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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: ABC Series
- Sprache: Englisch
ABC of Resuscitation is a practical, illustrated guide to the latest resuscitation advice for the non-specialist and provides the core knowledge on the treatment of cardiopulmonary arrest.
This edition provides a guide to the European Resuscitation Council Guidelines for Resuscitation 2010 and the Resuscitation Council (UK) 2010 Resuscitation Guidelines.
It Includes:
- the causes and prevention of cardiac arrest
- basic and advanced life support for adults, children and newborns
- resuscitation in a range of contexts (in-hospital and out-of-hospital, including drowning, pregnancy, sport and trauma)
- important aspects of implementation of guidelines including human factors and education
ABC of Resuscitation, 6th Edition is ideal for all healthcare professionals including junior doctors, medical students, general practitioners, paramedics and nurses. It is also useful for pre-hospital care practitioners, emergency medicine trainees, resuscitation officers and all those who teach resuscitation.
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Seitenzahl: 286
Veröffentlichungsjahr: 2012
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Table of Contents
Series Page
Title Page
Copyright
List of Contributors
Foreword
Chapter 1: Cardiac Arrest and the Chain of Survival
Epidemiology of cardiac arrest
The chain of survival
Resuscitation guidelines
Further Reading
Chapter 2: Sudden Cardiac Death
Introduction
Causes of sudden cardiac death
How do people present?
Inherited cardiac conditions
Prevention of sudden cardiac death
Further Reading
Chapter 3: Causes and Prevention of Cardiac Arrest in Hospital
Introduction
Demographics of IHCA
Outcome following in-hospital cardiac arrest
Predisposing factors
Structuring systems to prevent patient deterioration and cardiac arrest in hospital
The role of ‘do not attempt cardiopulmonary resuscitation’ decisions in reducing the cardiac arrest rate in hospital
Suggested guidelines for the prevention of in-hospital cardiac arrest
Further Reading
Chapter 4: Basic Life Support
Introduction
Diagnosing cardiac arrest
Circulatory support
Ventilatory support
Adult basic life support sequence
Compression-only CPR
CPR in children
Further Reading
Chapter 5: Advanced Life Support
Introduction
ALS algorithm (Figure 5.1)
Post-resuscitation care
Stopping resuscitation and confirmation of death
Informing the next of kin following a failed resuscitation attempt
Further Reading
Chapter 6: Defibrillation
Introduction
Defibrillators
Factors influencing defibrillation
Safety
Internal defibrillation
Further Reading
Chapter 7: Airway Management and Ventilation
Introduction
Causes of airway obstruction
Recognition of airway obstruction
Basic techniques for opening the airway
Adjuncts to basic airway techniques
Oxygen
Ventilation
Supraglottic airway devices
Tracheal intubation
Cricothyroidotomy
Further Reading
Chapter 8: Post-Resuscitation Care
Introduction
The post-cardiac arrest syndrome
Optimising organ function
Prognostication
Organ donation
Further Reading
Chapter 9: Paediatric Resuscitation
Introduction
Paediatric basic life support
Automated external defibrillator (AED) use in children
Paediatric advanced life support
Parental presence
Choking
Further Reading
Chapter 10: Resuscitation at Birth
Introduction
Equipment and temperature control
Procedure at delivery
Resuscitation procedure
Pre-term babies
Further Reading
Chapter 11: -of-Hospital Resuscitation
Introduction
Emergency Medical System (EMS) response
EMS dispatch
Initial assessment
Pre-hospital interventions
Performance
National guidelines
Chain of survival
Termination of resuscitation attempts
Further Reading
Chapter 12: In-Hospital CPR
Introduction
Recognising cardiac arrest
Start resuscitation
Activate the emergency resuscitation team
Handover to the resuscitation team
Resuscitation team
Planning for the emergency response
Further Reading
Chapter 13: Peri-arrest Arrhythmias
Introduction
Adverse features
Tachyarrhythmia
Bradyarrhythmia
Acknowledgement
Further Reading
Chapter 14: Pacemakers and Implantable Cardioverter-Defibrillators
