Vincent R N, Lang P, Elixson E M, Jonas R, Castaneda A R
Am J Cardiol. 1985 Sep 15;56(8):536-9. doi: 10.1016/0002-9149(85)91180-4.
Extravascular lung water (EVLW) was measured in 16 patients with congenital heart disease by the cold green dye, double indicator dilution technique. Five patients with optimally corrected tetralogy of Fallot served as controls, and EVLW in this group was 4.7 +/- 0.5 ml/kg (111 +/- 13 ml/m2) (mean +/- standard deviation). In 5 asymptomatic patients with atrial septal defect (ASD), normal pulmonary artery (PA) pressure and increased pulmonary blood flow, EVLW was 5.7 +/- 2.8 ml/kg (132 +/- 63 ml/m2), which was not significantly different from the value of control patients. However, in 6 patients with ventricular septal defect, PA hypertension, normal left atrial pressure and an equivalent left-to-right shunt to ASD patients, EVLW was 15.9 +/- 3.8 ml/kg (270 +/- 60 ml/m2). This was significantly different from values in both control and ASD patients (p less than 0.01). It is concluded that in the face of normal pulmonary vascular resistance, PA pressure is transmitted to the microvasculature, causing hydrostatic pulmonary edema. Other factors that may be implicated in the pathogenesis of pulmonary edema, such as increased pulmonary blood flow and relative lymphatic insufficiency in infants, cannot be excluded.
采用冷绿染料双指示剂稀释技术对16例先天性心脏病患者的血管外肺水(EVLW)进行了测量。5例法洛四联症矫正良好的患者作为对照,该组患者的EVLW为4.7±0.5 ml/kg(111±13 ml/m²)(均值±标准差)。5例无症状房间隔缺损(ASD)患者,肺动脉(PA)压力正常且肺血流量增加,其EVLW为5.7±2.8 ml/kg(132±63 ml/m²),与对照组患者的值无显著差异。然而,6例室间隔缺损、PA高血压、左心房压力正常且左向右分流与ASD患者相当的患者,其EVLW为15.9±3.8 ml/kg(270±60 ml/m²)。这与对照组和ASD患者的值均有显著差异(p<0.01)。结论是,在肺血管阻力正常的情况下,PA压力会传递至微血管,导致静水压性肺水肿。其他可能与肺水肿发病机制有关的因素,如婴儿肺血流量增加和相对淋巴功能不全,不能排除。