Javaheri S, Shore N S, Rose B, Kazemi H
Chest. 1982 Mar;81(3):296-301. doi: 10.1378/chest.81.3.296.
Although hyperventilation is a well-known compensatory mechanism in metabolic acidosis, compensatory hypoventilation has been inconsistent and controversial in metabolic alkalosis. Six healthy subjects were studied under baseline conditions and during steady-state metabolic acidosis (seven episodes) and alkalosis (14 episodes). Minute ventilation (VE) fell in metabolic alkalosis and rose in metabolic acidosis. These changes in ventilation were entirely due to reduction and elevation of tidal volume (VT) respectively, while respiratory frequency (f) remained unchanged. Alveolar ventilation fell during metabolic alkalosis and resulted in elevation of arterial PCO2 in all subjects. The ventilatory response to arterial PCO2 in all subjects. The ventilatory response to CO2 breathing was also diminished. There was a linear relationship between PaCO2 and plasma [HCO-3] in metabolic acidosis and alkalosis which was defined as PaCO2 (mm Hg = 0.7 [HCO-a] + 20 (+/- SEM), r = 0.95. Although arterial PO2 and plasma [K+] fell during metabolic alkalosis, minute ventilation did not change upon breathing oxygen and there was no correlation between changes in plasma [K+] and plasma H+ regulation.
尽管过度通气是代谢性酸中毒中一种广为人知的代偿机制，但代偿性通气不足在代谢性碱中毒中一直存在争议且情况不一。对6名健康受试者在基线条件下以及稳态代谢性酸中毒（7次发作）和碱中毒（14次发作）期间进行了研究。分钟通气量（VE）在代谢性碱中毒时下降，在代谢性酸中毒时上升。这些通气变化分别完全是由于潮气量（VT）的减少和增加所致，而呼吸频率（f）保持不变。在代谢性碱中毒期间肺泡通气量下降，导致所有受试者动脉血二氧化碳分压（PCO2）升高。所有受试者对动脉血PCO2的通气反应。对二氧化碳呼吸的通气反应也减弱。在代谢性酸中毒和碱中毒中，动脉血二氧化碳分压（PaCO2）与血浆[HCO3-]之间存在线性关系，定义为PaCO2（mmHg）=0.7[HCO3-]+20（±标准误），r=0.95。尽管在代谢性碱中毒期间动脉血氧分压（PO2）和血浆[K+]下降，但吸氧时分钟通气量并未改变，并且血浆[K+]的变化与血浆H+调节之间没有相关性。
