Overall plan and functions of the cardiovascular

system (CVS). Functional anatomy of the heart:

Recapitulation of cardiac muscle properties;
Med & Surg 200, Nursing 200, Med Lab 200,
Opt 300.
 INTRODUCTION
• Cardiovascular system is the system of heart and blood vessels that circulate
blood throughout the body. It constitutes one of the coordinating and integrating
systems of the body.
• It consists of the heart, blood and blood vessels (arteries, veins, and capillaries).
The arteries carry blood (oxygenated) from the heart to the rest of the body, and
the veins carry deoxygenated blood back to the heart with the exception of the
pulmonary vessels.
• The heart works continuously without a break throughout the life span of an
individual. Cessation of 3-5mins is called cardiac arrest and leads to sudden death
without resuscitation. The heart beats an average of 70beats/minute.
The heart works as a pump that pushes blood to the organs,
tissues, and cells of the body. Blood performs the following
functions:
Delivery of oxygen and nutrients to the tissues.
Transport of waste products of metabolism to the excretory
organs.
 Circulation of electrolytes and hormones.
Body temperature regulation- thermoregulation.
Transport of immune substances for body defense
mechanisms.
 THE HEART
• The heart is located between the lungs in the middle of the
chest, behind and slightly to the left of the sternum (breast
bone).

• The heart weighs between 200 and 425g, a little larger than the
fist.

• The heart beats about 72 times in a minute pumping about

5liters of blood and 100,000 times a day, pumping about 7,571
liters( 2 gallons) of blood.
 Functional anatomy of the Heart
• The heart is a muscular organ that pumps blood throughout the
circulatory system. It is situated between the 2 lungs in the
mediastinum.
• The heart itself is made up of 4 chambers, 2 atria and 2 ventricles. The
musculature is thicker in the ventricles, than the atria. The wall of the
L ventricle is 3 times thicker than the R ventricle.
• The heart is made up of 3 layers: outer pericardium, middle
myocardium and Inner endocardium.
• The pericardium is made of 2 layers; outer parietal pericardium and
inner visceral pericardium.
• The 2 layers are separated by a space called the pericardial cavity
which is just a potential space.
 SEPTA OF THE HEART
• Atria are separated from one another by a
fibrous septum called interatrial septum.

• The ventricles are separated by the

interventricular septum which is muscular.
 Valves of the heart
There are 4 heart valves
• The two atrioventricular (AV) valves, the
mitral valve (bicuspid valve), and the tricuspid valve, which are
between the upper chambers (atria) and the lower chambers
(ventricles). They control blood flow from the atria to the
ventricles.

• The two semilunar (SL)valves namely the aortic valve and the
pulmonary valve, which are in the arteries leaving the heart.
These control blood flow out of the ventricles.
 Vessels of the Cardiovascular system
• Aorta
• Arteries
• Arterioles
• Capillaries
• Venules
• Veins
• Venae Cavae
S/N CHARACTERISTICS ARTERIES VEINS
1 Arteries carry blood Veins carry blood
away from the heart from the tissues of
Blood Circulation
to the tissues of the the body back to the
body. heart.
2 Arteries carry Veins carry
oxygenated blood deoxygenated blood
Blood Type
expect pulmonary except pulmonary
artery. vein.
3 Arteries have thick Veins have thin non
Thickness elastic muscular elastic less muscular
walls. walls.
4 Veins are usually
Arteries are usually
positioned closer
Position positioned deeper
beneath the surface
within the body.
of the skin.
5 Valves Valves are absent. Valves are present.
6 These possess These possess wide
Lumen
narrow lumen. lumen
7 Blood flows under Blood flows under
Pressure
high pressure. low pressure.
8 These are reddish in These are bluish in
Color
color. color.
9 Superficial veins,
Pulmonary and deep veins,
Types
systemic arteries. pulmonary veins and
systemic veins.
10 Internal Diameter Narrower (4mm) Wider (5mm)
11 Volume Low (15%) High (65%)
12 These show spurty
These show sluggish
Movement movement of blood
movement of blood.
giving pulse.
•The cardiovascular system is composed of two
circulatory paths: pulmonary circulation, the circuit
through the lungs where blood is oxygenated; and
systemic circulation, the circuit through the rest of
the body to provide oxygenated blood. The two
circuits are linked to each other through the heart,
creating a continuous cycle of blood through the
body.
 PULMONARY CIRCULATION
• Pulmonary circulation is the movement of blood from the heart to
the lungs for oxygenation, then back to the heart again. Oxygen-
depleted blood from the body leaves the systemic circulation when it
enters the right atrium through the superior and inferior venae cavae.
The blood is then pumped through the tricuspid valve into the right
ventricle. From the right ventricle, blood is pumped through the
pulmonary valve and into the pulmonary artery. The pulmonary
artery splits into the right and left pulmonary arteries and travel to
each lung.
• At the lungs, the blood travels through capillary beds on the alveoli
where gas exchange occurs, removing carbon dioxide and adding
oxygen to the blood. The oxygenated blood then leaves the lungs
through pulmonary veins, which returns it to the left atrium,
completing the pulmonary circuit. As the pulmonary circuit ends, the
systemic circuit begins.
 SYSTEMIC CIRCULATION
• Systemic circulation is the movement of blood from the
heart through the body to provide oxygen and nutrients
to the tissues of the body while bringing deoxygenated
blood back to the heart. Oxygenated blood enters the
left atrium from the pulmonary veins. The blood is then
pumped through the mitral valve into the left ventricle.
From the left ventricle, blood is pumped through the
aortic valve and into the aorta, the body’s largest artery
to other parts of the body.
• The arteries branch into smaller arteries, arterioles, and finally
capillaries. Gas and nutrient exchange with the tissues occurs within
the capillaries that run through the tissues. Metabolic waste and
carbon dioxide diffuse out of the cell into the blood, while oxygen and
glucose in the blood diffuses out of the blood and into the cell.
Systemic circulation keeps the metabolism of every organ and every
tissue in the body alive, with the exception of the parenchyma of the
lungs, which are supplied by pulmonary circulation.

