Formulary
Digoxin: Uses, Dosing, Side Effects and Indian Brand Names
Digoxin is a cardiac glycoside with a narrow therapeutic index used for rate control in atrial fibrillation and symptomatic heart failure, notable for its complex toxicity profile that is potentiated by electrolyte disturbances.
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Digoxin: Uses, Dosing, Side Effects and Indian Brand Names
Digoxin is a cardiac glycoside with a narrow therapeutic index used for rate control in atrial fibrillation and symptomatic heart failure, notable for its complex toxicity profile that is potentiated by electrolyte disturbances.
NEET PG High-Yield: Narrowest therapeutic index of common cardiac drugs. Toxicity precipitated by hypokalaemia, hypomagnesaemia, hypercalcaemia, hypothyroidism, renal failure. Bidirectional VT is pathognomonic. Xanthopsia. DIG trial: reduces hospitalisations but NOT mortality. Amiodarone and quinidine DOUBLE digoxin levels. Contraindicated in WPW with AF. Antidote: digoxin-specific antibody fragments (Digibind). Gynaecomastia (steroid-like structure).
Clinical overview
Digoxin is derived from Digitalis lanata and has been used in cardiac medicine for over 200 years since William Withering's original description. Despite the development of numerous newer agents, digoxin retains a specific niche in modern practice: rate control in atrial fibrillation (particularly in heart failure where negative inotropes like beta-blockers may worsen haemodynamics) and symptomatic relief in heart failure with reduced ejection fraction (HFrEF) that remains symptomatic despite optimal therapy with ACE inhibitors, beta-blockers, and diuretics. The DIG trial showed digoxin reduces hospitalisations for heart failure but does not reduce mortality -- a frequently tested distinction. Digoxin has the narrowest therapeutic index of any commonly used cardiovascular drug, with a therapeutic range of 0.5-2.0 ng/mL (current guidelines recommend 0.5-0.9 ng/mL for heart failure). Toxicity is potentiated by hypokalaemia, hypomagnesaemia, and hypercalcaemia -- hence the critical importance of monitoring electrolytes in patients on digoxin, especially those also receiving diuretics. Digoxin toxicity classically causes a combination of cardiac (any arrhythmia, but bidirectional ventricular tachycardia and atrial tachycardia with AV block are highly characteristic), GI (nausea, vomiting, anorexia), and neurological (xanthopsia -- yellow vision, confusion) symptoms. Treatment of severe toxicity is with digoxin-specific antibody fragments (Digibind/DigiFab). In India, digoxin remains widely used, particularly in resource-limited settings where rate control options are constrained.
Pharmacological class
Digoxin belongs to the Cardiac Glycosides class. Inhibits the sodium-potassium ATPase (Na+/K+ pump) in cardiac myocytes, increasing intracellular sodium, which reduces the sodium-calcium exchange, leading to increased intracellular calcium and enhanced contractility (positive inotropic effect). Also increases vagal tone to the AV node (negative chronotropic/dromotropic effect) and sensitises the carotid baroreceptor, reducing sympathetic outflow.
Indian brand names and formulations
Available as: Digox (Glaxo/GSK), Lanoxin (Aspen/GSK), Cardioxin (Samarth Pharma).
Tablets: 0.0625 mg, 0.125 mg, 0.25 mg. Oral solution: 0.05 mg/mL (paediatric). Injection: 0.5 mg/2 mL (IV digitalisation).
Regulatory status
Digoxin is classified under Schedule H in India under the Drugs and Cosmetics Act, 1940. Prescription-only. Requires careful dose titration and therapeutic drug monitoring.
