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Practical Approach to Pediatric Electrocardiogram

BRJ Kannan MD (Ped) DM (Card) DNB (Card)

Assistant Professor

Department of Pediatric Cardiology

Amrita Institute of Medical Sciences and Research Center, Kochi, Kerala

E mail: kannanbrj@gmail.com
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Electrocardiogram (ECG) is a simple and useful investigation that is often under

utilized. It records changes in the electrical activity of the heart and the information

provided by ECG is not readily obtained by any other method. Apart from ischemia

detection, ECG plays an important role in arrhythmia detection and management. Its role

is somewhat limited in the diagnosis of structural heart disease. However, it does provide

important clues regarding the changes in cardiac chambers and supplements information

required for diagnosis along with clinical examination and chest radiography.

Some of the limitations of pediatric electrocardiography are as follows:

- Age dependent changes occur, therefore, single set of criteria cannot be applied to

children in various age groups

- Absence of specific guidelines for chest lead placement

- ‘Borrowed’ criteria for chamber hypertrophy from adult experience

- Poor sensitivity i.e., a child with large VSD might not have large LV forces

- Complexity of congenital heart diseases with very few lesion specific changes

Nonetheless, ECG has an important role to play and this chapter will address its practical

utility in the diagnosis and management of children with heart diseases.

Basics of recording and interpretation:

While recording ECG in a small child, limb lead electrodes should be placed more

proximally to reduce motion artifacts. The usual ‘12 lead ECG’ is not enough; additional

V3R or V4R leads have to be recorded in children with suspected congenital heart

disease. Standard gain (10mm/mV) is used. If the QRS voltages are very large, then the

gain might be halved.

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The ECG is recorded at a paper speed of 25 mm per second. The time or duration

of a wave is measured in milliseconds or seconds. Each small square represents 40

milliseconds (0.04 seconds). The voltage is measured in small squares or millivolts (mV).

Each small square represents 0.1mV. Intervals should be hand measured, as the

computerized systems are often inaccurate, especially in the neonates. Intervals in

children increase with increasing age, reaching the adult normal values by 7-8 years of

age. The PR interval is measured from the onset of the P wave to the Q wave or R wave

if no Q wave is present. It is often best measured in lead II. The duration of QRS complex

is measured in the lead with an initial Q wave. The QT interval is often best measured in

leads II, V5 and V6 and the longest value should be used. Corrected QT (QTc) is

calculated using Bazett’s formula.

Corrected QT = QT interval / √RR

Rate calculation:
1500
Heart rate =
Number of small squares in a RR interval

For example, if there are 15 small squares between two consecutive R’s, then the heart

rate is 100/min (1500/15).

Axis detection:

Select leads aVF and I. Determine if the net QRS voltage is positive or negative in these

leads. For example, if the R wave height is 10 mm (above the isoelectric line) and S wave

height is 3 mm (below the isoelectric line), then the net QRS voltage is positive (+7). If

the R wave is short and S wave is longer, the net QRS voltage would be negative (Fig 1).

The QRS axis can be located using the following simple rule:
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Lead I Lead Interpretation Comment

aVF
Positive Positive Normal axis Abnormal in neonates and early infancy
Negative Positive Right axis deviation Normal in neonates and in early infancy
Positive Negative Left axis deviation Abnormal at any age
Negative Negative North-west axis Abnormal at any age

Normal variations and related abnormalities:

Many tables of ECG standards for various measurements are available (1,2). However,

the practical utility of these tables is limited. The salient age related changes that one

needs to know are as follows:

1. Normal HR in the neonates vary between 120-230/min, it increases further by

first or second month of life and gradually decreases over the next 6 months.

Resting heart rate is about 120 beats/min at 1 year, 100 at 5 years and reaches

adult values by 15 years (2).

2. Appearance of secondary r waves (r’ or R’) in right chest leads is normal in

neonates.

3. At birth, right axis deviation of mean QRS vector is the rule. The axis becomes

normal by 1 year of age. Hence, normal or leftward QRS axis is abnormal in the

neonatal period and early infancy. Common conditions with leftward axis of QRS

vector are tricuspid atresia and AV canal defects.

4. Dominant R in right precordial leads can persist up to 6 months to 8 years; in the

majority, the R/S ratio in lead V1 becomes less than 1 by 4 years.

5. Q waves are normally seen in leads II, III, aVF, V5 and V6.

o If Q waves are seen in other leads, it is abnormal.

