It has the unique characteristic of increasing contractility (positive inotropy) while decreasing heart rate (negative chronotropy). It enhances an increase in intracellular ionized free calcium which in turn enhances myocardial contractility. Digoxin increases contractility without increasing ventricular rate. Sites of clearance are liver and kidney.

Indications of digoxin include congestive heart failure, atrial fibrillation and paroxysmal atrial tachycardia. The usual dose of digoxin is about 0.25 mg/d, with half that dose prescribed for the elderly (age > 65) and patients with renal insufficiency. When acute therapy is necessary, a loading dose of 1–1.5 mg is given over 24 hours

Digitalis toxicity includes anorexia, nausea, fatigue, visual disturbances, and confusion, severe conduction disturbances. The ECG manifestations may include sinus bradycardia, AV block, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, and fibrillation.

Factors such as renal insufficiency, electrolyte abnormalities (hypokalemia and hypercalcemia), hypothyroidism, pulmonary disease, drugs that can affect digoxin metabolism (quinidine, cyclosporine, verapamil, rifampin), can increase the risk of digitalis intoxication

Anesthetic consideration:

Some data suggest that halothane, ketamine, and curare may reduce the likelihood of digitalis-induced ventricular dysrhythmias.
Thiopental and fentanyl have no effect, whereas
Succinylcholine, neostigmine, and diazepam may induce dysrhythmias in patients taking digitalis.
More important to any discussion of digitalis-associated dysrhythmias and toxicity is prevention of hypokalemia, acid–base imbalance, hypoxia, hypercalcemia, and catecholamine excess states, and avoidance of medications that acutely increase digitalis serum levels.

4.5 Digitalis: