Personal O2 Toxicity Concern question..

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Falcon99

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Dr. Deco,

I've studied all the technical data and theory I could find on Nitrox like a good little engineer and am ready to take the certification, but have a rather technical concern about toxicity.

I know it is a rather individual thing, but I am concerned I may be one of those at high risk - bear with me here..

I always have had a high MCV when they did routine blood tests in the military. It isn't grossly high, just bouncing around on the upper limit. I read all I could on the subject, but not much detail was available. During flight training in 1998, I had my first experience with the altitude chamber to learn my hypoxia symptoms and that of others... Here's where it gets interesting. My symptoms were VERY minimal at most - a slight coldness in the fingers and a pressure feeling on my neck. That was it. I lasted nearly 10 minutes at 25,000 feet before any degradation of mental task ability was significant. Everyone else was gone in about 5. The lead instructor was pretty miffed, along with the observing flight surgeon. They just brushed it off saying I was lucky to have the ability to last longer than others and that it was probably a genetic trait. Here's my concern.. My blood's oxygen transport ability seems very, very efficient at low PPO2 levels. This leads me to think high caution is warranted with nitrox - i.e. I may not be so lucky at high PPO2 values. Any ideas?

James
 
Hi james:

Mean Corpuscular Volume

The volume measures the amount of hemoglobin in each red cell. However, the number that one is most interested in , I believe, is total hemoglobin. This is given, if I remember correctly, in grams hemoglobin per 100 cc of blood.

It is this number that athletes attempt to increase when they go to high altitudes for several weeks to train. It is this that they also attempt to change through “blood doping.” The amount of hemoglobin determines the amount of oxygen carried by the blood and hemoglobin is essentially saturated in room air.

It diving, when pressurized air us employed, the added amount of oxygen in dissolved in the plasma, the fluid portion of the blood (as contrasted with oxygen carried by the formed elements of the blood.

I suspect that while you might be resistant to hypoxia, this will not translate directly into sensitivity to CNS oxygen toxicity.

Dr Deco :doctor:

Please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm
 
Good to hear the details! So CNS toxicity is caused by the excess O2 dissolved in the plasma? Now that I thought about it, it makes sense since once the Hemoglobin is saturated, not much more can be transported in that meduim.

I really appreciate the response. Thanks!

James
 
Falcon99 once bubbled...
Good to hear the details! So CNS toxicity is caused by the excess O2 dissolved in the plasma? Now that I thought about it, it makes sense since once the Hemoglobin is saturated, not much more can be transported in that meduim.

I really appreciate the response. Thanks!

James

HI J:

An interesting interpretation, but I wish it were that simple. CNS toxicity is not caused by excess 02 dissolved in the plasma, but on how the brain responds to the high partial pressure of 02 once it diffuses in nervous tissue.

As all tissues require blood and hemoglobin to carry gases to and away from it, measuring the concentration of gases here is an indirect measure of what tissues receive.
 
As Saturation rightly states, CNS oxygen toxiciy is due to the effects of molecular oxygen at the intracellular level of brain tissue, where it is thought to generate nasties such as free radicals and the hydrogen ion, in consequence of the locally ambient ppO2.

There are as many theories about the actual cause of CNS oxtox as there are diving physiologists (and I tend to believe that a major contibutory factor is that a high ppO2 disables the carbaminohaemoglobin pH buffer since little CO2 can be deactivated if oxygen preferentially occupies the haemoglobin's carrier sites, which remains saturated with O2 - and CO2 retention increases the risks of a hit) but one factor that must always be remembered is the unpredictability of CNS oxygen "hits", both from person to person and within an individual person, from day to day.

As a general rule of thumb, if the inspired ppO2 is kept below 1.4 bar CNS oxtox is unlikely while a ppO2 of 3 bar will effectively guarantee a convulsion, in time. In the relatively safe environment of a recompression chamber oxygen is most often delivered at a partial pressure of 2.8 bar and CNS hits are relatively common, but entirely benign.
 
