THE CARDIOVASCULAR

SYSTEM

Gulnura Sadykova
PhD
Gulnura.sadykova76@
gmail.com
▶ Identify the major components of the cardiovascular system, and
describe their functions.
▶ Identify the major structures of the heart, and describe the path of
blood flow through the heart and blood vessels.
▶ Explain the events in the cardiac cycle: changes in ventricular, aortic,
and atrial pressure; changes in ventricular volume; and heart sounds.
▶ Trace the path of action potentials through the conduction system of the
heart, and relate the heart’s electrical activity to its pumping action.
▶ Describe how the phases of the electrocardiogram relate to the events of
the cardiac cycle.
▶ Explain the extrinsic and intrinsic regulation of the cardiac.

GOALS:
 THE CARDIOVASCULAR SYSTEM

∙A closed system of the heart and blood vessels

∙ The heart pumps blood
∙ Blood vessels allow blood to circulate to all
parts of the body
∙ The function of the cardiovascular system is to
deliver oxygen and nutrients and to remove
carbon dioxide and other waste products
1. Functional anatomy of the heart
2. Cardiac muscle properties
3. Intrinsic conduction system of the heart.
Pacemaker potential

LESSON 1. THE HEART. ELECTRICAL

ACTIVITY OF THE HEART
 BLOOD
VESSELS—cond
uits through
which the blood
THE HEART— flows
BLOOD—a fluid
a muscular pump that circulates
that drives the around the body,
flow of blood carrying materials
through blood to and from the
vessels cells.

THE
CARDIOVASCULAR
SYSTEM
 THE HEART

▶ The heart is a cone-shaped, hollow muscular organ.

▶ Function of the heart is to generate the force
that pumps blood through blood vessels to various
organs.
▶ It performs sensory and endocrine (APH) functions
that help regulate cardiovascular variables such as
blood volume and pressure (Na+).
 Heart pumps blood into
two circuits in sequence
• Pulmonary circuit
To and from the lungs
• Systemic circuit
To and from the rest of the
body

HEART’S PLACE IN THE CIRCULATION

Thickness of right and left
ventricles
▶ is located centrally in the thoracic cavity
▶ is about the size of a closed fist
▶ 300–350 grams in males and 250–300
grams in females.

THE HEART
THE LOCATION OF THE HEART IN THE THORACIC CAVITY
THE HEART
 A thin, inner layer, the endocardium, an epithelial
tissue that lines chambers end valves of the heart

The heart wall has

three distinct layers:

A middle, ticker, muscular layer, the A thin, outer layer, the epicardium,
myocardium, which is composed of includes pericardium – the membrane
cardiac muscle fibers. that covers the heart.

THE HEART WALLS ARE COMPOSED PRIMARILY OF

CARDIAC MUSCLE FIBERS
▶ Have striations (sarcomere
organization), typical myofibrils
that contain actin and myosin
filaments
▶ Have single nucleus
▶ Short, branched and
interconnected
▶ They contract by the sliding
filament mechanism.
▶ Autorhythmicity

CARDIAC MUSCLE CHARACTERISTICS

▶ Cardiac muscle fibers are made up of many individual cells connected in series and in parallel with
one another by intercalated discs
▶ The intercalated discs form permeable “communicating” junctions (gap junctions) that allow rapid
diffusion of ions.
▶ Action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.
▶ Cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so
interconnected that when one of these cells becomes excited, the action potential spreads to all of
them
▶ The heart actually is composed of two syncytiums: the atrial syncytium, which constitutes the walls
of the two atria, and the ventricular syncytium
▶ This division of the muscle of the heart into two functional syncytiums allows the atria to contract a
short time ahead of ventricular contraction, which is important for effectiveness of heart pumping.

DIFFERENCES BETWEEN CARDIAC AND

SKELETAL MUSCLE CELLS
FUNCTIONAL SYNCYTIUM
 Myocardial - contract and share characteristics
contractile cells within skeletal muscles.
(atrial and - pump blood through the body
ventricular muscle
fibers)
Major types of
cardiac
muscle fibers: - contract only feebly because they
contain few contractile fibrils;
- generation or conduction of the action
specialized potentials through the heart,
excitatory or
- providing an intrinsic conduction
nodal cells
system
- share characteristics within smooth
muscles
▶ Initiates and spreads electrical impulses in heart
▶ Two types of autorhythmic cells
• Nodal or Pacemaker cells
Reach threshold first
Set heart rate
▶ Conducting cells
Distributes stimuli to myocardium
▶ Functions: generating rhythmical electrical impulses to cause rhythmical
contraction of cardiac muscle (SAN) and
▶ conducting these impulses rapidly through the heart (AVN, AVB, PCs).

THE INTRINSIC CONDUCTION

SYSTEM OF THE HEART
 INTRINSIC CONDUCTION SYSTEM OF THE HEART

Figure 11.5
▶ The sinus node (also called sinoatrial node) is a small, flattened, is
located in the superior posterolateral wall of the right atrium immediately
below and slightly lateral to the opening of the superior vena cava.
▶ Have almost no contractile muscle filaments, but composed of excitatory
autorhythmic fibers.
▶ Connect directly with the atrial muscle fibers by internodal and
Bachmann pathways.
▶ Have the capability of self-excitation, a process that can cause automatic
rhythmical discharge and contraction.
▶ Controls the rate of beat of the entire heart.
▶ The velocity of conduction in atrial is high (0.3-1m/sec).

SINUS (SINOATRIAL) NODE

▶ The “resting” potential is
much less negative—only -55
millivolts in the nodal fiber
instead of the -90 millivolts in
the ventricular muscle fiber
and unstable
▶ The fast Na+ channels become
closed
▶ Only the slow Na/Ca channels
can open

ACTION POTENTIAL IN
THE SINUS NODE
 Internodal
Pathways

Sinus
(Sinoatrial) AV bundles Purkinje fibers
Atrioventricular node
Node • Proceeds On the base of
• the A-V node and its the hearthigh
controls the rate adjacent conductive through the
of beat of the interventricula velocity of
fibers delay conduction
entire heart transmission into the r septum
ventricles • Divided into Allows
The velocity of two branches ventricular
conduction • This delay allows time
• One-way contraction
0.3-1m/sec for the atria to empty
their blood into the conduction
ventricles before • The velocity of
ventricular contraction conduction
begins 0,03m/sec
• The velocity of
conduction 0,16m/sec
• Small diameter & less
number of gap junctions
Transmission of the cardiac
impulse through the heart,
showing the time of
appearance (in fractions of
a second) in different parts
of the heart.
▶ The velocity of
conduction in atrial is
high (0.3-1m/sec)
▶ The AVN - 0,13m/sec
▶ The BoH - 0,03m/sec
▶ The PFs - 1.5 -4m/sec
▶ RMP in the atrial -90mV
in the ventricles -80mV
▶ Cardiac action potential has
long plateau phase
▶ Cardiac muscle has long, slow
twitch
▶ Cardiac muscle has long
refractory period (0.25-0/3
sec)
▶ Can’t be tetanized

ACTION POTENTIAL OF CONTRACTILE

CARDIAC MUSCLE FIBERS
Correlation of the myocardial
action potential with
myocardial contraction.
The time course for the myocardial
action potential is compared with
the duration of contraction. Notice
that the long action potential
results in a correspondingly long
absolute refractory period and
relative refractory period. These
refractory periods last almost as
long as the contraction, so that the
myocardial cells cannot be
stimulated a second time until they
have completed their contraction
from the first stimulus.
▶ A long refractory period prevents tetanus of cardiac muscle.
▶ Like other excitable tissues, cardiac muscle has a refractory period. During the refractory
period, a second action potential cannot be triggered until an excitable membrane has
recovered from the preceding action potential. In skeletal muscle, the refractory period is
very short compared with the duration of the resulting contraction, so the fiber can be
restimulated before the first contraction is complete to produce summation of contractions.
Rapidly repetitive stimulation that does not let the muscle fiber relax between stimulations
results in a sustained, maximal contraction known as tetanus.
▶ In contrast, cardiac muscle has a long refractory period that lasts about 250 msec because
of the prolonged plateau phase of the action potential. This is almost as long as the period
of contraction initiated by the action potential; a cardiac muscle fiber contraction averages
about 300 msec. Consequently, cardiac muscle cannot be restimulated until contraction is
almost over, precluding summation of contractions and tetanus of cardiac muscle. This is a
valuable protective mechanism, because pumping of blood requires alternate periods of
contraction (emptying) and relaxation (filling). A prolonged tetanic contraction would
prove fatal: The heart chambers could not be filled and emptied again.
 The skeletal muscles The cardiac muscle
The action potential is caused by opening of two types of channels:
(1) the fast Na+ channels as those in skeletal muscle
is caused almost entirely by sudden (2) the slow Ca++ channels, which are
opening of large numbers of fast Na+ also called calcium-sodium channels
channels that allow tremendous
numbers of sodium ions to enter the
Ca++ channels are slower to open and, even more important, remain
skeletal muscle fiber from open for several tenths of a second. During this time, a large quantity
the extracellular fluid. of both calcium and sodium ions flows through these channels, and
this maintains a prolonged period of depolarization, causing the
plateau
Na+ channels remain open for only a
few thousandths of a second and the
Immediately after the onset of the action potential, the
action potential is over within another
permeability of the cardiac muscle membrane for K+ ions
thousandth of a second or so
decreases about fivefold

