Week 5 Heart Failure and Cardiomyopathy Flashcards

1
Q

In a heart with HF

A

:impaired ventricular contractility, increased afterload, or impaired filling of ventricles can lead to systolic or diastolic dysfunction

Systemic compensation occurs, including increases sympathetic activity, increase in specific hormone circulation, vasoconstriction, ventricular remodeling

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2
Q

Cardiac output

A

volume of blood ejected from left ventricle each minute

typically 4-6 L/min

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3
Q

CO =

A

HR x stroke volume

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4
Q

Preload is also called

A

left ventricle end-diastolic pressure (LVEDP)

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5
Q

Preload measures

A

stretch on L ventricle at the end of diastole

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6
Q

Increased preload may occur in HF which can

A

increase cardiac muscle O2 requirement

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7
Q

Many HF medications work to decrease preload

A

nitrates, diuretics, ACE inhibitors, ARB’s, calcium channels blockers

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8
Q

Afterload

A

the force against which the L ventricle is contracting to eject blood

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9
Q

Higher afterload =

A

lower cardiac output

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10
Q

Lower afterload =

A

higher cardiac output

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11
Q

Aortic pressures and peripheral pressures/resistance can

A

increase afterload

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12
Q

Increase afterload =

A

decreased stroke volume = increase blood left in chambers of heart after systole

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13
Q

In HFL elevated afterload leads to

A

long-term ventricular hypertrophy. While the body initial compensates with other systems, over time this leads to diastolic dysfunction (due to decreased compliance of ventricles – EF preserved) and eventually systolic dysfunction (EF reduced)

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14
Q

Contractility is affect by

A

HR, afterload, preload, sympathetic/parasympathetic activation

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15
Q

Contractility is decsribed as

A

the heart’s inherent ability to contract

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16
Q

Contractility is related to the Frank-Starling mechanism

A

force of cardiac muscle contraction is proportional to resting length of the muscle fibers

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17
Q

Increase preload =

A

increase contractility = increased stroke volume

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18
Q

Ejection fraction

A

“A ratio or percentage of the volume of blood ejected out of the ventricles relative to the volume of blood received by the ventricles prior to contraction.”
Normal=60-70%

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19
Q

Reduced ejection fraction – systolic dysfunction
(HFrEF)

A

impaired contractility, increase afterload

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20
Q

Preserved ejection fraction – diastolic dysfunction
(HFpEF)

A

impaired ventricular filling

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21
Q

Systemic compensations in HF

A

Increased blood volume (to increase preload)
Increased sympathetic nervous system activation
Increased HR
Decreased vagal/parasympathetic activation
Increased antidiuretic hormone
Increased renin-angiotensin-aldosterone mechanism activation (RAAS) – regulates blood volume and peripheral resistance
Increased peripheral resistance

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22
Q

HFrEF

A

CAD**
MI
Valvular regurgitation
Dilated cardiomyopathy
Aortic stenosis HTN

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23
Q

HFpEF

A

Left ventricular hypertrophy
Fibrosis of heart musculature
MI
Cardiac tamponade
Cardiomyopathies

24
Q

Class A

A

at high risk for HF but w/o structural heart disease or symptoms

25
Class B
structural heart disease but w/o signs and symptoms of HF
26
Class c
structural heart disease with current or prior symptoms of HF
27
Class D
Refractory HF requiring specialized interventions
28
Class I
no limitations of physical activity. Ordinary physical activity does not cause symptoms of HF
29
Class II
Slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in symptoms of HF
30
Class III
Marked limitation of activity. Comfortable at rest but less than ordinary activity causes symptoms of HF
31
Class IV
Unable to carry on any physical activity w/o symptoms of HF or symptoms of HF at rest
32
HF common presentation
Dyspnea Orthopnea Fatigue JVD Peripheral edema Tachycardia Cachexia
33
HF prognosis
HF prognosis is generally poor 5-year mortality ranges from 45-60% Patients with severe HF have a 1-year mortality rate of 60%
34
Dilated
Dilation of heart chambers, particularly L ventricle
35
Dilated causes
genetics (40%), toxins (chemo, drugs, alcohol), pregnancy, metabolic conditions involving the thyroid, myocarditis
36
Dilated patho
L ventricle enlargement leading to decreased contractility and stroke volume
37
Dilated symptoms similar to HF
dyspnea, orthopnea, edema, fatigue
38
Restrictive
Stiffness of myocardium resulting in decreased/impaired filling and diastolic dysfunction
39
Restrictive causes
amyloidosis (protein build-up) and sarcoidosis (inflammatory disease resulting in granulomas) Caused by increased fibrotic tissues in the heart
40
Hypertrophic
Thickening of walls of heart chamber
41
Hypertrophic interesting fact
accounts for 1/3 of sudden cardiac deaths in young athletic population, especially in football and basketball IOK(-p=[0
42
Hypertrophic symptoms often present at
a younger age, but some people are asymptomatic
43
Hypertrophic common symptoms
dyspnea and angina
44
Valve disease is more common on
L side due to elevated pressures
45
Risk factors for valve disease
RA, IVDA, smoking, obesity, congenital heart defects, family hx, autoimmune disorders, age
46
Mitral valve stenosis
most cases caused by rheumatic fever
47
Mitral valve regurgitation
caused by calcification, rupture of chordae tendinae or papillary muscles
48
Mitral prolapse
leaflets prolapse into L atrium
49
Mitral valve presentations
dyspnea, pulm HTN, pulmonary edema, fatigue, weakness
50
Aortic regurgitation
aortic insufficiency
51
Aortic regurgitation causes
congenital (2 instead of 3 leaflets to valve), ankylosing spondylitis, Marfan syndrome, HTN, endocarditis, rheumatic disease
52
Aortic regurgitation common s&s
syncope, angina, SOB, weakness/fatigue
53
Aortic stenosis
very common in older adults >65 y/o
54
Aortic stenosis causes
calcification/atherosclerosis or rheumatic disease
55
Aortic stenosis common s&s
syncope, angina, fatigue, dyspnea, decreased activity tolerance