Asst Prof Dr Ghaith Ali Jasim Al Zubaidy PhD Pharmacology MSc Physiology amp Pharmacology drghaithaliyahoocom Cardiovascular System Function Functional components of the cardiovascular system ID: 785093
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Slide1
The Heart & Circulation
Asst. Prof. Dr.
Ghaith Ali Jasim Al
Zubaidy
PhD Pharmacology
MSc
Physiology & Pharmacology
dr.ghaithali@yahoo.com
Slide2Cardiovascular System Function
Functional components of the cardiovascular system:
Heart
Blood Vessels
Blood
General functions these provide:
Transportation
Everything transported by the blood
Regulation
Of the cardiovascular system
Intrinsic v extrinsic
Protection
Against blood loss
Production/Synthesis.
Slide3To create the “pump” we have to examine the Functional Anatomy of
:
Cardiac muscle
Chambers
Valves
Intrinsic Conduction System
Slide4Functional Anatomy of the Heart
Cardiac Muscle
Characteristics
Striated
Short branched cells
Uni
-nucleate
Intercalated discs
T-tubules larger and
over z-discs
Slide5Functional Anatomy of the Heart
(Continued)
Chambers
4 chambers
2 Atria
2 Ventricles
2 systems
Pulmonary
Systemic
Slide6Functional Anatomy of the Heart
(Continued)
Valves
Function is to prevent backflow
Atrioventricular
Valves
Prevent backflow to the atria
Prolapse
is prevented by the
chordae
tendinae
Tensioned by the papillary musclesSemilunar ValvesPrevent backflow into ventricles
Slide7Functional Anatomy of the Heart
(Continued)
Intrinsic Conduction System
Consists of “pacemaker” cells and conduction pathways
Coordinate the contraction of the atria and ventricles
Slide8The heart circulates the blood round the body.
The left side of the heart transfers blood from the pulmonary veins to the aorta.
Slide9whilst the right side of the heart transfers blood from the great veins, the superior and inferior venae cavae, to the pulmonary artery.
Slide10Each side of the heart consists of two chambers, an atrium, previously known as the auricle, and a ventricle.
Slide11Valves exist between the atria and the ventricles, and between the ventricles and the aorta and pulmonary artery.
The
left
atrioventricular
valve has
two cusps
and is termed the
mitral
valve.
The
right
atrioventricular valve known as the tricuspid valve has
three
cusps;
so also
have the
aortic
and
pulmonary
valves.
Slide12Slide13These valves
enabl
e
the alternate
contraction
and
relaxation
of the ventricles to
pump blood round
the body.
If a valve becomes
faulty, the efficiency of the heart as a pump is greatly impaired.
Slide14The Structure of the Heart:
The heart lying in the thorax resembles an
inverted cone
.
The
superior
aspect of the heart, where the vessels enter, is called its
base
.
The
extremity
of the ventricles is termed the
apex.
Slide15The two atria and the two ventricles of the heart lie side-by side.
Slide16When the heart is beating the
atria contract simultaneously
, then, after a short pause,
both the ventricles contract
.
There
is then a
longer pause
during which time the whole heart is in a
state of relaxation.
Slide17The inlet and outlet valves of each ventricle lie alongside one another. All the four valves lie in the same plane, in the fibrous septum or ring which separates the atria from the ventricles.
Slide18This
property is developed to the greatest
extent
in a region known as the
sino-atrial
node (S.A. node)
which is
situated
in the wall of the right atrium
near the entrance of the superior vena cava.
Slide19The heart is composed of
cardiac muscle
, and
such muscle has
the inherent
property
of
rhythmicity
, that is, the muscle fibres contract and relax alternately in a rhythmical manner
.
Slide20This property is developed to the greatest
extent
in a region known as the
sino-atrial
node (S.A. node)
which is
situated
in the wall of the right atrium
near the entrance of the superior vena cava.
Slide21The
S.A
-node
originates
each heart beat
...It
is known as the
pacemaker
.
Cardiac muscle cells, known as fibres, are
cylindrical in shape with central nuclei and faint cross-striations.
The fibres
branch to form a network or sheet of muscle
in which it is difficult to see
where one cell ends and another begins.
Slide23It behaves like a syncytium. (If it were a true syncytium, there would be no cell boundaries at all.) This
syncytial
-like arrangement
enables a contraction wave to spread rapidly from cell to cell
until the whole muscle mass is in a state of contraction.
