(S-277) Hoffman, W.E., Tuesday 7:00

INTRODUCTION: Clinical studies show that brain oxygen reactivity is increased during cerebral injury. It is possible these measures are altered by the ventilation state in each patient. In 8 dogs, we evaluated brain oxygen reactivity in cerebral veins and tissue. Oxygen reactivity was determined by stepwise increases in oxygen ventilation and evaluated at 3 different levels of arterial CO2 pressure (PaCO2).
METHODS: After a craniotomy, a Neurotrend probe that measures tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), pH and temperature was inserted into cortex tissue. A small vein was catheterized that drained the same tissue for separate oxygen reactivity measures. Brain tissue oxygen reactivity was measured at 4 levels of inspired oxygen (40%, 60%, 80%, 95%) in relation to a control state of room air according to the formula: tissue O2 reactivity = ((PO2-control PO2)/control PO2*100)/(PaO2-control PaO2). Cerebral venous oxygen reactivity was determined in the same manner. This was repeated at three different end tidal PCO2 (20 mmHg, 40 mmHg, 60 mmHg). End tidal CO2 levels and FIO2 were tested in random order.
RESULTS: Median tissue oxygen reactivity at PCO2 of 20, 40 and 60 mmHg was 0.14%, 0.25% and 0.25% respectively (P < 0.05)(figure 1). Venous oxygen reactivity at PCO2 = 20, 40 and 60 mmHg was 0.07%, 0.08% and 0.30% respectively (P < 0.05). Oxygen reactivity did not change at different inspired oxygen levels.
DISCUSSION: These results show that oxygen reactivity does not change as inspired oxygen concentrations increase. However, tissue oxygen reactivity increases from hypocapnia to normo- capnia. This demonstrates the importance of comparing oxygen reactivity with the same PCO2 between different groups of patients. Venous oxygen reactivity is not closely related to tissue oxygen reactivity until hypercapnic levels are obtained.