Digoxin Like digitoxin, it is extracted from the foxglove (Digitalis lanata or Digitalis purpurea), which is why both are assigned to the digitalis glycosides. Cardiac glycosides increase the strength of the heart muscle and at the same time lower the heart rate.
Digoxin is a substrate of P-glycoprotein from the group of so-called cardiac glycosides (also cardiac glycosides).
Digoxin is a substrate of P-glycoprotein from the group of so-called cardiac glycosides (also cardiac glycosides). The active ingredient is obtained from Digitalis lanata (woolly thimble) and is used in particular for heart failure (cardiac insufficiency) and atrial flutter and fibrillation.
The cardiac glycoside increases the contractile force and excitability of the heart muscle, while at the same time slowing down the frequency and conduction of excitation. Digoxin itself is either in the form of crystals or as a crystalline, whitish powder that practically cannot be dissolved in water.
As a cardiac glycoside Digoxin various effects on the myocardium (heart muscle). On the one hand, the active ingredient increases the impact force and speed of contraction of the myocardium (positive inotropic effect).
On the other hand, it lowers the heartbeat frequency (negative chronotropic effect) and slows down the conduction of the cardiac muscle from the area of the atrium (atrium) to that of the ventricle or heart chambers (negative dromotropic effect). In addition, digoxin increases the 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 + absorption. The effect of digoxin is based on the inhibition of the membrane-bound α-subunits of Na + / K + -ATPase in the myocardial cells. Na + / K + -ATPase is a type of pump that transports ions (sodium, potassium, calcium, chloride) into the cell interior, resp. transported to the outside in order to maintain the specific ionic balance of the cell. The inhibition of 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 the contraction speed and impact force, because heart muscle cells require 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 sensory bodies) and correspondingly to neurohormonal effects. Digoxin is primarily excreted renally, via the kidneys, and has a half-life of 2 to 3 days.
Digoxin is primarily used in the context of the therapy of acute and chronic heart failure (cardiac muscle weakness) as well as certain cardiac arrhythmias (atrial fibrillation, atrial flutter) that can be attributed to delayed conduction of excitation.
The active ingredient is usually administered orally in tablet form or, more rarely, intravenously as an injection solution. 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 (enlargement of the aortic vessel wall at chest level), an AV block (bradycardic cardiac arrhythmia) second and third degree, and hypertrophic cardiomyopathy (thickened heart muscles) with increasing obstruction, treatment is a digoxin therapy contraindicated.
Hypercalcemia, hypokalaemia, hypomagnesaemia, and oxygen deficiency 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 on chronic or acute myocardial ischemia (e.g. in the context of coronary heart disease).
In addition, various interactions with other drugs must be taken into account in the context of therapy with digoxin. Calcium (especially intravenous) 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 strong increase in the digoxin concentration.
In addition, the bradycardizing effect is increased by beta blockers and cardiac arrhythmias are favored by certain drugs (including suxamethonium chloride, sympathomimethics, phosphodiesterase inhibitors). Drugs that cause an increase in potassium levels reduce the positive inotropic effect of digoxin.
As a result of the severely limited therapeutic range of Digoxin this can quickly be overdosed and lead to intoxication, which can manifest themselves symptomatically on the basis of cardiac arrhythmias (AV block, ventricular fibrillation, extrasystoles).
Individual therapy control is accordingly important. In addition, side effects such as loss of appetite, vomiting (vomiting), diarrhea, nausea, weakness, headache, facial pain and drowsiness can often be observed in the context of digoxin therapy.
In rare cases, digoxin therapy leads to perception disorders, visual disturbances, disorientation and / or psychoses. Digoxin therapy is very rarely accompanied by cramps, an enlargement of the male mammary gland, blood count disorders and / or hypersensitivity reactions.