Anda di halaman 1dari 58


The Cardiac Conduction System: Clinical Electrophysiology and Cardiac Ablation

Jessica Schucht

A Senior Thesis submitted in partial fulfillment

of the requirements for graduation
in the Honors Program
Liberty University
Fall 2011


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

distributes blood throughout the cardiovascular system. Heart contraction is controlled by

an electrical conduction system within the heart. The electrical activity can be visualized

in a recording known as an electrocardiogram (ECG). This conduction system can

malfunction causing a heart arrhythmia. Some heart arrhythmias can be dangerous,

causing illness or death. Improved techniques in imaging have allowed the growth of the

clinical discipline interventional electrophysiology. Medical personnel can now change

some abnormal electrical patterns thorough a procedure known as the ablation technique.

The Cardiac Conduction System: Clinical Electrophysiology and Cardiac Ablation

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

estimated that every thirty-eight seconds an American dies of cardiovascular disease

(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

must be diagnosed, assessed, and treated.

Although a few types of arrhythmias are harmless if untreated, the seriousness of

these electrical malfunctions eventually led to the development of a relatively new field

of medicine known as interventional cardiac electrophysiology. Since its inception in

1979, interventional cardiac electrophysiology has arisen as a medical sub-specialty and

is quickly developing very influential therapies. The electrocardiogram and various

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

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

many different forms of arrhythmias.

Because of the novelty of the cardiac ablation, there is a lack of research

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

system, which is vital to human survival. Electrophysiology is a relatively new field,

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

performing the ablation procedure in order to cure patients arrhythmias.

The Hearts Anatomy and Its Importance

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

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

rhythmic contraction is controlled by the cardiac conduction system in the heart. A

malfunction in this system could lead to improper or insufficient contractions, which

would hinder the normal propulsion of blood through the heart.

Figure 1. Pericardium Layers.

The pericardium consists of various layers. These include the fibrous, parietal,
and visceral layers. Figure obtained and modified from (Marieb, 2001)

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

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

cardiovascular system, the heart.

Figure 2. Cellular components of the myocyte.

These components are vital to the myocytes function, especially in relation to the
ECS. Figure obtained and modified from (Cummings, 2004).

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

functioning properly, these anatomical structures can malfunction.

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

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).

Figure 3. Heart Anatomy.

The hearts anatomy can help to explain its various functions. Figure
obtained and modified from (UK Health Care, 2007).

Action Potentials Drive the Cardiac Cycle

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

ions such as Ca2+, Na+, and K+.

Figure 4. Action Potential Propagation. Figure 5. Muscle Cell Components.

Action potential propagation occurs through The intercalated discs allow for
ion currents. Figure obtained and modified increased flow of ions. Figure obtained
from (Bulman-Fleming, 2000). and modified from (Doohan, 2000).

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

enters the cell causing it to become depolarized even further. Because the connexin

protein in cardiac gap junctions offers a low-resistance connection between cells, it

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).

Figure 6. Fast Response Depolarization and Repolarization Curve.

The repolarization and depolarization of the heart muscle can be seen in this type
of curve. Figure obtained and modified from (Zubieta-Calleja & Paulev, 2004).

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

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

that could lead to an arrhythmia (Klabunde, 2007).

The Electrical Components of the Heart Control the Cardiac Cycle

The SA node is a group of cells approximately 2 mm thick and 8 mm long that

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

depolarized, repolarized, and depolarized again, they spread a wave of depolarization

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

(Mohrman & Heller, 2010).


Figure 7. Cardiac Conduction System Components.

The cardiac conduction system contributes to the correct functioning of the
heart muscle. Figure adapted and modified from (Cunningham & Saunders,

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

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,


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

propagation of an impulse to continue. This is known as the atrioventricular node (AV

node). Therefore, after some delay, the AV node receives the impulse that began in the

SA node (Mohrman & Heller, 2010).

The AV node is a group of cells about 22 millimeters long, 10 millimeters wide,

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

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

complex arrangement of cells, which eventually stimulate the contraction of the

ventricles of the heart (Levy & Pappano, 2007).

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

parasympathetic stimulation, it is even possible to obtain a complete AV block, when no

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.

Sympathetic innervation enhances the rhythmicity of conduction cells and therefore

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

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-

ventricular pacemakers, which contribute to the automaticity of these fibers. However,

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,

heart failure can follow.

