Blood Pressure I, II, III Flashcards
Would you expect pulse pressure to be higher in the aorta or in muscular arteries?
• what about mean arterial pressure?
- PULSE pressure is higher in MUSCULAR ARTERIES - because they have less compliance (they don’t give as much as the Elastic Aorta)
- HOWERVER, MEAN ARTERIAL PRESSURE is HIGHER in the AORTA because the sum of the lumen sizes of aortic branches is larger than the aorta itself
What is the main difference between rapid responding systems to arterial pressure and slower responding systems?
RAPID RESPONSE:
• these are mostly buffered changes, no levels are being reset, the system is just trying to COMPENSATE
SLOW RESPONSE:
• Set LEVELS or pressure
Differentiate between specific timing of Rapidly Responding, Less Rapidly Responding, and Slowly Responding systems.
Rapid - 5 second to 1 minute:
• mostly buffer changes
Less Rapid - 1 minute - 30 mintues:
• Buffer changes AND set leves
Slow - days to months:
• Set long-term levels and pressures
What are the 4 Rapidly Responding Systems?
- BARORECEPTORS
- CHEMORECEPTORS
- STROKE VOLUME REGULATION BY AFTERLOAD
- CEREBRAL ISHEMIA-INDUCED RESPONSE
Where are the Baroreceptors that control arterial pressure located?
• what path do they take to get there?
- Carotid SinuS => Hering’s nerve => Glossopharyngeal (IX) => CNS
- Aortic Baroreceptors => Vagus Nerve (XI) => CNS
Where is the chemoreceptor that controls arterial pressure located?
• Carotid BO2dy
What nerve mediates vasocontriction and cardiac acceleration?
• what mediates cardiac deceleration?
- Acceleration/Vasoconstriction - Sympathetic nn.
* Decceleration - Vagus n.
What parts make up the sensor and effector in the body system that measures arterial PRESSURE?
- Pressure - measured by BARORECEPTORS
* Effector - Nucleus Tractus Solitarius in Medulla
What measure is used to tell us at how good a system is a compensating for changes in arterial pressure (or anything)?
• formula?
GAIN = Correction of Error Signal/Error Still remaining
e.g. increased in 10mmHg in BP, body compensates by decreasing this value by 1mmHg. Gain = 1/9
What information do Baroreceptors Provide to the CNS?
- Mean Arterial Pressure
- Pulse Pressure
- Heart Rate
WHEN does the Baroreceptor measure pressure?
• how does increasing mean arterial pressure affect this?
- Measures during the ASCENDING portion of the pressure profile not the TOP (unless…)
- At HIGH mean arterial pressures baroreceptors will start firing more and more (signal going to the tractus solitarius in the CNS)
What happens when the carotid sinus senses a loss in blood pressure?
• Heart
• Veins
• Arteries
SYMPATHETIC RESPONSE IS LAUNCHED
Heart:
• Increased Inotropy (strength of contraction)
• Increased Chronotropy (heart rate)
Veins:
• Constricted by Sympathetic Tone (less compliance)
Arterioles:
• RESISTANCE arterioles constrict
What accounts for the sensitivity of Baroreceptors to compensate for changes in blood pressure, pulse pressure, and heart rate?
The “Set point” or NORMAL value for the baroreceptor lies on the center of the steepest part of the SYSTEMIC ARTERIAL PRESSURE vs. ISOLATED CAROTID SINUS PRESSURE graph
this means that the sensitivity of the system is greatest when the system is experiences changes away from the norm
T or F: PULSE pressure in the carotid sinus is regulated INDEPENDENTLY of the MEAN pressure.
True, at a constant mean pressure it can be shown that changes in the pulse pressure will influence SYSTEMIC arterial pressure
How does the baroreceptor respond to changes in heart rate?
An action potential is felt in the Baroreceptor with each heartbeat
- with more action potentials being felt by the NTS (tractus solitarius) the more it will DECREASE sympathetic activity
What role do Baroreceptors play in setting the mean arterial pressure?
