CARDIOVASCULAR SYSTEM

Concept of the Cardiovascular System

We are more conscious of our heart than we are of most organs, and more wary of its failure.
Speculation about the heart is at least as old as written history. Some ancient Chinese, Egyptian Greek, and
Roman scholars correctly surmised that the heart is a pump for filling the vessels with blood.
Aristotle’s views, however, were a step backward. Perhaps because the heart quickens its pace when we
are emotio- nally aroused, and because grief causes “heartache,” he regarded it primarily as the seat of
emotion, as well as a source of heat to aid digestion.
During the Middle Ages, Western medical schools clung dogmatically to the ideas of Aristotle. Perhaps
the only significant advance came from Muslim medicine, when thirteenth-century physician Ibn an-Nafis
described the role of the coronary blood vessels in nourishing the heart. The sixteenth century dissections
and anatomical charts of Vesalius, however, greatly improved knowledge of cardiovascular anatomy and
set the stage for a more scientific study of the heart and treatment of its disorders—the science we now call
cardiology.

Cardiovascular system includes heart and blood vessels. Heart pumps blood into the blood vessels.\
Blood vessels circulate the blood throughout the body. Blood transports nutrients and oxygen to the tissues
and removes carbon dioxide and waste products from the tissues.

THE HEART

Heart is a muscular organ that pumps blood throughout the circulatory system. It is situated in between
two lungs in the mediastinum. It is made up of four chambers, two atria and two ventricles. The
musculature of ventricles is thicker than that of atria. Force of contraction of heart depends upon the
muscles.

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 Figure A: Section of the heart

SIZE, SHAPE, AND POSITION OF THE HEART

The heart is located in the thoracic cavity in the mediastinum, the area between the lungs. About two-
thirds of it lies to the left of the median plane. The broad superior portion of the heart, called the base, is
the point of attachment for the great vessels (arteries and veins). Its inferior end, the apex, tilts to the left
and tapers to a blunt point. The adult heart is about 9 cm wide at the base, 13 cm from base to apex, and 6
cm from anterior to posterior at its thickest point—roughly the size of a fist. It weighs about 300 g.

RIGHT SIDE OF THE HEART

Right side of the heart has two chambers, right atrium and right ventricle. Right atrium is a thin walled
and low-pressure chamber. It has got the pacemaker known as sinoatrial node that produces cardiac
impulses and atrioventricular node that co- nducts the impulses to the ventricles. Right atrium receives
venous (deoxygena- ted) blood via two large veins:
1. Superior vena cava that returns venous blood from the head, neck and upper limbs,
2. Inferior vena cava that returns venous blood from lower parts of the body.
Right atrium communicates with right ventricle through tricuspid valve. Wall of right ventricle is thick.
Venous blood from the right atrium enters the right Ventri-
cle through this valve. From the right ventricle, pulmonary artery arises. It carries the venous blood from
right ventricle to lungs. In the lungs, the deoxygenated blood is oxygenated.

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LEFT SIDE OF THE HEART

Left side of the heart has two chambers, left atrium and left ventricle. Left atrium is a thin walled and
low-pressure chamber. It receives oxygenated blood from the lungs through pulmonary veins. This is the
only exception in the body, where an artery carries venous blood and vein carries the arterial blood.
Blood from left atrium enters the left ventricle through mitral valve (bicuspid valve). Wall of the left
ventricle is very thick. Left ventricle pumps the arterial blood to different parts of the body through
systemic aorta.

THE HEART WALL

The heart wall consists of three layers of tissues:

1. Outer pericardium
2. Middle myocardium
3. Inner endocardium.
The epicardium is a serous membrane composed of a simple squamous epithelium overlying a thin layer
of areolar tissue. Over much of the heart, it has
thick deposits of fat that fill grooves in the heart surface and protect the coronary blood vessels.
The myocardium by far the thickest layer, is composed of cardiac muscle and performs the work of the
heart. Its muscle cells spiral around the heart and are
bound together by collagenous and elastic fibers that make up the fibrous skeleton. The fibrous skeleton
helps to provide structural support for the heart, especially around the valves and the openings of the great
vessels.
The endocardium consists of a simple squamous endothelium overlying a thin areolar tissue layer. It
forms the smooth inner lining of the chambers and valves and is continuous with the endothelium of the
blood vessels.

VALVES OF THE HEART

There are four valves in human heart. Two valves are in between atria and the ventricles called
atrioventricular valves. Other two are the semilunar valves, placed at the opening of blood vessels arising
from ventricles, namely systemic aorta and pulmonary artery. Valves of the heart permit the flow of blood
through heart in only one direction.

ATRIOVENTRICULAR VALVES

Left atrioventricular valve is otherwise known as mitral valve or bicuspid valve. Right atrioventricular
valve is known as tricuspid valve. Cusps of the valves are attached to papillary muscles by means of
chordae tendineae. Papillary muscles arise from inner surface of the ventricles. Papillary muscles play an
important role in closure of the cusps and in preventing the back flow of blood from ventricle to atria
during ventricular contraction.
Atrioventricular valves open only towards ventricles and prevent the backflow of blood into atria.

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 Figure B: Valves of the heart

SEMILUNAR VALVES

Semilunar valves are present at the openings of systemic aorta and pulmonary artery and are known as
aortic valve and pulmonary valve respectively. Because of the half-moon shape, these two valves are
called semilunar valves.
Semilunar valves open only towards the aorta and pulmonary artery and prevent the backflow of blood
into the ventricles.

