Departments of Medicine, Anesthesia, and Respiratory Care, University of California, San Francisco, San Francisco, CA.
Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University, Nashville, TN.
Chest. 2016 Oct;150(4):927-933. doi: 10.1016/j.chest.2016.03.043. Epub 2016 Apr 8.
Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. Pulmonary edema fluid collected from most patients with NPPE has a low protein concentration, suggesting hydrostatic forces as the primary mechanism for the pathogenesis of NPPE. Supportive care should be directed at relieving the upper airway obstruction by endotracheal intubation or cricothyroidotomy, institution of lung-protective positive-pressure ventilation, and diuresis unless the patient is in shock. Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact. In this review, we discuss the clinical presentation, pathophysiology, and management of negative-pressure or postobstructive pulmonary edema.
负压性肺水肿(NPPE)或后阻塞性肺水肿是一种描述明确的急性呼吸衰竭的原因,发生在强烈吸气努力对抗阻塞性气道后,通常是由于上呼吸道感染、肿瘤或喉痉挛。NPPE 患者会产生非常负的气道压力,这会增加跨血管液体过滤,并引发间质和肺泡水肿。从大多数 NPPE 患者中收集的肺水肿液蛋白浓度较低,提示静水压是 NPPE 发病机制的主要机制。支持性护理应通过气管插管或环甲膜切开术来缓解上呼吸道阻塞,实施肺保护性正压通气和利尿,除非患者处于休克状态。肺水肿的消退通常很快,部分原因是肺泡液体清除机制完整。在这篇综述中,我们讨论了负压或后阻塞性肺水肿的临床表现、病理生理学和治疗。