Mechanisms of pulmonary gas exchange abnormalities during experimental group B streptococcal infusion.

Group B streptococcal sepsis in newborns produces pulmonary arterial hypertension and hypoxemia. The purpose of this study was to investigate the mechanisms by which hypoxemia occurs. Ten anesthetized, ventilated piglets were infused with 2 X 10(9) colony forming units/kg of Group B streptococci over a 30-min period. Pulmonary arterial pressure rose from 14 +/- 2.8 to 38 +/- 6.7 torr after 20 min of the bacterial infusion (p less than 0.01). During the same period, cardiac output fell from 295 to 184 ml/kg/min (p less than 0.02). Arterial PO2 declined from 97 +/- 7 to 56 +/- 11 torr (p less than 0.02) and mixed venous PO2 fell from 39.6 +/- 5 to 28 +/- 8 torr (p less than 0.05). The multiple inert gas elimination technique was used to detect increases in shunt and alterations in ventilation-perfusion matching. Intrapulmonary shunt did not increase during or after the infusion with group B streptococci. However, there was a significant increase (p less than 0.05) in the SD of pulmonary blood flow, an index of VA/Q mismatching, 20 min after initiation of the infusion of bacteria. All the above changes reverted toward baseline during the 2-h period following discontinuation of the infusion. We conclude that the hypoxemia occurring in the early phase of group B streptococcal sepsis does not develop solely because of increased shunt, but rather is produced by a decline in cardiac output in conjunction with mismatching of pulmonary perfusion to alveolar ventilation.