SUPRAVENTRICULAR TACHYCARDIA

Compiled By:

HARASTHA KHAIRI AFINA 090100028

ANNISSA AUDREA ARYANI 090100166
FINA FADILA MAYASARI 090100185

Supervisor : dr. Nizam Akbar Sp.JP (K)

DEPARTEMENT OF CARDIOLOGY
H. ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINE
SUMATERA UTARA UNIVERSITY
MEDAN
2013
 TABLE OF CONTENTS

CHAPTER I INTRODUCTION ................................................ 1

1.1. Background ............................................................ 1
1.2. Objective ............................................................ 1
CHAPTER II LITERATURE REVIEW .................................... 2
2.1. Origin and Spread of Excitation in the Heart ................ 2
2.2. Abnormalities of Cardiac Rhythm (Arrythmia) ............. 6
2.3. Pathophysiology of Supraventricular Tachicardia (SVT) 12
2.4. SVT Classification and Appereance ............................ 25
2.5. Differential Diagnose.................................................... 39
2.6. Clinical Presentation ..................................................... 39
2.7.Interpretation of ECG Finding in PSVT......................... 40
2.8. Treatment ....................................................................... 47
2.9. Electrophysiology .......................................................... 56

CHAPTER III CASE REPORT ................................................ 68

CHAPTER IV CONCLUSION ................................................ 79

REFERENCES ........................................................................ 80
 PREFACE

Praise God for his gratitude and blessings so that we can finally be able to
complete the case report entitled "Supraventricular Tachycardia" well. This case report is
written in order to fulfill the duty of senior clinical assistant of clinical rotation in
pediatric department. This paper is expected to increase the knowledge and insight,
especially about SVT.

The authors would also like to thank the supervisor, dr.Nizam Akbar, Sp.JP (K) to
give guidance, suggestions, and assessment for this case report.

Last of all, we realize despite the effort we have put into this case report, there
are still errors and flaws in our work. Therefore we encourage and welcome suggestion,
advice and critics that will facilitate the improvement of this paper. Hopefully this
scientific work can contribute to development of medical science in particular.
 CHAPTER I
INTRODUCTION

1.1. Background

Arrhythmias result from disorders of impulse generation, disorders of

impulse conduction or the combination of both. The trigger for a run of
ventricular tachycardia, where the disorder is predominantly due to conduction
abnormalities secondary to myocardial disease, may be a premature ventricular
beat due to a disorder of impulse generation. There are two described types of
disorders of impulse generation; abnormal automaticity and triggered activity.

The narrow QRS tachycardias or supraventricular tachycardias (SVTs) as

they are more popularly known, generate considerable academic interest.
Supraventricular arrhythmia are relatively common, ocasionally persistent and
rarely life threatening. The participants of supraventricular arrhythmia vary with
age, sex, and associated comorbidity.

In the last few years the fundamental mechanism of each has been
elucidated and many have been shown to be based upon reentry whether
anatomical or functional. As the ultimate inmanagement strategies, curative
radiofrequency ablation has forced a reappraisal of what the aim of treatment
should be and its success has focused attention on our new knowledge of
arrhythmia anatomy. Yet there is much that remains to be established.

1.2. Objective
The aim of this study is to explore more about the theoritical aspects on
arrhythmia supraventricular tachycardia, and to integrate the theory and
application of supraventricular tachycardia cases in daily life.
 CHAPTER II
LITERATURE REVIEW

2.1. Origin and Spread of Excitation in the Heart

The heart contains muscle cells (fibers) that produce and distribute
excitation impulses (conducting system), as well as working myocardium, which
responds to the excitation by contracting. Contrary to the situation in skeletal
muscle, excitation originates within the organ (autorhythmicity or autonomy of
the heart). Atrial and ventricular myocardium each consists functionally of a
syncytium, i.e., the cells are not insulated from one another but connected through
gap junctions. A stimulus that originates somewhere within the atria or ventricles
thus always leads to complete contraction of both atria or of both ventricles,
respectively (all-or-nothing contraction).10

Normal excitation of the heart originates within the sinus node, the hearts
pacemaker. Excitation spreads from there through both atria to the
atrioventricular node (AV node) and from there, via the His bundle and its two
branches, reaches the Purkinje fibers, which transmit the excitation to the
ventricular myocardium.
 The potential in the cells of the sinus node is a pacemaker potential. It has
no constant resting potential, but rises after each repolarization. The most negative
value of the latter is called maximal diastolic potential (MDP: 70 mV). It rises
steadily until the threshold potential (TP:. 40 mV) is reached once more and an
action potential (AP) is again triggered. The following changes in ionic
conductance of the plasma membrane and thus of ionic currents cause these
potentials.

Once the TP has been reached, gCa now rises relatively rapidly, the
potential rising more steeply so that an increased influx of Ca2+ (ICa) produces
the upstroke of the AP. While the potential overshoots to positive values, leading
to an outward K+ flux IK, the pacemaker cell is again repolarized to the MDP.

Each AP in the sinus node normally results in a heart beat, i.e., the impulse
frequency of the pacemaker determines the rate of the heart beat. The rate is lower
if
The rise of the slow depolarization becomes less steep
The TP becomes less negative
The MDP becomes more negative so thatspontaneous depolarization
begins at a lower level
Repolarization in an AP starts later or is slower.
 All parts of the excitation/conduction system have the capacity of
spontaneous depolarization, but the sinus node plays the leading role in normal
cardiac excitation (sinus rhythm is ca. 7080 beats per minute). The reason for
this is that the other parts of the conduction system have a lower intrinsic
frequency than the sinus node

Excitation starting from the sinus node will thus arrive at more distal parts
of the conducting system, before their spontaneous depolarization has reached the
TP. However, if conduction of the sinus impulse is interrupted, the intrinsic
frequency of more distal parts of the conduction system take over and the heart
then beats in AV rhythm (4060 beats per minute) or, in certain circumstances, at
the even lower rate of the so-called tertiary (ventricular) pacemakers (2040 beats
per minute).

Although the heart beats autonomously, adaptation of cardiac activity to

changing demands is mostly effected through efferent cardiac nerves. The
following qualitites of cardiac activity can be modified by nerves:10
Rate of impulse formation of the pacemaker and thus of the heart beat
(chronotropism);
Velocity of impulse conduction, especially in the AV node (dromotropism);
The force ofmyocardial contraction at a given distension, i.e., the hearts
contractility (inotropism);
Excitability of the heart in the sense of changing its excitability threshold
(bathmotropism).

These changes in cardiac activity are caused by parasympathetic fibers of

the vagus nerve and by sympathetic fibers. Heart rate is increased by the activity
of sympathetic fibers to the sinus node (positive inotropic effect via "1-receptors)
and decreased by parasympathetic, muscarinic fibers (negative chronotropic
effect).
 This is due to changes in the slow depolarization rise and altered MDP in
the sinusnode. Flattening of the slow depolarization and the more negative MDP
under vagus action are based on an increased gk, while the increased steepness of
slow depolarization under sympathetic action or adrenalin influence is based on an
increase in gCa and, in certain circumstances, a decrease in gK.

The more subordinate (more peripheral) parts of the conduction system are
acted on chronotropically only by sympathetic fibers, which gives the latter a
decisive influence in any possible takeover of pacemaker function by the AV node
or tertiary pacemakers.

The parasympathetic fibers of the left vagus slow down while the
sympathetic fibers accelerate impulse transmission in the AV node (negative or
positive dromotropic action, respectively). The main influence is on the MDP and
the steepness of the AP upstroke. Changes in gK and gCa play an important role
here as well.

In contrast to chronotropism and dromotropism, the sympathetic nervous

system, by being positively inotropic, has a direct effect on the working
myocardium. The increased contractility is due to an increase in Ca2+ influx,
mediated by "1-adrenergic-receptors, from outside the cell that allows an increase
in the Ca2+ concentration in the cytosol of the myocardial cells. This Ca2+ influx
can be inhibited pharmacologically by blocking the Ca2+ channels (so-called
Ca2+ antagonists).

Contractility is also increased by prolonging the AP (and as a result

lengthening Ca2+ influx), as well as inhibiting Na+-K+-ATPase, for example,
bymeans of the cardiac glycosides digoxin and digitoxin (smaller Na+ gradient
across the cell membrane ! lower efficiency of 3 Na+/Ca2+ exchange !decreased
Ca2+ extrusion !increased cytosolic Ca2+ concentration).
 At a lower heart rate the Ca2+ influx over time is low (few APs), so that
there is a relatively long period in which Ca2+ outflux can take place between
APs. Thus, the mean cytosolic concentration of Ca2+ becomes lower and
contractility is held low as a result. The vagus nerve can also act via this
mechanism; however, it does so indirectly through negative inotropy (frequency
inotropism). The converse is true for sympathetic stimulation.

2.2. Abnormalities of Cardiac Rhythm ( Arrythmia)

The resting heart normally beats with a regular rhythm, 60 to 100 times
per minute. Because each beat originates with depolarization of the sinus node,
the usual, everyday cardiac rhythm is called normal sinus rhythm.

The term arrhythmia refers to any disturbance in the rate, regularity, site of
origin, or conduction of the cardiac electrical impulse. An arrhythmia can be a
single aberrant beat (or even a prolonged pause between beats) or a sustained
rhythm disturbance that can persist for the lifetime of the patient.

Not every arrhythmia is abnormal or dangerous. For example, heart rates

as low as 35 to 40 beats per minute are common and quite normal in well-trained
athletes. Single abnormal beats, originating elsewhere in the heart than the sinus
node, frequently occur in the majority of healthy individuals. Many arrhythmias,
however, can be dangerous, and some require immediate therapy to prevent
sudden death. The diagnosis of an arrhythmia is one of the most important things
an EKG can do, and nothing yet has been found that can do it better.

2.2.1. The Clinical Manifestations of Arrhythmias

Frequently, however, arrhythmias elicit one of several characteristic
symptoms.First and foremost are palpitations, an awareness of one's own
heartbeat. Patients may describe intermittent accelerations or decelerations of their
heartbeat, or a sustained rapid heartbeat that may be regular or irregular. The
sensation may be no more than a mild nuisance or may be a truly terrifying
experience.

More serious are symptoms of decreased cardiac output, which can occur
when the arrhythmia compromises cardiac function. Among these are light-
headedness and syncope (a sudden faint). Rapid arrhythmias can increase the
oxygen demands of the myocardium and cause angina (chest pain). The sudden
onset of an arrhythmia in a patient with underlying cardiac disease can also
precipitate congestive heart failure.
 Sometimes, the first clinical manifestation of an arrhythmia is sudden
death. Patients in the throes of an acute myocardial infarction are at a greatly
increased risk for arrhythmic sudden death, which is why they are hospitalized in
cardiac care units where their heart rate and rhythm can be continuously
monitored.

2.2.2.Pathophysiology of Arrythmia
The heart is capable of only five basic types of rhythm disturbances:9
The electrical activity follows the usual conduction pathways we have
already outlined, but it is either too fast, too slow, or irregular. These are
arrhythmias of sinus origin.
The electrical activity originates from a focus other than the sinus node.
These are called ectopic rhythms.
The electrical activity is trapped within an electrical racetrack whose shape
and boundaries are determined by various anatomic or electrical
myocardial features. These are called reentrant arrhythmias. They can
occur anywhere in the heart.
The electrical activity originates in the sinus node and follows the usual
pathways but encounters unexpected blocks and delays.
The electrical activity follows accessory conduction pathways that bypass
the normal ones, providing an electrical shortcut, or short circuit. These
arrhythmias are termed preexcitation syndromes.
 Disorders of rhythm (arrhythmias or dysrhythmias) are changes in the
formation and/or spread of excitation that result in a changed sequence of atrial or
ventricular excitation or of atrioventricular transmission. They can affect rate,
regularity, or site of action potential formation.12

Normal sinus rhythm is the normal rhythm of the heart. Depolarization

originates spontaneously within the sinus node. The rate is regular and between 60
and 100 beats per minute. If the rhythm speeds up beyond 100, it is called sinus
tachycardia; if it slows down below 60, it is called sinus bradycardia.
Sinus tachycardia and sinus bradycardia can be normal or pathologic.
Strenuous exercise, for example, will speed the heart rate over 100 beats per
minute, whereas resting heart rates below 60 beats per minute are typical in well-
conditioned athletes. On the other hand, alterations in the rate at which the sinus
node fires can accompany significant heart disease. Sinus tachycardia can occur in
patients with congestive heart failure or severe lung disease, or it can be the only
presenting sign of hyperthyroidism. Sinus bradycardia is the most common
rhythm disturbance seen in the early stages of an acute myocardial infarction; in
otherwise healthy individuals, it can result from enhanced vagal tone and can
cause fainting.
Mechanism of Arrythmia

2. Common Arrhythmia
Location Bradyarrhythmias Tachyarrythmias
SA nodes Sinus Bradycardia Sinus tachycardia
Sick sinus syndromes
Atria Atrial premature beats

Atrial flutter

Atrial fibrillation

PSVT

Focal atrial tachycardia

Multifocal atrial tachycardia

AV node Conduction blocks Paroxysmal reentrant
Junctional escape rhythm tachycardia (AV or AV nodal)
Ventricles Ventricular escape rhythm Ventricular premature beats

Ventricular tachycardia

Torsades de pointes

Ventricular fibrilation
2.3. Pathophysiology of Supraventricular Tachicardia (SVT)
Supraventricular tachycardias (SVTs) include all tachyarrhythmias that
either originate from or incorporate supraventricular tissue in a reentrant circuit.
The ventricular rate may be the same or less than the atrial srate, depending on the
atrioventricular (AV) nodal conduction.