NO role in SETTING the mean Arterial Pressure
Main Role is Controlling Variability
Suppose Mean Arterial Pressure is consistently 200 mmHg for 15 hours. Will your Baroreceptor correct this back to normal?
NO, it will reset after a long period and think that 200 mmHg is the new norm
So it does us no good at fixing chronically altered Hypertension
What is the relationship between diastolic pressure and sympathetic activity stimulated by the baroreceptor?
• at LOWER THAN NORMAL diastolic pressures Sympathetic activity will be INCREASE (to try to get BP back up in the normal range)
What is the range of the Carotid Baroreceptor?
• is this greater or less than the Aortic Baroreceptor?
Functional at 50mmHg to 200mmHg
• Aortic has a slightly smaller range
What is a MAJOR difference in the way that chemoreceptors and Baroreceptors Respond to Sympathetic activity?
Chemoreceptors can stimulate BOTH sympathetic AND parasympathetic activity SIMULTANEOUSLY
What is the net affect of chemoreceptors, how does this differ from Baroreceptors?
- Chemoreceptors: ONLY detect HYPOtension
* Baroreceptors will detect hyper- or hypotension.
If both sympathetic and parasympathetic activity kick in simultaneously in Chemoreception, then how can the body ever leave the hypotensive state?
SYMPATHETIC activity overrides the Parasympathetic activity
When do chemodetectors kick in?
• what are they looking for?
Kick in:
• Mean Arterial Pressure below 80mmHg activates Chemoreceptors
What:
• look for Decreased O2
• Increased CO2
What is the effect of increased afterload on cardiac output?
note: this is what happens during the SHORT TERM response where Arterial Pressure is increased
Increased Afterload causes DECREASED cardiac output because the AORTIC valve is open for less time because it doesn’t open until later in systole
What is the CEREBRAL ISCHEMIA INDUCED RESPONSE?
• When arterial pressure gets below 60mmHg BOTH SYMPATHETIC AND PARASYMPATHETIC systems are discharged simultaneously with the Sympathetic system being the predominant force
***Presents like the Cushing Reaction??
What is the CUSHING REACTION?
Overall this is a response to ISCHEMIA
- Increased Intracranial pressure (too much CSF) compresses CEREBRAL RESISTANCE ARTERIES
- Increased Arterial Pressure is induced to COUNTERACT the decreased blood flow caused by increased intracranial pressure
PRESENTS AS HYPERTENSION COMBINED WITH BRADYCARDIA*
What are the 4 rapidly responding systems to changes in blood pressure?
- Baroreceptors
- Chemoreceptors
- Regulation of Stroke Volume by Arterial Pressure
- Cerebran Ischemia-Induced Response
What are the 5 LESS rapidly responding systems to changes in Blood Pressure?
- Low Pressure Receptor-Mediated Reflex Mechanisms
- Atrial Natriuretic Factor
- Capillary Fluid Transfer
- Vascular Stress Relaxation
- Renin-Angiotensin-Aldosterone System
How does the Pressure Receptor-Mediated Reflex Mechanism work?
• aka what are all the downstream effects
Remember this all happens in 1-30 minutes
- Increased Plasma Volume => Increased FILLING PRESSURE
- Increased filling pressure leads to:
a. INCREASED Arterial pressure via increased CO
b. Increased ARTIAL pressure
(I) DECREASED Sympathetic stimulation
(II) DECREASED vasopressin
(III) INCREASED FLUID OUTPUT => volume correction
How does Regulation of Arterial pressure via Release of Atrial Natriuretic Peptide (ANP) work?
- Increased Plasma Volume
- Increased Filling Pressure
a. Aterial Pressure via Increased CO
b. Increased ATRIAL stretch
(I) INCREASED Release of ANP
(II) Increased Renal Fluid Output
(III) DECREASED plasma volume
How does Regulation of Arterial pressure via Capillary filtration work?
- Several Step but MAIN IDEA is increased plasma volume will lead to increased hydrostatic pressure in the capillaries
- Increased hydrostatic pressure tends to push fluid into the periphery correcting for the gain in plasma volume
What is the effect of increasing lumen size in veins in order to reduce blood pressure?
