Thome Ulrich H, Carlo Waldemar A
Division of Neonatology and Pediatric Critical Care, Children's Hospital, University of Ulm, 89070 Ulm, Germany.
Semin Neonatol. 2002 Oct;7(5):409-19. doi: 10.1053/siny.2002.0135.
Although lifesaving, mechanical ventilation can result in lung injury and contribute to the development of bronchopulmonary dysplasia. The most critical determinants of lung injury are tidal volume and end-inspiratory lung volume. Permissive hypercapnia offers to maintain gas exchange with lower tidal volumes and thus decrease lung injury. Further physiologic benefits include improved oxygen delivery and neuroprotection, the latter through both avoidance of accidental hypocapnia, which is associated with a poor neurologic outcome, and direct cellular effects. Clinical trials in adults with acute respiratory failure indicated improved survival and reduced incidence of organ failure in subjects managed with low tidal volumes and permissive hypercapnia. Retrospective studies in low birth weight infants found an association of bronchopulmonary dysplasia with low PaCO(2). Randomized clinical trials of low birth weight infants did not achieve sufficient statistical power to demonstrate a reduction of BPD by permissive hypercapnia, but strong trends indicated the possibility of important benefits without increased adverse events. Herein, we review the mechanisms leading to lung injury, the physiologic effects of hypercapnia, the dangers of hypocapnia, and the available clinical data.
尽管机械通气能挽救生命，但它可能导致肺损伤，并促使支气管肺发育不良的发生。肺损伤的最关键决定因素是潮气量和吸气末肺容积。允许性高碳酸血症可通过较低的潮气量维持气体交换，从而减少肺损伤。进一步的生理益处包括改善氧输送和神经保护，后者既通过避免与不良神经结局相关的意外低碳酸血症，也通过直接的细胞效应来实现。针对成人急性呼吸衰竭的临床试验表明，采用低潮气量和允许性高碳酸血症管理的受试者生存率提高，器官衰竭发生率降低。对低出生体重婴儿的回顾性研究发现支气管肺发育不良与低动脉血二氧化碳分压（PaCO₂）有关。针对低出生体重婴儿的随机临床试验没有获得足够的统计效力来证明允许性高碳酸血症可降低支气管肺发育不良的发生率，但有力的趋势表明在不增加不良事件的情况下可能有重要益处。在此，我们综述导致肺损伤的机制、高碳酸血症的生理效应、低碳酸血症的危害以及现有的临床数据。
