Lanoxin (Digoxin) Tablet

Brand name: Lanoxin Generic name: Digoxin Drug class: Cardiac glycoside

Mechanism of Action

Digoxin inhibits the Na+/K+-ATPase pump in cardiac myocyte cell membranes. This inhibition raises intracellular sodium, which in turn stimulates Na+/Ca2+ exchange, increasing intracellular calcium. The result:

Positive inotropic effect - increased force and velocity of myocardial contraction
Vagomimetic (parasympathomimetic) effect - slows heart rate and decreases conduction velocity through the AV node
Neurohormonal deactivation - decreases activation of the sympathetic nervous system and renin-angiotensin system
Renal effect - inhibits Na+/K+-ATPase in the kidney, blunting tubular sodium resorption

It also shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period in the AV node.

Braunwald's Heart Disease, p. 160
Lippincott Illustrated Reviews: Pharmacology, p. 405

Indications (FDA-Approved)

Indication	Population
Chronic heart failure with reduced ejection fraction (HFrEF)	Adults and pediatric patients
Rate control in atrial fibrillation (AF)	Adults
Atrial flutter	Adults

Digoxin is recommended as a Class IIa agent for patients with symptomatic HFrEF who remain symptomatic despite optimal therapy with ACEi/ARNI, beta-blockers, and mineralocorticoid receptor antagonists, to reduce hospitalizations.

Dosage Forms

125 mcg (0.125 mg) scored tablet - yellow, imprint Y3B
250 mcg (0.25 mg) scored tablet - white, imprint X3A

Dosing

Setting	Dose
Heart failure (maintenance)	0.125 mg daily (most patients)
Maximum	0.25 mg daily
Elderly (>70 yrs)	0.125 mg daily or less
Renal impairment (CrCl <60 mL/min)	0.0625-0.125 mg daily, adjust by response
AF - acute (IV)	0.25 mg IV every 2 hrs up to 1.5 mg, then maintenance
AF - non-acute or maintenance	0.125-0.375 mg PO daily

Target serum levels:

Heart failure (HFrEF): 0.5-0.9 ng/mL
Atrial fibrillation/flutter: 1.0-2.0 ng/mL (trough)
Serum level should be <1.0 ng/mL in elderly and renal-impaired patients

Contraindications

Ventricular fibrillation
Wolff-Parkinson-White (WPW) syndrome / accessory AV pathway
Acute myocardial infarction (use with caution)
Myocarditis

Warnings / Precautions

Sinus bradycardia and sinoatrial block
Pre-existing AV block
Planned electrical cardioversion (risk of ventricular arrhythmias)
Preserved LV systolic function (may decrease cardiac output)
Hypocalcemia reduces efficacy
Thyroid disorders and hypermetabolic states alter response
Hypokalemia and hypomagnesemia increase toxicity risk

Digoxin Toxicity

The therapeutic window is narrow. Toxicity risk is elevated with serum levels >2 ng/mL.

Risk factors for toxicity:

Hypokalemia, hypomagnesemia, hypercalcemia
Renal impairment (digoxin is renally cleared)
Elderly patients
Drug interactions (see below)

Signs and symptoms:

Cardiac: Bradycardia, heart block, ectopic ventricular beats, ventricular tachycardia/fibrillation, virtually any arrhythmia
GI: Nausea, vomiting, anorexia, abdominal pain
Neurological: Confusion, mental status changes, delirium, seizures
Visual: Yellow/green vision (xanthopsia), blurred vision, halos, scotomata
Hyperkalemia is common in acute toxicity; hypokalemia in chronic toxicity

Treatment of toxicity: Digoxin-specific Fab fragments (Digibind or Digifab) - anti-digoxin monoclonal antibody fragments that bind digoxin and remove it from tissues. Indicated for life-threatening arrhythmias, hyperkalemia (>5 mEq/L in acute toxicity), or ingestion of >10 mg in adults.

Lippincott Illustrated Reviews: Pharmacology, p. 406
Washington Manual of Medical Therapeutics

Key Drug Interactions

Interacting Drug/Class	Effect
P-glycoprotein inhibitors (amiodarone, verapamil, clarithromycin, quinidine)	Increased digoxin levels - toxicity risk
P-glycoprotein inducers (rifampin, St. John's Wort)	Decreased digoxin levels - reduced efficacy
Diuretics (thiazides, loop)	Electrolyte loss (hypokalemia/hypomagnesemia) increases toxicity risk
Antacids	Reduced digoxin absorption

Pharmacokinetics

Absorption: Oral bioavailability ~70-80%; affected by P-glycoprotein
Distribution: Wide; significant tissue binding (skeletal muscle, heart)
Elimination: Primarily renal (unchanged); half-life ~36-48 hours (prolonged in renal failure)
Protein binding: ~25% (relatively low)

Monitoring

Serum digoxin concentration (draw trough, 6-8 hours post-dose)
Renal function (BMP/CMP) - dose must be adjusted for kidney disease
Electrolytes (especially K+, Mg2+) - correct abnormalities before and during therapy
ECG for signs of toxicity

Lanoxin has one of the oldest histories in cardiology, first described from the foxglove plant (Digitalis lanata) by William Withering in 1775. Despite newer heart failure therapies, it still has a role as add-on therapy for symptom control and hospitalization reduction in HFrEF, and for ventricular rate control in AF, particularly in patients with concomitant heart failure.

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