CHF Flashcards

1
Q

Most common cause of HF in US

A

Ischemia

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2
Q

Sx of HF include

A

dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, fatigue

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3
Q

Signs of HF include

A

rales, JVD, pitting edema

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4
Q

Right Sided HF physiology

A

blood pools in right atrium, back up of blood in SVC and IVC

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5
Q

S/S of Right Sided HF

A

JVD, peripheral edema

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6
Q

Left Sided HF physiology

A

blood pools in Left atrium and backs up into the pulmonic vein congesting to lungs

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7
Q

S/S of Left Sided HF

A

Classic pulmonary congestive changes

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8
Q

High-Output HF physiology

A

abnormally elevated metabolic demands of tissues and CO cannot meet demands

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9
Q

Low-Output HF physiology

A

insufficient output to meet normal tissue metabolic demands

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10
Q

Causes of High-Output HF

A

Anemia, Thyrotoxicosis

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11
Q

Systolic HF physiology

A

inability to expel sufficient amount of blood

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12
Q

Diastolic HF physiology

A

failure to relax and fill normally

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13
Q

heart failure with preserved left ventricular ejection fraction (LVEF)

A

aka Diastolic HF

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14
Q

Functional Classification: NYHA Class I

A

Sx w/ strenuous activity

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15
Q

Functional Classification: NYHA Class II

A

Sx w/ ordinary activity (2 blocks or flight of stairs)

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16
Q

Functional Classification: NYHA Class III

A

Sx w/ minimal activity (<1 city block)

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17
Q

Functional Classification: NYHA Class IV

A

Sx w/ rest

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18
Q

Non-cardiogenic HF

A

ARDS, caused by shock, trauma, infection, transfusions

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19
Q

Adaptations of the heart in HF

A

change in LV volume and pressure, LV remodeling, neurohormonal activation

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20
Q

Remodeling of heart in HF

A

Hypertrophy, chamber dilation

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21
Q

Remodeling of the heart is a change in ventricular

A

shape, size, and mass secondary to myocyte loss

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22
Q

First change in remodeling of the heart

A

hypertrophy

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23
Q

Frank-Starling Law

A

Increasing EDV results in increased force of contraction

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24
Q

Frank-Starling Law as it applies to HF

A

EDV continues to increase and the heart is forced to increase contractility, until it plateaus and results in heart failure

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25
Second change in remodeling of the heart
chamber dilation---as myocyte loss increases
26
RAAS activation in HF is due to
RAAS and ADH are activated bc sensors indicate low perfusion/low O2
27
RAAS activation causes
functions to increase volume (Na+/H2O reabsorption) and vasoconstriction
28
SNS activation in HF is due to
Sensors indicating low perfusion/low O2
29
SNS activation in HF causes
HR increase, vasoconstriction, increased contractility
30
PE findings of HF
Increased HR, narrowed pulse pressure, crackles, rales, hepatojugular reflex, S3
31
Diagnosis
CXR (pulmonary edema), BNP, ECHO (EF of LV, valve function), BUN/Creatinine elevation, Na decreased, elevated LFT
32
ECHO showing systolic HF
reduced EF and increased chamber size
33
CXR findings w/ HF
Cardiomegaly and Bilateral lung infiltrates (back-up of blood in the venous vasculature of the lungs, increased transudation of fluid)
34
Kerley B Lines
short parallel lines at the lung periphery, usually seen at the costophrenic angle on CXR; commonly caused by pulmonary edema
35
Elevated BNP
can indicate many pathologies, HF included
36
Non-pharmacologic Treatment for HF
Fluid restriction, Na+ restriction, weight reduction, cardiac rehab
37
Pharmacologic Treatment for HF
loop diuretics (furosemide/lasix), spironolactone, ACE-I, ARB, Hydralazine+Nitrate, b-blocker
38
ACE-I treat HF by
decrease vasoconstriction -> decreased afterload; decreases preload (decreased volume)
39
ACE-I reduce mortality by
40%
40
Side effects of ACE-I
Dry cough, hypotension, angioedema, hyperkalemia, azotemia
41
ARB is ________ effective than/as ACE-I
equally
42
Unlike ACE-I, ARBs are not associated w/
dry cough
43
If HF pts cannot tolerate ACE-I or ARBs, consider
Hydralazine + Nitrates (vasodilation)
44
Hydralazine + Nitrates is ________ effective than/as ACE-I
less
45
Beta-blocker help treat HF by
decreasing Sympathetic tone (reduce vasoconstriction to decreased afterload)
46
3 b-blocker agents known to be effective
metoprolol, bisoprolol, carvedilol all improve LVEF and mortality
47
Aldosterone Antagonist are used for
severe HF to decrease mortality
48
Which drug/s is used in HF Tx, but is not associated w/ decreased mortality?
Loop diuretics and digoxin make ppl feel better, but do not make them live longer
49
Digoxin is used for _________, bc it causes what effect?
systolic HF; increased myocardial contractility
50
Dobutamine is a
IV inotropic agent (increases contractility)
51
Patients with EF <30-35% are at increased risk of
fatal arrhythmias (Vfib, Afib)
52
ICD (implanted defibrillator) are implanted in pts w/
NYHA III-IV with EF <30%
53
ICD (implanted defibrillator) are implanted when
40d post-MI, 3mo post-revascularization, 3mo on Optimal Drug therapy
54
Stage I
Lasix, ACE-I, b-Blocker
55
Pathology of pulmonary edema would show what type of cells?
"Heart Failure" cells: hemosiderin laden macrophages
56
What electrolyte finding is associated w/ HF?
Decreased Na+ (d/t increased free water)
57
Stage 1 of CHF
Redistribution of pulmonary vessels, cardiomegaly, broad vascular pedicle
58
Stage 2 of CHF
Kerley Lines, peribronchial cuffing, hazy contour of vessels, thickened inter lobar fissure
59
Stage 3 of CHF
consolidation, air bronchogram, cottonwood appearance, pleural effusion
60
What HF drug is not used acutely?
b-blocker