Digoxin toxicity

Learning objectives

Digoxin is a cardiac glycoside indicated for the treatment of chronic heart failure and persistent atrial fibrillation as it has inotropic effects
Digoxin toxicity can present acutely after an overdose or chronically
Toxicity can also occur from exposure to a number of plants and animals that contain cardioactive corticosteroids, including dogbane, foxglove, lily of the valley, oleander, yellow oleander, red quill, and the Bufo species toad
In therapeutic doses (0.5-0.9 ng/mL), digoxin increases cardiac contractility and controls the heart rate
Because of the narrow therapeutic index, chronic toxicity is more likely in the elderly and those with renal impairment
Digoxin inhibits by poisoning the sodium-potassium ATPase and the subsequent increase in intracellular sodium leads to increased intracellular calcium as calcium expulsion through the sodium-calcium, cation exchanger is reduced because of this
Higher intracellular calcium increases inotropy which can be of symptomatic benefit in CHF

Acute ingestion
Gastrointestinal tract	Anorexia Nausea Vomiting Diarrhea Abdominal pain
Metabolic system	Hyperkalemia
Cardiovascular system	Enhanced automaticity: atrial tachycardia (e.g. flutter, Atrial fibrillation (AF)) with AV block, VF, VT, ventricular ectopic beats Bradyarrhythmias: conduction delays/blocks, slow or regularised AF Hypotension Shock
Central nervous system	Lethargy Confusion
Chronic ingestion
	Fatigue Malaise Visual disturbances: blurred vision, color disturbances, haloes, and scotomas

ECG
- Premature ventricular betas (PVCs)
- Sinus bradycardia
- Trigeminal rhythms
- Ventricular bigeminy
- Bidirectional ventricular tachycardia
Laboratory tests
- Hyperkalemia is characteristic of digoxin toxicity
- Digoxin levels

Digoxin toxicity, dysrhythmias, hyperkalemia, Digibind, atropine, digoxin-specific Fab, DigiFab, DSFab