The study identifies local block and irregular spread of excitation as key electrophysiologic mechanisms initiating ventricular fibrillation in animal models.
Transition from a regular supraventricular or ventricular mechanism to fibrillation was recorded utilizing 2 ultramicroelectrodes.Fibrillation in the hypothermic dog heart was preceded by asynchronous repolarization of individual fibers. An early premature beat caused incomplete depolarization of some fibers (local block) and irregular spread of excitation, rapidly disorganizing the ventricles. A similar sequence of events was demonstrated in the development of ventricular fibrillation due to desacetyl lanatoside C. Focal injection of aconitine engendered a sustained, regular ventricular tachycardia characterized by a decreased rate of depolarization and electrical alternation in some fibers. A gradual transition to fibrillation occurred when the timing and configuration of individual action potentials became irregular.Common factors observed at the onset of ventricular fibrillation were the development of local block and an irregular spread of excitation, demonstrating electrophysiologic inhomogeneity of the ventricles.During spontaneous ventricular fibrillation in isolated puppy hearts, the Purkinje-ventricular muscle junction was shown to be a possible site of conduction failure in the genesis of local block and irregular spread of excitation.
Watanabe et al. (Sat,) studied this question.