Abstract Ventricular fibrillation, which is a common cause of sudden death following anesthesia, coronary occlusion, electric shock, etc., cannot be adequately described as an asynchronous, incoordinate contraction of ultimate cardiac fractions. The process is an evolution of changes from the moment of its inception until it ceases completely, which is within thirty to forty-five minutes. The visible spread of waves and punctate unipolar electrocardiograms are reviewed. The available evidence favors the conclusion that, after a single premature systole, the phenomenon is caused by re-entry of circulating wave fronts which involve smaller and smaller blocks of myocardium, each of which develops an independent excitation. As a result of the anoxia which develops progressively after the cessation of coronary flow, conduction is slowed and the vigor of fractionate contractions decreased. The resultant of these changes causes, in succession, the undulatory, convulsive, tremulous, and atonic stages of its evolution. The theory which best explains these sequential changes and the initiation of fibrillation by the application of a brief, strong, localized shock during the vulnerable period of late systole may be stated briefly as follows: In order to initiate fibrillation, an electrical stimulus or noxious influences with a “fibrillation threshold” must be applied during the vulnerable period of late systole, at which time certain elements have passed out of the refractory phase. Such a stimulus excites impulses in a number of nonrefractory fractions. These weave their way slowly through local, nonrefractory tissue to form a small wave front, from which a massive excitation wave sweeps over comparatively large portions of the myocardium in sequential order. This constitutes the first premature systole. If the wave front is large enough, and the mode of spread favorable for re-entry at, or near, the point of excitation, several circuits are formed through the ventricles; this is the undulatory stage. In some way—possibly by collision of different excitation fronts, combined with slow conduction-these masses of myocardium are broken into smaller and smaller ones, in which divided waves reenter more frequently. Thus the process passes successively into the convulsive and tremulous stages; during the latter there are innumerable avenues of re-entry. The atonic stage is characterized by progressive enfeeblement of contraction and gradual failure of conduction, which are the result of anoxia caused by cessation of the coronary circulation. This theory is obviously incomplete in many details and can be expanded only through the development of more perfect methods for following the spread of impulses over the cardiac surface.