physiology

2. By
Dr Ahmed El_Sayed Said
Nour Eden
Lecturer of Physiology Department
Faculty of Medicine Al Azhar
University(Assiut)
PHSIOLOGY OF THE
CARDIOVASCULAR
SYSTEM (CVS)

3. Arterial blood
pressure (ABP)

4. Definitions:
Blood pressure is the force exerted by the blood against a vessel wall.
- The maximum pressure exerted in the arteries when blood is ejected into them during systole, the
systolic pressure, averages 120 mm Hg.
- The minimum pressure within the arteries when blood is draining off into the rest of the vessels during
diastole, the diastolic pressure, averages 80 mm Hg.
- Although ventricular pressure falls to 0 mm Hg during diastole, arterial pressure does not fall to 0 mm
Hg, because the next cardiac contraction occurs and refills the arteries before all the blood drains off.
Mean arterial pressure:
It is defined as the average arterial pressure during a single cardiac cycle.
Mean arterial pressure = (diastolic pressure + 1/3 pulse pressure.)
Pulse pressure: is the difference between the systolic and diastolic pressure readings

5. Functions of the Arterial Blood Pressure:
1. It maintains tissue perfusion {i.e. blood flow) throughout various
tissues, including those lying above the heart level {in spite of the
force of gravity).
2. It produces the capillary hydrostatic pressure, which is the main
force concerned with tissue fluid formation.
3. The diastolic BP performs the following functions:
1) It maintains blood flow to the tissues during ventricular diastole.
2) It is essential for the normal coronary blood flow.
3) It prevents blood stasis in the arteries during ventricular diastole

6. Physiological Variations in Arterial BP
1. Body region: The arterial BP is normally higher in the lower limbs than in the upper
limbs.
2. Age: The arterial BP is very low at birth {about 70/40 mmHg) then it rises
progressively till about 120/80 mmHg at the age of 20 years. Its rise continues
gradually after that age, but its rate increases markedly after the age of 40 years due to
the normal gradual loss of arterial elasticity, so that it becomes normally about
150/90 mmHg after the age of 60 years. ABP is 90/60 mmHg in one year old children
and 100/70mmHg in 5 years old children
3. Sex: ABP is slightly higher in adult males (byl0%) than females. However, it becomes
slightly higher in females after menopause.
4. Body built: The arterial BP is usually high in obese persons,

7. Physiological Variations in Arterial BP
6- Meals: ABP increases slightly after meals due to vasodilatation (VD) in the
splanchnic area—* f VR—*■ f COP —> systolic BP.
7- Exercise: ABP increases during exercise, especially the systolic BP due to
sympathetic activity and VR then returns to normal due to VD.
8- Diurnal variation: ABP is normally lowest in the early morning and highest
in the afternoon.
9- Sleep: ABP decreases during quite sleep due to decreased sympathetic
activity, and increases during night mares.
10- Emotions: The systolic BP increases in most emotions due to increased
sympathetic stimulation. However, in certain emotions, V.D and hypotension
occur.

8. Physiological Variations in Arterial BP
11- Temperature: In hot environments, the systolic pressure is not or slightly
increased, but the diastolic pressure decreases due to cutaneous (V. D.) On
exposure to cold, both the systolic and diastolic pressures increase due to
cutaneous vasoconstriction (V. C).
12- Position: ABP is more in recumbent position than sitting which is more
than standing.
13- Gravity: On standing, the force of gravity increases the mean arterial
pressure below a reference point in the heart {in the right atrium near the
tricuspid valve} and decreases it above that point.
14- Respiration: ABP shows rhythmic fluctuation during the respiratory cycle.
It is decreased during inspiration.

9. gulation of the arterial blood pressu

10. Regulation of the arterial blood pressure
Mean arterial blood pressure is the main driving force for propelling blood to
the tissues. This pressure must be closely regulated for two reasons:
1. It must be high enough to ensure sufficient driving pressure.
Without this pressure, the brain and other tissues will not
receive adequate flow.
2. The pressure must not be so high that it creates extra work for
the heart and increases the risk of vascular damage and
possible rupture of small blood vessels.
Various mechanisms involving the integrated action of various components of
circulatory system and other body systems are vital in regulation of the mean
arterial pressure.

11. Regulation of the arterial blood pressure
1.Rapidly acting mechanism:
A.Baroreceptor feedback mechanism
B. Chemoreceptor mechanism
C. Central nervous system ischemic mechanism

12. 1. Ultra rapid Neural Control:
 It is characterized by its rapidity of response. It begins within seconds and often increasing the pressure to
two times normal within 5-15 seconds.
 Neural control of blood pressure is directed primarily at two main goals:
{1} they alter blood distribution to respond to specific demands. For example, during exercise blood
is shunted temporarily from the digestive organs to the skeletal muscles.
{2} they maintain adequate MAP by altering blood vessel diameter. Under conditions of low blood
volume, all vessels except those supplying the heart and brain are constricted to allow as much blood
as possible to flow to those vital organs.
 Most neural control operates via reflex arcs the center of which is the vasomotor center.
 Vasomotor activity is modified by inputs from
 {1} baroreceptors
 {2} chemoreceptors
 {3} higher brain centers {hypothalamus and cerebrum}, as well as by certain hormones and other blood- borne chemicals.

13. Baroreceptor Reflex
• Baroreceptors are the most important receptors involved in moment to moment regulation of
arterial blood pressure.
• They are located not only in the carotid sinuses and aortic arch but also in the wall of nearly
every large {elastic} artery of the neck and thorax.
• They are mechanoreceptors, sensitive to changes -in both mean arterial blood pressure and
pulse pressure.
• Baroreceptors continuously generate action potential in response to ongoing pressure within
the arteries.
• If for any reason the arterial pressure {either mean or pulse pressure} becomes elevated above
normal, the carotid sinus and aortic arch baroreceptors increase the rate of discharge in their
respective afferent neurons to vasomotor center leading to its inhibition resulting in:

14. Baroreceptor Reflex
1. Inhibition of vasomotor center resulting in:
a) Vasodilatation of the arterioles decreasing peripheral resistance.
b) Venodilatation shifting blood to venous reservoirs, causing a decline in venous return and
cardiac output.
2. Stimulation of the cardioinhibitory center resulting in:
a) Reducing the heart rate
b) Decreasing the contractile force and the cardiac output.
Therefore excitation of the baroreceptors by pressure in the arteries reflexly causes the arterial pressure
to decrease because of both a decrease in peripheral resistance and cardiac output.
Conversely, a decline in mean arterial pressure initiates reflex vasoconstriction and increases cardiac
output, causing blood pressure to rise. Thus, baroreceptors are called the pressure buffer system.

17. B. Chemoreceptor Reflex
• When the oxygen content or pH of the blood drops sharply or carbon dioxide levels
rise, chemoreceptors transmit impulses to the vasomotor center, and reflex
vasoconstriction occurs.
• The rise in blood pressure that follows speeds the return of blood to the heart and
lungs.
• The most prominent of these receptors are the carotid and aortic bodies located
close to the baroreceptors in the carotid sinus and aortic arch.
• They are more important in regulating respiratory rate and depth than in blood
pressure regulation {for more details see respiratory system chapter V.

19. Central Nervous System Ischemic
Response
• When blood flow to vasomotor center in the lower brain stem becomes decreased
enough(down to 60 and below) to cause nutritional deficiency i.e. to cause cerebral
ischemia, the neurons in the vasomotor center itself respond directly to ischemia
and become strongly excited and the systemic arterial blood pressure rises.
• This occurs because failure of the slowly flowing blood to carry CO2 away from
vasomotor center causing increase in local concentration of CO2 stimulating the
vasomotor center which stimulates the sympathetic nervous system causing
vasoconstriction and increased ABP.
• Other factors such as building of lactic acid and other acidic substances, also
contribute to marked stimulation of the vasomotor center and elevation of ABP.

20. CNS Ischemic Response
Severe decrease blood flow to brain
↓
Cerebral hypoxia
↓
Vasomotor center stimulated – causes powerful
Vasoconstriction
( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine)
Increase blood pressure & blood flow↓

21. Rapid {Hormonal} Control
1. Adrenal Medulla Hormones:
 During periods of stress, the adrenal gland releases norepinephrine {NE} and epinephrine into the blood, and both
enhance the sympathetic response.
 NE has a vasoconstrictive action.
 Epinephrine increases cardiac output and promotes generalized vasoconstriction {except in skeletal and cardiac
muscles, where it generally causes vasodilatation}.
 It is interesting to note that nicotine, an important chemical in tobacco and one of the strongest toxins known,
mimics the effects of catecholamines. It causes intense vasoconstriction not only by directly stimulating
postganglionic sympathetic neurons but also by promoting release of large amount of epinephrine and NE
2. Antidiuretic Hormone {ADH, Vasopressin}:
• Antidiuretic hormone is produced by the hypothalamus and stimulates the kidneys to conserve water. ADH is not
usually important in short-term blood pressure regulation. However, when blood pressure falls to dangerously low
levels (as during severe hemorrhage}; much more ADH is released and helps to restore arterial pressure by causing
intense vasoconstriction.

