Park's Pediatric Cardiology for Practitioners, 6th Ed.

Electrocardiography

In the clinical diagnosis and management of congenital or acquired heart disease, the presence or absence of electrocardiographic (ECG) abnormalities is often helpful. Hypertrophies (of ventricles and atria) and ventricular conduction disturbances are the two most common forms of ECG abnormalities. The presence of other ECG abnormalities such as atrioventricular (AV) conduction disturbances, arrhythmias, and ST segment and T-wave changes, is also helpful in the clinical diagnosis of cardiac problems.

Throughout this chapter, the vectorial approach will be used whenever possible. The vectorial approach is preferred to “pattern reading,” which has infinite number of possibilities. The following topics will be discussed in the order listed.

• What is the vectorial approach?

• Comparison of pediatric and adult ECGs

• Basic measurements and their normal values that are necessary for correct interpretation of an ECG. The discussion will include rhythm, heat rate, QRS axis, P and T axes, and so on.

• Atrial and ventricular hypertrophy

• Ventricular conduction disturbances

• ST-segment and T-wave changes, including myocardial infarction (MI)

Cardiac arrhythmias and AV conduction disturbances will be discussed separately in Chapters 24 and 25.

What Is the Vectorial Approach?

The vectorial approach views the standard scalar ECG as three-dimensional vector forces that vary with time. Vector is a quantity that possesses magnitude and direction, but scalar is a quantity that has magnitude only. A scalar ECG, which is routinely obtained in clinical practice, shows only magnitude of the forces against time. However, by combining scalar leads that represent the frontal projection and the horizontal projections of the vectorcardiogram, one can derive the direction of the force from scalar ECGs.

The limb leads (leads I, II, III, aVR, aVL, and aVF) provide information about the frontal projection (reflecting superior-inferior and right-to-left forces), and the precordial leads (leads V1 through V6, V3R, and V4R) provide information about the horizontal plane, which reflects forces that are right-to-left and anterior–posterior (Fig. 3-1). It is important for readers to become familiar with the orientation of each scalar ECG lead. After they have been learned, the vectorial approach helps readers retain the knowledge gained.

Hexaxial Reference System

It is necessary to memorize the orientation of the hexaxial reference system (see Fig. 3-1A). The hexaxial reference system is made up by the six limb leads (leads I, II, III, aVR, aVL, and aVF) and provides information about the superoinferior and right–left relationships of the electromotive forces. In this system, leads I and aVF cross at a right angle at the electrical center (see Fig. 3-1A). The bipolar limb leads (I, II, and III) are clockwise with the angle between them of 60 degrees. Note the positive poles of aVR, aVL, and aVF are directed toward the right and left shoulders and the foot, respectively. The positive limb of each lead is shown in a solid line and the negative limb in a broken line. The positive pole of each lead is indicated by the lead labels. The positive pole of lead I is labeled as 0 degree, and the negative pole of the same lead as ±180 degrees. The positive pole of aVF is designated as +90 degrees, and the negative pole of the same lead as −90 degrees. The positive poles of leads II and III are +60 and +120 degrees, respectively, and so on. The hexaxial reference system is used in plotting the QRS axis, T axis, and P axis.

The lead I axis represents the left–right relationship with the positive pole on the left and the negative pole on the right. The aVF lead represents the superior-inferior relationship with the positive pole directed inferiorly and the negative pole directed superiorly. The R wave in each lead represents the depolarization force directed toward the positive pole; the Q and S waves are the depolarization force directed toward the negative pole. Therefore, the R wave of lead I represents the leftward force, and the S wave of the same lead represents the rightward force (see Fig. 3-1A). The R wave in aVF represents the inferiorly directed force, and the S wave the superiorly directed force. By the same token, the R wave in lead II represents the leftward and inferior force, and the R wave in lead III represents the rightward and inferior force. The R wave in aVR represents the rightward and superior force, and the R wave in aVL represents the leftward and superior forces.

An easy way to memorize the hexaxial reference system is shown in Figure 3-2 by a superimposition of a body with stretched arms and legs on the X and Y axes. The hands and feet are the positive poles of electrodes. The left and right hands are the positive poles of leads aVR and aVL, respectively. The left and right feet are the positive poles of leads II and III, respectively. The bipolar limb leads I, II, and III are clockwise in sequence for the positive electrode.

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FIGURE 3-1 Hexaxial reference system (A) shows the frontal projection of a vector loop, and horizontal reference system (B) shows the horizontal projection. The combination of A and B constitutes the 12- (or 13-) lead electrocardiogram. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

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FIGURE 3-2 An easy way to memorize the hexaxial reference system. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

Horizontal Reference System

The horizontal reference system consists of precordial leads (leads V1 through V6, V3R, and V4R) (see Fig. 3-1B) and provides information about the anterior–posterior and the left–right relationship. The leads V2 and V6 cross approximately at a right angle at the electrical center of the heart. The V6 axis represents the left–right relationship, and the V2 axis represents the anterior–posterior relationship. The positive limb of each lead is shown in a solid line and the negative limb in a broken line. The positive pole of each lead is indicated by the lead labels (V4R, V1, V2, and so on). The precordial leads V3R and V4R are at the mirror image points of V3 and V4, respectively, in the right chest, and these leads are quite popular in pediatric cardiology because right ventricular (RV) forces are more prominent in infants and children.

Therefore, the R wave of V6 represents the leftward force and the R wave of V2 the anterior force. Conversely, the S wave in V6 represents the rightward force and the S wave of V2 the posterior force. The R wave in V1, V3R, and V4R represents the rightward and anterior force, and the S wave of these leads represents the leftward and posterior force (see Fig. 3-1B). The R wave of lead V5 in general represents the leftward force, and the R waves of leads V3 and V4 represent a transition between the right and left precordial leads. Ordinarily, the S wave in V2 represents the posterior and thus the left ventricular (LV) force, but in the presence of a marked right axis deviation, the S wave of V2 may represent RV force that is directed rightward and posteriorly.

Information Available on the 12-Lead Scalar Electrocardiogram

There are three major types of information available in the commonly available form of a 12-lead ECG tracing (Fig. 3-3):

1. The lower part of the tracing is a rhythm strip (of lead II).

2. The large upper left portion of the recording gives frontal plane information, and the upper right side of the recording presents horizontal plane information. The frontal plane information is provided by the six limbs leads (leads I, II, III, aVR, aVL, and aVF) and the horizontal plane information by the precordial leads. In Figure 3-3, the QRS vector is predominantly directed inferiorly (judged by predominant R waves in leads II, III, and aVF, so-called inferior leads) and is equally anterior and posterior, judged by equiphasic QRS complex in V2.

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FIGURE 3-3 A common form of routine 12-lead scalar electrocardiogram. There are three groups of information available on the recording. Frontal and horizontal plane information is given in the upper part of the tracing. Calibration factors are shown on the right edge of the recording. A rhythm strip (lead II) is shown at the bottom.

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FIGURE 3-4 Electrocardiogram from a normal 1-week-old infant.

3. A calibration marker usually appears at the right (or left) margin, which is used to determine the magnitude of the forces. The calibration marker consists of two vertical deflections 2.5 mm in width. The initial deflection shows the calibration factor for the six limb leads, and the latter part of the deflection shows the calibration factor for the six precordial leads. With the full standardization, one millivolt signal introduced into the circuit causes a deflection of 10 mm on the record. With the ½ standardization, the same signal produces 5 mm of deflection. The amplitude of ECG deflections is read in millimeters rather than in millivolts. When the deflections are too big to be recorded, the sensitivity may be reduced to ¼. With ½ standardization, the measured height in millimeters should be multiplied by 2 to obtain the correct amplitude of the deflection. In Figure 3-3, ½ standardization was used for the precordial leads.

Thus, from the scalar ECG tracing, one can gain information of the frontal and horizontal orientations of the QRS (or ventricular) complexes and other electrical activities of the heart as well as the magnitude of such forces.

Comparison of Pediatric and Adult Electrocardiograms

Electrocardiograms of normal infants and children are quite different from those of normal adults. The most remarkable difference is RV dominance in infants. RV dominance is most noticeable in newborns, and it gradually changes to LV dominance of adults. By 3 years of age, the child’s ECG resembles that of young adults. The age-related difference in the ECG reflects an age-related anatomic differences; the RV is thicker than the LV in newborns and infants, and the LV is much thicker than the RV in adults.

Right ventricular dominance of infants is expressed in the ECG by right axis deviation (RAD) and large rightward or anterior QRS forces (i.e., tall R waves in lead aVR and the right precordial leads [V4R, V1, and V2] and deep S waves in lead I and the left precordial leads [V5 and V6]) compared with an adult ECG.

A normal ECG from a 1-week-old neonate (Fig. 3-4) is compared with that of a young adult (Fig. 3-5). The infant’s ECG demonstrates RAD (+140 degrees) and dominant R waves in the right precordial leads. The T wave in V1 is usually negative. Upright T waves in V1 in this age group suggest right ventricular hypertrophy (RVH). Adult-type R/S progression in the precordial leads (deep S waves in V1 and V2 and tall R waves in V5 and V6; as seen in Fig. 3-5) is rarely seen in the first month of life; instead, there may be complete reversal of the adult-type R/S progression, with tall R waves in V1 and V2 and deep S waves in V5 and V6. Partial reversal is usually present, with dominant R waves in V1 and V2 as well as in V5 and V6, in children between the ages of 1 month and 3 years.

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FIGURE 3-5 Electrocardiogram from a normal young adult.

The normal adult ECG shown in Figure 3-5 demonstrates the QRS axis near +60 degrees and the QRS forces directed to the left, inferiorly and posteriorly, which is manifested by dominant R waves in the left precordial leads and dominant S waves in the right precordial leads, the so-called adult R/S progression. The T waves are usually anteriorly oriented, resulting in upright T waves in V2 through V6 and sometimes in V1.

Basic Measurements and Their Normal and Abnormal Values

In this section, basic measurements and their normal values that are necessary for routine interpretation of an ECG are briefly discussed in the order listed. This sequence is one of many approaches that can be used in routine interpretation of an ECG. The methods of their measurements will be followed by their normal and abnormal values and the significance of abnormal values.

1. Rhythm (sinus or nonsinus) by considering the P axis

2. Heart rate (atrial and ventricular rates, if different)

3. The QRS axis, the T axis, and the QRS-T angle

4. Intervals: PR, QRS, and QT

5. The P wave amplitude and duration

6. The QRS amplitude and R/S ratio; also abnormal Q waves

7. ST-segment and T-wave abnormalities

Rhythm

Sinus rhythm is the normal rhythm at any age and is characterized by P waves preceding each QRS complex and a normal P axis (0 to +90 degrees); the latter is an often neglected criterion. The requirement of a normal P axis is important in discriminating sinus from nonsinus rhythm. In sinus rhythm, the PR interval is regular but does not have to be of normal interval. (The PR interval may be prolonged as seen in sinus rhythm with first-degree atrioventricular [AV] block.)

Because the sinoatrial node is located in the right upper part of the atrial mass, the direction of atrial depolarization is from the right upper part toward the left lower part, with the resulting P axis in the lower left quadrant (0 to +90 degrees) (Fig. 3-6A). Some atrial (nonsinus) rhythms may have P waves preceding each QRS complex, but they have an abnormal P axis (Fig. 3-6B). For the P axis to be between 0 and +90 degrees, P waves must be upright in leads I and aVF or at least not inverted in these leads; simple inspection of these two leads suffices. A normal P axis also results in upright P waves in lead II and inverted P waves in aVR. A method of plotting axes is presented later for the QRS axis.

Heart Rate

There are many different ways to calculate the heart rate, but they are all based on the known time scale of ECG papers. At the usual paper speed of 25 mm/sec, 1 mm = 0.04 second, and 5 mm = 0.20 second (Fig. 3-7). The following methods are often used to calculate the heart rate.

1. Count the R-R cycle in six large divisions (1/50 minute) and multiply it by 50 (Fig. 3-8).

2. When the heart rate is slow, count the number of large divisions between two R waves and divide that into 300 (because 1 minute = 300 large divisions) (Fig. 3-9).

3. Measure the R-R interval (in seconds) and divide 60 by the R-R interval. The R-R interval is 0.36 second in Figure 3-8: 60 ÷ 0.36 = 166.

4. Use a convenient ECG ruler.

5. An approximate heart rate can be determined by memorizing heart rates for selected R-R intervals (Fig. 3-10). When R-R intervals are 5, 10, 15, 20, and 25 mm, the respective heart rates are 300, 150, 100, 75, and 60 beats/min.

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FIGURE 3-6 Comparison of P axis in sinus rhythm (A) and low atrial rhythm (B). In sinus rhythm, the P axis is between 0 and +90 degrees, and P waves are upright in leads I and aVF. In low atrial rhythm, the P wave is superiorly oriented, and P waves are inverted in lead aVF.

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FIGURE 3-7 Electrocardiographic paper. Time is measured on the horizontal axis. Each 1 mm equals 0.04 second, and each 5 mm (a large division) equals 0.20 second. Thirty millimeters (or six large divisions) equals 1.2 second or 1/50 minute.

When the ventricular and atrial rates are different, as in complete heart block or atrial flutter, the atrial rate can be calculated using the same methods as described for the ventricular rate; for the atrial rate, the P-P interval rather than the R-R interval is used.

Because of age-related differences in the heart rate, the definitions of bradycardia (<60 beats/min) and tachycardia (>100 beats/min) used for adults do not help distinguish normal from abnormal heart rates in pediatric patients. Operationally, tachycardia is present when the heart rate is faster than the upper range of normal for that age, and bradycardia is present when the heart rate is slower than the lower range of normal. According to age, normal resting heart rates per minute recorded on the ECG are as follows (Davignon et al, 1979/1980).

Newborn

145 (90–180)

6 mo

145 (105–185)

1 yr

132 (105–170)

2 yr

120 (90–150)

4 yr

108 (72–135)

6 yr

100 (65–135)

10 yr

90 (65–130)

14 yr

85 (60–120)

QRS Axis, T Axis, and QRS-T Angle

QRS Axis

The most convenient way to determine the QRS axis is the successive approximation method using the hexaxial reference system (see Fig. 3-1A). The same approach is also used for the determination of the T axis (see later discussion). For the determination of the QRS axis (as well as T axis), one uses only the hexaxial reference system (or the six limbs leads), not the horizontal reference system.

