Fig: The Failing Heart
ACE INHIBITORS AND AT-1 ANTAGONISTS :
ACEIs block formation of AII and inhibit bradykinin metabolism decrease aldosterone ->decrease fluid
retention -> increase vasodilation -> decrease preload and afterload.
In addition to improving symptoms and exercise tolerance, they slow progression of heart failure and prolong survival. In addition, ACEIs have prophylactic value post-MI because they oppose "remodeling" that can lead to heart failure.
Fig: Effects Resulting From Inhibition of Cardiac Membrane Na+/K+ATPase
The increase in contractility improves cardiac output, reversing the compensatory tachycardia
and the increases in BP and PVR that occur in heart failure. Renal perfusion and diuresis are also
improved, providing additional beneficial effects in heart failure. However, cardiac glycosides do
not improve survival; thus, ACEIs are now considered drugs of first choice in most situations.
Cardiac glycosides exert electrophysiologic effects on the heart (via PANS) that include central
vagal stimulation, facilitation of muscarink activity, and sensitization of baroreceptors. These
effects occur at conventional doses and in the absence of heart failure lead to a decrease in CO
without effects on BP and PVR.
Cardiac Effects of Digitalis
Table the Cardiac Effects of Digitalis
Table . Properties of Digoxin
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