Digoxin

Digoxin is a cardiac glycoside used to treat certain heart conditions. It acts primarily by inhibiting the Na+/K+-ATPase pump on cardiac cells, which increases intracellular calcium and enhances myocardial contractility (positive inotropy). In addition, digoxin increases vagal tone and slows conduction through the atrioventricular (AV) node, which helps control ventricular rate in atrial fibrillation and flutter.

Pharmacology and pharmacokinetics are marked by a narrow therapeutic index. Digoxin is absorbed orally with variable bioavailability, and it distributes widely in body tissues. Its elimination is predominantly renal, so dosing must be adjusted in kidney impairment. The typical half-life is about 1 to 2 days in individuals with normal renal function but can be prolonged in renal failure. Serum levels are influenced by age, kidney function, and drug interactions.

Indications include heart failure with reduced ejection fraction (as add-on therapy in optimized treatment) and atrial fibrillation or flutter with rapid ventricular response when rate control is desired. In practice, digoxin is often considered when symptoms persist despite guideline-directed medical therapy or when other rate-control agents are not suitable.

Monitoring and dosing require careful attention. Start with a low dose and adjust for renal function, electrolytes, and interactions. Therapeutic serum concentrations typically range from about 0.5 to 0.9 ng/mL for heart failure, and somewhat higher for atrial fibrillation, though targets vary by guidelines. Regular monitoring of renal function and electrolytes (especially potassium and magnesium) is important, as abnormalities can increase toxicity risk.

Toxicity can present with gastrointestinal symptoms, neurological changes, visual disturbances, and a variety of arrhythmias, particularly in the setting of hypokalemia, renal failure, or drug interactions (notably with amiodarone, verapamil, macrolides, and certain diuretics). Management may involve dose adjustment, electrolyte correction, and, in severe cases, digoxin-specific antibody fragments.