Digoxin
Digoxin can be a drug typically employed inside the treatment of many different heart conditions. Classified as a cardiac glycoside, it really is derived from the foxglove plant (scientific name: Digitalis lanata), and is as a result also referred to as digitalis.
Digoxin increases heart contractility (good inotropic effect), lessens the heart rate (negative chronotropic impact) and slows atrioventricular (AV) conduction (negative dromotropic impact). This is accomplished indirectly by way of the autonomic nervous program as a vagomimetic effect and through inhibition of Na -K -ATPase in heart muscle.
Primary indications consist of chronic heart problems, specifically inside the presence of systolic dysfunction; supraventricular arrhythmia in which the influence of AV conduction is considerable; and atrial fibrillation and flutter accompanied by a fast ventricular rhythm. It may possibly be administered orally or intravenously.
Most unwanted effects of digoxin are due to overdose, despite the fact that anorexia, nausea, vomiting and headache might also happen at therapeutic doses after fast absorption. Other non-cardiac unwanted effects contain diarrhea, weakness, apathy, fatigue, and CNS effects for example dizziness, confusion, depression, delirium, psychosis and visual disturbances (specially impaired color perception). Rarely, abdominal pain, intestinal necrosis, allergic reactions for example rashes and thrombocytopenia, and gynecomastia might also occur.
Frequent cardiac negative effects contain a variety of varieties of arrhythmias (specially ventricular extrasystoles), heart block and atrial tachycardia having a specific degree of AV block. Fast intravenous (IV) injection might outcome in vasoconstriction with hypertension and reduced coronary perfusion. In children, unwanted effects and related arrhythmias (specially conduction disturbances and supraventricular tachyarrhythmias) are distinct from these in adults, with bradycardia getting the initial and most frequent manifestation of overdose.
Digoxin must not be given to individuals with pheochromocytoma or tachyarrhythmias. Other contraindications incorporate hypertrophic obstructive cardiomyopathy, arrhythmias brought on by cardiac glycoside intoxication, 2nd- or 3rd-degree AV block, hypersensitivity to digitalis, ventricular tachycardia or ventricular fibrillation. Extra caution is advised in individuals with constrictive pericarditis and 1st-degree AV block.
Continuous monitoring of blood pressure, and central venous pressure if possible, is necessary immediately after beginning therapy. The suggested initial infusion rate is 2-5 mcg/kg physique weight/min, with the dose steadily increased until blood pressure and diuresis happen to be corrected. The desired therapeutic effect usually happens at an infusion rate of significantly less than 20 mcg/kg/min. In some circumstances of severe circulatory insufficiency, even so, doses of as much as 50 mcg/kg/min may possibly be required. Inside the presence of shock caused by heart failure, the dose ought to be kept as low as you possibly can. The desired therapeutic impact is generally achieved at an infusion rate of 500-1000 mcg/min.
Simply because it has no known adverse effects on the fetus, digoxin could be employed in the course of pregnancy whilst the maternal digoxin blood level is inside standard limits. Nonetheless, it may cross the placenta and reach fetal circulation in the very same plasma concentration as that on the mother. The fetal heart rate ought to as a result be meticulously monitored, specifically in the peripartal period. Dosages could must be adjusted because of fast excretion of digoxin throughout pregnancy. Digoxin is excreted in breast milk in such modest levels that no adverse effects on breastfeeding infants are expected.
Hypokalemia-inducing substances including particular laxatives and diuretics, amphotericin B, corticosteroids and lithium salts can accelerate the occurrence of cardiac glycoside intoxication. Parenteral calcium administration and suxamethonium also enhance the toxicity of digoxin.
Quinidine, hydroxychloroquine, propafenone, spironolactone, amiodarone, cyclosporine, verapamil, diltiazem, itraconazole, nitrendipine and nisoldipine can raise blood levels by inhibiting the excretion and/or displacement digoxin from tissue binding. Amiodarone and nefazodone can improve digoxin levels by 80% and 15-30%, respectively.
Prazosin, quinine, alprazolam, indomethacin along with other nonsteroidal anti-inflammatory drugs (NSAIDs) might enhance digoxin concentration. Conversely, rifampicin, phenytoin, and St. John's wort (Hypericum perforatum) could reduce digoxin levels. When using antibiotics (erythromycin, tetracycline), the degradation of digoxin by intestinal bacteria declines because of the alter in intestinal flora, so a lot more drug gets accessible for absorption. Simultaneous use of sympathomimetics increases the threat of arrhythmias.
When digoxin is offered orally, propantheline and possibly other parasympathicolytics could increase digoxin levels by growing gastrointestinal absorption. Cholestyramine, neomycin, penicillamine, metoclopramide, sulfasalazine, kaolin, adsorptive carbon, cytostatics and liquid antacids decrease absorption.
Kinetic information for digoxin are as follows:
Absorption: Oral 55-75%.
Tmax = 1-2 hours orally.
Protein binding = 20-30%.
Therapeutic plasma levels: 0.5-2 ng/mL.
Vd = 7.3 L/kg, the concentration within the heart is roughly 30 occasions higher than that within the systemic circulation.
Concomitant intake of food slows absorption.
Digoxin is eliminated 60-75% unchanged in the urine.
T1/2 = about 36 hours with regular renal and thyroid function.
To get a far more comprehensive review of cardioactive pharmacologic agents such as digoxin as well as other essential topics in vital care, please visit ExpertCollege.com.