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Physiology > Venous Structure/Hemorrhage > Flashcards

Venous Structure/Hemorrhage Flashcards

0
Q

Systemic veins act as…

A

blood reservoir

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1
Q

Vein wall structure

A

Little inherent tone, low R, high distensibility, stretch to accommodate excess volume, little elasticity, valves

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2
Q

When does the venous reservoir need to be tapped?

A

to increase venous return or cardiac output

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3
Q

Venoconstriction

A

increases VR

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4
Q

Venous sympathetic constriction

A

small change in P but no change in R => increased flow back to heart and increased flow downstream

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5
Q

Compliance

A

ability of vessel to distend & increase volume with little change in transmural pressure

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6
Q

vessel compliance…

A

true up to a certain volume. with a higher volume, there is only so much distention the vein can do and then it starts acting like an artery.

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7
Q

What does sympathetic discharge do to venous tone?

A

INCREASES it.

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8
Q

How does sympathetic discharge increase venous tone?

A

decreases BV => decrease MAP => CNS sympathetic discharge => venoconstriction

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9
Q

Venoconstriction allows

A

body to tolerate 20% BV loss & maintain normal circulatory function
(restore MAP to normal levels)

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10
Q

Factors that enhance short term venous return

A
  1. Cardiac contraction generated driving pressure
  2. Sympathetically induced venous vasoconstriction
  3. Skeletal mm. activity
  4. Venous valves
  5. Respiratory activity
  6. Cardiac suction
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11
Q

Sympathetically induced venoconstriction occurs based on

A

norepinephrine binds to adrenergic receptors => constrictions

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12
Q

Skeletal muscle activity (muscle pump)

A

contraction compresses veins which decreases venous capacity which increases venous pressure.

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13
Q

Venous valves

A
  • prevent back flow of blood
  • spaced at 2-4 cm intervals
  • effective against gravitational influences
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14
Q

Respiratory activity (respiratory pump)

A
  • chest activity P~3 to 5 mmHg < Patm
  • peripheral vv. at Patm
  • change P promotes VR
  • breath faster & deeper during excercising -> ^ VR
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15
Q

Cardiac suction (during exercise)

A
  • during vigorous ventricular contraction, AV valve drawn downward
  • enlarges atrial cavity => drop in atrial P transiently
  • CREATES change in P from venous system into atria
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16
Q

Factors that facilitate venous return in the long term

A

increase in blood volume

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17
Q

How does an increase in blood volume facilitate venous return?

A
  • passive bulk flow shift of fluid from ISF into plasma

- salt and water retention in kidney

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18
Q

ST BP Regulation control mechanisms

A
  • high pressure baroreceptors
  • chemoreceptors
  • cardiopulmonary baroreceptors (low pressure)
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19
Q

LT BP Regulation control Mechanisms

A
  • Anti-diuretic hormone (vasopressin)
  • Renin-angiotensin-aldosterone
  • Natriuretic peptides
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20
Q

What is the primary variable controlled by the CV system?

A

MAP

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21
Q

basis for Korotkoff sounds

A

indirect auscultatory measurement of bp.

noise = spurt of blood hitting a static column of blood downstream (systolic P)
Diastolic P = when it stops making noise

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22
Q

Physical determinants of MAP

A

blood volume and elasticity of large aa.

rate of inflow from heart vs. rate of outflow to periphery

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23
Q

What happens to systolic pressure if the artery is rigid?

A

it is higher!

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24
Q

What are the physiological determinants of MAP?

A

CO and SVR

MAP = CO x SVR

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25
Q

SVR’s purpose in determining MAP

A

when a vascular bed needs more blood it can dilate & get more blood. P upstream is high enough to allow this!

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26
Q

If you ^ SVR,

A

Flow decreases downstream to organs while elevating upstream P

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27
Q

ST MAP adjustments occur based on

A

autonomic influences on heart, vessels, and adrenal medulla

changes CO and SVR

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28
Q

LT adjustments to MAP based on

A

changes to salt & H2O balance to restore BLOOD VOLUME

-alters mechanisms of urine output and thirst

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29
Q

High Pressure Baroreceptors

A

sense stretch in vascular walls

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30
Q

Location of barareceptors

A
  1. Carotid sinus

2. Aortic arch

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31
Q

Why do 2 baroreceptors exist?

A

for redundancy and for serving the brain & rest of body.

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32
Q

Carotid sinus baroreceptor

A

sends signals to medulla of brain

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33
Q

Aortic arch baroreceptor

A

send signal via vagus n. to medulla

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34
Q

Where are baroreceptor impulses sent to?

A

cardiovascular control center in MEDULLA of brainstem

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35
Q

Frequency of baroreceptor impulses do what?

A

relay MAP info to CV control center

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36
Q

How does baroreceptor impulse firing increase?

A

stretch in vessel walls increases which leads to ^AP to ^CO

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37
Q

Which baroreceptors are the most effective in the reflex?

A

carotid sinus baroreceptors

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38
Q

Why do carotid sinus baroreceptors do a good job maintaining MAP?

A

the signals go to the brain, which is IMPORTANT

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39
Q

What downstream effectors respond to baroreflex to maintain MAP

A

heart, arterioles, veins, adrenal medulla, kidney

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40
Q

What happens in heart when baroreflex fires?

A

it pumps harder and CO increases

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41
Q

What happens in the adrenal medulla when baroreflex fires?

A

it reduces epinephrine and norepinephrine

42
Q

What happens in kidney when baroreflex fires?

A

norepinephrine stimulates B-1 on kidneys => release of renin => Angiotensin II made

43
Q

What happens in veins when baroreflex fires?

A

venous return increases

44
Q

peripheral chemoreceptors are…

A

proximal to but DISTINCT from arterial baroreceptors

45
Q

Types of Peripheral Chemoreceptors

A

aortic bodies

carotid bodies

46
Q

What do the aortic and carotid bodies do?

A

sense O2, CO2, pH and send signals to respirating centers.

-can effect MAP though-

47
Q

When do chemoreceptors play a role in MAP regulation?

A

ONLY during severe hypoxia

48
Q

chemoreceptors are…

A

secondary receptors.

49
Q

baroreceptors are

A

primary receptors

50
Q

Primary role of chemoreceptors

A

regulate respiration to ^ O2 intake or blow off more CO2

51
Q

peripheral chemoreceptors are MOST sensitive to…

A

changes in O2

52
Q

how do peripheral chemoreceptors work?

example

A

decrease PO2, ^PCO2 or decrease blood pH => ^SVR

53
Q

Central chemoreceptor Types

A

Medulla

54
Q

central chemoreceptors are most sensitive to…

A

changes in CO2 & pH

55
Q

central chemoreceptor mechanisms

example

A

^PCO2 or decrease pH of CSF => ^ SVR

56
Q

What do low-pressure (volume) baroreceptors detect?

A

‘fullness’ of circulation

57
Q

low-pressure (volume) baroreceptors are…

A

long term regulators

58
Q

purpose of low-pressure baroreceptors

A
  • eliminate or retain fluid at kidneys.

- distention depends on VR

59
Q

What happens if there is a high volume detected by low-pressure baroreceptors?

A

high V => decrease in renal SNA => ^GFR => decrease renal reabsorption of fluid => decreased renin release => decreased SVR

60
Q

What happens if there is a low volume detected by low-pressure baroreceptors?

A

low V => ^ renal SNA => decreased GFR => ^renal absorption of fluid => ^renin release => ^SVR

61
Q

types of LT humoral control mechanisms for MAP

A

~Anti-diuretic hormone (vasopressin)
~Renin-angiotensin-aldosterone
~Natriuretic peptides

62
Q

Function of LT humoral control mechanisms for MAP

A

to maintain normal MAP via regulation of ECV

63
Q

GFR =

A

glomerular filtration rate

64
Q

Effective circulating blood volume (ECV)

A

functional blood volume that is effectively perfusing the tissues
(volume of blood in arterial system)

65
Q

Anti-diuretic hormone secretion determined by…

A

high- and low-pressure baroreceptors & osmoreceptors

66
Q

Where are Anti-Diuretic Hormones (ADH) made?

A

hypothalamus

67
Q

Where are ADHs stored?

A

in pituitary

68
Q

What does ADH cause?

A

water reabsorption at kidney & vasoconstriction

69
Q

Renin-angiotensis-aldosterone system does what?

A

increases SVR, wather, & salt retention at kidney

70
Q

What happens when perfusion pressure decreases or NaCl increases?

A

^ renin

71
Q

What happens when perfusion pressure increases or NaCl decreases?

A

renin decreases

72
Q

What do juxtaglomerular cells of kidney do?

A

synthesize, store, & release renin

73
Q

ACE =

A

angiotensin converting enzyme

74
Q

Natriuretic peptides are secreted in response to

A

cardiac distention

75
Q

What would be the predicted physiologic response to cardiac distention/NP secretion?

A

LT: Stimulate H2O & Na excretion in kidney
ST: 1. Decrease renin, ADH, Ang II, Aldosterone
2. Vasodilation to decrease MAP & @ arteriole => ^ filtration & fluid removal

76
Q

Hemorrhage is most common cause of

A

hypovolemic circulatory shock

77
Q

hypovolemic circulatory shock

A

inability to get enough blood to tissue

78
Q

how does hemorrhage cause hypovolemic circulatory shock?