PROPERTIES OF CARDIAC MUSCLE

1. EXCITABILITY
Excitability is defined as the ability of a living tissue to give response to a stimulus. In all the tissues,
initial response to a stimulus is electrical activity in the form of action potential. It is followed by
mechanical activity in the form of contraction, secretion, etc.

SPREAD OF ACTION POTENTIAL THROUGH CARDIAC MUSCLE

Action potential spreads through cardiac muscle very rapidly because of the presence of gap junctions
between the cardiac muscle fibers. Gap junctions are permeable junctions and allow free movement of
ions and so the action potential spreads rapidly from one muscle fibre to another fibre. Action potential is
transmitted from atria to ventricles through the fibers of specialized conductive system.

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2. RHYTHMICITY
Rhythmicity is the ability of a tissue to produce its own impulses regularly. It is also called auto-
rhythmicity or self-excitation. Property of rhythmicity is present in all the tissues of heart. However, heart
has a specialized excitatory structure, from which the discharge of impulses is rapid. This specialized
structure is called pacemaker. From here, the impulses spread to other parts through the specialized
conductive system.

PACEMAKER
Pacemaker is the structure of heart from which the impulses for heartbeat are produced. It is formed
by the pacemaker cells called P cells. In mammalian heart, the pacemaker is sinoatrial node (SA node). It
was Lewis Sir Thomas, who named SA node as pacemaker of heart, in 1918.
Sinoatrial Node Sinoatrial (SA) node is a small strip of modified cardiac muscle, situated in the superior
part of lateral wall of right atrium, just below the opening of superior vena cava. The fibers of this node do
not have contractile elements. These fibers are continuous with fibers of atrial muscle, so that the impulses
from the SA node spread rapidly through atria.

Spread of Impulses from SA Node

Mammalian heart has got a specialized conductive system, by which the impulses from SA node
spreads to other parts of the heart.

3. CONDUCTIVITY
Human heart has a specialized conductive system, through which impulses from SA node are
transmitted to all other parts of the heart.

CONDUCTIVE SYSTEM IN HUMAN HEART

Conductive system of the heart is formed by the modified cardiac muscle fibers. These fibers are the
specialized cells, which conduct the impulses rapidly from SA node to the ventricles. Conductive tissues
of the heart are also called the junctional tissues. Components of Conductive System in Human Heart
includes;
1. AV node
2. Bundle of His
3. Right and left bundle branches
4. Purkinje fibers.
SA node is situated in right atrium, just below the opening of superior vena cava. AV node is situated
in right posterior portion of intra-atrial septum. Impulses from SA node are conducted throughout right

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 and left atria. Impulses also reach the AV node via some specialized fibers called Internodal fibers. There
are three types of internodal fibers:
1. Anterior internodal fibers of Bachman
2. Middle internodal fibers of Wenckebach
3. Posterior internodal fibers of Thorel.
All these fibers from SA node converge on AV node and interdigitate with fibers of AV node. From
AV node, the bundle of His arises. It divides into right and left branches, which run on either side of the
interventricular septum. From each branch of bundle of His, many Purkinje fibers arise and spread all over
the ventricular myocardium.

Sinoatrial node and conductive system of the heart.

4. CONTRACTILITY
Contractility is ability of the tissue to shorten in length (contraction) after receiving a stimulus. Various
factors affect the contractile properties of the cardiac muscle.

CARDIAC CYCLE
Cardiac cycle is defined as the succession of (sequence of) coordinated events taking place in the heart
during each beat. Each heartbeat consists of two major periods called systole and diastole. During systole,
heart contracts and pumps the blood through arteries. During diastole, heart relaxes and blood is filled in
the heart. All these changes are repeated during every heartbeat, in a cyclic manner.

EVENTS OF CARDIAC CYCLE

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Events of cardiac cycle are classified into two:
1. Atrial events
2. Ventricular events.

DIVISIONS AND DURATION OF CARDIAC CYCLE

When the heart beats at a normal rate of 72/minute, duration of each cardiac cycle is about 0.8 second.

ATRIAL EVENTS
Atrial events are divided into two divisions:
1. Atrial systole = 0.11 (0.1) sec
2. Atrial diastole = 0.69 (0.7) sec.

VENTRICULAR EVENTS
Ventricular events are divided into two divisions:
1. Ventricular systole = 0.27 (0.3) sec
2. Ventricular diastole = 0.53 (0.5) sec.
In clinical practice, the term ‘systole’ refers to ventricular systole and ‘diastole’ refers to ventricular
diastole. Ventricular systole is divided into two subdivi sions and ventricular diastole is divided into five
subdivisions.

VENTRICULAR SYSTOLE
Time (second)
1. Isometric contraction = 0.05
2. Ejection period = 0.22
0.27
VENTRICULAR DIASTOLE
1. Protodiastole = 0.04
2. Isometric relaxation = 0.08
3. Rapid filling = 0.11
4. Slow filling = 0.19
5. Last rapid filling = 0.11

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 0.53
Among the atrial events, atrial systole occurs during the last phase of ventricular diastole. Atrial
diastole is not considered as a separate phase, since it coincides with the whole of ventricular systole and
earlier part of ventricular diastole.

DESCRIPTION OF ATRIAL EVENTS

ATRIAL SYSTOLE;
Atrial systole is also known as last rapid filling phase or presystole. It is usually considered as the last
phase of ventricular diastole. Its duration is 0.11 second.
During this period, only a small amount, i.e. 10% of blood is forced from atria into ventricles. Atrial
systole is not essential for the maintenance of circulation. Many persons with atrial fibrillation survive for
years, without suffering from circulatory insufficiency. However, such persons feel difficult to cope up
with physical stress like exercise.