The Cardiac Cycle and Its Components

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

components of the heart (Klabunde, 2005). A malfunction of any of these components

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

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 cardiac cycle begins (Mohrman & Heller, 2010).

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

blood into the ventricles.


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

increasingly important to ventricle filling. Any number of malfunctions in the electrical

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


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

cycle, the volume in the heart remains constant. For this reason, it is termed the

isovolumetric phase. The ventricles contain about one hundred-twenty milliliters of

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

multiplied by 100 percent. An efficiency of 50 to 70 percent is normal for a healthy adult.

However, if there is a malfunction in the cardiac cycle due to disease, damage, or an

arrhythmia, this number can be much smaller and be an indication of a cardiac

malfunction (Cleveland Clinic, 2011).

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

gradient. The semilunar valves are once again closed due to the backflow of blood from

the aorta and pulmonary trunk (Potter, 2011).

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

these components is malfunctioning, there could be severe consequences. The cardiac

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.

The Clinical Use of Cardiac Electrophysiology

The Electrocardiogram Contributes to Clinical Diagnosis

The cardiac cycle and cardiac conduction system can be visualized in an

electrocardiogram (Figure 8). An electrocardiogram (ECG) is a powerful tool that is used

to evaluate cardiologic functions such as heart rate, rhythm, and the conduction

characteristics of heart tissues (Mohrman & Heller, 2010). It was first performed in

humans in 1887 and grows increasingly important as the science of interventional

electrophysiology develops (Luderitz, 2009). It is such a powerful tool because it can be

used to diagnose conduction problems that would go unnoticed otherwise. Some of the

main problems that can be diagnosed by an ECG include: cardiac rhythm disturbances,

heart attacks, and myocardial ischemia.

Figure 8. Typical ECG Reading.

The ECG is a very useful tool in clinical electrophysiology. Figure adapted
and modified from (Dahan & Sade, 2004).

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

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).

Figure 9. Einthovens Lead Placement and Explanation.

The three lead placement records the electrical potentials from different
perspectives across the heart. Figure adapted and modified from (The
McGill Physiology Virtual Laboratory, 2011)

However, for clinical purposes, a more intensive lead placement provides a more

accurate diagnostic tool. This placement is based on Einthovens original triangle of

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.

They provide a view of the heart at a different angle than the bipolar and augmented

placements, and therefore provide a recording of a different plane of electrical activity in

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

voltage difference between any two of the leads (Klabunde, 2005).

Figure 10. The augmented and precordial lead placements.

The placement of the augmented leads (left) generates a view of the frontal plane of the
heart. The placement of the unipolar precordial provides a view of the heart from several
different angles. Figure adapted and modified from (Klabunde, Cardiovascular
Physiology, 2007).

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

Figure 8). Throughout variations in these complexes, electrophysiologists have learned to

detect and treat heart arrhythmias.

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

largest spike because it represents the coordinated depolarization of many ventricular

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

repolarization is not synchronous. The synchronous depolarization of the ventricle cells

completely overshadows the atria repolarization; therefore, the ECG does not detect this

voltage difference (Mohrman & Heller, 2010).

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

unlike ventricular depolarization, ventricular repolarization does not occur synchronously

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 leads. Second, because the electrical wave has not yet reached the AV node, the

ventricle cells are still resting (Mohrman & Heller, 2010).

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

blood (Mohrman & Heller, 2010).

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

exist (Mohrman & Heller, 2010).

Because it encompasses many cardiac functions, is simple to perform, and

represents universal readings in healthy adults, the electrocardiogram has become a

powerful tool in the field of electrophysiology. Various pathologies can be determined by

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

of the reading represents one second of time. When evaluating the electrocardiogram

reading, a diagnostician examines each complexs duration, frequency, and amplitude to

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

system in the ventricles.

Cardiac Malfunctions That Can Be Detected by the Electrocardiogram

Abnormalities in the electrical conduction system can severely undermine the

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

known as arrhythmias. Various arrhythmias of the heart include tachycardia, bradycardia,

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,


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

fibrillation (Levy & Pappano, 2007).

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

die because it cannot repolarize these tissues (Klabunde, 2007).

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

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

rate, causing various types of tachycardia.

Sinus tachycardia (Figure 11) occurs when there is an increased firing of the

sinoatrial node (normally due to sympathetic stimulation). It normally occurs during

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).

Another form of tachycardia that can be inconsequential is known as

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

nodes pacemaker function. Supraventricular tachycardia can be diagnosed from looking

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

waves. Symptoms of supraventricular tachycardia include dizziness and low blood


pressure. It can be treated many different ways; however, recently the ablation procedure

has been used as a curative measure (Mohrman & Heller, 2010).

Figure 11. A normal ECG (top) compared to an ECG reading of Sinus Tachycardia
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).

Ventricular tachycardia (VT) is a common arrhythmia that describes a condition

in which the ventricles depolarize and contract apart from atrial contraction (Segal,

2002). This accelerated ventricular depolarization is generally caused by re-entry

mechanisms or ectopic foci. Ventricular tachycardia is clinically defined as the presence

of three or more consecutive QRS complexes on the ECG, occurring at an accelerated

rate (over 100bpm). If these accelerated complexes last for a duration longer than thirty

seconds, or elicit symptoms, the condition is described as sustained ventricular

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

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).

Polymorphic VT (Figure 12) is a very serious problem because it can lead to

idiopathic ventricular fibrillation. Ventricular fibrillation is the most common cause of

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

procedures has become very important.

Figure 12. An ECG reading for a case with polymorphic VT.

The complexes are not defined, and the QRS complexes are near
unrecognizable. Figure adapted and modified from (Krusor, 2009).

Figure 13. The activity of the ECS during polymorphic VT.

Various ectopic foci can contribute to increased ventricular contraction. Figure
adapted and modified from (Washington Heart Rhythm Associates, LLC).

Monomorphic ventricular tachycardia describes the condition in which each

frequently occurring QRS complex is similar. This is generally indicative of ventricular

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).

Monomorphic VT can also be caused by surgical incisions as well as Purkinje disease.

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.

Monomorphic VT can also occur in patients without known structural damage.

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

in the area of electrophysiology (Josephson, 2003).

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

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

palpitations, shortness of breath, discomfort, fatigue, and dizziness. In infrequent

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).

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

treatment to resume normal pacing activity. Finally, permanent AF describes a condition

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).

Bradycardia is yet another type of arrhythmia caused by a malfunction in the ECS

(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

through the new science of clinical cardiac electrophysiology.


Figure 15. Bradycardia ECG Reading.

Bradycardia is characterized by a larger time gap between each QRS complex in
the ECG. Figure adapted and modified from (, 2008)

The Development of Clinical, Interventional Cardiac Electrophysiology


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

arrhythmias but did not cure them (Josephson, 2003).

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

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

discoveries were made, electrophysiology grew. Physicians went from completely

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.

Figure 16. Catheter entrance into the heart.

The heart catheter has allowed physicians to gain a deeper understanding of
the functions of the heart. Figure adapted and modified from (United
Therapeutics, 2011)

The Catheter Ablation Procedure

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,

2003). Ablation is an ideal treatment for arrhythmias, as it is curative, unlike

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

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).

Figure 17. Diagram of a Radiofrequency Ablation Procedure.

This procedure uses radiowaves to create the lesions and cure the arrhythmia.
Figure adapted and modified from (Medical University of South Carolina).

As ventricular arrhythmias are the most common cause of sudden death in

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

been shown to successfully cure various forms of ventricular tachycardia. In 1970,

Guiraduon and his colleagues developed the first ablation technique to cure patients

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,


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

amount of re-entrant circuits available due to the damaged tissue. Monomorphic

ventricular tachycardias are very favorable to the ablation process. The triggers are

generally easy to determine. Bundle-branch VT is an example of this; it is generally

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

spite of the success of the ablative procedure in monomorphic VT, polymorphic VT is

only treated with ablation in certain circumstances (such as an ectopic trigger in the

Purkinje system, which leads to random stimulation). Polymorphic ventricular

tachycardia is controlled with an implanted defibrillator or the use of pharmaceuticals

(Josephson, 2003).

Two other modes of treatment for ventricular tachycardia are defibrillator

implantation and anti-arrhythmic pharmaceuticals. Although defibrillators have been

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).

