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Digoxin Mechanism and Indication
Cardiac glycosides, also called digitalis glycosides, are medications derived from the foxglove plant, Digitalis purpurea. They are commonly used for the treatment of atrial arrhythmias, such as atrial flutter and atrial fibrillation, which are caused by rapid, uncoordinated contractions of the atria. In addition, cardiac glycosides can be prescribed for congestive heart failure when other medications fail.
Now, the most commonly used cardiac glycoside is digoxin, which can be given orally, intravenously, and intramuscularly. Once administered, digoxin works by reversibly inhibiting the sodium-potassium ATPase located in the cell membrane of cardiomyocytes.
Normally the sodium-potassium ATPase pumps three sodium ions out of the cell for every two potassium ions that it pumps in, and to do this, it consumes one ATP molecule for energy.
When the sodium-potassium ATPase is inhibited by digoxin, sodium builds up inside the cell. This interrupts the sodium-calcium exchanger on the cell membrane, which normally pumps one calcium ion out in exchange for three sodium ions.
As a result, digoxin causes calcium to build up within cardiomyocytes, allowing the cardiac muscle fibers to contract more efficiently, which leads to an increase in the force of the heart’s contractions and cardiac output. In turn, the increase in cardiac output increases the renal blood flow and urine output, which also helps reduce peripheral edema.
Digoxin also stimulates the vagus nerve, which provides the parasympathetic supply to the heart, and reduces the conduction velocity through the AV node. These two effects combined result in a decreased heart rate. But because parasympathetic innervation is much richer in the atria, these effects mainly involve the atria.
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