Indications
- Rate control in atrial fibrillation (especially with coexisting heart failure)
- Heart failure with reduced ejection fraction (add-on when symptomatic despite ACEI + beta-blocker + diuretic)
- Atrial flutter (rate control)
- Supraventricular tachycardia (not first-line; adenosine preferred)
Dosing
Oral loading (rapid digitalisation): 0.75-1.5 mg over 24 hours in divided doses (e.g., 0.5 mg, then 0.25 mg every 6-8 hours). Maintenance: 0.125-0.25 mg once daily. Elderly: 0.0625-0.125 mg daily. Renal impairment: reduce dose (digoxin is 70% renally excreted unchanged). Target trough level: 0.5-0.9 ng/mL for heart failure.
Contraindications
- Hypertrophic obstructive cardiomyopathy (HOCM) -- may worsen outflow obstruction
- Ventricular tachycardia or ventricular fibrillation
- Second- or third-degree AV block (without pacemaker)
- Wolff-Parkinson-White (WPW) syndrome with atrial fibrillation (may accelerate conduction down the accessory pathway)
- Hypertrophic subaortic stenosis
Adverse effects
- Cardiac arrhythmias (virtually any arrhythmia; bidirectional VT and atrial tachycardia with AV block are pathognomonic of toxicity)
- Nausea, vomiting, and anorexia (often earliest signs of toxicity)
- Xanthopsia (yellow-green visual disturbance -- classic but not invariable)
- Fatigue, weakness, and confusion
- Gynaecomastia (with chronic use -- oestrogen-like steroid structure)
Drug interactions
- Amiodarone: doubles digoxin levels (reduces renal clearance and volume of distribution); halve digoxin dose when starting amiodarone
- Verapamil: increases digoxin levels by ~70%; reduce digoxin dose
- Hypokalaemia-inducing drugs (thiazides, loop diuretics, corticosteroids): potentiate digoxin toxicity by increasing binding to Na+/K+ ATPase
- Erythromycin and tetracycline: increase digoxin absorption by killing gut flora that inactivate digoxin
- Quinidine: doubles digoxin levels by displacing from tissue binding and reducing renal clearance
- Spironolactone: may increase digoxin levels and interfere with digoxin assays
Pregnancy and lactation
Category C. Crosses the placenta. Used in foetal SVT when other options fail. Monitor foetal heart rate closely.
Exam-style clinical scenario
A patient on digoxin and furosemide presents with nausea, yellow vision, and irregular pulse. ECG shows atrial tachycardia with varying AV block. Serum K+ is 2.8 mEq/L. Diagnosis? Digoxin toxicity precipitated by diuretic-induced hypokalaemia. Management: stop digoxin, correct hypokalaemia, consider Digibind if haemodynamically unstable.
Cost in India
Rs 10-25 for a strip of 10 tablets (0.25 mg). One of the cheapest cardiac drugs available.
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
Why does hypokalaemia worsen digoxin toxicity?
Digoxin and potassium compete for the same binding site on the Na+/K+ ATPase alpha subunit. When serum potassium is low, less potassium competes with digoxin for binding, so more digoxin binds to the pump even at therapeutic serum digoxin levels. This increases the intracellular calcium accumulation that drives toxicity. Always check and correct K+ and Mg2+ in any patient on digoxin.
Why does the DIG trial matter for NEET PG?
The DIG trial (1997) is a landmark study showing that digoxin reduces heart failure hospitalisations by approximately 28% but has NO effect on mortality. This is a favourite MCQ distinction: digoxin improves symptoms and reduces hospitalisations but does not prolong life. Contrast with ACEI (CONSENSUS, SOLVD), beta-blockers (MERIT-HF, CIBIS-II), and spironolactone (RALES), which DO reduce mortality in HFrEF.
What ECG changes does digoxin cause?
Therapeutic levels cause the characteristic reverse-tick/Salvador Dali moustache ST-segment depression (downsloping ST depression with scooped appearance) and shortening of the QT interval. These are EXPECTED and do NOT indicate toxicity. Toxicity causes arrhythmias: PVCs (most common), atrial tachycardia with block, bidirectional VT, and AV block.
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