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
What drugs make up ARNi
Sacubitril and valsartan
26
What is the MOA of ARNis
Inhibits endopeptidase that degrades BNP,ANP promotes diuresis and promotes vasodilation
27
Why are ARNis combined with ARBs
Neprilysin degrades A2 so the ARB will block those effects
28
Where are beta 1 receptors found
Heart and kidneys
29
Where are beta 2 receptors found
lungs and vascular smooth muscle
30
What is the MOA of beta blockers
blocks sympathetic activity decrease after load decrease heart rate decrease renin release
31
Which beta blockers are approved for heart failure in the US
Carvedilol metoprolol succinate Bisoprolol
32
What type of HF can beta blockers NOT be used in
acute HF
33
What is the benefit of using beta blockers in HF
improved survival in CHF cardioprotective improved LV hemodynamic function decreased cardiac O2 demand
34
What are the adverse effects of beta blockers
fatigue dizziness AV block bronchoconstriction sexual dysfunction changes glucose metabolism
35
What are common symptoms of HF
SOB LE swelling fatigue PND loss of appetite swollen or tender abdomen cough w/ frothy sputum polyuria at night impaired memory
36
What are the benefits / indications of diuretics
relief in pulmonary congestion relief of peripheral edema
37
Which diuretics are used in managing HF
loop diuretics
38
What is the MOA of hydralazine
decrease after load
39
What is the MOA of isosorbide dinitrate
decrease pre-load and after load by being converted to nitric oxide in the body leading the ventilation
40
When are vasodilators useful in HF
In patients with current or previous symptomatic HFrEF who cant tolerate ACEi & ARB ** mortality benefit in African Americans
41
What is the adverse reactions to vasodilators
H/A Hypotension Tachycardia ***Hydralazine.. malar rash and glomerulonephritis
42
What is the MOA of Digoxin
Inhibits Na-K-ATPase -increase intracellular Ca2+ increase cardiac contractility **parasympathomimetic effects
43
When is digoxin recommended in HF
In stage C and D with EF<25% NO EFFECT ON MORTALITY
44
What are the benefits of digoxin
decrease HF symptoms increase exercise tolerance decrease hospitalization rate use in atrial arrhythmia tx
45
If a patient has HF and Afib what is the best drug to give them
digoxin
46
What are the adverse reactions of digoxin
Narrow TI food decreases reabsorption crosses placenta
47
What are signs of digoxin toxicity
bradycardia (m/c) AV block tachyarrythmias/ ventricular automaticity delirium N/V
48
What type of HF is digoxin typically used in
decompensated heart failure
49
What groups of drugs are short term IV inotropic therapies
PDEi B1 agonist
50
Which drugs are PDEi inotrope
milrinone
51
What is the MOA go milrinone
decrease breakdown of cAMP -increase cAMP allows for increase Ca2+ in myocytes and vasodilation of vasc smooth muscle
52
What drug is a B1 adrenergic agonist
dobutamine
53
What is the MOA of dobutamine
Agonizes B1 to increase heart rate
54
When is dobutamine used
increase cardiac rate and output w/ few vascular side effects **pressor in states of acute heart failure (inotropic post CT surgery)
55
What are the adverse effects of dobutamine
same as Epi **use in caution with afib
56
When is ranolazine used
stable angina arrhythmias used when other drugs have failed
57
What is the MOA of ranolazine
inhibits late stage Na+ current and improves O2 supply and demand
58
what are the side effects of ranolazine
prolonged QT many drug interactions