原发性(高通透性)肺水肿

K. Brigham
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引用次数: 3

摘要

虽然当肺微循环滤过压力增加和肺损伤时,会发生水肿,即肺中过量液体的积聚,但两种形式的水肿在病理上是不同的。前两篇文章为研究这些差异提供了基础。高通透性肺水肿的诊断是通过临床推断得出的。如果胸片上肺水肿明显,肺动脉楔压正常或低,则推断水肿一定是肺交换血管通透性增加的结果。通常需要诊断成人呼吸窘迫综合征(ARDS)的附加标准包括严重低氧血症和肺顺应性降低。从符合这些标准的患者收集的其他数据支持血管通透性增加的推断:水肿液中的蛋白质浓度高;血管内蛋白与水肿液的平衡是迅速的。正常情况下,肺通过增加肺淋巴流量(排出多余的过滤液)和降低间质肿瘤压力(抵消血管静水压力增加的影响)来防止积液。当肺微血管通透性增加时,这些保护机制受损。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Primary (High Permeability) Pulmonary Edema
Although edema, that is, accumulation of excess fluid in the lungs, occurs when filtration pressures are increased in the lung microcirculation and in response to lung injury, pathogenetically the two forms of edema are different. The previous two articles provide the basis for examining the differences. The diagnosis of high permeability pulmonary edema is made clinically by inference. If pulmonary edema is evident on chest radiograph and pulmonary arterial wedge pressure is normal or low, it is inferred that the edema must be a result of increased permeability of exchange vessels in the lung. Additional criteria usually required for diagnosis of the adult respiratory distress syndrome (ARDS) include severe hypoxemia and decreased lung compliance. Other data collected from patients who meet these criteria support the inference of increased vascular permeability: protein concentrations in edema fluid are high; equilibration of intravascular proteins with edema fluid is rapid. Normally, the lungs are protected against accumulation of fluid by increasing lung lymph flow (draining away excess filtered fluid) and decreasing interstitial oncotic pressure (counteracting the effects of increased vascular hydrostatic pressure). When permeability of lung microvessels is increased, these protective mechanisms are compromised.
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