Algren J T, Price R D, Buchino J J, Stremel R W
Department of Anesthesiology, Baylor College of Medicine, Houston, Texas 77030.
Pediatr Emerg Care. 1993 Dec;9(6):332-7. doi: 10.1097/00006565-199312000-00002.
In order to evaluate the effect of acute upper airway obstruction upon pulmonary edema (PE) formation, we studied seven dogs that were subjected to inspiratory obstruction for three hours. Hypoxia was avoided by the administration of supplemental oxygen during the study period. Six dogs developed pulmonary vascular congestion, and four developed histologic findings of PE. Inspiratory intrapleural pressure decreased to -28 +/- 4 mmHg in dogs that developed PE and to -23 +/- 2 mmHg in dogs that did not. Transmural pulmonary artery pressure and pulmonary artery wedge pressure did not increase significantly. Central venous pressure during inspiration (CVPi) increased in all dogs, and CVP at end expiration (CVPe) was significantly higher in dogs with PE. Dogs that developed PE experienced a decrease in cardiac output and an increase in systemic vascular resistance. Furthermore, alveolar ventilation declined in dogs with PE, ultimately resulting in ventilatory failure. Pulmonary edema formation was not preceded by an increase in pulmonary vascular pressures but was associated with higher CVP, pulmonary vascular congestion, and hypercarbia.
为了评估急性上气道阻塞对肺水肿（PE）形成的影响，我们对7只狗进行了3小时的吸气性阻塞研究。在研究期间通过补充氧气避免了缺氧。6只狗出现了肺血管充血，4只出现了肺水肿的组织学表现。发生肺水肿的狗吸气时胸腔内压降至-28±4 mmHg，未发生肺水肿的狗降至-23±2 mmHg。跨壁肺动脉压和肺动脉楔压没有显著升高。所有狗吸气时中心静脉压（CVPi）均升高，发生肺水肿的狗呼气末中心静脉压（CVPe）显著更高。发生肺水肿的狗心输出量减少，全身血管阻力增加。此外，发生肺水肿的狗肺泡通气量下降，最终导致呼吸衰竭。肺水肿的形成并非先有肺血管压力升高，而是与较高的中心静脉压、肺血管充血和高碳酸血症有关。
