Why hydration?

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ebbdiver

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I always see good hydration before diving recommended for DCS prevention. Why does good hydration help prevent DCS biologically speaking? Thanks.
 
1) changes the solubility coefficient of the divers blood (affecting absorbsion rates)

2) increases density of fluid increasing clotting (clotting around small groups of inert gas bubbles cause a blockage which increases as more clotting occurs around this initial blockage)

3) having less available plasma within the circulatory system makes transport of CO2 from the tissues much less efficient)

4) increased CO2 levels in the blood and tissues:

a) increase in narcotic effect of nitrogen
b) increased pulse and respiration (air supply consumption and increased gas uptake)


Just to get the ball rolling here...

Jeff Lane
 
ebbdiver once bubbled...
I always see good hydration before diving recommended for DCS prevention. Why does good hydration help prevent DCS biologically speaking? Thanks.
 
Dear MonkSeal:

Hydration

The classical reason given is that fluid volume increases the perfusion and will assist in elimination of inert gas. I am not certain that fluid volume in the absence of exercise (the muscle pump) would be of that much benefit, but this has not been tested to my knowledge.

My personal felling is that hydration will change the concentration of surface-active biomacromolecules in the tissue fluids. This is speculation based on an old study of Dennis Walder (1948). It has never been proven one way or the other.:coke:

The ATTACHMENT does illustrate a study by Canadian researchers during World War II showing that increasing the number of glass of water imbibed will reduce DCS from exposure to altitude. The latter implies decompression with all gas loads being equal in all individuals.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm
 
rmediver2002 once bubbled...
2) increases density of fluid increasing clotting (clotting around small groups of inert gas bubbles cause a blockage which increases as more clotting occurs around this initial blockage)

I see where you were headed, but I don’t know that I buy it yet. What mechanism are you suggesting is involved whereas the clotting cascade is activated by exposure to nitrogen? Perhaps a bubble of substantial size could irritate the intima of a vessel badly enough to stimulate the release of kinins (factor XII is what I’m really thinking of) or is it an extrinsic pathway? I could see a growing bubble lodged in capillary causing damage and the associated inflammatory response. Either way, if simple irritation and not capillary bed destruction from a bubble “cluster” does indeed start the clotting cascade, wouldn’t DCS patients typically have DIC (to a certain extent) as well? Interesting thoughts indeed. Thanks for provoking thought and making me clear those cobwebs in attic.

Dr. Deco,

Do we commonly get D-Dimer and FSP on DCS patients as an indicator of factor useage?
 
I see where you were headed, but I don’t know that I buy it yet. What mechanism are you suggesting is involved whereas the clotting cascade is activated by exposure to nitrogen? Perhaps a bubble of substantial size could irritate the intima of a vessel badly enough to stimulate the release of kinins (factor XII is what I’m really thinking of) or is it an extrinsic pathway? I could see a growing bubble lodged in capillary causing damage and the associated inflammatory response. Either way, if simple irritation and not capillary bed destruction from a bubble “cluster” does indeed start the clotting cascade, wouldn’t DCS patients typically have DIC (to a certain extent) as well? QUOTE]

Hmm, I was speaking about indirect bubble effects but you bring up a good point about DIC.

You also draw attention to the fact that although stated as factual information in my post these are theoretical responses within the divers tissues.

Interesting thoughts indeed. Thanks for provoking thought and making me clear those cobwebs in attic.[/[/QUOTE

I am by no means an expert but do enjoy the stimulating discussion!! I would love to see some additional input on this subject...

Jeff Lane


Taylor WF., Chen S, Barshtein G, Hyde DE, Yedgar S. Enhanced
aggregability of human red blood cells by diving. Undersea Hyper Med
1998; 25(3)167-170.

Reggiani E, et al. Blood coagulation processes in decompression
sickness and hyperbaric therapy. Minerva Med. 1981 May
31;72(22):1383-90.




http://www.scuba-doc.com/brdprpDCSrx.html Dr. Cambell's site
 
Hi H2O Head:

Blood Factors

I am actually not a big believer in biochemical theories of DCS. I must temper this with the comment that this applies to rapid-onset DCS that is quickly treated. This type responds to treatment within a few minutes of repress in a chamber.

The type that has persisted for hours, allowing other changes to occur than simple bubble growth, are different. These do not respond rapidly to repress and oxygen. Repetitive treatments are often needed, and then the recovery is often not complete.

Most observation of biochemical factors in DCS pathophysiology relates to severe DCS in animals (and sometimes humans) Pharmacological countermeasures have not worked as expected. [Possibly because the hypothesis is incorrect and the role is minimal.]

Dr Deco :doctor:

Please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm
 
https://www.shearwater.com/products/perdix-ai/

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