Digoxin is a cardiac glycoside derived from the foxglove plant (see Digitalis). It strengthens the force of heart muscle contractions (positive inotropic effect) and slows the heart rate by reducing conduction through the atrioventricular (AV) node (negative chronotropic effect).
In modern cardiology, digoxin is used primarily for rate control in atrial fibrillation, particularly in patients with concurrent heart failure with reduced ejection fraction where beta-blockers or calcium channel blockers are insufficient or poorly tolerated. It may also be used as an add-on therapy in heart failure when symptoms persist despite other treatments. Its use has declined significantly as more effective agents (ACE inhibitors, beta-blockers, aldosterone antagonists, SGLT2 inhibitors) have become the cornerstone of heart failure treatment.
Digoxin has a narrow therapeutic index: the effective dose is close to the toxic dose, requiring careful monitoring. Signs of toxicity include nausea, vomiting, visual disturbances (characteristic yellow-green halos around lights), confusion, and dangerous arrhythmias including heart block and ventricular tachycardia. Toxicity is worsened by low potassium and magnesium, which are common in patients taking diuretics.
Digoxin levels can be measured in the blood using a trough level taken at least 6 hours after the last dose. Digoxin toxicity is treated by withholding the drug, correcting electrolyte abnormalities, and in severe cases, with digoxin-specific antibody fragments (Digibind). Kidney function should be monitored regularly in all patients taking digoxin, as it is renally excreted and dose reduction is needed in impaired kidney function.
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