So let's talk some basic pulmonary physiology here so we can communicate better on this forum. In arterial blood, 98.5% of O2 is bound to hemoglobin Hgb. It contains a porphyrin structure containing iron in its center which binds to O2. 1.5% of O2 dissolved in blood is not bound to Hgb. This is known as PO2. O2 sat % is the amount of hemoglobin with O2 bound to it. With a healthy person this is usually around 99%.
O2 binds to Hgb in the deoxygenated pulmonary arterioles as it is absorbed in the pulmonary alveoli. Hgb carries O2 peripherally thru the arterial blood supply to tissue were it is delivered/unloaded for oxidative phosphorylation or energy metabolism.
The relationship of PO2 to Hgb saturation has been thoroughly described. This is known as the O2/Hgb dissociation curve. Shown above. If one plots PO2 on X-axis and Hgb saturation on Y-axis, there is a sigmoidal shape to the curve. The critical level of PO2 is 60 mm Hg or 90% saturation. Below PO2 60mm Hg there is a precipitous decline in Hgb saturation %. Hence it is why it is so important in oxygen therapy to keep PO2> 60. Above PO2 60, the Hgb saturation curve is flat. Hence there is no need to drive PO2 > 80-90 mm Hg, as Hgb sat % peaks at 100%.
Certain disease states can shift the curve left and right. Shown above. Carboxy Hgb or carbon monoxide poisoning is a classic example of shifting the curve left. Hgb binds more avidly to O2 and less O2 is delivered peripherally to tissues, leading to peripheral ischemia. Sepsis is a classic example of the curve shifting to the right, unloading O2 easier peripherally during stress.
In COVID-19 patients PO2 is low due to pulmonary type 2 cell injury, inflammation and ARDS like physiology as we've discussed. I theorize that if COVID-19 is interfering with porphyrin O2 binding it is doing its damage peripherally in tissues and organs. Not in the lung primarily. Hence shifting the curve left, when it should be shifted right.
Hope that helps to understand.
