“Your Blood is Black”: My ME/CFS Experience with HELP Apheresis in Germany

[LarsSG]

More or less would suggest something is out of homeostatic control. Why the arterial O2 sats should be normal and the peripheral venous O2 sats very low is the question though. If it were simply a matter of "microclots are impairing oxygen transfer" that doesn't easily hold. Why wouldn't there be a similar problem on the pulmonary side so that lung capillaries weren't allowing oxygen to be onloaded, and so make for low arterial sats? I wonder whether the observation might indicate a contribution from circulating lymphocytes (metabolically reprogrammed) in the venous blood pool using more O2 - but I don't know if that's possible or whether it could explain this degree.

Naive perspective here, but the oxygen has to go somewhere, doesn't it? So if the theory is normal arterial oxygen and low venous oxygen, then you would pretty much have to find higher venous carbon dioxide and higher exhaled carbon dioxide than you would expect for a given effort, which I feel like we would have already seen in CPET results. I suppose you could have some level of build up of carbon dioxide in the blood (which would then lead to the dyspnea that some observe), but that seems like it would be fairly limited and only on a short time scale (and surely we would have seen that by now in blood pH).