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o Presence of Q wave in inferior leads (II, III and aVF) is due to clockwise

loop of initial QRS vector. This finding is seen in majority of congenital

heart diseases also.

o When Q waves are absent in inferior leads but are seen in Leads I and

aVL, it is due to counterclockwise loop of the initial QRS vector. This is a

feature of tricuspid atresia, AV canal defects and inlet VSD.

o Deep Q waves in lateral leads might point towards underlying anomalous

origin of left coronary artery from pulmonary artery.

6. QT interval is highly variable in the first 3 days of life. If the corrected QT is

more than 0.44 seconds (440 ms), it is abnormal (3).

o Hypokalemia, hypocalcemia, hypothermia, and cerebral injury are

common causes of prolonged QT interval.

o Drug induced QT prolongation has to be ruled out and the drugs

commonly implicated are macrolide antibiotics, trimethoprim, cisapride

etc (Fig 2).

o Consider Long QT syndrome, if clinically relevant. A comprehensive

discussion on congenital long QT syndromes and the management flow

chart is available in the guidelines given by European society of

cardiology (4).

7. T wave in lead V1 can be upright at birth and it inverts by 7 days and typically

remains inverted until 7 years of age.

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o Upright T waves in right precordial leads (V1-V3) between ages 7 days

and 7 years usually indicate right ventricular hypertrophy even if the

voltage criterion is not fulfilled.

8. Atrial and ventricular extra systoles are common and are typically abolished with

exercise. Also, sinus arrhythmia is very common and there could be irregularly

irregular rhythm (Fig 3). The heart rate slows in expiration and speeds up in

inspiration. Some children would present with significant sinus bradycardia. Both

these conditions are due to excessive vagal tone. Exercise consistently increases

the heart rate and the rhythm becomes regular in these children.

9. Sinus pauses as long as 800-1000 ms can be seen especially during feeding, sleep,

defecation or other times of increased vagal tone. At times, periods of junctional

rhythm, i.e. narrow QRS complexes without preceding P waves can be seen.

10. Wandering pacemaker: Change in P wave axis and morphology in different beats

due to the shift of pacemaker from the sinus node to other sites. It is a non-

pathological finding.

11. Early repolarization: Some children especially in the adolescent age group would

show ST segment elevation of 1-4mm with the concavity facing upwards (Fig 3).

They can also have terminal T wave inversion.

12. Premature children, especially those <28 weeks gestation, may not show RV

dominance. Chest leads may show LV dominance and QRS axis can be normal or

leftward even at birth.

Analysis of P wave:
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 P wave amplitude varies very little with age. Unlike QRS axis, P wave axis is

normal (positive in both lead I and aVF) from birth due to sinus nodal origin of

the atrial impulse.

 If the P axis is different, it indicates ectopic atrial rhythm, i.e. the atrial impulse

arises from some other site. Low atrial origin of the rhythm is common in

congenital heart disease where the P waves are typically negative in inferior leads

(II, III and aVF).

 In children with situs inversus, right axis deviation of the P wave is seen (Fig 4).

Right atrial enlargement:

 P wave amplitude is increased to >0.25 mV (2.5 mm) with a relatively normal P

wave duration (‘tall and peaked P waves’). The changes are best visualized in lead

II.

 Tricuspid atresia, pulmonary atresia with intact ventricular septum and severe

pulmonary stenosis are commonly associated with right atrial enlargement.

Left atrial enlargement:

 The changes are best visualized in lead V1 where the terminal negative deflection

is increased (>0.1 mV) and prolonged (>40 ms). Prolonged P wave duration with

increased notching can be seen in lead II due to left atrial enlargement but it is

less specific.

 Mitral atresia and post tricuspid shunts (VSD, PDA, aorto pulmonary window)

show left atrial enlargement.

Analysis of PR segment:
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PR segment reflects the time taken by the depolarization impulse to travel across the

atrium and the atrioventricular node. AV block results in prolongation of the PR interval.

 First degree block: Prolonged AV interval

 Second degree block, Mobitz Type I (Wenkebach type): With each successive

beat, the PR interval lengthens resulting in a ‘dropped’ QRS. This could be a

normal finding and does not usually indicate an adverse prognosis.

