Conduction System of the Heart

The cardiac muscle beats with an intrinsic rhythm. This permits the heart to beat without extrinsic
stimulation. The heart begins its rhythm and continues its rhythm, basically until something interrupts it.
Interconnecting cardiac muscle tissue which is specially designed to continue the rhythm of the heart’s
contraction creates the heart’s system of conduction. These strands of cardiac muscle tissue keep the
heart beating in the rhythm that it begins with without interruption through coordinating action. The
cardiac cycle refers to the process which fills and empties the individual chambers of the heart. The
system of the heart’s conduction enables this cycle to continue without interruption.

Via a complex system of cardiac energy, which is the generation and distribution of electrical impulses,
the muscle tissue is “in charge” of the rate the heart beats. The heart’s conduction system is comprised
of various components. The sinoatrial node is the body’s natural pace maker. It is positioned along the
posterior wall of the right atrium. More specifically, it is positioned where the superior vena cava creates
its connection with the heart. The electrical impulses generated by the sinoatrial node initiates the
entire cardiac cycle. The electrical impulses which the sinoatrial node is responsible for creating affects
the right and left atria and controls their contraction. By controlling the unison contraction, the
sinoatrial node keeps the heart beating with its depolarization rate of 70 to 80 times per minute. The
electrical impulses are then distributed to the atrioventricular node.

The atrioventricular node is positioned in the inferior section of the interatrial septum. The
atrioventricular bundle then picks up the following electrical impulses which is positioned on the tops of
the interatrial bundle. The atrioventricular bundle then branches off into two separate bundles, the right
and the left. Each individual branch runs ad infinitum with conduction myofibers that are just internal of
the ventricular wall. The unified ventricular contraction is caused by the stimulation of these fibers.
Systole is the term given to the simultaneous contraction of the ventricles.

Systolic pressure inside the arteries is produced by the conjunction of systole, tension of the supple
fibers, and the contraction of the smooth muscle within the systemic arteries. Diastole is the term given
to the action of ventricular relaxation. Diastolic pressure within the arteries is measured when the
ventricles are relaxed.

Despite the heart’s ability to maintain its self generated beat, there are times when the heart needs to
adjust in response to the varying demands of the physical human body. This is controlled by intervention
of the automic nervous system. Both the atrioventricular node and the sinoatrial node are innervated
with sympathetic and parasympathetic innervation. When the heart responds to the increased needs of
the body, as well as its own increased need, this is known as sympathetic stimulation. It is marked by the
acceleration of the heart rate and dilation of the coronary arteries. Parasympathetic stimulation refers
to the heart’s ability to slow down in response the decreased needs of both the body and the heart.
Fibers from the cervical as well as the upper thoracic ganglia are responsible for the sympathetic
innervation. Branches of the vagus nerves stimulate the parasympathetic innervation. The sinoatrial
node is innervated by the branches coming from the right vagus nerves while the branches from the left
vagus nerves are responsible for the innervation of the atrioventricular node.
The heart is a muscle with a special electrical conduction system. The system is made of two nodes
(special conduction cells) and a series of conduction fibers or bundles (pathways).

The normal heart begins with an electrical impulse from the SA (sinoatrial) node, located high in the
right atrium. The SA node is the pacemaker of the normal heart, responsible for setting the rate and
rhythm. The impulse spreads through the walls of the atria, causing them to contract. Next, the impulse
moves through the AV (atrioventricular) node, a relay station, into the conduction bundles which are
located in the ventricles themselves. As the impulse travels down the bundles, the ventricles contract.
The cycle then repeats itself.

This regular cycle of atrial and ventricular contractions pumps blood effectively out of the heart.
Problems may occur anywhere in the conduction system and interfere with effective pumping of blood.
The heart may beat too fast (tachycardia), too slow (bradycardia), or irregularly. These abnormal beats
are known as arrhythmias. Special studies of the heart's electrical system may be needed to accurately
diagnose the type and cause of the arrhythmia. Therapy for arrhythmias is based on their type and
difficulties they cause the child. Treatment may include medication, placement of a pacemaker, catheter
ablation of extra pathways, or even surgery. Most arrhythmias require no treatment as they cause no ill
effects to the child.

