Some Issues Related to Non-Arrhythmia Electrocardiography in Pediatrics

Jerome Liebman

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This is a critical time for clinical non arrhythmia electrocardiography for a large number of distinguished cardiologists believe that non-arrhythmia electrocardiography is only marginally necessary because of the excellence of echocardiography. In addition, very few electrocardiographers utilize or are even aware of the exciting newly recognized basic science knowledge. This group also includes many if not most of the many superb clinical electrophysiologists for whom newly known basic science immediately gets into the clinical arena. Many of these issues were recently delineated and discussed.⁽¹⁾

The newly known basic science, of which there has been considerable in the past 25 years is referenced^(2-8) but many other papers and reviews could have been quoted. Tragically, it is not just the newly known basic science that is not understood or properly utilized by many. An understanding of the meaning of the standard leads for example should be self evident by interpreters, but appears often not to be. Wilson’s chest leads⁽⁹⁾ obviously provided a great advance over Einthoven’s three limb leads, and of course the Wilson central terminal is used in most body surface potential mapping (BSPM) systems with large numbers of electrodes.⁽¹⁰⁾ But the fact that the chest leads (as well as aVR, aVL and aVF) are called “unipolar” is not only incorrect but has contributed to a lack of understanding of what the leads represent. Electricity obviously needs positive and negative poles in order to flow so that all leads are bipolar. Perhaps because of the statement “unipolar”, many believe that a chest electrode reflects the tissue only directly under the electrode, whereas it reflects all of the ventricle, for example, distorted by proximity effect.⁽⁷⁾ In order to understand the meaning of the leads the classic papers of Burger and Van Milan⁽¹¹⁾ are “must reading” as well as is Brody and Arzbaecher’s paper ⁽¹²⁾ on intrinsic properties of uncorrected and highly corrected leads.

QRS Axis

Perhaps the poorest use of the standard electrocardiogram is the calculation of the QRS axis. “The axis” is the mean vector in the frontal plane. For QRS this makes very little sense. There are five major areas being depolarized at about the same time early in the QRS; then at each instant of time throughout the QRS, different areas of the two ventricles are being activated. Although the QRS can be averaged at each instant of time, it cannot be averaged for the entire QRS.^{(3, 7, 8) that} lead I is such a poor lead is a separate problem.^{(3, 7, 8)}

VCG

Orthogonal electrocardiography (VCG), perhaps unwisely, is not being utilized at this time although it has certain advantages over standard ECG where we have documented significantly greater accuracy in interpreting hypertrophy. We quantitatively analyzed 100 consecutive children with pure hypertrophy who had cardiac catheterization and had not yet had cardiac surgery.⁽¹³⁾ The Frank system performed better than Mcfee-Parungao and both performed better than the standard ECG in predicting hemodynamics.

A very detailed analysis of the standard ECG, as well as VCG in congenital heart disease has demonstrated their usefulness in both diagnosis and correlations with hemodynamics.⁽¹⁴⁾

BSMP

In a series of papers, Kornreich used body surface potential mapping (BSPM) to demonstrate clearly that the six standard chest leads were often inadequate and was able to identify specific lead placements not part of the standard ECG to identify specific pathology.⁽¹⁵⁾

