Beruflich Dokumente
Kultur Dokumente
Jessica Schucht
Abstract
The cardiovascular system is vital for human survival. It has many functions and many
components; the most important is the heart. The heart is a muscular organ that
an electrical conduction system within the heart. The electrical activity can be visualized
causing illness or death. Improved techniques in imaging have allowed the growth of the
some abnormal electrical patterns thorough a procedure known as the ablation technique.
THE CARDIAC CONDUCTION 3
The heart is the hollow, fibro-muscular organ that is the driving component of the
cardiovascular system (Levy & Pappano, 2007). This system is vital to human life, and
contributes to the function of every other part of the human body. Damages to the heart,
heart disease, and heart malfunction affect many adults and youth in America. It is
(American Heart Association, 2009). Various factors can contribute to heart disease, and
many of these occur within the electrical conduction system in the heart. A minor
complication in this conduction system can lead to an arrhythmia (heart contraction out
of rhythm), which can cause severe malfunctions within the heart. It is estimated that
nearly forty percent of the people who die from cardiovascular disease suffer from an
arrhythmia (American Heart Association, 2009). For this reason, these heart malfunctions
these electrical malfunctions eventually led to the development of a relatively new field
mapping techniques have been adapted to easily diagnose arrhythmias. The increasing
development of these technologies has even allowed physicians to invade the heart tissue
and eliminate such arrhythmias. This is a minimally invasive procedure known as the
catheter ablation. If the ablation is performed accurately, it can correct arrhythmias with
THE CARDIAC CONDUCTION 4
only a minor complication rate (Lim, Singleton, Alasady, & McGavigan, 2010). It has a
first-time success rate of over 60 percent and a repeat success rate of up to 77 percent
(Stiles, 2009). This accuracy is allowing the ablation to become a popular treatment for
regarding its long-term effects (Lakshmanadoss, Aggarwal, Huang, Daubert, & Shah,
2009). For this reason, it is not always seen as a primary treatment option. Many people
would rather seek pharmaceutical treatment. However, others believe that because of the
curative nature of the ablation procedure, it is an ideal treatment for arrhythmias. Many
physicians are conducting research that supports the idea that it should be considered a
curative treatment for cardiac arrhythmias. The heart is the impetus behind the cardiac
which searches to cure previously incurable heart ailments. A malfunction in the heart
can be deadly, and a lack of long-term research should not stop physicians from
The heart is one of the most important organs in the human body. Without its
function, nutrients would not be delivered to other systems. This would cause the
cessation of bodily activities and eventually death. The hearts anatomy and location are
directly linked to its function, which is ultimately controlled by the cardiac conduction
system. The heart is situated so that the majority of the organ lies on the left side of the
bodys midline. Its anterior surface faces toward the sternum and intercostal muscles, and
THE CARDIAC CONDUCTION 5
its inferior surface faces the diaphragm (Mahadevan, 2008). The various surfaces of the
heart all meet at the apex. The entire organ is enclosed in the pericardium, or the
outermost tissue layer (Aaronson & Ward, 2007). The pericardium attaches the heart to
both the diaphragm and the sternum, allowing it to be situated in place in the chest cavity.
In this position, the heart is able to contract and distribute blood to the rest of the body
(Mahadevan, 2008). Most of the heart is composed of a special kind of contractile tissue
called cardiac muscle, which contracts regularly every day of a persons life. This
Aside from the fibrous pericardial layers, the heart also contains various other
layers of cells. These include the endocardium, epicardium, and the myocardium. The
endocardium is the thin, inner lining of the heart, while the epicardium is the thin layer of
cells on the outside of the heart (Aaronson & Ward, 2007). The largest of the epicardial
THE CARDIAC CONDUCTION 6
cell layers is the myocardium, which is composed of myocytes. Myocytes are small,
mononucleated cardiac muscle cells that are full of mitochondria (for generating energy).
Myocardial cells contain intercalated discs, which connect the myocytes to each other.
The intercalated discs contain adheren, desmosomes, and connexins, which all greatly
contribute to the cells functionality (Figure 2) (Mohrman & Heller, 2010). These discs
are very important to the electrical conduction system in the heart. They connect the
myocardial cells to one another, and facilitate the spread of electrical current from cell to
cell. This electrical current causes the contraction of the heart. The speedy conduction
through the myocardial cells allows them to contract together as one unit. All of these
cellular, fibrous, and muscular layers come together to form the major organ of the
The heart is divided into four chambers: the right atrium, the left atrium, the right
ventricle, and the left ventricle. Each chamber of the heart is influenced by electrical
stimulation from the heart conduction system. The activity of these chambers affects the
other components of the heart, including the vessels and valves. The heart contains many
vessels and valves, which control the movement of blood. Blood leaves the heart, enters
systemic circulation, travels through the body, and is eventually fed into the right atrium
via the superior and inferior vena cava. These veins allow blood to flow into the right
atrium. Within the right atrium, directly above the right ventricle, lies the tricuspid valve.
This valve allows blood flow from the right atrium to the right ventricle (Mohrman &
Heller, 2010). The right ventricle feeds into the pulmonary artery, which sits atop the left
atrium. The pulmonic valve (pulmonary semilunar valve) separates the pulmonary artery
from the ventricle. A pressure gradient during the cardiac cycle controls the opening and
closing of this valve. This allows the heart to be sufficiently filled before ejecting blood
into the pulmonary artery. If the electrical conduction system of the heart is not
The left atrium is the smaller of the two atria. Through the regulation of the
cardiac conduction system, it receives blood from the pulmonary veins (from the lungs)
and is connected to the left ventricle via the mitrial (bicuspid) valve (Aaronson & Ward,
2007). Both the mitrial and tricuspid valves are important because they prevent the
backflow of blood from the ventricles into the atria during cardiac contraction. They are
connected to the cusps of the chordae tendineae (fine chords), which are attached to the
papillary muscles inside the ventricles. This attachment couples their contraction to the
THE CARDIAC CONDUCTION 8
ventricle muscles, causing these valves to close upon ventricular contraction. The closed
valves can then prevent backflow into the atria when the pressure of blood in the
ventricle rises. The left ventricle is thicker and more muscular which allows it to generate
more pressure to the blood during cardiac contraction. This ventricle is connected to the
aorta by the aortic semilunar valve. The semilunar valves differ from the mitrial and
tricuspid because they do not have chordae tendineae connections that control their
opening/closing (Klabunde, 2005). However, all of these structures are similar in that
their function is necessary for the proper operation of the cardiac cycle. This cycle is
ultimately controlled by the action potentials of the electrical conduction system of the
heart (ECS).