 Second degree block, Mobitz Type II: The PR interval is normal or mildly

prolonged but it is constant in successive beats. There is sudden, intermittent loss

of conduction resulting in ‘dropped’ QRS. This is always pathological, carries

high risk to progress to complete AV block.

 Third degree AV block: This is also called as complete heart block (CHB) where

no atrial impulse is conducted to the ventricles. Atrial rate would be higher than

the ventricular rate with complete AV dissociation (Fig 5). If the escape rhythm

originates near the His bundle, the resulting QRS would be narrow. If the escape

focus is lower down, the resultant QRS complex would be broad. Congenital

complete heart block is often not associated with any underlying congenital heart

disease. 2-5% of mothers with autoimmune antibodies have children with CHB

and this condition carries a high mortality risk especially in the first 3 months (7).

CHB can be also seen in children with congenitally corrected transposition of

great arteries and AV canal defects. Acquired CHB can be seen in myocarditis,

digitoxicity, following cardiac surgery and rarely, after interventional procedures

such as catheter closure of the membranous VSD.

Causes of short PR interval:

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Common causes are Wolff Parkinson White syndrome (WPW syndrome), ectopic

atrial pacemaker from the low right atrium, mannosidosis, Fabry’s disease and Pompe’s

disease.

WPW syndrome (Preexcitation):

It is due to premature conduction of atrial impulses to ventricles through

accessory pathways resulting in delta wave and a fusion complex in the ECG (Fig 6). The

preexcitation may be subtle and only detected in the mid precordial leads. The prevalence

in children has been estimated to be 0.15 to 0.3%, higher in those with structural heart

disease (5). Congenital heart diseases with higher prevalence of WPW syndrome are:

Ebstein’s anomaly of tricuspid valve, congenitally corrected transposition of great

arteries, hypertrophic cardiomyopathy and cardiac rhabdomyoma.

WPW syndrome is the commonest cause of paroxysmal supraventricular

tachycardia in children. The incidence of sudden death has been estimated to be as high

as 0.5% and cardiac arrest may be the initial presentation (6). Hence it is very important

to identify this electrical abnormality. Digoxin and Verapamil have to be avoided in this

condition and beta-blocker therapy is the ideal choice.

Analysis of QRS complex:

Bundle branch blocks:

Intraventricular conduction abnormalities due to bundle branch blocks (BBB) are

uncommon in normal children. BBB result in wide QRS duration of >0.14 sec or more.

Right BBB is diagnosed if V1 shows tall wide notched R (rSR’ pattern) and the lateral

oriented leads (lead I, V5 and V6) show notched wide S wave (Fig 7). In left BBB, the
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lateral leads show tall notched R wave and V1 shows wide notched QS or rS complex.

Right BBB is commonly seen following open-heart surgery.

Right ventricular hypertrophy:

 Many congenital heart diseases are associated with right ventricular hypertrophy.

Tall R in V1 (R/S >1), deep S in V6 and upright T wave in right precordial leads

indicate the presence of right ventricular hypertrophy.

 Conditions with pressure overload of right ventricle, e.g. valvar pulmonary

stenosis show small q and tall R pattern or only tall R could be seen (Fig 8)

 Conditions with volume overload of right ventricle, e.g. atrial septal defect show

rSR’ pattern.

Left ventricular hypertrophy:

It produces increased voltages in the left sided leads and manifest as tall R wave

in leads V5, V6 and deep S wave in lead V1 (Fig 9). No definite criteria based on the

voltages are available to diagnose ventricular hypertrophy in children. Another important

clue for the presence of left ventricular hypertrophy is the presence of T wave

abnormalities in leads V5 and V6.

 Tall T waves would indicate underlying volume overloading condition (VSD, PDA)

 ST depression and T inversion in lateral leads could result from pressure overloading

of left ventricle (Aortic stenosis, coarctation of aorta).

 Peculiarly, neonates with coarctation of aorta have ECG features of right ventricular

hypertrophy (and not left ventricular hypertrophy) as the right ventricle receives a

greater proportion of systemic venous return from the SVC and faces the systemic

vascular resistance in the fetal period through the ductus arteriosus.

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 In children with post tricuspid shunts, large amplitude equi-phasic QRS complexes

could be seen in the mid precordial leads suggestive of biventricular hypertrophy

(Katz-Wachtel phenomenon).

