Professional Documents
Culture Documents
doi:10.1016/j.jemermed.2007.09.039
Selected Topics:
Cardiology Commentary
Figure 1. 12-lead ECG of 3-year-old girl demonstrating normal sinus rhythm at a rate of 112 beats/min and inverted T waves in
leads V1, V2, and V3 normal for patient’s age.
inverted T waves in leads V1, V2, and V3. These findings Examination revealed a well-developed infant in mild
were consistent with a normal juvenile pattern appropriate distress, pulse rate ⬎ 200 beats/min, but otherwise he-
for the patient’s age. A subsequent outpatient echocardio- modynamically stable with a clear chest on auscultation.
gram demonstrated no significant abnormalities. A 12-lead ECG was remarkable for a regular narrow
complex tachycardia at 280 beats/min (Figure 3). The
Case 2 patient was diagnosed with a supraventricular tachycar-
dia (SVT) and subsequently treated with intravenous
An 11-year-boy presented to the ED complaining of chest adenosine, at which point she converted to sinus rhythm.
pain after playing baseball. The patient denied trauma, Case 4
weakness, cough, or fever, but did report transient shortness
of breath. On examination, the patient had normal vital A 6-week-old infant was referred to the ED by her
signs and no remarkable physical findings. An ECG dem- pediatrician for poor feeding and irritability over the past
onstrated a sinus rhythm at 74 beats/min with normal axis week. On examination, the patient was hemodynamically
and inverted T waves in leads V1, V2, and V3 (Figure 2). stable, but was noted to have rales on chest auscultation
These findings were consistent with a juvenile ECG pattern, and a grade 3/6 systolic murmur and higher pitched 2/6
possibly persistent in this pre-adolescent patient. The pa- diastolic murmur on cardiac examination. An ECG was
tient workup in the ED was otherwise unremarkable. notable for an abnormal left ventricular hypertrophy
(LVH) and possible left axis deviation for her age (Fig-
Case 3 ure 4). Her chest radiograph was remarkable for cardio-
megaly and increased pulmonary vascular markings. Af-
An 11-month-old girl was brought to the ED by her ter admission, the patient was ultimately found to have a
caretakers for poor feeding, irritability, and lethargy. ventricular septal defect (VSD) on echocardiogram.
Figure 2. 12-lead ECG of 11-year-old boy demonstrating juvenile ECG pattern with inverted T waves in leads V1, V2, and V3.
Pediatric ECG 423
Figure 3. 12-lead ECG from 11-month-old girl revealing supraventricular tachycardia with regular narrow QRS complex
tachycardia at a rate of 280 beats/min.
Figure 4. 12-lead ECG from a 6-week-old infant with a large ventricular septal defect. The ECG reveals an abnormal left axis
deviation and left ventricular hypertrophy.
424 T. C. Chan et al.
Figure 5. 12-lead ECG from a 1-week-old infant with hypoplastic left heart syndrome. The ECG demonstrates marked right
ventricular hypertrophy with strain.
delta wave before the QRS complex (Figure 7). The vealed sinus tachycardia, but no other significant ab-
patient was ultimately diagnosed with Wolff-Parkinson- normalities (Figure 8).
White syndrome with likely episodes of tachycardia.
Figure 6. 12-lead ECG from adolescent with repair of tetralogy of Fallot. The ECG demonstrates biatrial enlargement, right axis
deviation, and intraventricular conduction delay.
Pediatric ECG 425
Figure 7. 12-lead ECG from a 9-year-old boy with Wolff-Parkinson-White syndrome. Note the shortened PR interval and wide
QRS complex with slurred upstroke (delta wave) consistent with ventricular pre-excitation.
ratory event or apparent life-threatening event (16%), complex congenital abnormalities. Because the interpre-
ingestion or toxicologic evaluation (10%), and other tation software is often calibrated for analysis in adults,
cardiac evaluation (10%) (2). Although the great major- the computer analysis on many ECG machines may
ity of ECGs in the pediatric population are normal, a provide inaccurate interpretations in children. However,
significant percentage, as high as 20%, demonstrate sig- many machines now have pediatric analysis software
nificant abnormality (1). that is activated when the appropriate age is entered into
When evaluating a pediatric ECG, it is important to the ECG machine.
do so in a systematic and routine manner. Although
settings can be changed to highlight certain features, the AGE-RELATED PEDIATRIC ECG FINDINGS
standard 12-lead ECG set at the 10 mm/mV amplitude
standard and 25 mm/s paper speed is the one that should Rapid changes occur over the first year of life as a result
be referenced against normal values. Additional right of the dramatic evolution in circulation and cardiac phys-
ventricular and posterior left ventricular precordial leads iology. After infancy, subsequent changes are more grad-
(V3R, V4R, and V7) can be included with pediatric ual until late adolescence and adulthood. In the fetus,
ECGs to provide more information on patients with blood is shunted away from the lungs by the patent
Figure 8. 12-lead ECG from 7-month-old girl with Kawasaki disease. The ECG is essentially normal for age with the exception
of the sinus tachycardia.
426 T. C. Chan et al.
First week 90–160 60–180 0.08–0.15 0.03–0.08 5–26 0–23 0–12 0–10
1–3 weeks 100–180 45–160 0.08–0.15 0.03–0.08 3–21 0–16 2–16 0–10
1–2 months 120–180 30–135 0.08–0.15 0.03–0.08 3–18 0–15 5–21 0–10
3–5 months 105–185 0–135 0.08–0.15 0.03–0.08 3–20 0–15 6–22 0–10
6–11 months 110–170 0–135 0.07–0.16 0.03–0.08 2–20 0.5–20 6–23 0–7
1–2 years 90–165 0–110 0.08–0.16 0.03–0.08 2–18 0.5–21 6–23 0–7
3–4 years 70–140 0–110 0.09–0.17 0.04–0.08 1–18 0.5–21 4–24 0–5
5–7 years 65–140 0–110 0.09–0.17 0.04–0.08 0.5–14 0.5–24 4–26 0–4
8–11 years 60–130 ⫺15–110 0.09–0.17 0.04–0.09 0–14 0.5–25 4–25 0–4
12–15 years 65–130 ⫺15–110 0.09–0.18 0.04–0.09 0–14 0.5–21 4–25 0–4
⬎ 16 years 50–120 ⫺15–110 0.12–0.20 0.05–0.10 0–14 0.5–23 4–21 0–4
* Reprinted with permission from reference (8): Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am 2006;24:196.
ductus arteriosus (PDA), and systemic circulation relies show right ventricular dominance and right axis devia-
primarily on the right side of the heart. As a result, at tion. Across the precordium, the R wave amplitude will
birth the right ventricle is larger than the left ventricle. be increased in leads V1 and V2, and decreased in leads
Subsequently, as the PDA closes during infancy, there is V5 and V6. With the cardiac changes described above
increased work of the left ventricle from the systemic occurring in the first 1–3 years of life, the left ventricle
circulation. The left ventricle enlarges and thickens such increases in size and the QRS axis will shift from right-
that by late infancy and early childhood it is more than ward to a more leftward axis. Across the precordium, the
twice as thick as the right ventricle (2,3). R wave amplitude decreases in leads V1 and V2, and
With these changes, there is a progression of alter- increases in leads V5 and V6.
ations in the normal ECG findings, including rate, axis,
interval duration, and complex morphologies in pediatric
patients. Table 1 lists the normal pediatric ECG values
Intervals
seen in the newborn, infant, child, and adolescent, in-
cluding ranges for heart rate, QRS complex axis, PR QRS Complex. The normal QRS complex duration is
segment and QRS complex intervals, and R and S wave shorter in children than adults. This finding may be the
amplitudes, and their changes with age (4 – 8). result of the smaller cardiac muscle mass in children. For
neonates, the normal QRS complex duration can be as
short as 30 ms and increases progressively with age
Heart Rate (Table 1). Accordingly, conduction abnormalities may
be present in what appears as a normal or nearly normal
Normal heart rate varies with age and is generally higher QRS complex duration in young children.
in children than adults. Table 1 lists the normal ranges
for heart rate, which tends to peak at 3– 8 weeks and then PR Interval. The normal PR interval duration is shorter
decreases through adolescence. Due to the smaller stroke in children and increases with age. Similar to the change
volume in neonates and young children, cardiac output is in normal QRS complex duration, this finding may be the
maintained by the higher heart rate. With age, stroke result of smaller cardiac muscle mass. In neonates, the
volume increases and contributes more significantly to normal PR interval duration can be as short as 80 ms
overall cardiac output. When assessing heart rate, it is (Table 1). As a result, AV conduction delay may be
important to consider the patient’s activity and stress present in young children with minimal prolongation or
levels, which can result in physiologic elevations of heart a “normal”-appearing PR interval (4).
rate. Rates significantly outside the normal range for age,
however, should be closely scrutinized for dysrhythmias. QT Interval. The QT interval duration varies with heart
rate in both children and adults. Similar to adults, the QT
interval must be corrected for heart rate (which is nor-
Axis mally higher in children) to obtain the corrected QTc
interval. In infants, the normal QTc is longer than in
As discussed above, the right ventricle is larger than the older children and, in fact, can be as long as 490 ms. This
left ventricle in the newborn infant, and the ECG will discrepancy in the evaluation of the QTc interval in
Pediatric ECG 427
infants and children should be noted, particularly when repolarization ST segment/Twave abnormalities (Case 7,
relying on computer analysis of ECG intervals. Figure 7).
Although SVTs are more common in children, tachy-
T waves. T wave morphology can be difficult to interpret cardias from a ventricular origin do occur in pediatric
in neonates and children. At birth, the T wave may be patients. In fact, because the normal QRS complex is
upright, flat, or inverted. Within a few days after birth, shorter in duration in children than in adults, ventricular
however, the T wave can become inverted normally. In tachycardias can be even more difficult to diagnose in
fact, upright T waves at this age may indicate right young children. It is important to remember that what
ventricular hypertrophy (RVH). The “juvenile pattern” appears as a slightly prolonged QRS complex on ECG
of T wave inversion usually seen in the anterior leads may, in fact, represent a significantly prolonged or wide
(leads V1–V3) typically lasts up until 8 years of age complex tachycardia in infants and children. Similar to
(Case 1, Figure 1), but can persist into early adolescence adults, such a finding may be indicative of a sinus tachy-
(Case 2, Figure 2). cardia or SVT with bundle branch block or aberrancy,
AV reentry tachycardia (antidromic), ventricular tachy-
cardia (VT), or ventricular fibrillation (11).
PEDIATRIC ECG ABNORMALITIES
VT. Ventricular tachycardia in the pediatric patient is
Tachydysrhythmias uncommon. VT may go unrecognized until the child
acutely decompensates, presenting with syncope, mental
Tachydysrhythmias are common in pediatric patients status changes, congestive failure, or hemodynamic in-
seen in the ED. The normal range for heart rate decreases stability. Because VT may lead to ventricular fibrillation
with age and an increased rate can be normal, particu- and subsequent cardiopulmonary arrest, rapid recogni-
larly in young children (Table 1). In addition, because tion of this rhythm and knowledge of its treatment is
cardiac output is more dependent on heart rate than critical (12).
stroke volume in children, a fast heart rate can be a Ventricular tachycardia is defined as a series of three
normal physiologic response to stressors such as fever, or more repetitive excitations originating from an ectopic
dehydration, and pain, which are often related to the focus in the ventricle at a rate ⬎ 120 beats/min. The ECG
patient’s reason for presenting to the ED. will reveal a QRS complex that has a different morphol-
ogy or axis from the underlying sinus rhythm. The QRS
SVT. The most common pediatric tachydysrhythmia is complex duration is usually prolonged, exceeding 0.08 s
supraventricular tachycardia (SVT). SVT occurs with a in infants and 0.09 s in children older than 3 years (6).
frequency between 1 in 250 and 1 in 1000 pediatric Importantly, the QRS complex may not be absolutely
patients, most commonly during the first 2 months of life “wide,” even after adjustment is made for the patient’s
(9). Presenting symptoms are often non-specific and vary age. This is particularly true in infants in whom the QRS
with age, from “fussiness,” poor feeding, or lethargy in complex duration in VT may range from 0.06 s to 0.11 s.
infants to complaints of chest pain, shortness of breath, In older children, the QRS complex is more often pro-
or dizziness in older children. In infants, the heart rate is longed (⬎ 0.09 s). The clinician must recognize this
typically ⬎ 220 beats/min, and in children the heart rate age-related QRS complex width variation; failure to do
is ⬎ 180 beats/min (10). On the ECG, the rhythm is fast so may result in misidentification of a malignant ventric-
and extremely regular, and the QRS complex is narrow ular dysrhythmia as a sinus tachycardia or SVT. It should
with no preceding P wave activity (Case 3, Figure 3). be noted that although VT is uncommon in children,
SVT can be episodic in infants and children, often mak- SVT with aberrancy is even more uncommon (13). In
ing the diagnosis more difficult. In neonates and young addition to QRS complex width and morphology, other
children, the SVT is usually associated with an accessory criteria that can be helpful in distinguishing VT are
atrioventricular pathway. In adolescents and adults, the atrioventricular dissociation, intermittent fusion and cap-
most common cause of SVT is an atrioventricular nodal ture beats, and ventricular rate.
reentry tachycardia (6).
SVT can be associated with Wolff-Parkinson-White
(WPW) syndrome in children, when there is an accessory Conduction Abnormalities
pathway between the atria and the ventricles (9). Elec-
trocardiographic findings suggestive of WPW include a AV block—from first-degree to complete heart block—
wide QRS complex with slurred upstroke or delta wave can occur in infants and children, as well as in adults.
indicative of ventricular pre-excitation from the acces- However, the diagnosis of first-degree AV block can be
sory pathway, short PR interval for age, and evidence of difficult due to the normally shorter PR interval seen in
428 T. C. Chan et al.
infants and children (Table 1). Thus, normal-appearing Prolonged QT syndrome is rare in children, and when
PR intervals may actually be abnormally prolonged and present, is more likely associated with a congenital cause
indicative of first-degree AV block. Third-degree or rather than acquired in contradistinction to adults. Al-
complete heart block may be congenital or acquired in though there are now a number of identified congenital
children. Congenital causes of complete heart block in- long QT syndromes, the most common are Romano-
clude transposition of the great arteries (TGA) or mater- Ward syndrome (autosomal dominant) and Jervell-
nal connective tissue disorders. Acquired conditions that Lange-Nielsen syndrome (autosomal recessive with as-
can present with heart block include Kawasaki disease, sociated with congenital deafness).
Lyme disease, muscular dystrophies, and rheumatic fe-
ver (8,11). The ECG must be closely scrutinized for
complete heart block in pediatric patients presenting with Congenital Heart Disease
significant bradycardia. In these cases, P wave activity
will be faster and have no clear relationship to the Congenital heart disease (CHD) occurs in 8 of every
slower, regular QRS complexes on the ECG. 1000 live births, and the clinical presentation of these
Intraventricular conduction blocks can result in vari- patients can vary in terms of both symptomatology and
able QRS complex duration, though blocks located in the timing (14 –21). The ECG, although not diagnostic, can
provide important clues in patients suspected of having
bundle branches result in abnormally prolonged QRS
CHD. In particular, the ECG can show the presence of
complexes. In infants and young children, it is important
chamber enlargement or conduction abnormalities that
to remember that the normal QRS complex duration is
may be associated with specific CHDs. A number of
shorter than in adults and thus the diagnosis can be
ECG findings can be associated with specific congenital
difficult to make. In addition, incomplete right bundle heart diseases (Table 2). Although abnormalities on the
branch block (BBB) can be a normal part of the involu- ECG are found in the majority of cases, it is important to
tion of right ventricular forces during infancy and early remember that with some CHDs (such as PDA), the ECG
childhood. In pediatric patients, right BBB is more com- can appear age appropriate and normal.
mon than left BBB. Right BBB can be seen with atrial Evidence of RVH on ECG (increased R wave ampli-
septal defects (ASDs), complete atrio-ventricular de- tude in leads V1, V2) is the most common electrocar-
fects, ventriculoseptal defects (VSDs), and after repair of diographic finding in patients with CHD. Due to the RV
tetralogy of Fallot (ToF) and VSDs. Left BBB is rare in predominance in the early neonatal period however, the
children and the possibility of WPW should be consid- ECG findings for RVH may be overlooked until later
ered as this syndrome can mimic a left BBB pattern on infancy. ECG findings consistent with RVH can be seen
ECG. in CHDs including pulmonary stenosis, ToF, TGA, and
Table 2. Congenital Heart Abnormalities with Timing of Onset and Typical Abnormalities that May be Seen on ECG*
* Modified with permission from reference (8): Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am 2006;24:204.
CHD ⫽ congenital heart disease; RVH ⫽ right ventricular hypertrophy; LVH ⫽ left ventricular hypertrophy; RAE ⫽ right atrial
enlargement; LAE ⫽ left atrial enlargement; RAD ⫽ right axis deviation; LAD ⫽ left axis deviation; RBBB ⫽ right bundle branch block;
PDA ⫽ patent ductus arteriosus; ASD ⫽ atrial septal defect; VSD ⫽ ventricular septal defect; CoA ⫽ coarctation of aorta; ToF ⫽ tetralogy
of Fallot; TGA ⫽ transposition of great vessels; PA ⫽ pulmonary atresia; HLHS ⫽ hypoplastic left heart syndrome; AS ⫽ aortic stenosis;
PS ⫽ pulmonic stenosis; AVC ⫽ atrioventricular canal defects; HCM ⫽ hypertrophic cardiomyopathy.
Pediatric ECG 429
VSD with pulmonary stenosis or pulmonary hyperten- ing or inversion and low QRS complex voltage ⬍ 5 mm
sion, coarctation of aorta (CoA) (newborn), pulmonary in all limb leads. Acute pericarditis, an acute inflamma-
valve atresia, hypoplastic left heart syndrome (HLHS) tion in the pericardium, can present in children and have
(Case 5, Figure 5), and atrial septal defects (ASDs). typical ECG findings of diffuse ST segment elevation
Evidence of LVH on ECG (increased QRS complex and PR depression (with reciprocal changes in leads aVR
amplitude in the lateral leads I, avL, V5, V6) can be seen and V1).
in CHDs in lesions resulting in LV outflow tract obstruc-
tion. These CHDs include aortic stenosis and CoA. LVH Kawasaki disease. Kawasaki disease is an acute, self-
can also be seen in lesions that result in a small RV, limited vasculitis of unknown etiology that occurs in
including tricuspid atresia and pulmonary atresia with infants and young children. Presentation is character-
intact ventricular septum. LVH can also be seen with ized by fever, conjunctivitis, rash, erythema of the oral
large VSDs, AV canal defects, and PDA (older children) mucosa and lips, swelling of the extremities, and cer-
(Case 4, Figure 4). vical lymphadenopathy. Approximately 15–25% of
Electrocardiographic evidence of right atrial (RA) en- untreated children develop coronary artery aneurysms,
largement can be seen with ASD, AV canal defects, which may result in myocardial infarction and isch-
tricuspid atresia, Ebstein’s anomaly, and severe pulmo- emic heart disease (23). Myocarditis is a common
nary stenosis. These lesions result in large left-to-right
feature early in the course of the disease and in severe
shunts causing RA volume overload and enlargement.
cases. In fact, Kawasaki disease has surpassed acute
Similarly, left atrial (LA) enlargement can be seen with
rheumatic fever as the leading cause of acquired heart
MV stenosis or insufficiency, left heart obstruction, and
disease in children (24). ECG findings in these patients
complete AV canal defects (Case 6 – Figure 6).
can vary from normal to classic ST segment, T wave
Abnormal axis deviations are common with CHDs.
Right axis deviation, greater than what is expected for and Q wave changes associated with ischemia and
age, can occur with ASD, ToF, CoA, TGA, and pulmo- infarction (25) (Case 8, Figure 8). Other reported
nary stenosis. Left axis deviation can be seen with large findings include T wave flattening or peaking, and PR
VSDs, tricuspid atresia, TGA and complete AV canal and QT interval prolongation (23). These ECG abnor-
defects (Case 4, Figure 4). malities have been reported in up to 77– 80% of pa-
tients and may indicate more severe disease in chil-
dren (26,27).