure (although levels can be raised for other reasons) butvery high levels are associated with adverse outcomes and

therefore urgent referral to a heart failure specialist is required;the UK National Institute of Clinical Excellence (NICE) sug-gest within 2 weeks. Natriuretic peptide levels can also be uti-lised for monitoring in patients with established diagnosis ofheart failure as they correlate with morbidity and prognosis.

Electrocardiogram

Electrocardiograms (ECGs) are an important initial step inthe work-up of heart failure. Although there are no specificchanges related to heart failure, in the vast majority of casesthe resting 12 lead ECG exhibits abnormalities and thereforea normal ECG should raise the possibility of an alternativediagnosis for the breathlessness. It is useful to examine the

ECG systematically as outlined below:• What is the heart rate?

Tachycardia is common in untreated heart failure.• Is it regular or irregular?

Cardiac arrhythmias especially atrial fibrillation can them-selves cause breathlessness or they may be a manifestationof a secondary pathology such as heart failure.

• Are the QRS voltages normal?Voltage criteria for left ventricular hypertrophy may be inkeeping with long-standing hypertension, aortic stenosisor less commonly hypertrophic cardiomyopathy.Low QRS voltages may be in keeping with infiltrative dis-ease such as Amyloidosis.

• Are there pathological Q waves or T wave inversions?These can be suggestive of previous myocardial infarction

although non-specific T-wave inversions can be seen withunderlying primary cardiomyopathies.

• Are there underlying conduction system defects, for exam-ple left bundle branch block or non-specific interventricu-lar conduction delay?These findings may be seen in those with previous myocar-dial infarction, hypertensive heart disease or underlying

cardiomyopathy.



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Chest X-ray

Radiographic features suggestive of heart failure are dis-cussed in Table 2.5 .

Arterial Blood Gases

When dealing with patients with breathlessness especially inthe acute setting baseline blood gas analysis is important. It isimportant to ascertain if the patient is in type 1 or type 2respiratory failure. Common causes of type 1 respiratory fail-ure include pulmonary embolism, pleural effusions and con-

gestive cardiac failure whereas type 2 respiratory failure is

Table 2.5 Chest X-ray findings to distinguish between heart failureand respiratory causes of breathlessness

Heart failure Lung pathologyPulmonary congestionwith alveolar oedema

Hyper-expansion of the lung fields(COPD or asthma)

“Bat’s wing”shadowing

Reticulo-nodular shadowing (can belocalised or diffuse in pulmonary fibrosis)

Upper lobe diversion Focal consolidationa with air-bronchogramsb (usually pneumonia)

Small effusions:blunting of costo-phrenic angles

Large pleural effusions: uniformly densewhite opacification overlying the costro-phrenic angle and hemi-diaphragm witha meniscus

Kerley B lines andpleural effusions (usuallysmall and bilateral)

Cardiomegalya Although consolidation is often used to describe a lobar pneumo-nia it is not synonymous with it as consolidation can be caused bycancer, pulmonary haemorrhage and pulmonary oedemab In consolidation the small airways fill with dense material (which appearwhite) however there is relative sparing of the larger airways (theseappear darker) which gives the appearance of an air bronchogram



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most commonly seen in patients with exacerbations ofCOPD. In reality it is rarely that straightforward, as we often

see mixed metabolic and respiratory patterns.

Echocardiography

Echocardiography is mandatory for confirming the diagno-sis. Apart from documenting systolic and diastolic left ven-tricular function, the scan is useful in the identification of

various causes and complications of heart failure. If an echo-cardiogram identifies normal cardiac structure and function,despite strong clinical suspicion, consider an alternativediagnosis or referral for a specialist review. Below is a sum-mary of specific features that might be used to ascertain thecause of SOB:

• systolic function: usually documented as a percentage of

ejection fraction.• regional wall motion abnormalities (RWMA) or global

systolic impairment. Regional wall motion abnormalitiesare usually suggestive of ischaemia whereas global impair-ment suggests a more diffuse cardiomyopathic process

• chamber sizes especially LV dimensions (these are oftenenlarged in a dilated cardiomyopathy or reduced in size in

hypertrophic cardiomyopathy• diastolic dysfunction: usually documented as mild, moder-ate or severe (also referred to as grade II-IV diastolic fill-ing patterns)

• valvular pathology: most commonly mitral regurgitation,aortic stenosis

• pulmonary arterial pressures: to assess for pulmonaryhypertension (this may co-exist with left ventricular

disease, be a consequence of pulmonary pathology or maybe present on its own suggesting it is the primarypathology)

• Pericardial disease: due to acute or chronic pericarditis,pericardial constriction, pericardial effusion



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• Other pathology: congenital cardiac anomalies such asatrial or ventricular septal defects

• Other complications: intramural thrombus, ventricularaneurysms

Specialist Tests

Cardiac MRI

This modality is complementary to echocardiography. Itcan be crucial in deciphering the exact aetiology of heartfailure especially when a primary cardiomyopathy is sus-pected. It can give further information about cardiac struc-ture and function. Gadolinium contrast is usually used tolook for the presence of late gadolinium enhancementwhich is suggestive of myocardial fibrosis and scar. The pat-tern of the late gadolinium enhancement can help distin-guish from ischaemic heart failure, myocarditis or aninherited cardiomyopathy.

