Trade Names:Digoxin- Tablets, oral 125 mcg (0.125 mg)- Tablets, oral 250 mcg (0.25 mg)- Solution, pediatric, oral 50 mcg/mL (0.05 mg/mL)
Trade Names:Lanoxin- Tablets, oral 125 mcg (0.125 mg)- Tablets, oral 250 mcg (0.25 mg)- Injection, solution 250 mcg/mL (0.25 mg/mL)- Injection, solution, pediatric 100 mcg/mL (0.1 mg/mL)Apo-Digoxin (Canada)Digoxin Injection C.S.D. (Canada)Digoxin Pediatric Injection C.S.D. (Canada)PMS-Digoxin (Canada)
Increases force and velocity of myocardial systolic contraction (positive inotropic action), slows heart rate, decreases conduction velocity through AV node, and decreases the degree of activation of the sympathetic nervous system and renin-angiotensin system. All actions are mediated through effects on sodium-potassium ATPase.
T max is 1 to 3 h (tablets), 30 to 90 min (oral solution). Food slows the rate of absorption after oral administration (tablets).Bioavailability
100% (IV), 70% to 85% (oral solution), 60% to 80% (tablets).
6 to 8 h tissue-distribution phase. Large apparent Vd. Crosses blood-brain barrier and placenta. Approximately 25% protein bound.
Approximately 16% metabolized; metabolites formed by hydrolysis, oxidation, and conjugation.
Elimination follows first-order kinetics. 50% to 70% excreted unchanged in the urine (after IV administration). Half-life is 1.5 to 2 days.
0.5 to 2 h (oral), 5 to 30 min (IV).
2 to 6 h (oral), 1 to 4 h (IV).
Cl correlates with CrCl. Half-life is 3.5 to 5 days in anuric patients. Dosage adjustment recommended.Hepatic Function Impairment
Plasma digoxin concentrations not affected by acute hepatitis.Race
Pharmacokinetics not expected to be affected by race.
Treatment of mild to moderate heart failure; control of ventricular response rate in chronic atrial fibrillation.
Ventricular fibrillation; hypersensitivity to digoxin or to other digitalis preparations.
400 to 600 mcg (0.4 to 0.6 mg) IV 500 to 750 mcg (0.5 to 0.75 mg) PO as a single dose; additional doses of 100 to 300 mcg (0.1 to 0.3 mg) or 125 to 375 mcg (0.125 to 0.375 mg) PO may be given cautiously at 6- to 8-h intervals until clinical evidence of an adequate effect is noted.Gradual digitalization with a maintenance dose
Initial dosage of 250 mcg (0.25 mg) PO once daily. Increase doses every 2 wk according to clinical response. Usual maintenance dosage is 125 to 500 mcg (0.125 to 0.5 mg) PO once daily.American College of Cardiology/American Heart Association (ACC/AHA) guidelines
Loading dose not needed. Initial and maintenance dosage is 125 mcg (0.125 mg) to 250 mcg (0.25 mg) daily.Infants and Children
Individualize dosage. Usual doses are listed in the previous section.Special populations Elderly
Initial dosage of 125 mcg (0.125 mg) once daily for treatment of heart failure. Per ACC/AHA guidelines, the initial dosage is 125 mcg (0.125 mg) daily or every other day.Renal function impairment
Initial dosage of 125 mcg (0.125 mg) once daily; 62.5 mcg (0.625 mg) once daily in patients with marked renal impairment. Per ACC/AHA guidelines, the initial dosage is 125 mcg (0.125 mg) daily or every other day.Low lean body mass
Per ACC/AHA guidelines, the initial dosage is 125 mcg (0.125 mg) daily or every other day.Atrial FibrillationInfants and Children Usual Pediatric Digitalizing and Maintenance Dosages With Healthy Renal Function Based on Lean Body Weight Age Digitalizing dose (mcg/kg) Daily maintenance dose as % of loading dose (mcg/kg in 2 to 3 divided doses) PO IV Premature 20 to 30 15 to 25 20% to 30% Term 25 to 35 20 to 30 25% to 35% 1 to 24 mo 35 to 60 30 to 50 25% to 35% 2 to 5 yr 30 to 40 25 to 35 25% to 35% 5 to 10 yr 20 to 35 15 to 30 25% to 35% > 10 yr 10 to 15 8 to 12 25% to 35% Adults
Peak digoxin body stores greater than 8 to 12 mcg/kg are usually required. Titrate doses to the minimum dose. The following dosages are according to ACC/AHA guidelines.Acute setting
Loading dose of 250 mcg (0.25 mg) IV every 2 h (up to 1,500 mcg [1.5 mg]) (onset at least 60 min) followed by a maintenance dosage of 125 to 375 mcg (0.125 to 0.375 mg) daily IV or PO.Nonacute setting
Loading dose of 500 mcg (0.5 mg) daily PO (onset 2 days) followed by a maintenance dosage of 125 to 375 mcg (0.125 to 0.375 mg) daily PO .
