Brain tissue acid-base response to hypercapnia in neurosurgical patients.
These studies were conducted in neurosurgical patients to determine brain tissue nonbicarbonate buffering of pH changes during hypercapnia. Following a craniotomy, a sensor which continuously measures oxygen pressure, carbon dioxide pressure, pH and temperature was inserted into cortex tissue of nine subjects. Bicarbonate concentration was calculated from the Henderson-Hasselbach equation. Following baseline measures, PaCO2 was increased 10mmHg for 10 min. Tissue pCO2 increased 9 mmHg (p < 0.05) without a change in tissue pO2. In six patients, tissue 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 increase in tissue bicarbonate during hypercapnia; 2 had baseline tissue pH less than 6.5 and one displayed signs of tissue hypoxia during the CO2 challenge. In all patients, increases in tissue H+ during hypercapnia were related to baseline tissue bicarbonate concentration. Marked increases in H+ were seen when baseline bicarbonate decreased below 10 meq L-1. These results suggest that when tissue bicarbonate is depleted, the risk of H+ induced injury during hypercapnia is increased.
Hoffman
W E
WE
Department of Anesthesiology, University of Illinois at Chicago 60612, USA.
Charbel
F T
FT
Edelman
G
G
Ausman
J I
JI
D000137:Acid-Base Imbalance; D001639:Bicarbonates / Q000378:metabolism*; D002561:Cerebrovascular Disorders / Q000378:metabolism / Q000601:surgery*; D003399:Craniotomy / Q000009:adverse effects*; D005069:Evaluation Studies as Topic; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism*
D001639:Bicarbonates