Conduction abnormalities
All degrees of AV block may occur in pediatric patients. It is important
to remember that the normal PR interval in infants is shorter and lengthens
as cardiac tissue matures with age. A normal appearing PR interval of 0.20
sec may thus in fact represent a pathologic first-degree AV block in an infant
or young child.
Complete heart block is a common cause of significant bradycardia in
pediatric patients and may be acquired or congenital (Fig. 6). Causes of congenital
heart block include structural lesions like L-transposition of the
great arteries, or maternal connective tissue disorders. Acquired heart block
may result from disorders such as Lyme disease, systemic lupus erythematosus,
muscular dystrophies, Kawasaki disease, or rheumatic fever [11].
Bundle branch blocks (BBB) may be present when there is QRS complex
prolongation abnormal for a given age. Right BBB occurs with abnormal
rightward and anterior terminal forces, frequently manifesting on ECG as
an rSR# pattern in leads V1 and V2. Right BBB is more common than left
BBB and can be seen after surgical repair of congenital heart defects, particularly
ventricular septal defect repairs. Similarly, left BBB is seen with abnormal
leftward and posterior forces, best appreciated in leads V5 and V6. Left
BBB is rare in children, however, and the possibility of WPW should be considered,
because this syndrome can mimic a left BBB pattern.
Congenital heart
With an incidence of 8/1000 live births, many of the structural congenital
heart diseases present in the neonatal period [12]. The signs and symptoms
of congenital heart disease may be nonspecific, however. Infants may present
with tachypnea, sudden onset of cyanosis or pallor that may worsen with
crying, sweating with feeds, lethargy, or failure to thrive [13].
Congenital heart disease lesions that present in the first 2–3 weeks of life
are typically the ductal-dependent cardiac lesions. During this period the
ductus arteriosus had been sustaining blood flow for these infants. When
the ductus closes anatomically at 2–3 weeks of life, these infants suddenly
become ill. Depending on the underlying structural abnormality, these neonates
present with sudden cyanosis or signs of cardiovascular collapse.
These newborns have depended on the ductus arteriosus to supply blood
to the lungsdas with tetralogy of Fallot (ToF) or tricuspid atresia (TA)d
or to the systemic circulationdas in the case of coarctation of the aorta
(CoA) or hypoplastic left heart syndrome (HLHS). The main causes of
cyanotic congenital heart disease are ToF, TA, transposition of the great
arteries (TGA), truncus arteriosus, total anomalous pulmonary venous
return (TAPVR), and pulmonary atresia or stenosis. Time of onset and
the common associated ECG findings are listed in Table 3 [14–16].
The other class of congenital cardiac lesions that present in the first
month of life are the left-to-right intracardiac shunts, such as ventricular
septal or atrioventricular canal defects. As the normal pulmonary vascular
resistance falls over the first month of life, any pre-existing left-to-right
shunt sees a gradual increase in flow across the shunt, resulting in congestive
heart failure. The differential diagnosis of congenital heart diseases that
cause congestive heart failure include not only the left-to-right intracardiac
shunts, but also HLHS, CoA, TA, endocardial cushion defect, patent ductus
arteriosus (PDA), aortic stenosis, interrupted aortic arch, aortic atresia, and
mitral valve atresia [17,18].
An ECG should be obtained in all infants suspected of having congenital
heart disease. Although the ECG does not make the diagnosis, it can show
evidence of conduction abnormalities or chamber enlargement as a result of
the congenital defect. In addition, the ECG provides a means of assessing
the degree of cardiac flow obstruction, chamber hypertrophy, and the development
of dysrhythmias as a result of the congenital heart disease.
Several ECG findings can be associated with specific congenital heart diseases
(Table 3). The ECG can seem normal or age-appropriate for some
congenital heart diseases. These include cases of PDA, mild-moderate pulmonary
stenosis, TGA, ASD, VSD, and CoA, though the presence of abnormalities
on the ECG is generally the rule.
RVH is the most common abnormality seen with congenital heart disease
and can be seen with pulmonary stenosis, ToF, TGA, and VSD with pulmonary
stenosis or pulmonary hypertension, CoA (newborn), pulmonary valve
atresia, HLHS, and ASD. RVH may be difficult to distinguish during the
early neonatal period because of the normal right ventricular predominance
on the ECG at this age. The abnormality becomes clear, however, with later
infancy and early childhood.
LVH is seen in lesions with small right ventricles, such as tricuspid atresia,
pulmonary atresia with intact ventricular septum, and lesions with left
ventricular outflow track obstruction (AS, CoA, hypertrophic cardiomyopathy
[HCM]). LVH also can be seen in older children with PDA and larger
VSD or AV canal defects (Fig. 7).
In conjunction with ventricular changes, atrial abnormalities can be detected
on the ECG with congenital heart disease. RAE occurs with large
left-to-right shunts, causing RA volume overload, and can be seen with ASD,
atrioventricular canal defects, tricuspid atresia, Ebstein anomaly, and severe
pulmonary stenosis. LAE can be seen with mitral stenosis or insufficiency, left
heart obstruction, and complete AV canal defects.
Abnormal QRS axis deviations are seen commonly with congenital heart
defects. Right axis deviation can occur with ASD, ToF, CoA, TGA, and
pulmonary stenosis. Left axis deviation can be seen with large VSD, tricuspid
atresia, TGA, and complete AV canal defects (Fig. 7). Right BBB can be
seen with ASD, complete AV defects, small VSD, and after repair of ToF. It
is important to keep in mind, however, that incomplete right BBB can be
a normal part of the involution of right ventricular forces during infancy
and early childhood (Fig. 8).
Hypertrophic cardiomyopathy
Although most cases of HCM are diagnosed at 30–40 years of age, 2% of
cases occur in children younger than 5 years of age and 7% occur in children
younger than 10 years of age [19]. Clinical presentation varies, with patients
experiencing chest pain, palpitations, shortness of breath, syncopal or near
syncopal episodes, or sudden death. The hallmark anatomic finding in patients
who have HCM is an asymmetric, hypertrophied, nondilated left ventricle
with greater involvement of the septum than the ventricular free wall.
ECG findings include LAE and LVH, ST-segment abnormalities, T-wave
inversions, Q waves, and diminished or absent R waves in the lateral leads.
Premature atrial and ventricular contractions, supraventricular tachycardia,
multifocal ventricular dysrhythmias, or new onset atrial fibrillation also may
be present.
Myocarditis
An inflammatory condition of the myocardium, this disease has numerous
causes; the most common etiology in North America is viral (Coxsackie A
and B, ECHO viruses, and influenza viruses) [20,21]. The clinical presentation
varies depending on multiple factors, including etiology and patient age. Neonates
and infants may present with symptoms such as lethargy, poor feeding,
irritability, pallor, fever, and failure to thrive. Symptoms suggestive of heart
failure like diaphoresis with feeding, rapid breathing, tachycardia, or respiratory
distress also may be present. Older children may complain of weakness
and fatigue, particularly on exertion. Signs of poor cardiac function, including
signs of congestive heart failure, may be present on examination.
Multiple ECG findings may be present. Sinus tachycardia is the most
common dysrhythmia. A tachycardia faster than expected for the degree
of fever (10 bpm for each degree of temperature elevation) may indicate
myocarditis. Many other dysrhythmias may be associated with myocarditis,
including junctional tachycardias, ventricular ectopy, ventricular tachycardias,
and even second- and third-degree AV blocks. Morphologically there
may be T-wave flattening or inversion and low QRS complex voltage, less
than 5 mm in all limb leads.
source:
Pediatric ECG
Ghazala Q. Sharieff, MDa,b,*, Sri O. Rao, MDc
aChildren’s Hospital and Health Center/University of California–San Diego,
3020 Children’s Way, San Diego, CA 92123
bPediatric Emergency Medicine, Palomar-Pomerado Hospitals/California
Emergency Physicians, 555 East Valley Parkway, Escondido, CA 92025, USA
cDivision of Pediatric Cardiology, Children’s Hospital and Health Center,
3020 Children’s Way, San Diego, CA 92123, USA
All degrees of AV block may occur in pediatric patients. It is important
to remember that the normal PR interval in infants is shorter and lengthens
as cardiac tissue matures with age. A normal appearing PR interval of 0.20
sec may thus in fact represent a pathologic first-degree AV block in an infant
or young child.
Complete heart block is a common cause of significant bradycardia in
pediatric patients and may be acquired or congenital (Fig. 6). Causes of congenital
heart block include structural lesions like L-transposition of the
great arteries, or maternal connective tissue disorders. Acquired heart block
may result from disorders such as Lyme disease, systemic lupus erythematosus,
muscular dystrophies, Kawasaki disease, or rheumatic fever [11].
Bundle branch blocks (BBB) may be present when there is QRS complex
prolongation abnormal for a given age. Right BBB occurs with abnormal
rightward and anterior terminal forces, frequently manifesting on ECG as
an rSR# pattern in leads V1 and V2. Right BBB is more common than left
BBB and can be seen after surgical repair of congenital heart defects, particularly
ventricular septal defect repairs. Similarly, left BBB is seen with abnormal
leftward and posterior forces, best appreciated in leads V5 and V6. Left
BBB is rare in children, however, and the possibility of WPW should be considered,
because this syndrome can mimic a left BBB pattern.
Congenital heart
With an incidence of 8/1000 live births, many of the structural congenital
heart diseases present in the neonatal period [12]. The signs and symptoms
of congenital heart disease may be nonspecific, however. Infants may present
with tachypnea, sudden onset of cyanosis or pallor that may worsen with
crying, sweating with feeds, lethargy, or failure to thrive [13].
Congenital heart disease lesions that present in the first 2–3 weeks of life
are typically the ductal-dependent cardiac lesions. During this period the
ductus arteriosus had been sustaining blood flow for these infants. When
the ductus closes anatomically at 2–3 weeks of life, these infants suddenly
become ill. Depending on the underlying structural abnormality, these neonates
present with sudden cyanosis or signs of cardiovascular collapse.
These newborns have depended on the ductus arteriosus to supply blood
to the lungsdas with tetralogy of Fallot (ToF) or tricuspid atresia (TA)d
or to the systemic circulationdas in the case of coarctation of the aorta
(CoA) or hypoplastic left heart syndrome (HLHS). The main causes of
cyanotic congenital heart disease are ToF, TA, transposition of the great
arteries (TGA), truncus arteriosus, total anomalous pulmonary venous
return (TAPVR), and pulmonary atresia or stenosis. Time of onset and
the common associated ECG findings are listed in Table 3 [14–16].
The other class of congenital cardiac lesions that present in the first
month of life are the left-to-right intracardiac shunts, such as ventricular
septal or atrioventricular canal defects. As the normal pulmonary vascular
resistance falls over the first month of life, any pre-existing left-to-right
shunt sees a gradual increase in flow across the shunt, resulting in congestive
heart failure. The differential diagnosis of congenital heart diseases that
cause congestive heart failure include not only the left-to-right intracardiac
shunts, but also HLHS, CoA, TA, endocardial cushion defect, patent ductus
arteriosus (PDA), aortic stenosis, interrupted aortic arch, aortic atresia, and
mitral valve atresia [17,18].
An ECG should be obtained in all infants suspected of having congenital
heart disease. Although the ECG does not make the diagnosis, it can show
evidence of conduction abnormalities or chamber enlargement as a result of
the congenital defect. In addition, the ECG provides a means of assessing
the degree of cardiac flow obstruction, chamber hypertrophy, and the development
of dysrhythmias as a result of the congenital heart disease.
Several ECG findings can be associated with specific congenital heart diseases
(Table 3). The ECG can seem normal or age-appropriate for some
congenital heart diseases. These include cases of PDA, mild-moderate pulmonary
stenosis, TGA, ASD, VSD, and CoA, though the presence of abnormalities
on the ECG is generally the rule.
RVH is the most common abnormality seen with congenital heart disease
and can be seen with pulmonary stenosis, ToF, TGA, and VSD with pulmonary
stenosis or pulmonary hypertension, CoA (newborn), pulmonary valve
atresia, HLHS, and ASD. RVH may be difficult to distinguish during the
early neonatal period because of the normal right ventricular predominance
on the ECG at this age. The abnormality becomes clear, however, with later
infancy and early childhood.
LVH is seen in lesions with small right ventricles, such as tricuspid atresia,
pulmonary atresia with intact ventricular septum, and lesions with left
ventricular outflow track obstruction (AS, CoA, hypertrophic cardiomyopathy
[HCM]). LVH also can be seen in older children with PDA and larger
VSD or AV canal defects (Fig. 7).
In conjunction with ventricular changes, atrial abnormalities can be detected
on the ECG with congenital heart disease. RAE occurs with large
left-to-right shunts, causing RA volume overload, and can be seen with ASD,
atrioventricular canal defects, tricuspid atresia, Ebstein anomaly, and severe
pulmonary stenosis. LAE can be seen with mitral stenosis or insufficiency, left
heart obstruction, and complete AV canal defects.
Abnormal QRS axis deviations are seen commonly with congenital heart
defects. Right axis deviation can occur with ASD, ToF, CoA, TGA, and
pulmonary stenosis. Left axis deviation can be seen with large VSD, tricuspid
atresia, TGA, and complete AV canal defects (Fig. 7). Right BBB can be
seen with ASD, complete AV defects, small VSD, and after repair of ToF. It
is important to keep in mind, however, that incomplete right BBB can be
a normal part of the involution of right ventricular forces during infancy
and early childhood (Fig. 8).
Hypertrophic cardiomyopathy
Although most cases of HCM are diagnosed at 30–40 years of age, 2% of
cases occur in children younger than 5 years of age and 7% occur in children
younger than 10 years of age [19]. Clinical presentation varies, with patients
experiencing chest pain, palpitations, shortness of breath, syncopal or near
syncopal episodes, or sudden death. The hallmark anatomic finding in patients
who have HCM is an asymmetric, hypertrophied, nondilated left ventricle
with greater involvement of the septum than the ventricular free wall.
ECG findings include LAE and LVH, ST-segment abnormalities, T-wave
inversions, Q waves, and diminished or absent R waves in the lateral leads.
Premature atrial and ventricular contractions, supraventricular tachycardia,
multifocal ventricular dysrhythmias, or new onset atrial fibrillation also may
be present.
Myocarditis
An inflammatory condition of the myocardium, this disease has numerous
causes; the most common etiology in North America is viral (Coxsackie A
and B, ECHO viruses, and influenza viruses) [20,21]. The clinical presentation
varies depending on multiple factors, including etiology and patient age. Neonates
and infants may present with symptoms such as lethargy, poor feeding,
irritability, pallor, fever, and failure to thrive. Symptoms suggestive of heart
failure like diaphoresis with feeding, rapid breathing, tachycardia, or respiratory
distress also may be present. Older children may complain of weakness
and fatigue, particularly on exertion. Signs of poor cardiac function, including
signs of congestive heart failure, may be present on examination.
Multiple ECG findings may be present. Sinus tachycardia is the most
common dysrhythmia. A tachycardia faster than expected for the degree
of fever (10 bpm for each degree of temperature elevation) may indicate
myocarditis. Many other dysrhythmias may be associated with myocarditis,
including junctional tachycardias, ventricular ectopy, ventricular tachycardias,
and even second- and third-degree AV blocks. Morphologically there
may be T-wave flattening or inversion and low QRS complex voltage, less
than 5 mm in all limb leads.
source:
Pediatric ECG
Ghazala Q. Sharieff, MDa,b,*, Sri O. Rao, MDc
aChildren’s Hospital and Health Center/University of California–San Diego,
3020 Children’s Way, San Diego, CA 92123
bPediatric Emergency Medicine, Palomar-Pomerado Hospitals/California
Emergency Physicians, 555 East Valley Parkway, Escondido, CA 92025, USA
cDivision of Pediatric Cardiology, Children’s Hospital and Health Center,
3020 Children’s Way, San Diego, CA 92123, USA
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