Although a pressure gradient is influential in the control of the cardiac cycle, the
most important cardiac control is the electrical conduction system throughout the heart
(Figure 4). Cardiac tissue possesses the ability to initiate its own beat and regulate its
activity (automaticity and rhythmicity). Action potentials are rapid voltage changes that
are able to travel across the membranes of cells. Cells are designed in order to have a
resting membrane potential; there is a separation of electric charge across the cell
membrane. In cardiac cells, the inside of the cell is negative with respect to the positive
charges that lie on the membrane. This electric potential is caused by the presence of
In order for an action potential to occur, a cell must be depolarized (which can
occur from nervous stimulation). Once the cell reaches its threshold potential, massive
changes occur in the cells ion channels and permeability. A fast inward current of ions
THE CARDIAC CONDUCTION 10
enters the cell causing it to become depolarized even further. Because the connexin
allows the propagation of this current to adjacent cells (Figure 5). Eventually, when the
action potential has spread and many cells are depolarized, a large amount of tension is
created, which causes the heart muscle to contract. After depolarization and contraction
occurs, these cells must then be repolarized before another action potential can spread.
This keeps cardiac cells from continually being activated and contracted (Mohrman &
Heller, 2010).
Two types of action potentials occur in cardiac cells: the fast response and slow
response action potentials. In normal cardiac cells, the fast response action potential
allows for a uniform contraction throughout the heart. Because this is generally the goal
of heart tissue, the majority of action potentials in myocardial cells are fast response
(Figure 6). These cells can be rapidly depolarized and even become depolarized over
THE CARDIAC CONDUCTION 11
their normal limit. They are influenced by the intercalated discs and their components.
Fast action potentials are very important to the proper function of the electrical
conduction system. However, some cardiac cells require a slower action potential. These
action potentials are termed the slow response cells. They have an unstable resting
potential and require more time to depolarize. These slow responses occur in the cells
that contribute to the pacemaker function of the heart, protecting it from over-stimulation
initiate the contraction of the human heart (Levy & Pappano, 2007). The SA node is
located between the right atrium and superior vena cava (Aaronson & Ward, 2007), and
is divided into various regions. A few of these regions possess automaticity, which is the
ability of cardiac cells to initiate a heartbeat (Figure 7). This compilation of cells forms
the SA node, or the atrial pacemaker complex (Levy & Pappano, 2007). As these cells are
through the atrial tissue and cause the heart to begin contraction. The number of heart
contractions per minute is known as the heart rate. It is determined by the amount of time
it takes for the repolarization and depolarization of the SA node. In the absence of outside
stimulation, the SA node maintains a heart rate of approximately 100 beats per minute.
However, various outside sources influence the action potentials in the SA node
The main influence on the SA node is the autonomic nervous system. This system
is responsible for the bodys automatic responses. It contains two divisions: the
parasympathetic and sympathetic nervous systems. Both of these systems influence the
SA node, but they elicit very different responses. The parasympathetic nervous system is
activated in times of rest and digestion. Its main connection to the SA node is through the
vagus nerve. The vagus nerve is a cranial nerve that extends to the heart and directly
innervates the sinoatrial node. When the parasympathetic nervous system is stimulated,
the vagus nerve releases acetylcholine at the SA node. This has three main effects. First,
it decreases the firing rate of the SA node. Second, it decreases the conduction velocity of
the electrical potential in the myocytes. Finally, it decreases the contractility of the heart
muscle itself. These three effects cause the heart rate to slow from its intrinsic rate. The
sympathetic division of the nervous system acts to increase the heart rate. It accomplishes
THE CARDIAC CONDUCTION 13
this task through the release of norepinephrine onto the SA node. This increases the
contractility of the heart, increases the firing of the SA node, and increases the ion
currents that cause the wave of depolarization through the atria (Mohrman & Heller,
2010).
After an impulse spreads through the atria, it travels through the three intermodal
tracts: the Bachmann, Wenckebach, and Thorel. After spreading through these tracks, the
electrical wave reaches the annulus fibrous, where the quick depolarization through the
atria comes to a halt. The annulus fibrous are the fibers between the atria and ventricles
that inhibit conduction. There is only one opening within these fibers that will allow the
node). Therefore, after some delay, the AV node receives the impulse that began in the
and three millimeters thick that is located at the mouth of the coronary sinus in between
the right atrium and ventricle (Aaronson & Ward, 2007) (Figure 7). The AV node is an
important aspect of the ECS in the heart; it is divided into three main sections, the AN, N,
and NH regions. The N region, located in the middle of the node, ensures a slow rate of
conduction of the electrical impulse. The AN region, located between the atrium and the
beginning of the node, also offers a delay in conduction. However, this is due to the
length of the AN region, not a slow conduction velocity of the cells. The slow
conduction velocities of the N and AN regions work together to greatly hinder the speed
of the impulse through the AV node. This delay is critical because it allows the atrial
THE CARDIAC CONDUCTION 14
contraction to push blood into the ventricles before they contract and expel the blood
from the heart (Mahadevan, 2008). The NH region is the final region and serves as the
connection between the AV node and the Bundle of His. These three regions form a
Like the SA node, the AV node is also affected by innervation from the
autonomic nervous system. The vagus nerve of the parasympathetic system is able to
prolong conduction even greater than normal through the AV node. This prolonged
conduction increases the length of diastole and decreases the heart rate. Under intense
conduction is able to transverse into the ventricle. The sympathetic division also
innervates the AV node. However, its function is opposite that of the parasympathetic.
decreases conduction time through the AV node. This allows the impulse to rapidly
transverse the NH region into the Atrio-ventricular bundle of His (AV bundle) (Levy &
Pappano, 2007).
The AV bundle emerges out of the AV node and extends down the inter-
ventricular septum (tissue which separates the right and left ventricles) (Mahadevan,
2008). It is another component of the ECS in the heart and transmits the AV nodes
signal into the upper section of the inter-ventricular septum. After transmission through
this area, the bundle splits into the left and right bundle branches. These branches
transmit the electrical impulse towards their respective sides of the heart. The left bundle
THE CARDIAC CONDUCTION 15
branch again splits into the posterior and anterior fascicles (Levy & Pappano, 2007).
These branches form the upper portion of the conduction system in the ventricles. As the
bundle branches transverse the septum, they divide further into the Purkinje System.
The Purkinje System is the portion of the conduction system that transverses the
endocardium of the heart to stimulate the right and left ventricles. It is responsible for the
ventricles specialized conduction. Once the impulse reaches these fibers, the contraction
becomes fully initiated (Aaronson & Ward, 2007). The Purkinje System contains idoi-
they fire at a rate of around 30 to 40 beats per minute, which is not enough to sustain
cardiac function in the event of an AV block (Levy & Pappano, 2007). If an AV block
occurs, or other malfunctions stop the electrical impulse from reaching the ventricles,
All of these anatomical components, along with the electrical events that occur in
one heartbeat, form the cardiac cycle. This cycle revolves around the action of a pressure
gradient instigated by the contraction of the heart (Mahadevan, 2008). The two main
actions of the cardiac cycle are systole and diastole. These are the contraction and
relaxation of the heart, respectively, and they are ultimately controlled by the electrical
can lead to serious problems in the cardiac cycle. Diastole is an important aspect of the
cycle, because it allows the heart muscle to rest. Different aspects and problems of the
cardiac conduction system can shorten the time spent in diastole, which can cause
THE CARDIAC CONDUCTION 16
malfunctions in this cardiac cycle. Diastole is the period of time when the heart is
allowed to relax, refill, and prepare for the next systole. Its length varies depending on
factors including health, age, sex, and outside conditions (Mohrman & Heller, 2010). The
actions of the right and left pump divide the cardiac cycle into four separate stages.
The first stage encompasses both ventricular and atrial diastole. Both components
of the heart are at rest. The atrioventricular valves are open, while the semilunar valves
are closed, allowing both the atria and ventricles to fill with blood. The SA node has not
yet fired to begin a heart contraction. At this time the blood flows freely from the atria
into the ventricles. During this stage the heart is simply receiving blood; it is not
transmitting it to the rest of the body (Potter, 2011). As the atria fill, the pressure of the
blood inside them begins to rise. Once this pressure reaches its maximum, stage two of
The second stage marks the beginning of atrial systole, which is initiated by the
depolarization of the sinoatrial node. The ventricles are still in diastole, and the
atrioventricular valves are open. The semilunar valves are closed, which again allows
blood to enter the ventricles without escaping their compartment to the rest of the body.
At this time, a pressure gradient drives much of the blood flow in the heart. As the
pressure of the atria increases (in phase 1), eventually the atria must contract. This
increases the pressure even further, causing a pressure gradient between the atria and
ventricles (Mohrman & Heller, 2010). This creates the appearance of the atria milking
The efficient contraction of the atria allows blood to more quickly flow from the
atria to the ventricles in preparation for ventricle systole. In general, this atrial contraction
is only responsible for about ten percent of ventricle filling. In times of a normal heart
rate this is not required for effective filling of the ventricles. However, during an elevated
heart rate due to exercise, arrhythmia, or heart damage, atrial contraction can become
conduction system of the heart can lead to an increased atrial contraction or overall rapid
heart rate. Throughout these periods, the ventricles do not have adequate time to fill
passively. Therefore atrial contraction assumes about forty percent of filling duties
(Mohrman & Heller, 2010). A malfunction that interferes with either ventricle filling or
atrial contraction could lead to decreased blood output and other detrimental
consequences.
After atrial contraction occurs, stage three of the heart cycle commences. This
stage is divided into two different phases. The first phase is known as the isovolumetric
phase. The atria have reverted back to diastole; the impulse has traversed the atria, and
they have completed the filling of the ventricles. Their new responsibility is to repolarize
and once again fill with blood in preparation for their next contraction. At this point, the
signal enters the AV node, and the ventricles then begin systole. As with the atria, the
contraction of the ventricle causes a significant rise in the ventricle bloods pressure. This
causes the atrioventricular valves to snap closed and prevent backflow from the ventricles
into the atria. However, because the ventricles are not yet ready to expel the blood to the
rest of the body, the semilunar valves are still closed. During this phase of the cardiac
THE CARDIAC CONDUCTION 18
cycle, the volume in the heart remains constant. For this reason, it is termed the
blood, and they are ready to expel it to the rest of the body (Potter, 2011).
Phase two of stage three of the cardiac cycle also encompasses atrial diastole and
ventricular systole. The impulse has now entered the Purkinje System, and the ventricles
are in full contraction. However, the pressure in the ventricles has risen substantially,
causing the semilunar valves to open. Because the atrioventricular valves remain closed
to prevent backflow, ventricle contraction pushes blood out of the heart into the
pulmonary trunk and aorta. This action normally expels around 70 milliliters of blood,
which is less than the blood that was originally pumped into the ventricles (Potter, 2011).
The remaining blood in the ventricles is known as the end systolic volume. An important
measure of heart efficiency is the ejection fraction. This is the end systolic volume
(normally 70 milliliters) divided diastolic volume (normally about 120 milliliters) and
The final stage of the cardiac cycle, stage four, is marked by both atrial and
ventricular diastole once again. The atria are continuing to fill from the systemic
circulation, and the ventricles have just begun diastole. The cardiac cells are all in the
process of repolarizing and preparing for the next action potential. The atrioventricular
valves are once again open, and the blood flows into the ventricles via a pressure
THE CARDIAC CONDUCTION 19
gradient. The semilunar valves are once again closed due to the backflow of blood from
When the cardiac cycle ends, the heart has already started to prepare for another
cycle. This continuous cycle of systole and diastole is responsible for the pressure
gradient that pushes blood through the entire body. Although autonomic innervation
plays a part in the control of the duration of the contraction and relaxation cycles, the
ECS within the heart muscle elicits these functions. This system is driven by the
propagation of action potentials throughout heart muscle (Klabunde, 2005). If any one of
cycle can be viewed through an electrocardiogram. This machine can help diagnose these
malfunctions, lead to curative processes, and has been the impetus to the discipline of
clinical electrophysiology.
to evaluate cardiologic functions such as heart rate, rhythm, and the conduction
characteristics of heart tissues (Mohrman & Heller, 2010). It was first performed in
used to diagnose conduction problems that would go unnoticed otherwise. Some of the
THE CARDIAC CONDUCTION 20
main problems that can be diagnosed by an ECG include: cardiac rhythm disturbances,
Because of the efficacy of the ECG, it has greatly enhanced the field of
electrophysiology. In order for it to be accurate and uniform, a standard lead protocol was
developed. This first began with Einthoven, a Dutch physiologist, who proposed a
triangular bi-polar lead placement, in which electrodes are placed in the formation of an
equilateral triangle on the body (Mohrman & Heller, 2010). A bi-polar lead is one in
which electrodes have opposite polarity. Einthovens triangular placement allows each
bipolar lead to measure the potential difference from their respective position, which is
60 degrees away from the other leads. Lead I is placed on the left wrist and measures the
potential difference of activity between the right and left arm. Lead II is placed on the
THE CARDIAC CONDUCTION 21
right wrist and is able to measure the electrical activity between the right arm and left leg.
Finally, lead III, is placed on the left ankle and records the potential difference between
the left leg and left arm (Aaronson & Ward, 2007).
However, for clinical purposes, a more intensive lead placement provides a more
bipolar leads, but it also includes nine extra unipolar leads. Three of these are placed on
the left leg, right arm, and left arm at various vertices of Einthovens triangle (Figure 9).
Three more leads, known as the augmented leads, aVR, aVL, and aVF, generate an
augmented view of the frontal plane of electrical activity in the heart (Aaronson & Ward,
2007). Finally, the six precordial leads (V1-V6) are placed strategically on the chest of
the patient.
THE CARDIAC CONDUCTION 22
They provide a view of the heart at a different angle than the bipolar and augmented
the heart. Together, these twelve leads (the precordial, augmented, and bipolar leads)
provide a recording that is composed of at least six different perspectives on the electrical
activity in the human heart (Aaronson & Ward, 2007) (Figure 10). The recording that
forms is a wave of electrical current known as the ECG tracing, and it represents a
An upward deflection in the ECG normally depicts a difference between the left
leg and right shoulder leads. A negative deflection depicts a negative potential in the
patients left leg. Each portion of the ECG represents a specific part of the cardiac cycle
and allows physicians to pinpoint specific problems in the ECG that can relate to
electrical activity in the heart. A normal ECG is broken into three major portions. These
are the P wave, QRS complex, and T wave (Mohrman & Heller, 2010) (as shown in
The P wave represents the beginning of one cycle of the ECG (Figure 8). It is an
upward deflection in the reading that represents the depolarization of the atria. It begins
when the sinoatrial node is depolarized, and fires an action potential through the atria.
The P wave has small amplitude because the propagation of electrical potential through
the extracellular fluid of atrial cells is not synchronous. This is much different from the
amplitude of the next complex, the QRS (Mohrman & Heller, 2010).
The QRS complex begins with the downward deflection known as the Q wave,
and then flows into the sharp spike known as the R wave (Figure 8). The R wave is the
cells. Finally, the complex terminates with the S wave (Figure 8). This entire process
typically lasts from about 60 to 120 milliseconds. The QRS cooperatively represents the
spread of the electrical current from the AV node, through the bundle of His, and
eventually the Purkinje system. While the ventricles are depolarizing in the QRS, the
atria are simultaneously repolarizing. This is not seen in the ECG because atrial
THE CARDIAC CONDUCTION 24
completely overshadows the atria repolarization; therefore, the ECG does not detect this
The final portion of the ECG is the T wave (Figure 8). This wave represents
ventricle repolarization. The T wave is much smaller than the QRS complex, because
throughout the cells. Repolarization actually begins with the most recently depolarized
cells and spreads upward toward the atria. During this period of time the atria are resting
and preparing for the next action potential (Mohrman & Heller, 2010).
The ECG recording is also divided into various segments, which describe
physiological voltage differences during specific parts of the cardiac cycle. The first of
these is the PR segment, also known as the PR interval. It stretches from the beginning of
the P wave to the beginning of the QRS complex. This distance represents the time it
takes for an action potential to spread from the SA node, through the atria and to the AV
node. In a healthy adult, its normal duration is anywhere from 100 to 120 milliseconds.
This delay is normal because it indicates the proper delay between the excitation of the
SA node and the AV node. As shown in Figure 1, at the end of the PR interval, there is
no deflection in the ECG reading. The leads are not detecting any voltage change. Two
main reasons describe this absence. First, the atrial cells are depolarized as part of the
action potential. Because atrial cells do not depolarize simultaneously, the action
potential spreading through these cells is not strong enough at this point to be detected by
THE CARDIAC CONDUCTION 25
the leads. Second, because the electrical wave has not yet reached the AV node, the
The next segment of the ECG encompasses both ventricular depolarization and
ventricular systole. It is known as the QT interval, and under healthy, resting conditions
lasts less than 380 milliseconds. It stretches from the beginning of the Q wave to the
beginning of the T segment, and demonstrates normal ventricular repolarization. Like the
PR segment, the end of the QT interval is marked by a lack of electrical activity. This
allows for the heart cells to rest and prepare for the next contraction as the atria fill with
The final segment of the ECG represents the time from the beginning of the S
wave to the beginning of the T wave. At the time of the S wave, the ventricle cells are at
their maximum action potential. The atria are resting, and after the S wave, there are no
deflections in the electrocardiogram. The electrically silent part of this segment is the
same as that of the QT interval; no rapid changes in membrane potential of the heart cells
simply examining a reading from one electrical lead. After the development of the 12-
lead system, this tool became even more powerful. Because of its diagnostic ability, the
scale of the ECG has been standardized. Generally, every centimeter on the y-axis
represents a potential difference of one millivolt, and every 25 millimeters on the x-axis
THE CARDIAC CONDUCTION 26
of the reading represents one second of time. When evaluating the electrocardiogram
determine if it is within a normal range. For example, under normal conditions (heart rate
of 60 beats per minute) the QRS complex occurs once per minute, has high, sharp
amplitude, and lasts for less than 120 milliseconds. If there is any significant deviation
from these qualities, the diagnostician can deduce there is a problem with the conduction
function of the heart muscle. These aberrations tend to occur because of abnormal cardiac
excitation and cause rhythmic disturbances in cardiac contraction. These disturbances are
pre-mature ventricular contractions, atrial flutter, and atrial fibrillation (Klabunde, 2005).
Tachycardia can be divided into different types and is categorized by its origin. In
general, tachycardia describes an increased heart rate of around 100 to 200 beats per
minute (Aaronson & Ward, 2007). It can be problematic because it leads to increased
time between ventricular contractions, where there is not as much time for cardiac filling.
This limits the cardiac output, and therefore the amount of blood that is able to leave the
heart and reach the various tissues. In general, tachycardia is fairly harmless: it is only
responsible for deaths at a rate of 575 people per year (American Heart Association,
2009).
THE CARDIAC CONDUCTION 27
Tachycardia is generally caused by two main phenomena: ectopic foci and re-
entry. Re-entry occurs when the wave of atrial conduction does not terminate at the AV
node, but travels through an alternative route causing re-excitation of the atrial tissue
(Mohrman & Heller, 2010). This re-excitation pathway can occur in a localized area of
the heart, or it can even occur between a larger region such as the atria and ventricles.
