Low-dose ASA

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Cacia

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Dear Dr. Deco,

About ten years ago I used to dive with physicians (cardiac surgeons, anesthesiologists and a perfusionist) and they all took baby aspirin when doing repetitive day diving. They thought that its anticoagulation effect might thin the blood enough to prevent microbubbles from aggregating as readily or something like that..... It sort of made sense at the time and I have been popping baby aspirin daily when I dive a few days in a row. Since it is generally advised to take an aspirin if you are having chest pain, (to prevent myocardial ischemia by optimizing microcirculation) does this seem like a plausable theory?

Also, I was curious how big of a role the slight shifts in blood pH play in shifting the equations that determine at what point bubbles come out of solution.
 
If I may chime in: I did a quick google yesterday about this. I found no plausible documents supporting the use of aspirin to prevent DCS, and several (old ones, though) dismissing the idea.

There's a small discussion on the subject going on over here.

Art
 
Okay, thanks for that. There is a lot of material on this out there!
 
catherine96821:
Since it is generally advised to take an aspirin if you are having chest pain, (to prevent myocardial ischemia by optimizing microcirculation)

IIRC, ASA is indicated for CP because it changes how clotting factors work. The purpose of taking ASA is to discourage clot formation to prevent an existin clot or thrombis from further occluding the cardiac artery.

Also, I was curious how big of a role the slight shifts in blood pH play in shifting the equations that determine at what point bubbles come out of solution.
I would guess no as your blood pH needs to be in a fairly narrow margin anyways 7.35-7.45. I don't belive ASA affects pH significantly.
 
Hello Catherine:

Aspirin and DCS – the Origin

The original research on aspirin, and other biochemical modifiers of blood, was performed on rats in the late 1960s and early 70s. Unfortunately, the rat is not a good model for DCS in larger mammals [e.g., humans]. Because of the small size [I guess], nitrogen does not form bubbles in the connective tissues. The first presentation [observable effect] of decompression is a slowed gait [that could be true joint-pain DCS], labored breathing, paralysis, and lastly complete, cardiopulmonary collapse [that is, the rats die].

Virtually all researchers using the rat model exposed the critters to profiles that result in a large percentage of deaths. These deaths result from a right-heart air lock (too many gas bubbles in the ventricles) and sometimes arterialization and embolization of the coronary arteries. [All of this is easily determined by autopsy. ] This si not "the bends."

With such an abundance of gas bubbles in the venous system, some drugs were found to ameliorate the problem. Aspirin was one of these. Clearly, right-heart failure and joint-pain DCS [the “bends”] are not the same. They do not have the same etiology [cause] and they do not have the same consequence. With entirely different pathophysiologies, it can be seen that one drug might not help the other situation. When the meds were tried on humans, there was no effect on DCS incidence (all cases of joint pain). [Other DCS problems were too few.]

Joint Pain

The gas phase associated with joint pain is most likely extravascular. Compression eliminates the pain [were performed soon after the problem] and depressurization causes it to reappear in the same place. If were the result of bubbles in the vasculature, they most like would shrink and be swept away. The pain would not reappear in the exact same location, e.g., the elbow.

Since platelets and the like are not located outside of the circulatory system, anticoagulation agents would not have any effect on the “bends.” Were one to get an excessive gas bubble load from a missed decompression, such as that described in “The Last Dive,” this would be different. Aspirin is not the answer, of course to omitted decompression and the dose given might not be sufficient in any case.

Dr Deco :doctor:
 
There are some threads on TDS related that are somewhat related to this topic. They deal with the comon practice among certain cliques of tech divers of taking large doses of NSAIDs before exteneded range dives, in part to reduce RBC rigidity. The downside is that if you do end up bent and you have a spinal bleed (which is common) having a ton of an NSAID onboard is going to make things worse.
 
Dr Deco:
Hello Catherine:

Aspirin and DCS – the Origin

The original research on aspirin, and other biochemical modifiers of blood, was performed on rats in the late 1960s and early 70s. Unfortunately, the rat is not a good model for DCS in larger mammals [e.g., humans]. Because of the small size [I guess], nitrogen does not form bubbles in the connective tissues. The first presentation [observable effect] of decompression is a slowed gait [that could be true joint-pain DCS], labored breathing, paralysis, and lastly complete, cardiopulmonary collapse [that is, the rats die].

Virtually all researchers using the rat model exposed the critters to profiles that result in a large percentage of deaths. These deaths result from a right-heart air lock (too many gas bubbles in the ventricles) and sometimes arterialization and embolization of the coronary arteries. [All of this is easily determined by autopsy. ] This si not "the bends."

With such an abundance of gas bubbles in the venous system, some drugs were found to ameliorate the problem. Aspirin was one of these. Clearly, right-heart failure and joint-pain DCS [the “bends”] are not the same. They do not have the same etiology [cause] and they do not have the same consequence. With entirely different pathophysiologies, it can be seen that one drug might not help the other situation. When the meds were tried on humans, there was no effect on DCS incidence (all cases of joint pain). [Other DCS problems were too few.]

Joint Pain

The gas phase associated with joint pain is most likely extravascular. Compression eliminates the pain [were performed soon after the problem] and depressurization causes it to reappear in the same place. If were the result of bubbles in the vasculature, they most like would shrink and be swept away. The pain would not reappear in the exact same location, e.g., the elbow.

Since platelets and the like are not located outside of the circulatory system, anticoagulation agents would not have any effect on the “bends.” Were one to get an excessive gas bubble load from a missed decompression, such as that described in “The Last Dive,” this would be different. Aspirin is not the answer, of course to omitted decompression and the dose given might not be sufficient in any case.

Dr Deco :doctor:


The real qustion is that if all things are equal, is asprin an effective anticoagulate? the answer is yes.

Now, will that prevent the bends? At the present time, the answer is no.

But, if the question is will the result of micro-bubbles in the blood will be less likely to cause a larger clot, or thrombosis, the answer must be yes.

Stan
 
serambin:
The real qustion is that if all things are equal, is asprin an effective anticoagulate? the answer is yes.

Now, will that prevent the bends? At the present time, the answer is no.

But, if the question is will the result of micro-bubbles in the blood will be less likely to cause a larger clot, or thrombosis, the answer must be yes.

Stan
If you are the latter situation, you are in very big trouble ASA or no.
 
serambin:
The real qustion is that if all things are equal, is asprin an effective anticoagulate? the answer is yes.

Stan

False.


Anti-platelet drugs!
Not anticoagulate
 

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