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首页> 外文期刊>Respiratory physiology & neurobiology >Mechanics of airway and alveolar collapse in human breath-hold diving.
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Mechanics of airway and alveolar collapse in human breath-hold diving.

机译:在人类屏气潜水中气道和肺泡的力学崩溃。

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摘要

A computational model of the human respiratory tract was developed to study airway and alveolar compression and re-expansion during deep breath-hold dives. The model incorporates the chest wall, supraglottic airway, trachea, branched airway tree, and elastic alveoli assigned time-dependent surfactant properties. Total lung collapse with degassing of all alveoli is predicted to occur around 235m, much deeper than estimates for aquatic mammals. Hysteresis of the pressure-volume loop increases with maximum diving depth due to progressive alveolar collapse. Reopening of alveoli occurs stochastically as airway pressure overcomes adhesive and compressive forces on ascent. Surface area for gas exchange vanishes at collapse depth, implying that the risk of decompression sickness should reach a plateau beyond this depth. Pulmonary capillary transmural stresses cannot increase after local alveolar collapse. Consolidation of lung parenchyma might provide protection from capillary injury or leakage caused by vascular engorgement due to outward chest wall recoil at extreme depths.
机译:开发了人类呼吸道的计算模型,以研究深呼吸屏气潜水期间的气道和肺泡压缩和再扩张。该模型结合了胸壁,声门上气道,气管,分支气道树和弹性肺泡,它们具有随时间变化的表面活性剂特性。预计全部肺泡脱气导致的肺总塌陷发生在235m左右,比对水生哺乳动物的估计要深得多。由于渐进的肺泡塌陷,压力-体积环的磁滞随着最大潜水深度而增加。肺泡的重新打开是随机发生的,因为气道压力克服了上升过程中的黏附力和压缩力。气体交换的表面积在塌陷深度处消失,这意味着减压病的风险应超过该深度。局部肺泡塌陷后,肺毛细血管透壁应力不会增加。肺实质的巩固可提供保护,以防止由于极度深度的向外胸壁后坐力而引起的血管充血引起的毛细血管损伤或渗漏。

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