India · Heart Failure · AF Rate Control · Loading & Maintenance · TDM · Toxicity · Lanoxin · Digocin
Amiodarone — doubles digoxin level. Halve digoxin dose when adding amiodarone.
Verapamil / Diltiazem — increase digoxin level + additive bradycardia.
Erythromycin / Clarithromycin — increase digoxin absorption significantly.
⚠️ Diuretics → hypokalaemia → digoxin toxicity. Always replace K⁺.
⚠️ Hypothyroidism increases digoxin levels.
| Patient group | Maintenance dose | TDM target | Recheck level |
|---|---|---|---|
| Adult HF, normal renal function | 125–250 mcg once daily | 0.5–0.9 ng/mL | After 7 days (5 half-lives) |
| Adult AF rate control | 125–250 mcg once daily | 0.8–2.0 ng/mL | After 7 days |
| Elderly (>70 years) | 62.5–125 mcg once daily | 0.5–0.9 ng/mL | After 7–10 days |
| CKD eGFR 30–60 | 62.5–125 mcg once daily | 0.5–0.9 ng/mL | After 10–14 days |
| CKD eGFR <30 | 62.5 mcg every 48 hours | 0.5–0.9 ng/mL | After 14+ days — consider alternative |
| Dialysis | Avoid or use with extreme caution | — | Specialist input required |
| Oral loading (AF) | 0.25 mg every 6h × 4 doses then maintenance | Check after loading | 6–8h post-last loading dose |
| IV loading (rapid AF) | 0.25–0.5 mg IV over 30 min (max 1mg/24h) | Check 24h later | Trough next day |
Digoxin is a cardiac glycoside that inhibits Na⁺/K⁺-ATPase, increasing intracellular calcium and thus myocardial contractility (positive inotrope). It also slows conduction through the AV node (negative chronotrope), making it useful for rate control in atrial fibrillation. In heart failure, the DIG trial demonstrated that digoxin reduces hospitalisation but does not reduce mortality. Its role is now limited to patients with HFrEF and concurrent AF, or those with symptomatic HF despite optimal medical therapy. Its narrow therapeutic index and complex pharmacokinetics — particularly renal clearance and multiple drug interactions — make it one of the most challenging drugs to use safely.
Digoxin and potassium compete for the same binding site on Na⁺/K⁺-ATPase. When serum potassium is low, digoxin binds more avidly even at normal digoxin levels — causing toxicity at levels that would otherwise be sub-toxic. This is the most important clinical concept in digoxin management. Any patient on both digoxin and a diuretic (furosemide, hydrochlorothiazide) is at high risk of diuretic-induced hypokalaemia triggering digoxin toxicity. Always check potassium when requesting a digoxin level. If K⁺ is below 3.5 mmol/L, replace potassium before interpreting the digoxin level or making dose changes.
Amiodarone is one of the most important digoxin interactions in clinical practice. It inhibits P-glycoprotein-mediated renal tubular secretion of digoxin, approximately doubling the digoxin serum level over 1–4 weeks. When amiodarone is started in a patient already on digoxin, the digoxin dose must be halved immediately (not gradually), and levels rechecked after 1–2 weeks. Failure to do this is a common cause of digoxin toxicity in cardiac patients on combination antiarrhythmic therapy.
Digoxin toxicity classically presents with a triad of GI, visual, and cardiac symptoms. GI symptoms (nausea, vomiting, anorexia, abdominal pain) are typically the earliest. Visual disturbances — particularly xanthopsia (yellow-green halos around lights) — are pathognomonic but occur in fewer than 20% of cases. Cardiac toxicity is the most dangerous: almost any arrhythmia can occur, but classic patterns include bradycardia, AV block (particularly 2nd degree Mobitz type I/Wenckebach), accelerated junctional rhythms, and bidirectional ventricular tachycardia. Treatment: hold digoxin, correct hypokalaemia/hypomagnesaemia, cardiac monitoring, and for severe toxicity with haemodynamic compromise — digoxin-specific antibody fragments (Digibind/DigiFab) IV. Digibind is available at selected Indian tertiary centres.