Pleural pressure theory revisited: a role for capillary equilibrium
Pleural pressure theory revisited: a role for capillary equilibrium
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DOI：
10.21037/jtd.2017.03.112
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发表时间：
2017-04-01
影响因子：
2.5
通讯作者：
Scarci, Marco
中科院分区：
文献类型：
--
作者：
Casha, Aaron R.;Caruana-Gauci, Roberto;Scarci, Marco
背景：解释胸膜压力的理论应该解释所有的观察结果，包括胸壁和肺的相等和相反的后坐力，小于预期的胸膜流体静力梯度及其在大叶边缘的变化，为什么胸膜压力为负以及胸膜液体循环如何起作用。方法：提出一种描述浮力、流体静力和毛细力之间平衡的理论模型。所描述的毛细管平衡模型依赖于由主动胸腔泵提供动力的胸膜液体积和蛋白质含量的控制。结果：计算浮力、静水压力和毛细血管压力之间的相互作用，并根据文献中发现的表面张力、接触角、胸膜液和肺密度值确定胸膜厚度和压力值。根据阿基米德的流体静力悖论，模型可以解释胸膜液和漂浮在胸膜液中的肺之间的浮力在大叶边缘的不同流体静力垂直胸膜压力梯度的问题。毛细血管平衡模型满足了胸膜压力模型的所有重要要求，在顶点处负压最大，肺和胸壁上的力相等且相反，循环泵的作用。结论：该模型预测肺气肿不可能发生胸腔积液，除非合并心力衰竭增加肺密度。该模型还解释了肺与胸壁（例如，肺叶边缘）的不融合如何使胸膜压力更负，以及为什么上肺叶切除术后胸膜压力比下肺叶切除术后更高。病理改变的胸腔积液成分和肺密度改变毛细血管和浮力静水压力之间的平衡，促进胸腔积液的形成。
Background: Theories elucidating pleural pressures should explain all observations including the equal and opposite recoil of the chest wall and lungs, the less than expected pleural hydrostatic gradient and its variation at lobar margins, why pleural pressures are negative and how pleural fluid circulation functions.Methods: A theoretical model describing equilibrium between buoyancy, hydrostatic forces, and capillary forces is proposed. The capillary equilibrium model described depends on control of pleural fluid volume and protein content, powered by an active pleural pump.Results: The interaction between buoyancy forces, hydrostatic pressure and capillary pressure was calculated, and values for pleural thickness and pressure were determined using values for surface tension, contact angle, pleural fluid and lung densities found in the literature. Modelling can explain the issue of the differing hydrostatic vertical pleural pressure gradient at the lobar margins for buoyancy forces between the pleural fluid and the lung floating in the pleural fluid according to Archimedes' hydrostatic paradox. The capillary equilibrium model satisfies all salient requirements for a pleural pressure model, with negative pressures maximal at the apex, equal and opposite forces in the lung and chest wall, and circulatory pump action.Conclusions: This model predicts that pleural effusions cannot occur in emphysema unless concomitant heart failure increases lung density. This model also explains how the non-confluence of the lung with the chest wall (e.g., lobar margins) makes the pleural pressure more negative, and why pleural pressures would be higher after an upper lobectomy compared to a lower lobectomy. Pathological changes in pleural fluid composition and lung density alter the equilibrium between capillarity and buoyancy hydrostatic pressure to promote pleural effusion formation.