VSD and caves

[Dr Deco]

Hello wetvet:

Diastole

Curiously, between the times I read the initial responses and wrote my response, I did not see the other comments. The reply from “pufferfish” with respect to diastolic pressures deserves comment. When addressing the question of pressure differences in the heart chambers, most will think of differences between maximal pressures in the opposing chambers. This is not really the correct period in the heart cycle. It is necessary to consider the pressure cycle during the entire heart cycle. In the atria, there can sometimes be a momentary reversal during the cycle, usually end diastole. This can be especially true if such an instant corresponds to a certain point in the inspiration or expiration during breathing.

I do not know the specifics in a closed chest human; they are probably not the same in a quadruped lab preparation. Because of the PFO issue, more appears in the literature concerning this problem.

Recumbency

This will change the atrial preload and has been implicated in paradoxical embolism through a PFO. This, and immersion ( another form of recumbency) is not treated with high regard by barophysiologists, in my experience, but I believe I can back up my observations and concerns. What these effects are in the ventricular system, I do not know.

We will all be curious to see how this will play out.

Dr Deco :doctor:

Please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

 

[pufferfish]

Hi Dr. Deco,

It has been quite a while since I have thought about cardiac physiology but when I saw this question the first thing that came to mind was immersion or recumbency and resultant changes in preload in the right heart. Is there any data with your altitude work on how quickly these shifts occur from peripheral to central circulation and what kind of relative volume shifts are we talking about?

And yes it would be during inspiration when there is a increase in preload due to the higher negative intrathoracic pressure that one might look for paradoxical emboli during end diastole. The heart also usually increases its rate during this time because of the extra preload (sinus arrythmia).

I read an article this spring (link below) on pulmonary edema with scuba diving and they have a section on immersion effects and discuss preload. It appears there are other factors specific to diving which would enhance this effect far more than seen in soley a gravity-free state.

Preload is increased further with immersion due to the increased ambient pressure on the body and reduced pooling in the leg veins.

This redistribution is also dependent on water temperature and cold temperatures would cause peripheral vasocontriction and increased fluid shifts to the central blood volume from the periphery.

The authors also make reference to studies in rats (those poor rats again) which showed "significant increases in pulmonary artery pressures due to short-term cold exposure." Increases in pulmonary artery pressures would lead to increased right sided end diastolic pressures and increased likelihood of a paradoxical emboli.

Trying to assess the potential for a right to left shunt then all of a sudden becomes much like trying to predict the probability of the eastern electrical grid failure. When enough of the factors which each on its own likely would not cause an event do come together in time, the risk of occurence increases substantially.

A large VSD, deep decompression dive, cold water and poor thermal insulation, inspiration, end diastole, and a forced micturation (I gotta pee right now and valsalva) might just be the 'perfect storm' to allow the gas emboli to shunt to the arterial circulation. The risk of an event may be very low, but the risk of serious injury if it happens very high.

Just curious why don't the barophysiologists treat immersion and preload changes with high regard? Seems like an important factor to me

Pufferfish

Pulmonary Edema in Scuba

 

[wetvet]

This is what I love about science.....the more you know, the less you know.

Dr. Brose responded to my question.....extremely quickly, I might add. He stated a bunch of general things about my VSD, and then stated that as long as the shunt is left to right, it is not a contraindication to diving. I had explained to him that I was planning on caveing, with the resultant deco obligations, so I assume that he meant that the VSD is not a contraindication to THAT kind of diving. YAY FOR ME. (this is all based on the fact that I do not have any changes in heart structure ie: no LV dilatation, or RV hypertrophy)

Pufferfish makes some very good points, which definitely increase the risk for right to left shunts. If ANYONE has any information about the likelyhood of such flow reversals.....I'm kinda interested.

Sooooo......its off to the cardiologist to get my chest shaved , and hopefully get a letter and some reassurance.

Wetvet

 

[Dr Deco]

Hi Pufferfish:

Recumbency

These effects of null gravity and Recumbency were noted during my research at NASA concerning decompression in individuals while in space. Recumbency and zero gravity are roughly equivalent with respect to the fluid shifts (legs to thorax).

Since very few scientists are involved in null gravity decompression, they would not observe the effects. The other part is simply the general inertia that occurs in science over new ideas. The reduction of stress-assisted nucleation in space is another concept. When the legs are not used on the ground (or there is a refrain from strenuous activity), DCS is reduced. You can see in the new Bennett and Elliott (5th edition) that some authors comment on this effect, and with others, any mention of the effect is conspicuously absent.

