Article cardiology

Neonatal Supraventricular
Tachycardia (SVT)
Harinder R. Singh, MD,*
Swati Garekar, MD,*
Michael L. Epstein, MD, †
Thomas L’Ecuyer, MD‡
Author Disclosure
Drs Singh, Garekar,
Epstein, and L’Ecuyer
did not disclose any
financial relationships
relevant to this
article.
Case Report
A male neonate born at 31 weeks’ gestation had a history of fetal supraventricular tachycardia
(SVT) detected at 28 weeks’ gestation, with no hydropic changes noticed on ultrasonography.
The mother was started on enteral digoxin with instructions for weekly follow-up. On her first
return visit at 31 weeks’ gestation, ultrasonography revealed hydropic changes and persistent
SVT. An emergency cesarean section was performed, and the infant was found to have hydrops
and respiratory distress, with a heart rate of 270 beats/min. The patient was intubated and
mechanically ventilated and received a dose of intravenous (IV) adenosine, resulting in a
transient decrease in heart rate to 120 beats/min before increasing back to 260 to 270 beats/
min. SVT persisted despite institution of an esmolol drip at 500 mcg/kg per minute, and
cardioversion was performed when hemodynamic instability developed. Recurrent SVT,
associated with hypotension, developed within 45 minutes of successful cardioversion. The
patient was given a loading dose of amiodarone, followed by cardioversion, continuous
amiodarone, and dobutamine infusion. Echocardiography revealed normal anatomy
with moderately reduced function. The patient remained in sinus rhythm and was weaned
to oral amiodarone after 1 week of infusion. An echocardiogram revealed normal
function. The patient was discharged from the hospital receiving 3 mg/kg per day of oral
amiodarone.

Introduction
SVT is the most common symptomatic arrhythmia in childhood that can be a recurrent and
persistent condition. The quoted incidence of SVT in children of 1 in 25,000 is based on
an estimate made in 1967, (1) but with a higher index of suspicion and better methods of
detection, it now is estimated to be 1 in 100 for children of all ages and 1 in 200 to 250 for
neonates. (2) We report a case series of seven patients admitted to our neonatal nursery
recently who had a diagnosis of SVT and review the pathophysiology and acute and
chronic management of this condition in neonates.
Table 1 summarizes the clinical presentations and hospital courses of the seven neonates
in this report. The heart rate during SVT ranged from 230 to 340 beats/min. Three
neonates had Wolff-Parkinson White (WPW) syndrome, and one neonate presented with
atrial flutter. Six patients had normal cardiac anatomy. SVT
was diagnosed prenatally in three neonates, and they exhib-
ited hydrops at birth and tachyarrhythmia-induced decreased
Abbreviations cardiac function. Electrical cardioversion was attempted and
AET: atrial ectopic tachycardia successful in all three infants. Because of refractoriness to
AT: atrial tachycardia initial pharmacologic management and decreased cardiac
AV: atrioventricular function, amiodarone was used for chronic maintenance
AVNRT: atrioventricular nodal re-entry tachycardia therapy.
AVRT: atrioventricular re-entry tachycardia
ECG: electrocardiogram Neonatal Tachycardia
IV: intravenous Neonatal tachycardia is a common problem, either repre-
NAPA: N-acetyl procainamide senting arrhythmia or sinus tachycardia. Sinus tachycardia
SVT: supraventricular tachycardia can occur at a rate of 180 to 250 beats/min. The criteria that
TDD: total digitalizing dose may help to identify sinus tachycardia are a normal P-wave
WPW: Wolff-Parkinson White (syndrome) axis (upright P waves in leads I and aVF), gradual onset and
termination, variable rate, presence of a possible secondary

*Fellow, Division of Cardiology, Department of Pediatrics.

†
Professor and Chief of Staff, Department of Pediatrics.
‡
Associate Professor, Division of Cardiology, Department of Pediatrics, Children’s Hospital of Michigan, Detroit, Mich.

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 Table 1. Overview of Neonates Who Had Supraventricular Tachycardia (SVT)

e340 NeoReviews Vol.6 No.7 July 2005

Postnatal Age
of Presentation/ Prenatal Max Heart
cardiology supraventricular tachycardia

Gestational Age Diagnosis/ Rate Mechanism of Results of Sequence of Maintenance

At Birth Clinical Features Management (beats/min) Tachycardia Echocardiography Treatment Termination (Enteral)

