Digox Drug Interactions

There may be interactions between Digoxin and drugs that after its absorption, interfere with its excretion, or have additive effects on the myocardium. Drugs that cause electrolyte disturbances increase the risk of toxicity from cardiac glycosides. Thiazides and loop diuretics cause hypokalemia and also hypomagnesemia which may lead to cardiac arrhythmias. Other causes of hypokalemia include treatment with corticosteroids, beta-2 agonists (such as salbutamol), amphotericin B, sodium polystyrene sulfonate, carbenoxolone and dialysis. Hypercalcemia may also increase toxicity and intravenous use of calcium salts is best avoided in patients taking cardiac glycosides. Serum-digoxin concentrations may be significantly increased by quinidine, amiodarone and propafenone and reduction of Digoxin dosage may be required. Other antiarrhythmics may have additive effects on the myocardium increasing the likelihood of adverse effects; beta blockers may potentiate bradycardia due to Digoxin. Calcium-channel blockers may increase Digoxin concentrations.
Digoxin is a substrate for P-glycoprotein and interactions may occur with drugs that affect P-glycoprotein action.