Volume Delivered During Recruitment Maneuver Predicts Lung Stress in Acute Respiratory Distress Syndrome.
Volume Delivered During Recruitment Maneuver Predicts Lung Stress in Acute Respiratory Distress Syndrome.
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DOI：
10.1097/ccm.0000000000001355
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发表时间：
2016-01
影响因子：
8.8
通讯作者：
Talmor D
中科院分区：
文献类型：
--
作者：
Beitler JR;Majumdar R;Hubmayr RD;Malhotra A;Thompson BT;Owens RL;Loring SH;Talmor D
低潮气量通气治疗急性呼吸窘迫综合征（ARDS）时，整体肺应力变化很大。尽管潮气量低，但高压力可能会加重肺损伤并增加死亡风险。目前还没有广泛可用的参数来评估整体肺应力。我们的目的是确定在肺复张操作（VRM）期间输送的容量是否与ARDS的肺压力和死亡率呈负相关。食管压力引导PEEP滴定的ARDS临床试验的子研究。美国学术医疗中心。42例ARDS患者，在复张操作（RM）期间记录气流、气道压力和食管压力。在开始方案指导的呼吸机管理之前进行单次RM。RM包括在重度镇静或麻痹状态下，在40 cmH 2 O气道压力下屏气30秒。通过对机动过程中的流量-时间波形进行积分来计算VRM。吸气末压力定义为潮气呼吸吸气末暂停期间的跨肺（气道减去食管）压力，潮气压力定义为吸气末和呼气末暂停之间的跨肺压差。VRM范围为7.4 - 34.7 mL/kg预测体重（PBW）。较低的VRM预示着较高的吸气末和潮气肺应力（吸气末：P =-0.449，95%CI-0.664 to-0.234; p <0.001;潮气：P =-0.267，95%CI-0.423 to-0.111; p = 0.001）。在调整PaO 2/FIO 2和驱动压、潮气量或平台压和PEEP后，VRM仍然与吸气末和潮气应力独立相关。在未校正的分析中，低VRM预测死亡风险增加（OR 0.85，95% CI 0.72-1.00; p = 0.026）。调整研究组后，VRM仍与死亡率显著相关（OR 0.84，95% CI 0.71-1.00; p = 0.022）。低VRM独立预测高肺应力，并可能预测ARDS患者的死亡风险。
Global lung stress varies considerably with low tidal volume ventilation for acute respiratory distress syndrome (ARDS). High stress despite low tidal volumes may worsen lung injury and increase risk of death. No widely available parameter exists to assess global lung stress. We aimed to determine whether the volume delivered during a recruitment maneuver (VRM) is inversely associated with lung stress and mortality in ARDS. Substudy of an ARDS clinical trial on esophageal pressure-guided PEEP titration. U.S. academic medical center. 42 patients with ARDS in whom airflow, airway pressure, and esophageal pressure were recorded during the recruitment maneuver (RM). A single RM was performed before initiating protocol-directed ventilator management. RMs consisted of a 30-second breath hold at 40 cmH2O airway pressure under heavy sedation or paralysis. VRM was calculated by integrating the flow-time waveform during the maneuver. End-inspiratory stress was defined as the transpulmonary (airway minus esophageal) pressure during end-inspiratory pause of a tidal breath, and tidal stress as the transpulmonary pressure difference between end-inspiratory and end-expiratory pauses. VRM ranged between 7.4 and 34.7 mL/kg predicted body weight (PBW). Lower VRM predicted high end-inspiratory and tidal lung stress (end-inspiratory: ß = −0.449, 95% CI −0.664 to −0.234; p < .001; tidal: ß = −0.267, 95% CI −0.423 to −0.111; p = .001). After adjusting for PaO2/FIO2 and either driving pressure, tidal volume, or plateau pressure and PEEP, VRM remained independently associated with both end-inspiratory and tidal stress. In unadjusted analysis, low VRM predicted increased risk of death (OR 0.85, 95% CI 0.72–1.00; p = .026). VRM remained significantly associated with mortality after adjusting for study arm (OR 0.84, 95% CI 0.71–1.00; p = .022). Low VRM independently predicts high lung stress and may predict risk of death in patients with ARDS.