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The heart is a four-chambered double pump connected in a series. Each
“pump” consists of one atrium and one ventricle. A dense connective
tissue framework separates the muscular layer of the atria from those of
the ventricles. The right side (right heart) supplies blood to the
pulmonary circulation, the left side (left heart ) supplies blood to the
systemic circulation.

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.

B. The Ventricles - The ventricle walls are relatively somewhat thicker
than are the atrial walls and the left ventricular wall is much thicker
than that of the right ventricle. The relative thickness of the various
walls is directly related to the work performed by the various
chambers. The normal pressure against which the right ventricle has
to eject blood is only 4 to 25 mm Hg whereas the normal pressure
against which the left ventricle has to eject blood is 70 to 130 mm
Hg. This difference in pressure is caused by the difference in the
resistance to blood flow in the pulmonary and systemic vascular beds;
the pulmonary circulation having a low resistance whereas the
systemic circulation has a high resistance.

The ventricular muscle fibers are arranged in a spiral pattern so
that when the heart contracts, it exerts a wringing action. By virtue o
this, the heart rotates slightly to the right each time it contracts. This
causes the tip of the apex of the heart to also rotate giving rise to a tap
called the apex beat which can be felt in the left intercostals space
just below the nipple in the mid-clavicular line. It is useful as the

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.

The ventricular musculature may be separated into four bands
arranged in a criss –cross fashion like the cords in an automobile tire.
The left ventricle in addition is encircled by a thick, deep constrictor
layer of muscle.

The left ventricle eject blood by (1) movement of the base
towards the apex and (2) shortening of the constrictor fibers.

There are three distinct action by which blood is ejected by the
right ventricle. These are by: (1) movement of the base towards the
apex, (2) movement of the free wall of the right ventricle toward the
interventricular septum (bellows effect) due to spiral muscle
contraction, and (3) increase in the curvature of the septum as the
constrictor muscles of the left ventricle contracts (left ventricular aid)

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

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.

Functionally there are two general types of myocardial cells
namely :
1) Cells specialized for impulse formation and conduction. These
cells may be capable of spontaneously generating action
potentials. Examples are the P cells in the sinoatrial and
atrioventricular nodes, trantional cells which connect P cells
with the rest of the heart and the Purkinje cells.

2) Cells specialized for contraction. They form the bulk of cardiac
cells. These cells are inactive until stimulated by an impulse
generated elsewhere. They are structurally similar to skeletal
muscle with the following differences:

a) Adjacent cardiac muscle cells are joined by specialized
paired membrane junctions called intercalated discs.
The discs are located at the end of the cells and at the
level of a Z line. They provide pathways of low

resistance between cells which explain why the
myocardium functions as a syncitium.

b) Cardiac cells have more mitochondria

c) In the sarcoplasmic reticulum of cardiac cells, the T-
tubules are larger, lateral sacs wrap partly around the T-
tubule and the branching of the T-tubules is irregular.

E. The specialized cardiac Tissues

1) Nodal Tissues

a) Sino-atrial node (SA Node)
The SA node lies in the sulcus between the superior vena
cava and the right atrium. It is made up of slender spindle-
shaped cells which are more swollen than ordinary cardiac
muscle fibers. The node is liberally supplied with vagal and
sympathetic efferents. The SA node is the primary
pacemaker of the heart and rythms originating here are
desinated as SINUS RHYTHMS.

b) Atrioventricular node (AV node)
The AV node is located in the subendocardial region of the
right atrium near the orifice of the coronary sinus and also
close to the interatrial septum. Functionally, the AV node is
made up of three zones. AN (atrionodal or atrial end of the
node), the N (middle nodal) and the NH (nodal His or
ventricular end of the node). The fibers in the AN node zone
not only have very small diameters but also branch

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

2. The Internodal and Interatrial Pathways

There are three pathways connecting the sino-atrial node to the
atrio-ventricular node and one connecting the sino-atrial node of the left

( 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,

(b) The middle internodal tract (Wenchebach’s tract) - from the
postero-dorsal edge of the sinus node, pass over the
interatrial septum to reach the A-V node. Some small
branches are given off which reaches the left atrium.

( c ) The posterior internodal tract ( Thorel’s tract) - from the
posterior end of the sinus node passes to the intoratrial
septum to reach the A-V node.

Velocity of the conduction through these pathways is more rapid than
through the ordinary contracting atrial muscles.

3. The Bundle of His and its Branches: the Purkinje Fibers.
The common bundle (bundle of His) begins at the A V node
penetrates into the uppermost portion of the interventricular septum and then
splits into a single right bundle branch and a left bundle branch which gives
off septal branches and two fascicles, an arterior which supplies the anterior
papillary muscle and a posterior which supplies the posterior papillary
muscle. The bundle branches have extensive ramifications and
interconnection as they spread out through the endorcardial surface of the
myocardium of the two ventricles. Those which penetrate into the depths of
the ventricular muscle merge with working myocardial cells providing for a
ventricular conduction in the Purkinje fiber is fastest among cardiac tissues.

F. The Pericardium . The heart is surrounded
by an invaginated sac. One side of the sac, attached firmly to the exterior
of the heart, is called the epicardium. The sac is reflected back around
the outside of the heart as the pericardium which is attached to the heart
only at the point of entrance and exit of the great vessels . Between these

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.

The pericardial sac is composed of fairly stiff non-stretchable
substance and is just about large enough to accommodate the normal
heart when it is optimally filled in diastole. The pericardium therefore,
probably serves to limit over distension of the normal heart. However,
when it is necessary for the heart to enlarge (cardiac hypertrophy) the
pericardium can gradually grow bigger allowing for the accommodation
of a larger of a larger heart. This is a gross change which requires time
and represents a part of the compensatory process that goes along with
cardiac hypertophy.

Under certain circumstances, such as with knife wounds, or traumatic
injury to the heart by a blow on the chest wall, a blood vessel in the heart
may be torn. In diseases such as coronary thrombosis, i.e., occlusion of one
of the coronary arteries, a portion of the myocardial wall may die. The
myrocardial wall may then rupture. In any of these events, blood from the
ventricle or an artery may penetrate the pericardial sac. If the pericardial sac
becomes filled with fluid, proper filling of the atria and ventricles during the
diastole is prevented, This sequence of events is called cardiac tamponade.


A. Irritability: Excitation of the heart.
Contraction of the heart muscle results from electrical activation. The
heart does not depend on its autonomic nerve supply (extrinsic nerves)
for excitation. The heart generates its own stimulus. The heart
therefore, possesses the property of automaticity. Furthermore, these
excitatory impulses are generated at regular intervals. The property is
called rhythmicity.

1. Automatic cells are found in

(a) sino-atrial node
(b) around the opening of the coronary sinus
(c) AV node and its junction with the bundle of His
(d) Specialized conduction tissues of the ventricles

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.

3. The sino-atrial node (SA node) is the pacemaker because:

(a ) its frequency of discharge is the highest, thus it is able to
excite the heart earlier than the other potential pacemarkers.

(b ) of overdrive suppression; the greater rhythmicity of the SA
node forces the other automatic cells of fire off at a faster rate
than their natural discharge rate. This causes depression of
their rhythmicity. Explanation - faster discharger rate
increases the activity of the sodium pump thus increasing the
maximum diastolic potential.

4. The frequency of discharge of impulses from the pacemakers is a
function of:

(a) The slope of the slow diastolic depolarization, the pro-
potential. If the slope is steeper, the phase 4 depolarization
will reach threshold or firing level quicker and the action
potentials generated will be closer to one another.
Frequently of discharge increases and so does the heart rate.
(b) The value of the maximum diastolic potential (beginning of
phase 4). If this is reduced (lower resting membrane
potential) firing level is reached faster and the impulse
frequency increases.
(c) The value of the threshold voltage or the critical firing
level. If this is set to a value nearer the maximum diastolic
potential, frequency discharge will increase.
(d) Duration of the period recovery. If the period of recovery is
shorter, frequency of discharge will increase.

(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.

B. Conductivity spread of excitation

1. The excitation which originates from the SA node spreads into the
surrounding atrial tissue through the artial muscle and the
internode tracts.

Conduction velocity in atrial muscle is o.3 – 0.5 m/sec.
Conduction velocity in the specialized tissue is 0.9 -1.8 m/sec.

2. The excitation process reaches the AV node thru the internode
tracts traversing the three zone to reach the Bundle of His. At the AV
node, conduction is slowed down (AV nodal delay). The delay is due
to slow conduction velocity and delayed development of the action
potential in the AN zone. The delay is a physiologic advantage in that
it assures proper coordination between atrial and ventricular
contraction. Time is allowed for complete filling of the ventricle with

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.

Conduction velocity through the A-V node is around 0.1 to 0.2
m./sec. It is primarily uninteractional from atrium to ventricle
(antegrade or orthograde) conduction). The NH zone of the Av node
can assume pacemaker functions if the SA node is depressed. Some
contend that it is not the NH zone which can be automatic but the
transitional cells between the NH zone and the His cells or the Bundle
of His itself.

3. If the excitation passes through the AV node with a sufficient amplitude,
it reaches the bundle of His. Velocity of conduction increases (3-4 m/sec)
because of the greater diameter of the fibers and their frequent branching .
Likewise, there is increased magnitude of the action potential, increased
velocity of the phase O depolarization and increased duration of the action

4. Excitation of the ventricles begin at the Left side of the ventricular
septum, travels downwards to the epicardial surface of the right ventricle
near the apex. The it travels concentrically towards the base of the heart.
The last area to be depolarized is the posterobasal portion of the ventricle
near the septum. Conduction velocities in human ventricular myocardium is
about 0.35-0.40 m/sec.

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

5. Effects of Repetitive stimulations.
(a) Production of heart blocks. At normal heart rates, the frequency
of excitation allows for smooth sequential stimulation of the atria down to
the ventricles. However, if the frequency of stimulation increases, the
impulses may come so close to one another that the cardiac tissue may

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.

(b) Overdrive suppression . Rhythmicity or automatic cells is
reduced if they are stimulated at rates faster than their natural frequency.

( c ) Overdrive enhancement . A dormant automatic cell, for
example. A Purkinje fiber, when stimulated at one second interval may
spontaneously beat after some time. The changes observed in the action
potentials elicited are:
- increasing resting membrane potential which was initially low,
- increasing amplitude of action potentials
- increasing of phase 4 slow diastolic depolarization


Excitation, excitation contraction coupling and the mechanism of
cardiac muscle contraction are essentially similar to those of the skeletal
muscles with a few differences. (Please refer to the previous section of
nerve and muscle physiology, and the physiologic anatomy of cardiac
1. The beginning of the excitatory action potential precedes the
mechanical changes by about 15 msec. Peak force develops
during phase 2 of the action potential. Repolarization is complete
before relaxation of the muscle.
2. Depolarization of muscle membrane causes release of Ca++ ion
from the cisterns of the sarcoplasmic reticulum and more
importantly for cardiac muscle, causes influx of Ca++ from the
exrtracellular fluid. The Calcium binds with the troponin C and
the contractile mechanism begins . Ca++ ions enter the cell
during Phase 0 through phase 2 of the action potential. During

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,

4. Some characteristic of cardiac muscle contraction:

(a) All-or-none response. This is due to stimulation of all fiber in the
cardiac tissue. This is made possible through rapid spread of
excitation from cell to cell as discussed earlier.
(b) Tetanic contractions cannot be produced. The cardiac muscle
membrane is in its absolute refractory period up to early phase 3
of the action potential. Related to muscle contraction, the period
would extend to the end of muscle contraction. Therefore no
response can be elicited until the muscle is in the relaxation
period. That tetanus cannot produced is a physiologic advantage
since the sustained contraction would be detrimental to its
pumping action.
(c) Effect of initial stretch, the Frank- Starling law. Within certain
limits, stretching the muscle fiber results in increased force of
contraction. Translated to the ventricle, if more blood return to it
before it contracts (increased ventricular filling, increased end-

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)

1. Stroke volume. The stroke volume is determined by the
volume of blood in he heart at the beginning of systole (end
diastolic volume – EDV) minus the volume of blood which
remains in the ventricles at the end of systole (end diastolic

Thus: CO = (EDV – ESV) x HR

a) End Diastolic Volume. If the heart is to be an effective
pump, the ventricles must fill the before systole. The
adequate of filling is determined by 1) the filling time, 2) the
effective filling pressure, and 3) the distensibility of the

b) End Diastolic volume. The end diastolic volume is the
volume of blood remaining in the ventricle at the end of
systole after the semilunar valves are closed.. The volume is
determined primarily by the balance between the force of
contraction of the ventricle and aortic (distending ) force.

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.


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.

The effect of sympathetic nerve stimulation is mediated by
the release of norepinephrine at the sympathetic nerve
terminal (post ganglionic mediator). Norepinephrine is
believed to decrease the membrane permeability to

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


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.