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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.
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doi:10.1016/j.cupe.2004.02.008
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230 C. Mehta, R. Dhillon
(above the iso-electric line) and vice versa. A and the experienced interpreter will be drawn to
greater myocardial depolarisation (for example, specific abnormalities. Indeed, at the end of this
resulting from greater myocardial mass) will result article, we present some short cuts to commonly
in a larger deflection (higher voltage).1,2 From this encountered paediatric ECG abnormalities. If the
basic starting point, much can be logically deduced reader has a method that is quick, thorough and
from an individual’s ECG regarding their unique effective, they should continue to use it. If not, the
cardiac structure and function. Therefore the ECGs following framework is suggested for reading an
of children are different from those of adults. ECG:
Furthermore, changes in cardiac physiology with
growth are reflected in changes in the ECG. An 1. Rate
essential starting point, then, is to note the 2. Rhythm
patient’s age. Background clinical information is 3. Axis
of relevance, especially concurrent medication, 4. P waves
electrolyte imbalance and, importantly, the reason 5. QRS complexes
for the ECG being performed in the first place. 6. T waves and ST segments
Not surprisingly, the newborn ECG differs most 7. Intervals (PR, QT)
from that of an adult, and is subject to the greatest
rate of change with growth. To understand why, we There will be some overlap between these
need to understand foetal cardiac physiology, its stages. For example, it is difficult (if not impos-
transition at birth, and the effects of maturation sible) to interpret rhythm without noticing P-wave
towards the adult state. In foetal life, pulmonary morphology.
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 Rate
the term newborn has thicker walls than the left.
There is a reversal of vascular resistances after Conventionally, the ECG paper is set to run at
birth, with a fall in pulmonary vascular resistance 25 mm/s. Hence 1500 mm are covered in 1 min.
and increased systemic vascular resistance. Other Therefore, heart rate (in beats per minute,
important influences of ageing are decreasing heart bpm) ¼ 1500/RR interval (equivalent to the dura-
rate, increasing chest wall thickness and changing tion of a single beat) in millimetres. Bradycardia or
disease processes. These factors mean that, com- tachycardia is defined by a heart rate lower or
pared to adults, normal ECGs in babies and children higher, respectively, than the range of normal for
have: age (Fig. 1), i.e.125 bpm.
* right ventricular dominance, gradually changing
to left ventricular dominance with increasing
age; Rhythm
* large ventricular voltages, particularly in the
mid-precordial leads; Normal sinus rhythm originates from the sinoatrial
* rightward (more positive) frontal QRS axes; node, giving a P wave for every QRS complex, with
* faster rates with correspondingly shorter dura- a uniform PR interval and normal P-wave axis. If the
tions (P waves and QRS complexes) and intervals P waves are inverted in leads I or aVF it suggests
(PR and QT). that the rhythm is not originating at the sinoatrial
node (e.g. junctional rhythm with retrograde
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).
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.
q waves
Figure 9 Lead II in a patient with right atrial enlarge-
The q wave (note: ‘q’ to denote normal, as opposed
ment.
to pathological Q waves) represents septal depo-
larisation and is normally present in all the leads
facing the interventricular septum from the left (I,
duces characteristic changes. Tall, narrow and II, III, aVL and aVF). It is almost always present in
spiked P waves taller than 3 mm in any lead are V5 and V6. Except in the newborn, the q wave is
seen in atrial septal defect, Ebstein’s anomaly of absent in V4R and V1. The amplitude should be less
the tricuspid valve, tricuspid atresia and cor than 6 mm in leads aVF and V5, less than 5 mm in
pulmonale. These abnormal waves are due to right lead V6, and not more than 25% of the amplitude of
atrial hypertrophy and/or dilatation and are most the associated R wave in any lead. The duration
obvious in standard lead II and leads V4R and V1. does not normally exceed 0.03 s. Pathological Q
Similar appearances are sometimes seen in thyr- waves may be seen with ventricular hypertrophy
otoxicosis (Fig. 9). (right or left), left bundle branch block, or after
Widened P waves, commonly bifid with duration myocardial infarction. In congenitally corrected
greater than 0.10 s (0.08 s in infants), indicate transposition of the great arteries, the septum is
left atrial enlargement. They are seen in severe depolarised from right to left, resulting in q waves
mitral stenosis, large ventricular septal defects in the right precordial leads and their absence from
and with communications between the aorta the left precordial leads (Fig. 10). In conditions
and pulmonary circulation (e.g. patent arterial with a single functional ventricle (e.g. hypoplastic
duct). Flattened P waves may be found in hyperka- left heart syndrome) there may be no q waves in
laemia. the precordial leads.
RS progression
QRS complexes
In adults and children over 3 years of age there is
Duration smooth progression through the precordial leads,
with a dominant S wave in V4R and V1, comparable
The normal duration increases with age (ranging R and S voltages in V2 and V3 and dominant R waves
from 0.07 s in infants up to 0.12 s in adults). in V4–V6. In the neonatal period there may be a
Prolongation occurs with ventricular conduction complete reversal of this progression, with a
disturbances such as intraventricular block, bundle dominant R wave in the right precordial leads and
branch block and Wolff–Parkinson–White (WPW) a dominant S wave in V5 and V6. Typically, between
syndrome, ventricular rhythm disturbances, hyper- these ages there is a dominant R wave in leads V1
kalaemia, and artificial pacemaker. and V6. Abnormal RS progression may result from
ventricular hypertrophy, ventricular conduction
disturbances, functionally single ventricle or myo-
Amplitude cardial infarction.
Abnormally large R- and S-wave amplitudes (above
normal for age range) usually indicate right or R/S ratio
left ventricular hypertrophy, with tall R waves
in those leads directly ‘viewing’ the respective In normal infants this ratio is large in the right
ventricle and deep S waves in the inverse leads. precordial leads and small in the left precordial
For example, in left ventricular hypertrophy leads. This pattern is reversed in adults. In common
there are tall R waves in leads V5 and V6, with with abnormally large R and S voltages, abnormal
deep S waves in lead V1 (Fig. 8). These changes R/S ratios may be seen in ventricular hypertrophy
may be seen with ventricular conduction distur- (being greater than normal in the leads viewing the
bances (see above). Low voltages (limb lead respective ventricle, and lower than normal in the
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234 C. Mehta, R. Dhillon
ST segments
IntervalsFPR and QT
PR interval
Figure 10 Precordial leads in congenitally corrected
transposition of the great arteries. Note the absence of q Age and heart rate both affect the PR interval. It is
waves in the left precordial leads. 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
opposing leads) and ventricular conduction distur- adult upper limit of normal is 0.20 s. The causes of a
bances. 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
T waves and ST segments be produced by some forms of second-degree heart
block (Wenkebach phenomenon) and complete
T waves heart block (Fig. 11).
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.
so that important abnormalities are not missed. It is 2. Davignon A. Normal ECG standards for infants and children.
worth reiterating that every ECG must be inter- Ped Cardiol 1979;1:123–52.
preted in the light of clinical information about the
patient.
Further reading
Acknowledgements Garson A. The electrocardiogram in infants and children:
a systematic approach. Philadelphia: Lea and Febiger,
1983.
The authors would like to thank Mrs. Anne Pritchard Garson Jr A, Bricker JT, Mc Namara DG. The science and practice
and Mr. John Stickley for their help with collating of pediatric cardiology, vol. 2. London: Lea and Febiger: 1990
the example ECGs. p. 713–67.
Guntheroth WG. Pediatric electrocardiography. Philadelphia: W
B Saunders; 1965.
Liebman J, Plonsey R, Yoram R. Paediatric and fun-
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