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American Journal of Emergency Medicine (2008) 26, 348–358

Diagnostics

The pediatric electrocardiogramPart II: DysrhythmiasMatthew O'Connor MDa, Nancy McDaniel MDb, William J. Brady MDc,⁎

aDepartment of Pediatrics, Children's Medical Center, University of Virginia Health System, Charlottesville, VA 22908, USAbDivision of Cardiology, Department of Pediatrics, Children's Medical Center, University of Virginia Health System,Charlottesville, VA 22908, USAcDepartment of Emergency Medicine, University of Virginia Health System, Charlottesville, VA 22908, USA

Received 27 July 2007; accepted 31 July 2007

0d

bstract The following articopulation. Their definitions

A le in this series will describe common arrhythmias seen in the pediatricp and clinical presentations along with electrocardiogram (ECG) exampleswill be presented. In addition, ECG changes seen in acute toxic ingestions commonly seen in childrenwill be described, even if such ingestions do not produce arrhythmias per se. Disturbances of rhythmseen frequently in patients with unrepaired and corrected congenital heart disease will be more fullydiscussed in the third article of this series. Numerous classification schemes for arrhythmias exist; in thisarticle arrhythmias will be grouped based upon their major ECG manifestations.© 2008 Elsevier Inc. All rights reserved.

1. Introduction

The following article in this series will describe commonarrhythmias seen in the pediatric population. Their defini-tions and clinical presentations along with ECG exampleswill be presented. In addition, ECG changes seen in acutetoxic ingestions commonly seen in children will bedescribed, even if such ingestions do not produce arrhyth-mias per se. Disturbances of rhythm seen frequently inpatients with unrepaired and corrected congenital heartdisease will be more fully discussed in the third article of thisseries. Numerous classification schemes for arrhythmiasexist; in this article arrhythmias will be grouped based upontheir major ECG manifestations.

⁎ Corresponding author.E-mail address: wb4z@virginia.edu (W.J. Brady).

735-6757/$ – see front matter © 2008 Elsevier Inc. All rights reserved.oi:10.1016/j.ajem.2007.07.034

2. Bradyarrhythmias

Bradyarrhythmias are uncommon causes of ECGabnormalities in children without congenital heart disease;they are seen frequently in patients with congenital heartdisease who have undergone surgical manipulation of theatria (eg, Fontan procedure, atrial septal defect repair,atrioventricular [AV] canal repair, and older “atrial switch”operations for transposition of the great arteries). Sinusbradycardia is defined by the presence of a sinus rhythm thatis abnormal only in that it is slower than expected for thechild's age (Fig. 1). Specific age-related norms weredescribed in the previous article, but in general a heartrate less than 100 beats per minute (bpm) in childrenyounger than 3 years old, less than 60 bpm in children 3 to9 years old, less than 50 bpm in children 9 to 16 years old,and less than 40 in older children and adolescents shouldentertain the diagnosis of sinus bradycardia [1]. As in adults,several factors must be considered before making this

Fig. 1 Sinus bradycardia in a child with hypothyroidism. The heart rate varies between 30 and 40 bpm.

349The pediatric ECG

diagnosis, particularly with regard to sleeping vs the wakingstate and level of athletic training.

Sinus arrest (also known as sinus pause) reflects thefailure of the sinoatrial node to propagate impulses. If theperiod of arrest is prolonged, escape rhythms may “takeover” the function of the sinoatrial, and these escape rhythmsmay occur at the AV nodal, bundle of His, or ventricularlevel. In children, the mean maximum duration of sinuspause (F2 SD) was found to be 1.82 seconds [2].

Fig. 2 First-degree AV block in a young boy undergoing Hol

3. Atrioventricular block

The generic term AV block implies a disturbance ofimpulse conduction from the atria to the ventricles. Theanatomic locations of such disturbances vary depending onthe underlying mechanism of the arrhythmia. Generally, AVblock is categorized into first-degree (1°), second-degree(2°), and third-degree (3°) subtypes. First-degree block(Fig. 2) is identified electrocardiographically by a prolonged

ter monitoring. Note the markedly prolonged PR interval.