• The deoxygenated blood continues through the capillaries which

merge into venules, then veins, and finally the venae cavae, which
drain into the right atrium of the heart. From the right atrium, the
blood will travel through the pulmonary circulation to be oxygenated
before returning again to the system circulation, completing the cycle
of circulation through the body.
 CARDIAC MUSCLE
• Cardiac muscle (heart muscle) is an involuntary, striated
muscle that is found in the walls and histological foundation of
the heart, specifically the myocardium. Cardiac muscle is one of
three major types of muscle, the others
being skeletal and smooth muscle. The cells that constitute
cardiac muscle, called cardiomyocytes or myocardiocytes.

• The myocardium is the muscle tissue of the heart, and forms a

thick middle layer between the outer epicardium layer and the
inner endocardium layer.
• Coordinated contractions of cardiac muscle cells in the
heart pump blood out of the atria and ventricles to the
blood vessels.
• Although it is striated, cardiac muscle differs from skeletal
muscle in that it is highly branched with cells connected by
overlapping projections of the sarcolemma called
intercalated discs. These discs contain desmosomes and
gap junctions
• These cross striations are formed by rotating segments
of thick and thin protein filaments. Like skeletal muscle,
the primary structural proteins of cardiac muscle are
myosin and actin
 Cardiac Muscles are made up of
Intercalated discs
• Intercalated discs are small connections that join cardiac muscle cells (cardiomyocytes)
to each other.
Gap junctions
• Gap junctions are part of the intercalated discs. When one cardiac muscle cell is
stimulated to contract, a gap junction transfers the stimulation to the next cardiac cell.
This allows the muscle to contract in a coordinated way.
Desmosomes
• Like gap junctions, desmosomes are also found within intercalated discs. They help hold
the cardiac muscle fibers together during a contraction.
Nucleus
• The nucleus is the “control center” of a cell. It contains all of the cell’s genetic material.
While skeletal muscle cells can have multiple nuclei, cardiac muscle cells typically only
have one nucleus.
 ELECTROPHYSIOLOGIC PROPERTIES OF THE HEART/
CARDIAC MUSCLE
1. Automaticity – the ability to spontaneously generate and discharge an
electrical impulse.
2. Rhythmicity; the ability to send electrical impulses in a regularly, evenly
manner.
3. Excitability – the ability of the cell to respond to an electrical impulse.
4. Conductivity – the ability to transmit an electrical impulse from one cell to the
next.
5. Contractility – the ability of the cell to shorten and lengthen its fibers.
6. Refractoriness; Cells inability to respond to another electrical impulse.
 AUTOMATICITY/RHYTHMICITY
• Ability of a tissue to produce its own impulses regularly- also called
autorhythmicity or self excitation.
• This property is present in all tissues of the heart. However, the heart
has specialized excitatory structure from which discharge of impulses is
rapid. This specialized structures are called pacemakers.
Pacemaker; defined as part of the heart from which impulses for
heartbeat are produced normally.
In mammalian heart , the pacemaker is the Sinoatrial (SA)node named
by Lewis Sir Thomas in 1918.
 Location of the SA node
• SA node, is a small strip of modified cardiac muscle situated in
the superior part of the R atrium just below the opening of the
SVC.
Rhythmicity of other parts
• SA node 70-80/minute
• AV node 40-60/minute
• Atrial muscle 40-60/min
• Ventricular muscle 20-40/min
• Purkinje fibers 35-40/min
 CONDUCTIVITY
• It is the ability of cardiac muscle to spread excitatory impulses in the
heart tissue through a specialized conductive system in the cardiac
muscle namely SA node, AV node, Bundle of His, Right & Left bundle
branches and the Purkinje fibres.
Conductive pathway of the heart
• Sinoatrial (SA) node normally generates the action potential, i.e. the electrical
impulse that initiates contraction.
• The SA node excites the right atrium (RA), travels through Bachmann’s
bundle to excite left atrium (LA).
• The impulse travels through internodal pathways in RA to the atrioventricular
(AV) node.
• From the AV node, the impulse then travels through the bundle of His and down
the bundle branches, fibers specialized for rapid transmission of electrical
impulses, on either side of the interventricular septum.
• Right bundle branch (RBB) depolarizes the right ventricle (RV).
• Left bundle branch (LBB) depolarizes the left ventricle (LV) and
interventricular septum.
• Both bundle branches terminate in Purkinje fibers, millions of small fibers
projecting throughout the myocardium.
Velocity of Impulse at Different Parts of the
Conductive System
• Atrial muscle 0.3meter/second
• AV node 0.05m/s
• Bundle of His 0.12m/s
• Purkinje fibers 4m/s
• Ventricular muscle 0.5m/s
 EXCITABILITY
• In all tissues, the initial response to a stimulus is the
development of action potential. It is followed by the
physiologic action, in this case contraction, secretion etc.
 Cardiac Membrane potential
• The transmembrane potential (TMP) is the electrical potential
difference (voltage) between the inside and the outside of a
cell. When there is a net movement of +ve ions into a cell, the
TMP becomes more +ve, and when there is a net movement of
+ve ions out of a cell, TMP becomes more –ve.
• Ion channels help maintain ionic concentration gradients and
charge differentials between the inside and outside of the
cardiomyocytes.
 Properties of cardiac ion channels
• Selectivity: they are only permeable to a single type of ion based on their
physical configuration.
• Voltage-sensitive gating: a specific TMP range is required for a particular channel
to be in open configuration; at all TMPs outside this range, the channel will be
closed and impermeable to ions. Therefore, specific channels open and close as
the TMP changes during cell depolarization and repolarization, allowing the
passage of different ions at different times.
• Time-dependence: some ion channels (importantly, fast Na+ channels) are
configured to close a fraction of a second after opening; they cannot be opened
again until the TMP is back to resting levels, thereby preventing further excessive
influx.
Action potential: electrical stimulation created by a sequence of
ion fluxes through specialized channels in the membrane
(sarcolemma) of cardiomyocytes that leads to cardiac
contraction.
Action potential in cardiomyocytes
• The action potential in typical cardiomyocytes is composed of 5
phases (0-4), beginning and ending with phase 4.
Phase 4: The resting phase
• The resting potential in a cardiomyocyte is −90 mV due to a
constant outward leak of K+ through inward rectifier channels.
• Na+ and Ca2+ channels are closed at resting TMP.
Phase 0: Depolarization
• An action potential triggered in a neighbouring cardiomyocyte or pacemaker cell
causes the TMP to rise above −90 mV.
• Fast Na+ channels start to open one by one and Na+ leaks into the cell, further
raising the TMP.
• TMP approaches −70mV, the threshold potential in cardiomyocytes, i.e. the point
at which enough fast Na+ channels have opened to generate a self-sustaining
inward Na+ current.
• The large Na+ current rapidly depolarizes the TMP to 0 mV and slightly above 0
mV for a transient period of time called the overshoot; fast Na+ channels close
(recall that fast Na+ channels are time-dependent).
Phase 1: Early repolarization
• TMP is now slightly positive.
• Some K+ channels open briefly and an outward flow of K+ returns the TMP to
approximately 0 mV.
Phase 2: The plateau phase
• L-type Ca2+ channels are still open and there is a small, constant inward current of
Ca2+. This becomes significant in the excitation-contraction coupling process
described below.
• K+ leaks out down its concentration gradient through delayed
rectifier K+ channels.
• These two countercurrents are electrically balanced, and the TMP is maintained
at a plateau just below 0 mV throughout phase 2.
Phase 3: Repolarization

• Ca2+ channels are gradually inactivated.

• Persistent outflow of K+, now exceeding Ca2+ inflow, brings TMP back
towards resting potential of −90 mV to prepare the cell for a new cycle
of depolarization.
• Normal transmembrane ionic concentration gradients are restored by
returning Na+ and Ca2+ ions to the extracellular environment, and
K+ ions to the cell interior. The pumps involved include the
sarcolemmal Na+-Ca2+ exchanger, Ca2+-ATPase and Na+-K+-ATPase.
CONTRACTILITY
• The ability of the cell to shorten and lengthen its fibers(contraction) after
receiving a stimulus.
• Factors affecting the contractile properties of the cardiac muscle are;
i. All or none law; If strength of stimulus is below threshold level, no response.
ii. Staircase phenomenon; gradual increase in the force of contraction.
iii. Summation of subliminal stimuli; stimulus with sublingual strength no
response but few stimuli with same sublingual strength in succession, response
thru contraction.
iv. Refractory period; period in which the muscle does not respond to stimulus.
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, (strength of the stimulus not adequate),
the muscle does not give response.
• All or None Law is applicable to whole cardiac muscle. It is because of
syncytial arrangement of cardiac muscle. In the case of skeletal
muscle, all or none law is applicable only to a single muscle fiber.
Staircase Phenomenon
• Gradual increase in the force of contraction.
• It occurs because of the beneficial effect which facilitates the force of successive
contraction. So there is a gradual increase in force of contraction.

Summation of Subliminal Stimuli

• When a stimulus with a sublimal 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. It is due to the
summation of the stimuli.
Refractory period

• Defined as the time from phase 0 until the next possible

depolarization of a myocyte, i.e. once enough fast Na+ channels have
recovered (as TMP decreases below −50 mV).

• Cardiomyocytes have a longer refractory period than other muscle

cells given the long plateau from slow Ca2+ channels (phase 2). This is
a physiological mechanism allowing sufficient time for the ventricles
to empty and refill prior to the next contraction. Total duration is
0.53s
• Absolute refractory period (ARP): the cell is completely
unexcitable to a new stimulus. Duration 0.27sec.

• Relative refractory period (RRP): a greater than normal stimulus

will depolarize the cell and cause an action potential. Duration is
0.26 sec

• Supranormal period: a hyperexcitable period during which a

weaker than normal stimulus will depolarize the cells and cause an
action potential. Cells in this phase are particularly susceptible to
arrhythmias when exposed to an inappropriately timed stimulus,
which is why one must synchronize the electrical stimulus during
cardioversion to prevent inducing ventricular fibrillation.
Significance of long refractory period in cardiac
muscle

1. Summation of contractions does not occur

2. Fatigue does not occur
3. Tetanus does not occur
 CARDIAC CYCLE
• The cardiac cycle is the sequence of coordinated events that occurs
when the heart beats. As the heart beats, it circulates blood
through pulmonary and systemic circuits of the body.
• One cardiac cycle is completed when the heart chambers fill with blood
and blood is then pumped out of the heart.
• The cardiac cycle comprises a complete relaxation and contraction of
both the atria and ventricles, and lasts approximately 0.8 seconds.
• Thus, cardiac cycle is the period of time between the onset of atrial
contraction (atrial systole) and ventricular relaxation (ventricular
diastole).
• The cardiac cycle integrates pressure, volume, and electrocardiographic
and valvular movements during the systolic and diastolic periods
 CARDIAC CYCLE PHASES
• At the beginning of the cardiac cycle, both the atria and ventricles are
relaxed (diastole). Blood is flowing into the right atrium from the
superior and inferior venae cavae and the coronary sinus.
• Blood flows into the left atrium from the four pulmonary veins. The
two atrioventricular valves, the tricuspid and mitral valves, are both
open, so blood flows unimpeded from the atria and into the ventricles.
Approximately 70–80 percent of ventricular filling occurs by this
method. The two semilunar valves, the pulmonary and aortic valves,
are closed, preventing backflow of blood into the right and left
ventricles from the pulmonary trunk on the right and the aorta on the
left.
 Seven (7) events of the cardiac cycle

1. Atrial contraction
2. Isovolumetric ventricular contractions
3. Rapid ventricular ejection
4. Reduced ventricular ejection
5. Isovolumetric ventricular relaxation
6. Rapid ventricular filling(ventricular gallop and S3
7. Reduced ventricular filling (atrial gallop and S4
Atrial contraction (A-V Valves Open; Semilunar Valves
Closed) Phase 1
• Atrial depolarization initiates contraction of the atrial musculature. As
the atria contract, the pressure within the atrial chambers increases,
which forces more blood flow across the open atrioventricular (AV)
valves, leading to a rapid flow of blood into the ventricles.

• Atrial contraction (atrial kick) normally accounts for about 10- 20% of
left ventricular filling. It lasts for about 0.11s.

• Atrial contraction does produce a small increase in venous pressure

that can be noted as the "a-wave" of the left atrial pressure (LAP). Just
following the peak of the a-wave is the x-descent.
• After atrial contraction is complete, the atrial pressure begins to fall
causing a pressure gradient reversal across the AV valves. This causes
the valves to float upward (pre-position) before closure. At this time,
the ventricular volumes are maximal, which is termed the end-diastolic
volume (EDV). The left ventricular EDV (LVEDV), which is typically
about 120 ml, represents the ventricular preload and is associated with
end-diastolic pressures of 8-12 mmHg and 3-6 mmHg in the left and
right ventricles, respectively.

• A heart sound is sometimes noted during atrial contraction (fourth

heart sound, S4). This sound is caused by vibration of the ventricular
wall during atrial contraction. Generally, it is noted when the ventricle
compliance is reduced ("stiff" ventricle) as occurs in ventricular
hypertrophy and in many older individuals.
Pressure Changes in the Atria (The a, c, and v Waves)
• The a wave is caused by atrial contraction. Ordinarily, the right atrial
pressure increases 4 to 6 mm Hg during atrial contraction, and the left atrial
pressure increases about 7 to 8 mm Hg.
• The c wave occurs when the ventricles begin to contract; it is caused partly
by slight backflow of blood into the atria at the onset of ventricular
contraction but mainly by bulging of the A-V valves backward toward the
atria because of increasing pressure in the ventricles.
• The v wave occurs toward the end of ventricular contraction; it results from
slow flow of blood into the atria from the veins while the A-V valves are
closed during ventricular contraction. Then, when ventricular contraction is
over, the A-V valves open, allowing this stored atrial blood to flow rapidly
into the ventricles and causing the v wave to disappear.
Isovolumetric ventricular contractions (All Valves Closed)
(Phase 2)
• This phase of the cardiac cycle begins with the appearance of
the QRS complex of the ECG, which represents ventricular
depolarization. This triggers excitation-contraction coupling,
myocyte contraction and a rapid increase in intraventricular
pressure. Early in this phase, the rate of pressure development
becomes maximal. This is referred to as maximal dP/dt.
• The AV valves close when intraventricular pressure exceeds
atrial pressure.
• Closure of the AV valves results in the first heart sound (S1).
This sound is normally split (~0.04 sec) because mitral valve
closure precedes tricuspid closure.
• During the time period between the closure of the AV valves
and the opening of the aortic and pulmonic valves, ventricular
pressure rises rapidly without a change in ventricular volume
(i.e., no ejection occurs).
• Ventricular volume does not change because all valves are
closed during this phase. Contraction, therefore, is said to be
"isovolumic" or "isovolumetric.“
• The rate of pressure increase in the ventricles is determined by
the rate of contraction of the muscle fibers, which is determine
by mechanisms governing excitation-contraction coupling. The
maximal rate of pressure change during this phase is termed
"dP/dtmax."
 Rapid ventricular ejection (Aortic and Pulmonic Valves
Open) Phase 3
• Rapid ejection: This phase represents initial, rapid ejection of blood into the aorta
and pulmonary arteries from the left and right ventricles, respectively. Ejection
begins when the intraventricular pressures exceed the pressures within the aorta
and pulmonary artery, which causes the aortic and pulmonic valves to open.

