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Flashcards in Autonomic Control of Blood Pressure Deck (31)
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1
Q

what is the single most important mechanism providing short-term regulation of arterial pressure?

A

the arterial baroreceptor, most importantly high-pressure carotid sinus, then aortic arch

2
Q

how is MAP monitored?

A
  1. high-pressure arterial baroreceptors (on arterial side, most importantly carotid sinus then aortic arch)
  2. renal juxtaglomerular apparatus
  3. low-pressure baroreceptors (AKA volume or cardiopulmonary receptors, on venous side and atrium)
  4. chemoreceptors (although mostly for respiratory control)
3
Q

how are adjustments to MAP made?

A

via the ANS and release of specific hormones

4
Q

where do all baroreceptors feed back to?

A

the nucleus tractus solitarius (NTS) in medulla

5
Q

where do carotid baroreceptors feed back to?

A

from carotid sinus; transmitted thru Hering’s nerve to CN IX in high neck, then to NTS

6
Q

where do aortic baroreceptors feed back to?

A

from aortic arch; transmitted thru CN X to NTS

7
Q

what happens if there is stretching of distensible vessel walls at the high-pressure baroreceptors?

A

stretching at carotid sinus and oartic arch causes reflex vasodilation and bradycardia

8
Q

peripheral chemoreceptors

A

located in carotid and aortic bodies, and in close contact with arterial blood

  • when arterial pressure falls below a critical level, the receptors are stimulated b/c less blood flow causes less O2
  • signals transmitted from chemoreceptors and baroreceptors pass thru Hering’s and IX nerves (if carotid) and vagus (if aortic) to NTS to elevate MAP back to normal
9
Q

is the chemoreceptor reflex a powerful MAP controller?

A

not until MAP falls below 80 mmHg (like during hemorrhage)

-thus it’s at lower pressures that this reflex becomes important to prevent further decreases in MAP

10
Q

central chemoreceptors

A

in the medulla

  • sensitive to decreases in brain pH reflecting increase in arterial PCO2
  • causes increase in SNS output
11
Q

what do low PO2 and high PCO2 act on, what what is their effect?

A

low PO2 acts on peripheral chemoreceptors, and high PCO2 acts on central chemoreceptor
-they act in concert to enhance vasoconstriction

12
Q

low-pressure baroreceptors

A

in cardiovascular system

-detect changes in venous pressure/volu

13
Q

what happens to baroreceptor APs and receptor potentials in response to higher pressure?

A

higher pressure (steps) –> higher receptor potential (depolarization) –> more frequent APs

14
Q

structure of baroreceptors in carotid sinus and aortic arch, and what are they sensitive to?

A

branched terminals of myelinated and unmyelinated sensory nerve fibers, intermeshed within elastic layers
-they are sensitive to stretch

15
Q

what does an increase in transmural pressure difference do?

A

enlarges the vessel, deforming the receptors, and increasing firing rate of the baroreceptor’s sensory nerve
-the signal is frequency modulated

16
Q

to what do baroreceptors respond to, and when are they most sensitive?

A

they respond rapidly to changes in MAP and are most sensitive in normal operating range ~100 mmHg for carotid sinus, and 130 mmHg for aortic arch (less sensitive)
-the slope of dI/dP is maximum at this time

17
Q

when do carotid sinus baroreceptors not work?

A

they are not stimulated by pressures between 0 to 50 or 60 mmHg
-above these levels, they respond progressively more rapidly and reach a maximum at 180 mmHg, and are optimal at 100 mmHg

18
Q

what happens to the rate of impulse firing during systole and diastole?

A

the rate increases in the fraction of a second during each systole, and decreases again during diastole

19
Q

do baroreceptors respond more to rapidly changing pressures or stationary pressures?

A

they respond more to rapidly changing pressures
-ex: if MAP is 150 mmHg, but is rising rapidly, the rate of impulse transmission may be twice that when the pressure is stationary at 150 mmHg

20
Q

what happens to the baroreceptor reflex in HTN?

