论文标题
呼吸机波形损坏的信息肺模型
A damaged-informed lung model for ventilator waveforms
论文作者
论文摘要
急性呼吸窘迫综合征(ARDS)的特征是扩散肺泡损伤(DAD)导致血管通透性增加和肺泡气体交换降低。机械通气是一种潜在的救生干预措施,可改善氧气交换,但有可能引起呼吸机诱导的肺损伤(VILI)。减少VILI的一般策略是使用低潮汐量和低压通风,但是对于床边医生来说,为个别患者的最佳呼吸机设置难以确定和来自ARDS的死亡率仍然令人难以置信。由于需要最大程度地减少Vili的动机,科学家开发了不同复杂性的模型,以了解患病的肺部生理学。但是,简单模型通常无法捕获现实世界的损伤,而复杂模型往往无法通过临床数据进行估计,从而限制了现有模型的临床实用性。为了解决这一差距,我们提出了一个生理锚定的数据驱动模型,以更好地模型肺损伤。我们的方法依靠在呼吸机波形数据中使用临床相关的特征,该功能包含有关肺部生理学,患者 - 视频剂相互作用和呼吸机设置的信息。我们的肺模型可以重现受控小鼠模型数据和不受控制的人类ICU数据的不同受损肺的基本生理学和病理生理动力学。与已知的肺部生理量度相关的估计参数值与观察到的肺损伤一致。在将来的努力中,该模型可用于表型呼吸机波形,并作为预测ARDS和改善患者护理过程的基础。
The acute respiratory distress syndrome (ARDS) is characterized by the acute development of diffuse alveolar damage (DAD) resulting in increased vascular permeability and decreased alveolar gas exchange. Mechanical ventilation is a potentially lifesaving intervention to improve oxygen exchange but has the potential to cause ventilator-induced lung injury (VILI). A general strategy to reduce VILI is to use low tidal volume and low-pressure ventilation, but optimal ventilator settings for an individual patient are difficult for the bedside physician to determine and mortality from ARDS remains unacceptably high. Motivated by the need to minimize VILI, scientists have developed models of varying complexity to understand diseased pulmonary physiology. However, simple models often fail to capture real-world injury while complex models tend to not be estimable with clinical data, limiting the clinical utility of existing models. To address this gap, we present a physiologically anchored data-driven model to better model lung injury. Our approach relies on using clinically relevant features in the ventilator waveform data that contain information about pulmonary physiology, patients-ventilator interaction and ventilator settings. Our lung model can reproduce essential physiology and pathophysiology dynamics of differently damaged lungs for both controlled mouse model data and uncontrolled human ICU data. The estimated parameters values that are correlated with a known measure of lung physiology agree with the observed lung damage. In future endeavors, this model could be used to phenotype ventilator waveforms and serve as a basis for predicting the course of ARDS and improving patient care.