CARDIOVASCULAR

PHYSIOLOGY
AHMED SHERIF ISA Ph .D

Department of Human Physiology,

Faculty of Basic Medical Sciences,
College of Medical Sciences
Ahmadu Bello University, Zaria
 Course Outline
• Overall design of the Cardiovascular System
• Functional anatomy of the heart and the cardiac muscle.
• Properties of cardiac muscle
• The origin of heart cardiac cycle
• Electrocardiogram (ECG)
• Cardiac output, Stroke volume
• Haemodynamics: Basic Principles of pressure, flow and
resistance
• Arterial Blood Pressure: Measurement, control and regulation
• Hypertension.
• Circulation through special regions: Pulmonary, coronary,
cerebral and cutaneous circulaton
• Cardiovascular adjustments in exercise
• Haemorrhagic shock, hypotension and their complications
Learning objectives
• Explain cardiac action potential
 INTRODUCTION
• CVS comprises the heart and blood vessels
• The heart pumps blood through a series of
distributing and collecting tubes
• The major function of the CVS is to supply
• Oxygen
• Nutrients
• Other essential substances to the tissues of the body
and
• Remove CO2
FUNCTIONAL ANATOMY OF
THE HEART
• It is located in the thoracic region
• It weighs an average 300g
• The heart is muscular organ enclose in a fibrous sac
called PERICARDIUM
• The inner layer of the pericardium is called the
EPICARDIUM.
• The narrow space between the pericardium and
epicardium is filled with a fluid called
PERICARDIAL FLUID
• The wall of the heart is called MYOCARDIUM which is
composed of cardiac muscle cells.
• The surface of the cardiac chamber is lined by layer of cells called
endothelial cells
• The heart divided in to right and left halves, each consisting of an
atrium and a ventricle
• The ventricles are separated by a muscular wall called
interventricular septum
• Between the atrium and ventricles is the AV valves.
• The right AV valves is called the TRICUSPID VALVES
• While the left AV valves is called the BICUSPID VALVES
• The valves are fastened to muscular projections (PAPILLARY
MUSCLE) by fibrous strands called chordae tendinae.
• The opening of the right ventricles into the
pulmonary trunk and the left ventricle into the aorta
also have valves called
• PULMONARY AND AORTIC VALVES A.K.A
SEMILUNAR VALVES
THE HEART
THE VALVES OF THE HEART
 Pop Quiz
The role of the chordae tendinae is

A.to tense the interventricular septum green

B. to prevent the valves from bulging into the
pink
atria when the ventricles contracts

C.to lower the base of the heart as they contract

yellow

D.to open AV valves to allow flow of blood into orange

the ventricles
 Pop Quiz
The role of the chordae tendinae is
A. to tense the interventricular septum
B. to prevent the valves from bulging into the
atria when the ventricles contracts pink
C. to lower the base of the heart as they contract
D. to open AV valves to allow flow of blood into
the ventricles
 The vascular system
• Blood vessels form a tubular network that
permits blood to flow from the heart to all the
living cells of the body and then back to the
heart.
• Arteries carry blood away from the heart,
• Veins return blood to the heart.
• Arteries and veins are continuous with each
other through smaller blood vessels called
Capillaries.
 Arterial system
Comprises
• Aorta
• Arteries
• Arterioles
The wall of the arteries are made up of
three layers
• Outer tunica adventitia(connective tissue layer)
• Middle tunica media (smooth muscles & elastic
fibres)
• Inner tunica intima (endothelium)
 VENOUS SYSTEM
Comprises
• Venules
• Veins
• Vena Cavae
The walls of the veins are made up of
• Inner endothelium
• Elastic tissues
• Smooth muscles
• Outer connective tissues
Fig 4: The blood vessels of the cardiovascular
system
Circulation of blood in the cardiovascular
system
 Properties of the heart
• Excitability
• Autorhythmicity/Automaticity
• Conductivity
• Contractility
 EXCITABILITY
• This is the ability of a tissue to respond to
stimuli
• The response to stimuli means generation of
action potential (AP) followed by a
physiological action in the form of
contraction.
AP in the cardiac muscle occurs in five phases:
0-Depolarization
1-Initial repolarization
2-A plateau
3-Final repolarization
4-resting membrane potential
 0 - Depolarization
1 - Initial repolarization
2 - Plateau
3 - Final repolarization
4 - resting membrane
potential (RMP)

Fig 5: Action potential in cardiac muscle

 Ionic basis of cardiac action potential
Depolarization
• Open of fast sodium channels leading rapid influx of Na ions
Initial Repolarization
• Transient opening of K+
• Closure of fast Na ions
Plateau
• Opening of slow Ca2+ channels
• Opening of slow Na channels
• Balances efflux of K+ ions
Final Repolarization
• K+ ion efflux increases
• Closure of Ca2+ ion channels
Restoration of resting membrane potential (RMP)
• All the Na+ that entered the cell during AP will
move out and K+ move in
• 3 Na+ moves out
• 2 K+ moves in
 AUTORHYTHMICITY/AUTOMATICITY
• Rhythmicity is the ability of a tissue to generate its
own impulses regularly
• This is the property of all the tissues of the heart
• The heart has a specialized excitatory structure from
the discharge of impulse is rapid
• This specialized structure is the SA Node and it
produces what is called the PACEMAKER
POTENTIAL
• From this structure impulses spread to other parts
through a specialized conducting system
Rhythmicity of other parts of the heart
1. SA node 70 – 80/min
2. AV node 40 – 50/min
3. Atrial muscle 40 – 50/min
4. Purkinje fibers 35 – 40/m
5. Ventricular muscle 20 – 40 min
 Pacemaker potential(electrical potential in
the SA node)
• The electrical potential in the SA node is different
from the other cardiac muscle
• In the SA node each impulse triggers the next impulse
• It is mainly unstable resting membrane potential
• The RMP -55 to -60 mV
 Conductivity
• The human heart has a specialized conductive system,
through which the impulses from the SA node are
transmitted to all other parts of the heart
Conductive system in the human heart includes:
1. SA node
2. Internodal fibres:
• (a) Anterior internodal fibers of Bachman
• (b) Middle internodal fibers of Wenckebach
• (c) Posterior internodal fibers of Thorel
3. AV node
4. The bundle of HIS
5. Right and left bundle muscles
6. Purkinje fibers
Figure 7: Spread of cardiac excitation
 CONTRACTILITY
• This is the ability of the tissue to shorten in length after
receiving a stimulus.
All or none law
• When a stimulus is applied, and the strength is adequate
(i.e. not below the threshold level), the cardiac muscle
responds by contraction, or if the strength is not adequate,
it does not respond at all.

