Pharmacology · Cardiac glycosides
Digoxin !
A medicine from the foxglove plant that strengthens the heartbeat and slows the heart rate. The line between effect and toxicity is narrow.
Updated 2026-11-01
The figure shows digoxin bound to the Na⁺/K⁺-ATPase from pig kidney, in the E2P state; the binding site is very similar to the human pump.
Mechanism of action
Digoxin binds the outer face of the Na⁺/K⁺-ATPase and blocks it. Sodium builds up inside the heart cell, the sodium-calcium exchanger removes less calcium, and more calcium is released with each beat, so contraction is stronger. It also raises vagal tone, slowing the sinus node and conduction through the AV node.
- Digoxin blocks the Na⁺/K⁺ pump of the heart cell
- Sodium rises and the Na⁺/Ca²⁺ exchanger removes less calcium
- More calcium per beat: stronger contraction
- Vagal effect slows the AV node and the heart rate
Pharmacokinetics
- Absorption
- Absorbed by mouth; gut bacteria inactivate part of it in some people
- Distribution
- Very large volume of distribution: the drug concentrates in tissues, including skeletal muscle
- Elimination
- Mainly unchanged by the kidneys, so it accumulates in kidney failure
- Half-life
- About 36 to 48 hours with normal kidney function, much longer in kidney failure
- Onset and duration
- Without a loading phase, steady state takes about one to three weeks, depending on kidney function
Indications
- Heart failure with reduced ejection fraction that remains symptomatic despite standard treatment Heart failure →
- Ventricular rate control in atrial fibrillation, especially with heart failure Atrial fibrillation →
Adverse effects
Common
- Nausea, vomiting and loss of appetite
- Tiredness and confusion, especially in older adults
- Blurred, yellow or green-tinged vision
- Bradycardia
Contraindications
- Ventricular fibrillation
- Atrial fibrillation with an accessory pathway (Wolff-Parkinson-White), unless that pathway is blocked
- Hypertrophic cardiomyopathy with outflow obstruction (the stronger contraction worsens it)
Key interactions
- Loop or thiazide diuretics
- Hypokalaemia and hypomagnesaemia increase toxicity
- Amiodarone, verapamil or quinidine
- Higher digoxin levels and more toxicity
- Clarithromycin or erythromycin
- Higher digoxin levels from greater absorption
- Beta blockers or calcium channel blockers
- Additive AV node slowing, up to advanced heart block
What is monitored
- Potassium and magnesium
- Kidney function
- Heart rate and ECG
- Serum digoxin level when toxicity is suspected or kidney function changes
Test yourself
Think of the answer, then tap the question to see it.
Why does hypokalaemia increase digoxin toxicity?
Potassium and digoxin compete for the same site on the pump. With low potassium, digoxin binds more, so the same drug level produces a stronger, more toxic effect.
Which visual symptom is characteristic of digoxin toxicity?
Changes in colour vision, with a yellow-green tint or halos around lights, along with blurred vision.
How does digoxin slow the heart rate in atrial fibrillation?
It increases vagal tone on the AV node, slowing conduction and lengthening refractoriness, so fewer atrial impulses reach the ventricles.
Why does digoxin accumulate in older adults with kidney failure?
It is eliminated mainly unchanged by the kidneys; with lower filtration its half-life lengthens and levels rise.
Which drugs typically raise serum digoxin levels?
Amiodarone, verapamil and quinidine, and macrolides such as clarithromycin or erythromycin, which increase its absorption.
Related drugs
Related conditions
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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Digoxin: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2017); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026); eEML - Electronic Essential Medicines List (World Health Organization, 2025); DailyMed - DIGOXIN tablet (DailyMed (U.S. National Library of Medicine), 2026).
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Representative model, for educational purposes only.