Deco stops

[Dr Deco]

Dear Readers:

To my knowledge, there is not any experimental evidence that gas exchange in the lungs is adversely affected by these oxygen partial pressures and these exposure times. The explanation given by Mr Irvine in the attachment is more of a hypothesis than a laboratory-tested fact.

If oxygen makes the decompression longer (or air shortens it), than the explanation almost assuredly will not come from alveolar gas exchange. The off gassing of the slower compartments is only minimally affected by the slight variations in the alveoli. Redundancy is high in this organ and exchange is very good. Any nitrogen “leaking” through and appearing in the arterial circulation would but minimally influence the off gassing of a slow tissue.

This is something that we at NASA have examined as well as many others.

Dr Deco :doctor:

 

[wb416]

Dr Deco once bubbled...
Dear Readers:

To my knowledge, there is not any experimental evidence that gas exchange in the lungs is adversely affected by these oxygen partial pressures and these exposure times. The explanation given by Mr Irvine in the attachment is more of a hypothesis than a laboratory-tested fact.

[snip]

Isn't the reduction in the lung's "Vital Capacity" due to prolonged pure O2 exposure measurable with tools like the spirometer?

There is also a tool in use that tries to predict the reduction in vital capacity:

%change in VC=-.01(pO2-0.5)t

Subsequently, wouldn't it follow that if the measurable Vital Capacity of an individual decreases due to prolonged pure O2 exposure, that the ability to "off-gas" might also be effected?

Thanks for your comments,
wb

 

[Saturation]

cwb once bubbled...


Isn't the reduction in the lung's "Vital Capacity" due to prolonged pure O2 exposure measurable with tools like the spirometer?

There is also a tool in use that tries to predict the reduction in vital capacity:

%change in VC=-.01(pO2-0.5)t

Subsequently, wouldn't it follow that if the measurable Vital Capacity of an individual decreases due to prolonged pure O2 exposure, that the ability to "off-gas" might also be effected?

Thanks for your comments,
wb

Mr. Irvine's BAUE transcript has much grounding and provides insightful recommendations for diving practice, but as Dr. Deco eloquently put, Mr. Irvine's physiology of 02 breaks has a bit more hypothesis than fact.

Lambertsen's 1988 paper summarized much work. Breathing pp02 0.21 between pp02 2-3 can delay the onset of pulmonary toxicity. pp02 2.0 can be breathed up to 12 hours with ~ 20 min 02 with 5 min normoxic break. There is also some evidence for breathing at ratios of 60min 02 with 15 min normoxia may be as or more efficient as the shorter breaks.

In general decompression technical diving [200-300' for 30min], few schedules require breathing 02 to over 60 minutes, so whether Mr. Irvine is right or not, the breaks are strictly not necessary for pulmonary toxicity reasons.

HOWEVER, in practical terms, breathing pp02 1.6 does begin to cause a heartburn like sensation in many divers by 30 minutes which does not abate until some lower pp02 is taken. Since most backgas is generally hyperoxic at 20,' assuming trimix 16/60 for 250' dive, backgas pp02 ~ .26, so one may take a break sooner to reduce overall pp02 loads and this sensation. If you adjust the breaktime porportionate to the pp02 exposure and backgas, increasing the breaktime and shortening the pp02 exposure (e.g. 20min/ (.26/.21)) provides a break at 16min for 6min backgas.

Note, in biomedical studies, there is no data I know that adjusting the backgas breaks proportionately as I did here, has been tested to be as effective as the 20:5 ratio. However, this regimen at minimum, provides a comfortable deco stop on high pp02.

The big question is whether the absence of this burning sensation, or as Mr. Irvine suggests doing the break ~ 20 min, forestall physiologic changes that make 02 decompression less efficient. Disciples of Irvine swear by the dogma and will swear _at_ you for heresy. Its of critical concern in much longer 02 exposures since Irvine has included the breaks in calculating the total 02 time, thereby shortening the total 02 deco by 5:20 or 25%. One credible hypothesis is that it takes 1-3 minutes for blood gases to equilibrate with alveolar gas, so decompression time may be effectively reduced only say 5-15%.

Carl Edmonds M.D. is a proponent of emergency in-water recompression treatment, and at least successes with his protocol suggests 02 efficiency without breaks [30-60min pp02 1.9].

Until the Irvine hypothesis can be further tested, a break is clinically a more comfortable dive for certain, and the only penalties currently is added total decompression time [ such as extending your 20' stop by 20 min to account for 4 breaks] and the label, deco weenie.

WB, what is the source of your VC change formula? It seems to have missing pieces.

