The ratio of venoarterial CO₂ tension to arteriovenous O₂ content difference (P[v-a]CO₂/C[a-v]O₂) increases when lactic acidosis is due to inadequate oxygen supply (hypoxia); we aimed to verify whether it also increases when lactic acidosis develops because of mitochondrial dysfunction (dysoxia) with constant oxygen delivery. Twelve anaesthetised, mechanically ventilated pigs were intoxicated with IV metformin (4.0 to 6.4 g over 2.5 to 4.0 h). Saline and norepinephrine were used to preserve oxygen delivery. Lactate and P[v-a]CO₂/C[a-v]O₂ were measured every one or two hours (arterial and mixed venous blood). During metformin intoxication, lactate increased from 0.8 (0.6−0.9) to 8.5 (5.0−10.9) mmol/l (p < 0.001), even if oxygen delivery remained constant (from 352 ± 78 to 343 ± 97 ml/min, p = 0.098). P[v-a]CO₂/C[a-v]O₂ increased from 1.6 (1.2–1.8) to 2.3 (1.9−3.2) mmHg/ml/dl (p = 0.004). The intraclass correlation coefficient between lactate and P[v-a]CO₂/C[a-v]O₂ was 0.72 (p < 0.001). We conclude that P[v-a]CO₂/C[a-v]O₂ increases when lactic acidosis is due to dysoxia. Therefore, a high P[v-a]CO₂/C[a-v]O₂ may not discriminate hypoxia from dysoxia as the cause of lactic acidosis.

当乳酸性酸中毒是由于供氧不足（缺氧）时，静脉CO ₂张力与动静脉O ₂含量差的比值（P[va]CO ₂ /C[av]O ₂）增加；我们的目的是验证当由于线粒体功能障碍（缺氧）和持续的氧气输送而导致乳酸性酸中毒时，它是否也会增加。十二头麻醉、机械通气的猪被静脉注射二甲双胍（4.0 至 6.4 克，2.5 至 4.0 小时）。生理盐水和去甲肾上腺素用于保持氧气输送。乳酸盐和 P[va]CO ₂ /C[av]O ₂每隔一两个小时测量一次（动脉和混合静脉血）。在二甲双胍中毒期间，乳酸从 0.8 (0.6−0.9) 增加到 8.5 (5.0−10.9) mmol/l (p < 0.001)，即使氧气输送保持不变（从 352 ± 78 到 343 ± 97 ml/min，p = 0.098）。P[va]CO ₂ /C[av]O ₂从 1.6 (1.2–1.8) 增加到 2.3 (1.9-3.2) mmHg/ml/dl (p = 0.004)。乳酸和 P[va]CO ₂ /C[av]O ₂之间的组内相关系数为 0.72 (p < 0.001)。我们得出结论，当乳酸性酸中毒是由于缺氧时，P[va]CO ₂ /C[av]O _{2 会}增加。因此，高 P[va]CO ₂ /C[av]O ₂ 可能无法将缺氧与缺氧区分开来作为乳酸性酸中毒的原因。