Heart Failure Drugs Flashcards
1
Q
Aliskrein
A
-Blocks the Renin conversion of angiotensinogen to angiotensin I
2
Q
Captopril
A
- ACE inhibitor
- prevents conversion of angiotensin I to angiotensin II
- lowers blood pressure and prevents heart remodeling
- Risk of cough, angioedema, and fetal toxicity
- short t1/2: 1.7 hr
3
Q
enalapril
A
- ACE inhibitor
- prevents conversion of angiotensin I to angiotensin II
- lowers blood pressure and prevents heart remodeling
- Risk of cough, angioedema, and fetal toxicity
- prodrug used in IV only
4
Q
benazepril
A
- ACE inhibitor
- prevents conversion of angiotensin I to angiotensin II
- lowers blood pressure and prevents heart remodeling
- Risk of cough, angioedema, and fetal toxicity
- long t1/2, 1x dose/day
5
Q
lisinopril
A
- ACE inhibitor
- prevents conversion of angiotensin I to angiotensin II
- lowers blood pressure and prevents heart remodeling
- Risk of cough, angioedema, and fetal toxicity
- long t1/2, 1x dose/day
6
Q
losartan
A
- ARB (Angiotensin II receptor inhibitor)
- nonpeptide, with 1000x more affinity for the AT1 receptor
- treatment of HTN, diabetic nephropathy, and HF
- blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II
- does not affect the response to bradykinin
- risk of fetal toxicity, hypotension
7
Q
valsartan
A
- ARB (Angiotensin II receptor inhibitor)
- not a prodrug
- more affinity for the AT1 receptor
- treatment of HTN, diabetic nephropathy, and HF
- blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II
- does not affect the response to bradykinin
- risk of fetal toxicity, hypotension
8
Q
candesartan
A
- ARB (Angiotensin II receptor inhibitor)
- irreversible binding
- more affinity for the AT1 receptor
- treatment of HTN, diabetic nephropathy, and HF
- blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II
- does not affect the response to bradykinin
- risk of fetal toxicity, hypotension
9
Q
valsartan/sacubitril
A
- ARNI (angiotensin receptor/neprolysin inhibitor)
- sacubitril increases level of ANP and BNP
- used for HF
- risk of angioedema, fetal toxicity, orthostatic hypertension, and cough
10
Q
carvedilol
A
- β-blocker
- nonselective beta- and alpha-adrenergic blocker
- reduces CO, causes vasodilation
- used to prevent the down regulation of β-adrenergic receptors (keeps heart receptive to sympathetic drive)
- indicated in stable pts post-MI with rEF <40%, or pts with HFrEF
- risk of MI if abruptly discontinued
11
Q
ivabradine
A
- HCN channel blocker (hyperpolarization-activated cyclic nucleotide-gated channels )
- Blocks Funny channels in SA node
- prolongs diastole and slows HR
- indicated for pts with CHF and <35% rEF, who are on max betablockers or cant have betablockers
12
Q
spironolactone
A
- K+ sparing diuretic
- competitive antagonist of aldosterone inhibitors
- prevents fibrotic effect of aldosterone
- used to counteract loss of K+ by other diuretics, and reduces fibrosis in HFrEF
- risk of gynecomastia and hirsuitism
13
Q
eplerenone
A
- K+ sparing diuretic
- MORE SELECTIVE competitive antagonist of aldosterone inhibitors
- prevents fibrotic effect of aldosterone
- used to counteract loss of K+ by other diuretics, and reduces fibrosis in HFrEF
- risk of gynecomastia and hirsuitism
14
Q
furosemide
A
- Na+-K+-2Cl-cotransporter blocker
- directly Inhibits reabsorption of sodium and chloride in the thick ascending limb of the loop of Henle
- causes increased excretion of fluid and most electrolytes, excretes isotonic urine
- works in pts with low GFR!
- risk of hypocalcemia, hypochloremic metabolic alkalosis, ototoxicity, and sulfur allergy
15
Q
torsemide
A
- Na+-K+-2Cl-cotransporter blocker
- directly Inhibits reabsorption of sodium and chloride in the thick ascending limb of the loop of Henle
- causes increased excretion of fluid and most electrolytes
- longer t1/2, better oral absorption
- risk of hypocalcemia, ototoxicity, and sulfur allergy
16
Q
bumetanide
A
- Na+-K+-2Cl-cotransporter blocker
- directly Inhibits reabsorption of sodium and chloride in the thick ascending limb of the loop of Henle
- causes increased excretion of fluid and most electrolytes
- risk of hypocalcemia, ototoxicity, and sulfur allergy
17
Q
ethacrynic acid
A
- NON SULFA loop diuretic
- causes increased excretion of fluid and most electrolytes
- risk of hypocalcemia, ototoxicity, and sulfur allergy
18
Q
hydrochlorothiazide
A
- Na+-Cl-cotransporter blocker
- causes increased urinary excretion
- treatment of HTN
- not effective in pts with low GFR
- may cause hypokalemia, hypochloremic metabolic acidosis, and sulfa allergy
19
Q
isosorbide dinitrate + hydralazine
A
- isosorbide dinitrate dilates veins to decrease preload, and the hydralazine dilates arteries to decrease afterload
- formulated for african americans
- best for pts who cannot tolerate ACEis
20
Q
nitroglycerin
A
- Releases NO which increases levels of cGMP, which vasodilates peripheral veins and arteries
- reduces cardiac o2 demand by decreasing preload
- treatment for angina pectoris and acute decompensated HF
21
Q
hydralizine
A
- endothelium dependent MOA, which requires COX activation and may be mediated by PGI2 receptor
- causes direct vasodilation of arterioles
- used in HTN, HFrEF when intolerant to ACEi/ARB, HTN emergency in pregnancy
- risk of angina pectoris, flushing, itching, lupus like syndrome
22
Q
digoxin
A
- cardiac glycoside
- inhibits Na+-K+ ATPase
- positive inotrope, increases CO
- used to control ventricular response rate in adults with chronic aFib, and in HF
- administered orally and needs a loading dose
- decreases firing in the atria and increases firing in the ventricles
- risk of hypokalemia, and can cause visual disturbance
23
Q
dobutamine
A
- synthetic catecholamine
- selectively binds to β1-adrenergic receptors
- sympathomimetic, increases HR and contractility
24
Q
dopamine
A
- a catecholamine which activates β1-adrenergic receptors
- sympathomimetic, increases HR and contractility
25
Q
milrinone
A
- PDE-III inhibitor
- results in increased cAMP which leads to increased contractility in heart and vasodilation
- must be given IV
