BLOOD PRESSURE
Dr. Arifa Begum
Associate professor, Dept of Physiology,
Gazi Medical College
Khulna, Bangladesh.
Definition: Blood pressure is the lateral pressure
exerted by blood on the vessel walls while flowing through
it.
• B.P= cardiac output X total peripheral resistance.
• Systolic pressure is the measure of Cardiac output
• Diastolic pressure is the measure of peripheral resistance
 Types :Arterial blood pressure is expressed in four different terms:
 1. Systolic blood pressure
2. Diastolic blood pressure
3. Pulse pressure
4. Mean arterial blood pressure
Systolic and diastolic blood pressure are measured blood pressure and
remaining two are calculated pressure.
SYSTOLIC BLOOD PRESSURE: Systolic blood pressure (systolic
pressure) is defined as the maximum pressure exerted in the arteries
during systole of heart.
Normal systolic pressure: 120 mm Hg (110 mm Hg to
140 mm Hg).
 Significance of Systolic pressure undergoes The height
of systolic pressure indicates: (1) The extent of work done
by heart
(2) The force with which the heart is working.
(3) The degree of pressure which the arterial walls have
to withstand.
DIASTOLIC BLOOD PRESSURE: Diastolic blood pressure
(diastolic pressure) is defined as the minimum pressure
exerted in the arteries during diastole of heart.
 Normal diastolic pressure: 80 mm Hg (60 mm Hg to 80 mm
Hg).
 Increase of diastolic pressure indicates that the heart is
approaching towards its failure. Consequently, variations of
diastolic pressure are of greater prognostic importance than
those of systolic.
 PULSE PRESSURE: Pulse pressure is the difference
between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
 MEAN ARTERIAL BLOOD PRESSURE: Mean arterial blood
pressure is the average pressure existing in the arteries.
It is the diastolic pressure plus one third of pulse pressure. To
determine the mean pressure, diastolic pressure is considered
than the systolic pressure.
It is because, the diastolic period of cardiac cycle is
longer (0.53 second) than the systolic period (0.27
second).
Normal mean arterial pressure: 93 mm Hg (80 + 13 =
93).
Mean arterial blood pressure = Diastolic pressure + 1/3
of pulse pressure = 80 + 40/3 = 93.3 mm Hg
Factors controlling arterial blood pressure:
1. Pumping action of the heart: Effectual contraction of the
heart is the main factor for controlling
the cardiac output, blood pressure and flow within the blood
vessels
2.Cardiac output: Alterations of cardiac output will alter blood
pressure. Cardiac output depends upon venous return, force
and frequency of heart beat. Blood volume affects blood
pressure directly, by mainly modifying the cardiac output.
3. Elasticity of the arterial walls:
4.Blood volume: Increase in blood volume will raise
both the systolic and diastolic blood pressure.
5. Viscosity of the blood: Alteration in blood viscosity
will affect the diastolic pressure by its effect on the
peripheral resistance.
.6. Peripheral resistance: It is the resistance which
blood has to overcome while passing through the
periphery.
The chief seat of peripheral resistance is the arterioles
and to a smaller extent the capillaries
Peripheral resistance depends on the following:
 (a) Velocity of blood (b) Viscosity of blood (c) Elasticity of
arterial walls (d) Lumen of the blood vessels.
 The seat of peripheral resistance is found to be chiefly in
the arterioles, where the velocity is fairly high and the
lumen is narrow.
Cardiac
output
Arterial system
Total
peripheral
resistance
Peripheral
runoff to
capillaries
The arterioles are the smallest branches of the arteries. Their
walls have an extensive development of smooth muscle, and
they are the site of highest resistance to blood flow.
It is extensively innervated by sympathetic adrenergic nerve
fibers. α1-Adrenergic receptors are found on the arterioles of
several vascular beds (e.g., skin and splanchnic vasculature).
When activated, these receptors cause contraction, or
constriction, of the vascular smooth muscle. Constriction
produces a decrease in the diameter of the arteriole, which
increases its resistance to blood flow
Poiseuille's law: In 1841 the French Physician J . L. M.
Poiseuille studied the factors regulating the flow of viscous
fluids through the capillary tubes.
 He showed that: Resistance to blood flow in any blood vessel
proportionally varies
 directly with the viscosity of the blood and also with the length
of the blood vessel
and inversely with the fourth power of the radius of the blood
vessel.
 It can be represented by the following formula:
where R stands for resistance to blood flow, n for viscosity
of blood, L for length of blood vessels, r for radius of the
blood vessel, 8 for Hagen's integration and 𝝅 factor for a
cylindrical tube.
• Factors Affecting Peripheral Resistance: Peripheral resistance
is determined by two main factors:
• 1. Radius of Blood Vessel: The radius of the blood vessel
significantly affects peripheral resistance. This is called
vascular hindrance.
• 1. Vasoconstriction increases and vasodilation decreases
• peripheral resistance.
