Some COVID-19 patients with severe pneumonia have spoken or read at ease with so little oxygen in their blood that medical science recommends that they should pass out. It is an extremely dangerous condition, as it may result in the patient's death.
Researchers from the University of Seville (Spain) believe that the non-breathless but extremely low blood oxygenation level of some COVID-19 patients is due to infection by SARS-CoV-2 of the cervical glomerulus, informs the journal Function .
So-called silent hypoxemia, also known as "happy hypoxia", is one of the physiopathological features of COVID-19 that surprised scientists and doctors alike the most.
Decreased arterial oxygen levels (hypoxemia) usually cause a subjective feeling of breathlessness and rapid breathing (which increases the body's absorption of oxygen). It's more or less the same feeling as when you put on a lot of effort. Meanwhile, some COVID-19 patients with severe pneumonia spoke or read calmly, with so little oxygen in their blood that current medical knowledge is that they should pass out.
We recommend: The Neanderthal gene protects against the severe course of COVID-19. New research
The reflex acceleration of breathing and the feeling of shortness of breath are caused by the cervical lobules - round formations with a diameter of about 4-6 millimeters, lying on both sides of the neck at the bifurcation of the common carotid artery. They are sensitive to rising carbon dioxide levels (hypercapnia), falling oxygen levels (hypoxemia) and acidosis, and via the glossopharyngeal nerve branch they send signals to the brain to stimulate the respiratory center.
A group of researchers from the University of Seville, led by Dr. Javier Villadi, Dr. Juan José Toledo-Aral and Dr. José López-Barneo, specialists in the physiopathology of the cervical glomerulus, suggested in the journal Function that "silent hypoxemia" in cases of COVID -19 can be caused by infection of this organ with the coronavirus (SARS-CoV-2).
Good to know: Dyspnoea - causes. What causes breathlessness?
The hypothesis is based on the results of experiments that revealed a high presence of the ECA2 enzyme in the cervical glomerulus,a protein used by the coronavirus to infect human cells. In COVID-19 patients, the coronavirus is circulating in the blood. Therefore, researchers suggest that infection of the human carotid lobe by SARS-CoV-2 in the early stages of the disease may alter its ability to detect oxygen levels in the blood, resulting in its inability to "notice" a drop in oxygen in the arteries.
Confirmation of this hypothesis, which is currently being tested in new experimental models, would justify the use of oxygen-independent carotid activators as respiratory stimulators in patients with COVID-19.