Dr Deco once bubbled...
Hi james:

Mean Corpuscular Volume

The volume measures the amount of hemoglobin in each red cell. However, the number that one is most interested in , I believe, is total hemoglobin. This is given, if I remember correctly, in grams hemoglobin per 100 cc of blood.
Not stictly correct Dr Deco!

MCV is actually the mean corpuscular volume, which is independent of the amount of haemoglobin carried. Indeed there are many examples of macrocytic anaemia, where the disease state causes the production of large red blood corpuscles which contain reduced quanties of haemoglobin. liver disease being a prime example.

As you quite rightly state, Dr Deco, it is the amount of haemoglobin, measured in grams per decilitre, which determines the degree of anaemia and the relative ability of the blood to transport oxygen to the tissues.

I suspect that James not only has/had a higher than normal total Hb, I supect, in addition, he has a greater oxygen reserve due to higher concentrations of myoglobin in his body. As you also rightly state, his obvious ability to tolerate hypoxia is quite unrelated to the mechanisms at play in the generation of CNS oxtox.


The amount of haemoglobin carried by each red corpuscle is the mean corpuscular haemoglobin, MCHb, which has little general use in clinical practice.
 
Many thanks for the info. I was unaware of the corpuscular volume anomaly with a normal hemoglobin concentration.

As for CNS and oxygen in the blood, this must be translated over to oxygenation of the brain neurons. Certainly, you can oxygenate a beaker of blood till the cows come home, and that blood will never convulse.

Dr D. :doctor:
 
Dr Deco once bubbled...
. . . I was unaware of the corpuscular volume anomaly with a normal hemoglobin concentration.
You are very welcome Dr Deco, it is gratifying that our information exchange can occassionally reverse direction! :)

As an aside, our courts look for the abscence of various markers of liver disease when assessing whether to return a convicted drink driver's licence. One of these is a marker called gamma glutaryl transferase (GGT) another is macrocytosis.
 
Dr Paul Thomas once bubbled...
where it is thought to generate nasties such as free radicals and the hydrogen ion

and CNS hits are relatively common, but entirely benign.

Thank you for the information regarding hits and some of the mechanisms, I find this topic very interesting. I frequently deco on oxygen at 1.6 ppo2.

I am curious about some of the less intense effects of high ppo2. You mention free radicals and hydrogen ions, which I assume do some damage? I realize this may be on the order of breathing car exhaust or eating pesticides.

I assume there are also other effects, such as better oxygenation of areas in the body that may not "get enough" for some reason at a PO2 of .21

Also, I know some organisms are anaerobic, and exposing them to oxygen will kill them. Am I correct to assume that breathing high ppo2 gas will also have an effect on these?

Are there any other effects?
 
Braunbehrens once bubbled...
Thank you for the information regarding hits and some of the mechanisms, I find this topic very interesting. I frequently deco on oxygen at 1.6 ppo2.
I did too. Most agencies consider this level safe for deco.
I am curious about some of the less intense effects of high ppo2. You mention free radicals and hydrogen ions, which I assume do some damage? I realize this may be on the order of breathing car exhaust or eating pesticides.

I assume there are also other effects. . .
This is a pretty complex subject, Braunbehrens and I suggest you refer to a diving medicine text such as Bennett & Elliott or Edmunds et al. Perhaps a search on Scubaboard for oxygen toxicity, too?

You are ablsolutely right about some tissues getting inadequate oxygenation at 0.21 bar ppO2. This is seldom seen in diving practice but often seen in medical practice! Diabetics suffer considerable tissue damage from poor circulation = poor oxygenation. The organism that causes necrotising fasciitis is killed by high ppO2 so hyperbaric chambers are frequently, and successfully used for the treatment of surgical wounds, ulcers, anaerobic infections and CO poisoning with 2.8 bar ppO2.
 
https://www.shearwater.com/products/swift/

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