Kollisch-Singule Michaela, Emr Bryanna, Smith Bradford, Ruiz Cynthia, Roy Shreyas, Meng Qinghe, Jain Sumeet, Satalin Joshua, Snyder Kathy, Ghosh Auyon, Marx William H, Andrews Penny, Habashi Nader, Nieman Gary F, Gatto Louis A
Department of General Surgery, SUNY Upstate Medical University, Syracuse, NY.
Department of Medicine, University of Vermont, Burlington, VT.
J Am Coll Surg. 2014 Nov;219(5):968-76. doi: 10.1016/j.jamcollsurg.2014.09.011. Epub 2014 Sep 19.
Improper mechanical ventilation can exacerbate acute lung damage, causing a secondary ventilator-induced lung injury (VILI). We hypothesized that VILI can be reduced by modifying specific components of the ventilation waveform (mechanical breath), and we studied the impact of airway pressure release ventilation (APRV) and controlled mandatory ventilation (CMV) on the lung micro-anatomy (alveoli and conducting airways). The distribution of gas during inspiration and expiration and the strain generated during mechanical ventilation in the micro-anatomy (micro-strain) were calculated.
Rats were anesthetized, surgically prepared, and randomized into 1 uninjured control group (n = 2) and 4 groups with lung injury: APRV 75% (n = 2), time at expiration (TLow) set to terminate appropriately at 75% of peak expiratory flow rate (PEFR); APRV 10% (n = 2), TLow set to terminate inappropriately at 10% of PEFR; CMV with PEEP 5 cm H2O (PEEP 5; n = 2); or PEEP 16 cm H2O (PEEP 16; n = 2). Lung injury was induced in the experimental groups by Tween lavage and ventilated with their respective settings. Lungs were fixed at peak inspiration and end expiration for standard histology. Conducting airway and alveolar air space areas were quantified and conducting airway micro-strain was calculated.
All lung injury groups redistributed inspired gas away from alveoli into the conducting airways. The APRV 75% minimized gas redistribution and micro-strain in the conducting airways and provided the alveolar air space occupancy most similar to control at both inspiration and expiration.
In an injured lung, APRV 75% maintained micro-anatomic gas distribution similar to that of the normal lung. The lung protection demonstrated in previous studies using APRV 75% may be due to a more homogeneous distribution of gas at the micro-anatomic level as well as a reduction in conducting airway micro-strain.
不当的机械通气会加重急性肺损伤,导致继发性呼吸机相关性肺损伤(VILI)。我们假设通过改变通气波形(机械通气)的特定组成部分可以减少VILI,并且我们研究了气道压力释放通气(APRV)和控制指令通气(CMV)对肺微观解剖结构(肺泡和传导气道)的影响。计算了吸气和呼气期间的气体分布以及微观解剖结构中机械通气期间产生的应变(微应变)。
将大鼠麻醉、进行手术准备,并随机分为1个未受伤对照组(n = 2)和4个肺损伤组:APRV 75%(n = 2),呼气时间(TLow)设定为在呼气峰值流速(PEFR)的75%时适当终止;APRV 10%(n = 2),TLow设定为在PEFR的10%时不适当终止;PEEP为5 cm H2O的CMV(PEEP 5;n = 2);或PEEP为16 cm H2O的CMV(PEEP 16;n = 2)。通过吐温灌洗诱导实验组的肺损伤,并在各自设定条件下进行通气。在吸气峰值和呼气末期固定肺组织以进行标准组织学检查。对传导气道和肺泡气腔面积进行定量,并计算传导气道微应变。
所有肺损伤组均将吸入气体从肺泡重新分布到传导气道。APRV 75%使传导气道中的气体再分布和微应变最小化,并在吸气和呼气时提供了与对照组最相似的肺泡气腔占有率。
在损伤的肺中,APRV 75%维持了与正常肺相似的微观解剖气体分布。先前使用APRV 75%的研究中所证明的肺保护作用可能归因于微观解剖水平上更均匀的气体分布以及传导气道微应变的降低。