ARTICLE IN PRESS

Current Paediatrics (2004) 14, 229–236

www.elsevierhealth.com/journals/cuoe

Understanding paediatric ECGs

Chetan Mehta, Rami Dhillon*

Department of Cardiology, Birmingham Children’s Hospital, Steelhouse Lane, Birmingham B4 6NH, UK

KEYWORDS Summary The ability to interpret the paediatric electrocardiogram (ECG) correctly
Electrocardiogram; is a skill of value to all doctors who treat children, whether acutely or electively.
Diagnosis Furthermore, basic ECG interpretation is a common component of paediatric
postgraduate examinations. In this article we have aimed to arm the reader with the
essential principles of paediatric ECG interpretation, highlighting age-specific
variation. As with any other area of medicine, practice makes perfect. The reader
would do well to inspect a number of normal and abnormal ECGs across the
paediatric age range, keeping in mind the clinical background against which the
investigation was performed. A comprehensive assessment of the paediatric ECG can
then be made by cross-referencing ECG observations against the framework
presented herein.
& 2004 Elsevier Ltd. All rights reserved.

Practice points them worthwhile during routine assessment

(see main article for details):
* Superior QRS axisFdominant S wave in

* The ECG is best assessed in a systematic lead aVF

* Right ventricular hypertrophyFupright T
fashion. Although the method suggested in
this article is quick and thorough, there waves in lead V1 between 7 days and 10
may be equally effective alternatives years of age
* Increased left ventricular forcesFpara-
* Consideration of the clinical background
against which the ECG was performed is meters vary with age
* Increased left or right atrial forcesFre-
essential, especially the age of the child,
as there is considerable age-related normal spectively, broad or tall P waves
variation in the ECG
* Traditionally, ECG interpretation begins
with an assessment of rate, rhythm and
QRS axis Introduction

The electrocardiogram (ECG) is an investigation

While ECG interpretation should be thor-
ough, the following abnormalities are impor-
tant and encountered sufficiently often in
paediatric practice to make a rapid scan for
*Corresponding author. Tel.: þ 44-121-333-9444; fax: þ 44-
121-333-9441.
E-mail address: rami.dhillon@bch.nhs.uk (R. Dhillon).
which merges principles of physics with those of
biology, and has resulted in a relatively new
science: electrophysiology. For those less inclined
towards physics than biology, perhaps the most
important physical principle in understanding the
ECG is that myocardial depolarisation towards an
ECG electrode produces a positive deflection