Slide25No nerves are involved in the spread of a contraction wave
through cardiac muscle. This may be
confirmed
by making a series of
interdigitating
cuts
in a piece of atrial muscle.
Such cuts
would
sever any nerves
running in the muscle,
yet
when
one part of the muscle is made to
contract,
the
contraction wave spreads
through the
intact parts
of the muscle to
reach the whole muscle mass.
Slide26Slide27Furthermore,
in the embryo
the heart
beats
before the nerves have developed.
Although the
two atria are separate chambers,
the
muscle fibres are arranged in rings
round both atria.
Slide28The heartbeat, originating
as a contraction wave
at the
S.A. node
,
spreads rapidly through the atrial
muscle causing both atria
to contract simultaneously
.
Slide29The blood in the atria is
forced through
the
atrioventricular valves
into the ventricles.
Rings
of cardiac muscle
around the entry
of the
superior and inferior
venae
cavae
, and the
pulmonary veins
,
close off
the veins
with a sphincter-like action
so that
blood is not regurgitated back
into the
veins
when the
atria contract.
The
spread
of the contraction
wave
through the cardiac muscle
ceases
at the fibrous septum
between
the atria and the ventricles
which contains the four heart valves [plane A-B].
Slide31The
only pathway
through this non-conducting septum is
from
the atrioventricular node
(A.V. node)
down the atrioventricular bundle
(bundle of His)
named after the German physiologist Wilhelm His.
This bundle runs into the ventricles in the septum between the right and left ventricles.
Slide32Slide33The
passage of the contraction
wave down this bundle of modified cardiac muscle is
not visible
from the
surface of the heart
, and there
appears
to be a
slight pause
following the
atrial
contraction
,
The contraction
wave enters
the
ventricles near the apex
and
spreads upwards
towards the base. The
blood
in the ventricles is
forced upwards
towards the base of the heart
and out
through the
aortic and pulmonary valves.
Slide34Slide35Pericardium:
The heart lies in a
conical sac
known as the
pericardium
. This
consists
of an
inner serous
pericardium and
an outer
fibrous
pericardium. The inner serous pericardium is composed of
two smooth layers, the visceral and parietal layers,
one attached
to the
heart
and the
other
to the
fibrous sac
. These two smooth layers
allow
the heart
to beat
in the
mediastinum
of the thorax with
the minimum of friction
.
Slide36The pericardium:
1 -
Sets a limit
to the
maximum size
of the
chambers
of the heart.
2 -
Prevents
excessive stretching
of the
cardiac muscle fibres due to overfilling with blood. The pericardium is
attached
to the
diaphragm
, and when the
heart beats
, it behaves
as if the apex were relatively fixed.
Slide38Slide39Thus
when the ventricles contract
,
instead
of the
apex moving upwards
towards the base,
the base
, and
particularly the
atrioventricular
ring
, descends
towards the apex.
This
has the effect
of
increasing the size
of
the atria at the same time as blood is ejected from the ventricles.
Slide40Cardiac Cycle-The Heart as a Pump:
The sequence of events may, therefore, be summarized as follows:
The heart beat originates in the S.A. node, and shortly afterwards the atria contract.
This is followed by a short pause whilst the contraction wave is moving down the bundle of His.
Then the ventricles contract, the atrioventricular ring moves downwards and blood is ejected into the arteries.
The ventricular muscle relaxes and the atrioventricular ring returns to its initial position.
There is then a long pause, when all chambers are relaxed before the next beat occurs.
Slide41The ventricular contraction phase is termed systole (pronounced
sis'to.lee
). It lasts for 0·3 seconds.
The ventricular relaxation phase is termed diastole (pronounced
dye.ess'to.lee
) and this lasts for 0.5 seconds.
The complete sequence of events, the cardiac cycle, lasts for 0.8 seconds, so that there are:
60~70
cycles/minute. This is the heart rate.
The heart beats continuously for the whole of a person's life and its only period of rest is after each contraction, during diastole which becomes shorter.
Slide42The Heart Sounds
The
valves
in the heart
close passively
whenever there is a tendency for the
blood to flow in the reverse direction
.
Since
blood flows
from a
region of high Pressure
to a region of low pressure, it is the
relative pressures in the atria, ventricles and arteries that will determine the
opening and shutting
of the valves.
