The interpretation of the pediatric ECG, particularly from an infant, presents a unique challenge for the emergency physician. The difficulty arises because the ECG normally changes with age, and findings typically abnormal for adults may in fact be normal in young children and infants.
These progressive electrocardiographic changes are indicative of the maturation in cardiac physiology and the circulatory system with age. During the perinatal period, systemic circulation initially depends on the right side of the heart via the patent ductus arteriosus (PDA). As the PDA closes, the left side of the heart provides systemic circulation. The transition from a right-dominant to left-dominant system results in concomitant changes in QRS complex axis and morphology with age. Similarly with age, stroke volume increases with heart size and becomes a more important determinant of overall cardiac output. In infancy and early childhood, heart rate is higher to maintain cardiac output, but decreases as stroke volume increases with age.
The typical infant ECG (Fig. 2) will reveal a sinus tachycardia (up to 180 beats/minute) and right axis deviation. In addition, right ventricular precordial dominance also will be seen. The normal ECG will demonstrate evidence of increased R wave amplitude in leads V1 and V2, and decreased amplitude in leads V5 and V6. Over the first few years of life, as the left ventricle increases in size and prominence, the R wave will diminish and the S wave will increase slightly in prominence in leads V1 and V2, while the R wave will increase in amplitude and the S wave will diminish in leads V5 and V6.
The typical “juvenile” repolarization pattern of T wave inversion, usually seen in the anterior leads V1 through V3, can be present at birth or within a few days after birth and lasting until late childhood and early adolescence. (Fig. 3.) It also should be noted that the normal ECG intervals differ in children owing to the smaller muscle mass. Accordingly the QRS complex and PR interval are normally shorter in children than adults, but this increases with age.
The ECG in this case is notable for a number of reasons. (Fig. 4.) First, the 12-lead ECG demonstrates sinus rhythm at a rate of 138 beats/minute, which is tachycardiac but not abnormally so for a newborn. Second and more concerning is the presence of a left-ward axis deviation that could be normal for an adult, but definitely is abnormal for a newborn infant. In addition, there is left ventricular predominance across the precordium with large amplitude R waves in leads V4, V5, and V6 consistent with left ventricular hypertrophy (Fig. 4.). This finding is abnormal for a newborn; infant right-sided predominance would be expected. In addition, there is evidence of repolarization abnormality consistent with left ventricular hypertrophy with inverted T waves in the lateral leads V4 and V5, a distribution that is not consistent with the typical “juvenile” pattern.
These findings of left axis deviation and left ventricular hypertrophy in a newborn are worrisome for the presence of congenital heart disease. Congenital abnormalities that can present with left ventricular hypertrophy and left axis deviation within the first few weeks of life include ventricular septal defects, tricuspid atresia, and atrioventricular canal defects. Causes of left ventricular hypertrophy in older children and even later in life include patent ductus arteriosus, coarctation of the aorta, truncus arteriosis, aortic stenosis, pulmonic stenosis, and hypertrophic cardiomyopathy.
The patient was admitted to the hospital's infant special care unit. Additional examination was performed including four-extremity blood pressures showing marked decreases in the left arm and both legs. Pulse oximetry performed in all extremities demonstrated saturations of 98% to 100% in the right upper extremity, and 88% to 94% in the left upper extremity and both lower extremities.
The pediatric cardiology service was consulted because of the suspicion for a congenital heart condition and abnormality. An echocardiogram was performed and revealed a stage 1 interrupted aortic arch and ventricular septal defect. Prostaglandin therapy was initiated to maintain the patency of the ductus arteriosus. The patient was subsequently transferred to the local children's hospital for definitive cardiac surgery.
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Philadelphia; Elsevier Mosby; 2005; pp. 22–30.