Store at 59° and 86°F. Store in a dry place and protect from light. Immediate use of the diluted injection is recommended
Digoxin serum concentrations may be reduced, decreasing the efficacy. Monitor digoxin serum concentrations and adjust the dose as needed.Alprazolam, antiarrhythmic agents (ie, amiodarone, propafenone, quinidine), azole antifungal agents (ie, itraconazole, ketoconazole), calcium channel blockers (ie, diltiazem, nifedipine, verapamil), carvedilol, conivaptan, cyclosporine, epoprostenol, gatifloxacin, macrolide antibiotics (eg, clarithromycin, erythromycin), nefazodone, NSAIDs (eg, diclofenac, ibuprofen, indomethacin), protease inhibitors (ie, ritonavir, saquinavir), proton pump inhibitors (eg, lansoprazole, omeprazole, rabeprazole), quinine, ranolazine, serotonin reuptake inhibitors (eg, fluoxetine, paroxetine, sertraline), telithromycin, telmisartan, tetracyclines (eg, tetracycline)
Digoxin serum concentrations may be elevated, increasing the pharmacologic effects and risk of adverse reactions and toxicity. Observe the clinical response of the patient and monitor digoxin serum concentrations. Adjust the digoxin dose as needed.Aluminum salts (eg, aluminum hydroxide, kaolin-pectin, magaldrate), cholestyramine, colestipol, sucralfate
May decrease digoxin absorption, decreasing the efficacy. Administer digoxin at least 2 hours before the aluminum salt. Separate the administration times of digoxin and cholestyramine or colestipol by as much as possible. Separate the administration times of digoxin and sucralfate by at least 2 hours.Amiloride, spironolactone
The positive inotropic effect of digoxin may be attenuated. If an interaction is suspected, discontinue one or both drugs. In addition, spironolactone may interfere with digoxin assay, resulting in falsely elevated levels.Aminoglycosides, hydantoins (eg, phenytoin)
Digoxin pharmacologic effects may be increased or decreased. Observe the clinical response of the patient and monitor digoxin serum concentrations. Adjust the digoxin dose as needed.Amphotericin B
Amphotericin B injectable–induced hypokalemia may increase the risk of digoxin toxicity.Anticholinergics (eg, diphenoxylate, propantheline), metoclopramide
May increase digoxin absorption because of a decrease in GI motility. This interaction may be specific to the oral digoxin preparation and may be greater with slower dissolving tablets compared with digoxin elixir, or more recent tablet formulations.Dofetilide
Coadministration of digoxin and dofetilide has been associated with an increased rate of torsades de pointes.Food
Food, especially high-fiber meals, may decrease digoxin absorption.Loop diuretics (eg, furosemide), thiazide diuretics (eg, chlorothiazide)
Drug-induced electrolyte disturbances may predispose to digitalis-induced arrhythmias. Measure potassium and magnesium plasma concentrations and supplement low levels.Succinylcholine
May cause sudden extrusion of potassium from muscle cells, resulting in arrhythmias in digitalized patients.St. John's wort
Digoxin serum concentrations may be reduced, decreasing the efficacy. Monitor digoxin concentrations and adjust the digoxin dose as needed.Sympathomimetics
Coadministration of sympathomimetics and digoxin may increase the risk of cardiac arrhythmias.Thioamines (eg, methimazole, propylthiouracil)
Hyperthyroid patients may require a reduced dose of digoxin if they become euthyroid.Tramadol
Digoxin toxicity has been reported during postmarketing experience.
