Albert Scott P, DiRocco Joseph, Allen Gilman B, Bates Jason H T, Lafollette Ryan, Kubiak Brian D, Fischer John, Maroney Sean, Nieman Gary F
Department of Surgery, SUNY Upstate Medical University, Syracuse, New York 13210, USA.
J Appl Physiol (1985). 2009 Mar;106(3):757-65. doi: 10.1152/japplphysiol.90735.2008. Epub 2008 Dec 12.
Inappropriate mechanical ventilation in patients with acute respiratory distress syndrome can lead to ventilator-induced lung injury (VILI) and increase the morbidity and mortality. Reopening collapsed lung units may significantly reduce VILI, but the mechanisms governing lung recruitment are unclear. We thus investigated the dynamics of lung recruitment at the alveolar level. Rats (n = 6) were anesthetized and mechanically ventilated. The lungs were then lavaged with saline to simulate acute respiratory distress syndrome (ARDS). A left thoracotomy was performed, and an in vivo microscope was placed on the lung surface. The lung was recruited to three recruitment pressures (RP) of 20, 30, or 40 cmH(2)O for 40 s while subpleural alveoli were continuously filmed. Following measurement of microscopic alveolar recruitment, the lungs were excised, and macroscopic gross lung recruitment was digitally filmed. Recruitment was quantified by computer image analysis, and data were interpreted using a mathematical model. The majority of alveolar recruitment (78.3 +/- 7.4 and 84.6 +/- 5.1%) occurred in the first 2 s (T2) following application of RP 30 and 40, respectively. Only 51.9 +/- 5.4% of the microscopic field was recruited by T2 with RP 20. There was limited recruitment from T2 to T40 at all RPs. The majority of gross lung recruitment also occurred by T2 with gradual recruitment to T40. The data were accurately predicted by a mathematical model incorporating the effects of both pressure and time. Alveolar recruitment is determined by the magnitude of recruiting pressure and length of time pressure is applied, a concept supported by our mathematical model. Such a temporal dependence of alveolar recruitment needs to be considered when recruitment maneuvers for clinical application are designed.
急性呼吸窘迫综合征患者不适当的机械通气可导致呼吸机相关性肺损伤(VILI),并增加发病率和死亡率。重新开放萎陷的肺单位可能会显著降低VILI,但肺复张的机制尚不清楚。因此,我们研究了肺泡水平的肺复张动力学。将大鼠(n = 6)麻醉并进行机械通气。然后用盐水灌洗肺以模拟急性呼吸窘迫综合征(ARDS)。进行左胸廓切开术,并将体内显微镜置于肺表面。在持续拍摄胸膜下肺泡的同时,将肺复张至20、30或40 cmH₂O的三个复张压力(RP),持续40秒。在测量微观肺泡复张后,切除肺,并对宏观全肺复张进行数字拍摄。通过计算机图像分析对复张进行量化,并使用数学模型解释数据。分别在应用RP 30和40后的前2秒(T2)内,大部分肺泡复张(78.3±7.4%和84.6±5.1%)发生。使用RP 20时,到T2时只有51.9±5.4%的微观视野被复张。在所有复张压力下,从T2到T40的复张有限。大部分全肺复张也在T2时发生,并逐渐复张至T40。数据通过结合压力和时间影响的数学模型得到准确预测。肺泡复张由复张压力的大小和压力施加的时间长度决定,这一概念得到了我们数学模型的支持。在设计临床应用的复张操作时,需要考虑肺泡复张的这种时间依赖性。