Zapol W M, Jones R
Am Rev Respir Dis. 1987 Aug;136(2):471-4. doi: 10.1164/ajrccm/136.2.471.
Mild pulmonary artery hypertension (PAP, 29.6 +/- 10.6 mm Hg, mean +/- SD) due to a 3-fold elevation of pulmonary vascular resistance (PVR, 2.2 +/- 1.1 mm Hg X L/min) is a common finding in severe ARDS. A vasodilator such as nitroprusside (151 micrograms/kg X min) can be administered in early ARDS and will lower PAP and PAOP (capillary wedge pressure) while increasing cardiac output (CO) from 6.9 to 8.75 L/min X M2 and venous admixture from 23% to 31.6%. This suggests diffuse vasoconstriction is present in early ARDS. In 19 patients with severe ARDS, 13 had vascular occlusions on balloon occlusion angiography, and these occlusions correlated with increased post mortem counts of PA thrombi. At autopsy, there was a considerable increase of PA medial thickness and a reduction of lumen diameter. This hemodynamic and morphologic evidence suggests both vasoconstrictor and anatomic changes play major roles elevating the PVR in ARDS.
重度急性呼吸窘迫综合征（ARDS）常见轻度肺动脉高压（PAP，29.6±10.6 mmHg，均值±标准差），此时肺血管阻力（PVR，2.2±1.1 mmHg×L/min）升高3倍。在ARDS早期可使用血管扩张剂如硝普钠（151微克/千克×分钟），这会降低PAP和肺动脉楔压（PAOP），同时使心输出量（CO）从6.9升至8.75 L/min×M2，静脉血掺杂从23%增至31.6%。这表明ARDS早期存在弥漫性血管收缩。在19例重度ARDS患者中，13例在球囊闭塞血管造影时有血管闭塞，这些闭塞与死后肺动脉血栓计数增加相关。尸检时，肺动脉中层厚度显著增加，管腔直径减小。这种血流动力学和形态学证据表明血管收缩剂和解剖学改变在ARDS中升高PVR方面均起主要作用。
