Functional pathophysiology of SARS-CoV-2-induced acute lung injury and clinical implications

被引:48
作者
Habashi, Nader M. [1 ]
Camporota, Luigi [2 ]
Gatto, Louis A. [3 ]
Nieman, Gary [3 ]
机构
[1] Univ Maryland, R Adams Cowley Shock Trauma Ctr, Baltimore, MD 21201 USA
[2] Guys & St Thomas NHS Fdn Trust, Kings Hlth Partners, St Thomas Hosp, Dept Adult Crit Care, London, England
[3] Upstate Med Univ, Dept Surg, Syracuse, NY 13210 USA
关键词
ARDS; COVID-19; SARS-CoV-2; TCAV; RESPIRATORY-DISTRESS-SYNDROME; PRESSURE RELEASE VENTILATION; HYPOXIC PULMONARY VASOCONSTRICTION; END-EXPIRATORY PRESSURE; LOW TIDAL VOLUME; MECHANICAL VENTILATION; NONINVASIVE VENTILATION; COVID-19; PNEUMONIA; DRIVING PRESSURE; MORTALITY;
D O I
10.1152/japplphysiol.00742.2020
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 (Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure) and ESICM (European Society of Intensive Care Medicine) Trials Groups have shown that similar to 13% of the mechanically ventilated non-COVID-19 ARDS patients have the type-L phenotype. 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 dysregulation, 2) thrombosis caused by loss of endothelial barrier, 3) endothelial dysfunction causing loss of hypoxic pulmonary vasoconstriction perfusion control, and 4) hyperperfusion of collapsed lung tissue that has been directly measured and supported by a computational model. A flowchart has been constructed highlighting the need for personalized and adaptive ventilation strategies, such as the time-controlled adaptive ventilation method, to set and adjust the airway pressure release ventilation mode, which recently was shown to be effective at improving oxygenation and reducing inspiratory fraction of oxygen, vasopressors, and sedation in patients with COVID-19.
引用
收藏
页码:877 / 891
页数:15
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