CARDIOVASCULAR SYSTEM

The cardiovascular system consists of the heart (pump) and a closed system of
distensible vessels through which the heart pumps blood to all parts of the body.
The vessels which carry blood away from the heart are called arteries, and their
smallest divisions are called arterioles. Those that carry blood from the tissues
back to the heart are called veins, and their smallest divisions are called venules.
The capillaries connect arterioles to venules.
The cardiovascular system may conveniently be divided into five main parts viz;
-the pump (heart)
-the distribution system (arteries)
-the exchange system (capillaries)
-the collection system (veins)
-the fluid system (blood)

FUNCTIONS OF THE CVS

1. It serves as the major transport system for the body through the transport
of respiratory gases and nutrients to and from the cells and tissues of the
body.
2. It helps in excretion through transport of metabolic waste to excretory
organs hence it is indirectly involved in excretion.
3. It plays a role in the coordination and integration of body functions.
4. Plays a role in regulation of temperature
5. Protects the body from infection and blood loss.

PRINCIPLES OF CVS FUNCTION

The most important factor in CVS is blood flow. In this system, it is a requirement
to have a pressure to drive the blood around the circuit. This pressure is required
to overcome the resistance mounted by blood vessels and the viscosity of blood.
The CVS also incorporates a mechanism to regulate the amount of blood flowing
to the tissues. Increase in tissue metabolic rate leads to an increase in regulatory
mechanisms to meet the metabolic demands of the tissues and vice versa.
ARCHITECTURE OF THE CVS
The CVS is designed in such a way that if the blood flow to a particular organ is
interrupted, the flow to the other organs will not be affected. It is therefore
possible to cut off blood flow to any organ without affecting the blood flow to
other organs. This is made possible by the parallel arrangement of the blood
vessels.
The importance is that it permits variation in the distribution of regional blood
flow. If the vessels were in series, any interruption will block the flow of blood to
other organs which will not be compatible to life.

THE HEART
The heart is a hollow organ which acts as the pump in the cardiovascular system.
It works continuously without a break throughout the lifespan of an individual.
The sudden cessation of the heart is known as cardiac arrest and could lead to
death if no resuscitation occurs within 3-5 minutes.
The heart as a pump
In order for the heart to operate as a pump it has to exhibit certain features that
are consistent with its function in the cardiovascular system. For the functioning
of the heart, it must show these features;
-must be able to pump adequate blood into the circulation to meet metabolic
demand.
-must be able to pump continuously without a break
-must function as a unit
-must provide unidirectional flow of blood
-must be able to adjust its output in accordance with the metabolic demand of
the tissues
-must show no signs of fatigue
The heart consists of two pumps: the right pump and the left pump. The right
pump receives venous blood throughout the body into its atrium (venous return)
and pumps it from the ventricles to the lungs for oxygenation. This system is
known as pulmonary circulation. The left pump receives oxygenated blood from
the lungs into its atrium and pumps it from its ventricles to all parts of the body.
This system is known as systemic circulation.
PHYSIOLOGIC ANATOMY OF THE HEART
The heart is partitioned into four chambers: two atria (right and left) and two
ventricles (right and left). Each atrium empties its contents into the corresponding
ventricles through a one-way valve that has three cusps in the right (tricuspid
valve) and two cusps in the left (bicuspid/mitral valve). These are collectively
known as atrioventricular valves. The atria do not communicate with each other,
neither do the ventricles. This communication only occurs in the presence of
congenital defects; Atrial Septal Defects (ASD) or Ventricular Septal Defects (VSD)
—HOLE IN THE HEART.
The outflow of blood from the left ventricle into the aorta is guarded by the aortic
valve while that from the right ventricle into the pulmonary artery is guarded by
the pulmonary valves both collectively known as the semilunar valves.
The left ventricular walls are four times thicker than the right ventricular walls and
account for about 75% of the mass of the heart.

Diagram of the heart

Atria
 Primary receptive chambers
 Right atrium receives deoxygenated blood from upper extremities through
the superior vena cava and from lower extremities through the inferior
vena cava.
 Left atrium receives oxygenated blood from the lungs through the
pulmonary valve.
 Atria empties blood into the ventricles via two processes;
-passive process: involves passive gradient i.e blood flows from the
atrium down into the ventricles (makes up 80% of ventricular filling)
-active process: involves contraction of atrium to force blood into the
ventricles (makes up 20% of ventricular filling).

Ventricles
 Main pumps
 Generates pressure to drive the blood round the circuit
 The left ventricle pumps blood into the systemic circulation and the right
ventricle pumps into the pulmonary circulation.
 The balancing of the output of the two ventricles is important because any
mismatch leads to pooling of blood either in the pulmonary or systemic
circulation.
 The left ventricular wall is 4X thicker than the right ventricular wall because
left ventricle pump against a higher pressure (80mmHg) in the systemic
circulation while the right ventricle pumps against low pressure (8mmHg) in
the pulmonary circulation.
Diagram of the heart showing the layers of the heart

LAYERS OF THE HEART

The heart consists of three layers;
1) The Pericardium/Epicardium: this covers the heart and consists of a serous
layer adherent to the surface of the heart and separated from the outer
fibrous layer by a thin film of fluid. This layer prevents excess expansion or
movement of the heart.
2) The Myocardium: The myocardium is functionally the main constituent of
the heart and the thickest layer of all three heart layers. It is a muscle layer
that enables heart contractions.
3) The Endocardium: The endocardium is the innermost layer of the heart. It
lines the inner surfaces of the heart chambers, including the heart valves.
The endocardium has two layers. The inner layer lines the heart chambers
and is made of endothelial cells. Superiorly, is the second layer: a
subendocardial connective tissue which is continuous with the connective
tissue of the myocardium.
HISTOLOGY OF THE CARDIAC MUSCLE CELL
Cardiac muscle tissue – These are specialized involuntary, striated,
mononucleated, contractile cells/fibers and the specialized conduction or
pacemaker cells/fibers which comprise the bulk of the tissue of the heart; forming
the myocardium in which the contractile cells are connected to each other by
intercalated discs

Contractile fibers - One of the two types of cardiac muscle cells; the majority of
cardiac muscle cells which are involuntary, striated, branched, uninucleate cells
connected to each other by intercalated discs and specialized to constrict by means
of the sliding filament mechanism using actin and myosin proteins; contractile
fibers are rapid in contraction and relaxation, have a long refractory period, do not
readily fatigue, and are autorhythmic.

Cell nucleus - The large, membrane-bound, usually oval or spherical organelle

within the cytoplasm of (almost all) living cells, containing the cell's hereditary
material (DNA in the form of chromosomes) and controlling the cell's metabolism,
growth, and reproduction.

Sarcomere - One of the segments into which a myofibril of striated muscle is

divided; "the unit of contraction;" the sarcomere has dark central A band split in
the middle by the lighter H zone which contains the M line and, at each end, has
one half of a lighter I band which is split by the Z line; the borders of the
sarcomere are the Z lines.

Striations - The series of parallel lines or light and dark bands observed in the
cytoplasm of striated muscle cells, the bands are perpendicular to the long axis of
the muscle cell; the banding pattern is due to the orderly arrangement of contractile
myofilaments organized into repeating sarcomeres within each myofibril.

Myofibril - The non-membrane-bound cell organelle of skeletal and cardiac

muscle cells which is a long cylindrical mass of contractile protein fibers (actin +
myosin), organized as a series of repeating sarcomeres

Myofilament - Any of the ultramicroscopic protein filaments, made up of actin

and myosin, that are the structural units of a myofibril.
Intercalated disc- the specialized intercellular junction between individual cardiac
muscle cells which appears as a dark line in microscopic specimens; at the
molecular level it contains both electrical synapses provided by gap junctions and
structural connections provided by desmosomes and tight junctions.

Gap junction - An intercellular junction which consists of a network of integral

membrane protein channels called connexons which facilitate the cell-to-cell
passage of small molecules, e.g., ions, small second messengers, etc., because
these junctions are relatively non-selective in their permeability, i.e., they provide
direct cytoplasmic connections; they are common in cardiac muscle and in some
smooth muscle tissues.

Desmosome - the specialized cell junction which links two cells by tying their
outer cell membranes together with a tuft of intermediate filaments = tonofilaments
embedded in a mass of dense anchoring material; desmosomes are particularly
prevalent in tissues such as the epidermis and myocardium which have to
withstand mechanical stress; nicknamed the "spot weld" junction.
EXCITATORY AND CONDUCTING SYSTEMS OF THE HEART
This consists of the Sino-atrial node (S.A. Node), the Atrioventricular node (A.V.
Node) and the Purkinje system. The S.A. and A.V. nodes are excitatory while the
Purkinje fibers and the bundle of His are conductive. The S.A. node starts the
sequence by causing the atrial muscles to contract, next, the signal travels to the
AV node, through the bundle of HIS, down the bundle branches, and through the
Purkinje fibers, causing the ventricles to contract.

S.A. Node
This is located at the endocardial surface of the right atrium near the junction of
the superior vena cava and the right atrium. The fibers are continuous with atrial
wall so that any action potential that begins in the S.A. node spreads immediately
into the atria. As a result, the S.A. node is called the pacemaker of the heart
because it determines the rate of the heart and it is the point of origin for
producing a wave of electrical impulses that stimulates atrial contraction by
creating an action potential across myocardium cells. Upon destruction of this
pacemaker, the A.V. node or Purkinje fibers can assume the function of pacing the
heart. The S.A. node is an excitable tissue. The S.A. node displays automatic
rhythmicity and is the most developed in the conductive system of the heart. The
S.A. node fires rhythmically at a rate of approximately 75-100 beats per minute.

A.V. Node
This is located on the septal wall of the right atrium, immediately posterior to the
tricuspid valve. It is connected to the S.A. node by three Atrial internodal bundles
viz;
-Bachmann’s bundle—Anterior (fastest)
-Thorel’s bundle —Posterior
-Wenckebach’s bundle —Middle
The A.V. node has a slower conduction velocity compared to the S.A. node. The
A.V. node has the ability to delay the conduction of atrial impulses to the Bundle
of His known as the AV nodal delay. This lasts about 0.01sec. The AV nodal
delay is a feature, not a bug because it ensures that atrial contraction is finished
before ventricular contractions begins and hence allows for complete atrial
emptying into the ventricles before ventricular contractions begin. The A.V. node
fires at a rate of approximately 40-60 beats per minute.

Purkinje Fibers
The A.V. node is connected to a conducting tissue, the Bundle of His which runs
along the inter ventricular septum and divides at the top of the muscular portion
of the septum into left and right bundle branches of the Purkinje system. These
run under the endocardium on either side and terminate as the Purkinje fibers
that penetrate the endocardium of the of the corresponding ventricular muscle.
The Purkinje fibers fires at a rate of approximately 15-40 beats per minute.
ELECTRICAL ACTIVITIES OF THE HEART
The heart has an inherent rhythmicity that is self-exciting and does not depend on
nerve stimulation to contract unlike in skeletal muscle. The inherent rhythmicity
of the heart is due to the presence of certain myocardial cells in well defined
areas of the heart, which can spontaneously depolarize causing action potentials
to be fired.
There are differences in the shape, ionic mechanism and durations of action
potentials in different parts of the heart.

VENTRICULAR ACTION POTENTIALS

Action potentials in the ventricles have 5 phases named phases 0 - 4

Phase 0; Rapid Depolarization with Overshoot: The Resting membrane potential

the resting membrane potential (voltage when the cell is not electrically excited)
of ventricular cells, is around -90 mV that is the inside of the membrane is more
negative than the outside. The action potential begins with the voltage becoming
more positive mainly due to the opening of voltage-gated Na + channels with a
rapid influx of Na+ (and some Ca2+). The gates open when the RMP drops to about
-60mV, the threshold potential. This causes the RMP to rapidly drop from -90mV
to 0mV, and then reverses in polarity such that the inside is positive, about
+25mV relative to the outside. This is known as Depolarization.

Phase 1; Initial Rapid Repolarization: From the new positive membrane

potential, there is a rapid decline to 0mV, which is due to closure of Na + channels
and influx of Cl-. Phases 0 and 1 correspond with the QRS wave of the ECG.

Phase 2; Plateau Phase: The membrane potential then remains stable for about
150ms. This is due to a prolonged opening of voltage-gated Ca2+ channels allowing
a slow influx of Ca2+. This phase corresponds with the ST wave of the ECG.

