CARDIOVASCULAR

SYSTEM
Dr Narendra Yadnik
Associate Professor, PIA
• INTRODUCTION
• The primary function of the cardiovascular
system is to provide an adequate supply of
oxygen and nutrients to all cells of the body and
carry away the waste products of their
metabolism.
• It is a well organized transport system of the
body by which the blood being circulated within
a closed system under different pressure
gradients, created by the pumping mechanism
where heart acts as the central pump
• The cardiovascular system includes (a) heart, (b)
arteries, (c) capillaries and (d) veins. They all
differ in structures as well as in functions. Blood
is in circulation and is carried out to various
tissue delivering oxygen and nutrients to them.
Blood gets deoxygenated in the tissues and
oxygenated in the lungs.
• circulatory system has been divided into two
functionally opposite parts:
l. Systemic circulation (greater circulation)-passing
through the tissues.
2. Pulmonary circulation (lesser circulation)-passing
through the lungs. The two systems again meet
in the heart
• The main functions of circulation are to make
available to the tissues its different metabolic
needs and on the other hand to carry away from
the tissues the CO2 and other metabolic waste
products for elimination from the body. These
are done in two ways:
(1) By maintaining patent circulation, so that blood
is supplied adequately to every part of the body
(in rest and activity).
(2) By maintaining an optimum blood pressure
which is essential for capillary exchange.
• The course of circulation is as follows -
a. The left ventricle propels oxygenated blood to the
tissues. Here, it gives up oxygen and becomes
reduced. The reduced blood comes back to the
heart through the Superior and Inferior vena cava
and is received by the right atrium.
b. From the right atrium it passes into the right
ventricle, which then propels it into the lungs
through Right & Left Pulmonary artery. Here, it
becomes re-oxygenated, and is returned to the left
atrium through the Right & Left pulmonary veins.
c. From here it enters the left ventricle and is pumped
out into the greater circulation again. In this way
circulation goes on.
• Key Points
1. The systemic circulation, therefore, begins in
the left ventricle and ends in the right atrium.
The pulmonary circulation starts in the right
ventricle and ends in the left atrium.
2. The right half of the heart is concerned with
reduced blood, while the left half with
oxygenated blood.
3. Two technical terms are used in connection with
heart, e.g. systole and diastole. The term systole
means contraction and diastole means
relaxation.
FUNCTIONAL ANATOMY
 1) 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.
• The heart weighs 250–390 g in men and 200–275
g in women and is a little larger than the owner’s
closed fist, being approximately 12 cm long and 9
cm wide.
• Location - It is located in the thoracic cavity
(chest) in the mediastinum (between the
lungs), behind and to the left of the sternum.
 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 Sino-atrial node that produces
cardiac impulses and Atrio-ventricular node that
conducts the impulses to the ventricles.
• Right atrium receives venous (deoxygenated) 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 ventricle 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.

Right Atrium

tRicuspid valve

Right Ventricle
 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
Great aorta.
 SEPTA OF THE HEART
• Right and left atria are separated from one
another by a fibrous septum called interatrial
septum. Right and left ventricles are separated
from one another by Inter-ventricular septum.
The upper part of this septum is a membranous
structure, whereas the lower part of it is
muscular in nature.
 LAYERS OF WALL OF THE HEART
• Heart is made up of three layers of tissues:
1. Outer pericardium Hint – Peri My End
2. Middle myocardium
3. Inner endocardium.
• PERICARDIUM
• Pericardium is the outer covering of the heart. It is
made up of two layers:
i. Outer parietal pericardium
ii. Inner visceral pericardium.
• The space between the two layers is called
pericardial cavity or pericardial space and it
contains a thin film of fluid.
 PERICARDIUM

i. Outer Parietal Pericardium

• Parietal pericardium forms a strong protective
sac for the heart. It helps also to anchor the
heart within the mediastinum.

