Every heartbeat is controlled by electrical waves passing through the heart. The summation of this electrical activity results in the tracing seen on an electrocardiogram (ECG). The first ECG was performed in the 1880s through the work of August Waller and Willem Einthoven. The ECG has since been used as a simple and noninvasive method to screen patients for a variety of anatomic and electrical disorders. This chapter provides an overview for interpreting pediatric ECGs and identifying important rhythm disturbances in the pediatric population.

A standard ECG is made up of 12 leads, consisting of 6 limb leads and 6 precordial leads. This divides the heart into a frontal plane (leads I, II, III, aVR, aVL, aVF) and a transverse plane (leads V1–V6). Due to the predominance of the right ventricle during fetal life and in many types of congenital heart disease, a complete pediatric ECG consists of three additional precordial leads: V7 on the left, and V3r, V4r on the right. The combination of these leads creates a three-dimensional model on which the electrical waves of the heart can be plotted and tracked.

The first step in ECG reading is to check the standards by which it is obtained. Since ECG interpretation depends on pattern recognition, diagnostic accuracy requires that all tracings be obtained in standard fashion. The paper speed should be 25 mm/s and the amplitude 10 mm/mV. If the QRS deflection is large, the ECG machine may decrease the amplitude automatically. Failure to recognize this may lead to a missed diagnosis of ventricular hypertrophy (Figure 52-1).

Beyond this, the ECG should be analyzed systematically. The following can be used as a model for ECG interpretation.

Normal cardiac depolarization starts in the sinus node, high in the right atrium. This results in atrial depolarization, inscribed as the P wave on an ECG. Electricity then passes from the atria into the atrioventricular (AV) node, which relays the impulse to the ventricles via the right and left bundle branches. Ventricular depolarization results in the QRS complex on ECG. As the ventricles transition from depolarization to repolarization, there is an isoelectric ST segment. Repolarization is represented by the T wave.

RATE

The heart rate can be calculated in milliseconds (ms) by counting the squares between consecutive QRS complexes, and in beats per minute (bpm) by dividing milliseconds into 60,000. Each small square is 40 ms; each large square is 200 ms. As an example, three large squares between beats is 60,000/600 ms = 100 bpm. The normal heart rate range varies by age.¹ Rates above the age-related normal are described as tachycardia; rates below normal represent bradycardia (Table 52-1).

RHYTHM

Sinus rhythm requires a P wave before every QRS complex, with the P wave originating in the high right atrium. Normal atrial depolarization is inscribed as an upright P wave in leads I, II, and aVF (axis 0 to +90 degrees; see “Axis,” below), indicating that the impulse is directed inferiorly and to the left.

Normal Rhythm Variants

When the P wave axis differs from sinus, the rhythm is called ectopic atrial rhythm, a normal variant in the healthy child with a normal heart rate. Fluctuations in the heart rate may be noted during the respiratory cycle. Specifically, in healthy patients, the heart rate increases with inspiration and slows with expiration. This may be exaggerated under certain circumstances, especially during periods of increased vagal tone, such as during sleep. This is called sinus arrhythmia, and despite its name, is a normal finding in healthy patients.

Tachyarrhythmias

Tachyarrhythmias can be broadly divided into two categories: narrow or wide. In general, narrow complex rhythms are caused by supraventricular tachycardia (SVT) and originate at or above the AV junction, whereas wide complex rhythms are caused by ventricular tachycardia (VT) and include arrhythmias arising from below the bundle of His. This distinction is imprecise, however, as some forms of SVT conduct with wide complex beats, while some VTs can appear narrow.²

Ectopic Beats

Single atrial or ventricular premature beats are common, often benign findings on pediatric ECGs. They are frequently noted after an irregular heartbeat is detected on physical examination. A high burden of isolated ectopic beats is often noted in the neonatal period. This generally resolves in the first few weeks of life and requires no medical intervention in the absence of heart disease. Atrial premature beats are almost always benign. When frequent ventricular ectopy is noted, an echocardiogram can be done to rule out structural abnormalities or ventricular dysfunction. A Holter monitor is used to quantify the ectopic beats and determine whether higher grade ectopy exists. Exercise stress testing is useful in evaluating the response of the ectopy to catecholaminergic stress. Further evaluation is warranted in the presence of symptoms (e.g. palpitations, dizziness, or syncope), runs of tachycardia, ventricular dilation or dysfunction by echocardiography, or increased ectopy with stress/exercise. Occasionally, ventricular ectopy can signify the presence of underlying cardiac electrical disease. A careful family history is important to investigate the possibility of an inherited arrhythmia substrate, such as Long-QT syndrome (LQTS).

AXIS

The frontal leads divide the heart into quadrants, allowing the reader to ascertain the direction of any wave passing through the heart (Figure 52-2). The P wave axis, or predominant direction of atrial depolarization, can be determined by identifying the limb lead with the largest P wave deflection. Each lead correlates with a vector in the figure, and therefore with the direction of the atrial wave-front. Similarly, the predominant direction of ventricular depolarization can be determined by the largest QRS complex in the frontal plane. As both atria and ventricles depolarize inferiorly and leftward, the axes of the P wave and QRS complex usually fall in the southeast quadrant, between 0 and +90 degrees. In normal heart this results in a positive deflection in leads I, II, and aVF (Table 52-1).