Musch Guido, Harris R Scott, Vidal Melo Marcos F, O'Neill Kevin R, Layfield J Dominick H, Winkler Tilo, Venegas Jose G
Department of Anesthesia and Critical Care, CLN 309, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA.
Anesthesiology. 2004 Feb;100(2):323-30. doi: 10.1097/00000542-200402000-00022.
Sustained lung inflations (recruitment maneuvers [RMs]) are occasionally used during mechanical ventilation of patients with acute lung injury to restore aeration to atelectatic alveoli. However, RMs do not improve, and may even worsen, gas exchange in a fraction of these patients. In this study, the authors sought to determine the mechanism by which an RM can impair gas exchange in acute lung injury.
The authors selected a model of acute lung injury that was unlikely to exhibit sustained recruitment in response to a lung inflation. In five sheep, lung injury was induced by lavage with 0.2% polysorbate 80 in saline. Positron emission tomography and [13N]nitrogen were used to assess regional lung function in dependent, middle, and nondependent lung regions. Physiologic data and positron emission scans were collected before and 5 min after a sustained inflation (continuous positive airway pressure of 50 cm H2O for 30 s).
All animals showed greater loss of aeration and higher perfusion and shunting blood flow in the dependent region. After the RM, Pao2 decreased in all animals by 35 +/- 22 mmHg (P < 0.05). This decrease in Pao2 was associated with redistribution of pulmonary blood flow from the middle, more aerated region to the dependent, less aerated region (P < 0.05) and with an increase in the fraction of pulmonary blood flow that was shunted in the dependent region (P < 0.05). Neither respiratory compliance nor aeration of the dependent region improved after the RM.
When a sustained inflation does not restore aeration to atelectatic regions, it can worsen oxygenation by increasing the fraction of pulmonary blood flow that is shunted in nonaerated regions.
在急性肺损伤患者机械通气期间，偶尔会采用持续肺膨胀（复张手法[RMs]）来使萎陷肺泡恢复通气。然而，在部分此类患者中，RMs并不能改善气体交换，甚至可能使其恶化。在本研究中，作者试图确定RMs导致急性肺损伤患者气体交换受损的机制。
作者选择了一种不太可能因肺膨胀而出现持续复张的急性肺损伤模型。对5只绵羊，用0.2%聚山梨酯80生理盐水灌洗诱导肺损伤。采用正电子发射断层扫描和[13N]氮评估肺下垂部位、中间部位和非下垂部位的局部肺功能。在持续肺膨胀（气道持续正压50 cm H2O，持续30秒）前及之后5分钟收集生理数据和正电子发射扫描图像。
所有动物肺下垂部位均出现更严重的通气丧失、更高的灌注及分流血流量。RMs后，所有动物的动脉血氧分压（Pao2）下降35±22 mmHg（P<0.05）。Pao2的下降与肺血流从中部通气较好区域重新分布至下垂部位通气较差区域有关（P<0.05），且与下垂部位肺血流分流比例增加有关（P<0.05）。RMs后，肺下垂部位的呼吸顺应性和通气均未改善。
当持续肺膨胀不能使萎陷区域恢复通气时，可通过增加未通气区域的肺血流分流比例而使氧合恶化。