22. Regulation of the arterial blood
pressure
2. Intermediate acting mechanism:
A.Renin angiotensin vasoconstrictor mechanism
B.Stress relaxation of vasculature
C.Fluid shift across the capillary for adjustment of blood
volume

23. Intermediate acting mechanism
•Several pressure control mechanisms exhibit significant responses only after a few minutes following an acute arterial pressure
change.
1- Stress-Relaxation Mechanism:
 When the pressure in the blood vessels becomes too high, they become stretched, and they keep on stretching more and more for
minutes or hours; as a result, the pressure in the vessels falls toward normal.
 Reverse Stress Relaxation: When the pressure in the blood vessel decreases, the pressure on the vessel wall decreases. The
vessel wall gradually contracts increasing the intravascular pressure to normal.
2- The Capillary Fluid Shift Mechanism:
 Any time the capillary pressure falls too low, fluid is absorbed by osmosis from the tissues, into the circulation, thus building up
the blood volume and increasing the pressure in the circulation.
 Conversely, when the capillary pressure rises too high, fluid is lost out of the circulation into the tissues, thus reducing the blood
volume and also all the pressures throughout the circulation.
3- Renin-Angiotensin Vasoconstrictor System Mechanism:
 Angiotensin II is generated in response to renin release by the kidneys when renal perfusion is inadequate due to decreased ABP. It
causes intense vasoconstriction, promoting a rapid rise in systemic blood pressure. It also stimulates release of aldosterone and
ADH, which act in long-term regulation of blood pressure by enhancing blood volume as described shortly afterwards

24. Intermediate acting mechanism
3- Atrial Mechanisms{Atrial volume reflex}
 Both the atria have stretch receptors [type B] in their walls similar to baroreceptor stretch receptors of the large
systemic arteries. These low pressure receptors play an important role to minimize ABP changes in response to
change in blood volume as the following:
• An Increase in the blood volume stimulates the low pressure receptors [or volume receptors] in the atria causing:
a. Reflex dilatation of the afferent arterioles in the kidneys as well as the other peripheral arterioles but is usually potent in the
kidneys Decrease afferent arteriolar resistance causing the glomerular capillary pressure to rise with resultant increase in
filtration of fluid into kidney tubules.
b. Signals are transmitted simultaneously to the hypothalamus to decrease the secretion of antidiuretic hormone, thereby
indirectly affect kidney function by diminishing reabsorption of water from the tubules.
These two effects cause rapid loss of fluid into urine serving as a powerful mechanism to return the blood volume toward
normal.
4- Atrial Natriuretic Peptide {ANP}:
• The atria of the heart produce, as a result of stretch of their walls, a peptide hormone called atrial natriuretic
peptide, which causes blood volume and blood pressure to decline, ANP antagonizes aldosterone and stimulates the
kidneys to excrete more sodium and water from the body, causing blood volume to drop. It also causes a generalized
vasodilatation.

25. Regulation of the arterial blood
pressure
3. Long term mechanism:
A. Renal blood volume pressure control mechanism

26. Long-term Mechanisms {Renal
Regulation} Although the baroreceptors respond to short-term changes in blood pressure, they quickly adapt to
prolonged or chronic episodes of high or low pressure. This is where the kidneys step in to restore and
maintain blood pressure homeostasis by regulating blood volume through modifying salt and water
excretion. Although blood volume varies with age and sex, renal mechanisms usually maintain it at close
to 5 L.
 The kidneys act both directly and indirectly to regulate arterial pressure and provide the major long-term
mechanism of blood pressure control
1. The Direct Mechanism:
 It alters blood volume. When blood volume or blood pressure rises, the rate at which fluid filters from the
blood stream into the kidney tubules is speeded up. In such situations, the kidneys are unable to process
the filtrate rapidly enough, and more of this fluid leaves the body in urine. As a result, blood volume and
blood pressure fall.
 Conversely, when blood pressure or blood volume is low, water is conserved and returned to the blood
stream and blood pressure rises.
 Thus as blood volume goes, so goes the arterial blood pressure.

27. Long-term Mechanisms {Renal
Regulation}2. The Indirect Renal Mechanism:
• It involves the renin angiotensin mechanism. When arterial blood pressure declines, special cells {juxtaglumerular cells} in
the kidneys release the enzyme renin into the blood.
• Renin triggers a series of enzymatic reactions: Angiotensinogen from the liver is converted by renin into aingiotensin I which
is converted by angiotensin converting enzyme from the lungs into angiotensin II that has the following functions:
1. It is a potent vasoconstrictor which, by promoting an increase in systemic blood pressure, increases the rate of blood delivery
to the kidneys and renal perfusion.
2. It also stimulates the adrenal cortex to secrete aldosterone, a hormone that enhances renal reabsorption of sodium.
3. It stimulates the posterior pituitary to release antidiuretic hormone {ADH}, which promotes more water reabsorption. As
sodium moves into the blood stream, water follows; thus, both blood volume and blood pressure rise.
4. It stimulates the adrenal medulla to secrete norepinephrine which is a vasoconstrictor substance.
5. It acts directly on the kidneys to decrease salt and water excretion increasing the blood volume with subsequent increased
ABP.
• It stimulates thirst sensation by acting on the subfornical organ. This increaseswater intake leading to increased blood volume
and blood pressure.