Digoxin Toxicity

Authors: Sidra Ali, Nikki Abela / Editor: Nikki Abela / Reviewer:
Charlotte Davies / Codes: / Published: 28/09/2021 / Reviewed: 04/08/2026

Unlike most overdoses we are used to, digoxin toxicity is usually unintentional. This is because digoxin (or dig, as we commonly refer to it) has a narrow therapeutic index and its toxicity can be life-threatening. Although it may also exhibit itself more acutely after an an overdose, it more commonly is seen as a chronically creeping digoxin levels, as is often seen in the elderly population.

What is digoxin?

Today, Digoxin is primarily used to regulate the ventricular response in atrial fibrillation and atrial flutter. It is also an effective treatment for heart failure patients who have persistent symptoms of heart failure despite conventional pharmacologic therapy with diuretics, ACE inhibitors, and a beta-blocker.

Mechanism of action

Digoxin works to increase intracellular Na+ by inhibiting the Na+/K+ ATPase pump in cardiac muscle cells. The subsequent increase in calcium levels lead to a more forceful contraction of cardiac muscle and allow the heart to work more efficiently.

Now that we know how it works, what happens when we take too much of it? Symptoms of digoxin toxicity include:

GIT: Nausea, vomiting, anorexia, diarrhoea
CVS: Palpitations, syncope, dyspnoea
CNS: Confusion, dizziness, delirium, fatigue
Visual: Blurred vision, yellow/green discolouration, haloes

As a side note, it is speculated that Van Gough experienced digitalis toxicity as it is thought he may have been given digoxin for seizure treatment and his “yellow period” has been blamed on this.

The Starry Night (1889) by Vincent Van Gogh. Original from Wikimedia Commons. Digitally enhanced by rawpixel.

Back to the current century, it is important to highlight here that serum digoxin levels do not always directly correspond to clinical toxicity. Patients can be asymptomatic with elevated serum digoxin levels. Equally, therapeutic levels can be harmful. However, the likelihood of toxicity increases progressively through the range 1.5 to 3 micrograms/litre.

Diagnosis

The diagnosis of digoxin toxicity is primarily a clinical diagnosis based on symptoms, as well as ECG changes and potassium levels. The cardinal abnormality in acute digoxin toxicity is hyperkalemia. Digoxin levels can be obtained, however, as we said already, elevated serum digoxin levels do not directly translate to digoxin toxicity, and measuring them is not recommended by toxbase.

ECG Features of Digoxin Toxicity

LITFL have some excellent pics of what these look like and you really really should go and check them out here .

ST depression – down-sloping or scooped (often referred to as a reverse tick or the Salvador Sagging Sign)
T wave changes – flattening, inversion or biphasic T waves
QT shortening
Premature beats – atrial, junctional or ventricular
Tachyarrhythmias – atrial tachycardia, accelerated junctional tachycardia
Prolonged PR interval
Bradyarrhythmias – sinus bradycardia, bundle branch block, AV block

Management

1.In cardiac arrest, take sample for digoxin levels if possible, and administer DigiFab, and contact the poisons service. Transfer for ECMO may be appropriate to give the digoxin a chance to wear off.

Weight (Adults and children)	DIGIFab dose (each vial should be reconstituted with 4 mL of sterile water by gentle mixing)
>40 kg	5 vials (200 mg)
20-40 kg	2 vials (80 mg)
20 kg	Reduced hospital admission

2. Charcoal:

Up to four doses of activated charcoal 50 g for adults; 1 g/kg for children if:

the patient is symptomatic,
has ingested 20 micrograms/kg or more digoxin,
or ingested any amount of a toxic plant

Stop oral activated charcoal if:

There is evidence of ileus.
Severe clinical features and/or high plasma concentration have resolved.

3. For patients with acute digoxin toxicity, it is critical to obtain vital signs, an ECG and blood tests to obtain potassium and magnesium levels.

4. Observe patients for at least 6 hours.

5. Rapidly replace fluid to reduce plasma digoxin concentration – may require ITU support if co-existing heart failure.

6. Treat bradycardia, hyperkalaemia, hypokalaemia, metabolic acidosis and hypotension conventionally.

7. Consider checking digoxin at six hours post treatment

8. DigiFab or DigiBind indications: :

Cardiac Arrest
Severe bradyarrythmia or life-threatening ventricular arrhythmia.
Severe hyperkalaemia (e.g. K+ greater than 6.5 mmol/L) resistant to conventional treatments.
Digifab and digibinds effect may be seen in 15-30 minutes of administration, but repeated doses may be necessary. Monitor the potassium carefully.

9. Haemodialysis is unlikely to help as digoxin is protein bound.

Chronic Toxicity

In chronic toxicity, apart from giving the antidote, cause-finding is vital. Common causes include infection and renal failure.

The clever people at Toxbase would highly suggest you call NPIS for advice when managing such a patient with severe toxicity. [Editor: Whenever I have called for problems, I have found them humungously helpful]

Patients that are symptomatic of digoxin toxicity but display no overt signs concerning for severe poisoning will need cardiac monitoring. They can be observed until symptoms resolve and digoxin concentrations are therapeutic.

Take Home Message Digoxin toxicity is usually unintentional, often occurring as chronic toxicity in older adults due to the drugs narrow therapeutic index. Diagnosis is primarily clinical, based on symptoms, ECG changes and electrolyte abnormalities, as serum digoxin levels do not reliably predict toxicity. Management includes supportive care, cardiac monitoring, correction of electrolyte disturbances, and DigiFab/DigiBind for severe toxicity (e.g. life-threatening arrhythmias, cardiac arrest or severe hyperkalaemia).

References/Further reading:

Burns E, Buttner R. Digoxin Toxicity. Life in the Fast Lane (LITFL). 2024.
Toxbase: Digoxin
Patel K, Wright P. Digoxin monitoring and toxicity management. Pharm J. 2023.