Human Variability?

[gcbryan]

Dr. Deco,

What, in your opinion, is the biggest variable among divers regarding who gets DCS and who doesn't? I'm sure it's not as simple as some have PFO's of varying sizes and some don't.

Is that in fact the biggest difference?

I'm thinking of the caisson workers and the long exposures that far exceed anything we would expose someone to today. What explains how some divers get bent, some die, and some are fine from the same exposures?

If everyone had a test for PFO's is it possible those with negative results would be doing 2 hours at 100fsw and coming out OK? Is there that kind of conservatism built into the tables just to account for those with PFO's?

If it's not that simple what are the other material variables between divers? I understand exercise might be a factor with bubble formation and perhaps hydration although I doubt those factors (particularly hydration) would explain the large variations amount divers. (Actually, I fail to see why hydration is mentioned so often. We are made up of water. Can slight dehydration really impact this issue?)

If you have an opinion on this please not only list what you think the largest area of variability is but how that factor could significantly increase the chances of DCS.

If there isn't a fairly simple explanation of the large degree of human variability then it almost seems pointless to study the more commonly studied smaller variables. If staying hydrated would improve our chances 1% but if the standard deviation among individual was 50% then it kind of stops minor improvements right there if we have to live with a 50% safety margin anyway.

 

[Dr Deco]

Hello gcbryan:

There would be variety amongst barophysiology researchers in providing an answer to this question. The answer is long and complex – and fraught with hypotheses – but I shall provide a short answer here [and leave the long answer for my book].

Gas Loads

This is of course the most obvious. Without oversaturation of dissolved nitrogen, decompression bubbles could not form/grow. Nitrogen uptake and elimination at the tissue level is determined by blood flow [perfusion] in that tissue. Some tissues, e.g., nerves, have a constant blood supply. Other tissues, e.g., muscle have perfusion that is dependent on oxygen usage, i.e., physical activity. Nitrogen uptake is not dependent on surface breathing rate. Likewise, it is not a function of how fast you exhaust your SCUBA tank [other than when this is related to musculoskeletal activity such as strenuous swimming]. This is demonstrable in the laboratory and has been known for decades.

Experience from the field indicates that diver body temperature is a factor. Warm divers take up more nitrogen and cool divers release less nitrogen. Therefore, the dictum is “dive cool and decompress warm.” Do not chill your body during off gassing.

Nitrogen elimination is not retarded by gas bubbles in the lungs if the bubbles are present in the relatively small quantities encountered in normal SCUBA diving. This gas exchange is demonstrable in the lab, and it was tested at NASA by a colleague of mine in subjects with many decompression bubbles [Spencer/Johanson precordial Grade IV].

Bubble Formation or Growth

Without gas micronuclei, DCS could not occur except with the most severe of supersaturations - hundreds of atmospheres.

If a group of individuals is depressurized [after resting to eliminate activity-formed bubbles; more on this below], it will be found that a fraction will not produce any Doppler bubbles at all. [This is a part of what was called sixty years ago ‘The Systemic Hypothesis.”] If the subjects are depressurized at one-hour intervals following knee-flex exercise, it will be found that bubble Grades decrease with increasing interval between activity and depress.

There are many studies indicating that physical activity plays a very large role in both DCS and bubble formation. Activity exerts its greatest effect kin tissue that move, e.g., muscle, and less in those that are less mobile, e.g., kidney. This is demonstrable in the laboratory.

I believe that activity in the diver, post dive, is the biggest factor in DCS following gas loading.

Diver Differences

I do not know why some individuals have a proclivity to bubble formation and others appear to be resistant. I will posit that it is a biochemical or structural difference at the molecular level. I had plans to test this while I was a NASA, but the opportunity never arose; all proposals were rejected as being of relatively no interest.

Surface tension might be a factor. The evidence is unclear at this point.

Diver differences are poorly understood, and research is not being performed in this area.

Hydration

It has never been conclusively shown that hydration is a big factor within normal hydration limits. Intravenous fluid administration is a different matter and is helpful [I am told] is more serious cases of DCS.

Biochemical and Medicinal Adjuncts

Many ideas of using drugs, such as antiplatelet-clumping medications, developed from research with rats in the early 1970s. The end point of DCS was, unfortunately, death of the small animals. Death is not an endpoint in human diving; death is caused by egregiously large bubble loads to the heart and lungs in the rats and is not related to joint-pain DCS.

In a similar fashion, complement in the blood had its day, but the studies were performed on the wrong model.

PFO

While this is a factor in some DCS cases, it is apparent in a relatively minor fraction of divers. Neurologic DCS depends, in part, on arterialization of gas bubbles. This depends on [1] the number of bubbles in the heart, [2] reversal of normal pressure gradients [and the point in the breathing cycle], and where the arterialized bubbles go in the arterial circulatory system, as well as the number of bubbles.

Add to this the fact that pulmonary shunts in the capillaries can allow arterialization in the absence of a PFO. Passage through flaws in the heart wall is only one method, and it is a waste to test all divers.


Dr Deco :doctor: