Drugs for treating heart failure. A. Introduction. Heart failure (HF) is due to the inability of the ventricles to pump sufficient blood thru-out the body. There are a number of causes of heart failure:. diabetes. from:http://www.nhlbi.nih.gov/health/dci/images/heart_coronary_artery.gif.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
This results in an inability of the cardiovascular system to meet the body’s demands for oxygen.
the mainstay of heart failure treatment until the discovery of the ACE inhibitors
Digoxin stimulates the vagus nerve, which slows the activity of the sinoatrial (SA) and atrioventricular (AV) nodes
This reduced heart rate (known as a negative chronotropic effect) is seen as a lengthening of the PR interval on an ECG.
Na1+- K1+-ATPase pump.
They decrease both the heart rate and the force of contraction.
At first this appears to be the opposite of the effects needed in treating heart failure.
However, there is increased activation of the sympathetic nervous system in patients with heart failure that causes tachycardia and increases stress on the heart.
Beta blockers slow the heart rate, which allows the heart to both fill and function more effectively.
This reduces both venous return to the heart and preload, allowing the heart to pump more forcefully.
Diuretic therapy, as well as sodium restriction is recommended for patients with mild heart failure
Some studies have shown that treatment of heart failure with a potassium sparing diuretic reduces mortality.
These diuretics are more effective when the aldosterone level is elevated as they are either:
Potassium sparing diuretics used in the treatment of heart failure include:
They inhibit angiotensin II. Angiotensin II causes vasoconstriction, and release of aldosterone and ADH.
In addition, they decrease the inactivation of an endogenous vasodilator, bradykinin.