Why a COVID fever is bad

What we may ultimately find is that no one is truly asymptomatic on COVID-19.  But for most people, the walking hypoxia* can be accommodated through usual acid base balance mechanisms.  I always envisage this system by thinking of alcohol intoxication (which leads to hypoventilation) ending in nausea.  Hypoventilation creates excess acid (as CO2) and the body responds by emitting hydrochloric acid. Screenshot_20200425-043700~2

In COVID, dysventilation occurs, with effects ranging from Vasoconstriction to blood pH changes.  Altered pH controls the affinity of Hemoglobin for Oxygen (relative to CO2).  The hypoxia remains happy as long as relatively low levels of CO2 counteract this.

But higher temperatures also reduce the affinity of Hemoglobin for O2.  There are now 2:1 factors shifting the oxygen gradient rather than a balanced pair, and a collapse of compensatory mechanisms ensue.  It might even be that the kidneys’ compensation for respiratory alkalosis contributes to dehydration and fever.

Children are not immune, but they might take it in stride because they are still growing and have little opportunity for oxidative stress to occur.  Oxidative stress is a breakdown of the canonical cellular respiration from carbohydrate to water and CO2.  It increases with age and underlying conditions.  Oxidative stress is also a key to platelet cascades.


Image: detail from https://www.sciencedirect.com/science/article/pii/S1751722211002216

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