Coronary Angiography

Coronary angiography may be undertaken in those patients

with heart failure of presumed ischaemic aetiology or thosein whom the aetiology is unclear.

Cardiopulmonary Exercise Testing

It is widely established that exercise tolerance predicts out-come in patients with heart failure. Cardiopulmonary exercise

testing or CPET can be used in heart failure patients as anobjective measure of exercise tolerance through measurementof peak VO

2 (maximal oxygen consumption). It can also be

used in the context of advance heart failure in risk stratifica-tion of patients evaluated for potential heart transplantation.



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Other Tests to Consider

Investigations to consider for selected patients with heartfailure include

• Blood tests: Troponin I or T, iron studies, folate, vitaminB12, Autoimmune screen, Immunoglobulins and proteinelectrophresis, serum ACE.

• Viral titres• Urine sample: Albumin/Creatinine ratio, 24-h urine collec-

tion for protein, catecholamines, Bence-Jones protein.• Pulmonary function tests• Ambulatory ECG monitoring (Holter)• Stress imaging• Radionucleotide ventriculography• Coronary angiography (CT or conventional)• Myocardial biopsy• Right heart catheterisation

Management of Heart Failure (Fig. 2.2 )

The initial investigations of choice and the timing of these inpatients with presumed heart failure are dependent on thechronicity of the symptoms. In those with an acute presenta-

tion, admission to hospital may be the most appropriate step.In patients with a less fulminant presentation they can oftenbe worked up in the community. Caution needs to be taken inpatients with a history of ischaemic heart disease, valvularpathology and cardiomyopathies who should be referred forspecialist assessment. In most other patients an electrocardio-gram and a chest X-ray are performed in the first instance.Depending on the results, a decision is made to proceed tomeasure serum natriuretic peptides and perform echocar-diography (Fig. 2.3 ). In those with a typical history and inves-tigations suggestive of heart failure, initial pharmacological



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therapy such as loop diuretics, ACE-inhibitors and β-blockerscan be commenced by the primary care physician pendingreferral to secondary care. Some patients may have the diag-nosis and initial management started by their cardiologist orheart failure specialist but are subsequently referred back tothe primary care physicians for further management.Community heart failure nurses have an important role inmonitoring titration of medications, monitoring weight andfluid balance as well as giving psychological support.

Pharmacological

therapy

Device therapy

Palliation

Psycholigical

support

Empowerment of

patient

(education and

self-management)

Transplant

Management

of heart

failure

Figure 2.2 Overview of the management of heart failure



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Specific Role of the Cardiologist

Patients should be referred to a cardiologist or heart failurespecialist in the following settings:

• new diagnosis of heart failure• patients with NYHA III-IV symptoms• heart failure due to valve disease• heart failure refractory to treatment

• those who cannot manage at home• in women with heart failure who wish to or are pregnant

(the care of these patients should be shared between theheart failure specialist and obstetrician)

Suspected heart failure

Acute onset Non-acute onset

ECG + CXR

Echocardiography

Echocardiography

EchocardiographyBNP/NT-proBNP

• ECG normal• NT-proBNP


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Patient Education

It is important to educate patients and their relatives in orderto empower them to manage their condition in the commu-nity and prepare them for the lifelong healthcare interven-tions required (Fig. 2.2 ). Table 2.6 outlines all essential topicsthat should be addressed.

Pharmacological Therapy

Figures 2.3 and 2.4 summarise a treatment algorithm forpatients with symptomatic heart failure and reduced systolicfunction. As a general principle angiotension convertingenzyme inhibitors (ACEi), beta-blockers and loop diureticsform the first-line treatment. The mineralocorticoid antago-nists or angiotensin receptor blockers are reserved for those

who are still symptomatic despite optimal first-line treatmentor who cannot tolerate one or more of those agents. Otherpharmacological agents and device therapy is reserved forpatients with persistent symptoms or patients with specificcharacteristics as described below.

Loop Diuretics

Loop diuretics provide symptomatic relief from pulmonaryand systemic congestion by reducing fluid overload, however,they do not offer any prognostic benefit. Regular monitoringof renal function and electrolytes is required to avoid renalfailure, hyponatraemia, hypokalaemia and hypomagnesae-mia. It is important to start with a low dose, especially in

diuretic-naive patients and the elderly, and increase the doseuntil clinical improvement occurs. Once fluid overloadresolves the diuretic dose should be readjusted to avoiddehydration. Motivated patients should be educated about



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Table 2.6 Education topics that should be addressed in patientswith heart failure

Educational topics Skills and self-care behavioursEducation of thecondition and thecause

Explain to patients what the conditionis and why they have the symptoms theyhave.

Symptoms and signsof heart failure

Empower patients so they can recognizesigns and symptoms of decompensation.Allow the patient flexibility in adjustingtheir diuretic dose.

