Antiarrhythmics · Cardiovascular
Digoxin
Lanoxin® · Toloxin®(brand names vary by market)
The oldest drug on the ward, and still the one that catches people out.
Also: oral liquid, injection
Mechanism
Inhibits the sodium-potassium ATPase, raising intracellular sodium and, through the sodium-calcium exchanger, intracellular calcium: more forceful contraction. Separately, it increases vagal tone, which is where the rate control comes from.
Indications
- Rate control in atrial fibrillation, usually as a second agent
- Symptomatic heart failure with reduced ejection fraction
Formulations
Dosing concepts
Renal function
Renally cleared with a narrow therapeutic index, so a falling eGFR raises the level without anyone changing the dose. Most toxicity arrives this way.
Levels
A level is taken at least six hours after a dose, and is interpreted for toxicity rather than used to chase a target. Digoxin toxicity is a clinical diagnosis that a level supports.
Potassium
Hypokalemia potentiates it at the same concentration, because potassium and digoxin compete at the same pump. A 'normal' level in a hypokalemic patient can still be toxic.
Concepts, not prescribing instructions. Practice numbers live in current references and local protocols.
Pharmacokinetics
- Bioavailability
- 60 to 80% depending on formulation
- Half-life
- 36 to 48 h, much longer in renal impairment
- Elimination
- renal: P-glycoprotein substrate: amiodarone, verapamil, clarithromycin and others raise its level
- Protein binding
- ~25%
Adverse effects
- Nausea, vomiting, anorexiacommonUsually the first sign of toxicity, and routinely attributed to something else.
- Visual disturbance: blurring, yellow-green tinge, haloscommonClassic, specific, and worth asking about directly.
- Arrhythmia of almost any kindseriousBradyarrhythmias with increased automaticity are characteristic.
- Confusion, particularly in older adultscommon
Contraindications & precautions
Contraindications
- Ventricular fibrillation
- Atrial fibrillation with pre-excitation
- High-grade AV block without a pacemaker
Precautions
- Renal impairment
- Hypokalemia, hypomagnesemia, hypercalcemia
- Older adults and low body weight
- Concurrent P-glycoprotein inhibitors
Interactions
Monitoring
Renal function and potassium
The two variables that turn a stable dose toxic · Regularly, and with any acute illness
Heart rate and rhythm
Effect and toxicity are both here
Level, when toxicity is suspected
Not for routine titration; timing after the dose changes the interpretation
Counselling points
- Take it at the same time each day.
- Tell us about nausea, loss of appetite, or any change in your vision, particularly seeing halos or a yellow tinge.
- Let us know if you become unwell with vomiting or diarrhoea, because it affects this drug.
- Do not start any new medicine without checking, including over-the-counter ones.
Clinical pearls
- It controls rate at rest through vagal tone, and vagal tone disappears on exertion. A patient whose resting rate looks perfect can still be tachycardic climbing stairs, which is why it is rarely used alone in an active person.
- Digoxin-specific antibody fragments exist and work; the indications are haemodynamic instability, life-threatening arrhythmia, and severe hyperkalemia in acute poisoning.
- In acute toxicity the potassium is high, and giving calcium for it has traditionally been avoided. In chronic toxicity the potassium is often low. Two opposite pictures, one drug.
References & review
- Digoxin product monograph (consult the current version for your market) (monograph)
- Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed. (reference-work)
Last reviewed 2026-08-16 · jurisdiction: global · drug information changes; verify against current references before practice use.