Introduction
Indications for pacing and ICDs
Methods of pacing
Concepts in pacing and internal cardiac defibrillation
Troubleshooting devices
Further Reading
Chapter 15: Cardiorespiratory Arrest in Advanced Pregnancy
Introduction
Physiological changes
Cardiopulmonary resuscitation guidelines 2010
Perimortem caesarean section
Maternal collapse
Other rare causes of maternal collapse and cardiopulmonary arrest
Maternal Early Warning Systems (MEWS)
Further Reading
Chapter 16: Drowning
Introduction
Definition
The need for oxygen
The drowning victim
Basic life support
Cervical spine injury
Defibrillation
Advanced life support
Hypothermia and drowning
Stopping CPR
Further Reading
Chapter 17: Trauma
Introduction
Airway management
Breathing
Circulation and haemorrhage control
Disability
Traumatic cardiac arrest
Further Reading
Chapter 18: Human Factors
Introduction
Nature of accidents
The error chain
Communication
Situation awareness
Summary
Further Reading
Chapter 19: CPR Devices
The importance of high-quality cardiopulmonary resuscitation
Cardiopulmonary resuscitation feedback and prompt devices
Mechanical chest compression devices
Active compression–decompression CPR
Impedance threshold device
Further Reading
Chapter 20: Resuscitation in Sport
Resuscitation in sport
Non-traumatic cardiac arrest
Initial management of a collapsed athlete due to presumed cardiac cause
Cardiac arrest associated with trauma in sport
Summary
Further Reading
Chapter 21: Improving Outcomes from Cardiac Arrest: Quality, Education and Implementation
Introduction
Measuring patient outcomes
Patient safety incident reporting
Education and implementation
Further Reading
Chapter 22: Decisions Relating to Resuscitation
Introduction
Ethical principles
When are decisions about CPR appropriate?
Communication
Further Reading
Index
This edition first published 2013, © 2013 by John Wiley & Sons, Ltd.
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Library of Congress Cataloging-in-Publication Data
ABC of resuscitation. – 6th ed. / [edited by] Jasmeet Soar, Gavin D. Perkins,
Jerry Nolan.
p. ; cm. – (ABC series)
Includes bibliographical references and index.
Summary: “This book is a practical guide to the latest resuscitation advice for the non-specialist, and covers the core knowledge on the management of patients with cardiopulmonary arrest”–Provided by publisher.
ISBN 978-0-470-67259-4 (pbk.)
I. Soar, Jasmeet. II. Perkins, Gavin D. III. Nolan, Jerry. IV. Series: ABC series (Malden, Mass.)
[DNLM: 1. Cardiopulmonary Resuscitation. WA 292]
616.1–dc23
2012027833
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Cover image: Cover photograph reproduced with kind permission by Michael Scott and the Resuscitation Council (UK).
Cover design by: Meaden Creative
List of Contributors
Foreword
The birth of modern emergency first aid for cardiac arrest can be dated to the recognition that the newly described effective artificial ventilation together with chest compressions were ‘parts of a whole and complete approach to resuscitation’. This occurred at a celebrated meeting of the pioneers of these techniques in 1960. By then, external defibrillators were also available. All that was needed was widespread dissemination of the necessary skills to permit the successful treatment of cardiac arrest to become an everyday reality. An international meeting to that end was held during the following year in Stavanger. At that time, chest compression was to be practised only by ‘medical personnel, nurses, and recognised life savers’. Progress thereafter was inevitably slow. Guidelines for public use were first published in the USA in 1974, whilst in the UK a stimulus for healthcare professionals was provided by a series of articles published in the British Medical Journal during 1986 under the banner of ‘The ABC of Resuscitation’. These were put together for the first edition of the booklet under that very apt name published at the end of the same year. The appearance now of a sixth edition attests its importance. It is based on the 2010 Guidelines of the Resuscitation Council (UK), has been prepared by the experts responsible for them and is greatly to be welcomed.
