Conditions · Emergency medicine and toxicology
Digoxin toxicity !
Excess digoxin, a heart medicine, causes nausea, vision changes and dangerous heart rhythms. It is often triggered by kidney problems or low potassium.
Updated 2026-11-01
Structures involved
Tap one to see what it is and open it in 3D.
- Atrioventricular (AV) node
- Retina
- Sinoatrial (SA) node
- Bundle of His
- Left ventricle
- Right atrium
- Optic nerve
- Kidneys
Why it happens
- Cardiac excitation–contraction coupling
- How arrhythmias arise
- Potassium balance
- Na⁺/K⁺-ATPase (sodium pump)
What it is
Poisoning by digoxin or other cardiac glycosides, either from an acute overdose or, more often, from gradual accumulation during treatment of heart failure or atrial fibrillation. Its narrow therapeutic range makes toxicity common.
Who gets it
Mostly chronic toxicity in older adults with heart failure or atrial fibrillation, kidney impairment and several medicines. Plants containing cardiac glycosides (such as oleander) can cause similar poisoning.
Causes
- Reduced kidney clearance (acute kidney injury, chronic kidney disease, dehydration)
- Drug interactions that raise digoxin levels (amiodarone, verapamil, quinidine, some macrolides)
- Intentional or accidental acute overdose
- Ingestion of cardiac glycoside-containing plants
Risk factors
- Older age and low body mass
- Hypokalaemia (often from diuretics), hypomagnesaemia and hypercalcaemia
- Hypothyroidism and myocardial ischaemia
- Multiple medicines and dosing errors
Pathophysiology
Digoxin inhibits the sodium-potassium ATPase, raising intracellular calcium and contractility, and increases vagal tone, slowing the AV node. In toxicity, calcium overload causes delayed afterdepolarisations and increased automaticity, while vagal effects cause bradycardia and AV block. Acute overdose blocks the pump throughout the body and raises serum potassium.
Symptoms and signs
- Nausea, vomiting, loss of appetite and abdominal pain (often first)
- Visual disturbances: blurred vision, yellow-green colour tint (xanthopsia) and halos
- Confusion, fatigue and weakness, especially in older adults
- Palpitations, dizziness and fainting
Diagnosis
- Clinical
- Clinical suspicion in anyone taking digoxin who develops gastrointestinal, visual or neurological symptoms or a new arrhythmia, especially with kidney impairment or a new interacting drug.
- Tests
- Serum digoxin level taken at least 6 hours after the last dose (levels do not perfectly match toxicity), potassium, magnesium, calcium, creatinine and ECG. Typical arrhythmias: frequent ventricular ectopy and bigeminy, atrial tachycardia with block, AV block and bidirectional VT. The 'scooped' ST segment is a digoxin effect, not proof of toxicity.
- Imaging
- Not needed for diagnosis; echocardiography for the underlying heart disease.
Differential diagnosis
- Gastroenteritis or other causes of vomiting
- Other causes of bradycardia: AV node disease, beta-blocker or calcium-channel-blocker toxicity
- Hyperkalaemia from kidney failure
- Delirium from other causes in older adults
Goal of treatment
Stop exposure, correct electrolytes, treat dangerous arrhythmias and neutralise digoxin with specific antibody fragments when indicated.
Treatment
- Acute
- Stop digoxin and interacting drugs; activated charcoal after a recent acute ingestion.
- Medical
- Digoxin-specific antibody fragments (Fab) for life-threatening arrhythmias, hyperkalaemia in acute poisoning or very high levels with symptoms.
- Medical
- Correction of potassium and magnesium; atropine for symptomatic bradycardia; temporary pacing if needed. Haemodialysis does not remove digoxin.
- Follow-up
- Continuous cardiac monitoring and repeated potassium. Nurses check the apical pulse for a full minute before each dose and report bradycardia, nausea or visual changes.
Complications
- Ventricular tachycardia or fibrillation
- Complete heart block
- Severe hyperkalaemia
- Cardiac arrest and death
Prognosis
Most chronic cases recover once digoxin is stopped and electrolytes corrected. Antibody fragments have greatly reduced mortality of severe poisoning; high potassium in acute overdose is a marker of severity.
Prevention
- Adjusting the dose to kidney function and age, and periodic level and electrolyte checks
- Review of interacting drugs before prescribing
- Patient education on early symptoms of toxicity
Test yourself
Think of the answer, then tap the question to see it.
Which visual symptom is classic in digoxin toxicity?
Yellow-green colour vision (xanthopsia) or halos around lights, with blurred vision.
Which electrolyte disorder precipitates chronic digoxin toxicity?
Hypokalaemia (often from diuretics); hypomagnesaemia and hypercalcaemia also increase risk.
Which arrhythmia is almost pathognomonic of digoxin toxicity?
Bidirectional ventricular tachycardia; atrial tachycardia with AV block is also typical.
What is the antidote for life-threatening digoxin toxicity?
Digoxin-specific antibody fragments (Fab).
What does the nurse check before giving digoxin?
The apical pulse for one full minute, plus symptoms of toxicity and recent potassium levels.
Related conditions
- Heart failure
- Atrial fibrillation
- Atrioventricular (heart) block
- Ventricular tachycardia
- Acute kidney injury
- Chronic kidney disease
- Hypomagnesaemia
- Beta-blocker and calcium-channel-blocker overdose
- Delirium
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Digitalis toxicity (MedlinePlus, US National Library of Medicine, 2026).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.
