Woman dead, husband injured on 230 meter dive - Greece

[Duke Dive Medicine]

At last year's BTS, Dr. Sotis explained that at higher ambient pressures, sufficient O2 dissolves in the blood plasma to support the body's needs without any hemoglobin transport at all (with the numbers to show it). IIRC, this is linearly proportional to depth. However, as one ascends, the amount of dissolved O2 decreases, and one depends to a progressively greater extent on hemoglobin transport. Thus, CO problems often present on ascent even though we normally change to progressively higher PPO2 as we go. The higher PPO2 cannot compensate for the lower ambient pressure, the O2 reaching the tissues drops, and you pass out.

It takes an inspired oxygen partial pressure of nearly 3 ATA in order for the arterial oxygen content to increase to the point that deoxygenation of hemoglobin isn't necessary. That is not duplicated under normal diving conditions. Also (r/t John's comment), CO does in fact cause tissue damage by binding to citochrome C oxidase in the mitochondria (the metabolic organs of the cells) and disrupting cellular metabolism. It also binds to myoglobin in the muscle cells. This is why the carboxyhemoglobin level in a poisoning victim is a poor predictor of outcome. In practice, some CO toxicity effects could be overcome by hyperoxia while diving, but as more CO is bound to the molecules described above, this effect would be rapidly negated.

Best regards,
DDM

 

[boulderjohn]

. Also (r/t John's comment), CO does in fact cause tissue damage by binding to citochrome C oxidase in the mitochondria (the metabolic organs of the cells) and disrupting cellular metabolism. It also binds to myoglobin in the muscle cells. This is why the carboxyhemoglobin level in a poisoning victim is a poor predictor of outcome. In practice, some CO toxicity effects could be overcome by hyperoxia while diving, but as more CO is bound to the molecules described above, this effect would be rapidly negated.

Thanks--I stand corrected.

 

[TrimixToo]

It takes an inspired oxygen partial pressure of nearly 3 ATA in order for the arterial oxygen content to increase to the point that deoxygenation of hemoglobin isn't necessary. That is not duplicated under normal diving conditions. Also (r/t John's comment), CO does in fact cause tissue damage by binding to citochrome C oxidase in the mitochondria (the metabolic organs of the cells) and disrupting cellular metabolism. It also binds to myoglobin in the muscle cells. This is why the carboxyhemoglobin level in a poisoning victim is a poor predictor of outcome. In practice, some CO toxicity effects could be overcome by hyperoxia while diving, but as more CO is bound to the molecules described above, this effect would be rapidly negated.

Best regards,
DDM

And, going back to read my notes, that's what she said as well (3 ATA to replace Hb transport entirely), so it looks as though you're working from the same set of numbers. But in normal diving, I would think this is still pertinent. At PPO2s in the normal range for technical diving, isn't the amount of O2 dissolved in plasma in the 100-150/minute range? This would seem to compensate for a 50% or so deficit in Hb transport, and lead to LOC on ascent for CO hits (her main point).

 

[KevinNM]

It takes an inspired oxygen partial pressure of nearly 3 ATA in order for the arterial oxygen content to increase to the point that deoxygenation of hemoglobin isn't necessary. That is not duplicated under normal diving conditions. Also (r/t John's comment), CO does in fact cause tissue damage by binding to citochrome C oxidase in the mitochondria (the metabolic organs of the cells) and disrupting cellular metabolism. It also binds to myoglobin in the muscle cells. This is why the carboxyhemoglobin level in a poisoning victim is a poor predictor of outcome. In practice, some CO toxicity effects could be overcome by hyperoxia while diving, but as more CO is bound to the molecules described above, this effect would be rapidly negated.

Last I knew there really wasn’t any effective treatment for serious CO poisoning. Hyperbaric oxygen was as good as it got, and it wasn’t that good. Is there another more effective treatment these days?

 

[Duke Dive Medicine]

And, going back to read my notes, that's what she said as well (3 ATA to replace Hb transport entirely), so it looks as though you're working from the same set of numbers. But in normal diving, I would think this is still pertinent. At PPO2s in the normal range for technical diving, isn't the amount of O2 dissolved in plasma in the 100-150/minute range? This would seem to compensate for a 50% or so deficit in Hb transport, and lead to LOC on ascent for CO hits (her main point).

