One of the factors that favors the development of ventricular fibrillation is an increase in the dispersion of refractoriness. Experiments will be described in which an increase in dispersion in the recovery of excitability was determined during brief episodes of enhanced sympathetic nerve activity, known to increase the risk of fibrillation. Whereas in the normal heart ventricular fibrillation can be induced by a strong electrical shock, a premature stimulus of moderate intensity only induces fibrillation in the presence of regional ischemia, which greatly increases the dispersion of refractoriness. One factor that is of importance for the transition of reentrant ventricular tachycardia to ventricular fibrillation during acute regional ischemia is the subendocardial Purkinje system. After selective destruction of the Purkinje network by lugol, reentrant tachycardias still develop in the ischemic region, but they do not degenerate into fibrillation. Finally, attempts were made to determine the minimal mass of thin ventricular myocardium required to sustain fibrillation induced by burst pacing. This was done by freezing of subendocardial and midmural layers. The rim of surviving epicardial muscle had to be larger than 20 g. Extracellular electrograms during fibrillation in both the intact and the ''frozen'' left ventricle were indistinguishable, but activation patterns were markedly different. In the intact ventricle epicardial activation was compatible with multiple wavelet reentry, in the ''frozen'' heart a single, or at most two wandering reentrant waves were seen. © 1998 American Institute of Physics. ͓S1054-1500͑98͒00201-8͔It has been known for a long time that the normal rhythmic activity of the heart can be upset by applying a single, strong electrical shock to the heart during a short part of the cardiac cycle, the so-called vulnerable period. The ensuing rhythm is called ventricular fibrillation, in which the different parts of the two main chambers of the heart "the ventricles… are rapidly and asynchronously activated so that a coordinated contraction of the heart no longer occurs. This is a lethal condition, unless another strong electrical shock causes this abnormal electrical activity to cease, allowing the normal pacemaker of the heart to resume control and to initiate the normal, regular heartbeat. In this paper the vulnerability to ventricular fibrillation is described in terms of the ''dispersion of refractoriness,'' indicating a time window during which some parts of the ventricles are inexcitable "refractory…, others partially excitable, and still others completely excitable. An electrical stimulus delivered during this time window will initially be unable to activate those parts that are inexcitable, but will cause a wave front of electrical activity that slowly travels around the area of inexcitable tissue, exciting it after a delay when excitability has returned, to finally reenter the site of origin. This so-called reentrant activity, which continues to reexcite tissue that just has recover...