Sorry Charlie, Posting that paper would be a copyright violation so it is not in my "download" folder anymore. Hills did summarize that work in this paper though.
Oxygen Window: Explanation and Purpose?
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lamont
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AFAIK they don't agree.
I don't have v-planner installed right now. See if you can find a profile that ends with 100% O2 that has a different runtime based on setting the last stop depth to 10 fsw or 20 fsw. Last time I saw this argued out on TDS it didn't matter, and the conclusion by those who follow v-planner was that you should move up to 10 fsw when you can in order to reduce O2 exposure.
And..
Pyle:
Pyle's statement indicates he had no theoretical understanding of why he felt better on his deep stop profiles. Experiment clearly led theory for him.
Dr Deco
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Hello Readers:
Oxygen Window and Gas Exchange
It appears that the term oxygen window has expanded in the world of recreational diving compared to what I remembered it to mean in the 1970s. From what I am reading, today it appears that increased levels of oxygen are thought by some to allow the increased rate of exit of inert gas from the body. However, the dissolution of nitrogen is governed by Henrys Law and is dependent only on the partial pressure of that gas. Nitrogen will not exit any faster or slower if you breathe oxygen, argon, or helium. It is dependent only on the partial pressure of nitrogen in the arterial blood. The oxygen window will not assist in pulling dissolved nitrogen from tissues.
Naturally, the greater the percent of oxygen in the breathing mix, the smaller will be the percent of nitrogen (or other inert gas). There is not a biochemical mechanism for changing the rate. I guess this purported increase is what some are calling the voodoo oxygen effect.
Gas Bubbles and Inherent Unsaturation
It was known for decades that gas bubbles will dissolve faster in the body with oxygen breathing. This is true in the tissues and the venous system. It will not occur in the arterial system since oxygen is not metabolized. Bubbles contain gases in proportion to the surrounding liquid. In the tissues (and the venous system), bubbles will contain oxygen, carbon dioxide, water vapor, and some nitrogen. If the oxygen is metabolized, little is present to diffuse into the bubbles. This vacancy is the oxygen window and applies to bubbles and their shrinkage. Substituting oxygen for inert gas is simply a matter of control of partial pressure and Henrys Law.
The references below illustrate some material in the literature. Most material is quite old and not easily obtained without access to a large library. :umnik:
Richard Pyle
I have communicated with Richard in the past but do not know the extent of his understanding of this issue when he first encountered it while collecting fish. He would have been aware of the work of David Yount in Hawaii. At that time, the idea of gas bubbles in tissues was poorly understood by most barophysiologists. They were still invoking biochemical mechanism to explain the lag between decompression and the appearance of DCS. Slow grow of nuclei by diffusion was not in their minds.
Brian Hills PhD attempted to address this matter in the late 1960s, but his idea was not well received by the hyperbaric community. While slow ascents and deep stops were a part of the Hills' "thermodynamic method," his ideas were very marginal. They were appreciated by those with a background in physics not common among barophysiologists. Today, it would be difficult to imagine that there was any resistance to the idea although it was not well developed in the 1970s. Nonetheless, the ideas of critical radii, and a spectrum of bubbles sizes and a reservoir of nuclei were all a part of the concept.
Dr Deco :doctor:
References :1book:
[1] VARIABILITY OF THE INERT GAS PARTIAL PRESSURE IN BUBBLES AND TISSUES. Van Liew, HD
Abstract of the Undersea and Hyperbaric Medical Society, Inc. Annual Scientific Meeting held May 12-13, 1976. Carillon Hotel, Miami Beach, FL
This work is an attempt to reevaluate the factors that determine whether inert gas will diffuse into or out of a decompression bubble. a) The physiological basis of the "oxygen window" or "inherent unsaturation" is the same as the basis for 02 breathing during decompression or as a treatment for decompression sickness. Consider a man breathing an 02-N2 mixture. Bubbles will shrink rather than grow if PN2 in the tissue or blood is lower than PN2 inside the bubbles. There are five important variables: inspired P02, atmospheric pressure, surface tension in the bubble, P02 in the tissue, and temperature of the tissue. Outside a bubble, PN2 approaches the PN2 of blood which comes from the lungs; in the lungs, PN2 depends on atmospheric pressure and P02 of inspired gas. Inside a bubble, PN2 depends mainly on surface tension and on P02 in the bubble; the bubble's P02 is close to the tissue P02 that results from the tissue's 02 utilization. b) Because blood flow and metabolism differ from organ to organ, and even from point to point in a single tissue, there will be variability in the inherent unsaturation and in its relationship to washout halftime for inert gases. We have estimated this variability from two kinds of published data: from multiple P02 analyses in skeletal muscle, and from blood flow and venous 02 content measurements of various organs. c) Surface tension increases the PN2 enormously inside very small bubbles. Also, PN2 of cool or warm tissues of the body can be substantially different from PN2 of lung and arterial blood due to temperature effects on gas solubility. (Supported in part by NIH grant 5 POI HL 14414-04.)
[2] A FUNDAMENTAL APPROACH TO THE PREVENTION OF DECOMPRESSION SICKNESS. Hills, BA
Journal of the South Pacific Underwater Medicine Society. 1978
The inherent unsaturation is very important not only because it determines the position of phase equilibrium upon decompression, and hence the point at which the first bubbles can start to form, but it provides a permanent driving force for dissolving gas in the body. This includes not only bubbles but intrapleural gas, gas in an occluded bronchioles or a blocked sinus, etc. Moreover the unsaturation also provides the driving force for dissolving bubbles.
[3] GAS NUCLEI, THEIR ORIGIN, AND THEIR ROLE IN BUBBLE FORMATION.
Blatteau JE, Souraud JB, Gempp E, Boussuges A.
Aviat Space Environ Med. 2006 Oct;77(10):1068-76.
Gas bubbles are the primary agent in producing the pathogenic effects of decompression sickness. Bubble formation during decompression is not simply the consequence of inert gas supersaturation. Numerous experiments indicate that bubbles originate as pre-existing gas nuclei. Radii are on the order of 1 microm or less. Heterogeneous nucleation processes are involved in generating these gas entities. Musculoskeletal activity could be the main promoter of gas nuclei from stress-assisted nucleation. The half-life and faculty for nuclei to initiate bubble formation during decompression depend on many factors. Oxygen window and surface tension are involved in resolving bubbles. Two factors have been proposed to stabilize gas nuclei against dissolution: gas nuclei trapped in hydrophobic crevices and gas nuclei coated with surface-active molecules such as surfactants. Diffusion and surface tension could play an important role in the formation of gas nuclei crevices. However, while the concept of in vivo hydrophobic crevices remains a theoretical possibility, none have yet been identified in tissues and/or in microcapillaries. Moreover, while surfactants seem present in numerous tissues and could play a role in gas nuclei stabilization, they could also be involved in bubble elimination. The understanding of such mechanisms is of primary importance to neutralize nuclei and for modeling bubble growth. Here we present in a single document a summary of the original findings and views from authors in this field.
Oxygen Window and Gas Exchange
It appears that the term oxygen window has expanded in the world of recreational diving compared to what I remembered it to mean in the 1970s. From what I am reading, today it appears that increased levels of oxygen are thought by some to allow the increased rate of exit of inert gas from the body. However, the dissolution of nitrogen is governed by Henrys Law and is dependent only on the partial pressure of that gas. Nitrogen will not exit any faster or slower if you breathe oxygen, argon, or helium. It is dependent only on the partial pressure of nitrogen in the arterial blood. The oxygen window will not assist in pulling dissolved nitrogen from tissues.
Naturally, the greater the percent of oxygen in the breathing mix, the smaller will be the percent of nitrogen (or other inert gas). There is not a biochemical mechanism for changing the rate. I guess this purported increase is what some are calling the voodoo oxygen effect.
Gas Bubbles and Inherent Unsaturation
It was known for decades that gas bubbles will dissolve faster in the body with oxygen breathing. This is true in the tissues and the venous system. It will not occur in the arterial system since oxygen is not metabolized. Bubbles contain gases in proportion to the surrounding liquid. In the tissues (and the venous system), bubbles will contain oxygen, carbon dioxide, water vapor, and some nitrogen. If the oxygen is metabolized, little is present to diffuse into the bubbles. This vacancy is the oxygen window and applies to bubbles and their shrinkage. Substituting oxygen for inert gas is simply a matter of control of partial pressure and Henrys Law.
The references below illustrate some material in the literature. Most material is quite old and not easily obtained without access to a large library. :umnik:
Richard Pyle
I have communicated with Richard in the past but do not know the extent of his understanding of this issue when he first encountered it while collecting fish. He would have been aware of the work of David Yount in Hawaii. At that time, the idea of gas bubbles in tissues was poorly understood by most barophysiologists. They were still invoking biochemical mechanism to explain the lag between decompression and the appearance of DCS. Slow grow of nuclei by diffusion was not in their minds.
