Symposium on Pediatric Cardiology-II

Supraventricular Tachycardia in Children

Michal J. Kantoch

4C2 WMC Health Sciences Centre, Division of Pediatric Cardiology, Department of Pediatrics, University of
Alberta, Edmonton, Alberta, T6G 2B7. Canada

Abstract. Several different mechanisms are responsible for paroxysmal supraventricular tachycardia in children. Different
forms of tachycardia occur at different age. Atrio-ventricular reentry tachycardia results from the presence of congenital atrio-
ventricular bypass tracts and is frequently encountered at all ages. Infants may present with ectopic atrial tachycardia or atrial
flutter. Atrio-ventricular node reentry tachycardia becomes more frequent in adolescence. Atrial scarring resulting from open
heart surgery predisposes to complex intra-atrial reentry. Certain forms of congenital and acquired heart disease are associated
with specific types of arrhythmia. Many children with paroxysmal supraventricular tachycardia do not require any therapy. The
decision to proceed with treatment should be based on the frequency and severity of symptoms and on the effect of arrhythmia
on the quality of life. Infants require medical treatment because of the difficulty to recognize symptoms of tachycardia and a
risk of heart failure. Patients with Wolff-Parkinson-White syndrome as well as those with significant heart disease are at risk
of sudden death. Syncope in children with paroxysmal tachycardia may indicate a severe fall in cardiac output from extremely
rapid heart rate. Patients with potentially life-threatening arrhythmia should not participate in competitive physical activities.
Treatment options have undergone significant evolution over the past decade. Indications for the use of specific antiarrhythmic
medications have been refined. Contemporary catheter ablation procedures employ different forms of energy allowing for safe
and effective procedures. Catheter ablation is the treatment of choice for symptomatic paroxysmal tachycardia in school children
and in some infants who failed medical treatment. Surgery is the preferred treatment in few selected cases. The goal of this
review is to present the state of the art approach to the diagnosis and management of paroxysmal supraventricular tachycardia
in infants, children and adolescents. [Indian J Pediatr 2005; 72 (7) : 609-619] E-mail: michalkantoch@cha.ab.ca

Key words : Supraventricular tachycardia; Arrhythmia; Heart failure; Children

Paroxysmal supraventricular tachycardia (PSVT) is the
most common symptomatic arrhythmia in young
patients. It affects children of all ages. Its prevalence is
estimated at more than one in 500 children. A pediatrician
may see several new patients with PSVT in a year. A child
with new onset PSVT is likely to present with the same
paroxysmal tachycardia for at least 10 subsequent years.
Different forms of PSVT present at different patient age.1
The goal of this review is to provide practical
guidelines regarding diagnosis and management of
supraventricular tachycardia in infants, children and
adolescents. The review explains pathophysiology of
different forms of PSVT and risks of heart failure or
sudden death.
Presentation of PSVT in infants
Symptoms of PSVT in infancy differ from those in
childhood and adolescence. A newborn may present with
history of fetal tachycardia or with signs of left ventricular
dysfunction from tachycardia in fetal life. Hydrops fetalis
represents severe heart failure from persistent rapid
tachycardia. Frequently, PSVT becomes less frequent and
Correspondence and Reprint requests : Dr. Michal J. Kantoch, 4C2
WMC Health Sciences Centre, Division of Pediatric Cardiology,
Department of Pediatrics, University of Alberta, Edmonton, Alberta,
T6G 2B7. Canada. Fax: (780) 407 3954.
easier to manage after birth. 2 Conversely, neonates with
no history of fetal tachycardia may present with incessant
and difficult to treat pathological tachycardia after birth.
PSVT may occur in the first days of life or somewhat later
in the first year of life. Most infants with PSVT have
structurally normal hearts. In 15% of infants, paroxysmal
tachycardia is associated with heart disease, drug
administration or a febrile illness. Incessant tachycardia at
a rate of more than 200/min leads to progressive left
ventricular dysfunction. Persistent very rapid tachycardia
at a rate of 250/min or more may produce life threatening
heart failure within few days. Symptoms of PSVT in
infants are inconspicuous and include irritability, poor
feeding, tachypnea, diaphoresis and poor color. When
counseling parents about risks of recurrent PSVT, it is
important to stress that symptoms of tachycardia
masquerade those of many other common illnesses in
infancy. It is prudent to advise parents to check infants
heart rate when the child is quiet or asleep. Parents may
verify heart rate at the time of feeding by placing hand on
the childs chest or with an inexpensive stethoscope. In
infants, atrio-ventricular reentry tachycardia (AVRT)
resulting from the presence of an accessory atrio-
ventricular (A-V) bypass tract accounts for approximately
80% of all cases of PSVT. Permanent junctional
reciprocating tachycardia (PJRT) and automatic atrial

Indian Journal of Pediatrics, Volume 72July, 2005 609

 Michal J. Kantoch
tachycardia are much less common but they frequently
pose a therapeutic challenge. Atrial flutter may occur in
newborns and usually resolves within few days or with
administration of digoxin. When tachycardia is
recognized, it is important to obtain an echocardiogram in
order to rule out structural heart disease and to assess
ventricular function.
Presentation of PSVT in children and adolescents
While obtaining clinical history from children, physicians
have to inquire about the sensation produced by
arrhythmia, how frequently symptoms occur, how long
they persist each time and what other symptoms
accompany arrhythmia. It is important to learn in detail
about each episode of rhythm disturbance. Physicians
may choose to inquire about the most recent bout of
arrhythmia first and then ask about each previous
episode. Frequently physicians have to put much effort
into prompting their patients to report everything they
can remember regarding presentation and circumstances
surrounding each attack of arrhythmia. It is essential to
inquire if there is any family history of arrhythmia or any
family history of sudden death or a convulsive disorder
which may represent life threatening arrhythmia.
Typically, PSVT will produce impression of a very
rapid and regular heart beat that is very difficult or
outright impossible to count. Patients may describe that
the heart is fluttering in the throat. A sensation of
somewhat accelerated pounding (painful) heart beat in
the chest usually indicates sinus tachycardia. In general,
PSVT presents with heart rates well in excess of 150/min
while sinus tachycardia at rest does not exceed such rate
even in a stressful situation.