The term paroxysmal supraventricular tachycardia (PSVT) refers to a

clinical syndrome characterized by a rapid, regular tachycardia with abrupt onset
and termination. Approximately two-thirds of cases of PSVT result from AV nodal
reentrant tachycardia (AVNRT).

Orthodromic AV reciprocating tachycardia (AVRT), which involves an

accessory pathway, is the second most common cause of PSVT, accounting for
approximately one-third of cases. The term Wolff-Parkinson-White syndrome
(WPW) designates a condition comprising both preexcitation and
tachyarrhythmias. Atrial tachycardias, which arise exclusively from atrial tissue,
account for approximately 5 percent of all cases of PSVT.9

1. Paroxysmal Supraventricular Tachycardia

Paroxysmal supraventricular tachycardia (PSVT) is a very common

arrhythmia. Its onset is sudden, usually initiated by a premature supraventricular
beat (atrial or junctional), and its termination is just as abrupt. It can occur in
perfectly normal hearts; there may be no underlying cardiac disease at all. Not
uncommonly, alcohol, coffee, or just sheer excitement can elicit this rhythm
disturbance.

PSVT is an absolutely regular rhythm, with a rate usually between 150 and
250 beats per minute. There are several types of PSVT. The most common type is
driven by a reentrant circuit looping within the AV node. Retrograde P waves may
sometimes be seen in leads II or III, but your best chance would be to look in lead
V1 for what is called a pseudo-R', a little blip in the QRS complex that represents
the superimposed P wave. More often than not, however, the P waves are so
buried in the QRS complexes that they cannot be identified with any confidence.
As with most supraventricular arrhythmias, the QRS complex is usually narrow.
Another type of PSVT occurs in patients with anomalous conduction pathways
and will be discussed in Chapter 5.

1.a. Atrioventricular Nodal Reentrant Tachycardia

AVNRT is an important arrhythmia for several reasons. First, AVNRT is
extremely common. Studies report that AVNRT occurs in approximately 10
percent of the general population and accounts for up to two-thirds of all cases of
PSVT.4 Although AVNRT can occur at any age, it is extremely uncommon prior to
the age of 5 years. The usual age of onset is beyond the fourth decade and is later
than the usual age of onset of accessory pathway-mediated tachycardias. 410
Women are affected twice as often as men. A second reason for the importance of
AVNRT is the fact that it can result in significant debility and decreased quality of
life.

Pathophysiologic Basis of Atrioventricular Nodal Reentrant Tachycardia

Early descriptions of the AV nodal tissue came from Albert Kent more than
a century ago.12 The AV node is located epicardially, just underlying the right
atrial epicardium, anterior to the nodal artery and between the coronary sinus and
medial tricuspid valve leaflet. It comprises three different components: the
transitional cell zone, the compact node, and the penetrating bundle of His (. The
compact AV node refers to the most easily histologically distinguishable tissue
located at the apex of the triangle of Koch (TOK). A zone of transitional cells is
interposed between the compact node and the atrial myocardium. Transitional
cells enter the triangle of Koch to join the compact node superiorly, inferiorly,
posteriorly, and from the left. At its distal extent, the AV node is distinguished
from the penetrating bundle, not so much by cellular characteristics as by the
presence of a fibrous collar surrounding the specialized cells. Systematic anatomic
investigation of the AV node in patients with AVNRT is lacking. No obvious
histologic abnormalities have been identified among patients with AVNRT versus
patients without AVNRT. Several recent autopsy studies have reported that the
sites of successful slow pathway ablation were clearly away from the histologic
compact AV node, approximately 1 or 2 cm inferior and posterior to it.10

Types of Atrioventricular Nodal Reentrant Tachycardia

Three types of AVNRT have been described. Typical or slow/fast AVNRT

is the most prevalent type, accounting for 85 to 90 percent of cases. Representing
the other 10 to 15 percent of cases, atypical AVNRT can be further differentiated
into fast/slow and slow/slow (or intermediate) AVNRT. Induction of typical and
atypical AVNRT in the same patient is possible but unusual. The typical or
slow/fast AVNRT is thought to use the slow pathway for antegrade conduction and
the fast pathway for retrograde conducion. When an atrial premature complex
blocks the fast pathway and proceeds slowly along the slow pathway, the fast
pathway has enough time to recover from its refractoriness. This allows the
impulse to activate the fast pathway retrogradely and return to the atrium, giving
rise to an AV nodal reentrant echo beat. The impulse then travels down along the
slow pathway again, continuation giving rise to AVNRT. It has been proposed that
the fast/slow AVNRT uses the fast pathway for anterograde conduction and the
slow pathway for retrograde conduction. The slow/slow AVNRT, conversely,
requires presence of two or more slow pathways with different conduction
properties and refractory periods; one slow pathway is used for antegrade
conduction and the other slow pathway for retrograde conduction.
 An automatic focus may demonstrate progressive rate increase at tachycardia onset (warm up) and/or progressive rate decrease

before termination (cool down), does not respond to vagal maneuvers, and often displays an incessant nature. Focal atrial tachycardia caused

by reentry generally can be induced by programmed electrical stimulation. During the arrhythmia the criteria for either manifest or concealed

entrainment usually can be demonstrated, and the interval between the initiating beat and the first beat of the atrial tachycardia is usually

inversely related. Triggered activity is thought to be caused by delayed afterdepolarizations, and includes digitalis toxicity, but catecholamines

can also precipitate focal atrial tachycardia due to this mechanism.

1

Table 381 Differential Diagnosis for Types of Supraventricular

Tachycardia Based on ECG Characteristics

I. LongR-P tachycardia: R-P P-R

i. Atypical AV nodal reentrant tachycardia
ii. Atrial tachycardia
iii. AVRT with a slowly conducting pathway (e.g., PJRT)
iv. Sinus node reentry
v. Sinus tachycardia
II. ShortR-P tachycardia R-P < P-R
i. Typical AVNRT
ii. AV reentry
1.b. Atrioventricular Reentrant Tachycardia and Wolff-Parkinson-White
Syndrome

Accessory pathways (APs) are important because they provide a substrate

for antidromic and orthodromic AV reciprocating tachycardia, are associated with
sudden cardiac death, and may be detected in asymptomatic patients on a routine
screening ECG. The sections that follow cover the pathophysiology, diagnosis,
and management of this fascinating clinical entity.
Pathophysiology

The WPW syndrome was first described in 1930 in an article by Louis

Wolff, Sir John Parkinson, and Paul Dudley White. The authors described 11
patients with recurrent tachycardia associated with an ECG pattern of "bundle-
branch block with short P-R interval." Since publication of this initial report, our
understanding of the anatomic and pathophysiologic features of preexcitation
syndromes has improved enormously.

Accessory pathways are anomalous, typically extranodal connections that

connect the epicardial surfaces of the atrium and ventricle along the AV groove.
Accessory bypass tracts, which conduct antegrade from the atrium to the ventricle
and therefore are detectable on an ECG, are reportedly present in 0.15 to 0.25
percent of the general population. A higher prevalence of 0.55 percent has been
reported in first-degree relatives of patients with WPW syndrome.

Classification

Accessory pathways can be classified based on their site of origin and

insertion, location along the mitral or tricuspid annulus, type of conduction, and
properties of conduction (decremental or nondecremental) (see Table 382).
Accessory pathways usually exhibit rapid, nondecremental conduction, similar to
that which is present in normal His-Purkinje tissue and atrial or ventricular
myocardium. Approximately 8 percent of accessory pathways display decremental
antegrade or retrograde conduction. Accessory pathways, which are capable only
of retrograde conduction, are referred to as concealed, whereas those capable of
antegrade conduction are referred to as manifest, demonstrating preexcitation on a
standard ECG .Accessory pathways usually conduct both antegrade and
retrograde. Antegrade-only accessory pathways are particularly uncommon. When
present, they are usually right-sided and frequently demonstrate decremental
conduction (Mahaim fiber). Concealed accessory pathways are less common,
accounting for approximately 15 percent of all accessory pathways. Patients with
Ebstein anomaly who also have WPW syndrome frequently have more than one
accessory pathway.

The degree of shortening of the P-R interval and the extent of ventricular
preexcitation depend on several factors, including location of the accessory
pathway, the relationship between antegrade conduction times and refractory
periods of the AV bypass tract, and the normal AV conduction system. A bypass
tract that crosses the AV groove in the left lateral region may also result in
inapparent preexcitation and minimal P-Rinterval shortening during sinus
rhythm due to greater interatrial distance for impulse propagation from the sinus
node to this site of atrial input into the AP. Conversely, an AP on the right side is
more likely to demonstrate marked preexcitation. Preexcitation may be less
apparent during sinus tachycardia, when sympathetic tone is high and vagal tone
low, resulting in faster AV node conduction time than that in the AP. On the other
extreme, during conditions of slowed conduction through the AV node either by
intrinsic nodal factors, withdrawal of sympathetic tone, or increased vagal tone,
the amount of preexcitation apparent on the 12-lead ECG is maximized because of
relatively greater conduction through the AP. Rapid intravenous administration of
adenosine causing blocking or slowing of AV node conduction and exposing the
anterograde AP conduction has been used as a diagnostic maneuver. The degree of
preexcitation can also be enhanced with atrial pacing directly over the AP,
eliminating the intraatrial conduction delay from the sinus node to the atrial
insertion site of AP.

2. Sinus tachycardia
Sinus tachycardia is usually a response to physiological stress such as
exercise or anxiety, and it may be the result of an abnormally heightened
sympathetic tone. Abnormal pathological causes include fever, hypotension,
anemia, thyrotoxicosis, hypovolemia, pulmonary emboli, myocardial ischemia,
and shock. Nicotine, caffeine, alcohol, and some medications (sympathetic
agonists or parasympatholytic agents) are frequently the underlying cause of sinus
tachycardia.The QRS complexes are preceded by P waves of normal morphology,
duration, and axis. Sinus tachycardia alone does not require any treatment, but the
underlyingcause should be determined.

3. Atrial tachycardia
 Atrial tachycardia can occur in the presence of cardiac or pulmonary
disease at a rate varying from 140 to 240 bpm. P-wave morphology is generally
different from that during SR, but the PQRS relationship remains 1:1. Some
atrial tachycardias are catecholamine sensitive; in this case, a b-blocker
isappropriate therapy. Curative radiofrequency ablation of atrial tachycardia is e
fective in 70% of cases. For refractory cases, creation of complete heart block by
radiofrequency catheter ablation with implantation of a permanent dual-chamber
pacemaker provides control of the rate and avoids drug toxicity.13

4. Atrial Fibrillation
Atrial fibrillation (AF) is characterized by disorganized atrial electrical activation
and uncoordinated atrial contraction. The surface electrocardiogram
characteristically demonstrates rapid fibrillatory waves with changing
morphology and rate and a ventricular rhythm that is irregularly irregular. Most
AF originates in one or more of the pulmonary veins (PVs), and because of
disparate atrial refractory periods the rapid firing focus in the left atrium (LA)
cannot be conducted in a 1:1 manner to the right atrium, which leads to
fibrillatory conduction. Additionally, it is thought that a driver, perhaps a reentrant
focus in the LA, acts in a similar manner. Although the ECG has the characteristic
appearance of disorganized atrial activation, further analysis may reveal what
appears to be a regular rapid atrial rhythm, often seen best in lead. Careful
measurement will disclose variability in the P-P intervals, and this should not be
misinterpreted as atrial flutter, or so-called atrial fibrillation-flutter. Atrial flutter,
as discussed later, is a very regular rhythm with monotonous repetition of similar
P waves with each cycle.