• No heart sounds are ordinarily noted during ejection because the opening of
healthy valves is silent. The presence of sounds during ejection (i.e., systolic
murmurs) indicate valve disease or intracardiac shunts.

• Left atrial pressure initially decreases as the atrial base is pulled downward,
expanding the atrial chamber. Blood continues to flow into the atria from their
respective venous inflow tracts and the atrial pressures begin to rise. This rise in
pressure continues until the AV valves open at the end of phase 5.
Isovolumetric Relaxation (Phase 5)-All Valves Closed
• When the intraventricular pressures fall sufficiently at the end of phase 4, the
aortic and pulmonic valves abruptly close (aortic precedes pulmonic) causing the
second heart sound (S2) and the beginning of isovolumetric relaxation. Valve
closure is associated with a small backflow of blood into the ventricles and a
characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery
pressure tracings.
• After valve closure, the aortic and pulmonary artery pressures rise slightly
(dicrotic wave) following by a slow decline in pressure.
• Although ventricular pressures decrease during this phase, volumes do not
change because all valves are closed. The volume of blood that remains in a
ventricle is called the end-systolic volume and is ~50 ml in the left ventricle. The
difference between the end-diastolic volume and the end-systolic volume is ~70
ml and represents the stroke volume.
• Left atrial pressure (LAP) continues to rise because of venous return from the
lungs. The peak LAP at the end of this phase is termed the v-wave.
 Rapid Filling (Phase 6)- A-V Valves Open
• As the ventricles continue to relax at the end of phase 5, the
intraventricular pressures will at some point fall below their respective
atrial pressures. When this occurs, the AV valves rapidly open and
passive ventricular filling begins.
• The opening of the mitral valve causes a rapid fall in LAP. The peak of
the LAP just before the valve opens is the "v-wave." This is followed by
the y-descent of the LAP. A similar wave and descent are found in the
right atrium and in the jugular vein.
• Ventricular filling is normally silent. When a third heart sound (S3) is
audible during rapid ventricular filling, it may represent tensing of
chordae tendineae and AV ring during ventricular relaxation and filling.
This heart sound is normal in children; but is often pathological in
adults and caused by ventricular dilation.
 Reduced Filling (Phase 7)-A-V Valves Open
• As the ventricles continue to fill with blood and expand, they become
less compliant and the intraventricular pressures rise. The increase in
intraventricular pressure reduces the pressure gradient across the AV
valves so that the rate of filling falls late in diastole.

• In normal, resting hearts, the ventricle is about 90% filled by the end of
this phase. In other words, about 90% of ventricular filling occurs
before atrial contraction (phase 1) and therefore is passive.

• Aortic and pulmonary arterial pressures continue to fall during this

period.
 Volume changes in the cardiac cycle
• End diastolic volume ( EDV): Maximum volume of blood in each ventricle after
filling(ie at the end of diastole). It is about 130—150mL
• End Systolic volume (ESV): Minimum volume of blood in each ventricle at the end
of ejection(ie at the end of Systole) . It is about 70-90mL
• Stroke volume (SV): Amount of blood ejected from the ventricles per beat.
SV=EDV-ESV. It is usually about 70 mL
• Ejection fraction (Ef): Is the fraction (or portion) of end diastolic volume that is
ejected out by each ventricles per beat. It is expressed in %tage. Ef= SV/EDV%
• Cardiac output (CO) is the total volume of blood pumped by the heart per
minute. It is the product of blood pumped by each heart beat (stroke volume or
SV) and the number of beats (heart rate). CO=HRxSV
ACTIONS OF THE HEART
FOUR TYPES

1. Chronotropic action
2. Inotropic action
3. Dromotropic action
4. Bathmotropic action
CHRONOTROPIC ACTION
• Is the frequency of heart beat or heart rate. There are 2 types
Tachycardia- increase in HR
Bradycardia- decrease in HR

INOTROPIC ACTION
• Is the force of contraction of the heart. There are 2 types
Positive inotropic- Increase in the force of contraction
Negative inotropic- Decrease in the force of contraction
DROMOTROPIC ACTION
• Is the conduction of impulse through the heart. There are 2 types
Positive dromotropic action : Increase in velocity of conduction
Negative dromotropic action: Decrease in Velocity of conduction

BATHMOTROPIC ACTION
• Is the excitability of cardiac muscle. There are 2 types
Positive bathmotropic action: Increase in the excitability of cardiac
muscle
Negative bathmotropic action: Decrease in the excitability of cardiac
muscle
• Preload can be defined as the initial stretching of the cardiac
myocytes prior to contraction. Preload, therefore, is related to
muscule sarcomere length. Because sarcomere length cannot
be determined in the intact heart, other indices of preload are
used such as ventricular end-diastolic volume or pressure.

