Pathophysiology of re-entrant dysrhythmias.
Re-entry was demonstrated as a self-perpetuating mechanism as early as 1906. It may lead to single-cycle electrocardiographic phenomena as well as reciprocating tachycardias. Factors favouring re-entry are as follows. Unidirectional or temporary local block of conduction, a mechanism always involved in initiation of reciprocating rhythms but also of importance for the maintenance of the arrhythmia. Increased myocardial mass. Decreased conduction velocity. Accelerated repolarization, e.g. short refractoriness. Increased dispersion of refractoriness. Regular reciprocating tachycardias utilize re-entrant mechanisms and are found in all components of the excitable cardiac tissue. Examples of such arrhythmias are reciprocating sinus tachycardia (RST), reciprocating atrial tachycardia (RAT), reciprocating junctional tachycardia (RJT), reciprocating atrioventricular tachycardia in connection with accessory pathways and ventricular tachycardia in the chronic stages of myocardial infarction. Re-entry mechanisms are also involved in fibrillation and flutter, in atria as well as in ventricles.
D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001281:Atrial Fibrillation / Q000503:physiopathology; D001283:Atrioventricular Node / Q000503:physiopathology; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology; D006329:Heart Conduction System; D006801:Humans; D012849:Sinoatrial Node / Q000503:physiopathology; D013614:Tachycardia, Paroxysmal / Q000503:physiopathology; D014927:Wolff-Parkinson-White Syndrome / Q000503:physiopathology