Arterial blood pressure

Blood pressure is the force exerted by blood

against a vessel wall.

It maintains blood flow through capillaries.

It depends on blood volume & compliance

(destinsibility) of blood vessels.

Arterial BP is not constant, it rises during

ventricular systole (contraction) & falls during
ventricular diastole (relaxation).
Systolic BP
Is the peak (highest) BP measured during
ventricular systole = 120 mmHg, in a young
Person at rest.

Diastolic BP
Is the minimum B.P. at the end of ventricular
diastole = 80 mmHg, in a young person at
rest.

Pulse pressure
Is the difference between systolic and
diastolic BP
Mean BP

Calculated by adding one-third of the pulse

pressure to the diastolic BP.

If BP = 120/90 mmHg.
The mean BP = 90 + 120 – 90
3
= 90 + 10 = 100 mmHg.

Mean arterial BP = C.O. x total peripheral

resistance.

C.O. determines systolic BP.

Total peripheral resistance determines diastolic BP.

 Blood Pressure Must Be Regulated

• Low Blood Pressure • High Blood Pressure

Blood will not reach all – Heart is placed under
Tissues specifically those great stress
Where gravity is acting
against flow. – Excess plasma leakage

Most importantly the brain.

– At the extreme,
capillaries burst
 Physiological variations in BP
• Age
• Sex
• Body mass index
• Meals
• Exercise
• Posture
• Anxiety
• ↓ Slightly during inspiration and ↑
Slightly during expiration
 Determinants of arterial BP

• Total peripheral resistance (TPR)

• Cardiac output (CO)

• Blood viscosity.

• Blood volume.

Arterial BP = CO X TPR
 Factors affecting diameter of arterioles
(resistance)

• Vasodilator agents:
– Adenosine
– Atrial natriuretic peptide (ANP)
- ↑ potassium or Hydrogen ions.
- ↓ Oxygen or ↑ CO2
– Histamine
– Nitric oxide and lactic acid
– Prostacyclin

• Vasoconstrictor agents:
– Noradrenaline
– Sympathomimetic drugs.
– Vasopressin (ADH)
– Angiotensin II
– Endothelin-1
Blood viscosity: Hematocrit
Effect of hematocrit on blood viscosity. Above-normal hematocrits produce a
sharp increase in viscosity. Because increased viscosity raises vascular
resistance, hemoglobin and oxygen delivery may fall when the hematocrit rises
above the normal range.
 Blood Viscosity

↓ Plasma protein → ↓ blood viscosity

Hypoalbumenimia:
Burns.
Malnutrition
 REGULATION OF ARTERIAL
BLOOD PRESSURE

Regulation of Blood Pressure

Nervous Renal Hormonal Local

Mechanism Mechanism Mechanism Mechanism

By By By By Local
Vasomotor Regulation Vasocons- Vasocons-
Center and of ECF -trictor and -trictors and
Impulses Volume and Vasodilator Vasodilators
from renin – Hormones
Periphery angiotensin
mechanism
 Effect of Blood Volume

Changes in blood volume affect arterial pressure

by changing cardiac output:

An increase in blood volume increases end–diastolic

volume → ↑ ventricular preload → ↑ ventricular stroke
volume by the Frank-Starling mechanism. 

↑ Stroke volume → ↑ cardiac output and ↑ arterial blood

pressure.  
 Hemodynamics

Is the branch of physiology concerned with

The physical principles governing:
Pressure, Flow, Resistance, Volume, and
Compliance as they relate to the CVS.

Resistance to blood flow results from the

inner friction & viscosity of blood.
Pressure flow and resistance are related by:
(Ohm’s Law), Q = ΔP/R .

Q = blood flow.
ΔP = the pressure difference between the
two ends of the vessel.
R = Resistance.

Resistance depends on the radius & length

of the blood vessel & the viscosity of
blood (Poiseuilleʾs law).
Q = ΔP / R .
R = V x L / ᷊4
Q = ΔP x ᷊4 / V x L .
Length does not change, and viscosity
rarely changes enough to have a
significant effect on resistance.

There for small changes in arteriolar

radius can cause large changes in blood
flow.
Q ~ ᷊4

R ~ 1 / ᷊4
The influence of tube length and
radius on flow. Because flow is
determined by the fourth power of
the radius, small changes in radius
have a much greater effect than small
changes in length. Furthermore,
changes in blood vessel length do
not occur over short periods of time
and are not involved in the
physiological control of blood flow.

The pressure difference (P) driving

flow is the result of the height of the
column of fluid above the openings
of tubes A and B.
Flow rate as a function of resistance
Arterioles & small arteries are
called (resistance vessels).