Trends

As with most things in the world, science has its trends. While “biochemical mechanisms of DCS pathophysiology” have prevailed for almost three decades in barophysiology, I notice that they virtually absence from the 5th addition of Bennett and Elliott. I have argued against these hypothesizes for decades, at personal hazard, but now see that they have set into, what I believe to be, a well-deserved obscurity.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

 

[pufferfish]

Dr Deco once bubbled...
Hi Pufferfish:

Trends

As with most things in the world, science has its trends. While “biochemical mechanisms of DCS pathophysiology” have prevailed for almost three decades in barophysiology, I notice that they virtually absence from the 5th addition of Bennett and Elliott. I have argued against these hypothesizes for decades, at personal hazard, but now see that they have set into, what I believe to be, a well-deserved obscurity.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

Dr. Deco,

I am just curious as to what you mean when you say "biochemical mechanisms of DCS pathophysiology?" I'm always interested in the evolution of trends and obscure ideas

Thanks,
Pufferfish

 

[Saturation]

wetvet once bubbled...
This is what I love about science.....the more you know, the less you know.

Dr. Brose responded to my question.....extremely quickly, I might add. He stated a bunch of general things about my VSD, and then stated that as long as the shunt is left to right, it is not a contraindication to diving. I had explained to him that I was planning on caveing, with the resultant deco obligations, so I assume that he meant that the VSD is not a contraindication to THAT kind of diving. YAY FOR ME. (this is all based on the fact that I do not have any changes in heart structure ie: no LV dilatation, or RV hypertrophy)

Pufferfish makes some very good points, which definitely increase the risk for right to left shunts. If ANYONE has any information about the likelyhood of such flow reversals.....I'm kinda interested.

Sooooo......its off to the cardiologist to get my chest shaved , and hopefully get a letter and some reassurance.

Wetvet

Thanks WV, Dr. Bove's expert opinion certainly emodies a great deal of experience. Please keep up posted on your progress.

Clinical theory is one thing, but the practical results ofyour exploits could help other VSD patients in the future.

 

[Dr Deco]

Dear pufferfish:

Biochemical Mechanisms of DCS

The idea for a biochemical mechanism for DCS arose from observations that DCS does not occur immediately after a reduction of pressure. A period of time (tens of minutes) intervenes. Since bubbles are thought to form as soon as pressure is reduced (as in the opening of a carbonated beverage), or when the “metastable limit” is exceeded, there arose in researcher’s minds the idea that there was a “missing link.” The free-gas phase was referred to as a “trigger” to instigate other biochemical processes. This supposedly required a period of time and would account for the delay between the pressure drop and DCS signs and symptoms.

Bubble Growth

Concurrent with this were my early ultrasound studies on gas phase formation/growth instigated in 1970 [References below, #1 and 2]. These indicate that the time course for bubble development (growth) paralleled the development of DCS signs in rats and that that an “intermediary” was not needed as a separate postulate.

Concurrent with this was the observation that rats were not really acquiring DCS in the form associated with human DCS. That is, humans commonly acquire joint pain and, in contrast, rats commonly die (of pulmonary gas embolism). While these are related (gas uptake, pressure reduction, bubble growth), they are separate phenomena with differing pathophysiologies.

Rats as far as I can tell, do not actually get “the bends” (first pointed out by Kindwall in 1964). This fact is probably related to the small size and diffusion distances of the connective tissues. It is easy to work with rats, however, and death is a very clear, convenient endpoint. Wrong, yes, but very convenient.

Countermeasures

Since very large gas loads are required to produce (what I termed) “decompression death,” it was certainly possible that all manner of blood changes could be found in animals (rats especially), and some drug interventions might be of utility. Only when large venous bubble loads were encountered did some of these changes appear in large animal models (references 3, 4, 5). Interventions were minimal to absent in humans (where DCS is very mild compared to the animal models employed). However, the enormous venous return gas loads encountered in animals are not found in humans (References 6 and 7).

Recompression

Other reseachers , in addition, pointed out the recompression reverse DCS signs and symptoms almost immediately if the time to treatment has been only a couple of hours. Biochemical methods of DCS would not be thought to be pressure responsive.

At this point it is necessary to emphasize that, when DCS remains untreated for several hours, other processes will develop (e.g., edema) and pressure reversal will not occur since the gas phase is now probably absent. Late-treated DCS is not the same as pressure reversal of DCS within the first hour. It has progressed now to a “different beast.”
Complement Factor

This is another example of small animal studies being extrapolated to humans. Nothing ever worked as it should, but it sure seemed as if it were a wonderful idea. It was, again, another alternative to the “bubble etiology” of DCS. In the face of so much negative results, it is finally going away.