Refractory period
• It is the period in which the muscle does not show any
response to a stimulus. Refractory period is of two types:
• Absolute refractory period
• Relative refractory period
Absolute refractory period
• Is period during which the muscle does not show any
response at all whatever may be the strength of the
stimulus. The absolute RP in cardiac muscle extends
throughout the contraction period
Relative refractory period
• It is the period during which the muscle show response if
the strength of stimulus is increased to maximum. RRP
extends during the first half of relaxation period.

Significance of long refractory period in cardiac muscle

• Summation of contractions does not occur
• Fatigue does not occur
• Tetanus does not occur
Figure: The refractory period in the heart, ARP:;Absolute refractory
period, RRP; relative refractory period
Pop quiz II
• Which of the following sequence is correct on spread of
cardiac excitation
A) B) SA node→ internodal pathways→ Bundle of His→ AV
node→ Bundle branches→ Purkinje fibres green

B) SA node→ internodal pathways→ AV node→ Bundle

branches→ Bundle of His→ Purkinje fibres pink

C)SA node→ internodal pathways→ AV node→ Bundle of

His→ Bundle branches→ Purkinje fibres yellow

D) SA node→ internodal pathways→ AV node→ Bundle of

His→Purkinje fibres→ Bundle branches orange
Pop quiz II
• Which of the following sequence is correct on spread of
cardiac excitation
A) B) SA node→ internodal pathways→ Bundle of His→ AV
node→ Bundle branches→ Purkinje fibres

B) SA node→ internodal pathways→ AV node→ Bundle

branches→ Bundle of His→ Purkinje fibres

C)SA node→ internodal pathways→ AV node→ Bundle of

His→ Bundle branches→ Purkinje fibres yellow

D) SA node→ internodal pathways→ AV node→ Bundle of

His→Purkinje fibres→ Bundle branches
Pop Quiz III
• The SA node is the normal pacemaker
because of its

A) Location in the atrium green

B) Rate of impulse discharge pink

C) neural control yellow

D) relative position to the AV node. orange

Pop Quiz III
• The SA node is the normal pacemaker
because of its

A) Location in the atrium

B) Rate of impulse discharge pink

C) neural control

D) relative position to the AV node.

 CARDIAC CYCLE
• Cardiac cycle is defined as the sequence of
coordinated events which takes place during
heartbeat. Each heartbeat consists of two major
periods called systole and diastole.

• During systole, there is contraction of the

cardiac muscle and pumping of blood from the
heart through arteries.

• During diastole, there is relaxation of cardiac

muscle and filling of blood.
Divisions of cardiac cycle

• The contraction and relaxation of atria are

called atrial systole and atrial diastole
respectively. The events of cardiac cycle are
classified into 2 division:
1. Systole
2. Diastole
Systole
• 1. Isometric contraction = 0.05
• 2. Ejection period = 0.22
0.27

Diastole
• 1. Protodiastole = 0.04
• 2. Isometric relaxation = 0.08
• 3. Rapid filling = 0.11
• 4. Slow filling = 0.19
• 5. Atrial systole = 0.11
0.53
 EVENTS OF THE CARDIAC CYCLE
Atrial systole
• Atrial systole is also known as second or last rapid
filling phase. It is considered as the last phase of
ventricular diastole.
• During this period, only a small amount i.e. 10% of the
blood is forced from atria into ventricles. Atrial systole
is not essential for the maintenance of circulation.

