Digoxin toxicity (2019)

Digoxin is derived from the purple foxglove plant (Figure 1), and was discovered 200 years ago (British Heart Foundation (BHF), 2019). It is not usually the first choice when prescribing for people with arrhythmia or heart failure, as it carries many risks owing to its narrow therapeutic range (BHF, 2019). Thus, its potential for toxicity—which often can have highly problematic effects, including dysrhythmia—may be fatal in cases of massive overdose.

Digoxin is a cardioactive corticosteroid and is used therapeutically to increase cardiac contractility and to control the heart rate (British Medical Journal (BMJ), 2019). Cardiac arrhythmias resulting from digoxin toxicity account for most digoxin toxicity-associated deaths (Kanji and MacLean, 2012).

Pincus (2016), a cardiologist, outlines how hyperkalaemia is often seen in digoxin toxicity; he notes that digoxin increases intracellular calcium in myocardial cells indirectly as a result of inhibiting the sodium-potassium pump in the cell membrane. This leads to an increase in cardiac contractility, thus resulting in risk of tachyarrhythmia, but also in hyperkalaemia. Another result of digoxin is an increase in vagal activity, reducing the activity seen in the sinus node and prolonging conduction in the atrioventricular (AV) node (Pincus, 2016)