Retamal J, Borges J B, Bruhn A, Feinstein R, Hedenstierna G, Suarez-Sipmann F, Larsson A
Hedenstierna Laboratory, Department of Surgical Sciences, Section of Anaesthesiology & Critical Care, Uppsala University, Uppsala, Sweden.
Departamento de Medicina Intensiva, Pontificia Universidad Católica de Chile, Santiago, Chile.
Acta Anaesthesiol Scand. 2016 Sep;60(8):1131-41. doi: 10.1111/aas.12735. Epub 2016 Apr 25.
We recently reported that a high respiratory rate was associated with less inflammation than a low respiratory rate, but caused more pulmonary edema in a model of ARDS when an ARDSNet ventilatory strategy was used. We hypothesized that an open lung approach (OLA) strategy would neutralize the independent effects of respiratory rate on lung inflammation and edema. This hypothesis was tested in an ARDS model using two clinically relevant respiratory rates during OLA strategy.
Twelve piglets were subjected to an experimental model of ARDS and randomized into two groups: LRR (20 breaths/min) and HRR (40 breaths/min). They were mechanically ventilated for 6 h according to an OLA strategy. We assessed respiratory mechanics, hemodynamics, and extravascular lung water (EVLW). At the end of the experiment, wet/dry ratio, regional histology, and cytokines were evaluated.
After the ARDS model was established, Cdyn,rs decreased from 21 ± 3.3 to 9.0 ± 1.8 ml/cmH2 O (P < 0.0001). After the lung recruitment maneuver, Cdyn,rs increased to the pre-injury value. During OLA ventilation, no differences in respiratory mechanics, hemodynamics, or EVLW were observed between groups. Wet/dry ratio and histological scores were not different between groups. Cytokine quantification was similar and showed a homogeneous distribution throughout the lung in both groups.
Contrary to previous findings with the ARDSNet strategy, respiratory rate did not influence lung inflammatory response or pulmonary edema during OLA ventilation in experimental ARDS. This indicates that changing the respiratory rate when OLA ventilation is used will not exacerbate lung injury.
我们最近报道，在急性呼吸窘迫综合征（ARDS）模型中，当采用ARDSNet通气策略时，高呼吸频率比低呼吸频率炎症反应轻，但会导致更多的肺水肿。我们假设开放肺通气（OLA）策略将抵消呼吸频率对肺部炎症和水肿的独立影响。在OLA策略期间，使用两种临床相关的呼吸频率在ARDS模型中对这一假设进行了验证。
12只仔猪建立ARDS实验模型，随机分为两组：低呼吸频率组（LRR，20次/分钟）和高呼吸频率组（HRR，40次/分钟）。根据OLA策略对它们进行6小时的机械通气。我们评估了呼吸力学、血流动力学和血管外肺水（EVLW）。实验结束时，评估湿/干比、局部组织学和细胞因子。
ARDS模型建立后，动态顺应性（Cdyn,rs）从21±3.3降至9.0±1.8ml/cmH2O（P<0.0001）。肺复张操作后，Cdyn,rs升至损伤前值。在OLA通气期间，两组之间在呼吸力学、血流动力学或EVLW方面未观察到差异。两组之间的湿/干比和组织学评分无差异。细胞因子定量相似，两组在整个肺内均呈均匀分布。
与先前ARDSNet策略的研究结果相反，在实验性ARDS的OLA通气期间，呼吸频率并未影响肺部炎症反应或肺水肿。这表明在采用OLA通气时改变呼吸频率不会加重肺损伤。