Slide43Since the valves are
passive structures
and contain
no contracting muscle
, diseased valves may be
replaced
by mechanical valves (prosthetic valves) which have been
specially designed
with
smooth surfaces to minimize the risk of blood clotting and
red cell haemolysis
.
Slide44With the
onset of ventricular systole
, the
pressure
in the ventricles
starts to rise
. As soon as it
exceeds
that in the corresponding
atrium, the A-V valves will shut. This simultaneous
closure
of the mitral and tricuspid valves
with the onset of systole can be heard by applying the ear to the chest wall of a subject (or by stethoscope). The sound
heard may be likened to the word 'lub
'
spoken very softly. It is termed the
first heart
sound
Slide45The
sound
of the
valvular closure
may be
augmented
by the
impact
of the
heart against the chest wall
and
by the
noise produced by the contraction of the ventricular muscle fibres.
It lasts for 0.15 seconds and the principal
frequencies
of the sound produced are in the range of
25-45 cycles/second
.
Slide46The
impact of the apex
of the heart
against
the
chest wall
with each
systo1e
can be
felt
, and frequently
seen
, in the 5
th left intercostal space. It is termed the apex beat.
The
intercostal spaces
are named
according
to the
rib that lies immediately above
. Thus the
5
th
interspace
lies between
the 5
th
and 6
th
ribs.
Slide48The apex beat lies about 3-3.5 in. from the midline. A line through the apex beat to the midline passes through the middle of the clavicle (mid-clavicular line).
As soon as the
ventricular pressures exceed
those
in the aorta
and the
pulmonary artery
, the
aortic and pulmonary valves will open
.
The
opening
of the valves
does not
produce any
detectable sound
. (A clapping sound is produced when we bring our bands sharply together, but there is no sound when we take them apart again).
During the
short interval
of time,
between the closure
of the
mitral
valve and the
opening of the aortic
valve, the
left ventricle is a closed chamber
.
At
the same time
the
right
ventricle will be
closed off
by the
closure of the tricuspid and pulmonary valves
.
Blood is incompressible and although the contraction
of the ventricular muscle is
increasing the pressure
in the ventricles there is no actual change in volume during this phase. It is known as the isometric contraction phase
.
Slide52As soon as the
aortic and pulmonary valves open
, the
ventricles decrease
in
size
as the blood is ejected into the aorta and pulmonary artery.
At
the end
of
ventricular systole
the
pressure in the ventricles drops
and the
aortic and pulmonary valves close
since the
pressure
in these
vessels
now
exceeds
that in
the ventricles
.
Slide53There is a
short isometric relaxation phase
during which time the
ventricles are once again closed
chambers,
but
as soon as the ventricu1ar
pressure
has
fall
to
below that in the atria
the mitral and tricuspid valves will open.
Slide54The closure of the aortic and pulmonary valves
gives rise to
the second heart sound
. This is a
shorter and sharper
sound and has been likened to the word
'dup'.
It
lasts for 0.1
seconds. The principal
frequency
is of the order of
50 cycles/second.
Slide55Since
systole is shorter than diastole
the
rhythm when listening
to the heart is:
'LUB' 'DUP' 'LUB' 'DUP'
I - II Pause I - II Pause
with a
shorter interval
between the
first and next second heart sound
than
between
the second and next first sound.
Slide56Under
suitable conditions
a
3
rd
heart sound
can be heard. This is
caused
by the
blood rushing
into the ventricles
during diastole
.
The third heart sound is probably
due to vibrations
of the
mitral valve cusps
since it is
no longer
heard in patients with
prosthetic mitral valves.
Slide57The
sound of atrial contraction
is
sometimes audible
and
when present
is
termed the A sound
or
the 4
th
heart
sound.
The
contribution of each valve to the heart sounds
is usually
heard best at
the sites shown in the Figure, known as the
valve areas
.
Slide58It follows that the
1
st
heart sound will usually be
heard loudest at the mitral and tricuspid areas
, whilst the
2
nd
heart sound will be
heard loudest at the pulmonary and aortic areas
.
Slide59Slide60Blood Flow Round the Circulation
* With each
systole 70 ml
. of blood are ejected from each ventricle.
* This quantity is termed the
stroke volume
.