A Healthy Heart

The heart is a beating muscle that continually pumps blood to the rest of the body. What we commonly
call a heartbeat is actually the rhythmic contraction of the heart's four chambers. Each heartbeat is
stimulated by electrical signals that travel through a specific nerve pathway in the heart. These signals
can be tracked and recorded by an electrocardiogram, or EKG.

The Heart's Electrical Signal

The heart's electrical signal begins at the sino-atrial node, or SA node, which is located in the top right
chamber, or atrium. The signal then travels to both the right and left atria, causing them to contract and
push blood into the lower chambers, or ventricles.

The electrical signal continues into the ventricles via the atrioventricular node, or AV node, and then
into the tissue that separates the ventricles, called the bundle of His. The signal continues down the
bundle and into the left and right bundle branches, located within the ventricles. When the signal
reaches bundle branches, it causes the ventricles to contract and pump blood to the lungs and body,
completing the heartbeat.

What Is the Conduction System?

The conduction system functions as the body's own pacemaker and keeps the heart beating at a normal
rate of 60 to 100 beats per minute. If the activity of this system is interrupted due to heart damage or
other medical conditions, it can cause the heart to beat at an abnormal rate or with an irregular rhythm.
Should this occur, blood flow to the brain and other parts of the body could be compromised.
Heart Conduction System

The sinoatrial node (SAN), located within the wall of the right atrium (RA), normally generates electrical
impulses that are carried by special conducting tissue to the atrioventricular node (AVN).

Upon reaching the AVN, located between the atria and ventricles, the electrical impulse is relayed down
conducting tissue (Bundle of HIS) that branches into pathways that supply the right and left ventricles.
These paths are called the right bundle branch (RBBB) and left bundle branch (LBBB) respectively. The
left bundle branch further divides into two sub branches (called fascicles).

Electrical impulses generated in the SAN cause the right and left atria to contract first. Depolarization
(heart muscle contraction caused by electrical stimulation) occurs nearly simultaneously in the right and
left ventricles 1-2 tenths of a second after atrial depolarization. The entire sequence of depolarization,
from beginning to end (for one heart beat), takes 2-3 tenths of a second.

All heart cells, muscle and conducting tissue, are capable of generating electrical impulses that can
trigger the heart to beat. Under normal circumstances all parts of the heart conducting system can
conduct over 140-200 signals (and corresponding heart beats) per minute.

The SAN is known as the "heart's pacemaker" because electrical impulses are normally generated here.
At rest the SAN usually produces 60-70 signals a minute. It is the SAN that increases its' rate due to
stimuli such as exercise, stimulant drugs, or fever.

Should the SAN fail to produce impulses the AVN can take over. The resting rate of the AVN is slower,
generating 40-60 beats a minute. The AVN and remaining parts of the conducting system are less
capable of increasing heart rate due to stimuli previously mentioned than the SAN.

The Bundle of HIS can generate 30-40 signals a minute. Ventricular muscle cells may generate 20-30
signals a minute.

Heart rates below 35-40 beats a minute for a prolonged period usually cause problems due to not
enough blood flow to vital organs.

Problems with signal conduction, due to disease or abnormalities of the conducting system, can occur
anyplace along the heart's conduction pathway. Abnormally conducted signals , resulting in alterations
of the heart's normal beating, are called arrhythmias or dysrrythmia.

By analyzing an EKG a doctor is often able to tell if there are problems with specific parts of the
conducting system or if certain areas of heart muscle may be injured.
THE CONDUCTION SYSTEM

The conduction system is responsible for the characteristic of autorythmicity of the myocardium. This
page will include the anatomy and physiology of this specialized system. First let's examine the anatomy
of the conduction system.

THE ANATOMY OF THE CONDUCTION SYSTEM

The heart's conduction system consists of the sinoatrial node, the atrioventricular node, internodal
fasiculus, and the atrioventricular bundle, which divides into right and left branches. These two branches
teminate into the purkinje fibers, otherwise called the subendocardial plexus. These fibers will become
contiuous with the ventricular myocardial fibers. The above structures mentioned are all specially
differentiated cardiac muscle fibers, separated from the normal myocardium by delicate envelopes of
connective tissue.

The sinoatrial node is located in the superior lateral wall of the right atrium immediately below and
slightly lateral to the opening of the superior vena cava. This structure is usually five to eight millimeters
in length, and occupies the whole thickness of the wall in the right atrium. The fibers of the sinoatrial
node connect directly with the atrial fibers, so the action potential beginnning in the node speads
immediately into the atria.