ii. Inner Visceral Pericardium

• Inner visceral pericardium lines the surface of
myocardium. It is made up of flattened epithelial
cells. This layer is also known as epicardium.
 MYOCARDIUM
• Myocardium forms the bulk of the heart and it is
responsible for pumping action of the heart.
Unlike skeletal muscle fibers, the cardiac muscle
fibers are involuntary in nature.
 ENDOCARDIUM
• Endocardium is the inner most layer of heart wall.
It is a thin, smooth and glistening membrane. It is
formed by a single layer of endothelial cells, lining
the inner surface of the heart including the heart
valves. Endocardium continues as endothelium of
the blood vessels.
• The endocardium is lined by endothelium just like
the blood vessels, and it's the innermost layer of
the heart which means that it's in direct contact
with the blood.
• It forms the cusps of the Bicuspid Valve, Tricuspid
Valve, Pulmonary Valve and the Aortic Valve as
well as the other valves we have like the valve of
the inferior vena cava. Cusps of these valves are
made up of double layer of Endocardium.
Without any type of Covering With layer of serous pericardium
With layer of fibrous pericardium
 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 Great aorta and Pulmonary artery.
• Valves of the heart permit the flow of blood
through heart in only one direction.
 A) Atrioventricular Valves

Left Right
atrioventricular atrioventricular

Bicuspid Valve (Mitral) 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.
• Role of the left A-V valve (Mitral) will open as a
result of increased pressure of left atrium as it
fills with blood.
 B) Semilunar Valves

Aortic Valve Pulmonary Valve

Three flaps Three flaps

Between the left ventricle and Between the Rt ventricle and

systemic aorta pulmonary artery
• 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.
ACTIONS OF THE HEART

IBCD
1) CHRONOTROPIC ACTION
• Chronotropic action is the frequency of
heartbeat or heart rate. It is of two types:
i. Tachycardia or increase in heart rate
ii. Bradycardia or decrease in heart rate.
2) INOTROPIC ACTION
• Force of contraction of heart is called inotropic
action. It is of two types:

i. Positive inotropic action or increase in the force

of contraction Ex – Digitalis
ii. Negative inotropic action or decrease in the
force of contraction.

Action – By Changing concentration of Ca2+ Ions

 3) DROMOTROPIC ACTION
• Dromotropic action is the conduction of impulse
through heart. It is of two types:
i. Positive dromotropic action or increase in the
velocity of conduction Ex Adrenalin
ii. Negative dromotropic action or decrease I the
velocity of conduction. Ex Cardiac Glycoside

Action - This action happens at AV Node

 4) BATHMOTROPIC ACTION
• Bathmotropic action is the excitability of cardiac
muscle.
• It is also of two types:
i. Positive bathmotropic action or increase in the
excitability of cardiac muscle Ex. Adrenalin
ii. Negative bathmotropic action or decrease the
excitability of cardiac muscle. Ex Acetylcholine
2) Blood Vessels
• Vessels of circulatory system are the aorta,
arteries, arterioles, capillaries, venules, veins and
venae cavae.

• ARTERIAL SYSTEM
• Arterial system comprises the aorta, arteries and
arterioles. Walls of the aorta and arteries are
formed by three layers:
1. Outer tunica adventitia, which is made up of
connective tissue layer. It is the continuation of
fibrous layer of parietal pericardium.
2. Middle tunica media, which is formed by
smooth muscles.
3. Inner tunica intima, which is made up of
endothelium.
• Arterial branches become narrower and their
walls become thinner while reaching the
periphery. Aorta has got the maximum diameter
of about 25 mm. Diameter of the arteries is
gradually decreased and at the end arteries, it is
about 4 mm.
• It further decreases to 30 μ in the arterioles and
ends up with 10 μ in the terminal arterioles.
Resistance (peripheral resistance) is offered to
blood flow in the arterioles and so these vessels
are called resistant vessels.
• Arterioles are continued as capillaries, which are
small, thin walled vessels having a diameter of
about 5 to 8 μ.
• Capillaries are functionally very important
because, the exchange of materials between the
blood and the tissues occurs through these
vessels.
• VENOUS SYSTEM
• From the capillaries, venous system starts and it
includes venules, veins and venae cavae.
• Capillaries end in venules, which are the smaller
vessels with thin muscular wall than the
arterioles. Diameter of the venules is about 20 μ.
• At a time, a large quantity of blood is held in
venules and hence the venules are called
capacitance vessels.
• Venules are continued as veins, which have the
diameter of 5 mm. Veins form superior and
inferior venae cavae, which have a diameter of
about 30 mm.
• In the veins and venae cavae, the elastic tissue is
less but the smooth muscle fibers are more.
Concept of Resistance of Arteriole

IMP - Resistance
of Single capillary
is high but
Collective
resistance of All
capillaries is Low
 Capillary

Artery

Capillary

Artery
 Concept of Capacitance of Venules

They can dilate more, and don’t squeeze.

