Digoxin - clinical toxicology
A cardiac glycoside with a narrow therapeutic index, digoxin is now used mainly for rate control in atrial fibrillation and occasionally for symptomatic heart‑failure management. Toxicity is an important emergency department (ED) problem because of drug-drug interactions, age‑related pharmacokinetic changes and impaired renal clearance.
Mechanism (why toxicity causes the findings)
- Inhibits the Na+/K+ ATPase in cardiac myocytes → increased intracellular Na+, reduced Na+/Ca2+ exchange and increased intracellular Ca2+ → positive inotropy.
- Increases vagal tone and depresses AV nodal conduction → slower ventricular response in atrial fibrillation/flutter.
- Excess pump inhibition predisposes to conduction block, atrial/junctional/ventricular arrhythmias and disturbed cellular K+ handling (acute toxicity may cause hyperkalaemia).
Clinical features
- Non‑specific systemic: malaise, lethargy, anorexia, nausea, vomiting, abdominal pain, confusion, delirium.
- Visual: blurred or yellow‑green vision (classical but not universal).
- Cardiac: spectrum from sinus bradycardia and progressive AV block to atrial tachycardia with block, ventricular ectopy, ventricular tachycardia/fibrillation.
- New or frequent ectopy (bigeminy, trigeminy, recurrent PVCs) in a patient taking digoxin is suspicious for toxicity.
- Chronic exposure: gynaecomastia and more subtle neurocognitive effects.
ECG features
- “Scooped” / downsloping ST depression (classically described as sagging).