0957-5839/$ - see front matter & 2004 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cupe.2004.02.008
 ARTICLE IN PRESS
230
(above the iso-electric line) and vice versa. A
greater myocardial depolarisation (for example,
resulting from greater myocardial mass) will result
in a larger deflection (higher voltage).1,2 From this
basic starting point, much can be logically deduced
from an individual’s ECG regarding their unique
cardiac structure and function. Therefore the ECGs
of children are different from those of adults.
Furthermore, changes in cardiac physiology with
growth are reflected in changes in the ECG. An
essential starting point, then, is to note the
patient’s age. Background clinical information is
of relevance, especially concurrent medication,
electrolyte imbalance and, importantly, the reason
for the ECG being performed in the first place.
Not surprisingly, the newborn ECG differs most
from that of an adult, and is subject to the greatest
rate of change with growth. To understand why, we
need to understand foetal cardiac physiology, its
transition at birth, and the effects of maturation
towards the adult state. In foetal life, pulmonary
vascular resistance is high (fluid-filled lungs not
participating in gas exchange), with low systemic
vascular resistance by virtue of the placental
circulation. As a result, the right ventricle (RV) of
the term newborn has thicker walls than the left.
There is a reversal of vascular resistances after
birth, with a fall in pulmonary vascular resistance
and increased systemic vascular resistance. Other
important influences of ageing are decreasing heart
rate, increasing chest wall thickness and changing
disease processes. These factors mean that, com-
pared to adults, normal ECGs in babies and children
have:
* right ventricular dominance, gradually changing
to left ventricular dominance with increasing
age;
* large ventricular voltages, particularly in the
mid-precordial leads;
* rightward (more positive) frontal QRS axes;
* faster rates with correspondingly shorter dura-
tions (P waves and QRS complexes) and intervals
(PR and QT).
Although the range of normal varies considerably
at different ages, readers will be encouraged to
know that tables of normal values are readily
available.2 Even career paediatric cardiologists
need to refer to these from time to time! There is
no universally accepted order in which to interpret
a paediatric ECG, just as there is no rigid order in
which to examine a toddler. However, most
clinicians favour beginning with the ‘rate, rhythm,
axis’ approach. Inevitably, in keeping with other
areas of medicine, pattern recognition develops,
C. Mehta, R. Dhillon
and the experienced interpreter will be drawn to
specific abnormalities. Indeed, at the end of this
article, we present some short cuts to commonly
encountered paediatric ECG abnormalities. If the
reader has a method that is quick, thorough and
effective, they should continue to use it. If not, the
following framework is suggested for reading an
ECG:
1. Rate
2. Rhythm
3. Axis
4. P waves
5. QRS complexes
6. T waves and ST segments
7. Intervals (PR, QT)
There will be some overlap between these
stages. For example, it is difficult (if not impos-
sible) to interpret rhythm without noticing P-wave
morphology.
Rate
Conventionally, the ECG paper is set to run at
25 mm/s. Hence 1500 mm are covered in 1 min.
Therefore, heart rate (in beats per minute,
bpm) ¼ 1500/RR interval (equivalent to the dura-
tion of a single beat) in millimetres. Bradycardia or
tachycardia is defined by a heart rate lower or
higher, respectively, than the range of normal for
age (Fig. 1), i.e.125 bpm.
Rhythm
Normal sinus rhythm originates from the sinoatrial
node, giving a P wave for every QRS complex, with
a uniform PR interval and normal P-wave axis. If the
P waves are inverted in leads I or aVF it suggests
that the rhythm is not originating at the sinoatrial
node (e.g. junctional rhythm with retrograde
Figure 1 ECG trace of a normal 5-month-old child.
 ARTICLE IN PRESS
Paediatric ECG 231

conduction, ectopic atrial rhythm). Tachycardias or situs inversus), the P wave may be inverted in
are usefully classified into those with normal lead I.
(p0.08 s) or broad duration QRS complexes
(40.08 s). Normal complex tachycardias are usual-
QRS axis
ly sinus tachycardia or ‘supraventricular tachycar-
dia’ (Fig. 2), whilst those with broad complexes
The frontal QRS axis is determined graphically using
should be regarded as ventricular tachycardia until
limb leads I and aVF, which ‘view’ the heart at right
proven otherwise, particularly in the presence of
angles to each other, as shown in Fig. 5. The net RS
haemodynamic compromise. A tachycardia with
deflection is determined for each lead and plotted
wide QRS complexes and absent or dissociated P
on the respective axis. The graphical coordinate
waves is virtually diagnostic of ventricular tachy-
thus generated is joined to the origin, creating an
cardia (Fig. 3). Bradycardias may represent sinus
angle against the zero axis. This angle (y) is the
node dysfunction (sinus node disease or depression
by extrinsic influences), or defects of atrioventri-
cular conduction (heart block of first, second or
third degree) (Fig. 4).

Axis Figure 4 First degree heart block with PR interval 0.20 s

in lead II.
P-wave axis

P waves are normally upright in leads I and aVF at

all ages, with a frontal axis of 0 to þ 901 with a
normal position of the atria and sinus rhythm. With
atrial inversion (mirror image atrial arrangement,

Figure 2 Lead II showing narrow complex (supraven- Figure 5 Calculating the frontal QRS axis (y) using limb
tricular) tachycardia in a newborn. leads I and aVF.

Figure 3 Sinus rhythm followed by broad complex (ventricular) tachycardia.

 ARTICLE IN PRESS
232 C. Mehta, R. Dhillon

Figure 7 Upright T waves in lead V1 suggestive of right

ventricular hypertrophy in a 5-year-old child with
untreated multiple ventricular septal defects.

