Fremont Richard D, Kallet Richard H, Matthay Michael A, Ware Lorraine B
Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University, T1218 MCN, 1161 Twenty-First Ave S, Nashville, TN 37232-2650, USA.
Chest. 2007 Jun;131(6):1742-6. doi: 10.1378/chest.06-2934. Epub 2007 Apr 5.
Postobstructive pulmonary edema is a well-recognized complication of upper airway obstruction. The mechanisms of edema formation are unclear and may be due to increased hydrostatic forces generated by high negative inspiratory pressure or by increased permeability of the alveolar capillary membrane. Measurement of the edema fluid/plasma protein ratio and the rate of net alveolar fluid clearance are two well-validated methods for classifying the underlying mechanism of edema formation. The goal of the current study was to investigate the mechanisms of pulmonary edema formation in patients with postobstructive pulmonary edema by serial sampling of undiluted pulmonary edema fluid.
A retrospective review of 341 patients who had pulmonary edema fluid collected prospectively after the acute onset of pulmonary edema. All patients had serial samples of edema fluid and plasma collected over the first 8 h after intubation.
Ten of the 341 patients with acute pulmonary edema were identified as having postobstructive pulmonary edema. The mean (+/- SD) edema fluid/plasma protein ratio in these patients was 0.54 +/- 0.15. The mean rate of alveolar fluid clearance over 8 h was 14.0 +/- 17.4% per hour. Nine of the 10 patients survived the hospitalization.
Measurement of the edema fluid/plasma protein ratio and the presence of net alveolar fluid clearance in 10 patients with postobstructive pulmonary edema supports a hydrostatic mechanism for edema fluid formation. The predominantly fast rates of alveolar fluid clearance may explain the rapid resolution of clinical postobstructive pulmonary edema that is typically described.
梗阻后肺水肿是上气道梗阻一种公认的并发症。水肿形成机制尚不清楚,可能是由于高负压吸气压力产生的静水压增加,或肺泡毛细血管膜通透性增加所致。测量水肿液/血浆蛋白比值和肺泡净液体清除率是两种用于明确水肿形成潜在机制的有效方法。本研究的目的是通过对未稀释的肺水肿液进行系列采样,探讨梗阻后肺水肿患者肺水肿形成的机制。
回顾性分析341例肺水肿急性发作后前瞻性收集肺水肿液的患者。所有患者在插管后的最初8小时内均采集了水肿液和血浆的系列样本。
341例急性肺水肿患者中有10例被确定为梗阻后肺水肿。这些患者的平均(±标准差)水肿液/血浆蛋白比值为0.54±0.15。8小时内肺泡液体清除的平均速率为每小时14.0±17.4%。10例患者中有9例住院期间存活。
对10例梗阻后肺水肿患者的水肿液/血浆蛋白比值及肺泡净液体清除情况的测量,支持了水肿液形成的静水压机制。肺泡液体清除率大多较快,这可能解释了通常所描述的梗阻后肺水肿临床症状的快速缓解。