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https://www.selleckchem.com/products/cu-cpt22.html A significative proportion of patients with pulmonary-related COVID-19 initially present with « silent » or « happy » hypoxemia, a term denoting an absence of dyspnea or other respiratory distress symptoms in face of profound hypoxemia. COVID-19 is a multisystemic disease characterized by the diffusion of SARS-COV-2 through the blood and a widespread secondary immune response. Most of the organs are involved, including the brain and this translates into the development of acute encephalopathy and other complications. Silent hypoxemia and the consequent "vanishing dyspnea" represent a loss of warning signal and may be associated with a rapid clinical worsening and a fatal outcome. In this article, we will describe the physiological basis of ventilation and we will elucidate the different pathophysiological mechanisms underlying the phenomenon of silent hypoxemia in COVID-19.Various neuromuscular complications have been described in SARS-CoV-2 infection, especially Guillain-Barré syndrome (GBS) and Critical Illness neuromyopathy (CI-NM). Two representative cases are discussed below. It appears that GBS shares most of the characteristics of classical post-infectious GBS, but SARS-CoV-2 may contribute to the increased incidence of CI-NM. Other rare complications have been described, including Tapia Syndrome and Kawasaki-like multiple system inflammatory syndrome. The question of vaccination and the risk of immune-mediated neuropathies remains open, but the lack of reported cases is reassuring as these complications usually occur within 6 weeks after vaccination.Among the long-COVID symptoms, neuropsychological sequelae are frequent after an infection by SARS-CoV-2, whatever the severity of the respiratory disease in the acute phase. These deficits seem to result from a neurological disorder, but also from psychiatric symptoms. Not only inflammatory components, which can play a major role in the genesis of the neuropsych

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