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FIGURE 3-8 Heart rate of 165 beats/min. There are about 3.3 cardiac cycles (R-R intervals) in six large divisions. Therefore, the heart rate is 3.3 × 50 = 165 (by method 1). By method 2, the RR interval is 0.36 sec. 60 ÷ 0.36 = 166. The rates derived by the two methods are very close.

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FIGURE 3-9 Heart rate of 52 beats/minute. There are 5.8 large (5 mm) divisions between the two arrows. Therefore the heart rate is 300 ÷ 5.8 = 52.

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FIGURE 3-10 Quick estimation of heart rate. When the R-R interval is 5 mm, the heart rate is 300 beats/min. When the R-R interval is 10 mm, the rate is 150 beats/min, and so on.

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FIGURE 3-11 Locating quadrants of mean QRS axis from leads I and aVF. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

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FIGURE 3-12 A, Set of six limb leads. B, Plotted QRS axis is shown.

Successive Approximation Method

Step 1: Locate a quadrant using leads I and aVF (Fig. 3-11). In the top panel of Figure 3-11, the net QRS deflection of lead I is positive. This means that the QRS axis is in the left hemicircle (i.e., from –90 degrees through 0 to +90 degrees) from the lead I point of view. The net positive QRS deflection in aVF means that the QRS axis is in the lower hemicircle (i.e., from 0 through +90 degrees to +180 degrees) from the aVF point of view. To satisfy the polarity of both leads I and aVF, the QRS axis must be in the lower left quadrant (i.e., 0 to +90 degrees). Four quadrants can be easily identified based on the QRS complexes in leads I and aVF (see Fig. 3-11).

Step 2: Among the remaining four limb leads, find a lead with an equiphasic QRS complex (in which the height of the R wave and the depth of the S wave are equal). The QRS axis is perpendicular to the lead with an equiphasic QRS complex in the predetermined quadrant.

Example: Determine the QRS axis in Figure 3-12.

TABLE 3-1

MEAN AND RANGES OF NORMAL QRS AXES BY AGE

Age

Mean (Range)

1 wk–1 mo

+ 110° (+30 to +180)

1–3 mo

+ 70° (+10 to +125)

3 mo–3 yr

+ 60° (+10 to +110)

Older than 3 yr

+ 60° (+20 to +120)

Adult

+ 50° (–30 to +105)

Step 1: The axis is in the lower left quadrant (0 to +90 degrees) because the R waves are upright in leads I and aVF.

Step 2: The QRS complex is equiphasic in aVL. Therefore, the QRS axis is +60 degrees, which is perpendicular to aVL.

Normal QRS Axis

Normal ranges of QRS axis vary with age. Newborns normally have RAD compared with the adult standard. By 3 years of age, the QRS axis approaches the adult mean value of +50 degrees. The mean and ranges of a normal QRS axis according to age are shown in Table 3-1.

Abnormal QRS Axis

The QRS axis outside normal ranges signifies abnormalities in the ventricular depolarization process.

1. Left axis deviation (LAD) is present when the QRS axis is less than the lower limit of normal for the patient’s age. LAD occurs with left ventricular hypertrophy (LVH), left bundle branch block (LBBB), and left anterior hemiblock.

2. RAD is present when the QRS axis is greater than the upper limit of normal for the patient’s age. RAD occurs with RVH and right bundle branch block (RBBB).

3. “Superior” QRS axis is present when the S wave is greater than the R wave in aVF. The overlap with LAD and left anterior hemiblock should be noted. Left anterior hemiblock (in the range of –30 to –90 degrees is seen in congenital heart diseases such as endocardial cushion defect and tricuspid atresia) or with RBBB. It is rarely seen in otherwise normal children.

T Axis

The T axis is determined by the same methods used to determine the QRS axis. In normal children, including newborns, the mean T axis is +45 degrees, with a range of 0 to +90 degrees, the same as in normal adults. This means that the T waves must be upright in leads I and aVF. The T waves can be flat but must not be inverted in these leads. The T axis outside of the normal quadrant suggests conditions with myocardial dysfunction similar to those listed for abnormal QRS-T angle (see below).

QRS-T Angle

The QRS-T angle is formed by the QRS axis and the T axis. A QRS-T angle of greater than 60 degrees is unusual, and one greater than 90 degrees is certainly abnormal. An abnormally wide QRS-T angle with the T axis outside the normal quadrant (0 to +90 degrees) is seen in severe ventricular hypertrophy with “strain,” ventricular conduction disturbances, and myocardial dysfunction of a metabolic or ischemic nature.

Intervals

Three important intervals are routinely measured in the interpretation of an ECG: PR interval, QRS duration, and QT interval. The duration of the P wave is also inspected (Fig. 3-13).

PR Interval

The normal PR interval varies with age and heart rate (Table 3-2). Davignon et al’s data are unsuitable for clinical use because they are presented separately according to age and heart rate. The PR interval is longer in older individuals and with a slower heart rate.

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FIGURE 3-13 Diagram illustrating important intervals (or durations) and segments of an electrocardiographic cycle.

TABLE 3-2

PR INTERVAL ACCORDING TO AGE AND RATE: MEAN (AND UPPER LIMITS OF NORMAL)

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From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.

Prolongation of the PR interval (i.e., first-degree AV block) is seen in myocarditis (rheumatic, viral, or diphtheric), digitalis or quinidine toxicity, certain congenital heart defects (endocardial cushion defect, atrial septal defect, Ebstein’s anomaly), some myocardial dysfunctions, hyperkalemia, and otherwise normal heart with vagal stimulation.

A short PR interval is present in Wolff-Parkinson-White (WPW) preexcitation, Lown-Ganong-Levine syndrome, myocardiopathies of glycogenosis, Duchene’s muscular dystrophy (or relatives of these patients), Friedrich’s ataxia, pheochromocytoma, and otherwise normal children. The lower limits of normal PR interval are shown under the topic of WPW preexcitation (see later discussion).

Variable PR intervals are seen in the wandering atrial pacemaker and the Wenckebach phenomena (Mobitz type I second-degree AV block).

QRS Duration

The QRS duration varies with age (Table 3-3). It is short in infants and increases with age.

The QRS duration is prolonged in conditions grouped as ventricular conduction disturbances, which include RBBB, LBBB, preexcitation (e.g., WPW preexcitation), and intraventricular block (as seen in hyperkalemia, toxicity from quinidine or procainamide, myocardial fibrosis, and myocardial dysfunction of a metabolic or ischemic nature). Ventricular arrhythmias (e.g., premature ventricular contractions, ventricular tachycardia, implanted ventricular pacemaker) also produce a wide QRS duration. Because the QRS duration varies with age, the definition of bundle branch block (BBB) or other ventricular conduction disturbances should vary with age (see the section on ventricular conduction disturbances).

QT Interval

The QT interval varies primarily with heart rate. The heart rate–corrected QT (QTc) interval is calculated by the use of Bazett’s formula:

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TABLE 3-3

QRS DURATION ACCORDING TO AGE: MEAN (UPPER LIMITS OF NORMAL) (IN SECONDS)

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 Upper limit of normal refers to the 98th percentile.

Derived from percentile graphs in Davignon A, Rautaharju P, Boisselle E, Soumis F, Megelas M, Choquette A. Normal ECG standards for infants and children. Pediatr Cardiol 1:123-131, 1979/1980.