DIFFERENCES BETWEEN CARDIAC AND

SKELETAL MUSCLE CELLS
▶ Excitability
▶ Autorythmicity - is the ability of the heart to beat regularly without
external stimulation, measured in imp/min

▶ Conductivity - is ability of CMs to conduct impulses from one to

others

▶ Contractility - is the ability of CMs to change length, shape and

tension of contraction

CARDIAC MUSCLE PROPERTIES

▶ Systole & diastole
▶ The Cardiac cycle, it’s phases
▶ Stroke volume. ESV&EDV
▶ Cardiac output and its control
▶ Heart sounds. Murmurs
▶ ECG, waves. ECG and cardiac cycle
▶ Cardiac abnormalities

LESSON 2. THE CARDIAC CYCLE.

CARDIAC OUTPUT.
▶ Explain the events in the cardiac cycle: changes in
ventricular, aortic, and atrial pressure; changes in
ventricular volume; and heart sounds.
▶ Trace the path of action potentials through the
conduction system of the heart, and relate the
heart’s electrical activity to its pumping action.
▶ Describe how the phases of the electrocardiogram
relate to the events of the cardiac cycle.

GOALS:
 THE HEARTBEAT. SYSTOLE &DIASTOLE

▶ When the heart beats, the two atria contract together,

then the two ventricles contract; then the whole heart
relaxes.
▶ Systole is the contraction of heart chambers;
diastole is the relaxation of the heart chambers.
▶ Each heartbeat is called a cardiac cycle.
Duration of cardiac cycle depend on heart beat and calculated by formula:

Cardiac cycle = 60sec/HR=60/75=0.8 sec

0.1sec 0.7sec

0.33sec 0.47sec

CARDIAC CYCLE TIMING

 Cardiac cycle
phases
1. Atrial systole

• AV valve open,
• SL valve close
• BP in the right atria -4-5mmHg
left atria 6-8mmHg
ventircles 0-3mmHg
aorta – 80mmHg
pulmonary trunk – 15mmHg
• Duration – 0.1 sec
End diastolic volume – amount of blood filling
the ventricles during diastole (80% during
ventricular filling phase +20% during atrial
contraction phase)
EDV=110-120 ml

END DIASTOLIC VOLUME

 Isovolumetric
contraction

• AV valve close,
• SL valve close,
• BP in the right and atrium -
0 mmHg
left venticle –
60-80mmHg
right ventricle- 15mmHg
aorta – 60mmHg
pulmonary trunk –
15mmHg
• Duration -
 Ejection

• AV valve close,
• SL valve open,
• BP in the right and atrium -
0 mmHg
left venticle –
81-120 mmHg
right ventricle- 15-30
mmHg
Duration – 0,25msec
▶ Contraction of the ventricles in systole ejects about two thirds
of the blood, this amount of blood pumped out of each
ventricle with each contraction is called THE STROKE
VOLUME (SV).
SV =70ml/beat.
▶ The ventricle does not empty completely during ejection. The
remaining amount of blood in each ventricles at the end of
ventricular systole is called THE END SYSTOLIC
VOLUME (ESV), which averages about 50 ml.
ESV = 40-50ml
EDV-ESV=SV = 120-50=70ml/beat
 Isovolumetric
relaxation

