PEDIATRICS Vol. 28 No. 4 October 1961, pp. 545-565
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FAILURE OF THE HEART AFTER UNDUE ASPHYXIA AT BIRTH

E. D. Burnard M.B., M.R.C.P., M.R.A.C.P.1 and L. S. James M.B.1

1 Anesthesiology Service of the Presbyterian Hospital, Sloane Hospital for Women, Babies Hospital, and the Departments of Anesthesiology and Pediatrics, College of Physicians and Surgeons, Columbia University

Thirty-three mature infants became ill in the neonatal period after suffering undue asphyxiation at birth. Dyspnea was a prominent symptom. Nineteen died and 14 recovered.

The transverse diameter of the cardiac silhouette in most cases was greater than the average in healthy infants. The progressively increasing size of the heart between 1) healthy infants, 2) those who appeared healthy, but had suffered undue asphyxiation at birth, and 3) those in whom signs of illness developed after asphyxia, indicated that the illness and cardiac enlargement were related. Dilatation rather than hypertrophy was the likely cause of the greater roentgenographic size. This was most obvious on the right. There was also evidence suggestive of left ventricular dilatation. The size of the heart diminished as the infants recovered. In three infants who died serial films showed that enlargement remained or increased, and hypertrophy of both ventricles was present at necropsy in the one who survived the longest time. Roentgenographic changes in the lungs did not correlate well with either the signs of illness or with the presence of cardiac enlargement. The possibility existed that vascular congestion and transudation could be responsible for abnormal appearances in the lungs, when these were present.

Biochemical changes resulting from severe asphyxia were observed soon after birth in four cases, and their presence in the others at this time was inferred from the depressed state of the infant as judged by the Apgar score. The quick recovery of the deranged acid base status which occurs after normal birth was not seen in most of the patients. Exceptions were those in whom the illness was brief. The abnormal biochemical status was characterized by arterial hypoxia and metabolic acidosis. The partial pressure of arterial carbon dioxide was distributed over a wide range. These findings are compatible with the presence of left ventricular failure.

The left atrial pressure was high in comparison with that of healthy newborn infants. Venous pressure was also increased on the right. Consideration of the results of the three different kinds of investigation led to the suggestion that left ventricular failure occurred early in the illness. Disproportion between different signs in individual cases might have been related to attempted compensation by the heart and to the rate at which failure of the right heart might follow, as well as to the severity of the illness and the rate of recovery. While atelectasis and infection may have been present, there was evidence that heart failure could be the explanation of dyspnea in life and pulmonary vascular congestion at necropsy. The cause of failure is not known. It is related to the metabolic disorder from undue birth asphyxia. A disturbance in hemodynamics that requires more investigation is present.