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Digoxin

Digoxin is a cardiac glycoside that has been used for centuries to manage heart failure and atrial fibrillation. Despite the advent of newer medications, digoxin remains a valuable therapeutic option due to its unique mechanism of action and clinical benefits. This article synthesizes information from the British National Formulary (BNF)Lippincott Textbook of Pharmacology, and Lange Basic & Clinical Pharmacology to provide a detailed overview of digoxin, including its mechanism, uses, dosing, side effects, precautions, and drug interactions.

Digoxin exerts its effects through two primary mechanisms:

  1. Positive Inotropic Effect:
    • Digoxin inhibits the Na-K-ATPase pump in cardiac myocytes, leading to increased intracellular sodium levels. This results in a secondary increase in intracellular calcium via the Na-Ca exchanger, enhancing myocardial contractility (LippincottLange).
  2. Negative Chronotropic Effect:
    • Digoxin increases vagal tone and reduces conduction through the atrioventricular (AV) node, making it effective in controlling ventricular rate in atrial fibrillation (BNF).
  1. Heart Failure with Reduced Ejection Fraction (HFrEF):
    • Improves symptoms and reduces hospitalizations in patients with HFrEF, particularly in those with persistent symptoms despite optimal therapy (BNF).
  2. Atrial Fibrillation (AF):
    • Controls ventricular rate in AF by slowing AV nodal conduction (Lippincott).
  • Heart Failure:
    • Loading dose (if rapid digitalization is needed): 0.75–1.5 mg in divided doses over 24 hours.
    • Maintenance dose: 125–250 mcg once daily (adjust based on renal function and serum digoxin levels) (BNF).
  • Atrial Fibrillation:
    • Maintenance dose: 62.5–250 mcg once daily (adjust based on heart rate response and serum levels) (Lippincott).

Administration:

  • Can be taken with or without food.
  • Regular monitoring of serum digoxin levels (therapeutic range: 0.5–2.0 ng/mL) is essential to avoid toxicity (Lange).
  • Common: Nausea, vomiting, anorexia, and fatigue (Lippincott).
  • Serious: Cardiac arrhythmias (e.g., bradycardia, AV block, ventricular tachycardia), visual disturbances (e.g., yellow-green halos), and confusion (BNF).
  • Renal Impairment: Digoxin is primarily excreted by the kidneys; reduce dose in patients with renal dysfunction (Lange).
  • Electrolyte Imbalances: Hypokalemia, hypomagnesemia, and hypercalcemia increase the risk of digoxin toxicity (Lippincott).
  • Pregnancy: Use only if benefits outweigh risks; monitor closely (BNF).
  • Contraindications: Ventricular fibrillation, hypertrophic obstructive cardiomyopathy (HOCM), and Wolff-Parkinson-White (WPW) syndrome (Lange).
  • Diuretics: Thiazides and loop diuretics can cause hypokalemia, increasing the risk of digoxin toxicity (BNF).
  • Amiodarone: Increases digoxin levels by reducing renal clearance; reduce digoxin dose by 50% (Lippincott).
  • Calcium Channel Blockers (e.g., verapamil): Increase digoxin levels and risk of toxicity (Lange).
  • Antibiotics (e.g., erythromycin, tetracycline): Alter gut flora, increasing digoxin absorption (BNF).

Digoxin is the generic name for this medication. It is marketed under the brand name Lanoxin® in some regions. Generic versions are widely available and cost-effective

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