* The aorta and large arteries are
elastic vessels
and they accommodate this blood with a relatively small rise in pressure. During the ensuing
diastole
, there
is no output from the heart, and the pressure in the arteries falls. The blood now in the arteries is pulsatile, and if an artery is cut, the blood shoots out in spurts.
Slide61*
The blood flow
to the tissues
is maintained by the
elastic recoil
of the arterial walls, and by the time the
capillaries
have been
reached
, the flow has
ceased to be pulsatile
; the
steady flow
of blood through these vessels shows no variation
in
systole or diastole
.
Slide62The blood
returns
to the heart along
the veins
, and the venous
flow
is a
steady
one. If a
vein is cut
the blood
oozes out
from the distal end
without any pulsation.
On
approaching
the heart, the flow
again becomes pulsatile
as the ventricles are
unable
to receive the
venous blood during systole
Function of the Atria:
*The blood
returning
to the heart during ventricular
diastole
passes through the atria and enters the ventricles
.
*The blood
returning during systole is
unable to do this
as the
A-V valves are closed. *The atria act as a storage reservoir for this blood until the end of systole when the A-V valves open. With the opening of these valves the
ventricles fill rapidly with the waiting blood.
Slide64*
Further filling
occurs as
blood returns during diastole
.
One-tenth
of a second
before
the onset of
systole
, when the
ventricles
are already
70% full of blood, the
atria contract and complete the filling of the ventricles
by
adding
the remaining
30%.
*Atrial contraction is
not essential
for life, but the
heart
is a much more
efficient pump
when the atria are contracting.
*The
flow
of blood through the
lungs and tissues
is
continued
but the flow is
intermittent through the heart
.
Slide65Pressure Changes In The Heart:
Although the
pressures
could be
expressed
in dyne/cm.
2
or lb. per in.
2
, it is usual to express blood pressure
in terms of
the height of a corresponding column
of mercury measured in millimeters. The units are mm. Hg. These pressures are measured with
reference to the atmospheric pressure.
Slide66The
pressure
in the
intra-thoracic part
of the circulation
may be less than
the
atmospheric
pressure. This is due to the
elastic recoil
of the lungs.
The pressure in the atria,
for example
, may be
755 mm. Hg
(absolute) whilst the
outside
barometric pressure is
760 mm. Hg.
Such a pressure
is denoted as -5 mm. Hg
meaning
5 mm.
Hg
less than
atmospheric.
Such a pressure
is referred to as a
negative pressure
.
Slide67The
atria are thin-walled vessels
and the
pressure of blood
in them is
never very far
from the
pressure outside
in the surrounding
mediastinum
.
This pressure is slightly negative (-2 mm. Hg) and it becomes more negative when breathing in (-8 mm. Hg).
Slide68Respiratory variations
in atrial pressure are
seen
in records of
atrial pressure
which are
obtained
with the
chest closed
by passing
a catheter
along the veins
into the heart
and
into the right atrium
. They
disappear
when the chest is
opened
as, for example, in thoracic surgery.
Slide69When the
A-V valves
(mitral and tricuspid) are
open
during diastole
(up to 0.1 and from 0.45 to 0.9 seconds), the
atrial pressure
is very
slightly greater
than the
ventricular
pressure
,
otherwise
the blood
would not enter
the
ventricles
. But to all intents and purposes the atrial and ventricular pressures are identical during this phase.
Slide70Similarly during
ventricular systole
, when the
aortic and pulmonary valves are open
, the
pressures
in the
ventricles
will be
equal
to those in the
aorta and pulmonary artery
(
from 0.15 to 0.4 and from 0.95 seconds onwards).
Slide71Ventricular Pressure Changes:
The left ventricle
develops a
maximum pressure of 120 mm. Hg
during
systole
and
therefore
the
aortic pressure reaches the same peak value
.
During
diastole the ventricular pressure falls to that in the thorax
which is approximately 0 mm. Hg (atmospheric pressure). The ventricular changes are thus
120/0 mm. Hg
.
Slide72The
pressure in the aorta
, however, is
maintained
by the
elastic recoil
of the
arterial walls
. Due to
this elastic
recoil the
pressure in the aorta has only fallen to 80 mm. Hg
by the
time the next systole occurs.
Thus
the pressure
in
the aorta fluctuates
between
120 mm. Hg and 80 mm. Hg.
These
changes are denoted as 120/80 mm. Hg.
