Management Of Cardiac Arrhythmias

By | 2013-08-04

Abnormalities in the generation and / or the conduction of electrical impulses in the heart can give rise to an overall reduction in the heart rate (bradydysrhythmias) or a rapid heart rate (tachydysrhythinias). In both circumstances, cardiac function may be compromised. Slow rates (<50 bpm) lead to inadequate output despite a very large stroke volume and fast irregular rhythms lead to insufficient time for adequate filling of the heart during diastole, thus giving rise to low stroke volume. In addition, tachycardias which encroach on diastole will reduce the time for myocardial blood flow and lead to ischaemia of the heart muscle. In any situation where cardiac function is already compromised, the development of an arrhythmia will tend to lead to decompensation and result in clinical signs of heart failure. Severe arrhythmias may give rise to an acute decrease in cardiac output and poor perfusion of the brain leading to loss of consciousness (syncope). It is important to remember that the presence of a cardiac arrhythmia does not necessarily indicate a primary cardiac problem; it may be an indication of a number of systemic problems (for example electrolyte, neurological, gastrointestinal disorders and circulatory shock of non-cardiac origin).

In some circumstances, the underlying cause of the arrhythmia will be amenable to specific treatment or will be self-limiting and the arrhythmia will resolve without anti-arrhythmic drug treatment. In other cases, the effects of the arrhythmia may be life-threatening or the underlying cause cither cannot be diagnosed or is not amenable to treatment. Here, symptomatic anti-arrhythmic drug therapy is indicated. It is important to recognize those situations where cardiac arrhythmias may occur so that they can be detected early and the patient can be monitored to determine whether anti-arrhythmic therapy is necessary.

In the following discussion of the management of different cardiac arrhythmias, a brief overview of the possible underlying causes is given followed by practical decisions concerning therapy and the realistic goals of such therapy. The diagnostic electrocardiographic features of specific cardiac arrhythmias are described in site.



The sinus node can be driven by excessive stimulation of sympathetic tone to discharge at a rate which begins to compromise cardiac function leading to sinus tachycardia. Rapid heart rates may also result from abnormalities in automaticity and or conduction which lead to cardiac arrhythmias. Electrophysiological mechanisms involved in the pathogenesis of tachydysrhythmias include:

Ectopic foci, which reach threshold before the sinus nodal tissue causing premature beats or sustained tachycardia.

Afterdepolarizations, which occur in the repolarization phase of a normal beat (hence are described as triggered activity).

Re-entry which occurs when an electrical impulse circulates around a conduction pathway, exciting the rest of the heart each time it does. If the circulation of a re-entrant rhythm is continuous, a sustained ectopic rhythm will develop (for example atrial fibrillation). Intermittent circulation will lead to paroxysmal episodes of tachycardia.

A surface ECG does not distinguish which electrophysiological mechanism predominates in the arrhythmia but consideration of the cellular mechanisms responsible for arrhythmogenesis does enable an appreciation of the mechanism of action of antidysrhythmic drugs. Site shows a schematic diagram of the pathogenesis of tachydysrhythmias and the sites at which antidysrhythmic drugs act to suppress such arrhythmias. Hypoxic, damaged heart tissue has a less negative resting membrane potential and hence could reach threshold and fire more quickly than the sinoatrial node and so, potentially, could give rise to ectopic foci. Catecholamines will speed the rate at which the diastolic membrane potential drifts towards threshold and so can contribute to the generation of ectopic impulses. Triggered activity is thought to occur when cardiac muscle cells become overloaded with calcium in their cytoplasm. Hypoxia will reduce the efficiency with which calcium is extruded from the cytoplasm or pumped into intracellular stores. Drugs, such as digoxin, will lead to cellular overload with calcium, hence their arrhythmogenic potential. Conditions which favour re-entry include a long conduction pathway (stretched myocardium), slow conduction (a low safely margin for conduction leading to a unidirectional block as occurs in damaged, hypoxic tissue) and rapid repolarization (an effect of catecholamine stimulation).

Supraventricutar tachydysrhythmias

Ventricular arrhythmias