Cardiac position related QRS changes:

In levocardia, the major portion of the ventricles is positioned to the left of the

midline with the apex pointing to the left. The chest leads show a progressive change

from a dominant S wave in lead V1 to a dominant R wave in leads V5 and V6. In

children with dextrocardia where the major portion of the ventricles is to the right of

midline, this normal progression is not seen. Instead, there is progressive reduction in the

amplitude of QRS from V2-V6 (Fig 4). In these children, right-sided leads are commonly

taken in the positions corresponding to the left sided leads that would show ‘normal’

progression of QRS complexes. However, further interpretation of the right-sided leads

regarding chamber enlargement is not possible.

Analysis of ST segment:

ST segment elevation is commonly due to early repolarization as mentioned

above. The next common cause is pericarditis. Other causes are: Hyperkalemia,

intracranial hemorrhage, pneumothorax or pneumopericardium. Structural anomalies that

can cause ST segment elevation are anomalous origin of left coronary artery from

pulmonary artery and Kawasaki disease related coronary arteritis. The former more

commonly presents with deep Q waves in leads I, aVL, V5 and V6 with associated T

wave inversion. Brugada syndrome is a genetic disorder associated with a high incidence

of sudden death due to ventricular fibrillation. ECG in this condition shows ST segment

elevation with RBBB pattern in the right precordial leads.

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ST segment depression is seen secondary to pressure over load strain. In right

ventricular strain, ST depression is seen in right precordial leads while it is seen in left

precordial leads in left ventricular strain.

Analysis of T wave:

In children, T wave is inverted in V1-V3 between 7 days to 7 years. At times, T

remains inverted in older children and adolescents (‘persistent juvenile T’). As mentioned

above, upright T wave in V1 would indicate right ventricular hypertrophy even in the

absence of high amplitude R wave.

 T wave inversion in lateral leads represent relative or absolute ischemia and is a

feature of ventricular pressure overload strain, ALCAPA and Kawasaki disease with

coronary involvement.

 Tall T wave is one of the ECG manifestations of hyperkalemia. Other manifestations

of hyperkalemia are disappearance of P wave, broadening of QRS wave, ST segment

disappearance resulting in sine wave.

 In hypokalemia, there is gradual reduction in the amplitude of T wave with eventual

disappearance of T wave while U wave appears.

Some disease specific ECG changes:

Most of the common congenital heart diseases like tetralogy of Fallot, D-

transposition of great arteries, total anomalous pulmonary venous connection, truncus

arteriosus, pulmonary atresia, hypoplastic left heart syndrome show Q waves in inferior

leads (leads II, III and aVF), RVH and right axis deviation of the QRS vector. The ECG

pattern does not help distinguish one condition from the other. However, absence of

above mentioned features point towards some other diagnosis.

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Tricuspid atresia (Fig 10):

Q wave in leads I and aVL

Left axis deviation of QRS

Right atrial enlargement

Dominant LV forces in the chest leads

Common AV canal defect:

Q wave in leads I and aVL

Left axis deviation of QRS

Both right ventricular and left ventricular forces are seen (biventricular

hypertrophy pattern)

Corrected transposition of great arteries:

Normally interventricular septum is depolarized from left to right that results in Q

waves in lateral leads (leads V5 and V6). In this condition, as the ventricles are

inverted, the septal depolarization is also reversed. Hence q waves are absent in

V5 and V6, but can be seen in right precordial leads (V3R, V1).

Ebstein’s anomaly (Fig 11):

Giant P waves, RBBB pattern, low voltage complexes (especially in limb leads)

Look for the presence of delta wave, as WPW syndrome is commonly associated.

The accessory pathway is usually right sided and hence V1 will show deep S

wave.

Pompe’s disease (Fig 12):

This condition produces apparent hypertrophy of the ventricles due to

accumulation of glycogen.
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Short PR interval

Very tall QRS complexes in multiple leads

Dilated cardiomyopathy:

In idiopathic dilated cardiomyopathy, ECG may be normal or show broad QRS

complexes in sick patients. However, in any case of cardiomyopathy, two common

treatable causes that need to be ruled out are ALCAPA and Tachycardiomyopathy. ECG

signs of ALCAPA are ST depression and Q waves in lateral leads (leads V5, V6, I and

aVL) (Fig 13). Persistent high heart rate should make one to suspect the ongoing

tachycardia. Even when the suspicion is small, it is useful to administer adenosine and

record the effect on the rhythm (See chapter on Arrhythmias)

Arrhythmias in children:

In any child presenting with tachycardia, it is important to document the

rhythm with a 12 lead ECG unless the child is hemodynamically compromised. It is

particularly useful to record the effects of administration of medications such as

adenosine because important clues to the underlying arrhythmia are unraveled.