The ventricular rate during AF can be quite variable, and depends on autonomic
tone, the electrophysiologic properties of the atrioventricular (AV) node, and the
effects of medications that act on the AV conduction system. The ventricular rate
may be very rapid (>300 beats/min) in patients with the Wolff-Parkinson-White
(WPW) syndrome, with conduction over accessory pathways (wide preexcited
QRS complexes) having short antegrade refractory periods. A regular, slow
ventricular rhythm during AF suggests a junctional rhythm, either as an escape
mechanism with complete AV block or as an accelerated junctional pacemaker.

Two concepts of the underlying mechanism of AF have received considerable

attention: factors that trigger the onset and factors that perpetuate this arrhythmia.
Triggering foci of rapidly firing cells within the sleeve of atrial myocytes
extending into the pulmonary veins have been clearly shown to be the underlying
mechanism of most paroxysmal AF. In animal models these pulmonary vein foci
manifest delayed afterpotentials and triggered activity in response to
catecholamine stimulation, rapid atrial pacing, or acute stretch. . The pulmonary
veins of patients with paroxysmal AF demonstrate abnormal properties of
conduction such that there is a markedly reduced effective refractory period
within the pulmonary veins, progressive conduction delay within the pulmonary
vein in response to rapid pacing or programmed stimulation, and often conduction
block between the pulmonary vein and the LA. Rapidly firing foci can often be
recorded within the pulmonary veins with conduction block to the LA.
Discontinuous properties of conduction within the pulmonary vein may also
provide a substrate for reentry within the pulmonary vein itself . Although most
triggering foci that are mapped during electrophysiologic studies occur in the
pulmonary veins in patients with paroxysmal AF, foci within the superior vena
cava, the ligament of Marshall, and the musculature of the coronary sinus have
been identified. Other sites of initiating foci may be recorded in the left atrial wall
or along the crista terminalis in the right atrium.

5. Atrial Flutter

There are several types of atrial flutter, all having rapid, regular atrial
rates, generally 240 to 340 beats/min, because of a reentrant mechanism in the
atria. Typical, also called counterclockwise atrial flutter is characterized by
negative sawtooth flutter waves and reverse typical, also called atypical or
clockwise atrial flutter by positive flutter waves in ECG leads II, III, and aVF
These two atrial flutter types share the same right atrial reentrant circuit. In typical
atrial flutter, the reentrant wavefront travels up the interatrial septum and down
the right atrial free wall, and vice versa in reverse atypical atrial flutter. Both types
use the sub-Eustachian or cavotricuspid isthmus (i.e., the isthmus between the
tricuspid annulus on one side and the inferior vena cavaEustachian ridge-
coronary sinus on the other) as a part of the reentrant circuit,

An important conceptual point is that the atrial flutter reentrant circuit

usually is not simply present and waiting to be engaged. Almost always missing is
the critical line of functional block between the venae cavae. In fact, it can be
considered that the difference between the clinical development of AF and atrial
flutter is whether or not this functional line of block between the venae cavae
develops. Moreover, this is an important part of the intricate relationship between
AF and atrial flutter and may explain why, following successful ablation of the
atrial flutter reentrant circuit, AF often becomes clinically manifest.

More recently, left atrial flutter, double wave reentry atrial flutter (two
reentrant wave fronts simultaneously circulating in the same reentrant circuit),
lower loop and upper loop reentry atrial flutter (variants of typical atrial flutter),
and atrial flutter caused by reentry around a surgical incision (lesion reentry) have
also been described. Left atrial flutter may be caused by reentry around the mitral
valve annulus, the pulmonary veins, or a region of block (usually anatomic) in the
LA, such as secondary to the presence of a scar caused for any reason, including
prior surgery or an ablation line. Atrial flutter caused by a surgical lesion is
common in patients after repair of congenital heart defects that involve one or
more right atrial free wall incisions. It has now been shown that most
(approximately two thirds) recurrent atrial flutter in patients following open heart
surgical repair of congenital heart defects indeed uses the classical atrial flutter
reentrant circuit.

6. Focal Atrial Tachycardia

The term atrial tachycardia refers to rapid (usually 130250 beats/min),

relatively regular rhythms that originate in the atria, do not require participation of
either the sinus node or the AV node for maintenance, and are neither AF nor atrial
flutter. Focal atrial tachycardia is characterized by atrial activation starting
rhythmically at a small area (focus). Potential mechanisms include reentry,
automaticity, and triggered activity. Foci are most frequently found in the
pulmonary veins in the LA, and the crista terminalis in the right atrium but can
occur at various sites in both atria. When incessant, they may be associated with a
dilated cardiomyopathy and CHF.

An automatic focus may demonstrate progressive rate increase at

tachycardia onset (warm up) and/or progressive rate decrease before termination
(cool down), does not respond to vagal maneuvers, and often displays an incessant
nature. Focal atrial tachycardia caused by reentry generally can be induced by
programmed electrical stimulation. During the arrhythmia the criteria for either
manifest or concealed entrainment usually can be demonstrated, and the interval
between the initiating beat and the first beat of the atrial tachycardia is usually
inversely related. Triggered activity is thought to be caused by delayed
afterdepolarizations, and includes digitalis toxicity, but catecholamines can also
precipitate focal atrial tachycardia due to this mechanism.

2.4. SVT Classification and Appereance

Arryhtmias can be classified according to their site of origin, their
mechanism and their electrocardiographic features.

1
Tachyarrythmias
When the heart rate is 100 bpm for three beats or more, a tachyarrhythmia
is present. Tachyarrhythmias result from one of the three mechanisms: enhanced
automaticity, reentry, or triggered activity. Tachyarrhythmias are categorized into
those that arise above the ventricles (supraventricular) and those that arise within
the ventricles.1

Differentiation of common supraventricular tachyarrhythmias.2

1. Regular Rhythm
A. Sinus Tachycardia
Sinus tachycardia is characterized by an SA node discharge rate
100 bpm to 180 bpm) with normal P waves and QRS complexesThis
rhythm most often results from increased sympathetic and/or decreased
vagal tone. Sinus tachycardia is an appropriate physiologic response to
 exercise. However, it may also result from sympathetic stimulation in
pathologic conditions, including fever, hypoxemia, hyperthyroidism,
hypovolemia, and anemia. In disease states, sinus tachycardia is
usually a sign of the severity of the primary pathophysiologic process
and treatment should be directed at the underlying cause.2

Sinus tachycardiawith normal P waves and QRS Complexes are

normal, but the rate is 100 bpm.

B. Atrial Flutter
Atrial flutter is characterized by rapid, regular atrial activity at a
rate of 180 to 350 bpm. Many of these fast impulses reach the AV node
during its refractory period and do not conduct to the ventricles,
resulting in a slower ventricular rate, often an even fraction of the
atrial rate. Thus, if the atrial rate is 300 bpm and 2:1 block occurs at
the AV node (i.e., every other atrial impulse finds the AV node
refractory), the ventricular rate is 150 bpm. Because vagal maneuvers
(e.g., carotid sinus massage) decrease AV nodal conduction, they
increase the degree of block, temporarily slowing the ventricular rate,
which allows better visualization of the underlying atrial activity.

In general, atrial flutter is caused by reentry over a large

anatomically fixed circuit. In the common form of atrial fl utter, this
circuit is the atrial tissue along the tricuspid valve annulus: the
circulating depolarization wave propagates up the interatrial septum,
across the roof and down the free wall of the right atrium and fi nally
along the fl oor of the right atrium between the tricuspid valve annulus
and inferior vena cava. Because large parts of the atrium are
depolarized throughout the cycle, P waves often have a sinusoidal or
sawtooth appearance. Large fl utter circuits can occur in other parts
of the right or left atrium as well, usually associated with areas of atrial
scarring from disease, prior heart surgery, or ablation procedures.
Atrial flutter generally occurs in patients with preexisting heart
disease. It may be paroxysmal and transient, persistent (lasting for days
or weeks), or permanent. Symptoms of atrial flutter depend on the
accompanying ventricular rate. If the rate is 100 bpm, the patient may
be asymptomatic. Conversely, faster rates often cause palpitations,
dyspnea, or weakness. Paradoxically, antiarrhythmic medications that
reduce the rate of atrial flutter by slowing conduction in the atrium
may paradoxically make the rhythm more dangerous by allowing the
AV node more time to recover between impulses. In this situation, the
AV node may begin to conduct in a 1:1 fashion, producing very rapid
ventricular rates. For example, a patient with atrial flutter at a rate of
280 bpm and 2:1 conduction block at the AV node would have a
ventricular rate of 140 bpm. If the atrial rate then slows to 220 bpm,
the AV node may be able to recover sufficiently between
depolarizations to conduct every atrial impulse, causing the ventricular
rate to accelerate to 220 bpm. In patients with limited cardiac reserve,
this acceleration may result in a profound reduction of cardiac output
and hypotension. Atrial flutter also predisposes to atrial thrombus
formation.2
 Atrial flutter is typified by rapid saw-toothed atrial activity (arrows).

C. Paroxysmal Supraventricular Tachycardias

Paroxysmal supraventricular tachycardias (PSVTs) are manifested:
sudden onset and termination
atrial rates between 140 and 250 bpm
narrow (normal) QRS complexes
unless aberrant conduction is present, as summarized later. The mechanism
of PSVTs is most often reentry involving the AV node, atrium, or an
accessory pathway between an atrium and ventricle. Enhanced
automaticity and triggered activity in the atrium or AV node are less
common causes.2

AV Nodal Reentrant Tachycardia

The ECG in AVNRT shows a regular tachycardia with normal-
width QRS complexes. P waves may not be apparent, because
retrograde atrial depolarization typically occurs simultaneously with
ventricular depolarization. Thus, the retrograde P wave and QRS are
inscribed at the same time and the P is typically hidden in the QRS
complex. When P waves are visible, they are superimposed on the
terminal portion of the QRS complex and inverted (negative
deflection) in limb leads II, III, and aVF because of the caudocranial
direction of atrial activation. Rarely, the reentrant loop revolves in the
reverse direction, with anterograde conduction down the fast pathway
and retrograde conduction up the slow pathway. This is known as
uncommon AVNRT and, unlike the more common rhythm, results in
clearly visible retrograde P waves following the QRS complex on the
ECG. AVNRT often presents in teenagers or young adults. It is usually
well tolerated but causes palpitations that many patients fi nd
frightening, and rapid tachycardias can cause lightheadedness or
shortness of breath. In elderly patients or those with underlying heart
disease, more severe symptoms may result, such as syncope, angina, or
pulmonary edema.

Acute treatment of AVNRT is aimed at terminating reentry by

impairing conduction in the AV node. Transient increases in vagal tone
produced by the Valsalva maneuver or carotid sinus massage may
block AV conduction, terminating the tachycardia. The most rapidly
effective pharmacologic treatment is intravenous adenosine, which
impairs AV nodal conduction and often aborts the reentrant rhythm .
Other drug options include intravenous calcium channel antagonists
(verapamil and diltiazem) or beta-blockers. Most patients with AVNRT
have infrequent episodes that terminate with vagal maneuvers and do
not require other specifi c interventions. Frequent symptomatic
episodes, particularly when requiring visits to the emergency
department for treatment, warrant preventive therapy: oral _-blockers,
calcium channel blockers, or digoxin are often successful for this
purpose. Catheter ablation of the slow AV nodal pathway is also an
effective option but is associated with a small risk (_2%) of heart
block owing to unintended damage to the fast AV nodal pathway, a
complication that requires permanent pacemaker implantation. Chronic
class IA or IC antiarrhythmic drugs are also effective, but are often less
desirable than catheter ablation, because of associated potential drug
toxicities.
only the fast pathway impulse makes its way forward to the ventricles (A).
In contrast, consider what happens when an APB spontaneously occurs (B)

Atrioventricular Reentrant Tachycardias

Atrioventricular reentrant tachycardias (AVRTs) are similar to AVNRTs
except that in the former, one limb of the reentrant loop is constituted
by an accessory pathway (bypass tract), rather than by separate fast
and slow pathways within the AV node itself. An accessory pathway is
an abnormal band of myocytes that spans the AV groove and connects
atrial to ventricular tissue separately from the normal conduction
system . Approximately 1 in 1,500 people has such a pathway.
Accessory pathways allow an impulse to conduct from atrium to
ventricle (anterograde conduction), from ventricle to atrium
(retrograde conduction), or in both directions.2

Depending on the characteristics of the pathway, one of two

characteristic entities can result:
1. the ventricular pre-excitation syndrome
2. PSVT resulting from a concealed accessory pathway.

