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Assessing why COVID-19 can cause silent hypoxia

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To utilize the digital aspect of the investigation, biomedical engineers deployed computer models in order to test out three different scenarios. These were designed to explain how and why the lungs stop providing oxygen to the bloodstream with some patients infected with coronavirus.

It is not fully known why some people become sicker than others when infected with the coronavirus, or why some people experience longer, ongoing symptoms (the so-termed ‘long COVID’ syndrome). What is evident is that as the COVID-19 pandemic has progressed through communities and nations, many survivors of infection will continue to experience a range of health problems. these health problems persist for a long period following the initial infection. More concerning, many survivors with additional complications experience an increased risk of death for the first six months following the initial diagnosis with the virus.

One ill-health effect is hypoxia, which is a condition where the body is deprived of an adequate oxygen supply at the tissue level. Hypoxia is either more generalized in terms of affecting the whole body, or it can local, instead affecting a region of the body. The physiological impact is with headaches and shortness of breath, although more severe cases can be fatal. in coronavirus patients, there is a risk of lasting lung damage. By ‘silent hypoxia’, this refers to the condition whereby a person has reduced pulse oximetry readings without signs of respiratory distress (hence the symptoms being ‘silent’).

In terms of why this is the case, Boston University researchers have discovered that hypoxia is caused by a combination of biological mechanisms. These can occur simultaneously in the lungs of COVID-19 patients. Primarily, the lungs lose the ability to restrict blood flow to damaged tissue. in addition, the lining of blood vessels in the lungs also become inflamed from COVID-19 infection, and this can lead to small blood clots. These factors account for hypoxia.

The research appears in Nature Communications, titled “Modeling lung perfusion abnormalities to explain early COVID-19 hypoxemia.”

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