• COMPLICATIONS IN BLOOD VESSELS
• Arteriosclerosis is the disease of the arteries,
associated with hardening, thickening and loss of
elasticity in the wall of the vessels.

• Atherosclerosis is the disease marked by the

narrowing of lumen of arterial vessel due to
deposition of cholesterol. Atherosclerosis is a
specific type of arteriosclerosis.
• Thrombosis –
• Inflammation of the wall of veins leads to the
formation of intravascular clot called thrombosis.
• The clot gets dislodged, as thrombus. The
thrombus travels through blood and causes
embolism. Embolism obstructs the blood flow to
vital organs such as brain, heart and lungs,
leading to many complications.
• Two types – 1) Arterial 2) Venous
ARTERIAL THROMBOSIS
• DEEP VEIN THROMBOSIS
PROPERTIES OF CARDIAC MUSCLE

1. EXCITABILITY
2. RHYTHMICITY
3. CONDUCTIVITY
4. CONTRACTILITY
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.
• Resting Membrane Potential
• Resting membrane potential in:
1. Single cardiac muscle fiber : – 85 to – 95 mV
2. Sinoatrial (SA) node : – 55 to – 60 mV
3. Purkinje fibers : – 90 to – 100 mV

• Action Potential
• Action potential in cardiac muscle is different
from that of other tissues such as skeletal
muscle, smooth muscle and nervous tissue.
• Phases of action potential
• Action potential in a single cardiac muscle fiber
occurs in four phases:
1. Initial depolarization (Phase 0)
2. Initial repolarization (Phase 1)
3. A plateau (Phase 2)
4. Final repolarization. (Phase 3)
5. Resting membrane potential (Phase 4)
• Depolarization - Process of becoming positive

• Repolarization – Process of becoming negative

• Influx of sodium – process of entry of Na+ ions from

outside to inside by voltage gated channels
• Efflux – Exit of ions from cell towards outside

• General Rule – Na+ ion concentration is higher

outside the cell and K+ ion concentration is higher
inside the cell.

