Developmental Changes

The marked changes that occur in cardiac physiology and chamber dominance during the perinatal transition (Chapter 415) are reflected in the evolution of the ECG during the neonatal period. Because vascular resistance in the pulmonary and systemic circulations is nearly equal in a term fetus, the intrauterine work of the heart results in an equal mass of both the right and left ventricles. After birth, systemic vascular resistance rises when the placental circulation is eliminated, and pulmonary vascular resistance falls when the lungs expand. These changes are reflected in the ECG as the right ventricular wall begins to thin.

The ECG demonstrates these anatomic and hemodynamic features principally by changes in QRS and T-wave morphologic features. It is recommended that a 13-lead ECG be performed in pediatric patients, including either lead V₃R or V₄R, which are important in the evaluation of right ventricular hypertrophy. On occasion, lead V₁ is positioned too far leftward to reflect right ventricular forces accurately. This problem is present particularly in premature infants, in whom the electrocardiographic electrode gel may produce contact among all the precordial leads.

During the 1st days of life, right axis deviation, large R waves, and upright T waves in the right precordial leads (V₃R or V₄R and V₁) are the norm (Fig. 417-2). As pulmonary vascular resistance decreases in the 1st few days after birth, the right precordial T waves become negative. In the great majority of instances, this change occurs within the 1st 48 hr of life. Upright T waves that persist in leads V₃R, V₄R, or V₁ beyond 1 wk of life are an abnormal finding indicating right ventricular hypertrophy or strain, even in the absence of QRS voltage criteria. The T wave in V₁ should never be positive before 6 yr of age and may remain negative into adolescence. This finding represents one of the most important, yet subtle differences between pediatric and adult ECGs and is a common source of error when adult cardiologists interpret pediatric ECGs.

Figure 417-2 Electrocardiogram in a normal neonate <24 hr of age. Note the dominant R wave and upright T waves in leads V₃R and V₁ (V₃R paper speed = 50 mm/sec).

In a newborn, the mean QRS frontal-plane axis normally lies in the range of +110 to +180 degrees. The right-sided chest leads reveal a larger positive (R) than negative (S) wave and may do so for months because the right ventricle remains relatively thick throughout infancy. Left-sided leads (V₅ and V₆) also reflect right-sided dominance in the early neonatal period, when the R : S ratio in these leads may be <1. A dominant R wave in V₅ and V₆ reflecting left ventricular forces quickly becomes evident within the 1st few days of life (Fig. 417-3). Over the years, the QRS axis gradually shifts leftward, and the right ventricular forces slowly regress. Leads V₁, V₃R, and V₄R display a prominent R wave until 6 mo to 8 yr of age. Most children have an R : S ratio >1 in lead V₄R until they are 4 yr of age. The T waves are inverted in leads V₄R, V₁, V₂, and V₃ during infancy and may remain so into the middle of the 2nd decade of life and beyond. The processes of right ventricular thinning and left ventricular growth are best reflected in the QRS-T pattern over the right precordial leads. The diagnosis of right or left ventricular hypertrophy in a pediatric patient can be made only with an understanding of the normal developmental physiology of these chambers at various ages until adulthood is reached. As the left ventricle becomes dominant, the ECG evolves to the characteristic pattern of older children (Fig. 417-4) and adults (Fig. 417-5).

Figure 417-3 Electrocardiogram of a normal infant. Note the tall R and small S waves in V₄R and V₁ and the inverted T wave in these leads. A dominant R wave is also present in V₆.

Figure 417-4 Electrocardiogram of a normal child. Note the relatively tall R waves and inversion of the T waves in V₄R and V₁.

Figure 417-5 Normal adult electrocardiogram. Note the dominant S wave in lead V₁. This pattern in an infant would indicate the presence of left ventricular hypertrophy.

Ventricular hypertrophy may result in increased voltage in the R and S waves in the chest leads. The height of these deflections is governed by the proximity of the specific electrode to the surface of the heart; by the sequence of electrical activation through the ventricles, which can result in variable degrees of cancellation of forces; and by hypertrophy of the myocardium. Because the chest wall in infants and children, as well as in adolescents, may be relatively thin, the diagnosis of ventricular hypertrophy should not be based on voltage changes alone.

The diagnosis of pathologic right ventricular hypertrophy is difficult in the 1st wk of life because physiologic right ventricular hypertrophy is a normal finding. Serial tracings are often necessary to determine whether marked right axis deviation and potentially abnormal right precordial forces or T waves, or both, will persist beyond the neonatal period (Fig. 417-6). In contrast, an adult electrocardiographic pattern (see Fig. 417-5) seen in a neonate suggests left ventricular hypertrophy. The exception is a premature infant, who may display a more “mature” ECG than a full-term infant (Fig. 417-7) as a result of lower pulmonary vascular resistance secondary to underdevelopment of the medial muscular layer of the pulmonary arterioles. Some premature infants display a pattern of generalized low voltage across the precordium.

Figure 417-6 Electrocardiogram of an infant with right ventricular hypertrophy (tetralogy of Fallot). Note the tall R waves in the right precordium and deep S waves in V₆. The positive T waves in V₄R and V₁ are also characteristic of right ventricular hypertrophy.

Figure 417-7 Electrocardiogram of a premature infant (weight 2 kg and age 5 wk at the time of the tracing). The cardiovascular system was clinically normal. Left ventricular dominance is manifested by R-wave progression across the chest, similar to tracings obtained from older children. Compare with the tracing from a normal full-term infant (see Fig. 417-3).

The ECG should always be evaluated systematically to avoid the possibility of overlooking a minor, but important abnormality. One approach is to begin with an assessment of rate and rhythm, followed by a calculation of the mean frontal-plane QRS axis, measurements of segment intervals, assessment of voltages, and, finally, assessment of ST and T-wave abnormalities.

Rate and Rhythm

A brief rhythm strip should be examined to assess whether a P wave always precedes each QRS complex. The P-wave axis should then be estimated as an indication of whether the rhythm is originating from the sinus node. If the atria are situated normally in the chest, the P wave should be upright in leads I and aVF and inverted in lead aVR. With atrial inversion (situs inversus), the P wave may be inverted in lead I. Inverted P waves in leads II and aVF are seen in low atrial, nodal, or junctional rhythms. The absence of P waves indicates a rhythm originating more distally in the conduction system. In this case, the morphologic features of the QRS complexes are important in differentiating a junctional (usually a narrow QRS complex) from a ventricular (usually a wide QRS complex) rhythm.

P Waves

Tall (>2.5 mm), narrow, and spiked P waves are indicative of right atrial enlargement and are seen in congenital pulmonary stenosis, Ebstein anomaly of the tricuspid valve, tricuspid atresia, and sometimes cor pulmonale. These abnormal waves are most obvious in leads II, V₃R, and V₁ (Fig. 417-8A). Similar waves are sometimes seen in thyrotoxicosis. Broad P waves, commonly bifid and sometimes biphasic, are indicative of left atrial enlargement (Fig. 417-8B). They are seen in some patients with large left-to-right shunts (ventricular septal defect [VSD], patent ductus arteriosus [PDA]) and with severe mitral stenosis or regurgitation. Flat P waves may be encountered in hyperkalemia.

Figure 417-8 Atrial enlargement. A, Peaked narrow P waves characteristic of right atrial enlargement. B, Wide bifid M-shaped P waves typical of left atrial enlargement.

QRS Complex

Right Ventricular Hypertrophy

For the most accurate assessment of ventricular hypertrophy, pediatric ECGs should include the right precordial lead V₃R or V₄R, or both. The diagnosis of right ventricular hypertrophy depends on demonstration of the following changes (see Fig. 417-6): (1) a qR pattern in the right ventricular surface leads; (2) a positive T wave in leads V₃R-V₄R and V₁-V₃ between the ages of 6 days and 6 yr; (3) a monophasic R wave in V₃R, V₄R, or V₁; (4) an rsR′ pattern in the right precordial leads with the 2nd R wave taller than the initial one; (5) age-corrected increased voltage of the R wave in leads V₃R-V₄R or the S wave in leads V₆-V₇, or both; (6) marked right axis deviation (>120 degrees in patients beyond the newborn period); and (7) complete reversal of the normal adult precordial RS pattern. At least 2 of these changes should be present to support a diagnosis of right ventricular hypertrophy.

Abnormal ventricular loading can be characterized as either systolic (as a result of obstruction of the right ventricular outflow tract, as in pulmonic stenosis) or diastolic (as a result of increased volume load, as in atrial septal defects [ASDs]). These two types of abnormal loads result in distinct electrocardiographic patterns. The systolic overload pattern is characterized by tall, pure R waves in the right precordial leads. In older children, the T waves in these leads are initially upright and later become inverted. In infants and children <6 yr, the T waves in V₃R-V₄R and V₁ are abnormally upright. The diastolic overload pattern (typically seen in patients with ASDs) is characterized by an rsR′ pattern (Fig. 417-9) and a slightly increased QRS duration (minor right ventricular conduction delay). Patients with mild to moderate pulmonary stenosis may also exhibit an rsR′ pattern in the right precordial leads.

