A very interesting discussion.
Thanks guys.
Milo
Thanks guys.
Milo
Diving With Nitrox and Blood Donation
- Thread starter LittleBug
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There is a theoretical and functional difference between arterial ppO2 and arterial O2 CONTENT. The ppO2 is only dependent on alveolar pO2, as plasma comes into equilibrium in the lungs. O2 CONTENT is dependent on hemoglobin. We are taught in physiology that O2 is poorly soluble in plasma, and that major increases in inspired pO2 do not significantly add usable oxygen to plasma, which is why even patients put on 100% O2 by ventilator do poorly if their hematocrit is too low (which is something we see with Jehovah's witnesses who refuse transfusion). How much that plasma content can be increased when you go beyond 1 ATA, I don't know, but my guess is that, within the ranges where we dive, hemoglobin content is going to exceed dissolved content many times.
The question is whether CNS oxygen toxicity is related to ppO2 or the O2 content. It stands to reason that, if there is little hemoglobin, then diffusion of oxygen into tissues will quickly lower ppO2 in plasma, whereas with high hemoglobin levels, there will be a buffering effect as oxygen moving out of plasma is replaced by oxygen moving off hemoglobin. So it would be tempting to believe that higher hemoglobin levels might potentiate O2 toxicity by keeping the ppO2 higher.
The question is whether CNS oxygen toxicity is related to ppO2 or the O2 content. It stands to reason that, if there is little hemoglobin, then diffusion of oxygen into tissues will quickly lower ppO2 in plasma, whereas with high hemoglobin levels, there will be a buffering effect as oxygen moving out of plasma is replaced by oxygen moving off hemoglobin. So it would be tempting to believe that higher hemoglobin levels might potentiate O2 toxicity by keeping the ppO2 higher.
If we go to theory of O2 transport, we should just move on to the anemia data...
A systematic review of the application of hyperbaric oxygen in the treatment of severe anemia: an evidence-based approach.
Van Meter. Undersea Hyperb Med. 2005 Jan-Feb;32(1):61-83.
RRR ID: 4038
I guess if we really wanted to let this spiral out of control we would start talking about fluid shifts from immersion and thermal changes.
This was an interesting read on fluid shifts "post-dive".
Hematologic changes after daily asymptomatic dives.
Diercks and Eisman. Undersea Biomed Res. 1977 Dec;4(4):325-31.
RRR ID: 2776
Too much theory for me today... Have a good evening!
A systematic review of the application of hyperbaric oxygen in the treatment of severe anemia: an evidence-based approach.
Van Meter. Undersea Hyperb Med. 2005 Jan-Feb;32(1):61-83.
RRR ID: 4038
I guess if we really wanted to let this spiral out of control we would start talking about fluid shifts from immersion and thermal changes.
This was an interesting read on fluid shifts "post-dive".
Hematologic changes after daily asymptomatic dives.
Diercks and Eisman. Undersea Biomed Res. 1977 Dec;4(4):325-31.
RRR ID: 2776
Too much theory for me today... Have a good evening!
CameronMartz
Fitness Instructor
TSandM:
Just to restate something from my previous post- blood reaching CNS tissues is very near untouched by metabolism. Thus, it seems that peak PPO2 at the CNS tissue is determined by the PPO2 of inspired gas, which as we both stated, is independent of hematocrit level. Metabolic action will only serve to reduce plasma PPO2, and there will be no RBC dissociation of O2 beyond that needed to bring tissue PPO2 into equilibrium with inspired PPO2. O2 bound to an RBC is metabolically inert- it can only function after becoming dissolved into the plasma, thus exerting a partial pressure allowing it to diffuse throughout the tissues in need.
That said, RBCs are flowing to CNS tissues for a reason, and O2 will eventually be metabolized away. Certainly, the higher the hematocrit, the higher the venous PPO2 and the higher the average PPO2 of the blood while in contact with CNS tissue. If either of these figures are of importance to oxtox, this is where hematocrit could have an influence. However, there is more to the story.
