Abstract
The review presents the results of experimental and clinical studies and observations. It allows to draw conclusions about the causes and mechanisms of the development of acute respiratory failure in severe COVID-19. The paper compares SARS-CoV-2, MERS-CoV and SARS-CoV. It explores the role of angiotensin-converting enzyme 2 in the pathogenesis of COVID-19, the mechanisms of the development of acute respiratory distress syndrome and hypoxemia, the adverse consequences of hypercytokinemia (cytokine storm), and the neurogenic mechanism of respiratory failure. It is emphasized that the adverse processes in the lungs of patients with COVID-19 are caused not so much by the direct action of the virus, but, rather, by the hyperreactivity of the immune system. The paper also focuses on the ability of SARS-CoV-2 for neuroinvasion, which leads to the spread of infection to the brain stem and structures of the respiratory center. Finally, based on the literature data, it is concluded that the pathogenesis of respiratory failure in COVID-19 has multiple causes and is characterized by diffuse and exudative damage to the alveoli, deterioration of ventilation-perfusion relations, development of fibrosis, thrombus formation, and hypoxemia. It is emphasized that the study of the central, neurogenic mechanisms of respiratory failure as well as their correlation with neurological symptoms contributes to a deeper understanding of the pathogenesis of COVID-19 and may be essential for the prevention and treatment of respiratory failure caused by SARS-CoV-2.
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