Rudolph's Pediatrics, 22nd Ed.

CHAPTER 493. Electrocardiography

George F. Van Hare

Normal electrical activation of the heart begins pacemaker activity in the sinoatrial node, and the wave of activation spreads through the right and left atria (Fig. 493-1). In the right atrium the wave of depolarization passes inferiorly, and the left atrium is activated via Bachmann bundle, which also triggers an inferiorly directed activation front. These activation fronts generate a potential that is detected on the body surface as the P wave. The impulse is delayed at the atrioventricular (AV) node, producing the PR interval. This allows ventricular filling to be completed before ventricular contraction begins. Beyond the AV node, the impulse moves rapidly down the bundle of His into the right and left bundle branches. As the impulses pass down the septum, they activate septal muscle predominantly from the left side, so that the initial ventricular vector passes from left to right, anteriorly and superiorly (Fig. 493-2), and begins the Q wave in lead V6 or the first part of the R wave in lead V1.1 After reaching the apex, the impulse activates the ventricular free walls from endocardium to epicardium and from apex toward the base, thus inscribing the R and S waves; the last part of the heart to be activated is the posterior ventricular muscle just under the AV ring. In adults and older children, there is more left than right ventricular muscle, so the major cardiac vectors point to the left and posteriorly and produce a tall R wave in V6 and a deep S wave in V1. In a normal newborn infant with a thick right ventricle, the major cardiac vectors pass to the right and anteriorly and produce a dominant R wave in V1 and a large S wave in V6. After depolarization has occurred, there is slower repolarization that produces the T wave.

The “scalar” electrocardiogram is a recording of voltage against time, usually made at a paper speed of 25 mm/s, with 1 mV giving 10 mm of deflection.  The limb leads (I, II, III, aVR, aVL, aVF) represent forces in the frontal plane, and the precordial leads essentially represent forces in the horizontal plane (Fig. 493-3B); of these, the right chest leads (V4R,V3R,V1,V2) indicate anteroposterior forces, and the left chest leads (V5,V6) indicate left-to-right forces. Furthermore, certain parts of the left ventricle can be roughly reflected in certain groupings of leads: leads V1 and V2 show activity in the anteroseptal muscle; V2 to V5 in the anterior wall; V5 and V6 in the apex; I and aVL in the anterolateral wall; and II, III, and aVF in the inferior (diaphragmatic) wall.


The routine pediatric electrocardiogram involves the recording of 15 leads, the standard 12 plus leads to the right of V1 (V3R, V4R), and at least 1 lead (V7) to the left of V6; if no Q wave is seen in V7, then leads to the left of V7should be recorded as well. Ideally, the electrocardiogram should be interpreted knowing the history; physical examination; drug therapy; and heart size, shape, and position as seen on the chest roentgenogram, as part of the standardized cardiac evaluation. However, the electrocardiographer often does not have access to this information. At a minimum, the reason for the study should be given.

It is best to read the electrocardiogram systematically. First, measure atrial and ventricular rates and define the rhythm. Then record the PR interval, QRS duration, and QT interval. Measure the frontal-plane mean axes of the P waves, QRS complex, and T waves. Finally, look for abnormalities of pattern in the waves and their interconnecting segments and note the voltages of P, Q, R, S, and T waves.

The electrocardiogram can provide information about arrhythmias, hypertrophy of cardiac chambers, electrolyte changes, myocar-dial or pericardial infections, and myocardial ischemia and infarction. Specific electrocardiogram (ECG) patterns occur in certain congenital heart diseases. The electrocardiogram gives little information about myocardial function or ventricular cavity size.

FIGURE 493-1. Diagram of conduction system. AV, atrioventricular node; His, bundle of His, dividing into right and left bundles; LA, left atrium; RV and LV, right and left ventricles; SA, sinoatrial node; SVC and IVC, superior and inferior venae cavae.


