Treatment of HF Flashcards

1
Q

ACE inhibitors

A

“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)

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2
Q

ARB

A

“sartan”
block AT1 receptor: vasodilation and Na/water excretion
reduce preload/afterload
SE: hypotension, hyperkalemia, hepatic, FETOTOXICITY
olmesartan AE: spruelike enteropathy

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3
Q

aliskiren

A

renin inhibitor: inhibits protease activity
vasodilation and natriuresis
ZE: hypotension, hyperkalemia, angiodema, FETOXICITY
DI: inhibit p-gp

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4
Q

Tx for class I HF

A

no symptoms, EF

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5
Q

Tx for class II HF

A

dyspnea on exertion, edema

add diuretic

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6
Q

Tx for class III HF

A

dyspnea, orthopnea, PND, edema

add digoxin and spironolactone

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7
Q

Tx for class IV HF

A

refractory edema

add combination diuretics, IV vasodilators, transplant/assist devices

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8
Q

digitalis

A

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

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9
Q

digibind

A

Ab to digoxin

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10
Q

B-blockers

A

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

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11
Q

NE/Epi effects on CHF

A

B-AR down regulation, arrhythmias, increased myocardial consumption/ischemia, mycyte apoptosis followed by cardiac fibrosis

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12
Q

B blockers approved for CHF

A

metoprolol
carvedilol
bisprolol
nebivolol (Europe ONLY)

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13
Q

Tx Stage A CHF

A
at risk
preventative measures (HTN, lipids, smoking, diabetes, EtOH)
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14
Q

Tx Stage B CHF

A
class I CHF
add ACE I/ARB: prevent metabolic stress, apoptosis, remodeling stimulated by angiotensin, aldosterone and NE (prevent decline in cardiac function)
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15
Q

Tx Stage C CHF

A
class II and III CHF
add B blocker, diuretic, digoxin, spironolactone
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16
Q

Tx Stage D CHF

A

class IV CHF
add IV inotrope, transplant
STOP B-blockers

17
Q

diuretics

A

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)

18
Q

spironolactone/eplerenone

A

ONLY diuretics that improve prognosis of CHF
K sparing
block aldosterone effects
use in combo with loop diuretics

19
Q

furosemide/ bumetanide

A
high ceiling (loop) diuretic
AE: ototoxicity
20
Q

triamterene, amioloride

A

K sparing diuretics
amioloride NOT used in CHF
used in combo with loop diuretics

21
Q

nitrate

A

venodilator: reduce preload/afterload

reduce pulmonary congestion and LV filling pressure/wall stress

22
Q

hydralazine

A

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)

23
Q

nitroprusside

A

veno and vasodilator: reduce preload and afterload

24
Q

dobutamine

A

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

25
Q

milirinone

A

IV
PDE inhibitor: cAMP is not degraded: inotropic
decrease after load
long term use: increases mortality in CHF

26
Q

nesiritide

A

recombinant B-type natriuretic peptide
reduce preload and after load
use: limited to those that do not respond to nitroglycerin
AE: hyoptension

27
Q

B-type natriuretic peptide and Atrial natriuretic peptide

A

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