早期急性呼吸窘迫综合征肺泡死腔增加的生理机制和空间分布：一项实验研究。
Physiological mechanism and spatial distribution of increased alveolar dead-space in early ARDS: An experimental study.
机构信息
Postgraduate Program of Electrical Engineering, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
出版信息
Acta Anaesthesiol Scand. 2021 Jan;65(1):100-108. doi: 10.1111/aas.13702. Epub 2020 Sep 28.
BACKGROUND
We aimed to investigate the physiological mechanism and spatial distribution of increased physiological dead-space, an early marker of ARDS mortality, in the initial stages of ARDS. We hypothesized that: increased dead-space results from the spatial redistribution of pulmonary perfusion, not ventilation; such redistribution is not related to thromboembolism (ie, areas with perfusion = 0 and infinite ventilation-perfusion ratio, ), but rather to moderate shifts of perfusion increasing in non-dependent regions.
METHODS
Five healthy anesthetized sheep received protective ventilation for 20 hours, while endotoxin was continuously infused. Maps of voxel-level lung ventilation, perfusion, , CO partial pressures, and alveolar dead-space fraction were estimated from positron emission tomography at baseline and 20 hours.
RESULTS
Alveolar dead-space fraction increased during the 20 hours (+0.05, P = .031), mainly in non-dependent regions (+0.03, P = .031). This was mediated by perfusion redistribution away from non-dependent regions (-5.9%, P = .031), while the spatial distribution of ventilation did not change, resulting in increased in non-dependent regions. The increased alveolar dead-space derived mostly from areas with intermediate (0.5≤ ≤10), not areas of nearly "complete" dead-space ( >10).
CONCLUSIONS
In this early ARDS model, increases in alveolar dead-space occur within 20 hours due to the regional redistribution of perfusion and not ventilation. This moderate redistribution suggests changes in the interplay between active and passive perfusion redistribution mechanisms (including hypoxic vasoconstriction and gravitational effects), not the appearance of thromboembolism. Hence, the association between mortality and increased dead-space possibly arises from the former, reflecting gas-exchange inefficiency due to perfusion heterogeneity. Such heterogeneity results from the injury and exhaustion of compensatory mechanisms for perfusion redistribution.
背景
我们旨在研究 ARDS 死亡率的早期标志物——生理死腔增加的生理机制和空间分布。我们假设：死腔的增加是由于肺灌注的空间再分布引起的，而不是通气引起的；这种再分布与血栓栓塞无关（即，灌注=0 和无限通气-灌注比的区域），而是与非依赖区灌注适度增加有关。
方法
5 只健康麻醉绵羊接受保护性通气 20 小时，同时持续输注内毒素。在基线和 20 小时时，通过正电子发射断层扫描估计体素水平肺通气、灌注、 、CO 分压和肺泡死腔分数的图谱。
结果
肺泡死腔分数在 20 小时内增加（+0.05，P=0.031），主要在非依赖区（+0.03，P=0.031）。这是由灌注从非依赖区重新分布引起的（-5.9%，P=0.031），而通气的空间分布没有变化，导致非依赖区的增加。增加的肺泡死腔主要来自中等 （0.5≤ ≤10）的区域，而不是几乎“完全”死腔（ >10）的区域。
结论
在这个早期 ARDS 模型中，肺泡死腔的增加发生在 20 小时内，是由于灌注的区域性再分布而不是通气。这种适度的再分布表明主动和被动灌注再分布机制（包括缺氧性血管收缩和重力效应）之间的相互作用发生了变化，而不是血栓栓塞的出现。因此，死亡率与增加的死腔之间的关联可能来自前者，反映了由于灌注异质性导致的气体交换效率低下。这种异质性是由于灌注再分布的补偿机制的损伤和衰竭引起的。
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