Digoxin Toxicity
Digoxin inhibits the myocardial sodium-potassium pump, so in excess it both blocks conduction and provokes ectopic firing, giving bradycardia, heart block and ventricular arrhythmia.
Definition
Digoxin toxicity is the clinical syndrome of cardiac glycoside excess: gastrointestinal, visual and neurological symptoms with disturbed cardiac automaticity and conduction. There is no concentration that defines it. The diagnosis rests on the exposure history, the ECG, the potassium and the renal function, with the serum level as supporting evidence only.
First principles
One pump explains the therapeutic effect and the poisoning
Digoxin inhibits myocardial sodium-potassium adenosine triphosphatase (Na+/K+-ATPase). Intracellular calcium rises, so contractility rises, and vagal tone increases, so the atrioventricular (AV) node conducts more slowly. In excess the same two actions collide: calcium-loaded myocytes fire ectopically while conduction is blocked, which is why a toxic patient can be bradycardic and tachyarrhythmic at once.
This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.