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NSCC 7320 - Critical Care Theory 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

what is heart failure

A

condition in which the heart cannot pump blood at a volume required ot meet the bodys needs

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2
Q

is heart failure a primary or secondary disease

A

secondary occurs after the heart becomes damaged or weakened

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3
Q

what is end diastolic volume or EDV

A

volume that is in the ventricles before the heart contracts

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4
Q

what does EDV tell us

A

preload

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5
Q

what is ESV

A

End systolic volume

amount of blood in te ventricles at the end of systole

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6
Q

what is a normal EF

A

60-80%

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7
Q

what is HFpEF

A

preserved EF >50%

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8
Q

What is HFmEF

A

mid-range EF 41-49%

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9
Q

what is HFref

A

reduced EF <40

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10
Q

recovered EF is

A

EF previously <40 now >40

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11
Q

what is systolic HF

A

dilated heart failure
problem with pumping and ventricular emptying
reduced contractility

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12
Q

what happens to the left ventricle in systolic HF

A

large dilated congested and overloaded

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13
Q

what type of remodeling is seen in systolic dysfunction

A

eccentric as cardiomyocgyes are elognated

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14
Q

what happens to contractility, EF and CO in systolic HF

A

reduced

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15
Q

what is the most common type of HF

A

systolic

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16
Q

what type of EF does systolic typically have

A

HFrEF <40%

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17
Q

what heart sound is likely heard in systolic HF

A

S3

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18
Q

what does BP typically look like in systolic HF

A

low

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19
Q

is systolic HF more common in men or women

A

men

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20
Q

what happens to preload, afterload and contracility in systolic Hf

A

increased preload
increased afterload - compsneatory
contractility decreased as heart stretched too far

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21
Q

what type of V/Q mismatch would you see in systolic HF

A

shunt like as increased hydostatic pressure in pulm capillaries causes fluid to back up into lungs
deadspace with decreased CO

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22
Q

what happens to lung compliance in systolic HF

A

decreased resulting in inc WOB

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23
Q

what type of meds are you likely to see in systolic HF

A

vasodialtors, diuretics, inotropes

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24
Q

what is diastolic HF

A

problems with inadequate ventricular filling d/t inability to relax/fill

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25
Q

what happens to the ventricles in diastolic HF

A

thick, stiff and noncompliant

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26
Q

what type of remodeling occurs in diastolic HF

A

concentric remodelling

cardiomyocytes increase in diameter not length

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27
Q

what happens to LVEDV and LVEDP in diastolic HF

A

LVEDV (preload) decrased

LVEDP increased

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28
Q

Causes of Diastolic HF

A

HTN
hypertrophic cardiomyopathy
aging

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29
Q

ER in Diastolic HF

A

Normal HFpEF

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30
Q

Ventricles in systolic HF vs Diastolic HF

A

S: large, dilated, overloaded problem with emptying/pumping
D: Thick, stiff, non compliant problem with filling adequately