• Afterload is related to the pressure that the ventricle must

generate in order to eject blood into the aorta. An increase in
afterload (e.g., increased aortic pressure) decreases SV, and
causes ESV to increase. Conversely, a decrease in afterload
augments SV and decreases ESV.
Factors that increase Preload
Heart Sounds
• Heart sounds are the sounds produced b the mechanical activities of
the heart during each cardiac cycle. Heart sounds are produced by
movements of
• Blood through the chambers of the heart
• Cardiac muscle
• Valves of the heart
• Heart sound are heard by placing the ear over the chest, stethoscope,
microphone.
 HEART SOUNDS
Four (4) heart sounds are produced during each cardiac cycle
1. First Heart Sound S1
2. Second Heart Sound S2
3. Third Heart Sound S3
4. Fourth Heart Sound S4
Features 1st Heart Sound 2nd Heart Sound 3rd Heart Sound 4th Heart Sound
Occurs during Isometric Protodiastole and part Rapid Filling Phase Atrial Systole
contraction period of isometric relaxation (considered physiologic
and part of ejection atrial sound.
period
Cause Closure of A-V Closure of Semilunar Rushing of blood into Contraction of atrial
valves valves ventricle musculature
Characteristics Long, soft and low Short, sharp and high Low pitched (can be Inaudible sound
pitched. Resembles pitched. Resembles the heard with the
the word “LUBB” word ‘DUB’ stethoscope in children
and athletes)
Duration (Sec) 0.10-0.17 0.10-0.14 0.07-0.10 0.02-0.04
Frequency (cycles per unit) 25-45 50 1-6 1-4

Relation with ECG Coincides with peak Precedes or appears Between ‘T’ wave and Between ‘T’ wave and
of ‘R’ 0.09s after peak of ‘T’ ‘P’ wave ‘Q’ wave
wave
No. of vibrations in 9-13 4-6 1-4 1-2
phonocardiogram

Conditions when it Children, athletes, Ventricular

Electrocardiogram (ECG)
• When the cardiac impulse passes through the heart, electrical current
also spreads from the heart into the adjacent tissues surrounding the
heart. A small portion of the current spreads all the way to the
surface of the body. If electrodes are placed on the skin on opposite
sides of the heart, electrical potentials generated by the current can
be recorded; the recording is known as an electrocardiogram
 Electrocardiogram (ECG)

• Electrocardiography is the technique by which the electrical activities of the heart

are studied. This technique was discovered by Dutch physiologists, Einthoven
Willem who is considered the father of ECG.
• Electrocardiograph is the instrument (ECG machine) by which the electrical
activities of the heart are recorded.
• Electrocardiogram is the record or graphical registration of electrical activities of
the heart, which occur prior to the onset of mechanical activities. ECG is recorded
in 12 leads.
• The paper used for recording ECG is called ECG paper. ECG grid refers to the
markings (lines) on ECG paper.
 ECG GRID
• The ECG paper has horizontal and vertical lines at regular intervals of
1mm. Every 5th line (5mm) is thickened.
• Duration: The duration of different ECG waves is denoted by the
vertical lines.
Interval b/w 2 thick lines (5mm)=0.2s
Interval b/w 2 thin lines (1mm)=0.04s
• Amplitude: The amplitude of ECG waves is denoted by horizontal lines
Interval b/w 2 thick lines (5mm)=0.5mV
Interval b/w 2 thin lines (1mm)=0.1mV
 The 12 leads of the ECG are classified into
1. Bipolar leads
2. Unipolar leads

Bipolar leads, also called standard limb leads

Two active electrodes ( positive and negative) are connected to get these leads.
They are three
1. Limb lead 1
2. Limb lead 11
3. Limb lead 111
 Limb Leads
Limb Lead 1 Right arm connected to negative terminal
Left arm connected to positive terminal

Limb Lead 11 Right arm connected to negative terminal

Left leg connected to the positive terminal

Limb Lead 111 Left arm connected to negative terminal

Left leg connected to the positive terminal
UNIPOLAR LEADS
• They are of two types
1. Unipolar Limb leads
2. Unipolar Chest leads
Unipolar Limb leads

• Also called augmented limb leads. One electrode is active while the
other is an indifferent electrode.
• There are three unipolar limb leads
1. aVR lead
2. aVL lead
3. aVF lead
aVR lead Active electrode from R arm, Indifferent connected to R arm and L leg

aVL lead Active electrode from L arm, Indifferent connected to R arm and L leg

aVF lead Active electrode from L leg, Indifferent connected to R arm and L arm
Unipolar Chest Leads
• Chest leads are also called Precardial leads. The indifferent electrode
is obtained by connecting the three limbs- L leg, Larm and R arm
through a resistance of 5000 ohms. The active electrode is placed on
six points over the chest called V1, V2, V3, V4, V5 and V6. V indicates
vector
 Unipolar Chest leads
Lead Position

V1 Over the 4th Intercostal Space (4ICS) near right sternal margin

V2 4ICS near left sternal margin

V3 Between V2 and V4

V4 5th Intercostal space midclavicular line (5ICSMCL)

V5 5th Intercostal space anterior axillary line (5ICSAAL)

V6 5th Intercostal space mid axillary line (5ICSMAL)

