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Abstract
The toxic effects of digitalis are attributable in part to poisoning of the enzyme
Na+-K+ ATPase and in part to the interactions of digitalis with the sympathetic and
parasympathetic nervous systems. Additional modifiers of the toxic effects of digitalis
include the concentrations of ions such as K+ and Ca2+, the age of the subject and
the extent and type of cardiac disease. At the cellular electrophysiologic level,
digitalis toxicity is seen as a depolarization of the membrane with the occurrence--individually
or simultaneously--of abnormalities of impulse initiation (including delayed afterdepolarizations
and abnormal automaticity) and abnormalities of conduction. The afterdepolarizations
result in triggered arrhythmias that differ partially in their characteristics of
onset and termination from automatic and reentrant arrhythmias. The cellular electrophysiologic
basis for these arrhythmias induced by toxic concentrations of digitalis and their
implications with respect to arrhythmogenesis in the in situ heart are explored in
detail.