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Pharm2: Module 2 > Heart Failure > Flashcards

Heart Failure Flashcards

(59 cards)

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1
Q

What is heart failure

A

inability of the heart to maintain enough cardiac output to meet the metabolic demands of the body

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2
Q

What are causes of Heart failure

A

Ischemia (CAD)(m/c)
valvular defect
ETOH
viral
peripartum
Stress
chemo
familial
congenital
idiopathic

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3
Q

What are the AHA/ACC classifications

A

Stage A - D

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4
Q

what is stage A

A

cardiac risk factors

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5
Q

what is stage B

A

structural heart disease without HF

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6
Q

what is Stage C

A

structural heart disease with HF

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7
Q

what is Stage D

A

end-stage HF

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8
Q

what is AHA

A

American Heart Association

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9
Q

what is ACC

A

American College of Cardiology

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10
Q

What are the functional classification NYHA

A

Class 1-4 (symptoms)
starts at AHA/ACC stage B/C

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11
Q

what is class 1 NYHA classification

A

asymptomatic or mild sx with strenuous exercise, no limitations

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12
Q

what is class 2 NYHA classification

A

symptoms with ordinary activity; slight limitation

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13
Q

what is class 3 NYHA classifications

A

marked symptoms with ordinary activity; no symptoms at rest

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14
Q

what is class 4 NYHA classification

A

symptoms at rest

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15
Q

what are the goals of HF therapy

A

improve mortality
slow disease production
alleviate symptoms

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16
Q

what are the physiological goals of HF therapy

A

reduce myocardial work - afterload and preload reduction
improve output - contractility
reduce morphological changes - remodeling

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17
Q

What is systolic dysfunction

A

decreased ability of the heart to eject blood - due to impaired contractility or pressure overload
elevated ESV
reduced EF
eccentric ventricular remodeling and increased EDV and mass (myocytes elongate)

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18
Q

what is diastolic dysfunction

A

decreased relaxation (stiffness) of the heart with reduced SV
elevated EDV/EDP
EF may be preserved
concentric ventricular remodeling and increased ventricular mass (myocytes thicken)

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19
Q

what is the bodies natural response to HF

A

baroreceptor response
increase sympathetic tone - increased HR and contractility, increase peripheral vasoconstriction, increase release of renin

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20
Q

what does the activation of RRAS lead to

A

sodium and water retention
increase peripheral vascular tone (vasoconstriction)

