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CP2 > Regulation of Arterial Pressure > Flashcards

Regulation of Arterial Pressure Flashcards

1
Q

What is Mean Arterial Pressure equation?

what’s normal?

how is it regulated?

A

CO x TPR = ( HR x SV ) x TPR

normally its 93.3 round up to 100 or something

baroreceptor
hormonally

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2
Q

What does the detector of the baroreceptor detect?

what happens after it detects something?

A

it detects the plasma membrane stretch (passive) and that will change the firing rate (afferent neural pathway)

this then coordinates this to the brain and then sends it to the efferent neural pathway and it corrects the deviation

if I move left, it’ll move it right. bringing the stretch back to wear it should be

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3
Q

What do we care about in the carotid sinus?

Aortic sinus?

What does our afferent neuron go through on its way up to the brain?

A 
Glossopharyngeal nerve (10)
Sinus nerve of Hering
Vagus Nerve (9)
Aortic Nerve

nucleus tractus solitarius (NTS)

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4
Q

What are the detectors of the baroreceptor reflex (2 of them)?

A

Chemoreceptors that respond to PO2, PCO2, pH

Mechanoreceptors that respond to the stretch.

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5
Q

What if we have an increase of the stretch?

what if the pressure falls?

A

increasing the firing rate of the nerve that connects the receptor to the NTS.

decrease the firing rate.

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6
Q

What is the cardioinhibitory area?

A

The carotid sinus and aortic sinus sends afferent signals up to the brain to the NTS and the NTS decides if it needs to do anything about it.

it could send its signal to the DORSAL NUCLEUS of the vagus and the nucleus ambiguous –> has a parasympathetic outflow which innervates on the heart.

Rostral ventrolateral medulla (C1 and A1 regions) which is outflow through the sympathetic nervous system –> going to the preganglionic synapse and then back up to the heart and the arteries/veins and the adrenal medulla!

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7
Q

What is the control center of the baroreceptor reflex?

how does this act on an increase in firing?

A

NTS

we activate our baroreceptors and increase the firing rate (stretched these) and its sensed by the NTS. I want to decrease heart rate so it’s going to activate the cardiac decelerator + inhibit the sympathetic side.

I want to slow down heart rate which causes the PNS to slow down heart rate and act on the SA node.

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8
Q

how would this work if we have a decrease in firing? (for the baroreceptor reflex)

A

our NTS knows that there is less firing and it’ll want to increase heart rate. so it’s going to activate the cardiac accelerator and vasoconstrictor and inhibit the cardiac decelerator.

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9
Q

What is TPR dependent on?

A

sympathetic stimulation of the arterioles

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10
Q

what is Stroke volume dependent on?

A

sympathetic stimulation of the heart

Preload

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11
Q

What is HR dependent on?

A

sympathetic and parasympathetic stimulation

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12
Q

What are the carotid bodies sensitive to? what happens if you go above that? below what?

what about the aortic bodies?

wtf is he getting at?

A

up to 200 mmHg. if you go higher you have a problem and your firing rate is going to level off

below 40, the same thing occurs on the flip side.

much higher threshold for activation, continues to respond above saturation, continues to respond above saturation.

increased frequency of stimulation increases the strength of the AP

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13
Q

Sympathetic:

Baroreceptor firing?

Influence and mediation?

A

lower

constriction of arterioles / veins (alpha 1 receptor)

increased HR and contractility (B1)

fluid retention by kidney due to afferent arteriole constriction and renin secretion

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14
Q

Parasympathetic:

Baroreceptor firing

Influence and mediation?

A

increased baroreceptor firing

decreased HR (M2/M3)

Vagus nerve signal to AV

indirect vasodilation on blood vessels by NO

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15
Q

Decrease in Mean Arterial Pressure leads to what baroreceptor firing?

what is the result?

A

less firing

so you increase SNS (C1 + A1) activity and decrease PNS (nucleus ambiguous + dorsal activation) activity

this increases TPR (alpha 1 receptors constrict blood vessels) and increases CO (product of stroke volume = increase in inotropic effect)

you’re going to contract harder through b1 receptors

heart rate increases through chronotropic effects

funny sodium channels in phase 4, more sodium coming in, phase 4 slope a little higher, SA a little sooner.

the overall is you’re wanting to INCREASE MAP

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16
Q

Increase MAP will result in what?

A

increased baroreceptor

Decreased SNS activity, increased PSNS activity

Changes in TPR + CO

closing the loop

decreasing it back down!

17
Q

What does hypertension do to MAP?

A

it resets the baroreceptors to regulate pressure at a HIGHER set point

your shift in blood pressure is the new norm! so the set point is readjusted so it sees that new value is normal.

18
Q

What is the RAAS system?

A

Renin-Angiotensin II - Aldosterone system

this is for long term changes in blood volume and helps control blood pressure.

has an influence from the baroreceptors.

19
Q

Of the RAAS, what is the order of what is produced?

A

Angiotensin

then Angiotensin 2 and then aldosterone around the same time but Angiotensin 2 is a bit earlier

20
Q

What is Renin?

A

secreted by the kidney to the bloodstream due to a decrease in BP

if BP goes higher than normal then less renin is secreted

21
Q

what is the secretion of renin stimulated by?

A

B1 adrenergic receptors on the kidney

22
Q

What does renin do?

A

takes angiotensinogen to be converted to angiotensin 1 and ACE converts this to Angiotensin 2 (active form)

this happens in the lungs and kidneys to begin compensation

23
Q

What cells are secreting renin?

A

juxtaglomerular cells

24
Q

What does angiotensin 2 do? (3 things)

A

causes secretion of aldosterone from adrenal cortex. aldosterone acts to reabsorb water and sodium

stimulates the secretion of ADH, which reduces urine production (fluid retention)

causes global vasoconstriction of arterioles by binding to specific receptors

25
Q

Because you’re increasing aldosterone, what happens to blood volume, preload, SV, CO, and BP?

A

increasing aldosterone increases blood volume.

increases preload

increases Stroke volume

increases CO

increases BP

26
Q

What does vasopressin do?

A

(ADH)

secreted in response to angiotensin II + atrial receptors (lower blood coming to the atria or higher amounts of blood) + (increased osmolarity of the blood)

acts at V1 receptors (smooth muscle) and V2 receptors (collecting ducts)

27
Q

What are Natriuretic peptides?

what is their function?

what does it cause?

A

sensing the levels of blood coming back to the blood.

Also BNP (brain) and C-type (CNP)

Atrial (ANP)… if we increase this secretion you’re trying to bring back balance. too much blood coming back so you’ll decrease everything to balance it all out.

It causes arteriolar dilation (decreases TPR), increases fluid loss (decreases preload), inhibits renin (decreases both TPR and preload)

it’s protecting against over dilation or overstitching of cardiac chambers

28
Q

What happens during a hemorrhage?

A

we lose a lot of blood volume

see a decrease in venous return, decrease in preload, stroke volume and CO decrease, and MAP decreases.

vascular function curve shifts left. –> activate responses to bring it back up.

Carotid sinus nerve firing lowers

heart rate, contractility, cardiac output increases

redistribute blood

increase TPR

Renin, angiotensin II, aldosterone, epinephrine, ADH up

29
Q

Atrial A fibers?

B fibers?

A

line up with the P wave… this is the atrial contraction

During ventricular contraction

30
Q

If I’m going to start an exercise, my initial response comes from what? what happens?

A

Brain.

Increased sympathetic output (B1 receptors) and DECREASED parasympathetic output

increased HR/contractility

Increased venous return

selective arteriolar vasoconstriction due to alpha 1 receptor activation (overall slight increase in MAP) –> constriction to skin, kidney, inactive muscle –> vasodilation of active muscle and coronary circulation due to release of lactate, K+ ions, and adenosine –> pulse pressure increases, SBP increases, DBP shouldn’t change

TPR deceases

31
Q

what happens when you’re standing for a long time?

A

if there’s no movement then venous return accumulates in lower limbs increasing venous and capillary hydrostatic pressure.

Venous pooling can result in edema and or hypotension

reflexes will attempt to bring BP back to normal

32
Q

With regards to MAP, what happens to changes in posture?

A

MAP lowers, no change in HR and TPR

SV and CO lower (from decreased venous return)

central venous pressure is lower (blood pools in lower extremities)

Compensatory: all above increases towards normal.

Baroreceptor reflex changes

Hormonal reflex will also be initiated but probably too slow to have an impact

orthostatic hypotension

CP2 (8 decks)

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