Digoxin remains a cornerstone in the management of select cardiovascular conditions, offering a unique inotropic and chronotropic profile that supports heart failure treatment and controls certain arrhythmias. As a cardiac glycoside derived from Digitalis lanata, it exerts its therapeutic effects by inhibiting the sodium-potassium ATPase pump, increasing intracellular calcium, and enhancing myocardial contractility. Its ability to slow conduction through the atrioventricular node also makes it valuable in rate control for atrial fibrillation. Despite the advent of newer agents, digoxin maintains a defined role in contemporary cardiology due to its well-characterized pharmacokinetics and hemodynamic benefits when used judiciously in appropriate patient populations.

Features

• Contains digoxin as the active pharmaceutical ingredient
• Available in oral tablets (62.5 mcg, 125 mcg, 250 mcg) and intravenous formulation
• Demonstrated narrow therapeutic index requiring careful monitoring
• Long half-life permitting once-daily dosing in most patients
• Well-established pharmacokinetics with primarily renal elimination
• Standardized bioavailability across manufactured formulations

Benefits

• Enhances myocardial contractility, improving cardiac output in heart failure patients
• Provides effective rate control in atrial fibrillation and atrial flutter
• Reduces hospitalizations for heart failure exacerbations when used appropriately
• Offers flexible dosing options with both oral and intravenous administration
• Maintains stable therapeutic effects with once-daily dosing convenience
• Complements contemporary heart failure regimens including beta-blockers and ACE inhibitors

Common use

Digoxin is indicated for the treatment of mild to moderate heart failure in patients who remain symptomatic despite optimal standard therapy, particularly those with reduced ejection fraction. It is also approved for controlling ventricular response rate in patients with chronic atrial fibrillation. The medication finds particular utility in patients with concomitant heart failure and atrial fibrillation, where it addresses both contractility impairment and rate control needs. Clinical use typically follows failure or intolerance to first-line agents, with careful consideration of the risk-benefit profile in each individual case.

Dosage and direction

Dosing must be individualized based on patient factors including age, renal function, body weight, and concomitant medications. For most adults with normal renal function, the typical maintenance dose ranges from 125 to 250 mcg once daily. Loading doses may be employed in urgent situations but require careful calculation and monitoring. Administration should occur at approximately the same time each day, with or without food. Renal function must be assessed before initiation and periodically during therapy, with dosage adjustments made for impaired renal function. Therapeutic drug monitoring with serum digoxin levels is essential, with target concentrations typically between 0.5 and 0.9 ng/mL for heart failure and 0.8 to 1.2 ng/mL for atrial fibrillation.

Precautions

Careful assessment of renal function is mandatory before initiation and during therapy, as digoxin is primarily eliminated renally. Electrolyte imbalances, particularly hypokalemia, hypomagnesemia, and hypercalcemia, can potentiate digoxin toxicity and must be corrected before and during treatment. Thyroid function should be evaluated as both hyperthyroidism and hypothyroidism can alter digoxin requirements. Advanced age, low body weight, and underlying conduction system abnormalities require particular caution. Concomitant use of drugs that affect renal function or interact with digoxin necessitates close monitoring and possible dosage adjustment.

Contraindications

Digoxin is contraindicated in patients with ventricular fibrillation or known hypersensitivity to digoxin or other digitalis preparations. Additional contraindications include second- or third-degree atrioventricular block without a functioning pacemaker, Wolff-Parkinson-White syndrome with atrial fibrillation, and known digoxin toxicity. It should not be used in patients with amyloid cardiomyopathy or constrictive pericarditis unless specifically indicated by a cardiologist familiar with these conditions.

Possible side effect

Common adverse effects include nausea, vomiting, diarrhea, headache, dizziness, and visual disturbances such as yellow-green halos around lights or objects. Cardiac effects may include various arrhythmias, particularly premature ventricular contractions, paroxysmal atrial tachycardia with block, and advanced heart block. Neurological effects can include fatigue, malaise, weakness, and rarely psychosis or seizures. Endocrine effects may include gynecomastia in males. Most side effects are dose-related and often indicate elevated serum concentrations.

Drug interaction

Digoxin interacts significantly with multiple medication classes. Diuretics, particularly loop and thiazide diuretics, can cause hypokalemia and increase toxicity risk. Amiodarone, verapamil, quinidine, and cyclosporine can increase digoxin concentrations. Concomitant use with beta-blockers or calcium channel blockers may potentiate bradycardia and conduction abnormalities. Antibiotics such as erythromycin and tetracycline may increase digoxin bioavailability in some patients. Antacids, cholestyramine, and certain antineoplastic agents may decrease digoxin absorption.

Missed dose

If a dose is missed, it should be taken as soon as remembered unless it is nearly time for the next scheduled dose. In that case, the missed dose should be skipped and the regular dosing schedule resumed. Patients should never double the dose to make up for a missed administration. Consistent timing is important for maintaining stable serum concentrations, so efforts should be made to establish a routine that minimizes missed doses. If multiple doses are missed, medical advice should be sought before resuming therapy.

Overdose

Digoxin overdose constitutes a medical emergency requiring immediate attention. Symptoms may include severe nausea and vomiting, visual disturbances, marked bradycardia, ventricular arrhythmias, and hyperkalemia. Management includes discontinuation of digoxin, cardiac monitoring, correction of electrolyte abnormalities, and administration of digoxin-specific antibody fragments (Digibind) for life-threatening toxicity. Activated charcoal may be effective if administered soon after ingestion. Supportive care including atropine for bradycardia and appropriate antiarrhythmic therapy may be necessary.

Storage

Store at controlled room temperature (20-25°C or 68-77°F) in the original container with the lid tightly closed. Protect from light and moisture. Keep out of reach of children and pets. Do not transfer tablets to other containers as this may affect stability. Do not use if the product appears discolored or shows signs of deterioration. Proper disposal of unused medication is important to prevent accidental ingestion.

Disclaimer

This information is provided for educational purposes only and does not constitute medical advice. Digoxin is a prescription medication that should only be used under the supervision of a qualified healthcare provider. Individual patient needs may vary, and therapeutic decisions should be based on professional medical judgment. Always consult with a healthcare professional before starting, stopping, or changing any medication regimen.

Reviews

Clinical studies consistently demonstrate digoxin’s efficacy in improving symptoms and reducing hospitalizations in heart failure patients when used within appropriate serum concentration ranges. The DIG trial, a landmark study, established its role in modern heart failure management. Many cardiologists note its particular value in specific patient subsets, especially those with difficult-to-control atrial fibrillation and concomitant systolic dysfunction. However, experts emphasize the necessity of careful patient selection, appropriate dosing, and vigilant monitoring due to its narrow therapeutic index and potential for serious toxicity.