Happy hypoxia is one of the physiopathological characteristics of Covid-19 that has most baffled the scientific and medical community.
For a normal person, the blood oxygen saturation level (the amount of hemoglobin carrying oxygen) is around 95 percent or more. Hypoxemia is a condition in which the blood saturation levels drop below 94 percent.
Patients with blood oxygen levels below 90 percent, which is considered too low, may experience symptoms like shortness of breath and chest pain.
They may need oxygen therapy. If blood oxygen levels continue to fall, their organs may shut down, which could be life threatening. However, despite low blood oxygen levels, some Covid-19 patients do not feel any symptoms and feel fine, until eventually, they collapse.
This unusual phenomenon gave rise to the term “silent hypoxemia” or “happy hypoxia.”
Patients with this condition often suffer a sudden imbalance, reaching a critical state that can be fatal.
Researchers and doctors have been trying to understand the causes of happy hypoxia in Covid-19 patients.
Now, researchers from the University of Seville in Spain have come up with an explanation for the condition.
They say that infection in carotid bodies by SARS-CoV-2, the virus responsible for the pandemic, may be the cause of the decreased blood oxygen levels in many Covid-19 cases.
Carotid bodies are sensory organs located on either side of the neck next to the carotid artery.
They detect the drop in blood oxygen and send signals to the brain to stimulate the respiratory centre.
In their study, detailed in the journal Function, the researchers suggest that infection of this carotid body by SARS-CoV-2 in the early stages of the disease could alter its ability to detect blood oxygen levels, resulting in the silent drop in oxygen in the arteries.
They have also found a high presence of the enzyme ECA2, the protein the coronavirus uses to infect human cells, in the carotid body.
The hypothesis support the use of activators of the carotid body independent of the oxygen sensing mechanism as respiratory stimulants in patients with Covid-19.
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