Oxygen cannot bind to RBCs without a partial pressure of dissolved O2 "pushing" on it. The higher the saturation of an RBC, the harder dissolved O2 must push to get another molecule to bind to the RBC.
In reverse, the partial pressure of dissolved O2 must drop more to release a molecule of O2 from a highly saturated RBC. In other words, at higher partial pressures of dissolved O2, more O2 must be metabolized from plasma in order to liberate a given quanty of O2 from RBCs.
So again, the higher the plasma PPO2, the less O2 bound to RBCs supplies our metabolic demand. Even if you were to increase hematocrit, the drop in plasma PPO2 from oxygen metabolism will still be high. This is half of the proverbial "oxygen window" that divers take advantage of when decompressing on 100% O2 at depth, and we know that the difference is significant at levels comfortably below CNS oxtox risk.
I also want to reiterate for anyone that has cared to read this far that I think it is the understanding of the oxygen transport system that is of value here, and that the original question serves as a nice way of framing the discussion. I think we are all in agreement with the ultimate answer to the original post.
Cameron
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Hi LittleBug,
No need to apologize. This discussion has clearly lost sight of the original question and audience.
The answer is, yes, donating blood prior to diving on EAN is safe provided that one waits 24 hrs and completely rehydrates over that time, is physically fit for scuba and feels fully up to the activity.
Regards,
DocVikingo
No need to apologize. This discussion has clearly lost sight of the original question and audience.
The answer is, yes, donating blood prior to diving on EAN is safe provided that one waits 24 hrs and completely rehydrates over that time, is physically fit for scuba and feels fully up to the activity.
Regards,
DocVikingo
Right. The loss of one unit of blood in the average person results in a fairly small hematocrit change. A change which, in the healthy person, is almost totally compensated for by increases in heart rate and respiratory rate. The difference in oxygen delivery to the tissues (which is correlated with oxygen toxicity) after transfusion is probably effectively nil.
For the technically obsessed (which is apparently most of us {good natured lol}):
There are a couple exceptions:
This would not be true for people who were very sick such as heart failure patients or people with lung disease, because these people are already living at the limits of their ability to respond to increased metabolic demand. Of course these people wouldn't be donating blood either.
Another exception (this one is key) is people who are maximally exerting themselves. The problem with normal physiology, is that we are all capable of pushing the limits of it by exercising very hard. If you are at 100 feet on nitrox and swimming away from a shark as fast as you can (or more likely: if you are panicking while struggling with an excessively task loaded situation) you might have a lower partial pressure of oxygen in your tissues if you had just given blood. The net result of which, theoretically, would be that you would be somewhat protected from O2 toxicity.... EXCEPT for the fact that if you were struggling at your physiologic limits, you would also be retaining carbon dioxide which is known to potentiate O2 toxicity! In other words, it's really hard to say. By which I guess I mean, until someone does the definitive study on this particular question (don't hold your breath), as always, don't push the limits.
That said, 24 hours sounds like a pretty good margin of error to me.
For the technically obsessed (which is apparently most of us {good natured lol}):
There are a couple exceptions:
This would not be true for people who were very sick such as heart failure patients or people with lung disease, because these people are already living at the limits of their ability to respond to increased metabolic demand. Of course these people wouldn't be donating blood either.
Another exception (this one is key) is people who are maximally exerting themselves. The problem with normal physiology, is that we are all capable of pushing the limits of it by exercising very hard. If you are at 100 feet on nitrox and swimming away from a shark as fast as you can (or more likely: if you are panicking while struggling with an excessively task loaded situation) you might have a lower partial pressure of oxygen in your tissues if you had just given blood. The net result of which, theoretically, would be that you would be somewhat protected from O2 toxicity.... EXCEPT for the fact that if you were struggling at your physiologic limits, you would also be retaining carbon dioxide which is known to potentiate O2 toxicity! In other words, it's really hard to say. By which I guess I mean, until someone does the definitive study on this particular question (don't hold your breath), as always, don't push the limits.
That said, 24 hours sounds like a pretty good margin of error to me.
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