Cover Page

Rapid Cardiac Care

Emma Menzies-Gow

Senior Lecturer – Cardiac Care
Kingston University and St George’s, University of London, UK

Christine Spiers

Principal Lecturer – Cardiac Care
School of Health Sciences, University of Brighton, UK





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Dedication

Heidi Simpson (née Clinton)

This book is dedicated to our much loved friend Heidi, an outstanding nurse whose contribution to healthcare education has influenced the clinical practice of many nurses and practitioners working in acute and intensive care

List of Abbreviations

ABGs
Arterial blood gases
ACE-I
Angiotensin-converting-enzyme inhibitors
ACLS
Advanced Cardiac Life Support
ACS
Acute coronary syndromes
AED
Automated external defibrillator
AF
Atrial fibrillation
ALP
Alkaline phosphatase
ALT
Alanine transaminase
APTT
Activated partial thromboplastin time
ARB
Angiotensin receptor blocker
ARVC
Arrhythmogenic right ventricular cardiomyopathy
AS
Aortic stenosis
AST
Aspartate transaminase
AV
Atrio-ventricular
AVNRT
A-V nodal re-entry tachycardia
AVRT
A-V re-entry tachycardia
BBB
Bundle branch block
BNP
B-type natriuretic peptides
BP
Blood pressure
bpm
beats per minute
CCBs
Calcium channel blockers
CK-MB
Creatinine kinase myocardial isoenzyme
CMR
Cardiac magnetic resonance
COPD
Chronic obstructive pulmonary disease
CPAP
Continuous positive airway pressure
CPR
Cardiopulmonary resuscitation
CRP
C-reactive protein
CRT
Cardiac resynchronisation therapy
CRT-D
Cardiac resynchronisation therapy – defibrillator
CRT-P
Cardiac resynchronisation therapy – pacemaker
CT
Computed tomography
CXR
Chest X-ray
DCCV
Direct current cardioversion
DCM
Dilated cardiomyopathy
ECG
Electrocardiogram
EDV
end diastolic volume
eGFR
Estimated glomerular filtration rate
ESR
Erythrocyte sedimentation rate
FBC
Full blood count
GTN
Glyceryl trinitrate
HbA1c
Glycated haemoglobin
HCM
Hypertrophic cardiomyopathy
HF
Heart failure
HF-PEF
Heart failure with Preserved Ejection Fraction
HF-REF
Heart failure with Reduced Ejection Fraction
ICD
Implantable cardioverter defibrillator
IE
Infective endocarditis
JVD
Jugular venous distension
LAD
Left anterior descending coronary artery
LAFB
Left anterior fascicular block
LBB
Left bundle branch
LBBB
Left bundle branch block
LCx
Left circumflex
LDL
Low-density lipoproteins
LMWH
Low molecular weight heparin
LPFB
Left posterior fascicular block
LQTS
Long QT syndrome
LV
Left ventricle
LVEDP
Left ventricular end diastolic pressure
LVEDV
Left ventricular end diastolic volume
LVF
Left ventricular failure
LVH
Left ventricular hypertrophy
LVOT
Left ventricular outflow tract
mV
millivolts
MR
Mitral regurgitation
NOAC
Non-vitamin K oral anti-coagulant
NSAIDs
Non-steroidal anti-inflammatory drugs
NSTEMI
Non ST-segment elevation myocardial infarction
NT-proBNP
N-terminal prohormone of brain natriuretic peptide
NYHA
New York Heart Association
PA
Posterior-anterior
P-PCI
Primary percutaneous coronary intervention
PCI
Percutaneous coronary intervention
PDA
Posterior descending artery
PEA
Pulseless electrical activity
PMH
Past medical history
PVCs
Premature ventricular contractions
QTc
Corrected QT
RAAS
Renin-angiotensin-aldosterone system
RBB
Right bundle branch
RBBB
Right bundle branch block
RCA
Right coronary artery
RV
Right ventricle
RVH
Right ventricular hypertrophy
RVOT
Right ventricular outflow tract
SA
Sino-atrial (node)
SCN5A
Sodium channel gene 5A
STEMI
ST-segment elevation myocardial infarction
SVT
Supraventricular tachycardia
TAVI
Transcutaneous aortic valve implantation
TEVAR
Thoracic endovascular aortic repair
TOE
Trans-oesophageal echocardiogram
TC
Takotsubo cardiomyopathy
TOE
Transoesophageal echocardiogram
TTE
Trans-thoracic echocardiogram
UA
Unstable angina
U&E
Urea and electrolytes
UFH
Unfractionated heparin
VF
Ventricular fibrillation
VT
Ventricular tachycardia
WPW
Wolff-Parkinson-White

Preface

Many cardiac conditions present suddenly, requiring a rapid response from healthcare practitioners. ‘Rapid Cardiac Care' provides a concise text to guide the assessment and management of patients experiencing a variety of cardiac conditions. A systematic approach has been used to structure your assessment of the patient data and to prioritise management interventions. An overview of cardiac anatomy and physiology precedes sections on cardiac assessment, investigations, history taking, physical examination, symptom review and cardiac rhythm evaluation. The 12-lead ECG is a pivotal investigation in the evaluation of many cardiac conditions and therefore a tool to guide rapid interpretation is also provided. The care of patients with a range of cardiac conditions is presented in an A–Z format, which will direct the reader straight to the relevant sections.

