Digoxin is currently the most widely used digitalis preparation. It is rapidly absorbed from the gastrointestinal tract and is primarily eliminated through renal excretion. It has a volume of distribution of 6 L/kg. The half-life of a therapeutic dose is 36 to 48 hours.
Digitalis has a narrow therapeutic-toxic margin. Toxicity results from an exaggeration of its therapeutic actions. Digitalis binds to a specific receptor site on the cardiac cell membrane, inactivating the sodium-potassium adenosine triphosphate pump (Na-K ATPase).3 This pump concentrates sodium extracellularly and potassium intracellularly to maintain the electrochemical membrane potential vital to conduction tissues. When Na-K ATPase is inhibited, the sodium-calcium exchanger removes accumulated intracellular sodium in exchange for calcium. This exchange increases sarcoplasmic calcium and is the mechanism thought to be responsible for the positive inotropic effect of digitalis. Inhibition of the Na-K ATPase pump also results in an increase in extracellular potassium. 3 Digitalis increases vagal tone and decreases conduction through the AV node. In toxic doses, these effects result in various bradydysrhythmias. Automaticity is increased due to slowing of conduction in the electrical system along with a shortened refractory period in the myocardium. Intracellular calcium overload can create delayed after-depolarizations, causing electrical oscillations in cell membranes that give rise to triggered dysrhythmias. 4
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