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THE HEART
A. The Atria - The atria are relatively thin walled structures which
have a fair amount of elasticity or distensibility. This arrangement
allows the atria to accept the blood that is returning to the heart by
way of the veins during ventricular contraction (systole) without
much rise in pressure. The atria elastically recoil and empty that
blood in the ventricle during early ventricular relaxation (diastole).
Contraction of atrial muscle (atrial systole) forces some more blood
into the ventricles.
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fairly accurate measure of how far a heart project to the left sternum
and serves as a clinical measure of the degree of enlargement
(hypertrophy) of the heart in cardiac diseases.
C. The Cardiac Valves - There are no valves between the veins and the
atria. During contraction of the atria, blood flows from the atrium to the
ventricle as well as back into the veins. As a result atrial contraction is not a
very effective method of filling the ventricle. Valves are located between
the atria and the ventricle. The right atrioventricular valve is the tricuspid
and the left is the mitral valve. The openings of these valves are quite large
so as to allow a rapid inflow of blood into the ventricle without requiring
any large pressure difference between the two chambers. The leaflets are
relatively thin and freely movable so that they are easily pushed aside during
the filling, phase of the ventricle . When the ventricle contracts, the valves
leaflets are pushed together preventing fluid from flowing from the ventricle
back into the atrium. To prevent eversion of the leaflets the edges are
supported by the chordae tendinae which are connected to the papillary
muscles. Contraction of the latter during ventricular systole keeps the
chordae tindenae at a constant tension. These valves sometimes become
scarred so that they no longer meet in the middle, or the chordae tindinae
scarred and shortened. As a result, the valves cannot fully close, producing a
mitral valvular insufficiency in which the valve is unable to prevent the
passage backward of the blood from the ventricle to the atrium. On the other
hand, the valves, as a result of scarring may tend to adhere together so that
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they are not able to swing apart freely when blood is flowing normally
through them. The result is valvular stenosis which interferes with the proper
filling of the ventricle.
The pulmonary and aortic valves are relatively small, the cup-like
arrangements, which project into the stream. There are three cusps or cups in
the pulmonary and three in the aortic valves. These cups are relatively small
and light, but quite strong. Because of their shape they do not any
mechanical support such as provided by the chordae tindinae for the
tricuspid and metal valves. The cups is pushed back against the wall when
the ventricle contracts. With the onset of ventricular relaxation the blood
tends to floe back into the ventricle, but the regurgitant stream catches the
cusps and pushes them out into the center of the stream till the three meet
and prevent further return of the fluid into the chamber from which it came.
D..The Myocardial Cell – Myocardial cells are discrete cells with intact
plasma membrane. Though structurally separate from one another, the
behaviour of these cells has been described that of a functional syncitium.
This is attributed to the presence of tight junctions or gap junctions of
very low electrical resistance which enables them to transmit electrical
changes very rapidly.
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resistance between cells which explain why the
myocardium functions as a syncitium.
1) Nodal Tissues
The cells in the N zone are similar to those in the SA node. The NH zone
merges with the atrioventricular bundle (bundle of His), therefore, this zone
is the upper portion of the conduction system which spreads the impulses
throughout the ventricles. The AV node also receives vagal and sympathetic
efferents,
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There are three pathways connecting the sino-atrial node to the
atrio-ventricular node and one connecting the sino-atrial node of the left
atrium.
( a) The anterior internodal tract - travels from the left tip of the
sinus node a short distance then divides into branches, the
Bachmann’s bundle which goes through the dorsal aspect of
the inter-atrial band to each the left atrium, and another
branch which goes down to the A-V node,
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two is the pericardial space which contains only a few milliliters of fluid.
The space provides a lubricating surface which allows the heart to turn
and move freely. The pericardium is attached to the diaphragm at the
apical portion,. Since the pericardial space contains only small amount
of fluid, the apex of the heart cannot move away from the apical portion
of the pericardium. As a result, the basilar portion of the heart, attached
to the more distensible mediastinal structures, moves downward with
ventricular systole.
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THE PHYSIOLOGIC PROPERTIES OF THE HEART
2. The normal pacemaker which sets the heart rate or the rhythm
of the heart is the S_A node. It is the automatic cells with the
highest frequency of discharge. Other cells with low frequencies
of discharge are called latent of potential pacemakers.
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4. The frequency of discharge of impulses from the pacemakers is a
function of:
(Both (a) and (b) may be observed upon stimulation of the sympathetic
nerve supply. (See section of nervous regulation or cardiac activity).
An agent which alters the frequency of discharge thus altering the heart is
called a chronotropic agent.
1. The excitation which originates from the SA node spreads into the
surrounding atrial tissue through the artial muscle and the
internode tracts.
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blood before actual contraction takes place. Furthermore, as the
action potential spreads to the N zone, there is progressive reduction
in the (a) resting membrane potential, (b) amplitude and overshoot of
the action potential, (c) velocity of phase O depolarization and (d)
conduction velocity. These characteristics are what is called
decremental conduction. This makes the N zone a most likely site for
the production of A-V blocks.
It should be noted that action potentials of endocardial cells lasts longer than
that of epicardial cells so that depolarization proceeds from endocardial to
epicardial surface but repolarization travels from epicardial to endocardial
surface.
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receive some of the excitatory impulse during its refractory period and thus
are not able to respond. While it is true that at faster heat rates, the
refraction period of cardiac tissues shorten, the shortening is not the same for
all tissues. For example, the refractory period of the AV node is least
affected by heart rate. Thus at heart rates of 240/min. or more impulse may
reach the AV node during its refractory period and therefore some impulse
are not transmitted to the ventricles. In which case the atria will be
contracting at faster rates than the ventricle. This is called A-V block.
Disease may prolong the refractory period of any part of he conduction
pathway so that blocks may occur even at normal heart rates.
C. CONTRACTILITY
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repolarization, calcium ions are pumped activity into the
sarcoplasmic reticulum and then out of the cell.
3. In normal cardiac activity, blood flows into the ventricle from the
atrium. Pressure in the ventricle rises and the walls are stretched.
The stretching force will determine how long the muscle fibers
would be before the ventricle contracts. This total stretching force
before contraction is called the pre-load,
When the ventricle contracts the A-V close (please refer to section
on the cardiac cycle). At this time the semilunar valves are still
closed so that no blood goes in or out of the ventricle. Since fluid
is incompressible, the volume of blood within the ventricle does
not change. The cardiac muscle fibers therefore cannot shorten
significantly (some actually lengthen and a change in shape of the
ventricles occurs) The type of contraction is almost isometric.
When the intra-ventricular pressure rises high enough to force
open the semilunar valves, blood is ejected, pressure falls and the
muscle fibers are able to shorten. Contraction then becomes
isotonic in type. The ventricle now pumps against the artic
pressure. This pressure is called the after-load,
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diastolic volume), the subsequent contraction (ventricular systole)
is more forceful and more blood is ejected into the circulation.
A. Cardiac output
The cardiac output is the volume of blood pumped by the heart
each minute, and this is the product of the volume of each beat
(stroke volume – SV), and the number of the heart beats per
minute (heart rate – HR)
2. Heart Rate.
If the stroke volume were held constant, an increase in heart rate
should cause a proportionate increase in the cardiac output. However, an
increase in heart rate in denervated or isolated heart, permits less time for
filling, so the EDV is decreased. If the ESV does not decrease
proportionally, the SV decreases.
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INNEVATION OF THE HEART
1. Sympathetic fibers
Preganglionic sympathetic fibers capable of affecting the
heart, leave the spinal cord by way of the upper five thoracic
roots. The synapses are found in the corresponding
paravertebral and the stelate ganglia and the post-ganglionic
fibers then proceed to the heart by way of the cardiac nerves.
They are distributed to the SA and AV nodes, conduction
tissue and the atrial and ventricular musculatures and the
coronary arteries.
2. Parasympathetic fibers
Parasympathetic pre-ganglionic fibers are conveyed to the
heart in the vagi. The synapses with the post-ganglionic
fibers are found in the intrinsic cardiac ganglia. Post-
ganglionic fibers of parasympathetic origin are distributed to
the SA node and the AV nodes, to the upper portion of
special conduction tissue, and the atrial myocardial fibers,
but none are known to be distributed to the ventricular
myocardium. The post-ganglionic mediator is acethylcholine
which is believed to increase the membrane permeability to
potassium.
BLOOD PRESSURE
The blood pressure is the force exerted by the blood per unit area of
the blood vessel wall. It is due to the fact that the volume of blood contained
in the vessels is larger than the capacity of distended vessels. The distention
of the vessel causes it to elastically recoil around the blood causing the
building up of the pressure in the system.
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