Digoxin
also: cardiac glycoside
Overview
Rate control in AF (esp. sedentary / coexisting HF) and a positive inotrope in heart failure. Narrow therapeutic index — a classic toxicity exam topic.
Mechanism
Inhibits the myocyte Na⁺/K⁺-ATPase → ↑intracellular Na⁺ → less Na⁺/Ca²⁺ exchange → ↑intracellular Ca²⁺ → positive inotropy. Increases vagal (parasympathetic) tone → slows AV-node conduction (rate control). Competes with K⁺ at the ATPase — so hypokalaemia worsens toxicity.
Indications
- AF rate control (sedentary patients, or add-on)
- Heart failure with reduced EF (symptom control)
Adverse effects
Nausea, vomiting, confusion, xanthopsia (yellow-green vision), arrhythmias.
Classically ventricular ectopy; "reverse tick" ST on ECG is a digoxin EFFECT, not toxicity.
Cautions & contraindications
Potentiates toxicity (less competition at Na⁺/K⁺-ATPase). Diuretics raise risk.
Enhances accessory-pathway conduction.
Renally cleared → accumulation; reduce dose.
Interactions
- Diuretics (hypokalaemia) → toxicity
- Amiodarone, verapamil, quinine → ↑digoxin levels (halve dose)
- Spironolactone
Monitoring & kinetics
U&E (esp. K⁺), renal function,Digoxin level only if toxicity suspected (sample ≥6 h post-dose),Toxicity treated with Digifab (digoxin-specific antibody fragments)
Renally excreted; long t½. Loading dose for rapid effect.
Choosing it
true
Source: BNF — Digoxin