• Generation of Action potential is positive feedback

mechanism.
• Process of generation of Action potential
1) It happens in ventricular muscle cell
2) The ionic composition around the cell is similar
to all other cells of the body.
3) The Na+ concentration is higher outside the cell,
so it tends to diffuse inside.
4) K+ concentration is higher inside the cell, so it
tends to diffuse outside.
5) With that, Ca+ concentration is higher outside
the cell, so it tends to diffuse inside.
6) Now, resting membrane potential in ventricular
muscle is -90mv. We know that, impulse are
generated at SA node of the heart. As the
impulse reaches at ventricular muscle cell, the
action potential will start here.
7) It begins with voltage-gated fast sodium
channels. The incoming impulse, opens this
channel. This opening allows the rapid influx of a
large number of sodium ions. As sodium is a
positively charged ion, it makes inside of the cell
electropositive, and the potential reaches about
+15 mV very rapidly. This phase is called phase 0,
upstroke, or initial depolarization.
8) Next, the fast sodium channels close. This
prevents the rapid influx of Na. Also... a small
quantity of potassium leaks out through K
channels. This leads to a little bit of
repolarization. This is called phase 1 or initial
repolarization.
9) One another thing, the cardiac muscles have L-
type Ca2+ channel. L means long-lasting ( lazy
channels.) They are lazy because they are slow to
open and slow to close. They are activated
during the depolarization and opens slowly.
• Now they allow the influx of Ca2+ into the
myocyte. Because of their slow nature, they stay
open for a longer time and close very slowly. This
allows an influx of Ca2+ for quite some time.
• Thus two things are going on at present.
Potassium is moving out and at the same time,
Ca2+ is continuously moving in. This loading of
positive ions inside and outside keeps the
membrane at same potential for some time i.e.
depolarized for some time and thus creates a
plateau in the action potential. Due to this long
plateau, the contraction time is also longer in
cardiac muscle. So this is phase 2 or plateau.
10) Eventually though, the Ca channels do close, so
the influx of Ca stops. And slow potassium
channels open so the efflux of potassium starts.
Due to the exit of the net positive charge, the
membrane returns to resting negative potential.
This repolarization phase is called phase 3 or
final repolarization.
11) Then of course we have resting membrane
potential till the next action potential. This is also
called phase 4.
12) Now let's talk about, how the ionic balance is
restored. We have seen that during an action
potential, sodium moves in, K moves out and Ca
moves in. To restore the balance, we have Na-K
pump, Na-Ca exchanger and Ca - ATPase pump
on the membrane.
13) Na-K pump moves sodium out and K in, using
energy from ATP.
• Na-Ca exchanger actively moves Ca out using the
downhill entry of Na into the cell. No worry
about the Na entering here. It will be moved out
again by Na-K pump.
• And finally Ca pumps that move Ca out using
energy directly from ATP.
• 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.
• Action potential is transmitted from atria to
ventricles through the fibers of specialized
conductive system, which is explained later in
this chapter.
 2) RHYTHMICITY
• Rhythmicity is the ability of a tissue to produce
its own impulses regularly. It is also called
autorhythmicity or self-excitation.
• 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).
• 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.
• These fibers are continuous with fibers of atrial
muscle, so that the impulses from the SA node
spread rapidly through atria.
• In mammalian heart, though the other parts of
the heart like AV node, atria and ventricle can
also produce the impulse, but SA node acts as a
pacemaker because the rate of impulse
generation by SA node is the highest.
• Rhythmicity of Different Parts of Human Heart
1. SA node : 70 to 80/minute
2. AV node : 40 to 60/minute
3. Atrial muscle : 40 to 60/minute
4. Purkinje fibers : 35 to 40/minute
5. Ventricular muscle : 20 to 40/minute
• ELECTRICAL POTENTIAL IN SA NODE
• Pacemaker potential is the unstable resting
membrane potential in SA node.
• Electrical potential in SA node is different from
that of other cardiac muscle fibers. In SA node,
each impulse triggers the next impulse. It is
mainly due to the unstable resting membrane
potential.
• Resting membrane potential in SA node has a
