|Classification and external resources|
Digitalis purpurea drawings by Franz Köhler
Digoxin toxicity is a poisoning that occurs when excess doses of digoxin (from plants of the genus Digitalis) are consumed acutely or over an extended period. The classic features of digoxin toxicity are nonspecific: fatigue, blurred vision, change in color vision (e.g. "yellow vision"), anorexia, nausea, vomiting, diarrhea, abdominal pain, headache, dizziness, confusion, delirium.
Characteristic EKG changes include bradycardia (the most frequent vital sign abnormality in toxicity), a prolonged PR interval. An accelerated junctional rhythm or bidirectional ventricular tachycardia suggests digoxin toxicity until proven otherwise.
Digoxin toxicity is often divided into acute or chronic. The therapeutic level for digoxin is 0.5-2 ng/mL. Low serum potassium increases the risk of digoxin toxicity and cardiac dysrhythmias. The classic arrhythmia is a paroxysmal atrial tachycardia with block. Digoxin toxicity occurs because it is very easy to overdose. Overdose commonly occurs because its therapeutic effect works only within a very narrow window. The most common source of digoxin is from the Foxglove plant.
Symptoms include hypersalivation, fatigue, nausea/vomiting, changes in heart rate and rhythm, loss of appetite (anorexia), diarrhea, visual disturbances (yellow or green halos around objects), confusion, dizziness, nightmares, agitation, and/or depression, as well as a higher acute sense of sensual activities.
The primary treatment of digoxin toxicity is digoxin immune Fab. Digoxin should not be given if the apical heart rate is below 60 BPM (beats per minute).
Atropine is also used in cases of bradyarrhythmias.