Congenital heart disease: An analysis of electrocardiographic patterns in forty-four patients with elevated right ventricular pressure

Abstract

Our purpose in this communication has been to describe the electrocardiogram in the presence of known right ventricular hypertrophy. Calculation of the total work of the right ventricle showed that in all patients work was elevated above the normal. Thus the presumption was made that a degree of right ventricular hypertrophy was present. All patients in this series showed elevation of right ventricular systolic pressure, some with increased flows, and an occasional normal to reduced flow. In two patients not included in this series the electrocardiogram showed right ventricular hypertrophy in the presence of increased cardiac output but with normal right ventricular and pulmonary artery pressures. Correlation coefficients were calculated relating mean right ventricular pressure and right ventricular work with the R S ratio in V 1 and the preintrinsicoid deflection time in V 1. None of these factors appear to be mathematically related since the highest correlation coefficient between the right ventricular mean systolic ejection pressure and the height of R in V 1 was plus 0.334, a barely significant figure. Even this degree of correlation is open to question because of the markedly skewed distribution of RV 1. These low correlations in no way negate the clinical significance of the patterns themselves. The electrocardiogram in congenital heart disease, as recently noted by Uhley 12 and previously by Schnitker, 13 shows few etiologically specific patterns. Predominant involvement of the right side of the heart is a classic characteristic of most types of congenital heart disease. Therefore, in this series, it is not surprising that thirty-five patients have shown electrocardiographic evidence of predominantly right ventricular involvement. Etiologically, the catheterization findings in these thirty-five patients have confirmed the diagnoses of tetralogy of Fallot, tetralogy of Eisenmenger, atrial septal defect, pure pulmonary stenosis, transposed pulmonary veins, atrial or ventricular septal defects with pulmonary stenosis, and the high ventricular septal defect. All of these thirty-five patients, it should be emphasized, belong in our electrocardiographic Groups I and II. Thus, the electrocardiographic pattern of predominantly right ventricular hypertrophy may show one of two general forms: the classic pattern, with tall RV 1 and marked reversal of the R S ratio of V 1, may be present; or alternately, a pattern of partial right bundle branch block may appear. If left ventricular enlargement is subordinate, the electrocardiogram of right ventricular hypertrophy should be present in one of these two forms. These two electrocardiographic patterns are not specific for a particular structural diagnosis, and do not appear to be related to the height of the ventricular pressure or work. It should be emphasized that in this series when right ventricular work is increased in “right-sided” congenital heart disease the electrocardiogram has always been abnormal. Conversely, when the pattern of right ventricular hypertrophy appears in congenital heart disease we may assume an elevated right ventricular pressure or flow. This series, thus, is not comparable with Johnson and associates' 2 group of patients with chronic pulmonary disease, where normal electrocardiograms were present in some patients having a moderate elevation of mean pulmonary artery pressure. It is to be expected that patients with congenital heart disease would demonstrate more abnormal electrocardiographic findings. For example, the upper limits of our R S ratios in V 1 are higher than those of either Johnson's or Myers'. The electrocardiographic pattern of partial right bundle branch block is a relatively new concept and introduces a real problem. We are only prepared to say that it appears with great frequency in the presence of elevated right ventricular work. Whether it represents a mild conduction defect in the right bundle branch, or whether it is a secondary result of the hypertrophy, cannot be decided on the evidence at hand. We do have a larger percentage of tracings in this category than has been reported by Johnson or Myers and their associates. We doubt whether the presence of septal defects is a significant contributory factor in these tracings. The anatomic diagnoses in Group III differ from those in Groups I and II. Of these nine patients, two tracings were normal, and the one patient with coarctation of the aorta showed left ventricular hypertrophy. Electrocardiograms in the remaining six patients showed findings suggestive of both right and left ventricular enlargement. Because of this bilateral involvement, the typical right ventricular hypertrophy pattern did not appear, being modified significantly by the presence of electromotive forces simultaneously arising from the enlarged left ventricle. Thus, a so-called “balanced” electrocardiogram was inscribed.