1. 2 d/31 wk Hydrops Fetal SVT (28 wk)/ 270 Pre-excitation/ Normal anatomy/ Adenosine/Esmolol/ Adenosine (transient) Amiodarone
Digoxin atrioventricular decreased Cardioversion Amiodarone/
re-entry function Cardioversion
tachycardia
(AVRT)
2. 1 d/34 wk Hydrops Fetal SVT (30 wk)/ 260 Pre-excitation/AVRT Normal anatomy/ Adenosine/ Adenosine (transient) Amiodarone
Digoxin decreased Procainamide/ Cardioversion
function Digoxin/ Amiodarone/
Propranalol/ Digoxin
Esmolol/
Cardioversion
3. 1 d/term Hydrops Presumed fetal 340 Pre-excitation/AVRT Normal anatomy/ Adenosine/Esmolol/ Cardioversion Amiodarone
SVT (hydrops at decreased Cardioversion Amiodarone
birth)/- function
4. 1 d/35 wk SVT on cardiorespiratory -/- 230 Atrial flutter Normal anatomy/ Adenosine/Esmolol Amiodarone Amiodarone
(CR) monitoring Normal
function
5. 1 d/28 wk SVT on CR monitoring -/- 320 No pre-excitation/ Normal anatomy/ Ice pack/ Adenosine Propranolol
AVRT Normal Adenosine/ Digoxin (oral)/
function Digoxin (oral)/ Propranolol (oral)
Propranolol
(oral)
6. 3 d/term SVT on CR monitoring -/- 280 No pre-excitation/ Normal anatomy/ Ice pack Adenosine -
AVRT Normal
function
7. 6 d/term SVT Congenital heart 250 No pre-excitation/ D transposition Ice pack Ice pack Digoxin
defect AVRT of the great Digoxin (oral)
arteries
Normal function

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 cardiology supraventricular tachycardia

results from a re-entry circuit be-

tween the atria and the ventricles
and is called atrioventricular re-
entry tachycardia (AVRT) (Fig. 1)
(Table 2). In this circuit, the AV
node generally forms the antegrade
pathway, and an accessory connec-
tion between the ventricle and the
atria serves as the retrograde path-
way for conduction of impulses.
This is referred to as orthodromic
AV reciprocating tachycardia. In
some patients, the accessory con-
nection can serve as the antegrade
pathway, and the AV node or a
second accessory pathway serves as
the retrograde pathway. This is re-
Figure 1. Mechanism of atrioventricular re-entry tachycardia.
ferred to as antidromic (antegrade)
AV reciprocating tachycardia.
WPW syndrome is SVT with evi-
cause (eg, fever, sepsis, catecholamine excess), and no dence of pre-excitation. It is identified from a surface
response to maneuvers used to convert SVT to normal electrocardiogram (ECG) in sinus rhythm by a short P-R
sinus rhythm. interval and a “delta wave.” The short P-R interval in
SVT is a tachyarrhythmia originating proximal to the WPW syndrome represents impulse conduction ante-
bundle of His. The typical infant who has SVT has a grade through the accessory pathway without AV nodal
regular R-R interval, with rates often greater than delay. The delta wave is caused by fusion of ventricular
230 beats/min and commonly 260 to 300 beats/min. complexes resulting from a portion of ventricular myo-
The normal cardiac impulse originates in the sinus cardium initially depolarized by antegrade conduction
node and travels antegrade through the atria to the through the accessory pathway along with depolarization
atrioventricular (AV) node, where the impulse is delayed of the rest of the myocardium through the normal path-
and is then propagated through the His bundle into the way. WPW syndrome comprises 12% to 56% of AVRTs.
right and left bundle branches. Normal conduction uses (2)(3)(4)(5)(6)(7)(8)(9) Patients 1 and 2 from Table 1
the AV node as the only connection between atria and showed evidence of WPW syndrome.
the ventricles. The most common type of SVT in infancy The second type of SVT is AV nodal re-entry tachy-
and childhood, representing approximately 70% of SVT, cardia (AVNRT) (Fig. 2) (Table 2), which represents

Table 2. Electrocardiographic (ECG) Features of SVT

Type QRS Complex P-R interval and
of SVT Baseline ECG During SVT P Wave During Tachycardia R-P interval Effect of Adenosine
AVRT Delta wave may Usually Inverted P wave may be seen P-R interval is longer Termination
be present narrow following the QRS than R-P interval
complex
AVNRT Normal Narrow Often not seen in typical Fast-slow AVNRT: Termination
AVNRT; seen after QRS R-P interval is
complex in “fast-slow” longer than P-R
(atypical) AVNRT interval
AT Normal Narrow Flutter or ectopic P waves R-P interval is longer Usually will not terminate;
may be seen than P-R interval may “uncover” atrial
rhythm
AVRT⫽atrioventricular re-entry tachycardia, AVNRT⫽atrioventricular nodal re-entry tachycardia, AT⫽atrial tachycardia

