Derick M. Wenning
Many different presentations to the pediatric emergency department (ED) warrant electrocardiogram (ECG) evaluation. These include common complaints such as chest pain, syncope, palpitations, drug exposure, and electrical burns. In young infants and neonates, an ECG may be indicated for poor feeding, cyanotic spells, or an acute life-threatening event. There are age-related changes that dramatically alter the appearance of the “normal” ECG in children (Table 8.1), and the first step in interpretation of the pediatric ECG should be noting the patient’s age. The normal range for heart rate for a newborn to an infant 6 months of age is 125 to 145 beats per minute (bpm). The mean adult resting heart rate of 80 bpm is not reached until adolescence. In neonates, due to fetal circulation, the right ventricle is dominant. This leads to a normal right axis deviation in ECGs of infants. Smaller muscle mass also leads to a shorter PR interval as well as QRS duration. In younger children, the PR interval ranges between 0.08 and 0.15 seconds and in adolescents between 0.120 and 0.2 seconds. QRS duration in patients aged less than 8 years should not exceed 0.08 seconds. Adolescent QRS intervals range from 0.1 to 0.12 seconds, the latter being the normal duration for adults. The QT interval in infancy is also slightly longer. Since the QT interval varies with heart rate, calculation of the corrected QT interval is indicated. The upper limit of normal for the QT interval in infancy is 490 milliseconds, and decreases to 440 milliseconds after 6 months of age. In addition, R-wave progression does not follow the normal adult pattern until the patient is approximately 6 to 8 years of age.
NORMAL PEDIATRIC ECG VALUES
| Age | HR (bpm) | QRS Axis (Degrees) | PR Interval (sec) | QRS Interval (s) | R in V1 (mm) | S in V1 (mm) | R in V6 (mm) | S in V6 (mm) |
|---|---|---|---|---|---|---|---|---|
| 1st week | 90–180 | 60–180 | 0.08–0.15 | 0.03–0.08 | 5–24 | 0–18 | 0–12 | 0–10 |
| 1–3wks | 100–185 | 45–160 | 0.08–0.15 | 0.03–0.08 | 3–21 | 0–16 | 2–15 | 0–10 |
| 1–2 mo | 120–185 | 30–135 | 0.08–0.15 | 0.03–0.08 | 3–18 | 0–15 | 5–21 | 0–9 |
| 3–5 mo | 105–185 | 0–135 | 0.08–0.15 | 0.03–0.08 | 3–19 | 0–15 | 6–22 | 0–9 |
| 6–11 mo | 110–170 | 0–135 | 0.07–0.16 | 0.03–0.08 | 2–20 | 0.5–18 | 6–23 | 0–7 |
| 1–2 yr | 90–165 | 0–110 | 0.08–0.16 | 0.03–0.08 | 2–18 | 0.5–21 | 6–23 | 0–7 |
| 3–4 yr | 70–140 | 0–110 | 0.09–0.17 | 0.04–0.08 | 1–16 | 0.5–23 | 4–26 | 0–5 |
| 5–7 yr | 65–135 | 0–110 | 0.09–0.17 | 0.04–0.08 | 0.5–14 | 0.5–23 | 4–26 | 0–4 |
| 8–11 yr | 60–130 | −15–110 | 0.09–0.17 | 0.04–0.09 | 0–12 | 0.5–25 | 4–25 | 0–4 |
| 12–15 yr | 65–120 | −15–110 | 0.09–0.18 | 0.04–0.09 | 0–10 | 0.5–21 | 4–23 | 0–4 |
T-wave changes in pediatric ECGs are nonspecific, and absolute rules for age-related changes have not been determined. The right precordial leads (V1–V3) should have upright T waves in the first week of life and inverting thereafter through early childhood. Upright T waves in leads V1 and V2 in a young child over the age of 1 week should raise suspicion for right ventricular hypertrophy (RVH) and further investigation is warranted. Inverted T waves in V1–V3 persist to 6 to 8 years of age and occasionally into adolescence.
Any abnormality found on ECG should be explored as a possible reason for the presenting complaint; however, a normal ECG does not rule out potential cardiac causes (see also Table 8.2). Depending on the severity of the presentation and results of other laboratory and radiographic testing, disposition may vary from inpatient hospitalization to urgent follow-up with possible cardiology consultation.
