Digoxin Toxicity
Digoxin's inhibition of the myocyte Na/K-ATPase pump raises intracellular calcium to boost contractility, but the same mechanism becomes arrhythmogenic in excess, and hypokalaemia potentiates toxicity because potassium and digoxin compete for the same binding site.
In a nutshell
Digoxin inhibits the Na/K-ATPase pump, raising intracellular calcium for inotropy but risking arrhythmia in excess. Potassium and digoxin compete for the same pump binding site, so hypokalaemia (classically from diuretics) potentiates toxicity even at therapeutic drug levels. DigiFab neutralises circulating digoxin directly.
Classic presentation
A patient on digoxin, often with diuretic-induced hypokalaemia or renal impairment, presenting with nausea, yellow-green visual disturbance, confusion and a bradyarrhythmia or ectopic tachyarrhythmia.
Key points
- Hypokalaemia potentiates digoxin toxicity through competitive binding at the Na/K-ATPase pump: correct potassium as part of treatment.
- The rhythm disturbance can be paradoxically both slow (AV block from vagal tone) and fast (ectopics from calcium-driven automaticity) in the same patient.
- Hyperkalaemia in acute massive overdose is a marker of severity, not a separate problem.
- DigiFab/Digibind is indicated for life-threatening arrhythmia, significant hyperkalaemia, or large ingestions.
First-line investigation
Serum digoxin level with U&E (particularly potassium) and a 12-lead ECG.
First-line management
Stop digoxin, correct precipitants (especially potassium and renal function), and give DigiFab in severe or life-threatening toxicity.
Exam traps
- A 'normal' digoxin level does not exclude toxicity if potassium is low: the competitive binding shifts the effective toxic threshold.
- Yellow-green vision (xanthopsia) is a classic but easily forgotten early clue in an exam stem.
- Diuretic therapy is a common but easily overlooked precipitant in a patient stable on digoxin for years.
Educational content pending clinical review. Not medical advice.