Diagnosis and treatment of digoxin toxicity.

Cardiac glycosides are unusual in having a narrow therapeutic range, which is idiosyncratic to the individual. In view of this it is perhaps not surprising that toxicity is a common occurrence, being reported in up to 35% of digitalized patients.' There are several mechanisms which can lead to this problem. Firstly, digoxin is excreted mainly by the kidneys, and therefore, any impairment ofrenal function may lead to higher than expected plasma concentrations. Congestive cardiac failure, renal failure and advanced age can also cause toxicity by reducing the volume of distribution of the drug. Concomitant electrolyte imbalance, notably hypokalaemia, hypomagnesaemia and hypercalcaemia can potentiate digoxin toxicity. Approximately 30% of digoxin is plasma protein bound and thus certain other drugs such as amiodarone and calcium antagonists can lead to higher than expected plasma concentrations. Lastly, several clinical conditions such as hypothyroidism, chronic lung disease and cardiac amyloid are associated with an abnormally high myocardial sensitivity to digoxin. Despite all of this, however, there is often still no clear relationship between these factors and manifest toxicity.