Enhanced cardiac automaticity
- Philip J Podrid, MD, FACC
Philip J Podrid, MD, FACC
- Professor of Medicine, Professor of Pharmacology and Experimental Therapeutics
- Boston University School of Medicine
- Lecturer, Harvard Medical School
Enhanced cardiac automaticity refers to the accelerated generation of an action potential by either normal pacemaker tissue (enhanced normal automaticity) or by abnormal tissue within the myocardium (abnormal automaticity). The discharge rate of normal or abnormal pacemakers may be accelerated by drugs, various forms of cardiac disease, reduction in extracellular potassium, or alterations of autonomic nervous system tone. Enhanced normal automaticity accounts for the occurrence of sinus tachycardia, while abnormal automaticity may result in various atrial or ventricular arrhythmias, for example, an accelerated idioventricular rhythm or an ectopic atrial tachycardia.
This topic will review the physiologic principles underlying both enhanced normal automaticity and automatic automaticity. The diagnosis and treatment of arrhythmias resulting from enhanced cardiac automaticity are discussed separately. (See "Sinus tachycardia: Evaluation and management" and "Focal atrial tachycardia".)
ENHANCED NORMAL AUTOMATICITY
Enhanced normal automaticity is best understood by beginning with a brief review of the physiology and hierarchy of stimulation of normal cardiac automaticity. This will be followed by a discussion of the electrophysiologic principles underlying the normal and enhanced automaticity of the SA node, the subsidiary atrial pacemakers, the atrioventricular (AV) node, and the ventricles.
Normal automaticity — Normal automaticity involves the slow, progressive depolarization of the membrane potential (spontaneous diastolic depolarization or phase four depolarization) until a threshold potential is reached, at which point an action potential (figure 1 and figure 2) is initiated. Although automaticity is an intrinsic property of all myocardial cells, the occurrence of spontaneous activity is prevented by the natural hierarchy of pacemaker function. (See "Myocardial action potential and action of antiarrhythmic drugs".)
The spontaneous discharge rate of the sinoatrial (SA) nodal complex exceeds that of all other subsidiary or latent pacemakers. As a result, the impulse initiated by the SA node depresses the activity of subsidiary pacemaker sites, before they can spontaneously depolarize to threshold. However, slowly depolarizing and previously suppressed pacemakers in the atrium, AV node, or ventricle can become active and assume pacemaker control of the cardiac rhythm if the SA node pacemaker becomes slow or unable to generate an impulse or if impulses generated by the SA node are unable to activate the surrounding atrial myocardium. The emergence of subsidiary or latent pacemakers under such circumstances is an appropriate fail-safe mechanism which assures that ventricular activation is maintained.
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