Ventricular tachycardia is a common phenomenon, and if it can be cured it seems

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

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

effective and influential in curing ventricular tachycardias (Josephson, 2003).

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.

Figure 18. The ablation procedure for AF.

The mapping catheter is used to find the area, while the ablation catheter is used to
create lesions. Figure adapted and modified from (Shapira, 2009).

Figure 19. After cardiac ablation.

After cardiac ablation the impulses cannot transverse the lesions. Figure
adapted and modified from (Beth Israel Deaconess Medical Center, 2010).

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

condition can be managed pharmaceutically. Pharmaceutical treatment is often believed

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

serious cardiac malfunctions, and it is important that a curative option be offered to

patients with AF (Singh & Murphy, 2009). Ablation offers this cure, and it should be

prescribed more to treat this illness.

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,

studies have shown that His bundle pacing may be safer and more effective during AV

nodal ablation.

Figure 20. AV Nodal ablation.

The AV nodal ablation is used as a treatment for AF. Figure adapted and
modified from (Healthwise, 2010).

One study performed on a 66-year-old woman helps to demonstrate an effective

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

studies performed in this area. Although many would say this study was an exciting

breakthrough, it is not sufficient to determine a procedures effectiveness solely based on

short-term follow up visits. It is necessary to monitor patients.

Another ablative technique used to cure atrial fibrillation is termed segmental

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

procedure should still be recognized.


Figure 21. Fluoroscope image taken during a PV ostial ablation procedure.

This type of ostial ablation technique can be used to treat paroxysmal AF. The
figure depicts the HRA (high right atrium), ABL (ablation catheter), CS (coronary
sinus,), His catheter, and Lasso guidance. Figure adapted and modified from (Lee
et al., 2010)

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 &

Morady, 2006). Ablation still remains to be the most curative and preferential procedure

when treating AF.

Because of the lack of information regarding long-term and residual effects

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

(Weerasooriya et al., 2011).

The vast amount of research performed by the pioneers of electrophysiology has

greatly contributed to the success of the ablation procedure. These scientists have

significantly improved the discipline of interventional electrophysiology. In less than 30

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

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

the efficacy of ventricular tachycardia (Josephson, 2003).

There is still much unknown about ventricular tachycardia and the causes of other

arrhythmias. In addition, the long-term efficacy of the catheter ablation procedure is

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

making corrections to the procedure. As they incorporate more research into their

practices, the ablation procedure will become more curative and accurate.

This has been evidenced through physicians responsiveness to complications and

recurrences. Thus far, when a repetitive complication arises within the ablation

procedure, a group of physicians has determined a method to overcome the difficulty. It

was determined that a magnesium deficiency resulted due to combination of anti-

arrhythmic medication and the ablation procedure. A group of physicians eventually

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

heparin could cause other types of bleeding complications, a group of physicians

proposed the administration of protamine post-op to reduce these problems. This

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

allowed for an increase in its overall safeness and efficacy.

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

in place of sole right ventricular pacing (Lakshmanadoss et al., 2009). Post-operative

care is also an issue that must be addressed. Often after an ablation, a patient must be

treated with pharmaceuticals to reduce the risk of a recurrent abnormal rhythm.

Electrophysiologists are in the process of determining how to reduce this need for

pharmaceuticals (Sachin et al., 2008). In spite of a lack of long-term research, physicians

continue to make improvements to the ablative procedure. Although it is able to treat

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


Although some view interventional electrophysiology as an under-researched

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,

and reveals many exciting results from the ablation procedure. As many fear that

mortality related to ablation could be a long-term complication, this study showed a 0%

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

the benefits of this technique.

Due to the importance of the cardiac electrical conduction system, the

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

treating an arrhythmia. More research conducted in the discipline of interventional

electrophysiology, especially on the ablation procedure and its techniques, will greatly

benefit the health of many Americans. As Americans continue to age and obesity

continues to rise, there will be a significant increase in the number of arrhythmias

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.


Aaronson, P. I., & Ward, J. P. (2007). The cardiovascular vascular system at a glance

(3rd ed.). Malden, MA: Blackwell Publishing.

American Heart Association. (2009, December 17). Heart disease and stroke statistics --

2010 update: A report from the American Heart Association. Circulation: Journal

of the American Heart Association, 120, 46-215.

Andrews, M., & Nelson, B. P. (2006). Atrial fibrillation. The Mount Sinai Journal of

Medicine, 73(1), 482-492.

Beth Israel Deaconess Medical Center. (2010). Treatments - Beth Israel Deaconess

Medical Center. Retrieved October 31, 2011, from Beth Israel Deaconess Medical

Center :



Boyle, N. G., Fleming, P. M., & Hale, K. L. (2011). Atrial fibrillation. Retrieved 9 2011,

September, from E Medicine Healthy:

Bulman-Fleming, D. B. (2000). Action potential propagation. Outline for Sept. 21, 2000.

Children's Hospital of Wisconsin. (2011). Arrhythmias. Retrieved November 14, 2011,

from Children's Hospital of Wisconsin:

Chugh, A., & Morady, F. (2006). Atrial fibrillation: Catheter ablation. Journal of

Interventional Cardiac Electrophysiology, 16, 15-26.

Cleveland Clinic. (2010, June). Treatment: Catheter ablation. Retrieved September 10,

2011, from Cleveland Clinic Institutes and Services:

Cleveland Clinic. (2011). Understanding your ejection fraction. (M. Eileen Hscich, & M.

Bruce Wilkoff, Editors) Retrieved September 8, 2011, from Cleveland Clinic:

Cummings, B. (2004). Human anatomy & physiology. New York, NY: Pearson


Cunningham, J., & Saunders. (2002). Conduction system of the heart. Textbook of

veterinary physiology. New York, NY: Elsevier.

Dahan, T., & Sade, A. (2004). An ECG is a recording of the electrical activity that

initiates each heartbeat. Application of ICA in removing artifacts from the ECG.

(E. Klaiman, Ed.)

Dong-Hyeon Lee, M., Yong-Seog Oh, M., Woo-Seung Shin, M., Ji-Hoon Kim, M., Yun-

Seok Choi, M., Sung-Won Jang, M., et al. (2010, September 30). A transthoracic

echocardiographic follow-up study after catheter ablation of atrial fibrillation:

Can we detect pulmonary vein stenosis by transthoracic echocardiography?

Retrieved November 1, 2011, from Korean Circulation Journal:


Doohan, J. (2000). Cardiac muscle. BioMed 108: Human physiology. New York, NY:

McGraw-Hill Companies.

Eric Chudler, P. (2010). Action potential. Retrieved August 20, 2011 from Neuroscience

for kids:

Healthwise. (2010, November 2). AV nodal ablation. Retrieved November 1, 2011, from,,zm6205,00.html

Josephson, M. E. (2003, October). Electrophysiology of ventricular tachycardia: A

historical perspective. PACE, 26(10), 2052-2067.

Klabunde, R. E (2007, 04 06). Cardiovascular physiology. Retrieved August 30, 2011,

from Cardiovascular Physiology:

Klabunde, R. E. (2005). Cardiovascular physiology concepts. Philadelphia, PA:

Lippincott, Williams, & Wilkins.

Krusor, B. (2009, May 26). Timing of defibrillation shocks for resuscitation of rapid

ventricular tachycardia. Retrieved October 28, 2011, from Cardiac science:


Lakshmanadoss, U., Aggarwal, A., Huang, D. T., Daubert, J. P., & Shah, A. (2009). His

bundle pacing post AVN ablation. Pacing and Clincal Electrophysiology, 32(8),


Levy, M. N., & Pappano, A. J. (2007). Cardiovascular Physiology (9th ed.).

Philadelphia, PA: Mosby Elsevier.


Lim, H., Singleton, C., Alasady, M., & McGavigan, A. (2010). Catheter Ablation for

Ventricular tachycardia. Internal Medicine Journal, 40(10), 673-681.

Luderitz, B. (2009). Historical perspectives of cardiac electrophysiology. Hellenic

Journal of Cardiology, 50, 3-16.

Mahadevan, V. (2008). Anatomy of the heart. Surgery (Oxford), 26(12), 473-476.

Malmivuo, J., & Plonsey, R. (1995). Bioelectromagnitism - principles and applications of

bioelectric and biomagnetic fields. New York: Oxford University Press.

Marieb. (2001). Pericardium. Retrieved October 31, 2011, from Human anatomy &



Medical Disability Advisor. (2010). Atrial fibrillation. Retrieved October 31, 2011, from

MD guidelines:

Medical University of South Carolina. (n.d.). Thermal ablation research group.

