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
Q

Diastolic HF basics

A

stiff/noncompliant heart

26
Q

Diastolic HF problem

A

impaired filling

decr lusitropy

27
Q

hallmark of diastolic HF

A

normal ejection fraction

ventricular wall thickening

28
Q

PV loop in diastolic HF

A

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
Q

causes of diastolic HF

A

1) High afterload / pressure overload
2) Myocardial thickening / fibrosis
3) External compression

30
Q

causes of High afterload / pressure overload

A

longstanding HTN
aortic stenosis
dialysis

31
Q

causes of mycoardial thickening/fibrosis

A

HCM

primary restrictive cardiomyopathy

32
Q

causes of external compression

A

pericardial fibrosis/constrictive pericarditis

pericardial effusion

33
Q

Right sided HF

A

can’t pump blood through lungs adequately

34
Q

Right sided HF

what causes forward RV HF

A

decr circulating blood flow

35
Q

Right sided HF

what causes backward RV HF

A

incr venous pressure

36
Q

Primary causes of right sided HF

A

1) Left sided HF
2) lung disease/pulmonary HTN/RV pressure overload
3) RV volume overload
4) damage to RV myocardium

37
Q

why does left heart failure cause right heart failure

A

backward HF stresses right side by incr pulm venous pressures

38
Q

Do HF forms coexist?

A

Yes

with fibrosis and ischemia

39
Q

Body’s compensatory responses to decr cardiac output in heart failure

A

1) neurohormonal activation
2) frank-starling (incr preload)
3) ventricular hypertrophy and dilation

40
Q

Normal response to decr cardiac output (JGA route)

A

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
Q

Normal response to decr cardiac output

A

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
Q

Neurohormonal compensatory mechanism- additional effect

A

supranormal filling pressures

43
Q

HF effect on SV vs. ventricular end diastolic pressure curve

A

shift down

given pressure, less stroke volume

44
Q

Frank Starling compensation

A

incr LV filling

incr SV

stroke volume preserved by increasing end diastolic filling and pressure

45
Q

Vascular remodeling via hypertrophy and dilation

Long term incr in cardiac workload and metab demand
4 things

A

1) ventricular hypertrophy
2) ventricular dilation
3) myocardial damage/apoptosis
4) myocardial fibrosis

46
Q

Vascular remodeling via hypertrophy and dilation

Overtime remodeling causes (3)

A

1) decr contractile force
2) decr dynamic function
2) incr diastolic stiffness