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Updated: Jul 2, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Pathophysiology of silent hypoxia in COVID-19: Truth and mystery
Abrar S Alsulami1, Hayder M Al-Kuraishy2, Ali I Al-Gareeb2
1Department of Microbiology, College of Medicine, Taif University, Taif, Saudi Arabia.
Abstract:
Coronavirus disease 2019 (COVID-19) is a highly infectious viral disease caused by the SARS-CoV-2. COVID-19 commonly leads to mild flu-like illness in most of cases. However, severe COVID-19-induced pneumonia and associated acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) may lead to ventilation-perfusion mismatch and the development of silent hypoxia. Silent hypoxemia is observed in critically COVID-19 patients without signs of subjective dyspnea that is often linked with poor clinical outcomes. Proposed mechanisms include impairment of peripheral carotid chemoreceptors, attenuation of the sensitivity of the respiratory center, and the development of acute vascular distress syndrome (AVDS). However, it should be noted that while AVDS is supported by imaging and pathological evidence, the roles of carotid body dysfunction and other proposed mechanisms remain incompletely validated and require further investigation. The pathophysiology of silent hypoxia in COVID-19 and other viral infections is a complex condition. Accordingly, this review aims to explain and discuss the pathophysiology of silent hypoxia, and its critical role in COVID-19.
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