BSPM with large numbers of electrodes is not being extensively utilized in clinical medicine but there is optimism that it will return to clinical usage. Taccardi,⁽¹⁶⁾ as part of the Einthoven celebration in 2002, summarized what we have learned from body surface maps during the last fifty years. Large numbers of BSPM’s in children have been published to great clinical efficacy with the extensive biography recently summarized.^(17,18) A few examples are included: In patients with severe coarctation of the aorta many years after successful surgery, the BSPM clearly demonstrated that there was persistent RVH as manifested by prominent late potentials, right anterior lateral or right anterior superior. There was clear evidence as well that there was epicardial right ventricular breakthrough so that right bundle branch block was not present. Another example of the great worth of BSPM is in the analysis of severe aortic stenosis (AS) and severe pulmonic stenosis (PS) in each of which the initial QRS is usually to the left. In AS the cause is marked hypertrophy of the posterior free wall and in PS the mechanism appears to be strong activation of the anterior right ventricle near the septum (plus perhaps right septal activation). We have in the past stressed that there is an Electrocardiogram of the Future^(18,19) which, in our opinion, utilizes a large number of electrodes on the body surface (at least 100) and records the BSPM conveniently and rapidly. Then an online calculation of the epicardial map would be obtained by an accurate inverse calculation so that when recording the surface electrocardiogram one is actually recording the epicardial map. The exact computation of epicardial maps from multielectrode BSPM has been termed by Oster “Non Invasive Electrocardiographic Imaging”^(20,21) The two recent papers by Ramanathan and Rudy^(22,23) expanded Oster’s concept of ECGI. They used the same human shaped torso tank as did Oster, into which had been suspended a dog heart. In addition, accurate geometry of torso inhomogeneities, including stylized lungs, were utilized and digitalized into a computer model for both forward and inverse measurements and calculations. Recently the work of Rudy’s group has expanded to include repolarization.^(24,26)

Repolarization in Infants and Children

There is no evidence that the principles of the electrophysiology of repolarization in infants and children are any different from that of any age. However, there is no question that there are clinical differences and it is very likely that the differences are not related to propagation. In the normal, the ST-T does not appear to follow the QRS. The differences begin in the newborn period. Ziegler⁽²⁷⁾ was the first to point out differences and great variability in the newborn period and judged that after one week of life, an upright T in the right chest leads indicated right ventricular hypertrophy. Michaelson⁽²⁸⁾ noted unusually low voltage of ST-T in the first days and Stern and Lind⁽²⁹⁾ noted positive T waves in lead V₁ in the first five minutes after birth which changed rapidly and variably in the next hours and days. Sodi Pallares’⁽³⁰⁾data demonstrated anterior left T’s at birth and the first hours of life. Datey and Bharoucha⁽³¹⁾ noted that by 24 hours of age the T waves in the right chest leads were positive and usually negative by one week. At 24 hours, they were positive in 59%, borderline in 29% and negative in 2%, and by one week were borderline positive in 29%, negative in 71%. Sutin and Schrire⁽³²⁾ described the electrocardiogram in various racial groups in the first 48 hour of life, although their judged differences in the group were not statistically significant. Grouping all three ethnic groups together, the T wave was to the right in 50/180 in the first 24 hours and usually to the left at 24-48 hours. The T was also posterior in 22% in the first 24 hours and posterior in 48% at 24-48 hours. A more comprehensive analysis was recorded by Hait and Gasul,⁽³³⁾ during which 20 newborns were studied in the first hours and days longitudinally. In the first hours of life, changes were remarkably rapid. Four distinct stages in the newborn were noted.

1.      birth (0-5 minutes)

2.      transient phase-defined as the period until the T waves reached their maximal rightward and anterior displacement (1-6 hours after birth)

3.      restitution phase (sometime before 7 days)

4.      final phase (by 3 to 7 days)

In phase 1 the T was always to the left and anterior but could be inferior or superior.

In phase 2 the T was to the right and anterior and inferior. In phase 3 by three days the T vector was always to the left and usually inferior, but could be anterior or posterior. In phase 4, by 7 days, the T was always to the left and inferior and always posterior. Castellanos⁽³⁴⁾ performed a Frank system vectorcardiography study and noted that immediately after birth and for a few hours the T was left and anterior. Later in the first day (approximately 16 hours) the T loop was anterior and to the right. After 24 hours and always by one week, the T loop was posterior and to the left. Hait and Gasul postulated that stage 1 was related to right ventricular hypertension and that phase 2 related to left ventricular volume overload from the patent ductus arteriosus with left to right shunt plus that the left ventricle, for the first time, was handling a full cardiac output. Why the T vector afterward is to the left and posterior could not be postulated and is still not known.

In our own work^(35-36) and building upon the above we found it useful to state that by 72 hours of age and surely by seven days of life, the normal T is well posterior and slightly to the left so that the T in the right chest leads is negative and in the left chest leads positive. After that there is a very gradual and variable change with the T becoming more anterior. It usually takes well into late teenage or early adulthood before the

T is reliably anterior. Thus if the T is anterior and to the left throughout childhood after seven days of life, RVH is diagnosed (with no correlation to severity). One caution must be made. If there is severe LVH with St & T abnormality, the T in the right chest leads may be anterior. Diagnosing additional RVH would be an error. Why the normal T is posterior throughout childhood is not known, but it is not related to the QRS. Davignon’s⁽³⁷⁾ comprehensive data confirms the above but expresses variability so that an occasional normal child after a year of age may demonstrate an anterior T vector.

In a very detailed body surface mapping (BSPM) study, Benson and Spach⁽³⁸⁾ reported on the QRS and ST-T from the first day throughout the first year. The above studies using standard ECG and Frank VCG could not be confirmed because exact hours of analysis were not delineated. However, after early infancy, the ST-T was stable and unrelated to changes in the QRS. This goes along with our concept that the ST-T in infancy and childhood is not a propagated entity in normals. It is evidently a primary change, the mechanism of which is not known. More confirmation of the above concept that the repolarization differences in early infancy are primary, is seen in our standard ECG and VCG in the premature infant^(39,40) where we showed that the prematurely born infant has less RVH then does the full term child. Yet the same repolarization waves are documented as in the full term child. Detailed, standard electrocardiographic and vectorcardiographic analysis for age 2-10 years^(41,42) through adolescence^(43,44) indicates the gradual anterior progression of the T vector with aging as described above.

Misnamed Concept of “Early Repolarization”

The second major issue related to repolarization early in life is the misnamed concept of “early repolarization.” Studies utilizing body surface potential maps^(45-49) have given insight into this issue. A recent editorial and earlier paper by Spodick^(49,50) discussed the issue as a misnomer, which we have always agreed with, although his judgment that there is both early and late repolarization together, implying that there is differential repolarization between parts of the left or both ventricles seems unlikely. In “early repolarization” there is ST elevation which begins before the QRS returns to baseline in lead avF and the left chest leads, then, rises to the peak of T. All agree that there is no pathology when this is recognized. The BSPM papers of Spach demonstrate that in the last 10% of the QRS, considerable repolarization is seen. Mirvis’s paper also documents that repolarization begins during the QRS and is evident before depolarization is completed. In our paper we documented that late in the QRS there may be so much repolarization that it distorts the end of the QRS causing the ST elevation. Obviously, since activation begins in the endocardium, repolarization normally begins early in the QRS. Later, activation begins in the epicardium but the transmembrane potential is completed before that of the endocardium. Furthermore, onset of activation of the left ventricle normally precedes onsets of activation of the right ventricle, adding to the complexity. The fact is that there is a lot of “late repolarization” near the end of the QRS, which distorts the QRS. Why this is recognized mostly in teenagers and young adults is not known and the exact mechanism is not known.

The landmark work of Antzelevich and his group^(51-53) where transmembrane potentials from various parts of the ventricles are measured using arterially perfused wedges of ventricle suggest that “ early repolarization” as seen in the surface electrocardiogram results from findings right after completion of phase 0 (phase 1). The recent paper of Demin⁽⁵⁴⁾ accepts the concept and believes that autonomic effects are responsible for the clinical finding. However, the fact that considerable repolarization at the end of the QRS appears to provide enough voltage to distort the end of the QRS and early ST segment on the surface electrocardiogram is not consistent with the above concept. Therefore, we believe that the term “early repolarization” is indeed a misnomer and should be discarded.

References

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54. Demin