Schaer H, Roth F
Anaesthesist. 1977 Oct;26(10):581-5.
Spontaneous respiration in the presence of upper airway obstruction causes considerable negative intra alveolar pressure which may lead to pulmonary oedema "ex vacuo". Four cases are presented of spontaneously breathing patients who sustained upper airway obstruction lastin from one to several hours, leading to manifest pulmonary oedema. The pathogenesis of pulmonary oedema ex vacuo is discussed on the basis of alteration of physiological parameters such as capillary, alveolar and pleural pressures, as well as the properties of lung liquid exchange. In contrast, pulmonary oedema occurring after re-expansion of a collapsed lung is reported in one patient. No negative intraalveolar pressure could be incriminated in this case since the patient was ventilated using intermittent positive pressure from the beginning of lung expansion. We tend to attribute the evolution of this second kind of pulmonary oedema to capillary damage, resulting from hypoperfusion of the atelectatic areas, altered alveolar surface lining layer, infection and other cases. The therapeutic measures used in pulmonary oedema "exvacuo" are briefly mentioned.
上气道梗阻时的自主呼吸会导致显著的肺泡内负压,这可能会引发“真空性”肺水肿。本文报告了4例自主呼吸患者,他们的上气道梗阻持续1至数小时,导致明显的肺水肿。基于毛细血管、肺泡和胸膜压力等生理参数的改变以及肺液体交换特性,对真空性肺水肿的发病机制进行了讨论。相比之下,本文还报告了1例肺萎陷复张后发生肺水肿的患者。由于该患者从肺扩张开始就使用间歇正压通气,因此在这种情况下不能归咎于肺泡内负压。我们倾向于将第二种肺水肿的发展归因于肺不张区域灌注不足、肺泡表面衬里层改变、感染等导致的毛细血管损伤。文中简要提及了用于“真空性”肺水肿的治疗措施。