Download cardiac muscle

CIRCULATION
The HEART
CARDIAC MUSCLE
Three types of cardiac muscle
exist:
-Atrial muscle (contractile);
- ventricular muscle (contractile);
-specialized muscle fibers (excitatory
and conductive).
SPECIAL PROPERTIES OF
CARDIAC MUSCLE
Syncytium:
There are intercalated discs between muscle fibers (unlike
skeletal muscle).
Electrical resistance through them is very low (only 1/400
the resistance of the cell membrane) because they have
permeable gap junctions (free diffusion of ions).
So action potential (AP) travels from one cardiac muscle cell
to another (unlike skeletal muscle). There are atrial
syncytium and ventricular syncytium in the heart.

NOTE: the atria are separated from the
ventricles by fibrous tissue (atrioventricular
septum). This allows the atria to contract ahead
of ventricles. AP can be conducted from the
atrial syncytium into the ventricular syncytium
only by way of a specialized conductive system
(the atrioventricular bungle).

Owing to the syncytial structure all cells of
syncytium are excited and participate in
contractile response (to each threshold and
super-threshold stimulus). So strength of cardiac
contraction does not depend on strength of
stimulus (principle “all or none”)- unlike skeletal
muscle.
Recording the depolarization wave (A and B) and the repolarization
wave (C and D) from a cardiacmuscle fiber.
Above, Monophasic action potential from a ventricular muscle
fibboer during normal cardiac function, showing rapid depolarization
and then repolarization occurring slowly during the plateau stage
but rapidly toward the end. Below, Electrocardiogram recorded
simultaneously.
Membrane potential

The resting MP of normal cardiac muscle is
about –90 mv (because of high Kpermeability and low Na-permeability of
the cell membrane).

Action potential is spike from –90 mv to
+20 mv (positive portion of AP is called
“overshoot potential”).

NOTE: membrane of ventricular cell
remains depolarized about 300 msec
(unlike skeletal muscle). This prolonged
phase of depolarization is called “plateau”.
It causes muscle contraction to last 3 to
15 times longer in cardiac muscle than in
skeletal one.
Three types of ion channels form the AP of cardiac
muscle:
 (1) fast sodium channels (that can be fast
activated and fast inactivated);

(2) slow calcium channels (that can be slow
activated and slow inactivated); they are called
also calcium- sodium channels because of
permeability for sodium ions; this type of ion
channel is absent in skeletal muscle;

(3)slow potassium channels (that have not
inactivated mechanism).

1. Firstly fast Na-channels become opened
and inward Na-current provokes
depolarization of the cell membrane and
overshoot. Then these channels become
inactivated and Na-current ceases.

2. Then slow Ca-channels become opened
and inward Ca-current (+ Na-current)
continue to depolarize the cell membrane
(phase “plateau”). During depolarization
the permeability of the cardiac muscle
membrane for K+ decreases (5-fold)
owing the excess of Ca-influx (This
prevents early return of the potential to its
resting level). Then Ca- channels become
inactivated and Ca-current ceases.

3. At last, slow potential-depended Kchannels become opened and outward Kcurrent provokes fast repolarization (to
resting level –90 mv).
Refractory period of cardiac muscle
During phase plateau fast Na-channels remain
inactivated and prolonged refractory period is
present (about 300 msec).
Duration of refractory period is equal duration
of systole. Therefore, cardiac muscle cannot
contract in form tetanus but it can contract
only in form single contraction (unlike skeletal
muscle).
 VELOCITY
OF CONDUCTION in cardiac
muscle (atrial and ventricular) is about
0.3-0.5 m/s (only 1/250 the velocity in
very large nerve fibers and 1/10 the
velocity in skeletal muscle).
 The
velocity of conduction in the
different parts of specialized
conductive system varies from 0.02
to 4 m/s.

EXCITATION-CONTRACTION COUPLING
mechanism is the same as that for skeletal
muscle. There are transverse tubules of
the cell membrane (very developed) and
longitudinal tubules of the sarcoplasmic
reticulum (much less developed) in the
cardiac muscle cell. So the strength of
contraction of cardiac muscle depends to a
great extant on the concentration of Ca in
the extracellular fluids (owing inward Cacurrent during phase plateau when the Ttubule action potential occurs).
SPECIAL PROPERTIES OF
CARDIAC MUSCLE
excitation
Phase plateau
Prolonged
refractory
period
conduction
Functional syncytium
cells are electrically
connected)
contraction
only single
contractionTetanus is
impossible
Contraction
principle “all
or none”
THE CARDIAC CYCLE
period from beginning of one heart beat to the
beginning of the next one (about 0.8 sec).

