Rodriguez-Roisin R, Hickey B P, Clark T J
Br J Dis Chest. 1976 Apr;70(2):138-40. doi: 10.1016/0007-0971(76)90022-x.
During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their CO2 responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood PCO2, and was not seen hypoxaemic patients with a normal PCO2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing durigng waking hours, and is linked to the arterial blood PCO2.
睡眠期间，一些气道阻塞和低氧血症患者会出现呼吸急促。这无法用他们肺功能异常的严重程度、二氧化碳反应性、肺部疾病的性质或他们的性格来解释。这种夜间呼吸急促与静息动脉血二氧化碳分压升高的相关性最强，而在二氧化碳分压正常的低氧血症患者中未见这种情况，这些患者在睡眠时呼吸频率会出现通常的下降。我们认为，在同时患有低氧血症和高碳酸血症的患者中，睡眠会消除一种在清醒时减缓呼吸的皮质抑制机制，且该机制与动脉血二氧化碳分压有关。