Brian Hills PhD attempted to address this matter in the late 1960s, but his idea was not well received by the hyperbaric community. While slow ascents and deep stops were a part of the Hills' "thermodynamic method," his ideas were very marginal. They were appreciated by those with a background in physics not common among barophysiologists. Today, it would be difficult to imagine that there was any resistance to the idea although it was not well developed in the 1970s. Nonetheless, the ideas of critical radii, and a spectrum of bubbles sizes and a reservoir of nuclei were all a part of the concept.
Dr Deco :doctor:
References :1book:
[1] VARIABILITY OF THE INERT GAS PARTIAL PRESSURE IN BUBBLES AND TISSUES. Van Liew, HD
Abstract of the Undersea and Hyperbaric Medical Society, Inc. Annual Scientific Meeting held May 12-13, 1976. Carillon Hotel, Miami Beach, FL
This work is an attempt to reevaluate the factors that determine whether inert gas will diffuse into or out of a decompression bubble. a) The physiological basis of the "oxygen window" or "inherent unsaturation" is the same as the basis for 02 breathing during decompression or as a treatment for decompression sickness. Consider a man breathing an 02-N2 mixture. Bubbles will shrink rather than grow if PN2 in the tissue or blood is lower than PN2 inside the bubbles. There are five important variables: inspired P02, atmospheric pressure, surface tension in the bubble, P02 in the tissue, and temperature of the tissue. Outside a bubble, PN2 approaches the PN2 of blood which comes from the lungs; in the lungs, PN2 depends on atmospheric pressure and P02 of inspired gas. Inside a bubble, PN2 depends mainly on surface tension and on P02 in the bubble; the bubble's P02 is close to the tissue P02 that results from the tissue's 02 utilization. b) Because blood flow and metabolism differ from organ to organ, and even from point to point in a single tissue, there will be variability in the inherent unsaturation and in its relationship to washout halftime for inert gases. We have estimated this variability from two kinds of published data: from multiple P02 analyses in skeletal muscle, and from blood flow and venous 02 content measurements of various organs. c) Surface tension increases the PN2 enormously inside very small bubbles. Also, PN2 of cool or warm tissues of the body can be substantially different from PN2 of lung and arterial blood due to temperature effects on gas solubility. (Supported in part by NIH grant 5 POI HL 14414-04.)
[2] A FUNDAMENTAL APPROACH TO THE PREVENTION OF DECOMPRESSION SICKNESS. Hills, BA
Journal of the South Pacific Underwater Medicine Society. 1978
The inherent unsaturation is very important not only because it determines the position of phase equilibrium upon decompression, and hence the point at which the first bubbles can start to form, but it provides a permanent driving force for dissolving gas in the body. This includes not only bubbles but intrapleural gas, gas in an occluded bronchioles or a blocked sinus, etc. Moreover the unsaturation also provides the driving force for dissolving bubbles.
[3] GAS NUCLEI, THEIR ORIGIN, AND THEIR ROLE IN BUBBLE FORMATION.
Blatteau JE, Souraud JB, Gempp E, Boussuges A.
Aviat Space Environ Med. 2006 Oct;77(10):1068-76.
Gas bubbles are the primary agent in producing the pathogenic effects of decompression sickness. Bubble formation during decompression is not simply the consequence of inert gas supersaturation. Numerous experiments indicate that bubbles originate as pre-existing gas nuclei. Radii are on the order of 1 microm or less. Heterogeneous nucleation processes are involved in generating these gas entities. Musculoskeletal activity could be the main promoter of gas nuclei from stress-assisted nucleation. The half-life and faculty for nuclei to initiate bubble formation during decompression depend on many factors. Oxygen window and surface tension are involved in resolving bubbles. Two factors have been proposed to stabilize gas nuclei against dissolution: gas nuclei trapped in hydrophobic crevices and gas nuclei coated with surface-active molecules such as surfactants. Diffusion and surface tension could play an important role in the formation of gas nuclei crevices. However, while the concept of in vivo hydrophobic crevices remains a theoretical possibility, none have yet been identified in tissues and/or in microcapillaries. Moreover, while surfactants seem present in numerous tissues and could play a role in gas nuclei stabilization, they could also be involved in bubble elimination. The understanding of such mechanisms is of primary importance to neutralize nuclei and for modeling bubble growth. Here we present in a single document a summary of the original findings and views from authors in this field.
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