Slide73The
right ventricle
pumps out
exactly
the
same quantity
of blood
as the lef
t ventricle
but
at a
much lower pressure
.
The
right ventricle
develops a
maximum pressure of 25 mm. Hg
. The
pressure falls to 0 mm. Hg
in
diastole
and the right ventricle
pressure changes are 25/0 mm. Hg.
The pressure in the
pulmonary artery falls to 8 mm. Hg
during
diastole
and the
pressure changes
in this vessel are, therefore
25/8 mm. Hg
.
Slide74Atrial Pressure Changes
The atrial pressure tracing follows a complex pattern due to the interplay of several factors.
Atrial contraction (atrial systole) is associated with a pressure rise in the atria. It lasts for only 0.1 seconds (time 0 to o.1 and 0.8 to 0.9 seconds).
For the reminder of the cardiac cycle the atrial muscle is in u state or relaxation (atrial diastole).
Slide75The isometric contraction of the ventricles causes the mitral and tricuspid valves to bulge into the atria causing a further increase in atrial pressure (time 0.1 to 0.15 and 0.9 to 0.95 seconds).
However, as soon as the aortic and pulmonary valves open, the ventricular volumes decrease rapidly.
Slide76The A-V ring descends increasing the volume of the atria. The atrial pressure falls sharply.
Blood returning to the heart cannot now enter the ventricles and the pressure in the atria builds up (time 0.2 to 0.45 seconds).
Slide77With the relaxation of the ventricles the atrioventricular ring moves upwards towards the base of the heart decreasing the volume of the atria and causing the atrial pressure to rise further (just before 0.45 seconds).
Slide78With the opening of the mitral and tricuspid valves at time 0.45 seconds the pressures in the atria and ventricles fall.
Blood returning to the heart enters the atria and ventricles and their pressures build up together till time 0.8 seconds is reached when another atrial contraction occurs.
Slide79Venous Pressure Changes:
The
veins near the heart
show
similar pressure
waves
to
those in the
right atrium
.
Since
the
veins and atria are in communication at all times
except during the brief atrial systole, the
atrial pressure changes
will be
transmitted back
to the
veins
.
Slide80There are
three
maxima in each
cardiac cycle lettered
a, c and v
.
The [a]
wave is
caused by
atrial systole
. The sphincter-like
action
of the
atrial muscle
round the
entry
of the veins
prevents this being
due simply to a
transmission of atrial systole to the veins
.
The
pressure builds up
because the
veins are unable to empty
their blood
into the atria.
Slide81The [c]
wave is
synchronous
with the
pulse wave
in
carotid artery
hence the letter c.
It
corresponds
to the atrial
pressure peaks
occurring
at 0.15 and 0.95 seconds
and
is duo to
the
bulging
of the
A-V valves
during the
isometric contraction phase
.
Slide82The [v]
wave corresponds
to the peak
in the
atrial pressure
, which
occurs
just
before 0.45 seconds
and is
due to
the
filling of the atria
whilst the
A-V valves are shut
and the upward
movemen
t of the
A-V ring
at the
end of ventricular systole.
These pressure changes
in the
veins
produce
the
venous pulse
which is
visible
in the
neck veins
when the subject is
lying down
.
Slide83All veins
above
the sternal angle are usually
collapsed
because their
pressure is sub-atmospheric
.
No pulsations
are therefore
visible in the neck veins
in the
upright posture
unless
venous congestion is present.
Slide84The
venous pulsations
are
seen
best in the
right external jugular
vein which is in direct
continuity
with the
superior vena cava and the right atrium. The venous pressure changes
are
too small
to be palpable.
Slide85Ventricular Volume Changes
The
ventricular volume
is
constant
during
both
the isometric
contraction
phase and the isometric
relaxation
phase.
Thus with the
onset of systole
, for the
first 0.05 second
there is
reduction in volume.
Slide86Slide87As soon as the
aortic valve
has
opened
the
ventricular volume decreases
as blood is ejected
into the aorta
. The ejection is
rapid at first
. Late in systole the ejection rate
is reduced
.
For the
first 0.05 second
of
diastole
there is
again no ventricular volume change
as the ventricular muscle fibers
relax
isometrically
.
Slide88As soon as the
mitral valve opens
the blood
rushes into the ventricle
, the ventricular
volume increases rapidly
at
first
and
later more slowly
.
