Furosemide-induced hypokalemia increases risk of digoxin toxicity (arrhythmias)
Management: Monitor serum potassium and digoxin levels closely. Supplement potassium if needed.
Diltiazem increases digoxin serum levels by 20-35% and both have additive AV nodal depression
Management: Reduce digoxin dose by 25-50% when adding diltiazem. Monitor digoxin levels and ECG.
Thiazide-induced hypokalemia increases sensitivity to digoxin toxicity
Management: Monitor potassium closely. Supplement potassium if needed. Watch for digoxin toxicity signs.
Amiodarone increases digoxin levels by 70-100% via P-glycoprotein inhibition, CYP3A4 inhibition, and reduced renal clearance.
Management: Reduce digoxin dose by 50% when initiating amiodarone. Monitor digoxin levels closely.
Quinidine reduces renal and non-renal digoxin clearance and displaces digoxin from tissue binding sites, increasing digoxin levels by ~100% (doubled).
Management: Reduce digoxin dose by 50% when adding quinidine. Monitor digoxin trough levels. Watch for digoxin toxicity (anorexia, arrhythmias).
Calcium increases myocardial sensitivity to digoxin by enhancing Na+/K+-ATPase binding. IV calcium in digitalized patient can precipitate fatal ventricular arrhythmias.
Management: Extreme caution with IV calcium in patients on digoxin. Give very slowly with continuous ECG. Correct hypokalemia first.
Isoproterenol increases myocardial excitability and automaticity. In digitalized myocardium, this greatly increases risk of fatal ventricular arrhythmias.
Management: Use extreme caution. If isoproterenol needed in patient on digoxin, continuous ECG monitoring mandatory. Consider temporary pacing instead.
Succinylcholine causes transient hyperkalemia (K+ release from muscle depolarization). In digitalized patients, hyperkalemia potentiates digoxin toxicity, risking fatal arrhythmias.
Management: Avoid succinylcholine in digitalized patients. Use non-depolarizing NMBA (rocuronium) instead.