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Cardiac arrhythmias due to digoxin toxicity

INTRODUCTION

Cardiac glycosides (digitalis preparations including digoxin and digitoxin) are used clinically in two situations: heart failure due to systolic dysfunction, and in certain supraventricular tachyarrhythmias [1]:

The ability to enhance cardiac contractility and modulate neurohumoral activation can lead to symptomatic improvement in systolic heart failure, although it is unclear if survival is prolonged. (See "Use of digoxin in heart failure due to systolic dysfunction".)

Digoxin also slows conduction through the atrioventricular (AV) junction (node) by increasing vagal tone. It may also have a sympathoinhibitory effect in therapeutic doses. As a result, it is sometimes used (usually adjunctively with beta blockers or calcium channel blockers) for controlling the ventricular response in atrial fibrillation and atrial flutter when there is excessively rapid transmission of stimuli from the atria to the ventricles through the AV junction. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and "Control of ventricular rate in atrial flutter".)

Digoxin may also be effective in the treatment of certain types of reentrant paroxysmal supraventricular tachycardia involving the AV node.

Digoxin toxicity is an important clinical problem which may be life-threatening [2]. The incidence of digoxin excess and toxicity, along with the potential associated arrhythmias, are presented here. The management of digoxin intoxication, including the treatment of cardiac arrhythmias associated with digoxin toxicity, is discussed separately. (See "Digitalis (cardiac glycoside) poisoning" and "Cardioversion for specific arrhythmias", section on 'Cardioversion in patients with digitalis toxicity'.)

               

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Literature review current through: Sep 2014. | This topic last updated: Apr 30, 2014.
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