negativity of –55 to –60 mV. It is different from
the negativity of –90 mV in other cardiac muscle
fibers.
• Action Potential in SA Node (Steps)
1) The heart generates impulses on its own to
trigger a heartbeat. For this, the heart has
three pacemaker tissues: the SA node, the AV
node and the Purkinje fibers.
• They all can generate impulse on their own.
However, their rate of impulse generation is
different. Normally the SA node generates
impulses faster than other tissues. Because of
the slower rate in other tissues, an interesting
thing happens.
2) Let's assume, this is time zero and the SA node
and AV node both start generating impulses on
their own at the same time. Because of the faster
rate in the SA node, impulse first appears in the
SA node and quickly spreads to the AV node.
• This incoming impulse stimulates the AV node
even before the AV node has generated its own
impulse. And this happens every time. The same
applies to the entire conductive system.
• So normally impulses from the SA node override
all other tissues and the SA node controls the
heart rate.
3) But for any reason, if the SA node gets slower
than the inherent frequency of other tissues, the
other tissue will generate its own action
potential before the impulse from the SA node
reaches it.
• In that case that tissue overrides all other tissue
and becomes pace maker of the heart. Thus the
fastest of the pacemaker tissues controls the
heart rate.
4) But normally the fastest one is the SA node. Now
let's move towards action potential in the SA node.
But before that, see the basics behind it.
• So there are 3 main ions involved in the rhythmicity
of the SA node. Na, Ca and K.
• Na and Ca concentration is higher outside the cell
and they tend to diffuse in. As they are positively
charged ions, their entry takes the membrane
potential to electro positivity.
• K concentration is higher inside the cell, so it tends
to diffuse outside. And the exit of positively charged
K ions makes the cell electronegative.
• The balance between the movement of these ions
controls the rhythmicity.
5) Starting with the resting membrane potential. It
is about -60 mV.
• However, this resting membrane potential is not
so resting in pacemaker tissues. It is in fact
unstable.
• The reason is slow sodium channels that allow an
influx of Na even without any external stimuli.
• This slow sodium entry raises the membrane
potential. This is Called funny current.
6) Along with sodium, slow entry of Ca also
contributes to the rise in membrane potential.
• The contribution of Ca increases gradually.
Eventually, the potential reaches the threshold
which is about -40 mV.
• So this was the phase of slow pacemaker
potential.
7) Next, at the threshold, more Ca channels open
resulting in a rapid influx of Ca. This produces
upstroke which is also called phase 0.
8) Then the Ca channels close and K channels open.
So Ca influx ceases and K starts leaving the cell.
• Exit of positive ions brings the membrane
potential towards electronegativity. Thus the
action potential is terminated. This is phase 3.
• But Where is Phase 1 & Phase 2 ? Well, the
phase 1 of initial repolarization and phase 2 is
the plateau.
• But they are seen in ventricular myocytes. They
are not seen in the SA node. So we have directly
phase 3 of repolarization.
9) The K efflux continues for some time even after
this. So the membrane is hyperpolarized. Now
reached a potential from where it started i.e.
- 60 mV
10) Now, the K channels start closing. So efflux of K
decreases.
• At the same time, Na and Ca influx that we
discussed earlier once again over-balances the K
efflux.
• So there is a net entry of positive charge into the
cell. So the membrane potential again moves
toward the electro positivity. This is called phase
4. Its nothing but the same as “Pacemaker
Potential”
• The potential reaches the threshold and action
potential generated again. In this way the SA
node keeps generating impulses on its own.
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 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.
• Components of Conductive System in Human
Heart
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 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.
• VELOCITY OF IMPULSES AT DIFFERENT PARTS OF
CONDUCTIVE SYSTEM
1. Atrial muscle fibers : 0.3 meter/second
2. Internodal fibers : 1.0 meter/second
3. AV node : 0.05 meter/second
4. Bundle of His : 0.12 meter/second
5. Purkinje fibers : 4.0 meter/second
6. Ventricular muscle fibers : 0.5 meter/second.