The booklet is not intended for the general public but rather for junior doctors, medical students, general practitioners, nurses and other healthcare professionals. There will be few healthcare professionals even with a major interest in resuscitation who will not benefit from its broad scope and the strong emphasis on key points. These are presented succinctly with commendable clarity that is aided by helpful illustrations. The 22 chapters include epidemiology, prevention, aetiology, clinical presentations, immediate managements, aftercare, devices, quality and ethics, all covering many situations through different ages from the newborn to adults.
Although all healthcare professionals do now receive training in resuscitation—and generally feel committed to good quality care—the skills are not easy to master. This is most true of chest compression which is performed to an excellent standard only rarely, as examination of tracings from real-time transmission or subsequent electronic downloads can attest. But it is not only compressions that are performed inadequately. All aspects of the prevention, management and aftercare of cardiac arrest suffer because they are practised infrequently, often in difficult environments, inevitably accompanied by anxiety and sometimes hindered by lack of confidence in the would-be rescuers. Constant revision of the principles and the details are needed if care is to be of a truly acceptable quality. No one strategy suffices to counter these difficulties but revision training, feedback and the ability readily to browse over the basics are all of paramount importance. The ABC of Resuscitation offers an excellent resource for the last of these requirements—as well as for initial training—to be valued by all who use it, and that will certainly include the writer of this Foreword.
Douglas ChamberlainJune 2012
Chapter 1
Cardiac Arrest and the Chain of Survival
Jasmeet Soar1, Gavin D. Perkins2, and Jerry Nolan3
1Southmead Hospital, North Bristol NHS Trust, Bristol, UK
2Warwick Medical School, University of Warwick, Coventry, UK
3Royal United Hospital, Bath, UK
OVERVIEW
Cardiovascular disease is the commonest cause of cardiac arrestEarly recognition of warning signs and a call for help can prevent cardiac arrestIf cardiac arrest occurs, immediate cardiopulmonary resuscitation (CPR) improves chances of survivalShockable cardiac arrest rhythms (ventricular fibrillation/pulseless ventricular tachycardia, VF/VT) are treated with attempted defibrillationNon-shockable rhythms (asystole and pulseless electrical activity (PEA)) are treated by identifying and treating the underlying cause.Post-cardiac arrest care in successfully resuscitated patients determines the final outcomeEpidemiology of cardiac arrest
In 2006, coronary heart disease accounted for 1 of every 6 deaths (a total of 425,425) in the United States and one-third of these deaths occurred within 1 h of symptom onset. In Europe, the annual incidence of emergency medical system (EMS)-treated, out-of-hospital cardiopulmonary arrest (OHCAs) for all rhythms is 40 per 100,000 population, with ventricular fibrillation (VF) arrest accounting for about one-third of these. However, data from recent studies indicate that the incidence of VF is declining: it was reported most recently as 23.7% among EMS-treated arrests of cardiac cause. Survival to hospital discharge is 8–10% for all-rhythm and around 21–27% for VF cardiac arrest; however, there is considerable regional variation in outcome.
The incidence of in-hospital cardiac arrest (IHCA) is difficult to assess because it is influenced heavily by factors such as the criteria for hospital admission and implementation of a Do Not Attempt Resuscitation (DNAR) policy. There are an estimated 200,000 treated IHCAs each year in the United States—approximately one per 1000 bed days. Of these patients undergoing CPR, 17.6% survive to hospital discharge and 13.6% have a favourable neurological outcome (Cerebral Performance Category (CPC) 1 or 2). Many patients sustaining an IHCA have significant comorbidity, which influences the initial rhythm and, in these cases, strategies to prevent cardiac arrest are particularly important.
The chain of survival
The key steps for improving survival are shown in the chain of survival (Figure 1.1).
Figure 1.1 Chain of survival.
