Lung Inhomogeneity in Patients with Acute Respiratory Distress Syndrome
Lung Inhomogeneity in Patients with Acute Respiratory Distress Syndrome
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DOI：
10.1164/rccm.201308-1567oc
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发表时间：
2014-01-15
影响因子：
24.7
通讯作者：
Gattinoni, Luciano
中科院分区：
文献类型：
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作者：
Cressoni, Massimo;Cadringher, Paolo;Gattinoni, Luciano
基本原理：在健康肺中诱导呼吸机诱导的肺损伤所需的压力和容量远远大于在患病肺中应用的压力和容量。一个可能的解释可能是存在的局部不均匀性作为压力倍增器（应力raisers）。目的：定量肺不均匀性在急性呼吸窘迫综合征（ARDS）患者。方法：回顾性定量分析148例ARDS患者和100例对照组的CT扫描图像。理想的均质肺在所有区域中具有相同的扩张;肺扩张通过CT扫描测量为气体/组织比，并且肺不均匀性测量为具有比其相邻肺区域更低的气体/组织比的肺区域。我们将肺不均匀性的程度定义为显示充气比大于对照组第95百分位数的肺的分数（1.61）.测量和主要结果：肺不均匀性的程度随着ARDS的严重程度而增加（14 +/- 5，18 +/- 8，23 +/- 10%的肺容积在轻度、中度和重度ARDS中; P< 0.001）并且与生理死腔相关（r（2）= 0.34; P< 0.0001）。从5 cm H2O气道压至45 cm H2O气道压，应用呼气末正压可将肺不均匀性程度从18 +/- 8降低至12 +/- 7%（P 0.0001）。肺不均匀性在非存活患者中比在存活患者中更大（20 +/- 9 vs. 17 +/- 7%的肺体积; P = 0.01），并且是唯一与死亡率独立相关的CT扫描变量，在后向logistic regression.Conclusions：肺不均匀性与总体疾病严重程度和死亡率相关。增加气道压力降低，但没有消除肺不均匀性的程度。
Rationale: Pressures and volumes needed to induce ventilator-induced lung injury in healthy lungs are far greater than those applied in diseased lungs. A possible explanation may be the presence of local inhomogeneities acting as pressure multipliers (stress raisers).Objectives: To quantify lung inhomogeneities in patients with acute respiratory distress syndrome (ARDS).Methods: Retrospective quantitative analysis of CT scan images of 148 patients with ARDS and 100 control subjects. An ideally homogeneous lung would have the same expansion in all regions; lung expansion was measured by CT scan as gas/tissue ratio and lung inhomogeneities were measured as lung regions with lower gas/tissue ratio than their neighboring lung regions. We defined as the extent of lung inhomogeneities the fraction of the lung showing an inflation ratio greater than 95th percentile of the control group (1.61).Measurements and Main Results: The extent of lung inhomogeneities increased with the severity of ARDS(14 +/- 5, 18 +/- 8, and 23 +/- 10% of lung volume in mild, moderate, and severe ARDS; P< 0.001) and correlated with the physiologic dead space (r(2) = 0.34; P< 0.0001). The application of positive end-expiratory pressure reduced the extent of lung inhomogeneities from 18 +/- 8 to 12 +/- 7% (P 0.0001) going from 5 to 45 cm H2O airway pressure. Lung inhomogeneities were greater in nonsurvivor patients than in survivor patients (20 +/- 9 vs. 17 +/- 7% of lung volume; P = 0.01) and were the only CT scan variable independently associated with mortality at backward logistic regression.Conclusions: Lung inhomogeneities are associated with overall disease severity and mortality. Increasing the airway pressures decreased but did not abolish the extent of lung inhomogeneities.