Download 22 Physiological properties of heart

Physiological
properties of the heart
Location of the heart in Circulation scheme of the
venous and arterial blood
the thorax
Anatomical structure of
the heart
Points of auscultation of
the heart
Functional properties of the heart
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Automaticm: ability to initiate an electrical impulse
Conductiblity: ability to transmit an electrical impulse from
one cell to another
Excitability: ability to respond to an electrical impulse
Refractoriness: cardiac muscle can not be exited during the
whole period of systole and early part of diastole. This period
prevents waves summation and tetanus
Contractility: Contractility is the ability of the cardiac muscle
to contract. In this way flowing of blood is provided.
Electrophysiological properties of
myocadial contractile cells
The level of the resting potential in contractile
cardiomyocytes is within -90 - 95 mV and it is stable.
Resting potential of myocardial contractile cells arises
due to diffusion of K-ions from the cell and entrance of
Cl-ions to cardiomyocytes, but in contrast to the phase
cross-lined muscles chloric permeability of their
membrane is more small than potassium and plays a
minor role in the formation of the resting potential of
contractile cardiomyocytes.
Phases of action potential
0 – depolarization
1 – beginning of
rapid repolarization
2 – slowly
repolarization
or plateau
3 – ending rapid
repolarization
4 – rest period.
Action Potential
The Action Potential in Skeletal
and Cardiac Muscle
Ionic bases of
transmembrane potentials
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The RMP is attributed mainly to the
equilibrium potential of potassium. The RMP
is affected more by potassium than by any
other ion.
 Cardiac tissues may be classified as:
 slow fiber
 fast fiber
Scheme of the conduction system of
the heart
1 – sine-atrial node ;
2 - atrial bundle of Bachmann ;
3 - interstitial conducting paths (
Bachmann’, Venkebah’, Torel’ );
4 atrioventricular node ;
5 - Hys node;
6 - right bundle of Hys node;
7 - anterior branch of the left
bundle of Hys node;
8 - posterior branch of the left
bundle Hys node;
9 - bundle of Kent ;
10 - James’ bundle ;
11 - Maheym’ bundle.
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Automatism of heart - the ability of cells of the heart conducting
system to produce independently bioelectric impulses, that cause its
excitement.
 Structures of conducting system have different degrees of
automaticity. It is established the so-called gradient of
automaticity . It manifests itself in a reduced ability to automatism
of different structures of the conducting system according to their
distance from the sine-atrial node. Thus, if the sine-atrial node
number of action potentials riches the level of 60-90 imp / min, and
in the cells of Hys node - 30-40 imp / min, so in the fibers of
Purkin'ye – less than 20 imp / min. Gradient of automaticity caused
by different spontaneous permeability cell membrane of conduction
system to Ca2 +. Based on the fact, that the sine- atrial node
imposes its rhythm to the departments of conduction system, that
lying lower, it is called pacemaker or pacemakers of first order.
Pacemaker of second order is atrio-ventricular node. Pacemaker
third order – it is Hys node and its ramifications.
Automaticity
– 60-90 /min
AV – node – 40-60 /min
Hiss bungle – 30-40 /min
Purkinje fibers - <20 /min
SA-node
The assimilation of rate
Under normal circumstances, the
automaticity of all sections of the
conduction system is suppressed by
sine-atrial node, which enforces its
own rhythm. That is why all parts of
the conduction system begin to work
at the same pace although they have
their own rhythm.
The phenomenon in which the
structure with slow pace of
generating of action potentials
assimilate more frequent rhythm from
other parts of the conducting system
called the assimilation of rate.
Setting of the artificial pacemakers
The spread of excitation in the atria and
AV node
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The spread of excitation in the atria
The excitement that arose in Sino- atrial node, is
conductesthrouht the atria at a speed of 0,8-1,0 m / s. At
first depolarization covers the right atrium , and then –
left atrium. Time of coverage by excitation of both atria –
0,1 sec.
 Conduction of excitation in the atrioventricular node
With the transfer of excitation from the atria to the
ventricles its delay in atrio -ventricular node is observed.
It is associated with features of geometrical structure of
node and the specifics development electrical potential in
it. This is due to the low density of Na + channels. This
delay is important for sequential excitation and
contraction of atria and then the ventricles. The speed of
excitation spread through atrio-ventricular node is about
0,02 m / s.
The spread of excitation in the
ventricles
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The speed of the excitation throught the His-node and
the Purkinje fibers is 1-1,5 m / s. The process of
ventricular depolarization begins at the middle third of the
interventricular septum and extends to the top and side
walls of the right and left ventricle. Basal parts of the
ventricles and the upper third of the interventricular
septum are depolyaryzate at last.
 Next delay of excitation - in the place of contact of
Purkinje fibers with contractile myocytes . It is the
result of summation of action potentials, which
contributes to the synchronization of myocardium’
excitation. The speed of excitation conduction within
ventricles averages 0,3-0,9 m / s.
Conduction of excitation in the heart
Conduction on the Heart
The sino-atrial node in humans is in the shape of a
crescent and is about 15 mm long and 5 mm wide.
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• The S-A nodal cells are self-excitatory, pacemaker cells.
• They generate an action potential at the rate of about 70 per
minute.
• From the sinus node, activation propagates throughout the
atria, but can not propagate directly across the boundary
between atria and ventricles.
 Even
more distally the bundles ramify into
Purkinje fibers (named after Jan
Evangelista Purkinje (Czech; 1787-1869))
that diverge to the inner sides of the
ventricular walls.
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Propagation along the conduction system
takes place at a relatively high speed once it
is within the ventricular region, but prior to
this (through the AV node) the velocity is
extremely slow.
Propagation from the AV node to the ventricles is
provided by a specialized conduction system.