• 2. Decrease in radius of vessels to half increases peripheral
• resistance by 16 times.
Viscosity of Blood: Viscosity of blood also affects
peripheral resistance. Viscosity mainly depends on
the factors like hematocrit, composition of plasma,
resistance of red cells to deformation and
temperature.
• Hematocrit: Hematocrit is the single most factor
that greatly affects viscosity of blood. Hematocrit is
the packed cell volume, which depends mainly on
the number of red cells in the blood.
Viscosity increases in polycythemia and decreases
in anemia.
In anemia, circulation is hyperdynamic due to
decreased peripheral resistance.
• Composition of Plasma: In plasma, it is mainly the
concentration of plasma proteins that affects
viscosity. Viscosity increases in conditions in which
concentration of plasma protein is more, Viscosity
decreases in hypoproteinemia.
• Resistance of Red Cells to Deformation: When the
red cells become rigid as seen in hereditary
• spherocytosis, viscosity increases.
• Temperature: increase temperature decreases
viscosity, decrease temperature increases viscosity.
Blood
Pressure
Cardiac
output
Stroke
volum
e
Preload
E.D.V
Venous
return
Total
peripheral
resistance
Heart
rate
Contr
actilit
y
After
load
Filling
time
Filling
pressure
Veno
motor
tone
Blood volume
 Measurement and recording of blood pressure:
 Indirect method: very convenient clinically in human being.
Riva-Roci (1896) first introduced this indirect method and
afterwards Korotkoff (1905) introduced a convenient method by
which the systolic and diastolic pressure could be ascertained
only through listening to a sound.
This is the standard method of recording blood pressure all
throughout the world.
 The instrument used is known as Sphygmomanometer.
Auscultatory method: The instrument is kept at the
level of the heart and the cuff is tied round the upper arm.
Pressure is raised to 200 mm of Hg and then gradually
released.
Variations of sounds are heard with a Stethoscope
placing its chest piece on the brachial artery, a little below
the cuff.
 the sounds are heard due to occurrence of turbulence in
the flow of blood through the narrowed blood vessels
when the manometric pressure just coincides with the
systolic blood pressure.
When the pressure is further released, normal streamline
flow sets in and the sound is no longer heard. At this point
manometric pressure coincides with the diastolic blood
pressure.
as the pressure is released the following variations of
sounds are heard: : First phase—sudden appearance of a
clear tapping sound. This indicates systolic pressure.
Second phase—the tap sound is replaced by a murmur
persisting for another 15 mm of Hg.
Third phase- the murmur is replaced by a clear loud
gong sound
Fourth phase—the loud sound suddenly becomes
muffled and rapidly begins to fade. This point indicates
diastolic pressure.
fifth phase— absence of all sounds.
REGULATION OF ARTERIAL BLOOD PRESSURE:
Arterial blood pressure varies even under physiological
conditions. However, immediately it is brought back to normal
level because of the presence of well organized regulatory
mechanisms in the body. The regulatory mechanisms are:
 A. Nervous mechanism or short term regulatory mechanism
B. Renal mechanism or long term regulatory mechanism
C. Hormonal mechanism
D. Local mechanism or intermediate - term mechanism
Short term regulation mechanism: 1. Baroreceptor
reflex mechanism
• 2. chemoreceptor mechanism
• 3. CNS ischemic response
Long term mechanism: 1. renal body fluid
mechanism
 2. Renin angiotensin mechanism
• Intermediate term mechanism:
• 1. vasoconstrictor mechanism
• 2.capillary fluid shift mechanism
• 3. Stress relaxation changes in vasculature
• Hormonal mechanism: 1. Epinephrin-nor epinephrin
mechanism
• 2. Vasopressin vasoconstrictor mechanism
• Cardiovascular centers are mainly located in the
medulla.
• These centers primarily control the autonomic
output on heart and blood vessels, which is the
major cardiovascular regulatory pathway.
Nervous control of arterial pressure, beginning within
seconds and often increasing the pressure to two times
normal within 5 to 10 seconds. Conversely, sudden
inhibition of nervous cardiovascular stimulation can
decrease the arterial pressure to as little as one-half
normal within 10 to 40 seconds.
Therefore, nervous control of arterial pressure is by far
the most rapid of all our mechanisms for pressure control.
. Baroreceptor Mechanism: Baroreceptors are the
receptors, which give response to change in blood
pressure.
Location: The baroreceptors are located in the walls of
the carotid sinus, where the common carotid artery
bifurcates into the internal and external carotid arteries,
and in the aortic arch.
The baroreceptors are mechanoreceptors, which are
sensitive to pressure or stretch.
Increases in arterial pressure cause increased stretch on
the baroreceptors and increased firing rate in the afferent
nerves. Decreases in arterial pressure cause decreased
stretch on the baroreceptors and decreased firing rate in
the afferent nerves.
