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PHYSIOLOGICAL PROPERTIES OF HEART.

FORMATION OF NORMAL ELECTROCARDIOGRAM.
PUMPING WORK OF THE HEART.
NEURO-HUMERAL REGULATION OF THE HEART.
Objectives for Students’ Independent Studies
You should prepare for the practical class using the existing textbooks
and lectures. Special attention should be paid to the following:
List:
1. PHYSIOLOGICAL PROPERTIES OF HEART
1. Morphology and functional organization of heart
2. Automaticity of the heart
3. Conductibility of the heart
4. Excitability of heart
5. Contractibility of the heart
6. Mechanism of contraction and relaxing of the heart muscle.
Formation of normal electrocardiogram
7. Separate myocardial cell electricity.
8. Electrogram and action potential of one myocardial cell.
9. Formation of EEG waves
10. ECG correspondence of heart depolarization
Electrocardiography as a method of observation
1. ECG leads
2. Algorithm of ECG registration:
3. ECG analysis
4. ECG analysis begins with estimation of control voltage and paper speed.
Another analysis at usual performs in this order.
5. Investigation of conductive system in the heart
6. ECG registration
7. ECG analysis
2. PUMPING WORK OF THE HEART
1. Listening ( auscultation ) of heart tones
2. The projection of the heart valves on the front chest wall
3. Cardiohaemodynamic
4. Physiological analysis of cardiac output
3. NEURO-HUMERAL REGULATION OF THE HEART
1. Nerve regulation of heart activity
2. Humeral regulation of heart activity
3. Intracardial regulatory mechanisms

1. PHYSIOLOGICAL PROPERTIES OF HEART

1. Morphology and functional organization of heart
a) Structure of heart.
The heart contains four chambers: two upper atria, which receive
venous blood and two lower ventricles, which eject blood into arteries. The
right ventricle pumps blood to the lungs, where the blood becomes
oxygenated. The left ventricle pumps oxygenated blood to the entire body.
The right and left atria receive blood from the venous system. The
right atrium and ventricle are separated from the left one by septum, which
is the muscular wall. This septum normally prevents mixture oxygenated and
not oxygenated blood.
Between the atria and ventricles there is a layer of dense connective
tissue known as fibrous skeleton of the heart. The connective tissue of
skeleton also forms rings, called annuli fibroses around two pairs of one-way
valves.
VIDEO
b) Structure of myocardium.
Bundles of myocardial cells in the atria attach to the upper margin of
this fibrous skeleton and form a myocardium. The myocardial cell bundles
of the ventricles attach to the lower margin and form a different myocardium.
As a result, the myocardium of the atria and ventricles are structurally and
functionally separated from each other.
Weight of whole myocardium consist 250-300g. Atria myocardium
has two layers of muscle cells - circular and longitudinal. Circular cells
layers surround mouth of vessels, which fall into atria and may cover again
it in constriction.
 Ventricles myocardium has three layers of muscle cells. External and
internal layer have spiral form and are common for both ventricles. Middle
layer has circular orientation and is separated in every ventricle.

c) Functional specialties of myocardial cells.

Myocardial cells contain actin and myosin filaments and contracts by
means of the sliding filament mechanism. Myocardial cells are joined by gap
junctions, due to which electrical impulses can spread to all cells in the mass.
Sarcoplasmatic reticulum in myocardial cells is developed slightly. That is
why some amount of calcium may enter the myocardial cell from the outside.
Besides contractive myocardial cells there are modified cells of the
conduction system of the heart. They can generate and conduct impulses
through myocardium.

d) Electrophysiological properties of the contractive myocardium.

The main electrophysiological properties of the contractive
myocardium are automaticity, contractility, conductability and excitability.
Automaticity is property to contract replying to electrical impulses,
originated in pacemaker cells of the conduction system of the heart.
Contractility is property to contract replying to irritation.
Conductibility is property to spread electrical impulses through the
conduction system and contractive myocardium.
Excitability is property to reply the irritation.

2. Automaticity of the heart

a) Structure of conduction system.
Action potentials that originate in the sinoatrial node (SA-node)
spread to adjacent myocardial cells of the right and left atria through the gap
junction between these cells.
Since the myocardium of the atria is separated from the myocardium
of ventricles by the fibroses skeleton of the heart, the impulse cannot be
conducted directly from the atria to the ventricles. Besides that atria have to
contract before ventricles to guarantee pumping of blood.
Once the impulses spreads through the atria, it passes to the atrio-
ventricular node (AV-node), which is located on the inferior portion of the
 internal septum. From here, the impulse continues through the atrio-
ventricular bundle, or bundle of His, beginning at the top of the
interventricular septum. The atrio-ventricular bundle divides into right and
left bundle branches, which are continues with Purkinje fibers within the
ventricular walls.
Specialized excitatory and conductive system of the heart: consists of:
1. Sinus node "SA" node: also called sinoatrial node, located in the right atrium.
It is concerned with the generation of rhythmical impulse; it is the pacemaker
of the heart that initiates each heart beat. This automatic nature of the heart
beat is referred to as automaticity.
2. Internodal pathways conduct the impulse generated in SA node to the AV
node.
3. The AV node (atrioventricular node), located near the right AV valve at the
lower end of the interatrial septum, in the posterior septal wall of the right
atrium. At which impulse from the atria is delayed before passing into the
ventricles.
4. The AV bundle (bundle of His) conducts the impulse from the atria into
ventricles.
5. The left and right bundles of purkinje fibers, which conduct the cardiac
impulse to all parts of the ventricles. The purkinje fibers distribute the
electrical excitation to the myocytes of the ventricles.

Figure: The cardiac conduction system.

Figure: organization of the AV node.

The SA node as the pacemaker of the heart:
(Automaticity & rhythmicity)
Automaticity is the property of self-excitation (i.e. the ability of spon-
taneously generating action potentials independent of any extrinsic stimuli)
while rhythmicity is the regular generation of these action potentials. In other
words, the cardiac impulse normally arises in the SA node, which has the
capability of originating action potentials and functioning as pacemaker.
This action potential then spreads from the SA node throughout the atria and
then into and throughout the ventricles.
 The contractile cardiac muscle cells don't normally generate action potentials
but they can do in certain pathological conditions. This mean that all parts of
the conduction system are able to generate a cardiac impulse;
(autorhythmicity), but the normal primary pacemaker is the SA node, while
the AV node is a secondary pacemaker and the Purkinje system is a tertiary
(or latent) pacemaker. The AV node acts only if the SA node is damaged or
blocked, while the tertiary pacemaker takes over only if impulse conduction
via the AV node is completely blocked.
The SA node discharges at an intrinsic rhythmical rate of 100-110 times per
minute (sinus rhythm). Under abnormal condition; the AV nodal fibers can
exhibit rhythmical discharge and contraction at a rate of 40 to 60
times/minute. While those of purkinje fibers discharge at a rate between 15
and 40 times/minute.
Autorhythmicity is a myogenic property independent of cardiac
innervation. This is evidenced by the following:
 Completely denervated heart continues beating rhythmically.
 Hearts removed from the body and placed in suitable solutions
continue
beating for relatively long periods.
 The transplanted heart (denervated heart) has no nerve supply but
they beat regularly.
Self-excitation of SA node:
What causes the SA node to fire spontaneously?
Although the SA node discharges at an intrinsic rhythmical rate of 100-110
times per minute but the pulse rate averages 70 or 80 times per minute, this
is because of the effect of vagal tone. SA node does not have a stable resting
membrane potential which starts at about – 60 mV. This is due to the inherent
leakiness of the SA nodal fibers to Na+ ions that causes this self-excitation
(Na+ influx). in other words, because of the high Na+ ions concentration in
the ECF as well as the negative electrical charge inside the resting sinus
nodal fibers, the positive Na+ ions outside the fibers tend to leak to the inside,
rising the membrane potential up to a threshed to fire an action potential.
Atrioventricular node (AV node):
The conductive system is organized, so that cardiac impulse will not
travel from the atria into ventricles too rapidly. There is a delay of
transmission of the cardiac impulse in the AV node to allow time for the atria
to empty their blood into the ventricles before ventricular contraction begins.
 VIDEO
b) Electrophisiological properties of conduction system.
The cells of SA-node do not keep a resting membrane potential in the
manner of resting neurons or skeletal muscle cells. The membrane potential
begins at about -60 mV and gradually depolarizes to -40 mV, which is the
threshold for producing an action potential in these cells. This spontaneous
depolarization is produced by the diffusion of Ca²+through openings in
membrane called slow calcium cannels. At the threshold level of
depolarization, other channels, called fast calcium channels, open and
calcium rapidly diffuses into the cells. The opening of voltage regulated
sodium gates, and the inward diffusion of sodium that results, may also
contribute to the upshot phase of the action potential in pacemaker cells.
The opening of potassium gates and outward diffusion of potassium,
as in the other excitable tissues produce repolarization.
Once repolarization to -60 mV has been achieved, a new pacemaker
potential begins, again culminating with a new action potential.
Action potential of SA node
The resting membrane potential of SA node is of -55 to -60 mV
(millivolts). The cause of this reduced negativity "less negative" is that the
cell membrane of the sinus fibers are naturally leaky to sodium ions
"Na+ influx". Therefore; Na+ influx causes a rising membrane potential
"gradual depolarization" which when reaches a threshold voltage at about -
40 mV, the fast calcium and sodium channels opened, leading to a rapid
entry of both Ca+2 and Na+ ions causing the action potential to about 0 mV
(zero), to be followed by repolarization which is induced by K+ efflux out of
the fiber because of the opening of K+ channels. This repolarization carries
the resting membrane potential down to about -55 to -60 mV at the
termination of action potential.

Figure: Action potentials of the SA node.

Action potential of ventricular cardiac muscle fiber

The membrane potential of cardiac ventricular muscle fiber cells is
about -90 mV; the interior of the cell is electrically negative with respect to
the exterior due to disposition; distribution of ions mainly Na +, K+ and
Ca+2 ions across its membrane.
 The action potential (AP) is an electrical signal or impulse produced
by ionic redistribution that the potential changes into positive inside the cell
(depolarization), to be followed by restoration of the ions; returning back to
the resting potential (repolarization). Stimulation of cardiac muscle cells by
SA produces a propagated action potential, that is responsible for muscle
contraction i.e., excitation-contraction coupling. In other words, stimulation
of cardiac muscle cells specifically those of the ventricles is performed by
the propagated AP of the SA node from which the electrical impulses
originating and propagated over the heart. According to the figure (a), the
propagated AP of the SA node depolarized the ventricular muscle fiber cells
rapidly with an overshoot (phase 0), followed by a plateau at around zero
potential level (phase 2). This plateau is unique for the heart muscle; and is
followed by phase 3 and 4; as final repolarization i.e., for the potential to
return to baseline.

Ionic basis of the action potential of the cardiac ventricular muscle fiber
cell:
The action potential of cardiac ventricular muscle fiber cell includes the
following phases :

 Phase 0 (upstroke): initial rapid depolarization with an overshoot to

about +20 mV are due to opening of the voltage-gated Na+ channels with
rapid Na+ influx.
 Phase 1 (partial repolarization): initial rapid repolarization is due to
K efflux (K+ outflow) followed the closure of Na+ channels when the
+

voltage reaches at nearly +20 mV.

 Phase 2 (plateau): subsequent prolonged plateau is due to slower
and prolonged opening of the voltage-gated Ca+2 channels with Ca+2 influx,
Ca+2 enter through these channels prolong depolarization of the membrane.
 Phase 3 (rapid repolarization): final repolarization is due to opening
of the voltage-gated K+ channels at zero voltage with rapid K+ outflow
(K+ efflux) followed the closure of Ca+2 channels and, this restores the
membrane to its resting potential.
 Phase 4 (complete repolarization): The membrane potential goes
back to the resting level (-90 mV) i.e., restoration of the resting potential.
This is achieved by the Na+-K+pump that works to move the excess K+ in
and the excess Na+ out.
 c) Function of
pacemaker centers.
Some other
regions of the heart,
including the area
around SA-node and the atrio-ventricular bundle can potentially produce
pacemaker potentials. The rate of spontaneous depolarization of these cells
however is slower, than that of SA-node.
As it determined SA-node produce 60-90 impulses per minute, AV-
node - 40-50, bundle of His - 20-30 and Purkinje fibers 10-20 impulses per
minute. The potential pacemaker cells are stimulated by action potential
from SA-node before they can stimulate themselves through their own
pacemaker potentials. If action potentials from the SA-node are prevented
from reaching these areas (through blockade of conduction), they will
generate pacemaker potentials at their own rate and save as sites for the
origin of action as pacemakers.
A pacemaker other than SA-node is called as ectopic pacemaker or
ectopic focus.
If the heart of a frog is removed from the body, and put in
physiological solution, it will still continue to beat as long as the myocardial
cells remained alive.
At a result of experiments with isolated myocardial cells and clinical
experience with patients who have specific heart disorders, many regions
within the heart have been shown to be capable of originating action
potentials and functioning as pacemakers.
In a normal heart, however, only one region demonstrates spontaneous
electrical activity and by this means functions as a pacemaker - SA-node.
 3. Conductibility of the heart
a) Conduction of impulses in atria. After excitation of SA-node
impulses conduct by bundle of Thorel, Venkenbuh and Buhman to AV-node.

Action potentials from SA-node spread at a rate of 0,8-1,0 m/s across

the myocardial cells of both atria. At first the right atrium is excited and left
is the second.
b) Peculiarities of conduction through AV-node. The conduction
rate slows considerably as the impulse passes into the AV-node. Slow
conduction of impulses (0,03-0,05 m/s) through the AV-node is caused by
special form of AV-node and peculiarities of impulse development in cells
of AV-node, as absence of rapid diffusion of ions. Slow conduction in AV-
node is necessary for proper order of contracting atria and ventricles.
c) Excitation of ventricles. After the impulses spread through the
AV-node, the conduction rate increases in the atrio-ventricular bundle and
reaches 5 m/s in the Purkinje fibers. As a result of this rapid conduction of
impulses, ventricular contraction begins 0,1-0,2 s after the contraction of
atria.
High velocity of impulses in ventricles is caused by rapid Na+-gates.
At first middle part of septum is excited, than impulses spread to apex
of heart, than to the right ventricle wall, to the left ventricle wall and to basal
parts of ventricles myocardium.
4. Excitability of heart
a) Excitability changing during excitation.
Once contractive myocardial cell has been stimulated by action potentials
origin in SA-node, it produces its own action potentials. The majority of
myocardial cells have resting membrane potentials of about -90 mV. When
stimulated by action potentials from a pacemaker region these cells become
depolarized to threshold. At this point their voltage - regulated Na+-gates
open.
The upshot phase of the action potential of no pacemaker cells is due
to the inward diffusion of Na+. This period called depolarization.
Following the rapid reversal of the membrane polarity, the membrane
potential quickly declines to about -15 mV. Opening K+ and Cl- gates and
inward diffusion of K+ and Cl- causes it. This period called quickly initial
repolarization.
 Then this level potential maintained for 200-300 ms and cells plato
phase. It's due to opening of slow Ca2+ gates. Gradually slow Ca2+ diffusion
stops and than diffusion of K+ increases. Rapid repolarization at the end of
the plato is achieved by rapid outward diffusion of K +. During last phase of
rest initial distribution of ions inwards and outwards is recovered by function
of the sodium-potassium pumps. The heart normally cannot be stimulated
until after it has relaxed from its previous contraction because myocardial
cells have long refractory periods. It corresponds to the long duration of their
action potentials. Summation of contractions is thus prevented and
myocardium must relax after each contraction. The rhythmic pumping action
of the heart is thus ensured.
Refractory period:
 Absolute refractory period (ARP), it is the interval during which
no action
potential can be produced, regardless of the stimulus intensity i.e., no
stimulus however strong, can produce a propagated action potential. It lasts
the upstroke plus plateau and initial repolarization till mid-repolarization at
about -50 to -60 mV. It means that the cardiac muscle can not be exited
during the whole period of systole and early part of diastole.This period
prevents waves summation and tetanus.
 Relative refractory period (RRP), it is the interval during which a
second
action potential can be produced but at higher stimulus intensity i.e., the heart
responds only to stronger stimuli. It lasts from the end of ARP
(midrepolarization) and ends shortly before complete repolarization i.e., it
lasts for a short period during diastole.

b) Excitability of the heart and skeletal muscles. Electrical impulses

that originate at any point of myocardium can spread to all cells, according
to ruler "all or nothing". Because all cells in myocardium are electrically
joined a myocardium behaves as a single functional unit. Unlike it, in skeletal
muscle contraction depends on number of excited neurons, which stimulate
 motor unit. Unlike skeletal muscles, cardiac muscle capable to produce
action potentials by pacemaker cells. The rate of heartbeat is regulated by
autonomic nervous system. In difference, skeletal muscles are regulated by
somatic nervous system.
5. Contractibility of the heart
a) Mechanism of contraction and relaxing of the heart muscle.
Like skeletal muscle cells, cardiac muscle cells are striated. They
contain actin and myosin filaments arranged in the form of sarcomeres. They
contract by means of the sliding filament mechanism. Myocardial cells are
short, branched and interconnected. Gap junctions join adjacent myocardial
cells. That is why a myocardium contracts to its full extent each time and all
of its cells contribute to the contraction. After opening Ca 2+- gates
contraction begins. The mechanism of contraction is similar to skeletal
muscles. Sliding on thin filaments they produce shortening of the
sarcomeres. In the process of contraction, the thin filaments slide deeper and
deeper toward the center, producing increasing amounts of overlap with
thick filaments. Sliding of the filaments is produced by the action of
numerous cross brigs that extend out from the myosin toward the action.
Before the cross brigs combine with actin the globular head function as
myosin ATP-ase enzymes. Then cross brigs combine with actin and can
attach to actin.

VIDEO
6. Mechanism of contraction and relaxing of the heart muscle.

b) Contractibility cardiac and skeletal muscles:

Contractility is the ability of the cardiac muscle to contract.
The effect of various factors on contractility is called inotropism; a
positive (+ve) inotropic effect means an increase in myocardial contractility,
whereas a negative (-ve) inotropic effect means a decrease in myocardial
contractility.
 - In skeletal muscles long fibrose cells are separated from each other
functionally and structurally. But myocardial cells are short, branched and
interconnected by gap junctions.
- Skeletal muscle produce contractions, which are graded depending
on the number of cells stimulated. But a myocardium contracts as a single
functional unit.
- Skeletal muscles require external stimulation by somatic motor
nerves before they can produce action potentials and contract. But cardiac
muscle is able to produce action potentials automaticity.
- Skeletal muscle capable to summation of contraction, but myocardial
muscle pumps the blood by rhythmic contractions.
Excitation-Contraction coupling in the heart muscle:
As in skeletal muscles, the depolarization wave reaching via the T
tubules causes the opening of Ca+2 channels in the sarcoplasmic reticulum
adjacent to the T-tubules. The released Ca+2 from the cisternae of the
sarcoplasmic reticulum (activator Ca+2; aCa+2) binds to troponin C, leading
to cross bridge formation between actin and myosin, which results in
contraction.
In cardiac muscle, the amount of this activator Ca +2 is often
insufficient to initiate contraction, but it can be increased indirectly by the
following mechanism:
The depolarization wave in the T-tubules opens the long-lasting Ca+2 chann-
els in the T-tubule membrane, and sarcolemma, Ca+2 diffuses from the ECF
through these channels into the cardiac muscle fibre cell causing a small
increase in the cytosolic (fluid of the cytoplasm) calcium concentration in
the region of the T-tubules and adjacent sarcoplasmic reticulum. This Ca+2 is
called depolarizing Ca+2, and although its amount is normally very small, yet
it is important because it acts as a signal for the release of large amount of
activator Ca+2 from the cisternae of sarcoplasmic reticulum, it is mainly this
cytosolic Ca+2 that causes the contraction, i.e. once Ca+2 is in the cytoplasm,
it binds to troponin and stimulates contraction. As a result, myocardial cells
contract when they are depolarized. The force of contraction is directly
proportional to the amount of cytosolic Ca+2.
Contraction ends when the cytosolic Ca+2 concentration restored to its
original level. In other words, relaxation of the cardiac muscle occurs as a
result of release of the actin-myosin combination, this is achieved by
decreasing the intracellular Ca+2 to its pre- contraction level, which occurs
by:
1- Active re uptake of Ca+2 into the sarcoplasmic reticulum by Ca+2 pump
(primary active transport of Ca+2).
2- Active pumping of excess Ca+2 outside the fibres by Na+- Ca+2 exchanger
carrier protein (secondary active transport ; counter transport).

The heart normally cannot be stimulated again until after it has relaxed from
its previous contraction because myocardial cells have long refractory
periods that correspond the long duration of their action potentials.
Summation of contractions and tetanus are thus prevented, and the
myocardium must relax at each contraction to ensure the rhythmic pumping
action of the heart.
FORMATION OF NORMAL ELECTROCARDIOGRAM
1. Electrogram and action potential of one myocardial cell.
An electrocardiograph is an instrument that measures and records the
electrocardiogram (ECG), the electrical activity generated by the heart.
Electrodes placed on various anatomical sites on the body help conduct the
ECG to the electrocardiograph. The ECG alone is not sufficient to diagnose
all abnormalities possible in the pacing or conduction system of the heart.
The interpretation of the 12-lead ECG provides a differential diagnosis for
many arrhythmias
During the depolarization phase the rapid Na+ gates open and inward
diffusion of Na+ occur. This event corresponds to formation upward part of
positive wave on electro gram line. The next fast initial repolarization begins
with inward Cl- diffusion. Then electro gram returns to baseline level. When
opening slow Ca2+ gates the potential difference temporarily isn’t essential
and baseline continues. During the next phase outward K+ diffusion
increases and external surface of membrane becomes positive. Voltage
fluctuation leads to deflection of electro gram downward further returning to
baseline level. In rest period all the membrane has positive charge on
external surface and baseline is recorded. Through this period ion pumps
restore initial distribution of ions.

2. Formation of EEG waves

Unexcited part of cell has already positive charge. Depolarized part
has already negative charge. Between positive and negative charges the
electrical power is recorded. Electrical power directs towards positive
voltage. When changing polarity, electrical power of entire heart has
different volume and direction in every moment of cardiac cycle.
 To understand formation of ECG waves in different leads it is
necessary to remember some rulers of this process:
- When electrical power directs towards positive pole of lead the
upward wave is recorded;
- When electrical power directs towards negative lead pole, the
downward wave occurs;
- If electrical power directs perpendicular to lead axis the baseline is
recorded.

3. ECG as a representation of heart depolarization

Every cardiac cycle produces ECG waves designated as P, Q, R, S and T.
These waves are not action potentials. They represent potentials between
rested and depolarized or depolarized and repolarized parts of whole heart.
Amplitude and duration of these waves correspond to electrical power
fluctuation in entire heart.
After producing impulse in SA-node depolarization begins at first in
cells of right atrium and ascend part of P wave is recorded. When
depolarization spreads into left atrium, the ECG line returns to baseline level.
Delay of depolarization in AV-node recorded as PQ-interval in baseline.
Then impulse spreads into middle part of septum and heart apex. This event
recorded as descend part of Q wave. In next depolarization of right ventricle
wall ECG line deflexed upward and formation of R wave begins. When
impulse spreads into left ventricle wall, the ECG line returned in contrary
side towards the lowest point of S wave. Depolarization of ventricles basis
afterwards caused formation of S wave, which continues to baseline.

Repolarization of atria is failed to record in ECG because of greater

depolarization of ventricles. Repolarization of ventricles develops firstly in
right part of heart and then in left one. That is why ascend and descend parts
of T wave are formed.
In diastole normally baseline is recorded but U wave may occur.

ELECTROCARDIOGRAPHY AS A METHOD OF OBSERVATION

 1. ECG leads:
The electrical current generated by the heart is conducted through the
pairs of electrodes and leads, and is amplified, recorded, and processed by
the electrocardiograph. The wires connecting the pairs of electrodes on the
surface of the body to the electrocardiograph are called leads. The different
features and modules of a typical electrocardiograph include the protection
circuitry, lead selector, calibration signal, preamplifier, isolation circuit,
driver amplifier, memory system, microcomputer, and recorder or printer.
Twelve leads usually comprise a diagnostic ECG recording: six limb
leads (three bipolar and three unipolar), and six unipolar precordial leads.
The instantaneous cardiac scalar voltages resulting from the electrical
activity in the heart is measured in each of the 12 leads. Since the cardiac
vector varies in magnitude with time over a three-dimensional space, it is
important to know its presentation (i.e. appearance or projection) in each of
the 12 leads of the ECG.
a) Bipolar limb leads.
The bipolar limb leads record the voltage between electrodes placed
on the wrists and legs. These leads were proposed by Einthoven in 1913.
I lead: left arm (+) - right arm (-);
II lead: left leg (+) - right arm (-);
III lead: left arm (+) - left leg (-).
For recording limb leads we put red electrode on right arm, yellow –
on left arm, green – on left leg and black – on right leg. Black electrode has
zero potential (ground).

b) The unipolar () limb leads were proposed by Goldberger in

1942. They record voltage between single “exploratory electrode” fro one
limb and zero joined electrode from two other limbs. So there are three leads
AVR, AVL, AVF. In fact zero electrodes records middle voltage of two
limbs. Bipolar limb leads and unipolar limb leads record electrical power in
frontal projection.

c) The unipolar chest leads were suggested in 1934 by Vilson. One

electrode, which is active, situated on the chest in six standard positions.
They labeled V1 - V6. Joined zero electrode records middle potential of right
arm, left arm and left leg. That is why every chest lead records voltage
between active chest electrode and Vilson’s joined zero electrode.
These standard positions of active chest electrode are:
 V1 - in crossing right IV right intercostal space and parasternal line;
V2 - in crossing left IV intercostal space and parasternal line;
V3 - between V2 and V4;
V4 - in crossing V left intercostal space and medioclavicular line;
V5 - in crossing V left intercostal space and anterior axilar line;
V6 - in crossing V left intercostal space and middle axilar line.
Unipolar chest leads records changes of heart polarity in horizontal
projection.

2. Algorithm of ECG registration:

Registration performs fare from electric motors and other electrical
devices.
Tested person may have rest before registration in 10-15 minutes. This
procedure needs 2-hour interval after eating or worm procedures.
For better contact between electrodes and skin use solution NaCl 5-10
% or special electrode past or electrode gel. Otherwise hindrances in ECG
curve may occur. They will stand in the way of ECG analysis

ECG registration performs in quiet breathing in patients.

Registration begins from standard voltage 1 mV from the
electrocardiograph for regulation of amplitude in ECG. Usually standard
voltage amplitude is 10 mm. Then continue registration of bipolar limb
leads, the next - unipolar limb leads and afterwards - unipolar chest leads.

3. ECG analysis:
In order to interpret the 12-lead ECG and use it to diagnose abnormalities,
it is important to know the normal characteristics of the ECG, and
understand the mechanisms underlying the generation of each segment of
the ECG. Figure 1 shows the various fiducial points in the ECG, and
typical values of the various intervals measured from the ECG.

Fig. 1. - Points various and intervals in the ECG

The main elements of ECG curve are:

- Waves P, Q, R, S and T. Sometimes U wave may occur;
- Segments - P-Q (from the end of P wave to beginning of Q wave),
S-T (from the end of S wave until beginning of T wave);
 - Intervals, which characterize certain time period of heart activity -
P-Q (from the beginning of P wave to beginning of Q wave), Q-T (from
beginning of Q wave to end of T wave);
- Complexes - atrial, which is presented by P wave, and ventricular -
QRST.
a) P wave in healthy persons, is obligatory positive in I, II, AVF, V2-
V6 leads. P wave may be negative in III, AVL and V1, either positive or
biphasic. If it is diphasic, then the negative component comes after the
positive component and is not excessively broad or deep. An absent P wave
in the ECG may signify sinoatrial block, an abnormality in which the impulse
from the SA node is not conducted to the AV node. Normally in II lead its
amplitude is 2,5 mm, duration – 0,1 s (not greater than 110 ms).
The P wave is caused by atrial depolarization. The normal shape of the
P wave does not include any notches or peaks.
b) P-Q interval reflects duration of AV-conduction, which is
spreading of potential by AV node, His bundle and its branches. This interval
lasts 0.12-0.20 s and depends on heartbeat rate.
c) QRST complex reflects spreading of excitation by ventricles. It
hole amplitude is higher 5 mm of the waves are signed by capital letters.
Otherwise it used little letters. ORS duration in II lead is not more than 0.1
s.
d) Q wave normally in II lead is less then 1/4 of R amplitude duration
is 0.03 s. Normally in AVR deep and wide Q waves may be recorded. In V1,
V2 - Q wave is particularly absent.
e) R-wave usually is recorded in all leads; exalt AVR, which may be
absent. In unipolar chest leads R amplitude gradually increases from V 1 to
V4 and some decreases in V5 and V6. So normally in unipolar chest leads
both increasing R-amplitude and S-amplitude occurs. S-wave has amplitude
not more than 20 mm, but it varies from lead to lead.

j) S-T-segment corresponds to excitation of both ventricles. Normally

in bipolar and unipolar leads it lies on baseline and don’t move more than 0.5
mm. In V1-V3 deviation upward to 2 mm may occur.
h) T-wave normally is positive in I, II AVF, V2-V6, TI>TIII, TV6>TV1.
T-wave has sloping ascend part and sleep descending part. In III, AVL, V1 T-
wave may either be positive, negative or bipolar. In II lead T-amplitude is 5-
6 mm, duration – 0.16-0.24 s.
i) Q-T interval is electrical systole of ventricles. Its duration directly
depends on heartbeat rate. Proper duration may calculated by Buzett
formula:h0
Q-T=K√¯R-R¯, where
K=0.37 in male or 0,40 in female
f) U-wave may be recorded in unipolar chest leads, which reflects
excitation fare of excitability after electrical systole of ventricles
myocardium. U-wave usually is positive and small.

4. ECG analysis begins with estimation of control voltage and

paper speed. Another analysis at usual performs in this order.
1) Determining of impulse origin. Pay attention to proper order of
waves in ECG. If P wave in II lead is positive and recorded before QRS
complex is believed to determine pacemaker in SA node.
2) Heart rhythm evaluation by measuring of R-R duration. Normally
adjacent R-R intervals duration may differ from each other not more 0.1 s.
Usually II lead is examined.
3) Determining of heart rate. In proper rhythm 60 s is divided to R-R
duration in seconds, which is calculated using paper speed.
4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R
wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG
voltage is decreased. Otherwise it is normal.
5) EMP direction determining.
- Visual method: needs measuring R amplitude in all bipolar limb
leads. If true, that RII>RI>RIII, the EMP direction is near 30º-69º, that is
normal;
- Graphic method use Baily co-ordinate. If in Einthoven’s triangle put
through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than
in any two bipolar limbs leads it is necessary to determine summary
amplitude of QRS waves. Upward waves have positive meaning and
downward are negative. Summary amplitude put on corresponding axis with
(+) or (-) sign. In this point lined perpendicular to lead axis. Next time
determined cross point of two drown perpendiculars. When join this point to
Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.
6) ECG elements analysis. Pay attention to form, amplitude and
duration of waves and intervals. Measure deviation from baseline if it occurs.
Compare the results with normal rate.

5. Investigation of conductive system in the heart

After distraction brain in spinal cord by probe enter to thoracic cavity.
Calculate rate of heartbeat in intact heart. Put the first Stannius’s ligature and
calculate heartbeat upper and lover this one. Also put the II and III ligature.
Every case calculate rate of heartbeat for venous sinus, atria and ventricles.
In the conclusion note would the automaticity gradient is characteristic
for heart of frog. Describe, what is automaticity gradient.
6. ECG registration
Registration performs fare from electric motors and other electrical
devices.
Tested person may have rest before registration in 10-15 minutes. This
procedure needs 2-hour interval after eating or worm procedures.
VIDEO ECG 1
For better contact between electrodes and skin use pieces of bandage,
wet by solution NaCl 5-10 % or special electrode past or electrode gel.
Otherwise hindrances in ECG curve may occur. They will stand in the way
of ECG analysis
ECG registration performs in quiet breathing in patients.
Registration begins from standard voltage 1 mV from the
electrocardiograph for regulation of amplitude in ECG. Usually standard
voltage amplitude is 10 mm. Then continue registration of bipolar limb
leads, the next - unipolar limb leads and afterwards - unipolar chest leads.
 Video ECG 2

Relationship of the ECG to the cardiac cycle (Timing):

The ECG (electrocardiogram) shows the P, QRS and T waves. They are
electrical voltages generated by the heart and recorded by the ECG:
 P-wave is caused by atrial depolarization; this is followed by atrial
contraction, which causes a slight rise in the atrial pressure curve after the P
wave.
 About 0.16 second after the onset of the P wave, the QRS
waves appear as a
result of electrical depolarization of the ventricles, which initiates
contraction of the ventricles and causes the ventricular pressure to begin
rising, as shown in the figure. Therefore, the QRS complex begins slightly
before the onset of ventricular systole.
 T-wave represents ventricular repolarization at which the ventricles
begin to
relax. Therefore, the T wave occurs slightly before the end of ventricular
contraction.

Relationship of the Heart Sounds to Heart Pumping

When listening to the heart with a stethoscope, one does not hear the opening
of the valves because this is a relatively slow process that normally makes
no noise. However, when the valves close, the cusps of the valves and the
surrounding blood vibrate under the influence of sudden pressure changes,
giving off sound that travels in all directions through the chest.
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 heart sound. 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 heart sound.

2. PUMPING WORK OF THE HEART

1. Listening ( auscultation ) of heart tones .
Listening of Heart allows you to get an impression about the
symptoms of sounds that occurs in it. Auscultation of the heart need to follow
a number of rules that increase the efficiency of the method:
1) need to listen to the heart in two positions – standing and supine
(sometimes on the left side );
2) cardiac auscultation can be performed without breath-holding , with
quiet breathing (if needed clarifying a number of points you can hear in
breath-hold , at an inches of inhalation or exhalation in height);
3) Auscultation need to keep silence in the room, should be warm, in
the presence of hair on body it's necessary to moisten with water;
4) follow a certain sequence of auscultation of the heart.
Indirect and direct auscultation of the heart. The most profitable and
common way of listening to the heart is mediated by auscultation with a
stethoscope or phonendoscope, because it permits to select the sound effects
from various points of the heart, which is especially important due to their
proximity to one another. However, some sound effects from the heart (III
physiological heart sound, gallop rhythm ) better to listen directly to the ear,
so in some cases it is necessary to use both indirect and direct auscultation.
You must pay attention to the advisability of using one and the same
stethoscope.
Places of auscultation of the heart not always coincide with the
projection of the valve seats on the front chest wall.
2.. The projection of the heart valves on the front chest wall.
The projection of the mitral valve – is on the left of the chest in the
area of attachment of the third rib, tricuspid valve – on the sternum, in the
middle of the distance between the place of attachment to the sternum
cartilage of the third rib (from the left side) and cartilage of 5 rib (from the
right side). Valve of pulmonary trunk is projected in the second intercostal
space on the left part of chest , aortic valve – in the middle of the sternum
at the level of the third costal cartilage. Perception of sounds, that occur in
the heart depends on the proximity of the projections valves, which appear
sound vibrations, from conduction of these fluctuations in blood flow, from
adjacent to the chest of the heart, in which these fluctuations are formed. This
allows you to find specific areas on the chest, where the best auscultated
sound phenomena associated with the activities of each valve.
In the heart there are sound effects , called heart tones.

During the heart activity there are sound effects, called cardiac tones.
Movement of heart structures in heart contraction produces heart
sounds. First heart sound occurs at beginning of systole, mainly due to
closure of AV valves. Second heart sound occurs at the end of systole,
mainly due to closure of semi lunar valves. Third heart sound occurs at
beginning of middle third diastole is produced by oscillation of blood back
and forth between walls of ventricles initiated by inrushing blood from atria.
Fourth heart sound occurs when atria contracts. First and second heart sounds
can head by ear. Abnormal heart sounds are known as heart murmurs.
Functional murmurs appear because of insufficient function of heart valves.
To listen first and second heart sounds a stethoscope or
phonendoscope should be used . Consistently one of the devices attached to
the place of listening of heart tones .In the V-th left intercostal space at 1-1,5
cm from midclavicular line to the sternum (part of the apical impulse ) you
can listen the first tone of the left half of the heart, in the II th intercostal
space on the right and left of the sternum the II sound can be listened.

Video

The first tone of the right half of the heart listened at the site of
attachment to the sternum xiphoid process, the second tone of the right half
of the heart - in the II th intercostal space to the left of the sternum.
Auscultation of heart tones involves choice of the best listening position
, detection of relationship with the apical impulse and the carotid pulse ,
and compare their duration

Sound file ( Cardiac normal)

Auscultation of the heart takes place in the following order:

1). At first listen to mitral valve on top of the heart ( first point )
2). Followed by aortic valve - in the second intercostal space on the
right of the sternum (second point)
3). Pulmonary valve stem in the second intercostal space on the left of
the sternum ( the third point )
4). Tricuspid valve base near the sternum (xiphoid process) (the fourth
point)
5) And again the aortic valve in the point of Botkin -Erb ( fifth point).
If you notice any changes in these areas, should carefully listen all area
of the heart. This is the main point of auscultation of the heart.

3. Cardiohaemodynamic :
a) physiological analysis of the cardiac cycle ;
Cardiac cycle - the period from the beginning of one heartbeat to the
next heartbeat. It consists of systole and diastole.
1. Cardiac cycle
a) Functional analysis
Period fro end of one heart contraction to end of next, is called cardiac
cycle. There are two phases – systole and diastole.
Systole, when heart contracts.
Diastole, when heart dilates.
Diastole can be divided into:
- Period of isometric relaxation, during which ventricles begin to relax
and pulmonary valves close;
- Period of rapid filling of ventricles, when AV valves open;
- Atria systole, when atria contract and pump 20-30 % blood into
ventricles.
Systole is composed by:
- Period of isometric contraction, when ventricles begin to contract and
AV valves are closed;
 - Period of ejection: during rapid ejection 70 % empting occur and in
slow ejection last 30 % empting occur;

Protodiastole.
b) Intra cardiac pressure

During period of isometric relaxation intra ventricular pressure falls. In

period of rapid filling of ventricles atria pressure becomes grater than intra
ventricular pressure. In atria systole pressure in right atrium rises to 4-6
mm Hg, in left atrium - 7-8 mm Hg.
Systole begins. In period of isometric contraction ventricular pressure
rises. In period of ejection left ventricular pressure rises to 125 mm Hg and
right ventricular pressure to25 mm Hg. In protodiastole ventricular pressure
falls, below aortic and pulmonary pressure.
c) Cardiac volumes
During period of isometric relaxation ventricular volume does not
change. During rapid filling of ventricles period blood flows rapidly into
respective ventricles. In atria systole ventricle volume increases on 20-30 %.
Systole begins. In period of isometric contraction there is no volume change.
In period of ejection stroke volume output occur. In protodiastole blood
flows into aorta and pulmonary trunk, due to momentum.
4. Physiological analysis of cardiac output
Also, when considering the cardiac cycle using the terms " time ", "
phase " and " interval" . The term "period" represent milestones systole and
diastole. The term " phase " is used to refer to parts of the period. The term
" interval" are characterized by the so-called transitional mizhfazovi states.
Stroke work output is the amount of blood that left ventricle pump to
aorta during each cardiac cycle.
Volume of blood on each ventricle at end of diastole is called end-
diastolic volume and measures 120-140 ml.
Volume of blood in the each ventricle at end of systole is called end
systolic volume and measures 50-60 ml.
Blood volume, which heart pumps per minute called as minute blood
volume. It may be calculated by multiply stroke volume to rate of heartbeat
and normally equal to 4-6,5 l/min. In physical exercises it rises to 10 l/min
and more.
 3. Characteristics heart tones:
a) the first tone ;
The first tone be heard as a short , fairly intense sound over the heart ,
but he is best expressed in the apex region of the heart. March 1 ton of cardiac
systole begins .
In the formation of tone and lead a valve component that was first
experimentally demonstrated prominent Moscow physician
O.A.Ostroumovym .
It is caused by fluctuations wings atrioventricular valves and
tendinous strands in the phase of isometric contraction.
The second component - muscle - resulting from fluctuations
associated with ventricular myocardial strain during isometric contraction.
The third component - Vascular - fluctuations in the initial sections of
the aorta and pulmonary artery, venous valves in the opening phase of rapid
expulsion.
The fourth component - atrial - arises from fluctuations associated
with atrial contraction . Auscultation of the first tone starts with this
component as fluctuations caused by atrial systole merge with the sound
vibrations caused by ventricular systole and auscultatory perceived as a tone.
b) the second tone ;
The second tone optimally be heard in the second intercostal space on
the left ( of the pulmonary artery ) and the right ( the aorta ) from the sternum
during diastole .
Formed by fluctuations occurring in early diastole at the close of
venous valves of the aorta and pulmonary artery blood flow , which hits the
them. This is the first valve component.
The second component - due to fluctuations in vascular walls of the
aorta and pulmonary artery.
c) The third and fourth tones ;
ÚTretiy tone you can hear sometimes in children or in patients with a
thin chest .
ÚVin due to rapid filling of the ventricles with blood during the phase
of rapid filling.
Normal third tone described VPObraztsov that recommended for its
detection using direct listening .
Tons of healthy heart is easily distinguished. VPObraztsov wrote:
"The first of them relative to the other low, long, dull, and the second relative
to the first tall, short, clear. The first sound coincides with the beginning of
systole of the heart, and the second - to the end of systole and early diastole
."
Change of heart tones . At various physiological and pathological
conditions may occur strengthening or weakening of the sonority of one or
two colors, change their timbre, duration, splitting or split, any additional
colors.
Easing I and II tones
Under physiological conditions, there may be a strengthening or
weakening of the volume of the first tone. Strengthening the ringing tone
may occur in people with thin chest wall, exertion, nervous excitement,
forward inclination of the trunk . Reducing the volume of the first tone is
associated with thickening of the chest wall due to delay significant amount
of adipose tissue, development of severe chest muscles.
In addition to changing the volume psrshoho tone may experience a
physiologically split ( instead of one heart sound listen two consecutive short
tones).
Bifurcation and splitting tones the heart. Often, instead of a single I or
II t listen two sounds of identical strength from barely noticeable gap
between them. Depending on the size of the interval distinguish splitting and
splitting and if the second heart sound . Then instead of sound "and" we hear
the sound of " May ". The difference between splitting and split a quantitative
and separation of these two phenomena to some extent due to the experience
and subjective sense of doctor.
Bifurcation and second tone can be both physiological and
pathological . Physiological split tone is more common in young people , it
is associated with the act of breathing or physical activity and is changeable
. Most often it is caused by asynchronous ventricular activity , namely delay
completion of right ventricular systole .
Bifurcation and tone depends on the non-simultaneous closing of two-
and tricuspid valves. In physiological conditions, this phenomenon can
sometimes occur during exhalation when, due to increased pressure in the
chest , blood with great force enters the left atrium and thus slows the closure
of the mitral valve. This leads to the fact that the sound effects of the
atrioventricular valves are perceived as a single tone.
d) functional murmurs.
They arise due to violation laminarnosti blood flow in the cavities of
the heart and blood vessels . These noises can listen to or between the first
and second tones, ie during the systolic pause , or between the second and
following the first tone, ie during the diastolic pause. In the first case, the
noise is called systolic and the second - diastolic .
Heart murmurs are also divided into functional and organic.
Functional heart murmurs occur when you change the aspect ratio of
the cavities of the heart and valve openings to the formation of the so-called
relative stenosis or insufficiency of valves. There is in childhood and young
age. Also functional murmurs occur in intact heart due to acceleration of
blood flow , reducing its density anemia , changes in papillary muscle tone .
Organic noises occur in the presence of anatomic changes in the heart
(change whole heart valves or holes ) or vessels that depart from the heart (
in the aorta or pulmonary artery).
By the time of occurrence of noise during systole or diastole
distinguish between systolic and diastolic murmurs. Systolic noise occurs
when the blood during systole , moving from one department to another heart
or the heart of a large vessel encounters an obstacle .
Systolic noise be heard at the mouth of aortic stenosis or pulmonary
trunk , as in these defects during the expulsion of blood from the ventricles
into the path of blood flow vasoconstriction occurs ( systolic murmur exile
). Systolic noise and listen for failure of mitral and tricuspid valves. Its origin
is explained by the fact that during ventricular systole blood goes only into
the aorta and pulmonary trunk, but back to the atrium through the
atrioventricular not completely closed hole, ie through a narrow slit (
regurgitant systolic murmur ).
Systolic noise appears along with the first tone during short breaks
hearts, it coincides with the apical impulse and the carotid pulse .
Diastolic murmur appears in those cases where there is narrowing of
the left or right atrioventricular opening, inasmuch as in these defects during
diastole is narrowing towards the flow of blood from the atria to the
ventricles . There is a diastolic murmur and with aortic valve insufficiency ,
pulmonary trunk - due to reverse flow of blood vessels in the ventricles
through the gap formed by the incomplete closing of shutters modified valve.
Diastolic murmur occurs after the second tone during long breaks your
heart. There are three types of diastolic noise : 1) protodiastolichnyy that
occurs in early diastole , immediately after the second tone , 2)
mezodiastolichnyy that occurs in diastole , 3) presistolic that appears at the
end of diastole.
 Functional murmurs of extremely rare exception is the systolic and
frequently listened over the pulmonary artery. This is due to the fact that in
children the difference between right ventricular lumen and lumen
pulmonary artery is larger than the corresponding difference between the left
ventricle and the aorta. Also pulmonary artery in children is easily
compressed with a deep exhalation due to increased intrathoracic pressure.
Functional murmurs differ significantly instability : they then appear ,
then disappear , originating in one body position of the subject , they can
disappear in a second. Their appearance is associated with mental
stimulation , or with physical activity. With a deep breath they either
drastically weakens or completely disappear at the end of the same breath ,
however, appear or increase .
3. NEURO-HUMERAL REGULATION OF THE HEART

NERVE REGULATION OF HEART ACTIVITY

1. Influence of central nervous system
Conditioned-reflex regulation of the heart.
The fact, that different emotions cause changes in cardiac activity,
indicating the importance of the cerebral cortex in the regulation of the heart
. Proof of this is that changes in rhythm and force of heart contractions. It
can be observed in humans at the mere mention or recollection of the factors
that cause it certain emotions.
The most convincing data on the presence of cortical regulation of the
heart obtained experimentally by the method of conditioned reflexes. If any
such sound , combining multiple stimulus by pressing on the eyeballs , which
causes a decrease in heart rate, then it is a stimulus that causes a decrease in
cardiac activity - conditioned eye- heart reflex.
Conditioned reflex’ reactions underlying the phenomena that
characterize the so-called pre-start condition athletes. Before the race they
observed changes in respiration, metabolism, cardiac activity of the same
nature , as well as during the actual race. As skaters at the start heart rate
increases by 22-35 contractions per minute.
The bark of the brain provides an adaptive response not only to the
current , but also to future events. On the mechanism of conditioned reflexes
signals go ahead occurrence of these events or substantial likelihood of their
occurrence , can cause adjustment functions of the heart and the entire
cardiovascular system in so far as this is necessary to ensure that future
activities of the body.
 In extremely difficult situations (action "emergency stimulus " according
to Pavlov ) possible violations and failures of higher cortical regulatory
mechanisms (neurosis in Pavlov). This, along with the disorder behavioral
responses (and neurotic changes in psychological status of a person) may be
significant disturbance of the heart and cardiovascular system. In some cases,
these disorders can be fixed by the type of pathological conditioned reflexes.
It cardiac abnormalities may occur under the influence of mere conventional
signals.
The activity of the heart is regulated by two centers present in the
medulla oblongata.
1) Cardiac Inhibitory centre, which is connected with the vagus nerve
i.e. parasympathetic nervous system: C.I.C. It is a part of the dorsal nucleus
of vagus, the axons of their neurons leave the medulla as preganglionic
fibers. They relay in terminal ganglia present in the heart.
2) Cardiac accelerator (activation) centre, which is connected with the
sympathetic nervous system: CAC. It lies near the inhibitory center, the
axon of their neurons descend in the white matter of the spinal cord and
synapse in lateral horn cells (L.H.C) of upper 5 thoracic segment.
Preganglionic fibers arise from L.H.C and relay in the three cervical
sympathetic ganglia. Postganglionic fibers pass from these ganglia to supply
the whole heart.

These two centers receive impulses from the following sites:

a). Afferent impulses from the higher centers:
1). Cerebral cortex: Cerebral cortex affects HR as in the following
conditions:
Conditioned reflexes; in certain conditions; seeing, hearing or smelling lead
to  in HR e.g. seeing the examiner or hearing about the exam leads to  HR.
Voluntary; yoga players can increase or decrease their HR voluntarily.
Emotions: Most types of emotions ( fear, anger anxiety etc) leads to  HR.
Sudden unexpected news leads to HR or may stop the heart.
2). Hypothalamus:
- Stimulation of anterior nuclei (which control the parasympathetic activity)
leads to  HR as in quite sleep, and severe emotions ( sudden unexpected
news).
- Stimulation of posterior nuclei (which control the sympathetic activity)
leads to  HR as in mild emotions and stress, and muscular exercise.
b). Afferent impulses from the circulatory system:
 1). Afferent from the venous side (Rt. Side of the heart):
Bainbridge reflex:  venous pressure caused by  venous return
(VR) in the right atrium leads to HR.  VR stimulates stretch receptors
present in the wall of the tight atrium. These receptors send impulses along
vagus nerve to the medulla causing stimulation of CAC and inhibition of
CIC. CAC sends efferent impulses through sympathetic fibers to the SAN
causing  HR.
Some authors believe that the increase in HR results from stretch of the SAN
leading to  rate of discharge from it. So, it is a local effect and not a true
nervous reflex.
Significance: The increased HR pumps the excess VR to the arterial side
and prevents stagnation of blood in veins.
Mc Dowel's reflex:  VR (or  pressure in right atrium) as in
haemorrhage leads to reflex  HR and V.C of arterioles.
Significance: During haemorrhage the increased HR and VC help to raise
ABP and maintain circulation to the vital organs (brain, heart kidneys and
liver).
2). Afferent impulses from arterial side (carotid sinus and aortic
arch):
Mary's law: The HR is inversely proportional to the arterial blood
pressure provided that other factors affecting HR remain constant.
 ABP  HR ,  ABP  HR
Mechanism:  ABP stimulates baroreceptors present in carotid sinus and
Aortic arch from which afferent impulses pass through sinus nerve and aortic
nerve. These impulses cause stimulation of CIC leading to  HR.  ABP as
in haemorrhage reduce the inhibitory impulses from the baroreceptors
leading to  HR.
Significance: These reflex buffers the excessive changes in ABP. In case
of  ABP, the decreased HR helps to  ABP to normal. In case of  ABP
(during haemorrhage) the increased HR helps to raise the ABP again to
normal.
3). Afferent from the respiratory system:
Respiratory sinus arrhythmia: During inspiration, the HR  while
during expiration the HR . It is commonly seen in infants:
Mechanism: During inspiration the HR increases due to:
1. The respiratory center radiates impulses to the CAC causing its
stimulation.
2. Lung inflation stimulates stretch receptors in the alveoli which send
impulses (through the vagus nerve) that stimulate CAC leading to  HR.
3. Bainbridge reflex, during inspiration the VR  (due to negativity of the
intra-pleural pressure), this leads to  pressure in right which causes  in
HR.
During expiration the HR decreases due to decreased activity of respiratory
center, elastic recoil of the lung, and  VR.
4) Afferent from the other parts of the body:
1. From the muscles: Alam Smirk reflex: Contraction of any
voluntary muscle leads to  HR. Muscle contraction stimulates
proprioceptors in the muscles and joints These receptors send impulses
which stimulate CAC   HR, to supply the active muscle with excess
blood.
2. From the skin and viscera: Mild or moderate pain from the skin
leads to  HR (due to stimulation of CAC). Severe pain from the skin (e.g.
massive burn) or any pain from the viscera leads to  HR (due to stimulation
of CIC).
3. From The trigger zones: Pain from the trigger zones (sensitive
areas) e.g. larynx, epigastrium, pericardium and tests produces sever
decrease in HR and even stop the heart. These areas are richly supplied by
parasympathetic fibers.
4. From they eye: Oculo-cardiac reflex: Pressure over the eyeball
produces reflex  HR.
( II ) Physical regulation:
In hyperthermia e.g. fever, the rise in body temperature by 1OC
increases the HR by 10 beats / min, due to direct stimulation of SAN and
stimulation of CAC by impulses coming from the heat regulating center in
the hypothalamus.
In hypothermia, the HR decreases by 10 beats / min for each 1 OC
decrease in body temperature.
( III ) Chemical regulation:
1-  O2 (Hypoxia): Mild or moderate hypoxia   HR due to
stimulation of CAC, both directly and indirectly (through the
chemoreceptors present in carotid body and aortic body). Severe
hypoxia   HR, then the heart stops due to damage of the medullary
centers and SAN.
 2-  CO2 and also  H+ ( acidosis ): causes initial  in HR due to
stimulation of CIC followed by  in HR due to direct stimulation of CAC
and paralysis of CIC.
3- Blood hormones:
a. Adrenaline: Small dose of adrenaline  HR due to direct
stimulation of SAN. Large does of adrenaline  HR because it produces VC
and  ABP (Mary's law).
b. Noradrenaline: Small or large dose of noradrenaline  HR
because of the generalized V.C which leads to  ABP (Mary's law).
c. Thyroxin:  HR due to direct stimulation of SAN. and  sensitivity
of SAN to the circulating adrenaline. Thyroxin also  the general
metabolism of the body which leads to  Body temperature   HR.
4- Other chemicals:
a. Chemicals  HR:
* Sympathomimetic drugs e.g. ephedrine and amphetamine.
* Parasympatholytic drugs e.g. atropine which inhibits the vagal effect on
the heart.
* Histamine  marked capillary VD   ABP  HR ( Mary's law).
b. Chemicals  HR:
* Parasympathomimetic drugs e.g. acetylcholine and pilocarpine.
* Bile salts cause direct inhibition of SAN and stimulation of CIC.
* Morphine stimulates CIC.
* Toxins e.g. typhoid and diphtheria toxins.
c). Efferent innervation of heart
The heart is regulated to a large extent through the central nervous
system. The heart nerve branches from the vagus nerve (from the medulla
oblongata) and thesympathetic nerve fibres from the spinal cord.
The vagus nerves are cardiac inhibitory nerves. When the vagus
nerve is stimulated, the activity of the heart is inhibited. The inhibitory action
of the vagus nerve is brought about as follows.
a) The heart rate is slowed down
b) The conductivity of the heart bundle is reduced.
c) The force of contraction is diminished.
d) The duration of systole is diminished but that of the diastole is increased.
e) Excitability of the heart is also reduced.
The sympathetic nerves are accelerator nerves. These fibres
stimulate the SA node, AV node and also the muscles of the auricles and the
ventricles Stimulation of the sympathetic nerves causes
a) Increase in frequency of heart rate
b) Increase in force of contraction
c) Increases excitability and irritability of the heart
d) Increases the conductivity of the cardiac muscle and bundle of His
thermal regulation.

Nerve supply to the heart:

I. Parasympathetic innervation: (vagus nerve)
Preganglionic fibers of vagus arise from the neurons of C.I.C. They reach
the heart as preganglionic fibers and relay in terminal ganglia present in the
substance of the atrial muscle particularly the nodal tissues. Postganglionic
fibers supply SA node, A-V node and main stem of A-V bundle (but not its
branches), atrial muscle, and coronary blood vessels. Vagus nerve does not
supply the ventricles, branches of A-V bundle and Purkinje fibers.
a) Specialties of vagal innervations of the heart. Right n. vagus controls
mainly right atrium and SA node. Left n. vagus control AV node, His bundle
and all contractile myocardium. So irritation of right nerve causes
bradycardia. Effects of left nerve lead to decrease of contractility and
conductibility.

b) Effects of nn. vagus on the heart activity.

Parasympathetic stimulation causes decrease in heart rate and
contractility, causing blood flow to decrease. It is known as negative
inotropic, dromotropic, bathmotropic and chronotropic effect.

Function of vagus nerve: (Parasympathetic supply to the heart)

It inhibits all cardiac properties; contractility, rhythmicity, excitability,
and conductivity.
Constriction of coronary blood vessels.
Vagus escape phenomenon: Stimulation of vagus slow HR, strong
stimulation of vagus stops the heart completely. If the strong stimulus is
maintained, the ventricles begin to beat by its own rhythm "Idio-ventricular
rhythm" (25 – 40 / min). This phenomenon is called vagus escape. It means
escape of the ventricle from the inhibitory effect of vagus. It is a proof that
the vagus does not supply the ventricles.
Physiological significance of absent vagal supply to the ventricles:
 In case of idio-ventricular rhythm, the ventricular rhythm is (25-40
beats/min) which is inadequate to maintain sufficient circulation. If vagus
supplies the ventricle, it will further the rate which is not desirable.
Vagus tone: During rest vagus nerve continuously discharge inhibitory
impulses to the heart to  the high rhythm of S-A node ( from 110-120 beat
/ min 70 beat/ min), this is called "Vagus tone".
Mechanism of vagus tone:
It is a reflex mechanism in which the stimulus is the resting
A.B.P. Receptors: baroreceptors or pressure receptors present in carotid
sinus and Aortic arch.
Afferents: through sinus nerve which is a branch of Glossopharyngeal
nerve (IX.C) and Aortic nerve which is a branch of vagus nerve
(X.C). Centre : C.I.C.
Efferent: vagus nerve which  the high rhythm of S-A node.
Proof: Cutting of both vagi in animal result in  in HR. ( from 70 to 120).
Stimulation of the cut end of vagus   in HR.
Vagus tone  : In man more than women, in athletes more than non
athletes, and in adult more than children.
Physiological significance of vagus tone: Vagus tone  HR from 120 –
to 70 beat / min. This  in HR will be a reserve to be used at times of need
as in muscular exercise.
II. Sympathetic supply to the heart:
It begins at C.A.C in the medulla oblongata near C.I.C. The axons of their
neuron descend in the white matter of the spinal cord, and relay at L.H.C of
upper 5 thoracic segment. Preganglionic fibers of L.H.C pass in sympathetic
chain and ascend upwards to relay in the three cervical sympathetic ganglia
(superior, middle and inferior cervical sympathetic ganglia. Postganglionic
fibers pass from the ganglia to the heart where they supply all the structures
of the heart including the ventricles.

Function of sympathetic supply to the heart:

1- It increases all cardiac properties; contractility, rhythmicity, excitability,
and conductivity.
2- Vasodilatation of coronary vessels.
c) Sympathetic effects.
Sympathetic nerves from Th1-5 control activity of the heart and large
vessels. First neuron lays in lateral horns of spinal cord. Second neuron
locates in sympathetic ganglions. Sympathetic nerve system gives to the
heart vasoconstrictor and vasodilator fibers. Vasoconstrictor impulses are
transmitted through alfa-adrenoreceptors, which are most spread in major
coronary vessels. Transmission impulses through beta-adrenergic receptors
lead to dilation of small coronary vessels.

Sympathetic influence produces positive inotropic, chronotropic,

dromotropic, bathmotropic effects, which is increase of strength, rate of
heartbeat and stimulating excitability and conductibility also.

d) Control of heart activity by vasomotor center. Lateral portion of

vasomotor center transmit excitatory signals through sympathetic fibers to
heart to increase its rate and contractility. Medial portion of vasomotor center
transmit inhibitory signals through parasympathetic vagal fibers to heart to
decrease its rate and contractility. Neurons, which give impulses to the heart,
have constant level of activity even at rest, which is characterized as nervous
tone.

Characteristics of reflexes from receptors of the heart

Reflex effects on the heart. There are three categories of cardiac
reflexes:
1). own, caused by irritation of receptors cardio - vascular system ;
2). extracardiac due to the activity of any other reflex zones ;
3). nonspecific which played in response to nonspecific effects ( in
physiological experiments , as well as pathology).
The most important physiological reflexes are own cardio-vascular
system, which often occur during stimulation of mechanoreceptors arteries
due to changes in system pressure. Thus, when the pressure in the aorta and
carotid sinus reflex is spovыlnennya heart rate.
A special group of their own cardiac reflexes are those that occur in
response to stimulation of arterial chemo - receptor changes in oxygen
tension in the blood. Under hypoxia develops reflex of tachycardia , while
breathing pure oxygen - bradycardia. These reactions are characterized by
extremely high sensitivity : a person increase in heart rate has been observed
at low oxygen tension by only 3 % when no signs of hypoxia in the body to
detect even impossible.

HUMERAL REGULATION OF HEART ACTIVITY

Adrenaline secreted by the adrenal medulla of
adrenal gland accelerates the rate of
heart beat during emergency
conditions.
Noradrenaline increases the heart beat during
normal condition
Thyroxine also influence heart rate.
Sex hormones

a) Effects of catecholamynes are transmitted by alfa- and bita-

adrenoreceptors.
Adrenalin and noradrenalin stimulate heat activity and cause positive
regulatory effects:
- Positive inotropic effect - increasing strength of heart contractions;
- Positive chrono-tropic effect - increasing heartbeat rate;
- Positive dromo-tropic effect - increasing heart conductibility;
- Positive bathmo-tropic effect - increasing excitability of heart muscle.
Nor-epinephrine increases permeability of cardiac fiber membrane to
Na and Ca2+.
+

b) Effects of acetylcholin leads to increase of K+ permeability through

cell membrane in conductive system, which leads to hyper-polarisation and
cause such effects to the heart activity:
- Negative inotropic effect - decreasing strength of heart contractions;
- Negative chrono-tropic effect - decreasing heartbeat rate;
-Negative dromo-tropic effect - decreasing heart conductibility;
- Negative bathmo-tropic effect - decreasing excitability of heart
muscle.
c) Effects of ions:
VIDEO
(Effects of Ca2+ - ions)
-Ca2+ causes spastic contraction of heart. Decreasing Ca2+ causes
cardiac flaccidity.
Excessive concentration of K+ causes decreasing heart rate. Impulse'
transmission through AV bundle is blocked. If K+ level was previously
decreased, increasing Concentration of K+ capable normalize cardiac
rhythm. Na+ competes Ca2+ in contractile process. So increasing Na+ may
depress cardiac contraction.

d) Effects of thyroid hormones.

