Nowadays hyperbaric oxygenation is generally accepted as the treatment of choice and is applied routinely in most general hospitals in Korea. The purpose of this study is to clarify in the therapeutic mechanism and the effect of hyperbaric oxygen through a sectional analysis of blood gas changes during the exposure to carbon monoxide and the treatment with hyperbaric oxygen.
Twenty two rabbits were exposed to carbon monoxide gas of 4,500 ppm for one hour. The half of the rabbits (experimental group) were treated with hyperbaric ox-ygen of 3 ata for one hour and then were observed for the next hour in the room air. Another half (control group) were left in the room air for two hours after CO exposure. Blood sampling was done from both internal carotid artery and external jugular vein shortly before CO exposure and then in every twenty minutes for the first two hours and every thirty minutes for the last hour.
The findings were as follows.
1. While the arterial PO2 increased by 29 mmHg during CO exposure, PCO2 decreased by 12´ mmHg suggesting that the rabbit´hyperventilated to compensate hypoxia.
2. At the end of CO exposure, pH (7.16), PCO2 (16mmHg), HC03 (1.57 mEq/L) and base excess (-21 mEq/L), all decreased suggesting the condition to be partially compensated metabolic acidosis.
3. Elevation of PO2 in arterial blood (113 mmHg) with concomitant drop in venous blood (11 mmHg) is most likely the result of increased utilization of dissolved ox-ygen instead of hemoglobin combined oxygen. The significance of cytochrome a3 inactivation as the mechanism of CO poisoning should be re-evaluated.
4. The half life of HbCO in experimental and control group were 7.8 and 17.2 minutes respectively; in other words, dissociation of HbCO in hyperbaric oxygen (3 ata) environment was 2.2 times as fast as that in the room air.
5. With hyperbaric oxygenation, arteriovenous difference of PO2 increased to 1,350 mmHg, which means about 4.2 volume percent of dissolved oxygen was utilized to result in almost immediate relief of tissue hypoxia.
6. Comparing the changes in pH and base excess of experimental and control group, it is obvious that hyperbaric oxygen accelerates the relief of metabolic acidosis in CO poisoning.
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