B4.004 Cardiovascular Control Mechanisms Flashcards

1
Q

how do veins differ from arteries?

A

more distensible
more compliant
ability to store blood

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2
Q

which vessels do sympathetic axon varicosities act upon?

A

BOTH arterioles and venules

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3
Q

sympathetic action on arteries

A

noradrenergic- a1
decreases diameter by smooth muscle contraction
increased resistance = increased MAP

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4
Q

sympathetic action on veins

A

noradrenergic- a1
decreases diameter by smooth muscle contraction
decreased capacitance = increased venous return = increased cardiac output

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5
Q

which vessels do parasympathetic nitrergic axon varicosities act upon?

A

arterioles

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6
Q

parasympathetic action on arterioles

A
NO- guanylate cyclase
-increased diameter
Epinephrine- b2 (non-neural)
-decreased resistance
-increased flow
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7
Q

difference between sympathetic and parasympathetic effects on vasculature

A
parasympathetic = very discrete, local control mechanism within limited vessels
sympathetic = overall function regulation
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8
Q

3 ranges for changing blood vessel diameter

A
  1. to change local blood flow
  2. to change total peripheral resistance (TPR)
  3. to change cardiac output (CO)
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9
Q

purpose of changing local blood flow

A

important for discrete reflexes (genital erection, GI vasodilation during a meal)
local resistance is decreases so local flow increases
no significant change in TPR or MAP

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10
Q

why does TPR need to be adjusted?

A

if MAP decreases (blood loss, pooling while standing, etc) this will reduce brain perfusion because the brain is at the top of the hydrostatic column
leads to syncope
compensated for by changing TPR

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11
Q

how is TPR determined

A

by arterial blood vessel diameters in vascular beds (renal, GI, skeletal)
TPR increased by arterial vascular constriction
-renal and GI by a1 receptors
-skeletal by b2 receptors

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12
Q

effects of TPR on MAP

A

increased TPR increases MAP

increased TPR normally will not significantly decrease CO

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13
Q

process of changing cardiac output

A

venules/veins store 2/3 of total blood volume
venous smooth muscle contraction forces blood back to the heart (increased venous return)
increased venous return = increased CO
increased CO = increased MAP

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14
Q

what is tone

A

level of activity of nerves and targets

high nerve discharge rate or contractile state = high tone

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15
Q

vascular tone

A

determined by balance between vasoconstrictors influences (mainly sympathetic a1) and vasodilatory factors

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16
Q

cardiac tone

A

determined by concurrent discharge of excitatory sympathetic and inhibitory parasympathetic nerves
HR increased by increasing symp or decreasing parasym discharge

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17
Q

describe the process of changing from supine to upright posture and the effect on MAP

A

increased hydrostatic pressure causes venous distention in lower body and venous pooling of about 700 mL of blood
decreased venous return > decreased CO > decreased MAP

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18
Q

process of increasing cardiac tone

A

increasing cardiac sympathetic tone and decreasing vagal parasympathetic tone increased HR and force of contraction
makes heart a more effective pump
this can help restore cardiac output

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19
Q

what initiated cardiovascular reflexes?

A

baroreceptors

  • cardiopulmonary
  • arterial
20
Q

baroreceptors

A

stretch receptors located on vessel walls that tell the brain to modulate autonomic cardiovascular tone
high pressure = high firing of baroreceptor nerves

21
Q

cardiopulmonary baroreceptors

A

measure venous return
located in right atria, vena cava, pulm vessels
stretch w more venous return
venous pressure range 0-20 mmHg

22
Q

arterial baroreceptors

A

located on aortic arch and carotid sinus
assess blood flow to the body and brain respectively
increased pulse pressure and MAP result in increased discharge rates over 60-180 mmHg

23
Q

which nerve connects the carotid sinus to the brain stem?

A

glossopharyngeal (9th cranial)

24
Q

which nerve connects the aortic arch to the brain stem

A

vagus nerve (10th cranial)

25
Q

which nerve connects the cardiopulmonary baroreceptors to the brain stem

A

vagus nerve (10th cranial)

26
Q

where do the afferent axons (vagus, glossopharyngeal) fire to?

A

nucleus of the tractus solitaries (NTS)

27
Q

what is the effect of decreased firing in the NTS (due to decrease in BP)?

A

decreased STIMULATION of preganglionic cardiac parasympathetic axons in dorsal motor nucleus of the vagus (DMV) and nucleus ambiguous (NA)
decreased INHIBITION of C1

28
Q

action of DMV/NA

A

preganglionic neurons for parasympathetic cardiac fibers

decreased stim = decreased cholinergic inhibition of heart = better pumping

29
Q

action of C1

A

sympathetic preganglionic neurons

decreased inhibition = increased firing of sympathetic nerves to heart and vasculature

30
Q

summarize the action of the NTS

A

stimulate DMV/NA which stimulate parasympathetic system

inhibits C1 which stimulates sympathetic system

31
Q

how does baroreflex selectivity influence different arteriolar beds

A

baroreflex activates the SNS without large effects on adrenomedullary secretion
thus…predominating vasoconstrictive effects mediated by NE (a1 with little to no b2 dilation)
most effective on renal and mesenteric arterioles
little change in cardiac and cerebral vascular beds

32
Q

how are baroreceptors “buffer” nerves

A

if cut, more variability in BP but no change in ‘set point’

avg not changed

33
Q

what are some factors that can override the baroreflex

A

pain

emotions

34
Q

chemoreflex

A

involved in respiration
active when MAP falls below 60 mmHg
low blood flow detected as low O2 in carotid and aortic body chemoreceptors

35
Q

central ischemic response

A

reduced perfusion of the medulla results in discharge of sympathetic centers (C1)
final line of defense to restore MAP and CO

36
Q

cushing reaction

A

when intracranial pressure is abnormally high, cerebral vessels collapse, perfusion stops and the central ischemic response is initiated even though systemic arterial pressure is normal or elevated

37
Q

orthostatic hypotension

A

inability to compensate for reduced CO associated with upright posture (autonomic failure)

38
Q

3 causes of orthostatic hypotension

A
  1. baroreflex pathway diseases
  2. degeneration of postganglionic sympathetic neurons (autonomic failure)
  3. postganglionic axon degeneration (neuropathy)
39
Q

carotid sinus syndrome

A

abnormal sensitivity of the carotid sinus receptors to touch or stretch

40
Q

vasovagal syncope

A

abnormally robust response to emotional stimuli leading to withdrawal of vasomotor tone and vagal parasympathetic activation
“playing possum”

41
Q

how does ADH exert intermediate cardiovascular control

A

baroreceptor mediated release
potent vasoconstrictor for both arterioles and veins
increases plasma volume by reducing urine output (long term regulatory mechanism)

42
Q

how does angiotensin II exert cardiovascular control

A

intermediate effects via direct actions on arteriolar smooth muscle
mediates long term volume increases by directly suppressing urine formation and indirectly by causing aldosterone release from the adrenal cortex
augments NE release from sympathetic varicosities

43
Q

what is renin?

A

converts angiotensinogen to angiotensin II

44
Q

how is renin regulated

A

diminished renal blood flow and SNS activation increase renin

45
Q

what is ANP

A

atrial natriuretic peptide

stored in atrial myocardial cells

46
Q

what elicits ANP release

A

increased plasma volume and resulting atrial stretching

47
Q

how does ANP work?

A

acts on the kidney to induce sodium excretion (and coupled water excretion)
reduces plasma volume and BP