Thyroid hormones increase transmission process in ribosome and
nucleus of cells. Intracellular enzymes are stimulated due to increasing
protein synthesis. Also increases glucose absorption and uptake of glucose
by cells, increases glycolisis and gluconeogenesis. In blood plasma increases
contents of free fatty acids. All these effects of thyroid hormones lead to
increase activity of mitochondria in heart cells and ATP formation in it. So,
both activity of heart muscle and conduction of impulses are stimulated.
e) Effects of adrenocortical hormones.
Aldosterone causes increasing Na+ and Cl- in blood and decreases K+.
This is actually for producing action potential in the heart. Cortisol stimulates
gluconeogenesis and increase blood glucose level. Amino acids blood level
and free fatty acids concentration in blood increases also. Utilization of free
fatty acids for energy increases. These mechanisms actual in stress reaction.
So heart activity is stimulated.
f) Hormones of islets of Langerhans effects.
Insulin promotes facilitated diffusion of glucose into cells by activation
glucokinase that phosphorilates glucose and traps it in the cell, promotes
glucose utilization, causes active transport of amino acids into cells, promote
translation of mRNA in ribosome to form new proteins. Also insulin
promotes glucose utilization in cardiac muscle, because of utilization fatty
acids for energy. Clucagone stimulate gluconeogenesis, mobilizes fatty acids
from adipose tissue, promotes utilization free fatty acids foe energy and
promotes gluconeogenesis from glycerol. So both hormones can increase
strength of heartbeat.
g) Endocrine function of heart. Myocardium, especially in heart
auricles capable to secretion of regulatory substances as atria Na-ureic
peptide, which increases loss of Na+ in increase of systemic pressure, or
digitalis-like substances, which can stimulate heart activity.
Effect on the activity of isolated frog hearts of adrenaline,
acetylcholine, potassium and calcium ions
In a state of anesthesia, destroy the frog brain, fix it on a
table preparuvalnomu belly side up. Riven chest, cut the pericardium.
 Scheme of frog dissection thoracic cavity
Under the left aortic arch take two ligatures, under the right -
one. Right hand should be tied. On the left arc from ligatures, located more
nearlyto the heart, make a loopwithout tightening of it.

Eye-cardiac reflex in humans

On the subject determined by cardioscope heart rate. Then it Close
your eyes first and second fingers to press on the eyeballs for 20 s. It
should not have any pain. Simultaneously with the start rate for 40-60
seconds (10 seconds for each separately). If the frequency changes were
observed, repeat the test, increasing the force pressing on the eyeballs.
Monitoring of respiratory arrhythmia in humans
With cardioscope determine the heart rate during deep inspiration
and expiration. The examination should be repeated.

respiratory arrhythmia

Exspiration

Inspiration

MECHANISMS OF HEART AUTO REGULATION

a). Intracellular metabolic changes
In cardiomyocytes intracellular metabolism characterized by cycles of
metabolic processes associated with cardiac activity. So the fastest decay of
energy-rich compounds - ATP and glycogen - is at the time of systole and
corresponds electrocardiogram QRS complex . Resynthesis and recovery of
these substances is in diastole . In addition , there is increased protein
synthesis, to rebuild structures damaged during systole and restoring ionic
balance. Cardiomyocytes can, depending on the activity, selectively adsorb
with blood and accumulate in the cytoplasm of substances that maintain
and regulate their bioenergy.
Greater rate of metabolism or less blood flow causes decreasing
O2 supply and other nutrients
Therefore rate of formation vasodilator substances (CO2, lactic acid,
adenosine, histamine, K+ and H+) rises. When decreasing both blood flow
and oxygen supply smooth muscle in precapillary sphincter dilate, and blood
flow increases. Moderate increasing temperature increases contractile
strength of heart. Prolonged increase of temperature exhausts metabolic
system of heart and causes cardiac weakness. Anoxia increases heart rate.
Moderate increase CO2 stimulates heart rate. Greater increase CO2 decreases
heart rate.
Intrinsic regulation is performed in response changes of blood
volume, flowing into the heart.
It is known as Frank Starling low. Within physiological limits heart
pumps all blood that comes to it without allowing excessive damming of
blood in veins. Cardiac contraction is directly proportional to initial length
of its fibers. In end-diastolic volume over 180 ml excessive stretching heart
fibers occurs and strength of next cardiac contraction decreases.

Anrep's low. Increase of blood flow in aorta and so coronary

arteries leads to excessive stretching surrounding myocardial cells.
According to Frank Starling low cardiac contraction is directly
proportional to initial length of its fibers. So increase of coronary blood flow
leads to stimulation heartbeat.
d) Boudichi phenomenon.
In evaluation heart beat rate increase of every next heart contraction is
observed. It caused by rising of Ca2+ influx into myocardial cells without
perfect outflow, because of shortening of cardio cycle duration.
b). Mechanisms of intercellular regulation of the heart
In cardiac muscle intercellular regulation is associated with the
presence of intercalated discs - Nexus providing the necessary transport of
substances , compounds myofibrils , transfer of excitation from cell to cell.
This arrangement allows the myocardium to respond to stimulation as
syntsytiyu . Intercellular regulation also includes the interaction of
cardiomyocytes from connective tissue cells that make up the stroma of the
heart muscle . Along with mechanical support, connective tissue cells is the
source of funds cardiomyocytes macromolecular organic compounds.
c). Role of cardiac Nexus in the regulation of heart
The basis of cell-cell interactions are kreatorni (creatura - create )
relationships. The essence of these relationships is that between cells is a
continuous exchange of macromolecules , the regulatory function of the
genetic apparatus of cells, the intensity of protein synthesis and cell
differentiation . Kreatornyy relationship is between contractile and
connective tissue cells of the myocardium. It provides normal contractile
function of the myocardium.
Violation of cell-cell interactions leads to asynchronous excitation of
myocardial cells and the appearance of cardiac arrhythmias.
By intercellular interactions and relationships include cardiomyocytes
of connective tissue cells of the myocardium. The latter is not simply a
mechanical supporting structure. They supply to the contractile cells of the
myocardium number of complex macromolecular products necessary to
maintain the structure and function of contractile cells. This type of cell-cell
interactions known kreatornyh links ( GI Kosytskyy .
d). Reflex regulation of heart activity from heart receptors.
Location of receptors in the heart.
Heart muscle contains, both chemical and stretch receptors in coronary
vessels, all heart cameras and pericardium. Stretch receptors are irritated by
changing blood pressure in heart cameras and vessels. Chemo sensitive
cells, which are stimulated by decrease O2, increase of CO2, H+ and
biological active substances also, are called as chemoreceptors.
When atria pressure increase due to increasing blood volume, atria
stretched.
Signals pass to afferent arterioles in kidneys to cause vasodilatation and
glomerullar capillary pressure, thereby increasing glomerullar filtration.
Signals also pass to hypothalamus to decrease antidiuretic hormone secretion
and so fluid reabsorbtion. It causes decreasing both blood volume and arterial
pressure to normal.
 Other reflex reaction is known as atria and pulmonary artery reflex.
When atria pressure increase due to increasing blood volume, atria stretched.
Low-pressure receptors, similar to baroreceptors, in atria and pulmonary
arteries stretched and stimulated. Signals pass to vasomotor center and
inhibit vasculomotor area. Arterial pressure decreases to normal.
Reflex reactions from receptors of pericardium, endocardium and
coronary vessels lead to stimulation n. vagus.
It leads to parasympathetic stimulation of the heart.
Parasympathetic stimulation causes decrease in heart rate and
contractility, causing blood flow to decrease. It is known as negative
inotropic, dromotropic, bathmotropic and chronotropic effect.

Reflexes from extracardial receptors.

1). Baroreceptor reflexes.
Increasing arterial pressure stretched and stimulated baroreceptors
in carotid sinus and aortic arc. Signals pass through glossopharyngeal and
vagal nerve to tractus solitarius in medulla. Secondary signals from tractus
solitarius inhibit vasoconstrictor center and excite vagal center. Peripheral
vasodilatation and decrease both heart rate and contractility occur. Arterial
pressure decreases to normal. When arterial pressure decreases, whole
process occurs, causing.

2). Irritation of visceroreceptors results in stimulation of vagal

nuclei, which cause decreasing blood pressure and heartbeat.
Parasympathetic stimulation causes decrease in heart rate and
contractility, causing blood flow to decrease. It is known as negative
inotropic, dromotropic, bathmotropic and chronotropic effect. This
mechanism is important for doctor in performing diagnostic procedures,
when probes from apparatuses are attached into visceral organs. This may
cause excessive irritation of visceral receptors.
3). Regulation of heart activity during physical exercises.
Motor areas of cerebral cortex are activated to cause exercise most of
reticular activating system is also activated. Increase stimulation of
vasoconstrictor and cardio acceleratory areas of vasomotor center leads to
increasing arterial pressure. Contraction of skeletal muscles during exercises
cause compression of blood vessels. It leads to translocation blood from
peripheral vessels into heart. Cardiac output increases, because of rising
arterial pressure.
Irritation of thrigeminal nerve, otherwise leads to excitation vagal
nucleus through interneuronal connection. So, parasympathetic effects
develop.
4). Atria and pulmonary artery reflex.
When arterial pressure increases due to increasing blood volume, atria
stretched. Low-pressure receptors, similar to baroreceptors, in atria and
pulmonary arteries stretched and stimulated. Signals pass to vasomotor
center and inhibit vasculomotor area. Arterial pressure decreases to normal.
Excessive stretching of lung tissue causes excitation of n. vagus. It leads
to parasympathetic stimulation of the heart. Parasympathetic stimulation
causes decrease in heart rate and contractility, causing blood flow to
decrease.

5). Danini-Ashner's reflex

Measure initial pulse rate in sitting body position in the examinee. Than
perform slight pressure to the one eye-boll by finger through 20 s. Continue
calculation pulse rate during irritation. In conclusion explain the difference,
which was revealed.

e). The cardiac system is self-regulating.

