Choi Goda, Wolthuis Esther K, Bresser Paul, Levi Marcel, van der Poll Tom, Dzoljic Misa, Vroom Margreeth B, Schultz Marcus J
Dept. of Intensive Care Medicine, Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Anesthesiology. 2006 Oct;105(4):689-95. doi: 10.1097/00000542-200610000-00013.
Alveolar fibrin deposition is a hallmark of acute lung injury, resulting from activation of coagulation and inhibition of fibrinolysis. Previous studies have shown that mechanical ventilation with high tidal volumes may aggravate lung injury in patients with sepsis and acute lung injury. The authors sought to determine the effects of mechanical ventilation on the alveolar hemostatic balance in patients without preexistent lung injury.
Patients scheduled for an elective surgical procedure (lasting > or = 5 h) were randomly assigned to mechanical ventilation with either higher tidal volumes of 12 ml/kg ideal body weight and no positive end-expiratory pressure (PEEP) or lower tidal volumes of 6 ml/kg and 10 cm H2O PEEP. After induction of anesthesia and 5 h later bronchoalveolar lavage fluid and blood samples were obtained, and markers of coagulation and fibrinolysis were measured.
In contrast to mechanical ventilation with lower tidal volumes and PEEP (n = 21), the use of higher tidal volumes without PEEP (n = 19) caused activation of bronchoalveolar coagulation, as reflected by a marked increase in thrombin-antithrombin complexes, soluble tissue factor, and factor VIIa after 5 h of mechanical ventilation. Mechanical ventilation with higher tidal volumes without PEEP caused an increase in soluble thrombomodulin in lavage fluids and lower levels of bronchoalveolar activated protein C in comparison with lower tidal volumes and PEEP. Bronchoalveolar fibrinolytic activity did not change by either ventilation strategy.
Mechanical ventilation with higher tidal volumes and no PEEP promotes procoagulant changes, which are largely prevented by the use of lower tidal volumes and PEEP.
肺泡纤维蛋白沉积是急性肺损伤的一个标志,由凝血激活和纤维蛋白溶解抑制引起。先前的研究表明,高潮气量机械通气可能会加重脓毒症和急性肺损伤患者的肺损伤。作者试图确定机械通气对无既往肺损伤患者肺泡止血平衡的影响。
计划进行择期外科手术(持续时间≥5小时)的患者被随机分配接受机械通气,一组采用12ml/kg理想体重的较高潮气量且无呼气末正压(PEEP),另一组采用6ml/kg的较低潮气量和10cmH₂O的PEEP。麻醉诱导后5小时,获取支气管肺泡灌洗液和血样,并测量凝血和纤维蛋白溶解标志物。
与采用较低潮气量和PEEP的机械通气(n = 21)相比,采用较高潮气量且无PEEP的机械通气(n = 19)导致支气管肺泡凝血激活,机械通气5小时后凝血酶 - 抗凝血酶复合物、可溶性组织因子和因子VIIa显著增加即反映了这一点。与较低潮气量和PEEP相比,采用较高潮气量且无PEEP的机械通气导致灌洗液中可溶性血栓调节蛋白增加,支气管肺泡活化蛋白C水平降低。两种通气策略均未改变支气管肺泡纤维蛋白溶解活性。
采用较高潮气量且无PEEP的机械通气促进促凝变化,而采用较低潮气量和PEEP在很大程度上可预防这些变化。