This larger pattern is known as global re-entry, and generally leads to tachycardias within
the ventricles (Klabunde, 2007). Another way to describe the route of re-entry is through
its pattern: ordered or random. An ordered re-entry route continually travels in a fixed
path. A random re-entry occurs when the route of re-excitation continues to change. The
tachycardia can then seem random and out of control. This type of re-entry is known as
In order for re-entry to effectively occur, three conditions must be met. First, there
must be the presence of a block in the conduction pathway. This block must stop
conduction in only one direction, allowing the stimulus to return through it in only one
direction. Second, the re-entry must have the correct timing. If the conduction pathway is
too fast, the re-entry will be halted because the tissues are still in their absolute refractive
period, and therefore unable to propagate the action potential. Third, the tissue through
the re-entry loop must have a short absolute refractory period. Once again, if the stimulus
reaches already excited tissues during their absolute refractory period, the stimulus will
Ectopic foci are also responsible for various types of tachycardia. They are
electrical regions in the heart other than the SA node and are sometimes referred to as
THE CARDIAC CONDUCTION 28
ectopic pacemakers. Under special circumstances, such as SA node failure, they are able
to initiate the heartbeat. However, sometimes these ectopic foci become easily excitable
and take over the SA nodes function unnecessarily. They tend to fire at a more rapid
Sinus tachycardia (Figure 11) occurs when there is an increased firing of the
exercise or times of stress; however, it can be caused by cardiac disease (Aaronson &
Ward, 2007). Sinus tachycardia is generally harmless, but it does lead to a decreased
cardiac output (per each heartbeat). This decreased output can lead to dizziness, fatigue,
or the feeling of heart palpitations. Sinus tachycardia generally returns to normal when
the exercise is ended or the stress is removed (Children's Hospital of Wisconsin, 2011).
supraventricular tachycardia (SVT). It causes less than 150 deaths per year.
Supraventricular refers to an abnormality that occurs above the ventricles. In SVT the
atrial cells become abnormally excited and fire at an accelerated rate. The excitation of
atrial cells in SVT could be caused by various deficiencies. One of which is the presence
of an ectopic focus outside the SA node that becomes excited and takes over the SA
at the ECG. The QRS complex appears to be normal; however, it actually occurs more
frequently. Also, the increase in heart rate can cause the superimposition of the P and T
pressure. It can be treated many different ways; however, recently the ablation procedure
Figure 11. A normal ECG (top) compared to an ECG reading of Sinus Tachycardia
(bottom).
During sinus tachycardia, the heart beats at a faster rate due to the faster repolarizing
of the atria. Figure adapted and modified from (Malmivuo & Plonsey, 1995).
in which the ventricles depolarize and contract apart from atrial contraction (Segal,
rate (over 100bpm). If these accelerated complexes last for a duration longer than thirty
tachycardia (SVT). This type of tachycardia generally needs medical attention (Singh &
Murphy, 2009).
There are two main categories of SVT: polymorphic and monomorphic. They are
defined by their appearance on the ECG as well as their etiology. Polymorphic describes
THE CARDIAC CONDUCTION 30
a condition in which the QRS complexes take different shapes and varieties on the ECG.
It has three main causes (Lim, Singleton, Alasady, & McGavigan, 2010). First, it can be
due to an acute, periodic restriction of blood flow to cardiac tissues. This can cause a
diversion of the electrical impulse through various pathways, leading to the appearance of
different QRS complexes on the ECG. It can also be caused by abnormalities of ion
channels that lead to other disturbances in the ECG such as the Long and Short QT
syndromes. Finally, polymorphic SVT can result from structural diseases within the heart
that affect the normal path of the ECS current (Stevenson & Kyoko Soejima, 2007).
death in developed nations (Lim, et al., 2010). It occurs when the ventricular cells begin
to depolarize and contract at random (Figure 13). The ECG is scattered and has no
discernable complexes, and there is no pulse during this rhythm. It is very dangerous, and
as of late there are not many treatment options available. The American Heart
Association estimates that nearly 310,000 people die as a result of V-fib per year
(American Heart Association, 2009; Torpy, 2010). For this reason, research on curative
damage or excess scar tissue within the heart. The excess scar tissue and damaged zones,
can cause a uni-directional block or a decrease in conduction. This paves the way for re-
entry and ectopic foci mechanisms that lead to arrhythmias (Lim et al., 2010).
Purkinje disease allows for the re-entry of mechanisms below the His-bundle, allowing
for a continual current conduction (Stevenson & Soejima, 2007). Because these
mechanisms generate frequent and uniform currents, they all produce monomorphic VT.
THE CARDIAC CONDUCTION 32
This is known as idiopathic (without a known cause), and can be once again evidenced in
the ECG (Stevenson & Soejima, 2007). There are two main categories of VT: those that
arise from ectopic focal mechanisms and those that occur in the left ventricle septum next
to the posterior papillary muscle in the heart. Ectopic foci are the most common cause of
idiopathic VT; they are able to stimulate conduction because of the automaticity of heart
cells (Josephson, 2003). VT associated with the left ventricular septum is less common
and has a less defined cause. Some physicians suggest it is caused by re-entry within the
Purkinje system. However, the exact function of the conductive system in these pathways
is ultimately unknown. This leaves another example of the importance of further research
Atrial fibrillation (AF) is the most common form of arrhythmia. It affects nearly
two million people in the United States (Boyle, Paul Fleming, & Hale, 2011). It is a type
of tachycardia that occurs when the atria begin to beat uncontrollably. It is described as
presenting as irregularly irregular (Neal, 2007). This is because the normal conduction
system in the heart goes from being systematic and coordinated to a highly disorganized
system. The atria contract at rates of 350-900 beats per minute, and because the impulse
is conducted slower through the AV node to the ventricles, they only contract 90-170
beats per minute. Sometimes this number is higher, but this unequal contraction in the
heart causes the heart to flutter (Andrews & Nelson, 2006). The mechanisms for atrial
fibrillation are still under question. However it is thought that much of AF is initiated and
THE CARDIAC CONDUCTION 33
maintained through re-entrant circuits in the pulmonary veins and right atrium (Chugh &
Morady, 2006).
The disorganized, rapid contraction does not generate enough force to supply the
body with blood. People with atrial fibrillation experience symptoms such as heart
occurrences atrial fibrillation is not harmless. However, prolonged episodes can increase
the risk of serious problems including blood clots, stroke, and heart failure. Atrial
fibrillation presents with an irregular pulse rate and recording on the electrocardiogram.
