Phys Lecture 7, 8, 9: Regulation of BP Flashcards
What are the 4 rapidly responding system (for the control of BP)?
- baroreceptors
- chemoreceptors
- regulation of SV by atrial pressure
- cerebral ischemia induced pressure
Where are the baroreceptors in our body?
- aortic arch
2. bilaterally in the carotid arteries (carotid sinuses/at the split of the carotid into external and internal branches)
Where do the barocrecptors send their signals when BP rises?
glossopharyngeal N –> Vasomotor center of CNS
What is feedback gain? (defn and formula)
it defines the power that a particular mechanism has to resist changes in BP
Gain = correction / error (abnormality still remaining)
Baroreceptors provide info to the CNS about…
- MAP (counter increases in MAP)
- Pulse pressure (Psystolic - Pdiastolic)
- HR
**these are reported INDEPENDENTLY of e/o
What determines the activity of impulses from carotid baroreceptors?
rate of stretch/changes in stretch
-they fire more frequently as pressure increases
they are more sensitive to CHANGES in MAP than just an increase in MAP
T or F: baroreceptors counter decreases in MAP
F (increases)
In a study of an isolated carotid sinus, when the pressure in the carotid sinus decreases, the systemic arterial pressure (increases, decreases, or stays the same).
How is this possible?
increases
baroreceptor decreases nerve impulses to CNS –> CNS thinks BP is dropping so it activates sympathetic NS to elevate it –> TPR inc, CO inc –> systemic arterial pressure increases
An increase in pulse pressure will (inc, dec, or maintain) systemic arterial pressure.
How is this possible?
decrease arterial pressure
Inc PP –> para > symp activity –> dec systemic arterial pressure (MAP is held constant though)
Inc in HR will causes (inc, dec, or maintain) systemic arterial pressure.
How is this possible?
decrease
Para > sympathetic activity
If baroreceptors are nonfunctional MAP will (inc, decrease, stay the same)
Stay they same
**there will be more fluctuations in systemic arterial pressure (these changes will not be buffered) but the mean arterial pressure will be constant
T or F: baroreceptors can effectively manage changes in MAP that lasts for more than a day (i.e. chronic changes in MAP)
F: eventually the baroreceptors will reset to a new BP (they cannot control the system for longer than a day)
**baro receptors are NOT the ultimate regulator of BP
T or F: baroreceptors only increase BP
F: increase or decrese
What is the range of BP that baroreceptors are able to function?
50 to 200 mmHg
Summarize how barorecptors buffer an increase in MAP
- sense strech
- Inc firing rate to CNS
- vasomotor center increases vagus N firing rate (parasymp) and decreases cardiac symp firing rate which act on the heart to decrease HR and decrease contractility
- vasomotor center also acts on VSM to dec TPR (vasodilate) and increase unstressed volume
- decrease in CO and MAP
What effect does activation of baroreceptors (in response to increase in MAP) have on the cardiac function curve?
down and to the right (bc sympathetic activity decreases)
What is the chemoreceptor?
carotid sinus
What activates carotid sinus?
ONLY a decrease in MAP to below 80 mmHg
What is the carotid sinus sensitive to? (what is it actually sensing)
low O2 and/or high CO2
Activation of carotid sinus stimulates..and leads to (inc, dec MAP)
sympathetic AND parasympathetic activity BUT the sympathetic > parasympathetic activity
leads to inc in MAP (remember hypotension <80 mmHg activates it) due to inc TPR
What is the effect of an increase of afterload on SV?
decreased SV (or CO) to decrease BP
T or F: There are more mechanisms in place to buffer decreases in BP than increases in BP.
Explain why this wou;d be T/F
True: bc there are more clinical manifestations at low BP than high BP (~worse to have drop in BP)
Cerebral ischemia response is activated when MAP drops below ____ mmHg. It activates ________ response.
60 mmHg
both symp and para but sympathetic prevails
What is the cushing reaction?
related to cerebral ischemia response
*inc CSF/intracranial pressure –> inc resistance of cerebral arteries –> induces cerebral ischemia response
TPR then is increased to inc P –> restore Q to brain
How is the cushing reaction treated?
not by fixing the arterial HTN! need to fix the hypotension in the brain… the inc in MAP is the compensatory response and is what is maintained Q to brain = if you “fix” this you will hurt the patient
What is the effect of hypervolemia on atrial pressure and CO?
