The development of an arrhythmia is believed to result from the superimposition of a 'transient' factor on a pre-existing or static factor. owever, an arrhythmic death may occur in the absence of clinically detectable cardiac disease. Only 20 per cent of cardiac arrest patients with coronary heart disease are subsequently shown to have developed an acute myocardial infarct with an acute plaque fissure causing platelet aggregation and subsequent thrombus formation. Transient myocardial ischemia-reperfusion causes the transient factor in the remainder, and in the presence of left ventricular hypertrophy or a previously healed myocardial infarction is particularly liable to be arrhythmogenic.
A model relating the transient and static factors is shown in Fig 1. It incorporates the chance development of ventricular tachycardia or fibrillation due to randomly occurring premature ventricular contractions (electrogenic component) ( Myerburg ef^a/ 1989).
Fig. 1 Biological model of sudden cardiac death. Short- or long-term structural abnormalities and functional modulations interact to influence the propensity for premature ventricular contractions (PVCs) to initiate a ventricular tachycardia or fibrillation (VT/VF). The four major categories of structural abnormalities may be influenced by one or more functional events, as shown. (Reproduced with permission from Myerburg,jelâL (.1989))
The cellular electrophysiological changes and the tendency for arrhythmias induced by acute ischemia develop within seconds. An initial peak relates to early cell injury with calcium and potassium shifts and developing electrochemical gradients as a direct result of ischemia. The second peak may be due to reperfusion injury or to different responses to ischemia in epicardial or endocardial cells, with the creation of an arrhythmogenic substrate. These changes promote disorders of myocardial electrical impulse conduction with local blocks and re-entry circuits.
Arrhythmias can result from disorders of electrical impulse formation (automaticity), disorders of electrical conduction, or a combination of both. After acute infarction, arrhythmias tend to be re-entrant in character in the first 30 min. Later, disorders of automaticity supervene, but after 3 days re-entrant arrhythmias again predominate.
The vulnerable period at which a premature ventricular contraction may trigger ventricular tachycardia or fibrillation is at the end (phase 3/4) of the myocardial action potential. In clinical practice this vulnerability is demonstrated by the association of the 'R on T' phenomenon with the development of ventricular arrhythmias.
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