• Intra-atrial pressure-increases slightly

• Intra-ventricular pressure – increases slightly
• Ventricular volume – increases slightly
1. Isovolumetric/Isometric contraction
period
Isometric is the first phase of ventricular systole. It occurs
immediately after atrial systole.
• The atrioventricular valves are closed due to increase in
ventricular pressure
• The semilunar valves are already closed
• The ventricles contract as closed cavities in such a way that
there is no change in the volume of ventricular chambers or
in the length of muscle fibers. Only the tension increases in
ventricular musculature
• Because of the increased tension in ventricular musculature
during isometric contraction, the pressure increases sharply
inside the ventricles.
2. Ejection period
Due to the opening of semilunar valves and the
contraction of ventricles, the blood is ejected out of
both the ventricle hence this period is called ejection
period.
Ejection period is of 2 stages:
• First stage is called the rapid ejection period this
occurs immediately after the opening of semilunar
valves.
• Second stage is called the slow ejection period.
During this stage, the blood is ejected slowly with
much less force.
Diastole
1. Protodiastole
It is the first stage of ventricular diastole, so it is called
protodiastole.
• Due to the ejection of blood, the pressure in aorta and
pulmonary artery increases and pressure in ventricles drops
• When the intra ventricular pressure becomes less than the
pressure in aorta and pulmonary artery the semilunar valves
closes.
• The AV valves are already closed
• No other change occurs in the heart during this period
• Thus, protodiastole indicates the end of systole and
beginning of diastole.
2. Isometric relaxation period
• During this period, all the valves of the heart are closed.
• Both ventricles are relaxed as closed cavities without any
change in volume or length of the muscle fiber, so it is
called isometric or isovolumetric relaxation period.
• The intra-ventricular pressure decreases during this time.
• The AV valves open.
Rapid filling phase
• When the AV valves open, there is a sudden rush of
blood (which has accumulated in the atria during atrial
diastole) from atria into ventricles.
• So this is called the first rapid filling phase.
• About 70% of filling takes place during this phase.
Slow filling phase (Diastasis)
• After the sudden rush of blood, the ventricular
filling becomes slow.
• It is also responsible for 20% of ventricular filling.
Atrial systole
• After slow filling period, the atria contracts, a small
amount of blood enters the ventricle from the atria
and the cycle is repeated.
Pop Quiz IV
The second heart sound is caused by

A. closure of the aortic and pulmonary valves. green

B. vibrations in the ventricular wall during systole. pink

C. ventricular filling. yellow

D. closure of the mitral and tricuspid valves. orange

Pop Quiz IV
The second heart sound is caused by

A. closure of the aortic and pulmonary valves. green

B. vibrations in the ventricular wall during systole.

C. ventricular filling.

D. closure of the mitral and tricuspid valves.

Pop Quiz V

The third heart sound is caused by

A. closure of the aortic and pulmonary valves. green

B. vibrations in the ventricular wall during systole. pink

C. ventricular filling. yellow

D. closure of the mitral and tricuspid valves. orange

Pop Quiz IV

The third heart sound is caused by

A. closure of the aortic and pulmonary valves.

B. vibrations in the ventricular wall during systole.

C. ventricular filling. yellow

D. closure of the mitral and tricuspid valves.

 Electrocardiogram (ECG)
• The activity of the cardiac chambers gives rise to
electrical potential differences that can be recorded
from the body surface. This signal can be amplified
and recorded by electrocardiogram (ECG).
Importance of ECG
• ECG information on heart rate and rhythm
• Electrical conduction
• Cardiac position
• It can be used to diagnose and roughly localize
pathological disturbances such as myocardial
ischemia.
• Prognosis
• Electrocardiography is the techniques by
which electrical activities of the heart are
studied.
• Electrocardiograph: The instrument by
which the electrical activities of the heart are
recoded is called electrocardiograph.
• Electrocardiogram: This is the record or
graphical representation of electrical
activities of the heart.
 ECG LEADS
The recording of ECG on the surface of the body
is done by connecting the ECG machine to two
electrodes called ECG leads.
ECG leads are of two types:
• Bipolar leads
• Unipolar leads
• The electrodes are fixed on the limbs, usually
the right arm, left arm and left leg.
• The heart is said to be in the centre of an
imaginary equilateral triangle drawn by
connecting the roots of these three limbs.
• This triangle is called Einthoven’s image.
• Bipolar leads
• They are otherwise known as standard limb
leads.
• Two limbs are connected to obtain these
leads and both electrodes are active. These
standard limb leads are:
• Limb lead I
• Limb lead II
• Limb lead III
• Unipolar leads
• Here, one electrode is active and the other is
indifferent or exploring electrode.
• The unipolar leads are of two types:
• Unipolar limb leads
• Unipolar chest leads
Unipolar limb leads
• They are also referred to as augmented limb
leads. The active electrode is connected to
one of the limbs, while the indifferent
electrode is obtained by connecting the other
two limbs through a resistance.
Unipolar limb leads are of 3 types:
• aVR lead
• aVL lead
• aVF lead
 Unipolar chest leads
• This electrodes are known as chest electrodes, and the
points over the chest are called V1, V2, V3, V4, V5, V6.
Position of the chest leads
• V1 - 4th intercostal space near the right sternal margin
• V2 - 4th intercostal space near the left sternal margin
• V3 - In-between V2 and V4
• V4 - left 5th intercostal space mid-clavicular line
• V5 - 5th intercostals space anterior auxiliary line
• V6 - 5th intercostals space mid auxiliary line
Bipolar limb leads
Position of electrodes for unipolar chest
leads
WAVES OF NORMAL ELECTROCARDIOGRAM
• The normal ECG consists of 5 main waves
called P, Q, R, S, T wave and sometimes the
U-wave. These waves are separated by
segments which starts and ends on the
isoelectric line.

P wave
• It is a positive wave, which is produced by
the electrical activity due to atrial
depolarization.
• It lasts for 0.1 second.
QRS complex

