Cellular and tissue responses to recurrent ventricular tachycardia and fibrillation.
The effects of rapid rhythms on cellular electrical activity depend on the rate of the rhythm, the cell type, and its condition prior to the arrhythmia. Rapid rates can cause major changes in transmembrane ion concentration gradients and the magnitude of these is a function of the transport capacity of the sodium-potassium pump. Thus digitalis can be expected to exert a prominent effect on rate-induced changes. Some of the rate-induced changes can lead to the generation of arrhythmias, as through calcium overload and the development of delayed afterdepolarizations. Since the actions of antiarrhythmic drugs often show use-dependence, the presence in the heart of local anesthetics or certain slow channel blockers will further modify the effect of rapid and irregular rhythms on cellular electrical activity.
D000889:Anti-Arrhythmia Agents / Q000378:metabolism; D004071:Digitalis Glycosides / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006352:Heart Ventricles / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D008564:Membrane Potentials; D011690:Purkinje Fibers / Q000378:metabolism; D012008:Recurrence; D013610:Tachycardia / Q000378:metabolism*; D014693:Ventricular Fibrillation / Q000378:metabolism*
D000889:Anti-Arrhythmia Agents; D004071:Digitalis Glycosides; D007473:Ion Channels