Unknown Tourist dead, Dive Master ill - Ambergris Caye, Belize

[DandyDon]

Since the fractions of both O2 and CO are constant, both partial pressures decrease during ascent.

No, not as I understand it. "When carbon monoxide is inhaled, it combines with hemoglobin (an iron-protein component of red blood cells), producing carboxyhemoglobin (COHb), which greatly diminishes hemoglobin's oxygen-carrying capacity. Hemoglobin's binding affinity for carbon monoxide is 300 times greater than its affinity for oxygen." Carbon Monoxide | NIOSH | CDC.

At depth, the increase in PPO can offset the toxicity to an extent, but this decreases at PPO decreases and PPCO doesn't.

 

[dmaziuk]

No, not as I understand it. "When carbon monoxide is inhaled, it combines with hemoglobin (an iron-protein component of red blood cells), producing carboxyhemoglobin (COHb), which greatly diminishes hemoglobin's oxygen-carrying capacity. Hemoglobin's binding affinity for carbon monoxide is 300 times greater than its affinity for oxygen." Carbon Monoxide | NIOSH | CDC.

At depth, the increase in PPO can offset the toxicity to an extent, but this decreases at PPO decreases and PPCO doesn't.

PPCO changes together with PPO2, it's just that CO doesn't matter to metabolism, whereas dissolved O2 does -- at high enough PPO2. This has been explained in dive medicine forums by medical doctors many times.

 

[inquis]

At depth, the increase in PPO can offset the toxicity to an extent

I can't see this being due to ambient pressure because the *inspired* PP of both change in lockstep.

My conjecture is the hemoglobin preferentially releases the O2. Over time, there are fewer and fewer available receptors upon returning to the lungs. (Those available receptors are still filled at the ~300:1 ratio in the lungs. Repeat every pulmonary cycle.) This would result in an increased fraction (and therefore the partial pressure) of CO in the blood. Eventually, there are just not enough O2 molecules being transported. Equivalently, the *dissolved* PO2 is below life-sustaining levels.

I'd say this deteriation is time-dependent, not depth-dependent, and the fact SHTF upon ascent is just because the ascent happens later.

 

[tarponchik]

I can't see this being due to ambient pressure because the *inspired* PP of both change in lockstep.

My conjecture is the hemoglobin preferentially releases the O2. Over time, there are fewer and fewer available receptors upon returning to the lungs. (Those available receptors are still filled at the ~300:1 ratio in the lungs. Repeat every pulmonary cycle.) This would result in an increased fraction (and therefore the partial pressure) of CO in the blood. Eventually, there are just not enough O2 molecules being transported. Equivalently, the *dissolved* PO2 is below life-sustaining levels.

I'd say this deteriation is time-dependent, not depth-dependent, and the fact SHTF upon ascent is just because the ascent happens later.

If the given 300:1 ratio refers to binding constants, then it is PP dependent. So you'll observe the 300:1 occupation ration only when PPO2 and PPCO are equal.

 

[dmaziuk]

Why doesn't oxygen cause decompression sickness?

Out of curiosity what is the tipping point where partial pressure (moles) of O2 is greater than the metabolic capacity? I think you're getting at arterial oxygen content, which is a function of hemoglobin level, O2 saturation (percentage of hemoglobin taken up by O2, normally 95-100%), and...

scubaboard.com

 

[DandyDon]

CO is a odd gas in that not everything is totally understood. It is a complicated issue how it all works, but I am sticking with this basic understanding explained at Safety Is In The Air

Carbon monoxide (CO) is an odourless, colourless and tasteless gas, usually produced by the incomplete combustion of carbon containing compounds.

It is absorbed 200 times more by haemoglobin than oxygen is. This reduces the oxygen carrying capacity and can eventually lead to hypoxia and even death.

The severity of CO poisoning depends on its concentration in the breathing gas and the exposure time. A long exposure to relatively low concentrations can therefore result in serious CO poisoning.

In diving, the partial pressure of CO will increase with depth, and even a low concentration of CO contamination, which at normal atmospheric pressure and after a prolonged exposure time would have no toxic effect, will become dangerous with increasing depth. When descending, the haemoglobin can get saturated with CO, impairing its ability to bind with oxygen, but the increased oxygen partial pressure may also result in enough oxygen in the blood keeping cells oxygenated. During the dive, the decreased oxygen transportation (through the haemoglobin) is also partially compensated by the amount of dissolved oxygen in the blood plasma. But during the ascent, when the partial oxygen pressure is reduced, and the amount of dissolved oxygen also reduces, this can lead to hypoxia. This might be the reason why the symptoms of poisoning may become worse during or after ascent.

 

[TrimixToo]

At a BTS seminar several years ago, Dr. Claudia Sotis* pointed out that O2 dissolves in blood plasma, just like inert gases do. 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. She showed the math. Of course, there are (a) a threshold above which one would effectively have a hard ascent ceiling and (b) different degrees of how much hemoglobin has been bound to CO, which changes that ceiling.

The interesting part of this is that it's one of the reasons she believes CO exposure crises present themselves on ascent. I found her arguments persuasive but cannot find my notes (two or three computers later), I'm afraid.

This is perhaps straying a bit off topic, but I'm not sure how many people have thought about this.

* Yes, I know. But let's leave her husband out of it, shall we? Not pertinent.

 

[tarponchik]

CO is a odd gas in that not everything is totally understood. It is a complicated issue how it all works, but I am sticking with this basic understanding explained at Safety Is In The Air

Phrases like "It is absorbed 200 times more by haemoglobin than oxygen is" make me wonder, who wrote this? A specialist in Medieval French poetry or a pro bassoon player, maybe? What does this actually mean? This is utter nonsense, like "a magpie has two wings, especially the left one".

 

[inquis]

If the given 300:1 ratio refers to binding constants, then it is PP dependent. So you'll observe the 300:1 occupation ration only when PPO2 and PPCO are equal.

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.

The issue that I see is there must be (my opinion) a decreasing number of available receptors as time goes on. Whether one ascends or not does not impact that.

 

[tarponchik]

At a BTS seminar several years ago, Dr. Claudia Sotis* pointed out that O2 dissolves in blood plasma, just like inert gases do. 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. She showed the math. Of course, there are (a) a threshold above which one would effectively have a hard ascent ceiling and (b) different degrees of how much hemoglobin has been bound to CO, which changes that ceiling.

The interesting part of this is that it's one of the reasons she believes CO exposure crises present themselves on ascent. I found her arguments persuasive but cannot find my notes (two or three computers later), I'm afraid.

This is perhaps straying a bit off topic, but I'm not sure how many people have thought about this.

* Yes, I know. But let's leave her husband out of it, shall we? Not pertinent.

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.