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Maria physio > week 9 > Flashcards

week 9 Flashcards

1
Q

at rest what is skeletal muscle primarily regulated by?

A

sympathetic innervation

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2
Q

what are the receptor types in vascular smooth muscle cells ?

A

a1 and b2 receptors

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3
Q

what are a1 receptors activated by?

A

NE from Sym neurons

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4
Q

what are b2 receptors activated by?

A

E fro sym neurons

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5
Q

what do a1 receptors lead to?

A

vasoconstriction

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6
Q

what do b2 receptors lead to?

A

vasodilation

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7
Q

what predominates vasoconstriction or vasodilation?

A

vasoconstriction predominates because sym adrenergic neurons primarily activate a1 receptors

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8
Q

what happens during exercise or fight or flight response?

A

epinephrine released from adrenal glands activates b2 receptors causing vasodilation to increase blood flow to the muscles

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9
Q

during exercise, what are the main regulators of blood flow in skeletal muscles and what do they promote?

A

local metabolites byproducts promoting vasodilation

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10
Q

what’s functional hyperemia?

A

increased blood flow to meet the metabolic demands of active tissue

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11
Q

what’s reactive hyperemia?

A

increased blood flow after a temporary reduction (ischemia), such as when a muscle temporarily compresses blood vessels during contraction

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12
Q

what are the key metabolic signals triggering vasodilation?

A

decreased pO2
increased pCO2
increased lactate (lower pH)
increased potassium (K+)
increased adenosine (from ATP metabolism)

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13
Q

mechanical compression*****?????

A

exercise-induced compression of blood vessels temporarily restricts flow, causing brief ischemia, followed by reactive hyperemia and vasodilation to restore blood supply

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14
Q

at rest, how much blood flows to skeletal muscles?

A

1L/min (20% of cardiac output)

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15
Q

during exercise, how much blood flows to skeletal muscles?

A

20-30 L/min (20-30x resting level)

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16
Q

what’s the arteriovenous difference in O2 at rest and during exercise?

A

rest - 60 mL O2/L
during exercise - 150 mL O2/L (due to increased oxygen extraction)

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17
Q

what’s considered dynamic exercise?

A

cycles of continuous muscle contraction and relaxation and contraction again

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18
Q

what does contraction do to arterial inflow?

A

inhibits arterial inflow due to vessel compression

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19
Q

what does relaxation do to arterial inflow?

A

increases arterial inflow as vessels are no longer compressed

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20
Q

what does contraction do to venous outflow?

A

increases venous outflow, enhancing venous return

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21
Q

what does relaxation do to

A

reduces venous pressure creating a larger pressure gradient supporting increased blood flow

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22
Q

what’s considered static exercise?

A

keeping the weight in 1 position when muscles are contracted

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23
Q

what’s the impact of muscle contraction in static exercise?

A

resistance in vessels increases and blood flow decreases

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24
Q

what happens to total peripheral resistance (TPR) in static exercise?

A

increases.

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25
Q

what happens to mean arterial pressure in static exercise?

A

increases (systolic and diastolic pressure increase)

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26
Q

with increased cardiac output and metabolic activity , what increases in consumption?

A

higher oxygen consumption

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27
Q

what are the metabolic changes leading to vasodilation?

A

decreased PCO2
increased pCO2
increased. H+ (lower pH)
increased K+
increased adenosine from ATP metabolism

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28
Q

effect of K+ channels

A

activation of k+ channels causes smooth muscle hyperpolarizatoin, reducing ca2+ influx leading vasodilation

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29
Q

effect of calcium reduction

A

increased adenosine raises cAMP levels, which further reduces IC ca2+, promoting muscle relaxation and vasodilation

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30
Q

from muscles when Ca increases what happens?

A

increase in ca, leads to NO synthase activation so NO produced by endothelial cells, leading to vsmr so also vasodilation

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31
Q

effect of NO release

A

muscle contraction raises Ca2+ which activates oxide synthase in endothelial cells, NO causes relaxation of VSMC further aiding vasodilation

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32
Q

what’s splanchnic circulation?

A

blood flow to abdominal organs, including GI tract, liver, spleen, pancreas

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33
Q

flow rate of splanchnic circulation?

A

1500 mL/min

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34
Q

blood supply origins

A

celiac artery, sup mesenteric artery, inferior mesenteric artery

35
Q

splanchnic circulation functions? (2)

A

-site of adjustable resistance
-major reservoir of blood
–> extensive interconnections between arterial branches provide collateral pathways through which blood can reach different parts
–> decreases the risk of ischemia during arterial occlusion

36
Q

type regulation in splanchnic circulation

A

autoregulation

37
Q

postprandial circulation

A

an increase in blood flow through GI tract after a meal

38
Q

what type of innervation do splanchnic blood vessels receive?

A

sympathetic innervation

39
Q

during sympathetic contraction of splanchnic arterials, what happens to blood flow?