"%change in VC=-.01(pO2-0.5)t"

Does a change in VC act as an index of lung damage from 02 exposure and does this reflect reduced deco efficiency? I'm not sure how significant it is, all patients recompressed will complain of burning lungs, and each treatment reduces VC by ~ 2%. Gas exchange is not highly influenced by VC, but lung elasticity suffers, and can be compensated for by higher minute ventilation.

 

[wb416]

Let me start by saying "Thanks for your detailed comments". As I continue to learn more about this area, I appreciate the insight into the physiological impacts and subsequent studies regarding O2 exposures.

Saturation once bubbled...


Mr. Irvine's BAUE transcript has much grounding and provides insightful recommendations for diving practice, but as Dr. Deco eloquently put, Mr. Irvine's physiology of 02 breaks has a bit more hypothesis than fact.

Lambertsen's 1988 paper summarized much work. Breathing pp02 0.21 between pp02 2-3 can delay the onset of pulmonary toxicity. pp02 2.0 can be breathed up to 12 hours with ~ 20 min 02 with 5 min normoxic break. There is also some evidence for breathing at ratios of 60min 02 with 15 min normoxia may be as or more efficient as the shorter breaks.

It looks like there were studies across wide ppO2 ranges. While the document here doesn't contain the abstract, I still found it interesting.

Extension of O2 tolerance by Intermittent Exposure

In general decompression technical diving [200-300' for 30min], few schedules require breathing 02 to over 60 minutes, so whether Mr. Irvine is right or not, the breaks are strictly not necessary for pulmonary toxicity reasons.

Remember, the context of Irvine's dives aren't those with "simple" 30 minutes bottom time. Rather, on his record-setting push he had 420 minutes of BT @ 300ft and a 7 hour deco schedule. 150 minutes of the deco is done on 100% O2 @ 30ft (in a trough).

Maximum Deco

HOWEVER, in practical terms, breathing pp02 1.6 does begin to cause a heartburn like sensation in many divers by 30 minutes which does not abate until some lower pp02 is taken. Since most backgas is generally hyperoxic at 20,' assuming trimix 16/60 for 250' dive, backgas pp02 ~ .26, so one may take a break sooner to reduce overall pp02 loads and this sensation. If you adjust the breaktime porportionate to the pp02 exposure and backgas, increasing the breaktime and shortening the pp02 exposure (e.g. 20min/ (.26/.21)) provides a break at 16min for 6min backgas.

For reference, Irvine was using 12 minutes on 100% O2, and 6 minutes on backgas (11/65).

Note, in biomedical studies, there is no data I know that adjusting the backgas breaks proportionately as I did here, has been tested to be as effective as the 20:5 ratio. However, this regimen at minimum, provides a comfortable deco stop on high pp02.

Perhaps some of the "recovery" ratios are derivations based upon studies regarding "Recovery" Equations.

Pulmonary & CNS O2 Toxicity & Estimation Parameters

The big question is whether the absence of this burning sensation, or as Mr. Irvine suggests doing the break ~ 20 min, forestall physiologic changes that make 02 decompression less efficient. Disciples of Irvine swear by the dogma and will swear _at_ you for heresy. Its of critical concern in much longer 02 exposures since Irvine has included the breaks in calculating the total 02 time, thereby shortening the total 02 deco by 5:20 or 25%. One credible hypothesis is that it takes 1-3 minutes for blood gases to equilibrate with alveolar gas, so decompression time may be effectively reduced only say 5-15%.

I think that Irvines' actual dive parameters bear out your references of "critical concern" regarding extended O2 exposures. 100% O2 @ 30ft has a PP of how much? ;-)

Carl Edmonds M.D. is a proponent of emergency in-water recompression treatment, and at least successes with his protocol suggests 02 efficiency without breaks [30-60min pp02 1.9].

Until the Irvine hypothesis can be further tested, a break is clinically a more comfortable dive for certain, and the only penalties currently is added total decompression time [ such as extending your 20' stop by 20 min to account for 4 breaks] and the label, deco weenie.

It would seem to me that the discomfiture or burning sensation in the lungs is an indication that the lungs are already reacting to the prolonged high ppO2 event.

WB, what is the source of your VC change formula? It seems to have missing pieces.

"%change in VC=-.01(pO2-0.5)t"

In the GUE Tech 1 manual there is a reference in Ch7 to Harabin's equation, however, much more detailed equations are available in the link I provided above regarding "Estimation Parameters".

Does a change in VC act as an index of lung damage from 02 exposure and does this reflect reduced deco efficiency? I'm not sure how significant it is, all patients recompressed will complain of burning lungs, and each treatment reduces VC by ~ 2%. Gas exchange is not highly influenced by VC, but lung elasticity suffers, and can be compensated for by higher minute ventilation.

