article neonatal supraventricular tachycardia...

Neonatal SupraventricularTachycardia (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 ReportA 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 firstreturn visit at 31 weeks’ gestation, ultrasonography revealed hydropic changes and persistentSVT. An emergency cesarean section was performed, and the infant was found to have hydropsand respiratory distress, with a heart rate of 270 beats/min. The patient was intubated andmechanically ventilated and received a dose of intravenous (IV) adenosine, resulting in atransient 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, andcardioversion was performed when hemodynamic instability developed. Recurrent SVT,associated with hypotension, developed within 45 minutes of successful cardioversion. Thepatient was given a loading dose of amiodarone, followed by cardioversion, continuousamiodarone, and dobutamine infusion. Echocardiography revealed normal anatomywith moderately reduced function. The patient remained in sinus rhythm and was weanedto oral amiodarone after 1 week of infusion. An echocardiogram revealed normalfunction. The patient was discharged from the hospital receiving 3 mg/kg per day of oralamiodarone.

IntroductionSVT is the most common symptomatic arrhythmia in childhood that can be a recurrent andpersistent condition. The quoted incidence of SVT in children of 1 in 25,000 is based onan estimate made in 1967, (1) but with a higher index of suspicion and better methods ofdetection, it now is estimated to be 1 in 100 for children of all ages and 1 in 200 to 250 forneonates. (2) We report a case series of seven patients admitted to our neonatal nurseryrecently who had a diagnosis of SVT and review the pathophysiology and acute andchronic management of this condition in neonates.

Table 1 summarizes the clinical presentations and hospital courses of the seven neonatesin this report. The heart rate during SVT ranged from 230 to 340 beats/min. Threeneonates had Wolff-Parkinson White (WPW) syndrome, and one neonate presented with

atrial flutter. Six patients had normal cardiac anatomy. SVTwas diagnosed prenatally in three neonates, and they exhib-ited hydrops at birth and tachyarrhythmia-induced decreasedcardiac function. Electrical cardioversion was attempted andsuccessful in all three infants. Because of refractoriness toinitial pharmacologic management and decreased cardiacfunction, amiodarone was used for chronic maintenancetherapy.

Neonatal TachycardiaNeonatal tachycardia is a common problem, either repre-senting arrhythmia or sinus tachycardia. Sinus tachycardiacan occur at a rate of 180 to 250 beats/min. The criteria thatmay help to identify sinus tachycardia are a normal P-waveaxis (upright P waves in leads I and aVF), gradual onset andtermination, 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.

Abbreviations

AET: atrial ectopic tachycardiaAT: atrial tachycardiaAV: atrioventricularAVNRT: atrioventricular nodal re-entry tachycardiaAVRT: atrioventricular re-entry tachycardiaECG: electrocardiogramIV: intravenousNAPA: N-acetyl procainamideSVT: supraventricular tachycardiaTDD: total digitalizing doseWPW: Wolff-Parkinson White (syndrome)

Article cardiology

NeoReviews Vol.6 No.7 July 2005 e339

Tab

le1.

Ove

rvie

wof

Neo

nate

sW

hoH

adSu

prav

entr

icul

arTa

chyc

ardi

a(S

VT)

Post

nata

lAge

ofPr

esen

tatio

n/Ge

stat

iona

lAge

AtBi

rth

Clin

ical

Feat

ures

Pren

atal

Diag

nosi

s/M

anag

emen

t

Max

Hea

rtRa

te(b

eats

/min

)M

echa

nism

ofTa

chyc

ardi

aRe

sults

ofEc

hoca

rdio

grap

hySe

quen

ceof

Trea

tmen

tTe

rmin

atio

nM

aint

enan

ce(E

nter

al)

1.2

d/31

wk

Hyd

rops

Feta

lSVT

(28

wk)

/Di

goxi

n27

0Pr

e-ex

cita

tion/

atrio

vent

ricul

arre

-ent

ryta

chyc

ardi

a(A

VRT)

Nor

mal

anat

omy/

decr

ease

dfu

nctio

n

Aden

osin

e/Es

mol

ol/

Card

iove

rsio

nAd

enos

ine

(tra

nsie

nt)

