Repetitive Nitrox Dives and O2 Clock

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I think PADI is just trying to simplify the issue as in practice it is difficult to exceed the 24 hour NOAA limit at a 1.6 PPO2 and virtually impossible at a 1.4 PPO2 as NDL's impose a limit long before total O2 exposure does.

I'd encourage you to plan several repetitive nitrox dives and see where you go both in terms of nitrogen loading and the CNS clock to get a feel for how the two add up. If you do that you will see that you'd really have to work at it to blow the total exposure limit with recreational no decompression nitrox diving.

For decompression divers, especially those at deeper depths and using accellerated deco at a 1.6 PPO2 for long periods, it is a different story. In those cases many divers will be figuring percentages for each dive and taking half life into account rather than relying on a NOAA chart.
 
I posted this a few weeks ago; it applies here as well:
---
Viewing oxygen in terms of "half life" is a bit of a red herring, because oxygen physiology and inert gas physiology are so very different.
In the first place, when the oxygen pressure in the breathing gas is reduced, high oxygen tissue tensions are extremely short-lived because oxygen is both metabolized by the cells and scavenged constantly by hemoglobin. In other words, as soon as the inspired oxygen pressure drops to anywhere near normal, excess oxygen is very quickly used or removed - it is no longer "free," and oxygen tissue tensions very quickly return to normal. This is not the case with inert gasses (Nitrogen or Helium) which depend on pressure gradients to move them out of the tissues, through the circulation to the lungs for elimination through breathing.
In the second place, inert gas damage to tissue doesn't occur simply due to high "loads," and if damaging bubbles can be avoided by sound decompression profiles then long-term and/or high exposures to inert gas don't do any damage. Not so with oxygen - it is the mere presence of high oxygen levels in the tissues that causes damage (injury), and that damage continues to build and get worse with exposure time - in other words there is no "saturation" point at which the damage will stop.
To distill the complex into the simple, the easiest way to view the difference is this:
For inert gasses, the surface interval is for offgassing.
For oxygen, the surface interval is for healing.
Very different animals
Rick
---
Rick
 
jiveturkey:
Is this an issue for me at this point, doing only non-deco dives with mixes under 40%? I haven't noticed my body reacting in anyway really.

In short, Yes it is an issue. Keep monitoring and paying attention to your body without becoming paranoid.

To further explain:
Although we don't refer to them as such all dives are decompression dives. That is a diver's body is subject to the effects of increased water pressure and breathing compressed gas on all dives. On what we call NDL dives these effects are adequately coped with by observing rate of ascent limits and "safety stops". The effects become serious enough on other dives that formal planning is needed to insure adequate decompression. So, just because you are doing relatively shallow and short duration dives doesn't mean they are without risk, or that the pressure and gas effects can be ignored.

Basic nitrox diving is limited to 40% mixes as much for mechanical reasons as anything else. Oxygen itself doesn't burn. What it does is lower the ignition temperature of flammable items it surrounds. Without going into detail that is why over that percentage a diver's kit needs to be Oxygen Clean. Plus, once a diver is using over 40% MODs start getting very shallow. That places in increased premium on good planning and good bouyancy control even when in rough seas.

Unfortunately although we do pretty well understand the underlying science; its' application to diving and to each individual diver's body is very much an art. That makes each of us an artist responsible for our own creation.
 
The rules may have been changed for some agencies for recreational diving within the NDL limits because DAN concluded you cannot reach the whole body exposure limit unless you are doing deconpression diving. Of course the CNS limits must still be tracked and observed.


from: http://www.si.edu/dive/ds_research.htm
Lang, M.A. (ed) 2001. DAN Nitrox Workshop Proceedings. Divers Alert Network, Durham, N.C., 197p.Available from Divers Alert Network (919) 684-2948Workshop Recommendations:
  • No evidence was presented that showed an increased risk of DCS from the use of oxygen enriched air (nitrox) versus compressed air.
  • A maximum PO2 of 1.6 atm was accepted based on its history of use and scientific studies.
  • Routine CO2 retention screening is not necessary.
  • Oxygen analyzers should use a controlled-flow sampling device.
  • Oxygen analysis of the breathing gas should be performed by the blender and/or dispenser and verified by the end user.
  • Training agencies recognize the effectiveness of dive computers.
  • For recreational diving, there is no need to track whole body exposure to oxygen (OTU/UPTD).
  • Use of the "CNS Oxygen Clock" concept, based on NOAA oxygen exposure limits, should by taught. However, it should be noted that CNS Oxygen toxicity could occur suddenly and unexpectedly.
  • No evidence was presented, based on history of use, to show an unreasonable risk of fire or ignition when using up to 40% nitrox with standard scuba equipment. The level of risk is related to specific equipment configurations and the user should rely on the manufacturer's recommendations
{emphasis is mine}

Ralph
 
Rick Murchison:
I posted this a few weeks ago; it applies here as well:
---
Viewing oxygen in terms of "half life" is a bit of a red herring, because oxygen physiology and inert gas physiology are so very different.

