In acute respiratory distress syndrome (ARDS), respiratory drive often differs among patients with similar clinical characteristics. Readily observable factors like acid–base state, oxygenation, mechanics, and sedation depth do not fully explain drive heterogeneity. This study evaluated the relationship of systemic inflammation and vascular permeability markers with respiratory drive and clinical outcomes in ARDS. ARDS patients enrolled in the multicenter EPVent-2 trial with requisite data and plasma biomarkers were included. Neuromuscular blockade recipients were excluded. Respiratory drive was measured as PES0.1, the change in esophageal pressure during the first 0.1 s of inspiratory effort. Plasma angiopoietin-2, interleukin-6, and interleukin-8 were measured concomitantly, and 60-day clinical outcomes evaluated. 54.8% of 124 included patients had detectable respiratory drive (PES0.1 range of 0–5.1 cm H2O). Angiopoietin-2 and interleukin-8, but not interleukin-6, were associated with respiratory drive independently of acid–base, oxygenation, respiratory mechanics, and sedation depth. Sedation depth was not significantly associated with PES0.1 in an unadjusted model, or after adjusting for mechanics and chemoreceptor input. However, upon adding angiopoietin-2, interleukin-6, or interleukin-8 to models, lighter sedation was significantly associated with higher PES0.1. Risk of death was less with moderate drive (PES0.1 of 0.5–2.9 cm H2O) compared to either lower drive (hazard ratio 1.58, 95% CI 0.82–3.05) or higher drive (2.63, 95% CI 1.21–5.70) (p = 0.049). Among patients with ARDS, systemic inflammatory and vascular permeability markers were independently associated with higher respiratory drive. The heterogeneous response of respiratory drive to varying sedation depth may be explained in part by differences in inflammation and vascular permeability.

中文翻译：

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急性呼吸窘迫综合征中与全身炎症和血管通透性相关的呼吸驱动异质性

在急性呼吸窘迫综合征（ARDS）中，具有相似临床特征的患者的呼吸动力通常有所不同。酸碱状态、氧合作用、力学和镇静深度等容易观察到的因素并不能完全解释驱动力的异质性。本研究评估了 ARDS 中全身炎症和血管通透性标志物与呼吸动力和临床结果的关系。参加多中心 EPVent-2 试验的 ARDS 患者具有必要的数据和血浆生物标志物。神经肌肉阻滞接受者被排除在外。呼吸动力的测量值为 PES0.1，即吸气努力的前 0.1 秒内食道压力的变化。同时测量血浆血管生成素 2、白细胞介素 6 和白细胞介素 8，并评估 60 天的临床结果。 124 名患者中的 54.8% 有可检测到的呼吸动力（PES0.1 范围为 0–5.1 cm H2O）。血管生成素 2 和白细胞介素 8（而非白细胞介素 6）与呼吸驱动相关，与酸碱、氧合、呼吸力学和镇静深度无关。在未调整的模型中或调整力学和化学感受器输入后，镇静深度与 PES0.1 没有显着相关性。然而，在模型中添加血管生成素 2、白细胞介素 6 或白细胞介素 8 后，较轻的镇静与较高的 PES0.1 显着相关。与较低驱动力（风险比 1.58，95% CI 0.82–3.05）或较高驱动力（2.63，95% CI 1.21–5.70）相比，中等驱动力（PES0.1 为 0.5–2.9 cm H2O）的死亡风险较低（ p = 0.049）。在 ARDS 患者中，全身炎症和血管通透性标志物与较高的​​呼吸动力独立相关。呼吸驱动对不同镇静深度的异质反应可以部分地用炎症和血管通透性的差异来解释。