Acknowledgements

We would like to thank the team at Wiley for their assistance throughout the production of this book.

Sincere thanks are extended to our families, for their constant support, patience and encouragement. We would especially like to acknowledge our fathers who influenced our lives immensely.

Part 1
Cardiac Anatomy and Physiology

1
Anatomy

The heart is a cone-shaped, muscular organ with four chambers that propel blood through the circulatory system (Figure 1.1). The two upper chambers, the atria, and the ventricles below are separated by the annulus fibrosus (AV ring), a layer of connective tissue that forms the cardiac skeleton, seen on the external surface of the heart as the atrio-ventricular (AV) groove. The mitral and tricuspid (AV) valves and aortic and pulmonary (semilunar) valves form part of the AV ring. Each valve consists of two or three cusps arising from an annulus. Healthy valves maintain forward blood flow through the heart, opening and closing in response to changes in pressure between the chambers. The interatrial septum separates the two atria; the ventricles are separated by the interventricular septum, which is visible on the outside of the heart as anterior-posterior interventricular groove.

Schematic of the heart with lines pointing at its parts labeled superior vena cava, aorta, pulmonary artery, right atrium, left atrium, mitral valve, aortic valve, pulmonary valve, tricuspid valve, etc.

Figure 1.1 Cardiac anatomy.

The heart wall is formed from three layers of tissue that provide different functions. The external layer is the pericardium, which surrounds the heart and the roots of the aorta and pulmonary arterial trunk. It consists of two distinct layers: the outermost fibrous layer and serous layer beneath. The serous pericardium has a visceral layer, known as the epicardium, which surrounds the myocardium and doubles back on itself to form the parietal pericardium, which lines the tough, outer fibrous layer. The space between the two layers contains a small volume of fluid to reduce friction during myocardial contraction. The central, thickest layer of the heart wall is the myocardium. It contains clusters of cardiac muscle cells known as myocytes, each surrounded by connective tissue and a network of capillaries. The internal surface of the heart is lined with a single, continuous layer of endothelial cells known as the endocardium. This facilitates smooth blood flow through the chambers and across the valves and provides some protection from the formation of thrombi.

Cardiac cycle

Cardiac output is the volume of blood ejected from the left ventricle (LV) in one minute, i.e. heart rate × stroke volume. It is approximately 4–7 L/min. The cardiac conduction system controls heart rate variability and co-ordinated systolic (contraction) and diastolic (relaxation and filling) activity of the cardiac chambers to maximise cardiac output.

The superior and inferior vena cava empty into the right atrium, enabling the return of deoxygenated blood to the heart. The coronary sinus, a large cardiac vein, also drains deoxygenated blood from the myocardium into the right atrium. The tricuspid valve opens to permit blood to enter the right ventricle (RV); atrial contraction provides extra force to expel blood from the chamber, known as the ‘atrial kick’, to optimise the end diastolic volume (EDV) of the ventricles.

During systole, the three papillary muscles in the RV contract, tightening the chordae tendineae, attached to the cusps of the tricuspid valve to ensure the valve leaflets remain closed, preventing regurgitation of blood into the right atrium. Pressure within the RV will rise until it exceeds the pressure within the pulmonary circulation beyond, forcing the pulmonary valve to open and blood to flow into the pulmonary arterial trunk. During ventricular diastole, the pulmonary arteries will rapidly recoil to enable blood to fall back towards the RV, closing the pulmonary valve.

Having completed gaseous exchange within the alveoli and pulmonary capillaries, oxygenated blood returns to the left atrium via four pulmonary veins. The increase in pressure within the atrial chamber forces the mitral valve to open and ventricular filling to begin. During diastole, the ventricular myocytes will stretch to accommodate the volume of blood, which directly correlates with the force of contraction that occurs during systolic contraction (Frank Starling’s Law). The two papillary muscles contract first, once systole begins, tightening the chordae tendineae attached to the two cusps of the mitral valve to prevent regurgitation. The LV and septum then contract to increase the pressure (preload) within the LV. Once the preload pressure exceeds the pressure in the aorta beyond the aortic valve (afterload), blood will leave the LV, referred to as the stroke volume, crossing the aortic valve into the aorta to supply the arterial circulation. The term ‘ejection fraction’ refers to the stroke volume as a percentage of the left ventricular EDV (LVEDV), usually approximately 60–70% at rest. As systole ends, diastole begins again and a small volume of blood in the aorta will return towards the LV, closing the aortic valve cusps and simultaneously perfusing the coronary arteries originating at the aortic root.