• You will get a DECREASE in ATRIAL pressure which will lead to a decrease in Cardiac Output
What is Vascular Stress Relaxation?
• when stretched venous smooth muscle cells have the capacity to relax
How does Regulation of Arterial Pressure via Stress Relaxation work?
- Increased Plasma Volume
a. **Increased Arterial Pressure
b. Increased Venous Pressure
(I) Increased Venous Pressure
(II) Increased Stress Relaxation
(III) Increased Unstressed Volume (Bigger veins)
(IV) Decreased Cardiac output
(V) **DEcreased ARTERIAL pressure
How does Renin system work on blood vessels?
- Decreased Arterial Pressure
- Increased Renin (peptidase)
(I) Angiotensinogen => Angiotensin I
(II) Angiotensin I => Angiotensin II (via Angiotensin Converting Enzyme ACE)
(III) Arteriolar and Venous constriction
(IV) Increased TPR and Filling pressure
(V) INCREASED CARDIAC OUTPUT (TPR)
What is the net effect of the renin system kicking in?
• You raise Arterial Pressure by raising TPR and FIlling Pressure which allows for greater CO
Besides acting alone on blood vessels to vasoconstrict, what can angiotensin also do?
• Stimuate Aldosterone Release from Adrenal which DECREASES URINE output leading to an INCREASE in blood volume
What does a Renal Function Curve graph?
Renal Fluid Output as a Function of Arterial Pressure
T or F: the renal function curve should have a very steep slope.
True, this means the VERY small changes in arterial pressure should cause HUGE changes in Renal Fluid output
What is determined by the intersection of the renal curve with the fluid intake line?
• Steady State Arterial Pressure is DEFINED by the point of intersection of the Renal Curve with the Fluid Intake line (horizontal)
**This is similar to determining Cardiac Output by looking at the intersection of the Cardiac and Venous Function lines
What happens if your fluid output is greater than your fluid intake on the renal curve?
• what if your input exceeds your output?
• you will become Hypovolemic
- Decreased Filling Pressure (left shift of Venous Func.)
- Decreased Cardiac output
• You become Hypervolemic
- Increased Filling Pressure (right shift on Venous Func)
- Increased Cardiac output
What are some factors that would cause your renal curve to shift to the right?
ANYTHING THAT INCREASES BLOOD PRESSURE • Angiotensin II • Aldosterone • Sympathetic Activity • Vasopressin • Renal Disease • Obestity
What are some factors that would cause your renal curve to shift to the left?
ANYTHING THAT DECREASES BLOOD PRESSURE • ANP • Nitric Oxide • Some Prostaglandins • Diuretics • Beta Blockers
T or F: increased salt leads to decreased fluid intake via thrist control mechanisms in the CNS.
FALSE, more salt = more fluid intake, this is governed via thirst control in the CNS
What does the renal curve look like for someone that gets Hypertensive from eating a lot of salt?
• It is SHALLOW, this means that as you move up on the fluid intake y-axis (controlled by Na+ intake) you will move higher up on the arterial pressure x-axis
What happens to the renal curve in disease and as we age?
- SHIFTS RIGHT (higher arterial pressure)
* Becomes more SHALLOW (salt sensitive)
In the experiment performed on rats in which the kidney was removed, the initial responses were as follows: • Increased Extracellular Fluid Volume • Increased CO • Increased Arterial Pressure • Decreased TPR
Increased Extracellular Fluid Volume
• Increased hydrostatic pressure pushes fluid to the periphery
Increased CO
• More Fluid in = More Fluid out (Frank-Sterling: the increased stretch will promote increased output)
Increased Arterial Pressure
• More Volume in the Cardiovascular System = Increased Pressure
Decreased TPR
• BARORECEPTORS in the Carotid Sinus respond by DECREASING SYMPATHETIC activity
In the experiment performed on rats in which the kidney was removed, the final responses were as follows: • Decreased Extracellular Fluid Volume • Decreased CO • Increased Arterial Pressure • Increased TPR
WHOLE BODY AUTOREGULATION HAPPENED
Decreased Extracellular Fluid
Decreased CO
• the end SYSTOLIC pressure will be increased (from autoreg.) causing increased SV and (SV x HR = CO)
Increased Arterial Pressure:
• caused by INCREASED TPR not c.o.
