The effect of varying arterial oxygen tension on neonatal acid-base balance.

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 PaO2 is decreased and, if severe, arterial partial pressure of CO2 is increased. Three-d-old swine were anesthetized, intubated, and mechanically ventilated. Ventilation with a gas mixture of medical air and 95% N2:5% CO2 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. Acid-base status was evaluated via changes in arterial blood partial pressure of CO2, pH, HCO3-, and base excess at 0, 30, 60, and 120 min. Only the severe hypoxia group had significantly elevated (p less than 0.0001) arterial partial pressure of CO2 compared to the other groups at 60 and 120 min [8.7 +/- 0.5 and 8.0 +/- 0.5 kPa (65.5 +/- 3.7 and 60.0 +/- 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 HCO3-, base excess, and pH at 60 and 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)