Electrophysiological mechanisms involved in ventricular fibrillation.
This report reviews the electrophysiological mechanisms involved in the initiation, maintenance, and termination of ventricular fibrillation. Ventricular fibrillation may be defined as chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge. The capacity to fibrillate is inherent in ventricular muscle because the electrophysiological properties of the various segments of the ventricle are not uniform. Factors that enhance electrical asynchrony facilitate, while factors that decrease electrical asynchrony hinder, the development of fibrillation. Ventricular fibrillation may result following stimulation during the vulnerable period; under certain circumstances, rapid ventricular rates produced by ventricular or supraventricular arrhythmias may provoke ventricular fibrillation. Once fibrillation is initiated, a large mass, brief refractory period, and slow conduction velocity favor perpetuation. Reducing the excitable ventricular mass to a value less than the amount necessary to support spontaneous fibrillation causes fibrillation to terminate. Depolarization of every cell in both ventricles is not necessary to terminate ventricular fibrillation in the entire heart.
D000200:Action Potentials; D000818:Animals; D001283:Atrioventricular Node / Q000503:physiopathology; D006328:Cardiac Catheterization; D003326:Coronary Circulation; D004285:Dogs; D004554:Electric Countershock; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology; D010138:Pacemaker, Artificial; D011690:Purkinje Fibers / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000503:physiopathology* / Q000628:therapy