Department of Anesthesiology, Osaka University Graduate School of Medicine and Pathology, Suita, Japan.
Crit Care Med. 2012 May;40(5):1578-85. doi: 10.1097/CCM.0b013e3182451c40.
We investigated whether potentially injurious transpulmonary pressure could be generated by strong spontaneous breathing and exacerbate lung injury even when plateau pressure is limited to <30 cm H2O.
Prospective, randomized, animal study.
University animal research laboratory.
Thirty-two New Zealand White rabbits.
Lavage-injured rabbits were randomly allocated to four groups to receive low or moderate tidal volume ventilation, each combined with weak or strong spontaneous breathing effort. Inspiratory pressure for low tidal volume ventilation was set at 10 cm H2O and tidal volume at 6 mL/kg. For moderate tidal volume ventilation, the values were 20 cm H2O and 7-9 mL/kg. The groups were: low tidal volume ventilation+spontaneous breathingweak, low tidal volume ventilation+spontaneous breathingstrong, moderate tidal volume ventilation+spontaneous breathingweak, and moderate tidal volume ventilation+spontaneous breathingstrong. Each group had the same settings for positive end-expiratory pressure of 8 cm H2O.
Respiratory variables were measured every 60 mins. Distribution of lung aeration and alveolar collapse were histologically evaluated. Low tidal volume ventilation+spontaneous breathingstrong showed the most favorable oxygenation and compliance of respiratory system, and the best lung aeration. By contrast, in moderate tidal volume ventilation+spontaneous breathingstrong, the greatest atelectasis with numerous neutrophils was observed. While we applied settings to maintain plateau pressure at <30 cm H2O in all groups, in moderate tidal volume ventilation+spontaneous breathingstrong, transpulmonary pressure rose >33 cm H2O. Both minute ventilation and respiratory rate were higher in the strong spontaneous breathing groups.
Even when plateau pressure is limited to <30 cm H2O, combined with increased respiratory rate and tidal volume, high transpulmonary pressure generated by strong spontaneous breathing effort can worsen lung injury. When spontaneous breathing is preserved during mechanical ventilation, transpulmonary pressure and tidal volume should be strictly controlled to prevent further lung injury.
研究在平台压限制在<30cmH2O 以下时，强烈自主呼吸是否会产生潜在的肺损伤压力，并加重肺损伤。
前瞻性、随机、动物研究。
大学动物研究实验室。
32 只新西兰白兔。
对肺损伤兔进行随机分组，分别接受低或中潮气量通气，同时结合弱或强自主呼吸努力。低潮气量通气的吸气压力设定为 10cmH2O，潮气量为 6mL/kg。中潮气量通气时，压力值为 20cmH2O，潮气量为 7-9mL/kg。分组为：低潮气量通气+弱自主呼吸、低潮气量通气+强自主呼吸、中潮气量通气+弱自主呼吸、中潮气量通气+强自主呼吸。每组的呼气末正压（positive end-expiratory pressure，PEEP）均为 8cmH2O。
每 60 分钟测量一次呼吸变量。通过组织学评估肺充气和肺泡萎陷的分布。低潮气量通气+强自主呼吸显示出最佳的氧合和呼吸系统顺应性，以及最佳的肺充气。相比之下，中潮气量通气+强自主呼吸时，观察到最大的肺泡萎陷和大量中性粒细胞浸润。虽然我们设置了所有组的平台压<30cmH2O，但在中潮气量通气+强自主呼吸组，跨肺压升高>33cmH2O。强自主呼吸组的分钟通气量和呼吸频率均较高。
即使平台压限制在<30cmH2O 以下，同时增加呼吸频率和潮气量，强自主呼吸产生的高跨肺压也会加重肺损伤。在机械通气时保留自主呼吸时，应严格控制跨肺压和潮气量，以防止进一步的肺损伤。
