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Special Alerts

Digoxin 0.25 mg Tablet Recall by Repackaging Company Due to Size Variability - May 2009

A-S Medication Solutions, a drug repackaging company, has issued a voluntary recall of all 0.25 mg Caraco brand digoxin tablets (white scored tablet with 441 imprint; NDC 54569-5758-0; 30 count) distributed prior to March 31, 2009 and within the expiration date of August 2011. The manufacturer states that the tablets may be of differing sizes, thus posing a risk of variable digoxin content.

For additional information, please refer to:

http://www.fda.gov/Safety/Recalls/ArchiveRecalls/ucm150734.htm

http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm128096.htm

Digoxin Tablet Recall Due to Potentially Variable Content of Active Ingredient - March 2009

Caraco Pharmaceutical Laboratories, Ltd, with awareness by the U.S. Food and Drug Administration (FDA), has issued a voluntary recall of all unexpired lots of 0.125 mg and 0.25 mg digoxin tablets distributed prior to March 31, 2009, and within expiration of September 2011. The manufacturer states that the tablets may be of differing sizes, thus posing a risk of variable digoxin content.

For additional information, including the product NDC numbers affected, please refer to:

http://www.fda.gov/Safety/Recalls/ArchiveRecalls/2009/ucm128443.htm

http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm128096.htm

Medication Safety Issues

Sound-alike/look-alike issues:

Digoxin may be confused with Desoxyn®, doxepin

Lanoxin® may be confused with Lasix®, levothyroxine, Levoxyl®, Levsinex®, Lomotil®, Lonox®, Mefoxin®, naloxone, Xanax®

High alert medication: The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs which have a heightened risk of causing significant patient harm when used in error.

International issues:

Dilacor®: Brand name for diltiazem in the U.S.; brand name for verapamil in Brazil; brand name for barnidipine in Argentina

Lanoxin® may be confused with Lemoxin® which is a brand bane for cefuroxime in Mexico

Lanoxin® may be confused with Limoxin® which is a brand name for amoxicillin in Mexico

Pronunciation

(di JOKS in)

U.S. Brand Names

• Lanoxicaps® [DSC]
• Lanoxin®

Generic Available

Yes: Excludes capsule

Canadian Brand Names

• Apo-Digoxin®
• Digoxin CSD
• Lanoxicaps®
• Lanoxin®
• Novo-Digoxin
• Pediatric Digoxin CSD

Pharmacologic Category

• Antiarrhythmic Agent, Class IV
• Cardiac Glycoside

Pharmacologic Category Synonyms

• Class IV Antiarrhythmic Agent
• Vaughan-Williams Class IV Antiarrhythmic
• Digitalis Glycoside

Use: Labeled Indications

Treatment of congestive heart failure and to slow the ventricular rate in tachyarrhythmias such as atrial fibrillation, atrial flutter, and supraventricular tachycardia (paroxysmal atrial tachycardia); cardiogenic shock

Pregnancy Risk Factor

C

Lactation

Enters breast milk (small amounts)/compatible

Contraindications

Hypersensitivity to digoxin or any component of the formulation; hypersensitivity to cardiac glycosides (another may be tried); history of toxicity; ventricular tachycardia or fibrillation; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; amyloid disease; second- or third-degree heart block (except in patients with a functioning artificial pacemaker); Wolff-Parkinson-White syndrome and atrial fibrillation concurrently

Warnings/Precautions

Concerns related to adverse effects:

• Proarrhythmic effects: Watch for proarrhythmic effects (especially with digoxin toxicity)

Disease-related concerns:

• Acute MI: Use with caution in patients with an acute MI (within 6 months).

• Electrolyte imbalance: Correct electrolyte disturbances, especially hypokalemia or hypomagnesemia, prior to use and throughout therapy.

• Heart failure (HF): Withdrawal in HF patients may lead to recurrence of HF symptoms.

• Hypermetabolic states: Atrial arrhythmias associated with hypermetabolic states are very difficult to treat.