As a rule, atrio-ventricular node reentry tachycardia
(AVNRT) is triggered by vigorous physical activity while
AVRT mediated by an A-V bypass may also occur at rest.
Patients may recognize a sudden onset of PSVT even
during sinus tachycardia. They report that the heart rate
suddenly accelerates and does not slow down for several
minutes or longer even though they stop physical activity
and lie down. Typical PSVT also terminates suddenly as
if turned off with a switch. Gradual acceleration and
deceleration of tachycardia usually indicate sinus
tachycardia or ectopic (automatic) atrial tachycardia.
Infrequently, children affected by paroxysmal tachycardia
of truly sudden onset and offset may still report that the
tachycardia starts suddenly but terminates gradually or it
begins and wanes gradually.
The majority of older children and adolescents provide
very precise description of their symptoms allowing for a
secure diagnosis of PSVT (although it is always preferred
to record a rhythm strip with arrhythmia). Even children
as young as 3 years of age may recognize symptoms of
PSVT. My heart is racing, beeping, skipping, hurting,
jumping up and down these are only few of many
descriptions that young children may use to explain their
sensation of tachycardia. Sometimes, children are able to
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give merely nebulous history of vague palpitations
especially if they cannot recognize when and how their
arrhythmia starts or what it feels like. Preschool children
may only say that their heart hurts. At times, children
may complain of general malaise or indistinct pressure or
discomfort in the throat. Some children may complain of
isolated headaches. Few patients might deny any
symptoms.
Tachycardia may be accompanied by fatigue, chest
discomfort, shortness of breath or lightheadedness.
Severe cardiovascular compromise produces more
pronounced dyspnea and lightheadedness. Syncope is
unusual and may indicate life threatening arrhythmia
which necessitates rapid diagnosis and treatment. Older
children and adolescents may present with two or more
forms of arrhythmia and it is important to distinguish
what symptoms represent each heart rhythm disturbance
such as paroxysmal tachycardia, accelerated sinus rhythm
or premature contractions. It is very important to
remember that clinical symptoms of relatively benign
PSVT are not different from those produced by life
threatening ventricular tachycardia.
Risk of Cardiac Arrest
The risk of cardiac arrest from PSVT in children and
adolescents is very low. Three general groups of children
at risk of life threatening heart failure or sudden death are
neonates with PSVT, patients with Wolff-Parkinson-
White (WPW) syndrome and children with heart disease.
Nonspecific presentation of PSVT in infants makes it
difficult to recognize. It is essential to remember that
cardiac reserve in neonates is very small and typical
supraventricular tachycardia with heart rate exceeding
200/min may lead to life threatening myocardial
dysfunction within several days.3 Neonates may already
present with subclinical heart failure from tachycardia
before birth. Every neonate with PSVT should be
evaluated with an echocardiogram in order to rule out
structural heart disease and to assess ventricular function.
Administration of intravenous adenosine in order to
terminate PSVT or to make precise diagnosis of
tachycardia is safe. It is important to remember that all
antiarrhythmic medications with the exception of digoxin
exert a negative inotropic effect on the myocardium and
therefore may produce significant hypotension and lead
to cardiac arrest. Even oral administration of a beta
blocker in an infant with impaired ventricular function
may lead to life threatening arterial hypotension. All
newborns should be hospitalized and their vital signs
should be closely monitored during initial therapy with
all antiarrhythmic agents.
The risk of sudden death in adult patients with WPW
syndrome is well recognized. Cardiac arrest is usually
precipitated by atrial fibrillation which is transmitted into
ventricles through a rapid conducting A-V bypass tract.
Atrial fibrillation is uncommon in children, nevertheless
sudden death is a well known complication of WPW
Indian Journal of Pediatrics, Volume 72July, 2005
 Supraventricular Tachycardia in Children
syndrome in young patients as well (Fig. 1A, 1B and 2).
Patients at high risk are those in whom the shortest
interval between two subsequent preexcited ventricular
beats during atrial fibrillation is less than 220
milliseconds.4, 5 This measurement could be taken from an
ECG or a rhythm strip recorded at the time of atrial
fibrillation or during electrophysiologic testing of the A-
V bypass tract. Syncope in patients with WPW syndrome
may indicate high risk of sudden death although sudden
death may be the very first presentation of life-
threatening arrhythmia. Even a single attack of syncope in
a child with WPW syndrome should lead to
electrophysiology studies and ablation of the bypass tract.
Successful ablation of the A-V bypass tract eliminates the
risk of sudden death from WPW syndrome.6 Strenuous
physical activities shorten the refractory period of the
bypass tract and may precipitate atrial fibrillation or
flutter. Sometimes, ventricular preexcitation resolves
during physical activity, for instance during an exercise
stress test. It is not known, however, if these patients are
at low risk of cardiac arrest. Competitive sports should be
discouraged in children with ventricular preexcitation on
a surface ECG.
Fig. 1A. Rapid, irregular tachycardia with wide QRS complexes in
a 9 year old boy who presented with syncope. Atrial
fibrillation produced very rapid ventricular response
mediated by an A-V bypass tract with short anterograde
effective refractory period.
Fig. 1B. After electric cardioversion, an ECG showed sinus rhythm
with ventricular preexcitation. Note that in each lead QRS
complexes are similar during tachycardia (Fig 1A) and
during preexcited sinus rhythm.
Many forms of congenital and acquired heart disease
may impair ventricular function or disturb coronary
circulation and thus increase risks associated with PSVT.
