Enjoyable post Brian, I like the way you explain it.
Jeff Lane
Jeff Lane
Elimination of body N2 using Nitrox
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Thanks Jeff ... I'm usually told I only make things worse 
Brian
Brian
OP
ScubaJorgen
Contributor
This is one of the moment I am proud to be member of this board!! Thanks a lot for the information. Jeff, especally the article you refer to is enlightening.
Summarizing:
- The author of my book refers to the oxygen window.
- The oxwindow increases when using Nitrox
- The oxygen window itself does not influence N2 transport
- N2 transport only depends on difference in partial pressure/tension between lungs and tissue, not on concentrations/partial pressures of other gasses like O2 or CO2
- The statement of the author of my book suggesting O2 being absent leaves 'space' for N2 in the transport is not quite correct.
Alveolar N2 pressure and Nitrox
It is interesting to look what the influence is of Nitrox on the alveolar N2 partial pressure. The alveolar ventilation equation states:
Palv_n2 = [Pamb - Ph20 - dPco2 + dPo2]Q
Palv_n2 - partial pressure N2 in alveoli
Q - fraction N2 in the inhaled air
Pamb - ambient pressure
Ph20 - water vapour pressure
dPco2 - pressure due to CO2 increase in alveoli
dPo2 - pressure due to O2 uptake by alveoli
The ratio of dPco2/dPo2 is called repiratory coefficient and is 0-7-1.0
Palv_n2 = [Pamb - Ph20 + (1-RQ) dPo2]Q
If the O2 uptake increases (due to increased ox window) when using Nitrox (and RQ<=1), then this dampens the effect of decreasing Q value! Fortunately (1-RQ)dPo2 is a small factor in the equation (~1/100 Pamb)......
So the increased ox window might even lead to less N2 transport than one would expect based on the inspired N2 percentage....
Interesting as well
From Jeffs link:
Enlarging the oxygen window may have another effect, which is subtler than tissue on- or off-gassing. The following discussion is conjecture based on data available in the literature, and has not been directly studied. During decompression of animals from air dives, venous blood becomes supersaturated with N2 during the early stages of decompression, and venous blood supersaturation appeared related to venous bubble formation (2). Venous blood N2 supersaturation occurred following a relatively mild decompression stress of ascent from 33 FSW to surface. Once bubble formation had occurred, gas removal was slowed, possibly by bubbles in the venous circulation (2). By limiting the speed with which ambient pressure is changed, deep stops may function to limit venous blood supersaturation and limit bubble formation related to the supersaturation. Increasing the oxygen window during decompression will also limit venous blood supersaturation by limiting the amount of non-metabolic gas in blood. In essence, the presence or absence of a second non-metabolic gas will not alter the amount of gas evolved from tissue. However, the presence of an inspired non-metabolic gas could increase the severity of venous blood supersaturation.
I definitely have to read this a couple of times.....
Summarizing:
- The author of my book refers to the oxygen window.
- The oxwindow increases when using Nitrox
- The oxygen window itself does not influence N2 transport
- N2 transport only depends on difference in partial pressure/tension between lungs and tissue, not on concentrations/partial pressures of other gasses like O2 or CO2
- The statement of the author of my book suggesting O2 being absent leaves 'space' for N2 in the transport is not quite correct.
Alveolar N2 pressure and Nitrox
It is interesting to look what the influence is of Nitrox on the alveolar N2 partial pressure. The alveolar ventilation equation states:
Palv_n2 = [Pamb - Ph20 - dPco2 + dPo2]Q
Palv_n2 - partial pressure N2 in alveoli
Q - fraction N2 in the inhaled air
Pamb - ambient pressure
Ph20 - water vapour pressure
dPco2 - pressure due to CO2 increase in alveoli
dPo2 - pressure due to O2 uptake by alveoli
The ratio of dPco2/dPo2 is called repiratory coefficient and is 0-7-1.0
Palv_n2 = [Pamb - Ph20 + (1-RQ) dPo2]Q
If the O2 uptake increases (due to increased ox window) when using Nitrox (and RQ<=1), then this dampens the effect of decreasing Q value! Fortunately (1-RQ)dPo2 is a small factor in the equation (~1/100 Pamb)......
So the increased ox window might even lead to less N2 transport than one would expect based on the inspired N2 percentage....
Interesting as well
From Jeffs link:
Enlarging the oxygen window may have another effect, which is subtler than tissue on- or off-gassing. The following discussion is conjecture based on data available in the literature, and has not been directly studied. During decompression of animals from air dives, venous blood becomes supersaturated with N2 during the early stages of decompression, and venous blood supersaturation appeared related to venous bubble formation (2). Venous blood N2 supersaturation occurred following a relatively mild decompression stress of ascent from 33 FSW to surface. Once bubble formation had occurred, gas removal was slowed, possibly by bubbles in the venous circulation (2). By limiting the speed with which ambient pressure is changed, deep stops may function to limit venous blood supersaturation and limit bubble formation related to the supersaturation. Increasing the oxygen window during decompression will also limit venous blood supersaturation by limiting the amount of non-metabolic gas in blood. In essence, the presence or absence of a second non-metabolic gas will not alter the amount of gas evolved from tissue. However, the presence of an inspired non-metabolic gas could increase the severity of venous blood supersaturation.
I definitely have to read this a couple of times.....
Yes, bubbles reduce the driving force for gas elimination. Think of it this way, a bubble expands until the pressure inside the bubble is equal to the surrounding atmospheric pressure. Thus there is no driving force for the gas to be eliminated when a bubble is present. Instead it must be absorbed which can be a time consuming process. So if the gas remains in solution (i.e. no bubbles) the driving force for gas elimination is maintained. Now this was an overly simplistic example, so lets add to it. Really, a diver wants to keep bubbles small. When a bubble is small, its bubble skin exerts more pressure and thus the internal pressure is greater. So smaller bubbles have a greater internal pressure than bigger bubbles. When a bubble gets too big, the skin pressure cant keep the bubble in check and the bubble will then start expanding. Thus, the smaller the bubble, the greater the skin pressure is driving the bubble to be even smaller and helping with gas elimination. I like to use Eric Maikens balloon example for a bubble analogy. A balloon is hardest to blow up when you start the process. As you get more air into the balloon, it becomes easier to fill up. This shows that when the balloon is small, its skin tension is exerting more pressure and trying to make the balloon (bubble) shrink and contract. So the idea is to keep the bubble within an acceptable size so that it does not just start expanding, hence what I call an efficient bubble one on the verge of expanding, but where it is still small and will choose to maintain an acceptable size or actually contract and become smaller. This is one of the principals of doing deep stops, i.e. more pressure equals smaller bubbles - which have greater internal pressure as compared to larger bubbles that may start expanding.ScubaJorgen:
Dr Deco
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Hello Readers:
Sorry to get around this so late. Other matters arose. My thanks to those who wrote responses. :laghost:
- How do O2 and CO2 partial pressures influence each other?
In a living creature, the se two gases are controlled by metabolism. Any wide variations are an indication of disease. Oxygen and carbon dioxide dissolve separately in the body fluids and dont really influence each other that much (although they will moderate blood flow). In the blood, there is a chemical combination and there is an influence. There is not any particular influence on the dissolving capability of body fluids for inert gases.
- Do O2 molecules bound to hemoglobin contribute to the tissue tension (normally resulting from dissolving gas)?
The ones that are truly bound do not contribute, however, the bond is weak, and the oxygen does easily come off of the hemoglobin. While it is a small addition, it does contribute a bit to the total gas tissue pressure.
- How do O2 and/or CO2 partial pressures (tension) influence N2 partial pressure in tissue (tension) (guess no influence) or the amount of dissolved N2?
Oxygen and carbon dioxide do not directly influence the amount of nitrogen dissolved. These gases do modify blood flow and hence half times. The inert gases indirectly, therefore, have their tissue tensions controlled.
- Does the same number of molecules per volume of a gas always result in the same partial pressure (tension) at constant temperature? Or does the presence of other gasses influence this?
If two gases are equally soluble, then the partial pressure is related to the number of molecules dissolved. Insofar as gases differ in their solubility, the given number of molecules of a very soluble gas will produce a lower partial pressure than a poorly soluble one. In the limit, an infinitely soluble gas would have infinite dissolve molecules in the liquid and no partial pressure.