To evaluate the mean frontal plane QRS axis, the following features must be noted:

• Lead I records electrical activity from the left to the right arm; by agreement, a deflection passing toward the left arm is positive, and a deflection passing away from it is negative (Fig. 493-4A).

• Leads II and III are at 60° to each other and to lead I, and they can be superimposed on a common center (Fig. 493-4B). Note that the lower half of the frontal plane is assigned positive numbers and the upper half negative numbers.

• Lead aVF records electrical activity from the legs up to the heart and thus lies in the axis +90° to 90° (Fig. 493-4C). An impulse passing toward the leg thus gives a positive deflection.

• Leads aVR and aVL record electrical activity from the right and left shoulders, respectively, to the heart (Fig. 493-4D), and their axes are at 120° to each other and to lead aVF. Because they are unipolar leads, an impulse passing toward either shoulder will give a positive deflection despite the negative angles associated with the superior ends of the axes in the figure.

• All 6 leads may be superimposed on a central point (Fig. 493-4E) to give axes that are at 30° to each other.

• To use this hexaxial reference frame, first decide whether lead I is predominantly positive or negative. In general, this can be determined from the heights of the R and S waves. However, because it is actually area that is assessed, a tall but narrow R wave might contribute less positivity than the negativity contributed by a short but wide S wave; if the Q wave is large, it should also be included in the assessment. If the result is positive, the net vector is passing to the left; if it is negative, the net vector is passing to the right. If the net voltage is zero (that is, equiphasic R and S complexes), the vector must be passing up at 90° or down at +90° (Fig. 493-4A). Next, examine aVF for its net voltage: if positive, the vector is passing down; if negative, it is passing up; if zero, it is passing directly right or left (Fig. 493-4C). These 2 leads can be quickly integrated to assign the vector to 1 of 4 quadrants (Fig. 493-4F). Lead I+, aVF+ indicates the left lower quadrant; lead I+, aVF− indicates the left upper quadrant (left axis); lead I−, aVF+ indicates the right lower quadrant (right axis); lead I−, aVF− indicates the right upper quadrant, sometimes termed the northwest quadrant. The axis can be measured more closely by referring to the remaining leads; on modern electrocardiograms, the frontal plane axis is computed and reported in the ECG print-out.

FIGURE 493-2. Normal ventricular depolarization, starting with 1 and ending with 5. A: Section through ventricles with thicker-walled left ventricle and thinner-walled right ventricle. Arrows are vectors, indicating direction and magnitude of electrical forces at each time. B: Vectors are superimposed on common center, and their tips are joined by a dashed line. C: The dashed line remains to give a vector loop. The vector at any moment would be a line joining the central point to the corresponding part of the loop. The arrows represent the direction of movement of the instantaneous vectors. In practice, direction is indicated by having each dash shaped like a teardrop, with the blunt end leading, and the dashes occur every 0.0025 second of the cardiac cycle.

• Occasionally, the R and S waves are almost equiphasic in several limb leads, perhaps in 4 or in all 6. This implies that the QRS vector is mainly perpendicular to the frontal plane and in the frontal plane forms a rough circle so that there is no true mean axis. This is sometimes termed an indeterminate frontal plane axis. It has little specific clinical importance except insofar as it prevents the accurate determination of a mean QRS axis.

• The mean frontal axis of the P and T waves can be calculated in the same way.


By convention, the measured QT interval is reported as well as the “corrected” interval, termed the QTc, which is the raw QT divided by the square root of the R-R interval.


In normal sinus rhythm, the right atrium is activated before the left atrium so that the first part of the P wave is right atrial, the last part is left atrial, but forces from both atria make up the middle of the P wave. With right atrial hypertrophy, the duration of the P wave is not typically lengthened, but the P waves become taller and peaked, especially in lead II, and exceed the normal upper limit of 0.25 mV (2.5 mm at full standardization). In lead V1, too, there may be a large biphasic P wave. With left atrial hypertrophy, the initial part of the P wave is unaltered, but the later part is larger and often lasts longer, so that the P waves are wider than normal and bifid, with a large second component.