• Renal impairment: Use with caution in patients with renal impairment; dosage adjustment needed.

• Sinus nodal disease: Use with caution in patients with sinus nodal disease; may worsen.

Concurrent drug therapy issues:

• Amiodarone/quinidine/verapamil: Adjust dose when amiodarone, quinidine, or verapamil are added to a patient on digoxin.

• Calcium: Especially when administered rapidly I.V., calcium can produce serious arrhythmias in digitalized patients.

Other warnings/precautions:

• CAST trial: In the Cardiac Arrhythmia Suppression Trial (CAST), recent (>6 days but <2 years ago) myocardial infarction patients with asymptomatic, non-life-threatening ventricular arrhythmias did not benefit and may have been harmed by attempts to suppress the arrhythmia with flecainide or encainide. An increased mortality or nonfatal cardiac arrest rate (7.7%) was seen in the active treatment group compared with patients in the placebo group (3%). The applicability of the CAST results to other populations is unknown. Antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias.

• Elective electrical cardioversion: Reduce or hold dose 1-2 days before elective electrical cardioversion.

• Rate control: When using digoxin for rate control, it works best in a sedentary patient.

• Serum monitoring: Serum concentration monitoring should be done before the next dose (patient can hold AM dose for blood test) for an accurate assessment.

Adverse Reactions

Incidence not always reported.

Cardiovascular: Heart block; first-, second- (Wenckebach), or third-degree heart block; asystole; atrial tachycardia with block; AV dissociation; accelerated junctional rhythm; ventricular tachycardia or ventricular fibrillation; PR prolongation; ST segment depression

Central nervous system: Visual disturbances (blurred or yellow vision), headache (3%), dizziness (5%), apathy, confusion, mental disturbances (4%), anxiety, depression, delirium, hallucinations, fever

Dermatologic: Maculopapular rash (2%), erythematous, scarlatiniform, papular, vesicular or bullous rash, urticaria, pruritus, facial, angioneurotic or laryngeal edema, shedding of fingernails or toenails

Gastrointestinal: Nausea (3%), vomiting (2%), diarrhea (3%), abdominal pain

Neuromuscular & skeletal: Weakness

<1% (Limited to important or life-threatening): Gynecomastia, thrombocytopenia, palpitation, unifocal or multiform ventricular premature contractions (especially bigeminy or trigeminy), anorexia, abdominal pain, intestinal ischemia, hemorrhagic necrosis of the intestines, increase plasma estrogen and decreased serum luteinizing hormone in men and postmenopausal women and decreased plasma testosterone in men, vaginal cornification, eosinophilia, sexual dysfunction, diaphoresis

Children are more likely to experience cardiac arrhythmia as a sign of excessive dosing. The most common are conduction disturbances or tachyarrhythmia (atrial tachycardia with or without block) and junctional tachycardia. Ventricular tachyarrhythmia are less common. In infants, sinus bradycardia may be a sign of digoxin toxicity. Any arrhythmia seen in a child on digoxin should be considered as digoxin toxicity. The gastrointestinal and central nervous system symptoms are not frequently seen in children.

Metabolism/Transport Effects

Substrate of CYP3A4 (minor)

Drug Interactions

5-ASA Derivatives: May decrease the absorption of Cardiac Glycosides. Risk C: Monitor therapy

Acarbose: May decrease the serum concentration of Digoxin. Risk C: Monitor therapy

Aminoglycosides: May decrease the absorption of Cardiac Glycosides. Exceptions: Amikacin; Gentamicin; Streptomycin; Tobramycin. Risk C: Monitor therapy

Aminoquinolines (Antimalarial): May increase the serum concentration of Cardiac Glycosides. Risk D: Consider therapy modification

Amiodarone: May increase the serum concentration of Cardiac Glycosides. Risk D: Consider therapy modification

Antifungal Agents (Azole Derivatives, Systemic): May increase the serum concentration of Cardiac Glycosides. Exceptions: Miconazole. Risk D: Consider therapy modification

