Preemptive application of airway pressure release ventilation prevents development of acute respiratory distress syndrome in a rat traumatic hemorrhagic shock model.
Preemptive application of airway pressure release ventilation prevents development of acute respiratory distress syndrome in a rat traumatic hemorrhagic shock model.
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DOI：
10.1097/shk.0b013e31829efb06
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发表时间：
2013-09
期刊：
影响因子：
--
通讯作者：
Nieman GF
中科院分区：
文献类型：
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作者：
Roy SK;Emr B;Sadowitz B;Gatto LA;Ghosh A;Satalin JM;Snyder KP;Ge L;Wang G;Marx W;Dean D;Andrews P;Singh A;Scalea T;Habashi N;Nieman GF
背景：急性呼吸窘迫综合征(ARDS)一旦确诊，对治疗的抵抗力很强，死亡率也很高。我们假设，在创伤/失血性休克(T/HS)大鼠模型上先行应用气道压力释放通气机(APRV)可以预防ARDS。方法：麻醉后行血流动力学监测的大鼠，随机分为两组：(A)容量循环通气组(VC组，n=5，潮气量10mL/kg；呼气末正压0.5cmH2O)；(B)APRV组(n=4，P HIGH=15~20cmH2O；T HIGH=1.3~1.5 S，达到总循环时间的90%；TLOW=0.11~0.14 S，设为呼气峰值流量的75%；Plow=0cmH2O)。结果：压力释放通气组PaO2/FIO2(143.3±42.4 vs.APRV 426.8±2 6.9，P<；0.0 5)与肺泡灌洗组相比明显减轻。此外，APRV组大鼠肺泡灌洗液总蛋白显著减少，肺表面活性蛋白B浓度升高，上皮组织钙粘附素表达增加。活体显微镜显示，与VC组相比，APRV组显著改善了肺泡的通畅性和稳定性。结论：超前机械通气联合APRV可减轻T/HS相关的临床和组织学肺损伤。其预防损伤的机制与保持肺泡上皮细胞和内皮细胞的完整性有关。背景急性呼吸窘迫综合征(ARDS)是一个严重的临床问题，每年困扰着高达30%的严重创伤患者(1)；尽管数十年的治疗研究，这种疾病仍然具有令人不安的高死亡率(2)、护理费用(3)和对幸存者的严重后遗症(4)。创伤和出血导致大量全身性炎症，并伴随血管通透性增加，导致严重的肺损伤和肺水肿。失血性休克(HS)的复苏通常需要输血产品，而输血产品与全身炎症反应综合征、急性肺损伤(ALI)和ARDS(7)独立相关。因此，创伤后HS患者极易发生ALI和ARDS。
Background: Once established, the acute respiratory distress syndrome (ARDS) is highly resistant to treatment and retains a high mortality. We hypothesized that preemptive application of airway pressure release ventilation (APRV) in a rat model of trauma/hemorrhagic shock (T/HS) would prevent ARDS. Methods: Rats were anesthetized, instrumented for hemodynamic monitoring, subjected to T/HS, and randomized into two groups:(a) volume cycled ventilation (VC)(n= 5, tidal volume 10 mL/kg; positive end-expiratory pressure 0.5 cmH 2 O) or (b) APRV (n= 4, P high= 15–20 cmH 2 O; T high= 1.3–1.5 s to achieve 90% of the total cycle time; T low= 0.11–0.14 s, which was set to 75% of the peak expiratory flow rate; P low= 0 cmH 2 O). Study duration was 6 h. Results: Airway pressure release ventilation prevented lung injury as measured by PaO 2/FIO 2 (VC 143.3±42.4 vs. APRV 426.8±26.9, P< 0.05), which correlated with a significant decrease in histopathology as compared with the VC group. In addition, APRV resulted in a significant decrease in bronchoalveolar lavage fluid total protein, increased surfactant protein B concentration, and an increase in epithelial cadherin tissue expression. In vivo microscopy demonstrated that APRV significantly improved alveolar patency and stability as compared with the VC group. Conclusions: Our findings demonstrate that preemptive mechanical ventilation with APRV attenuates the clinical and histologic lung injury associated with T/HS. The mechanism of injury prevention is related to preservation of alveolar epithelial and endothelial integrity. These data support our hypothesis that preemptive APRV, applied using published guidelines, can prevent the development of ARDS.BACKGROUNDAcute respiratory distress syndrome (ARDS) is a grave clinical problem afflicting up to 30% of severely injured trauma patients annually (1); the disease retains disturbingly high mortality (2), costs of care (3), and severe sequelae for survivors (4) despite decades of therapeutic research (5). Trauma and hemorrhage result in massive systemic inflammation with attendant increases in vascular permeability leading to severe lung injury with pulmonary edema (6). Resuscitation for hemorrhagic shock (HS) often requires transfusion of blood products, which are independently associated with the systemic inflammatory response syndrome, acute lung injury (ALI) and ARDS (7). Thus, traumatically injured patients with HS are highly susceptible to development of ALI and ARDS.