Rapid Cardiac Care E-Book

Emma Menzies-Gow

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

Seitenzahl: 149

Veröffentlichungsjahr: 2017

Beschreibung

Rapid Cardiac Care is an indispensable resource for all frontline staff working with acutely ill patients. Offering easy access to the knowledge base needed to provide rapid, safe and effective cardiac care, it is ideal for newly qualified healthcare professionals including, nurses, paramedics, cardiac technicians, junior medics, and physiotherapists. Key features include: * Essential information to support the assessment of the cardiac patient including focused history taking and physical assessment, rhythm interpretation and 12-lead ECG assessment * Practical guidance on how to care for patients with cardiac emergencies, including acute coronary syndromes, arrhythmias, heart failure and cardiac arrest * A quick reference A-Z section that explores a wide range of conditions affecting the heart, each with a comprehensive overview of patient presentation and strategies to guide patient assessment and management * Diagrams and images are provided to facilitate learning

Leseprobe

Table of Contents

Cover

Title Page

List of Abbreviations

Preface

Acknowledgements

Part 1: Cardiac Anatomy and Physiology

Anatomy

Cardiac cycle

Cardiac conduction system

Coronary circulation

Part 2: Rapid Cardiac Assessment

Introduction

Cardiac history taking

Physical examination

Cardiac monitoring

Rapid rhythm recognition

Cardiac investigations

Part 3: Rapid 12-lead ECG Interpretation

Introduction

Cardiac vectors and axis

Rapid ECG analysis tool

Rate and rhythm assessment

QRS axis calculation

Pre-excitation syndromes

Bundle branch block and fascicular block

Myocardial ischaemia or infarction

Other abnormalities seen on the 12-lead ECG

Part 4: Cardiac Conditions A–Z

Acute coronary syndromes

Acute coronary syndromes: treatment and interventions

Acute heart failure

Aortic aneurysm

Aortic dissection

Aortic regurgitation

Aortic stenosis

Arrhythmogenic right ventricular cardiomyopathy

Atrial fibrillation

Atrial flutter

Brugada syndrome

Cardiac arrest

Cardiac arrhythmias: treatment and interventions

Cardiogenic shock

Dilated cardiomyopathy

Heart blocks

Hypertension

Hypertrophic cardiomyopathy

Infective endocarditis

Long QT syndrome

Marfan syndrome

Mitral regurgitation

Mitral stenosis

Myocarditis

Pericarditis

Supraventricular tachycardia

Takotsubo cardiomyopathy

Ventricular tachycardia

Wolff-Parkinson-White syndrome (Pre-excitation syndrome)

Index

End User License Agreement

List of Tables

Chapter 3

Table 3.1 Causes of axis deviation

Table 3.2 Possible complications due to 12-lead ECG changes

List of Illustrations

Chapter 1

Figure 1.1 Cardiac anatomy.

Figure 1.2 Cardiac conduction system.

Figure 1.3 Coronary circulation.

Chapter 2

Figure 2.1 Cardiac auscultation landmarks.

Figure 2.2 5-lead cardiac monitoring.

Figure 2.3 Normal ECG waveforms and sinus rhythm (lead II).

Chapter 3

Figure 3.1 Orientation of the 12 ECG leads.

Figure 3.2 Hexaxial reference system showing four quadrants – normal, left, right and indeterminate axis.

Figure 3.3 WPW pattern.

Figure 3.4 rSR’ pattern associated with RBBB as seen in V

1

.

Figure 3.5 QS pattern associated with LBBB as seen in V

1

.

Figure 3.6a ST elevation.

Figure 3.6b ST depression.

Figure 3.6c T wave inversion.

Chapter 12

Figure 12.1 Atrial fibrillation (AF) as seen in lead II.

Chapter 13

Figure 13.1 Atrial flutter.

Chapter 14

Figure 14.1 Brugada Sign: down-sloping ST elevation with right bundle branch block pattern (V

1

).

Chapter 15

Figure 15.1 The Chain of Survival.

Chapter 19

Figure 19.1 1st degree AV block.

Figure 19.2 2nd degree AV block Mobitz Type I (Wenckebach).

Figure 19.3 2nd degree AV block Mobitz Type II.

Figure 19.4 3rd degree (complete) AV block.

Chapter 23

Figure 23.1 Torsades de Pointes.

Chapter 29

Figure 29.1 Supraventricular tachycardia (SVT).

Figure 29.2 WPW pattern.

Chapter 31

Figure 31.1 Ventricular tachycardia.

Chapter 32

Figure 32.1 Characteristic ECG findings associated with WPW.

Guide

Cover

Table of Contents

Begin Reading

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Rapid Cardiac Care

Emma Menzies-Gow

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

Christine Spiers

Principal Lecturer – Cardiac CareSchool of Health Sciences, University of Brighton, UK

This edition first published 2018 © 2018 by John Wiley & Sons Ltd

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Library of Congress Cataloging-in-Publication Data

Names: Menzies-Gow, Emma, author. | Spiers, Christine, author.Title: Rapid cardiac care / by Emma Menzies-Gow, Christine Spiers.Description: Hoboken, NJ : Wiley, 2017. | Includes index. |Identifiers: LCCN 2017030441 (print) | LCCN 2017030987 (ebook) | ISBN 9781119220282 (pdf) | ISBN 9781119220343 (epub) | ISBN 9781119220275 (paper)Subjects: | MESH: Cardiovascular Diseases–therapy | Acute Disease–therapy | Cardiovascular Diseases–diagnosis | Diagnostic Techniques, CardiovascularClassification: LCC RC667 (ebook) | LCC RC667 (print) | NLM WG 166 | DDC 616.1–dc23LC record available at https://lccn.loc.gov/2017030441

Cover Design: WileyCover Image: © Caiaimage/Sam Edwards/Gettyimages

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 1Cardiac Anatomy and Physiology

1Anatomy

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.

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.

Cardiac conduction system

The cardiac conduction system lies beneath the endocardium within the myocardium and consists of specialised myocytes responsible for generating and transmitting an impulse across the heart (Figure 1.2). The sino-atrial (SA) node, located on the posterior wall of the right atrium, is the primary pacemaker of the heart and therefore determines heart rate. It is capable of regular spontaneous depolarisation without external stimulus. However, the autonomic nervous system controls the SA nodal firing rate, permitting heart rate variability in response to fluctuating metabolic demand. Increased sympathetic activity will cause an increase in the SA nodal firing rate, for example during exercise. The heart rate is slowed via the vagus nerve, part of the parasympathetic nervous system.

Figure 1.2 Cardiac conduction system.