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CP Test 1 > B4-004 Cardiovascular Control Mechanisms > Flashcards

B4-004 Cardiovascular Control Mechanisms Flashcards

1
Q

3 reasons for changing blood vessel diameter

A
  1. to change local blood flow
  2. to change TPR
  3. to change CO
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2
Q

changes in local blood flow allow for discrete arterial dilation such as

A

GI vasodilation during a meal
erection

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3
Q

local arterial dilation [….] resistance, so local flow is […]

A

decreases; increased

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4
Q

results in no significant change in TPR or MAP

A

change to local blood flow

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5
Q

TPR is determined by

A

arterial blood vessel diameters in vascular beds

mainly renal, GI, and skeletal muscle

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6
Q

changing TPR can compensate for

A

changes in aterial pressure due to standing or blood loss

causes reduced blood to brain

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7
Q

MAP=

A

CO x TPR

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8
Q

if TPR is increased by arterial vasoconstriction and CO stays the same, MAP will

A

increase

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9
Q

do increases in TPR normally decrease CO?

A

no

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10
Q

veins and venules store about […] of total blood volume

A

2/3

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11
Q

because the heart is a Starling pump, increased venous return increases

A

cardiac output

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12
Q

venous smooth muscle contractions return

A

blood to the heart

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13
Q

increased venous return and cardiac output will increase…

A

MAP

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14
Q

innervate arterial and venous smooth muscle

A

vasomotor nerves

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15
Q

only relevant constrictor nerves

A

sympathetic nerves

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16
Q

sympathetic noradrenergic nerves only

A

constrict

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17
Q

excite vascular smooth muscle by NE acting on a1 receptors

A

sympathetic nerves

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18
Q

increase MAP by increasing TPR

A

sympathetic nerves

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19
Q

increase MAP by increasing venous return

A

sympathetic nerves

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20
Q

induce discrete dilation via NO

A

parasympathetic nerves

won’t affect TPR under normal conditions

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21
Q

level of activity of nerves and targets

A

tone

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22
Q

determined by the balance between vasoconstrictor influences and vasodilation influences

A

vascular tone

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23
Q

determined by concurrent dischange of excitatory sympathetic and inhibitory parasympathetic nerves

A

cardiac tone

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24
Q

heart rate is increased by […] sympathetic discharge and/or […] parasympathetic discharge

A

increasing; decreasing

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25
Q

to change blood pressure/output, change

A

cardiovascular tone

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26
Q

when horizontal, the body is […] hydrostatic column

A

20cm

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27
Q

in upright position, hydrostatic column is

A

180 cm

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28
Q

as a result of increased hydrostatic pressure, veins in lower body

standing

A

distend leading to venous pooling

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29
Q

[…] mL of blood is lost from venous return in the first few minutes after standing

A

700

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30
Q

decreased venous return leads to

A

decreased cardiac output,
which leads to decreased MAP

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31
Q

arterial pressure below […] is insufficent to maintain neural activity

A

90/60 mmHg

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32
Q

result of lost somatic motor control due to diminshed cardiac output

A

syncope

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33
Q

when cardiac output is diminshed, arterial blood pressure can be maintained by

A

arterial vasoconstriction
venoconstriction
increased cardiac tone

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34
Q

sympathetic contraction of venous smooth muscle reduces

A

compliance and capacitance,
forces blood back to heart

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35
Q

arterial vasoconstriction increases TPR, leading to

A

increased MAP

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36
Q

venoconstriction causes increased CO, leading to

A

increased MAP

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37
Q

by increasing cardiac sympathetic tone and decreasing vagal parasympathetic tone, heart rate and force of contraction

A

increase,
making the heart a more effective pump

38
Q

increased cardiac tone leads to increased

A

CO

39
Q

stretch receptors located on vessel walls that tell the brain to modulate autonomic CV tone

A

baroreceptors

40
Q

measure venous return

A

cardiopulmonary baroreceptors

41
Q

located in right atria, vena cava, and pulmonary vessels

A

cardiopulmonary baroreceptors

42
Q

“low pressure” receptors

A

cardiopulmonary baroreceptors

43
Q

located in aortic arch and carotid sinus

A

arterial baroreceptors

44
Q

assess blood flow to entire body and brain

A

arterial baroreceptors

45
Q

“high pressure” receptors

A

arterial baroreceptors

46
Q

decreased MAP leads to […] baroreceptor stretch

A

decreased

47
Q

decreased baroreceptor stretch leads to

A

decreased vagal/glossopharyngeal afferent nerve firing

48
Q

decreased afferent axon firing leads to

A

decreased firing in nucleus of tractus solitarius

49
Q

decreased firing in nucleus of tractus solitarius leads to

A

decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA

50
Q

decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA leads to

A

decreased cholinergic inhibition of the heart

51
Q

decreased firing in NTS leads to

A

decreased inhibition of C1

52
Q

decreased inhibition of C1 leads to

A

firing of sympathetic nerves to the heart and vasculature

53
Q

baroreflex activates the SNS without

A

large effects on adrenomedullary secretion

54
Q

baroreflex selectively increases resistance in which arteriolar beds?