The atrioventricular node is located in the interatrial septum, resting with its inferior surface on the
fibrous atrioventricular ring. This is in the proximity of the attachment for the septal cusp of the tricuspid
valve. The atrioventricular node is oval in shape and a little smaller than the sinoatrial node. Within the
septum, the node extends forward from the opening of the coronary sinus, and continues anteriorly into
the atrioventricular bundle. The atrioventricular bundle will then pass through the fibrous ring
connecting the node to the ventricles.

Connecting the sinoatial node to the atrioventricular node are internodal fasciculi. These fasciculi are
thought to help transmit the impulse from the sinoatrial node to the atrioventricular node. However,
impulses generated in the sinoatrial node spead to the atrioventricular node uniformily through the
atrial myocardium. It is still somewhat unclear of the functioning of these fasciculi.

The atrioventricular bundle or fasciculus is responsible for the activation of the ventricles. The thickness
of this bundle is that of a wooden matchstick. This bundle is located in the posterior septal wall of the
right atrium immediately behind the tricuspid valve and adjacent to the opening of the coronary sinus.
The bundle passes through the fibrous ring in a hole located at the margin of the right trigone (this
trigone is located between the aortic valve and the tricuspid valve). This is the only connection between
the myocardium of the atria and the ventricles. On the ventricular side of the ring, the bundle runs
downward and forward, running along the posterior margin of the membranous part of the
interventricular septum. It then branches into a right and a left crus or bundle branch. These two
branches straddle the uppper border of the muscular part of the interventricular septum. Each branch
heads toward the apex of the ventricles under the endocardium of the septum.

The right branch of the atrioventricular bundle crosses from the septum to the ventricular wall along the
moderator band (or septomarginal bundle). The left branch, on the other hand, breaks up inpo branches
and reaches the ventricular wall along several trabeculae carneae. These branches spread out as the
subendocardial purkinje fibers over the ventricular wall and over the papillary muscles. Because of this
arrangement, the impulses dispatched from the atrioventricular node first activate ventricular muscle in
the region of the apex, assuring a "milking" action of the ventricles toward the openings of the aorta and
the pulmonary trunk.

THE PHYSIOLOGY OF THE CONDUCTION SYSTEM

The heart contains two specialized types of cardiac muscle cells. The majority, around 99 percent, of the
cardiac muscle cells are contractile cells and are responsible for the mechanical work of pumping the
heart. The second type of cardiac muscle cells are the autorhythmic cells. The function of these cells is
to initiate and conduct action potentials that are responsible for the contraction of the working cells.

The cardiac muscle displays a pacemaker activity as opposed to a nerve or skeletal muscle cell which
displays a membrane that remains at a constant resting potential unless stimulated. Pacemaker activity
is defined as the membranes of cardiac muscle cells slowly depolarizing between action potentials until
threshold is reached, at which time the membranes fire or has an action potential. These action
potentials, generated by the autorhythmic cardiac muscle cells, will then spread throughout the heart
triggering rhythmic beating without any nervous stimulation.

The specialized autorhythmic cells of cardiac muscle comprising the conduction system serve two main
functions:1.) to generate rhythmical impulses to cause rhythmical contraction of the heart muscle and
2.) conducting these impulses rapidly throughout the heart. When this system works properly, the atria
contract about one sixth of a second ahead of ventricular contraction. This will allow extra filling of the
ventricles before they pump the blood through the lungs and peripheral circulation. Another important
function of this system is it allows all portions of the ventricles to contract alomost simultaneously,
which is essential for effective pressure generation in the ventricular chambers. In order to assure the
rythmical beating of the heart the rates at which these autorhythmical cells are capable of generating
action potentials differ due to differences in their rates of slow depolarization to threshold. Please refer
to the table below.

TISSUE ACTION POTENTIAL PER MINUTE

SA NODE 70-80
AV NODE 40-60
BUNDLE OF HIS 20-40
PURKINJE FIBERS 20-40

As you can see from the above table, the sinoatrial node is capable of depolarizing the greatest extent.
For this reason, the sinus node usually controls the rate of beat of the entire heart.

