[1 ampoule $2.39; 1 tablet 6 cents]
- IV, PO
- atrial fibrillation
- cardiac failure
PRESENTATION AND ADMINISTRATION:
Lanoxin PG tablets 62.5mcg tablets (blue), Lanoxin 250mcg tablets (white), Lanoxin Paediatric Elixir 50mcg/ml.
Solution may be injected slowly over at least 10-20 minutes. Alternatively, dilute required dose to four or more times its volume (eg 2ml with at least 8ml of diluent) with dextrose 5%, normal saline, glucose and sodium chloride or water for injection and administer slowly over at least 10-20 minutes. The preferred method of administration is to add the required dose to 50-100ml of compatible IV fluid and to infuse over at least 10-20 minutes but preferably two or more hours. Discard any solution not used within 24 hours of preparation.
Store at room temperature and protect from light.
Compatible with the following IV fluids:
Normal saline, 5% dextrose, glucose and sodium chloride, Hartmanns
Digitalising (loading) dose: 500mcg; followed by 250mcg 6 hours later and a further 250mcg 6 hours after that
750-1500mcg 1-2 doses 6 hours apart
62.5mcg – 250mcg daily
Note: when converting from the oral to the IV formulation the dosage should be reduced by 33% to take account of the difference in bioavailability
DOSAGE IN RENAL FAILURE AND RENAL REPLACEMENT THERAPY:
- Dose in renal impairment [GFR (ml/min)]
<10: 62.5mcg three times a week to 62.5mcg daily
10-20: usually 125mcg daily
>20-50: usually 125mcg daily
- Dose in renal replacement therapy
Note: for patients with renal impairment interval between doses given during digitalisation should be lengthened to for example 8-10 hours.
DOSAGE IN PAEDIATRICS:
Digitalising (loading) dose:
15mcg/kg stat and then 5mcg/kg after 6 hours
3-5mcg/kg 12 hourly Note: – when converting from the oral to the IV formulation the dosage should be reduced by 33% to take account of the difference in bioavailability
CLINICAL PHARMACOLOGY: Lanoxin (digoxin) is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. Digoxin inhibits sodium- potassium ATPase, an enzyme that regulates the quantity of sodium and potassium inside cells. Inhibition of the enzyme leads to an increase in the intracellular concentration of sodium and thus (by stimulation of sodium-calcium exchange) an increase in the intracellular concentration of calcium. The beneficial effects of digoxin result from direct actions on cardiac muscle, as well as indirect actions on the cardiovascular system mediated by effects on the autonomic nervous system.
CONTRAINDICATIONS 1. hypersensitivitytodigoxin
Sinus Node Disease and AV Block
Because digoxin slows sinoatrial and AV conduction, the drug commonly prolongs the PR interval. The drug may cause severe sinus bradycardia or sinoatrial block in patients with pre-existing sinus node disease and may cause advanced or complete heart block in patients with pre-existing incomplete AV block. In such patients consideration should be given to the insertion of a pacemaker before treatment with digoxin.
Accessory AV Pathway (Wolff-Parkinson-White Syndrome)
After intravenous digoxin therapy, some patients with paroxysmal atrial fibrillation or flutter and a coexisting accessory AV pathway have developed increased antegrade conduction across the accessory pathway bypassing the AV node, leading to a very rapid ventricular response or ventricular fibrillation.
Use in Patients With Electrolyte Disorders In patients with hypokalemia or hypomagnesemia, toxicity may occur despite serum digoxin concentrations below 2.0 ng/ml, because potassium or magnesium depletion sensitizes the myocardium to digoxin. Therefore, it is desirable to maintain normal serum potassium and magnesium concentrations in patients being treated with digoxin.
62.5mcg three times a week to 62.5mcg daily 62.5mcg three times a week to 62.5mcg daily usually 125mcg daily
Hypercalcemia from any cause predisposes the patient to digitalis toxicity. Calcium, particularly when administered rapidly by the intravenous route, may produce serious arrhythmias in digitalized patients. On the other hand, hypocalcemia can nullify the effects of digoxin in humans; thus, digoxin may be ineffective until serum calcium is restored to normal.
Use in Thyroid Disorders and Hypermetabolic States Hypothyroidism may reduce the requirements for digoxin. Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states (e.g., hyperthyroidism, hypoxia, or arteriovenous shunt) are best treated by addressing the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment. Care must be taken to avoid toxicity if digoxin is used.
Digoxin toxicity may develop in the critically ill, particularly if the patient has renal impairment. Monitoring is not routinely required but should be considered. Spec Collection: Plain (Red) or SST (Yellow); Paediatric and Neonatal only: 0.4 mL green microtainer.
Therapeutic Range 0.6-1.2 nmol/L. Recommended sampling: 8-24 hours post dose. If a patient is commenced on digoxin in the ICU levels should not be measured until the drug has achieved steady state at 5-7 days.
Drug/Laboratory Test Interactions:
None if note
IMPORTANT DRUG INTERACTIONS FOR THE ICU Potassium-depleting diuretics are a major contributing factor to digitalis toxicity. Calcium, particularly if administered rapidly by the intravenous route, may produce serious arrhythmias in digitalized patients. Quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise the serum digoxin concentration due to a reduction in clearance and/or in volume of distribution of the drug, with the implication that digitalis intoxication may result. Erythromycin and clarithromycin (and possibly other macrolide antibiotics) and tetracycline may increase digoxin absorption in patients who inactivate digoxin by bacterial metabolism in the lower intestine, so that digitalis intoxication may result. Rifampin may decrease serum digoxin concentration, especially in patients with renal dysfunction, by increasing the non-renal clearance of digoxin.
Ventricular extrasystoles, tachycardia, bradycardias, heart block, cardiac arrest
Anorexia, nausea, vomiting, diarrhoea, abdominal pain
Headache, dizziness, mental disturbances, visual disturbances.
Infants and Children The side effects of digoxin in infants and children differ from those seen in adults in several respects. Although digoxin may produce anorexia, nausea, vomiting, diarrhea, and CNS disturbances in young patients, these are rarely the initial symptoms of overdosage. Rather, the earliest and most frequent manifestation of excessive dosing with digoxin in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia. The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia.
Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmia or alteration in cardiac conduction that develops in a child taking digoxin should be assumed to be caused by digoxin, until further evaluation proves otherwise.