💊 Digoxin

Digoxin is a cardiac glycoside derived from the foxglove plant, primarily used to improve myocardial contractility and slow the ventricular rate in atrial fibrillation.

Digoxin inhibits the Na+/K+-ATPase pump in myocardial cells, leading to an increase in intracellular sodium. This, in turn, reduces the activity of the Na+/Ca2+ exchanger, resulting in increased intracellular calcium. The increased calcium enhances myocardial contractility (positive inotropy). It also has vagomimetic effects, slowing conduction through the AV node and reducing heart rate.

Digoxin is indicated for the control of ventricular rate in chronic atrial fibrillation, especially when other rate-limiting agents are ineffective or contraindicated. It is also used in the treatment of chronic severe heart failure with reduced ejection fraction (HFrEF) in patients who remain symptomatic despite optimal standard therapy, particularly those with concomitant atrial fibrillation.

Absolute contraindications include ventricular tachycardia or fibrillation, hypertrophic obstructive cardiomyopathy, and Wolff-Parkinson-White syndrome with atrial fibrillation. It should be used with caution in patients with hypokalaemia, hypomagnesaemia, hypercalcaemia, and renal impairment, as these increase the risk of toxicity.

Digoxin has a narrow therapeutic index, and toxicity is common. Early signs include nausea, vomiting, anorexia, and visual disturbances (e.g., yellow-green halos). Cardiac arrhythmias (e.g., bradycardia, AV block, ventricular ectopics) are serious manifestations. Confusion and lethargy can also occur.

Serum digoxin levels should be monitored, especially during initiation, dose changes, or if toxicity is suspected. Electrolytes (potassium, magnesium, calcium) and renal function (creatinine, eGFR) must be checked regularly, as imbalances can precipitate toxicity. ECG monitoring is important to assess heart rate and rhythm.

When prescribing, always check renal function and current electrolyte levels. Counsel the patient on the narrow therapeutic window and the importance of reporting any signs of toxicity (nausea, visual changes, palpitations). Emphasise the need for regular blood tests.

Digoxin's mechanism involves Na+/K+-ATPase inhibition. Remember its narrow therapeutic index and the classic signs of toxicity (yellow vision, GI upset, arrhythmias). Hypokalaemia is a major risk factor for toxicity. It's used for rate control in AF and in severe HFrEF.

SBA questions frequently test the narrow therapeutic index and the signs of digoxin toxicity (GI, visual, cardiac). Scenarios involving electrolyte imbalances (especially hypokalaemia) precipitating toxicity are common. Questions might also explore its specific role in rate control for AF vs. contractility in heart failure.