• Q is a small negative wave, which is continued by a

tall positive R wave, then it is followed by a small
negative, the S wave. The QRS complex is obtained
due to ventricular depolarization.
• It lasts for 0.08 – 0.10 seconds.
• Q wave is due to depolarization of the basal portion of
the interventricular septum.
• R wave is due to the depolarization of the apex and
ventricular wall
• S is due to depolarization of the posterior basal part of
the left ventricle and the pulmonary conus.
T wave
• It is a positive wave.
• It occurs as a result of ventricular
repolarization.
• It lasts for 0.2 seconds.
U wave
• This wave is rarely seen.
• It is supposed to be due to repolarization of
the papillary muscles.
 Intervals and Segments
P – R Interval
• This is the interval between the onset of p wave and the
onset of Q wave or QRS complex.
• It signifies the atrial depolarization and the conduction of
impulses through AV node.
Q – T interval
• It is the interval between the onset of Q wave and the end
of T wave.
• The Q-T interval indicates the ventricular depolarization
and repolarization (i.e. electrical activity in the ventricle).
R – R interval
• This is the time interval between the consecutive R
waves. The R – R interval signifies the duration of one
cardiac cycle. it lasts for about 0.8 second.
Waves of the ECG
S-T segment
• The time interval between the end of S wave and
the onset of T wave is called the S-T segment.
• It is isoelectric.
• Any deviation of S-T segment from the isoelectric
base line indicates a pathological condition.
• Elevation of S-T segment (above the isoelectric
line) occurs in acute myocardial infarction.
• Its depression occurs in myocardial ischemia.
Waves of the normal ECG
 Abnormalities of P wave
• In the left atrial hypertrophy (due to initial stenosis)
the p waves become broadened (p mitrale) and their
duration increases because the hypertrophied
muscle takes more time than normal.

• In the right atrial hypertrophy (due to pulmonary

hypertension), the p wave becomes tall and peaked
with less normal duration (p pulmonale).

• The P waves are also inverted in AV nodal rhythm

and
• it disappears in atrial fibrillation.
Atrial fibrillation: 300-500
beats/min
Atrial flutter: 200-350 beats/min
Abnormalities of T wave
• The T wave becomes inverted in cases of
myocardial ischaemia, ventricular hypertrophy and
extrasystoles
• Its amplitude increases in cases of sympathetic,
overactivity muscular exercise and hyperkalemia,
the apical portion of interventricular septum.
Heart Blocks

First degree heart block: When conduction between the

atria and ventricles is slowed but not completely interrupted
Second degree heart block: Not all the atrial pulses are
conducted to the ventricles, so a ventricle may once every
2nd or 3rd atria beat
Third degree heart block: when impulses from the atria
are completely blocked/interrupted, the ventricles beat
independent of the atria.
Extrasystole: This is as a result of ectopic foci or
premature contraction before normal contraction
Cardiac Output
• Cardiac output is the amount of blood pumped from
each ventricle per minute.
• Usually, it refers to the left ventricular output through
aorta into various organs of the body. It is an important
factor in cardiovascular system because the rate of
blood flow through different parts of the body depends
upon the cardiac output.
• It is the amount of blood pumped out by each ventricle
in one minute. It is the product of stroke volume and
heart rate.

Cardiac output = stroke volume (SV) x heat rate (HR)

• The normal value is 5 litres/per ventricle/minute
Stroke volume
• This is defined as the amount of blood pumped out
by each ventricle during each heart beat.
• Its normal value is 70ml (60-80 ml) when the heart
rate is normal (72/minute).
VARIATIONS IN CARDIAC OUTPUT
Physiological variations
1. Age:
2. Sex:
3. Body build:
4. Diurnal variation:
5. Environmental temperature:
6. Emotional conditions:
7. After meals:
8. Exercise:
9. High altitude
10. Posture:
11. Pregnancy:
12. Sleep:
 Pathological variations
Factors that increase cardiac output
include:
• Fever – due to increased oxidative processes
• Anemia – due to hypoxia
• Hyperthyroidism
Factors that decrease in cardiac output
• Cardiac output decreases in the following conditions:
• Hypothroidism due to the decreased basal metabolism
rate
• Atrial fibrillation because of incomplete filling
• Shock due to poor pumping and circulation
• Hemorrhage because of decreased blood volume
 Distribution of cardiac output
• The fraction of cardiac output distributed to a
particular region or organ depends upon the
metabolic activities of that region or organ. The
distribution of blood pumped out of the left
ventricle.
• Liver 1500ml = 30%
• Kidneys 1300ml = 26%
• Skeletal muscle 900ml = 18%
• Brain 800ml = 16%
• Skin, bone & GIT 300ml = 6%
• Heart 200ml = 4%
• Total 5000ml 100%
Factors maintaining cardiac output
Cardiac output is maintained/determined
by four factors:
1. Venous return
2. Force of contraction
3. Heart rate
4. Peripheral resistance
Venous return
• It is the amount of blood, which is returned
to the heart from different parts of the body.
• When it increases, the ventricular filling and
cardiac output are increased.
• Thus, the cardiac output is direct proportional
to venous return provided other factors
remain constant.
• Venous return in turn depends on five factors:
a. Respiratory pump
b. Muscle pump
c. Gravity
d. Venous pressure
e. Sympathetic tone
Force of contraction
• The cardiac output is directly proportional to
the force of contraction provided the other
three factors remain constant.
• Force of contraction upon diastolic period
and ventricular filling. Frank Starling’s law
applies to this.
• According to Frank Starling’s law, the energy
liberated by the heart when it contracts is a
function of length of its muscle fibers at the
end of diastole (i.e. the force of contraction
of heart is directly proportional to the initial
length of muscle fibers before the onset of
contraction.
HEART RATE
• Cardiac output is directly proportional to heart rate
provided the other three factors remain constant.
Moderate changes in heart rate does not alter the
cardiac output, but if there is a marked increase in
heart rate, cardiac output is increased if there is
marked decreases in heart rate, cardiac output is
decreased.

PERIPHERAL RESISTANCE
• This is the resistance against which the heart has to
pump blood. So the cardiac output is inversely
proportional to peripheral resistance.
 HAEMODYNAMICS
INTRODUCTION
• Dynamics means study of motion. The term haemodynamics
refers to the study of movement of blood through circulatory
system.
• The major function of the cardiovascular system is to pump
the blood and to circulate it through different parts of the
body.
• It is essential for maintenance of pressure and other physical
factors within the blood vessels so that, the volume of blood
supplied to different parts of the body is adequate.
Mean volume of blood flow
• This is the volume of blood, which flows into a region of the
circulatory system in a given unit of time. It is the product of
mean velocity and cross-sectional area of the vascular bed.