Waves of the normal ECG
• A normal ECG consists of waves, complexes, intervals and segments
• Waves of ECG recorded by Limb Lead 11 are considered as the typical
waves
• The normal electrocardiogram is composed of a P wave, a QRS
complex, and a T wave.
 Waves of Normal ECG
Wave/Segment From-To Cause Duration(s) Amplitude (mV)
P wave Atrial depolarization 0.1 0.1-0.12
QRS Onset of Q wave to the Ventricular 0.08-0.10 Q=0.1-0.2
end of S wavw Depolarization R=1
S=0.4
T Ventricular 0.2 0.3
Repolarization
P-R interval Onset of P wave to Atrial depolarization 0.18-(0.12-0.2)
onset of Q wave and conduction
through AV node
Q-T interval Onset of Q wave and Electrical activity in 0.4-0.42
end of T wave ventricles. Indicates
ventricular
depolarization and
ventricular
repolarization.
S-T interval End of S wave and Isoelectric 0.08
onset of T wave.
 P-Wave
• P -wave is positive ( upright) in leads 1,11,aVF, V4, V5, and V6 and
negative (inverted) in aVR and variable in other leads
Clinical significance
Right Atrial Hypertrophy Tall P wave (>2.5mm) in lead 11
•
Left Atrial Hypertrophy -
Tall and broad P wave (M shape)
Hyperkalaemia Absent or small P wave

Atrial fibrillation Absent P wave

Sinoatrial block Inverted or absent P wave

QRS Complex

• Also called initial ventricular complex. It is usually as a result of

depolarization of ventricular musculature
• Q wave due to depolarization of basal portion of interventricular
septum
• R wave due to depolarization of apical portion of interventricular
septum
• S wave due to depolarization of basal portion of ventricular muscle
near the atrioventricular ring
Clinical significance of QRS waves
• Bundle branch block: QRS is prolonged or deformed
• Hyperkalaemis: QRS prolonged
 T wave
• Final ventricular wave, usually due to ventricular repolarization
• Usually positive in leads 1,11 and V5 &V6. It is normally inverted in aVR
and variable in other leads.
CLINICAL SIGNIFICANCE
• Acute myocardial ischemia; Tall, broad based T wave (Hyperacute T
wave)
• Old age, hyperventilation, anxiety, myocardial infarction, L ventricular
hypertrophy and pericarditis- T wave is small, flat or inverted.
• Hypokalaemia: T wave is small, flat or inverted.
• Hyperkalaemia: T ave is tall and tented.
U- wave
• Not always seen
• Insignificant but represents repolarization of papillary muscle
Clinical uses of ECG
• To obtain information about the structure and function of the heart.
• To obtain information about the function of its electrical conduction
system.
• To measure the rate and rhythm of heartbeats, the size and position of
the heart chambers.
• To assess the presence of any damage to the heart’s muscle cells or
conduction system.
• To assess the effects of drugs to the heart.
• To assess the function of implanted pacemakers.
 Indications for performing ECG
1. Suspected myocardial infarction(heart attack) or chest pain.
2. Suspected Pulmonary embolism or shortness of breath.
3. Perceived arrhythmia.
4. Fainting or collapse
5. Seizures
6. Monitoring the effects of medication on the heart.
7. Assessing the severity of electrolyte abnormalities eg hyperkalaemia.
8. Hypertrophic cardiomyopathy (e.g due to sports)
9. Perioperative assessments.
10. Cardiac stress testing.
 CARDIAC OUTPUT
• Cardiac output (CO) 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.
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.
 Definition of terms
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 INDEX
• Cardiac index is the minute volume expressed in relation to square
meter of body surface area. It is defined as the amount of blood
pumped out per ventricle/minute/ square meter of the body surface
area. Normal value: 2.8 ± 0.3 L/square meter of body surface
area/minute (in an adult with average body surface area of 1.734
square meter and normal minute volume of 5 L/minute).

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. 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
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.
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
PATHOLOGICAL VARIATIONS

Increase in Cardiac output

1. Fever: Due to increased oxidative processes
2. Anemia: Due to hypoxia
3. Hyperthyroidism: Due to increased basal metabolic rate.
Decrease in Cardiac Output

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. Hemorrhage: Because of decreased blood volume
 DISTRIBUTION OF CARDIAC OUTPUT
• The whole amount of blood pumped out by the right ventricle goes to lungs.
• 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
Organ Amount of blood Percentage
(mL/ minute) e
Liver 1,500 30

Kidney 1,300 26

Skeletal muscles 900 18

Brain 800 16

Skin, bone and GI 300 6

tract
Heart 200 4

Total 5000 100

FACTORS MAINTAINING CARDIAC OUTPUT
Cardiac output is maintained (determined) by four factors:

1. Venous return
2. Force of contraction
3. Heart rate
4. Peripheral resistance
 VENOUS RETURN
• Venous return is the amount of blood which is returned to 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 depends upon five factors:
i. Respiratory pump
ii. Muscle pump
iii. Gravity
iv. Venous pressure
v. Sympathetic tone.
Respiratory Pump
• Respiratory pump is the respiratory activity that helps the return of
blood, to heart during inspiration. It is also called abdominothoracic
pump.
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 muscular activity increases, the venous return is more. When the
skeletal muscles contract, the vein located in between the muscles is
compressed.
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.
Venous Pressure
• Venous pressure also affects the venous return. Pressure in the venules is 12 to
18 mm Hg. In the smaller and larger veins, the pressure gradually decreases. In
the great veins, i.e. inferior vena cava and superior vena cava, the pressure falls
to about 5.5 mm Hg. At the junction of venae cavae and right atrium, it is about
4.6mm Hg. Pressure in the right atrium is still low and it alters during cardiac
action. It falls to zero during atrial diastole. This pressure gradient at every part
of venous tree helps as a driving force for venous return