Fig. 3 A, Type I second-degree AV block from a Holter recording in a 7-year-old boy with congenital complete heart block. B, Type IIsecond-degree AV block with wide QRS complex.

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PR interval for age. The reader is referred to age-relatedpediatric norms as discussed in Part I and other age-relatednorms discussed in this article [3]. First-degree block istypically asymptomatic and generally does not implyunderlying disease of the conduction system. It may beseen in the sleeping state [4], in trained athletes with lowresting heart rates [5], and rarely in Lyme disease andmyocarditis [6].

Second-degree AV block is divided into 2 categories: typeI (Wenkebach), in which there is progressive prolongation ofthe PR interval until failure of AV conduction occurs

Fig. 4 Third-degree AV block seen in the same patient as in Fig. 3A. No

(Fig. 3A), and type II (Möbitz), in which random “dropping”or failure of AV conduction occurs without PR prolongation(Fig. 3B). Of the two, type II block is more ominous and mayprogress to complete (3°) heart block. Type I 2° block isagain a common variant of normal, particularly in trainedathletes [5]. It is also common after repair of structuralcongenital heart disease [7]. The presence of Möbitz block orany symptomatic 2° block warrants pediatric cardiologyconsultation with consideration given to pacing.

Complete or 3° heart block is defined by the absence ofconduction between the atria and ventricles. Complete heart

te that there is no relationship between P waves and QRS complexes.

351The pediatric ECG

block is manifested by AV dissociation in which regularlyspaced P waves are not related temporally to the ventricularescape rhythm (Fig. 4). The QRS duration may be normal orprolonged depending on the location of the block; moreproximal blocks (ie, near the AV node) will typically result ina normal QRS duration. Congenital complete heart blockoccurs in infants of mothers carrying anti-Ro and anti-Laantibodies; mothers may or may not have clinical symptomsof lupus [8]. Complete heart block is also a knowncomplication of surgery for congenital heart disease andhas a significant effect on morbidity and mortality [9].Complete heart block is almost always symptomatic andusually requires dual-chamber pacemaker implantation.

The bundle branches are the downstream limbs of thebundle of His and allow for nearly synchronous depolariza-tion of the left and right ventricles, which is important inmaintaining cardiac synchrony. Prolongation of conductionthrough the bundle branches results in QRS prolongation andis known as bundle branch block (BBB). Bundle branchblock can affect the right or left bundle branches (RBBB,LBBB) and be classified as complete or incomplete, based

Fig. 5 Incomplete RBBB in a 3-week-old male infant aftertetralogy of Fallot repair. Note the rSR′ pattern in leads V1 and V2

with minimal QRS prolongation.

Fig. 6 Complete RBBB in a 19-year-old adolescent girl withrepaired tetralogy of Fallot. Note the similarity of the rSR′ pattern tothe previous figure, with this ECG manifesting QRS prolongation.

upon whether there is QRS prolongation for age. IncompleteRBBB is commonly seen in pediatric ECGs and ismanifested by an rSR′ pattern in lead V1 and a small Swave in lead V6; the initial upstroke of the QRS is normalwith a delay in the terminal portion of the QRS complex(Fig. 5). Right bundle branch block is detected in V1; the

Fig. 7 Left bundle branch block. Note the prolonged QRSduration in the lateral precordial lead V5.

352 M. O’Connor et al.

initial upstroke of the QRS is delayed (Fig. 6) with theterminal portion of normal duration, whereas LBBB istypically manifested by QRS prolongation in V6 (Fig. 7).Bundle branch blocks may be seen in a variety of conditionsand is a frequent finding after surgery for congenital heartdisease, particularly in which there has been a ventriculot-omy (ie, tetralogy of Fallot) [10].

4. Normal QRS duration tachycardias

Numerous schemes exist for classifying tachycardias; auseful and simple way is to categorize them based upon theQRS duration. In general, tachycardias with a normal QRSduration for age can be considered as originating superior tothe AV node, whereas tachycardias associated with QRSprolongation typically originate at locations inferior to theAV node. This scheme is not perfect but allows for easeof organization.

