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CVR Biweekly 1 > Taylor- Blood Flow Distribution > Flashcards

Taylor- Blood Flow Distribution Flashcards

1
Q

blood flow is controlled by altering what

A

vascular resistance in arterioles

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2
Q

regulate bulk blood flow through the capillary bed

A

arterioles

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3
Q

regulate number of perfused capillaries for exchange

A

precapillary sphincters

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4
Q

vessel steady-state tone is regulated by what

A

vasoconstriction and vasodilation

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5
Q

play a key role in distribution of CO by controlling resistance

A

arterioles

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6
Q

2 extrinsic mechanisms of controlling arteriole diameter

A

autonomic (sympathetic-NE)
hormones

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7
Q

main role of this neurotransmitter is on blood vessels and binds a1

A

NE

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8
Q

3 intrinsic mechanisms controlling arteriole diameter

A

mechanical, metabolic, endothelial factors

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9
Q

meet demands of the whole body (pressure and volume)

A

extrinsic mechanisms

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10
Q

match flow to local demands (specific organ)

A

intrinsic mechanisms

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11
Q

these are released and cause relaxation and increased blood flow

A

metabolites

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12
Q

these mechanisms are set up to sense pressure or volume changes and correct it

A

extrinsic mechanisms

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13
Q

body wants to keep _____ high enough to perfuse organs

A

blood pressure

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14
Q

extrinsic mechanism that increases HR and contractility, causes increase in resistance and vasoconstriction, and, NE and Epi released from adrenal gland in response to low bp

A

baroreceptor reflex

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15
Q

filters blood, makes urine, corrects blood volume

A

kidneys

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16
Q

produces renin

A

juxtaglomerular apparatus

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17
Q

how body responds to low perfusion pressure and low blood volume

A

by constricting blood vessels until the body reaches a blood pressure that restores proper perfusion pressure AND fluid/Na+ retention

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18
Q

steps kidneys take to increase fluid retention and resistance in response to low renal perfusion pressure (5 main steps)

A

1.JG produces renin
2.renin converts angiotensinogen to angiotensin I
3. ACE converts angiotensin I to II
4. aldosterone increases Na retention
5. vasoconstrict/increase SVR in arterioles

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19
Q

conserve blood volume and increase resistance to correct low renal perfusion pressure

A

kidneys

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20
Q

powerful vasoconstrictor

A

angiotensin II

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21
Q

at level of blood vessel causes vasoconstriction

A

AVP (arginine vasopressin) (ADH)

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22
Q

at level of kidney causes Na+ and fluid retention

A

AVP (ADH)

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23
Q

at level of kidney causes a decrease in fluid retention

A

ANP (atrial natriuretic peptide)

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24
Q

at level of blood vessel causes vasodilation

A

ANP

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25
Q

steps taken for problem of low blood volume (5 steps)

A
  1. decrease in atrial filling causes B fibers to increases sympathetics
  2. decrease in myocyte stretch causes decrease in ANP
  3. brain increases AVP
  4. Na+ and fluid retention
  5. vasoconstriction (increase resistance)
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26
Q

increased intravascular pressure causes active _____ response

A

myogenic

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27
Q

increase in intravascular pressure causes what 2 things to happen: (myogenic response)

A

stretch and then vasoconstriction

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28
Q

high pressure surrounding tissue does what to vessels

A

compresses them

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29
Q

increased blood flow to tissue when metabolism increases/meet O2 demand (decrease in sympathetic tone of vessel)

A

Active hyperemia

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30
Q

exaggerated flow occurring after temporary ischemia (due to accumulation and washout of metabolites)

A

Reactive hyperemia

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31
Q

major metabolite causing vasodilation

A

Adenosine

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32
Q

comes from endothelium and is a critical component of homeostasis in vasculature

A

Nitric Oxide (NO)

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33
Q

major vasodilator from endothelium that converts GTP to cGMP and leads to vasodilation

A

NO

34
Q

this is a major cause in development of atherosclerosis

A

dysfunctional endothelium

35
Q

3 main factors of endothelial dysfunction

A
  1. decreased NO
  2. impaired vasodilation
  3. contraction
36
Q

intrinsic ABILITY of vascular. bed to regulate its own flow over a wide range of intravascular pressures

A

pressure-flow autoregulaton

37
Q

2 most tightly autoregulated circulations

A

coronary and cerebral

38
Q

pressure-flow autoregulation is mediated by what

A

myogenic and metabolic mechanisms

39
Q

the CAPACITY for increasing flow within a given vascular bed (organ) at any given pressure

