Do very deep freedives risk hyperoxia (ppO2>>1.6)?

[bubblemonkey2]

I don't see this topic in search results

What ppO2's are experienced by a deep freediver?
We are taught that a ppO2 above 1.6 ATM is risky, and seizures can be readily observed in the 2.0 to 3.0+ range.

A freediver in freefall might be running a ppO2 over 2.3+ ATM as they descend deeper than 100 metres. (0.21 ATM * 11)
Even if they metabolize some oxygen on the way down, they are still over 2.0 ATM at 100 metres (~0.18 ATM * 11)

Symptoms of hyperoxia in the central nervous system (CNS) include visual disturbances, tinnitus, nausea, twitching, irritability, dizziness, and convulsions
Do any of the 100+ metre freedivers experience this?

Or is there just simply not enough oxygen left in the compressed lungs to do any harm in this regard?
Do their very brief (<30 seconds) forays below 100 metres make them 'immune' to a CNS hit?

Pre-breathing with oxygen or nitrox before a freedive should be even more dangerous according to ox-tox CNS theory.

And what about nitrogen? 3.16 ATM (@30 metres) is considered a limit beyond which narcosis is progressively debilitating.
At 100+ metres, is a freediver experiencing 8.7+ ATM of ppN2?

 

[johndiver999]

Narcosis and bends are issues, not oxygen.

Narcosis occurs very quickly upon descent, most people say the faster you descend the more intense the effect. Freedivers are very significantly compromised in their ability to function at extreme depths due to the narcosis. Difficulty in doing very simple tasks is well known and documented, as it suffering from the bends.

 

[lostsheep]

This is an interesting question , maybe one of the experts can chime in here.

Similarly, how does hypercapnia affect a freediver?

How does depth affect the time a freediver can hold their breath? I used to think smaller volume less time but now that I dive CCR I don’t think that is correct; the number of o2 molecules in our lungs is fixed so volume / depth should be irrelevant.

@Dr Simon Mitchell ?

 

[PatW]

I suppose you could have oxygen toxicity problems. But I think it takes a little time to develop. And I think free divers are generally down less than 5 minutes and most of the time, they are not that deep. Now if you were a sperm whale and stayed down for 30 minutes and went to 2000’, you might have problems. I don’t know, are they Tec certified?

 

[boulderjohn]

The primary reason for oxygen toxicity during a scuba dive is a significant and prolonged increase in the partial pressure of oxygen. This happens because one is breathing compressed gas and inhaling multiples of the amount of oxygen you would inhale on the surface. If you are breathing air (as a free diver would) while on scuba, at 99 FSW, you are at 4 atmospheres of pressure and are therefore inhaling 4 times as many oxygen molecules as you would on the surface. That would give you a partial pressure of 0.21 X 4 = 0.84, which is not remotely considered dangerous. You would have to go to around 200 feet to reach a dangerous partial pressure of oxygen, and then you would have to stay there for a while. That's on scuba, not freediving.

 

[johndiver999]

This is an interesting question , maybe one of the experts can chime in here.

Similarly, how does hypercapnia affect a freediver?

How does depth affect the time a freediver can hold their breath? I used to think smaller volume less time but now that I dive CCR I don’t think that is correct; the number of o2 molecules in our lungs is fixed so volume / depth should be irrelevant.

@Dr Simon Mitchell ?

I don't think that bolded statement is correct?

 

[inquis]

How does depth affect the time a freediver can hold their breath? I used to think smaller volume less time but now that I dive CCR I don’t think that is correct; the number of o2 molecules in our lungs is fixed so volume / depth should be irrelevant.

By "fixed", I'm assuming you mean the number of O2 molecules doesn't increase, so for a fixed metabolism you would think you'd have a fixed amount of time. My understanding is that the time is actually less for a deeper dive, since the urge to breath is directly proportional to the partial pressure of CO2 in the lungs. (Actually, the urge is largely based on the pH of your blood, but again, related.) Partial pressure is equivalent to a density (molecules per volume), volume is dropping, so PCO2 increases faster when descending than at a fixed depth (metabolism alone). A higher PCO2 in the lungs inhibits the removal from your blood/tissues, and you hit your "gotta breath" threshold sooner.

Now there may be some mental aspects that kick in to lower the metabolism rate, so definitely restrict the above comment to the fixed metabolism assumption that I think you were considering.

 

[lostsheep]

I don't think that bolded statement is correct?

I should have said the number of o2 molecules in our body is fixed when we leave the surface and is only reduced by what we metabolize. The rate of O2 metabolizing is not affected by depth and therefore the time we can hold our breaths isn’t reduced.

That said, Inquis brings up a good point about CO2

 

[dmaziuk]

We are taught that a ppO2 above 1.6 ATM is risky, and seizures can be readily observed in the 2.0 to 3.0+ range.

As John said: for prolonged exposure.

Info - Oxygen Toxicity Limits & Symptoms

Oxygen Toxicity Limits & Symptoms Oxygen toxicity limits can be very confusing, especially for PPO2 (Partial Pressure of Oxygen) levels above 1.6 ATA used in chamber-based hyperbaric treatment (recompression) and decompression tables. For example, here is a chart of one of the most common DCS...

scubaboard.com

Calculated risk of pulmonary and central nervous system oxygen toxicity: a toxicity index derived from the power equation

The risk of oxygen toxicity has become a prominent issue due to the increasingly widespread administration of hyperbaric oxygen (HBO) therapy, as well as the expansion of diving techniques to include oxygen-enriched gas mixtures and technical diving. ...

www.ncbi.nlm.nih.gov

 

[Dr Simon Mitchell]

Hello,

A great question by the OP, though the prediction calculations are slightly off. We don't have 21% oxygen in our lung alveoli during normal breathing; it is about 13%. That's because there are gases other than nitrogen and oxygen present (including CO2 and water vapor). A bit of hyperventilation before the dive would increase the oxygen content a bit.

Anyway, the assumption that the pressure of oxygen in the alveoli and arterial blood passing them would increase during a breath-hold descent (even though the diver is not breathing and metabolizing oxygen) is correct. This occurs because the lungs get compressed so you are compressing a (slowly decreasing) number of oxygen molecules into a smaller space.

We confirmed this in a study of an elite breath hold diver who we instrumented with a radial arterial catheter and I took a blood gas specimen when he arrived at 60m / 200' and then another specimen was taken before he breathed on arrival back at the surface. His arterial PO2 increased from about 16 kPA (120 mmHg) at the surface to 43 kPa (322 mmHg) at 200'. This is equivalent to breathing about 50% oxygen at surface pressure. So, this would definitely not bring a danger of oxygen toxicity. Even if you assume that you could double that number for 120 m (~400') it would still not be sufficient to provoke oxygen toxicity.

Parenthetically, the opposite happens during ascent, so that as the lungs expand the alveolar and arterial oxygen levels decrease extremely rapidly (way faster than just holding your breath alone) which creates the risk of hypoxic blackout without warning as the diver approaches the surface.

We published all this in Journal of Applied Physiology. Article attached.

Simon M