Bacić A, Gluncić I, Drnasin-Buklijas J
Medicinskog fakulteta u Zagrebu.
Lijec Vjesn. 1992 Sep-Dec;114(9-12):249-51.
The development of pulmonary edema after the relief of upper airway obstruction in two patients is described. Pulmonary edema in those patients was the result of increased negative intrapleural and intra-alveolar pressure during forceful inspiration and in the course of upper airway obstruction. An increase in the venous return occurs and the established transpulmonary pressure gradient promotes transudation into the interstitium and alveoli. Consequent alveolar hyperventilation results in hypoxia and acidosis. All patients developing pulmonary edema should be treated with positive pressure ventilation within 24-36 hours. The aim of this study was to alert physicians that besides know factors for the development of cardiogenic and noncardiogenic pulmonary edema there are also other significant mechanisms that cause the accumulation of fluid in pulmonary tissue.
本文描述了两名患者在上气道梗阻解除后发生肺水肿的情况。这些患者的肺水肿是由于用力吸气时以及在上气道梗阻过程中胸膜腔内和肺泡内负压增加所致。静脉回流量增加,既定的跨肺压力梯度促使液体渗入间质和肺泡。随之而来的肺泡过度通气导致缺氧和酸中毒。所有发生肺水肿的患者均应在24至36小时内接受正压通气治疗。本研究的目的是提醒医生,除了已知的心源性和非心源性肺水肿的发病因素外,还有其他重要机制可导致肺组织内液体蓄积。