Toxicity from digitalis mostly occurs in older patients and patients with renal failure. Other comorbidities that may make someone sensitive to the effects of digitalis include hypothyroidism, hypokalemia, hypomagnesemia, and acute myocardial ischemia. Some drugs potentiate the effects of digitalis, e.g., quinidine, amiodarone, and spironolactone.

Digitalis toxicity leads to arrhythmias affecting the SA and AV conduction systems. For example, a patient with first-degree AV block in the presence of digitalis toxicity develops second-degree AV block (Wenckebach type). If left untreated, the rhythm will further progress into a 2:1 AV block and complete AV block. These patients present with an escape rhythm located above the bundle of His and small QRS complexes on ECG. 

If a patient has atrial fibrillation, digitalis toxicity impairs AV conduction and causes bradycardia. Digitalis toxicity also provokes sinus bradycardia. It can cause nearly all of the cardiac arrhythmias, even rare types such as tachycardic atrial fibrillation.

Patients develop arrhythmias because digitalis toxicity increases automaticity in the atrium, the AV junction, and the ventricles. Premature beats are usually produced—bigeminy is the most commonly occurring pattern of PVCs. 

Ventricular tachycardia is also common in digitalis toxicity. The ECG will show irregular, monomorphic, or polymorphic morphologies without torsades de pointes. 

Digitalis toxicity can also provoke ventricular fibrillation and cardiac standstill. Atrial tachycardia with 2:1 AV block represents enhanced automaticity and delayed conduction. QT interval shortening is also seen in digitalis toxicity.