A

since it adapts to long-term changes in MAP, the curve is parallel and shifts to right (meaning it’s not as sensitive)

21
Q

what would happen to MAP if baroreceptors were absent?

A

MAP would fluctuate wildly if the baroreceptors were denervated, and no longer be constantly monitored
-the MAP would have a very wide range, instead of the usual ~100mmHg

22
Q

what is the primary purpose of arterial baroreceptor system?

A

reduce the minute-by-minute variation in arterial pressure to about one-third that which would occur if the baroreceptor system was not present

23
Q

in general, how many vessels does the SNS innervate? what does this mean?

A

in most tissues they innervate all vessels except capillaries

  • precapillary spinchters and metarterials are innervated in some, but not as densely
  • innervation of small arteries/arterioles allows SNS stimulation to increase R and decrease Q
  • innervation of large vessels, especially veins, allows SNS to vasoconstrict to push blood into heart to regulate CO (decrease compliance of vessels)
24
Q

what does the vasoconstrictor area of the vasomotor center do?

A

it transmits signals continuously to the sympathetic vasoconstrictor nerve fibers over the entire body

  • causes slow firing of these fibers at a rate of about 1/2 to 2 impulses per second
  • these impulses normally maintain a partial state of contraction in blood vessels, called vasomotor tone
25
Q

what does total spinal anesthesia do? and how can it be reversed?

A

it blocks all transmission of sympathetic nerve impulses from the spinal cord to the periphery

  • thus, the MAP falls from 100 to 50 mmHg, demonstrating the effect of losing vasoconstrictor tone throughout the body
  • it can be reversed by injecting NE so vessels constrict and MAP rises to an even greater level (~140 mmHg, for several minutes) until the NE is metabolized, and MAP decreases again
26
Q

what does an increase in MAP cause?

A

activates negative feedback via high-pressure baroreceptors (detector)

  • go via their afferent pathways to coordinating center (NTS in medulla)
  • efferent pathways cause vasodilation of veins/arterioles thru peripheral circulatory system, and decreased HR and strength of contraction
  • bradycardia and vasodilation will decrease MAP
27
Q

what happens when one changes posture from standing to lying down?

A

there is an increase in (central) venous return and SV, which leads to an increase in MAP

  • increases firing rate of baroreceptor afferent fibers, which feed back to NTS in medulla
  • effectors increase PNS and decrease SNS, which feed back to SA node
  • work together to decreases HR and CO (thus decrease SV)
  • SNS decreases peripheral resistance in arterioles, decrease venous tone in veins, and decrease contractility in ventricles to decrease SV and CO
  • altogether, will decrease MAP
28
Q

what happens when one stands up from lying down?

A

pooling of blood in veins will decrease arteriolar pressure

  • the baroreceptor fires less, thus causing and increase in sympathetic outflow (increased HR, contractility, CO, arterolar and vein constriction to increase TPR
  • minimizes the decrease in pressure in head and upper body
29
Q

what does the carotid sinus massage, or release from a Valsalva maneuver do?

A

stimulates the baroreceptors and reflexly slows heart in people with atrial tachycardia (atria flutter or fibrillation) to decrease HR

30
Q

carotid sinus syndrome

A

patients have hyper-sensitive baroreceptors such that even mild external pressure to the neck causes a strong reflex, and may even stop the heart for 5-10 seconds (syncope)

31
Q

what is the Valsalva maneuver used for?

A

test the integrity of the baroreceptor reflex

  • patient expires against a closed glottis, which increases intrathoracic pressure, thus decreasing venous return to heart, CO, and MAP
  • intact baroreceptors sense decrease in MAP, and direct increase in SNS and decrease in PNS outflow to heart and vessels
  • HR is remeasured (should have gone up)
  • rebound decrease in HR is noted after release

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