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

Abstract

The pathogenic mechanisms underlying the symptomatology of coronavirus disease 2019 (COVID-19) patients are not well understood. An atypical and bewildering clinical manifestation found in many COVID-19 patients is that they exhibit severe hypoxemia, 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, patients with COVID-19 pneumonia may decompensate and as a consequence undergo a rapid deterioration of their clinical state that can eventually lead to death. The pathophysiology of this so-called “silent hypoxemia”3 or “happy hypoxia” is unknown.1,3,4 A decline in arterial O2 tension is normally detected by O2-sensing cells in the carotid body (CB), the main arterial chemoreceptor, 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 and 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 response.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 hypoxemia” observed in COVID-19 patients