From the Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil (R.S.S., L.d.A.M., M.V.O., C.L.S., L.M., E.F.P., C.d.S.S., J.A.M., A.C.C., M.V.d.S.F., V.M., P.L.S., P.R.M.R.) the Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil (V.M., V.L.C.) the Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil (M.M.M.) the Department of Anesthesiology and Intensive Care Therapy, Pulmonary Engineering Group, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany (T.K., M.G.d.A.) the San Martino Policlinico Hospital, IRCCS for Oncology, Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy (P.P.).
Anesthesiology. 2018 Jun;128(6):1193-1206. doi: 10.1097/ALN.0000000000002143.
The authors hypothesized that low tidal volume (VT) would minimize ventilator-induced lung injury regardless of the degree of mechanical power. The authors investigated the impact of power, obtained by different combinations of VT and respiratory rate (RR), on ventilator-induced lung injury in experimental mild acute respiratory distress syndrome (ARDS).
Forty Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, 32 rats were randomly assigned to be mechanically ventilated (2 h) with a combination of different VT (6 ml/kg and 11 ml/kg) and RR that resulted in low and high power. Power was calculated as energy (ΔP,L/E,L) × RR (ΔP,L = transpulmonary driving pressure; E,L = lung elastance), and was threefold higher in high than in low power groups. Eight rats were not mechanically ventilated and used for molecular biology analysis.
Diffuse alveolar damage score, which represents the severity of edema, atelectasis, and overdistension, was increased in high VT compared to low VT, in both low (low VT: 11 [9 to 14], high VT: 18 [15 to 20]) and high (low VT: 19 [16 to 25], high VT: 29 [27 to 30]) power groups. At high VT, interleukin-6 and amphiregulin expressions were higher in high-power than in low-power groups. At high power, amphiregulin and club cell protein 16 expressions were higher in high VT than in low VT. Mechanical energy and power correlated well with diffuse alveolar damage score and interleukin-6, amphiregulin, and club cell protein 16 expression.
In experimental mild ARDS, even at low VT, high mechanical power promoted ventilator-induced lung injury. To minimize ventilator-induced lung injury, low VT should be combined with low power.
作者假设，无论机械功率大小如何，小潮气量（VT）都将最大限度地减少呼吸机引起的肺损伤。作者研究了通过不同的 VT 和呼吸频率（RR）组合获得的功率对实验性轻度急性呼吸窘迫综合征（ARDS）中呼吸机引起的肺损伤的影响。
40 只 Wistar 大鼠接受大肠杆菌脂多糖气管内滴注。24 小时后，32 只大鼠被随机分为两组，分别接受小潮气量（6ml/kg 和 11ml/kg）和 RR 的机械通气（2 小时），以产生低功率和高功率。功率计算为能量（ΔP,L/E,L）×RR（ΔP,L=跨肺驱动压；E,L=肺弹性），高功率组比低功率组高三倍。8 只大鼠未进行机械通气，用于分子生物学分析。
弥漫性肺泡损伤评分（代表水肿、肺不张和过度膨胀的严重程度）在高 VT 组中高于低 VT 组，在低功率（低 VT：11[9 至 14]，高 VT：18[15 至 20]）和高功率（低 VT：19[16 至 25]，高 VT：29[27 至 30]）组中均如此。在高 VT 时，高功率组中白细胞介素-6 和 Amphiregulin 的表达高于低功率组。在高功率下，高 VT 组中 Amphiregulin 和 club 细胞蛋白 16 的表达高于低 VT 组。机械能和功率与弥漫性肺泡损伤评分以及白细胞介素-6、Amphiregulin 和 club 细胞蛋白 16 的表达密切相关。
在实验性轻度 ARDS 中，即使采用小潮气量，高机械功率也会加重呼吸机引起的肺损伤。为了最大限度地减少呼吸机引起的肺损伤，应将小潮气量与低功率相结合。