The normal P frontal plane axis is about +30° to +60°; any marked change from this axis suggests an abnormal focus of atrial activation.

The PR interval, from the beginning of the P wave to the onset of the QRS complex, is about 0.13 second in newborns; it increases to about 0.16 second at 16 years of age and can be up to 0.21 second in adults.


Because ventricular activation begins in the septum and generates a septal vector that normally passes to the right, anteriorly, and superiorly, a Q wave is normally present in V6 and absent in the right chest leads. A Q wave in right but not in left chest leads may indicate septal activation from right to left because of left bundle branch block or ventricular inversion (L-transposition of the great arteries).

FIGURE 493-3 A: Einthoven equilateral triangle is superimposed on the frontal plane of the thorax. A mean QRS vector is shown in the triangle, and its projection on each of the limb leads is obtained by dropping perpendiculars (dashed lines) from the vector to each lead. Note that the angle the vector makes determines the magnitude of its projection in each lead and that the magnitude is greatest in the lead almost parallel to the vector. B: The conventional sites for electrode placement on the thorax (V leads). V1 and V2 are in the fourth intercostal space. V4 is in the fifth space. V3 is halfway between V2 and V4, and V5 and V6 are in the fifth space in the anterior and midaxillary lines, respectively. V3R and V4R are the right-sided counterparts of V3 and V4. These precordial leads lie roughly in the horizontal plane. MCL, midclavicular line.

FIGURE 493-4. Measurement of mean frontal plane axes (see text).


At birth, with the relatively thick right ventricle of the term infant, the mean QRS axis points anteriorly and to the right, giving right axis deviation (95% limits, 90–190°) and large R waves in right precordial leads. The QRS axis gradually shifts to the left in the frontal plane, and by about 3 months of age averages +65°, with a range in normal infants of 0° to +105°. It normally remains in the left lower quadrant throughout life. In the horizontal plane, with development the axis gradually rotates posteriorly until it is pointing leftward at 0° at about 3 months of age and posteriorly at about 45° from age 3 years onward.1This explains why with age the R wave decreases in V1 and increases in V6, whereas V1 shows a large S wave after infancy. Although premature infants also show right ventricular dominance at birth, the QRS vector begins to swing posteriorly and to the left at about 1 month of age; this normal variant may cause overdiagnosis of left ventricular hypertrophy in pre-term infants.

The mean T vector undergoes rapid and marked changes after birth. For the first 12 hours it points to the left and posteriorly and has a frontal plane axis of about +60°; this gives a negative T wave in V1. The T vector then rotates anteriorly and to the right, giving a positive T wave in V1 by 24 hours after birth. It remains anterior for 2 to 7 days and then moves posteriorly and to the left, and the T wave again inverts in V1. The reasons for these rapid changes are not clear. At about 12 years of age, the T wave may become upright once again in V1 in some children. T waves normally may be inverted in leads V5 and V6during but not beyond the first day after birth; they may be inverted normally in V4 until 5 years of age and in V3 until 10 years of age. The frontal plane T axis stays at about +60° throughout childhood. Because the T and QRS vectors do not follow the same course in early childhood, the angle between them changes. At birth the frontal plane mean QRS-T angle is about +130°, and it slowly falls until it reaches 30° to 60° by about 3 years of age; thereafter, it remains under 60°, and any increase suggests a myocardial abnormality.


Ventricular hypertrophy is difficult to diagnose reliably by electrocardiography. Differences in heart position and chest shape affect how much of the cardiac potential is recorded from the body surface, and minor degrees of asynchrony of ventricular depolarization can alter the algebraic sum of the electrical forces at any moment. Because of the wide range of normality, it is impossible to diagnose slight hypertrophy, especially as the voltages before the onset of hypertrophy are seldom known. Furthermore, no single sign on its own can be considered reliable; in particular, neither an abnormal QRS axis nor increased voltage in a single lead should result in the reading of hypertrophy if there are no other supportive features.