By the time
0.4 of the 0.5 second
of
diastole
has elapsed
the filling has been such that the
ventricular volume
has
increased by 50 m1= 70%
of the
next stroke volume
.
Atrial contraction
in the
last 0.1 second
of
ventricular diastole completes the filling by the addition of a further 20 ml
.
Slide89Murmurs
Murmurs
are
sounds
heard
during the cardiac cycle
in addition to the normal
heart sounds
.
Those
occurring
during systole
are known as systolic murmurs. Those occurring during diastole
are termed diastolic murmurs. They are
caused by turbulence
in the
blood
as it flows through the
valve
.
Slide90Valvular disease
may
prevent adequate closure
of the
valves
, so that blood
regurgitates
back
through the partially closed valves. This will
occur during systole
in a case of
mitral or tricuspid incompetence, giving rise to a systolic murmur. It will occur during diastole if the aortic or pulmonary valve is
faulty-giving a diastolic murmur.
Slide91Murmurs are
also caused
by a
narrowing
of the valve
orifice
which is known as a
stenosis
. The murmur will occur during the
rapid passage
of
blood
through
the valve
.
Thus,
mitral and tricuspid stenosis
will give rise to a
diastolic murmur
which will
reach
a
maximum during late diastole
when atrial
contraction forces
blood through the valve into the ventricle.
Aortic and pulmonary stenosis
will give rise to a
systolic murmur
.
Slide92If the
turbulence produces vibrations
of the
chest wall
with
low frequency components
, the vibrations
can be felt
when the
flat of the hand
(or the ulnar border of the hand) is
applied to the chest
wall. Such a
palpable murmur
is termed
a thrill
.
In general,
low frequencies can be felt rather than heard
, whilst
high frequencies can be heard rather than felt.
Slide93Heart Block
The
duration of the P-Q
, or as it is often called
the P-R, interval
is
a measure of the conduction time in the bundle
. It is normally
(0.15- 0.2)
seconds.
Any
longer time
denotes delay in the transmission along the
bundle and maybe the forerunner of complete failure of conduction
along the bundle
known as heart block.
Slide94Complete
heart block occurs
when the ventricles
will be
cut off
from the
pacemaker
and will
stop beating
. However, they may restart at a
slow independent rate
due to the
inherent rhythmicity of the ventricular muscle. The rate (about 30 beats/minute) is often
too slow for an efficient circulation.
Slide95In all probability
the S.A. node and atria
will
continue
at their
original rate of 70 beats/minute
.
Atrial contractions will cease
to be
effective
in
aiding the circulation
as many will occur
whilst the A-V valves are shut.
The
ECG will show numerous P waves
but
few abnormal QRS complexes
and there will be
no time correlation between them
.
Slide96In such a case
an electrical stimulator
may be
implanted
in the axilla or abdominal wall and
connected
to electrodes in the
ventricle
.
Such a device
acts as an artificial pacemaker
and the ventricular contractions follow at the rate set by the electronic circuits. About 20 x 10
-6
joules of energy are needed for each pulse.
Slide97If a
ventricular beat originates
at some
ectopic focus,
an
abnormal QRST
complex will
appear
on the
E.C.G
.
Slide98This is a
common
occurrence in
young adults
and is known as an
extra-systole
or
dropped beat
.
The term dropped beat is used
because the
ectopic beat
may prevent the next pacemaker beat from contracting the ventricular muscle.
Slide99There is therefore
a pause
until the next successive beat arrives
[Fig-34B].
Slide100Atrial Fibrillation
Atrial
fibrillation occurs
when the
increased excitability of the atrial
muscle
leads
to
abnormal beats
arising from
ectopic loci
in the
atria. As a result, different parts of the atria are
contracting and relaxing out of phase with one another.
Slide101The
general appearance
of the
atria during fibrillation
has been
described
as
resembling a bag of wriggling worms
.
The atria never empty and the atrial wall
becomes a
quivering
sheet of muscle.
Slide102In
atrial fibrillation
the
atria cease to pump blood into the ventricles
.
In addition,
the beat originated
by the
pacemaker
is not transmitted to the ventricles
.
Instead,
impulses down the bundle of His in a haphazard fashion at a rate too fast
for the ventricle to respond to each impulse.
Slide103The
ventricular contractions
which do occur
are irregular
both
in rate and amplitude.