Sinus tachycardia is usually simple to recognize on theECG (Fig. 8). For the diagnosis of sinus tachycardia to beestablished, a P wave must precede every QRS complex andthe P waves must have a normal axis (discussed previously).In adults, a heart rate greater than 100 bpm is consideredtachycardia. In children, this rate is age dependent butgeneral guidelines exist; heart rates greater than 160 bpm ininfants and greater than 140 bpm in children suggest sinustachycardia [11]. Sinus tachycardia often reflects anxiety,dehydration, or fever, and can be considered an “appropriate”physiologic response to the underlying disturbance. “Inap-propriate” sinus tachycardia implies underlying primarycardiac disturbance and is often seen in myocarditis orcongestive heart failure. Although a wide range of heart ratesmay be seen in sinus tachycardia, the sinus node rarely pacesat heart rates greater than 220 bpm; when greater heart ratesare seen, sinus tachycardia is uncommon. Ectopic atrialtachycardias can be difficult to distinguish from so-calledsupraventricular tachycardias (SVTs; see below), particu-larly at high rates in which the P wave is “buried” within theT wave of the preceding QRS complex (Fig. 9).

Fig. 8 Sinus tachycardia detected on Holter monitoring of a 6-year-

Atrial flutter and atrial fibrillation are quite rare inpediatric patients. However, a form of atrial flutter can beseen after surgery for congenital heart disease, particularly inpatients with Fontan-type operations and atrial switchprocedures for transposition of the great arteries [12]. Atrialflutter is identified by so-called sawtooth waves representingthe rapid atrial rate with typically normal QRS duration.Atrial fibrillation demonstrates chaotic irregular atrialactivity with an “irregularly irregular” ventricular rate;QRS is usually normal in duration (Fig. 10).

Supraventricular tachycardia is one of the most commonarrhythmias encountered in pediatric patients (Fig. 11). Theterm supraventricular tachycardia is confusing and does notimply a single mechanism, however. Supraventriculartachycardia includes any arrhythmia that requires atrial orAV nodal tissue for their initiation and propagation, andincludes atrial tachycardias, atrial fibrillation, atrial flutter,nodal tachycardia, junctional ectopic tachycardia, and others[13] For the purposes of this discussion, SVTwill be definedas a paroxysmal tachyarrhythmia manifested by the absenceof P waves and by the presence of normal QRS complexes.In children, there are 2 common mechanisms of SVT [14].Both involve reentry mechanisms. In AV nodal reentrytachycardia the reentry mechanism involves the AV node,and in AV reentry tachycardia reentry proceeds via anaccessory pathway near, but not including, the AV node. Twomechanisms are often indistinguishable via ECG. Preexcita-tion syndromes are more common in children with AVreentry tachycardia and are discussed below. The treatmentof SVT involves vagal maneuvers, adenosine, and in rarecases synchronized cardioversion and is discussed in furtherdetail elsewhere [15].

Two additional SVTs occasionally encountered in pedia-trics include junctional ectopic tachycardia and permanentjunctional reciprocating tachycardia (Fig. 12). Junctionalectopic tachycardia is a common and frequently hemodyna-mically deleterious rhythm seen in postoperative patients andis discussed in a subsequent article. Permanent junctionalreciprocating tachycardia is a chronic, incessant form oftachycardia involving an accessory pathway that presents ininfants and is electrocardiographically manifested by a

old girl with near syncope. The heart rate is regular at 157 bpm.

Fig. 9 Ectopic atrial tachycardia captured on Holter monitoring of a young girl. Note how the P waves are difficult to separate from the QRScomplex owing to the high heart rate.

353The pediatric ECG

prolonged R-P interval [16]. It frequently causes a cardio-myopathy which responds to rate control, although achieve-ment of normal sinus rhythm can be extremely difficult.

5. Abnormal QRS duration tachycardias

Tachycardias demonstrating prolonged QRS duration forage imply a ventricular origin to the arrhythmia. Ventriculararrhythmias also demonstrate “bizarre” QRS morphologies.Ventricular arrhythmias are uncommon in children andusually arise in the setting of severe electrolyte disarray,ingestion, or rare inherited disorders of cardiac conduction.Ventricular arrhythmias, however, are poorly tolerated

Fig. 10 Atrial flutter in a neonate without structural congenital heart dseen best in leads aVR and aVF.

hemodynamically so prompt recognition and initiation oftherapy are vital.

Premature ventricular contractions (PVCs) are a frequentfinding in children and may be cause for concern in rarecases (Fig. 13). They are manifested on the ECG by bizarrelyshaped, wide QRS complexes with the associated T waveusually pointing in the opposite direction of the QRScomplex. A compensatory pause after the PVC will be seen.Premature ventricular contractions of uniform morphologyare less concerning than those of multiple forms. Ventriculartachycardia consists of 3 or more successive PVCs at aregular rate of 120 to 180 bpm (Fig. 14). As in adults, it candegenerate into ventricular fibrillation, a usually lethalrhythm unless promptly treated. Several special conditionsassociated with ventricular tachycardia in children should be

isease. Note the rapid ventricular rate and distinctive flutter waves

Fig. 11 Supraventricular tachycardia in a 10-year-old boy with palpitations and a rapid heart rate. Note the regular rate, narrow QRScomplex, and absence of P waves. The tachycardia resolved with intravenous adenosine. Final diagnosis was orthodromic reciprocatingtachycardia due to an accessory pathway.

354 M. O’Connor et al.

mentioned. The Brugada syndrome is a rare, autosomaldominant, and frequently lethal disorder associated withbouts of ventricular tachycardia and sudden death. A peculiar“saddle-form” ST-segment elevation in the right precordial

Fig. 12 Narrow complex tachycardia in an 8-month-old infant presentiElectrophysiologic study revealed the diagnosis of permanent junctional

leads with a family history suggests the diagnosis [17].Arrhythmogenic right ventricular dysplasia is another rareinherited disorder causing ventricular tachycardia andsudden death in affected individuals due to the replacement

ng with feeding difficulties, poor weight gain, and cardiomyopathy.reciprocating tachycardia.

Fig. 13 Multiple PVCs in a 17-year-old adolescent boy with a history of transposition of the great vessels after arterial switch procedure.Note the bizarre, wide QRS complexes interspersed with QRS complexes of normal configuration.

355The pediatric ECG

of right ventricular myocardium with fatty and fibrous tissue.Patients with this disorder typically present after pubertywith ventricular tachycardia, and the interval ECG is notablefor a persistent juvenile pattern of T-wave inversion and awidened QRS complex in right precordial leads.

6. Ventricular preexcitation syndromes

The term preexcitation refers to ventricular depolarizationthat is earlier than expected. Preexcitation can occur viaeither a reentry pathway or an accessory pathway [18]. In

Fig. 14 Unprovoked ventricular tachycardia from Holter m

either case, the potential for sustained and dangeroustachycardia exists because the AV node no longer “protects”the ventricles from excessively high atrial rates. Theelectrocardiographic appearance of preexcitation (Fig. 15)consists of (a) normal P-wave morphology and axis, (b)shortened PR interval, (c) prolonged QRS complex withinitial “slurring” (delta wave), and (d) Q waves and T-waveabnormalities in what is termed a pseudoinfarction pattern.The most common syndrome associated with preexcitationin children and adults is the Wolff-Parkinson-White (WPW)syndrome. In patients with WPW, the most commonlyencountered arrhythmia is a paroxysmal reentry SVT.Detection of the “WPW pattern” (ie, delta wave with a

onitoring in a 13-year-old adolescent girl with syncope.

Fig. 15 Delta waves seen in a child with WPW syndrome who presented with SVT; preexcitation did not manifest until the tachycardiaresolved.

356 M. O’Connor et al.

prolonged QRS complex) in an asymptomatic child warrantscardiology referral, although the actual risk of sudden deathin this population is likely quite low [19].

7. Tachycardias associated with a prolongedQT interval

Evaluation of the QT interval is an essential aspect ofECG interpretation. Norms for the corrected QT interval

Fig. 16 Prolonged QT interval in an 18-year-old adolescent girl withinterval calculated by Bazett's formula is 506 milliseconds.

have been published and were discussed in the previousarticle of this series. Prolongation of the QT interval is oftenasymptomatic but puts the patient at risk of ventriculararrhythmias, the most common of which is torsades depointes. Torsades de pointes is a form of polymorphicventricular tachycardia that has the ECG appearance of“twisting along a string.” Prolongation of the QT intervalcan be due to a multitude of factors, congenital andacquired. QT prolongation is associated with hypokalemiaand hypocalcemia; it is also seen with administration ofantiarrhythmic agents. Many medications are associated

familial long QT syndrome and a history of cardiac arrest. The QT

357The pediatric ECG

with QT prolongation as well, particularly antibiotics andolder antipsychotics.

Congenital forms of the long QT syndrome warrantdiscussion in pediatric patients. Congenital long QTsyndrome is a cause of pediatric sudden death and hasbeen associated with sudden death during sleep, exercise,and perhaps a small subset of infants dying of sudden infantdeath syndrome [20]. The 2 most common inherited long QTsyndromes are known eponymously as the Romano-Wardand Jervell/Lange-Nielsen syndromes and are caused byknown mutations in cardiac ion channels. Congenital longQT syndrome is a common cause of sudden deathattributable to cardiac causes in children; in an internationalregistry of long QT patients, 8% died suddenly during 5 yearsof follow-up [21]. Certainly, identification of a prolonged QTinterval in a pediatric patient warrants pediatric cardiologyreferral and close follow-up (Fig. 16).

8. Toxicology

Children frequently present to EDs after ingestion ofmedications or other toxins, unintentionally or otherwise.Obtaining an ECG is an important aspect of evaluating thesepatients. A number of agents cause QRS prolongation,mainly via blockade of the sodium channels responsible fordepolarization during phase 0 of the myocardial actionpotential. Examples of such agents include tricyclicantidepressants, diphenhydramine, propanolol, hydroxy-chloroquine, and many antiarrhythmic agents [22]. QRSprolongation in the setting of sodium channel blockade,when severe, may lead to asystole unless therapy with salineor sodium bicarbonate is administered.

Fig. 17 Sinus tachycardia with widened QRS complex, deep S wave ina lethargic adolescent with tricyclic antidepressant ingestion.

Tricyclic antidepressant ingestion warrants specialattention owing to the multitude of effects on the ECG[23]. The ECG presentation of such toxicity is dependenton the specific medication ingested as well as the ingesteddose. Tricyclic antidepressants have 4 important effects:(1) inhibition of presynaptic neurotransmitter reuptake; (2)α-adrenergic receptor blockade; (3) anticholinergic effects;and (4) sodium channel blockade. Collectively, these canlead to tachycardia, QRS prolongation, and QT prolonga-tion (Fig. 17).

β-Blockers and calcium-channel blockers are commonlyused medications in adults that not infrequently areunintentionally ingested by children. β-Blockers are phar-macologically heterogeneous with each agent exertingsingle or multiple effects at β1, β2, and α1 receptors. Someβ-blockers contain sodium-channel blocking ability and mayprolong the QRS interval. Sotalol, a class III antiarrhythmicagent, contains potassium channel blocking ability and cancause QT interval prolongation [24]. β1 Receptors, however,located in the myocardium, are largely responsible for thecardiovascular sequelae of β-blocker overdose. Electrocar-diogram manifestations of ingestion generally includebradycardia, various grades of AV block, and QRS complexwidening. [25].

Calcium channel blockers cause predictable but non-specific changes in the ECG. Common changes includehypotension, bradycardia, and AV blocks [26]. Becausemany current formulations of calcium channel blockers areof the extended-release variety, symptoms may be delayedfor up to several hours postingestion [27]. Anotherconsideration in evaluating calcium channel overdose is thecardioselectivity of the agent. Older agents such as nifedipinemay exert a predominantly vascular effect at lower doses,resulting in hypotension with reflex bradycardia. Newer

lead I, and prominent R wave in lead aVr. This ECG was recorded in

358 M. O’Connor et al.

agents such as verapamil or diltiazem may result inbradycardia and conduction disturbances without hypoten-sion. At sufficient doses, however, selectivity is lost.

In summary, arrhythmias in otherwise healthy children arerelatively uncommon in the pediatric population but promptrecognition will prevent excess morbidity and mortality. Theincidence of arrhythmias in patients with a history ofcongenital heart disease is markedly higher and the ECGmanifestations of such arrhythmias in this patient populationwill be described in the next article of this series.

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