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31
Q

remodeling in Systolic vs. Diastolic HF

A

S: eccentric and elongated
D: concentric and thicker diameter

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32
Q

Causes of systloic vs. Diastolic HF

A

S: CAD
D: Htn, aging, hypertrophic cardiomyopathy

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33
Q

Extra heart sounds heard in Systolic vs. diastolic Hf

A

S3 vs S4

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34
Q

preload in systolic vs diastolic HF

A

S: increased
D: normal - incrased

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35
Q

afterload in systolic vs diastolic HF

A

S: increased
D: incrased

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36
Q

contractility in systolic vs. diastolic Hf

A

S: decreased
D: normal-decreased

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37
Q

where is the increase in diastolic pressures in systolic and diastolic HF

A

LA, LA, pulmonary vessels

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38
Q

what are the three types of compensatory mechanisms for HF

A

neurological - ANS (SNS & PNS)
hormonal - RAAS
Chemical - chemoreceptors

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39
Q

Describe the pathway for ANS

A

medulla –> CN X (vagus) –> heart

40
Q

what is the synapse for PNS

what neurotransmitter

A

cholinergic

ACetylcholine

41
Q

where are the receptors for ANS

A

atria

AV junction

42
Q

what effect does the PNS have on O2 supply and demand

A

decreases HR
slows impulse generation at SA
slows impulse through AV

43
Q

what is the neural pathway for SNS

A

medulla –> spinal cord –> exits @ T1-L2

44
Q

what type of synapse is in the SNS

what neurotransmitters

A

adrenergic

norepi, epi

45
Q

what receptors are involved in SNS

A

alpha - smooth muscle, skin, gut, kidneys, peripheral circulation
B1 - SA/AV nodes and ventricles
B2 - bronchiole, smooth muscle, skeletal msucle, arterioles

46
Q

how is the SNS triggered in HF

A

decreased CO/BP activates barorecpors in the aortic arch and carotid sinus -> stimulates medulla to activate SNS; also triggers RAAS

47
Q

what happens when the SNS is triggered in HF

A

increased catecholmaines - vasoconstriction increase afterload, inc. HR/condution/contactility
increasecd myocardial O2 demand

48
Q

How does HF trigger RAAS

A 
dec CO
poor kidney perfusion --> activates RAAS
angiotensin II and aldosterone
vasoconstriction and Na/H20 retention
increases afterload and preload
49
Q

what are the 2 types of chemorecepors and where are they located

A

Peripheral: carotid body, aortic arch
Central: brain ventral surface of medulla close to CSF

50
Q

what are peripheral cehmoreceptors sensitive to

A

PaO2 <60 mm Hg

51
Q

what are central chemoreceptors sensitive to

A

PaCO2 >40

52
Q

what is endothelin

A

neurohormone invovled in ventricular remodelling in HF; produced by endothelin cells in the endotehlium of vessels

53
Q

what does endothelin do

A

potent vasoconstrictor

can cause renal vasoconstriction and Na retention

54
Q

what is apoptosis

A

controlled cell death w/o inflammation scarring
promoted by angiotenin II and catecholamines
decreases # and strength of myocytes contributing to remodelling

55
Q

what remodeling process to ACE and Beta blockers slow down

A

apoptosis

56
Q

why does ventricular remodeling place pts at risk for arrythmias

A

d/t atrial/ventricular stretching and dilation –> disrupts conduction pathways

57
Q

what is the most common arrhythmia seen in remodeling

A

Afib

58
Q

what does an EF <30 and a hx of ventricular arrythmias predict might happen to a person

A

sudden death

59
Q

what are the 2 natriuretic peptides and where are they released from

A

ANP - atrial natriuretic peptide - atrial wall in response to stretch
BNP - brain natriuretic peptide - ventricle wall in response to stretch

60
Q

what do natriuretic peptides do

A

counter effects of compensatory mechanisms
promote vasodilation reduce Na and H2O retention via diuresis
promote balanced vasodilation
reduce preload and afterload
limit hypertrophy from injury or ischemia

61
Q

what do we call an acute worsening of chronic heart failure

A

acute decompensated HF

62
Q

what would cause acute decompensated HF

A

MI, myocarditis
dysrhtymias, ischemia
not adhering to diet restrictions

63
Q

what are some common medical issues that lead to chronic HF

A 
DM
kidney disease
atherosclerosis
COPD
valve dysfunction
64
Q

what occurs in left sided HF (3)

A

left ventricle ineffective contractile fn
low CO –> inc. afterload
pulmonary congestion decreased perfusion to peripheries

65
Q

what occurs in rt sided HF (3)

A

rt ventricle has ineffective contractile fn
can be caused by an acute condition such as a PE or rt ventricular infarction
most commonly caused by left sided HF

66
Q

what are 3 specific to HF lab values

A

BNP, CK, trop

67
Q

other than HF what else can cause inc. in BNP

A

pulmonary HTN, CKD, sepsis, burns, COPD, OSA

68
Q

what are 4 imaging tests for HF

A

CXR, TTE, angio, 12 lead

69
Q

2 types of valve dysfunction

A

stenosis

regurg

70
Q

what is valve stenosis

A

can be congenital or calficifation
narrowing
results in mechanical obstruction
limits blood flow