It is nearly impossible to consciously increase or decrease contraction
rate due to its involuntary operation. The large number of influential factors
affecting cardiac performance combine in a complex manner, thus providing
the ability to adapt quickly and efficiently to the needs of the body. This is
accomplished by two pathways. The intrinsic pathway represents the
alterations occurring within the myocardial cells which do or do not depend
on a change in the initial myocardial fiber length. The extrinsic pathway
occurs primarily through neural and humoral adaptations. These discrete
interrelated biological interactions indicate that regulating any certain
physiological control pathway is not easy.

Valsalva test
Used to evaluate the reactivity of the two divisions of the autonomic
nervous system.
Methods of test :
After the background samples inspected in a horizontal position on the
team makes breath for 15-20 seconds and exhales air through a
narrow canal in mundshtuts, supporting intrapulmonary pressure of 40 mm.
Hg. according to the gauge.
Throughout the tests continuoual ECG is recording.
Betsold-Jarisch reflex
Definite effect on the heart can be produced by effects of nonspecific
irritation of some reflex zones. In experimental investigation Betsold-Jarisch
reflex that develops is especially studied. This reflex – is a response to
intrakoronar injection of nicotine , alcohol and some plant alkaloids.
Hemoreflekses have similar nature and called epicardial and coronary. In all
these cases, there are reflex response , called Betsold-Jarisch triad
(bradycardia, hypotension, apnea).
Reflex of Henry-Gower
Reflexes from the heart, that impact upon other visceral systems, are
described. These include, for example, Henry-Gower kardiorenal reflex,
which represents an increase of diuresis in response to stretching of the wall
of the left atrium.
The fact, that the acceleration of the heart rate during muscular activity
has long been known. It is shown, that increase of heart rate occurs within
seconds from the start of contraction of skeletal muscles.
 Mobilization of cardiac activity during muscular work is mainly a
reflex response to impulses from muscle receptors that muscle are contract.
In human, passive flexion and extension of limbs leading to increase of heart
rate.

Activity of the heart during changing of body position

The transition from horizontal to vertical position (orthostasis) leads
to changes in hydrostatic pressure in the vascular system . The action of
gravity makes it difficult to return blood to the heart from the veins to even
healthy individuals with paralyzed leg muscles , additional delay of 300 to
800 ml of blood.
As a result, venous return and thus cardiac stroke volume are reduced.
Consequently falls impulses from mechanoreceptors of the aorta, carotid
sinus, pulmonary artery trunk, leading to an increase in heart rate not more
than 20 beats / min.
In case of failure of compensatory responses to orthostatic stress
developing orthostatic circulatory disorders , dangerous for the brain.
Subjectively, it is shown as a dizziness , "darkening " in the eyes , maybe
even loss of consciousness.
In the transition from vertical to horizontal position ( klinostasis ) , a
decrease in heart rate observed, which up to the initial value of average for
20 seconds.
Later klinostatych effect leads to a decrease in heart rate below the
reference value on 4-6 per minute. Throughout the 10 minute of klinostasis
mainly a decrease below baseline of diastolic blood pressure is observed.
These reactions are caused by growth of impulses from the
mechanoreceptors of the aorta, carotid sinus, pulmonary artery trunk
Heart failure
Heart failure is called a condition in which the heart is unable to
transfer as much blood as is necessary for the body, although venous flow
and adequate compensatory mechanisms operate. This condition can occur
even at rest (" lack of peace "), but may become noticeable only during
exercise (" stress failure "). Lack of left ventricle accompanied by stagnation
of blood in the lungs, which is manifested by symptoms such as shortness of
breath and cyanosis , right ventricular failure also leads to stagnation in the
systemic veins , which occur edema and ascites. To discharge violations of
the heart can cause a variety of conditions that do not directly affect
myocardial contractility ( valvular heart disease, pericardial induration ,
severe bradycardia , etc. ). In a narrow sense during heart failure understand
the decrease contractility of the heart ( myocardial failure ). Such states are
observed in chronic cardiac pressure overload or volume , as well as its
hypoxia ( koronaroskleroz , myocardial infarction) , inflammation
(myocarditis ), poisoning by certain poisons and overdose of certain drugs.

Blood flow in the heart

Morphofunctional peculiarities
Myocardium receives blood through two coronary ( coronary ) arteries
, right and left , coming from the root of the aorta. In coronary artery receives
about 5% of cardiac output. Most of the blood ( 65%) flowing through the
left coronary artery that supplies blood left ventricle ventricular septal her ,
left and right atrium.
The branches of the right coronary artery penetrate the wall of the right half
of the heart. Both right and left coronary arteries are on the epicardial surface
of the heart and vessels give rise to two types - A and B.
Vessels A krovopostachayut outer half of the myocardium, they depart
from the epicardial artery at an acute angle and branching . Second-
generation vessels or vessels away from the vessel A at right angles to go in
depth infarction. Between the branches of arteries is anastomoses.
Bandwidth mizharterialnyh anastomosis under physiological conditions is
negligible. Number of anastomosis may increase with regular exercise.

The main types of myocardial perfusion

There are three main types of myocardial perfusion : middle , left and right .
This division is mainly based on variations of blood supply to the posterior
or diaphragmatic surface of the heart as the blood supply to the anterior and
lateral parts are fairly stable and not subject to significant variations .
With an average type of all three major coronary arteries are well developed
and quite evenly. Blood supply of the left ventricle as a whole, including
both papillary muscle and anterior 1/ 2 and 2 /3 of the interventricular septum
is through the left coronary artery. Right ventricle including papillary
muscles of both right and rear walls 1/2-1/3 receive blood from the right
coronary artery. This is perhaps the most common type of blood supply to
the heart.
When blood flow to the left type only the left ventricle and, moreover
, it is all part of the posterior septum and right ventricular wall at the expense
of developed branches left coronary artery , which reaches the posterior
longitudinal sulcus and ends here as the rear descending artery branches
giving part of the rear surface the right ventricle.
Right there is a weak type of envelope branches that either expire
before reaching the blunt edge or coronary artery becomes blunt edge, not
extending to the back of the left ventricle. In such cases, the right coronary
artery after discharge posterior descending artery usually gives several
branches to the posterior wall of the left ventricle. The entire right ventricle
posterior wall of the left ventricular posterior papillary muscle and the left
part of the tip of the heart receive blood from the right coronary artery.
Capillary network in the myocardium is very dense : the number of
capillaries per unit mass of the heart muscle is 3-4 times higher than in
skeletal . At each muscle fiber myocardial capillary account . Arteriovenous
anastomoses in the heart is not installed. A thin layer of myocardium, which
is directly adjacent to the endocardium, almost no blood vessels and oxygen
derives mainly from the ventricular cavity through the vessels V'yessena -
Tebeziya . Out of vascularized and conducting system of the heart.
Blood outflow is mainly in the coronary sinus , which opens into the
right atrium. Blood anterior right ventricle flows into the cavity of the right
half of the heart.
 Feature coronary blood flow is its dependence on the variable cardiac
cycle. The place vintsenyh discharge vessels from the aorta contributes some
limitation coronary perfusion : during systole of the heart valve aortic valve
partially closed, the entrance to the coronary vessels . During diastole , when
aortalni.klapany closed aortic diastolic pressure is transmitted without
interference coronary arteries. Therefore, diastolic blood pressure in the
aorta is crucial to coronary blood flow. In addition, the amount of blood flow
affects vnutrishnokardialnoho vnutrishnomiokardialnyy compression
pressure. In systole the pressure is much higher than in diastole and
compression forces by more vnutrishnomiokardialni acting on the vessel.
Because blood flow to the myocardium during systole is minimal, while the
diastolic phase of the peace - Max . Venous coronary blood flow , however
, the maximum in systole . Since the compressive pressure of the developing
myocardium of the right ventricle is much smaller than that of the left
ventricle , its perfusion in systole only partially reduced. Reduction of
coronary blood flow during systole increased by any additional increase in
intraventricular pressure. The same effect is observed in the case of an
increase in myocardial contractility . Increased heart rate also limits coronary
blood flow , as this decreases the duration of diastole and thus the value of
the diastolic flow.
The dependence of the mode of perfusion alternating phases of the
cardiac cycle is most pronounced in the subendocardial layers of the
myocardium, mainly due to higher values of systolic strain.

Regulation of coronary blood flow.

Normally between myocardial oxygen demand and the degree of
expansion of coronary vessels is a direct correlation . Increased metabolism
in the myocardium is accompanied by an increase in coronary blood flow
and oxygen postupannyam with blood. This phenomenon is called functional
( working ) hyperemia : With regard to the myocardium with its high
volumetric perfusion rate is generally so-called " adenosine " working
hypothesis flushing. According to this hypothesis , the accumulation of
adenosine in the myocardium is slowing as in the synthesis of adenosine
triphosphate by reducing oxygen delivery , and in accelerating its decay that
occurs with an increase of the heart. In both cases, the excess goes adenosine
in the interstitial space of the myocardium and causes coronary vasodilation
either directly or after conversion to cyclic adenosine monophosphate . It is
possible that adenosine partially blocking kaltsiyzalezhni processes reduce
coronary vascular smooth muscle cells due to blocking seizure of calcium
ions.
Allowed to participate in promoting the expansion of coronary vessels
, and potassium ions , hydrogen, lactic and pyruvic acid increased
concentration of CO2.
The Mighty vasodilators is histamine , endothelium expanding factor or
nitric oxide, which discharge occurs when activation of cholinergic
mechanisms. Acetylcholine via M- cholinergic receptors dilates coronary
arteries.
Many humoral factors can affect the coronary artery lumen , but the direct
role of hormones in the regulation of blood flow to the heart is relatively
small. Insulin dilates coronary arteries. Epinephrine and norepinephrine via
alpha- adrenergic receptors causing constriction through
betaadrenoretseptory expansion of the coronary arteries. Angiotensin II and
vasopressin only in large doses lead to narrowing of the coronary vessels.
Coronary inervuyutsya both adrenergic and cholinergic nerve fibers .
Stimulation of sympathetic efferent fibers that go to the heart is at first a brief
narrowing of the coronary vessels and their extensions . Narrowing of the
coronary arteries is due to direct activation of catecholamines, which evolved
from sympathetic endings , alpha -adrenergic smooth muscle cells.
Expansion of the coronary arteries in response to stimulation of the
sympathetic nerves of the heart is probably the secondary metabolic
pathways as sympathetic nerves increase heart function and release of
adenosine. It is difficult to eliminate with the role of beta- adrenergic
receptors of smooth muscle cells , stimulation of which causes expansion of
the coronary arteries.
Stimulation of the vagus nerve leads to a lengthening of diastole,
because coronary blood flow may thus increase. Also founded, that
stimulation of these nerves in artificial constant rhythm of the heart is
expanding coronary arteries.