Increased TPR:
• Body’s response to Long Term increased fluid volume
What is whole body autoregulation?
• Increased Organ Perfusion Rate caused an Autoregulatory Increase of organ vascular resistance
THUS -
TOTAL FLOW is REDUCED = less cardiac output
Increased Vascular Resistance = Increased TPR
T or F: elevated pressure necessarily predicts the actual underlying hemodynamic situation that results in a particular pressure.
FALSE, ARTERIAL PRESSURE ∆P = TPR x CO, so any combination of changes in these two variable can lead to a particular ∆P
*This explains the intitial and final responses in the Rat Experiment
• Intiatially CO was increased and TPR was decreased but ∆P was elevated
• Later TPR was increased thus CO was decreased but ∆P was STILL elevate
The value of ∆P tells us nothing about the underlying cause
**How do you calculate Mean Arterial Pressure?
2 formulas
MAP = [Systolic P + 2(diastolic P)] / 3
MAP = (Pulse Pressure/3) + Diastolic P
**How do you calculate pulse pressure?
• Pulse Pressure = Systolic - Diastolic
Why does it just make sense the that the Mean Arterial Pressure Should be greater in the Aorta than in the in Peripheral arteries (i.e. femoral artery)?
Pressure must move outward to the periphery, if pressure where are in a more peripheral vessel then you would get retrograde flow
What physically are the baroreceptors in the kidney detecting?
• Detect Stretch via Stretch Calcium Receptors
What parasympathetic nerves control vascular tone?
• Vascular tone is controlled mostly by SYMPATHETIC nerves NOT parasympathetic.
What increases the FREQUENCY of action potentials created by baroreceptors?
• The RATE of arterial pressure increase in the aortic and carotid sinsus baroreceptors
Suppose you increase pressure slightly in the carotid sinus, what do you expect systemic pressure to do?
• Systemic pressure will likely drop substantially to compensate for the increase
How would you expect the autonomic response to changes in pressure if the aorta became less elastic?
Less Elastic Aorta = HIGHER PULSE PRESSURE
• Higher Pulse Pressure
• BARORECEPTORS will respond by causing a temorporary reduction in BP
T or F: People with chronic hypertension will stimulate their baroreceptors less often even if their blood pressure drops below what is normal for them.
False, they adjust to long term changes in vascular pressure so if they drop at a level below their normal hypertensive levels, you will see increased baroreceptor firing
How does regulation of stroke volume by arterial pressure (one of the four quick response mechs) work?
- Increased AFTERLOAD means the heart will have to increase PRESSURE work causing a Reduction in volume work
- LESS volume work means SMALLER stroke volume = Less Cardiac Output
- This is not that Big of An effect
What is the general trend in our body’s corrective mechanisms for changes in blood pressure?
• there are more systems that are responsible for counteracting HYPOtension than Hypertension
**Because not getting volume to your organs is much more deadly
In what type of pathological process might you see the Cushing Reaction?
- People who have had a stroke
* More Resistance through vessels causes more Sympathetic Stimulation because of Ischemia
What is the relative time of effect for angiotensin II acting alone compared when it activates aldosterone?
• Angiotensin II can only act for a fairly short time but it can go stimulate release of Aldosterone leading to increased fluid retention that is longer term in its effect
What organ is the most important physiological regulator of blood volume?
• Speed?
The kidney - adjustment of blood volume via changes in kidney function is a fairly SLOW process compared to correction of blood volume by pushing fluid into interstitial spaces
What is the significance of healthy Renal Function Curves being steep?
Steeper Curves mean your kidney has better control over fluid levels because you will only get SLIGHT INCREASES in ARTERIAL pressure with HUGE increases in FLUID intake