Q = VxA
Where
Q = Quantity of blood
V = Velocity of blood flow
A = Cross-sectional area of the blood vessel
Types of blood flow

The flow of blood through a blood vessel is of two types:

• Streamline/laminar flow
• Turbulent flow
Streamline/laminar flow
• This is the normal smooth (streamlined flow of blood in the blood
vessels.
• It is silent and laminar (that is the blood flows in several layers or
laminae.
• The outermost layer of blood in contact with the vessel wall is
almost completely static, while the other layers move by velocities
that increase gradually from out–inwards becoming maximal in
the central layer of the stream.
 Turbulent flow
• This is disturbed blood flow in the form of eddies in
various directions. When the velocity of blood flow
increases above critical level, the blood flow
becomes turbulent. It produces sounds which can be
heard using a stethoscope.

Figure 5. Streamline and turbulent blood flow. Blood flow is streamlined until a critical flow velocity is reached.
The critical velocity at which blood flow becomes turbulent
is known as Reynold’s number. The formula to determine
Reynold’s number is:
NR = ρDV
η
NR = Reynold’s number
ρ = Density of blood.
D = Diameter of blood vessel
V = Velocity
η = Blood viscosity
Factors maintaining volume of blood
Blood flow is determined by five factors, thus:
1. Pressure gradient
2. Resistance to blood flow
3. Viscosity of blood
4. Diameter of blood vessels
5. Velocity of blood flow
1. Pressure gradient
• The pressure gradient is the pressure differences between two ends of the
blood vessel. The volume of blood flowing through any blood vessel is
directly proportional to the pressure difference (∆ρ). Pressure gradient is
expressed as follows:
Pressure gradient = P1 – P2
Where,
P1 = Pressure at proximal end of the vessel
P2 = Pressure at distal end of the vessel

• The maximum pressure gradient exists between the aorta and the inferior
vena cava. The pressure in the aorta is 120mmHg and the pressure in inferior
vena cava is 0mmHg. So the pressure gradient is 120 – 0 = 120mmHg. Thus,
the blood will flow from the aorta to the inferior vena cava.
2. Peripheral resistance
• Resistance is the friction, or hindrance against which
blood has to flow. Peripheral resistance means the
resistance offered to blood flow in peripheral blood
vessels. The blood flow is inversely proportional to the
resistance.
Three important factors determine peripheral resistance:
• Radius of blood vessels
• Pressure gradient
• Viscosity of blood
• Peripheral resistance is inversely related to radius of the
blood vessel. Viscosity and pressure gradient of blood is
directly proportional to peripheral resistance. The following
formula shows the relationship between peripheral
resistance, pressure gradient and blood flow:

Peripheral resistance = Pressure gradient

Volume of blood flow
Peripheral resistance = P1 – P2 = ∆ρ
Q Q
3. Viscosity of blood
• Viscosity is the friction of blood against the wall of the blood
vessel. It is described as the lack of slipperiness. Viscosity
influences the blood flow through peripheral resistance. The volume
of blood flow is inversely proportional to the viscosity of blood.
• The number of red blood cell, plasma protein and albumin, are the
main factors which determine the viscosity of the blood.

4. Diameter of blood vessels

• Volume of blood is directly proportional to the diameter. The larger
the diameter of a blood vessels, the higher the blood flow in that
vessel. The diameter of the aorta and arterioles depends on the
elasticity and sympathetic tone.
5. Velocity of blood flow
• Velocity of blood flow is the rate at which blood
flows through a particular region. The mean
volume of blood flow is directly proportional to the
velocity of blood flow.
 HAGEN-POISEUILLE EQUATION
Hagen and poiseuille postulated an equation that
explains the relationship between different variables
of dynamism. This equation can also be applied to
haemodynamics.
Hagen – poiseuille equation is as follows:
Q = (P1 – P2) πr4
8L x η
Where,
Q = Volume of blood flow
P1 – P 2 = Pressure gradient
r4 = Radius of the blood vessel
L = Length of the blood vessel
η = Viscosity of the blood
vessel
 Arterial blood pressure
• This is the lateral pressure exerted by a medium of
blood on the arterial walls. It is usually oscillated
during the cardiac cycle between when it is
maximum.
• It is called systolic BP (at the peak of maximum
ejection phase) and a minimum. It is called diastolic
BP (during isometric contraction phase just before
opening of the aortic valve).
The arterial blood pressure is expressed in four
different terms:
• Systolic BP
• Diastolic BP
• Pulse pressure
• Mean arterial blood pressure

• Systolic blood pressure is defined as the maximum

pressure exerted in the arteries during systole of the
heart. It occurs at the peak of maximum ejection
phase. The normal systolic pressure is 120mmHg, it
ranges between 110 – 140mmHg.
• Diastolic blood pressure is the minimum pressure
in the arteries during diastole. It occurs during the
isometric contraction phase just before opening of
the aortic valve. The normal diastolic blood
pressure is 80 mmHg, it ranges between 60-
80mmHg.
• Pulse pressure: This is the difference between the
systolic pressure and diastolic pressure. Its normal
valve is 40mmHg.
• Mean arterial blood pressure: It is the average
pressure in the arteries, but it is not the arithmetic
mean of systolic and diastolic blood pressure. This
is because systole occupies a smaller portion of the
cardiac cycle than the diastole. It is the diastolic
blood pressure plus one-third of pulse pressure.
• MABP = DP + 1/3 (PP)
• MABP = DP + 1/3 (SP – DP)
PP= Pulse pressure
DP= Diastolic pressure
SP= Systolic pressure
 Physiological variations
• Age
• Sex
• Body build
• Diurnal variation
• After meals
• During sleep
• Emotions and dreams
• Exercise
 Determinants of arterial blood pressure –
factors maintaining ABP
These are factors necessary for the maintenance of
normal BP. They include:
• Cardiac output
• Heart rate
• Peripheral resistance
• Blood volume
• Venous return
• Elasticity of blood vessels
• Velocity of blood flow
• Diameter of blood vessels
• Viscosity of blood
Summary of factors affecting ABP
Measurement of ABP