Retrieved October 31, 2011, from Medical University of South Cariolina:

Mohrman, D. E., & Heller, L. J. (2010). Cardiovascular physiology (7th ed.). New York,

NY: The McGraw-Hill Companies.

Neal, J. (2007). Atrial fibrillation. Practice Nurse, 33(11), 46-51.

Patel, A. A., Clyne, C. A., Henyan, N. N., White, C. M., Zembrowski, B. F., Migeed, M.,

Coleman, C. (2007). The use of protamine after radiofrequency catheter


ablation: A pilot study. Journal of Interventional Cardiac Electrophysiology, 18

(2), 155-158.

Potter, D. H. (2011). The heart. (U. C. College, Producer) Retrieved September 7, 2011,

from 106 Lecture: (2008). Sinus bradycardia - slow heart rate. Retrieved

October 30, 2011, from Preventing a heart attack: http://www.preventing-a-heart-

Rosenthal, L. M. (2011, August 11). Atrial fibrillation. Retrieved September 7, 2011,

from Medscape Reference:


Ryan, S. S. (2011, 01 01). Atrial fibrillation overview. Retrieved October 31, 2011, from

Atrial Fibrillation Resources for Patients:

Sachin, S. A., Clyne, C. A., Henyan, N., Migeed, M. M., Yarlagadda, R., Silver, B. B.

White, C. Michael (2008). The impact of magnesium sulfate on serum magnesium

concentrations and intracellular electrolyte concentrations among patietns

undergoing radio frequency catheter ablation. Connecticut Medicine, 72(5), 261-


Segal, A. (2002). EKG tutorial: Ventricular rhythms. Retrieved September 9, 2011, from

Shapira, Adam R. (2009, November 15). Catheter ablation of supraventricular

arrhythmias and atrial fibrillation. American Family Physician, 80(10), 1089-1094


Singh, R., & Murphy, J. J. (2009). Electrocardiogram and arrhythmias. Anaesthesia and

Intensive Care Medicine, 10(8), 381-384.

Stevenson, W. G., & Soejima, K. M. (2007). Interventional cardiac electrophysiology:

Catheter ablation for ventricular tachycardia. Circulation, 115, 2750-2760.

Stiles, S. (2009, June 11). Success, complication rates for ablation therapy of atrial fib

are consistent in meta-analysis. Retrieved October 2011, 28, from Arrhthmia &


Tamborero, D., Mont, L., Molina, I., Matiello, M., Berruezo, A., Sitges, M., Brugada,

Josep (2007). Selective segmental ostial ablation and circumferential pulmonary

veins ablation: Results of an individualized strategy to cure refractory atrial

fibrillation. Journal of Interventional Cardiac Electrophysiology, 19(1), 19-27.

The McGill Physiology Virtual Laboratory. (2011, November). Cardiovascular

laboratory. Retrieved November 6, 2011, from The McGill University physiology

virtual laboratory:

Torpy, J. M., Lynm, C., & Glass, R.M. (2010). Atrial fibrillation. The Journal of the

American Medical Association, 303(4), 380-380.

UK Health Care. (2007). Basic anatomy of the heart. Retrieved October 21, 2011, from

UK Healthcare Transplant Center:

United Therapeutics. (2011). About right heart catheterization. Retrieved October 31,

2011, from Living pah:


Washington Heart Rhythm Associates, LLC. (n.d.). Ventricular tachycardia. Retrieved

October 31, 2011, from Washington heart rhythm associates:

Weerasooriya, R., Khairy, P., Litalien, J., Macle, L., Hocini, M., Sacher, F., Jais, MD,

Pierre (2011). Catheter ablation for atrial fibrillation. Journal of the American

College of Cardiology, 57(2), 160-166.

Yale Medical Group. (2011). Electrocardiogram (EKG)/stress test/holter monitor.

Retrieved August 20, 2011, from Yale School of Medicine:

Zubieta-Calleja, G., & Paulev, P.-E. (2004). New human physiology. Fig. 11-2:

Recordings of ECG (above), intracellular membrane potential (red curve) and

contraction (blue curve) of one heart cycle in a ventricular fibre. , 2nd.