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Proximally, this system is composed of a common
bundle, called the bundle of His (after German
physician Wilhelm His, Jr., 1863-1934).
• More distally, it separates into two bundle branches
propagating along each side of the septum,
constituting the right and left bundle branches. (The
left bundle subsequently divides into an anterior and
posterior branch.)
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SA NODE PACEMAKER BECAUSE
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1) Highest frequency of discharge 2) Of overdrive suppression
The greater rhythmicity of the
Other cells with low frequency of
SA node forces the other
discharge.
automatic cells to fire off at a
Called latent or potential pacemakers;
abnormal
faster rate than their natural
or ectopic pacemakers
discharge rate. This causes
Become pacemaker when:
depression of their
Develop rhythmical discharge rate that is
rhythmicity.
more
SA node rhythmical
rapid than SA node
discharge rate = 70-80/min
Develop excessive excitability
AV node = 40-60/min
Blockage of transmission of the impulses
P fibers = 15-40/min
from the
SA node to other parts of the heart
Normal Impulse Conduction
Sino-atrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
CONDUCTIVITY
spread of excitation
Excitation – originates from the SA node
 Conduction velocity in atrial muscle = 0.3 to 0.5 m/sec
 Conduction is faster in the interatrial
 bundles (presence of specialized conduction fibers)
 0.03 m/sec internodal pathway to AV node
 0.09 m/sec AV node itself
 0.04 m/sec penetrating AV bundle
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Total delay in the AV nodal and AV bundle system = 0.13 m/sec +
0.03 m/sec from SA to AV node = 0.16 m/sec
Cause of slow conduction in the transitional,
nodal, and penetrating AV bundle fibers:
 1)
Their sizes are considerably smaller than
 the sizes of the normal atrial muscle fibers.
 2) All these fibers have RMP that are much
 less negative than the normal RMP of other
 cardiac muscle.
 3) Few gap junctions connect the successive
 muscle cells in the pathway.
Excitation reaches the
Bundle of His
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Velocity of conduction =3-4 m/sec
 Increased magnitude of the AP;
 increased velocity of phase 0 depolarization;
 increased duration of the AP
 Excitation transmitted to the RBB and LBB and fascicles then to the
ventricular muscle
Note:
 AP
of endocardial cells lasts longer than that of epicardial cells, so that
depolarization proceeds from endo- to epicardial surface but
 repolarization
travels from epicardial to endocardial surface.
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Excitability - the ability of heart to excitation (or move
to a state of physiological activity). The excitability is
typical for cells of the conducting system of the heart and
contractile myocardium.
Changes of heart’ excitability during excitation
The excitability of the heart muscle during excitation
changes. If you compare the action potential with
excitability, it showes that during the 0, 1 and 2 phases
cell completely nonexcitable or refractory . This is socalled the absolute refractory period, when the cell is
not able to respond to the stimulus of any strength (is
caused by inactivation of Na +- channels). During phase
3 relative refractory period take place. During this period
underthreshold irritation can cause excitement. That is, in
this period there is a recovery of excitability.
Correlation between active potential,
contraction, excitability of heart cells
0 – rapid depolarization
1 – rapid initial
repolarization
2 – slow repolarization
(plateau)
3 – rapid ending
repolarisation
4 – absolute
refractivity;
5 – relative refractivity;
6 – period of
increaseexcitability;
7 - exaltation
Mechanism of myocardium contraction
A series of successive actions in
myocardial cells, starting with the
trigger of contraction - the action
potential of the membrane with
the following intracellular
processes, followed by shortening
of myofibrils, called the coupling
of excitation and contraction.
The structural basis for coupling
of excitation and contraction of
cardiomyocytes is T-system, that
consists transverse and
longitudinal T-tubules and
sarcoplasmic reticulum cisterns
which stored Ca2 +.
Mechanism of myocardium contraction
Under the influence of the action
potential, Ca2 + from
extracellular space and from the
cisterns of the sarcoplasmic
reticulum entering the
myoplazma, where under its
influence protein troponin (which
pushes back tropomyosin from
actin active sites) konformes.
Therefore between actin and
myosin bridges are formed.
Thus, splitting of ATP takes place
in this period and its energy is
used for sliding of actin
filaments. The more calcium ions
from the troponin contacted, the
more actomyosine bridges
formed and the greater the force
of muscle contraction.
Mechanism of relaxation of the heart muscle
The relaxation of cardiomyocytes
occurs as a result of repolarization of
the membrane. It is based on the fact
that the impact of repolarization
removes Ca2 + from the contractile
proteins. After that Ca2 + captures by
pumps of cysternes of sarcoplasmic
reticulum. Ca2 + is also displayed in
the interstitial liquid due the pump
work of cell membranes. The main
process, that determines the relaxation
of cardiomyocytes – the removal of
calcium ions from the sarcoplasma,
resulting in decreasisng of Ca2 +
concentration in it. Thus , complexes
of Ca2 + with troponin C break,
tropomyosin shiftes according to actin
filaments and closes their active
centers – contraction is terminated.
Differences Between Skeletal and
Cardiac Muscle Physiology
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Action Potential
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Cardiac: Action potentials conducted from cell to cell.
Skeletal, action potential conducted along length of single fiber
Rate of Action Potential Propagation
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Slow in cardiac muscle because of gap junctions and small diameter of
fibers.
Faster in skeletal muscle due to larger diameter fibers.
Calcium release
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Calcium-induced calcium release (CICR) in cardiac
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Movement of extracellular Ca2+ through plasma membrane and T
tubules into sarcoplasm stimulates release of Ca2+ from sarcoplasmic
reticulum
Action potential in T-tubule stimulates Ca++ release from sarco-plasmic
reticulum
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