title: Digitalis arrhythmias: role of oscillatory afterpotentials.
abstract: Digitalis-induced OAP provide a mechanism of automaticity that may be responsible for many arrhythmias induced by cardiac glycosides. In response to digitalis, OAP occur in tissues of the specialized conducting systems of both ventricles and atria and, under the influence of tension, occasionally in ventricular myocardium. Digitalis, in toxic doses, suppresses "normal" pacemaker activity possibly in part by enhancing overdrive suppression. In contrast to "normal" pacemaker activity, OAP exhibit, both in magnitude and rate of depolarization, postpacing acceleration. This plus the coupled nature of OAP are important characteristics in the generation of complex arrhythmias by OAP. Conduction disturbances may also be related to OAP. At early stages of intoxication OAP may speed conduction of superimposed beats relative to earlier or later beats. More advanced stages of intoxication are associated with conduction block. The occurrence of digitalis-induced OAP is promoted by high concentrations of calcium, low concentrations of potassium, and moderate stretch. OAP can be suppressed by high concentrations of potassium, reduction of extracellular calcium, and exposure to antiarrhythmic agents including diphenylhydantoin, verapamil, and aprindine. The effectiveness of the latter two agents may be related to ability to block transmembrane calcium currents. Digitalis-induced OAP in atrial tissue can be abolished by acetylcholine. A transmembrane current possibly but not necessarily carried by calcium appears to underly the occurrence of OAP. This current demonstrates kinetic properties different from those of the slow inward current associated with the plateau of the cardiac action potential. Calcium is intimately involved in the mechanism causing OAP and may be responsible for aftercontractions observed in conjunction with OAP. Aftercontractions greatly affect contractility and may be responsible at least in part for some of the inotropic actions of digitalis. Thus the occurrence of OAP may be linked to the inotropic actions of digitalis. Digitalis-induced OAP provide a mechanism of automaticity with characteristics paralleling automatic behavior observed in intact animals intoxicated with digitalis. The relative importance of OAP in the genesis of clinically important arrhythmias awaits further investigation.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000503:physiopathology; D002118:Calcium / Q000502:physiology; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D004071:Digitalis Glycosides / Q000009:adverse effects* / Q000494:pharmacology; D004558:Electric Stimulation; D006325:Heart Atria / Q000503:physiopathology; D006327:Heart Block / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D007477:Ions; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology / Q000502:physiology; D011690:Purkinje Fibers / Q000503:physiopathology; D013327:Strophanthidin / Q000031:analogs & derivatives / Q000494:pharmacology; D014630:Vagus Nerve / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D004071:Digitalis Glycosides; D007477:Ions; D013327:Strophanthidin; D011188:Potassium; D002118:Calcium