Mnemonic

Digoxin Toxicity

A memory aid for recognising and treating digoxin toxicity.

Expansion

Nausea, confusion, yellow vision and arrhythmia, worsened by hypokalaemia

Expansion

Mechanism: inhibition of the sodium-potassium ATPase, raising intracellular calcium. This increases contractility and, through vagal stimulation, slows atrioventricular conduction.

Features

  • Gastrointestinal: nausea, vomiting, anorexia, diarrhoea. Often the earliest
  • Visual: blurred vision, xanthopsia (yellow-green vision), halos
  • Neurological: confusion, dizziness, weakness
  • Cardiac: almost any arrhythmia, classically bradycardia with ventricular ectopy, atrial tachycardia with block, and ventricular arrhythmia

Precipitants

  • Hypokalaemia, which is the most important. Digoxin and potassium compete for the same binding site, so a low potassium increases binding
  • Hypomagnesaemia, hypercalcaemia
  • Renal impairment, since digoxin is renally cleared
  • Drugs: amiodarone, verapamil, diltiazem, spironolactone, macrolides, quinine
  • Age, and hypothyroidism

The “reverse tick” (Salvador Dali) ST depression is a sign of digoxin effect, not toxicity, and does not indicate a raised level.

Treatment: stop digoxin, correct potassium and magnesium, treat arrhythmias, and give digoxin specific antibody fragments for life threatening arrhythmia, haemodynamic instability or a potassium above 5.5 in acute overdose. Avoid calcium in hyperkalaemia caused by digoxin toxicity.