Lambeth Christopher, Wang Ziyu, Kairaitis Kristina, Moshfegh Abouzar, Jabbarzadeh Ahmad, Amis Terence
Ludwig Engel Centre for Respiratory Research, The Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW, Australia.
School of Aerospace, Mechanical and Mechatronic Engineering, The University of Sydney, Sydney, NSW, Australia.
J Appl Physiol (1985). 2018 Dec 1;125(6):1821-1831. doi: 10.1152/japplphysiol.00233.2018. Epub 2018 Oct 4.
We previously published a unique methodology for quantifying human velopharyngeal mucosal surface topography and found increased mucosal surface roughness in patients with obstructive sleep apnea (OSA). In fluid mechanics, surface roughness is associated with increased frictional pressure losses and resistance. This study used computational fluid dynamics (CFD) to analyze the mechanistic effect of different levels of mucosal surface roughness on velopharyngeal airflow. Reconstructed velopharyngeal models from OSA and control subjects were modified, giving each model three levels of roughness, quantified by the curvature-based surface roughness index (CBSRI) (range 24.8-68.6 mm). CFD using the shear stress transport turbulence model was performed (unidirectional, inspiratory, steady-state, 15l/min volumetric flow rate), and the effects of roughness on flow velocity, intraluminal pressure, wall shear stress, and velopharyngeal resistance () were examined. Across all models, increasing roughness increased maximum flow velocity, wall shear stress, and flow disruption while decreasing intraluminal pressures. Linear mixed effects modeling demonstrated a log-linear relationship between CBSRI and , with a common slope (log()/CBSRI) of 0.0079 [95% confidence interval (CI) 0.0015-0.0143; = 0.019] for all subjects, equating to a 1.9-fold increase in when roughness increased from control to OSA levels. At any fixed CBSRI, the estimated difference in log() between OSA and control models was 0.9382 (95% CI 0.0032-1.8732; = 0.049), equating to an 8.7-fold increase in . This study supports the hypothesis that increasing mucosal surface roughness increases velopharyngeal airway resistance, particularly for anatomically narrower OSA airways, and may thus contribute to increased vulnerability to upper airway collapse in patients with OSA. Increased mucosal surface roughness in the velopharynx of patients with obstructive sleep apnea (OSA) has recently been identified, but its role in OSA pathogenesis is unknown. This is the first study to model the impact of increased roughness on airflow mechanics in the velopharynx. We report that increasing roughness significantly affects airflow, increasing velopharyngeal resistance and potentially increasing the vulnerability to upper airway collapse, particularly in those patients with an already compromised anatomy.
我们之前发表了一种独特的方法来量化人类腭咽黏膜表面形貌，并发现阻塞性睡眠呼吸暂停（OSA）患者的黏膜表面粗糙度增加。在流体力学中，表面粗糙度与摩擦压力损失和阻力增加有关。本研究使用计算流体动力学（CFD）来分析不同程度的黏膜表面粗糙度对腭咽气流的作用机制。对来自OSA患者和对照受试者的重建腭咽模型进行修改，使每个模型具有三个粗糙度水平，通过基于曲率的表面粗糙度指数（CBSRI）进行量化（范围为24.8 - 68.6毫米）。使用剪切应力输运湍流模型进行CFD模拟（单向、吸气、稳态、15升/分钟的体积流量），并研究粗糙度对流速、腔内压力、壁面剪切应力和腭咽阻力（）的影响。在所有模型中，粗糙度增加会使最大流速、壁面剪切应力和气流紊乱增加，同时腔内压力降低。线性混合效应模型显示CBSRI与之间存在对数线性关系，所有受试者的共同斜率（log（）/CBSRI）为0.0079 [95%置信区间（CI）0.0015 - 0.0143； = 0.019]，这意味着当粗糙度从对照水平增加到OSA水平时，增加1.9倍。在任何固定的CBSRI下，OSA模型和对照模型之间log（）的估计差异为0.9382（95% CI 0.0032 - 1.8732； = 0.049），相当于增加8.7倍。本研究支持以下假设：黏膜表面粗糙度增加会增加腭咽气道阻力，特别是对于解剖结构较窄的OSA气道，因此可能导致OSA患者上气道塌陷的易感性增加。最近已确定阻塞性睡眠呼吸暂停（OSA）患者的腭咽黏膜表面粗糙度增加，但其在OSA发病机制中的作用尚不清楚。这是第一项模拟粗糙度增加对腭咽气流力学影响的研究。我们报告称，粗糙度增加会显著影响气流，增加腭咽阻力，并可能增加上气道塌陷的易感性，特别是在那些解剖结构已经受损的患者中。
