The worldwide pandemic caused by the SARS-CoV-2 virus has resulted in over 84,407,000 cases with over 1,800,000 deaths when this paper was submitted, with comorbidities such as gender, race, age, body mass, diabetes, and hypertension greatly exacerbating mortality. This review will analyze the rapidly increasing knowledge of COVID-19 induced lung pathophysiology. Although controversial, the acute respiratory distress syndrome (ARDS) associated with COVID-19 (CARDS) seems to present as two distinct phenotypes: Type-L and Type-H. The 'L' refers to Low elastance, ventilation/perfusion ratio, lung weight, and recruitability, and the 'H' refers to High pulmonary elastance, shunt, edema, and recruitability. However, the LUNG SAFE and ESICM Trials Groups has shown that ~13% of the mechanically ventilated non-COVID-19 ARDS patients have the Type-L phenotype. However, other studies have shown that CARDS and ARDS respiratory mechanics overlap and that standard ventilation strategies apply to these patients. The mechanisms causing alterations in pulmonary perfusion could be caused by some combination of: 1) renin-angiotensin system (RAS) dysregulation, 2) thrombosis caused by loss of endothelial barrier, 3) endothelial dysfunction causing loss of hypoxic pulmonary vasoconstriction (HPV) perfusion control, and 4) hyper-perfusion of collapsed lung tissue that has been directly measured and supported by a computational model. A flow chart has been constructed highlighting the need for personalized and adaptive ventilation strategies, such as the time controlled adaptive ventilation (TCAV) method to set and adjust the airway pressure release ventilation (APRV) mode, which recently was shown effective at improving oxygenation and reducing FiO₂, vasopressors, and sedation in COVID-19 patients.

中文翻译：

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SARS-CoV-2 引起的急性肺损伤的功能病理生理学及其临床意义


截至本文提交时，SARS-CoV-2 病毒引起的全球大流行已导致超过 84,407,000 例病例，超过 1,800,000 人死亡，性别、种族、年龄、体重、糖尿病和高血压等合并症大大加剧了死亡率。本综述将分析快速增加的有关 COVID-19 引起的肺部病理生理学的知识。尽管存在争议，但与 COVID-19 (CARDS) 相关的急性呼吸窘迫综合征 (ARDS) 似乎表现为两种不同的表型：L 型和 H 型。 “L”是指低弹性、通气/灌注比、肺重量和复张性，“H”是指高肺弹性、分流、水肿和复张性。然而，LUNG SAFE 和 ESICM 试验组表明，约 13% 的机械通气非 COVID-19 ARDS 患者具有 L 型表型。然而，其他研究表明，CARDS 和 ARDS 呼吸力学有重叠，并且标准通气策略适用于这些患者。引起肺灌注改变的机制可能是由以下因素组合引起的：1) 肾素-血管紧张素系统 (RAS) 失调，2) 内皮屏障丧失引起的血栓形成，3) 内皮功能障碍导致缺氧性肺血管收缩 (HPV) 灌注丧失控制，4）塌陷肺组织的过度灌注，已直接测量并由计算模型支持。 我们构建了一个流程图，强调了个性化和适应性通气策略的需求，例如用于设置和调整气道压力释放通气（APRV）模式的时间控制适应性通气（TCAV）方法，该方法最近被证明可以有效改善氧合和减少 FiO ₂ 、血管升压药和对 COVID-19 患者的镇静作用。