Ppo2

[The Chairman]

if not in the alveoli, just where are the chemoreceptors located?

Now this goes against some of what my NitrOx training has indicated, which is OK. No one has ever accused PADI or NAUI of having a monopoly on the truth. So, might I clarify a few "concepts" here.

1- Metabolism does not increase... not one iota. The higher PP of Oxygen merely dissolves into your system just like Nitrogen and will subsequently come out of solution via off gassing when hyberbaric conditions are absent.

2- Ergo the EAD concept of NitrOx is invalid, as there is still quite a bit of gas (in the form of excess O2 and not N2) that must be off gassed safely in order to prevent DCS or AGE.

Your thoughts are eagerly anticipated...

We are in firm agreement though that CO2 and not O2 triggers the breathing reflex.

 

[cat]

Central CO2 chemoreceptors are in the brain (medullar surface near cranial nerve 9, I think). CO2 crosses the blood-brain barrier easily and bumps down the pH, which then triggers an increased ventilation rate.

There are also peripheral sensors in the aorta and carotids (these are also sensitive to O2). Happy breathing.

 

[rmediver2002]

2- Ergo the EAD concept of NitrOx is invalid, as there is still quite a bit of gas (in the form of excess O2 and not N2) that must be off gassed safely in order to prevent DCS or AGE

Couple things here:

The Equivilent air depth concept is valid, although the original intent of NITROX was diving it on normal air tables and accepting the advantages of having less N2 in the system when leaving the bottom.

1. Oxygen enters and leaves the system very rapidly... the levels absorbed on a dive readily exit the system through normal respiration. In fact on working mixed gas dives (commercial / surface supplied diving) the divers are given 100% O2 for several minutes at 40 FSW and then brought to the surface to be recompressed in a chamber to complete the decompression obligation, again on 100% oxygen.

2. If oxygen does get into the circulation system it is metabolised (reabsorbed) by the body. The oxygen bubble would be 100% oxygen having a far greater partial pressure than any tissue of the body and so it is absorbed quite readily into any fluid.

3. The majority of damage from DCS or AGE is from a lack of O2 to the tissues, blockages of O2 do not generally suffer this problem.



Just to clarify the original statement, decompression sickness is caused by insufficent removal of excess partial pressures of gas (gas in soulution at depth forming bubbles when pressure is decreased)

Arterial Gas Embolism or AGE is a much larger blockage caused by an over expansion of the lungs. This blockage normally effect the central nervous system with symptom onset being especially rapid and severe. It can occur with an amount of gas taken in at depth and is a function of Boyles law exclusively. Time has nothing to do with this injury.

Hope this clarifies it somewhat...

Jeff Lane

 

[rmediver2002]

1- Metabolism does not increase... not one iota. The higher PP of Oxygen merely dissolves into your system just like Nitrogen and will subsequently come out of solution via off gassing when hyberbaric conditions are absent.

It is best not to talk in absolutes here, normal cellular respiration may not increase but high partial pressures of O2 do metabolize in other ways... So in effect more O2 metabolism does take place...


http://www.vspn.org/vspnsearch/aow/oxygentoxicity.htm

Jeff Lane

 

[The Chairman]

and a departure from what agencies teach (at least beyond their scope)... which is great! I would rather understand the truth than only a half truth.

Cat... you da woman! Concise and to the point!

rmediver... one more clarification...

The oxygen bubble would be 100% oxygen

If we had a bubble... would it not consist of Nitrogen and Oxygen according to their partial pressure? I don't think we would be dealing with a nitrogen bubble here and an oxygen bubble over there. Thats where the issue of O2 only being dissolved (and not consumed) worries me. I can see that IF all cells were recieving all of the O2 they needed (or wanted) at 1ata that this would hold true. But is it possible that cells would like more oxygen than what they are currently getting? That is, could they utilize more oxygen than we supply them with at 1 ata?

 

[rmediver2002]

Hey Pete,

If we had a bubble... would it not consist of Nitrogen and Oxygen according to their partial pressure? I don't think we would be dealing with a nitrogen bubble here and an oxygen bubble over there.

It would depend on the mechanism of injury, if the diver had an overinflation injury then the bubble composition would be the same as the mixuture they were breathing.

If the injury were due to gas coming out of solution (DCS) the the bubbles would be coming out independant of each other. It is hard to imagine just how small these bubbles actually are inside the body, it takes a group of many bubbles to actually cause a blockage.

But is it possible that cells would like more oxygen than what they are currently getting? That is, could they utilize more oxygen than we supply them with at 1 ata

Yes they (or more appropriately the fluid they are comprised of) will continue to absorb O2 until they reach equilibrium with the partial pressure of the gas. The cells will not increase metabolic consumption of fuel (glycerin) just because excess O2 is available.

Jeff Lane

 

[The Iceni]

robjones once bubbled...
. . . Why then does my consumption of oxygen, say, 0.8 litres per minute, remain independent of depth and pressure? What happens to all those other molecules I must have taken on board but clearly haven't used, and if I don't use them how do they increase my partial pressure with all the difficult consequences that brings?

