Cardiopulmonary & Critical Care Laboratory, Department of Surgery, SUNY Upstate Medical University, Syracuse, New York 13210, USA.
J Trauma Acute Care Surg. 2012 Aug;73(2):391-400. doi: 10.1097/TA.0b013e31825c7a82.
Established acute respiratory distress syndrome (ARDS) is often refractory to treatment. Clinical trials have demonstrated modest treatment effects, and mortality remains high. Ventilator strategies must be developed to prevent ARDS.
Early ventilatory intervention will block progression to ARDS if the ventilator mode (1) maintains alveolar stability and (2) reduces pulmonary edema formation.
Yorkshire pigs (38-45 kg) were anesthetized and subjected to a "two-hit" ischemia-reperfusion and peritoneal sepsis. After injury, animals were randomized into two groups: early preventative ventilation (airway pressure release ventilation [APRV]) versus nonpreventative ventilation (NPV) and followed for 48 hours. All animals received anesthesia, antibiotics, and fluid or vasopressor therapy as per the Surviving Sepsis Campaign. Titrated for optimal alveolar stability were the following ventilation parameters: (1) NPV group--tidal volume, 10 mL/kg + positive end-expiratory pressure - 5 cm/H2O volume-cycled mode; (2) APRV group--tidal volume, 10 to 15 mL/kg; high pressure, low pressure, time duration of inspiration (Thigh), and time duration of release phase (Tlow). Physiological data and plasma were collected throughout the 48-hour study period, followed by BAL and necropsy.
APRV prevented the development of ARDS (p < 0.001 vs. NPV) by PaO₂/FIO₂ ratio. Quantitative histological scoring showed that APRV prevented lung tissue injury (p < 0.001 vs. NPV). Bronchoalveolar lavage fluid showed that APRV lowered total protein and interleukin 6 while preserving surfactant proteins A and B (p < 0.05 vs. NPV). APRV significantly lowered lung water (p < 0.001 vs. NPV). Plasma interleukin 6 concentrations were similar between groups.
Early preventative mechanical ventilation with APRV blocked ARDS development, preserved surfactant proteins, and reduced pulmonary inflammation and edema despite systemic inflammation similar to NPV. These data suggest that early preventative ventilation strategies stabilizing alveoli and reducing pulmonary edema can attenuate ARDS after ischemia-reperfusion and sepsis.
已确立的急性呼吸窘迫综合征（ARDS）通常对治疗有抗性。临床试验表明治疗效果有限，死亡率仍然很高。必须制定呼吸机策略以预防 ARDS。
如果呼吸机模式（1）维持肺泡稳定性和（2）减少肺水肿形成，早期通气干预将阻止 ARDS 的进展。
对 38-45 公斤的约克夏猪进行麻醉，并进行“两次打击”缺血再灌注和腹腔脓毒症。受伤后，动物随机分为两组：早期预防性通气（气道压力释放通气[APRV]）与非预防性通气（NPV），并随访 48 小时。所有动物均根据拯救脓毒症运动接受麻醉、抗生素和液体或血管加压药治疗。优化肺泡稳定性的通气参数如下：（1）NPV 组-潮气量 10 mL/kg+呼气末正压-5 cmH2O 容积循环模式；（2）APRV 组-潮气量 10-15 mL/kg；高压、低压、吸气时间（Thigh）和释放相时间（Tlow）。在整个 48 小时的研究期间收集生理数据和血浆，然后进行 BAL 和尸检。
APRV 通过 PaO₂/FIO₂ 比预防 ARDS 的发展（p<0.001 比 NPV）。定量组织学评分显示 APRV 可预防肺组织损伤（p<0.001 比 NPV）。支气管肺泡灌洗液显示 APRV 降低了总蛋白和白细胞介素 6，同时保留了表面活性剂蛋白 A 和 B（p<0.05 比 NPV）。APRV 显著降低了肺水（p<0.001 比 NPV）。两组间血浆白细胞介素 6 浓度相似。
APRV 的早期预防性机械通气可预防 ARDS 的发展，保留表面活性剂蛋白，并减少炎症和水肿，尽管全身炎症与 NPV 相似。这些数据表明，稳定肺泡和减少肺水肿的早期预防性通气策略可减轻缺血再灌注和脓毒症后的 ARDS。
