Raimondi Guillermo A
Instituto Raúl Carrea FLENI. Montañeses 2325, C1428AQK Buenos Aires, Argentina.
Medicina (B Aires). 2003;63(2):157-64.
The hypoxemia of acute respiratory distress syndrome (ARDS) depends chiefly upon shunt and ventilation-perfusion (VA/Q) inequality produced by fluid located in the interstitial space, alveolar collapse and flooding. Variables other tham inspired oxygen fraction and the underlying physiological abnormality can influence arterial oxygen partial pressure (PaO2). Changes in cardiac output, hemoglobin concentration, oxygen consumption and alcalosis can cause changes in PaO2 through their influence on mixed venous PO2. Gas exchange (GE) in ARDS may be studied using the inert gas elimination technique (MIGET) which enables to define the distribution of ventilation and perfusion without necessarily altering the FIO2 differentiating shunt from lung units with low VA/Q ratios and dead space from lung units with high VA/Q ratios. Different ventilatory strategies that increase mean airway pressure (positive end-expiratory pressure, high tidal volumes, inverse inspiratory-expiratory ratio, etc) improve PaO2 through increasing lung volume by recruiting new open alveoli and spreading the intra-alveolar fluid over a large surface area. Also prone-position ventilation would result in a marked improvement in GE enhancing dorsal lung ventilation by the effects on the gravitional distribution of pleural pressure and the reduction in the positive pleural pressure that develops in dorsal regions in ARDS. Inhaled nitric oxide (NO) has been shown to increase PaO2 in ARDS patients by inducing vasodilation predominantly in ventilated areas redistributing pulmonary blood flow away from nonventilated toward ventilated areas of the lung thus resulting in a shunt reduction. On the same way inhaled prostaglandins (PGI2 or PGE1) causes selective pulmonary vasodilation improving pulmonary GE. Intravenous almitrine, a selective pulmonary vasoconstrictor, has been shown to increase PaO2 by increasing hypoxic pulmonary vasoconstriction. A synergistic effect was found between inhaled NO and almitrine. In spite of the improval of GE shown by these different techniques on ARDS, no effect was demonstrated on mortality or duration of mechanical ventilation.
急性呼吸窘迫综合征（ARDS）的低氧血症主要取决于间质空间积液、肺泡萎陷和肺实质浸润所导致的分流以及通气-灌注（V̇A/Q̇）不均。除了吸入氧分数和潜在的生理异常外，其他变量也会影响动脉血氧分压（PaO₂）。心输出量、血红蛋白浓度、氧耗量和碱中毒的变化可通过影响混合静脉血氧分压进而导致PaO₂的改变。可采用惰性气体清除技术（MIGET）来研究ARDS中的气体交换（GE），该技术能够在不改变FIO₂的情况下确定通气和灌注的分布，区分分流与低V̇A/Q̇比值的肺单位以及高V̇A/Q̇比值的肺单位中的无效腔。不同的通气策略，如增加平均气道压（呼气末正压、大潮气量、反比通气等），通过募集新的开放肺泡增加肺容积，并将肺泡内液体分散到更大的表面积，从而改善PaO₂。此外，俯卧位通气可通过影响胸膜压力的重力分布以及降低ARDS患者背部区域出现的正胸膜压力，显著改善GE，增强背部肺通气。吸入一氧化氮（NO）已被证明可使ARDS患者的PaO₂升高，其机制主要是诱导通气区域的血管舒张，使肺血流从无通气区域重新分布到通气区域，从而减少分流。同样，吸入前列腺素（PGI₂或PGE₁）可引起选择性肺血管舒张，改善肺GE。静脉注射阿米三嗪是一种选择性肺血管收缩剂，已证明可通过增强低氧性肺血管收缩来增加PaO₂。吸入NO与阿米三嗪之间存在协同作用。尽管这些不同技术显示可改善ARDS中的GE，但对死亡率或机械通气时间并无影响。
