Digoxin mechanism of action?

How does digoxin work in the body?

Digoxin is a cardiac glycoside. Its main mechanism of action is inhibition of the sodium-potassium ATPase pump (Na+/K+-ATPase) in heart cells. This increases intracellular sodium, which reduces the activity of the sodium-calcium exchanger (NCX) that normally moves calcium out of the cell.

With the exchanger less active, intracellular calcium rises. Higher intracellular calcium increases cardiac muscle contraction strength (positive inotropy), which helps the heart pump more effectively.

Why does digoxin slow the heart rate?

Digoxin also affects the autonomic control of the heart. It increases vagal (parasympathetic) tone, which slows conduction through the atrioventricular (AV) node. Clinically, this is why digoxin is used to help control ventricular rate in atrial fibrillation by reducing AV nodal conduction.

What happens to calcium and cardiac contractility?

The Na+/K+-ATPase inhibition leads to:
- increased intracellular Na+
- reduced Ca2+ extrusion via NCX
- increased intracellular Ca2+
- stronger systolic contraction because more calcium is available in cardiomyocytes

How does digoxin differ from other heart-rate drugs?

Many rate-control options (for example, beta blockers or non-dihydropyridine calcium channel blockers) reduce heart rate mainly by directly slowing electrical activity through the AV node via different receptors and ion channels. Digoxin combines AV nodal slowing (via increased vagal tone) with inotropy (via calcium handling).