Basically, the book suggests nitrox's higher O2 level enhances the amount of N2 that is being transported (off-gassing), given a fixed gradient between N2 partial pressure in body and air. Is this true? How is this possible? Basically this means Nitrox lowers the half time of the tissue.
Yes, nitrogen is eliminated faster with nitrox. Nitrox will allow the loss of nitrogen from the body faster because there is less nitrogen in the breathing mix than air. The very best exchange will come from breathing pure oxygen, but this gas must be controlled because of toxicity issues.
It is not a matter of changing the halftime of the tissue; this is controlled by blood flow (and gas solubility). It is simply more nitrogen leaving than entering the body.
- If true, does it hold for on gassing?
When considering nitrogen uptake, the opposite is true. With less nitrogen in the breathing mix, uptake is slower. If the mix were pure oxygen, there would be no nitrogen uptake.
Dr Deco :doctor:
Sorry to get around this so late. Other matters arose. My thanks to those who wrote responses. :laghost:
- How do O2 and CO2 partial pressures influence each other?
In a living creature, the se two gases are controlled by metabolism. Any wide variations are an indication of disease. Oxygen and carbon dioxide dissolve separately in the body fluids and dont really influence each other that much (although they will moderate blood flow). In the blood, there is a chemical combination and there is an influence. There is not any particular influence on the dissolving capability of body fluids for inert gases.
- Do O2 molecules bound to hemoglobin contribute to the tissue tension (normally resulting from dissolving gas)?
The ones that are truly bound do not contribute, however, the bond is weak, and the oxygen does easily come off of the hemoglobin. While it is a small addition, it does contribute a bit to the total gas tissue pressure.
- How do O2 and/or CO2 partial pressures (tension) influence N2 partial pressure in tissue (tension) (guess no influence) or the amount of dissolved N2?
Oxygen and carbon dioxide do not directly influence the amount of nitrogen dissolved. These gases do modify blood flow and hence half times. The inert gases indirectly, therefore, have their tissue tensions controlled.
- Does the same number of molecules per volume of a gas always result in the same partial pressure (tension) at constant temperature? Or does the presence of other gasses influence this?
If two gases are equally soluble, then the partial pressure is related to the number of molecules dissolved. Insofar as gases differ in their solubility, the given number of molecules of a very soluble gas will produce a lower partial pressure than a poorly soluble one. In the limit, an infinitely soluble gas would have infinite dissolve molecules in the liquid and no partial pressure.
Basically, the book suggests nitrox's higher O2 level enhances the amount of N2 that is being transported (off-gassing), given a fixed gradient between N2 partial pressure in body and air. Is this true? How is this possible? Basically this means Nitrox lowers the half time of the tissue.
Yes, nitrogen is eliminated faster with nitrox. Nitrox will allow the loss of nitrogen from the body faster because there is less nitrogen in the breathing mix than air. The very best exchange will come from breathing pure oxygen, but this gas must be controlled because of toxicity issues.
It is not a matter of changing the halftime of the tissue; this is controlled by blood flow (and gas solubility). It is simply more nitrogen leaving than entering the body.
- If true, does it hold for on gassing?
When considering nitrogen uptake, the opposite is true. With less nitrogen in the breathing mix, uptake is slower. If the mix were pure oxygen, there would be no nitrogen uptake.
Dr Deco :doctor:
OP
ScubaJorgen
Contributor
Dr Deco:
Thank you for the clear explanation. Just one remark.
My question was:
Basically, the book suggests nitrox's higher O2 level enhances the amount of N2 that is being transported (off-gassing), given a fixed gradient between N2 partial pressure in body and air. Is this true?
I should have replaced 'air' by 'breathing mixture'.
On that question I think the answer is NO. At a given N2 gradient between tissue and lungs the N2 uptake/elimination is NOT influenced by breathing Air, Nitrox, Oxygen, apple juice, alcohol vapour, or what so ever.
Sorry for the confusion...
ScubaJorgen:
You have it right ... the only thing that matters is the gradient. If anything, oxygen could slow it down (for the same N2 gradient) ... vasoconstriction, etc. Oxygen is the necessary evil to reduce the other gasses and it has it's own problems as everyone knows.
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