Digoxin and digoxin toxicity

Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.

Mechanism of action

• decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
• increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
• digoxin has a narrow therapeutic index

Monitoring

• digoxin level is not monitored routinely, except in suspected toxicity
• if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose

Digoxin toxicity

Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.

Features

• generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
• arrhythmias (e.g. AV block, bradycardia)
• gynaecomastia

Precipitating factors

• classically: hypokalaemia
  • digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
• increasing age
• renal failure
• myocardial ischaemia