Jounieaux Vincent, Parreira Veronica F, Aubert Genevieve, Dury Myriam, Delguste Pierre, Rodenstein Daniel O
Pneumology Unit, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium.
Chest. 2002 Apr;121(4):1141-8. doi: 10.1378/chest.121.4.1141.
To confirm the hypothesis that the ventilatory response to hypoxia (VRH) may be abolished by hypocapnia.
We studied four healthy subjects during intermittent positive-pressure ventilation delivered through a nasal mask (nIPPV). Delivered minute ventilation (Ed) was progressively increased to lower end-tidal carbon dioxide pressure (PETCO(2)) below the apneic threshold. Then, at different hypocapnic levels, nitrogen was added to induce falls in oxygen saturation, a hypoxic run (N(2) run). For each N(2) run, the reappearance of a diaphragmatic muscle activity and/or an increase in effective minute ventilation (E) and/or deformations in mask-pressure tracings were considered as a VRH, whereas unchanged tracings signified absence of a VRH. For the N(2) runs eliciting a VRH, the threshold response to hypoxia (TRh) was defined as the transcutaneous oxygen saturation level that corresponds to the beginning of the ventilatory changes.
Thirty-seven N(2) runs were performed (7 N(2) runs during wakefulness and 30 N(2) runs during sleep). For severe hypocapnia (PETCO(2) of 27.1 +/- 5.2 mm Hg), no VRH was noted, whereas a VRH was observed for N(2) runs performed at significantly higher PETCO(2) levels (PETCO(2) of 34.0 +/- 2.1 mm Hg, p < 0.001). Deep oxygen desaturation (up to 64%) never elicited a VRH when the PETCO(2) level was < 29.3 mm Hg, which was considered the carbon dioxide inhibition threshold. For the 16 N(2) runs inducing a VRH, no correlations were found between PETCO(2) and TRh and between TRh and both Ed and E.
During nIPPV, VRH is highly dependent on the carbon dioxide level and can be definitely abolished for severe hypocapnia.
验证低碳酸血症可能消除对低氧通气反应（VRH）这一假说。
我们对4名健康受试者进行了研究，通过鼻罩进行间歇正压通气（nIPPV）。输送的分钟通气量（Ed）逐渐增加，以使呼气末二氧化碳分压（PETCO₂）降至低于呼吸暂停阈值。然后，在不同的低碳酸血症水平下，添加氮气以诱导氧饱和度下降，即低氧试验（N₂试验）。对于每次N₂试验，膈肌活动的再次出现和/或有效分钟通气量（E）的增加和/或面罩压力描记图的变化被视为VRH，而无变化的描记图则表示无VRH。对于引发VRH的N₂试验，低氧反应阈值（TRh）定义为与通气变化开始相对应的经皮氧饱和度水平。
共进行了37次N₂试验（清醒时7次，睡眠时30次）。对于严重低碳酸血症（PETCO₂为27.1±5.2 mmHg），未观察到VRH，而在PETCO₂水平显著较高（PETCO₂为34.0±2.1 mmHg，p<0.001）时进行的N₂试验中观察到了VRH。当PETCO₂水平<29.3 mmHg时，深度氧饱和度下降（高达64%）从未引发VRH，29.3 mmHg被视为二氧化碳抑制阈值。对于16次引发VRH的N₂试验，未发现PETCO₂与TRh之间以及TRh与Ed和E之间存在相关性。
在nIPPV期间，VRH高度依赖于二氧化碳水平，严重低碳酸血症时可完全消除。