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21
Q

What are the RAAS

A

ACE
ARBs
Aldosterone Antagonists
Renin inhibitors

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22
Q

what are Effective HF drug classes

A

RAAS
BB
Diuretics
Vasodilators
Inotropics

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23
Q

what is the MOA for ACEi

A

blocks the conversion of angiotension 1 to angitensin 2

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24
Q

what are the ACEi

Study These Flashcards
A

captopril, enalapril, lisinopril

25
what are the benefits of ACEi
improved morbidity and mortality outcomes reduces cardiac remodeling slows progression of kidney disease especially in diabetics increase K+ reabsorption improved survival decreased LVH slows progression of renal insufficiency, esp in diabetics
26
what are the AE of ACEi
dry cough hyperkalemia angioedema (rare) skin reactions contraindicated in pregnancy
27
what are ARBS
inhibitors of the RAAS Loasartan, valsartan, candesartan, olmesartain
28
what is the MOA of ARBs
directly blocks angiotensin II type 1 receptors does not affect bradykinin levels
29
what are the AE of ARBs
hypotension hyperkalemia worsening renal function angioedema contraindicated in pregnancy
30
what are the aldosterone antagonists that inhibit RAAS
spironolactone and eplerenone recommended for stage C and D HF
31
what is the MOA for aldosterone antagonists
blocks the aldosterone (mineralocorticoid receptor) decreases sodium and water retention
32
What are the AE of aldosterone antagonists
hyperkalemia hypovolemia gynecomastica hypertriglyceridemia induced CYP renal dysfunction/failure
33
What is the angiotensin receptor-neprilysin inhibitors (ARNi)
sacubitril and valsartain MOA: inhibits neprilysin - endopeptidase that degrades BNP, ANP, promotes diuresis and vasodilation
34
what are the AE of sacubitril
hypotension hyperkalemia dizziness renal failure cough angioedema contraindicated in pregnancy
35
where are B1 receptors
mainly on the heart and kidneys
36
where are B2 receptors
mainly on the lungs and vascular smooth muscle
37
when are BB not indicated in HF
NOT indicated for acute HF
38
what are the approved HF BBs in the US
carvedilol metoprolol bisoprolol
39
what are the benefits of BB
decreased cardiac O2 demand - increase HR, contractility and LV wall stress improves survival after MI improved LV hemodynamic function improved survival in CHF lowers BP
40
what are the AE of BB
cardiac: fatigue, dizziness, low exercise tolerance, bradycardia, sinus arrest, AV block, HF Pulmonary: bronchoconstriction CNS: sexual dysfunction, fatigue, depression MEtabolic: change in glucose metabolism, may mask early signs of hypoglycemia (tachy)
41
what are symptoms of HF
SOB Swelling of LE Fatigue Orthopnea anorexia/distended abdomen cough with frothy sputum increased urination at night confusion and/or impaired memory
42
what is the MOA for Loops diuretics
blocks reabsorption of Na+, Cl-, K+, HCO3-, Ca2+, Mg2+ promoted the excretion of water and electrolytes decreased plasma volume - decreased preload and afterload
43
inidcations for diuretics
sympatomatic relief - only -volume overload relief of pulmonary congestion relief of peripheral edema
44
what are the AE of diuretics
hypovolemia hypotension electrolyte imbalance - hypokalemia, hyponatremia, hypocholoremia, hypomagnesemia ototoxicity hyperuricemia (gout) hyperglycermia
45
what is Hydralazine
arteriole vasodilator decreases afterload
46
what is isosorbide dinitrate
venodilator converted to nitric oxide in the body causes vasodilation decreased preload and afterload
47
what are AE of vasodilators
headache hypotension tachy
48
what can hydralazine cause at high doses
rarely but may cause lupus-like syndrome including glomerulonephritis
49
what is the MOA of Digoxin
cardiac glycoside inhibits NA-K-ATPase alters Na+/Ca+ exchanger - increased intracellular Ca2+ and cardiac contractility increase in vagal tone (decrease sym/renin release) Parasympathomimetic effects - slows SA node firing and AV node conduction
50
when is digoxin indicated
Stage C and D and EF <25% at low concentrations: reduced morbidity - improved symptoms, decreased admissions
51
what are the benefits of digoxin
increased cardiac contractility - decrease symptoms of HF -increase exercise tolerance -decrease hospitalizations useful for treatment of atrial arrhythmias HF and AFib - win/win combo
52
what is higher levels of digoxin in the body associated with
decreased survival in HF goal is 0.5 - 1.1 in HF
53
what are the AE of Digoxin
narrow TRUTH IS factors that increase risk of toxicity: renal insufficiency, increased age, drug interactions (amiodarone, verapamil), metabolic factors (hypokalemia, hypomagnesemia, hypernatremia, hypercalcemia, acid-base disturbances)
54
what are signs and symptoms of Digoxin toxicity
Bradycardia (m/c) AV block tachyarrhythmia/ventricular automaticity fatigue, n/v, delirium, blurred vision, anorexia, Diarrhea, abd pain, HA, dizziness, confusion
55
What are short term IV inotropic therapies
PDEi and B1 agonists
56
what are PDEi drugs
milrinon and inamrinone (formerly amrinone)
57
what is the MOA for PDEi
inhibit PDE type III to decrease breakdown of cAMP: increase cAMP leads to enhanced activity of cAMP-dependent protein kinase (PKA), phosphorylation of voltage - dependent CA2+ channels and increase Ca2+ influx - vasodilation
58
what are the indications for Milrinone
acute hemodynamic and symptomatic relief in patients with advanced HFrEF (class III or IV) short term support routine use not supported
59
what is Dobutamine
B1 adrenergic receptor agonists

Pharm2: Module 2 (4 decks)

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