Period of contraction is called systole and period of
relaxation is called diastole (during which the heart
fills with blood).
Because atria contract ahead ventricles there are tree
basic phases in cardiac cycle:
 (1)
systole of atria (0.1 sec)
 (2)
systole of ventricles (0.3 sec)
 (3)
common diastole (common pause) (0.4
sec)

In summary, the systole of the ventricle can be subdivided into the
following phases:
1. Isovolumetric contraction
0.05 s
2. Rapid ejection
0.10 s
3. Reduced ejection
0.15 s
Total
0.3 s
The subdivisions of ventricular diastole are:
1. Prodiastole
2. Isovolumetric relaxation
3. First rapid filling phase
4. Diastasis
5. Last rapid filling phase
0.04 s
0.06 s
0.10 s
0.20 s
0.10 s
Total about
0.5
N.B Please note that diastasis strongly depends on heart rate
Phases and events of the cardiac cycle
cuspid valves
open while valves
of vena cava and
pulmonary veins
are closed
P wave
atrial
depolarization &
contraction
QRS complex
atrial
repolarization and
relaxation &
empties the
simultaneous
ventricles
ventricular
depolarization
and contraction
cuspid valves are
closed while
semilunar valves
are open
T wave
ventricular
repolarization and heart relaxes
relaxation
cuspid and
semilunar valves
are closed
pause
myocardium at
rest
fills the ventricles
atria fill after a
pause of some
length
valves of vena
cava and
pulmonary veins
open so atria can
fill
Cardiac Cycle (Pressure within the chambers of the
heart rises and falls) Three phases:
1. Ventricular Filling (SYSTOLE OF ATRIA)
-heart in total relaxation, mid-to-late diastole
-pressure in heart is low, blood returning to heart
-rapid ventricular filling (70% of ventricle filling), blood
flows
-passively into atrium through open AV valves into
ventricles
-AV valve flaps drift upward to closed position
-atriole systole, atrial pressure rises, propels blood into
resting ventricles
-ventricles now contain the maximum volume of blood
called the end-diastolic volume (EDV)
2. Ventricular Systole







blood is pushed up against AV valves,
forcing them shut
All four valves closed (isovolumetric
contraction)
Pressure rises
Semilunar valves open
Ventricular ejection occurs
Ventricles start to relax, semilunar valves
close
Blood remaining - end systolic volume
(ESV)
3. Relaxation/ Common
diastole(Quiescent) Period (from T
wave to P wave)
Ventricles start to relax, all four chambers in
diastole
 Pressure within chambers drops, blood starts to
flow from pulmonary trunk and aorta toward
ventricles
 Blood becomes trapped in semilunar cusps, valves
close
 Rebound of blood closed cusps (dicrotic wave on

aortic pressure curve)




Isovolumetric relaxation occurs --> interval when
ventricular blood volume does not change
because both semilunar and atrioventricular
valves are closed
As ventricles relax, space inside expands, and
pressure falls
When ventricular pressure drops below atrial
pressure, atrioventricular valves open and
ventricular filling begins
NOTE: CARDIAC OUTPUT = HR X SV. Stroke
volume is equal to the difference between EDV
and ESV. At rest CO = HR (75 beats/min) X SV (70
ml/beat) = 5250 ml/min
End-diastolic volume (EDV) - The typical volume of blood,
approximately 120-130 mL, found in the ventricles after they
are filled by atrial contraction during ventricular diastole
(before the ventricles contract); the actual volume will
depend on venous return of blood to the heart.
End-systolic volume (ESV) - The residual volume of blood,
approximately 50-60 mL, found in the ventricles after systole
(when the ventricles have contracted); the volume varies in
response to activity levels and to disease states.
Venous return - The amount of blood delivered to the atria by
the veins of the pulmonary and systemic circulations; venous
return is influenced by blood pressure, gravity, blood volume,
activity levels and by disease states.
The maximum pressure occurs after ventricular
systole and is known as the systolic pressure.
When the blood pressure in the aorta exceeds
that in the ventricle, the aortic valve closes; this
accounts for the dicrotic notch.
Summary of the cardiac cycle
I. SYSTOLE OF ATRIA

Atria are primer pumps.

During ventricular systole, large amount of blood accumulates
in the atria (because A-V valves are closed).

At the beginning of ventricular diastole (when pressure in the
ventricles fall and A-V valves open) blood enter rapidly into the
ventricles.