Bubble Etiologies of DCS

We are now back again to some semblance of "fairness" in DCS with bubble models based on two-phase systems. While not understood by many, they are gaining some respectability. In fact, to my surprise, my research is even mentioned in Bennett and Elliott, 5th edition. [I wrote a long piece about Doppler Bubbles in the 3rd edition. This was countered to the prevailing ideas, and I never was asked to write a section again.]

Caveat emptor

The idea of tissue micronuclei with short lives generated by hydrodynamic cavitation with a power function size-number distribution will eventually be found to correct, I believe. Until it is replaced by something better (by me or another researcher), this is what I write in this FORUM and that is what I teach in my classes.

It is not a mainstream concept – yet - not even in the RGBM.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology :grad:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

References
1. MR Powell. Leg pain and gas bubbles in the rat following decompression from pressure: monitoring by ultrasound: Aerospace Med., 43, 168-172 (1972).
2. MR Powell. Gas phase separation following decompression in asymptomatic rats: visual and ultrasound monitoring: Aerospace Med., 43, 1240-1244 (1972).
3. GF Doebbler, MR Powell, RW Hamilton, Jr. Biochemical indicators of decompression sickness. In: Proceedings: International Symposium on Blood-Bubble Interactions In Decompression Sickness, Toronto, August (1974).
4. MR Powell, GF Doebbler, RW Hamilton, Jr. Serum enzyme level changes in pigs following decompression trauma. Aerospace Med., 45, 519-524 (1974).
5. MR Powell. Doppler ultrasound monitoring of venous gas bubbles in pigs following decompression from helium, neon, and air. Aerospace Med., 45, 505-508 (1974).
6. MR Powell. The Physiological Significance of Doppler-detected Bubbles in Decompression Sickness. In: Early Diagnosis of Decompression Sickness, Undersea Medical Society, Bethesda (1977).
7. MR Powell and DC Johanson. Ultrasound Monitoring and Decompression Sickness. In: Proceedings. VI Symposium on Underwater Physiology, Undersea Medical Society, Bethesda (1978).

 

[Saturation]

Dr Deco once bubbled...
Dear pufferfish:
Bubble Etiologies of DCS

We are now back again to some semblance of "fairness" in DCS with bubble models based on two-phase systems. While not understood by many, they are gaining some respectability. In fact, to my surprise, my research is even mentioned in Bennett and Elliott, 5th edition. [I wrote a long piece about Doppler Bubbles in the 3rd edition. This was countered to the prevailing ideas, and I never was asked to write a section again.]

Caveat emptor

The idea of tissue micronuclei with short lives generated by hydrodynamic cavitation with a power function size-number distribution will eventually be found to correct, I believe. Until it is replaced by something better (by me or another researcher), this is what I write in this FORUM and that is what I teach in my classes.

It is not a mainstream concept – yet - not even in the RGBM.

(1978).

Hi Dr. Deco:

A most illuminating summary of the various counter-theories for the pathophysiology of bubble trouble.

Its most unfortunate that the political squabbles in diving prevent wider dissemination of alternative theories, which are covered in the 5th edition of Bennett & Eliott. The new authors, Tom Newman and Alf Brubakk inject new insights and are most flexible.

I hope to see your collected insight in B&E's 6th edition. I will discuss it with the current editors at the next meet.

Some insight:

From a clinicians viewpoint, their is some practical benefit of your theory in modern diving, exertion is detrimental, and while this is accepted and well known in clinical studies, there is mixed reception to the idea that nucleation is potentially a big culprit to DCI generation.

As a newcomer, it seems that older data support such contention, especially results in anesthetized animals exposed to inert gas loads fatal to non-anesthetized animals.

It would be good to see if partially anesthetized animals have fatality rates inbetween active and fully anesthetized animals.

 

[pufferfish]

Dr. Deco,

Thanks so much for taking the time to put together that post on your work on DCS over the years. Your contributions to this board are a real asset to divers trying to understand these processes.

At risk of personal hazard I don't think the idea of a 'biological' component to DCS is dead in the water yet. In fact I would predict that we will see more reference to DCS being an 'infectious' disease process with bubbles as the 'pathogen'. Just like a virus or bacteria induces a 'cytokine signature' which may further modulate the immune response up or down or in some cases cause direct tissue destruction, I suspect a bubble is seen by the immune system as a foreign invader and a vigourous immune attack ensues if not removed quickly.