According to Bazett’s formula, the normal QTc interval (mean ± standard deviation) is 0.40 (±0.014) second with the upper limit of normal 0.44 second in children 6 month and older. The QTc interval is slightly longer in newborn and small infants with the upper limit of normal QTc 0.47 second in the first week of life and 0.45 second in the first 6 months of life.

Long QT intervals may be seen in long QT syndrome (e.g., Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome), hypocalcemia, myocarditis, diffuse myocardial diseases (including hypertrophic and dilated cardiomyopathies), head injury, severe malnutrition, and so on. A number of drugs are also known to prolong the QT interval. Among these are antiarrhythmic agents (especially class IA, IC, and III), antipsychotic phenothiazines (e.g., thioridazine, chlorpromazine), tricyclic antidepressants (e.g., imipramine, amitriptyline), arsenics, organophosphates, antibiotics (e.g., ampicillin, erythromycin, trimethoprim-sulfa, amantadine), and antihistamines (e.g., terfenadine).

A short QT interval is a sign of a digitalis effect or of hypercalcemia. It is also seen with hyperthermia and in short QT syndrome (a familial cause of sudden death with QTc ≤300 millisecond).

JT Interval

The JT interval is measured from the J point (the junction between the S wave and the ST segment) to the end of the T wave. A prolonged JT interval has the same significance as a prolonged QT interval. The JT interval is measured only when the QT interval is prolonged or when the QRS duration is prolonged as seen with ventricular conduction disturbances. The JT interval is also expressed as a rate-corrected interval (called JTc) using Bazett’s formula. Normal JTc (mean ± SD) is 0.32 ± 0.02 second with the upper limit of normal 0.34 second in normal children and adolescents.

P-Wave Duration and Amplitude

The P-wave duration and amplitude are important in the diagnosis of atrial hypertrophy. Normally, the P amplitude is less than 3 mm. The duration of P waves is shorter than 0.09 second in children and shorter than 0.07 second in infants (see the section on criteria for atrial hypertrophy).

QRS Amplitude, R/S Ratio, and Abnormal Q Waves

A comment about normal ECG data for the QRS complex is in order. Normal data of Davignon et al (1979/1980) are not used in this chapter. Their data are severely handicapped because they provide almost no information on the frontal plane leads. Their data include the R wave and S wave voltages of only the aVR lead among the six limb leads; no data are provided for leads I, II, III, aVL, and aVF. Without the QRS amplitude of the frontal plane information, the interpretation of an ECG for ventricular hypertrophy would suffer greatly. In general, the limb leads (which are lacking in Davignon et al’s data) provides much more useful information than the precordial leads. In addition, the limb leads are more reproducible than the precordial leads because each precordial lead electrode must be placed precisely on the correct spot on the chest wall but the limb lead electrodes do not.

The QRS amplitude and R/S ratio are important in the diagnosis of ventricular hypertrophy. These values also vary with age (Tables 3-4 and 3-5). Because of normal dominance of RV forces in infants and small children, R waves are taller than S waves in the right precordial leads (i.e., V4R, V1, V2), and S waves are deeper than R waves in the left precordial leads (i.e., V5, V6) in this age group. Accordingly, the R/S ratio (the ratio of the R-wave and S-wave voltages) is large in the right precordial leads and small in the left precordial leads in infants and small children.

TABLE 3-4

R VOLTAGES ACCORDING TO LEAD AND AGE: MEAN (AND UPPER LIMIT) (IN MM)

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Voltages measured in millimeters, when 1 mV = 10 mm paper

 Upper limit of normal refers to the 98th percentile.

From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.

TABLE 3-5

R/S RATIO: MEAN AND UPPER AND LOWER LIMITS OF NORMAL ACCORDING TO AGE

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LLN, lower limits of normal; ULN, upper limits of normal.

From Guntheroth WB: Pediatric Electrocardiography. Philadelphia, WB Saunders, 1965.

Normal mean Q voltages and upper limits are presented in Table 3-6. The average normal Q-wave duration is 0.02 second and does not exceed 0.03 second. Abnormal Q waves may manifest themselves as deep or wide Q waves or as abnormal leads in which they appear. Deep Q waves may be present in ventricular hypertrophy of the “volume overload” type and in septal hypertrophy. Deep and wide Q waves are seen in MI. The presence of Q waves in the right precordial leads (e.g., severe RVH or ventricular inversion) or the absence of Q waves in the left precordial leads (e.g., LBBB or ventricular inversion) is abnormal.

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FIGURE 3-14 Criteria for atrial hypertrophy. BAH, biatrial hypertrophy; LAH, left atrial hypertrophy; RAH, right atrial hypertrophy. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

TABLE 3-6

Q VOLTAGES ACCORDING TO LEAD AND AGE: MEAN (AND UPPER LIMIT) (IN MM)

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Voltages measured in millimeters, when 1 mV = 10 mm paper

 Upper limit of normal refers to the 98th percentile.

From percentile graphs in Davignon A, Rautaharju P, Boisselle E, Soumis F, Megelas M, Choquette A. Normal ECG standards for infants and children. Pediatr Cardiol 1:123-131, 1979/1980.

ST Segment and T Waves

The normal ST segment is isoelectric. However, in the limb leads, elevation or depression of the ST segment up to 1 mm is not necessarily abnormal in infants and children. An elevation or a depression of the ST segment is judged in relation to the PR segment as the baseline. Some ST-segment changes are normal (non-pathologic), and others are abnormal (pathologic). (See the later section of nonpathologic and pathologic ST-T changes in this chapter.)

Tall peaked T waves may be seen in hyperkalemia and LVH (of the “volume overload” type). Flat or low T waves may occur in normal newborns or with hypothyroidism, hypokalemia, pericarditis, myocarditis, and myocardial ischemia.

Atrial Hypertrophy

Right Atrial Hypertrophy

Tall P waves (>3 mm) indicate right atrial hypertrophy (RAH) or “P pulmonale” (Fig. 3-14).

Left Atrial Hypertrophy

Widened and often notched P wave is seen in left atrial hypertrophy (LAH) or “P mitrale.” In V1, the P wave is diphasic with a prolonged negative segment (see Fig. 3-14). A notched P wave in V1 is not diagnostic of LAH; the P wave duration has to be abnormally prolonged (with the P duration >0.10 second in children and >0.08 second in infants).

Biatrial Hypertrophy

In biatrial hypertrophy (BAH), a combination of an increased amplitude and duration of the P wave is present (see Fig. 3-14).

Ventricular Hypertrophy

General Changes

Ventricular hypertrophy produces abnormalities in one or more of the following; the QRS axis, the QRS voltages, the R/S ratio, the T axis, and miscellaneous areas.

1. Changes in the QRS axis

The QRS axis is usually directed toward the ventricle that is hypertrophied. Although RAD is present with RVH, LAD is seen with volume-overload type but not with pressure-overload type of LVH. Marked LAD (such as that seen with left anterior hemiblock or “superior” QRS axis) usually indicates ventricular conduction disturbances, not hypertrophy.

2. Changes in QRS voltages

Anatomically, the RV occupies the right and anterior aspect, and the LV occupies the left, inferior, and posterior aspect of the ventricular mass. With ventricular hypertrophy, the voltage of the QRS complex increases in the direction of the respective ventricle.

In the frontal plane (Fig. 3-15A), LVH shows increased R voltages in leads I, II, aVL, aVF, and sometimes III, especially in small infants. RVH shows increased R voltages in aVR and III and increased S voltages in lead I (see Table 3-4 for normal R and S voltages).

In the horizontal plane (Fig. 3-15B), tall R waves in V4R, V1, and V2 or deep S waves in V5 and V6 are seen in RVH. With LVH, tall R waves in V5 and V6 or deep S waves in V4R, V1, and V2 are present (see Table 3-4).

3. Changes in R/S ratio

The R/S ratio represents the relative electromotive force of opposing ventricles in a given lead. In ventricular hypertrophy, a change may be seen only in the R/S ratio without an increase in the absolute voltage. An increase in the R/S ratio in the right precordial leads suggests RVH; a decrease in the R/S ratio in these leads suggests LVH. Likewise, an increase in the R/S ratio in the left precordial leads suggests LVH, and a decrease in the ratio suggests RVH (see Table 3-5).

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FIGURE 3-15 Diagrammatic representation of left and right ventricular forces on the frontal projection (hexaxial reference system) (A) and the horizontal plane (B). (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

4. Changes in the T axis

Changes in the T axis are seen in severe ventricular hypertrophy with relative ischemia of the hypertrophied myocardium. In the presence of other criteria of ventricular hypertrophy, a wide QRS-T angle (i.e., >90 degrees) with the T axis outside the normal range indicates a “strain” pattern. When the T axis remains in the normal quadrant (0 to +90 degrees), a wide QRS-T angle indicates a possible “strain” pattern.

5. Miscellaneous nonspecific changes

a. RVH

1) A q wave in V1 (qR or qRs pattern) suggests RVH, although it may be present in ventricular inversion.

2) An upright T wave in V1 after 3 days of age is a sign of probable RVH.

b. LVH

Deep Q waves (>5 mm) and tall T waves in V5 and V6 are signs of LVH of the “volume overload” type. These may be seen with a large-shunt ventricular septal defect (VSD).

Criteria for Right Ventricular Hypertrophy

In RVH, some or all of the following criteria are present.

1. RAD for the patient’s age (see Table 3-1).

2. Increased rightward and anterior QRS voltages (in the absence of prolonged QRS duration) (see Table 3-4); a wide QRS complex with increased QRS voltages suggests ventricular conduction disturbances (e.g., RBBB) rather than ventricular hypertrophy.

a. R waves in V1, V2, or aVR greater than the upper limits of normal for the patient’s age

b. S waves in I and V6 greater than the upper limits of normal for the patient’s age

In general, the abnormal forces to the right and anteriorly are stronger criteria than abnormal forces to the right or anteriorly only.

3. Abnormal R/S ratio in favor of the RV (in the absence of prolonged QRS duration) (i.e., BBB; see Table 3-5).

a. R/S ratio in V1 and V2 greater than the upper limits of normal for age

b. R/S ratio in V6 less than 1 after 1 month of age

4. Upright T waves in V1 in patients more than 3 days of age, provided that the T is upright in the left precordial leads (V5, V6); upright T waves in V1 are not abnormal in patients older than 6 years of age.

5. A q wave in V1 (qR or qRs patterns) suggests RVH. (The physician should ascertain that there is not a small r in an rsR′ configuration.)

6. In the presence of RVH, a wide QRS-T angle with T axis outside the normal range (in the 0 to –90 degree quadrant) indicates a “strain” pattern. A wide QRS-T angle with the T axis within the normal range suggests a possible “strain” pattern.

Figure 3-16 is an example of RVH. There is RAD for the patient’s age (+150 degrees). The T axis is –10 degrees, and the QRS-T angle is abnormally wide (160 degrees) with the T axis in an abnormal quadrant. The QRS duration is normal. The R-wave voltages in leads III and aVR and the S waves in leads I and V6 are beyond the upper limits of normal, indicating an abnormal rightward force. The R/S ratios in V1 and V2 are larger than the upper limits of normal, and the ratio in V6 is smaller than the lower limits of normal, again indicating RVH. Therefore, this tracing shows RVH with “strain.”

The diagnosis of RVH in newborns is particularly difficult because of the normal dominance of the RV during this period of life. Helpful signs in the diagnosis of RVH in newborns are as follows.

1. S waves in lead I that are 12 mm or greater

2. Pure R waves (with no S waves) in V1 that are greater than 10 mm Hg

3. R waves in V1 that are greater than 25 mm or R waves in aVR that are greater than 8 mm

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FIGURE 3-16 Tracing from a 10-month-old infant with severe tetralogy of Fallot.

4. A qR pattern seen in V1 (this is also seen in 10% of normal newborns)

5. Upright T waves seen in V1 after 3 days of age

6. RAD with the QRS axis greater than +180 degrees

Criteria for Left Ventricular Hypertrophy

In LVH, some or all of the following abnormalities are present.

1. LAD for the patient’s age in some cases (see Table 3-1)

2. QRS voltages in favor of the LV (in the absence of a prolonged QRS duration for age) (see Table 3-4)

a. R waves in leads I, II, III, aVL, aVF, V5, or V6 greater than the upper limits of normal for age

b. S waves in V1 or V2 greater than the upper limits of normal for age

In general, the presence of abnormal forces to more than one direction (e.g., to the left, inferiorly, and posteriorly) is stronger criterion than the abnormality in only one direction

3. Abnormal R/S ratio in favor of the LV: R/S ratio in V1 and V2 less than the lower limits of normal for the patient’s age (see Table 3-5)

4. Q waves in V5 and V6, greater than 5 mm, as well as tall symmetrical T waves in the same leads (“LV diastolic overload”)

5. In the presence of LVH, a wide QRS-T angle with the T axis outside the normal range indicates a “strain” pattern; this is manifested by inverted T waves in lead I or aVF. A wide QRS-T angle with the T axis within the normal range suggests a possible “strain” pattern.

Figure 3-17 is an example of LVH. There is LAD for the patient’s age (0 degrees). The R waves in leads I, aVL, V5, and V6 are beyond the upper limits of normal, indicating abnormal leftward force. The QRS duration is normal. The T axis (+55 degrees) remains in the normal quadrant. This tracing shows LVH (without “strain”).

Criteria for Biventricular Hypertrophy

BVH may be manifested in one of the following ways.

1. Positive voltage criteria for RVH and LVH in the absence of BBB or preexcitation (i.e., with normal QRS duration)

2. Positive voltage criteria for RVH or LVH and relatively large voltages for the other ventricle

3. Large equiphasic QRS complexes in two or more of the limb leads and in the midprecordial leads (i.e., V2 through V5), called the Katz-Wachtel phenomenon (with normal QRS duration)

Figure 3-18 is an example of BVH. It is difficult to plot the QRS axis because of large diphasic QRS complexes in limb leads. The QRS duration is not prolonged. The R and S voltages are large in some limb leads and in the midprecordial leads (Katz-Wachtel phenomenon). The S waves in leads I and V6 are abnormally deep (i.e., abnormal rightward force), and the R wave in V1 (i.e., rightward and anterior force) is also abnormally large, suggesting RVH. The R waves in leads I and aVL (i.e., leftward force) are also abnormally large, suggesting LVH. Therefore, this tracing shows BVH.

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FIGURE 3-17 Tracing from a 4-year-old child with a moderate ventricular septal defect. Note that some precordial leads are in ½ normal standardization.

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FIGURE 3-18 Tracing from a 2-month-old infant with large-shunt ventricular septal defect, patent ductus arteriosus, and severe pulmonary hypertension.

Ventricular Conduction Disturbances

Conditions that are grouped together as ventricular conduction disturbances have abnormal prolongation of the QRS duration in common. Ventricular conduction disturbances include the following:

1. BBB, right and left

2. Preexcitation (e.g., WPW-type preexcitation)

3. Intraventricular block

In BBBs (and ventricular rhythms), the prolongation is in the terminal portion of the QRS complex (i.e., “terminal slurring”). In preexcitation, the prolongation is in the initial portion of the QRS complex (i.e., “initial slurring”), producing “delta” waves. In intraventricular block, the prolongation is throughout the duration of the QRS complex (Fig. 3-19). Normal QRS duration varies with age; it is shorter in infants than in older children or adults (see Table 3-3). In adults, a QRS duration longer than 0.10 second is considered abnormally prolonged. In infants, a QRS duration of 0.08 second is the upper limit of normal. Depending on the degree of prolongation, complete versus incomplete block may be assigned.

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FIGURE 3-19 Schematic diagram of three types of ventricular conduction disturbances. A, Normal QRS complex. B, QRS complex in right bundle branch block with prolongation of the QRS duration in the terminal portion (black arrows, terminal slurring). C, Preexcitation with delta wave (open arrow, initial slurring). D, Intraventricular block in which the prolongation of the QRS complex is throughout the duration of the QRS complex.

By far the most commonly encountered form of ventricular conduction disturbance is RBBB. WPW preexcitation is uncommon, but it is a well-defined entity that deserves a brief description. LBBB is extremely rare in children, although it is common in adults with ischemic and hypertensive heart disease. Intraventricular block is associated with metabolic disorders and diffuse myocardial diseases.

Right Bundle Branch Block

In RBBB, delayed conduction through the right bundle branch prolongs the time required for a depolarization of the RV. When the LV is completely depolarized, RV depolarization is still in progress. This produces prolongation of the QRS duration, involving the terminal portion of the QRS complex, called “terminal slurring” (see Fig. 3-19B), and the slurring is directed to the right and anteriorly because the RV is located rightward and anteriorly in relation to the LV.

In a normal heart, synchronous depolarization of the opposing electromotive forces of the RV and LV cancels out the forces to some extent, with the resulting voltages that we call normal. In RBBB (and other ventricular conduction disturbances), asynchronous depolarization of the opposing electromotive forces may produce a lesser degree of cancellation of the opposing forces and thus results in greater manifest potentials for both ventricles. Consequently, abnormally large voltages for both RV and LV may result even in the absence of ventricular hypertrophy. Therefore, the diagnosis of ventricular hypertrophy in the presence of BBB (or WPW preexcitation or intraventricular block) is insecure.

In adults, when the QRS duration is longer than 0.12 second it is called complete RBBB, and when the QRS duration is between 0.10 and 0.12 second, it is called incomplete right bundle branch block (IRBBB). Normal QRS duration is shorter in infants and children. Therefore, dividing RBBB into complete and incomplete is generally arbitrary and is particularly meaningless in children. Furthermore, in most of pediatric cases of RBBB, the right bundle branch is intact.

Criteria for Right Bundle Branch Block

1. RAD, at least for the terminal portion of the QRS complex. (The initial QRS force is normal.)

2. The QRS duration clearly longer than the upper limit of normal for the patient’s age (see Table 3-3). When the prolongation of the QRS duration is only mild, it could be called incomplete RBBB.

3. Terminal slurring of the QRS complex that is directed to the right and usually, but not always, anteriorly:

a. Wide and slurred S waves in leads I, V5, and V6

b. Terminal, slurred R′ in aVR and the right precordial leads (V4R, V1, and V2).

4. ST-segment shift and T-wave inversion are common in adults but not in children.

Figure 3-20 is an example of RBBB. The QRS duration is increased (0.11 second), indicating a ventricular conduction disturbance. There is slurring of the terminal portion of the QRS complex, indicating a BBB, and the slurring is directed to the right (slurred S waves in leads I and V6, and slurred R waves in aVR) and anteriorly (slurred R waves in V4R and V1), satisfying the criteria for RBBB. Although the S waves in leads I, V5, and V6 are abnormally deep and the R/S ratio in V1 is abnormally large, it cannot be interpreted as RVH in the presence of RBBB.

Two pediatric conditions commonly associated with RBBB are ASD and conduction disturbances after open heart surgery involving right ventriculotomy. Other congenital heart defects often associated with RBBB include Ebstein’s anomaly, coarctation of the aorta in infants younger than 6 months of age, endocardial cushion defect, and partial anomalous pulmonary venous return; it is also occasionally seen in normal children. Rarely, RBBB is seen in myocardial diseases (cardiomyopathy, myocarditis), muscle diseases (Duchenne’s muscular dystrophy, myotonic dystrophy), and Brugada syndrome.

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FIGURE 3-20 Tracing from a 6-year-old boy who had corrective surgery for tetralogy of Fallot that involved right ventriculotomy for repair of a ventricular septal defect and resection of infundibular narrowing.

The significance of RBBB in children is different from that in adults. In several pediatric examples of RBBB, the right bundle is intact. In ASD, the prolonged QRS duration is the result of a longer pathway through a dilated RV rather than an actual block in the right bundle. Right ventriculotomy for repair of VSD or tetralogy of Fallot disrupts the RV subendocardial Purkinje network and causes prolongation of the QRS duration without necessarily injuring the main right bundle, although the latter may occasionally be disrupted.

Incomplete Right Bundle Branch Block

IRBBB is one of the more common ECG abnormalities reported by computer readouts and by physicians alike. Because some physicians are concerned with the rsR′ pattern in V1 or the diagnosis of IBBB, the topic deserves a little more attention.

Although the RSR′ (or rSr′) pattern in V1 is unusual in adults, this pattern is a normal finding in infants, toddlers, and children. From vectorcardiographic points of view, in order for a newborn ECG pattern to change to the adult pattern, it has to go through a stage in which rSr′ or RsR′ pattern appears. It is almost impossible for a newborn ECG to change to an adult pattern without going through the rSr′ (or rsR′) stage. (For those who are interested in learning about the reason, Park and Gunderoth, 2006, is recommended.)

The following clarifies some issues related to the rSr′ pattern in V1.

1. An rsR′ pattern in V1 is normal if it is associated with normal QRS duration and normal QRS voltage.

2. If the rSr′ pattern is associated with only slightly prolonged QRS duration (not to satisfy the criterion of RBBB), it is then incomplete RBBB. The QRS voltage may be slightly increased in some cases for the same reason as discussed under RBBB.

3. If the rsR′ pattern is associated with slightly prolonged QRS duration and an abnormal QRS voltage, it is still IRBBB, not ventricular hypertrophy.

4. RVH is justified only if an abnormal QRS voltage is present in the presence of normal QRS duration.

The pathophysiology and clinical significance of IRBBB are similar to that of RBBB as discussed earlier. Whether to call it “complete” or “incomplete” is arbitrary in children. When structural and functional cardiac anomalies are ruled out, IRBBB does not have much clinical significance in the pediatric population. Some cardiologists prefer the term “right ventricular conduction delay” rather than a “block” as in IRBBB. The prevalence of IRBBB in the pediatric population is not known, although a large epidemiologic study from Japan suggests it is around 1% among the normal pediatric population. The prevalence of IRBBB in the adult population is estimated to be 5% to 10%, and it tends to increase with advancing age. A recent report suggests it may be a marker for lone atrial fibrillation in adults (which is defined as atrial fibrillation in the absence of identifiable cardiovascular or pulmonary disease).

Left Bundle Branch Block

LBBB is extremely rare in children. In LBBB, the duration of the QRS complex is prolonged for age, and the slurred terminal portion of the QRS complex is directed leftward and posteriorly. A Q wave is absent in V6. A prominent QS pattern is seen in V1, and a tall R wave is seen in V6.

LBBB in children is associated with cardiac disease or surgery in the LV outflow tract, septal myomectomy, and replacement of the aortic valve. Other conditions rarely associated with LBBB include LVH, myocarditis, cardiomyopathy, MI, aortic valve endocarditis, and premature ventricular contractions (or ventricluar tachycardia [VT]) originating in the RV outflow tract.

LBBB alone may rarely progress to complete heart block and sudden death, but the prognosis is more dependent on associated disease than on the LBBB itself.

Intraventricular Block

In intraventricular block, the prolongation is throughout the duration of the QRS complex (see Fig. 3-19D). This usually suggests serious conditions such as metabolic disorders (e.g., hyperkalemia), diffuse myocardial diseases (e.g., myocardial fibrosis, systemic diseases with myocardial involvement), severe hypoxia, myocardial ischemia, or drug toxicity (quinidine or procainamide).

Wolff-Parkinson-White Preexcitation

Wolff-Parkinson-White preexcitation results from an anomalous conduction pathway (i.e., bundle of Kent) between the atrium and the ventricle, bypassing the normal delay of conduction in the AV node. The premature depolarization of a ventricle produces a delta wave and results in prolongation of the QRS duration (see Fig. 3-19C).

Criteria for Wolff-Parkinson-White Syndrome

1. Short PR interval, less than the lower limit of normal for the patient’s age. The lower limits of normal of the PR interval according to age are as follows.

Younger than 12 mo

0.075 second

1–3 yr

0.080 second

3–5 yr

0.085 second

5–12 yr

0.090 second

12–16 yr

0.095 second

Adults

0.120 second

2. Delta wave (initial slurring of the QRS complex)

3. Wide QRS duration beyond the upper limit of normal

Patients with WPW preexcitation are prone to attacks of paroxysmal supraventricular tachycardia (SVT) (see Chapter 24). When there is a history of SVT, the diagnosis of WPW syndrome is justified. WPW preexcitation may mimic other ECG abnormalities such as ventricular hypertrophy, RBBB, or myocardial disorders. In the presence of preexcitation, the diagnosis of ventricular hypertrophy cannot be safely made. Large QRS deflections are often seen in this condition because of an asynchronous depolarization of the ventricles rather than ventricular hypertrophy.

Figure 3-21 is an example of WPW preexcitation. The most striking abnormalities are a short PR interval (0.08 second) and a wide QRS duration (0.11 second). There are delta waves in most of the leads. Some delta waves are negative, as seen in leads III, aVR, V4R, and V1. The ST segments and T waves are shifted in the opposite direction of the QRS vector, resulting in a wide QRS-T angle. The leftward voltages are abnormally large, but the diagnosis of LVH cannot safely be made in the presence of WPW preexcitation.

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FIGURE 3-21 Tracing from an asymptomatic 2-year-old boy whose ventricular septal defect underwent spontaneous closure. The tracing shows the Wolff-Parkinson-White preexcitation (see text for interpretation).

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FIGURE 3-22 Algorithm for differentiating between ventricular hypertrophy (VH) and ventricular conduction disturbances (VCDs). LV, left ventricle; RV, right ventricle.

There are two other forms of preexcitation that can also results in extreme tachycardia (SVT).

1. Lown-Ganong-Levine syndrome is characterized by a short PR interval and normal QRS duration. In this condition, James fibers (which connect the atrium and the bundle of His) bypass the upper AV node and produce a short PR interval, but the ventricles are depolarized normally through the His-Purkinje system. When there is no history of SVT, the tracing cannot be read as Lown-Ganong-Levine syndrome; it should read simply as short PR interval.

2. Mahaim-type preexcitation syndrome is characterized by a normal PR interval and long QRS duration with a delta wave. There is an abnormal Mahaim fiber that connects the AV node and one of the ventricles, bypassing the bundle of His and “short circuiting” into the ventricle.

Ventricular Hypertrophy Versus Ventricular Conduction Disturbances

Two common ECG abnormalities in children, ventricular hypertrophy and ventricular conduction disturbances, are not always easy to distinguish; both present with increased QRS amplitudes. An accurate measurement of the QRS duration is essential. The following approach may aid in the correct diagnosis of these conditions (Fig. 3-22).

1. When the QRS duration is normal, normal QRS voltages indicate a normal ECG. Increased QRS voltages indicate ventricular hypertrophy.

2. When the QRS duration is clearly prolonged, a ventricular conduction disturbance is present whether the QRS voltages are normal or increased. An additional diagnosis of ventricular hypertrophy should not be made.

3. When the QRS duration is borderline prolonged, distinguishing between these two conditions is difficult. Normal QRS voltages favor a normal ECG or a mild (RV or LV) conduction disturbance. An increased QRS voltage favors ventricular hypertrophy.

ST-Segment and T-Wave Changes

Electrocardiographic changes involving the ST segment and the T wave are common in adults but relatively rare in children. This is because there is a high incidence of ischemic heart disease, BBB, MI, and other myocardial disorders in adults. Some ST-segment changes are normal (nonpathologic), and others are abnormal (pathologic).

Nonpathologic ST-Segment Shift

Not all ST-segment shifts are abnormal. A slight shift of the ST segment is common in normal children. Elevation or depression of up to 1 mm in the limb leads and up to 2 mm in the precordial leads is within normal limits. Two common types of nonpathologic ST-segment shifts are J-depression and early repolarization. The T vector remains normal in these conditions.

J-Depression

J-depression is a shift of the junction between the QRS complex and the ST segment (J-point) without sustained ST segment depression (Fig. 3-23A). The J-depression is seen more often in the precordial leads than in the limb leads (Fig. 3-24).

Early Repolarization

In early repolarization, all leads with upright T waves have elevated ST segments, and leads with inverted T waves have depressed ST segments (see Fig. 3-24). The T vector remains normal. This condition, seen in healthy adolescents and young adults, resembles the ST-segment shift seen in acute pericarditis; in the former, the ST segment is stable, and in the latter, the ST segment returns to the isoelectric line.

Pathologic ST-Segment Shift

Abnormal shifts of the ST segment often are accompanied by T-wave inversion. A pathologic ST segment shift assumes one of the following forms:

1. Downward slant followed by a diphasic or inverted T wave (see Fig. 3-23B)

2. Horizontal elevation or depression sustained for longer than 0.08 second (see Fig. 3-23C)

Pathologic ST segment shifts are seen in left or RVH with “strain” (discussed under ventricular hypertrophy); digitalis effect; pericarditis, including postoperative state; myocarditis (see under myocarditis, Chapter 19); MI; and some electrolyte disturbances (hypokalemia and hyperkalemia).

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FIGURE 3-23 Nonpathologic (nonischemic) and pathologic (ischemic) ST-segment and T-wave changes. A, Characteristic nonischemic ST-segment change called J-depression; note that the ST slope is upward. B and C, Examples of pathologic ST-segment changes; note that the downward slope of the ST segment (B) or the horizontal segment is sustained (C). (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

T-Wave Changes

T-wave changes usually are associated with the conditions manifesting with pathologic ST-segment shift. T-wave changes with or without ST-segment shift are also seen with BBB and ventricular arrhythmias.

Pericarditis

The ECG changes seen in pericarditis are the result of subepicardial myocardial damage or pericardial effusion and consist of the following:

1. Pericardial effusion may produce low QRS voltages (QRS voltages <5 mm in every one of the limb leads).

2. Subepicardial myocardial damage produces the following time-dependent changes in the ST segment and T wave (Fig. 3-25):

a. ST-segment elevation occurs in the leads representing the LV.

b. The ST-segment shift returns to normal within 2 to 3 days.

c. T-wave inversion (with isoelectric ST segment) occurs 2 to 4 weeks after the onset of pericarditis.

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FIGURE 3-24 Tracing from a healthy 16-year-old boy that exhibits early repolarization and J-depression. The ST segment is shifted toward the direction of the T wave and is most marked in II, III, and aVF. J-depression is seen in most of the precordial leads.

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FIGURE 3-25 Time-dependent changes of the ST segment and T wave in pericarditis. The initial change is ST-segment elevation (A), followed by return of ST segment elevation toward normal (B), and T wave inversion with isoelectric ST segment (C). (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

Myocardial Infarction

MI is rare in infants and children, but correctly diagnosing the condition is important for proper care. All conditions that have been associated with MI in adults have been described as causing MI in children, such as atherosclerosis, inflammatory disease of the myocardium, lupus erythematosus, polyarteritis nodosa, hypertension, and diabetes mellitus. Uncommon causes of MI in pediatric patients include anomalous origin of the left coronary artery from the pulmonary artery, endocardial fibroelastosis, coronary artery embolization resulting from infective endocarditis or from interventional or diagnostic catheterization procedures performed on the left side of the heart, and inadvertent surgical interruption of the coronary artery during cardiac surgery. In recent years, early and late sequelae of Kawasaki’s disease, surgical complications of the arterial switch operation for transposition of the great arteries, and dilated cardiomyopathy have emerged as important causes of MI in the pediatric population.

The ECG findings of adult MI are time dependent and are illustrated in Figure 3-26. Changes seen during the hyperacute phase are short lived. The more common ECG findings are those of the early evolving phase. These consist of pathologic Q waves (abnormally wide and deep), ST-segment elevation, and T-wave inversion. The duration of the Q wave is 0.04 second or greater in adults, and it should be at least 0.03 second in children. Over the next few weeks, the elevated ST segment gradually returns toward the baseline, but inverted T waves persist (late evolving phase). The pathologic Q waves persist for years after MI (see Fig. 3-26). Leads that show these abnormalities vary with the location of the infarction and are summarized in Table 3-7.

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FIGURE 3-26 Sequential changes of the ST segment and T wave in myocardial infarction. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed., Philadelphia, Mosby, 2006)

TABLE 3-7

LEADS SHOWING ABNORMAL ELECTROCARDIOGRAPHIC FINDINGS IN MYOCARDIAL INFARCTION

 

Limb Leads

Precordial Leads

Lateral

I, aVL

V5, V6

Anterior

 

V1, V2, V3

Anterolateral

I, aVL

V2–V6

Diaphragmatic

II, III, aVF

 

Posterior

 

V1–V3

 None of the leads is oriented toward the posterior surface of the heart. Therefore, in posterior infarction, changes that would have been present in the posterior surface leads will be seen in the anterior leads as a mirror image (e.g., tall and slightly wide R waves in V1 and V2, comparable to abnormal Q waves, and tall and wide, symmetric T waves in V1 and V2).

In most pediatric patients with MI, the time of onset is not clearly known, and the evolution of the different phases is difficult to document. Frequent ECG findings in children with acute MI include the following (Towbin et al, 1992):

1. Wide Q waves (>0.035 second) with or without Q-wave notching

2. ST segment elevation (>2 mm)

3. Prolongation of QTc interval (>0.44 second) with accompanying abnormal Q waves

The width of the Q wave is more important than the depth; the depth of the Q wave varies widely in normal children (see Table 3-6).

Figure 3-27 is an ECG of MI in an infant with anomalous origin of the left coronary artery from the pulmonary artery. The most important abnormality is the presence of a deep and wide Q wave (0.04 second) in leads I, aVL, and V6. A QS pattern appears in V2 through V5, indicating anterolateral MI (see Table 3-7).

Electrolyte Disturbances

Two important serum electrolytes that produce ECG changes are calcium and potassium.

Calcium. Calcium ion affects the duration of the ST segment and thus change the relative position of the T wave. Hyper- or hypocalcemia does not produce ST-segment shift or T-wave changes. Hypocalcemia prolongs the ST segment and, as a result, prolongs the QTc interval (Fig. 3-28). Hypercalcemia shortens the ST segment, resulting in shortening of the QTc interval (see Fig. 3-28).

Potassium. Hypokalemia produces one of the least specific ECG changes. When the serum potassium level is below 2.5 mEq/L, ECG changes consist of a prominent U wave with apparent prolongation of the QTc, flat or diphasic T waves, and ST-segment depression (Fig. 3-29). With further lowering of serum potassium levels, the PR interval becomes prolonged, and sinoatrial block may occur.

The earliest ECG abnormality seen in hyperkalemia is tall, peaked, symmetrical T waves with a narrow base, so-called tented T wave. In hyperkalemia, sinoatrial block, second-degree AV block (either Mobitz I or II), and accelerated junctional or ventricular escape rhythm may occur. Severe hyperkalemia may result in either ventricular fibrillation or arrest. The following ECG sequence is associated with a progressive increase in the serum potassium level (see Fig. 3-29):

1. Tall, tented T waves

2. Prolongation of the QRS duration (intraventricular block)

3. Prolongation of the PR interval (first-degree AV block)

4. Disappearance of the P wave

5. Wide, bizarre diphasic QRS complex (“sine wave”)

6. Eventual asystole

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FIGURE 3-27 Tracing from a 2-month-old infant who has anomalous origin of the left coronary artery from the pulmonary artery. An abnormally deep and wide Q wave (0.04 second) seen in I, aVL, and V6 and a QS pattern seen in V2 through V6 are characteristic of anterolateral myocardial infarction.

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FIGURE 3-28 Electrocardiographic findings of hypercalcemia and hypocalcemia. Hypercalcemia shortens and hypocalcemia lengthens the ST segment. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

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FIGURE 3-29 Electrocardiographic findings of hypokalemia and hyperkalemia. (From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)

These ECG changes are usually seen best in leads I and II and the left precordial leads.