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cardiology supraventricular tachycardia
Figure 2. Mechanism of AV nodal re-entry tachycardia.
about 13% of SVTs. The tachycardia circuit also involves
dual pathways, but both are situated within or near the
AV node. Typical AVNRT conducts in an antegrade
direction slowly down to the ventricles through one
pathway and has a rapid retrograde conduction via the
other pathway. It is, therefore, called “slow-fast”
AVNRT. On the ECG, this manifests as a QRS complex
followed by a T wave, with the P wave often not visible
(concealed in the QRS complex). Atypical AVNRT has a
comparatively slower retrograde conduction, so the P
wave is visible as an inverted complex after the QRS. This
is called “fast-slow” AVNRT. Other rarer forms are
“slow-slow” AVNRT and “fast-fast” AVNRT.
The third most common type of SVT is atrial tachy-
cardia (AT), comprising approximately 14% of SVTs
(Table 2). (3) AT includes atrial flutter and atrial ectopic
tachycardia (AET). Atrial flutter results from a re-entry
circuit within the atrial muscle, with flutter wave rates as
high as 400 to 500 beats/min. AET is due to ectopic
atrial foci that display abnormal automaticity. These foci
are reflected by an abnormal P-wave axis during tachy-
cardia. The atrial rates range from mild tachycardia to
300 beats/min. The onset of AET is characterized by
gradual acceleration of the atrial rate (ramping up) to
maximum. AET does not employ re-entry. The AV node
is not a part of the circuit in atrial flutter or atrial re-entry
tachycardia. The ventricular rate is dependent on con-
duction of the atrial impulse through the AV node.
Therefore, it can be as high as the atrial rate, with 1:1
conduction through the AV node or, more often, lower,
with variable degrees of AV conduction.
Of particular importance in the management of SVT
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is the fact that both AVRT and AVNRT require conduc-
tion through the AV node as a part of the circuit to
maintain tachycardia (Figs. 1 and 2). Natural history
studies in patients who have SVT have demonstrated that
approximately 70% of infants lose SVT inducibility by 1
year of age, and clinical recurrences are uncommon. (10)
Clinical Features
Presenting features of SVT in neonates can include fetal
SVT, unexplained nonimmune hydrops in the newborn
(patients 1, 2, and 3 from Table 1), sudden cardiovascu-
lar collapse, incidental detection during cardiorespiratory
monitoring (patients 4, 5, and 6 from Table 1), or
symptomatic heart failure developing over a few hours to
days. A cardiac cause is found in about 9% of nonimmune
hydrops, 60% of which is due to fetal SVT. (11) SVT can
occur in patients who have underlying congenital cardiac
defects, especially Ebstein anomaly and L-transposition
of the great arteries. Congenital heart disease is reported
in about 6.5% to 37% of neonates who have SVT.
(2)(3)(12) Patient 7 in Table 1 was diagnosed with
transposition of the great arteries and developed SVT
awaiting cardiac surgery. SVT has been reported as the
initial presenting feature of cardiac involvement in pa-
tients who have tuberous sclerosis with cardiac rhab-
domyomas. (13)(14)(15)(16)
ECG Features
As noted previously, the typical neonate who has SVT has
a regular R-R interval, with rates greater than 230 beats/
min and usually 260 to 300 beats/min. P waves are
discernible in only 60% of cases and usually differ mor-
phologically from those present in sinus rhythm. They
often are inverted and are seen just after the QRS com-
plex. In more than 90% of cases, the QRS morphology
has a normal complex similar to the baseline sinus QRS
(Fig. 3). Wide QRS complex is seen in patients who have
pre-existing or rate-dependent bundle branch block and
in antegrade AVRT (Fig. 1). Nevertheless, additional
consideration should be given to ventricular tachycardia
in all patients who have wide-complex tachycardia (Fig.
4), and treatment should be directed accordingly. A delta
wave (Fig. 5) and a short P-R interval seen on the
baseline ECG in sinus rhythm in a neonate who has SVT
makes the diagnosis of WPW syndrome.
A 12-lead ECG should be performed during tachycar-
dia and after sinus rhythm is achieved, but this should not
delay treatment. Once the patient is stable, an echocar-
diogram should be performed to evaluate ventricular
function, identify the presence of congenital heart dis-
ease, and look for cardiac rhabdomyomas. The response

