Wrigge Hermann, Zinserling Jörg, Neumann Peter, Defosse Jerome, Magnusson Anders, Putensen Christian, Hedenstierna Göran
Department of Anaesthesiology and Intensive Care Medicine, University of Bonn, Germany.
Anesthesiology. 2003 Aug;99(2):376-84. doi: 10.1097/00000542-200308000-00019.
Experimental and clinical studies have shown reduction in intrapulmonary shunt with improved oxygenation by spontaneous breathing with airway pressure release ventilation (APRV) in acute lung injury. The mechanisms of these findings are not clear. The authors hypothesized that spontaneous breathing results in better aeration of lung tissue and that improvement in oxygenation can be explained by these changes. This hypothesis was studied in a porcine model of oleic acid-induced lung injury.
Two hours after induction of lung injury, 24 pigs were randomly assigned to APRV with or without spontaneous breathing at a positive end-expiratory pressure of 5 cm H(2)O. Hemodynamics, spirometry, and end-expiratory lung volume by nitrogen washout were measured at baseline, after 2 h of lung injury, and after 2 and 4 h of mechanical ventilation in the specific mode. Finally, spiral computed tomography of the chest was performed at end-expiratory lung volume in 22 pigs.
Arterial carbon dioxide tension and mean and end-inspiratory airway pressures were comparable between settings. Four hours of APRV with spontaneous breathing resulted in improved oxygenation compared with APRV without spontaneous breathing (arterial oxygen tension, 144 +/- 65 vs. 91 +/- 50 mmHg, P < 0.01 for interaction time x mode), higher end-expiratory lung volume (786 +/- 320 vs. 384 +/- 148 ml, P < 0.001), and better aeration. End-expiratory lung volume and venous admixture were both correlated with the amount of lung reaeration (r(2) = 0.62 and r(2) = 0.61, respectively).
The results support the hypothesis that spontaneous breathing during APRV improves oxygenation mainly by recruitment of nonaerated lung and improved aeration of the lungs.
实验和临床研究表明,在急性肺损伤中,气道压力释放通气(APRV)下自主呼吸可降低肺内分流并改善氧合。这些发现的机制尚不清楚。作者推测,自主呼吸可使肺组织通气更好,氧合改善可由这些变化来解释。该假设在油酸诱导的猪肺损伤模型中进行了研究。
在诱导肺损伤2小时后,将24头猪随机分为两组,分别进行呼气末正压为5 cm H₂O的有或无自主呼吸的APRV。在基线、肺损伤2小时后以及特定模式机械通气2小时和4小时后,测量血流动力学、肺量计参数以及通过氮洗脱法测定的呼气末肺容积。最后,对22头猪在呼气末肺容积时进行胸部螺旋计算机断层扫描。
两种设置下的动脉二氧化碳分压、平均气道压和吸气末气道压相当。与无自主呼吸的APRV相比,有自主呼吸的APRV持续4小时可改善氧合(动脉氧分压,144±65 vs. 91±50 mmHg,交互作用时间×模式P<0.01),呼气末肺容积更高(786±320 vs. 384±148 ml,P<0.001),通气更好。呼气末肺容积和静脉血掺杂均与肺复张量相关(r²分别为0.62和0.61)。
结果支持以下假设,即APRV期间的自主呼吸主要通过使未通气肺复张和改善肺通气来改善氧合。