11 18 2014 Heart Failure Drugs Flashcards
Diuretics (mechanism)
- When to use?
- What are adverse effects?
promote the elimination of sodium and water through kidney = reduce intravascular volume and thus Venous Return.
- decrease preload
- out of range that promote pulmonary congestion
USE ONLY WHEN PULMONARY CONGESTION IS SEEN because they can cause an undesired decrease in CO.
Can also cause an electrolyte imbalance = arrhythmias
loop diuretics:
furosemide
Torsemide
bumetamide
MOST POTENT diuretics
Thiazide diuretics
hydrochlorothiazide and metolazone
less effective in the setting of decreased renal perfusion.
Vasodilators
(who are they)
(why use them?)
ACE inhibitors Nitrates (venous vasodilators) Hydralazine (arterial vasodilators) ARBs Nesiritide
- vasodilator regimens significantly extend survival in patients with heart failure.
- Ace is better than Nitrates or hydrazine
ACE inhibitors mechanism
block the metabolism of bradykinin and causes vasodilation of veins and arteries
Limit maladaptive remodeling of patients with chronic heart failure and acute myocardial infarction.
ARBs
angiontensin II receptor blockers
provide a more complete inhibition of RAAS .
Do not stimulate rise in bradykinin
Nesiritide
(effects) and issues
used for decompensated heart failure
- potent vasodilator
- reduces elevated intracardiac pressures
- augments forward cardiac output
- lessens RAAS
- promotes diuresis
- safety issue and expensive
Beta adrenergic agonists
dobutamine and dopamine and isopropanolol
Milrinone
Phosphodiesterase inhibitor
-limited to IV treatment of CHF
Digitalis
intraveously or orally
- enhances contractility and reduce cardiac enlargement
not useful in diastolic heart failure
beta blockers
helps with increasing CO
- reduce heart rate and blunting chronic sympathetic activation
- allow time for heart to fill up