Some pathways do not conduct impulses at rates suffi cient to cause

tachycardias and cause no symptoms at all.2
Ventricular Pre-excitation Syndrome
In patients with ventricular pre-excitation (also termed Wolff
ParkinsonWhite [WPW] syndrome; atrial impulses can pass in an
anterograde direction to the ventricles through both the AV node and
the accessory pathway. Because conduction through the accessory
pathway is usually faster than that via the AV node, the ventricles are
stimulated earlier than by normal conduction over the AV node.
During sinus rhythm, activation of the ventricle from the accessory
pathway causes a characteristic ECG appearance:
1. the PR interval is short (_0.12 sec) because ventricular stimulation
begins earlier than normal through the accessory pathway
2. the QRS has a slurred rather than a sharp upstroke (referred to as a
delta wave) because the initial ventricular activation by the
accessory pathway is slower than activation over the Purkinje
system
3. the QRS complex is widened because it represents fusion of two
excitation wave fronts through the ventricles, one from the
accessory pathway and one from the normal HisPurkinje system

Patients with WPW syndrome are predisposed to PSVTs because

the accessory pathway provides a potential limb of a reentrant loop.
The most common PSVT in these patients is orthodromic AVRT.
During this tachycardia, an impulse travels anterogradely down the AV
node to the ventricles and then retrogradely up the accessory tract back
to the atria. Because the ventricles in this situation are depolarized
exclusively via the normal conduction system (through the AV node
and the bundle of His), there is no delta wave during the tachycardia
and the width of the QRS is usually normal. Retrograde P waves are
often visible soon after each QRS complex because the atria are
stimulated from below via retrograde conduction through the accessory
pathway.2

In fewer than 10% of patients with AVRT involving an accessory

pathway, the reentrant arrhythmia travels in the opposite direction.
Impulses travel anterogradely down the accessory pathway and
retrogradely up the AV nodeTermed antidromic AVRT, its ECG
pattern is characterized by a wide QRS complex because the ventricles
are activated entirely from anterograde conduction over the accessory
pathway. From the ECG alone, such antidromic tachycardia is difficult
to distinguish from ventricular tachycardia.2

A third type of arrhythmia encountered in patients with WPW

syndrome is anterograde conduction over the accessory pathway when
AF or atrial fl utter is present. Some accessory pathways have short
refractory periods that allow faster rates of ventricular stimulation than
does the AV node. Thus, during AF or atrial fl utter, ventricular rates as
 fast as 300 bpm may result. Such rates are poorly tolerated and can
lead to ventricular fibrillation and cardiac arrest, even in a young,
otherwise healthy patient.

WolffParkinsonWhite syndrome. The delta wave (arrow) indicates pre-

excitation of the
ventricles. Note the shortened PR interval

Concealed Accessory Pathways

Accessory pathways do not always result in ECG findings of
ventricular pre-excitation (i.e., short PR, delta wave). Many are
capable of only retrograde conduction. In this case, during sinus
rhythm, the ventricles are depolarized normally through the AV node
alone and the ECG is normal (i.e., the accessory pathway is
concealed). However, because the accessory pathway is capable of
retrograde conduction, it can form a limb of a reentrant circuit under
appropriate circumstances and result in orthodromic AVRT.2

D. Focal Atrial Tachycardia

Focal atrial tachycardia (AT) results from either automaticity of an
atrial ectopic site, or reentry. The ECG has the appearance of sinus
tachycardia, with a P wave before each QRS complex, but the P-wave
morphology is different from that of sinus rhythm, indicating
depolarization of the atrium from an abnormal site. The arrhythmia can
be paroxysmal and of limited duration, or it can persist. Short,
 asymptomatic bursts of atrial tachycardia are commonly observed on
24-hour ECG recordings, even in otherwise healthy people. Atrial
tachycardia can be caused by digitalis toxicity and is also aggravated
by elevated sympathetic tone (e.g., during exertion or periods of
illness).2

- Atrial Premature Beats

Atrial premature beats (APBs) are common in healthy as well as
diseased hearts. They originate from automaticity or reentry in an atrial
focus outside the SA node and are often exacerbated by sympathetic
stimulation. APBs are usually asymptomatic but may cause
palpitations. On the ECG, an APB appears as an earlier-than-expected
P wave with an abnormal shape (the impulse does not arise from the
SA node, resulting in abnormal conduction through the atria). The
QRS complex that follows the P wave is usually normal, resembling
the QRS during sinus rhythm, because ventricular conduction is not
impaired. However, if the abnormal atrial focus fires very soon after
the previous beat, the impulse may encounter an AV node that is
refractory to excitation, resulting in a blocked impulse that does not
conduct to the ventricles. The premature P wave is then not followed
by a QRS complex and is termed a blocked APB. Similarly, if the
ectopic focus fi res just a bit later in diastole, it may conduct through
the AV node but encounter portions of the HisPurkinje system that are
still refractory. As a result, the impulse is conducted through those
territories and to the ventricular myocytes more slowly than normal,
producing QRS complexes that are abnormally wide (termed an APB
with aberrant conduction). APBs require treatment only if they are
symptomatic. Because caffeine, alcohol, and adrenergic stimulation
(e.g., emotional stress) can all predispose to APBs, it is important to
address these factors. Blockers are the initial preferred pharmacologic
treatment if needed.2
 The P wave occurs earlier than expected, and its shape is abnormal.

2. Irreguler Rhytm
A. Atrial Fibrillation
AF is a chaotic rhythm with an atrial rate so fast (350 to 600
discharges/min) that distinct P waves are not discernible on the ECG.
As with atrial fl utter, many of the atrial impulses encounter refractory
tissue at the AV node, allowing only some of the depolarizations to be
conducted to the ventricles in a very irregular fashion (indicated by a
characteristic irregularly irregular rhythm). The average ventricular
rate in untreated AF is approximately 140 to 160 bpm. Because
discrete P waves are not visible on the ECG, the baseline shows low-
amplitude undulations punctuated by QRS complexes and T waves.2

The mechanism of AF probably involves multiple wandering

reentrant circuits within the atria, and in some patients, the rhythm
repetitively shifts between fi brillation and atrial flutter. When
fibrillation is paroxysmal (i.e., sudden, unpredictable episodes), it is
often initiated by rapid fi ring of foci in sleeves of atrial muscle that
extend into the pulmonary veins. To sustain AF, a minimum number of
reentrant circuits is needed, and an enlarged atrium increases the
potential for this to occur. Thus, AF is often associated with right or
left atrial enlargement. Accordingly, diseases that increase atrial
pressure and size promote AF, including heart failure, hypertension,
coronary artery disease, and pulmonary disease. Thyrotoxicosis and
alcohol consumption can precipitate AF in some people.2
 AF is a potentially dangerous arrhythmia because:
1. Rapid ventricular rates may compromise cardiac output, resulting in
hypotension and pulmonary congestion (especially in patients with a
hypertrophied or stiff left ventricle in whom the loss of normal atrial
contraction can signifi cantly reduce left ventricular filling and stroke
volume)
2. The absence of organized atrial contraction promotes blood stasis in
the atria, increasing the risk of thrombus formation, particularly in the
left atrial appendage. Embolization of left atrial thrombi is an
important cause of stroke.

B. Multifocal Atrial Tachycardia

In multifocal atrial tachycardia (MAT), the ECG shows an irregular
rhythm with multiple(at least three) P-wave morphologies, and
theaverage atrial rate is >100 bpm An isoelectric (i.e., fl at) baseline
between P waves distinguishes MAT from the chaotic baseline of AF.
This rhythm is likely caused by either abnormal automaticity in
several foci within the atria or triggered activity and occurs most often
in the setting of severe pulmonary disease and hypoxemia. Because
patients with this rhythm are often critically ill from the underlying
disease, the mortality rate is high, and treatment is aimed at the
causative disorder. The calcium channel blocker verapamil is often
effective at slowing the ventricular rate as a temporizing measure.

Multifocal atrial tachycardia. The rhythm is irregular and each QRS is preceded
by a P
wave of varying morphology.
 Typically, the ECG shows rapid, irregular atrial activity, with, in the
case of normal atrioventricular conduction a rapid, irregular rhythm.
Characteristically, the former arrhythmia is found in middle-aged men and
begins at night, during rest, or after a meal. Catecholamine-sensitive atrial
fibrillation is less commonly encountered in clinical practice. The
arrhythmia is most often observed in young women. It is related to stress
and exercise, and can be provoked by caffeine and alcohol. Holter
recordings show the occurrence of the arrhythmia in the daytime, usually
in the morning, and preceded by an increase in sinus rate.1
Electrocardiographically, a supraventricular tachyarrhythmia is more likely
if the morphology of the QRS at the rapid rate
is similar to that on the patients ECG tracing obtained while in sinus
rhythm (i.e., the complex is widened because of an underlying bundle
branch block). Conversely, VT is more likely if:
there is no relationship between the QRS complexes and any observed P
waves (AV dissociation)
- the QRS complexes in each of the chest leads (V1 through V6) have a
similar appearance, with a dominant positive or negative defl ection
(i.e., there is concordance of the precordial QRS complexes).
- Other morphologic ECG features have been used to distinguish VT
from SVT with aberrancy, but the distinction is often very difficult.
Most patients with wide QRS tachycardiashould be managed as though
they have VT until proven otherwise.2
 2.5. Differential Diagnose

2.6. Clinical Presentation

Most patients with PSVT present clinically with episodes of palpitations
that are of sudden onset and, in some cases, also abrupt offset. The duration of
palpitations is highly variable among individuals, with episodes that may last from
a few seconds to several hours. Patients usually cannot identify a precipitating
trigger that provokes their sudden tachycardia. Patients with PSVT may present
either to the emergency department or to the physicians office. In patients who
have symptoms of tachycardia but no diagnosis based on ECG results, appropriate
steps need to be taken to ensure that the tachycardia is recorded and that a
symptom-rhythm correlation exists. Hence, the use of ambulatory monitoring and
event recorders may be required.
At presentation, PSVT may be associated with presyncope, syncope, chest pain,
and abnormal pulsations in the neck.6 Syncope may occur if an episode of PSVT
is extremely rapid, resulting in compromise in cardiac output, or it may follow a
prolonged pause immediately after spontaneous termination of tachycardia.
Syncope may also be related to the triggering of a vasovagal response caused by
the tachycardia itself. The mechanism of chest pain is unclear. Although chest
pain in PSVT is usually unrelated to coronary artery disease, such pain in older
patients raises the possibility of myocardial ischemia.

By definition, PSVT is paroxysmal, both starting and stopping abruptly.

However, it may be prolonged because of the cardiac adrenergic drive that builds
up during PSVT as a result of hypotension or anxiety. The build-up of adrenergic
drive results in a less perceptible transition to a sinus tachycardia after the PSVT
has terminated. An atrial tachycardia or junctional tachycardia may accelerate
more gradually and, thus, would be nonparoxysmal. Some patients with PSVT
may describe an urge to urinate, possibly as a result of atrionatriuretic peptide
release, which produces an intrinsic diuretic effect.

In a less common scenario, some patients with SVT may present with
chronic cardiac failure and cardiomyopathy. In such cases, patients generally do
not experience palpitations during tachycardia and will have excessive heart rates
until cardiac decompensation occurs. The tachycardia in these patients likely takes
weeks or months to cause heart failure, depending on the patients heart rate and
on the amount of time that the patient experiences tachycardia episodes.
Ventricular dysfunction is usually reversible, even, to some degree, in patients
who have not been treated for long-standing tachycardia.
 2.7. INTERPRETATION OF ECG FINDINGS IN PSVT
Most PSVTs are represented on ECGs as narrow QRScomplex
tachycardias, with the QRS duration being less than 90 ms (ie, normal QRS
duration). Tachycardia-contingent BBB (ie, aberrancy) is relatively frequent in
patients with PSVT. Many of these patients may have preexistent BBB,
interventricular conduction delays, or some other QRS abnormality. These
abnormalities carry over to the tachycardia.