Phase 3; Rapid Repolarization: The following rapid repolarization returns the

membrane potential to its resting level. This occurs as a result of the closure of
Ca2+ channels and opening of both voltage and ligand-gated K+ channels which
cause K+ efflux. This phase corresponds with the T wave of the ECG.
Phase 4: Without any further change in membrane potential, the K+ channels
close and the Na+-- K+ pump restores the Na+ and K+ to their original positions on
either side of the cell membrane.
 ELECTROCARDIOGRAM
This is a recording of the voltage produced by the electrical activity of
the heart. The SA node of the heart generates an electrical signal that
moves through the two atria into the AV node. The AV node delays the
signal and then sends it through the bundle of His and Purkinje fibres
which causes simultaneous contraction of the ventricles.
Now when electrodes are connected to the surface of the skin at
particular points around the heart, electrical signals can be picked up
using the electrocardiograph.

Terminologies
Electrocardiograph: equipment used for recording
Electrocardiogram: tracing/recording obtained on a paper
Electrocardiography: the procedure
Electrocardiographic grid: the paper on which it is recorded

Uses
Used in the diagnosis and management of myocardial infarction
Used in the diagnosis and management of rhythm and conduction
abnormalities
Used in diagnosis of pulmonary embolism
Used in diagnosis of atria and ventricular hypertrophy
Used in detection of drug intoxication.

ELECTROCARDIOGRAPHIC LEADS
The electrodes used in recording are called ECG leads. The heart is said
to be in the middle of an imaginary equilateral known as the
Einthoven’s triangle. This imaginary equilateral triangle is drawn by
connecting the roots of three limbs usually the right arm, left arm and
left foot. Three types of leads are used in ECG recording namely;
Bipolar limb leads or Standard limb leads
Unipolar limb leads or Augmented limb leads
Chest (Precordial) leads

Bipolar limb leads: Here the difference in potential between two active
electrodes are measured. There are three leads in the bipolar limb
leads system
Lead I: this measures the potential difference between the right arm
and left arm. It is obtained by connecting the negative terminal to the
right arm and the positive terminal to the left arm.
Lead II: this measures the potential difference between the right arm
and left leg. It is obtained by connecting the right arm to the negative
terminal of the instrument and the left leg to the positive terminal.
Lead III: this measures the potential difference between the left arm
and the left leg. It is obtained by connecting the left arm to the negative
terminal and the left leg to the positive terminal.

Unipolar leads: In addition to the three bipolar limb leads, there are
three augmented unipolar limb leads. They are termed unipolar limb
leads because there is a single positive electrode that is referenced
against two of the other two limb electrodes. The positive electrodes
for these augmented leads are located on the left arm (aVL), right arm
(aVR) and left leg (aVF).

Precordial leads: The precordial chest leads view the electrical activities
of the heart in a plane perpendicular to the frontal plane. Here the
active electrode is placed on six points over the chest. These points are
labelled V1 to V6.
Positions of chest leads are as follows;
V1: Over 4th intercoastal space near right sternal margin
V2: Over 4th intercoastal space near left sternal margin
V3: In between V2 and V3
V4: Over left 5th intercoastal space on mid clavicular line
V5: Over left 5th intercoastal space on the anterior axillary line
V6: Over left 5th intercoastal space on the mid axillary line

WAVES OF NORMAL ECG

Normal ECG consists of waves, complexes, intervals and segments.
Normal electrocardiogram has the following waves, P, Q, R, S, T and U.

P wave: the cardiac cells within the SA node depolarize and initiate an
action potential in the upper right atrium of the heart. As it spreads out
through the conduction channels in the right and left atrium, it causes
them to contract. This contraction leads to the opening of the av valves
so that blood is drained into the ventricles. Hence, P waves occurs due
to atrial depolarization.

P-R Segment: this segment indicates the arrival of the electrical signal
at the AV node where there is a delay of about 0.1sec. this delay allows
for complete emptying of the atria. After this the AV node depolarizes
and sends the signal through the bundle of His and Purkinje fibers.
Duration: 0.08s-0.11s

QRS Complex: this complex consists of three individual waves. It

represents the depolarization of the ventricles leading to ventricular
contraction. This contraction due to its high pressure causes the closing
of the AV valves thereby producing the first heart sound. Notice that
this produces a much higher amplitude than any other portion of the
electrocardiogram, this is because the ventricles are much thicker than
the atria and as a result produce a more forceful contraction. Hence
QRS complex signifies ventricular depolarization. Duration: 0.08s-0.10s