Antineoplastic Agents: May decrease the absorption of Cardiac Glycosides. This may only affect digoxin tablets. Exceptions: Alitretinoin; Altretamine; Aminoglutethimide; Anastrozole; Asparaginase; AzaCITIDine; Busulfan; Capecitabine; CARBOplatin; Chlorambucil; CISplatin; Cladribine; Cytarabine (Liposomal); Dacarbazine; DACTINomycin; DAUNOrubicin Citrate (Liposomal); DAUNOrubicin Hydrochloride; Denileukin Diftitox; Docetaxel; Epirubicin; Estramustine; Etoposide; Etoposide Phosphate; Exemestane; Fludarabine; Fluorouracil; Gemcitabine; Goserelin; Hydroxyurea; IDArubicin; Ifosfamide; Irinotecan; Letrozole; Leuprolide; Lomustine; Mechlorethamine; Megestrol; Mercaptopurine; Mitomycin; Mitotane; Mitoxantrone; Nilutamide; Paclitaxel; Pegaspargase; Pentostatin; Polyestradiol; Porfimer; RiTUXimab; Streptozocin; Tamoxifen; Temozolomide; Teniposide; Thioguanine; Thiotepa; Topotecan; Toremifene; Tretinoin (Systemic); Valrubicin; VinBLAStine; Vinorelbine. Risk C: Monitor therapy

Antineoplastic Agents (Anthracycline): Cardiac Glycosides may diminish the cardiotoxic effect of Antineoplastic Agents (Anthracycline). Antineoplastic Agents (Anthracycline) may decrease the serum concentration of Cardiac Glycosides. The effects of liposomal formulations may be unique from those of the free drug, as liposomal formulation have unique drug disposition and toxicity profiles, and liposomes themselves may alter digoxin absorption/distribution. Risk C: Monitor therapy

Atorvastatin: May increase the serum concentration of Digoxin. Risk C: Monitor therapy

Beta-Blockers: May enhance the bradycardic effect of Cardiac Glycosides. Exceptions: Levobunolol; Metipranolol. Risk C: Monitor therapy

Bile Acid Sequestrants: May decrease the absorption of Cardiac Glycosides. Exceptions: Colesevelam. Risk C: Monitor therapy

Calcitriol: May enhance the arrhythmogenic effect of Cardiac Glycosides. Risk C: Monitor therapy

Calcium Channel Blockers (Nondihydropyridine): May enhance the AV-blocking effect of Cardiac Glycosides. Calcium Channel Blockers (Nondihydropyridine) may decrease the metabolism of Cardiac Glycosides. Risk D: Consider therapy modification

Carvedilol: May increase the serum concentration of Digoxin. Risk C: Monitor therapy

Conivaptan: May increase the serum concentration of Digoxin. Risk C: Monitor therapy

CycloSPORINE: May decrease the metabolism of Cardiac Glycosides. Risk D: Consider therapy modification

Dronedarone: Digoxin may enhance the AV-blocking effect of Dronedarone. Digoxin may also enhance the other electrophysiologic effects of Dronedarone. Dronedarone may increase the serum concentration of Digoxin. Management: Avoid concurrent use of digoxin when possible. If concurrent use is necessary, reduce adult digoxin dose by 50% and increase monitoring for both clinical response to therapy and the occurrence of adverse effects. Risk D: Consider therapy modification

Kaolin: May decrease the absorption of Cardiac Glycosides. Risk C: Monitor therapy

Macrolide Antibiotics: May increase the serum concentration of Cardiac Glycosides. Risk D: Consider therapy modification

Midodrine: Cardiac Glycosides may enhance the bradycardic effect of Midodrine. Risk C: Monitor therapy

Milnacipran: May enhance the adverse/toxic effect of Digoxin. The risk of postural hypotension and tachycardia may be increased, particularly with IV digoxin. Management: Avoid concurrent use of intravenous (IV) digoxin in patients receiving milnacipran. Use caution when using oral digoxin and milnacipran together, monitoring closely for possible postural hypotension and tachycardia. Risk D: Consider therapy modification

