Cardiac arrhythmias afterdepolarization

Calcium overload is manifested as an early afterdepolarization of the cardiac action potential, which may result in premature depolarization of Purkinje fibers and the appearance of ventricular arrhythmias. With substantially increased calcium load, this may lead to ventricular tachyarrhythmias and death. 

Cardiac glycosides increase the influx of calcium, and decrease the outflow of potassium. Because there is little sequestration of calcium in cardiac cells, intracellular calcium may increase to toxic levels, particularly with high doses of the drug, and may exchange for sodium, via the sodium-calcium exchanger. This results in an overload of intracellular sodium and calcium, which, because of the decreased outflow of potassium, is not counterbalanced. Thus, calcium overload is manifested as an early afterdepolarization of the cardiac action potential, which may result in premature depolarization of Purkinje fibers and the appearance of ventricular arrhythmias, which may result in ventricular tachyarrhythmias and death. 

---