Vedrinne J M, Curtil A, Martinot S, Vedrinne C, Robin J, Franck M, Champsaur G
Department of Anesthesiology, Hôpital Edouard Herriot, Lyon, France.
Anesth Analg. 1998 Jul;87(1):21-6. doi: 10.1097/00000539-199807000-00006.
During hypoxemia, hypoxic pulmonary vasoconstriction and tachycardia are often observed in association with increases in pulmonary artery pressure and cardiac output. Nevertheless, the hemodynamic consequences of hypoxemia have never been evaluated by echocardiography and simultaneously compared with invasive hemodynamic variables. Fourteen open-chest, anesthetized piglets (weight 29-36 kg) were submitted to progressive hypoxemia and reoxygenation. Usual invasive hemodynamic variables were obtained from peripheral and central heart catheters. Direct epicardial echocardiography was used to measure right and left ventricular areas on a short-axis view at mid-papillary level. The mean pulmonary artery pressure (MPAP) increased with pulmonary vascular resistance in a dose-related manner as the fraction of inspired oxygen (FIO2) declined from 0.5 to 0.12. The MPAP correlated with right ventricular end-diastolic area (RVEDA) only at FIO2 0.08. There was a 49% reduction in left ventricular end systolic wall stress (LVESWS) between FIO2 0.5 and 0.08. Left ventricular ejection fraction area (LVEFA) increased by 33% above baseline and correlated with the decrease in LVESWS. No correlation was observed between left ventricular end-diastolic area and pulmonary artery occlusion pressure or left atrial pressure and between cardiac output and LVEFA. Systemic vascular resistance underestimates the magnitude of changes in LVESWS but overestimates the afterload compared with LVESWS. This study demonstrates that, for the lowest FIO2 (0.08), changes in MPAP correlated with changes in RVEDA but not in pulmonary vascular resistance. Moreover, LVESWS decreases significantly in a dose-related manner under progressive hypoxemia and normalizes immediately after reoxygenation. This study also shows that, under hypoxemic conditions, echocardiography enhances understanding of hemodynamic changes compared with right heart catheterization alone.
Acute hypoxemia in pigs is responsible for pulmonary vasoconstriction-induced pulmonary hypertension (which is restricted by the right ventricular failure), as well as a PaO2-dependent decrease in left ventricular afterload. These changes are better displayed by echocardiography than by right heart catheter.
在低氧血症期间,常观察到低氧性肺血管收缩和心动过速,同时伴有肺动脉压和心输出量增加。然而,低氧血症的血流动力学后果从未通过超声心动图进行评估,也未与有创血流动力学变量同时进行比较。14只开胸、麻醉的仔猪(体重29 - 36千克)接受了渐进性低氧血症和再氧合处理。从外周和中心心脏导管获取常规有创血流动力学变量。直接心外膜超声心动图用于在乳头肌水平短轴视图上测量右心室和左心室面积。随着吸入氧分数(FIO2)从0.5降至0.12,平均肺动脉压(MPAP)与肺血管阻力呈剂量相关增加。仅在FIO2为0.08时,MPAP与右心室舒张末期面积(RVEDA)相关。在FIO2从0.5降至0.08期间,左心室收缩末期壁应力(LVESWS)降低了49%。左心室射血分数面积(LVEFA)比基线增加了33%,并与LVESWS的降低相关。未观察到左心室舒张末期面积与肺动脉闭塞压或左心房压之间以及心输出量与LVEFA之间存在相关性。与LVESWS相比,体循环血管阻力低估了LVESWS的变化幅度,但高估了后负荷。本研究表明,对于最低FIO2(0.08),MPAP的变化与RVEDA的变化相关,但与肺血管阻力无关。此外,在渐进性低氧血症下,LVESWS以剂量相关方式显著降低,并在再氧合后立即恢复正常。本研究还表明,在低氧条件下,与单独的右心导管检查相比,超声心动图能增强对血流动力学变化的理解。
猪的急性低氧血症会导致肺血管收缩引起的肺动脉高压(受右心室衰竭限制),以及依赖于PaO2的左心室后负荷降低。这些变化通过超声心动图比通过右心导管检查显示得更好。