A
proportion
of these beats
fail to develop sufficient pressure
to
open the aortic valve
. As a result the radial pulse is "irregularly irregular"
and the
heart rate
measured
at the
heart
may be
higher than
if it is
measured by the pulse at the wrist
. This is known as a
pulse deficit
.
Slide104Ventricular Fibrillation
Should the
ventricular muscle fibrillate
, the
circulation stops immediately
. Unless immediate
cardiac massage
is
carried out
,
life will cease
.
Under suitable conditions ventricular fibrillation may be stopped by passing an electric current
through the heart. The apparatus is termed a cardiac defibrillator.
Slide105The
E
lectro
C
ardio
G
ram (
E.C.G
)
The
invasion
of the cardiac muscle
by the contraction wave is associated with
electrical changes. These potentials may be
recorded
at
points remote from the heart
and
after electronic amplification
may be
displayed
on a
pen recorder
or a cathode ray oscilloscope.
The
wave form
obtained is termed
ECG
.
The
various waves
present in the
waveform
are
lettered
starting with the
letter P
.
Slide106Each small box = 0.04 sec
Each large box = 0.2 sec
Each 5 large box = 1 sec
Slide107Slide108The
P
wave corresponds to the
spread
of
excitation
from the
S.A. node
over the
atrial muscle
and
therefore
represents
atrial systole.
Slide109The
propagation
of the contraction
wave down
the bundle
of His
does not produce any
detectable
external electrical change. It is denoted on the E.C.G. by the iso-electric
P-Q
interval where there
is no deflection. The QRS complex at the commencement of the ventricular excitation,
and the T wave at the end are all that remain of this algebraic summation. The relaxation phase
T-P
is
iso-electric
.
Slide110The detailed
waveform depends
on the
site
of the
recording electrodes
.
To record
the standard limb leads
, electrodes are applied to the left arm,
right arm
, and
left leg. These electrodes usually consist of a metal plate which is strapped over the flat part of the limb.Electrode
fluid or jelly is used between the electrode and the skin to ensure a good electrical connexion.
Leads I, II, Ill, aVR, aVL and aVF
Slide111The
right leg
is
not used
for
recording
the ECG, but a further electrode
is often applied to
this limb
to 'earth' the subject, and thus minimize interference from the mains and electrical apparatus.
In order to make a recording,
two input connexions
must be made to the amplifier and there is usually a switch on the
electrocardiograph apparatus which makes the appropriate connexions internally when a particular lead is chosen.
Slide112When the
switch is set at
Lead I
,
the
electrodes
on
the
right and left arms are
connected
to the amplifier. The
amplifier then records the potential difference between the right arm and the left arm.
When the switch is set to Lead II
,
the
potential difference
between the
right arm and left leg is recorded
.
When
set
to
Lead III
, the potential
difference
between
the left arm and left leg is recorded
.
Slide113An
alternative way
of
recording
the ECG is to
connect
one input
of the
amplifier to a limb electrode, and to
connect
the
other input of the amplifier to the other two limbs through two resistances. Such an
arrangement records the difference between the potential in one limb
and the
mean potential
in the other two.
If the
single limb
is the
right arm,
the
lead is termed 'aVR'
, if the
left arm,
it is
termed 'aVL'
, and if the
left leg
(or foot), it is
termed 'aVF
'.
Leads I, II III, aVR, aVL and aVF are the
six standard limb leads
which
are recorded clinically
.
Cardiac Vector
The figure shows the ECG recorded
using six limb leads.
They have been
arranged
to correspond to the figure below.
Chest Leads
The
six limb
leads (so far discussed) give
information
about the
'electrical axis of the heart'
in the
frontal plane.
To study the
activity
in a horizontal plane, chest leads are used.
These usually take the form of a single chest electrode which will
adhere
to the
chest wall by suction
, and which is
connected
to
one input
of the amplifier.
The
other input
of the amplifier
is connected
to an
electrically neutral point V
which is
obtained
by
joining
the
three limb leads together through resistances
.
Slide116It is found that
the point V
does not change
its
potential
during the
cardiac cycle
and this
potential may thus be used as a reference.
As the search
electrode is moved across
the chest, the ECG shows a dominant S-wave in chest positions 1 and 2, and a dominant
R-wave in chest positions 5 and 6.
Slide117