Pharmacologicaltreatment

Understand indications, dosing andeffects of drugs.Recognise the common side-effects ofeach drug.

Risk factormodification

Counsel the patient regarding smokingcessation.Monitor blood pressure if hypertensive.

Ensure good blood glucose control ifdiabetic.

Diet recommendation Salt restriction.Avoid excessive fluid intake.Modest intake of alcoholMonitor and prevent malnutrition

Exercise

recommendation

Be reassured, comfortable about physical

activityUnderstand the benefits of exercise.

Sexual activity Discuss problems with healthcareprofessionals.Be reassured about engaging in sex andunderstand specific sexual problems andvarious coping strategies.

Immunization Receive immunization against infectionssuch as influenza and pneumococcaldisease



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self-adjustment of their diuretic dose based on daily weightmeasurements and other clinical signs of fluid retention.

Angiotension Converting Enzyme Inhibitors (ACEi)

Unless contraindicated or not tolerated, all patients with

symptomatic heart failure or asymptomatic left ventriculardysfunction should receive an ACEi. Angiotension convert-ing enzyme inhibitors reduce morbidity (improve symptoms,exercise tolerance, quality of life and reduce the need forhospitalisation) and mortality and may improve or at leastprevent further deterioration of ventricular function. Themain concern relating to ACE-inhibitors is deterioration in

renal function and hyperkalaemia. This may or may not be inthe presence of renal artery stenosis. Some rise in urea andcreatinine (up to 10 %) is expected and should not causeconcern. An increase of ≤50 % from baseline or to an abso-lute concentration of 265 μmol/l, whichever is lower, isacceptable. If creatinine rises to >265μmol/l but is


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Heart failure confirmed

Commence ACEi/BB &

loop diuretic

Titrate BB to HR & BP

Titrate ACEi to BP

(ARB if ACEi not tolerated)

Still NYHA II-IV

Still NYHA II-IV

Still NYHA II-IV

• Ivabradline (if in SR, EF ≤ 35 %)• Digoxin• ARB (if ACEi or MRA not tolerated)

a

• Hydralzine & nitrate (especially if

Afro-Caribbean)b

Still NYHA II-IV & EF ≤ 35 %

No further treatment required

QRS duration ≥ 120 ms

Consider LVAD or

TransplantationConsider

CRT-P/CRT-D Consider ICDc

Consider:

YES NO

NOYES

Specialist

assessment

Rapid deterioration

despite therapy

YES NO

YES

YES

NO

NO

Add mineralocorticoid antagonist (MRA)

Figure 2.4 Algorithm to the management of heart failure (Adaptedfrom ESC 2012 Acute and Chronic Heart Failure guidelines – EurHeart J. 2012;33:1787–1847). a If mineralocorticoid receptor antago-nist not tolerated, an ARB may be added to an ACE inhibitor as an

alternative. b The combination of hydralazine and isosorbide dini-trate may also be considered earlier in patients unable to tolerate anACE inhibitor or an ARB. c ICD is not indicated for NYHAIV. Asymptomatic patients with an LVEF ≤35 % and a history ofmyocardial infarction should be considered for an ICD



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halve the dose of ACEi and monitor biochemistry. If creati-nine rises to ≥310 μmol/l, stop ACEi and monitor biochemis-

try. In case of hyperkalaemia, if potassium rises to >5.5 mmol/l,halve the dose of ACEi and monitor biochemistry. If howeverthe potassium rises to >6.0 mmol/l, stop the ACEi and review.Ensure that the patient is not on any other nephrotoxic drugsor drugs that could exacerbate hyperkalaemia.

A potentially life threatening side effect is the develop-ment of angioedema, but that occurs in only 0.1–0.7 % ofindividuals and usually resolves on discontinuation. Finally,

dry cough and hypotension may limit the drug’s utility.

Contraindications to ACEi

• history of angioedema• bilateral renal artery stenosis• serum creatinine >220 μmol/l

• severe aortic valve stenosis

Initiation of ACEi

Below is a simple guide on how to initiate and titrate ACEi

• check renal function and serum electrolytes.• start with a low dose and re-check renal function and

serum electrolytes within 1–2 weeks of commencing thetreatment.

• consider dose up-titration at 2–4 week intervals and re-check renal function and serum electrolytes within 1–2weeks of dose up-titration.

• more rapid dose up-titration can be carried out but closesupervision is required.

• once maintenance dose has been achieved re-check renalfunction and serum electrolytes at 1, 3, 6 months and 6monthly thereafter.

• aim for evidence-based target dose or the maximum toler-ated dose (in practical terms this is highest dose that BPwill allow).



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Angiotensin II Receptor Blockers

Angiotensin II receptor blockers (ARBs) should be used inpatients with heart failure or asymptomatic left ventricularsystolic dysfunction when an ACE-inhibitor is not tolerated(usually due to cough). As with ACE-inhibitors, ARBs reducemorbidity and mortality in

common cardiovascular dis

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