Sorbonne Université, UPMC Univ Paris 06, INSERM UMRS_1166-iCAN, Institute of Cardiometabolism and Nutrition, 75651 Paris Cedex 13, France.
Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Medical Intensive Care Unit, 75651 Paris Cedex 13, France.
Crit Care Med. 2019 Nov;47(11):1505-1512. doi: 10.1097/CCM.0000000000003894.
Ventilator settings for patients with severe acute respiratory distress syndrome supported by venovenous extracorporeal membrane oxygenation are currently set arbitrarily. The impact on serum and pulmonary biotrauma markers of the transition to ultra-protective ventilation settings following extracorporeal membrane oxygenation implantation, and different mechanical ventilation strategies while on extracorporeal membrane oxygenation were investigated.
Randomized clinical trial.
Nine-month monocentric study.
Severe acute respiratory distress syndrome patients on venovenous extracorporeal membrane oxygenation.
After starting extracorporeal membrane oxygenation, patients were switched to the bi-level positive airway pressure mode with 1 second of 24 cm H2O high pressure and 2 seconds of 12 cm H2O low pressure for 24 hours. A computer-generated allocation sequence randomized patients to receive each of the following three experimental steps: 1) high pressure 24 cm H2O and low pressure 20 cm H2O (very high positive end-expiratory pressure-very low driving pressure); 2) high pressure 24 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure-high driving pressure); and 3) high pressure 17 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure-low driving pressure). Plasma and bronchoalveolar lavage soluble receptor for advanced glycation end-products, plasma interleukin-6, and monocyte chemotactic protein-1 were sampled preextracorporeal membrane oxygenation and after 12 hours at each step.
Sixteen patients on ECMO after 7 days (1-11 d) of mechanical ventilation were included. "Ultra-protective" mechanical ventilation settings following ECMO initiation were associated with significantly lower plasma sRAGE, interleukin-6, and monocyte chemotactic protein-1 concentrations. Plasma sRAGE and cytokines were comparable within each on-ECMO experimental step, but the lowest bronchoalveolar lavage sRAGE levels were obtained at minimal driving pressure.
ECMO allows ultra- protective ventilation, which combines significantly lower plateau pressure, tidalvolume, and driving pressure. This ventilation strategy significantly limited pulmonary biotrauma, which couldtherefore decrease ventilator-induced lung injury. However, the optimal ultra-protective ventilation strategy once ECMO is initiated remains undetermined and warrants further investigations. (Crit Care Med 2019; 47:1505-1512).
目前，接受静脉-静脉体外膜肺氧合（ECMO）支持的严重急性呼吸窘迫综合征患者的呼吸机设置是任意设定的。本研究旨在探讨 ECMO 植入后向超保护性通气设置过渡以及在 ECMO 期间使用不同机械通气策略对血清和肺生物创伤标志物的影响。
随机临床试验。
为期 9 个月的单中心研究。
接受静脉-静脉 ECMO 的严重急性呼吸窘迫综合征患者。
在开始 ECMO 后，患者切换到双水平正压通气模式，高压为 24cmH2O（持续 1 秒），低压为 12cmH2O（持续 2 秒），持续 24 小时。计算机生成的分配序列将患者随机分配至以下三个实验步骤中的每一步：1）高压 24cmH2O 和低压 20cmH2O（超高呼气末正压-超低驱动压力）；2）高压 24cmH2O 和低压 5cmH2O（低呼气末正压-高驱动压力）；3）高压 17cmH2O 和低压 5cmH2O（低呼气末正压-低驱动压力）。在 ECMO 前和每个步骤 12 小时后采集血浆和支气管肺泡灌洗可溶性晚期糖基化终产物受体（sRAGE）、血浆白细胞介素-6（IL-6）和单核细胞趋化蛋白-1（MCP-1）。
纳入了 7 天（1-11 天）机械通气后接受 ECMO 的 16 名患者。与 ECMO 启动后的“超保护性”机械通气设置相比，血浆 sRAGE、IL-6 和 MCP-1 浓度明显更低。在每个 ECMO 实验步骤中，血浆 sRAGE 和细胞因子均无差异，但最低的支气管肺泡灌洗 sRAGE 水平是在最小驱动压力下获得的。
ECMO 允许采用超低保护性通气，其平台压、潮气量和驱动压显著降低。这种通气策略显著限制了肺生物创伤，因此可以降低呼吸机引起的肺损伤。然而，一旦启动 ECMO，最佳的超保护性通气策略仍未确定，需要进一步研究。（危重病医学 2019；47:1505-1512）。
