Contribution of variable entrance and exit block in protected foci to arrhythmogenesis in isolated ventricular tissues.
Automatic foci with membrane potentials in the range characterized by depolarization-induced automaticity exhibit entrance block. The present study demonstrates a role of variable entrance and exit block in arrhythmogenesis. We studied canine interventricular septa with the right bundle branch exposed, isolated false tendons and isolated feline papillary muscle using standard microelectrode techniques. Foci of automaticity were produced either by focal application of electric current or by exposure of the preparations to Tyrode's solution containing 1.5-2.0 mM KCl. Foci induced by mild depolarization exhibited entrance block with exit conduction and were subject to electrotonic modulation. With greater depolarization, varying degrees of exit block developed. Various rhythms, including Wenckebach periodicity, resulted. Delayed emergence of electrotonically accelerated activity led to closely coupled extrasystoles resembling reentrant activity. Exit conduction in some preparations was facilitated by enhanced normal pacemaker activity (membrane potentials -- 70 mV or greater) in tissue peripheral to the focus. Also, when there were two sites of automaticity separated by an area of depressed conduction, intermodulation between the two automatic regions generated complex arrhythmias. Shifts in maximum diastolic potential also changed conduction and led to changes in arrhythmic patterns. In some experiments, focal automaticity was terminated by single stimuli. We conclude that complex and variable behavior of automatic foci may result in activity with characteristics previously attributed to other arrhythmic mechanisms.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D002304:Cardiac Pacing, Artificial; D002415:Cats; D003327:Coronary Disease / Q000503:physiopathology; D004285:Dogs; D005260:Female; D006327:Heart Block / Q000209:etiology; D006329:Heart Conduction System / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials; D008839:Microelectrodes; D009200:Myocardial Contraction; D010210:Papillary Muscles / Q000503:physiopathology; D011690:Purkinje Fibers / Q000503:physiopathology