A
  • renal
  • splanchnic
  • cutaneous
  • skeletal muscle
55
Q

primary mechanism maintaining MAP under normal conditions

A

baroreflex

56
Q

nerves are “buffer nerves”

if cut, more variablity in BP, but no significant change in set point

A

baroreflex

57
Q

the baroreflex can be overridden by what?

A

pain and emotions

58
Q
  • mainly involved in respiration
  • active when MAP falls below 60 mmHg
  • detects low O2 in carotid and aortic body
A

chemoreflex

59
Q
  • reduced perfusion of the medulla
  • results in discharge of C1
  • final line of defense to restore MAP and CO
A

central ischemic response

60
Q

when ICP is abnormally high, cerebral vessels collapse, brain perfusion stops and CIR is initiated, this is called?

A

cushing reaction

61
Q

inability to compensate for reduced CO associated with upright posture

A

orthostatic hypotension

62
Q

orthostatic hypertension can be caused by:

A
  • CNS diseases
  • postganglionic axon degeneration
  • degeneration of postganglionic sympathetic neurons
63
Q
  • variant of orthostatic hypotension
  • characterized by rapid heart rate, dizziness and fatigue
A

POTS

64
Q

abnormal sensitivity of the carotid sinus baroreceptors to touch or stretch

A

carotid sinus syndrome

65
Q

slight pressure to the neck is perceived as high blood pressure, leading to vagal slowing of heart and fainting

A

carotid sinus syndrome

66
Q

abnormally robust response to emotional stimuli leading to withdrawal of vasomotor tone and vagal parasympathetic activation

A

vasovagal syncope

67
Q

may be a vestige of an adaptive response for dealing with danger

playing dead

A

vasovagal syncope

68
Q

represent short term regulator mechanism

A

nerves

69
Q

represent intermediate-term effects

A

circulating hormones

70
Q

represent long term regulatory effects

A

factors effecting volume

71
Q
  • released into circulation
  • augments sympathetic nervous system during “fight or flight”
A

epinephrine

72
Q
  • activates all adrenoreceptors, including b2 receptors
  • elicitis skeletal muscle vasodilation
A

epinephrine

73
Q

adrenomedullary catechloamine release is not strongly affected by

A

baroreceptors

74
Q

exerts intermediate CV control via baroreceptor mediated release

A

ADH

75
Q

potent vasocontrictor for both arterioles and veins

A

ADH

76
Q

increases plasma volume by reducing urine output

A

ADH

77
Q

increased by diminished renal blood flow and sympathetic activation

A

plasma renin (Ang II)

78
Q

intermediate effects on CV control via direct action on arteriolar smooth muscle

A

Ang II

79
Q

mediates long term volume increases by directly suppressing urine formation and indirectly by causing aldosterone release from adrenal cortex

A

Ang II

80
Q

augments NE release from sympathetic varicosities

A

Ang II

81
Q

stored in atrial myocardial cells

A

ANP

82
Q

elicited by increased plasma volume causing atrial stretching

A

ANP

83
Q

acts on kidney to induce sodium excretion into the urine to reduce plasma volume and blood pressure

A

ANP

84
Q

if sympathetic neurons are compromised what key function is lost?

A

vasoconstriction
–> decreased TPR

85
Q

after taking the drug:

  • cardiac output is increased
  • total peripheral resistance is unchanged
  • central venous pressure is increased
  • heart rate is unchanged

what kind of drug?

A

mineralcorticoid like volume expander

86
Q

an Alpha 1 adrenoreceptor agonist would increase

A

TPR

87
Q

a beta 2 adrenoreceptor agonist would decrease

A

TPR

88
Q

what kind of drug?

will decrease
* cardiac output
* TPR
* central venous pressure.

A

ganglionic blocker

89
Q
  • lost sensation in hands/feet
  • does not sweat
  • becomes light headed standing rapidly
A

elevated ADH

90
Q

sympathetic innervation to the kidney is the major means for

A

increasing TPR

91
Q

expansion of plasma volume will result in what hormone changes?

A
  • decreased Ang II
  • increased ANP
  • decreased epi
  • decreased ADH

CP Test 1 (16 decks)

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