hypervolemia causes an increase in atrial pressure and CO
atrial pressure =
CO x TPR
Describe the effect of inc in arterial pressure via stretch receptors and efferent renal reflex activity
- inc plasma volume
- increases filling pressure which increases arterial pressure via inc CO
- increased filling pressure also increases atrial pressure
- decreased renal sympathetic output –> inc fluid output –> dec plasma volume and arterial pressure
- decreased vasopressin –> inc fluid output –> dec plasma volume and arterial pressure
What are the systems that respons to change in BP less rapidly (1 to 30 mins) (5):
- lpw pressure receptor mediated reflex mechanisms (stretch receptors)
- ANP
- Capillary fluid transfer
- vascular stress relaxation
- renin-angio-aldo sys
Describe how ANP regulates arterial pressure in response to an inc in MAP
- inc PV –> inc filling pressure –> inc arterial pressure via inc CO
- inc atrial stretch
- release of ANP
- inc renal fluid output (and vasodilates/dec TPR)
- dec plasma volume and arterial pressure
Describe the regulation of arterial pressure (in response to an inc in MAP) via capillary filtration
- inc plasma volume
- inc ATRIAL pressure and venous pressure
- inc capillary pressure (HPc)
- inc capillary filtration (fluid into ISF)
- dec blood volume and dec arterial pressure
- inc plasma volume
- inc ARTERIAL pressure
- dec sympathetic activity
- dec TPR
- inc flow into capillaries
- inc capillary pressure
- inc capillary filtration (fluid into ISF)
- dec BV and arterial pressure
hiding volume in ISF
What happens to the veins when they are stretched?
they enlarge/relax
= “stress relaxation”
What happens to CO when veins are stretched?
decreases
Describe the effect of stretch relaxation to regulate MAP
- inc plasma volume
- inc venous pressure
- in stress relaxation
- in unstressed volume
- dec filling pressure
- dec CO
- dec MAP
Describe the effect of the renin-angiotensin system on MAP via blood vessels
- dec arterial pressure
- inc renin releasse
- angiotensinogen (liver) converted to angiotensin I –> angiotensin II (lung) –>
- inc TPR -> inc filling pressure
- inc CO
- inc MAP
Describe the effect of the renin-angiotensin system on MAP via effect of aldo on kidneys
- dec MAP
- renin released
- aldo released
- dec renal fluid output
- inc blood volume
- inc MAP
What are the rapid and slow ways blood volume is regulated?
rapid: capillary pressure/fluid transfer
slow: renal output, GI output, thirst
What evidence do we have that the kidney’s are important to regulation of blood volume
renal cross transplantation studies:
put kidney from HTN rat into normal rat –> rat became HTN
put kidney from normotensive rat into HTN rate –> rat became normotensive
What is the renal function curve?
fluid output (y) vs arterial pressure (x)
The renal function curve show that at MAP increases, kidney output (inc, dec, stays the same)
increases
What determines the long term/steady state MAP?
fluid intake line (aka how much water person drinks) point of intersection with the renal function curve
What happens to MAP/fluid intake line when a person eats a lot of salt?
the fluid intake lime rises/MAP rises
Why is the renal function curve very steep?
increasing salt/fluid intake will not inc MAP (very much) (in health, for most people)
Why would the renal function curve move to the right?
person becomes HTNsive!
- angiotensin II
- aldo
- sympathetic activity
- vasopressin
- renal disease
- obesity
Describe how the kidney adjusts to a shift in the renal function curve moving to the right (person becoming HTNsive)
- shift to right/inc MAP
- fluid output decreases (fluid intake > output)
- inc blood volume
- inc filling pressure
- inc zCO
- arterial pressure rises until fluid intake = output
What would shift the renal function curve to the left?
ANF, NO, some PGs
decrease in angio II, aldo, vasopressin, symp activity, renal disease, obesity
How is a salt sensitive renal curve different than a normal renal curve?
decreased slope = inc salt intake will have a more noticeable/bigger increase in MAP
How does the renal function curve change with disease and age?
to the right and starts leaning/dec slope
–> become HTNsive and more sensitive to salt
How does shifting renal function curve to the right (inc MAP), affect TPR and CO?
inc CO –> inc TPR* –> dec CO (to normal)
*inc CO -> inc organ perfusion/Q -> vessels constrict to correct perfusion/Q
T or F: Changes in TPR cause equal and opposite changes in CO but have NO effect on arterial pressure
T: MAP = CO x TPR
What is the difference between acute and chronic changes in blood vessels to increase TPR?
acute: change in tone and reactivity
chronic: hypertrophy, angiogenesis, rarefaction
What is the most rapid response to regulate a change in arterial pressure?
baroreceptors > chemoreceptors > CNS ischemic response > stress relaxation
What mechanism of MAP regulation has the highest gain?
renal-blood volume pressure control (gain is INFINITE!!!) bc it will always adjust MAP to set point/steady state
