De Pasquale Carmine G, Arnolda Leonard F, Doyle Ian R, Grant Robyn L, Aylward Phillip E, Bersten Andrew D
Cardiac Services, Flinders Medical Centre, Adelaide, South Australia, Australia.
Crit Care Med. 2003 Apr;31(4):1060-7. doi: 10.1097/01.CCM.0000059649.31659.22.
To determine whether acute cardiogenic pulmonary edema is associated with damage to the alveolocapillary barrier, as evidenced by increased leakage of surfactant specific proteins into the circulation, to document the duration of alveolocapillary barrier damage in this setting, and to explore the role of pulmonary parenchymal inflammation by determining if circulating tumor necrosis factor-alpha is increased after acute cardiogenic pulmonary edema.
Prospective, observational study.
Critical care, cardiac intensive care, and cardiology wards of a tertiary-care university teaching hospital.
A total of 28 patients presenting with acute cardiogenic pulmonary edema and 13 age-matched normal volunteers.
Circulating surfactant protein-A and -B and tumor necrosis factor-alpha were measured on days 0 (presentation), 1, 3, 7, and 14. Clinical markers of pulmonary edema were documented at the same times.
Surfactant protein-A and -B were elevated on day 0 compared with controls (367 +/- 17 ng/mL vs. 303 +/- 17 and 3821 +/- 266 ng/mL vs. 2747 +/- 157 [mean +/- sem], p <.05), and although clinical, hemodynamic and radiographic variables improved rapidly (p <.001), surfactant protein-A and -B rose further until day 3 (437 +/- 22, p <.001, 4642 +/- 353, p <.01). Tumor necrosis factor-alpha was elevated at presentation (p <.05), doubled by day 1 (6.98 +/- 1.36 pg/mL, p <.05), remained elevated on day 3 (5.72 +/- 0.96 pg/mL, p <.05), and peak levels were related to chest radiograph extravascular lung water score (r(p) = 0.64, p =.003).
Although the initial increase in plasma surfactant protein-A and -B may represent hydrostatic stress failure of the alveolocapillary barrier, the prolonged elevation, when hemodynamic abnormalities have resolved, and the delayed elevation of tumor necrosis factor-alpha are consistent with pulmonary parenchymal inflammation, which may further damage the alveolocapillary barrier. This prolonged physiologic defect at the alveolocapillary barrier after acute cardiogenic pulmonary edema may partly account for the vulnerability of these patients to recurrent pulmonary fluid accumulation.
确定急性心源性肺水肿是否与肺泡毛细血管屏障损伤相关,证据是表面活性物质特异性蛋白向循环中的渗漏增加;记录这种情况下肺泡毛细血管屏障损伤的持续时间;通过确定急性心源性肺水肿后循环肿瘤坏死因子-α是否升高来探讨肺实质炎症的作用。
前瞻性观察性研究。
一所三级大学教学医院的重症监护、心脏重症监护和心脏病病房。
共28例急性心源性肺水肿患者和13名年龄匹配的正常志愿者。
在第0天(就诊时)、第1天、第3天、第7天和第14天测量循环中的表面活性蛋白-A和-B以及肿瘤坏死因子-α。同时记录肺水肿的临床指标。
与对照组相比,第0天时表面活性蛋白-A和-B升高(分别为367±17 ng/mL对303±17以及3821±266 ng/mL对2747±157[平均值±标准误],p<.05),尽管临床、血流动力学和影像学变量迅速改善(p<.001),但表面活性蛋白-A和-B在第3天前进一步升高(分别为437±22,p<.001,4642±353,p<.01)。肿瘤坏死因子-α在就诊时升高(p<.05),第1天时翻倍(6.98±1.36 pg/mL,p<.05),第3天时仍升高(5.72±0.96 pg/mL,p<.05),峰值水平与胸部X线血管外肺水评分相关(r(p)=0.64,p=.003)。
尽管血浆表面活性蛋白-A和-B的最初升高可能代表肺泡毛细血管屏障的静水压性衰竭,但在血流动力学异常已缓解时其持续升高以及肿瘤坏死因子-α的延迟升高与肺实质炎症一致,这可能会进一步损害肺泡毛细血管屏障。急性心源性肺水肿后肺泡毛细血管屏障的这种长期生理缺陷可能部分解释了这些患者易发生反复肺积液的原因。