Rapid tachycardia shortens filling time of ventricles and
Indian Journal of Pediatrics, Volume 72July, 2005
Fig. 2. Ventricular fibrillation and cardiac arrest in a 12 year old girl
with WPW syndrome. Arrows point to 2 sinus beats with
ventricular preexcitation followed by a short burst of atrial
flutter which resulted in ventricular fibrillation.
decreases stroke volume and cardiac output. Coronary
blood flow is reduced. Patients with borderline left
ventricular function are at particularly high risk of life
threatening arterial hypotension from PSVT. Few
examples of heart disease leading to ventricular
dysfunction in children include myocarditis, dilated
cardiomyopathy, congenital defects producing large
shunts (in infants and small children) and complex heart
anomalies. Stenotic and regurgitant lesions of heart valves
significantly decrease stroke volume which is already
compromised during tachycardia because of abnormally
short ventricular filling and ejection times. PSVT in
patients with pulmonary hypertension is life threatening.
Physicians have to keep in mind that many patients with
operated heart disease are left with considerable
ventricular dysfunction even though parents may inform
them that the heart was fixed.
Certain forms of heart disease predispose to the
occurrence of certain types of PSVT. Patients with
hypertrophic cardiomyopathy are at risk of atrial
fibrillation which produces a major reduction in the left
ventricular stroke volume in a setting of a thick, non-
compliant myocardium and leads to myocardial ischemia.
Rheumatic disease of the mitral valve is also associated
with paroxysmal atrial fibrillation and a risk of
thromboembolic events. Children with the Ebstein
anomaly of the tricuspid valve present with AVRT which
may produce significant hemodynamic derangement in a
setting of severe tricuspid insufficiency. Children with
Kawasaki disease and coronary artery abnormalities are
at risk of myocardial ischemia and infarction. Children
and adults with operated congenital or acquired heart
disease may present with incisional atrial reentry
tachycardia (IART). This rapid tachycardia at atrial rates
of 180 250 resembles atrial flutter although it is more
difficult to manage. Detailed discussion of risks associated
with PSVT in patients with heart disease falls outside of
the scope of this review.
Presence of severe non-cardiac disease may augment
symptoms associated with PSVT.
Diagnosis
The diagnosis of PSVT is based on thorough clinical
history and electrocardiograms (ECGs) or rhythm strips
recorded at the time of tachycardia and during sinus
rhythm. It is very important to encourage patients and
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 Michal J. Kantoch
their care givers to go to the emergency room or to their
clinic in order to document prolonged attacks of
arrhythmia so that their physician can make a proper
diagnosis. An ECG has to be repeated after tachycardia
resolves. Resting ECGs have to be recorded on several
occasions since ventricular preexcitation may be
intermittent and may not be obvious on each tracing.
Different types of PSVT present differently on a 12 lead
ECG. An ECG recording of the tachycardia allows a
cardiologist to design the best possible treatment. A single
lead tracing should be recorded only if a complete 12 lead
ECG cannot be done. Clinicians should attempt to
identify P waves representing atrial activation during
tachycardia. Short PR tachycardia is such PSVT when the
PR interval is shorter than the RP interval. Short PR
tachycardia includes sinus tachycardia, ectopic atrial
tachycardia, PJRT and an atypical AVNRT. Short RP
tachycardia is such PSVT when the RP interval is short
and the PR interval is long. The P wave is usually
superimposed on the T wave and very close to the
preceding QRS complex. The P wave may be recognizable
in few leads only and usually in limb lead II and in
precordial leads V1 and V2. Short RP tachycardia includes
AVRT mediated by an A-V bypass tract (WPW
syndrome) and typical AVNRT.
An exercise stress test may induce tachycardia and
allow for its documentation. Ambulatory Holter
monitoring may be successful in recording paroxysmal
tachycardia in patients with frequent recurrences of
PSVT. Holter is not likely to document PSVT in patients
with very infrequent bouts of tachycardia although it may
show intermittent ventricular preexcitation pointing to
WPW syndrome. Clinicians are more likely to document
heart rhythm responsible for sporadic palpitations and
other symptoms suggestive arrhythmia if they choose
ambulatory event recorders which patients may keep at
home for several weeks.
Brief and infrequent attacks of palpitations even
accompanied by significant symptoms are very difficult
to record. Symptoms usually resolve by the time patients
arrive at the emergency room or in an ambulatory clinic.
Clinicians may choose to teach patients or their parents
how to take pulse rate or how to count heart rate with a
stethoscope. Patients may want to start a diary indicating
the date of their symptoms, their activity when
palpitations or tachycardia occurred, the pulse rate or the
heart rate as well as accompanying symptoms and
duration of symptoms.
PSVT with wide QRS complexes
Infrequently, an electrocardiogram recorded during PSVT
may show tachycardia with wide QRS complexes. This
may be the case in the following situations:
Antidromic reciprocating tachycardia in patients
with WPW syndrome (Fig. 3).
PSVT with right or left bundle branch block (aberrant
ventricular conduction).
612
Fig. 3. Antidromic AVRT in an adolescent boy with Ebstein
anomaly of the tricuspid valve and WPW syndrome. An
ECG does not allow differentiating this supraventricular
tachycardia from ventricular tachycardia.
PSVT with bystander participation of an accessory A-
V bypass tract
Electrocardiograms recorded during tachycardia and
in sinus rhythm frequently allow a clinician to establish
proper diagnosis. Presence of ventricular preexcitation
during sinus rhythm may point to antidromic
reciprocating tachycardia or bystander participation of an
accessory A-V bypass tract in patients with WPW
syndrome. The term bystander participation of a bypass
tract implies that a bypass tract transmits rapid atrial
activation to the ventricles but the mechanism of
tachycardia does not include a bypass tract (e.g. atrial
fibrillation, AVNRT, ectopic atrial tachycardia, etc.).
Infrequent presence of right or left bundle branch block
during sinus rhythm indicates that tachycardia with wide
QRS complexes represents aberrant conduction as long as
the morphology of QRS complexes is the same during
tachycardia and during sinus rhythm. Frequently
aberrant ventricular conduction is rate dependent which
means that right or left bundle branch block occurs only
at rapid heart rates. Rate dependent aberrant conduction
with right bundle branch block is more frequent than
aberrant conduction with left bundle branch block.
Ventricular tachycardia (VT) is uncommon in children
and adolescents. In general, idiopathic VT is not a life
threatening condition although it may produce syncope.
