Digoxin × Furosemide

Furosemide increases urinary loss of potassium and magnesium. Digoxin and potassium compete for the same binding site on the Na+/K+-ATPase: as potassium falls, the blocked fraction of the pump grows and the same blood concentration of digoxin produces a larger effect. The digoxin label states it plainly: agents that cause hypokalaemia or intracellular potassium depletion, among them some diuretics, lithium salts and corticosteroids, increase sensitivity to digoxin. Furosemide itself does not change the glycoside concentration; what changes is the electrolyte background.

Nausea, vomiting, loss of appetite and visual disturbance with a yellow or green halo before any cardiac symptom. Then bradycardia, AV block, ventricular ectopy and confusion in older people. Symptoms appear with potassium below 3.5 mmol/L, even when the digoxin level sits inside the therapeutic range.

Potassium and magnesium before the pair starts, at 1-2 weeks and periodically thereafter; sooner with vomiting, diarrhoea or hot weather. If potassium drops below 4 mmol/L in someone on digoxin, it is corrected with potassium or a potassium-sparing agent. Magnesium is replaced below 0.7 mmol/L, because without it hypokalaemia will not correct. The digoxin level is read together with potassium: a normal value against low potassium does not rule out toxicity.