• Thus, the velocity of impulses is maximum in

Purkinje fibers and minimum at AV node.
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.
• Following are the contractile properties:
a) ALL-OR-NONE LAW
• According to all-or-none law, when a stimulus is
applied, whatever may be the strength, the whole
cardiac muscle gives maximum response or it does
not give any response at all. Below the threshold
level, i.e. if the strength of stimulus is not adequate,
the muscle does not give response.
• All-or-none law is demonstrated in the quiescent
heart of frog.
• Procedure - Ventricle is stimulated by placing the
electrode at the base of ventricle.
• First, one stimulus is applied with a minimum
strength of 1 volt at the base of ventricle and the
contraction is recorded. Then, after 20 seconds,
the strength of stimulus is increased to 2 volt and
the stimulus is applied
• The procedure is repeated by increasing the
strength every time and applying the stimulus
with an interval of 20 seconds
• Amplitude of all contractions remains the same,
irrespective of increasing the strength of
stimulus. This shows that cardiac muscle obeys
all-or-none law.
b) STAIRCASE PHENOMENON
• When the ventricle of a heart of frog is
stimulated at a short interval of 2 seconds,
without changing the strength, the force of
contraction increases gradually for the first few
contractions and then it remains same. Gradual
increase in the force of contraction is called
staircase phenomenon.
c) SUMMATION OF SUBLIMINAL STIMULI
• When a stimulus with a subliminal strength is
applied, the quiescent heart does not show any
response. When few stimuli with same
subliminal strength are applied in succession, the
heart shows response by contraction, due to the
summation of stimuli.
Cardiac Cycle
• DEFINITION
1) Cardiac cycle is defined as the succession of
(sequence of) coordinated events taking place
in the heart during each beat.
2) Changes that occur in the heart during one beat
are repeated in the same order in the next beat.
This cyclical repetition of the various changes in
heart, from beat to beat, is called cardiac cycle.
 Things to Remember
• The cardiac cycle (heart beat) consists of
alternate periods of systole (contraction and
emptying) and diastole (relaxation and filling).
• The atria and ventricles go through separate
cycles of systole and diastole.
• Contraction happens with excitation, whereas
relaxation follows the subsequent repolarization.
• Blood flows from an area of high pressure to an
area of low pressure.
• The actual pump are the ventricles.
• Normally, diastole is longer than systole, systole
is shorter but strong.
• Cardiac Cycle Time
• This is the time required for one complete
cardiac cycle. With the normal heart rate of 75
per minute, this time will be 60/75 = 0.8 second.