Life threatening VT may complicate different forms of
cardiomyopathy or congenital heart defects (especially
repaired or palliated heart disease). Ventricular
tachycardia will always present with wide, abnormal
looking QRS complexes. Only in infants, VT may present
with relatively narrow QRS complexes. A-V dissociation
is not always the feature of VT and at times it is not
possible to distinguish VT from wide QRS complex PSVT
in patients with ventricular preexcitation. Patients with
wide QRS tachycardia should have an echocardiogram
and should be evaluated by a pediatric cardiologist.
Acute treatment
Regardless of the type of PSVT there are certain general
principles of therapy which apply to all patients.
Physicians should teach their patients maneuvers which
increase parasympathetic (vagal) tone, slow down
Indian Journal of Pediatrics, Volume 72July, 2005
 Supraventricular Tachycardia in Children
conduction through the A-V node and break the reentry
circuit responsible for PSVT in most cases. An ice-bag can
be used at any age with good success.7 It is important to
place an ice-bag around the nose and mouth in order to
make it effective. Immersion of the face in ice-cold water
may also terminate PSVT. In the Valsalva maneuver
patients are asked to take a deep breath and bear down.
Valsalva maneuver may be combined with other
measures such as an ice-bag or pressure on the abdomen.
Carotid sinus massage, retching or gagging induced by a
finger or a spoon, or blowing on a thumb may also be
effective. Different measures may be successful in
different children. Standing on the head (a rather tricky
operation) seems to work well for some adolescents.
Applying pressure on the eyes with closed eyelids must
never be used because of a significant risk of injury to the
eyes and retinal detachment.
Acute treatment in the emergency room depends on
patients symptoms. Children with unstable vital signs or
signs of heart failure require electric cardioversion. Stable
vital signs and normal blood pressure allow for less
aggressive measures such as those described above.
Intravenous administration of adenosine as a rapid bolus
is safe in children of all ages (Fig. 4). Adenosine is quickly
cleared from circulation by cellular uptake, mostly by
endothelial cells and erythrocytes. The half life in the
blood stream is less than 10 seconds. The standard dose
ranges from 50 to 200 micrograms per kilogram of body
weight. The most commonly observed side effects are
transient chest discomfort, dyspnea, facial flushing, sinus
pauses and A-V block. Significant bradycardia may occur
in patients with sinus node dysfunction, A-V conduction
defects or after concurrent administration of other
medications which affect the A-V node (e.g. beta blockers,
calcium channel blockers, amiodarone and other).
Adenosine may produce bronchoconstriction in patients
with asthma.
Fig. 4. Administration of adenosine during A-V node dependant
tachycardia terminates the tachycardia and results in a 7
second complete heart block.
Following administration of adenosine, it is not
unusual to see PSVT break for few seconds and resume
with vengeance. It is very important to print a rhythm
strip when adenosine is pushed in and review an ECG
tracing after each injection. A rhythm strip may show
sudden termination of tachycardia followed by merely
one or several normal sinus beats and resumption of
PSVT. In such cases a longer acting intravenous
medication could be considered such as a beta blocker
(propranolol), digoxin, procainamide, a calcium channel
blocker (verapamil) or amiodarone. Calcium channel
blockers should not be administered to children under 2
Indian Journal of Pediatrics, Volume 72July, 2005
years of age because of a risk of cardiovascular collapse.
One should remember that intravenous administration of
many antiarrhythmic agents may produce significant
arterial hypotension or induce life-threatening
arrhythmia. It is important to follow guidelines regarding
administration of each medication in regards to the
correct dose and rate of intravenous infusion.
Antiarrhythmic medications are grouped according to
their electrophysiologic properties which allows for their
proper use.8
A rhythm strip recorded during administration of
adenosine may uncover atrial flutter or P waves of atrial
tachycardia. Adenosine is not effective in converting atrial
flutter or fibrillation into sinus rhythm but it is helpful in
establishing correct diagnosis.
Chronic management
Chronic management of PSVT should be individualized.
In general, the decision to treat a child with PSVT
depends on the childs age, symptoms produced by
paroxysmal tachycardia and the effect of PSVT on the
quality of life. Prophylactic treatment with antiarrhythmic
medications is prescribed for infants younger than one
year of age because of nonspecific nature of symptoms
and the risk of life-threatening heart failure from
unrelenting rapid tachycardia. 9 Beta blockers are
prescribed most frequently. Digoxin may be used in
infants without ventricular preexcitation. One could also
prescribe sotalol, flecainide or amiodarone in selected
cases. At one year of age, prophylactic treatment could be
withheld in order to see if tachycardia recurs. More than
one half of toddlers with history of PSVT after birth will
be free from tachycardia at least until school age when
children are able to recognize symptoms of arrhythmia.
Prophylactic treatment with medications may be
extended into preschool years if tachycardia recurs or
parents are unable to recognize recurrent arrhythmia. The
dose of every medication should be increased over time in
order to keep up with the childs weight gain. Patients
compliance improves if prescribed medication could be
taken once or twice a day. Medications may become
ineffective over time and may have to be replaced by
other agents.
In school-aged children, the decision to treat PSVT
usually depends on its effect on the quality of life.
Infrequent PSVT accompanied by mild symptoms does
not warrant any treatment especially if a child is able to
interrupt tachycardia with appropriate maneuvers.
Consumption of caffeine (coffee, tea, soft drinks
containing caffeine) may increase the likelihood of
recurrent tachycardia. Physicians may advise patients
against taking such substances if it is clear that relapses of
PSVT are associated with their intake or PSVT produces
significant symptoms. Use of medications that augment
sympathetic tone or those that suppress vagal tone may
increase the likelihood of another attack of tachycardia.
Patients report more problems with PSVT if they take beta
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 Michal J. Kantoch
adrenergic medications (salbutamol) or certain
decongestants (pseudoephedrine, antihistamines). It is
crucial to treat all patients with WPW syndrome who
present with syncope or who participate in competitive
sports. This recommendation also applies to isolated
ventricular preexcitation with no history of paroxysmal
tachycardia. It is important to remember that prophylactic
treatment with medications does not cure the child from
tachycardia but merely suppresses arrhythmia.
Symptomatic relief from PSVT can be achieved by
implantation of a permanent anti-tachycardia pacemaker.
Such device can recognize occurrence of paroxysmal
tachycardia and interrupt it with overdrive atrial pacing.
Anti-tachycardia pacemakers are considered only in
selected symptomatic patients who failed medical
treatment and ablation procedures.
Catheter Ablation Procedures
Elimination of the arrhythmic substrate and permanent
cure from almost all forms of PSVT can be achieved
through percutaneous catheter ablation or by means of
surgery.10-12 Catheter ablation procedures are performed
in an electrophysiology laboratory and are similar to
cardiac catheterization with the use of fluoroscopy.
Radiofrequency current (RF) ablation is employed most
frequently. During the procedure, a small metal tip of the
catheter is heated to 50-60oC by alternating current at 350
kHz to 1 MHz.13 This relatively low temperature produces
a permanent small scar measuring approximately 4 mm
in diameter and 4 mm in depth. An RF application
directly to the arrhythmic substrate will destroy it
permanently and prevent recurrences of paroxysmal
tachycardia. A cardiologist has to apply from one to
several burns before an RF application lands directly on
the target. The initial success rate of RF ablation exceeds
90%. Infrequently, PSVT may recur if ablation lesions did
not damage but only temporarily injured the arrhythmic
focus. Large ablation lesions are produced by
radiofrequency irrigation catheters and are frequently
required for ablation procedures in patients with atrial
flutter or postoperative atrial tachycardia. Cryoablation is
employed in such cases when an arrhythmic substrate is
located close to the A-V node. Cooling a metal tip of the
catheter to minus 20 oC freezes the tip to the target and
allows the operator to make distinction between the
arrhythmic focus and the A-V node without producing
permanent damage. Cooling to minus 70oC produces a
small permanent scar. Other forms of energy for ablation
procedures are still under scientific investigation.
Sophisticated three dimensional mapping systems allow
for precise localization of arrhythmic foci and
identification of waves of myocardial depolarization.
Such mapping systems allow for successful ablation of
complex arrhythmia, especially IART following heart
surgery. Only very infrequently, a cardiologist may
choose to proceed with ablation of the A-V node and
implantation of a ventricular pacemaker for life
614
threatening PSVT refractory to medical therapy or
catheter ablation of the arrhythmic substrate.
Risks associated with ablation procedures depend on
patients age and location of the arrhythmic focus.
Ablation of an A-V bypass tract situated next to the A-V
node (para-hisian bypass tracts) carries a high risk of a
complete heart block. A smaller risk of a complete A-V
block is associated with ablation of microreentry circuits
responsible for AVNRT and ablation of automatic foci
located close to the A-V node. Generally, this risk is
smaller with the use of cryoablation compared to RF
current ablation. Ablation procedures in small children
and transseptal puncture for ablation of left atrial
arrhythmic foci carry a risk of atrial perforation and
cardiac tamponade. Catheter manipulation in the left
heart is associated with a risk of thrombosis and a stroke.
Other risks may be present in individual cases. As a rule,
ablation procedures are not recommended in children
under 3 years unless other treatments fail to prevent
recurrences of life threatening PSVT.
Surgical ablation of A-V bypass tracts and other
arrhythmic substrates may be considered in such cases
when arrhythmia is life threatening or severely
incapacitating and it cannot be controlled by other means.
Mechanisms of PSVT
Most frequently PSVT has to be differentiated from
accelerated sinus rhythm. Aside from physical activity,
sinus tachycardia can be produced by a febrile illness,
anemia, heart failure, hyperthyroidism, administration of
beta-adrenergic medications, emotion, anxiety and other
factors. Persistent inappropriate sinus tachycardia is
encountered very infrequently. Children at school age,
especially adolescents, may complain of a sensation of
accelerated and pounding heart beat which may occur for
no clear reason at rest and frequently at bed time. These
children may complain that abnormal heart beat does not
allow them to relax, makes them anxious and at times is
associated with chest pain or lightheadedness.
Accelerated heart rate usually does not exceed 120/min.
In the majority of patients, sinus tachycardia has a
functional background and does not require any therapy
aside from reassurance.
Some children and adolescents may provide history of
benign premature beats in such a way that a physician
will get an impression of paroxysmal tachycardia. This is
more likely to happen if a child presents with frequent
premature beats, especially in a form of bigeminy or
trigeminy. A biased physician may continue clinical
interview in a mislead direction.
PSVT in childhood may have different mechanisms.
The list below presents several types of PSVT in the
decreasing order of their prevalence:
Atrio-ventricular reentry tachycardia (Wolff-
Parkinson-White syndrome)
Atrio-ventricular node reentry tachycardia
Ectopic (automatic) atrial tachycardia
Indian Journal of Pediatrics, Volume 72July, 2005
 Supraventricular Tachycardia in Children

Atrial flutter and atrial fibrillation the accessory pathway. The reentry circuit allows for
Junctional tachycardia continuous alternate depolarization of atria and
ventricles. During typical orthodromic reciprocating atrio-
Wolff-Parkinson-White syndrome
ventricular tachycardia (orthodromic AVRT), the
The prevalence of WPW syndrome in the general macroreentry proceeds from the atria to the ventricles
population is estimated at 0.15 to 0.3%. Boys are affected through the A-V node, and back up to the atria from the
more frequently than girls. Occasionally, the syndrome ventricles in the retrograde direction via the A-V bypass
may be inherited. WPW is more prevalent in children tract (Fig. 5B). In most patients with WPW syndrome, an
with the Ebstein anomaly of the tricuspid valve, A-V accessory pathway behaves like a two-way street for
septal defects and ventricular septal defects. The electric conduction. In orthodromic AVRT, QRS
syndrome is produced by the presence of an A-V bypass complexes are narrow and the retrograde P wave may be
tract (accessory pathway) which is a thin and short seen embedded into the early portion of the T wave. The
muscular fiber connecting atria to the ventricles across the retrograde P wave is usually best seen in leads II and V2.
