ARTERIAL BLOOD PRESSURE

ARTERIAL BLOOD
PRESSURE
 ARTERIAL BLOOD PRESSURE
l Definition:
This is the lateral pressure exerted by the
blood on the arterial walls.
l - Maximum pressure is called: Systolic
B.P.{average(120mmHg) range(100-140)}.
l -Minimum pressure is called: Diastolic
B.P.{average(80mmHg) range(60-90)}.
l It is produced as a result of the elastic recoil
of the aorta.
l Mean ABP = Diastolic B.P. + 1/3 pulse pressure
 ARTERIAL BLOOD PRESSURE
l The Systolic B.P. is produced by ejection of blood
into the aorta during left ventricular systole.
l The Diastolic B.P. is produced as a result of the
elastic recoil of the aorta during ventricular diastole.
l The mean A.B.P.= Diastolic B.P. +1/3pulse
pressure (Systolic B.P. - Diastolic B.P. ).
l e.g.80 +(120-80)=93mmgH
ARTERIAL BLOOD PRESSURE
l Systolic & diastolic B.P.
 Physiological factors that
affect the A.B.P.
l 1-Age
l 2-Sex

l 3-Body weight

l 4-Race

l 5-Diurnal variation

l 6-Meals
Physiological factors that affect
the A.B.P.

l 7-Exercise
l 8-Emotions

l 9-Sleep

l 10-Temperature

l 11-Gravity

l 12-Respiration
Physiological variation of ABP

l 1. Age:
l - In newly - born infants the blood pressure is 80/40.
l - Then it increases gradually where
l ● at 4 years old it is 100/65.
l ● at 20 years it is 120/80.
l - It increases gradually after the age of 20 years to
reach 150/90 at the age of 60 years due to decrease
the elasticity of arteries.
 .
l 2. Sex:
l The blood pressure in adult male is higher
than in adult female, but after the menopause it
becomes higher in females this may be due to
hormonal changes during this period.
l 3. Body built:
l The blood pressure usually higher in obese
persons.
 .
l 4. Race:
l The blood pressure in Orientals is less than that
in Europeans and Americans may be due to:
l (a) Genetic factors
l (b) Environment
l (c) Less cholesterol in diet
l (d) Less stress in life.
 .
l 5. Sleep:
l During quiet sleep the ABP is decreased due to
parasympathetic activity. .

l 6. Emotions:
l In different emotional state (e.g. anger) the ABP
is elevated due to sympathetic overactivity.
• 7. Meals: .
• After meals the ABP increases due to:-
• (a) The contraction of smooth muscles of the gut
compress the blood vessels thus increasing VR and COP.
• (b) The vasodilatation occurs in the splanchnic area
increases the VR and also COP.
• 8. Gravity:
• - During standing, the blood pressure increases in all
vessels below the heart and decreases in vessels
above the heart level.
• - The rise or decrease in BP is equal to the weight of
blood column from the vessel to the heart (i.e. 0.77
mmHg per cm).
 9. Exercise

l ●In the isometric (static) exercise: both the diastolic and

the systolic pressures rise sharply and return immediately
to normal after stoppage of exercise.
l This is due to reflex action by impulses originate in the
contracting muscles proprioceptors to stimulate VMC.
l ● In the isotonic (dynamic exercise): The systolic blood
pressure increases sharply, while the diastolic blood
pressure remains constant or even decreases and this effect
remains for a time after exercise due to vasodilation of the
skeletal muscle vessels resulting from accumulation of
vasodilator metabolites.
 10. Respiration
(Respiratory pressure waves)

l - The changes in the blood pressure during

each respiratory cycle are called "respiratory
pressure waves".
l - "The ABP increases during the late part of
inspiration and the early part of expiration, while
it falls during the remainder of the respiratory
cycle".
l - Also, they are called "Traube-Hering wave ".
 Factors That Determine and
Maintain A.B.P.
l 1-Cardiac output (C.O.):
l 2-Peripheral Resistance (P.R.):
3-Elasticity of the blood vessels.
l 4-Blood Volume and Circulatory Capacity
l

l
 Factors That Determine and
Maintain A.B.P.
l 1-Cardiac output (C.O.):
l The A.B.P. is directly proportionate to the C.O.
{C.O.= S.V. x H.R.}
l Stroke volume (S.V.) affects mainly systolic B.P.
l Heart rate (H.R.) affects mainly diastolic B.P.
 .
l 2-Peripheral Resistance (P.R.):
It is essential for maintenance of A.B.P.
especially diastolic B.P.
v It is produced mainly by diameter of the
arterioles.
v Also by blood viscosity and length of blood vessel
l 3-Elasticity of the blood vessels.
l It is essential for production and maintenance
of a relatively high diastolic B.P.
4-Blood Volume and Circulatory Capacity

l They determine A.B.P. by controlling the mean

systemic filling pressure (MSFP) .
l The A.B.P varies directly with the MSFP.
l The mean systemic filling pressure (MSFP) is:-
l Increased by:-
an increase of blood volume or
l decrease of the circulatory capacity. and
l Decreased by:-
l decrease of the blood volume or
an increase of the circulatory capacity.
Regulation (Control) of A.B.P.

l 1. Rapidly acting mechanism:

