Abstract
The pathophysiologic mechanisms of cardiac arrhythmias include both structural abnormalities of cardiac tissue (e.g., healed infarction, hypertrophied or hemodynamically-stressed muscle) and transient functional changes in cardiac electrical properties (e.g., due to transient ischemia, reperfusion, autonomic or electrolyte fluctuations) . Clinical and experimental data suggest that both the chronic and the dynamic changes in electrical properties interact in the genesis of life-threatening arrhythmias. Experimental studies have demonstrated that the onset of ischemia, and its reversal by reperfusion, create dynamic changes in cellular membrane characteristics which may participate in the genesis of cardiac arrhythmias. Clinical observations at the onset of myocardial infarction, and reperfusion after coronary spasm or interventional procedures, are beginning to provide a parallel body of information. In both experimental and clinical studies, the characteristics and ionic mechanisms for ischemic arrhythmias appear to differ from those in reperfusion arrhythmias. Studies on the experimental influences of both α-and β-adrenergic activity on ischemic or normal myocardium demonstrate an arrhythmogenic effect, in parallel with limited information on autonomic fluctuations in clinical arrhythmias.It has long been recognized that experimental changes in electrolyte and metabolic status of ventricular muscle influence cellular electrophysiology and arrhythmogenesis, and recent clinical information is beginning to suggest similar influences in man. Specifically, transient changes in oxygen supply, pH, Ca++ flux, and superoxide radical formation may be responsible for the transient destabilization of the myocardium experimentally, and also may contribute to the genesis of potentially lethal arrhythmias in man. A thorough understanding of the factors which transpose a structurally diseased but stable myocardium into an electrically unstable mass of tissue is required for meaningful inroads into the prevention of potentially lethal arrhythmeas.