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High-Tidal-Volume Mechanical Ventilation and Lung Inflammation in Intensive Care Patients With Normal Lungs

机译:高潮量机械通风和肺部肺部肺炎患者正常肺部

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摘要

Background This study was conducted to investigate whether high-tidal-volume mechanical ventilation is associated with increased lung inflammation compared with low-tidal-volume mechanical ventilation in critically ill patients with no evidence of lung injury. Methods In this prospective, single-blind, randomized (1:1), parallel-group study, 18 critically ill patients with normal lungs were randomly assigned to receive mechanical ventilation with a tidal volume of either 6 mL/kg (low tidal volume) or 12 mL/kg (high tidal volume) during the first 4 days in the intensive care unit. Results At baseline and at 24, 48, and 96 hours, exhaled breath condensate was collected to measure interleukin 1 beta, interleukin 10, tumor necrosis factor alpha, and total nitric oxide metabolites. Interleukin 1beta levels in exhaled breath condensate were significantly increased at 24 hours compared with baseline in the high-tidal-volume group but not in the low-tidal-volume group. The interleukin 1 beta increase in the high-tidal-volume group was transient. Exhaled breath condensate levels of interleukin 1beta, interleukin 10, tumor necrosis factor alpha, and total nitric oxide metabolftes did not differ significantly between the high-tidal-volume and low-tidal-volume groups at any time point. Conclusion Short-term mechanical ventilation with a tidal volume of 12 mL/kg may trigger inflammatory responses in the lungs of intensive care unit patients without preexisting lung injury.
机译:背景技术该研究是为了研究高潮气体积机械通气是否与肺炎的肺炎患者的低潮量机械通气增加,没有肺损伤。在这种前瞻性,单盲,随机(1:1),平行群体研究中,18例患有正常肺部的患者的方法,随机分配了18例患者,以接收机械通风,以6ml / kg(低潮气量)的潮气量在重症监护病房的前4天内或12毫升/千克(高潮气体积)。结果在基线和24,48和96小时的情况下,收集呼出的呼吸冷凝物,以测量白细胞介素1β,白细胞介素10,肿瘤坏死因子α和总一氧化氮代谢物。与高潮气体积组中的基线相比,在24小时内,呼出呼吸缩合的白细胞介素1Beta水平显着增加,但在低潮气体积组中。高潮体组的白细胞介素1β增加是短暂的。呼出的呼吸抑制剂凝结水平的白细胞介素1Beta,白细胞介素10,肿瘤坏死因子α,以及在任何时间点之间的高潮气量和低潮气体内组之间的全氮氧化物Metabolftes没有显着差异。结论短期机械通气12ml / kg的潮量可能会引发重症监护单位患者的肺部炎症反应,而无需先存在的肺损伤。

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