An initial analysis of ECG findings for a patient with PSVT is best

followed by a methodical approach to ECG interpretation, in which the physician
reviews the elements of the differential diagnosis, either mentally or in writing,
and examines the evidence supporting each diagnostic possibility. A high-
quality12-lead ECG is much more useful in the clinical setting than limited
presentations or individual cardiac rhythm strips. The main ECG findings of
interest are compelling atrial activity and zones of transition, such as ectopy, cycle
length change, or intermittent aberrant conduction.
Interventions may be helpful if the mechanism of the tachycardia is
unclear from examination of the routine ECG or rhythm strips. Vagal stimulation
maneuvers, such as carotid sinus massage or Valsalva maneuver, are classic
procedures for assessing the role of the AV node in the tachycardia mechanism.
Pharmacologic interventions are most useful for quickly determining the
mechanism of an arrhythmia.

Features to consider in ECG interpretation include the following:

1. Tachycardia Rate
Careful analysis of the R-R interval should be performed to determine the
rate of the tachycardia. A rate of 150 beats/min raises the suspicion of
atrial flutter with 2:1 AV block because the usual atrial rate during flutter is
300 beats/min. In general, a tachycardia with an atrial rate of less than 160
to 170 beats/min and without a visible P wave implies the presence of the
 slow-pathway component of the AV node.
The most frequently encountered PSVT of this type is typical AV nodal
reentry (ie, AVNRT). Atrial tachycardia or AVRT involving a slow AV
nodal pathway for anterograde conduction are considerably less frequently
observed than AVNRT. Faster rates of tachycardia are not generally helpful
in narrowing the differential diagnosis.
2. Mode of Onset
Onset.
The physician should check if the onset of the patients tachycardia is
captured on the ECG. Most PSVTs are triggered by a premature atrial
complex (PAC). If the PAC conducts to the ventricle with a very long PR
interval at initiation of tachycardia (ie, a jump in the PR interval), the
physician can safely postulate that the tachycardia is dependent on
anterograde slow-pathway conduction of the AV node to the ventricle.
Atrioventricular nodal reentrant tachycardia is the typical tachycardia that
begins with this mechanism. It is important to remember that a PAC, if
coupled closely enough, generally results in a longer PR interval in the
premature cycle because of normal decremental AV nodal physiologic
factors. Supraventricular tachycardias that start with a ventricular
premature complex are usually AV nodedependent tachycardias.
Supraventricular tachycardias are almost never atrial tachycardias

Termination.
Tachycardias in which the last event at termination is a P wave are highly
unlikely to be atrial tachycardias. If such conditions were atrial
tachycardias, it would be necessary to postulate that the last atrial beat. Its
more logical to postulate that the block in the AV node caused the
tachycardia to terminate and, consequently, that the condition is an AV
nodedependent tachycardia. Although an atrial tachycardia almost always
terminates with a ventricular complex, this observation may not be helpful
in diagnosis because some AV nodedependent tachycardias also terminate
 in this manner.
caused the block in the AV node.

The top panel demonstrates PSVT terminating with a

ventricular complex.
The bottom panel shows PSVT terminating with an atrial
complex, indicating that this patient is highly unlikely to
have atrial tachycardia.

3. Relative Position of the P wave within the R-R interval

Physician should attempt to identify the presence of P waves. A widely
used classification nomenclature of PSVT morphology, as previously
mentioned, is the long RP tachycardia vs the short RP tachycardia. This
nomenclature is purely descriptive and in most cases does not help the
physician to narrow the differential diagnosis. Nevertheless, in cases in
which simultaneous atrial and ventricular activation occurs, this
classification system can be used to rule out AVRT, pointing to typical
slow-fast AVNRT.
 With any extremely rapid PSVT, both the RP interval and PR
interval become short, making it difficult to distinguish between the two.
However, at slower PSVT rates, a shorter RP interval is usually indicative
of AVRT, as shown in the top panel, and a long RP interval most
commonly represents atrial tachycardia. Long RP morphologies, shown in
the bottom panel may also represent atypical AVNRT or AVRT. Finally,
sinus tachycardia is technically a long RP tachycardia, but it can often be
differentiated from atrial tachycardia through close comparison of P-wave
morphology during sinus rhythm vs during the tachycardia. These
guidelines for ECG interpretation have been validated with
electrophysiologic data. Kalbfleisch et al reported that more than 90% of
AVNRTs and 87% of AVRTs are short RP tachycardias. By contrast, only
11% of atrial tachycardias present as short RP tachycardias.

4. Morphology of The P Wave

P waves may be difficult to distinguish in ECGs, especially during
more rapid tachycardia, because of overlap with the QRS and T waves. If
P waves are visible during tachycardia, comparison with P waves in sinus
rhythm is useful. Although all available ECG leads require inspection,
evaluation of the inferior ECG leads (particularly lead II), as well as lead
V1, is likely to be the most productive. A normal P wave has a positive
QRS morphology in the inferior leads because normal atrial activation
begins at the sinus node during sinus rhythm, with a wave of electrical
propagation moving toward the AV node (ie, high to low sequence). As
this impulse moves toward the inferior leads, it produces an upright P
wave in leads II, III, and aVF. By contrast, junctional-dependent rhythms,
such as AVNRT and AVRT, and atrial tachycardias with origins in the
lower atrium result in negative P waves in the inferior leads. The negative
P waves occur because these tachycardias activate the atrium in the
opposite direction (ie, low to high sequence).
 Careful analyses of other ECG leads can help physicians to
determine if the atria are being activated from left to right or vice versa.
This conclusion can be achieved by examining the morphology of the P
wave in leads I and aVL. In right atrial tachycardia foci, the P wave is
positive or biphasic (ie, first negative, then positive) in lead aVL. That is
because the right atrium is activated first, with the wave of depolarization
moving toward the left atrium and, thus, to lead aVL. In left atrial
tachycardia foci, the P wave is negative or isoelectric (ie, electrically
neutral) in lead aVL. In addition, a positive P wave (ie, from the back to
the front) is observed in lead V1 in left atrial foci. This contrasts with the
negative or biphasic P wave observed in lead V1 when the atrial
tachycardia is of right atrial origin. In the long RP tachycardias caused by
atrial tachycardias, the P-wave morphology provides the first
approximation of the site of the abnormal focus. These algorithms may be
useful if the physician attempts to ablate the tachycardia.

5. Change in QRS morphology

A ventricular rate that is irregularly irregular (ie, a rate that is
variable in unpredictable ways), including having an irregular baseline,
suggests a diagnosis of atrial fibrillation. The cycle length in most cases of
PSVT is reasonably regular; however, it may oscillate in a patient who has
dual or multiple anterograde AV nodal pathways. In fact, most oscillation
in cycle length occurs in the anterograde part of the circuit. Patients with
atrial tachycardias may present with a notably irregular ventricular rate if
there is variable block in the AV node. A more subtle oscillation in cycle
length can be diagnostically useful. If the ECG shows that the QRS change
initiates the P-wave change during SVT (ie, if the VV change precedes the
AA change), the patients condition cannot be an atrial tachycardia and
must be a junctional reentrant tachycardia instead. The converse (ie, if the
AA change precedes the VV change) is less useful for diagnostic purposes,
although such an observation usually suggests an atrial tachycardia.
 QRS alternans is a phasic alteration of the amplitude of the QRS
complex, of unclear mechanism, that is observed in 1 or more ECG leads.
It is a nonspecific finding in faster tachycardias regardless of mechanism.
Thus, it most commonly occurs in conjunction with AVRT (25%-38% of
orthodromic AVRT, in which the usual direction of traffic is to the AV
node). QRS alternans also occurs with AVNRT (13%-23% of AVNRT), but
it is virtually never seen with atrial tachycardia.3

6. Effect Of Intermittent BBB On Tachycardia

A change in AV rate with the development of BBB aberration can
mean only that a bundle branch is part of the tachycardia circuit. This
characteristic excludes every SVT mechanism except AV reentry.

Bundle branch block that occurs ipsilateral to an accessory

pathway results in prolongation of the ventriculoatrial conduction time,
which is generally reflected in the tachycardia cycle length. This
association exists because those bundle branches are active (if not
obligatory) components of the tachycardia circuit. The converse is also
true. If leftsided BBB resolves during tachycardia and the cycle length
decreases, an ipsilateral accessory pathway is suggested. By contrast, the
development of right-sided BBB with a left-sided accessory pathway, or
vice versa, will have no effect on the tachycardia cycle length because that
bundle is not an integral part of the tachycardia circuit.

Furthermore, BBB that occurs in either AVNRT or atrial

tachycardia has no effect on the tachycardia cycle length because the
bundle branches are not integral parts of these tachycardia mechanisms.
 Electrocardiograms indicative of paroxysmal supraventricular tachycardia, with
no visible P wave. Left, normal QRS morphology; right, sudden development of
right-sided bundle branch block (without any change in cycle length). The
tachycardia shown in this electrocardiogram was verified as atrioventricular nodal
reentrant tachycardia during electrophysiologic testing.
 2.8. Treatment
Short-Term Treatment7
If the diagnosis of SVT with aberration or SVT with preexcitation is not certain,
tachycardia with a wide QRS complex must be considered as an unknown
mechanism and treated as such.
SVT with preexcitation can be the result of either antidromic atrioventricular
reentry or, uncommonly, another type of SVT (e.g., atrial tachycardia) with an
accessory pathway that is no critical for the maintenance of the arrhythmia. BBB
denotes bundle-branch block, VT ventricular tachycardia, IV intravenous, and
ECG electrocardiogram. Adapted from Blomstrom-Lundqvistetal.7
 Most supraventricular tachycardias depend on the atrioventricular node for
maintenance of the reentry circuit and can be interrupted by vagal maneuvers or
pharmacologic agents that slow conduction through the atrioventricular node.

1. Non- Pharmacology
Vagal Maneuvers
Massage of the carotid sinus stimulates baroreceptors, which trigger a
reflexive increase in the activity of the vagal nerve and sympathetic with- drawal,
slowing conduction through the atrioventricular node. If the physical examination
does not reveal a carotid bruit and there is no history suggesting carotid artery
disease, pressure may be applied at the level of the cricoid cartilage for about five
seconds with a firm circular movement. If the tachyarrhythmia persists, the
procedure may be repeated on the opposite side. Other approaches to increasing
vagal tone include having the patient perform a Valsalva maneuver or (primarily
in children) apply an ice pack to the face. A continuous 12-lead ECG recording of
the episode should be obtained during vagal maneuvers, since the way in which
arrhythmias end may provide clues to their mechanism.

2. Pharmacology
Adenosine
As with vagal maneuvers, treatment with intravenous adenosine has both
diagnostic and therapeutic value. Data from randomized trials show that
supraventricular tachycardia is terminated in 60 to 80 percent of patients treated
with 6 mg of adenosine and in 90 to 95 percent of those treated with 12 mg. In
patients with atrial tachycardias, adenosine causes a transient atrioventricular
nodal block or interrupts the tachycardia ECG monitoring is required during the
administration of adenosine, and resuscitation equipment should be available in
the event that the rare complications of bronchospasm or ventricular fibrillation
occur. Adenosine is contraindicated in heart-transplant recipients and should be
used cautiously in patients with severe obstructive lung disease. Adenosine is also
contraindicated in patients with tachycardia with a wide QRS complex (unless the
diagnosis of supraventricular tachycardia with aberrancy is certain).

Other Agents
If supraventricular tachycardia is refractory to adenosine or rapidly recurs,
clinical experience indicates that the tachycardia can usually be terminated by the
administration of intravenous verapamil or a beta-blocker. As a next step,
procainamide, ibutilide, propafenone, or flecainide can be given intravenously if
the patients blood pressure is stable.15 However, sequential trials with different
antiarrhythmic agents should be undertaken only after careful consideration of
their possible negative hypotensive, bradycardic, and proarrhythmic effects. At
any point, electrical cardioversion is an alternative, but this technique is generally
considered in patients in hemodynamically stable condition only if
atrioventricular nodal-blocking agents fail. Table 3 reviews medications used for
acute supraventricular tachycardia. These agents are contraindicated in patients
with severe hypotension, a history of heart block, or congestive heart failure.

