digoxin and salbutamol

ModerateUsually manageable, but it must be recognised and monitored.

Mechanism

Salbutamol activates beta-2 adrenoceptors, stimulating Na+/K+ ATPase and promoting intracellular uptake of potassium, resulting in transient hypokalemia. Low extracellular potassium reduces the inhibitory effect of digoxin on the sodium-potassium pump in cardiac myocytes, thereby increasing digoxin's inotropic and arrhythmogenic effects.

What it means clinically

Hypokalemia can precipitate digoxin toxicity, manifesting as arrhythmias (e.g., ventricular ectopy, supraventricular tachycardia), nausea, vomiting, and confusion. Patients on digoxin who receive salbutamol, particularly in high doses or via nebulisation, are at increased risk of cardiac adverse effects.

What to do

Monitor serum potassium levels before and during concurrent therapy, especially in patients at risk of hypokalemia (e.g., those on diuretics). Correct hypokalemia promptly. Consider ECG monitoring in patients with symptoms of digoxin toxicity or if potassium falls below 3.5 mmol/L. Avoid excessive salbutamol doses in patients with digoxin toxicity.

Evidence

Well-established interaction based on case reports and clinical studies; mechanism is pharmacodynamic.

The two drugs

digoxinCardiac glycosidesRead the monograph salbutamolShort-acting beta-2 agonistsRead the monograph

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Other interactions involving digoxin or salbutamol

Educational reference for students and clinicians in training. It does not replace professional judgement, local protocols or current prescribing information.