Dembinski Rolf, Hochhausen Nadine, Terbeck Sandra, Uhlig Stefan, Dassow Constanze, Schneider Monika, Schachtrupp Akexander, Henzler Dietrich, Rossaint Rolf, Kuhlen Ralf
Department of Surgical Intensive Care Medicine, and Institute of Pharmacology and Toxicology, University Aachen, Aachen, Germany.
Crit Care Med. 2007 Oct;35(10):2359-66. doi: 10.1097/01.ccm.0000281857.87354.a5.
To test the hypothesis that ventilation with 3 mL/kg tidal volume combined with extracorporeal CO2 removal by arteriovenous interventional lung assist reduces ventilator-associated organ injury in experimental acute lung injury when compared with ventilation with 6 mL/kg tidal volume without interventional lung assist.
Prospective, randomized, controlled trial.
A university research laboratory.
A total of 14 pigs weighing 46 +/- 4 kg (mean +/- sd).
Acute lung injury was induced by repeated lung lavages until Pao2 was <100 mm Hg, with Fio2 of 1.0 and positive end-expiratory pressure of 5 cm H2O, for 1 hr without additional lavages. Animals were randomized to an interventional group with a tidal volume of 3 mL/kg with interventional lung assist (n = 7) or to a control group with a tidal volume of 6 mL/kg without interventional lung assist (n = 7) for 24 hrs. Organ function in vivo was determined by laboratory analyses, including calculations of pulmonary ventilation/perfusion distribution. Histologic assessment of organ injury was performed post mortem after 24 hrs.
In both groups, gas exchange improved in the course of the study (p < .05). However, in contrast to control animals, animals with lower tidal volumes and interventional lung assist had severe ventilation/perfusion mismatch, as indicated by increased perfusion to lung areas with a low ventilation/perfusion ratio (p < .05). Other variables of organ function in vivo and results of histologic examination post mortem did not reveal any statistical difference between groups.
Combined ventilation with lower tidal volumes and extracorporeal CO2 removal as compared with traditional low tidal volumes without extracorporeal CO2 removal is not associated with differences in organ injury. Obviously, ventilation with tidal volumes of <6 mL/kg may cause pulmonary de-recruitment when positive end-expiratory pressure is not adequately increased.
验证以下假设:与采用6 mL/kg潮气量且无介入肺辅助的通气相比,采用3 mL/kg潮气量联合动静脉介入肺辅助进行体外二氧化碳清除,可减少实验性急性肺损伤中呼吸机相关性器官损伤。
前瞻性、随机、对照试验。
大学研究实验室。
共14头体重46±4 kg(均值±标准差)的猪。
通过反复肺灌洗诱导急性肺损伤,直至动脉血氧分压<100 mmHg,吸入氧浓度为1.0,呼气末正压为5 cmH₂O,持续1小时且不再进行额外灌洗。将动物随机分为干预组(潮气量为3 mL/kg,采用介入肺辅助,n = 7)或对照组(潮气量为6 mL/kg,无介入肺辅助,n = 7),持续24小时。通过实验室分析,包括计算肺通气/灌注分布,来测定体内器官功能。24小时后进行尸检,对器官损伤进行组织学评估。
在两组中,气体交换在研究过程中均有所改善(p < 0.05)。然而,与对照动物相比,潮气量较低且采用介入肺辅助的动物存在严重的通气/灌注不匹配,表现为通气/灌注比低的肺区域灌注增加(p < 0.05)。体内器官功能的其他变量以及尸检组织学检查结果在两组之间未显示出任何统计学差异。
与传统的低潮气量且无体外二氧化碳清除相比,低潮气量联合体外二氧化碳清除通气与器官损伤差异无关。显然,当呼气末正压未充分增加时,潮气量<6 mL/kg的通气可能会导致肺复张不全。