Lec 16 Microcirculation Flashcards

1
Q

What controls flow to individual capillary beds?

A

precapillary sphincters control flow, constrict to turn off flow to capillary bed

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2
Q

What is metarteriole?

A

type of shunt pathway

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3
Q

What do shunts do in skin?

A
  • they are pathways to bypass capillaries and connect arterioles/venules
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4
Q

What is structure of a single capillary? What is the function of this structure?

A
  • capillary = 5-10 um diameter
  • surrounded by single endothelial cell
  • small size optimizes for gas and nutrient transfer [max surface area to volume ratio]
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5
Q

What is law of laplace?

A

Wall stress = (pressure * radius) / thickness

wall stress = P*r/w

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6
Q

Why do capillaries not burst?

A

reasonable wall stress since very small radius even with high P
= law of laplace

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7
Q

How does wall stress of capillary compare with that of aorta?

A

6x greater wall stress in aorta

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8
Q

What are two main mech of gas/nutrient movement across capillaries?

A
  • diffusion

- filtration

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9
Q

Where is most O2 transfer in capillary?

A

at beginning of capillary

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10
Q

What are 3 things that mainly transfer out of capillary by diffusion

A
  • O2
  • CO2
  • glucose
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11
Q

How does velocity in capillary allow effect?

A

slow velocity through capillaries allows diffusion

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12
Q

What are normal values of hydrostatic and oncotic pressures?

A

hydrostatic
- Pc: capillary hydrostatic P, high at beginning of capillary, low at end of capillary
- Pi: close to zero
oncotic
- πc: high through capillary since plasma proteins in capillary but not in interstitial space
- πi: close to zero

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13
Q

What is πc? Where is it high? Value?

A
  • πc is oncotic pressure in capillary created by plasma proteins [albumin]
  • πc = 25 mmHg
  • high through capillary since plasma proteins don’t exit capillary
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14
Q

What is Pc? Where is it high/low? Values?

A
  • Pc = hydrostatic pressure in capillary
  • high at beginning of capillary [35 mmHg]
  • low at end of capillary [15 mmHg]
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15
Q

What is normal value of πi?

A

close to zero since no plasma proteins in interstitial space

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16
Q

What is normal value of Pi?

A

close to zero

17
Q

What is the starling equation?

A

Q = k[(Pc - Pi) - (πc - πi)]

Q = fluid movement [mL/min]
k = filtration constant
18
Q

What does positive Q mean in starling equation?

A

movement out of capillary

19
Q

What does negative Q mean in starling equation?

A

movement into capillary

20
Q

What part of capillary has filtration and what has absorption?

A
  • filtration on arterial end

- absorption on venous end

21
Q

What is NFP?

A
  • net filtration pressure

- NFP = Pc - πi

22
Q

What causes increase in albumin in interstitial space? What effect?

A

cause: damage to capillary may allow filtration of protein from capillary to interstitium
effect: increased πi, decreased absorption, edema

23
Q

What causes increase in capillary hydrostatic pressure? What effect?

A

cause: increased pressure in veins, propagates back to capillaries and increases Pc
effect: increased Pc, increased filtration, edema

24
Q

What effect of decrease in plasma protein?

A

decreased πc, reduced absorption, edema

25
Q

Does increased arteriolar resistance alter Pc?

A

No!

26
Q

What happens to Pc and pressure drop across arterioles when you constrict arterioles?

A
  • same Pc
  • bigger pressure drop across arterioles
  • increased MAP
27
Q

What is autoregulation of blood flow? where does it occur?

A
  • in kideneys, heart, brain, muscle
  • way to keep flow through vessel relatively constant

if high local BP –> increased local flow –> vasoconstriction –> decreased flow

if low local BP –> decreased local flow –> vasodilation –> increased flow

28
Q

What are 3 ways of local regulation of blood flow?

A
  • autoregulation
  • active hyperemia
  • endothelial-vascular communication
29
Q

What is active hyperemia? Where does it occur?

A
  • usually in skeletal muscle

- metabolic activity –> releases agents that cause vasodilation –> increased blood flow

30
Q

What are a few important dilating factors in active hyperemia?

A
  • lactic acid
  • intravascular O2
  • adenosine
  • CO2
  • H+
  • extracellular K+
31
Q

What is endothelial-vascular communication?

A
  • turbulent flow –> increased shear stress causes endothelial cells to produce NO [Endothelium derived relaxing factor]
  • NO diffuses from endothelial to smooth muscle cell –> cGMP to inhibit MLCK –> vasodilation
32
Q

laminar flow vs turbulent flow

A
  • laminar flow is straight through
  • turbulent flow in all directions
  • most blood flow is laminar
33
Q

Is most blood flow laminar or turbulent?

A

laminar

34
Q

What 3 things encourage turbulent flow?

A
  • high velocities [v = Q/A]
  • low fluid viscosity [decreased hematocrit]
  • narrow blood vessels [bc increases velocity]
35
Q

What is path of function of NO [EDRF]

A

turbulent flow –> increased endothelial shear stress –> production endothelial NO –> vasodilation –> decreased endothelial shear stress

36
Q

What is ultimate fate of fluid filtered in capillaries?

A
  • returns to blood via lymphatic system, leads to edema