In the first place, when the oxygen pressure in the breathing gas is reduced, high oxygen tissue tensions are extremely short-lived because oxygen is both metabolized by the cells and scavenged constantly by hemoglobin. In other words, as soon as the inspired oxygen pressure drops to anywhere near normal, excess oxygen is very quickly used or removed - it is no longer "free," and oxygen tissue tensions very quickly return to normal. This is not the case with inert gasses (Nitrogen or Helium) which depend on pressure gradients to move them out of the tissues, through the circulation to the lungs for elimination through breathing.
.......

For inert gasses, the surface interval is for offgassing.
For oxygen, the surface interval is for healing.
Very different animals
But there are an awful lot of very different animals in this world that exhibit exponential decay.

I don't think anybody is trying to say that the 90 minute half life decay has anything to do with dissolved gas. Now THAT would be a red herring.

OTOH, exponential decay is a very common behavior pattern of physical systems, ranging from radioactive decay, to cooling of hot objects, to discharge of the voltage on a capacitor by a resistor. None of these involve offgassing. Exponential decay is also very common in chemical reactions, and it might very well be that the effect on the nervous system / body chemistry is why experiments measuring O2 sensitivy have shown such a halflife/exponential decay response.

Exponential decay of CNS toxicity buildup is an experimental observation, not a red herring.
 
jiveturkey:
I've also seen some discussions on here regarding the half life of o2. Any links for more information on this?

Modeling pulmonary and CNS O2 toxicity and estimation of parameters for humans .... "The power expression for cumulative oxygen toxicity and the exponential recovery were successfully applied to various features of oxygen toxicity". Not real human tests, but instead extrapolations from tests on rats. "The recovery time constant for CNS oxygen toxicity was calculated from the value obtained for the rat, taking into account the effect of body mass, and yielded the recovery equation: Kt = Ke × e^(-0.079t), where Kt and Ke are the values of K at time t of the recovery process and at the end of the hyperbaric oxygen exposure, respectively, and t is in minutes. "
( -0.079/min is a time constant of 13 minutes, or halflife of 9 minutes.)

This report seems consistent with the anectdotal reports of the successful use of airbreak on the order of 5 or 10 minutes during extended decompression stops at high ppO2.

I think the rat study they used is this one.

I found various other references to some work in Israel, but couldn't find any abstracts or texts online. http://maritime.haifa.ac.il/cms/newslett/cms24/cms24_17.htm

Another entry, not oxtox related, on the publications list by Dan Kerem caught my attention: "Study of the Alleged Side-benefits of Nitrox Breathing in Divers
The claims that Nitrox reduces narcosis and alleviates post-dive fatigue are studied in divers unaware of the composition of their breathing mixture. The research was carried out in cooperation with Adi Gonen, Israeli Naval Medical Institute and Stephen Breitstein, CMS."
 
As pointed out in the various posts there have been precious few studies of EAN effects on humans. And the few that have been done have either been very limited or have been deficient in their constrction.

For example, a study of the effects of EAN on the human body was reported by DAN. If memory serves, that study was a randomized, double-blind study using EAN and Air. That was good as far as it went. But the study failed when it reported how the divers felt instead of measured changes in the diver's chemistry or vital signs Feelings are a very poor measure of EAN's value, or lack of value.

So, given this lack, why use EAN and what precautions should someone take? The answer to me is pretty clear.

-For a given length dive there will be less nitrogen in a diver's system using EAN than air. There is no dispute about that being a good thing.
-Even with the lack of empirical studies we have enough anecdotal and experiental information to know that within the limits specified by NOAA and the Certifying Agencies there is little or no risk to the individual diver in using EAN.
-Each diver must pay attention to how EAN affects them, individually while staying within limits. That is unless the individual wants to conduct a biological experiment on themself.
 

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