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Pharm 2 module 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is the most common cause of HF

A

CAD (ischemia)

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2
Q

What are the stages of HF

A

Stage A
Stage B
Stage C
Stage D

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3
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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4
Q

What is Stage A heart failure

A

Cardiac risk factors

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5
Q

What is stage B HF

A

Structural heart disease W/O HF

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6
Q

What is stage C HF

A

Structural heart disease with HF

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7
Q

What is stage D HF

A

End-stage heart failure

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8
Q

What is the pathophys of HF

A

CAD
Hypertension
Cardiomyopathy
valvular dysfunction

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9
Q

What patients fall into Stage B HF

A

Previous MI
LV remodeling (LVH & low EF)
Asymptomatic valvular disease

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10
Q

What is class 1 of stage B/C HF

A

Asymptomatic / mild symptoms with strenuous exercise

no limitations

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11
Q

What is class 2 of B/C HF

A

sxs with ordinary activity but no symptoms at rest

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12
Q

What is class 3 of B/C HF

A

marked sxs with ordinary activity but no symptoms at rest

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13
Q

What is class 4 of stage B/C HF

A

Symptoms at rest

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14
Q

What are the patient goals of therapy

A

improve mortality
slow disease progression
alleviate symptoms

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15
Q

What are the ways you can reduce the myocardial work

A

afterload reduction
preload reduction

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16
Q

What are the physiological goals of HF therapy

A

reduce myocardial work
improve output
reduce morphological changes

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17
Q

How does the body react to a decrease in cardiac output

A

Baroreceptor response
Increased sympathetic tone

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18
Q

What occurs when the body activates the RAAS system

A

Sodium / water retention occurs which causes an increase in peripheral vascular resistance

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19
Q

how does the RAAS system lead to worsened HF

A

Short term it will initially boost CO but long term causes LV remodeling

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20
Q

What drug classes are useful for HF

A

RAAS
B-blockers
Diuretics
vasodilators
inotropics

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21
Q

What is the benefit of ACEi in HF

A

Decrease both preload and after load by decreasing TPR and H2O/Na retention

slows progression of renal insufficiency

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22
Q

What are the indications for ACEi in HF

A

Symptomatic / asymptomatic HFrEF

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23
Q

What is the MOA of ARBs

A

Prevents binding at the AT1 receptor site

Does NOT effect bradykinin levels (less incidence of cough /angioedema)

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24
Q

Which patients are aldosterone antagonists recommended

A

Stage C and D HF

25
Q

What drugs make up ARNi

A

Sacubitril and valsartan

26
Q

What is the MOA of ARNis

A

Inhibits endopeptidase that degrades BNP,ANP

promotes diuresis and promotes vasodilation

27
Q

Why are ARNis combined with ARBs

A

Neprilysin degrades A2 so the ARB will block those effects

28
Q

Where are beta 1 receptors found

A

Heart and kidneys

29
Q

Where are beta 2 receptors found

A

lungs and vascular smooth muscle

30
Q

What is the MOA of beta blockers

A

blocks sympathetic activity
decrease after load
decrease heart rate
decrease renin release

31
Q

Which beta blockers are approved for heart failure in the US

A

Carvedilol
metoprolol succinate
Bisoprolol

32
Q

What type of HF can beta blockers NOT be used in

A

acute HF

33
Q

What is the benefit of using beta blockers in HF

A

improved survival in CHF
cardioprotective
improved LV hemodynamic function
decreased cardiac O2 demand

34
Q

What are the adverse effects of beta blockers

A

fatigue
dizziness
AV block
bronchoconstriction
sexual dysfunction
changes glucose metabolism

35
Q

What are common symptoms of HF

A

SOB
LE swelling
fatigue
PND
loss of appetite
swollen or tender abdomen
cough w/ frothy sputum
polyuria at night
impaired memory

36
Q

What are the benefits / indications of diuretics

A

relief in pulmonary congestion
relief of peripheral edema

37
Q

Which diuretics are used in managing HF

A

loop diuretics

38
Q

What is the MOA of hydralazine

A

decrease after load

39
Q

What is the MOA of isosorbide dinitrate

A

decrease pre-load and after load by being converted to nitric oxide in the body leading the ventilation

40
Q

When are vasodilators useful in HF

A

In patients with current or previous symptomatic HFrEF who cant tolerate ACEi & ARB

** mortality benefit in African Americans

41
Q

What is the adverse reactions to vasodilators

A

H/A
Hypotension
Tachycardia

***Hydralazine.. malar rash and glomerulonephritis

42
Q

What is the MOA of Digoxin

A

Inhibits Na-K-ATPase
-increase intracellular Ca2+
increase cardiac contractility

**parasympathomimetic effects

43
Q

When is digoxin recommended in HF

A

In stage C and D with EF<25%

NO EFFECT ON MORTALITY

44
Q

What are the benefits of digoxin

A

decrease HF symptoms
increase exercise tolerance
decrease hospitalization rate
use in atrial arrhythmia tx

45
Q

If a patient has HF and Afib what is the best drug to give them

A

digoxin

46
Q

What are the adverse reactions of digoxin

A

Narrow TI
food decreases reabsorption
crosses placenta

47
Q

What are signs of digoxin toxicity

A

bradycardia (m/c)
AV block
tachyarrythmias/ ventricular automaticity

delirium
N/V

48
Q

What type of HF is digoxin typically used in

A

decompensated heart failure

49
Q

What groups of drugs are short term IV inotropic therapies

A

PDEi
B1 agonist

50
Q

Which drugs are PDEi inotrope

A

milrinone

51
Q

What is the MOA go milrinone

A

decrease breakdown of cAMP
-increase cAMP allows for increase Ca2+ in myocytes and vasodilation of vasc smooth muscle

52
Q

What drug is a B1 adrenergic agonist

A

dobutamine

53
Q

What is the MOA of dobutamine

A

Agonizes B1 to increase heart rate

54
Q

When is dobutamine used

A

increase cardiac rate and output w/ few vascular side effects

**pressor in states of acute heart failure (inotropic post CT surgery)

55
Q

What are the adverse effects of dobutamine

A

same as Epi
**use in caution with afib

56
Q

When is ranolazine used

A

stable angina
arrhythmias
used when other drugs have failed

57
Q

What is the MOA of ranolazine

A

inhibits late stage Na+ current and improves O2 supply and demand

58
Q

what are the side effects of ranolazine

A

prolonged QT
many drug interactions

Pharm 2 module 2 (4 decks)

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