Figure 3. Narrow QRS complex SVT at a rate of 300 beats/min.
to adenosine can facilitate an accurate diagnosis of SVT
as well as restore sinus rhythm in a significant percent of
cases. As shown in Figure 6, adenosine can terminate
SVT promptly if the AV node is a part of the circuit.
Acute Management of Neonatal SVT
SVT is a relatively common tachyarrhythmia in the neo-
natal intensive care unit. It may be recurrent or occasion-
ally persistent, but rarely is it life-threatening. Acute
termination of SVT is critical in patients who develop
signs and symptoms of hemodynamic instability, includ-
ing lethargy, pallor, poor perfusion, hypotension, acido-
sis, and signs of cardiac failure. Immediate restoration of
sinus rhythm is achieved best by cardioversion (patients
1, 2, and 3 in Table 1). If IV access is available, adenosine
may be tried while preparing for cardioversion.
Cardioversion refers to an electrical energy discharge
that is synchronized with the large R (or S) wave of the
QRS complex. Synchronization with the early part of the
QRS complex avoids energy delivery in the early phase of
Figure 4. Wide-complex SVT at a rate of 240 beats/min.
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cardiology supraventricular tachycardia
repolarization when ventricular fi-
brillation can be induced. Transient
delivery of electrical current causes
a momentary depolarization of
most cardiac cells. This allows the
sinus node to resume normal pace-
maker activity. The key compo-
nents in preparing the patient are
intravenous access, airway manage-
ment equipment, sedative drugs,
and a converter/defibrillator mon-
itoring device. Lack of IV access or
sedation should not delay cardio-
version in the critically ill neonate.
For neonates, a single paddle or
patch is placed immediately to the
right of the sternum, and the other paddle/patch is
placed between the tip of the left scapula and the spine to
place as much heart mass as possible between the two
paddles/patches. If a paddle is used, conductive gel
should be applied to ensure good contact because skin
can conduct away a significant portion of the current.
The patches are pre-gelled. The paddles should be ap-
plied firmly against the chest wall to avoid arcing and skin
burns. An initial synchronized shock of 0.5 J/kg is
recommended. In subsequent attempts, the energy is
doubled. Even under ideal circumstances, only 10% to
30% of the total current reaches the heart. If conversion
to sinus rhythm is not achieved after two attempts, drug
therapy should be initiated before attempting cardiover-
sion again. Although cardioversion can restore sinus
rhythm, it cannot maintain sinus rhythm. Therefore, it is
always prudent to have a pharmacologic agent available
to maintain sinus rhythm after conversion.
Adenosine can be administered if a neonate is hemo-
Figure 5. Wolff-Parkinson White syndrome characterized by
short P-R interval and delta wave (arrow).
NeoReviews Vol.6 No.7 July 2005 e343
cardiology supraventricular tachycardia

circuit. The advantages of adeno-

sine are its very short half-life (10 to
15 sec) and the onset of efficacy
(within 10 to 20 sec). Administra-
tion can be repeated immediately if
required, and the drug has no neg-
ative inotropic effect. The disad-
vantage is immediate recurrence of
tachycardia in approximately 30%
of cases. Adenosine can cause flush-
ing, bronchospasm, and transient
new rhythms at the time of conver-
sion, including premature ventricu-
lar contractions, premature atrial
contractions, sinus bradycardia,
tachycardia, as well as varying de-
grees of AV nodal block. (20)(21)
Figure 6. Responses of narrow complex tachycardia to adenosine. IVⴝintravenous, For patients who are hemody-
AVⴝatrioventricular, VTⴝventricular tachycardia, ATⴝatrial tachycardia, AVRTⴝ namically stable, a more graded ap-
atrioventricular re-entry tachycardia, AVNRTⴝatrioventricular node re-entry tachycardia, proach is appropriate. Initially, va-
AETⴝatrial ectopic tachycardia. Adapted from ACC/AHA guidelines for the management gal maneuvers, which are simple,
of patients with supraventricular arrhythmias. Circulation. 2003;108:1871–1909. Copy- quick, and safe to perform, can be
right 2004 The American College of Cardiology Foundation and American Heart attempted. Placement of an ice
Association, Inc. Permission granted for one time use. Further reproduction is not pack on the face and nose for 5 to
permitted without permission of the ACC/AHA. 10 seconds at a time is used com-
monly. This maneuver initiates a
dynamically stable and can be provided to the unstable “diving reflex” that has been described in certain species
neonate in whom IV access has been established while of animals in which diving into cold water induces a reflex
preparing for cardioversion. Adenosine is administered as peripheral vasoconstriction accompanied by a profound
a rapid IV bolus followed by a saline flush in doses of vagal discharge. (22) The afferent pathway of the reflex is
0.05 to 0.2 mg/kg, with continuous ECG monitoring the trigeminal nerve endings around the nose and
and availability of cardiopulmonary resuscitation equip- mouth, and the efferent pathway is the vagus nerve. In
ment. Adenosine is successful in terminating SVT in humans, bradycardia also is observed with these maneu-
about 42% to 86% of cases (Fig. 7). (4)(17)(18)(19) In vers. Success rates vary from 63% to 96%. (2)(5)(18)(23)
our case series, adenosine successfully terminated SVT in In our case series, an ice pack was used in three neonates
four of the six neonates (66%) in whom it was used. It and was successful in terminating SVT in only one (33%).
produces AV block (may appear as a brief episode of Esmolol is a very useful pharmacologic agent in pa-
asystole), thereby disrupting one limb of the re-entry tients who experience recurrent or sustained SVT. This
beta blocker has class II antiar-
rhythmic properties, an immediate
onset of action, and a very short
half-life of about 3 minutes. It is
administered IV at a dose that can
be titrated based on the response
and can guide long-term manage-
ment. (24)(25)(26) It acts by in-
creasing the refractory period of the
AV node, thus interrupting the re-
entry circuit. It usually is adminis-
tered as a loading dose of 100 to
Figure 7. Termination of SVT with adenosine. 500 mcg/kg over 1 minute fol-