John,

What units are you using? In a diver with healthy lungs the arterial pO2 at an inspired pO2 of 1.6 ATA would be over 700 mmHg. Under a very specific set of circumstances that would be possible, but I wouldn't make a blanket statement or use loss of consciousness on ascent to diagnose CO poisoning.

Best regards,
DDM

And, going back to read my notes, that's what she said as well (3 ATA to replace Hb transport entirely), so it looks as though you're working from the same set of numbers. But in normal diving, I would think this is still pertinent. At PPO2s in the normal range for technical diving, isn't the amount of O2 dissolved in plasma in the 100-150/minute range? This would seem to compensate for a 50% or so deficit in Hb transport, and lead to LOC on ascent for CO hits (her main point).

John,

I'm not sure what units you're working in. Arterial pO2 is expressed in mmHg and not as a function of time.

That aside, what you're saying is theoretically possible under a very specific set of circumstances, but unconsciousness on ascent is not diagnostic for CO poisoning and I don't think there are any data to support the statement that CO poisoning in divers often presents on ascent.

Best regards,
DDM

 

[Duke Dive Medicine]

Last I knew there really wasn’t any effective treatment for serious CO poisoning. Hyperbaric oxygen was as good as it got, and it wasn’t that good. Is there another more effective treatment these days?

Kevin,

Hyperbaric oxygen therapy is effective for severe CO poisoning. The UHMS website has some information:

Carbon Monoxide Poisoning - Undersea & Hyperbaric Medical Society

I don't know of a more effective treatment.

Best regards,
DDM

 

[RayfromTX]

I don't think there are any data to support the statement that CO poisoning in divers often presents on ascent.

Best regards,
DDM

Another factoid from my OW class shot to hell.

 

[TrimixToo]

John,

What units are you using? In a diver with healthy lungs the arterial pO2 at an inspired pO2 of 1.6 ATA would be over 700 mmHg. Under a very specific set of circumstances that would be possible, but I wouldn't make a blanket statement or use loss of consciousness on ascent to diagnose CO poisoning.

Best regards,
DDM


John,

I'm not sure what units you're working in. Arterial pO2 is expressed in mmHg and not as a function of time.

That aside, what you're saying is theoretically possible under a very specific set of circumstances, but unconsciousness on ascent is not diagnostic for CO poisoning and I don't think there are any data to support the statement that CO poisoning in divers often presents on ascent.

Best regards,
DDM

Please understand that I am not trying to make the argument, just relay it. She was not talking about arterial PO2 pressure, but about how much O2 can be transported to tissues via blood plasma at different pressures. What my notes say is that one needs about 250cc/minute of O2 (perhaps the depth-appropriate equivalent amount at 1 ATA), and that at 2 ATA PP02 about 100cc/minute can be dissolved in plasma and transported that way, and that at 3 ATA, about 300 cc/minute can be. These units seem wrong in retrospect (something like grams of O2/minute would be better...I think). As I understood the main point, it was that if some percentage of Hb were bound to CO, it could be replaced by dissolved O2 in the plasma until the *amount* (not PO2) of dissolved O2 declined due to the ascent so that the algebraic sum of transported O2 dropped below that 250cc/minute (presumably at 1 ATA) value. It's quite possible I misunderstood the details or mistranscribed the units, and I cannot find the presentation posted anywhere. However, the main point, which is that CO poisoning can often present on ascent, was clear enough.

You could always contact her for clarification...or I could ask her to send me or post the presentation.

 

[Duke Dive Medicine]

Another factoid from my OW class shot to hell.

Sorry! It’s not impossible and the mechanism is interesting to think about. Risking a hijack here so maybe if there’s more to add there should be a separate thread.

Best regards,
DDM

 

[Kay Dee]

Thank you for comprehending and re-articulating my original intent.

With all due respect to others, it wasn't very hard to do to make that 'leap'. Duh!

As I said elsewhere, maybe some of the folks here with an ingrained christian / judeo background should ponder the words of the 11th century Buddhist sage Milerapa "Life before death, life after death, and death itself – regard all three as one and believe this; all three are one single continuous path of life, which is subject to change and transience."