Digoxin, originally derived from the foxglove flower, blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear however is perhaps due to increased vagal tone.
Intracellular calcium within the cardiac myocytes is increased by digoxin (due to calcium channels opening allowing calcium influx) resulting in increased inotropy (contractility) and thus digoxin is frequently used when atrial fibrillation and left ventricular systolic dysfunction coexist. Digoxin toxicity is a concern and is discussed elsewhere. Digoxin causes a characteristic appearance on the ECG with “reverse check mark” sign, even in the absence of toxicity.
Digoxin is effective to reduce ventricular rates at rest, however not effective during physical activity and thus it is recommended to use digoxin in combination with a beta-blocker or non-dihydropyridine calcium channel blocker.
Digoxin therapy gets a class I indication for the treatment of symptomatic systolic congestive heart failure. The DIG (Digitalis Intervention Group) trial showed no mortality benefit, however there was improvement in symptoms and fewer hospitalizations for heart failure. Subanalysis showed that keeping levels between 0.5 - 1.0 in men and 0.5 - 0.8 in women reduce the risk of toxicity while maintaining clinical benefit.
Commonly, if systolic heart failure is present in combination with atrial fibrillation and an uncontrolled ventricular rate, digoxin therapy is utilized.
Digoxin is only used in diastolic heart failure if atrial fibrillation is present with uncontrolled ventricular rates.
Digoxin does have a class IIa indication to control heart rates in atrial fibrillation when used in conjunction with a beta-blocker or non-dihydropyridine calcium channel blocker.
Digoxin has a class IIb indication to be used a sole agent to control heart rates in patients with atrial fibrillation and a class III indication (may be harmful) to be used as a sole agent to control heart rates in patients with paroxysmal atrial fibrillation.