How does digoxin work in the body?
Digoxin is a cardiac glycoside that mainly works by inhibiting the Na⁺/K⁺-ATPase pump in heart cells. This inhibition raises intracellular sodium, which indirectly increases intracellular calcium through the Na⁺/Ca²⁺ exchanger. The higher calcium level strengthens heart muscle contraction (positive inotropy) and also slows electrical conduction through the atrioventricular (AV) node (negative dromotropy).
What does that do to heart rate and rhythm?
Because digoxin slows AV-node conduction, it can reduce the ventricular rate in conditions with rapid atrial firing, such as atrial fibrillation or atrial flutter. It does not typically “cure” atrial arrhythmias, but it helps control how fast the ventricles beat by slowing the signal that passes from atria to ventricles.
How does digoxin affect heart failure?
In heart failure, increased contractile force (from higher intracellular calcium) helps the failing heart pump more effectively. Digoxin can improve symptoms and reduce hospitalizations in some patients, largely by improving cardiac performance rather than by directly causing major changes in survival.
What is the Na⁺/K⁺-ATPase mechanism in one chain?
- Digoxin inhibits Na⁺/K⁺-ATPase.
- Intracellular Na⁺ rises.
- Na⁺/Ca²⁺ exchange slows, so intracellular Ca²⁺ rises.
- Ca²⁺ available in the cell increases contraction strength.
- AV-node conduction slows, reducing ventricular response rate.
What side effects are tied to its mechanism?
Digoxin has a narrow therapeutic window, and excess digoxin can lead to digoxin toxicity. Toxicity commonly shows up with:
- Gastrointestinal symptoms (nausea, vomiting, loss of appetite)
- Visual changes (classically yellow/green color perception)
- Cardiac effects (arrhythmias, conduction abnormalities)
These problems relate to how strongly digoxin can disrupt electrolyte balance and electrical activity in the heart when levels are too high.