A

decreases blood flow to GI tract, which increases blood for organs/ muscles needed for exercise

40
Q

effect of increase in TPR

A

increase blood to other organs

41
Q

what controls blood flow in coronary circulation

A

local metabolites

42
Q

most important local metabolite factors in coronary circulation

A

hypoxia
adenosine

43
Q

coronary blood flow Qc at rest

A

amount of blood heart gets in a minute
Qc=200-250 blood/min, 5% of CO 5,6L/min

44
Q

coronary blood flow Qc exercise

A

1250mL/min

45
Q

ADVO2 value

A

120-130mL O2/L blood

46
Q

ADVO2 during exercise

A

900-1200mL/min

47
Q

O2 consumption

A

30 mL O2/min

48
Q

formula for Qc

A

Qc = pp/R

49
Q

LCA during systole

A

-wall tension increases
-aortic valve closed
-high pressure in myocardium compresses coronary vessels

50
Q

increase in perfusion pressure on LCA during systole

A

increase in CO
increases Perfusion pressure

51
Q

blood flow during diastole

A

-wall tension decreases
-resistance decreases
-bood flow increase

52
Q

how is coronary blood flow regulated

A

myogenic, metabolic and neutral controls

53
Q

myogenic mechanism role in in coronary blood flow

A

myogenic mechanism (Bayliss effect) provides autoregulation, maintaining stable flow during perfusion pressure (60-160 mmHg)

54
Q

describe how Bayliss effect maintains coronary blood flow

A

increased arterial pressure causes vasoconstriction to limit blood flow, while decreased pressure causes vasodilation maintaining steady flow

54
Q

mechanism of Bayliss effect at cellular level

A

increased pressure raises wall tension, activating non-selective cation channels, leading to depolarisation and VDCC activation which increases Ca2+ and causes vasoconstriction

55
Q

what happens at cellular level in Bayliss effect when pressure decreases

A

decreased pressure reduces wall tension, decreasing activation of cation channels and VDCC leading to less Ca2+ and resulting in vasodilation

56
Q

metabolic regulation

A

process where factors from metabolism cause vasodilation

57
Q

what happens to o2 and co2 during exercise

A

o2 decreases, co2 increases which triggers vasodilation

58
Q

what effects cause vasodilation

A

decreased PO2, increased Co2, increased H+, increased K+ and increased adenosine

59
Q

how does increased heart rate indirectly cause vasodilation

A

higher heart rate increases CO leading to vasodilation

60
Q

difference between abrupt and gradual occlusion in coronary vessels

A

-abrupt occlusion leads to necrosis
-gradual occlusion allows new vessels to form, reducing damage

61
Q

what primarily controls cerebral circulation

A

local metabolites, auto regulation and hyperemia

62
Q

most important local vasodilator in brain

A

increased co2 sensed by central chemoreceptors

63
Q

what effect does increased co2 have on cerebral blood flow

A

causes vasodilation, increased blood flow to remove excess co2

64
Q

what happens to cerebral blood flow during hyperventilation

A

Co2 level drop, causing vasoconstriction

65
Q

blood flow in brain

A

750-800 mL/min & 15% of CO

66
Q

what happens if brain blood flow stops for 5 secs, for 5 mins

A

loss of consciousness
irreversible brain damage

67
Q

auto regulation in cerebral circulation

A

brains ability to maintain constant blood flow despite changes in pressure

68
Q

what metabolic changes increase cerebral blood flow

A

increased pCO2, decreased pO2, increased H+, K+ and adenosine lead to vasodilation

69
Q

key regulators of cerebral blood flow

A

pCO2 and EC K+

70
Q

how do brain vessels respond to high pCO2 levels

A

they vasodilate to increase blood flow to remove co2

71
Q

effect of hyperventilation on brain vessels

A

lowers pCO2, leading to vasoconstriction

72
Q

role of astrocytes near neurons

A

are in close contact with synapses, take up K+ and release them to cause vasodilation

73
Q

what happens if 1 volume component in brain increases

A

compresses brain tissue, which can cause damage

74
Q

what is Cushing reflex

A

increased intracranial pressure (ICP) compresses arteries leading to increased blood pressure and decreased heart rate

75
Q

what forms the blood brain barrier and function

A

capillaries with tight junction that restrict direct access to brain EC fluid, prevents harmful solutes in blood from reaching ec fluid

76
Q

volume and daily production of csf

A

volume - 150mL
production rate - 550 mL/day

77
Q

main functions of csf

A

provides mechanical protection , allows brain to float and maintains stable environment for neurons

78
Q

where is csf produced

A

by ependymal cells in choroid plexus

79
Q

how does csf compare to blood composition

A

csf has low k+, low protein concentration and slightly lower pH

80
Q

how is csf absorbed

A

passively absorbed through arachnoid vili driven by csf pressure to sup saggital sinus

81
Q

typical pressure of csf

A

100 mmH2O

82
Q

what happens if csf pressure increases

A

absorption increases, which leads to brain damage

Maria physio (2 decks)

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