Atrial fibrillation with rapid ventricular conduction can occur

spontaneously in patients with the WolffParkinsonWhite syndrome or during
treatment for supraventricular tachycardia. Emergency- resuscitation equipment
should be available, since the arrhythmia can degenerate into ventricular
fibrillation if the accessory pathway has a short refractory period (250 msec or
less). Treatment with an electrical shock is a safe option. If the patients condition
is hemodynamically stable, procainamide, ibutilide, propafenone, or flecainide
may be used; all have a rapid onset of action, lengthen antegrade refractoriness of
the accessory pathway, and terminate atrial fibrillation in the majority of cases.

Wide-QRS-Complex Supraventricular Tachycardia

Supraventricular tachycardia presents infrequently as a wide-complex
tachycardia, in which there is an associated bundle-branch block or conduction
over an accessory pathway. Wide-QRS-complex, regular tachycardia should
routinely be treated as ventricular tachycardia, unless the diagnosis of
supraventricular tachycardia with aberrancy or of supraventricular tachycardia
with preexcitation
is certain. Adenosine and other atrioventricularnodal blocking agents are
ineffective and potentially deleterious in patients with ventricular tachycardia.

Pharmacologic Agents for Short-Term Treatment of Supraventricular Tachycardia

(SVT).
Long-Time Treatment
 The risk of recurrence after a single episode of supraventricular
tachycardia is not well defined, and a single episode is not an indication for long
term therapy. For patients with recurrent episodes, options for long-term treatment
include medication and ablation therapy. However, not all patients with recurrent
supraventricular tachycardia need treatment. The severity of the symptoms and
patient preferences should be considered in decision making. In cases in which the
precise mechanism of tachycardia is uncertain, management is based on the
presence or absence of preexcitation on the baseline ECG.

Pharmacologic Therapy
Patients with recurrent episodes of supraventricular tachycardia without
preexcitation may be treated with prophylactic antiarrhythmic agents.

Patients with atrioventricular nodal reentrant tachycardia and

atrioventricular reentrant tachycardia mediated by a concealed accessory pathway
should primarily receive atrioventricular-nodeblocking agents such as verapamil,
beta-blockers, or digoxin. Clinical experience indicates that these agents decrease
the frequency of the episodes and the severity of symptoms in an estimated 30 to
60 percent of patients, but complete suppression of supraventricular tachycardia is
uncommon. A randomized, double-blind trial in which verapamil, propranolol,
and digoxin were compared failed to demonstrate the superiority of any one drug
over the others.19 If treatment with the above mentioned agents proves
unsatisfactory, pharmacologic options include a combination of two
atrioventricular node-blocking agents or a class IC or class III antiarrhythmic drug
(e.g., propafenone, sotalol, or amiodarone). In randomized, placebo-controlled
trials, class IC and class III antiarrhythmic drugs have prevented the recurrence of
supraventricular tachycardia in up to 80 percent of patients over a 60-day period
of follow-up; these agents also appear to be more effective in preventing
supraventricular tachycardia than are the atrioventricular-nodeblocking drugs,
although data from comparative trials are lacking. Despite the apparent safety of
class IC antiarrhythmic drugs in patients with supraventricular tachycardia, long-
term therapy with these drugs is generally not recommended because of their
potential adverse effects); catheter ablation is usually preferred if the patient
agrees to this approach.

The pharmacologic management of atrial tachycardiashas not been well

evaluated in controlled trials. Depending on the mechanism causing the
arrhythmia, beta-blockers, calcium-channel blockers, and class I or class III
antiarrhythmic drugs may reduce or eliminate symptoms.

Pill-in-the-Pocket Approach
For patients with infrequent (i.e., no more than a few per year) but
prolonged (i.e., lasting more than one to two hours) episodes of supraventricular
tachycardia that are well tolerated hemodynamically, or for patients who have had
only a single episode of supraventricular tachycardia, another option is to
prescribe single-dose pharmacologic therapy (the pill in the pocket) to be taken
when needed for an arrhythmic event. Drugs administered in this fashion include
calcium-channel blockers (e.g., 40 to 160 mg of verapamil), exclusively for
patients without preexcitation; various betablockers; flecainide (100 to 300 mg);
and propafenone (150 to 450 mg). In one study, 80 percent of episodes of
supraventricular tachycardia were in- terrupted within two hours with a
combination of diltiazem and propanolol or with flecainide.

Supraventricular Tachycardia with the WolffParkinsonWhite Syndrome

Verapamil and digoxin are contraindicated in patients with the Wolff
ParkinsonWhite syndrome, unless the accessory pathway has been shown to
have a long refractory period (300 msec or more), because these drugs may
increase the risk of rapid ventricular response, causing ventricular fibrillation in
patients with atrial fibrillation.24,25 Although catheter ablation is considered the
treatment of choice for these patients, both flecainide and propafenone are
effective and have been approved by the Food and Drug Administration for the
prevention of paroxysmal supraventricular tachycardias mediated by an accessory
pathway (with or without antegrade conduction).

Non- Pharmacologic Therapy

Catheter Ablation
patient with PSVT should be offered pharmacologic therapy or catheter
ablation for long-term treatment. Catheter ablation should be considered early in
the management of PSVT because of its proven efficacy and low procedural risk,
particularly if the patient has not responded to medication or is reluctant to take
medication.3

Catheter ablation is generally performed on an outpatient basis with a

combination of local anesthesia and conscious sedation. Catheters are introduced
into the heart via femoral and subclavian venous access, and an electrophysiologic
study is performed to fully elucidate the nature of the SVT. Catheter ablation has a
high procedural success rate of approximately 95% for patients with clinical
tachycardia, particularly AVNRT and AVRT. As many as 5% of patients may
experience a recurrence of tachycardia and require a second procedure.

In the case of AVNRT, the patient can be treated by performing careful

ECG mapping and delivering radiofrequency energy to the slow-pathway area of
the heart (ie, the posteromedial tricuspid annulus, near the coronary sinus ostium).
In patients with AVNRT and in some patients with accessory pathways, the site of
ablation is extremely close to the compact AV node. Therefore, these patients
should be informed of a small risk (0.1%-1%) of potential damage to the AV node.
Such damage would require implantation of a permanent pacemaker.3

Catheter ablation is highly effective in most cases of PSVT, regardless of

the mechanism. Research indicates that ablation may be more effective for AVRT
and AVNRT (>95% success rate) than for the atrial tachycardias (>80% success
rate). Nevertheless, certain considerations, such as a patients very advanced age
or comorbidities, may lead a physician to reject the use of catheter ablation.
Cryoablation (ie, using extreme cold to produce a lesion) is another procedure
that can be used to ablate either AVNRT or AVRT. Cryoablation may have a lower
risk of inadvertent AV block than catheter ablation.3

Some patients with PSVT may prefer using medications instead of

undergoing ablation. Traditionally, AV nodal blocking agents, such as verapamil
and diltiazem, or b- blockers are used first. Class I antiarrhythmic agents, such as
flecainide and propafenone, may also be effective. Such drugs are preferable for
patients with known Wolff- Parkinson-White syndrome because they generally
prolong the effective refractory period of the accessory pathway. Class I
antiarrhythmic agents may also have some efficacy in the prophylaxis of atrial
fibrillation.3
Patients with atrial tachycardia generally require the use of an AV nodal blocking
drug for atrial rate control. A membrane-active drug can be used for prevention of
atrial tachycardia. Sotalol is a b-blocker with antiarrhythmic properties that may
be useful in any case of PSVT. Amiodarone is effective in the management of
PSVT, but it is rarely indicated because of its potential toxicity over the long term
and because of the availability of effective alternatives.3

Pharmacology Prophylactic SVT

 2.9. Electrophysiology
Intracardiac electrophysiology study (EPS)5,6
Intracardiac electrophysiology study (EPS) is a test to look at how well the
hearts electrical signals are working.

It is used to check for abnormal heartbeats or heart rhythms.

 Electrophysiology studies test the electrical activity of your heart to find
where an arrhythmia (abnormal heartbeat) is coming from.
These results can help you and your doctor decide whether you need
medicine, a pacemaker, an implantable cardioverter defibrillator (ICD),
cardiac ablation or surgery.
These studies take place in a special room called an electrophysiology
(EP) lab or catheterization (cath) lab while you are mildly sedated.

EPS is used to see:

Where an arrhythmia is coming from.

How well certain medicines work to treat your arrhythmia.
If they should treat a problem by destroying the place inside your heart
that is causing the abnormal electrical signal. This procedure is called
catheter ablation.
If a pacemaker or implantable cardioverter defibrillator (ICD) might help
you.
You may need to have other tests before this study is done.
Test the function of your heart's electrical system
Pinpoint a known abnormal heart rhythm (arrhythmia) that is starting in
the heart, and help decide the best therapy for it
Determine whether you are at risk for future heart events, especially
sudden cardiac death
See if medicine is controlling an abnormal heart rhythm
If you are at risk for heart problems such as fainting or sudden cardiac
death due to cardiac arrest (when your heart stops beating).

How the Test is Performed

 Wire electrodes are placed in the heart to do this test. These electrodes
measure electrical activity in the heart. The procedure is done in a hospital
laboratory. The staff will include a cardiologist, technicians, and nurses.

To have this study:

Your groin or neck area will be cleaned and numbing medicine
(anesthetic) will be applied to the skin.
The cardiologist will then place several IVs (called sheaths) into the groin
or neck area. Once these IVs are in place, wires or electrodes can be
passed through the sheaths into your body.
The doctor uses moving x-ray images to guide the catheter into the heart
and place the electrodes in the right places.
The electrodes pick up the heart's electrical signals.
Electrical signals from the electrodes may be used to make the heart skip
beats or produce an abnormal heart rhythm. This can help the doctor
understand more about what is causing the abnormal heart rhythm or
where in the heart it is starting.
You may also be given medicines may also be used for the same purpose.

Other procedures that may also be done during the test:

Placement of a heart pacemaker
Procedure to destroy small areas in your heart that may be causing your
heart rhythm problems (called catheter ablation)

How to Prepare for the Test

At a hospital or clinic, doctors and nurses do EPS in a room that has special
equipment for the tests. You may hear this room called the electrophysiology
laboratory, or EP lab. Some call it the catheterization laboratory (cath lab). During
the test:
You will be told not to eat or drink for 6 - 8 hours before the test.
 You will wear a hospital gown. You must sign a consent form for the
procedure.
A nurse will put an IV (intravenous line) in your arm. Youll get medicine
(a sedative) that will calm youhelp you relax. But youll be awake and able
to follow instructions during the test.
Your nurse will clean and shave the part of your body where the doctor
will be working. This is usually in the groin but may be the arm or neck.
Youll be given a shot aA local anesthetic will be given to make the
area numb. Your doctor will make a needle puncture through your skin and
into your blood vessel. A small straw-sized tube called a sheath will be
inserted into your artery or vein. The doctor will gently guide several
specialized EP catheters into your blood vessel through the sheath and
advance them to your heart. A video screen will show the position of the
catheters. You may feel some pressure in the area where the sheath was
inserted, but you shouldnt feel any pain.
Your doctor will send small electric pulses through the catheters to make
your heart beat at different speeds. You may feel your heart beat stronger
or faster.
Electrical signals produced by your heart will be picked up by the special
catheters and recorded. This is called cardiac mapping and allows the
doctor to locate where arrhythmias are coming from,
Your doctor will remove the catheters and the IV line. Your nurse will put
pressure on the puncture site to stop any bleeding.
EPS usually last 1 to 4 hours.

How the Test Will Feel

You will be awake during the test. You may feel some discomfort when the
IV is placed into your arm. You may also feel some pressure at the site when the
catheter is inserted. You may feel your heart skipping beats or racing at times.