• It means that every event in the cycle will be

repeated at the interval of 0.8 second.

• It is obvious that the cardiac cycle time will be

inversely proportional to the heart rate
C.C. Time = 1/ H. R.
 EVENTS OF CARDIAC CYCLE

1. Atrial events 2. Ventricular events.

1. Atrial systole 1. Ventricular systole

2. Atrial diastole 2. Ventricular diastole.
 Atrial events
1) Atrial systole: Atrial systole initiates the cycle,
because the pacemaker SA node is situated in it.
It lasts for 0.1 second, and is followed by atrial
diastole, lasting for 0.7 second. At the end of
diastole, the atrial systole returns, and in this
way, the atrial cycle goes on (total duration 0.8
second).
2) Atrial diastole: Atrial systole is followed by atrial
diastole and its duration is 0.7 sec.
 Ventricular events
1) Ventricular systole: At the end of atrial systole,
ventricular systole starts and its duration is 0.3
second.
2) Ventricular diastole: This is immediately
followed by ventricular diastole and its duration
is 0.5 second.
At the end of diastole, ventricular systole repeats
and thus the ventricular cycle goes on.
(total duration 0.8 second).
Inner Ring Represents the Atrial Events &
Outer Ring Represents Ventricular Events
 Let us follow inner ring first
• Atrial systole: The one shaded division in it
denotes atrial systole (0.1 second). During this
period the atria contract and expel their contents
into the respective ventricles.
• Atrial diastole:
• After atrial systole, comes atrial diastole (0.7
second) being represented by seven unshaded
divisions in the ring. During this period the atria
relax and receive blood from the great veins-the
right atrium from the venae cavae, the left
atrium from the pulmonary veins. At the end of
this period, the atrial systole comes again and in
this way, the atrial events go on.
 Let us now follow the Ventricular Events in the Outer
Ring
• There are 3 shaded divisions on it, representing
ventricular systole (0.3 second).
• It is followed by 5 unshaded divisions, indicating
ventricular diastole (0.5 second).
• Ventricular systole: On comparing the two rings, it
would be found that ventricular systole commences
at the end of atrial systole. The reason for this is very
clear. The impulse originating at the SA node will
certainly overtake the atrium first, and then it will
travel down the junctional tissues, enter the
ventricles and stimulate their contraction. Naturally
then, ventricular systole will always come after atrial
systole.
• From these interrelations we can deduce one
fundamental rule of cardiac action that the
systoles of atrium and ventricle will never
overlap. In other words, when one chamber is
contracting, the other must be relaxing.
1. At the onset of ventricular systole, the first
sound occurs. It is caused by the sudden closure
of the AV valves.
2. The semilunar valves open a little later, because,
until the intraventricular pressure goes above
that in the aorta and pulmonary artery, the
semilunar valves will not open. Thus, at the
beginning of ventricular systole, there is a brief
period during which both the valves are closed
and the ventricles are contracting as closed
cavities
•
3. At the end of this period, the semilunar valves
open and the ejection period starts (0.25
second). During this period, blood is expelled
from the ventricles- a) from the left ventricle into
the systemic aorta, b) from the right ventricle
into the pulmonary trunk. In the first part of this
period (0.11 second) the outflow is very rapid.
Hence, it is known as the maximum ejection
period.
4) In the last part (0.14 second) the rate of outflow
slows down. Hence, it is called the reduced
ejection period. Here, the ventricular systole
ends and diastole begins.
 Let us follow the Outer Ring Further
• It will be seen that after the three shaded
divisions, come the five clear divisions-
representing the duration of ventricular diastole
(0.5 second).
• Ventricular diastole: As soon as ventricles relax,
the intraventricular pressure starts falling. The
blood columns in the aorta and pulmonary trunk
try to roll back towards ventricles but are
stopped by the sharp closure of the semilunar
valves. This produces the second sound of heart.
Thus, the onset of ventricular systole is marked
by the first sound and its termination by the
second sound (approximately).
 Let us Again follow the Ventricular Diastole on the
Outer Ring
1. As mentioned above, the second sound occurs
at the end of ventricular systole. But this
statement is not true because, till the falling of
intra-ventricular pressure goes below the intra-
aortic pressure, the semilunar valves will not
close. Consequently, there will be a short
interval between the onset of diastole and the
closure of the semilunar valves (i.e. the second
sound). This period is called the protodiastolic
period (0.04 second).
2. Although the semilunar valves have closed, yet
the AV valves are still not open. Because, the
falling intraventricular pressure takes a little time
to go below that of the atria, so that the AV
valves may open. Consequently, there will be a
brief interval during which both the valves
remain closed and ventricles are relaxing as
closed cavities. Since no blood enters the
ventricles there will be no lengthening of cardiac
muscle fibres. Owing to this, it is called the
isometric relaxation period (0.08 second)
3. At the end of isometric relaxation period, the AV
valves open. Blood rushes into the ventricles and
ventricular filling begins. The first part of this
period is known as the first rapid filling phase
(0.113 second).
• Because, as soon as the AV valves open, blood
accumulating so long in the atria, rushes into the
ventricles. Due to rapid rush of blood a sound is
produced, known as the 3rd sound of heart
4. In the next phase of ventricular diastole, the rate
of filling slows down. The ventricles are already
full to a large extent and ventricular pressure
slowly rises.
• Consequently, the rate of inflow from the atria
will be gradually slower. This period is called slow
inflow phase (0.167 second). Although this is the
longest phase of ventricular diastole, yet the
amount of filling during this period is minimum.
• If one looks into the heart during this time, one
will find that, the whole atrioventricular canal
contains a continuous column of blood, more or
less stagnant, in which the cusps of the AV valves
are passively floating.
5. After this period comes the last part of ventricular
diastole represented by the last unshaded division
on the outer ring. It is obvious that this phase
corresponds with atrial systole. Due to atrial
contraction, blood rushes into the ventricles and
ventricular filling again becomes rapid. This phase is
the last rapid filling phase (0.1 second) is responsible
for the last part of ventricular filling.
• Due to rapid rush of blood, again a sound is
produced-known as the fourth sound of heart. Thus,
the onset of filling period is marked by the third
sound and its termination by the fourth sound. Here
the ventricular diastole ends. They are completely
filled up, the impulse from the SA node arrives in the
mean time and the ventricles plunge into systole
again. Thus, the cycle goes on.
1. Thus, the onset of ventricular systole is
marked by the 1st sound and its termination
by the 2nd sound (approximately).
2. Thus, the onset of filling period is marked by
the 3rd sound and its termination by the 4th
sound.
• Heart sounds are the sounds produced by
mechanical activities of heart during each cardiac
cycle.
• Heart sounds are heard by placing the ear over
the chest or by using a stethoscope or
microphone. These sounds can also be recorded
graphically.
• DIFFERENT HEART SOUNDS
1. First heart sound
2. Second heart sound
3. Third heart sound
4. Fourth heart sound.