Figure 6 Left superior axis in an infant with atrioven-

tricular septal defect (leads I and aVF).

mean frontal plane QRS axis (Fig. 5). At birth the

mean QRS axis is þ 1251 (range þ 30 to þ 1801).
Thereafter the axis moves leftward, reaching the
adult mean value of þ 501 after 3 years of age
(adult range 30 to þ 901). The 6-week-old patient
whose ECG is shown in Fig. 6 has a complete
atrioventricular septal defect. Using the above
method we can see the net RS deflection (R
amplitude S amplitude) is positive 5 mm in lead
I and negative 10 mm in lead aVF. Plotting this on
the graph reveals left axis deviation, with a
‘superior’ frontal axis of 601.
The horizontal QRS axis is also useful, though
less widely applied, and can be similarly assessed
using the precordial leads. For this purpose, leads
V2 and V6 are perpendicular in their view of Figure 8 Left precordial leads showing severe left
ventricular hypertrophy with strain at 1/4th standardisa-
the heart.
tion.

T-wave axis include myocarditis, pericarditis and myocardial

The T-wave axis is assessed in the horizontal plane
using the precordial leads. The axis is anterior at
birth with upright T waves in the anterior precordial
leads, including V4R and V1. Beyond 7 days of age
the T waves invert in these leads and remain
inverted until about 10 years of age. Persistence of
upright T waves in V4R and V1 in this age group
suggests right ventricular hypertrophy (Fig. 7).
Inverted T waves in the left-sided precordial
leads are abnormal and can be seen with severe left
ventricular hypertrophy (Fig. 8). Other causes
infarction.
P waves
The P wave is generated by atrial depolarisation
and gives important information about the rhythm
(see P-wave axis, above) and atrial enlargement.
The right atrium is depolarised first, so that the
early portion of the P wave is generated by the
right atrium and the latter portion by the left
atrium. Enlargement of the atria therefore pro-
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Paediatric ECG
Figure 9 Lead II in a patient with right atrial enlarge-
ment.
duces characteristic changes. Tall, narrow and
spiked P waves taller than 3 mm in any lead are
seen in atrial septal defect, Ebstein’s anomaly of
the tricuspid valve, tricuspid atresia and cor
pulmonale. These abnormal waves are due to right
atrial hypertrophy and/or dilatation and are most
obvious in standard lead II and leads V4R and V1.
Similar appearances are sometimes seen in thyr-
otoxicosis (Fig. 9).
Widened P waves, commonly bifid with duration
greater than 0.10 s (0.08 s in infants), indicate
left atrial enlargement. They are seen in severe
mitral stenosis, large ventricular septal defects
and with communications between the aorta
and pulmonary circulation (e.g. patent arterial
duct). Flattened P waves may be found in hyperka-
laemia.
QRS complexes
Duration
The normal duration increases with age (ranging
from 0.07 s in infants up to 0.12 s in adults).
Prolongation occurs with ventricular conduction
disturbances such as intraventricular block, bundle
branch block and Wolff–Parkinson–White (WPW)
syndrome, ventricular rhythm disturbances, hyper-
kalaemia, and artificial pacemaker.
Amplitude
Abnormally large R- and S-wave amplitudes (above
normal for age range) usually indicate right or
left ventricular hypertrophy, with tall R waves
in those leads directly ‘viewing’ the respective
ventricle and deep S waves in the inverse leads.
For example, in left ventricular hypertrophy
there are tall R waves in leads V5 and V6, with
deep S waves in lead V1 (Fig. 8). These changes
may be seen with ventricular conduction distur-
bances (see above). Low voltages (limb lead
233
deflections of less than 5 mm) occur with pericar-
dial effusion, chronic constrictive pericarditis
and hypothyroidism, but may be normal in the
newborn.
q waves
The q wave (note: ‘q’ to denote normal, as opposed
to pathological Q waves) represents septal depo-
larisation and is normally present in all the leads
facing the interventricular septum from the left (I,
II, III, aVL and aVF). It is almost always present in
V5 and V6. Except in the newborn, the q wave is
absent in V4R and V1. The amplitude should be less
than 6 mm in leads aVF and V5, less than 5 mm in
lead V6, and not more than 25% of the amplitude of
the associated R wave in any lead. The duration
does not normally exceed 0.03 s. Pathological Q
waves may be seen with ventricular hypertrophy
(right or left), left bundle branch block, or after
myocardial infarction. In congenitally corrected
transposition of the great arteries, the septum is
depolarised from right to left, resulting in q waves
in the right precordial leads and their absence from
the left precordial leads (Fig. 10). In conditions
with a single functional ventricle (e.g. hypoplastic
left heart syndrome) there may be no q waves in
the precordial leads.
RS progression
In adults and children over 3 years of age there is
smooth progression through the precordial leads,
with a dominant S wave in V4R and V1, comparable
R and S voltages in V2 and V3 and dominant R waves
in V4–V6. In the neonatal period there may be a
complete reversal of this progression, with a
dominant R wave in the right precordial leads and
a dominant S wave in V5 and V6. Typically, between
these ages there is a dominant R wave in leads V1
and V6. Abnormal RS progression may result from
ventricular hypertrophy, ventricular conduction
disturbances, functionally single ventricle or myo-
cardial infarction.
R/S ratio
In normal infants this ratio is large in the right
precordial leads and small in the left precordial
leads. This pattern is reversed in adults. In common
with abnormally large R and S voltages, abnormal
R/S ratios may be seen in ventricular hypertrophy
(being greater than normal in the leads viewing the
respective ventricle, and lower than normal in the
 ARTICLE IN PRESS
234
Figure 10 Precordial leads in congenitally corrected
transposition of the great arteries. Note the absence of q
waves in the left precordial leads.
opposing leads) and ventricular conduction distur-
bances.
T waves and ST segments
T waves
These waves represent ventricular repolarisation.
The axis is discussed above. They may be of
abnormal amplitude in many pathological pro-
cesses, including ventricular hypertrophy, cardio-
myopathy, myocardial infarction and electrolyte
(particularly potassium) disturbance. In hyperka-
laemia the T waves are commonly of high voltage
and are tent-shaped. In any form of carditis simple
inversion of the T wave may occur. Hypothyroidism
C. Mehta, R. Dhillon
may produce flat or inverted T waves in association
with generalised low voltages.
ST segments
A shift (elevation/depression) of up to 1 mm may be
normal in limb leads, whereas up to 2 mm is normal
in left precordial leads attributed to early repolar-
isation of the heart. In generalised pericarditis,
superficial epicardial involvement may cause ST
segment elevation followed by abnormal T wave
inversion as healing progresses.
Administration of digoxin is associated with
sagging of the ST segment and abnormal inversion
of the T wave. Depression of the ST segment may
also occur in any condition that produces myocar-
dial damage, for example aberrant origin of the left
coronary artery from the pulmonary artery (ALCA-
PA), glycogen storage disease affecting the heart,
myocardial tumours, and mucopolysaccharidoses.
In ALCAPA changes may be indistinguishable from
those of acute myocardial infarction in adults.
Similar changes may occur in patients with other
rare abnormalities of the coronary arteries and
with cardiomyopathy without anatomic abnormal-
ities of the coronary arteries.
IntervalsFPR and QT
PR interval
Age and heart rate both affect the PR interval. It is
measured from the start of the P wave to the start
of the QRS complex. The lower limits of normal
vary from 0.08 s in infants up to 0.12 s in adults. The
adult upper limit of normal is 0.20 s. The causes of a
short PR interval include WPW syndrome, junc-
tional rhythm and glycogen storage disease. Causes
of first-degree heart block (long PR) include
inflammatory processes, electrolyte disturbances,
drugs and hypothermia. A variable PR interval can
be produced by some forms of second-degree heart
block (Wenkebach phenomenon) and complete
heart block (Fig. 11).
QT interval
Prolongation of the QT interval is associated with
ventricular arrhythmias (notably Torsade de
pointes), syncope and sudden death. The QT
interval represents both depolarisation and repo-
larisation of the ventricles. It is measured from the
onset of the QRS complex to the end of the T wave
(Fig. 12). The longest interval in any lead should be
 ARTICLE IN PRESS
Paediatric ECG
Figure 11 Rhythm strip in lead II showing complete heart block with an atrial rate of 75 bpm and ventricular rate of
45 bpm. The P waves (arrowed) are independent of the QRS complexes.
Figure 12 Prolonged QT interval.
used. The QT interval varies with heart rate, but
not with age except in infancy. Conventionally,
therefore, the QT interval is expressed in relation
to the heart rate, as the corrected QT interval
(QTc), using Bazett’s formula (with all durations in
seconds):
QTc ¼ QT=OR  R interval:
It is abnormal if 40.44 s (except in the first 6
months of life, when it may be normal up to 0.45 s).
The example in Fig. 12 shows a prolonged QTc, as
measured from lead V5, of 0.6/O1.12 ¼ 0.57 s.
Common patterns of abnormality
Abnormalities of QRS axis
* Superior axis
* in an acyanotic child suspect atrioventricular
septal defect;
* in a cyanotic child suspect tricuspid atresia.
* Abnormal right or left axis deviation (be aware
of wide variation of normal) should arouse
suspicion of
* chamber hypertrophy;
* univentricular physiology.
Chamber hypertrophy
Atrial enlargement
* Peaked P waves (P pulmonale) are seen in right
atrial enlargement: suspect heart or lung dis-
ease.
* Bifid, wide P waves (P mitrale) are seen in left
atrial enlargement: left-to-right shunts or mitral
stenosis.
235
Right ventricular hypertrophy
In infants with right ventricular hypertrophy the
following changes may occur singly or in combination:
* A qR pattern in the right ventricular leads.
* A positive T wave in leads V4R and V1 after the
first 7 days of life.
* A monophasic R wave in V4R and/or V1.
* rsR’ in the right precordial leads often with a tall
secondary R wave.
* Age-related voltage increase in V4R and V1 for R
and/or V5-6 for S.
* Marked right axis deviation (age related).
* Complete reversal of the normal adult precordial
RS pattern.
* Right atrial enlargement.
Left ventricular hypertrophy
* Depression of the ST segments and inversion of T
waves in the left precordial leads (V5, V6)
indicates a left ventricular strain pattern. These
findings suggest the presence of a severe lesion
and significant myocardial abnormality.
* Increase in magnitude of initial forces to the
right (deep Q in left precordial leads).
* Voltage increase in V4R and V1 for S wave and/or
V6 for R wave.
* It is important to emphasise that evaluation of
ventricular hypertrophy should not be based on
voltage criteria alone.
Conclusion
Very often ECGs are performed in children with
suspected congenital heart defects or arrhythmia.
In children with suspected arrhythmia, it is im-
portant to record the ECG not only during arrhyth-
mia but also in normal sinus rhythm. The
importance of ECG documentation during treat-
ment of arrhythmia (e.g. intravenous adenosine)
cannot be stressed enough.
The above scheme is not the only way to
interpret the ECG. However, a process should be
developed which is quick and simple, but complete,
 ARTICLE IN PRESS
236
so that important abnormalities are not missed. It is
worth reiterating that every ECG must be inter-
preted in the light of clinical information about the
patient.
Acknowledgements
The authors would like to thank Mrs. Anne Pritchard
and Mr. John Stickley for their help with collating
the example ECGs.
References
1. Hampton JR. The ECG made easy, 4th ed. London: Churchill
Livingstone; 1992.
C. Mehta, R. Dhillon
2. Davignon A. Normal ECG standards for infants and children.
Ped Cardiol 1979;1:123–52.
Further reading
Garson A. The electrocardiogram in infants and children:
a systematic approach. Philadelphia: Lea and Febiger,
1983.
Garson Jr A, Bricker JT, Mc Namara DG. The science and practice
of pediatric cardiology, vol. 2. London: Lea and Febiger: 1990
p. 713–67.
Guntheroth WG. Pediatric electrocardiography. Philadelphia: W
B Saunders; 1965.
Liebman J, Plonsey R, Yoram R. Paediatric and fun-
damental electrocardiography. Boston: Martinis Nijhoff;
1987.
Park MK, Guntheroth WG. How to read pediatric ECGs, 3rd ed.
Chicago: Year Book Medical Publishers; 1992.