The use of therapeutic doses of digoxin may cause prolongation of the PR interval and depression of the ST segment on the ECG. Digoxin may produce false-positive ST-T changes on the ECG during exercise testing. These electrophysiologic effects reflect an expected effect of the drug and are not indicative of toxicity.
Tachycardia (2%); heart arrest, ventricular extrasystole (1%); accelerated junctional (nodal) rhythm, atrial tachycardia with block, AV dissociation, bradycardia, PR interval prolongation, rhythm disturbances (eg, first-, second- [Wenckebach], or third-degree heart block [including asystole]), ST-segment depression, unifocal or multiform ventricular premature contractions (especially bigeminy or trigeminy), ventricular fibrillation, ventricular tachycardia. In children, the most common are conduction disturbances or supraventricular tachyarrhythmias (eg, atrial tachycardia [with or without block], junctional [nodal] tachycardia). Ventricular arrhythmias are less common.
Dizziness (6%); mental disturbances (eg, anxiety, delirium, depression, hallucination) (5%); headache (4%); apathy, confusion, disorientation, drowsiness, weakness.
Visual disturbances (eg, blurred or yellow vision, halo effect).
Diarrhea, nausea (4%); vomiting (2%); anorexia (1%).
Monitor apical pulse for 1 full min before administering. Withhold dose if pulse rate is less than 60 bpm in adult, less than 70 bpm in child, or less than 90 bpm in infant. Draw serum levels just before the next scheduled dose. If this is not possible, perform sampling at least 6 to 8 h after the last dose. About two-thirds of adults considered adequately digitalized (without evidence of toxicity) have serum digoxin concentrations ranging from 0.8 to 2 ng/mL. Monitor for signs of toxicity (eg, abdominal pain, anorexia, arrhythmias, bradycardia, ECG changes, headache, nausea, seizure, visual disturbance, vomiting). Be prepared to administer digoxin antibodies (digoxin immune fab) for severe overdose toxicity. Periodically assess serum electrolytes and creatinine.
Category C .
Excreted in breast milk.
Newborns show varying tolerance. Premature and immature infants are particularly sensitive; reduce and individualize dose as needed.
Use with caution; renal Cl likely to be reduced.
Excretion may be decreased, leading to digoxin accumulation and toxicity; adjust dosage.
Electrical conversion of arrhythmias may require dose reduction prior to electrical cardioversion. Digoxin may cause severe sinus bradycardia or sinoatrial block in patients with preexisting sinus node disease and may cause advanced or complete heart block in patients with preexisting incomplete AV block. Consider insertion of a pacemaker before treatment with digoxin in these patients. Unless conduction down the accessory pathway has been blocked (either pharmacologically or by surgery), do not use digoxin in patients with paroxysmal atrial fibrillation or flutter and a coexisting accessory AV pathway. Patients with certain disorders involving heart failure associated with preserved left ventricular ejection fraction may be particularly susceptible to toxicity of the drug. Such disorders include restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, and acute cor pulmonale. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction because of the inotropic effects of digoxin.
Anorexia, nausea, and vomiting may be associated with toxicity or CHF. Arrhythmias for which digoxin is indicated may also be a reflection of toxicity.
Maintain normal serum potassium, calcium, and magnesium levels. Hypokalemia, hypomagnesemia, and hypercalcemia may predispose the patient to digoxin toxicity.
Use with caution in patients with acute MI. The use of inotropic drugs may increase myocardial oxygen demand and ischemia.
Hypothyroidism may reduce the requirements for digoxin. Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states (eg, arteriovenous shunt, hyperthyroidism, hypoxia) are best treated by addressing the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment. Take care to avoid toxicity if digoxin is used.
Blurred or yellow vision, confusion, depression, disorientation, drowsiness, GI symptoms (ie, anorexia, diarrhea, nausea, vomiting), headache, heart block, progressive bradyarrhythmias, restlessness, ventricular arrhythmia, ventricular fibrillation, ventricular tachycardia, weakness. Conduction disturbances or supraventricular tachyarrhythmias are common manifestations of toxicity in children.
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