BRAIN-TISSUE ACID-BASE RESPONSE TO HYPERCAPNIA IN NEUROSURGICAL PATIENTS

These studies were conducted in neurosurgical patients to determine br ain tissue nonbicarbonate buffering of pH changes during hypercapnia. Following a craniotomy, a sensor which continuously measures oxygen pr essure, carbon dioxide pressure, pH and temperature was inserted into cortex tissue of nine subjects. Bicarbonate concentration was calculat ed from the Henderson-Hasselbach equation. Following baseline measures , PaCO2 was increased 10 mmHg for 10 min. Tissue pCO(2) increased 9 mm Hg (p < 0.05) without a change in tissue pO(2). In six patients, tissu e bicarbonate concentration increased from 18 to 20 meq L(-1) (p<0.05) indicating a 40-50% attenuation of the increase in hydrogen ion (H+) by nonbicarbonate buffering mechanisms. Three patients showed no incre ase in tissue bicarbonate during hypercapnia; 2 had baseline tissue pH less than 6.5 and one displayed signs of tissue hypoxia during the CO 2 challenge. In all patients, increases in tissue H+ during hypercapni a were related to baseline tissue bicarbonate concentration. Marked in creases in H+ were seen when baseline bicarbonate decreased below 10 m eq L(-1). These results suggest that when tissue bicarbonate is deplet ed, the risk of H+ induced injury during hypercapnia is increased.