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CSI Exam 4 > CHF > Flashcards

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
Q

Second change in remodeling of the heart

A

chamber dilation—as myocyte loss increases

26
Q

RAAS activation in HF is due to

A

RAAS and ADH are activated bc sensors indicate low perfusion/low O2

27
Q

RAAS activation causes

A

functions to increase volume (Na+/H2O reabsorption) and vasoconstriction

28
Q

SNS activation in HF is due to

A

Sensors indicating low perfusion/low O2

29
Q

SNS activation in HF causes

A

HR increase, vasoconstriction, increased contractility

30
Q

PE findings of HF

A

Increased HR, narrowed pulse pressure, crackles, rales, hepatojugular reflex, S3

31
Q

Diagnosis

A

CXR (pulmonary edema), BNP, ECHO (EF of LV, valve function), BUN/Creatinine elevation, Na decreased, elevated LFT

32
Q

ECHO showing systolic HF

A

reduced EF and increased chamber size

33
Q

CXR findings w/ HF

A

Cardiomegaly and Bilateral lung infiltrates (back-up of blood in the venous vasculature of the lungs, increased transudation of fluid)

34
Q

Kerley B Lines

A

short parallel lines at the lung periphery, usually seen at the costophrenic angle on CXR; commonly caused by pulmonary edema

35
Q

Elevated BNP

A

can indicate many pathologies, HF included

36
Q

Non-pharmacologic Treatment for HF

A

Fluid restriction, Na+ restriction, weight reduction, cardiac rehab

37
Q

Pharmacologic Treatment for HF

A

loop diuretics (furosemide/lasix), spironolactone, ACE-I, ARB, Hydralazine+Nitrate, b-blocker

38
Q

ACE-I treat HF by

A

decrease vasoconstriction -> decreased afterload; decreases preload (decreased volume)

39
Q

ACE-I reduce mortality by

A

40%

40
Q

Side effects of ACE-I

A

Dry cough, hypotension, angioedema, hyperkalemia, azotemia

41
Q

ARB is ________ effective than/as ACE-I

A

equally

42
Q

Unlike ACE-I, ARBs are not associated w/

A

dry cough

43
Q

If HF pts cannot tolerate ACE-I or ARBs, consider

A

Hydralazine + Nitrates (vasodilation)

44
Q

Hydralazine + Nitrates is ________ effective than/as ACE-I

A

less

45
Q

Beta-blocker help treat HF by

A

decreasing Sympathetic tone (reduce vasoconstriction to decreased afterload)

46
Q

3 b-blocker agents known to be effective

A

metoprolol, bisoprolol, carvedilol all improve LVEF and mortality

47
Q

Aldosterone Antagonist are used for

A

severe HF to decrease mortality

48
Q

Which drug/s is used in HF Tx, but is not associated w/ decreased mortality?

A

Loop diuretics and digoxin make ppl feel better, but do not make them live longer

49
Q

Digoxin is used for _________, bc it causes what effect?

A

systolic HF; increased myocardial contractility

50
Q

Dobutamine is a

A

IV inotropic agent (increases contractility)

51
Q

Patients with EF <30-35% are at increased risk of

A

fatal arrhythmias (Vfib, Afib)

52
Q

ICD (implanted defibrillator) are implanted in pts w/

A

NYHA III-IV with EF <30%

53
Q

ICD (implanted defibrillator) are implanted when

A

40d post-MI, 3mo post-revascularization, 3mo on Optimal Drug therapy

54
Q

Stage I

A

Lasix, ACE-I, b-Blocker

55
Q

Pathology of pulmonary edema would show what type of cells?

A

“Heart Failure” cells: hemosiderin laden macrophages

56
Q

What electrolyte finding is associated w/ HF?

A

Decreased Na+ (d/t increased free water)

57
Q

Stage 1 of CHF

A

Redistribution of pulmonary vessels, cardiomegaly, broad vascular pedicle

58
Q

Stage 2 of CHF

A

Kerley Lines, peribronchial cuffing, hazy contour of vessels, thickened inter lobar fissure

59
Q

Stage 3 of CHF

A

consolidation, air bronchogram, cottonwood appearance, pleural effusion

60
Q

What HF drug is not used acutely?

A

b-blocker

CSI Exam 4 (11 decks)

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