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Cardiopulmonary Exam 1 > Regulation of Arterial Pressure > Flashcards

Regulation of Arterial Pressure Flashcards

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

A

vagus nerve

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
Q

Three centers in the Vasomotor center

A

Vasoconstrictor center, Cardiac accelerator center, and cardiac decelerator center

26
Q

what happens when the cardiac decelerator center is positively stimulated?

A

it causes inhibition of SA node

27
Q

Renin-Angiotensin-II-Aldosterone System

sequence leading to RENIN release

A

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
Q

Renin-Angiotensin-II-Aldosterone System

sequence leading to Angiotensin II release

A

Renin converts angiotensinogen to angiotensin I

angiotensinogen

29
Q

angiotensin II in the heart and lungs specifically

A

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
Q

Angiotensin II

apart from heart and kidneys, where does this protein work?

A

vascular smooth muscle, brain, and adrenal cortex

it stimulates G coupled protein-couple angiotensin II receptors (ATi)

i

31
Q

Angiotensin II —> aldosterone

A

increases aldosterone, which increases sodium reabsorption

kidneys

32
Q

Angiotensin II –> Na-H exhcnager

A

increases their activity in the kidneys, stimulating sodium reabsorption

33
Q

Angiotensin II –> hypothalamus

A

increases thirst and release antidiuretic hormone

34
Q

Angiotensin II —> arterioles

A

increase TPR —> increasing arterial pressure

achieves this by binding to g coupled protein receptors and causing an upswing of cAMP–>IP3–>DAG—>Ca2+

35
Q

big picture theme of Pa’s relationship to angiotensin II

A

as Pa decreases, angiotensin II tries to restore it

36
Q

why is the baroreceptor induced over the hormone method of restoring Pa, and vice versa?

A

baroreceptors can work in seconds but are considered long term and short term mechanisms

hormones are needed for long term pressure maintenance

37
Q

from Ballam slides

angiotensin I is converted by ____ in the _____. (1)
angiotensin I is converted to ____ in the _____ as well (2)

A

angiotensin converting enzyme in the blood and in the kidneys as well

38
Q

“ultimate relationships”

angiotensin II —> aldosterone —>……

A

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
Q

ADH

A

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
Q

vasopressin

A

ADH

41
Q

side effect of ACE inhibitors

A

angiotensin converting enzyme convers angiotensin I to II, but it also breaks down bradykinin which accumulates and can make you cough

42
Q

ARBs

A

angiotensin receptor blockers

43
Q

cerebral ischemia

A

causes increased sympathetic outflow from vasomotor center

44
Q

Hemorrhage cause blood to

A

drop

means loss of blood volume

45
Q

Hemorrhage causes what parts of the vasomotor to work, and how

A

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
Q

Valsalva maneuver

A

expiring against a closed glottis
causes increase in intrathoracic pressure
decreases venous return

47
Q

Cushing reflex

A

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
Q

Vasopressin is released

A

in response to angiotensin II from brain
also released by r. atria in response to low preload
causes increased TPR and water retention

49
Q

Natriuretic peptide :ABC

A

Atrial, Brain, C-type
causes arteriolar dilation, increases fluid loss
inhibits renin
decrease TPR at atrioles
secreted by excessive preload of atria and ventricles

Cardiopulmonary Exam 1 (21 decks)

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