Satoh S, Matsukawa S, Hoshi K, Haga S, Kaise A, Hashimoto Y
Department of Anesthesiology, Tohoku University School of Medicine, Sendai.
Masui. 1990 Aug;39(8):1022-7.
Apnea and desaturation following nitrous oxide inhalation were studied in seven adult volunteers breathing spontaneously. Arterial oxygen saturation (SpO2), end-tidal CO2 concentration in the nasal cavity and respiratory patterns were measured in volunteers breathing air after N2O (50% or 67%) + O2. SpO2 was measured with Biox 3700 and end-tidal CO2 concentration was measured with Normocap, and respiratory patterns were recorded with RESPIGRAPH. After breathing N2O, two volunteers had frequent apnea (greater than 20 sec) accompanied by desaturation (SpO2 less than 90%). The lowest value of SpO2 was 82%. When the apnea occurred, the airway seemed to be open and end-tidal CO2 concentration values were lower than those before N2O inhalation. The authors considered that this kind of apnea was due to several factors, such as hypocapnia caused by hyperventilation during N2O anesthesia, dilution of alveolar O2 and CO2 during N2O excretion, loss of consciousness by N2O, and depression of CO2 ventilatory response by N2O. Inhalation of O2 at high concentrations for five minutes could improve the hypocapnia and prevent the apnea.
对7名自主呼吸的成年志愿者吸入氧化亚氮后的呼吸暂停和血氧饱和度下降情况进行了研究。在志愿者吸入50%或67%的N₂O + O₂后呼吸空气时,测量其动脉血氧饱和度(SpO₂)、鼻腔呼气末二氧化碳浓度及呼吸模式。SpO₂用Biox 3700测量,呼气末二氧化碳浓度用Normocap测量,呼吸模式用RESPIGRAPH记录。吸入N₂O后,两名志愿者频繁出现呼吸暂停(超过20秒)并伴有血氧饱和度下降(SpO₂低于90%)。SpO₂的最低值为82%。呼吸暂停发生时,气道似乎是开放的,呼气末二氧化碳浓度值低于吸入N₂O前。作者认为这种呼吸暂停是由多种因素引起的,如N₂O麻醉期间过度通气导致的低碳酸血症、N₂O排出过程中肺泡O₂和CO₂的稀释、N₂O导致的意识丧失以及N₂O对CO₂通气反应的抑制。高浓度吸入O₂ 5分钟可改善低碳酸血症并预防呼吸暂停。