HEART SOUNDS
Heart sounds are the sounds produced by mechanical activities of heart during each cardiac cycle.
Heart sounds are produced by:
1. Flow of blood through cardiac chambers
2. Contraction of cardiac muscle
3. Closure of valves of the heart.
Heart sounds are heard by placing the ear over the chest or by using a stethoscope or microphone. These
sounds are also recorded graphically.

DIFFERENT HEART SOUNDS

Four heart sounds are produced during each cardiac cycle:
1. First heart sound
2. Second heart sound
3. Third heart sound
4. Fourth heart sound.

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 First and second heart sounds are called classical heart sounds and are heard by using the stethoscope.
These two sounds are more prominent and resemble the spoken words ‘LUB, (or LUBB) and ‘DUBB’ (or
DUP), respectively.
Third heart sound is a mild sound and it is not heard by using stethoscope in normal conditions. But it
can be heard by using a microphone. Fourth heart sound is an inaudible sound. It becomes audible in
pathological conditions only. This sound is studied only by graphic registration, i.e. the phonocardiogram.

IMPORTANCE OF HEART SOUNDS

Study of heart sounds has important diagnostic value in clinical practice because alteration in the heart
sounds indicates cardiac diseases involving valves of the heart.

DESCRIPTION OF HEART SOUNDS

FIRST HEART SOUND
First heart sound is produced during isometric contraction period and earlier part of ejection period.
Causes
Major cause for first heart sound is the sudden and simultaneous closure of atrioventricular valves.
However, some other factors are also involve.
Characteristics
First heart sound is a long, soft and low-pitched sound. It resembles the spoken word ‘LUBB’. The
duration of this sound is 0.10 to 0.17 second.

SECOND HEART SOUND

Second heart sound is produced at the end of protodiastolic period.
Cause
Second heart sound is produced due to the sudden and simultaneous closure of the semilunar valves.
Characteristics
Second heart sound is a short, sharp and high-pitched sound. It resembles the spoken word ‘DUBB’ (or
DUP). Duration of second heart sound is 0.10 to 0.14 second. Its frequency is 50 cycles/second.
THIRD HEART SOUND
Third heart sound is a low-pitched sound that is produced during rapid filling period of the cardiac cycle.
It is also called ventricular gallop or protodiastolic gallop, as it is produced during earlier part of diastole.
Usually, the third heart sound is inaudible by stethoscope and it can be heard only by using microphone.
Causes
Third heart sound is produced by the rushing of blood into ventricles and vibrations set up in the
ventricular wall during rapid filling phase. It may also be due to vibrations set up in chordae tendineae.

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 Characteristics
Third heart sound is a short and low-pitched sound. Duration of this sound is 0.07 to 0.10 second. Its
frequency is 1 to 6 cycles/second.

FOURTH HEART SOUND

Normally, the fourth heart sound is an inaudible sound. It becomes audible only in pathological
conditions. It is studied only by graphical recording, i.e. by phonocardiography. This sound is produced
during atrial systole (late diastole) and it is considered as the physiologic atrial sound. It is also called
atrial gallop or presystolic gallop.
Causes
Fourth heart sound is produced by contraction of atrial musculature and vibrations are set up in atrial
musculature, flaps of the atrioventricular valves during systole. It is also due to the vibrations set up in the
ventricular myocardium because of ventricular distention during atrial systole.
Characteristics
Fourth heart sound is a short and low-pitched sound. Duration of this sound is 0.02 to 0.04 second. Its
frequency is 1 to 4 cycles/second.

METHODS OF STUDY OF HEART SOUNDS

Heart sounds are studied by three methods:
1. By using stethoscope
2. By using microphone
3. By using phonocardiogram.

BY STETHOSCOPE
First and second heart sounds are heard on the auscultation areas, by using the stethoscope. The chest
piece of the stethoscope is placed over four areas on the chest, which are called auscultation areas.
Auscultation Areas
i. Mitral area (Bicuspid area)
Mitral area is in the left 5th intercostal space, about 10 cm away from the midline (midclavicular line).
Sound produced by the closure of mitral valve (first heart sound) is transmitted well into this area. It is
also called apex beat area because apex beat is felt in this area.
ii. Tricuspid area
Tricuspid area is on the xiphoid process. Sound produced by the closure of tricuspid valve (first heart
sound) is transmitted well into this area.
iii. Pulmonary area

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 Pulmonary area is on the left 2nd intercostal space, close to sternum. Sound produced by the closure of
pulmonary valve (second heart sound) is heard well on this area.
iv. Aortic area
Aortic area is over the right 2nd intercostal space, close to the sternum. On this area, the sound produced
by the closure of aortic valve (second heart sound) is heard well.