About 75% of the blood flows directly through the atria into
ventricles before the atria contraction (passive filling of
ventricles). Atria contraction causes an additional 25% filling of
the ventricles (active filling of ventricles). Atria pressure rises 6
to 8 mm Hg during their contraction.
II. SYSTOLE OF VENTRICLES
(a)
period of isovolumic (isometric) contraction
After ventricular contraction begins the ventricular pressure abruptly
rises and A-V valves close.
Semilunar valves of aorta and pulmonary artery are closed too.
Volume of blood remains constant in the ventricles.
(b)
period of ejection
When the ventricular pressure rises above diastolic pressure in the
vessels (70-80 mm Hg in the left ventricle and 8-10 mm in the right
one) semilunar valves open.
Blood begins enter vessels: first third of the period of ejection –
70% of blood (period of rapid ejection) and remained 2/3 of the
period – 30% of blood (period of slow ejection).
III. COMMON DIASTOLE

Relaxation of ventricles begin suddenly,
intraventricular pressure falls rapidly, semilunar
valves close, A-V valves remain closed too
(period of isovolumic relaxation of the
ventricles).

Then A-V valves open and filling of the ventricles
begins (period of rapid filling, period of slow
filling). During common pause passive filling of
ventricles occurs (both atria and ventricles are
relaxed). Pressure in the ventricles is about zero
during this phase.
FUNCTION OF THE VALVES

They prevent backflow of the blood. They
close and open passively (owing to
gradient of pressure).

(Contraction of sphincters prevents
backflow of the blood from atria into
venous vessels).
CONDUCTING SYSTEM OF THE
HEART

There is specialized excitatory and conductive system in the heart:

sinus node (sinoatrial), in which the normal rhythmical impulses are

internodal pathways that conduct impulses from the sinus node to the A-V

A-V node (atrioventricular node) in which impulse from the atria is delayed

A-V bundle, which conducts impulse from the atria into the ventricles;

left and right bundles of Purkinje fibers, which conduct impulses to all parts
generated;
node;
before passing into the ventricles;
of the ventricles.

This system has the capability of self-excitation (so the heart can be
excited and contracts automatically).
SINUS NODE

Each cardiac cycle is initiated by spontaneous generation of action potential
in the sinus node. It is located in the wall of right atrium near the opening
of the superior vena cava.

“Resting” potential of the cell of the sinus node is about -55 mv (because
of low permeability for K-ions and high permeability for Na-ions at rest). At
this level of negativity fast Na-channels are inactivated. Only slow Cachannels can open (become activated) and thereby cause the AP. AP is
slower, with a slow decrement.

Self-excitation: At rest Na-ions outside the fibers tend to leak to the
inside. ”Resting” potential gradually rises between each two heart beats.
This is SDD -spontaneous diastolic depolarization. When it reaches a
threshold voltage (-40 mv), the slow Ca-channels become activated and the
AP is generated. Then Ca-channels are inactivated; K-ions diffuse out of the
fibers and membrane potential returns at “resting” level. Then K-channels
begin to close, leakage of Na-ions to the internal provokes SDD again and
all cycle is repeated.
ATRIOVENTRICULAR NODE

It is located in the posterior septal wall of
the right atrium. It occurs delay in impulse
conduction (about 0.13 sec)
CAUSES OF THE SLOW CONDUCTION:
 (1) small sizes of the cells
 (2) their resting potential is much less
negative that causes low voltage to drive
the ions
 (3) gap junctions has great resistance to
the movement of the ions.


A-V BUNDLE normally occurs one-way conduction
(from atria toward ventricles). [In rare instances,
abnormal muscle bridge does penetrate the fibrous
barrier between atria and ventricles besides at the A-V
bundle. Under such conditions the cardiac impulse can
re-enter the atria from the ventricles and cause
serious arrhythmia].

A-V bundle divides into left and right bundle brunches
that lie beneath endocardium. The terminal Purkinje
fibers penetrate about 1/3 of the way into the muscle
mass. Then impulse is transmitted by the ventricular
muscle fibers themselves. Direction of transmission is
(a) from the apex of the ventricles toward base and
(b) from the endocardium toward epicardium.
PACEMAKER OF THE HEART

NOTE: sinus node is the pacemaker of the heart.
The normal rate of the sinus node is 70-80 times
per min. (the rate of A-V node is 40-60; the rate
of Purkinje fibers is between 15 and 40).

Sinus node has a high velocity of its own
depolarization and emits its impulse before A-V
node can reach its own threshold for excitation.
So sinus node always excites other potentially
self-excitatory tissues before their self-excitation
can occur. Thus sinus node controls the beat of
the heart.

A pacemaker elsewhere than the sinus node is
called an ectopic pacemaker (abnormal).

When A-V block occurs the atria continue to beat
at the normal rate of rhythm of the sinus node,
while a new pacemaker develops in the Purkinje
system of the ventricles and drives the
ventricular muscle at a new rate between 15 and
40 beats per min.

NOTE: effective pumping by the two ventricular
chambers requires synchronous type of their
contraction. Slow transmission provokes much of
ventricular mass to contract before contraction
of the remainder. Pumping effectiveness of the
ventricles is decrease 20-30%.
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