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Cardio > Hemodynamic Disorders Lecture 1 > Flashcards

Hemodynamic Disorders Lecture 1 Flashcards

1
Q

What is the volume of blood in the left ventricle at the beginning of systole?

A

150 mL

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2
Q

What is the pressure of the blood in systole?

A

130 mmHg

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3
Q

What % and mL of blood in the left ventricle is ejected?

A

66% or 100 mL

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4
Q

What is the 2nd most common valvular disease? (male or female predominance)

A

calcific aoritc stenosis

male

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5
Q

What are the 3 causes of calcific aoritc stenosis

A
  1. anamalous bicuspid valve (50%) (insteasd of 3 cusps) = presents 10 years earlier
  2. “senile” regeneration (wear and tear)
  3. chronic rheumatic disease
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6
Q

What is the pathology of calcific aoritc stenosis?

A

Early: sclerosis (fibrosis) and thickening, lipid deposition, macrophages and lymphocytes (looks like athlerosclerosis!!–and has the same risk factors–smoking, obesity, HTN

–> inc afterload

Late: nodular heaped-up calcifications in minportion of each cusp, protruding into sinuses of valsalva
*arthlerosclerosis also calcifies

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7
Q

Describe the gross pathology of calcific aoritc stenosis

A

rocks in sinuses of valsalva squezzing lumen

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8
Q

Why does aoritc stenosis cause angina?

A

hypertrophic left ventricle has inc need for blood + rocks/calcification blocking coronary ostia = impedes blood flow to coronary arteries –> chest pain (even with normal coronary arteries

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9
Q

Where are the coronary ostia?

A

cusps of the valve

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10
Q

Why does aortic stenosis cause syncope?

A

impaired blood flow due to narrowed opening –> not enough blood flow/O2 to brain

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11
Q

When are pts with calcific aoritc stenosis likely to experience angina and syncope?

A

upon exertion

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12
Q

Why does aortic stenosis cause dyspnea?

A

blood cant get out of valve –> back up –> hypertrophy of left ventricle –> dilation of pulmonary veins –> inc pressure in pulmonary vessels/pulmonary HTN –> LHF

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13
Q

Dyspnea is a symptom of ______

A

LHF/pulmonary HTN

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14
Q

In what ways is aortic stenosis like HTN heart disease?

A

in both, there is narrowing of the lumen of the vessels (aorta)–> higher BP causes hypertrophy of the left ventricle bc the heart is trying to work harder to push an increased afterload

difference: valve is fucked up vs the vessels are fucked up, but they both cause increase in afterload

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15
Q

Factors that help

A

preload
afterload
contractility

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16
Q

How is CAD differentiated from aortic stenosis?

A

aortic stenosis has a MURMUR!

otherwise they present the exact same way (angina, dypnea, syncope)

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17
Q

What is the volume at the start of diastole? pressure?

A

50 mL

10 mmHg

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18
Q

What is the billowing of mitral valve into left atrium during systole called?

A

miral valve prolapse

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19
Q

What is the most common valvular disease?

male or female predominance

A

mitral valve prolapse; female

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20
Q

gross pathology of MVP?

microscopic pathology of MVP?

A

elongeted/thinned cordae tendinae
floppy, ballooning/hooding of valve leaflets

1) degeneration/thinned outer zona fibrosa and
2) expanded myxomatous inner zona spongiosa
* **can also have normal microscopic appearance = structural problem

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21
Q

Into what part of the heart do the prolapsed mitral valve protrude?

A

left atrium

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22
Q

A prolapsed mitral valve protrudes into the L atrium during (systole or diastole)?

A

systole

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23
Q

You are a heart with MVP that has a rupture of chordae tendinae which causes regurgitation of 70 mL of blood. How can your cope?
How quickly does this compensation occur after injury?

A

inc contractility!! (pump harder) and allow for blood to fill in ventricle (inc filling volume) to…

  • increased SV
  • increased EDV

** only 30 mL sent out in SV (normal is 100)

24
Q

You are a heart with MVP that has a rupture of chordae tendinae which causes regurgitation of 70 mL of blood.

Suppose the best you can do is 40% more SV and 13% moe EDV to compensate.

What is the total SV, forward SV, and EDV?

Will this be enough to avoid HF?

A

Total SV –> 140 mL
forward SV = 70 mL

EDV –> 170

25
Q

Symptoms of ruptured cordae tendinae (before compensation)

A

significant, immediate drop in SV –> dyspnea, syncope, angina upon exertion + murmur

26
Q

normal SV

A

100 mL

27
Q

____% reduction is forward stroke volume is the threshold for heart failure
RED SLIDE

A

25%

28
Q

____ mL SV is is threshold (max) for HF

A

75 mL

29
Q

What is the gross pathology of acute rheumatic heart disease?

microscopic?

