Welcome to ScubaBoard, the world's largest scuba diving community. Registration is not required to read the forums, but we encourage you to join. Joining has its benefits and enables you to participate in the discussions.
Benefits of registering include
Agreed, and the general statements don't give that sort of detail; it seems reasonable to assume that is at equal fractions (or partial pressures). So the actual take-up ratio depends on the ratio of the fractions in the tank, which is constant regardless of depth.
Actually, O2 is more soluble in water than N2 or inert gases, you can check the data available. The likely explanation for the CO/ascent phenomena can be hidden in the text you just printed. As PPO decreases during the ascent, so does the concentration of the dissolved O2, and this ruins the bypass mechanism of the O2 transport via O2 solubility.
I didn't mean to imply greater or lesser solubility, since I don't recall it being discussed and didn't look it up, so I plain don't know. I don't think it's hidden in what I wrote, which was mean to describe it. Perhaps I could have done that better (shrug). Your last sentence is precisely on point.
Dr Simon Mitchell has addressed this. The required PO2 levels for plasma to carry a reasonable amount of O2 is toxic (CNS).
And to clarify, this will be true only at equilibrium. Since it is very likely that the off rate of CO is extremely slow (think of the CO-treated ground beef that stays bright red on the shelf in a grocery for a month at least), it is unlikely that equilibrium state will be reached during a scuba dive and it is safe to assume that any CO absorbed by haemoglobin will stay absorbed forever.
I was referring to your phrase "there are depth/PPO2 combinations at which the dissolved O2 can deliver enough to the cells to offset the deficit caused by CO having bound to hemoglobin."
See @dmaziuk's post above, #207.
CO2 poisoning: Hypercapnia, also known as hypercarbia, is a condition where there is too much carbon dioxide (CO2) in the blood. It's caused by the body not being able to expel enough CO2 when it exhales. This can happen when there's insufficient oxygen respiration, or when breathing is repeatedly interrupted, such as during sleep apnea. Hypercapnia is defined as the PaCO2 being greater than 42 mm Hg. If the PaCO2 is greater than 45 mm Hg, and the PaO2 is less than 60 mm Hg, a patient is said to be in hypercapnic respiratory failure. Immediately Dangerous to Life or Health (IDLH) 50,000 ppm (5.0%) Strong respiratory stimulation, dizziness, confusion, headache, shortness. of breath. 80,000 ppm (8.0%) Dimmed sight, sweating, tremor, unconsciousness, and possible DEATH.
So as I understand what Simon wrote in that post, he is saying that dissolved O2 alone cannot fully replace Hb transport. I don't think what Dr. Sotis said or what I wrote contradicts that. If Hb transport is impaired enough to make a deficit in the amount of O2 required by the tissues, there are combinations of PPO2 and depth for which dissolve O2 can make up that deficit that are nontoxic. Maybe that's a narrow range--I didn't do the math--but it should nonetheless exist. Her essential point was that if you fall into this range your symptoms will most likely present on ascent because you can ascend out of it. If the required PPO2 is over 1 ATA, you will certainly fall out of it before the surface.
