PERMISSIVE HYPERCAPNIA IN ACUTE RESPIRATORY-FAILURE
PERMISSIVE HYPERCAPNIA IN ACUTE RESPIRATORY-FAILURE
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DOI：
10.1001/jama.272.12.957
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发表时间：
1994-09-28
影响因子：
120.7
通讯作者：
ZWISCHENBERGER, JB
中科院分区：
文献类型：
--
作者：
BIDANI, A;TZOUANAKIS, AE;ZWISCHENBERGER, JB
客观。-根据当前呼吸机相关肺损伤理论、系统性高碳酸血症的潜在并发症和现有的人类结局研究，评价压力限制伴允许性高碳酸血症治疗急性呼吸衰竭/成人呼吸窘迫综合征的潜在疗效。数据来源。文章通过MEDLINE、已发表数据的参考引文以及与各自领域权威机构的咨询进行识别。动物模型实验和人体临床试验的选择是基于它们是否解决了伴或不伴高碳酸血症的压力限制问题、高碳酸血症的病理生理学效应或呼吸机诱导的实质性肺损伤的概念。经常引用的参考文献优先包括。数据提取。分析数据时特别强调从临床研究中获得以下变量：吸气峰压、潮气量、每分钟通气量和PCO 2。呼吸生理学的定量方面用于分析允许性高碳酸血症对正常和受损肺的呼吸需求的理论影响。大量的动物模型数据支持这一假设，即呼吸机驱动的肺泡过度扩张可诱导显著的实质性肺损伤。成人呼吸窘迫综合征肺损伤的异质性，其生理肺容量小，可能使肺容易受到这种类型的损伤，通过使用传统的潮气量（10至15 mL/kg）。允许性高碳酸血症是一种通过压力或容量限制使肺泡过度扩张最小化的方法，并且可以接受呼吸性酸中毒的潜在有害后果。与预测死亡率的模型相比，外显或内隐允许性高碳酸血症的非对照人体试验显示出生存率的改善。基于动物模型和计算机模拟，通过压力或容量限制来避免肺泡过度扩张具有重要的支持。在初步的人体临床试验中，严重肺损伤中相关的高碳酸血症的有害作用似乎不是一个重要的限制因素。尽管目前的非对照研究表明了这种治疗的益处，但在批准采用这种治疗方法之前，迫切需要进行对照试验来证实这些发现。
Objective.-To evaluate the potential efficacy of pressure limitation with permissive hypercapnia in the treatment of acute respiratory failure/adult respiratory distress syndrome on the basis of current theories of ventilator-induced lung injury, potential complications of systemic hypercarbia, and available human outcome studies.Data Sources.-Articles were identified through MEDLINE, reference citations of published data, and consultation with authorities in their respective fields.Study Selection.-Animal model experimentation and human clinical trials were selected on the basis of whether they addressed the questions of pressure limitation with or without hypercapnia, the pathophysiologic effects of hypercapnia, or the concept of ventilator-induced parenchymal lung injury. Frequently cited references were preferentially included.Data Extraction.-Data were analyzed with particular emphasis on obtaining the following variables from the clinical studies: peak inspiratory pressures, tidal volumes, minute ventilation, and PCO2. Quantitative aspects of respiratory physiology were used to analyze the theoretical effects of permissive hypercapnia on ventilatory requirements in normal and injured lungs.Data Synthesis.-Extensive animal model data support the hypothesis that ventilator-driven alveolar overdistention can induce significant parenchymal lung injury. The heterogeneous nature of lung injury in adult respiratory distress syndrome, with its small physiologic lung volume, may render the lung susceptible to this type of injury through the use of conventional tidal volumes (10 to 15 mL/kg). Permissive hypercapnia is an approach whereby alveolar overdistention is minimized through either pressure or volume limitation, and the potential deleterious consequences of respiratory acidosis are accepted. Uncontrolled human trials of explicit or implicit permissive hypercapnia have demonstrated improved survival in comparison with models of predictive mortality.Conclusions.-Avoidance of alveolar overdistention through pressure or volume limitation has significant support based on animal models and computer simulation. Deleterious effects of the associated hypercarbia in severe lung injury do not appear to be a significant limiting factor in preliminary human clinical trials. Although current uncontrolled studies suggest benefit, controlled trials are urgently needed to confirm these findings before adoption of the treatment can be endorsed.