Biddle T L, Yu P N, Hodges M, Chance J R, Ehrich D A, Kronenberg M W, Roberts D L
Am Heart J. 1976 Dec;92(6):692-9. doi: 10.1016/s0002-8703(76)80004-x.
Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.
对88例急性心肌梗死患者测量了肺血管外容积或肺水（PEV）、动脉血气和心脏血流动力学。从I级（无并发症）患者到III级（明显肺水肿）患者，观察到PEV逐渐增加，动脉血氧分压（PaO2）降低。根据临床分类，随着心力衰竭严重程度的增加，心率和肺楔压（Pw）升高，心脏指数下降。PEV与Pw之间存在显著相关性，且与临床分级无关（r = 0.47，p < 0.01）。PaO2与Pw（r = -0.28，p < 0.01）以及PEV（r = -0.26，p < 0.02）呈负相关。因此，我们得出结论，急性心肌梗死患者继发于肺静脉高压的肺静水压升高是间质性水肿的主要决定因素。在PEV值较高时，PaO2较低。肺水过多时低氧血症的机制可能是多种因素所致，包括小气道功能障碍和肺内分流。
