Evidence for involvement of hypocapnia and hypoperfusion in aetiology of neurological deficit after cardiopulmonary bypass.

Arterial and jugular bulb pressures and blood gas tensions were recorded for later analysis in 65 patients having coronary artery graft surgery. In the first 35 (group A) routine peroperative monitoring was used; and in the next 30 (group B), similar in age and other characteristics, special measures were adopted to maintain normocapnia (PaCO2 35-45 mm Hg) by continuous monitoring during surgery. On the third postoperative day clinical neurological deficits were observed in 46% of group A and 27% of group B, and psychometric deficits in 71% and 40%, respectively. On analysis of the records, more than half of group A proved to have been hypocapnic immediately before onset of cardiopulmonary bypass, and those with postoperative deficits differed from the others in this group in having had greater changes in PaCO2 after onset of bypass and lower cerebral perfusion pressures in the first 10 minutes of bypass, usually because of a rise in cerebral venous pressure.