Heart Failure Flashcards

1
Q

Heart Failure Basic components

A

1) Poor forward blood flow = low flow (decr cardiac ouput)

2) Backward buildup of pressure = congestion (incr filling pressures) as a response to low flow

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2
Q

3 factors that affect stroke volume

A

1) preload (incr sv)
2) afterload (decr sv)
3) inotropy (incr SV)

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3
Q

2 factors affecting CO

A

1) HR (incr CO)

2) SV (incr CO)

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4
Q

Effect of Preload on Stroke volume vs. Ventricular EDP

A

increased filling of ventricle, incr ventricular output (SV)

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5
Q

the more LV is filled, the ____

A

more it will contract

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6
Q

the ____ the more it will contract

A

more LV is filled

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7
Q

incr ___ produces increased SV and CO for given inotropic state

A

Preload

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8
Q

incr preload increases ___ and ____ for given inotropic state

A

SV and CO

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9
Q

Effect of inotropy on SV vs. ventricular EDP curve

A

shifts curve upwards

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10
Q

Same filling (preload) of LV produces a ___

A

greater squeeze of contraction

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11
Q

Determinants of inotropy

A

catecholaminergic/adrenergic stim

calcium

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12
Q

incr inotropy produces increased ___ and ____ for the same preload

A

SV and CO

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13
Q

incr ____ produces increased SV and CO for the same preload

A

inotropy

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14
Q

Effect of increased preload on PV loop

A

increased end diastolic pressure (more filling on the LV)

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15
Q

Effect of increased inotropy on PV loop

A

increased pressure (height) and decr end systolic volume

pump with greater force and empty more of the LV

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16
Q

effect of increased afterload on PV loop

A

increased end systolic volume and increased pressure

have to pump with more force against higher resistance and empty LESS of LV

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17
Q

Systolic HF basics

A

weak/damaged myocardium (thinner walls)

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18
Q

Systolic HF problem

A

problem with squeeze

decr contraction and decr inotropy

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19
Q

hallmarks of systolic dysfunction

A

decreased ejection fraction

ventricular enlargement

20
Q

PV loop with systolic HF

A

decr top pressure line and shift curve to the right

decr inotropy, decr SV (pump out less) and lower systolic blood pressure b/c less force

incr end diastolic volume b/c walls are thinner

21
Q

Primary causes of systolic HF

A

1) direct destruction of heart muscle cells
2) overstressed heart muscle
3) volume overloaded heart muscle

22
Q

causes of Direct destruction of heart muscle cells

A
MI
viral myocarditis
peripartum
dilated cardiomyopathy
alcohol
23
Q

causes of Overstressed heart muscle

A

tachycardia mediated HF
meth use
stress provoked

24
Q

causes of volume overloaded heart muscle

A

mitral regurg
high cardiac output
- shunting of blood
- wet beriberi

25
Diastolic HF basics
stiff/noncompliant heart
26
Diastolic HF problem
impaired filling decr lusitropy
27
hallmark of diastolic HF
normal ejection fraction | ventricular wall thickening
28
PV loop in diastolic HF
incr bottom pressure line, decr top pressure line, decr end diastolic volume incr stiffness so need higher baseline pressure to keep stiff wall open can't fill as much blood due to thick walls decr top pressure line due to stiffer walls
29
causes of diastolic HF
1) High afterload / pressure overload 2) Myocardial thickening / fibrosis 3) External compression
30
causes of High afterload / pressure overload
longstanding HTN aortic stenosis dialysis
31
causes of mycoardial thickening/fibrosis
HCM | primary restrictive cardiomyopathy
32
causes of external compression
pericardial fibrosis/constrictive pericarditis | pericardial effusion
33
Right sided HF
can't pump blood through lungs adequately
34
Right sided HF | what causes forward RV HF
decr circulating blood flow
35
Right sided HF | what causes backward RV HF
incr venous pressure
36
Primary causes of right sided HF
1) Left sided HF 2) lung disease/pulmonary HTN/RV pressure overload 3) RV volume overload 4) damage to RV myocardium
37
why does left heart failure cause right heart failure
backward HF stresses right side by incr pulm venous pressures
38
Do HF forms coexist?
Yes | with fibrosis and ischemia
39
Body's compensatory responses to decr cardiac output in heart failure
1) neurohormonal activation 2) frank-starling (incr preload) 3) ventricular hypertrophy and dilation
40
Normal response to decr cardiac output (JGA route)
1) dehydration or bleeding 2) decr LV filling, decr CO 3) juxtaglomerular apparatus sense low flow and activ renin system 4) incr sodium retention 5) activate vasoconstriction 6) incr volume and incr LV filling
41
Normal response to decr cardiac output
1) dehydration or bleeding 2) decr LV filling, decr CO 3) baroreceptors sense lower pressure 4) adrenergic activation 5) incr HR and vasoconstriction 6) incr blood volume and incr LV filling
42
Neurohormonal compensatory mechanism- additional effect
supranormal filling pressures
43
HF effect on SV vs. ventricular end diastolic pressure curve
shift down given pressure, less stroke volume
44
Frank Starling compensation
incr LV filling incr SV stroke volume preserved by increasing end diastolic filling and pressure
45
Vascular remodeling via hypertrophy and dilation | Long term incr in cardiac workload and metab demand 4 things
1) ventricular hypertrophy 2) ventricular dilation 3) myocardial damage/apoptosis 4) myocardial fibrosis
46
Vascular remodeling via hypertrophy and dilation Overtime remodeling causes (3)
1) decr contractile force 2) decr dynamic function 2) incr diastolic stiffness