Preprint Hypothesis Version 2 Preserved in Portico This version is not peer-reviewed

The Role of Alveolar Edema in COVID-19

Version 1 : Received: 19 April 2020 / Approved: 20 April 2020 / Online: 20 April 2020 (08:30:29 CEST)
Version 2 : Received: 11 February 2021 / Approved: 11 February 2021 / Online: 11 February 2021 (11:40:30 CET)

A peer-reviewed article of this Preprint also exists.

Journal reference: Cells 2021, 10, 1897
DOI: 10.3390/cells10081897


The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threatening hypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation-perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (alcohol-oxygen vapor therapy and fluid management) may be great helpful for reducing occurrence of severe cases. Given that late mechanical ventilation may cause mucus (edema fluid) to be blown to the deep of the small airways, oxygen therapy should be given at the early stages. The optimal time and SpO2 threshold for oxygen therapy are also discussed.


SARS-CoV-2; acute respiratory distress syndrome; hypoxic pulmonary vasoconstriction; alveolar edema; early low-flow oxygen



Comments (1)

Comment 1
Received: 11 February 2021
Commenter: Shu Yuan
Commenter's Conflict of Interests: Author
Comment: Hypoxemia in patients with acute altitude sickness occurs through different pathophysiological mechanisms. Thus, the comparison between altitude sickness and COVID-19 has been removed, including the diagram in Figure 1.On 28 September 2020, Herrmann et al. published a research article on Nature Communications, which modeled lung perfusion abnormalities and suggested that early COVID-19 hypoxemia may be mainly attributed to severe ventilation-perfusion mismatch. Thus, the pathophysiological mechanisms behind COVID-19 proposed in the manuscript has been revised according to this reference (Figure 1 has also been revised).In previous version, we suggested early oxygen inhalation. However, increasing inspired oxygen results in enhanced oxygenation, but does not improve the ratio of arterial oxygen tension to fractional inspired oxygen (PaO2:FiO2). Simple oxygen therapy would not achieve adequate effects on alveolar edema clearance. In this revision, we propose that treatments to pulmonary edema (alcohol-oxygen vapor therapy and fluid management) may be great helpful for reducing occurrence of severe cases.In references, most review articles have been replaced by the primary sources, when possible.
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