Amio

daro

ne/

Card

iove

rsio

n

Amio

daro

ne

2.1

d/34

wk

Hyd

rops

Feta

lSVT

(30

wk)

/Di

goxi

n26

0Pr

e-ex

cita

tion/

AVRT

Nor

mal

anat

omy/

decr

ease

dfu

nctio

n

Aden

osin

e/Pr

ocai

nam

ide/

Digo

xin/

Prop

rana

lol/

Esm

olol

/Ca

rdio

vers

ion

Aden

osin

e(t

rans

ient

)Ca

rdio

vers

ion

Amio

daro

ne/

Digo

xin

Amio

daro

ne

3.1

d/te

rmH

ydro

psPr

esum

edfe

tal

SVT

(hyd

rops

atbi

rth)

/-

340

Pre-

exci

tatio

n/AV

RTN

orm

alan

atom

y/de

crea

sed

func

tion

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e/Es

mol

ol/

Card

iove

rsio

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rdio

vers

ion

Amio

daro

neAm

ioda

rone

4.1

d/35

wk

SVT

onca

rdio

resp

irato

ry(C

R)m

onito

ring

-/-

230

Atria

lflut

ter

Nor

mal

anat

omy/

Nor

mal

func

tion

Aden

osin

e/Es

mol

olAm

ioda

rone

Amio

daro

ne

5.1

d/28

wk

SVT

onCR

mon

itorin

g-/

-32

0N

opr

e-ex

cita

tion/

AVRT

Nor

mal

anat

omy/

Nor

mal

func

tion

Ice

pack

/Ad

enos

ine/

Digo

xin

(ora

l)/Pr

opra

nolo

l(o

ral)

Aden

osin

eDi

goxi

n(o

ral)/

Prop

rano

lol(

oral

)

Prop

rano

lol

6.3

d/te

rmSV

Ton

CRm

onito

ring

-/-

280

No

pre-

exci

tatio

n/AV

RTN

orm

alan

atom

y/N

orm

alfu

nctio

n

Ice

pack

Aden

osin

e-

7.6

d/te

rmSV

TCo

ngen

italh

eart

defe

ct25

0N

opr

e-ex

cita

tion/

AVRT

Dtr

ansp

ositi

onof

the

grea

tar

terie

sN

orm

alfu

nctio

n

Ice

pack

Ice

pack

Digo

xin

(ora

l)Di

goxi

n

cardiology supraventricular tachycardia

e340 NeoReviews Vol.6 No.7 July 2005

cause (eg, fever, sepsis, catecholamine excess), and noresponse to maneuvers used to convert SVT to normalsinus rhythm.

SVT is a tachyarrhythmia originating proximal to thebundle of His. The typical infant who has SVT has aregular R-R interval, with rates often greater than230 beats/min and commonly 260 to 300 beats/min.

The normal cardiac impulse originates in the sinusnode and travels antegrade through the atria to theatrioventricular (AV) node, where the impulse is delayedand is then propagated through the His bundle into theright and left bundle branches. Normal conduction usesthe AV node as the only connection between atria andthe ventricles. The most common type of SVT in infancyand childhood, representing approximately 70% of SVT,

results from a re-entry circuit be-tween the atria and the ventriclesand is called atrioventricular re-entry tachycardia (AVRT) (Fig. 1)(Table 2). In this circuit, the AVnode generally forms the antegradepathway, and an accessory connec-tion between the ventricle and theatria serves as the retrograde path-way for conduction of impulses.This is referred to as orthodromicAV reciprocating tachycardia. Insome patients, the accessory con-nection can serve as the antegradepathway, and the AV node or asecond accessory pathway serves asthe retrograde pathway. This is re-ferred to as antidromic (antegrade)AV reciprocating tachycardia.WPW syndrome is SVT with evi-

dence of pre-excitation. It is identified from a surfaceelectrocardiogram (ECG) in sinus rhythm by a short P-Rinterval and a “delta wave.” The short P-R interval inWPW syndrome represents impulse conduction ante-grade through the accessory pathway without AV nodaldelay. The delta wave is caused by fusion of ventricularcomplexes resulting from a portion of ventricular myo-cardium initially depolarized by antegrade conductionthrough the accessory pathway along with depolarizationof the rest of the myocardium through the normal path-way. WPW syndrome comprises 12% to 56% of AVRTs.(2)(3)(4)(5)(6)(7)(8)(9) Patients 1 and 2 from Table 1showed evidence of WPW syndrome.

The second type of SVT is AV nodal re-entry tachy-cardia (AVNRT) (Fig. 2) (Table 2), which represents

Figure 1. Mechanism of atrioventricular re-entry tachycardia.

Table 2. Electrocardiographic (ECG) Features of SVTTypeof SVT Baseline ECG

QRS ComplexDuring SVT P Wave During Tachycardia

P-R interval andR-P interval Effect of Adenosine

AVRT Delta wave maybe present

Usuallynarrow

Inverted P wave may be seenfollowing the QRScomplex

P-R interval is longerthan R-P interval

Termination

AVNRT Normal Narrow Often not seen in typicalAVNRT; seen after QRScomplex in “fast-slow”(atypical) AVNRT

Fast-slow AVNRT:R-P interval islonger than P-Rinterval

Termination

AT Normal Narrow Flutter or ectopic P wavesmay be seen

R-P interval is longerthan P-R interval

Usually will not terminate;may “uncover” atrialrhythm

AVRT�atrioventricular re-entry tachycardia, AVNRT�atrioventricular nodal re-entry tachycardia, AT�atrial tachycardia



about 13% of SVTs. The tachycardia circuit also involvesdual pathways, but both are situated within or near theAV node. Typical AVNRT conducts in an antegradedirection slowly down to the ventricles through onepathway and has a rapid retrograde conduction via theother pathway. It is, therefore, called “slow-fast”AVNRT. On the ECG, this manifests as a QRS complexfollowed by a T wave, with the P wave often not visible(concealed in the QRS complex). Atypical AVNRT has acomparatively slower retrograde conduction, so the Pwave is visible as an inverted complex after the QRS. Thisis 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 ectopictachycardia (AET). Atrial flutter results from a re-entrycircuit within the atrial muscle, with flutter wave rates ashigh as 400 to 500 beats/min. AET is due to ectopicatrial foci that display abnormal automaticity. These fociare reflected by an abnormal P-wave axis during tachy-cardia. The atrial rates range from mild tachycardia to300 beats/min. The onset of AET is characterized bygradual acceleration of the atrial rate (ramping up) tomaximum. AET does not employ re-entry. The AV nodeis not a part of the circuit in atrial flutter or atrial re-entrytachycardia. 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 1:1conduction through the AV node or, more often, lower,with variable degrees of AV conduction.

Of particular importance in the management of SVT

is the fact that both AVRT and AVNRT require conduc-tion through the AV node as a part of the circuit tomaintain tachycardia (Figs. 1 and 2). Natural historystudies in patients who have SVT have demonstrated thatapproximately 70% of infants lose SVT inducibility by 1year of age, and clinical recurrences are uncommon. (10)

Clinical FeaturesPresenting features of SVT in neonates can include fetalSVT, unexplained nonimmune hydrops in the newborn(patients 1, 2, and 3 from Table 1), sudden cardiovascu-lar collapse, incidental detection during cardiorespiratorymonitoring (patients 4, 5, and 6 from Table 1), orsymptomatic heart failure developing over a few hours todays. A cardiac cause is found in about 9% of nonimmunehydrops, 60% of which is due to fetal SVT. (11) SVT canoccur in patients who have underlying congenital cardiacdefects, especially Ebstein anomaly and L-transpositionof the great arteries. Congenital heart disease is reportedin about 6.5% to 37% of neonates who have SVT.(2)(3)(12) Patient 7 in Table 1 was diagnosed withtransposition of the great arteries and developed SVTawaiting cardiac surgery. SVT has been reported as theinitial presenting feature of cardiac involvement in pa-tients who have tuberous sclerosis with cardiac rhab-domyomas. (13)(14)(15)(16)

ECG FeaturesAs noted previously, the typical neonate who has SVT hasa regular R-R interval, with rates greater than 230 beats/min and usually 260 to 300 beats/min. P waves arediscernible in only 60% of cases and usually differ mor-phologically from those present in sinus rhythm. Theyoften are inverted and are seen just after the QRS com-plex. In more than 90% of cases, the QRS morphologyhas a normal complex similar to the baseline sinus QRS(Fig. 3). Wide QRS complex is seen in patients who havepre-existing or rate-dependent bundle branch block andin antegrade AVRT (Fig. 1). Nevertheless, additionalconsideration should be given to ventricular tachycardiain all patients who have wide-complex tachycardia (Fig.4), and treatment should be directed accordingly. A deltawave (Fig. 5) and a short P-R interval seen on thebaseline ECG in sinus rhythm in a neonate who has SVTmakes the diagnosis of WPW syndrome.

A 12-lead ECG should be performed during tachycar-dia and after sinus rhythm is achieved, but this should notdelay treatment. Once the patient is stable, an echocar-diogram should be performed to evaluate ventricularfunction, identify the presence of congenital heart dis-ease, and look for cardiac rhabdomyomas. The response

Figure 2. Mechanism of AV nodal re-entry tachycardia.



to adenosine can facilitate an accurate diagnosis of SVTas well as restore sinus rhythm in a significant percent ofcases. As shown in Figure 6, adenosine can terminateSVT promptly if the AV node is a part of the circuit.

Acute Management of Neonatal SVTSVT 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. Acutetermination of SVT is critical in patients who developsigns and symptoms of hemodynamic instability, includ-ing lethargy, pallor, poor perfusion, hypotension, acido-sis, and signs of cardiac failure. Immediate restoration ofsinus rhythm is achieved best by cardioversion (patients1, 2, and 3 in Table 1). If IV access is available, adenosinemay be tried while preparing for cardioversion.

Cardioversion refers to an electrical energy dischargethat is synchronized with the large R (or S) wave of theQRS complex. Synchronization with the early part of theQRS complex avoids energy delivery in the early phase of

repolarization when ventricular fi-brillation can be induced. Transientdelivery of electrical current causesa momentary depolarization ofmost cardiac cells. This allows thesinus node to resume normal pace-maker activity. The key compo-nents in preparing the patient areintravenous access, airway manage-ment equipment, sedative drugs,and a converter/defibrillator mon-itoring device. Lack of IV access orsedation should not delay cardio-version in the critically ill neonate.For neonates, a single paddle orpatch is placed immediately to the

right of the sternum, and the other paddle/patch isplaced between the tip of the left scapula and the spine toplace as much heart mass as possible between the twopaddles/patches. If a paddle is used, conductive gelshould be applied to ensure good contact because skincan 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 skinburns. An initial synchronized shock of 0.5 J/kg isrecommended. In subsequent attempts, the energy isdoubled. Even under ideal circumstances, only 10% to30% of the total current reaches the heart. If conversionto sinus rhythm is not achieved after two attempts, drugtherapy should be initiated before attempting cardiover-sion again. Although cardioversion can restore sinusrhythm, it cannot maintain sinus rhythm. Therefore, it isalways prudent to have a pharmacologic agent availableto maintain sinus rhythm after conversion.

Adenosine can be administered if a neonate is hemo-

Figure 3. Narrow QRS complex SVT at a rate of 300 beats/min.

Figure 4. Wide-complex SVT at a rate of 240 beats/min.Figure 5. Wolff-Parkinson White syndrome characterized byshort P-R interval and delta wave (arrow).



dynamically stable and can be provided to the unstableneonate in whom IV access has been established whilepreparing for cardioversion. Adenosine is administered asa rapid IV bolus followed by a saline flush in doses of0.05 to 0.2 mg/kg, with continuous ECG monitoringand availability of cardiopulmonary resuscitation equip-ment. Adenosine is successful in terminating SVT inabout 42% to 86% of cases (Fig. 7). (4)(17)(18)(19) Inour case series, adenosine successfully terminated SVT infour of the six neonates (66%) in whom it was used. Itproduces AV block (may appear as a brief episode ofasystole), thereby disrupting one limb of the re-entry

circuit. The advantages of adeno-sine are its very short half-life (10 to15 sec) and the onset of efficacy(within 10 to 20 sec). Administra-tion can be repeated immediately ifrequired, and the drug has no neg-ative inotropic effect. The disad-vantage is immediate recurrence oftachycardia in approximately 30%of cases. Adenosine can cause flush-ing, bronchospasm, and transientnew rhythms at the time of conver-sion, including premature ventricu-lar contractions, premature atrialcontractions, sinus bradycardia,tachycardia, as well as varying de-grees of AV nodal block. (20)(21)

For patients who are hemody-namically stable, a more graded ap-proach is appropriate. Initially, va-gal maneuvers, which are simple,quick, and safe to perform, can beattempted. Placement of an icepack on the face and nose for 5 to10 seconds at a time is used com-monly. This maneuver initiates a

“diving reflex” that has been described in certain speciesof animals in which diving into cold water induces a reflexperipheral vasoconstriction accompanied by a profoundvagal discharge. (22) The afferent pathway of the reflex isthe trigeminal nerve endings around the nose andmouth, and the efferent pathway is the vagus nerve. Inhumans, bradycardia also is observed with these maneu-vers. Success rates vary from 63% to 96%. (2)(5)(18)(23)In our case series, an ice pack was used in three neonatesand was successful in terminating SVT in only one (33%).

Esmolol is a very useful pharmacologic agent in pa-tients who experience recurrent or sustained SVT. This

beta blocker has class II antiar-rhythmic properties, an immediateonset of action, and a very shorthalf-life of about 3 minutes. It isadministered IV at a dose that canbe titrated based on the responseand can guide long-term manage-ment. (24)(25)(26) It acts by in-creasing the refractory period of theAV node, thus interrupting the re-entry circuit. It usually is adminis-tered as a loading dose of 100 to500 mcg/kg over 1 minute fol-

Figure 6. Responses of narrow complex tachycardia to adenosine. IV�intravenous,AV�atrioventricular, VT�ventricular tachycardia, AT�atrial tachycardia, AVRT�atrioventricular re-entry tachycardia, AVNRT�atrioventricular node re-entry tachycardia,AET�atrial ectopic tachycardia. Adapted from ACC/AHA guidelines for the managementof patients with supraventricular arrhythmias. Circulation. 2003;108:1871–1909. Copy-right 2004 The American College of Cardiology Foundation and American HeartAssociation, Inc. Permission granted for one time use. Further reproduction is notpermitted without permission of the ACC/AHA.

Figure 7. Termination of SVT with adenosine.



lowed by a continuous infusion of 50 to 100 mcg/kg perminute. Esmolol can be titrated upward by 50-mcg/kgper minute increments every 5 to 10 minutes to a maxi-mum dose of 1,000 mcg/kg per minute until eitherthere is control of the ventricular rate or hypotensiondevelops. (24)(25)(26) Other potential adverse effectsinclude bradycardia and bronchospasm. (27)

Digoxin has been the drug of choice for neonatal SVTin the past. Digoxin acts by decreasing conductionthrough the AV node. This agent is avoided in patientswho have WPW syndrome because of their predisposi-tion to develop atrial fibrillation, which may lead toventricular arrhythmias due to enhanced conductionthrough the accessory pathway. We tend to use digoxinin neonates who have SVT and poor cardiac function andhave not responded to beta blockade. Digoxin has anonset of action within 5 to 30 minutes, with the maxi-mum effects seen within 1 to 4 hours after parenteraladministration. After oral administration, the onset ofaction is within 30 minutes to 2 hours, with maximumeffects seen after 2 to 8 hours. The elimination half-life is61 to 170 hours in preterm neonates and 35 to 45 hoursin term neonates. The oral total digitalizing dose (TDD)is 20 to 30 mcg/kg in preterm neonates and 25 to35 mcg/kg in term neonates. The parenteral TDD is75% of the oral TDD. The dose is reduced by 50% inpatients receiving concomitant amiodarone or patientswho have end-stage renal disease. Therapeutic serumlevels are 0.8 to 2 ng/mL. Toxicity may be seen withconcentrations higher than 2 ng/mL. Adverse effectscommonly 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 therhythm, a class I antiarrhythmic agent may be appropri-ate. Procainamide is a class IA antiarrhythmic agent thathas anticholinergic and local anesthetic effects. It de-creases myocardial excitability and conduction velocityand depresses myocardial contractility. By decreasingatrial excitability, procainamide decreases the flutterwave rate, but it may increase flutter wave conductionrate across the AV node, potentially causing ventriculartachycardia. Therefore, it is recommended that the pa-tient be digitalized before receiving a loading dose ofprocainamide. Procainamide can be administered IV in aloading dose of 3 to 6 mg/kg over 5 minutes, repeatedevery 5 to 10 minutes to a maximum of 15 mg/kg, andfollowed by a continuous infusion of 20 to 80 mcg/kgper minute. The infusion should be stopped if the QRS

complex widens to more than 125% of baseline. It isimportant to monitor the patient for hypotension andarrhythmias during the infusion. The enteral dose ofprocainamide is 15 to 50 mg/kg per day divided every3 to 6 hours. Procainamide is metabolized to the activemetabolite N-acetyl procainamide (NAPA). The half-lifeof procainamide in infants is approximately 1.7 hours,and the half-life of NAPA is approximately 6 hours.Therapeutic concentrations of both procainamide andNAPA are 4 to 10 mcg/mL. Other potential adverseeffects are a lupuslike syndrome, nausea, vomiting, diar-rhea, and liver dysfunction. (31)

Flecainide is a class IC drug that exerts profoundeffects on the accessory connection and the AV node,which is unlike the action of the beta blockers adenosineand digoxin, which terminate SVT by blocking AV nodeconduction only. Flecainide is administered at a dose of2 mg/kg IV over 10 minutes during the acute phasefollowed by a dose of 3 to 6 mg/kg per day orally in twodivided 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 junctionaltachycardia. Its effects are similar to flecainide. An IVdose of 1 to 2 mg/kg can be used for acute control ofSVT. The oral dose of propafenone is 8 to 10 mg/kg perday divided in three to four equal doses, which may beincreased in increments of 2 mg/kg per day up to amaximum of 20 mg/kg per day. Peak plasma concentra-tions are reached after 2 to 3 hours, and steady-statelevels are achieved in 4 to 5 days. The elimination half-lifeis approximately 5 to 8 hours. The adverse effects re-ported with propafenone are negative inotropic effects,proarrhythmic effects, sinus node dysfunction, blooddyscrasias, 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 amiodaronemay 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 havedepressed cardiac function. Amiodarone is started withan IV loading dose of 5 mg/kg over 1 hour, followed bya continuous infusion of 5 mcg/kg per minute, with doseincreases until either conversion of SVT or attainment ofa maximum of 15 mcg/kg per minute. The onset ofeffect after parenteral administration is usually withinminutes, especially after a loading dose. Once SVT is



controlled with amiodarone infusion, the total daily dosecan be converted into an oral dose that is weaned slowlyto a maintenance dose of 3 to 5 mg/kg per day in twodivided doses. The half-life of amiodarone is about 40 to55 days. Amiodarone can cause new arrhythmias, hypo-thyroidism, liver dysfunction, pulmonary fibrosis, andcorneal opacities. (39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51) With the use of lower doses, suchadverse 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 withamiodarone. Various other combinations have been triedwith high success rates. The reported success rate for thecombination of amiodarone and propranolol is 80%,flecainide with amiodarone is 78%, and flecainide withsotalol is 100% in controlling single or multidrug refrac-tory SVT. (52)(53)(54)

Chronic Management of SVTChronic medical treatment is appropriate for neonateswho have hemodynamically significant SVT, frequentSVT requiring medical management, pre-excitation onECG, or congenital cardiac defect. For neonates whohave had self-terminating asymptomatic SVT with noevidence of pre-excitation on ECG and with normalcardiac anatomy, chronic medical treatment may be de-ferred.

A beta blocker such as propranolol is most appropriatefor patients responding to esmolol or who have evidenceof pre-excitation on ECG. Propranolol is a noncardio-selective class II antiarrhythmic agent that has propertiessimilar to esmolol. The starting dose of propranolol is0.25 mg/kg every 6 to 8 hours and can be increasedslowly to a maximum of 4 mg/kg per dose with closemonitoring 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 havepoor cardiac function and those who have hyperactiveairway disease. (27)

Patients who achieved control of SVT with class I orclass III agents are treated with oral preparations of thesame medications. Because 70% of neonates who haveSVT lose inducibility by 1 year of age, most cardiologiststreat for about 6 to 9 months, adjusting dosage for size,and subsequently allow the patient to outgrow the drugdose by about 1 year of age.

Figure 8 presents an algorithm for management of

neonatal SVT that can be modified based on institutionalpreferences.

Fetal SVTSVT is the most common symptomatic fetal cardiacarrhythmia. Atrioventricular re-entry tachycardia is themost common mechanism, occurring in more than 90%of fetal SVTs. Other, rare mechanisms for SVT in fetusesare atrial flutter or fibrillation, automatic tachycardia, andpermanent junctional reciprocating tachycardia. In fe-tuses that have SVT, the characteristic heart rate is 240 to260 beats/min. In fetuses that have atrial flutter, thecharacteristic atrial rate is 300 to 500 beats/min, withvarying ventricular response rates. (55)

Ultrasonography currently is the most commonlyused diagnostic tool to analyze heart rhythm in a fetus.A detailed study includes definition of cardiac structure,rhythm, function, hemodynamics, and presence of fetalhydrops. Structural malformations of the heart are seenin 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, orrhabdomyoma. (56)(57)

Figure 8. General algorithm for management of neonatalsupraventricular tachycardia. SVT�supraventricular tachycar-dia, IV�intravenous



Fetal SVT is associated with a fetal and neonatalmortality rate of 8% to 30%. Preterm delivery of an infantwho has hydrops and SVT is associated with high rates ofmorbidity and mortality. (56)(57)(58)(59) The goals oftherapy for fetal SVT are to restore sinus rhythm, resolveheart failure, and postpone delivery until term. The indi-cations to treat fetal SVT are prematurity or evidence ofsevere hemodynamic compromise of the fetus, such ashydrops. (55) The therapeutic goal is rate control (inatrial flutter) or complete control of the arrhythmia.Prior to initiating therapy, a complete maternal historyfor arrhythmia and a baseline maternal ECG to rule outlong 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 isimportant for all medications. (55) Therapy with antiar-rhythmics is initiated using low doses, with gradual doseincreases and careful monitoring of maternal and fetaldrug response in an inpatient setting. Fetuses that havehydrops are at a higher risk of adverse drug effects thanfetuses that do not have hydrops. A fetus treated for SVTusually requires therapy for at least 2 to 3 weeks afterconversion to sinus rhythm because of a predilection forrecurrence.

Digoxin is the most frequently used monotherapy inmothers whose fetuses do not have hydrops but do haveeither SVT or atrial flutter. (55)(56)(60) It is used at ahigher-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 to8 hours during the first 24 hours for rapid digitalization(maximum, 2 mg/d). The enteral loading dose ofdigoxin is 0.25 to 1.5 mg, followed by a maintenancedose of 0.25 mg to 0.5 mg/d. (62) The digoxin cordblood concentration varies widely, from 40% to 90% ofthe maternal level. Placental transfer of digoxin is as lowas 10% in fetuses that exhibit hydrops. The dose shouldbe titrated to achieve a maternal serum level of 1 to2 ng/mL. The effectiveness of digoxin monotherapy is32% 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 thesecond-line antiarrhythmic agents for fetal SVT that doesnot 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 isadministered for 1 to 7 days, with a single dose notexceeding 800 mg. Once sinus rhythm is obtained, thedose is decreased to the lowest effective dose necessary to

sustain sinus rhythm, usually 200 to 400 mg/d. Chronicmaintenance therapy is continued until hydrops resolvesand tachycardia is quiescent for 2 to 3 weeks. The half-lifeof amiodarone is 50 to 60 days. Maternal thyroid andliver profiles should be monitored before and duringamiodarone therapy. Fetal plasma concentrations of ami-odarone vary from 10% to 50% of the maternal level.During chronic treatment, the desired therapeutic serumconcentration is 0.5 to 2.5 mcg/mL. Amiodarone aloneor in conjunction with digoxin is successful in restoringsinus rhythm in approximately 60% to 75% of fetuses thathave SVT and 33% to 50% of fetuses that have atrialflutter. (45)(63)(65)(66)(67)

Flecainide is a sodium channel blocker (class 1C) thathas been used effectively in fetal SVT, both as mono-therapy and in combination with digoxin. Flecainideshould not be used as monotherapy in atrial flutterbecause it can increase the ventricular rate. Maternaldosing is initiated at 100 mg enterally twice a day. Thedose can be increased to 300 mg/d in two to threedivided doses. The half-life is 14 hours, and the time toreach 90% of a steady-state plasma concentration is ap-proximately three times the half-life. The fetomaternalplasma ratio of flecainide varies from 50% to 80%. Thetherapeutic flecainide plasma concentration is 0.4 to0.8 mcg/mL, and careful monitoring of values is re-quired to decrease the incidence of proarrhythmic effectsin the mother and fetus. Other maternal adverse eventsinclude dizziness, flushing, nausea, vomiting, and visualdisturbances. Flecainide has negative inotropic effectsand should be avoided when SVT is accompanied bystructural heart disease or depressed myocardial contrac-tility. Overall, the reported conversion rate to sinusrhythm has been 90% to 100% for fetuses that do nothave hydrops with SVT and 60% to 85% for fetuses thatdo have hydrops. (62)(63)(64)(68)(69)

Sotalol has both beta-blocking and class III antiar-rhythmic properties. Because of its potent antiarrhythmiceffect and excellent placental transfer, sotalol is effectivefor fetal SVT, particularly in atrial flutter. Its half-lifevaries 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, indicatingcomplete transplacental passage of sotalol. The oral ma-ternal dose should be initiated at 80 mg twice daily andincreased in incremental doses to a maximum of 160 mgthree times daily. The therapeutic plasma concentrationranges 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



is warranted during treatment with sotalol. Sotalol cancause temporary adverse effects in mothers, includingnausea, dizziness, and fatigue, and can be proarrhythmicin fetuses. (70) Sotalol monotherapy is effective in con-verting 80% to 85% of fetuses that have atrial flutter and60% to 70% of fetuses that have SVT to sinus rhythm. Infetuses that exhibit hydrops, the conversion rate is 40% to60% as monotherapy and 80% in combination withdigoxin. (63)(70)(71)(72)

SummarySVT, which can be recurrent and persistent, is the mostcommon symptomatic arrhythmia. The most commontype of SVT in infancy results from a re-entry circuitbetween the atria and the ventricles. SVT inducibility islost in 70% of infants by 1 year of age. Twelve-lead ECGduring 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 instabilitywarrants immediate restoration to sinus rhythm, bestachieved by synchronized electrical cardioversion. Med-ical management of SVT consists of a trial of vagalmaneuvers, adenosine, and medications to maintain si-nus rhythm such as beta blockers and class I or class IIIantiarrhythmic medications. For neonates who have he-modynamically significant SVT, frequent SVT requiringmedical 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, canoccur in infants who have underlying congenital heart defects. Of the following, the most commoncongenital 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 suchepisode, the heart rate is 280 beats/min. Electrocardiography reveals inverted P waves, most of whichfollow QRS complexes; normal QRS pattern; and P-R intervals that exceed R-P intervals. The infant ishemodynamically stable, has no echocardiographic evidence of congenital heart disease, and has noindwelling vascular catheters. Vagal maneuvers and intravenous adenosine are unsuccessful in restoringnormal heart rhythm. Of the following, the next pharmacologic agent recommended, according to thealgorithm 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, acombination of medications may be tried. Of the following, the combination of medications most successfulin 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.



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