Direct measurement
• The direct method of measuring ABP is usually done in
animals. It is performed by inserting a cannula into an
artery which is connected to a manometer. By using a
kymograph, the BP can be recorded continuously in
form of a graph.

Indirect measurement
• This is performed by an apparatus called the
sphygmomanometer which consists of a cuff, connected
to a mercury manometer. The cuff can be inflated with
air using a hand pump, and deflated by opening a release
valve. Alongside with the sphygmomanometer, the
stethoscope is necessary to measure blood pressure.
Principle
• When an external pressure is applied over the artery,
the artery, the blood flow through it is obstructed
and the pressure required to cause occultism of
blood flow indicates the pressure inside the vessel.
• Brachial artery is usually chosen because of
convenience. The arm cuff is tied around the upper
arm above the cubital fossa. The cuff should not be
two tight or too loose. The cuff is attached to the
sphygmomanometer. The blood pressure can be
measured by three methods:
• Palpation method
• Ausculatory method
• Oscillatory method
 Regulation of arterial BP

VASOMOTOR CENTRE
• Vasomotor center is bilaterally situated in the reticular
formation of medulla oblongata and the lower part of the
pons.
Vasomotor center consists of three areas:
i. Vasoconstrictor area
ii. Vasodilator area
iii. Sensory area.
 REGULATION OF ARTERIAL BP
• (a) Short-term mechanisms
• These are few seconds after alteration of the BP and their
action lasts for several hours. They are mostly nervous
reflexes, but adjust vascular capacity, resistance and cardiac
pump.

• (1) Arterial baroreflexes: The receptors of these reflexes

are located in the carotid sinus and wall of the aortic arch.
They are stretch receptors that discharge when arterial BP
rises, in which case they discharge signals that stimulate
vasodilation centre and inhibit the vasoconstrictor centre.
This results in reduction of the arterial BP by decreasing
• Rate and force of contraction
• Cardiac pumping
• Cardiac output
• Peripheral resistance
• Arterial chemoreflexes: The receptors are located in
the carotid and aortic bodies. They are stimulated
when the arterial BP is reduced below 60mmHg.
• They discharge signals leading to stimulation of the
vasoconstrictor centre and vasodilator centre.
• This causes elevation of the arterial BP by increasing
(a) the cardiac pumping power and CO (b) peripheral
resistance, (c) by the resulting generalized
vasoconstriction. Opposite effects occur when the
blood pressure is increased.
• CNS ischaemic response: When arterial BP below
60mmHg, brain ischemia occurs. The resulting local
hypoxia stimulate the vasoconstrictor centre resulting in
generalized vasoconstriction, which elevates the arterial BP
and maintains the cerebral blood flow. It could also be
referred to as Cushing’s reflex.
• Abdominal compression reflex: This is an important
mechanism to raise the arterial BP since it increases the
intra-abdominal pressure which compresses the abdominal
veins resulting in an increase in the venous return and
consequently CO, which helps elevation of the arterial BP.
 Intermediate-term mechanisms
These mechanisms control the arterial BP by adjusting the vascular
capacity, resistance and blood volume. The act within a few minutes
after alteration of the BP and their action lasts for several days.
• (1) Capillary fluid shift mechanism: This mechanism occurs
especially when the arterial BP is altered as a result of changes in
the blood volume. An increase in the blood volume increases the
capillary hydrostatic pressure, and thus helps fluid filtration into
the tissue spaces, thus the blood volume is decreased leading to
reduction in arterial BP toward the normal level.
• (2) Stress relaxation mechanism: A rise of the arterial BP
stretches the arteries and increase the tension in their walls.
However, after sometime the arteries relax and the tension in their
walls decreases. This is called stress relaxation of the arteries, and
it helps in lowering of the arterial BP.
• (3) Renin-angiotensin VC mechanism: A fall
of the arterial BP leads to renal ischaemia.
• (4) Right atrial mechanism: This occurs
especially when the arterial BP is altered as a result
of changes in the blood volume. An increase in the
blood volume stimulates the volume receptors in the
right atrium resulting in the following:
• Generalized vasodilatation which decreases the
peripheral resistance.
• Reflex inhibition of secretion of antidiuretic
hormone.
• Atrial natruetic pressure (ANP) is also secreted,
which increases salt and water excretion, therefore
reducing blood volume.
Regulation of blood pressure by renin-angiotensin
mechanism
 Long-term mechanism
• These mechanisms control the arterial BP by adjusting the
body fluids and blood volume through modifying the
excretion of water and salt by the kidneys.
• Glomerular filtration
• Secretion of aldosterone hormone
Pathological variations of arterial blood pressure
A. Hypertension: Hypertension is defined as the persistent high blood
pressure. Clinically, when the systolic pressure remains elevated
above 150 mm Hg and diastolic pressure remains elevated above 90
mm Hg, it is considered as hypertension.
Types of Hypertension
Hypertension is divided into two types:
• 1. Primary hypertension or essential hypertension
• 2.Secondary hypertension.
• Primary hypertension
• is the elevated blood pressure in the absence of any
underlying disease. It is also called essential hypertension.
Arterial blood pressure is increased because of increased
peripheral resistance, which occurs due to some unknown
cause.
• Secondary Hypertension
• Secondary hypertension is the high blood pressure due to
some underlying disorders. The different forms of secondary
hypertension are:
(1) Cardiovascular hypertension
• a. Atherosclerosis: Hardening of blood vessels due to fat
deposition
• b. Coarctation of aorta: Narrowing of aorta.
(2) Endocrine hypertension
• Endocrine hypertension is developed because of hyperactivity of
some endocrine glands:
• a. Pheochromocytoma: Tumor in adrenal medulla, resulting in
excess secretion of catecholamines
• b. Hyperaldosteronism: Excess secretion of aldosterone from
adrenal cortex
• c. Cushing syndrome: Excess secretion of glucocorticoids from
adrenal cortex.
(3) Renal hypertension
Renal diseases causing hypertension:
• a. Stenosis of renal arteries
• b. Tumor of juxtaglomerular cells, leading to excess
production of angiotensin II
• c. Glomerulonephritis.
(4) Neurogenic hypertension
Nervous disorders producing hypertension:
• a. Increased intracranial pressure
• b. Lesion in tractus solitarius
• c. Sectioning of nerve fibers from carotid sinus.
(5) Hypertension during pregnancy
• Some pregnant women develop hypertension because of toxemia
of pregnancy. Arterial blood pressure is elevated by the low
glomerular filtration rate and retention of sodium and water.
• TREATMENT OF HYPERTENSION
• 1. Beta adrenoceptor blockers
• 2. Alpha adrenoceptor blockers
• 3. Calcium channel blockers
• 4. Vasodilators
• 5. Diuretics
• 6. Inhibitors of angiotensin-converting enzyme (ACE inhibitors)
• 7. Angiotensin II receptor blockers
HYPOTENSION
• Hypotension is the low blood pressure. When the systolic pressure
is less than 90 mm Hg, it is considered as hypotension.
1. Primary hypotension
• Primary hypotension is the low blood pressure that develops in the
absence of any underlying disease and develops due to some
unknown cause. It is also called essential hypotension.
2. Secondary hypotension
• Secondary hypotension is the hypotension that occurs due to some
underlying diseases. Diseases, which cause hypotension are:
i. Myocardial infarction
ii. Hypoactivity of pituitary gland
iii. Hypoactivity of adrenal glands
iv. Tuberculosis
v. Nervous disorders.
Orthostatic Hypotension
• Orthostatic hypotension is the sudden fall in blood
pressure while standing for some time. It is due to the
effect of gravity. It develops in persons affected by
myasthenia gravis or some nervous disorders like
tabes dorsalis, syringomyelia and diabetic neuropathy.
Common symptom of this condition is orthostatic
syncope.
 HAEMORRHAGE
Hemorrhage is defined as the excess loss of blood due to rupture
of blood vessels.
COMPENSATORY EFFECTS OF HEMORRHAGE
Many effects are observed during and after hemorrhage. Effects
are different in acute hemorrhage and chronic hemorrhage.
Compensatory Effects
• After hemorrhage, series of compensatory reactions develop in
the body to cope up with the blood loss. Compensatory effects
of hemorrhage are of two types.
A. Immediate compensatory effects
B. Delayed compensatory effects
IMMEDIATE COMPENSATORY EFFECTS OF
HEMORRHAGE
1. On Cardiovascular System
2. On Skin
3. On Tissue Fluid
4. On Kidneys
5. On Renin Secretion
6. On Secretion of Antidiuretic Hormone
7. On Secretion of Catecholamines
8. On Respiration
9. On Nervous System
DELAYED COMPENSATORY EFFECTS OF HEMORRHAGE

• If hemorrhage is not severe, some delayed

compensatory reactions occur. These reactions help
to restore blood volume, blood pressure and blood
flow to different regions of the body.
Delayed reactions are:
• 1. Restoration of plasma volume
• 2. Restoration of plasma proteins
• 3. Restoration of red blood cell count and
hemoglobin content
 SHOCK
• Shock is a general term that refers to the depression or
suppression of body functions produced by any disorder.
• Circulatory shock refers to the shock developed by
inadequate blood flow throughout the body. It is a life
threatening condition and it may result in death if the
affected person is not treated immediately.
• Characteristic feature of all types of circulatory shock is the
insufficient blood flow to the tissues particularly the brain.
Major cause of decreased blood flow is the reduction in
cardiac output.
• Following are the manifestations of circulatory shock:
• 1. Whenever cardiac output is decreased, arterial blood
pressure drops down
• 2. Low blood pressure produces reflex tachycardia and
reflex vasoconstriction
• 3. Tachycardia decreases the diastolic period. So, filling of
the heart reduces leading to decrease in stroke volume and
systolic pressure.
• This decreases the pulse pressure below 20 mm Hg.
• Pulse also becomes feeble.
• 4. Stagnant hypoxia develops because of decreased velocity of
blood flow
• 5. Skin becomes pale and cold due to the vasoconstriction
• 6. Along with hypoxia, cyanosis also develops in many parts of
the body, particularly ear lobes and fingertips
• 7. Glomerular filtration rate (GFR) and urinary output are
reduced due to fall in blood pressure and constriction of renal
blood vessels
• 8. Metabolic activities of myocardium are accelerated because
of reduced blood flow and increased heart rate. A large amount
of lactic acid is produced, resulting in acidosis.
• 9. Acidosis decreases myocardial efficiency and pumping
action of the heart leading to further reduction in cardiac output
• 10. So, the blood flow to vital organs is severely
affected
• 11. Lack of blood flow to brain tissues produces
ischemia resulting in fainting and irreparable
damage of brain tissues
• 12. Finally the damage of brain tissues and cardiac
arrest kill the victim.
STAGES OF CIRCULATORY
SHOCK
Circulatory shock occurs in three stages:
1. First stage or compensated stage
2. Second stage or progressive stage
3. Third stage or irreversible stage.
TYPES AND CAUSES OF CIRCULATORY SHOCK
Circulatory shock is primarily classified into four
types
A. Shock due to decreased blood volume
B. Shock due to increased vascular capacity
C. Shock due to cardiac disease
D. Shock due to obstruction of blood flow.
SHOCK DUE TO DECREASED BLOOD VOLUME –
HYPOVOLEMIC SHOCK
• Shock due to decreased blood volume is called hypovolemic
shock or cold shock. It occurs when there is acute loss of at
least 10% to 15% of blood
• Important Manifestations of Hypovolemic Shock
• 1. Decrease in cardiac output
• 2. Low blood pressure
• 3. Thin thready pulse
• 4. Pale and cold skin
• 5. Increase in respiratory rate
• 6. Restlessness or lethargy.
Pathological Conditions when Hypovolemic
Shock Occurs

