Hemodynamic Disorders Lecture 1 Flashcards
What is the volume of blood in the left ventricle at the beginning of systole?
150 mL
What is the pressure of the blood in systole?
130 mmHg
What % and mL of blood in the left ventricle is ejected?
66% or 100 mL
What is the 2nd most common valvular disease? (male or female predominance)
calcific aoritc stenosis
male
What are the 3 causes of calcific aoritc stenosis
- anamalous bicuspid valve (50%) (insteasd of 3 cusps) = presents 10 years earlier
- “senile” regeneration (wear and tear)
- chronic rheumatic disease
What is the pathology of calcific aoritc stenosis?
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
Describe the gross pathology of calcific aoritc stenosis
rocks in sinuses of valsalva squezzing lumen
Why does aoritc stenosis cause angina?
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
Where are the coronary ostia?
cusps of the valve
Why does aortic stenosis cause syncope?
impaired blood flow due to narrowed opening –> not enough blood flow/O2 to brain
When are pts with calcific aoritc stenosis likely to experience angina and syncope?
upon exertion
Why does aortic stenosis cause dyspnea?
blood cant get out of valve –> back up –> hypertrophy of left ventricle –> dilation of pulmonary veins –> inc pressure in pulmonary vessels/pulmonary HTN –> LHF
Dyspnea is a symptom of ______
LHF/pulmonary HTN
In what ways is aortic stenosis like HTN heart disease?
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
Factors that help
preload
afterload
contractility
How is CAD differentiated from aortic stenosis?
aortic stenosis has a MURMUR!
otherwise they present the exact same way (angina, dypnea, syncope)
What is the volume at the start of diastole? pressure?
50 mL
10 mmHg
What is the billowing of mitral valve into left atrium during systole called?
miral valve prolapse
What is the most common valvular disease?
male or female predominance
mitral valve prolapse; female
gross pathology of MVP?
microscopic pathology of MVP?
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
Into what part of the heart do the prolapsed mitral valve protrude?
left atrium
A prolapsed mitral valve protrudes into the L atrium during (systole or diastole)?
systole
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?
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)
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?
Total SV –> 140 mL
forward SV = 70 mL
EDV –> 170
Symptoms of ruptured cordae tendinae (before compensation)
significant, immediate drop in SV –> dyspnea, syncope, angina upon exertion + murmur
normal SV
100 mL
____% reduction is forward stroke volume is the threshold for heart failure
RED SLIDE
25%
____ mL SV is is threshold (max) for HF
75 mL
What is the gross pathology of acute rheumatic heart disease?
microscopic?
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
foci of fibrinoid necrosis with histiocytes and anitschkow cells + lymphocytes
~granulomas
Aschoff bodies
ARHD
cellls with clumped chromatin resembling caterpillar
Anitschkow cells
ARHD
How can you prevent ARHD
Abx (penicillin) therapy for strep throat
Chronic RHD is common with
with recurrent and/or severe carditits at an early age
females > men
symptoms of chronic RHD appear _____ after cardities
20 years
mitral stenosis
chronic rheumatic heart disease
*female predominance
slit-like fishmouth or round buttonhole stenosis with fibrous thickening and rigidity of valve
gross pathology if rheumaric mitral stenosis
thickening, shortening, and fusion of cordae
chronic rheumaric mitral stenosis
how happens to the left atrium? Why?
dilation of L atrium behind stenoitc valve
You are heard with chronic mitral valve regurgitation of 95 mL. How does the heart cope?
- inc SV
- inc EDV
- left ventricular dilation (bc chronic and have lots of time)
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?
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)
part of SLE
Libman-Sacks endocarditis
small verrucous, berrylike or flat vegetations commonly on multiple valves and can be on either or both sides of valve
libman-Sacks endocarditites
necrotic debris, fibrinoid material, degenerating leukocytes, fibroblasts and hematoxylin bodies
libman-Sacks endocardititis
T or F: ibman-Sacks endocarditites tend to embolize
F
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)
marantic endocartitis
T or F: marantic endocarditis do not embolize
F: they do embolize
Predisposing conditions for marantic endocarditis
cancer (hyper coagulable state)
prolonged central venous catheterization
chronic inflammatory condition (hypercoagulable state)
Where are tge thrombiemboli from marantic endocardities most likely to go?
Why each of these organs
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)
What is the most important thing about marantic endocardititis?
RED SLIDE
it is the precursor for infective endocarditis
blood clot on a heart valve
marantic endocarditis
Early: sclerosis (fibrosis) and thickening, lipid deposition, macrophages and lymphocytes (looks like athlerosclerosis!!–and has the same risk factors–smoking, obesity, HTN
calcific aoritc stenosis
Late: nodular heaped-up calcifications in minportion of each cusp, protruding into sinuses of valsalva
*arthlerosclerosis also calcifies
calcific aoritc stenosis
elongeted/thinned cordae tendinae
floppy, ballooning/hooding of valve leaflets
mitral valve prolapse
1) degeneration/thinned outer zona fibrosa and
2) expanded myxomatous inner zona spongiosa
mitral valve prolapse
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
cute rheumatic heart disease
Which valve is most likely and 2nd most likely to have marantic endocarditis?
Is is on the line of closure or the leaflets?
most common: atrial side of mitral valve
second most common: ventricular side of aortic valve
*usually on line of closure