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lowed by a continuous infusion of 50 to 100 mcg/kg per
minute. Esmolol can be titrated upward by 50-mcg/kg
per minute increments every 5 to 10 minutes to a maxi-
mum dose of 1,000 mcg/kg per minute until either
there is control of the ventricular rate or hypotension
develops. (24)(25)(26) Other potential adverse effects
include bradycardia and bronchospasm. (27)
Digoxin has been the drug of choice for neonatal SVT
in the past. Digoxin acts by decreasing conduction
through the AV node. This agent is avoided in patients
who have WPW syndrome because of their predisposi-
tion to develop atrial fibrillation, which may lead to
ventricular arrhythmias due to enhanced conduction
through the accessory pathway. We tend to use digoxin
in neonates who have SVT and poor cardiac function and
have not responded to beta blockade. Digoxin has an
onset of action within 5 to 30 minutes, with the maxi-
mum effects seen within 1 to 4 hours after parenteral
administration. After oral administration, the onset of
action is within 30 minutes to 2 hours, with maximum
effects seen after 2 to 8 hours. The elimination half-life is
61 to 170 hours in preterm neonates and 35 to 45 hours
in term neonates. The oral total digitalizing dose (TDD)
is 20 to 30 mcg/kg in preterm neonates and 25 to
35 mcg/kg in term neonates. The parenteral TDD is
75% of the oral TDD. The dose is reduced by 50% in
patients receiving concomitant amiodarone or patients
who have end-stage renal disease. Therapeutic serum
levels are 0.8 to 2 ng/mL. Toxicity may be seen with
concentrations higher than 2 ng/mL. Adverse effects
commonly seen with digoxin include nausea, vomiting,
heart block, and rhythm disturbances. Monitoring potas-
sium concentrations is crucial, especially in patients re-
ceiving concomitant diuretic therapy because hypokale-
mia can potentiate digoxin toxicity. (2)(28)(29)(30)
If beta blockade is ineffective in controlling the
rhythm, a class I antiarrhythmic agent may be appropri-
ate. Procainamide is a class IA antiarrhythmic agent that
has anticholinergic and local anesthetic effects. It de-
creases myocardial excitability and conduction velocity
and depresses myocardial contractility. By decreasing
atrial excitability, procainamide decreases the flutter
wave rate, but it may increase flutter wave conduction
rate across the AV node, potentially causing ventricular
tachycardia. Therefore, it is recommended that the pa-
tient be digitalized before receiving a loading dose of
procainamide. Procainamide can be administered IV in a
loading dose of 3 to 6 mg/kg over 5 minutes, repeated
every 5 to 10 minutes to a maximum of 15 mg/kg, and
followed by a continuous infusion of 20 to 80 mcg/kg
per minute. The infusion should be stopped if the QRS
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cardiology supraventricular tachycardia
complex widens to more than 125% of baseline. It is
important to monitor the patient for hypotension and
arrhythmias during the infusion. The enteral dose of
procainamide is 15 to 50 mg/kg per day divided every
3 to 6 hours. Procainamide is metabolized to the active
metabolite N-acetyl procainamide (NAPA). The half-life
of procainamide in infants is approximately 1.7 hours,
and the half-life of NAPA is approximately 6 hours.
Therapeutic concentrations of both procainamide and
NAPA are 4 to 10 mcg/mL. Other potential adverse
effects are a lupuslike syndrome, nausea, vomiting, diar-
rhea, and liver dysfunction. (31)
Flecainide is a class IC drug that exerts profound
effects on the accessory connection and the AV node,
which is unlike the action of the beta blockers adenosine
and digoxin, which terminate SVT by blocking AV node
conduction only. Flecainide is administered at a dose of
2 mg/kg IV over 10 minutes during the acute phase
followed by a dose of 3 to 6 mg/kg per day orally in two
divided doses. (29)(32)(33)(34) The half-life in new-
borns is approximately 29 hours. Flecainide has a mod-
erate negative inotropic effect and can be proarrhythmic.
Propafenone is an alternate class IC agent that occa-
sionally is used in neonatal SVT, especially junctional
tachycardia. Its effects are similar to flecainide. An IV
dose of 1 to 2 mg/kg can be used for acute control of
SVT. The oral dose of propafenone is 8 to 10 mg/kg per
day divided in three to four equal doses, which may be
increased in increments of 2 mg/kg per day up to a
maximum of 20 mg/kg per day. Peak plasma concentra-
tions are reached after 2 to 3 hours, and steady-state
levels are achieved in 4 to 5 days. The elimination half-life
is approximately 5 to 8 hours. The adverse effects re-
ported with propafenone are negative inotropic effects,
proarrhythmic effects, sinus node dysfunction, blood
dyscrasias, and neurologic effects. (35)(36)(37)(38)
For patients who are unresponsive to the beta block-
ade or class I agents, a class III drug such as amiodarone
may be successful in terminating SVT. Amiodarone in-
hibits adrenergic stimulation, prolongs the action poten-
tial and refractory period in myocardial tissue, and de-
creases AV conduction and sinus node function.
Amiodarone is useful in patients who have SVT unre-
sponsive to beta blockers or class I agents or who have
depressed cardiac function. Amiodarone is started with
an IV loading dose of 5 mg/kg over 1 hour, followed by
a continuous infusion of 5 mcg/kg per minute, with dose
increases until either conversion of SVT or attainment of
a maximum of 15 mcg/kg per minute. The onset of
effect after parenteral administration is usually within
minutes, especially after a loading dose. Once SVT is
NeoReviews Vol.6 No.7 July 2005 e345
cardiology supraventricular tachycardia

controlled with amiodarone infusion, the total daily dose

can be converted into an oral dose that is weaned slowly
to a maintenance dose of 3 to 5 mg/kg per day in two
divided doses. The half-life of amiodarone is about 40 to
55 days. Amiodarone can cause new arrhythmias, hypo-
thyroidism, liver dysfunction, pulmonary fibrosis, and
corneal opacities. (39)(40)(41)(42)(43)(44)(45)(46)
(47)(48)(49)(50)(51) With the use of lower doses, such
adverse effects are infrequent.
For cases of SVT that do not respond to single phar-
macologic agents, a combination of different medica-
tions can be tried. Commonly used combinations in-
clude digoxin with propranolol (7) and digoxin with
amiodarone. Various other combinations have been tried
with high success rates. The reported success rate for the
combination of amiodarone and propranolol is 80%,
flecainide with amiodarone is 78%, and flecainide with
sotalol is 100% in controlling single or multidrug refrac-
tory SVT. (52)(53)(54)

Chronic Management of SVT

Chronic medical treatment is appropriate for neonates
who have hemodynamically significant SVT, frequent
SVT requiring medical management, pre-excitation on
ECG, or congenital cardiac defect. For neonates who
have had self-terminating asymptomatic SVT with no
evidence of pre-excitation on ECG and with normal
cardiac anatomy, chronic medical treatment may be de-
ferred.
A beta blocker such as propranolol is most appropriate
for patients responding to esmolol or who have evidence
of pre-excitation on ECG. Propranolol is a noncardio-
selective class II antiarrhythmic agent that has properties
similar to esmolol. The starting dose of propranolol is
0.25 mg/kg every 6 to 8 hours and can be increased
slowly to a maximum of 4 mg/kg per dose with close
monitoring of heart rate, heart size, and contractility.
Propranolol can cause bradycardia, hypotension, im-
paired myocardial contractility, hypoglycemia, and bron-
chospasm. It is contraindicated in patients who have
poor cardiac function and those who have hyperactive
airway disease. (27)
Patients who achieved control of SVT with class I or
class III agents are treated with oral preparations of the
same medications. Because 70% of neonates who have
SVT lose inducibility by 1 year of age, most cardiologists
treat for about 6 to 9 months, adjusting dosage for size,
and subsequently allow the patient to outgrow the drug
dose by about 1 year of age.
Figure 8 presents an algorithm for management of
Figure 8. General algorithm for management of neonatal
supraventricular tachycardia. SVTⴝsupraventricular tachycar-
dia, IVⴝintravenous
neonatal SVT that can be modified based on institutional
preferences.
Fetal SVT
SVT is the most common symptomatic fetal cardiac
arrhythmia. Atrioventricular re-entry tachycardia is the
most common mechanism, occurring in more than 90%
of fetal SVTs. Other, rare mechanisms for SVT in fetuses
are atrial flutter or fibrillation, automatic tachycardia, and
permanent junctional reciprocating tachycardia. In fe-
tuses that have SVT, the characteristic heart rate is 240 to
260 beats/min. In fetuses that have atrial flutter, the
characteristic atrial rate is 300 to 500 beats/min, with
varying ventricular response rates. (55)
Ultrasonography currently is the most commonly
used diagnostic tool to analyze heart rhythm in a fetus.
A detailed study includes definition of cardiac structure,
rhythm, function, hemodynamics, and presence of fetal
hydrops. Structural malformations of the heart are seen
in up to 5% of fetuses that have SVT, which most fre-
quently include Ebstein anomaly of the tricuspid valve,
AV canal defect, hypoplastic left heart syndrome, or
rhabdomyoma. (56)(57)

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Fetal SVT is associated with a fetal and neonatal
mortality rate of 8% to 30%. Preterm delivery of an infant
who has hydrops and SVT is associated with high rates of
morbidity and mortality. (56)(57)(58)(59) The goals of
therapy for fetal SVT are to restore sinus rhythm, resolve
heart failure, and postpone delivery until term. The indi-
cations to treat fetal SVT are prematurity or evidence of
severe hemodynamic compromise of the fetus, such as
hydrops. (55) The therapeutic goal is rate control (in
atrial flutter) or complete control of the arrhythmia.
Prior to initiating therapy, a complete maternal history
for arrhythmia and a baseline maternal ECG to rule out
long QT syndrome should be obtained. Daily monitor-
ing of maternal ECG for rate and rhythm, P-R interval,
and QRS and QTc duration as well as fetal monitoring is
important for all medications. (55) Therapy with antiar-
rhythmics is initiated using low doses, with gradual dose
increases and careful monitoring of maternal and fetal
drug response in an inpatient setting. Fetuses that have
hydrops are at a higher risk of adverse drug effects than
fetuses that do not have hydrops. A fetus treated for SVT
usually requires therapy for at least 2 to 3 weeks after
conversion to sinus rhythm because of a predilection for
recurrence.
Digoxin is the most frequently used monotherapy in
mothers whose fetuses do not have hydrops but do have
either SVT or atrial flutter. (55)(56)(60) It is used at a
higher-than-usual dose to maintain therapeutic concen-
trations because of increased clearance and shorter elim-
ination half-life during pregnancy. (61) A maternal load-
ing dose of 0.25 to 0.5 mg is administered IV every 6 to
8 hours during the first 24 hours for rapid digitalization
(maximum, 2 mg/d). The enteral loading dose of
digoxin is 0.25 to 1.5 mg, followed by a maintenance
dose of 0.25 mg to 0.5 mg/d. (62) The digoxin cord
blood concentration varies widely, from 40% to 90% of
the maternal level. Placental transfer of digoxin is as low
as 10% in fetuses that exhibit hydrops. The dose should
be titrated to achieve a maternal serum level of 1 to
2 ng/mL. The effectiveness of digoxin monotherapy is
32% to 71% in fetuses that do not have hydrops and 10%
to 20% in fetuses that have hydrops. (56)(57)(62)(63)
Amiodarone and flecainide are emerging as the
second-line antiarrhythmic agents for fetal SVT that does
not respond to digoxin therapy. (63)(64)(65)(66) Ami-
odarone is the most effective treatment for drug-
refractory fetal tachycardia accompanied by hydrops.
A maternal oral loading dose of 800 to 2,400 mg/d is
administered for 1 to 7 days, with a single dose not
exceeding 800 mg. Once sinus rhythm is obtained, the
dose is decreased to the lowest effective dose necessary to
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cardiology supraventricular tachycardia
sustain sinus rhythm, usually 200 to 400 mg/d. Chronic
maintenance therapy is continued until hydrops resolves
and tachycardia is quiescent for 2 to 3 weeks. The half-life
of amiodarone is 50 to 60 days. Maternal thyroid and
liver profiles should be monitored before and during
amiodarone therapy. Fetal plasma concentrations of ami-
odarone vary from 10% to 50% of the maternal level.
During chronic treatment, the desired therapeutic serum
concentration is 0.5 to 2.5 mcg/mL. Amiodarone alone
or in conjunction with digoxin is successful in restoring
sinus rhythm in approximately 60% to 75% of fetuses that
have SVT and 33% to 50% of fetuses that have atrial
flutter. (45)(63)(65)(66)(67)
Flecainide is a sodium channel blocker (class 1C) that
has been used effectively in fetal SVT, both as mono-
therapy and in combination with digoxin. Flecainide
should not be used as monotherapy in atrial flutter
because it can increase the ventricular rate. Maternal
dosing is initiated at 100 mg enterally twice a day. The
dose can be increased to 300 mg/d in two to three
divided doses. The half-life is 14 hours, and the time to
reach 90% of a steady-state plasma concentration is ap-
proximately three times the half-life. The fetomaternal
plasma ratio of flecainide varies from 50% to 80%. The
therapeutic flecainide plasma concentration is 0.4 to
0.8 mcg/mL, and careful monitoring of values is re-
quired to decrease the incidence of proarrhythmic effects
in the mother and fetus. Other maternal adverse events
include dizziness, flushing, nausea, vomiting, and visual
disturbances. Flecainide has negative inotropic effects
and should be avoided when SVT is accompanied by
structural heart disease or depressed myocardial contrac-
tility. Overall, the reported conversion rate to sinus
rhythm has been 90% to 100% for fetuses that do not
have hydrops with SVT and 60% to 85% for fetuses that
do have hydrops. (62)(63)(64)(68)(69)
Sotalol has both beta-blocking and class III antiar-
rhythmic properties. Because of its potent antiarrhythmic
effect and excellent placental transfer, sotalol is effective
for fetal SVT, particularly in atrial flutter. Its half-life
varies from 9 to 12 hours. Sotalol accumulates in amni-
otic fluid but not in the fetus. Maternal sotalol concen-
trations increase linearly with increasing dose. The feto-
maternal plasma ratio of sotalol is nearly 1, indicating
complete transplacental passage of sotalol. The oral ma-
ternal dose should be initiated at 80 mg twice daily and
increased in incremental doses to a maximum of 160 mg
three times daily. The therapeutic plasma concentration
ranges from 1.27 to 1.63 mg/L, but the maternal con-
centration does not correlate with clinical efficacy. Ma-
ternal ECG monitoring for prolongation of QTc interval
NeoReviews Vol.6 No.7 July 2005 e347
cardiology supraventricular tachycardia
is warranted during treatment with sotalol. Sotalol can
cause temporary adverse effects in mothers, including
nausea, dizziness, and fatigue, and can be proarrhythmic
in fetuses. (70) Sotalol monotherapy is effective in con-
verting 80% to 85% of fetuses that have atrial flutter and
60% to 70% of fetuses that have SVT to sinus rhythm. In
fetuses that exhibit hydrops, the conversion rate is 40% to
60% as monotherapy and 80% in combination with
digoxin. (63)(70)(71)(72)
Summary
SVT, which can be recurrent and persistent, is the most
common symptomatic arrhythmia. The most common
type of SVT in infancy results from a re-entry circuit
between the atria and the ventricles. SVT inducibility is
lost in 70% of infants by 1 year of age. Twelve-lead ECG
during and after SVT along with the response to adeno-
sine can facilitate accurate diagnosis. SVT can have vary-
ing clinical presentations, ranging from incidental detec-
tion to hemodynamic collapse. Hemodynamic instability
warrants immediate restoration to sinus rhythm, best
achieved by synchronized electrical cardioversion. Med-
ical management of SVT consists of a trial of vagal
maneuvers, adenosine, and medications to maintain si-
nus rhythm such as beta blockers and class I or class III
antiarrhythmic medications. For neonates who have he-
modynamically significant SVT, frequent SVT requiring
medical management, pre-excitation on ECG, or con-
genital cardiac defect, chronic medical treatment is ap-
propriate.
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NeoReviews Quiz
6. Supraventricular tachycardia (SVT), a tachyarrhythmia that originates proximal to the bundle of His, can
occur in infants who have underlying congenital heart defects. Of the following, the most common
congenital heart disease that predisposes to SVT is:
A. Coarctation of the aorta.
B. Ebstein anomaly of the tricuspid valve.
C. Pulmonary atresia with intact ventricular septum.
D. Tetralogy of Fallot.
E. Total anomalous pulmonary venous return.

7. A term newborn has recurrent episodes of tachycardia that began at 12 hours of age. During one such
episode, the heart rate is 280 beats/min. Electrocardiography reveals inverted P waves, most of which
follow QRS complexes; normal QRS pattern; and P-R intervals that exceed R-P intervals. The infant is
hemodynamically stable, has no echocardiographic evidence of congenital heart disease, and has no
indwelling vascular catheters. Vagal maneuvers and intravenous adenosine are unsuccessful in restoring
normal heart rhythm. Of the following, the next pharmacologic agent recommended, according to the
algorithm for management of neonatal supraventricular tachycardia, is:
A. Amiodarone.
B. Digoxin.
C. Esmolol.
D. Procainamide.
E. Propafenone.

8. In neonatal cases of supraventricular tachycardia nonresponsive to a single pharmacologic agent, a

combination of medications may be tried. Of the following, the combination of medications most successful
in controlling refractory supraventricular tachycardias is:
A. Amiodarone and propranolol.
B. Digoxin and amiodarone.
C. Digoxin and propranolol.
D. Flecainide and amiodarone.
E. Flecainide and sotalol.

e350 NeoReviews Vol.6 No.7 July 2005

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 Neonatal Supraventricular Tachycardia (SVT)
Harinder R. Singh, Swati Garekar, Michael L. Epstein and Thomas L'Ecuyer
NeoReviews 2005;6;e339
DOI: 10.1542/neo.6-7-e339

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 Neonatal Supraventricular Tachycardia (SVT)
Harinder R. Singh, Swati Garekar, Michael L. Epstein and Thomas L'Ecuyer
NeoReviews 2005;6;e339
DOI: 10.1542/neo.6-7-e339

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