Figure 417-9 Electrocardiogram showing right ventricular conduction delay characterized by an rsR′ pattern in V₁ and a deep S wave in V₆ (V₃R paper speed = 50 mm/sec).

Left Ventricular Hypertrophy

The following features indicate the presence of left ventricular hypertrophy (Fig. 417-10): (1) depression of the ST segments and inversion of the T waves in the left precordial leads (V₅, V₆, and V₇), known as a left ventricular strain pattern—these findings suggest the presence of a severe lesion; (2) a deep Q wave in the left precordial leads; and (3) increased voltage of the S wave in V₃R and V₁ or the R wave in V₆-V₇, or both. It is important to emphasize that evaluation of left ventricular hypertrophy should not be based on voltage criteria alone. The concepts of systolic and diastolic overload, though not always consistent, are also useful in evaluating left ventricular enlargement. Severe systolic overload of the left ventricle is suggested by straightening of the ST segments and inverted T waves over the left precordial leads; diastolic overload may result in tall R waves, a large Q wave, and normal T waves over the left precordium. Finally, an infant with an ECG that would be considered “normal” for an older child may, in fact, have left ventricular hypertrophy.

Figure 417-10 Electrocardiogram showing left ventricular hypertrophy in a 12 yr old child with aortic stenosis. Note the deep S wave in V₁-V₃ and tall R in V₅. In addition, T-wave inversion is present in leads II, III, aVF, and V₆.

P-R and Q-T Intervals

The duration of the P-R interval shortens with increasing heart rate; thus, assessment of this interval should be based on age- and rate-corrected nomograms. A long P-R interval is diagnostic of a 1st-degree heart block, the cause of which may be congenital, postoperative, inflammatory (myocarditis, pericarditis, rheumatic fever), or pharmacologic (digitalis).

The duration of the Q-T interval varies with the cardiac rate; a corrected Q-T interval (Q-Tc) can be calculated by dividing the measured Q-T interval by the square root of the preceding R-R interval. A normal Q-Tc should be <0.45. It is often lengthened with hypokalemia and hypocalcemia; in the former instance, a U wave may be noted at the end of the T wave (Fig. 417-11). There are a number of medications that can also lengthen the Q-T interval. A congenitally prolonged Q-T interval (Fig. 417-12) may also be seen in children with one of the long Q-T syndromes. These patients are at high risk for ventricular arrhythmias, including a form of ventricular tachycardia known as torsades de pointes, and sudden death (Chapter 429.5).

Figure 417-11 Electrocardiogram in hypokalemia (serum potassium, 2.7 mEq/L; serum calcium, 4.8 mEq/L at the time of the tracing). Note the prolongation of electrical systole as evidenced by a widened TU wave, as well as depression of the ST segment in V₄R, V₁, and V₆.

Figure 417-12 Prolonged Q-T interval in a patient with long Q-T syndrome.

ST Segment and T-wave Abnormalities

A slight elevation of the ST segment may occur in normal teenagers and is attributed to early repolarization of the heart. In pericarditis, irritation of the epicardium may cause elevation of the ST segment followed by abnormal T-wave inversion as healing progresses. Administration of digitalis is sometimes associated with sagging of the ST segment and abnormal inversion of the T wave.

Depression of the ST segment may also occur in any condition that produces myocardial damage or ischemia, including severe anemia, carbon monoxide poisoning, aberrant origin of the left coronary artery from the pulmonary artery, glycogen storage disease of the heart, myocardial tumors, and mucopolysaccharidoses. An aberrant origin of the left coronary artery from the pulmonary artery may lead to changes indistinguishable from those of acute myocardial infarction in adults. Similar changes may occur in patients with other rare abnormalities of the coronary arteries and in those with cardiomyopathy, even in the presence of normal coronary arteries. These patterns are often misread in young infants because of the unfamiliarity of pediatricians with this “infarct” pattern, and thus a high index of suspicion must be maintained in infants with dilated cardiomyopathy or with symptoms compatible with coronary ischemia (e.g., inconsolable crying).

T-wave inversion may occur in myocarditis and pericarditis, or it may be a sign of either right or left ventricular hypertrophy and strain. Hypothyroidism may produce flat or inverted T waves in association with generalized low voltage. In hyperkalemia, the T waves are commonly of high voltage and are tent-shaped (Fig. 417-13).

Figure 417-13 Electrocardiogram in hyperkalemia (serum potassium, 6.5 mEq/L; serum calcium, 5.1 mEq/L). Note the tall, tent-shaped T waves, especially in leads I, II, and V₆.