Hi Rob,

Very interesting and useful replies above, but can I revert to answering the question as asked?

The answer is, your body will only use the amount of oxygen it requires for its metabolism and this rate is very carefully controlled by a large number of enzymes at all levels in the tissues, much like the accelerator on a car. Consequently all oxygen surplus to requirements is passively distributed in solution throughout the body, in a similar manner to nitrogen, only to be later excreted unaltered by the lungs.

The body is not a passive user of fuel and oxygen. If it were, we would spontaneous combust at depth as the energy generated by the burning of the body's fuel created more and more heat energy, much like a furnace supplied with pure oxygen!

Yes the excess oxygen remains in solution in the blood, tissues and veins where it does indeed cause problems. If the inspired partial pressure of oxygen greatly exceeds 1.4 bar it becomes toxic to the central nervous system and can cause grand mal convulsions without warning (not a good idea underwater). In addition prolonged exposure to a ppO2 in excess of 0.5 bar causes irritation to the tissues of the lungs - pulmonary oxygen toxicity.

By the way, if the inspired partial pressure of oxygen exceeds 3 bar sufficient oxygen is carried in simple solution in the plasma to meet all the body's metabolic needs so the haemoglobin remains completely saturated, even in the veins!

I hope that helps. :doctor:

 

[The Iceni]

NetDoc once bubbled...
2- Ergo the EAD concept of NitrOx is invalid, as there is still quite a bit of gas (in the form of excess O2 and not N2) that must be off gassed safely in order to prevent DCS or AGE.

Your thoughts are eagerly anticipated...

I will probably regret this!

I think you will find few accept that oxygen is a problem for DCI because it is not an inert gas. I will try not to go into too much detail but if you think at the level of a capillary blocked by a bubble of oxygen and another blocked by a bubble of nitrogen (or air).

Both will cause an air lock and stop tissue perfusion and offgassing at least at first, but in the case of the oxygen bubble, the tissues will rapidly use it to generate highly soluble CO2 (no bubbles) molecule for molecule (the tissue cannot get oxygen from blood because the blood supply has been blocked by the bubble!) and thus the bubble's size is quickly reduced to zero, restoring perfusion and allowing further offgassing.

In the case of a nitrogen bubble (or an air bubble once the oxygen in the air is used up) as nitrogen is not metabolised the bubble will continue to block the blood supply to the affected tissue for much longer, and indeed it may even grow in size as the tissues offgas into it, causing local tissue damage we know as DCI.

Now, if I am wrong can you explain how recompression to 2.8 bar oxygen on therapeutic tables works in the treatmant of DCI, Netdoc?

In a nutshell, DCI is only caused by inert gas so the concept of EAD is quite valid. It considers the partial pressure of the inert gas in any Nitrox mix with reference to air and allows the diver to use air tables at a greater depth using Nitrox.

For example EAN 32% at 30 metres has a ppN2 of 2.72 bar, which is the same as air at 24 metres. Thus a dive to 30 metres on Nitrox 32% can be treated as a dive to 24 on air for the purposes of decompression.

This is not to be confused with END which considers the theoretical narcotic potential of a gas mix.

 

[robjones]

Dear Paul

My thanks to you and everyone else who contributed for the exponential increase in my knowledge and understanding of what's going on here.

 

[The Chairman]

I am not trying to argue one side or the other... I am trying to reconcile what you are saying with my incredibly limited understanding. As Rob put it, my learning in this one thread has been exponential to say the very least. That doesn't mean I won't ask hard and pointed questions that are intended to push the envelope of my understanding even further.

However, it is hard for me to conceptualize bubbles that are not homogenous. While bubbles might be incredibly tiny, I would venture that molecules are tinier still and the Van Der Wall forces that they possess would show little discrimination over which other molecule they would form bubbles with. Hence it would follow that we would not have discrete bubbles of nitrogen and oxygen but bubbles that would be comprised of both in similar proportions as their PP in the plasma.

It would also make sense to me that Oxygen, once out of solution, would probably exhibit the same resistance to re-enter solution as nitrogen. Since lung tissues (surfactant et al) are optimized to increase the transfer of Oxygen into the blood, they might keep plasma blood oxygen saturation high enough to inhibit a quick re-adsorption of oxygen in bubble form.

This brings yet another question to mind... IF oxygen displaces CO2 in the red blood cell. Would this happen continually throughout the bloodstream? Is this a function of perfusion that occurs only in the alveoli? Would this cause an increase of CO2 levels dissolved in plasma? Do red blood cells transport CO2 at all? If they don't then this starts to make a lot more sense. Once free of it's oxygen load (taken by a cell) would the cell then absorb another free roaming oxygen molecule with the resultant being released in to the blood stream as a free molecule???

So many questions....

BTW, Dr Paul... THANKS for the enzyme explanation. That was worth it's weight in gold.

One last thing... lest I am mis-cast here and since I have not done it in a while. I heal sick networks and not people. I am NOT in any sense a medical doctor. However, the doctor for your Network is always in!