In infancy, with the increased mass of left ventricular muscle in left ventricular hypertrophy, the mean QRS axis moves to the left and posteriorly. Therefore, in the frontal plane the QRS axis moves to between 0° and –90°; an axis less than 30° is uncommon in infancy and suggests the possibility of left ventricular hypertrophy. This leftward shift of the QRS axis increases the R wave and decreases the S wave in V5and V6, and the posterior shift of the QRS axis decreases R waves and increases S waves in V1. In older children and adults, the QRS axis is normally to the left, posterior, and inferior, so that with left ventricular hypertrophy there is no further axis shift but only an increase in voltage.

In practice, the reading of left ventricular hypertrophy is based largely on voltage changes and T wave abnormalities. It should be noted here that the normal standards used in children derive from a study by Davignon et al in which the subjects were predominantly of European descent.3 There are clear data showing that in the African American population mean QRS voltages are higher without a higher incidence of actual left ventricular hypertrophy.4Therefore, the diagnosis of ventricular hypertrophy should be made with caution when the only indicator is increased voltage.

Increased posterior forces are suggested by R waves below the fifth percentile or S waves above the 95th percentile in V3R and V1 (Fig. 493-5A).3 The increased left forces are suggested by R waves above the 95th percentile in V5and V6 (Fig. 493-5B); smaller than normal S waves in V5 and V6 are not helpful because they can normally be very small. In addition, because the septum is usually involved in the hypertrophy, there is often an enlarged Q wave, which, when greater than 0.4 mV (4 mm at full standardization), suggests left ventricular hypertrophy. T-wave changes in the absence of voltage changes do not indicate left ventricular hypertrophy, but if the two changes are associated, they suggest either myocardial ischemia, as in severe aortic stenosis, or else what is termed left ventricular strain.

FIGURE 493-5. Normal values for R and S waves in (A) right and (B) left precordial leads at different ages. Lines represent percentiles, with the dotted line the 50th percentile. (Source: Davignon A, Rautaharju P, Boiselle E, et al. Normal ECG standards for infants and children. Pediatr Cardiol. 1979/1980;1:123.)


At birth the term infant has a right ventricular wall as thick as, or slightly thicker than, that of the left ventricle. Thus, the newborn has a pattern of physiological right ventricular hypertrophy compared with the older child or adult. If there is pathological right ventricular hypertrophy, the mean QRS vector may move farther right and anteriorly, so that frontal plane QRS axes more than 190° under 1 week of age or 105° over 1 month of age suggest right ventricular hypertrophy, provided that there is no conduction defect. The increased anterior and rightward forces produce taller R waves and smaller S waves in right chest leads and smaller R waves and larger S waves in left chest leads.

In addition, a pure R wave or a qR pattern in the right chest leads strongly suggests pathologic right ventricular hypertrophy, as does an upright T wave in V4R and V1 between 7 days and about 8 years of age. Note that neither left nor right ventricular hypertrophy can be diagnosed confidently if there is an abnormally wide QRS complex, as occurs in bundle branch block or Wolff-Parkinson-White syndrome.


If the right bundle is interrupted, septal activation from left to right is unchanged, and then the left ventricle is depolarized to give a force to the left and posteriorly; this force is more marked than usual because the counteracting right ventricular forces have not yet begun. As left ventricular depolarization is ending, the impulse eventually penetrates the right ventricular muscle and spreads slowly through it to give late-onset slow right and anterior forces. Therefore, in right chest leads there is a normal initial R wave followed by a deep narrow S wave and then a tall and wide R’ that brings the QRS duration to over 0.12 second in adults. (By convention, a deflection under 5 mm is written as a lowercase letter, for example, r, and a deflection over 5 mm is written as a capital letter, for example, R. Also, a second positive deflection is described as r’ or R’.) In left chest leads the pattern is of a qRS type, with a deep and wide terminal S wave. The terminal right and anterior forces, being unopposed by left ventricular forces, are large and serve to produce a marked right-axis shift in the frontal plane.

Because in the newborn infant the normal QRS duration is about 0.05 to 0.06 second, it is possible for complete right bundle branch block to widen the QRS but still be under the limit of 0.12 second that pertains to adults. Finally, many normal children have an rSr pattern that results from a delayed but otherwise normal terminal deflection caused by late depolarization of the posterior part of the right ventricle under the AV groove. This pattern has been termed incomplete right bundle branch block, but in children it usually has nothing to do with conduction changes in the right bundle and its major branches. Therefore, it is better to refer to this as a minor right ventricular conduction delay, and this pattern does not prevent one from reading the ECG as normal. A similar but more marked pattern of delayed terminal rightward conduction may also be seen in children with atrial septal defects and other causes of right ventricular volume overload.


ST-segment and T-wave changes other than those related to maturation have similar causes in children and adults. Frequently, they are secondary to changes in the QRS complex, such as widening of the QRS complex in conduction abnormalities or an increased QRS amplitude in hypertrophy. These secondary changes of T waves are usually associated with a normal QRS-T angle in the frontal plane.


Hypocalcemia lengthens and hypercalcemia shortens the QT interval. Because the QT interval normally varies with heart rate, a rate-independent corrected QT interval (QTc) is calculated as QT/√R-R. The normal value is 0.40, with a range of 0.36 to 0.44. A low magnesium level may intensify the effects of low calcium; clinically, the long QT interval of hypocalcemia in infancy may remain after the calcium level has been restored to normal and improve only after magnesium is given. Other factors can also alter the QT interval: Digitalis glycosides and pericarditis may shorten it slightly, and myocarditis and certain genetic syndromes may lengthen it.

A high serum potassium level gives high, peaked T waves that are clearly abnormal at concentrations above 7 meq/L. Higher potassium concentrations not only raise T waves further, but reduce QRS amplitude, widen QRS duration, and lengthen PR interval. Above 9 meq/L there are usually atrial arrest and very wide QRS complexes that may lead to ventricular fibrillation. Preterm infants may be more resistant to these changes. Low serum potassium levels lower T waves, the effect being detectable below 3.5 meq/L. As potassium falls more, a U wave appears, and the ST segment becomes depressed.


Physiologic changes are important because, if not appreciated, they may lead to the incorrect diagnosis of heart disease. Drinking iced liquids may cool the inferior wall of the left ventricle and cause transient deep T-wave inversion in the left chest leads. After heavy meals, there can be T-wave inversion in left chest leads that some clinicians associate with hyperglycemia. A history of recent ingestion of food or iced drinks will suggest these causes of T-wave changes, and a repeat ECG while fasting should then show normal T waves.

Two other important normal variants should be considered. Some children and young adults have large upright T waves and elevated S-T segments in precordial or even limb leads, thus pericarditis might be suspected. This pattern is termed early repolarization,  and it should not be considered abnormal. What distinguishes this variant from pericarditis is that here the T waves are very large and do not evolve as they do in pericarditis. The second variant is that of isolated inversion of the T waves in leads over the left ventricular apex, although the T waves are upright in earlier and later leads. This finding occurs most often in young men; it can vary from time to time and has no accepted explanation. Like other physiological T-wave changes, the T waves usually return to normal after oral potassium salts are ingested. Finally, athletes in peak training condition can have not only increased voltages diagnostic of left or right ventricular hypertrophy but also T-wave inversion in left ventricular leads. These can be normal findings in this setting, but hypertrophic cardiomyopathy must be ruled out, ideally by echocardiography.