Ma Haoran, Fujioka Hideki, Halpern David, Bates Jason H T, Gaver Donald P
Department of Biomedical Engineering, Tulane University, New Orleans, LA, United States.
Center for Computational Science, Tulane University, New Orleans, LA, United States.
Front Netw Physiol. 2023 Nov 2;3:1257710. doi: 10.3389/fnetp.2023.1257710. eCollection 2023.
This study developed and investigated a comprehensive multiscale computational model of a mechanically ventilated ARDS lung to elucidate the underlying mechanisms contributing to the development or prevention of VILI. This model is built upon a healthy lung model that incorporates realistic airway and alveolar geometry, tissue distensibility, and surfactant dynamics. Key features of the ARDS model include recruitment and derecruitment (RD) dynamics, alveolar tissue viscoelasticity, and surfactant deficiency. This model successfully reproduces realistic pressure-volume (PV) behavior, dynamic surface tension, and time-dependent descriptions of RD events as a function of the ventilation scenario. Simulations of Time-Controlled Adaptive Ventilation (TCAV) modes, with short and long durations of exhalation ( and , respectively), reveal a higher incidence of RD for despite reduced surface tensions due to interfacial compression. This finding aligns with experimental evidence emphasizing the critical role of timing in protective ventilation strategies. Quantitative analysis of energy dissipation indicates that while alveolar recruitment contributes only a small fraction of total energy dissipation, its spatial concentration and brief duration may significantly contribute to VILI progression due to its focal nature and higher intensity. Leveraging the computational framework, the model may be extended to facilitate the development of personalized protective ventilation strategies to enhance patient outcomes. As such, this computational modeling approach offers valuable insights into the complex dynamics of VILI that may guide the optimization of ventilation strategies in ARDS management.
本研究开发并研究了一个机械通气的急性呼吸窘迫综合征(ARDS)肺的综合多尺度计算模型,以阐明导致呼吸机相关性肺损伤(VILI)发生或预防的潜在机制。该模型基于一个健康肺模型构建,该健康肺模型纳入了真实的气道和肺泡几何结构、组织扩张性以及表面活性剂动力学。ARDS模型的关键特征包括肺复张和肺萎陷(RD)动力学、肺泡组织粘弹性以及表面活性剂缺乏。该模型成功再现了逼真的压力 - 容积(PV)行为、动态表面张力以及作为通气方案函数的RD事件的时间依赖性描述。对呼气时间分别为短和长的时间控制自适应通气(TCAV)模式的模拟显示,尽管由于界面压缩表面张力降低,但呼气时间短时RD的发生率更高。这一发现与强调时机在保护性通气策略中关键作用的实验证据一致。能量耗散的定量分析表明,虽然肺泡复张仅占总能量耗散的一小部分,但其空间集中和短暂持续时间可能因其局部性质和更高强度而对VILI进展有显著贡献。利用该计算框架,该模型可扩展以促进个性化保护性通气策略的开发,从而改善患者预后。因此,这种计算建模方法为VILI的复杂动力学提供了有价值的见解,可指导ARDS管理中通气策略的优化。