MECHANISM OF SINUS NODAL RHYTHMICITY

The potential of the sinoatrial node fibers between discharges has a negativity o fonly -55 to -60
millivolts in comparison with a ventricular muscle fiber which depolarizes at -85 to -90 millivolts. The
cause of this reduced negativity is that the cell membranes of the sinus fibers are naturally leaky to
sodium ions.
Before going any further a quick review of the role that membrane ion channels play in the
depolarization and repolarization of cardiac muscle will be provided. There are three types of membrane
ion channels that play important roles in causing the voltage changes of the action potential. They are as
follows:

1. fast sodium channels

2. slow calcium-sodium channels
3. potassium channels

Opening of the fast sodium channels is responsible for the rapid spikelike onset of the action potential
observed in ventricular muscle because of the rapid influx of positive sodium ions to the interior of the
fiber. Next you have a plateau of the ventricular action potential caused primarily by a slower opening of
the slow calcium-sodium channels. Lastly, increased opening of the potassium channels and diffusion of
large amounts of positive potassium ions out of the fiber return the membrane potential to its resting
level.

There is a difference in the function of the above mentioned channels in the sinoatrial node fibers. The
reason for this is the much lesser negativity of teh "resting" potential, -55 millivolts. At this level of
negativity, the fast sodium channels have basicly become "inactivated", meaning they have become
blocked. The reason for this is any time the membrane potential remains less negative than around -60
millivolts for more than a few milliseconds, the inactivation gates on the inside of the cell membrane
that close the fast sodium channels become closed and remain so. Therefore, only the slow calcium-
sodium channels can open or become "activated", and cause the action potential. As a result, the action
potential is slower to develop than that of the ventricular muscle, and it also recovers with a slow
decrement of the potential rather than the abrupt recovery that occurs for the ventricular fiber.

INTERNODAL PATHWAYS AND TRANSMISSION OF THE CARDIAC IMPULSE THROUGH THE ATRIA

The ends of the sinoatrial node fibers fuse with the surrounding atrial muscle fibers, and action
potentials originating in the sinus node travel outward into these fibers. Therefore, the action potential
travels through the entire atrial muscle mass and, eventually, reaching the atrioventricular node. The
velocity of conduction in most of the atrial muscle is around .3 milliseconds. However, the velocity of
conduction will be faster in several other pathways in the right atrial muscle. One of these, the anterior
interatrial band, passes through the anterior walls of the atria to the left atrium and conducts the
cardiac impulse at a velocity of around one millisecond. Three other similar pathways exist. These
pathways curve through the atrial walls and terminate in the atrioventricular bundle (refer to anatomy
of conduction system). These pathways also conduct the impulse at a faster rate.

The impulse initiating in the sinoatrial node travels through the internodal pathways and reaches the
atrioventricularbundle. Here the impulse is delayed a total of around .16 seconds. The cause of this slow
conduction through the atrioventricular bundle is partly due to the small fiber size as compared to
normal atrial muscle fibers. However, two other factors will contribute more to the delay. First, all of
these fibers have resting membrane potentials that are much less negative than the normal resting
potential of other cardiac muscle. Secondly, few gap junctions connect these muscle cells in the
pathway, so there is a large resistance to the conduction of excitatory ions from one cell to the next.
Thus, with both low voltage to drive the ions and great resistance to the movement of the ions, you can
see why each succeeding cell is slow to be excited.

TRANSMISSION IN THE PURKINJE SYSTEM

The fibers located in the purkinje system are very large, even larger than ventricular muscle fibers, and
transmit action potentials at a velocity of 1.5 to 4.0 milliseconds. This velocity translates to 6 times that
in normal cardiac muscle. This high rate of transmission of action potentials could be caused by a high
level of permeability of the gap junctions at the intercalated discs between the successive cardiac cells
that make up these purkinje fibers.

Once the impulse reaches the purkinje fibers, it is transmitted through the ventricular muscle mass by
the ventricular muscle fibers themselves. The velocity of transmission is now only around 0.3 tp 0.5
milliseconds, equating to one sixth that in the purkinje sysem.

The cardiac muscle wraps around the heart in a double spiral. Fibrous septa exist between the spiraling
layers. The cardiac impulse, therefore, does not travel directly outward toward the surface of the heart
but instead angulates toward the surface along the directions of the spirals.

For effective pumping of the ventricles to exist the purkinje sysem must send the action potential to
almost all portions of the ventricles within in a short amount of time. This will allow both ventricles to
begin contracting at around the same time.