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Trying again without typos:
(1/n) While COVID-19 is indeed a humbling disease, this image almost certainly represents a measurement artifact rather than "happy" or "silent" anything. https://twitter.com/srrezaie/status/1291950866946314240
(1/n) While COVID-19 is indeed a humbling disease, this image almost certainly represents a measurement artifact rather than "happy" or "silent" anything. https://twitter.com/srrezaie/status/1291950866946314240
(2/n) An arterial saturation of 23% implies an arterial O2 content <50mL.O2/L, even assuming a normal [Hbg], which is atypical in the types of people at highest risk of severe COVID-19. So the real CaO2 is likely even lower....
(3/n) To maintain a resting VO2 >200mL.O2/min (bare minimum to maintain the described state of "no distress") with a normal cardiac output (HR on monitor of 83) would require 100% extraction of oxygen from the blood (MVO2 of 0%). Such a state is plainly impossible (see attached)
(4/n) In fact, even arterial saturations measured in acclimatized climbers on Everest operating near human performance limits remain in the 40s-50s%. Untrained people brought to similar levels of hypobaric hypoxemia lose consciousness in minutes. (see https://nejm.org/doi/full/10.1056/NEJMoa0801581…)
(5/n) So what's going on? Hard to say without being there, but I wonder whether malperfusion and/or venous pulsations (say from TR, etc.) are causing a venous saturation to be erroneously captured.... https://www.sciencedirect.com/science/article/pii/S095461111300053X#bib4
6/n) In any case, nothing about SARS-CoV-2 gives reason to believe the resultant hypoxemia would behave differently than all hypoxemia that has preceded it - and there is nothing in mammalian physiology that would allow an organism to "silently" tolerate such a state regardless.
