Cardiovascular system

Cardiovascular system
This chapter consist of three main topic:
1-the heart .
2-circulatory system
3- ECG
 The heart
Is muscular organ , located in the chest cavity
and cover by a moist fibrous sac, the
pericardium, which allows .the heart to move
freely during each contraction
 Function of the heart

The purpose of the heart is to

function as a pump to produce
pressure, which in turn causes
the blood to flow through the
.blood vessels
Anatomy of the heart
 THE HEART
• Anatomy of the heart:
 Characterization of the conducting
system
This system is characterize by:
1- autorhythmicity : has the ability to generate
action potential spontaneously at regular
interval.
2- it’s a specialized conducting system: which
conduct the pulse very rapidly to ensure
simultaneous contraction of both atria
followed by simultaneous contraction of both
ventricles.
 Conducting system of the heart
S-A node ( pacemaker of
the heart , this node is
located in the superior
lateral wall of the right
atrium near the opening
of the superior vena cava
has the highest intrinsic
rate of impulse
generation (90/ min)( the
rate of A.P generation
determine the H.R)
• and the action potential travels from SA node
rapidly through both atria and then through the A-V
bundle into the ventricles. Because of this special
arrangement of the conducting system from the
atria into the ventricles, there is a delay of more
than 0.1 second during passage of the cardiac
impulse from the atria into the ventricles. This
allows the atria to contract ahead of ventricular
contraction, thereby pumping blood into the
ventricles before the strong ventricular contraction
begins. Thus, the atria act as primer pumps for the
ventricles, and the ventricles in turn provide the
major source of power for moving blood through
the body’s vascular system
• A-V node has the second rate of impulse
generation ( 60/ min).
 Sequence of excitation
AP (wave of depolarization) SA RA and LA
(intranodular and cardiac muscle cell (1 -0.3 m/sec)
total 0.4 to reach AVN.

AVN (0.1-0.2m/sec) purkinji system (1.5-4 m/sec )

subendocardium epicardium (0.3-0.5m/sec).

0.3m/ sec AVN to reach terminal peripheral end and

another 0.3m/sec from the endocardium to the
epicedium (0.6m/sec).
 SHORT NOTE
1-Functional synncytium:
A- Intercalated disc ,the dark areas crossing the cardiac
muscle fibers are actually cell membranes that separate
individual cardiac muscle cells from one another.
cardiac muscle fibers are made up of many individual cells
connected in series and in parallel with one another two
cardiac muscle cells by gap junctions has a very low
electrical resistance, this specific character allows the AP to
spread easily from one cell to another causing the atria/
and or ventricles to function as a single unit.
• B-the rapid conduction along the purkinjie
fibers and their highly diffused distribution
cause depolarization of all right and left
ventricular cell more or less simultaneously
and ensure single force of ventricular
contraction.
2-AV node delayed:
The propagation of AP through the AV node is
delayed for about 0. 1 sec , to allow the atria to
contract and empty their blood content to the
ventricles before ventricular contraction (atria
contraction precedes ventricular contraction).
 Action Potentials in Cardiac Muscle

The action potential recorded in a ventricular muscle fiber averages

about 105 millivolts, which means that the intracellular potential
rises from a very negative value, about -85 millivolts, between beats
to a slightly positive value, about +20 millivolts, during each beat.
After the initial spike, the membrane remains depolarized for about
0.2 second, exhibiting a plateau, followed at the end of the plateau
by abrupt repolarization. The presence of this plateau in the action
potential causes ventricular contraction to last as much as 15 times
as long in cardiac muscle as in skeletal muscle
What Causes the Long Action Potential
and the Plateau?
• At least two major differences between the
membrane properties of cardiac and skeletal
muscle account for the prolonged action
potential and the plateau in cardiac muscle.
• First, the action potential of skeletal muscle is caused
almost entirely by sudden opening of large numbers of
so-called fast sodium channels that allow tremendous
numbers of sodium ions to enter the skeletal muscle
fiber from the extracellular fluid.
• These channels are called “fast” channels because they
remain open for only a few thousandths of a second
and then abruptly close. At the end of this closure,
repolarization occurs, and the action potential is over
within another thousandth of a second or so
• In cardiac muscle, the action potential is caused by
opening of two types of channels: (1) the same fast
sodium channels as those in skeletal muscle and (2)
another entirely different population of slow calcium
channels, which are also called calcium-sodium
channels. This second population of channels differs
from the fast sodium channels in that they are slower
to open and, even more important, remain open for
several tenths of a second. During this time, a large
quantity of both calcium and sodium ions flows
through these channels to the interior of the cardiac
muscle fiber, and this maintains a prolonged period of
depolarization, causing the plateau in the action
potential. Further, the calcium ions that enter during
this plateau phase activate the muscle contractile
process, while the calcium ions that cause skeletal
muscle contraction are derived from the intracellular
sarcoplasmic reticulum
• The second major functional difference : Immediately
after the onset of the action potential, the permeability
of the cardiac muscle membrane for potassium ions
decreases about fivefold, an effect that does not occur
in skeletal muscle. This decreased potassium
permeability may result from the excess calcium influx
through the calcium channels just noted. Regardless of
the cause, the decreased potassium permeability
greatly decreases the outflux of positively charged
potassium ions during the action potential plateau and
thereby prevents early return of the action potential
voltage to its resting level. When the slow calcium-
sodium channels do close at the end of 0.2 to 0.3
second and the influx of calcium and sodium ions
ceases, the membrane permeability for potassium ions
also increases rapidly; this rapid loss of potassium from
the fiber immediately returns the membrane potential
to its resting level, thus ending the action potential
 Cardiac cycle
The cardiac events that occur from the beginning of
one heartbeat to the beginning of the next are
called the cardiac cycle.

The cardiac cycle: divided into two major phases :

1- ventricular contraction (systole).

2- ventricular relaxation (diastole).

Each cardiac cycle represents one beat.

The event of cardiac cycle depend on:
1- changes in the blood volume.
2- changes in the pressure.
3- closure and opening of the heart valve.
The events that occurs in the RV and LV is the same,
except that the pressure in the RV is smaller than the
LV.
 EVENTS IN THE VENTRICALS DURING SYSTOLE AND
DIASTOLE
LT VENTRICAL SYSTOLE DIASTOLE
EVENT CONTRACTION RELAXATION
PRESSURE
HEART SOUND FIRST HEART SOUND SECEND HEART SOUND

