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急性心肌梗死后患者胶体渗透压和肺动脉楔压变化相关的肺水肿

Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction.

作者信息

Luz da P L, Shubin H, Weil M H, Jacobson E, Stein L

出版信息

Circulation. 1975 Feb;51(2):350-7. doi: 10.1161/01.cir.51.2.350.

Abstract

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.

摘要

对26例急性心肌梗死患者进行了肺动脉楔压和血浆胶体渗透压及其与肺水肿关系的研究,其中14例发生了肺水肿。在无肺水肿时,肺动脉楔压和血浆胶体渗透压均在正常范围内;肺水肿发生后,观察到肺动脉楔压中度升高,血浆胶体渗透压降低。计算血浆胶体渗透压与肺动脉楔压之间的梯度时,显示出高度显著差异(P小于0.002)。在无肺水肿时,该梯度平均为9.7(±1.7标准误)托;肺水肿出现后,降至1.2(±1.3)托。在用洋地黄和速尿治疗期间,肺水肿的逆转与胶体渗透压-流体静压梯度的相应变化密切相关。这些观察结果表明,肺水肿发生后可能出现肺毛细血管压力升高和胶体渗透压降低。胶体渗透压的这种下降,尤其是胶体渗透压-流体静压毛细血管压力梯度的降低,可能有利于液体渗入肺部。

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