right or left A-V ring. Approximately 10% of patients may In orthodromic AVRT, QRS complexes may become wide
have two or more A-V bypass tracts. Accessory pathways because of aberrant conduction with a right or left bundle
behave like electric conduits between atria and ventricles branch block. At times, one can see PSVT begin with wide
but they do not carry the same specialized electro- QRS complexes for several beats followed by narrow QRS
physiologic properties as a normal A-V node. Location of tachycardia (Fig. 6).
an accessory bypass tract can be predicted from a 12-lead Only infrequently, the reentry circuit may proceed in
ECG.14 the opposite, antidromic direction allowing for ventricular
WPW syndrome is a congenital heart defect since depolarization through the A-V bypass tract and return of
accessory bypass tracts are already present at birth. An A- the depolarization wave back to the atria through the A-
V bypass tract may be responsible for paroxysmal V node. Antidromic AVRT presents with very abnormal,
tachycardia in a fetus. Relatively infrequent and brief
bouts of fetal tachycardia do not affect fetal well being, yet
incessant tachycardia may result in heart failure, non-
immune hydrops and fetal demise. A-V bypass tracts may
produce tachycardia in the first weeks or months of life. It
is important to treat PSVT at this age because it is difficult
for parents to recognize tachycardia and the cardiac
reserve in infants is small. PSVT resolves in more than
50% of infants by one year of age at which time a
physician may choose to discontinue medications. In
some preschool children it is necessary to continue
medical treatment because PSVT recurs or because of
social reasons. After grace period during preschool and
early school years, PSVT may recur in adolescence when
ablation procedures rather than medications become the Fig. 5A. A 4 month old infant with ventricular preexcitation due to
treatment of choice. Majority of individuals born with A- a right postero-lateral A-V bypass tract. Note that the delta
wave is negative in leads aVR and V1, and positive in all
V bypass tracts do not experience any tachycardia until other leads.
adolescence or adulthood. Some may never present with
any PSVT.
A typical ECG recorded during sinus rhythm in a
patient with WPW syndrome shows ventricular
preexcitation which is manifested by a short PR interval,
a wide QRS complex and presence of a delta wave (Fig.
5A). In many patients, ventricular preexcitation is present
at all times and at all heart rates. In some patients,
ventricular preexcitation may be intermittent. In such
cases, preexcitation is usually present at lower heart rates
and it may be documented with ambulatory Holter
monitoring. Ventricular preexcitation during sinus
rhythm is produced by a wave of depolarization which
enters one of the ventricles through a bypass tract in the
anterograde direction (from atria to ventricles). Fig.5B. Orthodromic AVRT in the same infant as in figure 5A.
The macroreentry circuit of PSVT is produced by the Arrows (lead V2) point to retrograde P waves just behind
atrial muscle, the A-V node, the ventricular muscle and narrow QRS complexes.

Indian Journal of Pediatrics, Volume 72July, 2005 615

 Michal J. Kantoch
Fig. 6. A rhythm strip showing four beats of sinus rhythm followed
by a burst of 13 beats of regular PSVT. The first 5 beats
present with wide QRS complexes because of aberrant
ventricular conduction (bundle branch block). Disregard
letter labels of each QRS complex Holter systems
frequently label cardiac events wrong.
wide QRS complexes which resemble ventricular
tachycardia (Fig. 3). Presence of ventricular preexcitation
on a resting ECG points toward antidromic AVRT.
Sudden death in patients with WPW syndrome is
discussed in the section Risk of Cardiac Arrest.
In many patients, a bypass tract behaves like a one way
street only. A bypass tract which conducts exclusively in
the anterograde direction from atria to ventricles
manifests itself by ventricular preexcitation and may
allow for antidromic reentry tachycardia. Even patients
with isolated ventricular preexcitation and no history of
PSVT are at risk of cardiac arrest from paroxysmal atrial
fibrillation if the bypass tract is capable of very rapid
conduction.
A concealed A-V bypass tract is an accessory pathway
capable of conducting solely in the retrograde direction
from ventricles to atria. An electrocardiogram recorded
during sinus rhythm is normal; there is no ventricular
preexcitation. Concealed A-V bypass tracts participate in
orthodromic AVRT. Concealed bypass tracts are very
common.
Certain infrequently encountered accessory pathways
have unusual conduction properties that may resemble
those of an A-V node. Most of these unusual bypass tracts
cross the tricuspid valve in the septal or inferior half of the
valve ring. Permanent Junctional Reciprocating
Tachycardia (PJRT) is produced by a slow-conducting A-
V bypass tract which renders the A-V reciprocating
tachycardia very stable and unremitting. In PJRT, an ECG
shows inverted P waves in inferior limb leads that
precede QRS complexes. PJRT may lead to heart failure in
neonates and in older children. A Mahaim fiber is another
example of an unusual A-V bypass tract which presents
with slow conduction properties and connects to the right
branch of the bundle of His. Mahaim fibers produce
ventricular preexcitation that resembles left bundle
branch block with a normal PR interval.
The general rules regarding prophylactic treatment of
PSVT were already described in another section. Patients
with WPW syndrome should not be treated with
medications which enhance conduction along the bypass
tract such as calcium channel blockers and digoxin. These
medications increase the risk of cardiac arrest precipitated
by atrial fibrillation. Class III antiarrhythmic agents such
as amiodarone and sotalol are effective and safe. Class Ic
agents (propafenone, flecainide) and beta adrenergic
616
blockers are also effective. A physician may consider
prophylactic treatment with digoxin in infants without
ventricular preexcitation. Calcium channel blockers may
be used for prevention of AVRT mediated by concealed
A-V bypass tracts but must not be prescribed for children
younger than 2 years of age. Ablation of the accessory
pathway may be considered as the primary treatment
option at school age and in small children who failed
medical treatment for significant arrhythmia.
Atrio-ventricular node reentry tachycardia (AVNRT)
AVNRT is the most common form of paroxysmal
tachycardia in adolescence and adulthood (Fig. 7).
AVNRT is very unusual in infants and toddlers and only
school aged children may present with AVNRT for the
first time. AVNRT is typically triggered by physical
activity. This form of PSVT is not associated with a risk of
cardiac arrest unless a patient has significant heart
disease.
Fig. 7. AVNRT in a 16 year old girl. Activation of atria and
ventricles occurs at the same time therefore P waves are
embedded in QRS complexes and cannot be seen at all.
The anatomic substrate for AVNRT is a dual electric
input from the right atrium into the A-V node.15 This dual
input is a normal, physiologic finding and consists of a
fast pathway and a slow pathway. The fast
pathway is located in the low interatrial septum near the
His bundle recording site. The slow pathway is found
above the ostium of the coronary sinus and close to the
ring of the tricuspid valve. Both pathways are connected
by a broad area of tissue at the site of their input to the A-
V node. In patients with AVNRT, physiologic conduction
properties of both pathways are such that they allow for
a microreentry circuit at the entrance to the A-V node. The
most common direction of the reentry is such that the
slow pathway conducts toward the A-V node and the
fast pathway allows for retrograde activation of the
atria. In an unusual atypical form of AVNRT, the
direction of reentry is opposite.
An ECG recorded during sinus rhythm is normal. An
ECG recorded during AVNRT shows normal, narrow
QRS complexes unless tachycardia produces a functional
bundle branch block. P waves are not clearly seen because
activation of atria and ventricles occurs at the same time
and P waves are embedded within QRS complexes.
All medications that slow conduction through the A-V
Indian Journal of Pediatrics, Volume 72July, 2005
 Supraventricular Tachycardia in Children
node are effective in preventing recurrences of AVNRT.
Beta adrenergic blockers and calcium channel blockers are
frequently used. Digoxin usually does not control PSVT.
Ablation procedures for AVNRT are associated with a 1-
2% risk of a heart block which requires implantation of a
permanent pacemaker. At the time of an ablation
procedure, an operator usually disrupts the slow pathway
leading into the A-V node.
Ectopic (automatic) atrial tachycardia
Atrial tachycardia is an uncommon variety of PSVT in
children and adolescents.16 In infants, atrial tachycardia is
more prevalent and may account for 15% of all cases of
supraventricular tachycardia. Atrial tachycardia may be
paroxysmal or incessant. The tachycardia usually
originates from a small ectopic focus or from an area of
abnormal atrial muscle in the right or in the left atrium.
The electrophysiologic basis of atrial tachycardia is either
increased automaticity of myocardial cells in the atrium or
reentry within the atrial myocardium. Atrial tachycardia
may produce rapid heart rates and may prove refractory
to medical treatment. Incessant atrial tachycardia may
lead to life-threatening heart failure.
As opposed to the AVRT and AVNRT, atrial
tachycardia may have a relatively slow onset and a
gradual offset. Patients may report that their tachycardia
begins suddenly or the heart rate increases rather
gradually. Many patients are asymptomatic. An ECG
usually shows regular tachycardia with narrow QRS
complexes unless the tachycardia produces a functional
bundle branch block in which case QRS complexes are
wide. Ventricular rhythm is irregular in such cases when
atrial rate is so rapid that not every atrial beat is
conducted to ventricles (Fig. 8). P waves are usually best
seen in leads II, V1 and V2. When every atrial beat is
conducted to ventricles, the PR interval is usually shorter
Fig. 8. A 6 day old newborn with ectopic atrial tachycardia. Small
arrows point to P waves produced by atrial tachycardia.
Tachycardia breaks to allow a single sinus beat (larger
arrow) and restarts with a beat bearing incomplete right
bundle branch block morphology. Note that tachycardia P
waves are best seen in lead V1.
Indian Journal of Pediatrics, Volume 72July, 2005
than the RP interval and the morphology of P waves is
abnormal. P waves produced by atrial tachycardia may
resemble normal P waves of sinus rhythm when the
ectopic focus is located in close proximity to the sinus
node.
Chaotic (multifocal) atrial tachycardia is very unusual
in children. Atrial activation from multiple foci in the
atrial myocardium produces P waves of different
morphologies and atrial rate may exceed 400/min. An
echocardiogram frequently shows normal structure and
function of both atria and ventricles.
Vagal maneuvers do not interrupt atrial tachycardia.
Adenosine usually does not terminate tachycardia,
however it will produce a higher degree A-V block
allowing for clear visualization of rapid atrial P waves.
Infrequently, adenosine may terminate atrial tachycardia
which makes correct diagnosis more difficult.
Short, asymptomatic and even relatively frequent
bouts of atrial tachycardia might not require any
antiarrhythmic therapy since brief spells of rapid heart
rate do not impair ventricular function. Digoxin, beta
adrenergic blockers and calcium channel blockers may
not prevent recurrences of tachycardia. Medications that
belong to class Ia, Ic and III are more effective. One may
consider therapy with propafenone or flecainide alone or
in combination with digoxin or a beta blocker. Flecainide
must not be used in patients with heart disease other than
PSVT. Sotalol is used as monotherapy, in combination
with digoxin or cautiously in combination with class Ic
agents. Amiodarone may be effective but long term
therapy is associated with several side effects.
Medications that belong to class I and III should be
prescribed by an experienced physician since their
administration is associated with a risk of significant side
effects and proarrhythmia. An ablation procedure should
be considered in children at school age when it allows for
permanent cure in more than 80% of cases. An ablation
procedure may be effective in infants with rapid heart
rates or ventricular dysfunction who failed medical
therapy.
Intermittent ectopic atrial rhythms at rates close to the
normal heart rate for age are common in children of
school age and in adolescence. Ectopic atrial rhythms
produce abnormal P wave morphology but they do not
represent any heart disease and they do not lead to any
ventricular dysfunction. As a rule, even very frequent
premature atrial beats and ectopic atrial rhythms do not
predict occurrence of PSVT and do not degenerate into
ectopic atrial tachycardia. An exercise stress test will show
normalization of P waves as the sinus rhythm takes over
even with mild physical activity. Ectopic atrial beats and
intermittent ectopic atrial rhythms do not require any
treatment.
Atrial flutter, IART and atrial fibrillation
Atrial flutter is an unusual arrhythmia in children. It may
occur in a fetus when it presents with ventricular rates of
617
 Michal J. Kantoch
150 220/min. Atrial flutter may be present at birth or it
may occur in the first days of life. Intravenous
administration of adenosine does not terminate this
tachycardia but it allows for clear visualization of saw
tooth flutter waves (Fig. 9). Electric cardioversion should
be done in a neonate with heart failure. Treatment with
digoxin is frequently effective in an infant with preserved
heart function but it may take several days before atrial
flutter terminates. Class Ia (procainamide), Ic
(propafenone, flecainide) or class III (sotalol, amiodarone)
antiarrhythmic medications can be used if digoxin fails to
restore sinus rhythm. All antiarrhythmic agents with the
exception of digoxin exert negative inotropic effect on
ventricular myocardium and may precipitate life
threatening hypotension. Electromechanical dissociation
has been reported after intravenous administration of
amiodarone. Once neonatal flutter terminates it usually
does not recur. It is advisable to continue treatment with
digoxin for six months.
Fig. 9. Atrial flutter in a newborn. Administration of adenosine
allowed for clear visualization of flutter waves (first several
beats) before 2:1 A-V conduction returns making it difficult
to diagnose atrial flutter.
Atrial flutter is very unusual in older children and
adolescents with normal hearts. It is more common in
children with congenital heart disease. In typical atrial
flutter, repetitive atrial activation results from continuous
flow of a depolarization wave around the tricuspid valve
(macroreentry). This reentry circuit becomes very stable
in patients with a dilated right atrium. Antiarrhythmic
medications are only infrequently successful in
converting atrial flutter back to sinus rhythm. Ablation
procedures for typical atrial flutter target the isthmus
between inferior vena cava and the ring of the tricuspid
valve.
Patients with heart disease and especially those after
open heart surgery often present with atrial tachycardia
resulting from several different reentry circuits in the
right or left atrium.17 The right astronomy scar, scaring
from repair of septal defects as well as other suture lines
in atrial walls produce obstruction to uniform
propagation of atrial activation during sinus rhythm and
create complex pathways for intra-atrial reentry
tachycardia (IART). Electric cardioversion is generally
effective in restoring sinus rhythm although IART may
recur within a short period of time. Atrial surgery
predisposes to sinus node dysfunction which further
increases risk of recurrent IART. Incisional atrial
tachycardia is consistently resistant to medical therapy
618
and should be treated in specialized cardiac centers. At
times IART can be suppressed with sotalol or amio-
darone. Infrequently, a patient with atrial scarring may
present with automatic atrial tachycardia from an ectopic
focus rather than with IART.
Paroxysmal atrial fibrillation is even less prevalent
than atrial flutter. An ECG recorded during atrial
fibrillation shows an irregularly irregular rapid heart
rhythm. QRS complexes are narrow although some may
become wide because of intermittent aberrant ventricular
conduction. Infrequent bouts of atrial fibrillation in
patients with normal heart function do not require any
treatment except for administration of aspirin to prevent
thromboembolic complications. Children with congenital
or acquired (rheumatic) heart disease are more likely to
develop atrial fibrillation. Treatment should address the
cause of hemodynamic dysfunction before targeting
arrhythmia. The efficacy, safety and long term outcomes
of catheter ablation procedures for atrial fibrillation in
children are unknown. Electric cardioversion for
sustained atrial flutter, fibrillation or IART must be
preceded with several weeks of anticoagulation.
Junctional tachycardia
Congenital junctional ectopic tachycardia (JET) is also
very uncommon. It generally presents in the first 6
months of life. An ECG shows regular tachycardia at
heart rates ranging from 150 to 200 per minute and
narrow QRS complexes. Retrograde P waves are found
just behind QRS complexes or there may be complete A-
V dissociation with the atrial rate slower than the
ventricular rate. Incessant JET at a rapid heart rate may
lead to heart failure. Electric cardioversion does not
terminate this tachyarrhythmia. JET is difficult to treat
although it may yield to therapy with amiodarone at a
dose as high as 250-500 mg/m2 per day orally. Patients
with severe ventricular dysfunction who fail medical
treatment should be considered for catheter ablation
therapy. Transient postoperative JET is commonly seen in
small children during the first week following open heart
surgery for complex heart disease.
Slow escape junctional rhythms during sinus
bradycardia as well as transient accelerated junctional
rhythms are common in healthy children and adolescents.
These rhythms are a normal finding and do not require
any therapy.
CONCLUSION
PSVT in children may have several different underlying
mechanisms. General rules regarding acute and chronic
therapy are similar for most forms of paroxysmal
tachycardia, however clear understanding of
pathophysiology of different tachyarrhythmias will assist
a physician in selecting the best possible treatment. PSVT
is usually benign and patients with asymptomatic and
infrequent tachycardia do not require any intervention.
Indian Journal of Pediatrics, Volume 72July, 2005
 Supraventricular Tachycardia in Children
Conversely, frequent and symptomatic tachycardia or
PSVT presenting with syncope should be treated.
Neonates, patients with ventricular preexcitation and
those with impaired ventricular function from heart
disease are at risk of cardiovascular collapse or sudden
death. Patients with ventricular preexcitation must not be
allowed to participate in competitive sports until a bypass
tract is interrupted with an ablation procedure. Medical
treatment is the preferred option for infants and toddlers
while ablation procedures are very effective and safe in
older children and adolescents. Patients with less
common forms of PSVT as well as those with heart
disease should be referred to a pediatric cardiology clinic.
Rapid administration of adenosine not only terminates
most common forms of PSVT but also allows establishing
correct diagnosis in refractory cases; it is essential to
record a rhythm strip within seconds after adenosine
push.
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