Early recognition and call for help
Out-of-hospital, early recognition of the importance of chest pain will enable the victim or a bystander to call the EMS and the victim to receive treatment that may prevent cardiac arrest. In-hospital, early recognition of the deteriorating patient who is at risk of cardiac arrest and a call for the resuscitation team or medical emergency team (MET) will enable treatment to prevent cardiac arrest. If cardiac arrest occurs, early recognition and a call for help are essential. Agonal breathing (gasping) often occurs immediately after cardiac arrest and is often mistaken for a sign of life—this can cause delays in starting CPR.
Early CPR
If cardiac arrest occurs, the victim will be unconscious, unresponsive and not breathing or not breathing normally (agonal breathing). Cardiopulmonary resuscitation (CPR) with chest compressions and ventilation of the victim's lungs will slow the deterioration of the brain and heart. Bystander CPR doubles the chances of long-term survival. Interruptions to chest compressions must be minimised and should occur only briefly during defibrillation attempts and rhythm checks.
Early defibrillation
Ventricular fibrillation (VF) is the commonest initial rhythm after a primary cardiac arrest although this often deteriorates to a non-shockable rhythm by the time it is first monitored. Early defibrillation can be effective at restoring a circulation. Public Access Defibrillation (PAD) programs using automated external defibrillators (AEDs) enable a wide range of rescuers to treat OHCA caused by VF. Most IHCAs tend to have an initial rhythm of pulseless electrical activity (PEA) or asystole but most survivors are among those with VF arrest. Hospital staff should therefore be trained and authorised to use a defibrillator (AED or manual) to enable the first responder to a cardiac arrest to attempt defibrillation when indicated, without delay.
Post resuscitation care
Return of a spontaneous circulation (ROSC) is an important phase in the continuum of resuscitation; however, the ultimate goal is a patient with normal cerebral function, a stable cardiac rhythm and normal haemodynamic function, so that they can leave hospital in good health and at minimum risk of a further cardiac arrest. The quality of the treatment given in the post-cardiac arrest phase will influence outcome—there is considerable inter-hospital variation in outcome among patients admitted to an intensive care unit after cardiac arrest (Box 1.1).
Resuscitation guidelines
The Resuscitation Council (UK) (www.resus.org.uk) provides healthcare professionals and laypeople with evidence-based guidelines for all patient groups (adults, children, newborn) and all settings. The scientific evidence supporting these guidelines is reviewed every 5 years (most recently in 2010). The UK Guidelines are based on the European Resuscitation Council (www.erc.edu) Guidelines. The European Guidelines are in turn derived from the International Liaison Committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations (CoSTR). ILCOR (www.ilcor.org) therefore establishes the scientific evidence for the guidance and creates treatment recommendations (Figure 1.2).
Figure 1.2 Resuscitation guidelines development process.
Further Reading
Meaney PA, Nadkarni VM, Kern KB, et al. Rhythms and outcomes of adult in-hospital cardiac arrest. Crit Care Med 2010;38:101–8.
Merchant RM, Yang L, Becker LB, et al. Incidence of treated cardiac arrest in hospitalized patients in the United States. Crit Care Med 2011;39:2401–6.
Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA 2008;300:1423–31.
Nolan JP, Soar J, Zideman DA, et al. on behalf of the ERC Guidelines Writing Group. European Resuscitation Council Guidelines for Resuscitation 2010: Section 1. Executive summary. Resuscitation 2010;81:219–76.
Nolan JP, Hazinski MF, Billi JE, et al. Part 1: Executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation 2010 Oct;81(Suppl 1):e1–25.
Nolan J, Soar J, Eikeland H. The chain of survival. Resuscitation 2006;71:270–1.
Resuscitation Council (UK). Resuscitation Guidelines 2010. Available at http://www.resus.org.uk/pages/guide.htm.
Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes 2010;3:63–81.
