PCO2 threshold for CNS oxygen toxicity in rats in the low range of hyperbaric PO2

Central nervous system (CNS) oxygen toxicity, as manifested by the first el ectrical discharge (FED) in the electroencephalogram, can occur as convulsi ons and loss of consciousness. CO2 potentiates this risk by vasodilation an d pH reduction. We suggest that CO2 can produce CNS oxygen toxicity at a Po -2 that does not on its own ultimately cause FED. We searched for the CO2 t hreshold that will result in the appearance of FED at a Po-2 between 507 an d 253 kPa. Rats were exposed to a Po-2 and an inspired PCO2 in 1-kPa steps to define the threshold for FED. The results confirmed our assumption that each rat has its own PCO2 threshold, any PCO2 above which will cause FED bu t below which no FED will occur. As Po-2 decreased from 507 to 456, 405, an d 355 kPa, the percentage of rats that exhibited FED without the addition O f CO2 (F-o) dropped from 91 to 62, to 8 and 0%, respectively. The percentag e of rats (F) having FED as a function Of PCO2 was sigmoid in shape and dis placed toward high PCO2 with the reduction in Po-2. The following formula i s suggested to express risk as a function Of PCO2 and Po-2 F = F-o + (100 - Fo)/[1 + (P-50/P-CO2)(N)] [GRAPHICS] where P-50 is the PCO2 for the half response and N is power. A small increa se in PCO2 at a Po-2 that does not cause CNS oxygen toxicity may shift an e ntire population into the risk zone. Closed-circuit divers who are CO2 reta iners or divers who have elevated inspired CO2 are at increased risk of CNS oxygen toxicity.