S-T Segment: within this segment, the contraction continues to

increase as hydrostatic pressure continues to increase. This causes the
opening of the semi lunar valves so that blood flows from these valves
into their respective arteries. So now all the cardiac cells within the
ventricles have been depolarized and repolarization begins. Hence, this
segment marks the beginning of ventricular repolarization. Duration:
0.12s-0.2s

T wave: repolarization continues in this phase and takes place fully

here. Here the cells of the ventricles repolarize and essentially empty
out all the blood into the arteries. The hydrostatic pressure in the
ventricles now decreased causes the closing of the semi lunar valves.
This brings about the second heart sound. Duration: 0.20s-0.30s

U wave: this is a small peaked wave that follows the T wave. The U
wave is believed to describe the repolarization of the cells of the
intraventricular septum. It’s almost never seen and mostly considered
as abnormal.

CLINICAL CORRELATES OF ECG

Diseases of the heart are classified into four main groups;
1. Conduction and Rhythm abnormalities
2. Diseases of the cardiac muscle
3. Valvular diseases
4. Septal defects
Conduction abnormalities
i. S-A node block: here the impulses are not conducted to the
atrium. When this happens, AV node takes over as the pacemaker
and since the AV node has low rhythmicity the heart will beat at a
slower rate hence the absence of P wave
ii. A-V block: here the conduction of impulses may be delayed more
than normal or the impulses may not pass through at all. Three
degrees of AV block exists.
-1st Degree Heart block where AV nodal delay is more than normal
leading to a prolonged PR segment
-2nd Degree Heart block where some of the impulses from the
atria do not reach the ventricles
-3rd Degree Heart block where all the impulses pass through the
AV node so that the atria are completely dissociated from the
ventricles. Hence there are two P waves to one QRS complex.

Rhythm abnormalities
i. Sinus rhythm abnormalities
ii. Atrial rhythm abnormalities
CARDIAC CYCLE
Cardiac cycle is a succession of coordinated mechanical events that
take place in the heart during each heartbeat. This represents the
period from the end of a heart contraction to the beginning of the next.
Each heartbeat consists of an alternate period of diastole and systole.
During systole, the heart contracts and blood is pumped through the
arteries while during diastole the heart relaxes and blood fills the heart.

The cardiac cycle is initiated by impulses originating from the S.A. node
which spreads all over the atrium and is delayed by 0.1s in the A.V.
node which permits the ventricles to be filled with blood from the
atrium. At a resting heart rate of 72 beats per min, the cardiac cycle
lasts a total of 0.83secs.

EVENTS IN CARDIAC CYCLE

Two major events exist in cardiac cycle: Systole and Diastole

SYSTOLE
This represents the period of cardiac contractions. It occurs in two
stages viz:
-Isovolumic contraction period
-Ejection period

Isovolumic contraction period

This occurs at the onset of ventricular systole. There is increase in intra
ventricular pressure which causes immediate closure of the Atrio-
ventricular valves causing the first heart sound to be heard. Since both
the Atrio-ventricular valves and semilunar valves are closed at this
phase, intra ventricular pressure continues to increase approaching
80mmHg in the left ventricle and 8mmHg in the right ventricle.
Ejection period
Following the period of isovolumic contraction of the ventricles, with all
the valves closed, ventricular pressure continues to rise until the left
ventricular pressure is above 80mmHg and right ventricular pressure is
above 8mmHg then ventricular ejection begins. This developed
ventricular pressure pushes the semilunar valves open and blood
begins to pour out of the ventricles.

DIASTOLE
This represents the period of cardiac relaxation. It occurs in four stages
viz;
-Isovolumic relaxation period
-Rapid filling
-Diastasis
-Atrial systole

Isovolumic relaxation period

Now the valves are closed, there’s no change in volume and ventricles
are now relaxed. This stage is referred to as the Isovolumic relaxation
stage. The relaxation causes a rapid fall in intra ventricular pressure.
The intra ventricular pressure continues to reduce until the AV valves
are now pushed open and blood begins to flow into the ventricles from
the atria.

Rapid Filling
The filling of the ventricles beginning of diastole is very rapid. It is
preceded by the opening of the AV valves and rapid inflow of blood
occurs from the atria to the ventricles. This phase accounts for about
70-80% of ventricular filling. This phase is also associated with the third
heart sound.

Diastasis
The rapid filling is followed by a period of slower filling of ventricles
known as diastasis. The flow in this phase is almost at a stand still.

