A self-protecting servo-model for explanation of the mechanism involved in spontaneous ventricular defibrillation.

Ventricular fibrillation (VF) is the most life-threatening arrhythmia. It has been suggested that VF in humans is always sustained. Recent publications indicated that VF can be either sustained (SVF) or transient (TVF), reverting spontaneously into sinus rhythm. In previous studies we have hypothesized that TVF requires, during VF, a high cardiac catecholamine level ([CA]). Since during VF sympathetic activity is enhanced, the question arises of why VF is sustained in the majority of cases. Looking on the living body as a self-protecting servo-mechanism, we propose a servo-model that on the one hand describes the mechanism involved in TVF and on the other proposes a therapeutic procedure which can help the heart in its effort to transform VF into TVF. Our model has been examined by various experimental studies. The results obtained strongly support our hypothesis.