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U N I V E R S I T Y O F M I N N E S O T A A m p l at z C H I L D R E N ’ S H O S P I T A L
Supraventricular Tachycardia in Children and Adolescents
from the body—on the right from the body and on the left from
the lungs. Atria contracts to advance blood into the ventricles
(pumping chambers). The ventricles pump blood out of the
heart—on the right to the lungs (pulmonary ventricle) and on the
left (systemic ventricle) to the body.
Parvin Dorokstar, M.D., Pediatric Cardiologist
Overview
Supraventricular tachycardia (SVT) is a type of heart rhythm
disorder that can be found in healthy children and adolescents
as well as those with underlying heart disease. SVT affects as
many as 1:250-300 children. Tachycardia refers to any heart
rhythm where the heart beats faster than normal for age and
environmental factors. Supraventricular means “above the
ventricles,” thus describing any tachycardia that originates and/
or involves structures above the ventricles of the heart. The
term supraventricular tachycardia is often used differently in
different settings. Properly, SVT refers to any tachycardia that
is not ventricular in origin. This definition would include sinus
tachycardia.
In a clinical setting, supraventricular tachycardia is used loosely as
a synonym for paroxysmal supraventricular tachycardia (PSVT).
This term refers to those SVTs that have a sudden, abrupt or
immediate onset. A person experiencing PSVT may see their
heart rate go from 90 to 180 beats per minute instantaneously.
Because sinus tachycardias (and some other SVTs) have a gradual
(i.e., non-immediate) onset, they are usually excluded from the
PSVT category.
The heart consists of 4 chambers – 2 upper chambers called atria,
that function as receiving chambers for the blood and 2 lower
chambers called ventricles that function as pumping chambers.
The atria (receiving chambers) receive blood from venous vessels
There are specialized heart cells that create and coordinate
electrical activity and contractions. Even though most cells of the
myocardium are capable of impulse formation, the fastest ones
are located in the sinoatrial node (SAN) or sinus node, which is
located in the right atrium. The created impulse is transmitted
to the atrioventricular node (AVN) and the bundle of His, which
transmits the impulse to the His-Purkinje system supporting
impulse propagation to the right and left ventricles. Once the
impulse gets transmitted through the atrioventricular node and
the bundle of His and its branches, electromechanical association
results in contraction of the heart muscle and the ventricles.
The atria and ventricles contract in quick sequence and in a
coordinated fashion, supporting a heart rhythm. This rhythm is
responsive to all sorts of stimulation both positive and negative,
such as stress, exercise, fever, hormones, drugs and nervous system
signals. Nervous system input and the level of hormones in the
blood strongly influence the rate of the heart’s contraction. An
arrhythmia can occur when there is an electrical problem with
any of the cells of the heart or their response to the environment.
During the expression of supraventricular tachycardia, the heart
rate is sped up by an abnormal electrical impulse and the heart
beats so fast that the heart muscle cannot relax completely
between contractions. Thus, the ventricles fill with less blood and
the patient becomes symptomatic. Due to the ineffective filling or
contractions of the heart, the brain receives less blood and oxygen
and patients become light-headed, dizzy, or feel like they may
faint or pass out (syncope).
Supraventricular tachycardia can be found in healthy young
children, in adolescents, and in people with a history of heart
disease. Most people who experience SVT live a normal life
without restrictions. However, tachycardia can impose an
altered life style and compromise, especially in adolescents
where sports are so important. Supraventricular tachycardia
often occurs as sporadic episodes with stretches of normal heart
rhythm in between. This is typically referred to as paroxysmal
supraventricular tachycardia (PSVT). Supraventricular
tachycardia may also be chronic (ongoing, long term). Symptoms
can come on suddenly and may go away without treatment.
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They can last a few minutes or as long as 1-2 days. Inadequate
filling of the heart during SVT can make the heart less effective so
that the cardiac output is decreased and the blood pressure drops.
Signs and symptoms
Supraventricular tachycardia is the most common abnormal
tachycardia in the pediatric age group. The most common types
of SVT in children include atrioventricular reentrant tachycardia
(AVRT)—including Wolff-Parkinson-White syndrome (WPW),
and AV nodal reentrant tachycardia (AVNRT).
SVT usually has its onset at rest but may initiate during exercise.
The precipitating factors are often difficult to identify but
occasionally a febrile illness may precipitate an episode. The heart
rate is usually in the 160 to 300 beats per minute range. In general,
the younger the patient the more rapid the SVT heart rate, but
the longer the tachycardia is tolerated before symptoms (usually
congestive heart failure) becomes obvious. As a rule, episodes of
SVT onset and terminate abruptly, and may last anywhere from a
few minutes to several hours, which is why it is called paroxysmal.
The following symptoms are typical (but not always present) with a
rapid pulse of 150-300 beats per minute:
• Pounding chest (palpitations)
• Shortness of breath
• Chest pain / heavy chest
• Rapid breathing
• Dizziness
• Loss of consciousness (in serious cases)
In infants, symptoms of SVT may not become apparent until
the patient has been in SVT for 24 hours, or longer. They will
often present with symptoms of congestive heart failure such as
tachypnea, pallor, poor feeding, fussiness or lethargy. In children
and adolescents, symptoms may include palpitations, chest pain,
shortness of breath, dizziness, syncope or near syncope, pallor,
and diaphoresis. It is unusual for older patients to present in heart
failure, as they will usually become symptomatic soon after the
onset of SVT. They will often complain of intermittent episodes of
palpitations, with mild associated symptoms.
In a healthy child, supraventricular tachycardia usually presents
with palpitations but rarely, it may present as syncope or near
syncope. This may occur in patients with WPW who develop atrial
fibrillation and rapid conduction down the accessory pathway to the
ventricles. The onset of SVT can also cause a decrease in cardiac
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output with resultant hypotension, decreased cerebral perfusion
pressure, and syncope.
In the pediatric age group, the most common cause of syncope
is neurocardiogenic syncope (also called a vasovagal faint).
Syncopal episodes associated with palpitations should raise the
suspicion of a possible tachyarrhythmia contributing to the
patient’s symptoms. Nearly any type of cardiac arrhythmia can
cause syncope if a sudden fall in cardiac output occurs. Cardiac
dysrhythmias to consider should include—SVT, ventricular
tachycardia, advance degree AV block, sick sinus syndrome
in patients with previous cardiac surgery, and pacemaker
malfunction in those patients who are pacer dependent.
Other cardiac related disease to consider in patients presenting
with syncope include outflow tract obstruction (hypertrophic
cardiomyopathy, aortic stenosis, pulmonic stenosis, pulmonary
hypertension), coronary artery anomalies, cardiomyopathies,
and mitral valve prolapse. The diagnosis can often be made
with a thorough history and physical examination performed
as close to the time of the syncopal episode as possible.
Cases, which should arouse increased concern, include those
not consistent with neurocardiogenic syncope, syncope
with exercise, a family history of sudden death, and those
patients with known structural cardiac disease. All patients
who present with syncope should, at the minimum, have an
EKG performed. In most cases of neurocardiogenic syncope,
symptoms will improve or resolve with increased fluid and salt
intake. Treatment for other causes of syncope should address
the underlying etiology.
The differential diagnosis of a pediatric patient who presents in
a narrow complex tachycardia includes SVT, sinus tachycardia,
atrial flutter, atrial fibrillation, junctional ectopic tachycardia,
ectopic atrial tachycardia, and chaotic atrial rhythm. Some
patients with SVT and a bundle branch block or antidromic
WPW, may present with a wide complex tachycardia, which
if often difficult to distinguish from ventricular tachycardia
(VT).
Types of SVT
Supraventricular tachycardia can be divided into two broad
categories based on the mechanism of the tachycardia—
abnormalities in impulse propagation, otherwise known as
reentrant tachycardias and abnormalities in impulse formation
or automatic tachycardias.
S u p raventricu l ar T achycardia in C hi l dren and A do l escents
The following are types of supraventricular tachycardias,
each with a unique mechanism of impulse expression and
maintenance:
• SVTs involving sinoatrial tissue
- Sinus tachycardia
- Inappropriate sinus tachycardia
- Sinoatrial node reentrant tachycardia (SANRT)
• SVTs involving atrial tissue:
- Atrial tachycardia (Unifocal) (AT)
- Multifocal atrial tachycardia (MAT)
- Atrial fibrillation (with or without a rapid ventricular
response)
- Atrial flutter (with or without a rapid ventricular response)
• SVTs involving the atrioventricular node:
- AV nodal reentrant tachycardia (AVNRT)
- AV reentrant tachycardia (AVRT)
- Junctional ectopic tachycardia
The individual subtypes of SVT can be distinguished from
each other by certain physiological and electrical characteristics,
many of which can be present in the patient’s ECG. Some of the
distinguishing features are more subtle and require further testing
for delineation.
evidence of a delta wave, and therefore most will have normal PR
intervals. Most patients with SVT have normal cardiac anatomy.
Congenital heart defects in which SVT is most commonly
encountered are Ebstein’s anomaly and L-transposition of the
great arteries.
Atrioventricular reentrant tachycardia (AVRT) results from a
reentry circuit that involves an accessory pathway. This reentrant
circuit is physically much larger than that associated with
AVNRT. One portion of the circuit is usually the AV node,
and the other, an abnormal accessory pathway that crossed the
atrioventricular groove from atria to the ventricle. Accessory
pathways occur in basically 2 different types—bidirectional
conduction associated with Wolff-Parkinson-White syndrome
and unidirectional conduction usually associated with a normal
baseline electrocardiogram. SVT supported by AVRT is the most
common cause of tachycardia in children. AVRT occurs in two
forms—orthodromic where the impulse uses the atrioventricular
node antegradely and the accessory pathway retrogradely and
antidromic where the impulse uses the atrionventricular node
retrogradely and the accessory pathway antegradely.
Manifest
Variations
Most of the narrow complex tachyarrhythmias may be
distinguished from their electrocardiogram findings.
Supraventricular tachycardia ranges in heart rate from 160 to 300
beats per minute. The diagnosis of AVRT or AVNRT requires the
presence of 1:1 A-V conduction. The heart rate usually remains
in a very narrow range regardless of the patient’s physiologic state.
P-waves, which are oftentimes retrograde, are visible only majority
of cases. Upon conversion to a sinus rhythm, patients with WPW
(or, rarely Mahaim fibers which are accessory pathways that are
able to conduct only antegrade, with slow conduction, connecting
the atrium directly to a portion of the right bundle branch)
will demonstrate the classical delta waves as evidenced by an
upsloping or slurring of the initial portion of the QRS complex.
Delta waves are secondary to rapid antegrade conduction from
the atrium to the ventricles through the accessory pathway, thus
causing ventricular pre-excitation. With WPW the PR interval
is short. Forms of SVT with concealed accessory pathways (i.e.,
those capable of only retrograde conduction) will not show
During sinus rhythm
During SVT
During orthodromic AVRT, the electrical impulse is conducted
down through the AV node antegradely, like ususal, and and
uses an accessory pathway retrogradely to re-enter the atrium.
A distinguishing characteristic of orthodromic AVRT can
therefore be a p-wave that follows each of its regular, narrow QRS
complexes, due to retrograde conduction.
In antidromic AVRT, electrical impulses are conducted
down through the accessory pathway and re-enter the atrium
retrogradely via the AV node. Because the accessory pathway
arrived in the ventricles outside of the bundle of His, the QRS
complex in is wider than usual.
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Concealed
During sinus rhythm
During SVT
Atrial flutter is caused by a reentry rhythm in the atria, with a
regular rate of approximately 300 beats per minute when there
is one to one conduction. On the ECG, this appears as a line of
“sawtooth” p-waves. The AV node will not usually conduct such
a fast rate, and so the P:QRS usually involves a 2:1 or 4:1 block
pattern, (though rarely 3:1, and sometimes 1:1 in setting of class
IC anti-arrhythmic drug use). Since the ratio of P to QRS is
usually consistent, A-flutter is often regular in comparison to its
irregular counterpart, A-fib. Atrial flutter may not express itself as
a tachycardia unless the AV node permits a ventricular response
greater than 100 beats per minute. Atrial flutter usually presents
with a regular or regularly irregular tachycardia with an atrial
rate in the range of 250 to 400 beats per minute. The classic
sawtooth flutter waves may be seen, or revealed following a dose
of adenosine. The ventricular rate will depend on the degree of
A-V conduction (e.g. 2:1, 3:1, etc.).
Atrial flutter will most often be encountered in the setting of
congenital heart disease, presence of significant mitral or tricuspid
valve regurgitation with atrial dilatation; and rarely in fetuses or
newborns with normal hearts (i.e., it sometimes occurs in normal
fetuses and newborns), or in pacents with myocarditis.
AV nodal reentrant tachycardia (AVNRT) sometimes used
to be referred to as a junctional reciprocating tachycardia.
It involves a reentry circuit forming within or around the AV
node itself. The circuit most often involves two pathways one
faster than the other, within the AV node. Because the AV node
is immediately between the atria and the ventricle, the re-entry
circuit often stimulates both, meaning that a retrogradely
conducted p-wave is buried within or occurs just after regular,
narrow QRS complexes.
Reentry tachycardia within
the artioventricular node
(AVNRT)
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In the above two ECGs you can diagnose atrial flutter, first with 2:1
conduction (shown above) and then with 1:1 conduction (shown below)
once the patient received an intravenous line.
S u p raventricu l ar T achycardia in C hi l dren and A do l escents
Reentry tachycardia
involving atrial tissue
Atrial fibrillation, when it is associated with a rapid ventricular
response greater than 100 beats per minute, becomes a type
of SVT. Atrial fibrillation is characteristically an “irregularly
irregular rhythm” both in its atrial and ventricular depolarizations.
It is distinguished by fibrillatory p-waves that, at some point in
their chaos, stimulate a response from the ventricles in the form of
irregular, narrow QRS complexes.
Atrial fibrillation demonstrates a rapid atrial rate (300-500
beats per minute) with a very chaotic pattern, and an irregularly
irregular ventricular rhythm. Atrial fibrillation is most often seen
in older children following palliative surgery for congenital heart
defects, especially those involving atrial surgery (e.g., Fontan,
Mustard, or Senning procedures), and those children with
significant atrioventricular valve disease.
Ectopic atrial tachycardia and chaotic atrial rhythm are rare
tachyarrhythmias in the pediatric age group. On EKG, ectopic
atrial tachycardia will show the presence of a variable (and
sometimes misleadingly regular) atrial rate with an abnormal
P-wave axis indicating a single atrial focus.
(Unifocal) Atrial tachycardia is tachycardia resultant from one
ectopic foci within the atria, distinguished by a consistent p-wave
of abnormal morphology that fall before a narrow, regular QRS
complex.
Multifocal atrial tachycardia (MAT) is tachycardia resultant
from at least three ectopic foci within the atria, distinguished
by p-waves of at least three different morphologies that all fall
before irregular, narrow QRS complexes. During this tachycardia
the three non-sinus P-wave morphologies are associated with
an irregular ventricular response, and variable PR, PP, and RR
intervals. Both types of dysrhythmias occur most often in patients
with structurally normal hearts, at times with concomitant
myocarditis or diminished myocardial funtion.
Junctional ectopic tachycardia or JET is a rare tachycardia
caused by increased automaticity of the AV node itself initiating
frequent heart beats. On the ECG, junctional tachycardia often
presents with abnormal morphology p-waves that may fall
anywhere in relation to a regular, narrow QRS complex. This
tachycardia is most commonly seen after surgery for congenital
heart disease. Junctional ectopic tachycardia is most commonly
encountered in children less than 2 years of age, in the immediate
post-operative period following corrective surgery for a congenital
heart defect involving the region around the AV node (e.g., VSD
or tetralogy of Fallot repair). This is one of the most common
post-operative arrhythmias encountered. The ECG typically
demonstrates a narrow complex tachycardia with a regular
ventricular rhythm, and a ventricular rate, which is often rapid
than the atrial rate. When the atrium is captured retrograde
the p-wave morphology is negative in leads II, III and AVF,
supporting the notion that this dysrhythmia originates from a
focus of enhanced automaticity in the peri-AV nodal region. The
heart rate typically rises and decreases gradually (warms up and
cools down). This feature helps differentiate it from a reentrant
type of tachyarrhythmia.
Sinus tachycardia is considered “appropriate” when a reasonable
stimulus, such as the catecholamine surge associated with
fright, stress, or physical activity, provokes the tachycardia. It
is distinguished by a presentation identical to a normal sinus
rhythm except for its fast rate (>100 beats per minute in adults).
Inappropriate sinus tachycardia, then, is a rhythm originating
form around the sinus node that is inappropriately fast.
Sinoatrial node reentrant tachycardia (SANRT) is caused by
a reentry circuit localised to or near the SA node, resulting in a
normal-morphology p-wave that falls before a regular, narrow
QRS complex. It is therefore impossible to distinguish on the
ECG from ordinary sinus tachycardia. It may, however, be
distinguished by its prompt response to vagal manoeuvres.
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Irregular heart beat
Diagnosis
An irregular heart rhythm is not an unusual finding in children
with or without known cardiac disease. Some irregular rhythms
are normal findings in healthy children. If the heart rate is not too
slow or too fast, as to limit the cardiac output, then an arrhythmia
may be well tolerated. Most children can be satisfactorily evaluated
with a 12 lead electrocardiogram and rhythm strip, with possible
supplementation by a chest x-ray, echocardiogram, Holter or
event monitor, or an exercise study. There are several important
determinants of arrhythmias, which should be considered. These
include the arrhythmogenic substrate (e.g., accessory conduction
pathway, automatic ectopic focus), modulating factors, and triggers
of the arrhythmia.
Making an diagnosis can sometimes be difficult, especially when
there is no dcocumented record of the tachycardia. Several tests
can be performed to attempt to document the tachycardia and
therefore a more accurate diagnosis.
Changes in sinus rhythm (P-wave preceding each QRS complex,
with a normal P-wave axis) are most commonly seen with a sinus
arrhythmia, sinus bradycardia, or sinus tachycardia. In pediatrics,
sinus arrhythmia is usually secondary to a variation in vagal tone
during the normal respiratory cycle. This causes an increase in
heart rate during inspiration and a decrease in heart rate during
exhalation. It is most pronounced when the heart rate is slower
and resolves with an increase in heart rate.
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Holter monitor
Imaging with start (red arrow) and end (blue arrow) of a SVTtachycardia with a pulse frequency of about 128/min. Usually,
most supraventricular tachycardias have a narrow QRS complex
on ECG. Rarely, supraventricular tachycardia with aberrant
conduction can produce a wide-complex tachycardia that can
mimic ventricular tachycardia, such as antidromic AVRT.
In the clinical setting, it is important to determine whether a
wide-complex tachycardia is an SVT or a ventricular tachycardia,
since they are treated differently. Ventricular tachycardia has to be
treated appropriately, since it can quickly degenerate to ventricular
fibrillation and death. A number of different algorithms have
been devised to determine whether a wide complex tachycardia is
supraventricular or ventricular in origin. In general, a history of
S u p raventricu l ar T achycardia in C hi l dren and A do l escents
structural heart disease dramatically increases the likelihood that
the tachycardia is ventricular in origin.
Event recorder
Since it is often difficult to capture an episode of tachycardia when
it is happening and a patient may not have an episode during a
scheduled Holter evaluation, an event recorder can be prescribed.
This device is able to document a heart rhythm after the push of a
button. This heart rhythm can be electronically transmitted to the
doctor.
Exercise testing
Sometimes the tachycardia is associated with exercise. In this case
the evaluating doctor may choose to perform an exercise test to
evaluate the expression of tachycardia.
Acute treatment
In general, SVT is not life threatening but episodes should be
treated or prevented. While some treatment modalities can be
applied to all SVTs with impunity, there are specific therapies
available to cure some of the different sub-types. Cure requires
intimate knowledge of how and where the arrhythmia is initiated
and propagated.
The SVTs can be separated into two groups, based on whether
they involve the AV node for impulse maintenance or not. Those
that involve the AV node can be terminated, acutel by slowing
conduction through the AV node with a drug like adenosine,
that transiently blocks atrioventricular conduction. Those that do
not involve the AV node as a critical component of the reentrant
loop will not/or may tansiently respond to AV nodal blocking
manuevres. These manuevres are still useful however, as transient
AV block will often unmask the underlying rhythm abnormality,
which usually originates from somewhere in the atria.
AV node block can be achieved in at least three different ways:
Physical maneuvers
A number of physical maneuvers cause slowing of conduction
across the AV node, principally through activation of the
parasympathetic nervous system and its relation to the heart
via the vagus nerve. These physical manipulations are therefore
collectively referred to as vagal maneuvers.
The valsalva maneuver is a popular vagal maneuver used. It works
by increasing intra-thoracic pressure and affecting baro-receptors
(pressure sensors) within the arch of the aorta. It is carried out
by asking the patient to hold their breath and “bear down” as
if straining to pass a bowel motion, or by getting them to hold
their nose and blow out against it. There are many other vagal
maneuvers including—holding ones breath for a few seconds,
coughing, plunging the face into cold water, (via the diving reflex),
drinking a glass of ice cold water, and standing on one’s head.
Carotid sinus massage, carried out by firmly pressing the bulb at
the top of one of the carotid arteries in the neck, is effective but is
often not recommended due to risks of stroke in those with plaque
in the carotid arteries. If necessary, the act of defaecation can
sometimes halt an episode, again through vagal stimuation.
Drug treatment
Another modality that slows conduction in the atrioventricular
node involves treatment with medications. Adenosine, an ultrashort acting AV nodal blocking agent, is indicated if vagal
maneuvers are not effective. If this works, follow up therapy with
diltiazem, verapamil or metoprolol may be helpful. When the
supraventricuar tachycardia that does NOT involve the AV node
as a critical part of its expression, the patient may not respond
to this drug or respond only transiently with heart rate slowing.
Other anti-arrhythmic drugs such as sotalol or amiodarone can
also slow conduction in the atrioventricular node. In pregnancy,
metoprolol is the treatment of choice as recommended by the
American Heart Association.
Electrical cardioversion
If the patient is unstable or other treatments have not been
effective, cardioversion may be used, and is almost always
effective.
Prevention & cure
Once the acute episode has been terminated, ongoing treatment
may be indicated to prevent a recurrence of the arrhythmia.
Patients who have a single isolated episode, or infrequent and
minimally symptomatic episodes usually do not warrant any
aggressive or invasive treatment except observation.
Patients who have more frequent or disabling symptoms from their
episodes generally warrant some form of preventative therapy. A
variety of drugs including simple AV nodal blocking agents like
beta-blockers and verapamil, as well as anti-arrhythmics may
be used, usually with good effect, although the risks of these
therapies need to be weighed against the potential benefits and
side effects.
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For most tachycardia caused by a re-entrant pathway, radiofrequency ablation is probably the best option. This is a low risk
procedure that uses a catheter inside the heart to deliver radio
frequency energy to locate and destroy the abnormal electrical
pathways. Ablation has been shown to be highly effective—up
to 98% effective in eliminating AVNRT. Similar high rates of
success are achieved with radio-frequency ablation in eliminating
AVRT and typical atrial flutter.
Management and care
The management approach for SVT depends upon the age and
condition of the patient on presentation. If the patient is clinically
stable, vagal maneuvers may be initially attempted to convert the
tachycardia. Such vagal maneuvers may include bearing down
(as though having a bowel movement, i.e., valsalva maneuver),
or inducing the diving reflex using an ice bag to the face or
submerging the patient’s face into a container of ice water. Other
vagal maneuvers such as eyeball pressure and unilateral carotid
massage are less effective and may be harmful.
If the patient appears clinically unstable, then an intravenous line
should be immediately started in a centrally located peripheral
vein (antecubital preferred over a hand vein) through which an IV
bolus of adenosine may be given. It must be remembered that this
medication has a very short half life of approximately 10 seconds;
therefore it should be administered via bolus injection followed by
an immediate bolus of saline utilizing either a 3 way stopcock or
simultaneous needles within the same IV hub (the IV push and
immediate flush technique). A 12 lead electrocardiogram should
be obtained before and after conversion, if possible, and a rhythm
strip should be continuously run during attempted conversion.
External pacing equipment should be available since some patients
go into sinus arrest following administration of adenosine.
Adenosine causes a transient AV block and sinus bradycardia
thus interrupting the reentrant circuit involving the AV node and
accessory pathway. Potential side effects with adenosine include
hypotension, bronchospasm, and flushing.
In rare cases, a patient will present in very unstable condition.
Immediate electrical cardioversion may be required in such cases,
especially if an IV cannot be started in an expedient manner or
the patient fails to convert with IV adenosine.
Other modes of acute treatment include use of digoxin, verapamil,
propranolol, transesophageal or transvenous pacing. Conversion
to a sinus rhythm with these medications will usually be slower;
therefore most are utilized for chronic control once the SVT has
been converted by other means. If adenosine fails to convert the
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SVT, but the patient is hemodynamically stable, they may be
started on one, or more, of these medications (with the exception
of verapamil which should be avoided in infants) and monitored
for conversion. It is important to remember not to use digoxin
on patients with ventricular pre-excitation (e.g., WPW), as it
may increase antegrade conduction down the accessory pathway.
Patients with WPW are more prone to develop atrial flutter or
fibrillation, and are therefore at risk for 1:1 conduction to the
ventricles while on digoxin, potentially sending the patient into
ventricular tachycardia or fibrillation.
Long-term management of SVT depends on the severity and
frequency of episodes. In those patients with no ventricular preexcitation and infrequent, mild episodes that can be converted
with vagal maneuvers, no treatment is required. Patients with
frequent episodes, or severe symptoms, and those with ventricular
pre-excitation, medical management should be started with a betablocker, digoxin, or calcium channel blocker. Patients diagnosed
in infancy often will not require continued treatment beyond 1
year of age, but may have recurrent episodes later in life. With the
presence of severe symptoms, syncope, difficult to control SVT, or
other situations, e.g., patient preference, an electrophysiology study
and radiofrequency ablation can be performed with a high success
rate for cure.
The majority of fetuses and infants who present in SVT will have
no recurrences off medication after 6 to 12 months of age. Patients
who present in later childhood or during adolescence will likely
have recurrent episodes of SVT throughout their lifetime. Many
of these patients will require medical treatment and will eventually
seek curative treatment with radio frequency ablation. Radio
frequency ablation involves mapping out accessory conduction
pathways in the heart with the use of electrodes placed in the
atria, coronary sinus, and ventricles through central venous access.
Upon localization of the pathway a specialized ablation catheter
(tip is heated using radio frequency energy) is used to burn and
cause irreversible tissue injury to the accessory conduction tissue.
With the recent advancements in pediatric electrophysiology, the
prognosis for patients with SVT is very good. The success rate
with radio frequency ablation continues to improve, especially
when performed at centers with experienced specialists (> 90%
of the time the procedure is successful). Death or significant
morbidity is rare with the present state of medical management.
Most patients can be expected to live a normal life expectancy
with little or no lifestyle alteration due to this condition.
S u p raventricu l ar T achycardia in C hi l dren and A do l escents
Chris and Eddie pose for a photo at the
Twin Cities Ronald McDonald House
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7. Chun T.U., Van Hare G.F. Curr Cardiol Rep. 2004 Sept: 6(5):
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20. Manole M.D., Saladino R.A. Pediatric Emergency Care. 2007
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16. Tada H., Kaseno K., Kubota S., Naito S., Yokokawa M.,
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18. K nirsch W., Kretschmar O., Vogel M., Uhlemann F., Bauersfield
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Successful Treatment of Atrial Flutter with Amiodarone in a
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