They determine the mean arterial

blood pressure.
 Types of blood flow
Laminar (Streamline) flow :
Smooth flow at a steady rate. The central portion of
blood stays in the center of the vessel → Less
friction.

Turbulent flow :
High flow rate in all directions (Mixing) → increase
resistance & slow flow rate.

In restricted blood flow or valvular lesions bruits or

murmurs can be heard.
Streamline and turbulent blood flow. Blood flow is streamlined until a critical
flow velocity is reached. When flow is streamlined, concentric layers of fluid
slip past each other with the slowest layers at the interface between blood and
vessel wall. The fastest layers are in the center of the blood vessel. When the
critical velocity is reached, turbulent flow results. In the presence of turbulent
flow, flow does not increase as much for a given rise in pressure because
energy is lost in the turbulence.
Axial streamline and flow velocity. The distribution of red blood cells in blood
vessel depends on flow velocity. As flow velocity increases, red blood cells
move toward the center of the blood vessel (axial streaming), where velocity is
highest. Axial streaming of red blood cells lowers the apparent viscosity of
blood
Measurement of B.P.
Systolic pressure can also be estimated by palpating
the radial artery and noting the cuff pressure at which
the first pulsation is felt.
Hypertension in adults is a BP greater than 140/90.

BP at or below 120/80 is normal.

Values between 121/81 and 139/89 indicate a state

of pre-hypertension.

Hypertension increases the work load of the heart →

enlargement of the left ventricle → ↑ muscle mass → ↑
oxygen demand.

Insufficient coronary circulation → symptoms of

ischemic heart disease.
 Dangers of hypertension
Silent killer:
Patients are asymptomatic until substantial
vascular damage occurs.

Atherosclerosis increases afterload.

Increase workload of the heart.

Congestive heart failure.

Damage cerebral blood vessels.

Cerebral vascular accident (stroke)

Chronic renal failure.

 Elastic rebound

During systole the arterial walls expand to

accommodate the extra amount of blood
pumped by the ventricles.

During diastole the BP falls, the arteries recoil to

their original dimensions (Elastic rebound) →
maintains blood flow in the arteries when the
ventricle is in diastole.
 If the blood pressure drops suddenly

 Two problems confronts the pressure

control system:

 The first is survival,

 to return the arterial pressure immediately

to near a normal level that the person can
live trough the acute episode.
 The second is to return the blood volume
eventually to its normal level

 So that the circulatory system can

re-establish full normality,

 Including return of the arterial pressure

back to its normal value
Three mechanisms in regulating the blood
pressure

 React rapidly, within seconds or minutes;

 Respond over an intermediate time period,

minutes or hours

 Provide long-term pressure regulation, days,

months, and years.
 Effects of Rapidly Acting Pressure Control
Mechanisms

 To cause constriction of the veins and provide

transfer of blood into the heart.

 To cause increased heart rate and contractility of the

heart and provide greater pumping capacity by the
heart

 To cause constriction of the peripheral arterioles to

impede the flow of the blood out of the arteries.

 All these effects occur almost instantly to raise the

arterial pressure back into a survival range.
Rapidly Acting Pressure Control Mechanisms

1- The baroreceptors:
Stretch receptors in large systemic arteries
(particularly the carotid artery and aorta).

2- Carotid and aortic chemoreceptors:

Monitor changes of oxygen, carbon
dioxide, and hydrogen ions.

3- CNS ischemic responses.

Sudden increase in BP → ↑ activity of the baroreceptors
:which produces
H.R. & ↓ C.O. due to ↓ sympathetic & ↑parasympathetic ↓ -1
.activity

Widespread peripheral vasodilatation due to inhibition of -2

.the vasomotor center

Sudden decrease in BP → ↓ activity of the baroreceptors

: which produces
H.R. & ↑ C.O. due to ↑ sympathetic & ↓ parasympathetic ↑ -1
.activity

Widespread peripheral vasoconstriction due to stimulation -2

. of the vasomotor center
 Importance of the baroreceptor reflex

 To keep the arterial pressure relatively

constant in the rang of 70 mmHg to 150
mmHg, maintain the mean blood pressure
at about 100 mmHg

 Pressure buffer system – reduce the blood

fluctuation during the daily events, such as
changing of the posture, respiration,
excitement etc.
 Baroreceptor Resetting

 Baroreceptor will adapt to the long term

change of blood pressure.

 If the blood pressure is elevated for a long

period of time, several days or years, the set
point will transfer to the elevated mean blood
pressure.