Nefazodone: May increase the serum concentration of Cardiac Glycosides. Risk C: Monitor therapy

Neuromuscular-Blocking Agents: May enhance the arrhythmogenic effect of Cardiac Glycosides. Risk C: Monitor therapy

Penicillamine: May decrease the serum concentration of Digoxin. Risk C: Monitor therapy

P-Glycoprotein Inducers: May decrease the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy

P-Glycoprotein Inhibitors: May increase the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy

Potassium-Sparing Diuretics: May diminish the therapeutic effect of Cardiac Glycosides. In particular, the inotropic effects of digoxin appear to be diminished. Potassium-Sparing Diuretics may increase the serum concentration of Cardiac Glycosides. This particular effect may be unique to Spironolactone. Risk C: Monitor therapy

Propafenone: May increase the serum concentration of Cardiac Glycosides. Risk C: Monitor therapy

Protease Inhibitors: May increase the serum concentration of Digoxin. Increased serum concentrations of digoxin may increase risk of AV nodal blockade. Risk C: Monitor therapy

QuiNIDine: May increase the serum concentration of Cardiac Glycosides. Risk D: Consider therapy modification

QuiNINE: May increase the serum concentration of Cardiac Glycosides. Risk D: Consider therapy modification

Ranolazine: May increase the serum concentration of Digoxin. Risk C: Monitor therapy

Spironolactone: May increase the serum concentration of Digoxin. Spironolactone (and/or its metabolites) may also interfere with the assays used to determine Digoxin concentrations, falsely increasing or decreasing Digoxin concentrations. Risk C: Monitor therapy

St Johns Wort: May decrease the serum concentration of Cardiac Glycosides. Risk C: Monitor therapy

Sucralfate: May decrease the serum concentration of Digoxin. Specifically, sucralfate may decrease the absorption of digoxin. Management: Administer digoxin at least 2 hours before or at least 6 hours after sucralfate. Risk D: Consider therapy modification

Telmisartan: May increase the serum concentration of Cardiac Glycosides. Risk C: Monitor therapy

Ethanol/Nutrition/Herb Interactions

Food: Digoxin peak serum levels may be decreased if taken with food. Meals containing increased fiber (bran) or foods high in pectin may decrease oral absorption of digoxin.

Herb/Nutraceutical: Avoid ephedra (risk of cardiac stimulation). Avoid natural licorice (causes sodium and water retention and increases potassium loss).

Storage

Protect elixir and injection from light.

Compatibility

Stable in D₅1/2NS with KCl 20 mEq, D₅W, D₁₀W, LR, 1/2NS, and NS. May be diluted fourfold in D₅W, NS, or SWFI for direct injection (or may be administered undiluted).

Y-site administration: Compatible: Ciprofloxacin, cisatracurium, diltiazem, famotidine, gatifloxacin, heparin with hydrocortisone sodium succinate, inamrinone, linezolid, meperidine, meropenem, midazolam, milrinone, morphine, potassium chloride, remifentanil, tacrolimus, vitamin B complex with C. Incompatible: Amphotericin B cholesteryl sulfate complex, fluconazole, foscarnet, propofol. Variable (consult detailed reference): Insulin (regular).

Compatibility in syringe: Compatible: Heparin, milrinone. Incompatible: Doxapram.

Compatibility when admixed: Compatible: Bretylium, cimetidine, floxacillin, furosemide, lidocaine, ranitidine, verapamil. Incompatible: Dobutamine.

Mechanism of Action

Congestive heart failure: Inhibition of the sodium/potassium ATPase pump which acts to increase the intracellular sodium-calcium exchange to increase intracellular calcium leading to increased contractility

Supraventricular arrhythmias: Direct suppression of the AV node conduction to increase effective refractory period and decrease conduction velocity - positive inotropic effect, enhanced vagal tone, and decreased ventricular rate to fast atrial arrhythmias. Atrial fibrillation may decrease sensitivity and increase tolerance to higher serum digoxin concentrations.

