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.