Chapter 2
Sudden Cardiac Death
David Pitcher
University Hospital Birmingham, UK
OVERVIEW
SCD can occur at any age, but its frequency increases with increasing age and its causes vary with ageIschaemic heart disease is the commonest cause of SCD in people older than 35 yearsInherited conditions are more common in people below the age of 35Warning signs are often absent, but can include chest pain, shortness of breath and syncopeIdentification and treatment of the underlying condition under specialist guidance can prevent SCDIntroduction
Sudden cardiac death (SCD) is defined as ‘Natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of acute symptoms; pre-existing heart disease may have been known to have been present but the time and mode of death are unexpected’. In this chapter we shall consider causes of sudden cardiac death in adults, how to identify those at potential risk of sudden death, and what treatment options may prevent or reduce the risk of sudden death.
Causes of sudden cardiac death
Sudden cardiac death may occur at any age, but its frequency increases with age and its causes vary with age. Causes may be inherited or acquired (or a combination of both). Coronary atheroma and resulting ischaemic heart disease are the commonest cause of SCD in adults over the age of 35 but other, predominantly acquired, conditions can cause SCD in this age group. Inherited conditions are a less common cause in older adults but predominate as the cause of SCD in people below the age of 35. Table 2.1 lists some of the important causes.
Table 2.1 Some causes of sudden cardiac death.
Condition
Causes
Further detail
Long QT syndromes (LQTS)
Inherited (autosomal dominant) ion channel disorders Many different genotypes but types 1–3 are most common
Predispose to
torsade de pointes
VT and VF
Acquired QT interval prolongation
Drug therapy Ischaemic heart disease Myocarditis
Predisposes to
torsade de pointes
VT and VF
Brugada syndrome
Inherited (autosomal dominant) ion channel disorder
Occurs worldwide but more common in SE Asia. Risk of SCD higher in young males
Short QT syndrome (SQTS)
Rare, inherited (autosomal dominant) ion channel disorder
Predisposes to
torsade de pointes
VT and VF
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Rare, inherited (autosomal dominant) ion channel disorder
Predisposes to
torsade de pointes
VT and VF, especially on exercise
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Inherited (autosomal dominant)
Predisposes to VT and VF
Hypertrophic cardiomyopathy (HCM)
Inherited (autosomal dominant) Several different genotypes
SCD risk is due to VT and VF. Risk varies with genotype and with individual factors
Wolff–Parkinson–White (WPW) syndrome
Mostly sporadic Infrequent familial incidence
Not all WPW patients are at risk of SCD. Risk is due to rapid transmission of AF to the ventricles, triggering VT or VF
High-grade atrioventricular block
Conducting system fibrosis Calcific aortic stenosis Myocardial diseases including ischaemic heart disease Cardiac surgery Drug therapy Occasionally congenital
Predisposes to ventricular standstill (asystole). Some people with extreme bradycardia develop
torsade de pointes
VT and VF
Severe aortic stenosis
Congenital bicuspid valve (becomes severe at age 50–70 or younger) Degenerative (becomes severe in elderly patients)
If untreated may progress to heart failure or SCD, probably mostly due to VT or VF
Dilated cardiomyopathy
Probably multiple causes Familial in a minority of cases
Many develop progressive heart failure but there is risk of SCD due to VT or VF
Ischaemic heart disease due to coronary atheroma
Partly genetic, partly acquired
SCD risk is mainly due to VT or VF, which may be in response to acute ischaemia or infarction or may be due to previous myocardial scarring
Other myocardial diseases
Hypertensive heart disease, sarcoid heart disease, etc.
May predispose to ventricular arrhythmia or AVB in some patients
Anomalous coronary artery anatomy
Congenital
Rare cause of SCD in young people, often on exercise. Risk varies with the anomalous anatomical pattern
SCD = sudden cardiac death; VT = ventricular tachycardia; VF = ventricular fibrillation; AF = atrial fibrillation.
How do people present?
Sadly, many people present by dying suddenly; the first doctor to assess them is the coroner's pathologist. The autopsy is really important in this tragic situation, because it may provide information that will allow prevention of SCD in other family members. Some inherited conditions that predispose to SCD, such as hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC), may not be easy to confirm or exclude at a routine autopsy and detailed examination of hearts of SCD victims by an expert cardiac pathologist is recommended. When an autopsy identifies an inherited abnormality, there is an opportunity to screen family members to identify others at risk, in whom treatment may prevent SCD. When autopsy finds no abnormality to explain death, this is regarded as sudden adult death syndrome (SADS). This should always trigger consideration of whether or not there may have been a purely ‘electrical’ inherited cardiac condition that may be present in other family members.