Sympathetic Tone
• Venous return is aided by sympathetic or vasomotor tone which causes
constriction of venules. Venoconstriction pushes the blood towards heart.
2. FORCE OF CONTRACTION
Cardiac output is directly proportional to the force ofcontraction,
provided the other three factors remain constant. According to Frank-
Starling law, force of contraction of heart is directly proportional to the
initial length of muscle fibers, before the onset of contraction. 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. force of contraction of heart and
cardiacoutput are directly proportional to preload
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. Thus, the afterload for left
ventricle is determined by aortic pressure and afterload for right
ventricular pressure is determined by pressure in pulmonary artery.
• Force of contraction of heart and cardiac output are inversely
proportional to afterload.
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
 MEASUREMENT OF CARDIAC OUTPUT
Cardiac Outout can be measured through
Direct methods used to measure cardiac output in animals:
1. By using cardiometer
2. By using flowmeter.
Indirect methods used to measure cardiac output (Used for
animals and humans):
1. By using Fick principle
2. Indicator (dye) dilution technique
3. Thermodilution technique
4. Ultrasonic Doppler transducer technique
5. Doppler echocardiography
6. Ballistocardiography.
• Adolph Fick described Fick principle in 1870. According to this
principle, the amount of a substance taken up by an organ (or by the
whole body) or given out in a unit of time is the product of amount of
blood flowing through the organ and the arteriovenous difference of
the substance across the organ.
Amount of substance taken or given= Amount of blood flow /minute x
Arteriovenous difference
Eg. Amount of blood flowing through lungs is 5,000 mL/minute
O2 content in arterial blood = 20 mL/100 mL of blood
O2 content in venous blood = 15 mL/100 mL of blood
Amount of O2 moved from lungs to blood= Amount of blood flow /minute x
Arteriovenous difference of O2
5,000 x 20-15/ 100 = 250 mL/minute
• Amount of oxygen moved from lungs to blood= 250 mL/minute
 Modification of Fick principle to
measure cardiac output
• Fick principle is modified to measure the cardiac output or a
part of cardiac output (amount of blood to an organ).Thus,
cardiac output or the amount of blood flowing through an
organ in a given unit of time is determined by the formula:

Cardiac output= Amount of substance taken or given by the organ/ minute

Arteriovenous difference of the substance across the organ
By modifying Fick principle, cardiac output is measured in two
ways:
• i. By using oxygen consumption
• ii. By using carbon dioxide given out.

Measurement of Cardiac Output by Using Oxygen Consumption

• Fick principle is used to measure the cardiac output by
determining the amount of oxygen consumed in the body in a
given period of time and dividing this value by the
arteriovenous difference across the lungs.
• Cardiac Output = O2 consumed (in mL/minute)
Arteriovenous O2 difference
• Oxygen consumption: Amount of oxygen consumed is measured by
using a respirometer or BMR apparatus (Benedict Roth apparatus).
Oxygen content in arterial blood: Blood is collected from any artery to
determine the oxygen content in arterial blood. Oxygen content is
determined by blood gas analysis.
• Oxygen content in venous blood: Only mixed venous
• blood is used to determine the oxygen content of venous
• blood, since oxygen content is different in different
• veins. Mixed venous blood is collected from right atrium
• or pulmonary artery. It is done by introducing a catheter
• through basilar vein of forearm. Oxygen is determined
• from this blood by blood gas analysis
• Calculation
• For example, in a subject, the following data are
• obtained:
O2 consumed (by lungs) = 250 mL/minute
O2 content in arterial blood = 20 mL/100 mL of blood
O2 content in venous blood = 15 mL/100 mL of blood
Cardiac Output = O2 consumed (in mL/minute)
Arteriovenous O2 difference
CO= 250 250x100
5/100 5
= 5,000ml/min

5 mL of oxygen is taken by 100 mL of blood while passing through the

lungs. Thus, 250 mL of oxygen is taken by 5,000 mL of blood. Since
cardiac output is equivalent to the amount of blood passing through
pulmonary circulation, the cardiac output = 5 L/minute.
Measurement of Cardiac Output by Using Carbon Dioxide
• Cardiac output is also measured by knowing the arteriovenous
difference of carbon dioxide and amount of carbon dioxide given out
(removed) by lungs

Cardiac Output = CO2 evolved (in mL/minute)

Arteriovenous CO2 difference
 Calculation

For example, in a subject CO2 removed by lungs = 200 mL/minute

• CO2 content in arterial blood = 56 mL/100 mL of blood
• CO2 content in venous blood = 60 mL/100 mL of blood
200
60-56 mL/100mL

200 x 100 = 5,000mL = 5L/min.

4
• Since cardiac output is equal to the amount of blood passing through
lungs (pulmonary circulation), the
cardiac output = 5 L/minute
• Nitrous oxide is also used to measure cardiac output by applying Fick
principle.
Advantage of measurement of cardiac output by Fick principle
• The results are accurate.
Disadvantage
• Fick principle is an invasive method and involves the insertion of
catheter through subject vein.