Pharmacodynamics/Kinetics

Onset of action: Oral: 1-2 hours; I.V.: 5-30 minutes

Peak effect: Oral: 2-8 hours; I.V.: 1-4 hours

Duration: Adults: 3-4 days both forms

Absorption: By passive nonsaturable diffusion in the upper small intestine; food may delay, but does not affect extent of absorption

Distribution:

Normal renal function: 6-7 L/kg

V_d: Extensive to peripheral tissues, with a distinct distribution phase which lasts 6-8 hours; concentrates in heart, liver, kidney, skeletal muscle, and intestines. Heart/serum concentration is 70:1. Pharmacologic effects are delayed and do not correlate well with serum concentrations during distribution phase.

Hyperthyroidism: Increased V_d

Hyperkalemia, hyponatremia: Decreased digoxin distribution to heart and muscle

Hypokalemia: Increased digoxin distribution to heart and muscles

Concomitant quinidine therapy: Decreased V_d

Chronic renal failure: 4-6 L/kg

Decreased sodium/potassium ATPase activity - decreased tissue binding

Neonates, full-term: 7.5-10 L/kg

Children: 16 L/kg

Adults: 7 L/kg, decreased with renal disease

Protein binding: 30%; in uremic patients, digoxin is displaced from plasma protein binding sites

Metabolism: Via sequential sugar hydrolysis in the stomach or by reduction of lactone ring by intestinal bacteria (in ~10% of population, gut bacteria may metabolize up to 40% of digoxin dose); metabolites may contribute to therapeutic and toxic effects of digoxin; metabolism is reduced with CHF

Bioavailability: Oral (formulation dependent): Elixir: 75% to 85%; Tablet: 70% to 80%

Half-life elimination (age, renal and cardiac function dependent):

Neonates: Premature: 61-170 hours; Full-term: 35-45 hours

Infants: 18-25 hours

Children: 35 hours

Adults: 38-48 hours

Adults, anephric: 4-6 days

Half-life elimination: Parent drug: 38 hours; Metabolites: Digoxigenin: 4 hours; Monodigitoxoside: 3-12 hours

Time to peak, serum: Oral: ~1 hour

Excretion: Urine (50% to 70% as unchanged drug)

Dosage

When changing from oral (tablets or liquid) or I.M. to I.V. therapy, dosage should be reduced by 20% to 25%. Refer to the following: See table.

Dosing adjustment/interval in renal impairment:

Cl_cr 10-50 mL/minute: Administer 25% to 75% of dose or every 36 hours

Cl_cr <10 mL/minute: Administer 10% to 25% of dose or every 48 hours

Reduce loading dose by 50% in ESRD

Hemodialysis: Not dialyzable (0% to 5%)

Administration: I.M.

Inject no more than 2 mL per injection site. May cause intense pain.

Administration: I.V.

May be administered undiluted or diluted fourfold in D₅W, NS, or SWFI for direct injection. Less than fourfold dilution may lead to drug precipitation. Inject slowly over ?5 minutes

Administration: I.V. Detail

pH: 6.8-7.2

Monitoring Parameters

When to draw serum digoxin concentrations: Digoxin serum concentrations are monitored because digoxin possesses a narrow therapeutic serum range; the therapeutic endpoint is difficult to quantify and digoxin toxicity may be life-threatening. Digoxin serum levels should be drawn at least 4 hours after an intravenous dose and at least 6 hours after an oral dose (optimally 12-24 hours after a dose).

Initiation of therapy:

If a loading dose is given: Digoxin serum concentration may be drawn within 12-24 hours after the initial loading dose administration. Levels drawn this early may confirm the relationship of digoxin plasma levels and response but are of little value in determining maintenance doses.

If a loading dose is not given: Digoxin serum concentration should be obtained after 3-5 days of therapy.

Maintenance therapy:

Trough concentrations should be followed just prior to the next dose or at a minimum of 4 hours after an I.V. dose and at least 6 hours after an oral dose.