Some people present with ‘failed sudden death’, when a person suffers cardiac arrest from which cardiopulmonary resuscitation (CPR) is successful. Increased public access to effective CPR and early defibrillation has increased the incidence of this situation. This provides an important opportunity to assess and offer preventative treatment to the survivor of the arrest and, when there is an inherited cause, to family members at risk. Healthcare professionals involved in successful resuscitation from cardiac arrest and in post-resuscitation care have a unique opportunity to identify individuals with a high risk of further cardiac arrest and those who have an inherited basis for cardiac arrest, with implications for family members.
Some people at risk of SCD experience warning symptoms. In people with severe coronary disease the warning symptom is likely to be angina or an acute coronary syndrome. In people with severe aortic stenosis it may be angina, breathlessness or syncope. People at risk of sudden death from cardiac arrhythmia may experience syncope. When someone presents after syncope, they should be assessed to identify features of common problems that do not carry a significant risk of death (such as uncomplicated faints) and to identify a small minority in whom syncope is the only prior warning of a life-threatening but treatable problem. This problem might be, for example, high-grade atrioventricular block (AVB), as shown in Figure 2.1, in which a pacemaker will protect against SCD, or an inherited cardiac condition predisposing to ventricular arrhythmia, requiring an implanted cardioverter-defibrillator (ICD) in some patients.
Figure 2.1 ECG showing broad-complex complete atrioventricular block.
Other modes of presentation are by screening or by chance identification of a potential risk. In addition to screening relatives of SCD or cardiac arrest victims, there is an increasing focus on screening participants in competitive sport to try to prevent sudden death on the sports field, and some people are found to have clinical evidence of structural heart disease or an ECG abnormality when being assessed for other reasons.
Inherited cardiac conditions
Although relatively uncommon as a cause of SCD, it is important that those providing CPR are aware of inherited cardiac conditions and are able to recognise those who may have them. They cause SCD by predisposing to sudden ventricular arrhythmia: ventricular tachycardia (VT), including torsade de pointes (Figure 2.2), and ventricular fibrillation (VF). Ion channel disorders such as long QT syndromes (LQTS), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT) and short QT syndrome occur without any structural heart disease; some of these can be identified from typical ECG features. An example of an ECG in LQTS is shown in Figure 2.3 and a typical Brugada syndrome ECG is shown in Figure 2.4. Some people with these conditions may have a normal resting ECG and diagnosis may require provocative testing, such as exercise testing or catecholamine challenge for CPVT or flecainide or ajmaline testing for Brugada syndrome.
Figure 2.2 ECG showing torsade de pointes ventricular tachycardia.
Figure 2.3 ECG showing prolonged QT interval in a patient with long QT syndrome.
Figure 2.4 ECG showing typical features of Brugada syndrome. Note the right bundle branch block morphology and unusual ST segment elevation in leads V1-V3.
Other inherited conditions involve abnormalities of cardiac structure and function. These include HCM and ARVC, and a minority of cases of dilated cardiomyopathy (DCM) also has a familial basis.
Consideration of genetic testing is appropriate when an inherited cardiac condition is identified in an individual. Patients who have been resuscitated from unexplained cardiac arrest or who have unexplained syncope should undergo specialist assessment in a unit with expertise in detecting and treating inherited cardiac conditions.
Prevention of sudden cardiac death
In some people, reducing risk of SCD requires avoidance of specific activities or circumstances that predispose to SCD.