ELECTROCARDIOGRAM (ECG)
DEFINITIONS 0F TERMS;
1. Electrocardiography
Electrocardiography is the technique by which electrical activities of the heart are studied. The spread
of excitation through myocardium produces local electrical potential. This low-intensity current flows
through the body, which acts as a volume conductor. This current can be picked up from surface of the
body by using suitable electrodes and recorded in the form of electrocardiogram. This technique was
discovered by Dutch physiologist, Einthoven Willem, who is considered the father of electrocardiogram
(ECG).
2. Electrocardiograph
Electrocardiograph is the instrument (machine) by which electrical activities of the heart are recorded.
3. Electrocardiogram
Electrocardiogram (ECG) is the record or graphical registration of electrical activities of the heart, which
occur prior to the onset of mechanical activities. It is the summed electrical activity of all cardiac muscle
fibers recorded from surface of the body.
USES OF ECG
Electrocardiogram is useful in determining and diagnosing the following:
1. Heart rate
2. Heart rhythm
3. Abnormal electrical conduction
4. Poor blood flow to heart muscle (ischemia)
5. Heart attack
6. Coronary artery disease
7. Hypertrophy of heart chambers.

4- ELECTROCARDIOGRAPHIC GRID
The paper that is used for recording ECG is called ECG paper. ECG machine amplifies the electrical
signals produced from the heart and records these signals on a moving ECG paper.

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Electrocardiographic grid refers to the markings (lines) on ECG paper. ECG paper has horizontal and
vertical lines at regular intervals of 1 mm. Every 5th line (5 mm) is thickened.

DURATION
Time duration of different ECG waves is plotted horizontally on X-axis.
On X-axis
1 mm = 0.04 second
5 mm = 0.20 second
AMPLITUDE
Amplitude of ECG waves is plotted vertically on Y-axis.
On Y-axis
1 mm = 0.1 mV
5 mm = 0.5 mV

ECG LEADS
ECG is recorded by placing series of electrodes on the surface of the body. These electrodes are called
ECG leads and are connected to the ECG machine.
Electrodes are fixed on the limbs. Usually, right arm, left arm and left leg are chosen. Heart is said to
be in the center of an imaginary equilateral triangle drawn by connecting the roots of these three limbs.
This triangle is called Einthoven triangle.
ECG is recorded in 12 leads, which are generally classified into two categories.
I. Bipolar leads
II. Unipolar leads.
BIPOLAR LIMB LEADS
Bipolar limb leads are otherwise known as standard limb leads. Two limbs are connected to obtain these
leads and both the electrodes are active recording electrodes, i.e. one electrode is positive and the other
one is negative.
Standard limb leads are of three types:
a. Limb lead I
b. Limb lead II
c. Limb lead III.
Lead I

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Lead I is obtained by connecting right arm and left arm. Right arm is connected to the negative terminal of
the instrument and the left arm is connected to the positive terminal.
Lead II
Lead II is obtained by connecting right arm and left leg. Right arm is connected to the negative terminal of
the instrument and the left leg is connected to the positive terminal.

Lead III
Lead III is obtained by connecting left arm and left leg. Left arm is connected to the negative terminal of
the instrument and the left leg is connected to the positive terminal.

Position of electrodes for standard limb leads, RA = Right arm, LA = Left arm, LL=Left leg.

WAVES OF NORMAL ECG

Normal ECG consists of waves, complexes, intervals and segments. Waves of ECG recorded by limb
lead II are considered as the typical waves. Normal electrocardiogram has the following waves, namely P,
Q, R, S and T. Einthoven had named the waves of ECG starting from the middle of the English alphabets
(P) instead of starting from the beginning (A).
Major Complexes in ECG
1. ‘P’ wave, the atrial complex
2. ‘QRS’ complex, the initial ventricular complex
3. ‘T’ wave, the final ventricular complex
4. ‘QRST’, the ventricular complex.

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 Waves
of normal ECG
CARDIAC OUTPUT
Cardiac output is the amount of blood pumped from each ventricle. Usually, it refers to left ventricular
output through aorta. Cardiac output is the most important factor in cardiovascular system, because rate of
blood flow through different parts of the body depends upon cardiac output.

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 DEFINITIONS AND NORMAL VALUES
Usually, cardiac output is expressed in three ways:
1. Stroke volume
2. Minute volume
3. Cardiac index.
However, in routine clinical practice, cardiac output refers to minute volume.
STROKE VOLUME
Stroke volume is the amount of blood pumped out by each ventricle during each beat. Normal value: 70
mL (60 to 80 mL) when the heart rate is normal (72/minute).
MINUTE VOLUME
Minute volume is the amount of blood pumped out by each ventricle in one minute. It is the product of
stroke volume and heart rate:
Minute volume = Stroke volume × Heart rate
Normal value: 5 L/ventricle/minute.

CARDIAC RESERVE
Cardiac reserve is the maximum amount of blood that can be pumped out by heart above the normal value.
Cardiac reserve plays an important role in increasing the cardiac output during the conditions like exercise.
It is essential to withstand the stress of exercise.
Cardiac reserve is usually expressed in percentage. In a normal young healthy adult, the cardiac reserve is
300% to 400%. In old age, it is about 200% to 250%. It increases to 500% to 600% in athletes. In cardiac
diseases, the cardiac reserve is minimum or nil.

VARIATIONS IN CARDIAC OUTPUT

(A) PHYSIOLOGICAL VARIATIONS
1. Age: In children, cardiac output is less because of less blood volume. Cardiac index is more than that in
adults because of less body surface area.
2. Sex: In females, cardiac output is less than in males because of less blood volume. Cardiac index is
more than in males, because of less body surface area.
3. Body build: Greater the body build, more is the cardiac output.

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4. Diurnal variation: Cardiac output is low in early morning and increases in day time. It depends upon the
basal conditions of the individuals.
5. Environmental temperature: Moderate change in temperature does not affect cardiac output. Increase in
temperature above 30°C raises cardiac output.
6. Emotional conditions: Anxiety, apprehension and excitement increases cardiac output about 50% to
100% through the release of catecholamines, which increase the heart rate and force of contraction.
7. After meals: During the first one hour after taking meals, cardiac output increases.
8. Exercise: Cardiac output increases during exercise because of increase in heart rate and force of
contraction.
9. High altitude: In high altitude, the cardiac output increases because of increase in secretion of
adrenaline. Adrenaline secretion is stimulated by hypoxia (lack of oxygen).
10. Posture: While changing from recumbent to upright position, the cardiac output decreases.
11. Pregnancy: During the later months of pregnancy, cardiac output increases by 40%.
12. Sleep: Cardiac output is slightly decreased or it is unaltered during sleep.

(B) PATHOLOGICAL VARIATIONS

(i) Increase in Cardiac Output
Cardiac output increases in the following conditions:
1. Fever: Due to increased oxidative processes
2. Anaemia: Due to hypoxia
3. Hyperthyroidism: Due to increased basal metabolic rate.
(ii) Decrease in Cardiac Output
Cardiac output decreases in the following conditions:
1. Hypothyroidism: Due to decreased basal metabolic rate
2. Atrial fibrillation: Because of incomplete filling of ventricles
3. Incomplete heart block with coronary sclerosis or myocardial degeneration: Due to defective pumping
action of the heart
4. Congestive cardiac failure: Because of weak contractions of heart
5. Shock: Due to poor pumping and circulation
6. Haemorrhage: Because of decreased blood volume.

DISTRIBUTION OF CARDIAC OUTPUT

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 The whole amount of blood pumped out by the right ventricle goes to lungs. But, the blood pumped by
the left ventricle is distributed to different parts of the body. Fraction of cardiac output distributed to a
particular region or organ depends upon the metabolic activities of that region or organ.
Distribution of Blood Pumped out of Left Ventricle
Distribution of blood pumped out of left ventricle to different organs and the percentage of cardiac output.
Heart, which pumps the blood to all other organs, receives the least amount of blood. Liver receives
maximum amount of blood.
Organs Amount of blood (mL/minute). Percentage
Liver 1,500 30
Kidney 1,300 26
Skeletal muscles 900 18
Brain 800 16
Skin, bone and GI tract 300 6
Heart 200 4
Total 5,000 100

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.

1. VENOUS RETURN
Venous return 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, cardiac output is directly
proportional to venous return, provided the other factors (force of contraction, heart rate and peripheral
resistance) remain constant. Venous return in turn, depends upon five factors:
i. Respiratory pump ii. Muscle pump iii. Gravity iv. Venous pressure v. Sympathetic tone.
i. Respiratory Pump
Respiratory pump is the respiratory activity that helps the return of blood, to heart during inspiration. It
is also called abdominothoracic pump. During inspiration, thoracic cavity expands and makes the
intrathoracic pressure more negative. It increases the diameter of inferior vena cava, resulting in increased
venous return. At the same time, descent of diaphragm increases the intra-abdominal pressure, which

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compresses abdominal veins and pushes the blood upward towards the heart and thereby the venous return
is increased.
ii. Muscle Pump
Muscle pump is the muscular activity that helps in return of the blood to heart. During muscular
activities, the veins are compressed or squeezed. Due to the presence of valves in veins, during
compression the blood is moved towards the heart.
When the skeletal muscles contract, the vein located in between the muscles is compressed. Valve of
the vein proximal to the contracting muscles is opened and the blood is propelled towards the heart. Valve
of the vein distal to the muscles is closed by the back flow of blood. During relaxation of the muscles, the
valve proximal to muscles closes and prevents the back flow of blood. The valve distal to the muscles
opens and allows the blood to flow upwards.
iii. Gravity
Gravitational force reduces the venous return. When a person stands for a long period, gravity causes
pooling of blood in the legs, which is called venous pooling. Because of venous pooling, the amount of
blood returning to heart decreases.
2. FORCE OF CONTRACTION
Cardiac output is directly proportional to the force of contraction, provided the other three factors
remain constant. Force of contraction depends upon preload and afterload.
Preload;
Preload is the stretching of the cardiac muscle fibers at the end of diastole, just before contraction. It
is due to increase in ventricular pressure caused by filling of blood during diastole. Stretching of muscle
fibers increases their length, which increases the force of contraction and cardiac output.
Afterload;
Afterload is the force against which ventricles must contract and eject the blood. Force is
determined by the arterial pressure. At the end of isometric contraction period, semilunar valves are
opened and blood is ejected into the aorta and pulmonary artery. So, the pressure increases in these two
vessels. Now, the ventricles have to work against this pressure for further ejection.
3. HEART RATE
Cardiac output is directly proportional to heart rate provided, the other three factors remain constant.
Moderate change in heart rate does not alter the cardiac output. If there is a marked increase in heart rate,
cardiac output is increased. If there is marked decrease in heart rate, cardiac output is decreased.

4. PERIPHERAL RESISTANCE
Peripheral resistance is the resistance offered to blood flow at the peripheral blood vessels. Peripheral
resistance is the resistance or load against which the heart has to pump the blood. So, the cardiac output is
inversely proportional to peripheral resistance. Resistance is offered at arterioles so, the arterioles are
called resistant vessels.

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 HEART RATE
NORMAL HEART RATE
Normal heart rate is 72/minute. It ranges between 60 and 80 per minute.
A- TACHYCARDIA
Tachycardia is the increase in heart rate above 100/ minute.
 Physiological Conditions when Tachycardia Occurs;
1. Childhood
2. Exercise
3. Pregnancy
4. Emotional conditions such as anxiety.
 Pathological Conditions when Tachycardia Occurs;
1. Fever
2. Anaemia
3. Hypoxia
4. Hyperthyroidism
5. Hypersecretion of catecholamines
6. Cardiomyopathy
7. Diseases of heart valves.

B- BRADYCARDIA
Bradycardia is the decrease in heart rate below 60/ minute.
 Physiological Conditions when Bradycardia Occurs;
1. Sleep
2. Athletes.
 Pathological Conditions when Bradycardia Occurs
1. Hypothermia
2. Hypothyroidism
3. Heart attack
4. Congenital Heart Disease

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5. Degenerative process of aging
6. Obstructive jaundice
7. Increased intracranial pressure.

REGULATION OF HEART RATE

Heart rate is maintained within normal range constantly. It is subjected for variation during normal
physiological conditions such as exercise, emotion, etc. However, under physiological conditions, the
altered heart rate is quickly brought back to normal. It is because of the perfectly tuned regulatory
mechanism in the body.

ARTERIAL BLOOD PRESSURE

Arterial blood pressure is defined as the lateral pressure exerted by the column of blood on wall of
arteries. The pressure is exerted when blood flows through the arteries. Generally, the term ‘blood
pressure’ refers to arterial blood pressure.
NORMAL VALUES
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 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).
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).
PULSE PRESSURE
Pulse pressure is the difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).

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 MEAN ARTERIAL BLOOD PRESSURE
Mean arterial blood pressure is the average pressure existing in the arteries. It is not the arithmetic
mean of systolic and diastolic pressures. 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).

(Mean arterial blood pressure = Diastolic pressure + 1/3 of pulse pressure)

Normal mean arterial pressure: 93 mm Hg (80 + 13 = 93).

VARIATIONS
Blood pressure is altered in physiological and pathological conditions. Systolic pressure is subjected
for variations easily and quickly and its variation occurs in a wider range. Diastolic pressure is not
subjected for easy and quick variations and its variation occurs in a narrow range.
PHYSIOLOGICAL VARIATIONS
1. Age
Arterial blood pressure increases as age advances.
Systolic pressure in different age At 70 years: 90 mm Hg
New-born: 70 mm Hg At 80 years: 95 mm Hg
After 1 month: 85 mm Hg
After 6 months: 90 mm Hg
After 1 year: 95 mm Hg
At puberty: 120 mm Hg
At 50 years: 140 mm Hg
At 70 years: 160 mm Hg
At 80 years: 180 mm Hg
Diastolic pressure in different age
New-born: 40 mm Hg
After 1 month: 45 mm Hg
After 6 months: 50 mm Hg
After 1 year: 55 mm Hg
At puberty: 80 mm Hg
At 50 years: 85 mm Hg

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2. Sex
In females, up to the period of menopause, arterial pressure is 5 mm Hg, less than in males of same age.
After menopause, the pressure in females becomes equal to that in males of same age.
3. Body Built
Pressure is more in obese persons than in lean persons.
4. Diurnal Variation
In early morning, the pressure is slightly low. It gradually increases and reaches the maximum at noon. It
becomes low in evening
5. After Meals
Arterial blood pressure is increased for few hours after meals due to increase in cardiac output.
6. During Sleep
Usually, the pressure is reduced up to 15 to 20 mm Hg during deep sleep. However, it increases slightly
during sleep associated with dreams.
7. Emotional Conditions
During excitement or anxiety, the blood pressure is increased due to release of adrenaline.
8. After Exercise
After moderate exercise, systolic pressure increases by 20 to 30 mm Hg above the basal level due to increase
in rate and force of contraction and stroke volume. Normally, diastolic pressure is not affected by moderate
exercise. It is because, the diastolic pressure depends upon peripheral resistance, which is not altered by
moderate exercise.
PATHOLOGICAL VARIATIONS
Pathological variations of arterial blood pressure are hypertension and hypotension.

FACTORS MAINTAINING ARTERIAL BLOOD PRESSURE

Some factors are necessary to maintain normal blood pressure. These includes;
1. Cardiac Output
Systolic pressure is directly proportional to cardiac output. Whenever the cardiac output increases, the
systolic pressure is increased and when cardiac output is less, the systolic pressure is reduced. Cardiac output
increases in muscular exercise, emotional conditions, etc. So in these conditions, the systolic pressure is

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increased. In conditions like myocardial infarction, the cardiac output decreases, resulting in fall in systolic
pressure.

2. Heart Rate
Moderate changes in heart rate do not affect arterial blood pressure much. However, marked alteration in the
heart rate affects the blood pressure by altering cardiac output.
3. Peripheral Resistance
Peripheral resistance is the important factor, which maintains diastolic pressure. Diastolic pressure is
directly proportional to peripheral resistance. Peripheral resistance is the resistance offered to the blood flow
at the periphery. Resistance is offered at arterioles, which are called the resistant vessels. When peripheral
resistance increases, diastolic pressure is increased and when peripheral resistance decreases, the diastolic
pressure is decreased.

4. Blood Volume
Blood pressure is directly proportional to blood volume. Blood volume maintains the blood pressure
through the venous return and cardiac output. If the blood volume increases, there is an increase in venous
return and cardiac output, resulting in elevation of blood pressure.

5. Venous Return
Blood pressure is directly proportional to venous return. When venous return increases, there is an
increase in ventricular filling and cardiac output, resulting in elevation of arterial blood pressure.

6. Elasticity of Blood Vessels

Blood pressure is inversely proportional to the elasticity of blood vessels. Due to elastic property, the
blood vessels are distensible and are able to maintain the pressure. When the elastic property is lost, the blood
vessels become rigid (arteriosclerosis) and pressure increases as in old age. Deposition of cholesterol, fatty
acids and calcium ions produce rigidity of blood vessels and atherosclerosis, leading to increased blood
pressure.
7. Velocity of Blood Flow
Pressure in a blood vessel is directly proportional to the velocity of blood flow. If the velocity of blood flow
increases, the resistance is increased. So, the pressure is increased.

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8. Diameter of Blood Vessels
Arterial blood pressure is inversely proportional to the diameter of blood vessel. If the diameter decreases,
the peripheral resistance increases, leading to increase in the pressure.

9. Viscosity of Blood
Arterial blood pressure is directly proportional to the viscosity of blood. When viscosity of blood increases,
the frictional resistance is increased and this increases the pressure.

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. Body has
four such regulatory mechanisms to maintain the blood pressure within normal limits;
A. Nervous mechanism or short term regulatory mechanism
B. Renal mechanism or long term regulatory mechanism
C. Hormonal mechanism
D. Local mechanism.

NERVOUS MECHANISM FOR REGULATION OF BLOOD PRESSURE –

SHORT-TERM REGULATION
Nervous regulation is rapid among all the mechanisms involved in the regulation of arterial blood pressure.
When the pressure is altered, nervous system brings the pressure back to normal within few minutes.
Although nervous mechanism is quick in action, it operates only for a short period and then it adapts to the
new pressure. Hence, it is called short term regulation.

RENAL MECHANISM FOR REGULATION OF BLOOD PRESSURE –LONG-TERM REGULATION

Kidneys play an important role in the long term regulation of arterial blood pressure. When blood pressure
alters slowly in several days/months/years, the nervous mechanism adapts to the altered pressure and loses the

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sensitivity for the changes. It cannot regulate the pressure any more. In such conditions, the renal mechanism
operates efficiently to regulate the blood pressure. Therefore, it is called long term regulation.
Kidneys regulate arterial blood pressure by two ways:
1. By regulation of ECF volume
2. Through renin-angiotensin mechanism.
BY REGULATION OF EXTRACELLULAR FLUID VOLUME
When the blood pressure increases, kidneys excrete large amounts of water and salt, particularly sodium,
by means of pressure diuresis and pressure natriuresis. Pressure diuresis is the excretion of large quantity of
water in urine because of increased blood pressure. Even a slight increase in blood pressure doubles the water
excretion. Pressure natriuresis is the excretion of large quantity of sodium in urine.
Because of diuresis and natriuresis, there is a decrease in ECF volume and blood volume, which in turn
brings the arterial blood pressure back to normal level.
When blood pressure decreases, the reabsorption of water from renal tubules is increased. This in turn,
increases ECF volume, blood volume and cardiac output, resulting in restoration of blood pressure.

THROUGH RENIN-ANGIOTENSIN MECHANISM

Actions of Angiotensin II
When blood pressure and ECF volume decrease, renin secretion from kidneys is increased. It converts
angiotensinogen into angiotensin I. This is converted into angiotensin II by ACE (angiotensin converting
enzyme).
Angiotensin II acts in two ways to restore the blood pressure:
i. It causes constriction of arterioles in the body so that the peripheral resistance is increased and blood
pressure rises. In addition, angiotensin II causes constriction of afferent arterioles in kidneys, so that
glomerular filtration reduces. This results in retention of water and salts, increases ECF volume to normal
level. This in turn increases the blood pressure to normal level.
ii. Simultaneously, angiotensin II stimulates the adrenal cortex to secrete aldosterone. This hormone increases
reabsorption of sodium from renal tubules. Sodium reabsorption is followed by water reabsorption, resulting
in increased ECF volume and blood volume. It increases the blood pressure to normal level.

HORMONAL MECHANISM FOR REGULATION OF BLOOD PRESSURE

Many hormones are involved in the regulation of blood pressure. Hormones which increase or decrease the
arterial blood pressure are;

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 HORMONES WHICH INCREASE BLOOD PRESSURE
Hormones, which increase the arterial blood pressure have different mechanism of action.
1. Adrenaline
Adrenaline is secreted by the adrenal medulla. It is also released by sympathetic postganglionic nerve endings.
Adrenaline regulates the blood pressure by acting through heart and blood vessels. It increases systolic
pressure by increasing the force of contraction of the heart and cardiac output. It decreases diastolic pressure
by reducing the total peripheral resistance. Adrenaline causes constriction of blood vessels through alpha
receptors. It also causes dilatation of blood vessels through β2receptors in some areas of the body like skeletal
muscle, liver and heart. So, the total peripheral resistance is reduced leading to decrease in diastolic pressure.
2. Noradrenaline
Noradrenaline is secreted by the adrenal medulla. It is also released by sympathetic postganglionic nerve
endings. Noradrenaline increases diastolic pressure due to its general vasoconstrictor effect. It has stronger
effects on blood vessels than on the heart. It causes constriction of all blood vessels throughout the body via
alpha receptors. So it is called ‘general vasoconstrictor’. The action of noradrenaline is to increase the total
peripheral resistance and diastolic pressure. It also increases the systolic pressure slightly, by increasing the
force of contraction of heart.
3. Thyroxine
Thyroxine secreted from thyroid gland increases systolic pressure but decreases the diastolic pressure. It
increases the systolic pressure by increasing cardiac output. The cardiac output is increased because of
increase in the blood volume and force of contraction of the heart. Thyroxine has indirect action on diastolic
pressure. Large quantities of metabolites are produced during increased metabolic activity induced by
thyroxine. These metabolites cause vasodilatation, leading to decrease in peripheral resistance. It causes
decrease in diastolic pressure.
4. Aldosterone
Aldosterone is secreted from adrenal cortex. It causes retention of sodium and water and thereby, increases
the ECF fluid volume and blood volume, leading to increase in blood pressure. Thus, an increase in the
secretion of aldosterone increases the blood pressure by increasing the blood volume.

5. Vasopressin
Vasopressin or ADH, which is secreted by posterior pituitary has a potent action on the blood vessels,
particularly the arteries. It causes constriction of the arteries in all parts of the body. Due to the
vasoconstriction, the blood pressure is increased. However, the amount of this hormone required to cause the
vasopressor effect is very much high than the amount required to cause the antidiuretic effect.
6. Serotonin

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 Serotonin is otherwise known as 5-hydroxytryptamine (5-HT). It increases the blood pressure by
vasoconstriction.

HORMONES WHICH DECREASE BLOOD PRESSURE

Following hormones decrease the arterial blood pressure by causing vasodilatation:
1. Vasoactive Intestinal Polypeptide
Vasoactive intestinal polypeptide (VIP) is secreted in the stomach and small intestine. A small amount of
this hormone is also secreted in large intestine. VIP is a vasodilator and causes dilatation of peripheral blood
vessels and decrease in blood pressure.
2. Bradykinin
Bradykinin is produced in blood during the conditions like inflammation. During such conditions, the
enzyme in the blood called kallikrein is activated. It acts on α2globulin to form kallidin, which is converted
into bradykinin. Bradykinin is a vasodilator substance and causes reduction in blood pressure.
3. Prostaglandins
Prostaglandin PGE2 is a vasodilator substance. It is secreted from almost all tissues of the body. It
decreases blood pressure.
4. Histamine
Histamine is secreted in nerve endings of hypothalamus, limbic cortex and other parts of cerebral cortex.
Histamine is also released from tissues during allergic conditions, inflammation or damage. Histamine causes
vasodilatation and decreases the blood pressure.
5. Acetylcholine
Acetylcholine is the cholinergic neurotransmitter released from many sources. Acetylcholine causes
vasodilatation and decreases the blood pressure.

APPLIED PHYSIOLOGY
Pathological variations of arterial blood pressure:
A. Hypertension
B. Hypotension.
HYPERTENSION

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 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. If there is increase only in systolic pressure, it is called systolic hypertension.
Types of Hypertensions
Hypertension is divided into two types:
1. Primary hypertension or essential hypertension
2. Secondary hypertension.
Primary 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. Primary hypertension is of two types:
i. Benign hypertension
ii. Malignant hypertension.
Benign hypertension
Benign hypertension is the high blood pressure that does not cause any problem. It is defined as the
essential hypertension that runs a relatively long and symptomless course. In early stages of this condition,
there is moderate increase in blood pressure, with systolic pressure of 200 mm Hg and the diastolic pressure
of about 100 mm Hg. However, in resting conditions and sleep, the blood pressure returns to normal level.
Later, there is a further increase in blood pressure and it does not come back to normal level in resting
conditions. Persistent increase in pressure over the years causes development of vascular, cardiac or renal
diseases.
Malignant hypertension
Malignant hypertension is a severe form of hypertension with a rapid course leading to progressive cardiac
and renal diseases. It is also called accelerated hypertension. In this case, the blood pressure is elevated to a
great extent. Systolic pressure rises to about 250 mm Hg and diastolic pressure rises to 150 mm Hg. It is
always developed due to the combined effects of primary and secondary hypertension. Malignant
hypertension causes severe damage of tunica intima of small blood vessels and organs like eye (retina), heart,
brain and kidneys. It is a fatal disease, since it causes death within few years.

2. Secondary Hypertension
Secondary hypertension is the high blood pressure due to some underlying disorders. The different forms
of secondary hypertension are:

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 i. Cardiovascular hypertension
Cardiovascular hypertension is produced due to the cardiovascular disorders such as:
a. Atherosclerosis: Hardening of blood vessels due to fat deposition
b. Coarctation of aorta: Narrowing of aorta.
ii. 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.
iii. 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.
iv. Neurogenic hypertension
Nervous disorders producing hypertension:
a. Increased intracranial pressure.
v. 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. It may be because of some
autoimmune processes during pregnancy or release of some vasoconstrictor agents from placenta or due to the
excessive secretion of hormones causing rise in blood pressure. Hypertension is associated with convulsions
in eclampsia.

HYPOTENSION
Hypotension is the low blood pressure. When the systolic pressure is less than 90 mm Hg, it is considered
as hypotension.
Types
1. Primary hypotension

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2. Secondary hypotension.

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. Frequent fatigue and weakness
are the common symptoms of this condition. However, the persons with primary hypotension are not easily
susceptible to heart or renal disorders.

Secondary hypotension
Secondary hypotension is the hypotension that occurs due to some underlying diseases. Diseases, which
causes hypotension are:
i. Myocardial infarction
ii. Hypoactivity of pituitary gland
iii. Hypoactivity of adrenal glands
iv. Tuberculosis
v. Nervous disorders.

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