Abstract

Ramesh Ganpisetti*, Praneeth Chandluri*, Dr. B.V.S. Lakshmi, Dr. P. Aravinda Swami

ABSTRACT

Digitalis is a plant-derived cardiac glycoside commonly used in the treatment of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia. Direct inhibition of membrane-bound sodium- and potassium-activated adenosine triphosphatase (Na +/K + -ATPase), which leads to an increase in the intracellular concentration of calcium ([Ca 2+]. Approximately 0.4% of all hospital admissions in the United States are related to digitalis toxicity, while about 1.1% of outpatients on digoxin and 10-18% of people in nursing homes develop this toxicity. The most common precipitating cause of digitalis intoxication is depletion of potassium stores, which occurs often in patients with heart failure as a result of diuretic therapy and secondary hyperaldosteronism. Cardiac toxicity can also occur at therapeutic doses in patients who have conditions which may alter their sensitivity to digoxin. Quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise the serum digoxin concentration due to a reduction in clearance and/or i Digitalis glycosides are contraindicated in patients with ventricular fibrillation or in patients with a known hypersensitivity to digoxin n volume of distribution of the drug, with the implication that digitalis intoxication may result. The lethal dose of most glycosides is approximately 5-10 times the minimal effective dose and only about twice the dose that leads to minor toxic manifestations. Morbidity is usually 4.6-10%; however, morbidity is 50% if the digoxin level is greater than 6 ng/mL.