Supraventricular tachycardia (SVT) is much more common than ventricular tachycardia

(VT). QRS complex is narrow and similar to that of sinus rhythm in SVT. If the QRS

complex is different from sinus, VT should be diagnosed even if the QRS is relatively

narrow (4). Any wide QRS tachycardia should be considered as VT until proved

otherwise. (See chapter on arrhythmias)

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References:

1. Davignon A, Rautaharju P, Boisselle E, Soumis F, Megelas M, Choquette A.,

Normal ECG standards for infants and children. Pediatr Cardiol 1979;1:123-52.

2. Goodacre S, McLeod K. ABC of clinical electrocardiography: Pediatric

electrocardiography. BMJ 2002;324:1382-85.

3. Schwartz PJ, Stramba-Badiale M, Segantini A et al. Prolongation of the QT

interval and the sudden infant death syndrome. N Engl J med 1998;338:1709-14.

4. Schwartz PJ, Garson A, Paul T et al. Guidelines for the interpretation of the

neonatal electrocardiogram. European Heart J 2002;23:1329-44.

5. Sorbo MD, Buja GF, Miorelli M et al. The prevalence of the Wolff Parkinson

White syndrome in a population of 116542 young males. G Ital Cardiol

1995;25:681-7.

6. Munger TM, Packer DL, Hammill SC et al. A population study of the natural

history of Wolf Parkinson White syndrome in Olomsted County, Minnesota,

1953-1989. Circulation 1993;87:866-73.

7. Buyon JP, Hiebert R, Copel J et al. Autoimmune associated congenital heart

block: long term outcome of children and immunogenetic study. J am Coll

Cardiol 1998;31:1658-66.
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Legends for figures:

Figure 1:

The four quadrants representing various axes have been shown. The arrow shows a

normal QRS vector. Similarly, by determining the net voltage of P wave, one can locate

the ‘P axis’.

Figure 2:

QT prolongation: The measured QTc was 680 ms with deep inverted T waves in multiple

leads. This was secondary to the administration of Azithromycin.

Figure 3:

There is significant irregularity of the rhythm. However, all QRS complexes are preceded

by P waves with constant PR interval. This is due to sinus arrhythmia. Note the ST

segment elevation with concavity facing upwards due to early repolarization. Both the

findings are normal in children.

Figure 4:

There is right axis deviation of P wave (black arrows) as it is negative in lead I and

positive in lead aVF. This is consistent with atrial situs inversus. The chest leads show

progressive reduction of the QRS size without the normal progression of R wave, which

is suggestive of dextrocardia.
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Figure 5:

Complete heart block: Atrial rate is 90/min and the ventricular rate is 45/min. Arrows

indicate the P waves. Though apparently P wave is seen before each QRS complex, there

is PR interval is not constant suggestive of AV dissociation.

Figure 6:

WPW syndrome: Short PR interval is seen. The slurring of initial portion of R wave

(delta wave) is seen in all leads, especially II, III, aVF, V5 and V6 (black arrows)

Figure 7:

Right bundle branch block: Broad QRS complexes with rsR’ pattern in V1. The ST-T

changes are secondary to the bundle branch block. This is a common finding in children

following open-heart surgery.

Figure 8:

Right ventricular hypertrophy: There is right axis deviation of QRS. Tall R wave, ST

depression and T inversion in leads V1-3 is suggestive of right ventricular hypertrophy

with pressure overload strain

Figure 9:

Left ventricular hypertrophy: Tall QRS complexes in the lateral leads with ST depression

and T inversion due to pressure overload of LV

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Figure 10:

Tricuspid atresia: Left axis deviation of QRS, Q waves in leads I and aVL and absence of

RV forces in right sided leads.

Figure 11:

Ebstein’s anomaly: Tall P waves due to right atrial enlargement. Broad and bizarre QRS

complexes of RBBB morphology typically seen in this condition.

Figure 12:

Pompe’s disease: Very tall QRS complexes in all the leads with relatively short PR

interval

Figure 13:

ALCAPA: Note the deep Q waves in leads I, aVL, V5 and V6. These leads also show ST

depression and T wave inversion.