Brain stem cardiovascular centers: are located in the
reticular formations of the medulla and in the lower onethird of the pons. These centers function in a coordinated
fashion, receiving information about blood pressure from
the baroreceptors and then directing changes in output of
the sympathetic and parasympathetic nervous systems to
correct the blood pressure as needed.
Mechanism: blood pressure is sensed by baroreceptors
in the carotid sinus and aortic arch. Afferent information
about blood pressure is then sent to the medulla via the
glossopharyngeal (CN IX) and vagus (CN X) nerves.
This information is integrated in the nucleus tractus
solitarius, which then directs changes in the activity of
several cardiovascular centers
The parasympathetic outflow is the effect of the vagus
nerve on the SA node to decrease the heart rate.
The sympathetic outflow has four components: an effect
on the SA node to increase heart rate, an effect on
cardiac muscle to increase contractility and stroke
volume, an effect on the arterioles to produce
vasoconstriction and increase TPR.
An increase in Pa is detected by baroreceptors in the
carotid sinus and in the aortic arch.
 The glossopharyngeal and vagus nerve fibers synapse
in the nucleus tractus solitarius of the medulla
increase in parasympathetic outflow to the heart and a
decrease in sympathetic outflow to the heart and blood
vessels
• The increase in parasympathetic activity to the SA node (via
the vagus nerve) results in a decrease in heart rate
• The decrease in sympathetic activity to the SA node decrease
HR and also decreases cardiac contractility.
• the decreased heart rate and decreased cardiac contractility
produce a decrease in cardiac output
• decrease in sympathetic activity also affects the tone of the
blood vessels, decreased constriction of arterioles, decreases
TPR
these coordinated reflexes reduce Pa back to the setpoint pressure (i.e., to 100 mm Hg)
How BP is regulated in a person when stand
suddenly from lying position:
the carotid sinus baroreceptors are not stimulated at all
by pressures between 0 and 50 to 60 mm Hg, but above
these levels, they respond progressively more rapidly and
reach a maximum at about 180 mm Hg.
Note especially that in the normal operating range of
arterial pressure, around 100 mm Hg.
Chemoreceptor reflex: that operates in much the same way
as the baroreceptor reflex except that chemoreceptors.
The chemoreceptors are chemo sensitive cells sensitive to
oxygen lack ,carbon dioxide excess, and hydrogen ion excess.
this chemoreceptor reflex is not a powerful arterial pressure
controller until the arterial pressure falls below 80 mm Hg
Location: Peripheral chemoreceptors are situated in the
carotid body and aortic body.
Mechanism: Whenever blood pressure decreases,
blood flow to chemoreceptors decreases
Resulting in decreased oxygen content and excess of
carbon dioxide and hydrogen ion
 Excite the chemoreceptors, which send impulses to
stimulate vasoconstrictor center.
 Blood pressure rises and blood flow increases.
Chemoreceptors play a major role in maintaining
respiration rather than blood pressure.
Central nervous system (CNS) ischemic response:
the baroreceptors, the chemoreceptors, and the lowpressure receptors, all of which are located in the
peripheral circulation outside the brain.
when blood flow to the vasomotor center in the lower
brain stem becomes decreased
 Cause cerebral ischemia
the vasoconstrictor and cardioaccelerator neurons in the
vasomotor center become strongly excited
Stimulating the sympathetic vasomotor nervous control
areas in the brain's medulla.
The systemic arterial pressure often rises to a level as
high as the heart can possibly pump.
This arterial pressure elevation in response to cerebral
ischemia is known as the central nervous system (CNS)
ischemic response.
The ischemic effect on vasomotor activity can elevate the
mean arterial pressure dramatically, sometimes to as high as
250 mm Hg for as long as 10 minutes
he CNS ischemic response is one of the most powerful of all
the activators of the sympathetic vasoconstrictor system.
It is sometimes called the "last ditch stand" pressure
control mechanism.
Cushing Reaction: Cushing reaction is a special type of
CNS ischemic response that results from increased
pressure of the cerebrospinal fluid around the brain in the
cranial vault. It occurs when ICP raises.
Long term mechanism for blood pressure control:
Kidneys play an important role in the long term regulation of
arterial blood pressure.
Kidneys regulate arterial blood pressure by two ways:
1. By regulation of ECF volume or renal body fluid mechanism.
2. Through renin angiotensin mechanism.
 Long term mechanism for blood pressure control:
Renal body fluid mechanism: when body contains too
much extra cellular fluid
blood volume
Arterial pressure
The rising pressure in turn has a direct effect to cause the
kidney to excrete the excess ECF, thus returning pressure
 back toward normal.
So, When the blood pressure increases, kidneys excrete
large amounts of water and salt, particularly sodium, by
means of pressure diuresis and pressure natriuresis. This
is the mechanism for decreasing blood pressure.
Renin angiotensin aldosterone mechanism: