Jose Dianti MD , Idunn S. Morris MD , Thiago G. Bassi MD, PhD , Eddy Fan MD, PhD , Arthur S. Slutsky MD , Laurent J. Brochard MD , Niall D. Ferguson MD , Ewan C. Goligher MD, PhD
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Associations were evaluated using linear mixed-effects regression models including prespecified terms for potential interactions.</p></div><div><h3>Results</h3><p>The study included 223 individual measurements of P<sub>0.1</sub> and 235 individual measurements of |ΔPes| and ΔP<sub>L,dyn</sub> from 30 patients. Propofol-attenuated P<sub>0.1</sub> (–0.4 cm H<sub>2</sub>O; 95% CI, –0.3 to –0.1 cm H<sub>2</sub>O per 10-μm/kg/min increase), |ΔPes| (–2.5 cm H<sub>2</sub>O; 95% CI, –3.4 to –1.7 cm H<sub>2</sub>O per 10-μm/kg/min increase), and ΔP<sub>L,dyn</sub> (–1.6 cm H<sub>2</sub>O; 95% CI, –2.3 to –0.8 cm H<sub>2</sub>O per 10-μm/kg/min increase). The effect of inspiratory pressure on |ΔPes| varied depending on propofol dose: with higher propofol dose, inspiratory pressure resulted in higher ΔP<sub>L,dyn</sub>. 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引用次数: 0
摘要
研究问题吸气和呼气末正压(PEEP)、镇静和静脉体外膜肺氧合(VV-ECMO)对触发呼吸机的急性低氧血症呼吸衰竭(AHRF)患者的呼吸驱动力、用力和肺舒张压有哪些单独影响和相互作用?研究设计和方法在这项对 AHRF 肺和膈肌保护试验的二次探索性分析中,对吸气压力、镇静剂、PEEP 和 VV-ECMO 进行了滴定,同时记录了呼吸驱动力(前 100 毫秒的气道压力 [P0.1])、用力(食管压力摆动 [|ΔPes|])和肺舒张压(动态跨肺驱动压力 [ΔPL,dyn])。采用线性混合效应回归模型对相关性进行了评估,该模型包括针对潜在交互作用的预设项。丙泊酚可降低 P0.1(-0.4 cm H2O;95% CI,每增加 10-μm/kg/min 降低-0.3 至-0.1 cm H2O)、|ΔPes|(-2.5 cm H2O;95% CI,每增加 10-μm/kg/min 降低-3.4 至-1.7 cm H2O)和 ΔPL,dyn(-1.6 cm H2O;95% CI,每增加 10-μm/kg/min 降低-2.3 至-0.8 cm H2O)。吸气压力对|ΔPes|的影响因丙泊酚剂量而异:丙泊酚剂量越高,吸气压力导致的ΔPL,dyn越高。与未接受 VV-ECMO 的患者(n = 14)相比,接受 VV-ECMO 的患者(n = 16)的|ΔPes|(-10 cm H2O; 95% CI, -17.5 to -2.5 cm H2O)明显降低,并且需要更少的镇静剂来降低|ΔPes|。接受 VV-ECMO 的患者需要较少的镇静剂来控制呼吸强度。
Sedation-Ventilation Interaction in Acute Hypoxemic Respiratory Failure
Background
Ventilation and sedation are used for the management of acute hypoxemic respiratory failure (AHRF), but their optimal combination to minimize the risks of ventilation is not well understood.
Research Question
What are the individual effects and interactions of inspiratory and positive end-expiratory pressure (PEEP), sedation, and venovenous extracorporeal membrane oxygenation (VV-ECMO) on respiratory drive, effort, and lung-distending pressure in patients with AHRF triggering the ventilator?
Study Design and Methods
In this secondary exploratory analysis of a trial of lung and diaphragm protection in AHRF, inspiratory pressure, sedation, PEEP, and VV-ECMO were titrated while respiratory drive (airway pressure in the first 100 ms [P0.1]), effort (esophageal pressure swing [|ΔPes|]), and lung-distending pressure (dynamic transpulmonary driving pressure [ΔPL,dyn]) were recorded. Associations were evaluated using linear mixed-effects regression models including prespecified terms for potential interactions.
Results
The study included 223 individual measurements of P0.1 and 235 individual measurements of |ΔPes| and ΔPL,dyn from 30 patients. Propofol-attenuated P0.1 (–0.4 cm H2O; 95% CI, –0.3 to –0.1 cm H2O per 10-μm/kg/min increase), |ΔPes| (–2.5 cm H2O; 95% CI, –3.4 to –1.7 cm H2O per 10-μm/kg/min increase), and ΔPL,dyn (–1.6 cm H2O; 95% CI, –2.3 to –0.8 cm H2O per 10-μm/kg/min increase). The effect of inspiratory pressure on |ΔPes| varied depending on propofol dose: with higher propofol dose, inspiratory pressure resulted in higher ΔPL,dyn. With VV-ECMO, patients (n = 16) showed significantly lower |ΔPes| (–10 cm H2O; 95% CI, –17.5 to –2.5 cm H2O) and required less sedation to reduce |ΔPes| than without VV-ECMO (n = 14).
Interpretation
Mechanical ventilation, sedation, and VV-ECMO exert interdependent effects on respiratory drive, effort, and lung-distending pressure in AHRF. Patients receiving VV-ECMO require less sedation to control respiratory effort.