Bernard T E, Duker J
Am Ind Hyg Assoc J. 1981 May;42(5):361-4. doi: 10.1080/15298668191419884.
Acute carbon monoxide poisoning is the result of a diminished capacity of the blood to transport oxygen and sustain a level of metabolic activity. The diminished capacity is expressed in terms of the carboxyhemoglobin (COHb) level in the blood which is dependent upon the concentration of CO in the inhaled air. The rate of CO uptake or elimination is dependent upon the concentration of CO in the air as well as pulmonary diffusion capacity and alveolar ventilation which change with different metabolic rates. Coburn, Forster and Kane (CFK) developed a mathematical model to describe the uptake and elimination kinetics of CO in sedentary individuals. The CFK model was used in a mathematical simulation of CO uptake and elimination where the independent variables were inhaled CO concentration and metabolic rate. The metabolic rate was used to specify pulmonary diffusing capacity and alveolar ventilation. As the level of COHb increased the metabolic rate was decreased to a level compatible with the impaired oxygen transport. A physical fatigue limit was also included. The theoretical model was used to simulate conditions beyond the range of exposures permissible under experimental laboratory conditions.
急性一氧化碳中毒是血液输送氧气及维持一定代谢活动水平的能力下降的结果。这种能力下降通过血液中碳氧血红蛋白（COHb）水平来体现，而该水平取决于吸入空气中一氧化碳的浓度。一氧化碳的摄取或清除速率取决于空气中一氧化碳的浓度以及肺扩散能力和肺泡通气量，这些会随不同的代谢率而变化。科伯恩、福斯特和凯恩（CFK）开发了一个数学模型来描述久坐个体中一氧化碳的摄取和清除动力学。CFK模型被用于一氧化碳摄取和清除的数学模拟，其中自变量为吸入的一氧化碳浓度和代谢率。代谢率用于指定肺扩散能力和肺泡通气量。随着碳氧血红蛋白水平升高，代谢率会降至与受损的氧气输送相适应的水平。还纳入了身体疲劳极限。该理论模型用于模拟超出实验室内允许暴露范围的情况。