Atrial systole
In the last phase of the diastole, the atria begin to contract giving an
additional thrust to the filling of the ventricles. This phase contributes
to about 30% of ventricular filling in each cardiac cycle.
Events in cardiac cycle
VENOUS RETURN
Venous return refers to the flow of blood from all parts of the body (except the
lungs) to the right atrium. Since the circulatory system is a closed circuit, venous
return must equal cardiac output and as a result, factors which affect venous
return must affect cardiac output. The most important determinant of venous
return is the rate of body metabolism therefore, cardiac output is regulated to
match body metabolism.

CARDIAC OUTPUT
Cardiac output refers to the quantity of blood ejected per minute by each
ventricle. It is a very important factor in cardiovascular physiology because the
rate of blood flow through different parts of the body depends on the cardiac
output. The quantity of blood ejected per minute by each ventricle is the product
of the number of beats per minute (Heart rate) multiplied by the volume ejected
in each beat or stroke (Stroke volume)
Cardiac Output= Heart rate × Stroke volume
The heart has intrinsic mechanisms that enable it adjust its output but in times of
circulatory stress such as exercise, hemorrhage or severe dehydration, the
autonomic nervous control of the circulation ensures adequate blood supply to
vital organs such as the brain and the heart. Hence, adjustments of the cardiac
output depend on adjustments of the heart rate or the stroke volume or both.

Physiological Variations of Cardiac Output

The cardiac output in an individual depends on age, sex, body size, exercise,
pregnancy, emotional state and environmental temperature.
Age and sex: Cardiac Output decreases with advancing age, probably as a result
of decreased activity. The cardiac output in females is 10-20 per cent lower than
that of males.
Body size: Cardiac Output increases directly with the surface area of the body.
That is the greater the body build, the more the cardiac output.
Exercise: the commonest cause of increase in cardiac output is exercise. This is as
a result of increase in heart rate and force of contraction.
Pregnancy: during pregnancy especially towards the last phase, cardiac output
increases by about 40%. This is as a result of the increase in blood volume and
increase in metabolism associated with peripheral vasodilation.
Emotional conditions: such as anxiety, apprehension and excitement increase
cardiac output. This is as a result of catecholamines released during these
conditions that increase heart rate and force of contraction.

Pathological Variations
Cardiac output increases in the following conditions;
Fever
Anemia
Hyperthyroidism
Cardiac output decreases in the following conditions
Hypothyroidism
Atrial fibrillation
Congestive cardiac failure
Shock
Hemorrhage

Regulation of Cardiac Output

Regulation of cardiac output is either by an increase in either one or both of the
factors affecting it which are heart rate and stroke volume.
Heart rate can be defined as the number of beats per minute. This heart rate is
set by the SA node known as the pacemaker of the heart. Certain factors however
can affect the rate at which the heart beats inadvertently affecting the rate of
cardiac output. These factors are as follows;
Increase in production of sympathetic nervous system neurotransmitters: the
main effect of the sympathetic stimulation is to increase the heart rate and this is
called the Chronotropic effect. The production of epinephrine and norepinephrine
can have a chronotropic effect on the heart i.e. an increase in heart rate.
Hormones: production of hormones such as thyroid hormones (T 3 and T4) can
influence heart rate positively. Excessive production of thyroid hormones by the
thyroid gland can lead to a condition known as hyperthyroidism which causes
increased heart rate.
Body temperature: an increase in body temperature leads to an increase in basal
metabolic rate which also amounts to an increase in heart rate.
Chemoreceptors: stimulation of peripheral chemoreceptors due to situations that
cause decreased partial pressure of oxygen, increased partial pressure of carbon
dioxide or decrease in pH will stimulate the heart rate.

Stroke volume can be defined as the volume of blood pumped in one heartbeat.
The stroke volume is gotten when the total volume of blood left in the heart after
the ventricles have contracted (End Systolic Volume, usually about 50mls per
beat) is subtracted from the total volume of blood contained in the heart before
contractile activities begin (End Diastolic Volume, usually about 120mls per beat).
i.e. Stroke Volume= End Diastolic Volume – End Systolic Volume
Factors that affect stroke volume are as follows;

PRELOAD: is the degree of stretch of the cardiac muscle when it is filled with
blood. The myocardium has a length-tension relationship similar to that of
skeletal muscle i.e. the force of contraction is proportional to the initial length of
the muscle fibers. Hence the stronger the force of contraction, the higher the
diastolic stretch of muscle fibers.