Digoxin serum concentrations should be obtained within 5-7 days (approximate time to steady-state) after any dosage changes. Continue to obtain digoxin serum concentrations 7-14 days after any change in maintenance dose. Note: In patients with end-stage renal disease, it may take 15-20 days to reach steady-state.

Additionally, patients who are receiving potassium-depleting medications such as diuretics, should be monitored for potassium, magnesium, and calcium levels.

Digoxin serum concentrations should be obtained whenever any of the following conditions occur:

Questionable patient compliance or to evaluate clinical deterioration following an initial good response

Changing renal function

Suspected digoxin toxicity

Initiation or discontinuation of therapy with drugs (amiodarone, quinidine, verapamil) which potentially interact with digoxin; if quinidine therapy is started, the digoxin dose should be reduced by 25% to 50% and digoxin levels should be monitored closely. Any disease changes (hypothyroidism)

Any disease changes (hypothyroidism)

Heart rate and rhythm should be monitored along with periodic ECGs to assess both desired effects and signs of toxicity

Follow closely (especially in patients receiving diuretics or amphotericin) for decreased serum potassium and magnesium or increased calcium, all of which predispose to digoxin toxicity

Assess renal function

Be aware of drug interactions

Observe patients for noncardiac signs of toxicity, confusion, and depression

Reference Range

Digoxin therapeutic serum concentrations:

Congestive heart failure: 0.5-0.8 ng/mL

Arrhythmias: 0.8-2 ng/mL

Adults: <0.5 ng/mL; probably indicates underdigitalization unless there are special circumstances

Toxic: >2.5 ng/mL

Digoxin-like immunoreactive substance (DLIS) may cross-react with digoxin immunoassay. DLIS has been found in patients with renal and liver disease, congestive heart failure, neonates, and pregnant women (3rd trimester).

Dietary Considerations

Maintain adequate amounts of potassium in diet to decrease risk of hypokalemia (hypokalemia may increase risk of digoxin toxicity).

Patient Education

Take as directed; do not discontinue without consulting prescriber. Maintain adequate dietary intake of potassium (do not increase without consulting prescriber). Adequate dietary potassium will reduce risk of digoxin toxicity. Take pulse at the same time each day, hold medication as directed by prescriber. Notify prescriber of acute changes in pulse. Report loss of appetite, nausea, vomiting, persistent diarrhea, swelling of extremities, palpitations, "yellowing" or blurred vision, mental confusion or depression, or unusual fatigue. Pregnancy precaution: Inform prescriber if you are or intend to become pregnant.

Geriatric Considerations

Digitalis preparations (primarily digoxin) are frequently used to treat common cardiac diseases in the elderly (congestive heart failure, atrial fibrillation). Elderly are at risk for toxicity due to age-related changes; volume of distribution is diminished significantly; half-life is increased as a result of decreased total body clearance. Additionally, elderly frequently have concomitant diseases which affect the pharmacokinetics in digitalis glycosides; hypo- and hyperthyroidism and renal function decline will affect clearance of digoxin. Exercise in elderly will reduce serum concentrations of digoxin due to increased skeletal muscle uptake. Therefore, a knowledge of the physical activity of elderly helps interpret serum assays. Must be observant for noncardiac signs of toxicity in elderly such as anorexia, vision changes (blurred), confusion, and depression. Changes in dose may be necessary with declining renal function with age; monitor closely.

Anesthesia and Critical Care Concerns/Other Considerations

Clinical Pearls/Comments: Elderly are at risk for toxicity due to age-related changes; volume of distribution is diminished significantly; half-life is increased as a result of decreased total body clearance. Digoxin toxicity may be potentiated in patients with hypokalemia, hypomagnesemia, and hypercalcemia. Digoxin may also rapidly approach toxic levels in patients with renal failure. Signs of digoxin toxicity include both brady- and tachyarrhythmias. Bidirectional VT induced by digoxin indicates imminent development of ventricular fibrillation.