 That makes the baroreceptor system

unimportant for long-term regulation of arterial
pressure
Denervation of the baroreceptors can lead to
paroxysmal hypertension.
 Stimulation of chemoreceptors leads to a
reflex increase in vasomotor tone,

 which causes generalized

vasoconstriction and hence a rise in
blood pressure.

 Chemoreceptor mechanism is important

in regulation of blood pressure when it
fall below the range in which
baroreceptors act (70 mmHg).
 CNS ischemic response

 Chemoreceptor reflex is useful in

regulation of blood pressure when it falls
to a level between 40 and 70 mmHg.

 But if the blood pressure below 40 mmHg,

the last ray of hope for survival is the
central nervous system (CNS) ischemia
response.

 So it sometimes called the “last ditch

stand” pressure control mechanism.
 Pressure Control Mechanisms That Act
After Many Minutes
(Intermediate-control mechanism)

 The renin-angiotensin vasoconstrictor

mechanism

 Stress-relaxation of the vasculature

 Shift of fluid through the tissue capillary

wall in and out of the circulation to adjust
the blood volume as needed.
 REGULATION OF BLOOD PRESSURE BY
RENIN-ANGIOTENSIN MECHANISM

Decrease in Blood Pressure Normal Blood Pressure

Stimulation

Juxtaglomerular apparatus

Renin

Angiotensinogen Angiotensin I

Converting enzyme

Angiotensin II Vasoconstriction
 Stress-relaxation of the vasculature

 When the pressure in the blood vessels

becomes too high, they become stretched
and keep on stretching more and more for
minutes or hours.

 As a result, the pressure in the vessels falls

toward normal.

 This continuing stretch of the vessels, called

stress-relaxation, can serve as an
intermediate-term pressure control.
 Shift of fluid through the tissue capillary wall
in and out of the circulation

• Any time the capillary pressure falls too

low,.

• Fluid is absorbed by capillary osmosis from

the tissue into the circulation.

• Thus increasing the blood volume and the

pressure in the circulation.
 Long-term Regulation of Arterial Pressure
by the Kidneys

• The kidneys control the level of H2O and NaCl in the

body, thus controlling the volume of the extracellular
fluid and blood by:
1- Renal fluid shift through Antidiuretic hormone (ADH)

2- Renin- angiotensin- aldosterone mechanism.

 Importance
 It takes a few hours to show significant response
for these mechanisms.

 Return the arterial pressure back to normal.

 NaCl /  Extracellular fluid volume / Helps correct
 Arterial blood pressure
+ H2O
conserved

Na+ (and Cl¯)

+ + osmotically hold
more H2O in ECF
Angiotensin-
Renin converting
enzyme Na+ (and Cl¯)
conserved

Angiotensinogen Angiotensin I Angiotensin II Aldosterone  Na+ reabsorption

by renal tubules
Circulation ( Cl¯ reabsorption
follows passively)
+ + +
ADH Thirst Arteriolar
vasoconstriction

 H2O reabsorption  Fluid intake

by kidney tubules

Renin-Angiotensin-Aldosterone System
Renal Urinary Output Curve
 Atrial baroreceptors (low pressure receptors)

Respond to stretch of the wall of the right atrium.

↑ atrial pressure → stimulate CV center → ↑ H.R.& ↑ C.O

(Bainbridge reflex) → prevent damming of blood in veins,
atria & pulmonary Circulation.

Atrial stretch also → dilate afferent arterioles → ↑ GFR →

↓ ADH & ↑ ANP hormone secretion → ↑ urine output. →
↓ B.P.
 Hormonal regulation of CVS

The endocrine system provides both short-term and

long term regulation of CVS.

Epinephrine, and Norepinephrine, stimulate C.O. and

vasoconstriction.

Other hormones for long-term regulation of arterial

BP include:
1- Antidiuretic hormone (ADH).
2- Angiotensin II- Aldosterone system
3- Erythropoietin.
4- Atrial natriuretic peptides (ANP).
High BP Leads to:
1- ↓ Antidiuretic hormone (ADH) secretion.
2- ↓ Angiotensin II hormone secretion
3- ↓ Aldosterone hormone secretion
4- ↓ Erythropoietin hormone secretion.
5- ↑ Atrial natriuretic peptides (ANP) hormone secretion.

Low BP Leads to:

1- ↑ Antidiuretic hormone (ADH) secretion.
2- ↑ Aldosterone hormone secretion
3- ↑ Angiotensin II hormone secretion .
4- ↓ Natriuretic peptides (ANP) hormone secretion
5- ↑ Erythropoietin hormone secretion → ↑ RBCS,
take few days.