diagnosis, particularly with regard to sleeping vs the waking
state and level of athletic training.
Sinus arrest (also known as sinus pause) reflects the
failure of the sinoatrial node to propagate impulses. If the
period of arrest is prolonged, escape rhythms may “take
over” the function of the sinoatrial, and these escape rhythms
may occur at the AV nodal, bundle of His, or ventricular
level. In children, the mean maximum duration of sinus
pause (F2 SD) was found to be 1.82 seconds .
3. Atrioventricular block
The generic term AV block implies a disturbance of
impulse conduction from the atria to the ventricles. The
anatomic locations of such disturbances vary depending on
the underlying mechanism of the arrhythmia. Generally, AV
block 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
Fig. 1 Sinus bradycardia in a child with hypothyroidism. The heart rate varies between 30 and 40 bpm.
Fig. 2 First-degree AV block in a young boy undergoing Holter monitoring. Note the markedly prolonged PR interval.
349The pediatric ECG
PR interval for age. The reader is referred to age-related
pediatric norms as discussed in Part I and other age-related
norms discussed in this article . First-degree block is
typically asymptomatic and generally does not imply
underlying disease of the conduction system. It may be
seen in the sleeping state , in trained athletes with low
resting heart rates , and rarely in Lyme disease and
Second-degree AV block is divided into 2 categories: type
I (Wenkebach), in which there is progressive prolongation of
the PR interval until failure of AV conduction occurs
(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 may
progress to complete (3°) heart block. Type I 2° block is
again a common variant of normal, particularly in trained
athletes . It is also common after repair of structural
congenital heart disease . The presence of Möbitz block or
any symptomatic 2° block warrants pediatric cardiology
consultation with consideration given to pacing.
Complete or 3° heart block is defined by the absence of
conduction between the atria and ventricles. Complete heart
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 II
second-degree AV block with wide QRS complex.
Fig. 4 Third-degree AV block seen in the same patient as in Fig. 3A. Note that there is no relationship between P waves and QRS complexes.
350 M. O’Connor et al.
block is manifested by AV dissociation in which regularly
spaced P waves are not related temporally to the ventricular
escape rhythm (Fig. 4). The QRS duration may be normal or
prolonged depending on the location of the block; more
proximal blocks (ie, near the AV node) will typically result in
a normal QRS duration. Congenital complete heart block
occurs in infants of mothers carrying anti-Ro and anti-La
antibodies; mothers may or may not have clinical symptoms
of lupus . Complete heart block is also a known
complication of surgery for congenital heart disease and
has a significant effect on morbidity and mortality .
Complete heart block is almost always symptomatic and
usually requires dual-chamber pacemaker implantation.
The bundle branches are the downstream limbs of the
bundle of His and allow for nearly synchronous depolariza-
tion of the left and right ventricles, which is important in
maintaining cardiac synchrony. Prolongation of conduction
through the bundle branches results in QRS prolongation and
is known as bundle branch block (BBB). Bundle branch
block can affect the right or left bundle branches (RBBB,
LBBB) and be classified as complete or incomplete, based
upon whether there is QRS prolongation for age. Incomplete
RBBB is commonly seen in pediatric ECGs and is
manifested by an rSR′ pattern in lead V1 and a small S
wave in lead V6; the initial upstroke of the QRS is normal
with a delay in the terminal portion of the QRS complex
(Fig. 5). Right bundle branch block is detected in V1; the
Fig. 5 Incomplete RBBB in a 3-week-old male infant after
tetralogy 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 with
repaired tetralogy of Fallot. Note the similarity of the rSR′ pattern to
the previous figure, with this ECG manifesting QRS prolongation.
Fig. 7 Left bundle branch block. Note the prolonged QRS
duration in the lateral precordial lead V5.
351The pediatric ECG
initial upstroke of the QRS is delayed (Fig. 6) with the
terminal portion of normal duration, whereas LBBB is
typically manifested by QRS prolongation in V6 (Fig. 7).
Bundle branch blocks may be seen in a variety of conditions
and is a frequent finding after surgery for congenital heart
disease, particularly in which there has been a ventriculot-
omy (ie, tetralogy of Fallot) .
4. Normal QRS duration tachycardias
Numerous schemes exist for classifying tachycardias; a
useful and simple way is to categorize them based upon the
QRS duration. In general, tachycardias with a normal QRS
duration for age can be considered as originating superior to
the AV node, whereas tachycardias associated with QRS
prolongation typically originate at locations inferior to the
AV node. This scheme is not perfect but allows for ease
Sinus tachycardia is usually simple to recognize on the
ECG (Fig. 8). For the diagnosis of sinus tachycardia to be
established, a P wave must precede every QRS complex and
the P waves must have a normal axis (discussed previously).
In adults, a heart rate greater than 100 bpm is considered
tachycardia. In children, this rate is age dependent but
general guidelines exist; heart rates greater than 160 bpm in
infants and greater than 140 bpm in children suggest sinus
tachycardia . 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 primary
cardiac disturbance and is often seen in myocarditis or
congestive heart failure. Although a wide range of heart rates
may be seen in sinus tachycardia, the sinus node rarely paces
at heart rates greater than 220 bpm; when greater heart rates
are seen, sinus tachycardia is uncommon. Ectopic atrial
tachycardias can be difficult to distinguish from so-called
supraventricular tachycardias (SVTs; see below), particu-
larly at high rates in which the P wave is “buried” within the
T wave of the preceding QRS complex (Fig. 9).
Atrial flutter and atrial fibrillation are quite rare in
pediatric patients. However, a form of atrial flutter can be
seen after surgery for congenital heart disease, particularly in
patients with Fontan-type operations and atrial switch
procedures for transposition of the great arteries . Atrial
flutter is identified by so-called sawtooth waves representing
the rapid atrial rate with typically normal QRS duration.
Atrial fibrillation demonstrates chaotic irregular atrial
activity with an “irregularly irregular” ventricular rate;
QRS is usually normal in duration (Fig. 10).
Supraventricular tachycardia is one of the most common
arrhythmias encountered in pediatric patients (Fig. 11). The
term supraventricular tachycardia is confusing and does not
imply a single mechanism, however. Supraventricular
tachycardia includes any arrhythmia that requires atrial or
AV nodal tissue for their initiation and propagation, and
includes atrial tachycardias, atrial fibrillation, atrial flutter,
nodal tachycardia, junctional ectopic tachycardia, and others
 For the purposes of this discussion, SVT will be defined
as a paroxysmal tachyarrhythmia manifested by the absence
of P waves and by the presence of normal QRS complexes.
In children, there are 2 common mechanisms of SVT .
Both involve reentry mechanisms. In AV nodal reentry
tachycardia the reentry mechanism involves the AV node,
and in AV reentry tachycardia reentry proceeds via an
accessory pathway near, but not including, the AV node. Two
mechanisms are often indistinguishable via ECG. Preexcita-
tion syndromes are more common in children with AV
reentry tachycardia and are discussed below. The treatment
of SVT involves vagal maneuvers, adenosine, and in rare
cases synchronized cardioversion and is discussed in further
detail elsewhere .
Two additional SVTs occasionally encountered in pedia-
trics include junctional ectopic tachycardia and permanent
junctional reciprocating tachycardia (Fig. 12). Junctional
ectopic tachycardia is a common and frequently hemodyna-
mically deleterious rhythm seen in postoperative patients and
is discussed in a subsequent article. Permanent junctional
reciprocating tachycardia is a chronic, incessant form of
tachycardia involving an accessory pathway that presents in
infants and is electrocardiographically manifested by a
Fig. 8 Sinus tachycardia detected on Holter monitoring of a 6-year-old girl with near syncope. The heart rate is regular at 157 bpm.
352 M. O’Connor et al.
prolonged R-P interval . 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 for
age imply a ventricular origin to the arrhythmia. Ventricular
arrhythmias also demonstrate “bizarre” QRS morphologies.
Ventricular arrhythmias are uncommon in children and
usually arise in the setting of severe electrolyte disarray,
ingestion, or rare inherited disorders of cardiac conduction.
Ventricular arrhythmias, however, are poorly tolerated
hemodynamically so prompt recognition and initiation of
therapy are vital.
Premature ventricular contractions (PVCs) are a frequent
finding in children and may be cause for concern in rare
cases (Fig. 13). They are manifested on the ECG by bizarrely
shaped, wide QRS complexes with the associated T wave
usually pointing in the opposite direction of the QRS
complex. A compensatory pause after the PVC will be seen.
Premature ventricular contractions of uniform morphology
are less concerning than those of multiple forms. Ventricular
tachycardia consists of 3 or more successive PVCs at a
regular rate of 120 to 180 bpm (Fig. 14). As in adults, it can
degenerate into ventricular fibrillation, a usually lethal
rhythm unless promptly treated. Several special conditions
associated with ventricular tachycardia in children should be
Fig. 10 Atrial flutter in a neonate without structural congenital heart disease. Note the rapid ventricular rate and distinctive flutter waves
seen best in leads aVR and aVF.
Fig. 9 Ectopic atrial tachycardia captured on Holter monitoring of a young girl. Note how the P waves are difficult to separate from the QRS
complex owing to the high heart rate.
353The pediatric ECG
mentioned. The Brugada syndrome is a rare, autosomal
dominant, and frequently lethal disorder associated with
bouts of ventricular tachycardia and sudden death. A peculiar
“saddle-form” ST-segment elevation in the right precordial
leads with a family history suggests the diagnosis .
Arrhythmogenic right ventricular dysplasia is another rare
inherited disorder causing ventricular tachycardia and
sudden death in affected individuals due to the replacement
Fig. 12 Narrow complex tachycardia in an 8-month-old infant presenting with feeding difficulties, poor weight gain, and cardiomyopathy.
Electrophysiologic study revealed the diagnosis of permanent junctional reciprocating tachycardia.
Fig. 11 Supraventricular tachycardia in a 10-year-old boy with palpitations and a rapid heart rate. Note the regular rate, narrow QRS
complex, and absence of P waves. The tachycardia resolved with intravenous adenosine. Final diagnosis was orthodromic reciprocating
tachycardia due to an accessory pathway.
354 M. O’Connor et al.
of right ventricular myocardium with fatty and fibrous tissue.
Patients with this disorder typically present after puberty
with ventricular tachycardia, and the interval ECG is notable
for a persistent juvenile pattern of T-wave inversion and a
widened QRS complex in right precordial leads.
6. Ventricular preexcitation syndromes
The term preexcitation refers to ventricular depolarization
that is earlier than expected. Preexcitation can occur via
either a reentry pathway or an accessory pathway . In
either case, the potential for sustained and dangerous
tachycardia exists because the AV node no longer “protects”
the ventricles from excessively high atrial rates. The
electrocardiographic appearance of preexcitation (Fig. 15)
consists of (a) normal P-wave morphology and axis, (b)
shortened PR interval, (c) prolonged QRS complex with
initial “slurring” (delta wave), and (d) Q waves and T-wave
abnormalities in what is termed a pseudoinfarction pattern.
The most common syndrome associated with preexcitation
in children and adults is the Wolff-Parkinson-White (WPW)
syndrome. In patients with WPW, the most commonly
encountered arrhythmia is a paroxysmal reentry SVT.
Detection of the “WPW pattern” (ie, delta wave with a
Fig. 14 Unprovoked ventricular tachycardia from Holter monitoring in a 13-year-old adolescent girl with syncope.
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
prolonged QRS complex) in an asymptomatic child warrants
cardiology referral, although the actual risk of sudden death
in this population is likely quite low .
7. Tachycardias associated with a prolonged
Evaluation of the QT interval is an essential aspect of
ECG interpretation. Norms for the corrected QT interval
have been published and were discussed in the previous
article of this series. Prolongation of the QT interval is often
asymptomatic but puts the patient at risk of ventricular
arrhythmias, the most common of which is torsades de
pointes. Torsades de pointes is a form of polymorphic
ventricular tachycardia that has the ECG appearance of
“twisting along a string.” Prolongation of the QT interval
can be due to a multitude of factors, congenital and
acquired. QT prolongation is associated with hypokalemia
and hypocalcemia; it is also seen with administration of
antiarrhythmic agents. Many medications are associated
Fig. 16 Prolonged QT interval in an 18-year-old adolescent girl with familial long QT syndrome and a history of cardiac arrest. The QT
interval calculated by Bazett's formula is 506 milliseconds.
Fig. 15 Delta waves seen in a child with WPW syndrome who presented with SVT; preexcitation did not manifest until the tachycardia
356 M. O’Connor et al.
with QT prolongation as well, particularly antibiotics and
Congenital forms of the long QT syndrome warrant
discussion in pediatric patients. Congenital long QT
syndrome is a cause of pediatric sudden death and has
been associated with sudden death during sleep, exercise,
and perhaps a small subset of infants dying of sudden infant
death syndrome . The 2 most common inherited long QT
syndromes are known eponymously as the Romano-Ward
and Jervell/Lange-Nielsen syndromes and are caused by
known mutations in cardiac ion channels. Congenital long
QT syndrome is a common cause of sudden death
attributable to cardiac causes in children; in an international
registry of long QT patients, 8% died suddenly during 5 years
of follow-up . Certainly, identification of a prolonged QT
interval in a pediatric patient warrants pediatric cardiology
referral and close follow-up (Fig. 16).
Children frequently present to EDs after ingestion of
medications or other toxins, unintentionally or otherwise.
Obtaining an ECG is an important aspect of evaluating these
patients. A number of agents cause QRS prolongation,
mainly via blockade of the sodium channels responsible for
depolarization during phase 0 of the myocardial action
potential. Examples of such agents include tricyclic
antidepressants, diphenhydramine, propanolol, hydroxy-
chloroquine, and many antiarrhythmic agents . QRS
prolongation in the setting of sodium channel blockade,
when severe, may lead to asystole unless therapy with saline
or sodium bicarbonate is administered.
Tricyclic antidepressant ingestion warrants special
attention owing to the multitude of effects on the ECG
. The ECG presentation of such toxicity is dependent
on the specific medication ingested as well as the ingested
dose. 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 can
lead to tachycardia, QRS prolongation, and QT prolonga-
tion (Fig. 17).
β-Blockers and calcium-channel blockers are commonly
used medications in adults that not infrequently are
unintentionally ingested by children. β-Blockers are phar-
macologically heterogeneous with each agent exerting
single or multiple effects at β1, β2, and α1 receptors. Some
β-blockers contain sodium-channel blocking ability and may
prolong the QRS interval. Sotalol, a class III antiarrhythmic
agent, contains potassium channel blocking ability and can
cause QT interval prolongation . β1 Receptors, however,
located in the myocardium, are largely responsible for the
cardiovascular sequelae of β-blocker overdose. Electrocar-
diogram manifestations of ingestion generally include
bradycardia, various grades of AV block, and QRS complex
Calcium channel blockers cause predictable but non-
specific changes in the ECG. Common changes include
hypotension, bradycardia, and AV blocks . Because
many current formulations of calcium channel blockers are
of the extended-release variety, symptoms may be delayed
for up to several hours postingestion . Another
consideration in evaluating calcium channel overdose is the
cardioselectivity of the agent. Older agents such as nifedipine
may exert a predominantly vascular effect at lower doses,
resulting in hypotension with reflex bradycardia. Newer
Fig. 17 Sinus tachycardia with widened QRS complex, deep S wave in lead I, and prominent R wave in lead aVr. This ECG was recorded in
a lethargic adolescent with tricyclic antidepressant ingestion.
357The pediatric ECG
agents such as verapamil or diltiazem may result in
bradycardia and conduction disturbances without hypoten-
sion. At sufficient doses, however, selectivity is lost.
In summary, arrhythmias in otherwise healthy children are
relatively uncommon in the pediatric population but prompt
recognition will prevent excess morbidity and mortality. The
incidence of arrhythmias in patients with a history of
congenital heart disease is markedly higher and the ECG
manifestations of such arrhythmias in this patient population
will be described in the next article of this series.
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