Digoxin has been used for many years in treatment of heart failure. Digoxin therapy is associated with a decrease in frequency in hospitalizations for exacerbations of heart failure. Digoxin use for ventricular rate control in patients with atrial fibrillation is a particularly useful strategy in those patients with coexisting systolic dysfunction. While digoxin may control ventricular response rate for atrial fibrillation at rest, the medication is less effective for rate control during exercise.

Cardiovascular Considerations

Digoxin has been used for many years in treatment of heart failure. Even though digoxin has a very narrow therapeutic index, it remains an important therapeutic strategy when added to standard therapy. When used in heart failure, it should be used only for systolic dysfunction and not diastolic dysfunction. While the long-term trials show no convincing reduction in cardiovascular mortality, digoxin therapy is associated with a decrease in frequency in hospitalizations for exacerbations of heart failure. A potential mechanism of benefit in heart failure is that digoxin may improve baroreflex sensitivity.

Digoxin use for ventricular rate control in patients with atrial fibrillation is a particularly useful strategy in those patients with coexisting systolic dysfunction. It is important to consider, however, that while digoxin may control ventricular response rate for atrial fibrillation at rest, the medication is less effective for rate control during exercise.

Digoxin toxicity may be potentiated in patients with hypokalemia, hypomagnesemia, and hypercalcemia. Digoxin may also rapidly approach toxic levels in patients with renal failure. For patients with renal failure, the loading dose is unchanged but maintenance doses may be adjusted and levels should be monitored very carefully. Signs of digoxin toxicity include both brady- and tachyarrhythmias. Bidirectional VT induced by digitalis toxicity indicates imminent development of ventricular fibrillation. The recent development of digoxin antibodies (Digibind®) allows rapid intervention for acute digoxin toxicity. However, it is important to note that after administration of Digibind®, measured digoxin levels cannot be used to follow effectiveness of antibody therapy because they seem to rise rapidly.

Dental Health: Effects on Dental Treatment

Sensitive gag reflex may cause difficulty in taking a dental impression.

Dental Health: Vasoconstrictor/Local Anesthetic Precautions

Use vasoconstrictor with caution due to risk of cardiac arrhythmias with digoxin

Mental Health: Effects on Mental Status

May cause sedation

Mental Health: Effects on Psychiatric Treatment

Phenytoin may decrease levels of digoxin; monitor levels

Nursing: Physical Assessment/Monitoring

Closely assess effects and interactions with other prescriptions, OTC medications, or herbal products patient may be taking. Assess results of laboratory tests (when beginning or changing dosage, especially with I.V. administration and when patients are receiving diuretics or amphotericin). Monitor therapeutic effectiveness and adverse reactions at beginning of therapy, periodically throughout therapy, or when changing dosage. Monitor for signs of digoxin toxicity. I.V.: Monitor ECG continuously. Oral: Monitor apical pulse before administering any dose. Assess knowledge/teach patient appropriate use, adverse reactions to report, and appropriate interventions to reduce side effects.

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [CAN] = Canadian brand name; [DSC] = Discontinued product

Capsule:

Lanoxicaps®: 100 mcg [contains ethanol; DSC]; 200 mcg [contains ethanol; DSC]

Injection, solution: 250 mcg/mL (1 mL, 2 mL)

Lanoxin®: 250 mcg/mL (2 mL) [contains ethanol 10% and propylene glycol 40%]

Injection, solution [pediatric]: 100 mcg/mL (1 mL)

Solution, oral: 50 mcg/mL (2.5 mL, 5 mL [DSC], 60 mL)

Tablet: 125 mcg, 250 mcg

Lanoxin®: 125 mcg, 250 mcg

Apo-Digoxin® [CAN]: 62.5 mcg, 125 mcg, 250 mcg

Pricing: U.S. (www.drugstore.com)

Capsules (Lanoxicaps)

0.1 mg (100): $39.99

Solution (Digoxin)

0.05 mg/mL (60): $36.99

Tablets (Digoxin)

0.125 mg (30): $19.26

0.25 mg (30): $18.69

Tablets (Lanoxin)

0.125 mg (30): $21.88

0.25 mg (30): $19.69

References

“Consensus Recommendations for the Management of Chronic Heart Failure. On Behalf of the Membership of the Advisory Council to Improve Outcomes Nationwide in Heart Failure,” Am J Cardiol, 1999, 83(2A):1A-38A.

