The PR interval represents electrical impulse conduction from sinus node through atria, atrioventricular (AV) node, His bundle, bundle branches, and Purkinje system to ventricular myocyte (Fig. 8.3). PR interval measured from onset of P-wave to the onset of QRS complex, usually in lead II. Normal AV conduction defined as normal PR interval and normal association of each P-wave to the following QRS complex.

Normal PR interval duration is shorter in children and changes with age and heart rate. This finding may be due to the smaller cardiac mass in children. The neonatal PR interval may vary between 70 ms and 140 ms with mean of 100 ms (Schwartz et al. 2002). Therefore, AV conduction abnormality in young children may present with normal-appearing PR interval.

Short PR interval indicates that impulse generates from locations other than normal pacemaker (sinus node), the presence of accessory AV connections, or facilitated AV node conduction. PR prolongation represents impaired AV conduction. Injury to normal conduction pathway in atrium, AV node, His bundle, and bundle branches could increase PR duration.

For PR analysis, association of each QRS to previous P-wave is necessary. P-QRS evaluation in consecutive beats could help us to detect dissociation of the P-wave and QRS complex in disorders such as junctional rhythm and AV blocks.

QT interval reflects both ventricular depolarization and repolarization. It is measured from the onset of Q-wave to the end of T wave usually in leads II, V5, or V6 (Schwartz et al. 2002). QT is age and heart rate dependent. The increase of heart rate results in shorter QT interval. In the cases that T and U waves have overlap and discrimination of two waves is difficult or P-wave superimposes on T wave (usually in infant with higher heart rate), a line is drawn from the peak of the T-wave tangential to its downslope until it intersects the isoelectric line, and this point is considered as the end of T wave (Fig. 8.4).

For elimination of R-R interval variation on QT interval, QT should be corrected (QTc). Bazett’s formula is a practical method for QTc calculation: QTc = QT interval (ms)/√R-R interval (sec) (Bazett 1920).

Multiple studies were done to determinate cutoff point for QT prolongation. In first few days of neonatal period, upper limit (2 standard deviation above mean or 97.5 percentile) for QTc is 440 ms. After this period, there is an increase in QT interval duration. In the first 6 months of life, QTc interval can be as long as 490 ms; however, after 6 months the cutoff point for normal QTc is 440 ms (O’Connor et al. 2008). Anyway, if the QTc is greater than 50 % consecutive R-R interval, it is considered as abnormal.

The QT interval calculation is important because the presence of long QT predisposes the patients into malignant arrhythmia, i.e., torsades de pointes. The QT prolongation may have congenital and acquired types. Before evaluation for congenital disorders, acquired causes such as drugs and electrolyte abnormalities should be ruled out. In the presence of bundle branch block, JT segment is calculated, but there is a question about the accuracy of this measurement.

The P wave displays atrial depolarization. The first 0.04–0.06 s of the P-wave is related to RA depolarization and remainder related to the LA. RA enlargement is defined as tall and peaked P-wave in lead II. In infant and children, P-wave amplitude greater than 2.5–3.0 mV is considered abnormal. LA enlargement is characterized by a broad (≥0.12 s) and notched P-wave in lead II or wide (>0.04 s) and deep (>0.1 mV) terminal component (negative phase) in lead V1. In biatrial enlargement, both criteria for atrial enlargement are present.

The measurement of R-wave amplitude and QRS duration especially in precordial leads reflects ventricular depolarization status. Because of lower ventricular mass, the QRS duration is usually shorter in children than in adult: under 4 years of age, it is less than 0.09 s, less than 0.10 s up to 16 years of age, and less than 0.11 s by late adolescence (Deal et al. 2004).

Thin chest and proximity of the heart to ribs in neonate cause tall R or S wave in precordial leads in comparison to limb leads. Low QRS voltage may indicate myocarditis, pericardial effusion, and hypothyroidism.

Fetal circulation is mainly dependent on RV function; therefore, in neonatal period RV muscle mass increased in comparison to LV. This change on surface ECG reflects as high amplitude R wave in right precordial lead with R/S > 1 and deep S wave in left precordial leads with R/S < 1. Gradually after 1 month, the RV loses its dominancy and the LV is the dominant ventricle by the end of the first year of life. As a result, the R-wave amplitude will decrease in right precordial leads and increase in left precordial leads with advancing age (S-wave changes are reverse). Therefore, age-related R- and S-wave amplitude changes in precordial leads should be considered while assessing the ECG for ventricular hypertrophy.

The T-wave morphology and axis are changing during childhood. T wave represents ventricular repolarization. As opposed to ventricular depolarization, repolarization begins from the epicardium to the endocardium (QRS-T axis concordance). More than 90° difference between two axes may indicate myocardial injury. The T-wave amplitude value may vary from 0.5 mV in limb leads to 10 mV in precordial leads (Coviello 2016).

In the first week of life, T wave is upright in leads V1 and V3R. Then, it becomes inverted until 8 years and even may be continued to adolescence. In the first 3–5 years of life, 50 % of children have inverted T wave in lead V2, but this value decreases to 5–10 % in 8–12 years (Dickinson 2005). Persistent positive T wave after the first week may represent RVH. T wave is usually positive in left precordial leads in childhood except for the first few days of life that T wave may be flat or inverted. Although ST-T segment changes are nonspecific, but evaluation for diseases such as myocarditis, cardiomyopathy, pericarditis, and electrolyte disorders should be done.