• AV valve close,
• SL valve close,
• BP in the right-1-2 mmHg
and left atria 2-3 mmHg
left venticle and right
ventricles falls to 0 mmHg
• Duration – 0,12msec
 Filling

• AV valve open,
• SL valve close,
• BP in the
right-1-2
mmHg and left
atria 2-3
mmHg
left venticle
and right
ventricles -
2-3 mmHg
• Duration –
0,25msec
The Wigger's
diagram
shows the
relationship between
the ECG, the
pressure, and volume
changes in the left
ventricle and aorta.
▶ Cardiac output—Amount of blood pumped by
each side of the heart in one minute
Cardiac output = heart rate × stroke volume
= 70 beats/min × 70 ml/beat
= 4900 ml/min ≅ 5 L/min

CARDIAC OUTPUT
▶ S1. When the ventricles contract, one first hears a sound caused by closure of the A-V valves. The
vibration is low in pitch and relatively long-lasting and is known as the first (lub) heart sound.
▶ S2. When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because
these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the
second (dub) heart sound.
▶ S3. Occasionally a weak, rumbling third heart sound is heard at the beginning of the middle third of
diastole. Explanation of this sound is oscillation of blood back and forth between the walls of the
ventricles initiated by flowing blood from the atria. This sound is usually so low that the ear cannot hear
it, yet it can often be recorded in the phonocardiogram.
▶ S4. An atrial heart sound can sometimes be recorded in the phonocardiogram, but it can almost never be
heard with a stethoscope because of its weakness and very low frequency—usually 20 cycles/sec or less.
This sound occurs when the atria contract, and presumably, it is caused by the inrush of blood into the
ventricles.
• Indicate start/stop of systole
• Heard with stethoscope

HEART SOUNDS
▶ Listening to the sounds of the
body, usually with the aid
of a stethoscope, is called
auscultation.
▶ Figure shows the areas of the
chest wall from which the
different heart valvular sounds
can best be distinguished.
▶ If a microphone specially
designed to detect low-frequency
sound is placed on the chest, the
heart sounds can be amplified
and recorded by a high-speed
recording apparatus. The
recording is called a
phonocardiogram, and the heart
sounds appear as waves
▶ Heart murmurs are sounds that usually result from blood flowing
past the valves of the heart.
▶ Most of these murmurs are not pathological and are found in people
with healthy hearts. Many people have small defects that produce
detectable murmurs but do not seriously compromise the pumping
ability of the heart. Larger defects, however, may have dangerous
consequences and thus may require surgical correction.
▶ However, some types of murmurs are caused by the flow of blood past
diseased heart valves that may result from a defect present at birth, or
it may be due to other illnesses, such as heart disease, heart attacks,
heart failure or infection.

HEART MURMURS
▶ Is diagnostic tool used to assess the electrical and muscular function of the heart.
▶ The normal electrocardiogram is composed of a P wave, a QRS complex, and a T wave.
▶ The P wave is caused by electrical potentials generated when the atria depolarize before
atrial contraction begins.
▶ The QRS complex is caused by potentials generated when the ventricles depolarize before
contraction, that is, as the depolarization wave spreads through the ventricles.
▶ The T wave is caused by potentials generated as the ventricles recover from the state of
depolarization. This process normally occurs in ventricular muscle 0.25 to 0.35 second
after depolarization, and the T wave is known as a repolarization wave.

THE ELECTROCARDIOGRAM (ECG)

NORMAL ELECTROCARDIOGRAM
Representative heart conditions detectable
through electrocardiography
Rhythmicity Conductivity Contractility
Sinoatrial block
Tachycardia is fast heart rate, A premature contraction is
In rare instances, the impulse from the
usually defined in an adult sinus node is blocked before it enters the a contraction of the heart
person as faster than 100 atrial muscle. This phenomenon causes
beats/min. sudden cessation of P waves, with
before the time that
resultant standstill of the atria. normal contraction would
have been expected. This
condition is also called
Bradycardia is a slow heart Conditions that can either decrease
extrasystole, premature
rate, usually defined as the rate of impulse conduction in AV
bundle or block the impulse entirely beat, or ectopic beat
fewer than 60 beats/min are called AV block
▶ Intrinsic regulation
▶ Nervous regulation
▶ Humoral regulation

