Digoxin Toxicity

On this page
  1. Direct answer
  2. What you must remember
  3. A worked case of an elderly woman on digoxin with vomiting
  4. Where the exam tries to catch you
  5. Frequently asked questions
  6. Related topics

Direct answer

Digoxin toxicity occurs when raised levels of this cardiac glycoside inhibit the sodium potassium ATPase, producing arrhythmias and, in acute poisoning, hyperkalaemia. The classic arrhythmia is bidirectional ventricular tachycardia, and nausea, yellow-green visual halos and bradycardia are common clues. DigiFab, a digoxin-specific antibody fragment, reverses life-threatening toxicity, while hypokalaemia, hypomagnesaemia and renal impairment raise the risk.

What you must remember

  • Mechanism: Inhibition of the sodium potassium ATPase raises intracellular sodium and calcium, increasing automaticity and causing conduction block.
  • Classic arrhythmia: Bidirectional ventricular tachycardia, with atrial tachycardia with block and accelerated junctional rhythm also typical.
  • Visual and gastric features: Nausea, vomiting, anorexia and xanthopsia with yellow-green halos.
  • Precipitants: Hypokalaemia, hypomagnesaemia, hypercalcaemia, hypothyroidism and renal impairment, plus amiodarone, verapamil, quinidine and clarithromycin that raise levels.
  • Acute hyperkalaemia: Large acute ingestions cause hyperkalaemia, a sign of severe poisoning and an indication for antibody therapy.
  • DigiFab: Digoxin-specific Fab fragments treat life-threatening arrhythmias, marked hyperkalaemia and high levels, with dosing set by the product labelling.

A worked case of an elderly woman on digoxin with vomiting

A 72-year-old woman with atrial fibrillation and heart failure has taken digoxin and furosemide for years. For three days she has vomited, and now reports yellow halos around lights.

Her pulse is 38 per minute, potassium is 2.9 mmol/L and creatinine is raised. Diuretic-induced hypokalaemia and reduced renal clearance both increase digoxin's effect on the heart.

  1. Stop digoxin: digoxin is stopped, and a timed level is sent so that it can be read against the clinical picture.
  2. Correct electrolytes: potassium and magnesium are corrected, with monitoring.
  3. Treat bradycardia: bradycardia responds to atropine, and temporary pacing is considered if it persists.
  4. Avoid calcium: intravenous calcium is avoided in ordinary digoxin toxicity because it may worsen arrhythmia.
  5. Give antibodies if severe: if the arrhythmia is life threatening, or the level is high with clinical features, digoxin-specific antibody fragments are given.
  6. Recheck potassium: potassium is rechecked afterwards because it can fall sharply.

Where the exam tries to catch you

Examiners probe a few recurring distinctions.

  • Trap: calling bidirectional ventricular tachycardia torsades de pointes. Correct: bidirectional tachycardia alternates the QRS axis beat to beat and is characteristic of digoxin toxicity, whereas torsades is polymorphic and linked to a long QT interval.
  • Trap: deciding toxicity from the serum level alone. Correct: chronic toxicity can occur at modest levels, so clinical features and electrolytes matter as much as the number.
  • Trap: ignoring new drugs in a stable patient on digoxin. Correct: adding amiodarone, verapamil, quinidine or clarithromycin is a warning sign.
  • Trap: treating hyperkalaemia in acute poisoning with potassium-lowering measures alone. Correct: it reflects enzyme blockade, so antibody therapy addresses the cause, while potassium-lowering measures are only supportive.

Frequently asked questions

Which arrhythmia is characteristic of digoxin toxicity?

Bidirectional ventricular tachycardia is the arrhythmia most characteristic of digoxin toxicity, with the QRS axis alternating beat to beat. Atrial tachycardia with variable atrioventricular block and accelerated junctional rhythm are also typical.

Why does hypokalaemia increase the risk of digoxin toxicity?

Hypokalaemia increases digoxin binding to the sodium potassium ATPase, which enhances the drug's effect on the myocardium. Diuretic-induced potassium loss is therefore a common precipitant, and correcting potassium is central to safe management.

When is DigiFab indicated in digoxin toxicity?

DigiFab, a digoxin-specific antibody fragment, is indicated for life-threatening arrhythmias, marked hyperkalaemia and high serum concentrations with clinical features. Dosing depends on the serum level and body weight, according to the product labelling.

Which drugs raise digoxin levels and increase toxicity risk?

Amiodarone, verapamil, quinidine and clarithromycin raise serum digoxin levels, mainly by reducing its clearance. When such drugs are added, the digoxin dose is commonly reduced and levels are monitored closely.

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