In some this will mean abstaining from vigorous exercise. In most parts of the world, HCM is the commonest cause of SCD during sport (Figure 2.5). The exception is Italy, where pre-participation screening has been performed for many years, and people with HCM have not been permitted to engage in competitive sport. Although there is an ongoing debate regarding the optimal screening methods, increasing screening of sportspeople offers an opportunity to identify and protect those at highest risk; this will include those with other inherited cardiac conditions as well as HCM. When the ECG is used for screening, it should be interpreted by someone with expertise in distinguishing true abnormalities from features that represent physiological adaptation to high-level exercise training.
Figure 2.5 Echocardiogram showing an apical 4-chamber view from a patient with hypertrophic cardiomyopathy. He presented after a syncopal attack whilst running, was found to have features indicating a high risk of SCD, advised to refrain from vigorous exercise and to undergo ICD implantation. Note the very thick interventricular septum (normal up to 1.2 cm). IVS, interventricular septum; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
People with LQTS should avoid drugs that cause further QT prolongation (including amiodarone, which in a resuscitation setting would otherwise be used to treat VT) and avoid hypokalaemia (e.g. due to thiazide-like diuretics). The circumstances in which SCD occurs varies, depending on the underlying condition and by no means all are related to exercise. For example, in LQTS type 2, SCD may be triggered by a sudden noise (e.g. an alarm clock or fire alarm), whereas in LQTS type 3 and Brugada syndrome, SCD is more likely at rest, such as during sleep. Alterations of lifestyle or activity to reduce risk should be tailored to the specific condition in each individual.
Specific treatment will reduce risk of SCD in many of the situations outlined here.
Coronary atheroma and ischaemic heart disease
Detailed discussion of measures that may reduce progression of and risk of SCD from this condition is beyond the scope of this chapter. It is important to identify those at high risk of premature or severe coronary disease, such as those with familial dyslipidaemia, since early, effective treatment may prevent or delay development of severe, life-threatening coronary disease. In those with symptoms from coronary disease, prompt assessment and appropriate treatment can reduce the risk of SCD. This applies especially in those with acute ST-segment-elevation myocardial infarction in whom immediate reperfusion therapy and appropriate drug therapy will reduce the risk of future SCD, by minimising myocardial damage and resulting left ventricular impairment. The latest European guidance on both prevention and treatment of coronary disease can be accessed at www.escardio.org.
Heart failure and left ventricular systolic impairment
Detailed consideration of the treatment of heart failure is beyond the scope of this chapter. People who have experienced heart failure or who have substantial impairment of left ventricular systolic function are at increased risk of SCD; that risk can be minimised by appropriate treatment. For many that will involve optimal medical treatment, but for selected patients the use of an implanted device to provide cardiac resynchronisation therapy (biventricular pacing), with or without an ICD capability, will reduce further the risk of SCD. Patients with heart failure require risk assessment to determine the most appropriate treatment for each individual. The latest European guidance on treatment of heart failure can be accessed at www.escardio.org.
Long QT syndromes
In people with LQTS (especially types 1 and 2), treatment with a beta-adrenoceptor blocking drug will reduce SCD risk to a very low level. In some of these patients, SCD risk may also be reduced by pacemaker implantation.
Severe aortic stenosis
In people with severe aortic stenosis, the risk of SCD is reduced by valve replacement.
Atrio-ventricular block
In people with high-grade atrio-ventricular block (AVB), pacemaker implantation reduces the risk of SCD, so should be considered even in the absence of symptoms. Other causes of bradycardia (e.g. sinus node disease) are not associated with a high risk of SCD and the need for pacing is dictated by symptoms.
Wolff–Parkinson–White syndrome
Although a rare cause of SCD, this syndrome deserves mention. Some, but not all, patients with ventricular pre-excitation have an increased risk of SCD. This is believed to occur when atrial fibrillation (AF) develops and is transmitted rapidly to the ventricles via the accessory pathway, triggering VT and VF. People who present with pre-excited AF (Figure 2.6) with rapid heart rates are likely to be at risk in this way. Others with pre-excitation on their ECG in sinus rhythm (Figure 2.7) require risk assessment by electrophysiology studies. Radiofrequency ablation of the accessory pathway will prevent SCD due to AF in those at risk.
Figure 2.6