VALVE CLOSURE OF THE OPEN OF THE MITRAL VALVE

MITRAL VALVE
LVP >LAP LVP < LAP
OPEN OF THE AORTIC VALVE CLOSURE OF THE AORTIC
VALVE
LVP>LAP LVP < LAP
VOLUME ESV: THE VOUME OF BLOOD EDV: VOLUME OF BLOOD IN
REAMING IN THE THE VENTRICALS JUST
VENTRICALS AFTER BEFORE SYSTOLE
EJECTION
• During systole, the aortic pressure
increases reaching a maximum value of
120 mmHg known a systolic pressure,
then during the diastolic phase , as the
blood flows out of the aorta towards
periphery , the aortic pressure decreases
reaching a minimum value of 80 mmHg
at the end of diastole, known as diastolic
pressure.
Anatomy of the heart
• Venous blood enters the right
atrium (RA) of the heart
through the superior vena
cava (SVC) and inferior vena
cava (IVC). The right atrium
has a relatively thin muscular
wall and easily expand, Blood
passes from the RA to the RV
through the tricuspid valve.
The free wall of the right
ventricle is not as thick as the
left ventricle. As the RV
contracts and generates
pressure.
blood leaves the RV, flows
across an open
semilunar pulmonary valve,
and enters the pulmonary
artery that distributes the
output of the right ventricle
to the lungs where exchange
of oxygen and carbon dioxide
occur. The pulmonary valve,
like all healthy heart valves,
permits blood to flow in only
one direction. Blood returns
to the heart from the lungs
through four pulmonary
veins that enter the left
atrium (LA). This chamber is
similar to the RA in that it is
very distensible
• Blood flows from the LA,
across the mitral valve,
and into the left
ventricle (LV). The LV wall
is very thick so that it can
generate high pressures
when it contracts
(normally ~120 mmHg at
rest ). When the LV
contracts, blood is
expelled through the
semilunar aortic valve and
into the aorta, which then
distributes blood to the
arterial system.
The tricuspid and mitral valves (also called atrio
ventricular, or AV valves) have fibrous strands
(chordae tendineae) on their leaflets that
attach to papillary muscles located on the
respective ventricular walls. The papillary
muscles contract during ventricular
contraction and generate tension on the valve
leaflets via the chordae tendineae to prevent
the AV valves from bulging back into the atria
and becoming incompetent.
Cardiac cycle
 Diastole and Systole
Diastole:
represents the period of time when the ventricles are
relaxed (not contracting).Throughout most of this period,
blood is passively flowing from the left atrium (LA) and
right atrium (RA) into the left ventricle (LV) and right
ventricle (RV), respectively.
The blood flows through atrio-ventricular valves (mitral and
tricuspid) that separate the atria from the ventricles.
The RA receives venous blood from the body through the
superior vena cava (SVC) and inferior vena cava (IVC). The
LA receives oxygenated blood from lungs through four
pulmonary veins that enter the LA. At the end of diastole,
both atria contract, which eject an additional amount of
blood into the ventricles.
Systole:
represents the time during which the left and right
ventricles contract and eject blood into the aorta and
pulmonary artery, respectively. During systole, the aortic
and pulmonary valves open to permit ejection into the
aorta and pulmonary artery. The atrio-ventricular valves
are closed during systole, therefore no blood is entering
the ventricles; however, blood continues to enter the
atria though the vena cavae and pulmonary veins.
 EVENTS IN THE VENTRICALS DURING SYSTOLE AND
DIASTOLE
LT VENTRICAL SYSTOLE DIASTOLE
EVENT CONTRACTION RELAXATION
PRESSURE
HEART SOUND FIRST HEART SOUND SECEND HEART SOUND

VALVE CLOSURE OF THE OPEN OF THE MITRAL VALVE

MITRAL VALVE
LVP >LAP LVP < LAP
OPEN OF THE AORTIC VALVE CLOSURE OF THE AORTIC
VALVE
LVP>LAP LVP < LAP
VOLUME ESV: THE VOUME OF BLOOD EDV: VOLUME OF BLOOD IN
REAMING IN THE THE VENTRICALS JUST
VENTRICALS AFTER BEFORE SYSTOLE
EJECTION
 MECHANICAL EVENTS OF THE CARDIAC CYCLE

1-Ventricular systole subdivided into 4 phases:

atria systole. isovolumic contraction phase, rapid
ejection phase, reduced ejection phase.

2-Ventricular diastole subdivided into 3 phases:

Isovolumic relaxation phase, rapid filling phase,
slow filling phase (diastasis ),
 Phases of cardiac cycle
Atrial Contraction (Phase 1(

