Cardiac arrhythmias

S.M. Cobbe, A.D. McGavigan and A.C. Rankin

in Oxford Textbook of Medicine

Fifth edition

Published on behalf of Oxford University Press

Published in print May 2010 | ISBN: 9780199204854
Published online May 2010 | e-ISBN: 9780199570973 | DOI:

Series: Oxford Textbooks

Cardiac arrhythmias

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The term cardiac arrhythmia (or dysrhythmia) is used to describe an abnormality of cardiac rhythm of any type. The spectrum of cardiac arrhythmias ranges from innocent extrasystoles to immediately life-threatening conditions such as asystole or ventricular fibrillation.

The key to the successful diagnosis of cardiac arrhythmias is the systematic analysis of an ECG (see Chapter 16.3.1) of optimal quality obtained during the arrhythmia.

Continuous monitoring is necessary for identification when arrhythmias are intermittent. Ambulatory electrocardiographic recordings are of most value when they provide correlation between the patient’s symptoms and the cardiac rhythm at that moment. Alternative strategies for the detection of infrequent arrhythmias include the use of a patient-activated recorder, which is applied and activated during symptoms, or an external or implanted loop recorder.

More detailed investigation of cardiac arrhythmias is undertaken by invasive cardiac electrophysiological testing. Multipolar electrodes are inserted transvenously to record electrograms from the atrium, ventricle, His bundle, and commonly from the coronary sinus. Electrophysiological mapping is an essential part of radiofrequency ablation.


Bradycardia is defined as a ventricular rate of less than 60 beats/min. The principal indications for active intervention in bradycardia are symptomatic (disturbances of consciousness, fatigue, lethargy, dyspnoea, or bradycardia-induced tachyarrhythmias) or prognostic (prevention of sudden cardiac death).

In the presence of haemodynamic compromise, immediate attempts to increase heart rate should be employed, using atropine, isoproterenol (isoprenaline), and/or temporary cardiac pacing (transvenous or transcutaneous). Following stabilization, factors causing or contributing to the presentation should be sought and corrected—especially, acute ischaemia and infarction, concomitant drug therapy, or electrolyte disorders.

Specific disorders causing bradycardia include (1) sinoatrial disease (‘sick sinus syndrome’); (2) neurocardiogenic syncope (e.g. carotid sinus hypersensitivity); and (3) atrioventricular (AV) conduction disorders (‘heart block’).

AV block—the commonest cause of AV block is idiopathic fibrosis of the His–Purkinje system, and the severity (degree) of block can be classified as (1) first-degree—defined as a PR interval greater than 0.2 s, which produces no symptoms and does not require treatment; (2) second-degree—when there is intermittent failure of conduction from atrium to ventricle, either with (Mobitz type I, Wenckebach) or without (Mobitz type II) a characteristic pattern of increasing PR-interval duration preceding the nonconducted P wave; pacemaker implantation is not necessary for type I in most cases, but is required for type II; (3) third-degree (complete) AV block—when there is complete dissociation between atrial and ventricular activity, which is an indication for permanent pacemaker implantation, except in the context of an acutely reversible condition.


The principal mechanisms responsible for tachyarrhythmias are (1) abnormal automaticity; (2) triggered activity; or (3) re-entry. Most clinically important sustained tachycardias appear to arise on the basis of re-entry, which requires the presence of a potential circuit comprising two limbs with different refractoriness and conduction properties.

The first and most important step in the diagnosis and management of tachycardias is to determine whether the arrhythmia arises within the atria and/or AV junction, or from the ventricles, which can often be achieved by careful analysis of a 12-lead ECG.

Diagnosis—it is safe to assume that virtually all narrow-complex tachycardias have a supraventricular origin, but wide-complex tachycardias (QRS duration ≥0.12 s) may arise either from the ventricle or from supraventricular mechanisms, and few areas in cardiology cause more difficulty—or result in more mismanagement—than the diagnosis of wide-complex tachycardias. Careful scrutiny of the 12-lead ECG may reveal diagnostic features, but the commonest reason for error is that the clinical context is not considered, or erroneous conclusions are drawn from it: key issues to recognize are (1) elderly patients or those with a history of ischaemic heart disease are most likely to have ventricular arrhythmia; (2) the patient’s haemodynamic status is a poor predictor of the type of tachycardia; (3) ventricular tachycardia can present with a history of paroxysmal self-terminating episodes.

Treatment—R-wave synchronized, direct-current (DC) cardioversion under general anaesthesia or deep sedation is the most effective and immediate means of terminating sustained tachycardias, and should be employed when tachycardia is associated with haemodynamic compromise. In patients with tachycardia who are haemodynamically stable, manoeuvres that produce transient vagal stimulation, such as the Valsalva manoeuvre or carotid sinus massage, may be employed. The response to intravenous adenosine, which will often terminate arrhythmias dependent on the AV node, may be of therapeutic or diagnostic value, and should be considered in all patients with tolerated regular tachycardia. In the long term, tachycardias can be treated with antiarrhythmic drugs (usefully categorized by the Vaughan Williams classification), implantable cardioverter–defibrillators (ICDs), radiofrequency ablation, or arrhythmia surgery.

Atrial fibrillation

Cardioversion—if it is clinically appropriate to attempt cardioversion, the drugs of choice are the class Ic agents (e.g. flecainide) for patients without significant underlying heart disease; class III drugs are somewhat less effective but are safer in the presence of left ventricular dysfunction or ischaemic heart disease (e.g. sotalol or amiodarone). Normally, only one drug should be tried in any individual patient: if drug therapy fails, DC cardioversion is commonly effective.

Risk of thromboembolism—because atrial fibrillation is a risk factor for the development of intracardiac thrombus formation, cardioversion—by chemical or electrical means—should not be attempted if arrhythmia has been present for longer than 48 h. Anticoagulation plus rate control with a β-blocker, calcium-channel blocker, or digoxin should be considered in these circumstances. Prophylaxis against thromboembolism should be considered in all patients with atrial fibrillation.

Paroxysmal atrial fibrillation—drug therapy may not be necessary for patients with infrequent paroxysms, or a ‘pill-in-the-pocket’ approach can be used in those without structural heart disease, whereby they take a dose of an antiarrhythmic drug after the onset of arrhythmia. No drug is entirely satisfactory for recurrent paroxysmal atrial fibrillation: a β-blocker is often prescribed as first-line therapy.

Persistent atrial fibrillation—usually requires electrical cardioversion to achieve sinus rhythm and has a high recurrence rate even after successful cardioversion. The key decision is whether to employ a rhythm or rate-control strategy. In general, a rate-control strategy (AV nodal blocking drug, e.g. β-blocker, calcium channel blocker, or digoxin) should be employed in patients with few or minor symptoms, elderly patients, and those with contraindications to antiarrhythmic therapy or cardioversion. A rhythm-control strategy (elective cardioversion) may be best in more severely symptomatic or younger patients, or in those with atrial fibrillation due to a treated precipitant.

Atrial flutter

It is important to attempt to terminate atrial flutter since the ventricular rate is often poorly controlled by AV nodal blocking drugs: this may be achieved by chemical or electrical cardioversion. Prophylaxis against thromboembolism should be given as for atrial fibrillation.

Supraventricular tachycardias

The term supraventricular tachycardia (also called junctional re-entry tachycardia) is commonly reserved for those in which the AV node is an obligate part of a re-entry circuit—AV nodal re-entrant tachycardia (AVNRT) or AV re-entry tachycardia (AVRT).

Termination of an attack of AV nodal re-entrant tachyxardia is achieved by producing transient AV nodal block by vagotonic manoeuvres, adenosine or by verapamil. Drug prophylaxis is undertaken with β-blockers, a combined β-blocker/class III agent such as sotalol, or AV nodal blocking drugs such as verapamil or digoxin. Curative treatment is by radiofrequency ablation.

Attacks of AV re-entry tachycardia are treated in the same way as is AV nodal re-entrant tachycardia. Antiarrhythmic prophylaxis may be effective, but radiofrequency ablation offers high success rates with low incidence of complications and should be considered early.

Pre-excitation syndromes

The term ‘pre-excitation’ refers to the premature activation of the ventricle via one or more accessory pathways that bypass the normal AV node and His–Purkinje system. The commonest type is Wolff–Parkinson–White (WPW) syndrome, where a δ-wave is characteristically seen on the ECG, and the main prognostic concern is pre-excited atrial fibrillation, which can be very rapid and degenerate into ventricular fibrillation. Patients with symptomatic WPW syndrome should be offered radiofrequency ablation as first-line therapy.

Ventricular tachycardia

Ventricular tachycardia normally occurs in individuals with overt heart disease, but is also seen in young and apparently healthy subjects, when occult cardiac disease or cardiac genetic syndromes should be considered.

Sustained ventricular tachycardia is a medical emergency. Immediate DC cardioversion is necessary if the patient is hypotensive; haemodynamically tolerated VT may be terminated pharmacologically, with intravenous lidocaine (lignocaine) or sotalol being the usual first-choice options. Unless there is a clear precipitating factor, the risk of sudden death is high and patients should be considered for an implantable cardioverter-defibrillator.

Polymorphic ventricular tachycardia, of which torsades de pointes is a well-recognized type associated with acquired or congenital prolongation of the QT interval, is an unstable rhythm with varying QRS morphology that undergoes spontaneous termination or degenerates into ventricular fibrillation. In patients with this condition, it is essential to discontinue predisposing drugs or other agents and to avoid empirical antiarrhythmic drug therapy. Intravenous magnesium sulphate is a safe and effective emergency measure.

Ventricular fibrillation

The management of cardiac arrest due to ventricular fibrillation is discussed in Chapter 17.1. Patients who survive an episode should be assessed carefully to determine the risk of recurrence and may require an implantable cardioverter-defibrillator or antiarrhythmic therapy as for patients with ventricular tachycardia.

Genetic syndromes

The congenital long-QT syndromes are inherited conditions due to mutations in genes encoding ion-channel proteins: their prognosis, if untreated, is poor. β-Blockers are highly effective in the commonest form of the condition.

The Brugada syndrome is an autosomal dominant condition where there is an unusual pattern of variable ST-segment elevation and partial right bundle branch block in the right precordial leads, associated with a risk of polymorphic ventricular tachycardia and sudden death. Patients with congenital long QT or Brugada syndrome considered at high risk of sudden death should be considered for an implantable cardioverter-defibrillator.

Chapter.  19921 words.  Illustrated.

Subjects: Cardiovascular Medicine

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