A

reserve

40
Q

constricting influences establish persistent tone that can be intermittently overridden by what

A

local dilating influences (metabolic)

41
Q

main way blood flow is autoregulated in coronary circulation

A

myogenic tone

42
Q

key metabolic dilator in coronary circulation

A

Adenosine

43
Q

important for flow mediated dilation in coronary circulation

A

NO

44
Q

an excess of blood in the vessels supplying an organ or other part of the body

A

hyperemia

45
Q

coronary flow in coronary circulation is stimulated by what

A

sympathetics (active hyperemia)

46
Q

susceptible to ischemia due to vascular compression during systole

A

endothelium

47
Q

compromised in coronary artery disease (atherosclerosis) +/or vasospasm

A

blood flow

48
Q

brain metabolism

A

highly oxidative (glucose and O2)

49
Q

2 main ways brain gets blood flow

A

Circle of Willis and cortical anastomoses

50
Q

barrier in brain with tight junctions in endothelium

A

blood-brain barrier

51
Q

how blood flow is autoregulated in the brain

A

myogenic tone

52
Q

localized active hyperemia in the brain due to what

A

low pH

53
Q

major metabolic controller in the brain

A

pH

54
Q

causes global drop in brain pH and global brain hyperemia

A

hypercapnia (high blood PCO2)

55
Q

any disruption of brain blood flow

A

stroke

56
Q

disruption of brain blood flow due to thrombosis or embolism

A

ischemic stroke

57
Q

bleeding causes damage and can promote prolonged ischemia through vasoconstriction

A

hemorrhagic stroke

58
Q

in parallel AND series w/ other splanchnic organs (and why)

A

liver (b/c hepatic artery and portal vein)

59
Q

this specific capillary bed is a blood reservoir

A

splanchnic bed

60
Q

why do I get a cramp if I exercise after eating

A

b/c increase in sympathetic output causes vasoconstriction of splanchnic arteries and veins (limits blood flow)

61
Q

8 fold increase in blood flow following a meal (elderly susceptible)

A

postprandial hyperemia

62
Q

this circulation is due to counter current flow; interstitium of intestinal villi is hypertonic and hypoxic

A

mesenteric

63
Q

allows for villi in small intestine to be hypertonic (absorption of water and components) and hypoxic (O2 moving from arterial to venous side)

A

counter current flow

64
Q

perfused by hepatic artery (systemic pressure) and portal vein (low pressure)

A

liver

65
Q

liver fibrosis; increased resistance to outflow

A

Cirrhosis

66
Q

can ultimately lead to portal vein hypertension, esophageal varices and ascites

A

Cirrhosis

67
Q

fluid out of circulation into abdominal wall

A

ascites

68
Q

increased venous and sinusoid pressure in liver—> ascites can lead to

A

congestive heart failure

69
Q

Capacity to increase blood flow > 20-fold during aerobic exercise

A

skeletal muscle circulation

70
Q

at rest, this circulation experiences myogenic tone w/ high resistance and low flow; low O2 extraction

A

skeletal muscle circulation

71
Q

during exercise, tone is overridden by active hyperemia

A

skeletal muscle circulation

72
Q

experiences low resistance, high flow, and high O2 extraction

A

skeletal muscle during exercise

73
Q

facilitate flow in contracting muscle (pumping veins and allows blood to go to heart)
2 things

A

muscle pump and reactive hyperemia

74
Q

these in the skin experience vasoconstriction due to sympathetic _____ input

A

arterioles and venules; adrenergic

75
Q

these in the skin experience sweating and vasodilation due to sympathetic _____ input

A

sweat glands; cholinergic (Ach)

76
Q

what happens to nonapical skin vessels when it is cold and why

A

vasoconstriction (symp. adrenergic)

77
Q

what happens to nonapical skin vessels when body is hot and why

A

vasodilation (symp. adrenergic withdrawal)

78
Q

what happens to body in high heat/stress and why

A

sweating/vasodilation (symp. cholinergic)

79
Q

Mainly myogenic tone with metabolic override (local autoregulation)

A

Coronary and cerebral circulation

80
Q

Mainly sympathetic tone with metabolic override

A

skeletal and splanchnic muscle

81
Q

Predominant sympathetic tone with limited metabolic influence (sympathetic cholinergic override in non-apical skin)

A

cutaneous circulation

82
Q

local autoregulation with sympathetic control of glomerular filtration

A

renal circulation

CVR Biweekly 1 (19 decks)

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