A

tiny (1-2 mm) verrucous (wartlike) vegetations lined up on the line of valve closure. Fibrous pericarditis

Microscopic: fibrin-platelet vegetations/thrombi on valves
Aschoff bodies
Anitschkow cells

30
Q

foci of fibrinoid necrosis with histiocytes and anitschkow cells + lymphocytes
~granulomas

A

Aschoff bodies

ARHD

31
Q

cellls with clumped chromatin resembling caterpillar

A

Anitschkow cells

ARHD

32
Q

How can you prevent ARHD

A

Abx (penicillin) therapy for strep throat

33
Q

Chronic RHD is common with

A

with recurrent and/or severe carditits at an early age

females > men

34
Q

symptoms of chronic RHD appear _____ after cardities

A

20 years

35
Q

mitral stenosis

A

chronic rheumatic heart disease

*female predominance

36
Q

slit-like fishmouth or round buttonhole stenosis with fibrous thickening and rigidity of valve

A

gross pathology if rheumaric mitral stenosis

37
Q

thickening, shortening, and fusion of cordae

A

chronic rheumaric mitral stenosis

38
Q

how happens to the left atrium? Why?

A

dilation of L atrium behind stenoitc valve

39
Q

You are heard with chronic mitral valve regurgitation of 95 mL. How does the heart cope?

A
  1. inc SV
  2. inc EDV
  3. left ventricular dilation (bc chronic and have lots of time)
40
Q

You are heard with chronic mitral valve regurgitation of 95 mL.
Suppose the best this heart can do is double the normal SV and add 90 mL to the EDV. What will this be?

WIll this be enough to avoid HF?

A

SV: 200 mL
-forward = 100 mL and backward = 100 mL (~ spilt 50-50)
EDV: 240 mL

no (95 mL forward is enough not to have sympotms)

41
Q

part of SLE

A

Libman-Sacks endocarditis

42
Q

small verrucous, berrylike or flat vegetations commonly on multiple valves and can be on either or both sides of valve

A

libman-Sacks endocarditites

43
Q

necrotic debris, fibrinoid material, degenerating leukocytes, fibroblasts and hematoxylin bodies

A

libman-Sacks endocardititis

44
Q

T or F: ibman-Sacks endocarditites tend to embolize

A

F

45
Q

small (1-5 mm) fibrin + platelet thrombi commonly found on atrial side of mitral valve (2nd most commonly on ventricular side of aortic valve)
small and tan (can be partly red)

A

marantic endocartitis

46
Q

T or F: marantic endocarditis do not embolize

A

F: they do embolize

47
Q

Predisposing conditions for marantic endocarditis

A

cancer (hyper coagulable state)
prolonged central venous catheterization
chronic inflammatory condition (hypercoagulable state)

48
Q

Where are tge thrombiemboli from marantic endocardities most likely to go?

Why each of these organs

A

on atrial side –> systemic circulation

  • kidneys: they receive the largest fraction of CO
  • Heart: bc coronary ostia are right there)
  • spleen: bc is the filter for things in the blood)
  • brain: they get a large fraction of CO (blood supply)
49
Q

What is the most important thing about marantic endocardititis?
RED SLIDE

A

it is the precursor for infective endocarditis

50
Q

blood clot on a heart valve

A

marantic endocarditis

51
Q

Early: sclerosis (fibrosis) and thickening, lipid deposition, macrophages and lymphocytes (looks like athlerosclerosis!!–and has the same risk factors–smoking, obesity, HTN

A

calcific aoritc stenosis

52
Q

Late: nodular heaped-up calcifications in minportion of each cusp, protruding into sinuses of valsalva
*arthlerosclerosis also calcifies

A

calcific aoritc stenosis

53
Q

elongeted/thinned cordae tendinae

floppy, ballooning/hooding of valve leaflets

A

mitral valve prolapse

54
Q

1) degeneration/thinned outer zona fibrosa and

2) expanded myxomatous inner zona spongiosa

A

mitral valve prolapse

55
Q

tiny (1-2 mm) verrucous (wartlike) vegetations lined up on the line of valve closure. Fibrous pericarditis

Microscopic: fibrin-platelet vegetations/thrombi on valves
Aschoff bodies
Anitschkow cells

A

cute rheumatic heart disease

56
Q

Which valve is most likely and 2nd most likely to have marantic endocarditis?
Is is on the line of closure or the leaflets?

A

most common: atrial side of mitral valve

second most common: ventricular side of aortic valve

*usually on line of closure

Cardio (26 decks)

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