During atrial fibrillation, the complexes are not regularly formed, and the QRS
complexes are closer together indicating a rapid, irregular heartbeat (Torpy, 2010).
Figure 14. A normal heart and ECG (top) compared to a heart and ECG with atrial
fibrillation (bottom).
Re-entry and ectopic foci in the atria can lead to AF. Figures adapted and modified
from (Medical Disability Advisor, 2010) (Ryan, 2011).
THE CARDIAC CONDUCTION 34
Atrial fibrillation can be classified into four different types: lone, paroxysmal,
persistent, and permanent. Lone atrial fibrillation describes atrial fibrillation in younger
patients due to structural heart disease. Paroxysmal explains a condition that includes
periodic instances of atrial flutter. The patient normally returns to normal rhythm within
seven days, and the fibrillation episodes last for less than twenty-four hours. Persistent
AF occurs when episodes last more than seven days and require an outside influence or
in which the fibrillation persists for over a year. This generally only occurs when
interventional techniques have failed or not yet been attempted (Rosenthal, 2011).
(Figure 15). However, it elicits a slow heart rate. It occurs when the heartbeat is slowed
due to a failure of the electrical impulse to reach the atrioventricular node. Bradycardia
can be caused by pathologies. An example of this is Sick Sinus Syndrome. This is caused
by hardening of the SA node, and can result in escape beats in the ECG. These beats
come from ectopic foci that take over for the function of the SA node. Much research has
been done on this syndrome. It has become one of the more distinguished and explained
arrhythmias in the heart due to the research of JJ Wellens (Luderitz, 2009). It is generally
treated with a pacemaker, but the ablation procedure could offer a cure (Aaronson &
Ward, 2007). Many more arrhythmias exist: atrial flutter, atrioventricular block,
atrioventricular nodal re-entry tachycardia, and other conduction blocks associated with
the cardiac conduction system. Many of these arrhythmias have been cured and/or treated
History
Because of the wide range of malfunctions that occur within the conduction
system of the heart and the increase in technology available, physicians began to study
the mechanisms and treatment options for these arrhythmias. Eventually, a new clinical
discipline grew out of this research. This was known as interventional electrophysiology.
For many years doctors were unsure of the mechanisms and pathologies of heart
arrhythmias. In the 1960s, it was even believed that coronary bypass surgery was curative
for patients with ventricular tachycardia (Luderitz, 2009). The conduction mechanism
that occurs in heart issues was not yet completely understood. It is now clear that this
method was far too simplistic, but at that time other curative options were not available.
The only treatments that existed were pharmacological supplements, which suppressed
However, in the late 1960s and early 1970s many different discoveries allowed
the field of interventional electrophysiology to grow. Physicians began to use the catheter
(a thin, flexible tube) to examine, diagnose, and stimulate the conduction system of the
THE CARDIAC CONDUCTION 36
heart (Figure 16). This allowed scientists and physicians to come to a greater, less
simplistic understanding of the conduction system in the heart. As more and more
resecting damage tissues (in the 1970s), to repairing and restoring function (Luderitz,
2009). This was a complicated and invasive procedure, but it did provide an option for
those who could not undergo other treatments. In the 1980s the first curative catheter
ablation procedure was performed. At this time, however, the ablation procedure had
severe limitations. It could not treat ventricular tachycardia because physicians could not
make deep enough lesions in the tissue with the current technology (Josephson, 2003).
Mapping abilities were poor, leaving the performing physicians with less of an ability to
pinpoint the particular place to lesion (Lim et al., 2010). However, these mapping studies
generated enough research to allow physicians to further develop the ablation technique.
The catheter ablation is the most significant procedure to develop from the
science of electrophysiology (Figure 17). The techniques associated with this procedure
grew out of the mapping advances and studies during the 1970s and beyond (Josephson,
pharmaceuticals. It involves the insertion of a thin catheter into the heart (Cleveland
Clinic, 2010). Once vascular access is obtained, the physician must locate the critical site
of the arrhythmia. This is the area in which the arrhythmia originates or must pass
through to continue (Stevenson & Soejima, 2007). This could either be a location of
ectopic foci, over active pacemaker cells, or re-entry pathway. Depending on the patient,
type of arrhythmia, and source of arrhythmia, this part of the procedure varies from
patient to patient.
After determining the source of the origin of the arrhythmia, the physician must
be able to induce the arrhythmia from this site. During induction of the arrhythmia, the
physician must be able to pace the heart at a faster rate than the arrhythmia, at the same
rate as the arrhythmia, at a normal rate, and finally back to the rate of the arrhythmia
(Josephson, 2003). This confirms the diagnosis and assures that termination of the
arrhythmia is a potential result of the case. Without this conformation, the procedure
would be less accurate and successful. After induction, more mapping is performed in
order to pinpoint the source of the arrhythmia. Finally, the physician creates lesions with
a machine that delivers energy into the critical site. This is known as the ablation portion
of the procedure. The energy delivered disconnects the pathway, and therefore halts the
THE CARDIAC CONDUCTION 38
arrhythmia (Cleveland Clinic, 2010). Finally, after the lesions are created, the physician
tests the area to determine if the ablation was successful (Stevenson & Soejima, 2007).
developed nations, this procedure is becoming increasingly important (Lim et all, 2010).
Generally, ventricular tachycardia is not fatal in those with a healthy heart. However,
sustained VT has been shown as a leading cause of sudden death in patients with heart
disease (Stevenson & Soejima, 2007). Ablation has proven to be a successful cure for the
many that suffer from VT. The various techniques for ablation of ventricular tachycardias
grew out of the many mapping studies in the 1970s, and the ablation procedure has since
Guiraduon and his colleagues developed the first ablation technique to cure patients
THE CARDIAC CONDUCTION 39
suffering from SVT due to cardiac disease. This procedure was not ideal because it had a
high mortality rate. However, research continued, and the sources of most ventricular
arrhythmias were subsequently identified. He believed that they occur on the endocardial
surface of the heart. From this knowledge, Josephson implemented a technique that used
mapping capabilities to resect subendocardial areas of the heart. This proved successful,
and this technique is still used to eliminate VT in many different patients (Josephson,
2003).