The master hormone that likely regulates this process at many levels and can dampen the process is one's ability to produce sufficient levels of cortisol from the hypothalamic-pituitary-adrenal (HPA) system. Cortisol dampens the hypercytokinemia. In fact my hunch is that the key to keeping DCS tissue damage under control is the ability of one's HPA system to release sufficient cortisol in the face of a 'stressor' like a bubble or infectious particle. This adrenal reserve in fact is likely the basis to our 'constitution' and 'individual susceptibility' factor we see in DCS. In the critical care field evidence is emerging that one can predict accurately who will survive surgery or sepsis (blood infection) simply by assessing one's adrenal reserve. I see the Japanese have started to look at some of these adaptive repsonses in terms of hyperbaric stress.

Stress Hormones and Saturation Diving


Adrenal 'fitness' and the ability to release sufficient cortisol levels to counter the cytokines released by surgery, infection, or a large bubble load can be assessed by heavy exercise, insulin challenge, 35% CO2 challenge, or an ACTH challenge. Military physiologists are very interested in this prior to sending soldiers into theatre and I suspect in the future we will be assessing astronauts and diver's HPA fitness prior to long difficult missions. It really is the HPA axis where all the organism's stresses both psychological and physical feed down through. There must be a final common pathway to handle the multitude of stressors we are exposed to.

In effect I think your theory about bubble formation is right on the money, but once those bubbles are in the systemic circulation the immune system is activated just as it would be for a virus, bacteria, or other foreign particle. Early recompression would abate this process much like early antibiotics in gram negative sepsis can stop that cascading process up to a certain point. Once though the cytokines are released and become amplified in a cortisol deficient subject, antibiotics in the case of sepsis and recompression in the case of Type 2 DCS are likely of little help. Interestingly recently in the case of sepsis in those patients whose adrenal reserve was assessed on admission to be insufficent, and who were given physiologic doses of cortisone saw their complication and mortality rates fall substantially.
Has anyone looked at using physiological doses of hydrocortisone in neurological DCS during recompression? :wacko:

While these ideas have no research to back them up in the case of DCS and may just be that, ideas from out in left field I do see so many similarities between the pathogenisis of infectious diseases and DCS that one cannot help but wonder. The problem in the past it seems is we did not have the knowledge or assays of what to look for. In essence the 'eyes couldn't see what the brain didn't know' but things have changed very much in the last two years. Salivary cortisols, HPA axis fitness, cytokine assays have all come into the mainstream infectious disease literature in the last two years.

It is time to look at adrenal fitness with regards to 'individual susceptibility' in DCS and cytokine signatures (not complement but hormones like interleukin 1,6, tumor necrosis factor, etc) with bubble formation. I think in the end we may think of bubbles as 'bugs' and rather than giving antibiotics if early we give recompression. Later on once immune mediated tissue destruction is underway the treatment will be anti-TNF and similar antibodies as well as supplemental cortisone to further dampen that tissue destruction.

These concepts are becoming well established in the infectious disease community and I would like to know if any barophysiologists have started to look at this even if still in obscurity. Remember it was Louis Pasteur who said "chance favours the prepared mind"

 

[Dr Deco]

Hello Again Pufferfish:

Thanks for the comments. When I speak of “biochemical etiologies,” I am referring to those processes within the first hour that directly result in the pain of DCS. I have not seen evidence that a chemical pathway mediates this. A strain is another lesion to a ligament that can result in pain and will within a short time result in pain that is “biochemical” in origin. I do believe that the same will occur with gas bubbles, but only after a period of time. The joint pain is probably from extravascular bubbles and would not, most likely, be reflected in measurements made on blood.

The pain within the first hour can be made to appear and remit by decompression- compression cycles which indices that it is probably a mechanical process. After time passes, it is known that recompression is minimally effective and some more permanent process has ensued.

Within all of this are, naturally, the components of the blood, the third-space fluids, and the cytosol. I suspect that there are differences within individual genotypes and phenotypes causing a difference in resistance to DCS with a given depress. What these are, I do not know. Within the framework of the microbubble hypothesis, there are compounds responsible for the lifetimes of the nuclei, which I believe vary from person to person.

I have wondered if it is possible to determine resistance from a test as simple as blowing a set volume of air into a certain volume of serum through a fixed needle gauge. How many bubbles are formed, and how long do they persist? My colleagues and I have discussed something as simple as this, but we need human test subjects on fixed protocols; this requires suitable decompression runs to be available. It requires permission to perform studies (and, unfortunately, we are not catching NASA at her best).

In short, are there some biological differences? I am sure there are. Could I take ten individuals, test them, and tell you which are DCS sensitive and which resistant? I believe, yes, I could, and even many of my colleagues would believe this. This is not currently of interest to NASA management (because astronauts must always be in at least pairs, so fast depress and egress is not an advantage). Thus, this biology is lost. Whether we could find why some differ with respect to DCS is another question.

Dr Deco