Translational Medicine Program, Hospital for Sick Children, Peter Gilgan Centre for Research and Learning, 686 Bay St., 9th Floor, Toronto, ON, M5G 0A4, Canada.
The Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada.
Crit Care. 2022 Feb 18;26(1):47. doi: 10.1186/s13054-022-03924-2.
An abrupt lung deflation in rodents results in lung injury through vascular mechanisms. Ventilator disconnections during endo-tracheal suctioning in humans often cause cardio-respiratory instability. Whether repeated disconnections or lung deflations cause lung injury or oedema is not known and was tested here in a porcine large animal model.
Yorkshire pigs (~ 12 weeks) were studied in three series. First, we compared PEEP abruptly deflated from 26 cmHO or from PEEP 5 cmHO to zero. Second, pigs were randomly crossed over to receive rapid versus gradual PEEP removal from 20 cmHO. Third, pigs with relative volume overload, were ventilated with PEEP 15 cmHO and randomized to repeated ETT disconnections (15 s every 15 min) or no disconnection for 3 h. Hemodynamics, pulmonary variables were monitored, and lung histology and bronchoalveolar lavage studied.
As compared to PEEP 5 cmHO, abrupt deflation from PEEP 26 cmHO increased PVR, lowered oxygenation, and increased lung wet-to-dry ratio. From PEEP 20 cmHO, gradual versus abrupt deflation mitigated the changes in oxygenation and vascular resistance. From PEEP 15, repeated disconnections in presence of fluid loading led to reduced compliance, lower oxygenation, higher pulmonary artery pressure, higher lung wet-to-dry ratio, higher lung injury score and increased oedema on morphometry, compared to no disconnects.
Single abrupt deflation from high PEEP, and repeated short deflations from moderate PEEP cause pulmonary oedema, impaired oxygenation, and increased PVR, in this large animal model, thus replicating our previous finding from rodents. Rapid deflation may thus be a clinically relevant cause of impaired lung function, which may be attenuated by gradual pressure release.
在啮齿动物中,肺部突然瘪陷会通过血管机制导致肺损伤。在人类中,经气管内吸引时呼吸机断开连接常常导致心肺不稳定。目前尚不清楚重复断开连接或肺萎陷是否会导致肺损伤或水肿,本研究在猪大型动物模型中对此进行了测试。
研究共纳入了三个系列的约克夏猪(~12 周龄)。首先,我们比较了从 26cmH2O 快速放气与从 5cmH2O 逐渐放气至零的两种情况。其次,猪被随机交叉接受从 20cmH2O 快速或逐渐放气。第三,对于存在相对容量超负荷的猪,用 15cmH2O 的 PEEP 通气,并随机分为反复进行 ETT 断开连接(每 15 分钟断开 15 秒)或 3 小时不进行断开连接。监测血流动力学、肺功能,并研究肺组织学和支气管肺泡灌洗。
与 PEEP 5cmH2O 相比,从 PEEP 26cmH2O 突然放气增加了肺血管阻力,降低了氧合,并增加了肺湿干重比。从 PEEP 20cmH2O 开始,与突然放气相比,逐渐放气减轻了氧合和血管阻力的变化。在存在液体负荷的情况下,从 PEEP 15 开始,反复断开连接导致顺应性降低、氧合降低、肺动脉压升高、肺湿干重比升高、肺损伤评分升高和形态计量学上水肿增加,与不进行断开连接相比。
在该大型动物模型中,从高 PEEP 突然单一次肺萎陷和从中等 PEEP 反复进行短时间肺萎陷均可导致肺水肿、氧合受损和肺血管阻力增加,从而复制了我们之前在啮齿动物中的发现。因此,快速放气可能是导致肺功能受损的一个临床相关原因,而逐渐释放压力可能会减轻这种影响。