Most types of ventricular tachycardia can be treated with ablation. The technique
used by most physicians is fairly standard. First, the critical site for the current must be
located. Then pacing abilities must be obtained at this site. Finally, once a site is
determined, lesions are created. After the lesions are created, the success of the procedure
is evaluated, and the case ends (Josephson, 2003). Although the general procedure
remains constant, the various types of VT are attacked differently. In patients with
previous heart damage, VT is much more dangerous and can arise from many different
circuits. Many have so much damage to the tissue that eliminating all triggers is
impossible. The goal of the ablation is to eliminate the most important, clinically relevant
pathways. There is a lower success rate in patients with damage because of the great
ventricular tachycardias are very favorable to the ablation process. The triggers are
caused by re-entrant pathways through the bundle branches. Once this site is determined,
a lesion is created. This has been found very effective, and with little complication. In
THE CARDIAC CONDUCTION 40
only treated with ablation in certain circumstances (such as an ectopic trigger in the
(Josephson, 2003).
used to prevent sudden death in patients with VT, these devices are not curative. They
simply provide a restorative shock to the heart when it does jump out of rhythm. Patients
with defibrillators (ICD) have a decreased quality of life due to the anxiety and stress of
the chance of a recurrent attack. Defibrillators are also associated with an increased
mortality in patients after a heart attack (Lim et al., 2010). It seems obvious that they
should not be a first treatment priority in patients with cardiac malfunction. Yet, many
patients receive these devices after an attack or if they are thought to be candidates for
VT. A study showed that VT reappears in 40-60% of patients who received a defibrillator
after an attack of ventricular tachycardia, and 20% of patients who received an ICD prior
to their first attack (Stevenson & Soejima, 2007). In spite of these numbers, many people
still opt for this mode of treatment over catheter ablation (Josephson, 2003).
that it should be. It is an inconvenience to those with it, and in prolonged instances can
lead to heart damage and failure. Anti-arrhythmic drugs are a popular treatment for VT,
but they are not ideal for many patients. Many side effects are associated with these
THE CARDIAC CONDUCTION 41
medications; some prescriptions even increase the risk of mortality in patients after a
heart attack. Although there are some benefits to these medications (they do not involve a
surgical procedure), there are too many side effects to implement these as the main
treatment for VT. Although some physicians may utilize pharmacological techniques for
a short period of time, ablation seems to be a much better choice for patients with heart
damage or disease. Ideally, catheter ablation should be the first mode of treatment for
those with SVT because it offers a cure for patients. It has a high success rate, and
relatively few complications. Other modes of treatment for VT do not offer the same
benefits. As technology continues to expand, the ablation procedure will only get more
The ablation procedure has also been used to effectively treat atrial fibrillation
(Figure 18). A major discovery that led to the ablations effectiveness in this area occurred
when Michel Haissaguerre determined that the pulmonary veins play a role in the
initiation of atrial fibrillation. Physicians began to research this and enacted the trigger
approach to ablations. The goal of this procedure is to eliminate triggers in ectopic foci
and the pulmonary veins (Figure 19). When the trigger is eliminated through the ablation
procedure, the atrial fibrillation ceases. However, this procedure is yet to be perfected,
and there is not one fix for all forms of atrial fibrillation (Chugh & Morady, 2006).
Because of the diverse and even unknown mechanisms that lead to atrial fibrillation,
there are many different ablation treatments that need to be conformed for each patient.
THE CARDIAC CONDUCTION 42
Generally, when patients are diagnosed with atrial fibrillation they are first treated
with medication for a period of time. This allows the physician to determine if the
THE CARDIAC CONDUCTION 43
to be an ideal option, but in reality it does not offer a cure for atrial fibrillation.
Medications have many limitations. They function to suppress the stimulation of atrial
fibrillation and protect against blood clots, and they are only completely effective when
taken as part of a strict schedule. Because patients are often not compliant with
medications, the reported statistics are often inaccurate. Atrial fibrillation can lead to
patients with AF (Singh & Murphy, 2009). Ablation offers this cure, and it should be
AV nodal ablation is one of these techniques (Figure 20). This procedure has been
used for many years, and its efficacy has even been shown (Lakshmanadoss, Aggarwal,
Huang, Daubert, & Shah, 2009). Atrioventricular nodal ablation is often used in patients
with recurrent AF that has not been sufficiently managed with medications and/or
pacemaker activity. However, during this procedure it is necessary to pace the heart from
a separate site other than the atrioventricular node. For many years this was performed
thorough the right ventricle. However, recent studies have shown that pacing from the
right ventricle can lead to dysfunction in the left ventricle, heart failure, and an increased
risk of mortality. These findings have led physicians to look for other methods of pacing
during AV node ablation. Two more modes of pacing have proven to be accompanied
with less risk: His bundle pacing and Bi-ventricular pacing. However, bi-ventricular
pacing can be complicated, because left ventricle pacing is hard to obtain. Therefore,
THE CARDIAC CONDUCTION 44
studies have shown that His bundle pacing may be safer and more effective during AV
nodal ablation.
ablation. This procedure consisted of the main aspects of the normal ablative procedure.
The physicians obtained vascular access of the His bundle. After access was obtained,
pacing was initiated in the His bundle. It was determined that this was a critical and
acceptable site that was able to adequately mimic the arrhythmia. Finally, permanent
pacing was applied, and the effectiveness was tested and achieved. During this procedure,
there were no signs of the normal complications that occur during RV pacing
(Lakshmanadoss et al., 2009). As exciting as these findings are, these results originate
from only a six-month follow-up visit. It is clear that there must be more long-term
THE CARDIAC CONDUCTION 45
studies performed in this area. Although many would say this study was an exciting
ostial ablation (Figure 21). This technique can be used for patients with paroxysmal atrial
fibrillation, as well as those who suffer from atrial fibrillation due to ectopic foci in the
pulmonary veins (Tamborero et al., 2007). This procedure was the first interventional,
trigger catheter ablation technique used to treat atrial fibrillation. It utilizes a circular
mapping technique along with a larger tipped ablation catheter that allows the physician
to deliver higher energy near the critical site within the pulmonary vein. The high energy
current produces the risk of the hardening of the pulmonary vein. Although physicians
have taken measures to prevent vein hardening, it is still a problem associated with this
technique. Segmental ostial ablation is shown be effective in greater than fifty percent of
patients, with a complication rate of less than nine percent (Tamborero et al., 2007).