I found the following study very fascinating for a relative "pulmonary neophyte" like myself. While gas exchange may not be directly effected by VC (VC seems to be one of the most consistent measurable markers of O2 exposure insult), there is, however, tracking of negative effect on CO exchange after high ATA O2 exposures. It would seem inline that other pulmonary gas exchanges would be impaired as well. An earlier post indicated "no known experimental evidence" that gas exchange is effected. Perhaps this study touches on that.

Effects of Prolonged O2 Exposure

Thanks for your help.
wb

 

[Saturation]

cwb once bubbled...
Let me start by saying "Thanks for your detailed comments".

You're welcome. I hope my replies are not confusing. Its not easy to accurately represent the physiology without jargon.

It looks like there were studies across wide ppO2 ranges. While the document here doesn't contain the abstract, I still found it interesting. Extension of O2 tolerance by Intermittent Exposure

This paper and other excellent links mentioned below, continue to build on work Lambertsen summarized in 1988. Where provided, consider the reference section of papers in your links. An interested reader may buy the 4th edition [ to save money] or for $150 the 2003 5th ed. of Bennett & Elliott's "Physiology and Medicine of Diving" to provide a wider, if not thorough, perspective than just isolated papers.

Remember, the context of Irvine's dives aren't those with "simple" 30 minutes bottom time. Rather, on his record-setting push he had 420 minutes of BT @ 300ft and a 7 hour deco schedule. 150 minutes of the deco is done on 100% O2 @ 30ft (in a trough).

Maximum Deco


Worse case OTU in 'maximum deco' is ~ 1,300 units, about 2 recompression chamber rides. This results at worse, 10% reduction in VC [assuming no benefit from normoxic breaks], at best it was 1-2%. An unpleasant, but non-lethal exposure. Without physiologic studies done on Irvine before or after "maximum deco," its hard to make claims on its safety beyond he survived. What damage to his lungs occured after the schedule? did lungs fully recover? By OTU analysis its likely he did well, but hard data would be better.

What maybe 'record setting' about "maximum deco" is the aggressiveness of the schedule and the extent of the cave penetration. It could be a superb data point for the validation of bubble decompression theory, but NOT of some superhuman resistance to 02 toxicity.

For reference, Irvine was using 12 minutes on 100% O2, and 6 minutes on backgas (11/65).
Perhaps some of the "recovery" ratios are derivations based upon studies regarding "Recovery" Equations.Pulmonary & CNS O2 Toxicity & Estimation Parameters

Arieli's paper is fine tuning an equation to fit curves for existing VC reduction and recovery data spanning ~ 30 years, and adds more data point with their own Israeli studies. The basic curves were established by Lambertsen, Clark and others, again summarized in the 1988 paper or any diving physiology text. Arieli measures recovery via vital capacity, which is just one measure of 02 pulmonary toxicity. The 2002 Arieli paper changed [I'm recalling from memory, so there may be errors here]:

dVC% = .0082 x hours^2 x [ppO2 in ATA] ^ 4.57

In 1994 [ see the references] his estimate was:
dVC% = .0115 x hours^1.85 x [pp02 in ATA] ^ 4.56

The recovery rate is not critical, since most recovery is in ~ 24 hours.

I think that Irvines' actual dive parameters bear out your references of "critical concern" regarding extended O2 exposures. 100% O2 @ 30ft has a PP of how much? ;-)

The "critical concern" I raise is not tolerating a pp02 of 1.9 at 30' but that Irvine teaches that the air breaks are part of the calculated 02 time. If a schedule states an 02 deco is 20 minutes and you take a 5 min backgas break, Irvine effective states you do 15 minutes of 02 and 5 minutes of backgas and that = 20 min of 02. In the 12min 02 and 6 min backgas break in 'maximum deco', the 30' stop is effectively reduced from 150min of 02 to only 75 minutes. This causes a large reduction in pp02 exposure. The explanation for how this might work is in my prior post.

It would seem to me that the discomfiture or burning sensation in the lungs is an indication that the lungs are already reacting to the prolonged high ppO2 event. While gas exchange may not be directly effected by VC (VC seems to be one of the most consistent measurable markers of O2 exposure insult), there is, however, tracking of negative effect on CO exchange after high ATA O2 exposures. It would seem inline that other pulmonary gas exchanges would be impaired as well. An earlier post indicated "no known experimental evidence" that gas exchange is effected. Perhaps this study touches on that.
Effects of Prolonged O2 Exposure

Pulmonary toxicity begins when exposure pp02 > 0.5 ATA. The rate of injury increases with increased pp02 and time on this pp02. Diving air or nitrox, this means 02 related injury begins once dives are beyond 46' [ diving per se causes a persistent reduction in VC over years, and this maybe one of its mechanisms.] So, even before deco, injury has begun. In reference to Mr. Irvine's dive of 420 minutes bottom time at pp02 1.1, there is certain to be marked injury, as the studies you linked show changes at pp02 of 1.0 and up.