RVH is the most common abnormality seen with congenital heart disease (CHD). Additional right precordial leads (V3R and V4R) can be used to provide more information about the right ventricle in infants.
Correction of the QT interval can be done using the Bazett formula that divides the measured QT by the square root of the preceding R–R interval in which the QT is being measured (QTc = QT/√R–R).
P waves should be upright in leads I, II, and aVF. Other P wave orientations in these leads suggest a nonsinus atrial rhythm.
Q waves can be normal in the inferior and lateral leads in a child.
Michael J. Walsh
Congenital heart defects, affecting approximately 8 in 1000 live births, are the most common birth defects in newborns. With advances in fetal and postnatal echocardiography, an increasing number of diagnoses are made before newborns leave the hospital. However, in patients discharged with unrecognized cardiac disease, an accurate and timely diagnosis is essential for the reduction of morbidity and mortality.
Critical CHD commonly presents with closure of the patent ductus arteriosus (PDA) and can lead to a rapid decline in clinical status. PDA may close from the first day (most commonly) up to the 90th day (rarely) after birth in normal infants. Although echocardiography provides a definitive diagnosis, treatment often must be initiated before such a diagnosis is made. In the absence of an echocardiogram, clinicians should employ the physical examination, chest radiograph (CXR), ECG, four-extremity blood pressures, and pre- and postductal pulse oximetry in an effort to narrow the diagnosis (Table 8.3).
COMMON PRESENTATIONS OF NEONATAL CHD
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In patients with ductal-dependent systemic blood flow, ductal closure leads to a marked decrease in cardiac output, and thus, oxygen delivery—leading to metabolic acidosis and shock. Femoral pulses will be diminished or absent. Critical aortic stenosis, coarctation of the aorta (CoA), interrupted aortic arch, and hypoplastic left heart syndrome (HLHS) are the most common examples of ductal-dependent systemic blood flow.
When the pulmonary circulation is ductal dependent, PDA closure leads to profound cyanosis. This is evident in right-heart obstructive lesions, such as critical pulmonary stenosis or pulmonary atresia. Cyanosis that does not respond to oxygen therapy suggests a cardiac etiology. Cyanosis is also the most common presentation in patients with parallel circulations, as in transposition of the great arteries (TGA). Severe pulmonary edema can result from over-circulation of the lungs, as in truncus arteriosus, or from obstruction of pulmonary venous return, as seen with totally anomalous pulmonary venous return (TAPVR). Single ventricle lesions, such as double-inlet left ventricle and tricuspid atresia, can have any of the above presentations depending on the patency of the aorta and the pulmonary artery, as well as other intracardiac factors.
Prompt recognition and stabilization are essential for the reduction of morbidity and mortality. If cardiac disease is suspected, arrangements should be made to transfer the baby to a tertiary-care center for potential surgical or catheter-based interventions. Often, therapy must be initiated before a definitive diagnosis is made by echocardiography.
The mainstay of medical management for many of these patients is prostaglandin E1 (0.03–0.1 μg/kg/min). It is a life-saving treatment for patients with ductal-dependent lesions, and in those patients with TGA and inadequate mixing. There is a small subset of CHD patients for whom PGE makes the clinical status worse, including obstructed TAPVR. Clinicians must anticipate the side effects of apnea and hypotension. If a transfer is anticipated, consider the reliability of the airway and intravascular access before transport.
Left-sided obstructive lesions can be associated with severe heart failure after ductal closure. Catecholamines, such as dopamine and epinephrine, have an important role. Metabolic acidosis should be corrected. In patients with respiratory distress as a result of congestive heart failure, intravenous (IV) diuretics (ie, furosemide 1 mg/kg/dose IV) will be helpful.
In cases of TGA with intact ventricular septum and restrictive foramen ovale, medical management alone is often insufficient. Balloon atrial septostomy is essential to promote adequate mixing. Neurodevelopmental outcomes hinge on the speed with which this occurs. These patients underscore the need for prompt referral to a tertiary-care center. There, echocardiography can provide a definitive diagnosis and cardiothoracic surgeons can provide the lesion-specific palliation or repair.
CHD is common and has variable presentations in the neonate. Cyanosis, a single second heart sound, diminished femoral pulses, and poor perfusion may help to distinguish CHD from other neonatal illnesses.
If clinical suspicion for CHD is high, consultation with a pediatric cardiologist and initiation of prostaglandin E1 should be initiated without waiting for a definitive diagnosis. Neurodevelopmental outcomes can hang in the balance.
If a transfer is anticipated, consideration must be given to the reliability of the infant’s airway and intravascular access. Prostaglandin E1 must be run as a continuous infusion and can lead to apnea.
Michael D. Quartermain
The presentation of CHD in an infant and a child is mostly characterized by left to right shunts, left-sided outflow obstructive lesions, and cardiomyopathies (Table 8.4). The time frame of infancy and early childhood is a vulnerable period when normal decreases in the pulmonary vascular resistance (PVR) allow for the hemodynamic sequelae of CHD to become apparent. The most common defect to present to the ED in heart failure in this age range is a moderate to large ventricular septal defect (VSD). Another lesion presenting in this age group is a complete atrioventricular canal defect, which occurs in 40% of children with Trisomy 21. The defect includes a large VSD component in combination with an atrial septal defect and abnormalities of the mitral and tricuspid valves.
An isolated patent ductus arteriosis (PDA), if large, can present with similar left to right shunt symptoms of pulmonary over circulation. Coarctation of the aorta (CoA), while most common in the newborn period, can present during infancy and early childhood. Both anomalous left coronary artery from the pulmonary artery (ALCAPA) and cardiomyopathies (eg, viral, metabolic, and infectious) present with left ventricular dilation with systolic dysfunction and must be considered in this age group.
This assortment of heart defects present with overlapping features of congestive heart failure or low cardiac output. On physical examination, poor growth is evident often with height and weight less than 5th percentile and a history of feeding intolerance. Tachycardia and tachypnea with mild to moderate respiratory distress are common. Cardiac murmurs are often present along with a hyperdynamic precordium. Cool extremities with poor capillary refill and hepatomegaly are additional features often seen in these patients. Four-extremity blood pressures will identify the child with a significant CoA with gradients greater than 20 mmHg from right arm to lower extremity.
Pulse oximetry, accurate four-extremity blood pressure assessment, ECG, and CXRs are the initial diagnostic tools. Pulse oximetry readings are often normal or only mildly decreased secondary to pulmonary edema in these patients. ECG is valuable to rule out underlying arrhythmia, assess for prominent ventricular forces seen in large left to right shunts, and identify ischemia patterns consistent with ALCAPA. The majority of these lesions will have cardiomegaly and pulmonary edema present on CXRs. Consultation with a pediatric cardiologist is recommended for confirmatory echocardiography and development of the appropriate treatment plan for the lesion. The patient with a large left to right shunt from a VSD or PDA will benefit from diuretic therapy, usually 1 mg/kg IV furosemide. Oxygen therapy is not recommended for these patients because its vasodilatory effects may increase pulmonary blood flow and lead to worsening pulmonary edema. Admission for initiation of nasogastric feeds and digoxin therapy is often performed. Patients with a dilated cardiomyopathy often require more significant support with mechanical ventilation and IV medications such as dopamine and milrinone. If ALCAPA is suspected by echocardiography, some centers choose confirmation by cardiac catheterization prior to surgical treatment. If an arrhythmia, such as supraventricular tachycardia (SVT), is identified, then an initial treatment with adenosine (0.1 mg/kg per dose IV) to restore sinus rhythm and then hospitalization is required to begin maintenance therapy with either a beta-blocker or digoxin depending on the underlying mechanism.
Respiratory distress in an infant or a child may not be airway disease, a cardiac etiology must always be considered.
CXR is a simple and safe test to help identify significant CHD in this age group as most will have cardiomegaly and increased pulmonary vascular markings.
Absent or diminished femoral pulses strongly suggest the diagnosis of a CoA and should be evaluated in any child that presents to emergency room with possible cardiac disease or right arm hypertension. In the setting of low cardiac output, a typical pressure gradient from right arm to lower extremity may not be present.
FIGURE 8.18
Echo image of a PDA. The classic ductal (aka “3 vessel”) view demonstrates the right and left pulmonary arteries with antegrade (blue) flow and the large PDA (red) continuous flow from aorta to pulmonary artery. (RPA, right pulmonary artery; LPA, left pulmonary arter; MPA, middle pulmonary artery; DAo, descending aorta.)