As the atria contract, the

pressure within the atria
chambers increases, which
forces more blood flow across
the open atrio-ventricular (AV)
valves, leading to a rapid flow
of blood into the ventricles. A-
V Valves Open; Semilunar
Valves Closed
• Pressure Changes in the Atria—The a, c, and v Waves. In
the atrial pressure curve, three minor pressure elevations,
called the a,c, and v atrial pressure waves, are noted. 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 Contraction (Phase2)
Immediately after ventricular contraction
begins, the ventricular pressure rises
abruptly, causing the A-V valves to close.
Then an additional 0.02 to 0.03 second is
required for the ventricle to build up
sufficient pressure to push the semilunar
(aortic and pulmonary) valves open against
the pressures in the aorta and pulmonary
artery. Therefore, during this period,
contraction is occurring in the ventricles, but
there is no emptying. This is called the
period of iso volumic or isometric
contraction, meaning that tension is
increasing in the muscle but little or no
shortening of the muscle fibers is occurring.
 Period of ejection
• Period of Ejection. When the left ventricular
pressure rises slightly above 80 mm Hg (and the
right ventricular pressure slightly above 8 mm
Hg), the ventricular pressures push the semilunar
valves open. Immediately, blood begins to pour
out of the ventricles, with about 70 per cent of
the blood emptying occurring during the first
third of the period of ejection and the remaining
30 per cent emptying during the next two thirds.
Therefore, the first third is called the period of
rapid ejection, and the last two thirds, the period
of slow ejection
 3-Rapid ejection phase
Rapid Ejection (Phase 3)
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 intra-ventricular
pressures exceed the pressures
within the aorta and pulmonary
artery, which causes the aortic
and pulmonary valves to open
while AV remains closed.
 Reduced Ejection (Phase 4)
Aortic and Pulmonary Valves Open; AV
Valves Remain Closed the rate of
blood flow from the aorta to the
peripheral arteries exceeds the rate of
blood flow form the heart to the
aorta,
Aortic pressure decreases, produce 2nd
heart sound.
Closure of the aortic valve marks the
end of ventricular systole. And the
onset of ventricular diastole.
Dicrotic notch :is an incisura on the
descending limb of aortic pressure
curve due to closure of aortic valve
 Isovolumetric Relaxation (Phase 5)
At the end of systole, ventricular relaxation begins
suddenly, allowing both the right and left intra
ventricular pressures to decrease rapidly. The
elevated pressures in the dis tended large arteries
that have just been filled with blood from the
contracted ventricles immediately push blood back
toward the ventricles, which snaps the aortic and
pulmonary valves closed. For another 0.03 to 0.06
second, the ventricular muscle continues to relax,
even though the ventricular volume does not
change, giving rise to the period of isovolumic or iso
metric relaxation. During this period, the intraven
tricular pressures decrease rapidly back to their low
diastolic levels. Then the A-V valves open to begin a
new cycle of ventricular pumping.
 Rapid Filling (Phase 6)

The major part of

ventricular filling occur
occurs immediately upon
opening of AV valve, when
blood suddenly flow into
the relaxing ventricle.
In this stage the arterial
pressure is higher than the
ventricular pressure,
resulting in opening of the
av valve
• The period of rapid filling lasts for about the
first thirt
• During the middle third of diastole, only a
small amount of blood normally flows into the
ventricles; this is blood that continues to
empty into the atria from the veins and passes
through the atria directly into the ventricles.
• During the last third of diastole, the atria
contract and give an additional thrust to the
inflow of blood into the ventricles; this
accounts for about 20 per cent of the filling of
the ventricles during each heart cycle.
 Reduced Filling (Phase 7)
The rapid filling phase is
followed by a phase of slow
filling called Diastasis.
The blood that is coming from
the systemic circulation falls
into the Rt ventricle coming
from the Rt atrium, whereas
the blood coming from the
lungs flows into the Lt atrium
then to the Lt ventricle.
 End-Diastolic Volume, End-Systolic
Volume, and Stroke Volume Output
• . During
diastole, normal filling of the ventricles increases the volume
of each ventricle to about 110 to 120 milliliters. This volume is called
the end-diastolic volume. Then, as the ventricles empty during systole,
the volume decreases about 70 milliliters, which is called the stroke
volume output.
• The remaining volume in each ventricle, about 40 to 50 milliliters, is
called the end-systolic volume. The fraction of the end-diastolic
volume that is ejected is called the ejection fraction— usually equal to
about 60 per cent. When the heart contracts strongly, the end-systolic
volume can be decreased to as little as 10 to 20 milliliters. Conversely,
when large amounts of blood flow into the ventricles during diastole,
the ventricular end diastolic volumes can become as great as 150 to
180 milliliters in the healthy heart. By both increasing the end-diastolic
volume and decreasing the end-systolic volume, the stroke volume
output can be increased to more than double normal.