Regulation of Arterial Pressure Flashcards

(49 cards)

1
Q

TPR

effects of decreasing and increasing TPR

A

total peripheral resistance: determined by arterioles

a decrease in TPR causes an increase in venous return/CO
an increase in TPR will reduce venous return/CO

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2
Q

increasing TPR does what to arterial and venous pressure?

A

increases arterial pressure but decreases venous pressure

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3
Q

decreasing TPR does what to arterial and venous pressure

A

decreases arterial pressure and an increase in venous pressure

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4
Q

Increasing TPR effects CO or vasculature?

A

both: it INCREASES arterial pressure, so it must increase the afterload on the heart

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5
Q

Decreasing TPR effects CO or vasculature?

A

both: it DECREASES arterial pressure, to it decreases the afterload on the heart

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6
Q

Mean arterial pressure

A

the pressure in the major arteries delivering blood are basically the same: 100 mmHg. this pressure remains the same throughout major artery, but delivery pressure itself is controlled at the individual level by metabolic means

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7
Q

what is mean arterial pressure

A

100 mmHg

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8
Q

what is the formula for mean arterial pressure

A

P = CO x TPR

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9
Q

what is “deceptive” about the mean arterial pressure formula?

A

CO and TPR are not independent variables, so effecting one will effect the other. thus P won’t follow simple logic of an equation because it’s based on variables that alter one another.

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10
Q

Baroreceptors

A

located in carotid sinus and aortic arch

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11
Q

baroreceptors in the carotid sinus

A

respond to increases and decreases in pressure

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12
Q

baroreceptors in the aortic arch

A

respond to increases in pressure

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13
Q

baroreceptors are

A

“mechanoreceptors” which are sensitive to pressure or stretch

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14
Q

Which is the strongest stimulus on the baroreceptor:

Absolute pressure level
Rate of pressure changes
Changes in pressure

A

rate and changes

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15
Q

local arterial bed rely on a _____ input pressure to control how much blood the tissue receives

A

constant, high input pressure

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16
Q

Two control mechanisms for blood flow to local vascular beds

A

1) maintain a constant, high input pressure

2) ability to alter resistance to flow through individual vascular beds

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17
Q

Two general mechanisms for controlling blood flow

A

neuronal (baroreceptors) and hormonal

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18
Q

carotid sinus baroreceptors —>

A

herrings nerves —> CN IX

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19
Q

CN IX —>

A

+ stimulus at the Vasomotor center (medulla – nucleus tractus solitarus) —> cardiac decelerator —> (-) @ SA node

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20
Q

information from the aortic arch is carried by the

21
Q

information from the carotid sinus is carried by the

A

glossopharyngeal center

22
Q

Vasomotor Center

how it is stimulated and what it does

A

baroreceptor input (increased pressure) decreases sympathetic activity and increases parasympathetic activity (decreasing heart rate)

decrease pressure –> decreased firing —> increased sympathetic activity

23
Q

Increase in Pa —>

A

stimulation of X and IX —> vasomotor center in medulla —> increase in parasympathetics + decrease in sympathetics ———> negative stimulus of SA node + decrease sympathetic stimulation of contraction and SA —> relaxation of heart and vasodilation —> Pa brought down back to normal

24
Q

Sympathetic system causes (3 things)

Parasympathetic system causes (1 thing)

A

constriction of arterioles and veins via alpha receptors

increases HR and contractility via beta-1 receptors

causes fluid retention by kidney due to afferent arteriolar constriction and increased renin secretion

Decrease in heart rate (muscarinic receptors)

25
Three centers in the Vasomotor center
Vasoconstrictor center, Cardiac accelerator center, and cardiac decelerator center
26
what happens when the cardiac decelerator center is positively stimulated?
it causes inhibition of SA node
27
Renin-Angiotensin-II-Aldosterone System sequence leading to RENIN release
regulates Pa decreased renal profusion ---> mechanoreceptors in afferent arterioles --> decrease in Pa causes Prorenin to be converted to renin in juxtaglomerular cells OR beta-1 receptor stimulation on juxtaglomerular cells --> renin release
28
Renin-Angiotensin-II-Aldosterone System sequence leading to Angiotensin II release
Renin converts angiotensinogen to angiotensin I | angiotensinogen
29
angiotensin II in the heart and lungs specifically
catalyzed from angiotensin I by angiotensin converting enzyme (ACE) in the heart and lungs increase blood volume, preload, stroke volume, CO and therefore BP
30
Angiotensin II apart from heart and kidneys, where does this protein work?
vascular smooth muscle, brain, and adrenal cortex it stimulates G coupled protein-couple angiotensin II receptors (ATi) i
31
Angiotensin II ---> aldosterone
increases aldosterone, which increases sodium reabsorption kidneys
32
Angiotensin II --> Na-H exhcnager
increases their activity in the kidneys, stimulating sodium reabsorption
33
Angiotensin II --> hypothalamus
increases thirst and release antidiuretic hormone
34
Angiotensin II ---> arterioles
increase TPR ---> increasing arterial pressure achieves this by binding to g coupled protein receptors and causing an upswing of cAMP-->IP3-->DAG--->Ca2+
35
big picture theme of Pa's relationship to angiotensin II
as Pa decreases, angiotensin II tries to restore it
36
why is the baroreceptor induced over the hormone method of restoring Pa, and vice versa?
baroreceptors can work in seconds but are considered long term and short term mechanisms hormones are needed for long term pressure maintenance
37
from Ballam slides angiotensin I is converted by ____ in the _____. (1) angiotensin I is converted to ____ in the _____ as well (2)
angiotensin converting enzyme in the blood and in the kidneys as well
38
"ultimate relationships" angiotensin II ---> aldosterone --->......
angiotensin II ---> aldosterone from adrenal cotex ---> Na-H pump in the kidneys ---> Na retention ---> water reuptake ---> Pa ---> increased preload -->increased SV --> increased CO --> increased BP
39
ADH
released by hypothalamus in response to angiotensin II binds to receptors on arterioles and causes vasoconstriction (increasing TPR) binds to kidney cells and stimulate reabsorption remember: angiotensin II ---> site of action ---> increased blood volume --> increased preload ---> increased SV ---> increased CO ---> increased BP --> increased Pa
40
vasopressin
ADH
41
side effect of ACE inhibitors
angiotensin converting enzyme convers angiotensin I to II, but it also breaks down bradykinin which accumulates and can make you cough
42
ARBs
angiotensin receptor blockers
43
cerebral ischemia
causes increased sympathetic outflow from vasomotor center
44
Hemorrhage cause blood to
drop means loss of blood volume
45
Hemorrhage causes what parts of the vasomotor to work, and how
decreased blood volume ---> decreased stretch on baroreceptors at carotid sinus --> decreases signals to brain--> induce sympathetics in heart ---> heart rate/contractility increase ---> decreases unstressed volume
46
Valsalva maneuver
expiring against a closed glottis causes increase in intrathoracic pressure decreases venous return
47
Cushing reflex
as intracranial pressure increases, cerebral arteries are compressed --> decreased perfusion in the brain CO2 and therefore H is not removed from the brain, so the pH drops, which causes medullary chemoreceptors to cause sympathetic outflow toward brain in a nuttshell: intracranial pressure redues blood flow to medulla, activating sympathetics to increase outflow to brain. over all effect is increase in TPR and Pr
48
Vasopressin is released
in response to angiotensin II from brain also released by r. atria in response to low preload causes increased TPR and water retention
49
Natriuretic peptide :ABC
Atrial, Brain, C-type causes arteriolar dilation, increases fluid loss inhibits renin decrease TPR at atrioles secreted by excessive preload of atria and ventricles