A

loss of blood volume -> decreased cardiac filling pressure -> decrease in venous return -> decreased cardiac output

79
Q

Hemorrhage and MAP/CO

A

MAP/CO rapidly fall with respect to the amount of hemorrhage that occurs. They are inversely related at larger amounts of hemorrhage. (more hemorrhage, less CO/MAP)

80
Q

When the body loses a smaller amount of blood, a

A

sympathetic discharge keeps MAP @ fairly normal levels.

81
Q

When the body loses more blood, it

A

cannot compensate for the loss as well as when its lost a little bit of blood. MAP can be higher and even plateau, but eventually it will die completely.

82
Q

What is the plateau phase of CO/MAP that occurs during massive hemorrhage?

A

the body’s last effort to save itself via a massive sympathetic discharge. (chemoreceptor response)

83
Q

How does autoregulation play into hemorrhage?

A

it maintains flow to the brain and heart despite a 1/4 to 1/3 decrease in flow to other organs.
this doesn’t last forever

84
Q

Critical level

A

the MAP from below which the body cannot recover from during a hemorrhage without medical intervention.

85
Q

Levels of hemorrhagic shock

A
  1. Nonprogressive
  2. Progressive
  3. Irreversible
86
Q

Nonprogressive hemorrhagic shock

A

normal circulatory compensatory mechanisms eventually cause full recovery w/o outside therapy

87
Q

Progressive hemorrhagic shock

A

without therapy, shock becomes steadily worse until death

88
Q

Irreversible hemorrhagic shock

A

shock has progressed to such an extend that all forms of therapy are inadequate to save the patient.

AKA even without medical intervention you cant save animal

89
Q

What are the factors that compensate for nonprogressive hemorrhagic shock enough to prevent further deterioration of circulation?

A

baroreflex, central chemoreceptors when MAP < 50 (more powerful thanbaroreflex), ^ renin secretion, angiotensin II, ^ vasopressin secretion, ^ epin. & norep., restore BV

90
Q

How is BV restored during nonprogressive hemorrhagic shock?

A

conservation of salt & H2O at kidney, increased thirst, fluid flux from ISF to capillary

91
Q

Transcapillary refill

A

fluid from ISF entering capillary beds to aid in restoration of BV during hemorrhage

92
Q

hemodilution

A
  • evidence of fluid from ISF moving to vasculature.
  • cap. oncotic pressure decreases during bleed => dilution of plasma proteins in vascular space b/c H2O is pulled into vasculature & decreases [protein] in vasculature wrt ISF [protein]
93
Q

What causes progressive hemorrhagic shock?

A

vicious cycle of CV deterioration.

94
Q

Cardiac depression

A

-decrease in coronary blood flow (CBF) below that required to meet metabolic demands of heart
-weakens heart muscle => further decrease in CO (despite ^BP in RA)
=> Progressive deterioration of heart over time

95
Q

Methods of CV deterioration

A
  • Cardiac depression
  • Failure of constrictor response
  • Failure of transcapillary refill
  • CNS depression
96
Q

Failure of constrictor response

A

Occurs with prolonged hypertension:

  • Desensitization of a1-receptors (don’t respond well to norep. stimulus)
  • Norep. depletion in nerve terminals
  • Metabolic vasodilator build-up
97
Q

What is the effect of metabolic vasodilator build-up?

A
  • stimulates more vasodilation

- lose vasoconstrictor response

98
Q

Failure of Transcapillary Refill

A

-Precapillary sphincters fail b/c can’t stay constricted forever
-Arterioles lose resistance
-Venules retain tone for longer b/c of decrease R in aa. & ^R in vv.
=> ^capillary hydrostatic P

99
Q

An increase in capillary hydrostatic P leads to…

A

loss of fluid b/c hydrostatic P > colloid osmotic pressure

100
Q

CNS Depression

A

Occurs with cerebral ischemia:
-Decreased neural activity in brain
-Weakens sympathetic output
=> Decreased vascular and cardiac responses

101
Q

What is the MAIN issue with irreversible hemorrhagic shock?

A

even a transfusion is INCAPABLE of saving patient’s life

102
Q

What can therapy not overcome in irreversible hemorrhagic shock?

A
  • extensive tissue damage
  • destructive enzyme release
  • extensive acidosis
103
Q

What leads to irreversible hemorrhagic shock?

A

too much blood is lost and the animal has already gone through nonprogressive and progressive hemorrhagic shock WITHOUT any treatment

Physiology (10 decks)

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