Regulation of Arterial Pressure Flashcards
What is Mean Arterial Pressure equation?
what’s normal?
how is it regulated?
CO x TPR = ( HR x SV ) x TPR
normally its 93.3 round up to 100 or something
baroreceptor
hormonally
What does the detector of the baroreceptor detect?
what happens after it detects something?
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
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?
Glossopharyngeal nerve (10) Sinus nerve of Hering
Vagus Nerve (9) Aortic Nerve
nucleus tractus solitarius (NTS)
What are the detectors of the baroreceptor reflex (2 of them)?
Chemoreceptors that respond to PO2, PCO2, pH
Mechanoreceptors that respond to the stretch.
What if we have an increase of the stretch?
what if the pressure falls?
increasing the firing rate of the nerve that connects the receptor to the NTS.
decrease the firing rate.
What is the cardioinhibitory area?
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!
What is the control center of the baroreceptor reflex?
how does this act on an increase in firing?
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.
how would this work if we have a decrease in firing? (for the baroreceptor reflex)
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.
What is TPR dependent on?
sympathetic stimulation of the arterioles
what is Stroke volume dependent on?
sympathetic stimulation of the heart
Preload
What is HR dependent on?
sympathetic and parasympathetic stimulation
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?
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
Sympathetic:
Baroreceptor firing?
Influence and mediation?
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
Parasympathetic:
Baroreceptor firing
Influence and mediation?
increased baroreceptor firing
decreased HR (M2/M3)
Vagus nerve signal to AV
indirect vasodilation on blood vessels by NO
Decrease in Mean Arterial Pressure leads to what baroreceptor firing?
what is the result?
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
Increase MAP will result in what?
increased baroreceptor
Decreased SNS activity, increased PSNS activity
Changes in TPR + CO
closing the loop
decreasing it back down!
What does hypertension do to MAP?
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.
What is the RAAS system?
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.
Of the RAAS, what is the order of what is produced?
Angiotensin
then Angiotensin 2 and then aldosterone around the same time but Angiotensin 2 is a bit earlier
What is Renin?
secreted by the kidney to the bloodstream due to a decrease in BP
if BP goes higher than normal then less renin is secreted
what is the secretion of renin stimulated by?
B1 adrenergic receptors on the kidney
What does renin do?
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
What cells are secreting renin?
juxtaglomerular cells
What does angiotensin 2 do? (3 things)
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
Because you’re increasing aldosterone, what happens to blood volume, preload, SV, CO, and BP?
increasing aldosterone increases blood volume.
increases preload
increases Stroke volume
increases CO
increases BP
What does vasopressin do?
(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)
What are Natriuretic peptides?
what is their function?
what does it cause?
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
What happens during a hemorrhage?
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
Atrial A fibers?
B fibers?
line up with the P wave… this is the atrial contraction
During ventricular contraction
If I’m going to start an exercise, my initial response comes from what? what happens?
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
what happens when you’re standing for a long time?
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
With regards to MAP, what happens to changes in posture?
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
