Is Carotid Body Infection Responsible for Silent Hypoxemia in COVID-19 Patients?

Abstract

The pathogenic mechanisms underlying the symptomatology
\nof coronavirus disease 2019 (COVID-19) patients are not well understood. An atypical and bewildering clinical manifestation
\nfound in many COVID-19 patients is that they exhibit severe
\nhypoxemia, with arterial levels of oxygen (O2) tension even below 50 mmHg, without clear signs of distress (dyspnea) or significant acceleration of breathing.1,2 Under these conditions,
\npatients with COVID-19 pneumonia may decompensate and as
\na consequence undergo a rapid deterioration of their clinical
\nstate that can eventually lead to death. The pathophysiology of
\nthis so-called “silent hypoxemia”3 or “happy hypoxia” is unknown.1,3,4 A decline in arterial O2 tension is normally detected
\nby O2-sensing cells in the carotid body (CB), the main arterial
\nchemoreceptor, which rapidly activates sensory fibers impinging on neurons in the brainstem to induce compensatory hyperventilation and increased heart rate. In this way, both O2 uptake
\nand its distribution to the tissues are enhanced. Bilateral removal of the CB in humans leaves individuals unaware of hypoxemia, with complete abolition of the hypoxic ventilatory
\nresponse.5 Therefore, inhibition of CB responsiveness to hypoxia could be a plausible explanation for the impaired respiratory drive and reduced dyspnea that characterizes the “silent
\nhypoxemia” observed in COVID-19 patients

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