Pharmacology of Digoxin
Digoxin is a medicine used in the treatment of various heart conditions. Here, we review what digoxin is, how it works, what side effects its linked to, as well as a variety of other clinical considerations and drug interactions.
Digoxin was first isolated from the foxglove plant, Digitalis lanata, in 1930.
Digoxin is used to treat the following conditions:
- Atrial fibrillation / atrial flutter
- Heart failure
Digoxin is rarely used in isolation as a first-line agent. Instead, it is often reserved, in combination with other drugs, for second or third-line treatment.
For example – a beta-blocker or non-dihydropyridine calcium channel blocker is often more effective in treating atrial fibrillation or atrial flutter. Similarly, other medicines – such as triple therapy of an ACE inhibitor, beta-blocker and aldosterone antagonist – are used to treat heart failure before digoxin is brought out.
Mechanism of action
There are two modes of action that must be considered.
First, how digoxin works for atrial fibrillation and atrial flutter.
Digoxin works by increasing vagal tone; an effect that leads to reduced conduction through the AV node. With fewer impulses passing through the AV node, it has a knock-on effect on the ventricles, reducing ventricular rate.
Second, how digoxin works for heart failure.
Digoxin inhibits the Na+/K+-ATPase pump, meaning sodium ions accumulate in myocytes. This accumulation directly leads to calcium accumulation, too, increasing the force of cardiac contractions.
Side effects with digoxin include:
- Breast enlargement – though its incidence has been called into question
- Gastrointestinal effects – nausea, vomiting, diarrhea, abdominal pain
- Loss of appetite
- Skin rash
- Visual disturbances – including blurred /yellowed vision
- CNS effects – dizziness, drowsiness, headache
Arrythmias may also occur, though they are more likely in cases of digoxin toxicity.
Given that digoxin has a narrow therapeutic window (meaning the difference between therapeutic and toxic doses is small), the incidence of arrythmias is not an unlikely one.
When we talk about the clinical pharmacology of digoxin, we need to think about the following factors:
- That digoxin should be avoided in heart block, due to the increased risk of conduction abnormalities.
- That because digoxin is eliminated via the renal route, its dose should be reduced in patients with renal failure.
- That electrolyte abnormalities increase the risk of digoxin toxicity – these include hypokalemia, hypercalcemia and hypomagnesemia.
- That due to the development of hypokalemia, thiazide and loop diuretics increase the risk of digoxin toxicity.
- That amiodarone, calcium channel blockers and quinine all increase the risk of digoxin toxicity.
- That digoxin can be administered via the oral and IV routes. Effects from oral use present within 2 hours, whereas they take effect at 30 minutes after IV use. Due to digoxin’s large volume of distribution, loading doses are often administered.
Digoxin is an important medicine which, though its use has lessened in recent years, it remains an important second or third line treatment option for a variety of serious cardiac states.
For even more facts and pharmacology quiz questions on digoxin pharmacology, register with PharmaFactz today. Check back to our pharmacy blog soon for even more great articles on digoxin and other drugs used to treat atrial fibrillation!