71
Q

what does valve stenosis do to afterload

A

permanent increase

72
Q

what are signs and symptoms of valve steonsis

A 
dyspnea
fatigue
waekaness
resp symptoms
angina
activity intolerance
edema
73
Q

what is valve regurgitation

A

leaflets dont close adequately causing backflow during systole
increases pressure in chambers before affected vlave

74
Q

does valve regurgitation cause hypertorphy

A

yes to maintain adequate stroke volume and forward flow

75
Q

what caues regurg

A

dilated poorly contractile ventrilce

stretching of valvular tissue as dilation and remodelling occur

76
Q

what are signs and symptoms of valve regurgitation

A

fatigue
dyspnea
palpations
pulmonary edema

77
Q

what are some medicatoins we can use to decrease or redirect preload

A

diuretics - decrease total ciculating volume
vasodilators - inc. venous capitance decrease preload
improves contractility and reduces afterload

78
Q

aside from medication what can e do to reduce preload

A

CRRT

uses osmosis to remove water directly from pts blood

79
Q

what medication can we give to eliminate anxiety associated with pulmonary edema

A

morphine

80
Q

what are 4 ways we can improve oxygenation in HF

A

O2 therapy - inc driving pressure
CPAP or BiPAP - pushes fluid out decrease preload from pressure
high fowlers - dependent portions more perfused and better ventilated
diuretic - decreases preload improves oxygenation and ventilation

81
Q

3 medications for improving contractility

A

dobutamine -inotrope and vasodilator beta 1 and some beta 2
milrionoe -phophodiesterase III inhibitor with vasodilation effect
digoxin - HR control in acute HF as an inotrope for chronic HF

82
Q

what are 3 short term devices that can be used in the management of HF

A

intra aortic balloon pump
ECMO
Impella

83
Q

what is the goal with IABP

A

increase coronary artery perfusion and decrease afterload

should only be used for 5-7 days

84
Q

what does the impella do

A

sucks blood from LV and transfers to aorta offloads the LV allowing it to rest and recover

85
Q

what does ECMO do

A

functions as a heart and lungs giving organs a chance to recover

86
Q

What is the NYHA and what are the 4 classes

A

new york heart association heart failure classification
I no limitation
II slight limitation comfortable at rest
III comfortable at rest but any movement causes symptoms
IV SOB even with bedrest

87
Q

what do ACEI and BB do

A

slow remodelling and progression of HF

88
Q

what does Ivabradine do

A

SA node modulator slows HR
reduces hospilizations for HF and reduces mortality
used in comination with BB

89
Q

what are 3 devices that can be used for HF

A

implantable cardioverter defibrillators (ICDs)
Cardiac REsynchronization Therapy (CRT)
Left ventricular assistive device (LVAD)

90
Q

what is an ICD? when is it indicated

A 
implantable cardioverter defibrillator 
EF < 30
narros QRS
hx of sudden cardiac arrest
can overdrive pcae, cardiovert and defibrillate
91
Q

can an ICD cause PTSD

A

yes

92
Q

when would you implant CRT

A

for prolonged QRS or BBB any asyncrhonous contraction of ventricals
it uses biventricular pacing to synchroinize contraction and improve LV fn

93
Q

pateints who have what 3 things should get a cRT

A 
LBBB
EF <35 and NYHA class II/III
94
Q

what is an LVAD

A

left ventricular assistive device
provides CO or flow using an outflow cannula in the left atrium or ventricule
bypasses ventricle and augments/replaces pumping

95
Q

do pts with an LVAD have a palpable pulse

A

no

96
Q

when should a HF pt call for help

A 
weight gain >5lbs in a week
increaseing SOB with regular activities 
increasing orhtopnea
waking up in the night SOB
increasing edema

NSCC 7320 - Critical Care Theory 3 (5 decks)

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