Acute changes in arterial carbon dioxide tension and acid-base status and early neurologic characteristics in term infants following perinatal asphyxia.

BACKGROUND

Marked acute changes in arterial carbon dioxide tension (PaCO2) and acid-base status occur in the immediate postnatal period in infants delivered in the presence,of pathologic fetal acidemia (FA) in whom the risk for hypoxic-ischemic cerebral injury is high. The cerebral vasculature is extremely sensitive to changes in PaCO2. However, the relationship between the acute changes in PaCO2 and subsequent neonatal neurologic characteristics remains unclear.

OBJECTIVES

(1) To determine the extent of the acute changes in PaCO2 and acid-base status following birth in infants delivered in the presence of pathologic FA and (2) to determine the potential relationship of the initial changes in PaCO2 and neonatal neurologic characteristics.

METHODS

PaCO2 and acid base status of cord umbilical arterial blood and initial postnatal arterial blood were studied in 73 term infants admitted to the Neonatal Intensive Care Unit. Infants were categorized in three groups: I, no FA, no respiratory support and normal neonatal neurologic examination (n = 49); II, pathologic FA (umbilical artery pH < or = 7.00, base deficit > or = 12 mEq/l), no respiratory support and normal neonatal neurologic examination (n = 17); III, FA, intubated and with evidence of hypoxic ischemic encephalopathy (HIE) including seizures (n = 7).

RESULTS

Demographic characteristics were similar among the three groups, although 5-min Apgar score < or = 5 was more common in group II (47%) and group III (100%) than in group I (4%). Umbilical arterial pH was lower in group III (6.75 +/- 0.18) vs. group II (6.90 +/- 0.09) and in group II vs. group I (6.90 +/- 0.09 vs. 7.19 +/- 0.09) (P < 0.005) and the PaCO2 was higher in group III (141 +/- 37 mmHg) vs. group II (94 +/- 22 mmHg) and in group II vs. group I (94 +/- 22 vs. 60 +/- 13 mmHg) (P < 0.05). The mean base deficit was large but comparable between groups III and II, i.e. 18 +/- 6 vs. 18 +/- 5 mEq/l, respectively, and higher than in group I infants (6 +/- 4 mEq/l) (P < 0.00). At 1 h postnatal age, the mean arterial pH had increased in all groups, i.e. 7.06 +/- 0.15 (group III), 7.25 +/- 0.09 (group II), and 7.31 +/- 0.06 (group I); however, the differences amongst the groups remained significant (P < 0.005). The mean PaCO2 decreased from 94 +/- 22 mmHg (12.5 +/- 2.9 kPa) to 30 +/- 6 mmHg (4.0 +/- 0.8 kPa) for the spontaneously ventilating group II infants and from 141 +/- 37 mmHg (18.8 +/- 4.9 kPa) to 45 +/- 14 mmHg (6.0 +/- 1.9 kPa) in the intubated group III infants (P < 0.005). A repeat PaCO2 at 2 h of age in group III infants had decreased to 29 + 2 mmHg (3.9 +/- 0.3 kPa),which was not different from the PaCO2 at 2 h in group II infants (30 +/- 8 mmHg; 4.0 +/- 1.1 kPa). No significant differences were observed for pH or base deficit at this time.

CONCLUSIONS

Marked and rapid changes in PaCO2 and pH were observed in term infants delivered in the presence of pathologic FA. Initial postnatal PaCO2 values varied significantly with the lowest values noted in those infants breathing spontaneously and who exhibited an uneventful neonatal course; higher initial postnatal values, despite mechanical ventilation, were noted in infants with HIE including seizures. Further investigation in this area is imperative in order to better define the optimal respiratory management of the neurologically at-risk infant.