Physiopathology of ventricular tachyarrhythmias.
Ventricular arrhythmias may be the result of three mechanisms: abnormal automaticity, triggered activity complicating early or late after-depolarizations, and reentry by circular pathway or by reflection. These three fundamental mechanisms have been observed in the intact heart in experimental models of myocardial ischemia and digitalis intoxication. In man, the arguments in favor of a given mechanism are indirect and may be determined by their response to stimulation. It may be possible to state the following conclusions: (1) reentry is at the origin of ventricular fibrillation, certain ventricular tachycardias of bundle branch reentry and probably most chronic sustained ventricular tachycardias that are easily inducible; (2) the mechanism of certain other ventricular arrhythmias sustained remains unknown; (3) even when arrhythmias are associated with reentry, the triggering extrasystole can arise from a focal origin.
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D002908:Chronic Disease; D003327:Coronary Disease / Q000503:physiopathology; D004195:Disease Models, Animal; D004285:Dogs; D004594:Electrophysiology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology; D013552:Swine; D013610:Tachycardia / Q000503:physiopathology*