In children especially during tachycardia, P wave may be superimposed on T wave. Comparison of serial T-wave morphology in long strip of the ECG may be helpful. Notched T wave in leads V2 and V3 can be a normal variant in the children. It may be misdiagnosed with 2:1 atrioventricular block, but with careful examination, this pattern is not observed in other leads. Hyperkalemia causes tall and peaked T wave (tented T wave) in surface ECG.

It is measured from the end of the QRS complex to the onset of the T wave. J point is the beginning of ST segment. It represents termination of depolarization with onset of ventricular repolarization. It is elevated when it is at least 1 mm above the isoelectric line and depressed when it is 0.5 mm below the isoelectric line (Deal et al. 2004). ST-segment elevation as J-point elevation is very common in adolescents. It is related to early depolarization and may be considered in differential diagnosis of other diseases especially pericarditis. In early repolarization, ST segment returns to the baseline with exercise. Early repolarization usually better observed in mid-precordial leads. Special forms of the early repolarization may be a risk factor for sudden death. ST-segment elevation in children is usually related to the pericarditis; however, less common causes such as myocardial ischemia should be considered.

RVH in children mostly results from congenital heart diseases with pressure and volume overload mechanisms. Other causes include cardiomyopathy, hereditary myocardial disease, pulmonary vascular disease, and respiratory disease.

The ECG criteria for RVH (Table 8.1) include R wave >98th percentile in V1, S wave > 98th percentile in V6, R/S ratio > 98th percentile in V1, RAD according to age, upright T wave in V1 between the first week and 8 years, specific morphologies of QRS (R, QR, RsR) in right precordial leads, and neonatal R-wave progression in precordial leads in older children (Fig. 8.5) (Davignon et al. 1979). As a criterion for RVH, RAD should be considered with other criteria. In combination with right atrial enlargement and deep S wave in V6, cor pulmonale should be suspected.

Diagnosis of RVH in neonate may be difficult, but signs of RVH include QR complex in V1, upright T wave in V1 after the first week of life, increased R-wave amplitude in V1, and decreased S-wave amplitude in V6.

Left ventricular hypertrophy (LVH) interpretation at surface ECG is based on voltage and repolarization criteria. ECG criteria of the LVH (Table 8.2) include R wave > 98th percentile in V6, S wave > 98th percentile in V1, R/S ratio > 98th percentile in V6, Q wave > 98th percentile in V6 or lead III, inverted T wave in left precordial leads, increased T-QRS angle (>100°), and increased inferior forces (low specificity) (Fig. 8.6).

In normal conditions T-wave and QRS complex axes have similar directions, but two axes would shift to opposite directions in LVH. It is important to note that LAD in children is not a criterion for LVH. Although ST-segment and T-wave changes are nonspecific markers for myocardial disease, they should be considered as the signs of LVH after excluding ischemic and myocardial diseases.

In neonate the decreased RV dominancy may be the only sign of LVH; therefore, normal adult ECG pattern in neonate is indicative of the LVH. Of course in preterm infant, the LV force is more prominent.

Biventricular hypertrophy (BiVH) should be considered when criteria for both RVH and LVH are present (Table 8.3). In BiVH, increased R-wave and S-wave voltages are observed in leads V1 and V6. High amplitude R and S wave in mid-precordial leads may be seen in children with thin chest wall. If combination of R- and S-wave amplitudes in leads V3 and V4 is more than 60 mm, BiVH should be considered (Katz and Wachtel 1937).

AV block can occur in children as well as in adult. Underlying causes may be congenital or acquired. Based on the severity of conduction system disease, AV block is divided into first, second, and third degree.

First–degree AV block, defined as PR interval prolongation, is a benign condition in children. As it was mentioned before, PR interval is shorter in children than adult; therefore, a normal-appearing PR interval may be indicative of conduction system disease. This form of AV block is usually asymptomatic and no treatment is necessary (Fig. 8.7).

Second–degree AV block is characterized by intermittent failure of atrial impulse conduction to the ventricles (Fig. 8.8). There are two types of second-degree AV block: Mobitz type I (Wenckebach) and Mobitz type II. Mobitz type I AV block is defined as progressive prolongation of AV conduction leading up to a nonconducted P wave. This kind of AV block is usually located in the AV node and needs no treatment. Mobitz type II AV block is present when there is sudden loss of AV conduction without prior PR elongation. This type of AV block is usually located more distally in the His bundle, bundle branches, and Purkinje system. The treatment is pacemaker implantation.

Third–degree or complete AV block is presented by lack of association between atrial and ventricular depolarization (Fig. 8.9). In this situation, atrial activity will be faster than ventricular response with no clear association. The treatment is pacemaker implantation.

His bundle divided into left and right bundle branches. Left bundle is sheetlike structure that is divided to left anterior fascicle and left posterior fascicle. Right bundle branch is cord-like structure that runs along moderator band to anterior portion of RV. Impulse conduction in left bundle and its branches is faster compared with right-sided counterpart. Consequently depolarization of both ventricles is nearly simultaneous and QRS complex is narrow. Injury to bundle branches may cause ventricular conduction delay and wide QRS.