Treatment of HF Flashcards
ACE inhibitors
“pril”
natriuresis, decrease TPR and aldosterone (can have aldosterone escape)
advantages: decrease mortality post MI, preserve renal function in diabetics, little lipid/sexual effects, bradykinin (vasodilator)
decrease preload/afterload
AE: hypotension, Na depletion, dry cough (bradykinin), hyperkalemia, angiodema, renal insufficiency, hepatotoxicity, pancreatitis, increase PGs, FETOTOXICITY
AA/low renin hypertensives respond poorly: add diuretic
many are prodrugs (not captopril and lisinopril)
preferred over ARB (although the two are comparable)
ARB
“sartan”
block AT1 receptor: vasodilation and Na/water excretion
reduce preload/afterload
SE: hypotension, hyperkalemia, hepatic, FETOTOXICITY
olmesartan AE: spruelike enteropathy
aliskiren
renin inhibitor: inhibits protease activity
vasodilation and natriuresis
ZE: hypotension, hyperkalemia, angiodema, FETOXICITY
DI: inhibit p-gp
Tx for class I HF
no symptoms, EF
Tx for class II HF
dyspnea on exertion, edema
add diuretic
Tx for class III HF
dyspnea, orthopnea, PND, edema
add digoxin and spironolactone
Tx for class IV HF
refractory edema
add combination diuretics, IV vasodilators, transplant/assist devices
digitalis
also digoxin, digitoxin, ouabain
MOA: increase intercellular availability of Ca via inhibition of Na/K ATPase
toxicity: atrial, ventricular arrhythmias, yellow-green halo, headache, fatigue, drowsy, confusion, seizures
CI (digoxin toxicity): quinidine and amiodarone (decrease elimination), verapamil (slow HR), diuretics (hypokalemia)
does NOT effect mortality
digibind
Ab to digoxin
B-blockers
attenuate NE/Epi effects
short term: reduce CO, BP (get worsening of symptoms before improvement)
long term: increase CO, decrease LVEDP
improved mortality
CI: heart block, bradycardia, decompensated CHF/need for IV inotropes (dobutamine), volume overload
NE/Epi effects on CHF
B-AR down regulation, arrhythmias, increased myocardial consumption/ischemia, mycyte apoptosis followed by cardiac fibrosis
B blockers approved for CHF
metoprolol
carvedilol
bisprolol
nebivolol (Europe ONLY)
Tx Stage A CHF
at risk preventative measures (HTN, lipids, smoking, diabetes, EtOH)
Tx Stage B CHF
class I CHF add ACE I/ARB: prevent metabolic stress, apoptosis, remodeling stimulated by angiotensin, aldosterone and NE (prevent decline in cardiac function)
Tx Stage C CHF
class II and III CHF add B blocker, diuretic, digoxin, spironolactone
Tx Stage D CHF
class IV CHF
add IV inotrope, transplant
STOP B-blockers
diuretics
reduce preload, CO NOT increased
no improved survival
AE: electrolyte disturbance, hypokalemia, hyponatremia, hypochloremic metabolic alkalosis, azotemia (high NO in blood), dehydration, hypotension
DI: NSAIDs reduce efficacy (promote fluid retention)
reduce dose with ACE I/ ARB (both have mild diuretic effects)
spironolactone/eplerenone
ONLY diuretics that improve prognosis of CHF
K sparing
block aldosterone effects
use in combo with loop diuretics
furosemide/ bumetanide
high ceiling (loop) diuretic AE: ototoxicity
triamterene, amioloride
K sparing diuretics
amioloride NOT used in CHF
used in combo with loop diuretics
nitrate
venodilator: reduce preload/afterload
reduce pulmonary congestion and LV filling pressure/wall stress
hydralazine
arterial vasodilator: increase CO
reduce preload
effective in CHF but: stimulates RAS, variability in dose
AE: nausea, anorexia, +FANA, drug induced lupus, exacerbate angina (coronary steal)
use: limited to patients than are unable to tolerate ACE I
other vasodilators not effective in CHF (ex: parson, minoxidil, dihydropyrindine)
nitroprusside
veno and vasodilator: reduce preload and afterload
dobutamine
IV
B agonist (B1>B2), alpha 1 agonist, postive inotrope, vasodilator
limited by B-AR desensitization, arrhythmias
CI: B blocker prevents vasodilator effect of dobutamine and can cause vasoconstriction
milirinone
IV
PDE inhibitor: cAMP is not degraded: inotropic
decrease after load
long term use: increases mortality in CHF
nesiritide
recombinant B-type natriuretic peptide
reduce preload and after load
use: limited to those that do not respond to nitroglycerin
AE: hyoptension
B-type natriuretic peptide and Atrial natriuretic peptide
released from atria in response to volume/pressure increase
elevated in CHF
promotes vasodilation, venodilation, natriuresis
reduce preload, inhibit renin and aldosterone, afferent arteriolar vasodilation, inhibits Na reabsorption