Rohrs Elizabeth C, Bassi Thiago G, Nicholas Michelle, Wittmann Jessica, Ornowska Marlena, Fernandez Karl C, Gani Matt, Reynolds Steven C
Advancing Innovation in Medicine Institute, New Westminster, BC, Canada.
Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada.
Can J Respir Ther. 2023 Apr 11;59:103-110. doi: 10.29390/cjrt-2022-075. eCollection 2023.
Mechanical ventilator breaths provided to deeply sedated patients have an abnormal volume distribution, encouraging alveolar collapse in dependent regions and promoting alveolar overdistention in non-dependent regions. Collapse and overdistention both start with the first breath and worsen over time, driving ventilator-induced lung injury (VILI). This is exacerbated when the lung is already injured or has increased heterogeneity. Our study investigated the impact of a single episode of lung injury on lung mechanics and the risk factors for ventilator-induced injury, compared with non-injured lungs.
Two groups of pigs were sedated and ventilated using lung-protective volume-controlled mode at 8 mL/kg, positive end-expiratory pressure (PEEP) 5 cmHO, with respiratory rate and FiO2 set to maintain normal blood gas values. Animals in one group were ventilated for 50 h (50-Hour MV group, n=10). Animals in the second group had lung injury induced using oleic acid and were ventilated for 12 h post-injury (LI MV group, n=6). Both groups were compared with a never-ventilated control group (NV, n=6). Lung mechanics and injury were measured using electrical impedance tomography, esophageal pressure monitoring and tissue histology.
End-expiratory lung-volume loss was greater in the 50-Hour MV group (P<0.05). Plateau pressure, driving pressure and lung injury score were higher in the LI MV group, (P<0.05).
Risk factors for VILI developed three- to five-times faster in the group with injured lungs, demonstrating that a single lung-injury episode substantially increased the risk of VILI, compared with normal lungs, despite using a lung-protective mechanical ventilation protocol.
为深度镇静患者提供的机械通气呼吸具有异常的容积分布，促使依赖区域的肺泡萎陷，并导致非依赖区域的肺泡过度扩张。萎陷和过度扩张均始于首次呼吸，并随时间加重，从而引发呼吸机相关性肺损伤（VILI）。当肺部已经受损或异质性增加时，这种情况会加剧。我们的研究调查了与未受伤的肺相比，单次肺损伤对肺力学的影响以及呼吸机诱导性损伤的危险因素。
两组猪使用肺保护性容量控制模式进行镇静和通气，潮气量为8 mL/kg，呼气末正压（PEEP）为5 cmH₂O，设置呼吸频率和吸入氧分数以维持正常血气值。一组动物通气50小时（50小时机械通气组，n = 10）。第二组动物使用油酸诱导肺损伤，并在损伤后通气12小时（肺损伤机械通气组，n = 6）。将两组与未通气的对照组（NV，n = 6）进行比较。使用电阻抗断层扫描、食管压力监测和组织组织学测量肺力学和损伤情况。
50小时机械通气组呼气末肺容积损失更大（P<0.05）。肺损伤机械通气组的平台压、驱动压和肺损伤评分更高（P<0.05）。
与正常肺相比，肺损伤组中VILI的危险因素发展速度快三至五倍，这表明尽管采用了肺保护性机械通气方案，但单次肺损伤事件仍显著增加了VILI的风险。