Segmental ostial ablation is most effective in patients with paroxysmal AF; those
with persistent AF have less success during this procedure. The University of Michigan
has performed long-term studies (with a three year follow-up) on the efficacy of this
procedure (Chugh & Morady, 2006). However, there is a sufficient lack of data regarding
the effects of ablative procedures greater than five years post-operation. This is one of the
primary reasons some physicians are still hesitant to offer ablation as the primary
treatment option. In spite of this deficit, the curative and diverse benefits of the ablation
Because of the many different origins and mechanisms behind atrial fibrillation,
various modifications have been made when using to the catheter ablation procedure to
cure AF (Weerasooriya et al., 2011). Many of these involve ablation (the creation of
lesions) in areas of the pulmonary veins. This is because current research shows that
much of the atrial fibrillation is triggered inside these veins, or within their attachment to
the right atrium. Another influential ablation procedure, atrial circumferential ablation,
utilizes the new mapping technologies. This ablation technique has proven to be very
effective in curing paroxysmal atrial fibrillation. However, it also has the tendency to
transform atrial fibrillation into atrial flutter. Although this condition is less serious than
AF, this side effect prevents the complete curative nature of the procedure (Chugh &
THE CARDIAC CONDUCTION 47
Morady, 2006). Ablation still remains to be the most curative and preferential procedure
regarding the ablation procedure, many physicians still choose to treat atrial fibrillation
with more traditional methods. A number atrial fibrillation cases are managed with
pharmaceuticals for a period of time before the ablation procedure is even considered
(Singh & Murphy, 2009). Although it is clear that more research must be conducted on
the results of the ablation procedure, it remains the most effective, curative method for
treating atrial fibrillation. The catheter ablation procedure has been successfully used to
treat patients whose AF cannot be treated with medication alone (Weerasooriya et al.,
2011). This procedure has also been utilized in conjunction with pacemakers and
defibrillators, when they are not able to sufficiently manage a patients atrial fibrillation
(Lakshmanadoss et al., 2009). Physicians are performing novel procedures and adapting
techniques to treat a varying degree of patients. Although there is still a large gap in
information regarding these techniques, physicians are making strides to perform long-
term research that will lead to a greater efficacy during the ablation procedure
greatly contributed to the success of the ablation procedure. These scientists have
years, new ablative energies have been developed, new catheters have been developed,
and mapping abilities have greatly increased. Direct current was the first form of energy
THE CARDIAC CONDUCTION 48
used to create lesions in the tissue (Josephson, 2003). This was not ideal because it
created a mini explosion in the tissue, which led to less control of the procedure and
greater complications (Lim et al., 2010). This was replaced by cryoablation, which did
not have as high of a success rate (Josephson, 2003). Currently, physicians are using
radio-frequency ablation. This offers a more controllable and safe source of energy for
the creation of lesions in the heart muscle. The type of catheter tip has also evolved from
the beginning stages of interventional electrophysiology. Physicians are now able to use
irrigated tip catheters, which allows the control of temperature at the catheter tip. This
helps to eliminate blood pooling, increases power delivery, and reduces the risk of clot
formation. The mapping abilities available to physicians have also lead to an increase in
There is still much unknown about ventricular tachycardia and the causes of other
under-researched. However, physicians are currently reporting a 70% success rate, and
10-40% recurrence rate (Josephson, 2003). In those with recurrent arrhythmias, a second
ablative procedure is often more terminally curative (Lim et al., 2010). Sometimes,
inadequate mapping and pacing techniques can alter the efficacy of the ablative
procedure. There is clearly room for improvement within the catheter ablation
procedures, but its success thus far is undeniable (Josephson, 2003). The most recent
research shows a high success rate in most ablative procedures accompanied by a low
risk of complications (Lim et al., 2010). Physicians are in the process of perfecting and
THE CARDIAC CONDUCTION 49
making corrections to the procedure. As they incorporate more research into their
practices, the ablation procedure will become more curative and accurate.
recurrences. Thus far, when a repetitive complication arises within the ablation
demonstrated that the use of intravenous magnesium treatments could help buffer this
problem (Sachin et al., 2008). The threat of clot formation during RFCA was remedied
by the administration of heparin to thin the blood. When it was found that this same
treatment was found to be highly successful in the trial phase, and should significantly
reduce thrombotic events as well as other bleeding complications that may arise during
the ablation procedure (Patel et al., 2007). Research regarding the ablation procedure has
It is evident that the effectiveness of the ablation procedure would greatly benefit
from more research and innovation. The use of various pacing techniques is an example
of this. Pacing in some areas of the ECS has been shown to increase complications and
reduce the efficacy of the ablation (in permanently curing arrhythmias). Currently,
physicians are combatting these complications. They have discovered new methods for
pacing during the ablative procedure. These include His bundle and bi-ventricular pacing
THE CARDIAC CONDUCTION 50
care is also an issue that must be addressed. Often after an ablation, a patient must be
Electrophysiologists are in the process of determining how to reduce this need for
many different types of arrhythmias such as: AV nodal re-entrant tachycardia, accessory
pathways, atrial flutter, atrial fibrillation, and ventricular tachycardia, there are still
complications and side effects associated with this procedure. In order for some to
consider the ablation procedure a foremost treatment option, these issues must be
addressed.
field, its novelty is often forgotten. There have been many advances in the field of
electrophysiology since its inception in 1979. Physicians have learned the mechanisms
behind arrhythmias, as well as developed curative and preventive measures for such
problems. The most exciting development out of this field, the ablation procedure, arose a
little over 30 years ago. The majority of these years have been spent perfecting the
mapping, pacing, and ablation techniques that have led to the accuracy of the current
procedure (Josephson, 2003). This has left little room for significant long-term research
regarding the ablation techniques. As the procedure continues to develop, there will be an
increase in studies regarding its effectiveness, curative nature, and complication rate. One
such study reported by Lim, Singleton, Alasady, and McGavigan (2010) spans five years,
THE CARDIAC CONDUCTION 51
and reveals many exciting results from the ablation procedure. As many fear that
mortality rate after the procedure (Lim et al., 2010). In order to address skeptics of the
ablation procedure, this type of research is necessary and will increase the awareness of
significance of its malfunctions, and the high efficacy of the ablation procedure in curing
these aberrations, the catheter ablation procedure should be considered a priority when
electrophysiology, especially on the ablation procedure and its techniques, will greatly
benefit the health of many Americans. As Americans continue to age and obesity
diagnosed each year. One study has predicted that in the next fifty years, Americans will
see a three-fold increase in the number of patients with atrial fibrillation alone (Neal,
2007). This is just one of the many arrhythmias that can be cured through the ablation
procedure. Although there is currently not a great deal of long-term research regarding
this procedure, the efficacy of the ablation has yet to be disproven (Josephson, 2003). The
significance of the electrical conduction system in the heart is clear, and the further
development of the ablation procedure to treat its malfunctions will greatly benefit
cardiovascular medicine.
THE CARDIAC CONDUCTION 52
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