What Abnormal Results Mean

 Abnormal results may be due to abnormal heart rhythms that are too slow or
too fast. These may include:
Atrial fibrillation or flutter
Heart block
Sick sinus syndrome
Supraventricular tachycardia (a collection of abnormal heart rhythms that
start in the upper chambers of the heart)
Ventricular fibrillation and ventricular tachycardia
Wolff-Parkinson-White syndrome
There may also be causes that are not on this list.
The health care provider must find the location and type of heart rhythm problem
in order to determine the proper treatment.
Risks

The procedure is very safe in most cases. Possible risks include:

Arrhythmias; During EPS you may have abnormal heart rhythms that
make you dizzy. If this happens, your doctor may give your heart an
electric shock to bring back a regular heartbeat.
Bleeding
Blood clots that lead to embolism; clots sometimes can form at the tip of
the catheter, break off and block a blood vessel. Your doctor may give you
medicine to prevent blood clots.
Cardiac tamponade
Heart attack
Infection; bleeding and bruising at the site where the catheter went in
(groin, arm or neck)
Injury to the vein
Low blood pressure
Stroke
Catheter Ablation
Catheter-based ablation of a cardiac arrhythmia is performed in an
electrophysiology laboratory in conjunction with an electrophysiology study.
Catheter ablation is first-line therapy for many supraventricular arrhythmias,
including AVNRT, symptomatic AVRT, atrial flutter, and symptomatic or incessant
atrial tachycardia.

An electrophysiology study involves the percutaneous insertion of

catheters into the femoral veins and often the internal jugular vein. The catheter
tips are positioned at specific locations in the heart. Electrical stimulation is
delivered to the myocardium via these catheters to characterize cardiac conduction
and arrhythmias. Once the patients conduction system has been studied and the
rhythm disturbance diagnosed, an ablation catheter is used to thermally destroy
the pathogenic myocardial tissue underlying the arrhythmias initiation or
maintenance. Success and complication rates vary, depending on the individual
arrhythmia Introduction of catheters into the heart, with or without the delivery of
ablative energy, uniformly carries the risk of cardiac perforation and possibly
tamponade. If detected early and in the absence of systemic anticoagulation,
iatrogenic cardiac tamponade caused by catheter perforation uncommonly is a
life-threatening complication; however, it does require the percutaneous insertion
of a temporary subxiphoid pericardial drain if associated with hemodynamic
compromise.

One to four catheter electrodes are introduced into the cavities of the heart
through femoral (or, alternatively, internal jugular or subclavian) venous access
after local anesthesia is administered. Radiofrequency current a low-voltage,
high-frequency (500 kHz) form of electrical energy used for electrocautery in
surgery is delivered through a catheter electrode to create small lesions through
thermal injury in the myocardial tissue, the conduction system, or both, which
have been identified as critical for mediating the cardiac arrhythmia. In patients
with arrhythmias mediated by an abnormal accessory pathway, the catheter is
positioned so that it is in contact with the pathway, and the application of
radiofrequency current blocks conduction over the accessory pathway within a
few seconds. For left-sided accessory pathways, a retrograde approach through the
femoral artery and the aortic valve can be used. Alternatively, a transseptal
puncture can be performed to gain access to the left atrium. Cryothermal ablation
is an effective approach in patients with atrioventricular (AV) nodal reentrant
tachycardia or an accessory pathway close to a His bundle because of the
reversibility of the initial effect and the negligible risk of AV block. Most ablation
procedures take one to three hours. Catheter ablation of supraventricular
tachycardia can be performed as a one-day outpatient procedure, or it may require
overnight hospitalization. Treatment with aspirin is often recommended for
several weeks after ablation that has been performed in the left side of the heart to
reduce the potential risk of emboli. Patients need no special follow-up after the
intervention.

Characteristics of Catheter Ablation for Selected Cardiac Arrhythmias

 Atrial Tachycardia
Sustained atrial tachycardia is a relatively uncommon arrhythmia
diagnosed in about 5 to 15 percent of patients referred for supraventricular
tachycardia ablation, but with increasing age, it constitutes a larger
percentage of supraventricular tachycardias. It is a focal arrhythmia that
can arise from anywhere in the right or left atrium. For atrial tachycardia
ablation, success rates are 86 to 100 percent, with a recurrence rate of 0 to
8 percent. Uncommon complications (0 to 8 percent) include cardiac
perforation, phrenic nerve injury, and atrioventricular or sinus node
dysfunction. Catheter ablation of atrial tachycardia is reserved for
symptomatic cases refractory to medical therapy and for patients who have
developed a tachycardia-mediated cardiomyopathy because of
prolongedexposure to rapid heart rates.

Atrioventricular Nodal Reentrant Tachycardia

AVNRT is the most common supraventricular tachycardia referred for
treatment by catheter ablation and demonstrates a 2:1 predominance in
women. Catheter ablation of AVNRT is successful in approximately 96
percent of cases, with recurrence rates of 3 to 7 percent. The principal
potential complication related to AVNRT ablation is atrioventricular nodal
block (0.5 to 1 percent); palpitations and inappropriate sinus tachycardia
also have been described postablation.Ablation is recommended as first-
line therapy in most cases of AVNRT, but must be tailored to the individual
patients lifestyle and concomitant medical conditions.

Atrial Flutter
Atrial flutter constitutes approximately 15 percent of all supraventricular
arrhythmias and occurs in 25 to 35 percent of patients with atrial
fibrillation.1 Atrial flutter usually is more symptomatic than atrial
fibrillation because it is often associated with more rapid ventricular rates.
 The electrical circuit causing the most common forms of atrial flutter is
anatomically well defined and can be interrupted readily with ablation near
the junction of the inferior vena cava and the right atrium.

Longterm success rates for ablation of typical forms of atrial flutter range
from 88 to 100 percent,14-19 and patients treated with ablation have
lower hospitalization rates than patients treated with antiarrhythmic drugs.
Complications from ablation occur at a rate of 2.5 to 3.5 percent and
include heart block, cardiac perforation with tamponade, thromboembolic
events, and myocardial infarction. Catheter ablation is recommended in
most cases of atrial flutter.

Atrial Fibrillation
Atrial fibrillation is the most common clinically significant arrhythmia,
with an estimated prevalence of 0.4 to 1.0 percent in the general
population. Atrial fibrillation is associated with an increased risk of stroke,
heart failure, and all-cause mortality. Management principles focus on
adequate anticoagulation (to prevent embolic stroke occurrence),
ventricular rate control measures (to prevent symptomatic and pathogenic
tachycardia), and in selected patients, rhythm control strategies (to restore
and maintain sinus rhythm).
Atrial fibrillation ablation seeks to establish and maintain sinus rhythm by
targeting the tissue interface between the pulmonary veins and the left
atrium, an anatomic region that plays a critical role in initiating and
perpetuating atrial fibrillation.
 During catheter ablation of atrial fibrillation, a catheter ispassed
into the left atrium and is used to cauterize areas surrounding the orifices
of the pulmonary veins. The resulting scars prevent conductionof the extra
beats arising from the veins, which can trigger atrial fibrillation.

Patients who are most likely to benefit from atrial fibrillation

ablation are those with a normal left atrial size and in whom atrial
fibrillation is symptomatic and refractory to one or more antiarrhythmic
medications. Symptoms factor heavily in determining whether atrial
fibrillation ablation is worthwhile, because quality-of-life scores
demonstrate improvement after ablative therapy. As such, ablation of atrial
fibrillation is undertaken as an alternative to pharmacologic treatment to
prevent recurrent atrial fibrillation in symptomatic patients with minimal
or no left atrial enlargement.

A recent metaanalysis found that radiofrequency ablation after

failed antiarrhythmi drug therapy maintained sinus rhythm more than
continuation of drug therapy alone. Overall success rates for the
elimination of atrial fibrillation via catheter ablation vary depending on the
data examined, patient clinical factors, the number of atrial fibrillation
ablation procedures the patient has undergone, as well as the definition of
a successful ablation. Paroxysmal atrial fibrillation has higher elimination
rates at one year (roughly 75 to 80 percent) than persistent atrial
fibrillation (60 to 70 percent), with repeat ablations for atrial fibrillation
resulting in higher effectiveness rates. These differing ablation success
rates come from the observation that the longer atrial fibrillation is present,
the more the left atrium histologically is altered to promote and perpetuate
atrial fibrillation. The risk of a major complication with an atrial
fibrillation ablation procedure is approximately 6 percent.

The most common major complication is cardiac tamponade, and

the most common minor complication is groin hematoma formation at
catheter insertion sites (13 percent).

Patient Experience
Typically, a patient will present to his or her family physician with
palpitations. An externally worn, ambulatory ECG monitor commonly is
used to correlate symptoms of palpitations with a specific supraventricular
arrhythmia. These monitors can be worn for up to a month. If an
ambulatory monitor fails to identify a specific arrhythmia, an implantable
monitor can be inserted surgically to screen for arrhythmias for up to
several years. If and when a supraventricular arrhythmia is identified, the
patient is usually referred to a cardiologist, and subsequently, an
electrophysiologist. Ultimately, a decision is made regarding
pharmacologic rhythm control versus an electrophysiology study and
ablation.

If the patient elects for an electrophysiology study and ablation, he

or she should fast after midnight the night before the procedure and not
take medications that may interfere with tachycardia inducibility at the
electrophysiology study. On arrival to the electrophysiology laboratory,
routine preoperative care occurs, with insertion of an intravenous line and
often, assessment by an anesthesiologist. Analgesia protocols range from
conscious sedation to general endotracheal anesthesia. The former is used
when excess sedation threatens to render the clinical arrhythmia quiescent,
and thus, not ablatable. Heavier sedation may be needed for complex,
protracted ablations in which arrhythmia induction is not required or when
patient immobility is important.

During the procedure, the patient lies flat for several hours; the
exact length of time is dependent on the complexity of the arrhythmia.
AVNRT ablations tend to be shorter (less than three hours) than atrial
fibrillation ablations (which can last four to eight hours). During and after
the procedure, patients may have back pain and anxiety.
Chest pressure or pleuritic pain may be experienced during the delivery of
ablation energy (a relatively small percentage of the total procedural time).
On completion of the procedure, the catheters and sheaths are removed
from their insertion sites, and manual pressure is applied to achieve
hemostasis. Typically, the patient is discharged later the same day or the
next day. Full recovery typically takes two or three days, with longer
recuperation times for more complex procedures.
Radiation Exposure
As with cardiac catheterization and angioplasty, fluoroscopy is the
principal means of visualizing and modifying catheter position during an
electrophysiology study and arrhythmia ablation. The duration of
fluoroscopy (and thus, the degree of radiation exposure) varies depending
on the type and sophistication of the ablation procedure.
The measurement for radiation doses used in medical procedures,
including an electrophysiology study and ablation, is the millisievert
(mSv). Millisieverts can be converted into chest radiography equivalent
doses, which is the dose of radiation that is received from a single chest
radiograph. One chest radiography equivalent dose is 0.1 mSv.47 The
radiation doses for an electrophysiology study and ablation are estimated
to be 3.2 mSv (chest radiography equivalent dose = 32) and 15.2 mSv
(chest radiography equivalent dose = 152), respectively,48 with a range of
1.4 mSv (chest radiography equivalent dose = 14) to 49.75 mSv (chest
radiography equivalent dose = 497) for combined electrophysiology study
and ablation reported in several studies.

The potential long-term risks of radiation exposure that accompany

catheter ablation procedures are rare and include skin injury, malignancy,
and teratogenicity. Overall risk of fatal malignancy caused by radiation
from an electrophysiology study with ablation was found to be 0.03
percent for 60 minutes of fluoroscopy, and the risk of teratogenicity was
found to be one to 20 per 1 million births per 60 minutes of fluoroscopy.
Radiation exposure can be limited by the implementation of adjunctive
three-dimensional computer mapping software that creates a real-time
virtual map of the anatomic area of interest,as well as ablation catheter
position.
 CHAPTER III
CASE REPORT
STATUS OF THE PATIENT
Kepaniteraan Klinik Senior
Departemen Kardiologi dan Kedokteran Vaskuler
Fakultas Kedokteran USU / RS H Adam Malik Medan
Rekam Medik

No :00.56.69.89 Date : 1st December 2013 Day : Sunday

Name : Leni Artati Age : 37 years old Seks : Woman
Job : Housewife Address : Jl. Karya Bersama N0. 228 Medan
Religion : Islam Tlp: - Hp:

Chief Complaint : Dyspnoe

Anamnesis : Dyspnoe felt by patient since 6 month ago and consequence in

2 month. Dyspnoe connected with insignificant activity (during 15 minute).
History of dyspnoe constructed. History of applying pillow 2-3 to reduce dyspnoe
(+). Whezzing (-). History of asthma (-) allergy (-).
Cough (+), felt by patient during 2 month ago. Cough with phlegm and bloody
with colored rosy. Fever (-). History of perspiration at night (+). History of
consume cough medicine during 6 month (-). History of family link or
circumstance around with same disease (-)
Palpitations (+), felt by patient since 6 month ago. Appear suddenly when patient
did activity. Syncope (-). Pain on the head when palpitations (-). History of
consuming coffee (-).
History of swelling leg (+), since 2 month ago. Appear slowly swollen at first time
being hurt on leg. History of liver refuted by patient.
History of joint pain (+), felt by patient since 2 month ago. History of chest pain
refuted by patient. History of difficulty in swallowing (-)
On July month ago, patient has been treatment at Martha Friska hospital and being
suffered diagnose heart failure and pneumonia.
Urination and defecate within normal limits.
Risk Factor of CHD : Hypertension
Past History : Heart failure
History of Drug Use : Captopril, Furosemide

Presens status:
General state: moderate Sensorium: CM BP:90 /70 mmHg
HR : 101 x/i, irreguler RR: 20 x/i
Temperature: 35,8C Cyanosis : (-)
Ortopnu: (+) Dispnu: (-) Icterus: (+) Edema (-) Pale (-)

Physical Examination
Head : Eye : conjungtiva palpebra inferior anemia (+/+), icteric sclera (+/+),
isochoric pupil,
3 mm, Ear/Nose/Mouth normal in appearance
Neck : JVP : R-2 cmH2O
Thoracic wall :
Inspection : Symmetrical fusiformis
Palpation : Weakend in both lower lung. Ictus (+), anterior axillaris sinistra ICR
VII
Percussion : Dullness in both lower lung
Cardiac border : Superior range : ICR III mid clavicularis sinistra
Medial range : Linea parasternalis dekstra
Lateral range : Linea mid axilaris sinistra
Auscultation :
Heart : S1 (N) S2 (N) S3 (-) S4 (-) regular, HR 101x/irreguler
Murmur : (+), Type : PSM Grade : 3/6
Punctum maximum : anterior axillaris ICR VII Radiation : mid
axillaris
Lung : Respiratory sound : vesicular
Additional sound : ronchi (-/-) wheezing (-/-)
Abdominal : Palpation Hepar/Lien : Soepel, unpalpable acites (-)
Extremity : Superior : cyanosis (-) Clubbing : (-)
Inferior : edema (-) Arterial pulsation : (+/+)
Acral : warm

Interpretation of ECG record

SVT with abrance, P (-) visible, BAD , PR interval, QRS durasi : 0,20, P set
Interpretation of chest X-Ray
CTR 78%, aortic elongation (-), aortic dilatation (+), cardiac waist flat, cardiac
border : mid claviculasris dextra, apex down ward, infiltrat (+)
Impression : Cardiomegaly + pleural effusion
Laboratory results :
Hematologi
Hb 12,70 gr% Bilirubin total : 8,9 mg/dl
Ht 37,40 % Biribubin direct : 6,7 mg/dl
RBC 3,79 x 106 /mm3 SGOT : 2550
WBC 19,40 x 103/mm3 SGPT : 859
Trom 111 x 103/mm3 Albumin : 3.8
Globulin : 3.9

Carbohydrate Metabolism:
KGDS : 34,5 mg/dL
Kidney
Kreatinin 1.72 mg/dl ; Ureum 55 mg/dL
Elektrolit
Na/K/Cl : 131 mEq/L;6 mEq/L; 105 mEq/L

Working Diagnosis : CHF Fc III ec MR severe

1. Functional : CHF Fc III
2. Anatomy : Mitral valve
3. Etiology :

Differential Diagnosis :
- CHF fc III ec MR severe ec dd. RHD

Treatment :
- Bed Rest, semifowler
 - O2 2-4L/i
- IVFD NaCl 0,9% 10 gtt/i (micro)
- Furocemide 20 mg/8 hr
- Inj. Ceftriaxone 2 gr/12 hr
- Ambroxol 3x Ci
- Laxadin syr 1x Ci
- Spironolacton 1x25 mg
- Captopril 3x12,5 mg

Further Inspection Plan :

- Complete blood count
- Blood gas analysis
- Serial ECG
- Electrolyte

Prognosis :
Dubia ad malam

FOLLOW UP ( 2nd December 2013 7th December 2013)

Date Vital Sign & PE Diagnosis Management
2-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
Palpitations (-) unstable - O2 2-4L/i
Cough (+) hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc IV ec
Sputum (+) (micro)
MR severe
Blood (+) - Vascon 0,03 mg/kgBW/i >
- Lung infection
Head : eye: anemia (-/-), icteric AFF
sclera (+/+) - Dobutamin 5 mg/kgBW/i
Neck : JVP R + 3 cm H2O - Furocemide 5 mg/hr
Heart : S1(N), S2(N), Murmurs : (+) - Inj. Ceftriaxone 2 gr/12 hr
type PSM, grade 3/6 apex - Ambroxol 3x Ci
Lung : LS : Vesicular - Laxadin 1x Ci
AS : Crackles basal (+/+)
Coarse crackles (+/+) Lab results :
Abdomen : Acites (+) RBC : 3,79 106/mm3
Ekstremitas: warm acral, Oedem (+/ WBC : 19,40 103/mm3
+) Ht : 37,40%
UOP : 1000 cc/24 hr, TB : -687 cc Platelet : 111 103/mm3
EKG : ST + Anterolateral ischemic SGOT/SGPT : 2550/859
Bil. Tot/direct : 8,9/6,7
Albumin/globulin : 3.8/3.9
Blood gas analysis :
pCO2 : 23 mmHg
pO2 : 171,6 mmHg
HCO3 : 15,8 mmol/L
Total CO2 : 16,5 mmol/L
Carbohydrate metabolism :
Blood glucose during : 34,5
mg/dl
Kidney :
Ur : 55 mg/dl
Cr : 1,72 mg/dl
 Electrolyte :
Na : 131 mEq/L
K : 60 mEq/L

3-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
Palpitations (-) unstable - O2 2-4L/i
Cough (+) hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc IV ec
Sputum (+) (micro)
MR severe
Blood (+) - Furocemide 5 mg/hr
- Pneumonia
O: Sens: CM - Inj. Ceftriaxone 2 gr/12 hr
BP: 140/70 mmHg HR: 100x/i - Ambroxol 3x Ci
RR: 20 x/i Temp: 36C - Laxadin syr 1x Ci
Head : eye: anemia (-/-), icteric
sclera (-/-) Lab results :
Neck : JVP R + 3 cm H2O RBC : 3,70 g 106/mm3
Heart : S1(N), S2(N), Murmurs : (+) WBC : 13,8 103/mm3
type PSM, grade 3/6 apex, gallop (-) Ht : 35,5 %
Lung : LS : Vesicular Platelet : 50 103/mm3
AS : Crackles basal (+/+) Albumin :2,9
Coarse crackles (+/+) Ur/Cr : 107,2/1,42
Abdomen : Acites (+)
Extremity: warm acral, Oedem (+/+)
UOP : 5500 cc/24 hr, TB : 4700 cc
4-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 140/90 mmHg HR: 104x/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 20 x/i Temp: 36.8C (micro)
MR severe
 Head : eye: anemia (-/-), icteric - Pneumonia - Furocemide 20 mg/8 hr
sclera (+/+) - Inj. Ceftriaxone 2 gr/12 hr
Neck : JVP R + 2 cm H2O - Ambroxol 3x Ci
Heart : S1(N), S2(N), Murmurs : (+), - Laxadin syr 1x Ci
type PSM, grade 3/6 apex - Spironolacton 1x25 mg
Lung : LS : Vesicular - Captopril 3x12,5 mg
AS : Crackles basal (+/+)
Abdomen : Soepel Lab results :
Extremity : warm acral, Oedem (+/+) Na : 130 mEq/L
UOP : 9200 cc/24 hr K : 2,7 mEq/L
5-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
Cough (+) unstable - O2 2-4L/i
Blood (+) hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
O: Sens: CM (micro)
MR severe
BP: 100/90 mmHg HR: 110x/i - Furocemide 20 mg/8 hr >
- Pneumonia
RR: 20 x/i Temp: 36.5C - Jaundice ec 20 mg/12 hr
Head : eye: anemia (-/-), icteric ischemic - Inj. Ceftriaxone 2 gr/12 hr
sclera (+/+) hepatitis - Ambroxol 3x Ci
- AKI std injury
Neck : JVP R + 2 cm H2O - Laxadin syr 1x Ci
Heart : S1(N), S2(N), Murmurs : (+), - Spironolacton 1x25 mg
type PSM, grade 3/6 apex - Captopril 3x12,5 mg >
Lung : LS : Vesicular 3x25 mg
AS : Crackles basal (+/-)
Abdomen : Soepel Lab result :
Extremity : warm acral, Oedem (+/+) Albumin : 3,0 g/dl
UOP : 3500 cc/24 hr Echocardiography result :
Mitral valve : MR severe ec
remodeling LV
Aortic valve : normal
Tricuspid valve : TR mild
Pulmonary valve : normal
 Immpression : Global LV
systolic function decreases,
LVEF 35% of global
hipokinetik
MR severe ec LV dilatation
6-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 100/70 mmHg HR: 114/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 20 x/i Temp: 36.5C (micro)
MR severe
Head : eye: anemia (-/-), icteric - Furocemide 20 mg/8 hr >
- Pneumonia
sclera (+/+) - Jaundice ec 20 mg/12 hr
Neck : JVP R + 2 cm H2O ischemic - Inj. Ceftriaxone 2 gr/12 hr
Heart : S1(N), S2(N), Murmurs : (+), hepatitis - Ambroxol 3x Ci
type PSM, grade 3/6 apex AKI std injury - Laxadin syr 1x Ci
Lung : LS : Vesicular - Spironolacton 1x25 mg
AS : Crackles basal (+/-) - Captopril 3x12,5 mg >
Abdomen : Soepel 3x25 mg
Extremity : warm acral, Oedem (+/+) - Liver care 3x1
Hasil lab :
INR 3.7
7-12-13 S: Dyspnoe (+) reduce - Post SVT with - Bed Rest, semifowler
O: Sens: CM unstable - O2 2-4L/i
BP: 100/70 mmHg HR: 98/i hemodinamic - IVFD NaCl 0,9% 10 gtt/i
- CHF Fc III ec
RR: 28 x/i Temp: 36C (micro)
MR severe
Head : eye: anemia (-/-), icteric - Furocemide 20 mg/8 hr >
- Pneumonia
sclera (+/+) - Jaundice ec 20 mg/12 hr
Neck : JVP R + 2 cm H2O ischemic - Inj. Ceftriaxone 2 gr/12 hr
Heart : S1(N), S2(N), Murmurs (+), hepatitis - Ambroxol 3x Ci
type PSM, grade 3/6 apex AKI std injury - Laxadin syr 1x Ci
Lung : LS : Vesicular - Spironolacton 1x25 mg
AS : Crackles basal (+/-) - Captopril 3x12,5 mg >
 Abdomen : Soepel 3x25 mg
Extremity : warm acral, Oedem (+/+) - Liver care 3x1

CHAPTER IV
CONCLUSION

Arrhythmias result from disorders of impulse formation, impulse

conduction, or both.Abnormally slow rhythms are termed bradycardias (or
bradyarrhythmias). Fast rhythms are known as tachycardias (or tachyarrhythmias).
Tachycardias are further characterized as supraventricular when they involve the
atrium or AV node, and designated ventri cular when they originate from the His-
Purkinje system or ventricles. Disorders of heart rhythm result from alterations of
impulse formation, impulse conduction,or both.
 Supraventricular tachycardias frequently threaten the quality of life but
only rarely threaten life itself. In the one circumstance in which that occurs
Wolff-Parkinson-White syndrome and atrial fibrillation an aggressive curative
management strategy is appropriate. Radiofrequency ablation is the treatment of
choice for high risk accessory pathways. For all other supraventricular
tachycardias, the aim of management should be to abolish attacks or at the least to
minimize the impact of attacks. This latter maybe achieved by significant
lengthening of the interval between attacks'33' or by a significant reduction in
attack duration.

Tachyarrhythmias is directed at the mechanism responsible for the rhythm

disturbance. Forrefractory tachyarrhythmias, or in emergency situations, electric
cardioversion or defi brillation is used. Catheter-based ablative techniques are
useful for long-term control of certain tachyarrhythmias. ICDs are lifesaving
devices implanted in patients at high risk of sudden cardiac death because of
ventricular tachyarrhythmias.

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