• 1. Hemorrhage: Hemorrhagic shock

• 2. Trauma: Traumatic shock
• 3. Surgery: Surgical shock
• 4. Burns: Burn shock
• 5. Dehydration: Dehydration shock.
SHOCK DUE TO INCREASED VASCULAR
CAPACITY – VASOGENIC SHOCK

• In this case, the blood volume is normal. Shock occurs

because of inadequate blood supply to the tissues due to
increased vascular capacity. Capacity of the vascular system
increases by the extensive dilatation of blood vessels. It is
also known as vasogenic or low resistance or distributive
shock.
Causes and Types of Vasogenic Shock

• 1. Sudden loss of vasomotor tone: Neurogenic shock

• 2. Anaphylaxis: Anaphylactic shock
• 3. Sepsis: Septic shock.
• Neurogenic Shock
• Neurogenic shock is the type of shock characterized by
sudden depression of nervous system due to extensive
vasodilatation caused by loss of vasomotor tone.
• Conditions when neurogenic shock develops
• i. Ischemia of brain: Severe ischemia in medulla depresses
the activity of vasomotor center
• ii. General anesthesia
• iii. Spinal anesthesia
• iv. Emotional conditions: Extreme emotions cause sudden
and exaggerated activity of autonomic nervous system, the
subject faints because of neurogenic shock.
SHOCK DUE TO CARDIAC DISEASES –
CARDIOGENIC SHOCK
• Conditions when Cardiogenic Shock Occurs
• 1. Arrhythmia, particularly those which lead to
reduced
• cardiac output
• 2. Depressed activity of myocardium due to
ischemia
• 3. Congestive cardiac disease.
SHOCK DUE TO OBSTRUCTION OF
BLOOD FLOW – OBSTRUCTIVE SHOCK
• Shock developed due to the obstruction of blood flow
through circulatory system is called obstructive shock.
• Conditions when Obstructive Shock Occurs
• 1. Tumor in myocardium
• 2. Cardiac tamponade
• 3. Obstruction of blood vessels in lungs due to embolism.
 TREATMENT FOR CIRCULATORY SHOCK
Treatment for shock is based on the cause of the shock.
Following are the various measures taken during the treatment
of shock.
• Blood transfusion
• Plasma transfusion
• Administration of plasma substitutes
• Administration of sympathomimetic drugs
• Administration of glucocorticoids
• Oxygen therapy
• By changing the posture
FIRST STAGE OR COMPENSATED STAGE

• First stage is also called non-progressive stage. When blood loss is less
than 10% of total volume, the blood pressure decreases only
moderately. And the regulatory mechanisms in the body operate
successfully to reestablish normal blood pressure and normal blood flow
throughout the body. Thus the shock becomes nonprogressive
• and the person recovers. Regulatory mechanisms involve negative
feedback control.
• Regulatory mechanisms are:
• i. Baroreceptor mechanism
• ii. Renal mechanism
• iii. ADH mechanism.
SECOND STAGE OR PROGRESSIVE STAGE
• Second stage is also called decompensated stage. When the
shock is severe, positive feedback system develops so that
regulatory mechanisms become inadequate to compensate.
And the shock enters progressive stage.
• With immediate and appropriate treatment, this stage of
shock can be reversed.
THIRD STAGE OR IRREVERSIBLE STAGE
• Third stage is the last stage prior to the collapse. It is also
called refractory stage. Irreversible stage leads to death
regardless of type of treatment offered to the patient. It is
because the brain fails to function due to severe cerebral
ischemia. The blood pressure falls drastically. Even the
infusion of blood fails to restore blood pressure. Finally,
cardiac failure occurs due to decrease in the myocardial
activity and reduced.
CARDIOVASCULAR ADJUSTMENT TO EXERCISE
• During exercise, there is an increase in metabolic needs of
body tissues, particularly the muscles.
• Various adjustments in the body during exercise are aimed
at:
1. Supply of various metabolic requisites like nutrients and
oxygen to muscles and other tissues involved in exercise.
2. Prevention of increase in body temperature.
• 1. On blood
• 2. On blood volume
• 3. On heart rate
• 4. On cardiac output
• 5. On venous return
• 6. On blood flow to skeletal muscles
• 7. On blood pressure