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Digoxin is a cardiac glycoside that has been used for many years to treat congestive heart failure, atrial fibrillation and paroxysmal atrial tachycardia. The use of digoxin for the treatment of heart failure has decreased following the availability of more effective and less toxic therapies, including angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, neprilysin angiotensin-receptor inhibitors, beta-blockers, and mineralocorticoid-receptor antagonists. The use of digoxin therapy for the treatment of atrial fibrillation has also decreased as alternative therapies with greater efficacy and reduced toxic effects have been developed.

 Different digoxin products have significant bioavailability differences. Many drugs interact with digoxin, often requiring an adjustment of the digoxin dose. Clearance of digoxin is low in premature neonates, increases in full term neonates, reaches a maximum in infants and decreases slowly during childhood and adulthood.  Approximately 20 to 30% of digoxin is bound to blood albumin, and factors such as older age, congestive heart failure, and renal failure reduce the volume of distribution, contributing to an increased risk of toxic effects

The major route of elimination of digoxin is through renal excretion. Blood level can rise in patients with reduced glomerular filtration rate. Circulating half-life is 1 to 1.6 days in patients with normal renal function and 3.5 to 4.5 days in anuric patients.

Digoxin level is frequently monitored because of the narrow therapeutic range and the potential for serious adverse drug events. Digoxin toxicity is characterized by confusion, dizziness, nausea, vomiting, diarrhea, weakness, and visual disturbances. Life-threatening consequences of digoxin toxicity include ventricular tachycardia, severe bradycardia, complete heart block, and shock.

Although serum levels of 0.8 to 2.1 ng/mL have historically been considered therapeutic, there is considerable overlap between therapeutic and toxic concentrations. Patients may experience signs and symptoms of digitalis intoxication at serum levels less than 2.1 ng/mL. Conversely, some patients may require serum levels in excess of 2.1 ng/mL to control arrhythmia.  

Digoxin-like reactive factors encompass a broad range of substances, both exogenous and endogenous, that may interfere with digoxin immunoassays. They are small molecular weight endogenous substances that are universally present, but usually only identified in patients with renal or liver failure, pregnant women, and newborn infants. Endogenous digoxin-like reactive factors may occur in patients with volume expansion and appear to have natriuretic effects. Exogenous digoxin-like immunoreactive substances include spironolactone, canrenone, and Chinese herbal medications. Spironolactone and related medications are not known to interfere with digoxin measurement using current generation digoxin immunoassays.

Treatment with digoxin immune Fab fragments (Digibind), which bind to digoxin and clear the drug from tissues, is indicated for the treatment of life-threatening arrhythmias and shock, as well as for the prevention of these events when hyperkalemia is present.  A blood sample must be obtained before the administration of digoxin-binding antibody fragments to measure digoxin concentration. Clearance of antibody fragments may take days to more than a week in patients with severe kidney dysfunction.

Routine measurement of serum digoxin concentration is probably not necessary in stable patients.  Digoxin measurement is necessary in the following situations:

  • After a patient has reached steady state with a new digoxin dose
  • Following significant change in renal function
  • Following addition or discontinuation of a potentially interacting drug
  • Following signs or symptoms consistent with digoxin toxicity.

Therapeutic range (trough) is 0.8-2.1 ng/mL. Trough levels  >3.0 ng/mL are considered critical.     

Trough specimens should be drawn 6 hours after the last dose. Specimen requirement is one SST tube of blood.

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