Reid K H, Patenaude B, Guo S Z, Iyer V G
Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, KY 40292, USA.
Resuscitation. 1998 Sep;38(3):185-91. doi: 10.1016/s0300-9572(98)00096-3.
In the clinical literature there are reports of patients failing to breathe and becoming comatose when supplied with 100% oxygen for respiratory distress. This effect has been attributed to a loss of respiratory drive. Recent studies have established that this explanation is incorrect, but have left the phenomenon unexplained. We propose that the apnea and coma reported is due to carbon dioxide narcosis. We have reproduced this effect in an animal model and have documented PCO2 values in excess of 250 mmHg during the apneic period. Our results suggest that this level of PCO2 suppresses both brainstem auditory evoked potentials and spontaneous respiration. The high PCO2 is due to inadequate gas exchange, and is easily remedied by provision of adequate ventilation.
临床文献中有报道称，一些患者在因呼吸窘迫而接受100%氧气供应时，会出现呼吸停止并陷入昏迷的情况。这种效应被归因于呼吸驱动力的丧失。最近的研究已经确定这种解释是不正确的，但该现象仍未得到解释。我们认为所报道的呼吸暂停和昏迷是由二氧化碳麻醉引起的。我们已经在动物模型中重现了这种效应，并记录到呼吸暂停期间二氧化碳分压（PCO2）值超过250毫米汞柱。我们的结果表明，这种水平的PCO2会抑制脑干听觉诱发电位和自主呼吸。高PCO2是由于气体交换不足所致，通过提供充足的通气很容易得到纠正。