Nervous regulation.
l 2. Intermediately acting mechanism:
Capillary fluid shift mechanism.
The stress-relaxation mechanism.
l 3. Slowly acting mechanism:
Hormonal mechanism which acts through the
kidney.
 ARTERIAL BLOOD PRESSURE REGULATION
There are three basic mechanisms for regulation of
blood pressure:-
Short-term regulation:
– Baroreceptor reflexes.
– Chemoreceptor reflexes.
– Atrial reflexes.
– CNS-ischemic response.
Intermediate regulation:
– Capillary fluid shift
– The stress-relaxation mechanism
Long-term regulation:
– Role of the kidney.
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 Regulation (Control) of A.B.P.
l A-Short-term mechanisms:
l 1-Arterial baroreflexes :
by stimulation of baroreceptors (in carotid sinus
and aortic arch) when the A.B.P. increases.
l a- Increase the A.B.P.
Stimulates baroreceptors leads to decrease
H.R.,V.D.,& decrease catecholamine secretion
(from adrenal medullae), leads to decrease the
A.B.P.
l b- The opposite occurs when A.B.P. is decreased.
Higher Control of ABP

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 2- Arterial chemoreflexes stimulation
l a-Decrease the A.B.P.
stimulates chemoreceptors (in carotid and
aortic bodies), as a result of (hypoxia) leads to
increase H.R.,V.C.,& increase catecholamine
secretion (from adrenal medullae), leads to
increase the A.B.P.
l b- The opposite occurs when A.B.P. is
increased.
 3-CNS ischemic response
l Decrease the A.B.P. below 60 mmHg causes brain
ischemia resulting in local hypoxia which stimulates
the VCC resulting in generalized V.C. which elevates
the A.B.P. and maintain cerebral blood flow.
l N.B.:
l The same effect occurs in cases of increased
intracranial pressure (Cushing's reflex) in the
cerebral circulation.
4-The abdominal compression reflex:

l Decrease A.B.P.
stimulates VCC which stimulates the
medullary reticular formation (RF) and send
signals that increase skeletal muscle tone.
l The increase skeletal muscle tone in the
abdominal muscle raising A.B.P. (by
compressing the abdominal veins increasing
the venous return).
 B-Intermediate -term mechanisms
• 1-Capillary fluid shift mechanism:
Increase blood volume increases capillary hydrostatic pressure.
• This helps fluid filtration, and decrease blood volume, so A.B.P.
is decreased.
• 2-Stress relaxation mechanism:
• Increase A.B.P. stretches the arteries and increases tension in
their walls.
• After sometimes the arteries relax (Stress relaxation) helping
decrease A.B.P.
• 3-Renin-angiotensine V.C. mechanism.
• 4- Right atrial mechanism.
• Increase ABP causes (VD, reflex inhibition of ADH &
sec. of ANP)
3-Renin-angiotensin V.C. mechanism
l Decrease A.B.P. leads to renal ischemia
which stimulates secretion of renin (from the
kidneys) act on angiotensinogen (α2 globulin)
forming angiotensin I which is converted into
angiotensin II by angiotensin converting
enzyme (ACE) {especially in the lungs}.
l Angiotensin II has a potent V.C. effect leads
to increase A.B.P.
 4-Right atrial mechanism
l Increase blood volume stimulates volume
receptors in the right atrium ( type B
receptors) causing:
l 1-Generalized V.D.
l 2- Reflex inhibition of A.D.H. secretion
l 3- Secretion of ANP (helps salt and water
excretion by the kidneys .
These effects help lowering A.B.P.
C-Long-term mechanisms
l These mechanisms control A.B.P. by
modifying the excretion of water and salt
by the kidneys. Through:-
l 1-Glomerular filtration.
l 2-Aldosterone hormone secretion.
.
l A-Decrease A.B.P.:-
l Decreases glomerular filtration & urine
flow (so, the excretion of water and salt
by the kidneys is decreased).
l At the same time, renin is secreted and
angiotensin II is formed.
 .
l Angiotensin II stimulates aldosterone
hormone secretion (from the adrenal cortex),
which increases sodium & water
reabsorption (in the distal tubules of the
kidney).
l All these effects increase body fluids and
blood volume, raises the A.B.P. to the
normal level.
 .
l B-Increase A.B.P.:-
l Increases glomerular filtration & urine
flow (so, the excretion of water and salt by
the kidneys is increased). {called pressure
diuresis}.
l At the same time, renin secretion is
inhibited and angiotensin II is not formed.
 .
l Aldosterone hormone secretion (from the
adrenal cortex) is not formed [inhibited],
which lead to loss of sodium and water in
the urine.
l All these effects decrease body fluids and
blood volume, reduces the A.B.P. to the
normal level.
 Actions of Angiotensin II
l 1-Generalized V.C.
l 2- Stimulates aldosterone hormone secretion
(from the adrenal cortex), which increases sodium
& water reabsorption (in the distal tubules of the
kidney).
l 3-Increases sodium reabsorption (directly in the
proximal tubules of the kidney).
l 4-Decreases glomerular filtration
 .
l 5- Stimulation of the osmoreceptors and the
thirst & salt appetite centers (in the anterior
hypothalamus) leading to :-
a-Release of ADH
b- Increases thirst sensation
c- Increases salt intake
d-Secretion of ACTH which stimulates
secretion of glucocorticoids (from the
adrenal cortex), {which have pressor effect
and cause sodium& water reabsorption}.
 Angiotensin III
l It is formed from Angiotensin II
l But it has about :-
•40% of its pressor activity and
•100% of its aldosterone- stimulating
activity