Cardiac Medication Group Research Paper
Digoxin is a drug used to treat certain heart problems such as heart failure. Heart failure occurs when the heart cannot pump blood well enough to meet the body’s needs. If a person has heart failure (heart failure), digoxin can improve his or her heart’s ability to pump blood. This will often improve symptoms such as breathlessness (i.e., shortness of breath). Digoxin can also be useful for people who have an accelerated or irregular heart rate (pulse). This can be caused by a heart condition known as atrial fibrillation. Digoxin helps slowing and controlling the heart rate.Cardiac Medication Group Research Paper
Digoxin is a digitalis drug used to increase the force of contraction of both atrial and ventricular myocardial fibers (positive inotropic effect). It is able to reduce the sinus rate (negative chronotropic effect) and the speed of cardiac conduction in a particular way at the level of the atrioventricular node (AV); also possesses a modest direct effect on vascular smooth muscle. Important is the indirect vagomimetico effect, at least at therapeutic concentrations.
Pharmacology
The overall effects of digoxin also depend on the initial reflex responses to changes induced by the drug and the different situations in which they can pour heart and cardiovascular system. In fact, the response to digoxin is different in normal conditions and in case of cardiac failure. In heart failure, the positive inotropic effect leads to an increase in cardiac output, a decrease in cardiac volume, a reduction in venous pressure, end-diastolic pressure, the volume of circulating blood, of edema and, finally, an increase in diuresis.
In patients with atrial flutter or atrial fibrillation, digoxin lowers the ventricular rate. The direct effects of digoxin (especially vague but also on sympathetic) affect both the mechanical activity that electrical activity of the myocardium. It seems that the positive inotropic effect of digoxin, and likewise of all digitalis drugs, and following binding of the drug with the Na-K-ATPase (it would be a link with the subunit of the enzyme) involved in the maintenance of the level Optimum sodium inside the cell. The intracellular accumulation of sodium promotes the exchange of sodium with the extracellular calcium causing, ultimately, an increase of intracellular calcium and, therefore, a greater activation of the contractile apparatus (Hollman 2006, 912).Cardiac Medication Group Research Paper
Pharmacokinetics
The effects of digoxin occur 15-30 minutes after intravenous administration (maximum effect within 2-5 hours) and 1-2 hours after oral administration (maximum effect within 6-8 hours). In this way, the digoxin has a bioavailability ranging from 60% to 90%, depending on the types of preparation and with significant differences even between different commercial products. The plasma protein binding is 20-30%. Digoxin has a high volume of distribution (5.10 l/kg). The therapeutic plasma concentration is between 0.5 and 2 ng/ml and higher concentrations are toxic, toxicity effect even at lower concentrations of digoxin when coexisting hypokalemia, hypomagnesaemia, hypercalcemia and other conditions.Cardiac Medication Group Research Paper