Theme

Blood circulation system and its

regulation.
Blood circulation in facial region
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.

Automaticity of the heart
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.
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.
A pacemaker other than SA-node is called as
ectopic pacemaker or ectopic focus.
In a normal heart, however, only one region
demonstrates spontaneous electrical activity and
by this means functions as a pacemaker - 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.

Cardiac cycle
Period fro end of one heart contraction to end of next, is called cardiac
cycle. There are two phases systole, when heart contracts and 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.

Physiological analysis of cardiac
output
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.

Heart sounds
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.

Effects of catecholamynes are transmitted
by alfa- and beta-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 Ca
2+
.

Effects of acetylcholin
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.

Effects of ions
-Ca
2+
causes spastic contraction of heart.
Decreasing Ca
2+
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 Ca
2+
in
contractile process. So increasing Na
+
may depress
cardiac contraction.

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.

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.

Hormones of islets of Langerhans
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.

Endocrine function of heart.
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.

Mechanisms of heart auto
regulation
Greater rate of metabolism or less blood flow
causes decreasing O
2
supply and other nutrients.
Therefore rate of formation vasodilator substances
(CO
2
, 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 CO
2
stimulates heart
rate. Greater increase CO
2
decreases heart rate.
Laws of heart
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.

Laws of heart
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.
Boudichi phenomenon. In evaluation heart beat
rate increase of every next heart contraction is
observed. It caused by rising of Ca
2+
influx into
myocardial cells without perfect outflow, because
of shortening of cardio cycle duration.

General characteristic of central nervous
regulation of heart activity
Central nervous system affects regulation of blood
flow and pumping activity of the heart and
provides very rapid control of arterial pressure.
Cerebral cortex control heart activity to correct it
depending on body needs when performing
behavioral reactions. Secondary somatic sensory
zone takes part in analysis of afferent information
from the hart. Pre-motor cortex may correct heart
activity by descendant influences through
hypothalamus. Anterior hypothalamus promotes
parasympathetic control of heart activity. Posterior
hypothalamus realizes their effects through
sympathetic nervous system.

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.
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.

Sympathetic effects
Sympathetic nerves from Th
1-5
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.

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.