Abstract

Outline of Problem: Sudden unexpected cardiac death is one of the most important Public Health problems in the affluent societies. The apparent occurence is about 150, 000 per 100 million population/year. In about one-half of the victims, sudden cardiac death is the first manifestation of heart disease (usually coronary) . In the vast majority of persons with good ventricular function, the mechanism is ventricular fibrillation (VF) . In some victims with severely impaired ventricular function, additional (numerically less important) mechanisms include: ventricular tachycardia (VT), cardiac standstill, and electro-mechanical dissociation.Ventricular premature complexes are nearly ubiquitous and increase in frequency and“complexity”exponentially with age, and also with increasing severity of heart disease. I will examine the relation between these arrhythmias and sudden cardiac death, and will propose that the simple and“complex”ventricular arrhythmias, including nonsustained VT are not precursors of either sustained VT, or VF. Sustained VT is usually a marker of severely impaired ventricular function i.e. a breakdown of electrical safety mechanisms protecting the heart whereas VF is an electrical accident caused usually by severe myocardial ischemia, and sometimes by marked increase in the dispersion of ventricular repolarization (frequently associated with long QT interval) .Hypothesis: The apparent paradox of nearly perfect electrical safety in the presence of variety of ubiquitous ventricular arrhythmias, and the occurrence of fatal electrical accidents unrelated to these arrhythmias may be better understood if we examine the electrophysiologic mechanisms of experimental and clinical accidents encountered in practice and in the laboratory. Extrapolating from these accidents, the following safety factors appear to protect the healthy heart from electrical accidents; 1) Hierarchy of escape pacemakers, 2) Impulse delay in the A-V node + long refractoriness of the conducting system, 3) High (negative) stable resting membrane potential, 4) Fast and uniform ventricular conduction, 5) Long absolute and short relative refractory period of ventricular myocardium, 6) Small dispersion of ventricular repolarization, 7) Uniform ventricular polarization, and 8) Large safety factor inherent in a small ratio of the duration of impulse propagation to the duration of refractoriness in the ventricle.The following examples, and causes of the safety breakdown will be briefly presented: 1) Cardiac standstill—failure of escape pacemakers, 2) Ventricular flutter during atrial flutter and conduction through the Kent bundle—loss of normal protection afforded by the A-V nodal function, 3) Ventricular fibrillation in hypokalemia—diastolic depolarization as well as short absolute and long relative refractory period of the ventricular myocardium, 4) Electrocution—nonunif orm polarization, 5) Induced ventricular tachyarrhythmia by extrastimulation—shortening the refractory period and slowing conduction, 6) Ventricular tachyarrhythmia due to digitalis toxicity—induction of diastolic depolarization and afterdepolarizations, 7) Torsade de pointe in congenital long QT syndrome—increased dispersion of ventricular repolarization, 8) Primary VF in the presence of myocardial ischemia—nonunif orm polarization resulting in slow and nonunif orm conduction.Conclusions: The heart is remarkably well protected from electric accidents. They occur under unusual circumstances, representing mainly the consequences of modern lifestyle, and occasional congenital defects.

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