• 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.
• 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.
 1) FIRST HEART SOUND
• First heart sound is produced during isometric
contraction period
• Causes
• Major cause for first heart sound is the sudden
and synchronous closure of atrio-ventricular
valves. However, some other factors are also
involved.
1. Valvular factor - Synchronous closure of
atrioventricular valves set up the vibrations in
the valvular leaflets and chordae tendineae.
These vibrations are mainly responsible for the
production of the first heart sound.
2. Vascular factor - Rush of blood from the
ventricles into aorta and pulmonary artery
during ejection period
3. Muscular factor - contraction of ventricular
muscle during isometric contraction and the
ejection periods
• 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.

• First Heart Sound and ECG

• First heart sound coincides with peak of ‘R’ wave
in ECG.
 2) 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 synchronous 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.
• Second Heart Sound and ECG - It coincides with the
‘T’ wave in ECG.
 3) THIRD HEART SOUND
• Third heart sound is a low-pitched sound that is
produced during rapid filling period of the cardiac
cycle.
• 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 & chordae tendineae.
• Characteristics - Third heart sound is a short and
low-pitched sound. Duration of this sound is 0.07 to
0.10 second.
• Third Heart Sound and ECG - appears between ‘T’
and ‘P’ waves of ECG.
 4) 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.
• 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.
• Characteristics - Fourth heart sound is a short and
low-pitched sound. Duration of this sound is 0.02 to
0.04 second.
• Fourth Heart Sound and ECG - It coincides with the
interval between the end of ‘P’ wave and the onset
of ‘Q’ wave.
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.
• 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.
1) 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).
2) 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

= 70 ml × 72
= 5040 ml
~ 5 liter

• Normal value: 5 L/ventricle/minute.

3) CARDIAC INDEX

• In different people, the cardiac output is

different depending on their body size. So cardiac
output is usually normalized to body surface
area. The parameter thus we get is the cardiac
index.
• It is defined as the amount of blood pumped out
per ventricle/minute/square meter of the body
surface area.
• Cardiac index = Cardiac output / body surface
area
= 5 L / min
1.7 m2

= 3 L/min/m2
• EJECTION FRACTION
• Ejection fraction is the fraction of end diastolic
volume that is ejected out by each ventricle.
Normal ejection fraction is 60% to 65%
• 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.
• Normally it's about 300-400%. i.e. the cardiac
output can increase up to 3 to 4 times that of
resting condition when needed.
• Increases: In trained athletes.
• Decreases: With age & in pathological
conditions.
 VARIATIONS IN CARDIAC OUTPUT

1. PHYSIOLOGICAL VARIATIONS
2. PATHOLOGICAL VARIATIONS

1) 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. Gender: 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.
4. Diurnal variation: Cardiac output is low in early
morning and increases in day time. Because
temperature is low, Blood pressure is slightly low,
body is in the relaxed condition.
5. Environmental temperature: Moderate change in
temperature does not affect cardiac output. Increase
in temperature above 30°C raises cardiac output.
Because increased temperature increases slight
heart rate. So Cardiac output increases.
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 supine to upright
position, the cardiac output decreases. Because
blood pools in the veins of lower extremity. So
venous return to the heart decreases. If venous
return is low, cardiac output decreases
11. Pregnancy: During the later months of
pregnancy, cardiac output increases by 40%.
Because blood volume increases slowly. Because
plasma volume increases. It eventually increases
heart rate, stroke volume & Cardiac output.
12. Sleep: Cardiac output is slightly decreased or it
is unaltered during sleep.
2) PATHOLOGICAL VARIATIONS
• Increase in Cardiac Output
1. Fever: Due to increased heart rate.
2. Anemia: When the body senses an oxygen deficit,
the heart has to do more work to increase cardiac
output or accomplish the needed blood flow so as to
compensate for the low-oxygen carrying capacity of
red blood cells in anemia.
• Typically, the heart rate also increases and this gives
rise to the palpitation symptom reported in anemia.
3. Hyperthyroidism: Due to increased basal metabolic
rate.
• Decrease in Cardiac Output

1. Hypothyroidism: Due to decreased basal

metabolic rate and decreased contractility of
heart & decreased heart rate
2. Atrial fibrillation: Atrial fibrillation is the most
common type of heart arrhythmia (irregular
heartbeat) that can interrupt the normal flow of
blood. Because of incomplete filling of ventricles.
• With A.Fib, the two atria are affected. This
disrupts blood flow to the ventricles, and then
throughout the rest of your body.
3. Congestive cardiac failure: Because of weak
contractions of heart, heart can't pump blood well
enough to meet body's needs. Heart is still working.
But because it can't handle the amount of blood it
should, blood stays in other parts of the body
mostly in lungs, legs and feet
4. Shock: Body experiences shock when you don’t have
enough blood circulating through your system to
keep organs and tissues functioning properly.
• It can be caused by any injury or condition that
affects the flow of blood through your body. Shock
can lead to multiple organ failure as well as life-
threatening complications. So due to poor pumping
and circulation, cardiac output decreases.
5. Hemorrhage: Because of decreased blood volume.
• DISTRIBUTION OF CARDIAC OUTPUT
• 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.
• Heart, which pumps the blood to all other
organs, receives the least amount of blood.
• Liver receives maximum amount of blood.