Faber - Hemodynamics
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What is laminar flow?
Where is it fastest?
Slowest? -
*Fluid moving with a parabolic front.
*It is fastest at the center
*it is slowest at the edges -
Pouisielle's law can be reduced to an expression of R and radius. How are these two related?
What does this insinuate? -
*R = 1/r^4
*that radius is the primary determinant of resistance - What keeps changes in capillary bed resistance from having drastic effects on MAP?
- The fact that most beds are arranged in parallel circuits buffers the effects on MAP.
- What effects will dilation of a capillary bed have?
- Lower R and increased Q and P in that capillary, but small effects system-wide.
- What effects will constriction of a capillary bed have?
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*increased R and decreased Q and P in the capillary bed
*buffered effects systemwide - What is the equation for velocity of blood?
- v = Q/cross-sectional area
- What happens in a transition from a smaller vessel to a larger vessel?
- Velocity drops, which can result in pooling and increased pressure on the vessel walls.
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Why is velocity slowest in the capillaries?
What beneficial effect does this have? -
*Because the total cross-sectional area of the entire bed is taken into account.
*Slow velocity allows good exchange with tissues - In words, how is tension defined by the LaPlace relationship.
- Tension is the force a wall must generate to counteract the pressure inside.
- What is the equation for tension?
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T = Pr/h
*h = wall thickness - What happens to tension in the event of an aneurysm?
- The radius of the vessel inceases, thus tension increases.
- In arteries, there is both high pressure and a large radius. How do these vessels prevent a high tension?
- By their thick walls (high "h").
- How do capillaries withstand pressures up to 100mmHg?
- The radius is very small, this reduces tension and also allows the capillaries to have very thin walls.
- In HTN, pressure in the arteries increases greatly. How do the arteries compensate?
- There is hypertrophy of the wall and an increase in "h" - this reduces the tension on the artery.
- In aortic regurgitation, blood flows back into the LV and increases LVEDP. How is this exacerbated by the LV? How is it compensated for?
- A stretching or dilation of the LV increases "r" and thus increases T even more. The LV compensates through hypertrophy of the walls.
- What effect would a LV MI have on the tension in that area?
- The loss of myocytes would cause an aneurysm, thus increasing "r" and tension in that area. The risk for rupture increases.
- Define diastolic wall tension (as experienced by the LV).
- The distending force that must be overcome by contraction of the myocytes in order to compress the LV.
- What is atherosclerosis? What effects does it have on systolic pressure? Why?
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*stiffening of arterial walls
*increases systolic pressure
*vessels are less able to stretch and recoil - What is pulse pressure?
- PP = systolic P - diastolic P
- Name 3 determinants of systolic arterial P. How is each related to P?
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*SV, directly related
*diastolic P, which determines the starting P
*CPL, inversely related - How would an inotropic rx affect systolic and diastolic arterial P?
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*would increase SV (thru CTY)
*large rise in systolic P
*modest rise in diastolic P -
What are the three main determinants of diastolic arterial P?
How is each related to P? -
*SVR, directly related
*systolic P, determines starting P
*HR, directly related - determines time for draining before next surge in P - What happens to pulse pressure when SVR decreases?
- It increases. Decreased SVR means diastolic arterial P drops, but systolic pressure remains unchanged.
- What happens to pulse pressure when SV increases?
- It increases. Increased SV causes an lg increase in systolic arterial P, but only a modest increase in diastolic P.
- How would tx with an arteriolar vasoconstrictor affect pulse pressure?
- It would decrease. SVR increases, thus so does diastolic arterial P. Systolic P inceases only modestly.
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What are two synonyms for CPL?
How can it be defined? -
Distensibility or capitance.
The change in volume for a given change in pressure. - What is the equation for CPL?
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CPL = delta V/delta P
(the change in volume for a given change in pressure) - Which have greater CPL - veins or arteries?
- Veins - they are elliptical and not totally filled.
- What 2 things are the main determinants of CPL?
- Passive structural components and active vascular smooth muscle.
- How does contraction of VSM affect large arteries and veins?
- It stiffens walls, but normally does not decrease diameter.
- How does sympathetic excitation of veinous smooth muscle maintain SV?
- It decreases CPL, which maintains or increases veinous return to the heart.
- List the 6 main determinants of CVP.
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1.Constriction of venules and sm. veins
2.decreased CPL in lg veins
3.Total blood vol.
4.Gravity
5.Capillary P.
6.CO - How does gravity affect arterial pressure below and above the heart?
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*Below the heart, G can add 90mmHg of P
*above the heart, G can subtract 30mmHg -
Which is affected more by gravity, venous or arterial circulation?
Why? - Venous - b/c of the greater distensibility of the vessels.
- What are 4 mechanisms venous circulation uses to counteract the effect of gravity?
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1.Contriction of VSM reduces CPL
2.Increase arterial pressure
3.Skeletal muscle compression
4.movement of diaphragm - How does decreased CPL affect CVP?
- It increases it.
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How will constriction of small veins and venules increase return to the heart?
There are 2 reasons. -
1.Increase CVP
2.Reduce to volume of the venous reservoir - i.e. mobilize more blood - Why does a decrease in CO raise CVP?
- Decreased CO creates a backlog effect that translates into greater CVP.