Active Ingredients

Digoxin – Effect, Application & Risks


Like digitoxin , digoxin is extracted from the foxglove (digitalis lanata or digitalis purpurea), which is why both are assigned to the digitalis glycosides. Cardioactive glycosides increase the heart muscle’s ability to beat and at the same time lower the heart rate.

What is digoxin?

Digoxin is a substrate of P-glycoprotein from the group of so-called cardioactive glycosides (also cardiac glycosides). The active ingredient is obtained from digitalis lanata (woolly foxglove) and is used in particular for heart failure (heart weakness) as well as atrial flutter and fibrillation.

The cardiac glycoside increases the contractility and excitability of the heart muscle while slowing the rate and conduction. Digoxin itself is either in the form of crystals or a crystalline, off-white powder that is practically insoluble in water.

Pharmacological action

As a cardiac glycoside, digoxin has various effects on the myocardium (heart muscle). On the one hand, the active ingredient increases the impact and contraction speed of the myocardium (positive inotropic effect).

On the other hand, it reduces the heart rate (negative chronotropic effect) and slows down the conduction of the heart muscle from the area of ​​the atrium (courtyard) to the ventricle or heart chambers (negative dromotropic effect). In addition, digoxin increases excitability, especially that of the ventricular muscles (positive bathmotropic effect). The mechanisms of action mentioned cause an increased stroke volume, which in turn has a positive effect on the blood flow in the kidneys and increases urine excretion.

Digoxin also has a direct renal effect by inhibiting Na+ reabsorption. The effect of digoxin is based on the inhibition (inhibition) of the membrane-bound α-subunits of the Na+/K+-ATPase in the myocardial cells. Na+/K+-ATPase is a kind of pump that transports ions (sodium, potassium, calcium, chloride) into the cell interior or transported to the outside to maintain the specific ionic balance of the cell. The inhibition of the Na+/K+-ATPase in turn leads to an inhibited Na+ and Ca2+ exchange.

The increased Ca2+ concentration in the myocardial cells leads to Ca2+ uptake in the sarcoplasmic reticulum and thus to an increase in contraction speed and impact force, because heart muscle cells need calcium for their contraction activity and the contraction force increases with increasing calcium uptake.

The inhibited Na+/K+-ATPase can also lead to an improvement in the sensitivity of the so-called baroreceptors (also pressor receptors or pressure-sensitive corpuscles) and correspondingly to neurohormonal effects. Digoxin is primarily eliminated via the kidneys and has a half-life of 2 to 3 days.

Medical Application & Use

Digoxin is primarily used in the context of the therapy of acute and chronic cardiac insufficiency (cardiac insufficiency) as well as certain cardiac arrhythmias ( atrial fibrillation , atrial flutter), which can be traced back to a delayed excitation conduction.

The active ingredient is usually administered orally in tablet form or, more rarely, intravenously as a solution for injection. Due to the limited therapeutic range, carefully monitored and individual dosage adjustment is recommended, especially in the case of impaired renal function. In the presence of hypersensitivity, ventricular tachycardia and/or fibrillation, thoracic aortic aneurysm (widening of the aortic vessel wall at chest level), second and third degree AV block (bradycardia) and hypertrophic cardiomyopathy (thickened heart muscles) with increasing obstruction, digoxin therapy is recommended contraindicated.

Hypercalcemia , hypokalemia , hypomagnesemia, as well as hypoxia can also be contraindicators. Since the effect of digoxin increases the oxygen demand of the heart muscle cells, therapy with this active ingredient can have an unfavorable effect in chronic or acute myocardial ischemia (e.g. in the context of coronary heart disease ).

In addition, in the context of therapy with digoxin, various interactions with other drugs must be taken into account. Calcium (especially intravenously) as well as diuretics or laxatives ( laxatives ) increase the glycoside toxicity of digoxin. Parallel therapy with calcium channel blockers, antiarrhythmics (including amiodarone , quinidine ), itraconazole, captopril, spironolactone, atropine and certain antibiotics cause a sharp increase in the digoxin concentration.

In addition, the bradycardiac effect is increased by beta- blockers and cardiac arrhythmia is promoted by certain medications (including suxamethonium chloride, sympathomimetics, phosphodiesterase inhibitors). Drugs that increase the potassium level reduce the positive inotropic effect of digoxin.

Risks & side effects

As a result of the very limited therapeutic range of digoxin , it can quickly be overdosed and lead to intoxications, which can manifest themselves, among other things, in the form of cardiac arrhythmias (AV block, ventricular fibrillation, extrasystoles ).

Individual therapy control is correspondingly important. In addition, in the context of digoxin therapy, side effects such as loss of appetite , emesis ( vomiting ), diarrhea ( diarrhoea ), nausea and weakness , headaches , pain in the facial area and drowsiness can often be observed.

In rare cases, digoxin therapy leads to perceptual disturbances, visual disturbances, disorientation and/or psychoses. Very rarely, digoxin therapy is accompanied by cramps, enlargement of the male mammary gland, blood disorders and/or hypersensitivity reactions.

Lisa Newlon
 | Website

Hello! I am Lisa Newlon, and I am a medical writer and researcher with over 10 years of experience in the healthcare industry. I have a Master’s degree in Medicine, and my deep understanding of medical terminology, practices, and procedures has made me a trusted source of information in the medical world.