Schumacker P T, Rhodes G R, Newell J C, Dutton R E, Shah D M, Scovill W A, Powers S R
Am Rev Respir Dis. 1979 Jan;119(1):33-43. doi: 10.1164/arrd.1979.119.1.33.
To investigate the role of ventilation-perfusion (VA/Q) imbalance in the hypoxemia observed after head injury, 5 male subjects (17 to 26 years of age) with isolated head trauma and subsequent hypoxemia were studied. Disturbances of ventilation and perfusion were assessed using the steady-state elimination of six inert gases of different solubilities. Paired studies were conducted during mechanical ventilation with a volume-cycled ventilator and during spontaneous ventilation. Distributions recovered from studies of spontaneous ventilation show a mode of ventilation and perfusion near a VA/Q of 1.0. In addition, 41% of the cardiac output was distributed to a second population of lung units with low VA/Q (less than 0.1) and shunt. During mechanical ventilation, perfusion to these regions of low VA/Q decreased to 21% of the cardiac output, whereas shunt fraction was unchanged. This was associated with a marked broadening of the VA/Q mode near 1.0, relative to the studies during spontaneous ventilation. Mean functional residual capacity during mechanical ventilation was not different from that during spontaneous ventilation. These results suggest that head injury can lead to hypoxemia through a failure of VA/Q regulatory mechanisms.
为研究通气/灌注(VA/Q)失衡在颅脑损伤后低氧血症中所起的作用,我们对5名(年龄在17至26岁之间)患有单纯性颅脑外伤并继发低氧血症的男性受试者进行了研究。使用六种不同溶解度的惰性气体的稳态清除来评估通气和灌注的紊乱情况。在使用容量控制呼吸机进行机械通气期间和自主通气期间进行了配对研究。自主通气研究中恢复的分布显示通气和灌注模式接近VA/Q为1.0。此外,41%的心输出量分布到第二组肺单位,这些肺单位的VA/Q较低(小于0.1)且存在分流。在机械通气期间,流向这些低VA/Q区域的灌注减少至心输出量的21%,而分流分数不变。这与相对于自主通气期间的研究,VA/Q模式在1.0附近明显变宽有关。机械通气期间的平均功能残气量与自主通气期间无差异。这些结果表明,颅脑损伤可通过VA/Q调节机制的失效导致低氧血症。