DLCO is a sensitive marker for damage, and corroborated by the increase in (A-a)D02 which takes several days to normalize. Since lung injury was already initiated simply by diving past the critical depth, say 46', not to mention prolonged stay at depth, then the only thing gas breaks do is minimize further damage. If reduction in "efficiency" can be avoided by not having pulmonary injury, its too late, its already done.

 

[The Iceni]

In a related debate about the relative benefits/risks of 100% oxygen (as stongly advocated by GI with his Baker's Dozen) or Nitrox 80 as the final deco gas it was pointed out to me that breathing pure oxygen will slow down offgassing due to pulmonary and whole body toxicity and would therefore not be as efficient as 80% Nitrox.

I replied as follws.

I am not sure we will ever get the answer but offgassing with 100% oxygen may indeed deteriorate with time as these (temporary) effects develop. However all things are relative;-

The aim of decompression is to offgas nitrogen. In this context the oxygen in the breathing gas is the diluent!

If we look at the nitrogen offgassing counter pressure in the breathing gas alone;-

At 6 M (20 ft)

With oxygen ppN2 is close to zero
With 80% nitrox pp N2 = 0.32 bar
(with air (20%) pp N2 = 1.28 bar)

At 3 M (10 ft)

With oxygen ppN2 is close to zero
With 80% nitrox pp N2 = 0.26 bar
(with air (20%) pp N2 = 1.04 bar)

on the surface

With oxygen ppN2 is close to zero
With 80% nitrox pp N2 = 0.20 bar
with air (20%) pp N2 = 0.80 bar

Since blood has a half-time of seconds this is the ppN2 in arterial blood. In my opinion, the reduction in tissue offgassing as a consequence of vasoconstriction will have to be considerable to defeat the advantages of removing this nitrogen diffusion counterpressure.

As far as the lungs are concerned, gaseous exchange is remarkably efficient so I aver that pulmonary effects will never be sufficient to overcome the considearble advantages of a near zero arterial ppN2 c/w a ppN2 of 0.8 bar when breathing surface air.

So extended periods of decompression on 100% oxygen "will not be as efficient as you might think" but it is likely to be far more efficient than 80% Nitrox. (within NOAA limits, of course.)

**I have no research data to confirm this observation of what may occur in practice.**

A project worth doing?

 

[Genesis]

some SCIENTIFIC, peer-reviewed studies on this matter.

Right now all we have is anecdotes. That's unfortunate, but it is the way of the world for now....

One can only hope that there will, sometime in the future, be an OPEN study made by some of the proponents. Not "proprietary anecdotes", but real, honest-to-god study.

 

[Dr Deco]

Dear Readers:

Air Breaks

In the field of aviation and space medicine, there has been some interest in ancillary topic referred to as “break in prebreathe.” This appears in two forms, air interruption of oxygen, and breathing masks with a poor fit. There has not been a great deal of work on this topic, some is conflicting, and not all of it is entirely congruent with the diving question.

The paucity of findings indicates that the “payback” for air interruptions is equal to the duration of interruption or a bit longer. I have never seen data to indicate that the introduction of some nitrogen will increase the efficiency of the washout process.

Pulmonary Injury

There is the feeling by some technical divers that the pulmonary injury from oxygen will introduce gas exchange problems. Data indicates that considerable damage would be needed to produce much of an effect on arterial gas partial pressures. I would doubt that tech divers are in that range. I do not have any data on this however.

If there is success with the deco methods, I would bet that much has to do with the fact that the divers are “adynamic” in the same way that astronauts in space are. This effect will reduce DCS risk by several fold – not just several percent.

As far as more research goes, don't hold your breath.

Dr Deco :doctor:

 

[Genesis]

The advocates for one form or another are not going to be funding peer-reviewed, scientifically-valid studies anytime soon.

Particularly if there is a non-zero risk that the findings would mean that they'd have to recant YEARS of dogma and screed!

 

[Dr Deco]

Genesis:

That may be true regarding funding for the competition, but what I had in mind was the limited amount of research funds - period. Recreational diving is, well, recreational. It is not considered something that "deserves" funds since funds are limited. Diving is basically a choice and not in the same league as cancer, heart disease and stroke. Yes, many of these are the result of bad life style choices but the public does not see it that way. The arguments are extensive on both sides.:upset:

At one time (20 years ago) the US Navy had a research program that could supply such funding. That program has been long gone. While some money might be available for pulmonary studies, there would be little to none to study problems of divers per se. I too wish that it was different.

Dr Deco :doctor: