CHF therapy Flashcards
What is the most important therapy to start at risk CHF patients on?
ACE inhibitors/ARBs–> prevents cardiac remodeling associated with AngII/Aldosterone
What is the indication for Beta-blocker therapy in CHF patients?
The second the Ejection Fraction drops
What therapy is changed around in late, severe CHF?
Remove any beta-blockers, put the pt on beta-agonist (must preserve any remaining cardiac function)
Angiotensin II/Aldosterone mitogenic effects?
Hypertrophy of cardiac myocytes, hypertrophy of vascular smooth muscle, cardiac/vascular fibrosis and remodeling, and atherosclerosis
Detrimental effect of ventricular fibrosis?
Decreased compliance, less function
Pregnancy class of ACE inhibitors/ARBs?
Severely teratogenic, NEVER GIVE TO PREGNANT WOMEN
ADEs of ACE inhibitors not present in ARBs?
ARBs do not increase bradykinin levels or produce dry, irritating cough
Once a CHF patient begins having edema, what therapy needs to be started?
Diuretics (normally HCTZ first, then furosemide)
Main reason why beta-blockers are efficacious in heart failure?
reduce the deleterious effects of chronically elevated Norepi and Epi –> overactivity of SNS causes down regulation of B receptors –> B blocker therapy allows for a regeneration of the beta receptors, improving Cardiac function
Nebivolol special effect?
potentiates NO in the vasculature (only approved for HTN in the United States, not CHF)
Carvedilol special effect?
functions as an alpha1-antagonist, reduces reflex vasoconstriction
Best beta blocker for CHF?
Carvedilol
Aldosterone antagonists?
Spironolactone, eplerenone
What medication can you not take with diuretics?
NSAIDs
Hemodynamic effect of diuretics that is beneficial to CHF patients?
reduced preload
What is a high ceiling diuretic?
A diuretic that can cause a very high amount of diuresis (Furosemide)
Do ACE inhibitors/ARBs have diuretic effects?
Yes, they reduce Na+ retention by preventing aldosterone release
Spironolactone, Eplerenone beneficial effects besides diuresis?
prevent the mitogenic effects of aldosterone (combines with AngII–> fibrosis)
Mechanism of action of Hydralazine?
Vasodilator that acts directly on arterial smooth muscle (effective for CHF, reduced afterload)
What causes release of the natriuretic peptides (ANP/BNP)
volume and pressure expansion
What causes release of the natriuretic peptides (ANP/BNP)
volume and pressure expansion (elevated in CHF)
Effects of ANP/BNP?
Promote vasodilation, venodilation, natriuresis. Reduce preload, inhibit renin/aldosterone release, inhibit Na+ reabsorption, promote afferent arteriole dilation
What is Neseritide?
Recombinant human BNP
MOA of Neseritide?
binds to BNP receptor in vascular smooth muscle–> veno-and vasodilation via cGMP (reduce preload/afterload)
Naming system for ACE inhibitors?
End in “-pril” (Lisonopril)
Naming system for ARBs?
End in “-tan” (Losartan)
Where do ACE inhibitors work?
Block AngI–>AngII conversion in lung endothelium
Life threatining ADE seen in ACE inhibitors?
Severe angioedema due to inhibition of Bradykinin metabolism (more prevalent in African Americans)
Who respond less favorably to ACE inhibitors?
African Americans and low-renin hypertensives
Advantageous effect of ACE inhibitors for diabetics?
Preserves their renal function
Most common ADEs with ACE inhibitors?
1st dose hypotension, a dry, irritating cough
Direct Renin Inhibitor?
Aliskiren
Drug drug interactions seen with Aliskerin?
Inhibits p-glycoprotein pumps (don’t prescribe with erythromycin/amiodarone
What does Digoxin inhibit?
Na+/K+ ATPase
How does Digoxin cause its intended effect
Na+/K+ ATPase inhibition–> increase in intracellular Na+–>reversal of Na:Ca pump–> increase intracellular Ca2+ and therefore contractility
Ionotropes only increase what?
Stroke Volume
Unusual ADE seen in early Digoxin toxicity
Blurry blue-green halos in the eyes
What is Digibind?
anti-Digoxin antibody used in digoxin toxicity rescue
Digoxin’s therapeutic window?
Extremely narrow, toxicity is very easy to cause
