The correct answer is digitalis-induced delayed after depolarizations. Let's consider the observations and the reason. The observations here are that she did get ICD shocks for tachycardia in the setting of dilated cardiomyopathy. Her resting electrocardiogram is remarkable for PACs and nonspecific STT wave changes. Although these changes are present, they're not characteristic of digitalis intoxication, of course. Then the rhythm strip that was shown exhibited bidirectional ventricular tachycardia. A couple of things. Electrical remodeling in heart failure does include action potential duration prolongation. This often results in abnormalities of the QT interval and the T wave. The result of downregulation of many currents, but prominently potassium currents and aberrancies in calcium handling, downregulation of the sarcoplasmic, endoplasmic reticulum calcium transporter, and altered function of the sodium calcium exchanger. There are also problems with conduction, and conduction slowing prominently due to fibrosis in the myocardium, altered calcium current, and connexin intercellular ion channel, downregulation, and altered location. The bidirectional ventricular tachycardia is a digitalis-associated arrhythmia. Although many of these changes occur, bidirectional ventricular tachycardia and in the setting of these shocks, as well as the patient symptoms, are most consistent with digitalis-induced arrhythmias. As you are aware, digitalis is an inhibitor of the sodium potassium ATPase. When it inhibits this transporter, it increases intracellular sodium and functionally, alters the function of the sodium calcium exchanger. In particular, when intracellular sodium is increased, promotes the mode of function of the sodium calcium exchanger, where calcium is brought into the cell and sodium is removed. This is one of the reasons that digitalis has a positive inotropic effect. At therapeutic concentrations, digitalis is parasympathomimetic, both from the perspective of the central parasympathetic as well as a peripheral parasympathetic nervous system. Therefore, it slows conduction in the atrium and the AV node. Atrial fibrillation with a rapid ventricular response, less likely here in this circumstance. There's also little direct effect of digitalis on conduction in the AV node at therapeutic concentrations. However, when the concentration of digitalis is high, there's intracellular cytoplasmic calcium overload and sympathetic nervous system activation, in particular, in toxic doses. This can lead to the development of delayed after depolarizations and triggered arrhythmias and the bidirectional tachycardia that I showed you earlier.

digitalis

arrhythmia

cardiomyopathy

ventricular tachycardia

calcium overload