LESSON 3. REGULATION OF THE

CARDIAC ACTIVITY
REGULATION OF THE CARDIAC ACTIVITY

Intrinsic Extrinsic
regulation regulation
Frank-Starling Neural
law regulation
Cardiac
Humoral
output-venous
regulation
return
 INTRINSIC CONTROL OF HEARTBEAT
1. The SA (sinoatrial) node, or pacemaker, initiates the heartbeat and causes the
atria to contract on average every 0.85 seconds.
▶ The SA node controls the beat of the heart, because its rate of rhythmical
discharge is faster than other components of CSH.
▶ Normal rhythmicity of the SAN – 70-80imp/min.
2. The AV (atrioventricular) node conveys the stimulus and initiates contraction of
the ventricles, when not stimulated from outside can genetare impulses, 40-60
imp/min.
3. The signal for the ventricles to contract travels from the AV node through the
atrioventricular bundle to the smaller Purkinje fibers, 15-40 imp/min.
4. They are called abnormal-ectopic pacemakers.
The intrinsic ability of the heart to
adapt to increasing volumes of Within physiological limits the
inflowing blood is called heart pumps all blood, that
Frank-Starling law returns by the veins
Cardiac output=venous return

FRANK-STARLING
LAW

It means that the greater the heart The Frank-Starling law equalizes
muscle stretched during filling cardiac output of the right and left
phase, the greater is the force of ventricles and keeps the same
FRANK-STARLING LAW
contraction & the greater the volume of blood flowing to both
quantity of blood punped into the systemic and pulmonary
aorta curculations
 EXTRINSIC REGULATION OF THE CARDIAC ACTIVITY

Neural regulation
SAN – primary pacemaker
(70-80imp/min) • sympathetic
AVN&Purkinje fibers – • parasympathetic
secondary, abnormal
pacemakers

Humoral • Increase (norepinephrine, Na+, Ca+,

regulation thyroid hormones, high temperature)
• Decrease (acetylcholine, K+, low
by the hormones & ions
temperature)
Neural Cardioaccelera Cardioinhibitory
regulation tory center center
• Activation of • Governing of
• Basic control in sympathetic neurons parasympathetic neurons
medulla
• Are distributed to all • Are distributed mainly to
oblongata
parts of the heart the atria (SAN&AVN),
• Other inputs:
• Higher • Causes opposite little to the ventricles
centers effects: • Causes:
• Blood • increases the over all • Decreases HR
pressure activity of the heart
sensors • The rhythm rate of SAN
• Increase HR, CO & SV
• Oxygen,
carbon dioxide • The strength of heart
sensors contraction
Release Norepinephrin Release Acetylcholine

Increases permeability of the

Increases permeability of the membrane
membrane to K+
to Na+ & Ca+
RMP of SAN becomes more negative,
Accelerating self-excitation of SAN cells
that causes hyperpolarization
Decreasing HR
Increasing HR
Decreases the excitability of the
Short AV delay
SAN
▶ Parasympathetic innervation
• Releases acetylcholine (ACh)
• Lowers heart rate and stroke
volume
▶ Sympathetic innervation
• Releases norepinephrine
(NE)
• Raises heart rate and stroke
volume

AUTONOMIC CONTROL
OF THE HEART
CARDIAC OUTPUT REGULATION

Figure 11.7
1. Overview of the circulation. Functions of the circulation and their meaning for
organism functioning. Circulation as a component of different functional systems.
2. Physiological properties and peculiarities of heart muscle. Contemprary
conception about substratum, mechanism and gradient of heart automacity
(self-excitation rhythmicity).
3. Action potential of typical cardiomyocyte (contracting heart muscle) and atypical
cardiomyocyte (cells of specialized excitatory and conductive system of the heart).
4. Correlation between excitation, contractility and excitability of the heart in
different phases of cardiac cycle. Reaction of heart muscle on additional
stimulation. The extrasystole and it types.
5. Electrocardiogram (ECG). Formation of ECG components. ECG leads.
Characteristics of the normal ECG. Role of ECG interpretation in medicine.

POSSIBLE EXAM QUESTIONS: