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Tytuł pozycji:

Functional Pathophysiology of SARS-CoV-2 Induced Acute Lung Injury and Clinical Implications.

Tytuł :
Functional Pathophysiology of SARS-CoV-2 Induced Acute Lung Injury and Clinical Implications.
Autorzy :
Habashi NM; Adams Cowley Shock Trauma Center, University of Maryland, Baltimore, United States.
Camporota L; Department of Adult Critical Care, Guy's and St Thomas' NHS Foundation Trust, United Kingdom.
Gatto LA; SUNY Cortland.
Nieman GF; Department of Surgery, SUNY Upstate Medical University, United States.
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Źródło :
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2021 Jan 14. Date of Electronic Publication: 2021 Jan 14.
Publication Model :
Ahead of Print
Typ publikacji :
Journal Article
Język :
Imprint Name(s) :
Original Publication: Bethesda, MD : American Physiological Society, c1985-
Contributed Indexing :
Keywords: ARDS; COVID-19; SARS-CoV-2; TCAV
Entry Date(s) :
Date Created: 20210114 Latest Revision: 20210114
Update Code :
Czasopismo naukowe
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 FiO 2 , vasopressors, and sedation in COVID-19 patients.

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