1. Increase in End Diastolic Volume: this achieved by an increase in venous

return. Increased venous returns can be stimulated by the following
factors;
i. Increased Musculo-venous pump activity: rhythmical contractions of limb
muscles as occurs during walking, running or swimming promotes venous
return by the muscle pump mechanism.
ii. Respiratory Pump: during inspiration, the intrathoracic pressure is reduced
while the abdominal pressure is increased. This creates a pressure gradient
between the infra and supra diaphragmatic parts of the inferior vena cava
pulling the blood towards the right atrium and increasing venous return.
iii. Veno motor tone (Venoconstriction): because the sympathetic nervous
system controls the veins, through the release of nor-epinephrine, smooth
muscle contractility can be increased leading to a reduction in storage
capacity of the veins and as a result bring an increase in venous return.
 2. Atrial contribution to ventricular filling: the heart requires enough time to
fill with blood. A higher filling time would require a decrease in heart rate
as an increased heart rate would not afford the heart enough time to fill
and as a result less preload.

CONTRACTILITY: myocardial contractility represents the innate ability of the heart

muscles to contract. Factors that increase the contractility are said to be inotropic
agents. Contractility of the myocardium is dependent on a number of inotropic
factors namely;
i. Sympathetic impulses: the release of neuro transmitters such
epinephrine and nor-epinephrine increase contractility by acting on
beta1 adrenergic receptors to increase the calcium content in the cell
that leads to increase in cross bridges and as a result increased
contractility.
ii. Hormones: thyroid hormones T3 and T4 help to increase contractility
when they act on myocardial cells to increase the expression of beta1
adrenergic receptors that produce the neurotransmitters epinephrine
and nor-epinephrine that increase contractility. Another hormone with
the ability to provide this same effect is glucagon.
iii. Drugs: certain drugs have the ability to increase contractility of
myocardial cells. Examples of such drugs include digitalis, dopamine,
dobutamine, atropine etc
iv. Ions: certain ions have certain effects on the contractility of the heart.
An increase in Ca++ (Hypercalcemia) will obviously increase contractility
while a decrease will inhibit contractility. However high amounts of ions
such as K+ and Na+ inhibit contractility and vice versa. Also, during
acidosis, i.e. high amounts of protons, contractile state of myocardium
is greatly decreased.

AFTERLOAD: this is basically defined as the amount of resistance that must be

overcome in order for the ventricles to eject blood into the aorta or the
pulmonary trunk. Increase in afterload leads to decrease in stroke volume as
opposed to preload and contractility. Factors which increase afterload are as
follows;
i. Aortic valve dysfunction i.e. sclerosis or stenosis or its simply hard to open
 ii. Occlusion of the blood vessels
iii. High systemic vascular resistance

CARDIOVASCULAR RESPONSES TO EXERCISE

Strenuous exercise imposes the most stressful situation to be faced by the
cardiovascular system. Cardiac output may increase from 5L/min to about
35L/min especially in trained athletes.

Anticipatory Response
These are responses that take place even before the exercise has begun. These
originate from the higher centers and are mediated via the vasomotor centers.
The sympathetic nervous system responds to the anticipation of exercise by
releasing adrenaline into the system that provides a fight-or-flight response. This
causes the following effects;
a. Increased heart rate and force of contraction
b. Vaso constriction of blood vessels in cutaneous, renal and splanchnic
circulations
c. Stimulation of sympathetic cholinergic vasodilator nerves in skeletal muscle
causing increased blood flow to the muscles
d. Venoconstriction in most part of the body
e. Increased release of adrenaline from the adrenal medulla to further
reinforce all of the above sympathetic effects.

GENERAL CIRCULATORY CHANGES

Cardiac output
 Increases from about 5L/min to about 35L/min due to increased heart rate
as well as increased stroke volume.
 Sustenance of these effects is due to sympathetic stimulation and
hormones such as adrenaline.

Venous return
 Increases as cardiac output increases to supply the increased blood
necessary for the heart to increase its output.
Arterial blood pressure
 Changes in ABP depends upon sage, type and severity of exercise and
degree of training.
 Systolic pressure may increase from 120 to 180mmHg while diastolic
pressure may increase from 80 to 110mmHg