The Effect of Varying Arterial Oxygen Tension on Neonatal Acid-Base Balance

Abstract

ABSTRACT. Acute severe hypoxia, when the arterial partial pressure of O2 (Pao2) is sufficiently reduced, causes a shift from aerobic to anaerobic metabolism and can be fatal to neonates. The ability of the neonate to accommodate this shift, and prevent acidosis, could play a role in its ability to tolerate hypoxia. This study examines the effect of varying degrees of acute hypoxia on acid-base homeostasis in the neonate using a model of right to left shunting where Pa02 is decreased and, if severe, arterial partial pressure of C 0 2 is increased. Three-d-old swine were anesthetized, intubated, and mechanically ventilated. Ventilation with a gas mixture of medical air and 95% N2:5% COz resulted in four groups: 1) normoxia (n = 5); 2) mild hypoxia (n = 4); 3) moderate hypoxia (n = 3); and 4) severe hypoxia (n = 5), with Pao2 of 10.7, 8.0, 5.3, and 2.7 kPa (80, 60, 40, and 20 mm Hg), respectively. Acidbase status was evaluated via changes in arterial blood partial pressure of COz, pH, HC03-, and base excess at 0,30,60, and 120 min. Only the severe hypoxia group had significantly elevated (p < 0.0001) arterial partial pressure of C 0 2 compared to the other groups at 60 and 120 min [8.7 f 0.5 and 8.0 f 0.5 kPa (65.5 f 3.7 and 60.0 f 3.7 mm Hg), respectively]. Base excess was unaltered in the normoxic and mild and moderate hypoxic groups, indicating no change in metabolic acid-base status. The severe hypoxic group had progressively decreased HC03-, base excess, and pH at 60 and 120 min. Thus, neonates maintained acid-base homeostasis with a wide range of Pao2 from 12.0 to 5.3 kPa (90 to 40 mm Hg), although progressive acidosis occurred when the Pao2 was further decreased to 2.7 kPa (20 mm Hg). (Pediatr Res 31: 112-116, 1992)

Peripartum hypoxic risk and cognitive outcome: A study of term and preterm birth children at early school age.

“…Goldstein et al (1995) found metabolic acidosis to be the best biochemical predictor of outcome at the age of 24 months. In the current study, initial arterial pH, but not initial base excess (an indicator of metabolic acid-base status of the buffering system independent of respiratory acidosis or alkalosis; Golderger, 1986;Goldstein et al, 1995;Torrance & Wittnich, 1992) accounted for a larger proportion of outcome variance. The differential statistical effect of the two risk indexes on outcome may, in part, stem from the fact that the standard deviation of the base excess was large relative to the mean, whereas the standard deviation of pH was comparatively small (in our total sample, initial base excess ± SD = -6.47 ± 3.56 milliequivalent per liter (mEq/L) vs. initial pH = 7.23 ± 0.05, with coefficients of variation of .55 and .01, respectively).…”