Fuster V, Ryden LE, Asinger RW, et al, “ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation),” J Am Coll Cardiol, 2001, 38(4):1231-66.

“Guidelines for the Evaluation and Management of Heart Failure. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Committee on Evaluation and Management of Heart Failure,” Circulation, 1995, 92:2764-84.

Konstam MA, “Heart Failure Evaluation and Care of Patients With Left-Ventricular Systolic Dysfunction,” U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy Research, 1994. Clinical Practice Guideline: Number 940612.

Murgatroyd FD, Gibson SM, Baiyan X, et al, “Double-Blind Placebo-Controlled Trial of Digoxin in Symptomatic Paroxysmal Atrial Fibrillation,” Circulation, 1999, 99(21):2765-70.

Roberts SA, Diaz C, Nolan PE, et al, “Effectiveness and Costs of Digoxin Treatment for Atrial Fibrillation and Flutter,” Am J Cardiol, 1993, 72(7):567-73.

“The Effect of Digoxin on Mortality and Morbidity in Patients With Heart Failure. The Digitalis Investigation Group,” N Engl J Med, 1997, 336(8):525-33.

Ujhelyi MR and Robert S, “Pharmacokinetic Aspects of Digoxin-Specific Fab Therapy in the Management of Digitalis Toxicity,” Clin Pharmacokinet, 1995, 28(6):483-93.

International Brand Names

• Cardiacin (TW)
• Cardiogoxin (AR)
• Cardioxin (PH)
• Cardoxin (IL)
• Digomal (IT)
• Digosin (JP, KP)
• Digoxin (PL)
• Digoxin ”Dak” (DK)
• Digoxin-Sandoz (BF, BJ, CH, CI, ET, GH, GM, GN, ID, JP, KE, LR, MA, ML, MR, MU, MW, NE, NG, SC, SD, SL, SN, TN, TZ, UG, ZA, ZM, ZW)
• Digoxin-Zori (IL)
• Digoxina (ES, GT, HN, NI, PE)
• Digoxina Boehringer (ES)
• Digoxine Nativelle (LU)
• Digoxine Navtivelle (FR)
• Dilacor (BG)
• Dilanacin (CY, EG, IQ, JO, SD)
• Eudigox (IT)
• Fargoxin (ID)
• Grexin (TH)
• Lanacordin (ES)
• Lanicor (AE, AR, AT, BB, BF, BH, BJ, BM, BS, BZ, CI, CY, CZ, DE, EC, EG, ET, GH, GM, GN, GR, GY, HR, IL, IQ, IR, IT, JM, JO, KE, KW, LB, LR, LU, LY, MA, ML, MR, MU, MW, NE, NG, OM, QA, SA, SC, SD, SL, SN, SR, SY, TN, TT, TZ, UG, VE, YE, ZA, ZM, ZW)
• Lanikor (RU)
• Lanox (PH)
• Lanoxin (AE, AR, AU, BB, BE, BF, BH, BJ, BM, BR, BS, BZ, CI, CY, EG, ET, GB, GH, GM, GN, GR, GY, HK, ID, IE, IL, IN, IQ, IR, IT, JM, JO, JP, KE, KP, KW, LB, LR, LU, LY, MA, ML, MR, MU, MW, MX, MY, NE, NG, NL, NO, OM, PH, PK, PT, PY, QA, RU, SA, SC, SD, SE, SL, SN, SR, SY, TH, TN, TT, TW, TZ, UG, UY, YE, ZA, ZM, ZW)
• Lanoxin PG (NZ)
• Lenoxin (DE)
• Mapluxin (MX)
• Purgoxin (ZA)
• Sigmaxin (AU)
• Toloxin (TH)
• Vidaxil (MX)

Lexi-Comp.com

Last full review/revision October 2009

Content last modified October 2009