The Brain and Diving

[Bubbletrubble]

I see your point completely. What are your thoughts on Patent Foramen Ovale conditions? I mean apparently up to 20% of the adult population has the condition from birth (in varying degrees of severity) and that the only way to really test for it accurately is using Bubble Echocardiography (which hardly anyone is going to have done). If kept conservatively within a NDL in relatively shallow water (less than 50ft) even with a Patent Foramen Ovale, do you feel the risk of decompression stress is very high?

@Plane Trouble: I think one of the most even-handed, reasonable takes on PFOs in the context of diving is a short essay written in 2004 by Bove and Wood. The article is hosted on the DAN website, so check it out.

In general, I think that recreational divers are more worried about PFOs than they need to be. It sounds like a really serious condition involving a very important internal organ (the heart), so people tend to freak out over it. Assuming that the estimated prevalence of PFO in the general population is similar to that in the diving population (10 - 20%), if PFOs alone were responsible for a high percentage of DCS hits, I'd expect the incidence of DCS per dive in recreational divers to be much higher than the observed 0.005-0.08%. I see that Leadturn SD has similar thoughts on the matter.

Recreational divers should be far more concerned with staying physically fit, remaining well-hydrated, exercising good buoyancy control, moderating decompression stress (bubble load) by not coming close to NDLs, not ascending too quickly, and doing extended safety stops. For tech divers, commercial divers, and scuba instructors (people exposed to significantly higher decompression stress), PFO screening might prove to be interesting...especially if there's a history of probable DCS. I understand that there are cardiologists out there implanting the PFO occluders in divers. To evaluate the efficacy of this intervention, it's critical that the divers: (a) continue to dive the same profiles post-procedure as they did prior to treatment and (b) do a good job of following up with investigators so that outcomes can be tallied. Unfortunately, I suspect that condition (a) will not be met because it's human nature to want to dive more conservatively after a DCS incident. What really needs to be done is a long-term, blinded, prospective study on a population of divers subjected to high decompression stress (commercial divers, tech divers, scuba instructors, etc.). All participants would be screened for PFO. Of those with PFO, study participants would be stratified into a treatment group (PFO occlusion) and control group (sham procedure). Then, they should keep track of their dive profiles (using something like the Reefnet Sensus Ultra) and report back to investigators annually with that dive data and whether or not they experienced any DCS incidents. In an ideal world, both groups would be asked to dive identical profiles, but that kind of demand would not be logistically possible. Having such control in a human study is rather rare. With rodent studies, it's a totally different story.

Going forward, hopefully we'll be able to better track this potential risk factor since the diving public is now hyper-aware of it. I guess that's one advantage of divers obsessing about PFOs.

 

[farsidefan1]

As a diver who suffered an unprovoked DCS last August and had a PFO repaired December 23rd I'm hoping the PFO was a major contributor. As one who swam 1.5 mles 3 times a week and lifted weights 2 times a week I felt I had the conditioning thing down fairly well. I believe I was dehydrated, I think several factors were in play. I had some say they felt really the only factors were how long you were down and how fast you come up. I think they fail to pay attention to the term unprovoked.

 

[idocsteve]

As a diver who suffered an unprovoked DCS last August

The last thing you want to do is provoke a DCS hit. Best thing to do is look it in the eye, and slowly back away, as if it's some sort of stray dog.

 

[Lopaka]

Going forward, hopefully we'll be able to better track this potential risk factor since the diving public is now hyper-aware of it. I guess that's one advantage of divers obsessing about PFOs.

Losing your hearing and having areas of stroke found will do that to you..........

 

[diver 85]

To the OP, here's a list from DAN on possible ocular problems assoc with diving---

DAN Divers Alert Network : High-Pressure Ophthalmology

 

[Plane Trouble]

I noticed at the end of the article the authors mentioned the use of enriched air to decrease the risk of having issues with a possible PFO... Would use of Nitrox on a dive 35ft to the surface be measurably advantageous at eliminating these risks?

 

[Bubbletrubble]

I noticed at the end of the article the authors mentioned the use of enriched air to decrease the risk of having issues with a possible PFO... Would use of Nitrox on a dive 35ft to the surface be measurably advantageous at eliminating these risks?

@Plane Trouble: To clarify, you are referring to the following quote from the Bove and Wood PFO essay published on the DAN website:

In short, having a PFO is not necessarily a contraindication for diving. If it is proven with certainty that a PFO in a diver with VGE predisposes to DCI by providing a route through which bubbles can pass into the arterial circulation, then the safest strategy would be to reduce the venous bubble load by developing different decompression procedures, limiting bottom time or by the appropriate use of oxygen-enriched breathing mixes.

All other things being equal (bottom time, depth profile, etc.), diving an oxygen-enriched gas mix vs. air will result in decreased nitrogen load. If the majority (or entirety) of decompression stress is exerted by nitrogen bubbles, then this should decrease decompression stress in the presence or absence of PFO. Understand that even if nitrogen bubbles are present, they must still find a way to enter the high pressure arterial system and plug up the capillaries in the brain to cause AGE. As you know, the presence of PFO isn't the only medical condition that could cause AGE. Any condition that increases fragility of lung tissue or blocking of the small airways (lung cancer, cysts, infections, smoking, asthma, etc.) increases the probability of pulmonary barotrauma. Keeping an open airway during ascent and ascending under control at prescribed rates will protect against lung over-expansion injuries, which provide a mechanical means of gas entering the bloodstream.

You ask whether breathing nitrox for a relatively shallow dive 35 fsw would be "measurably advantageous at eliminating these risks." There is no such thing as "eliminating" risks altogether. That being said, your DCI risk would probably be very, very, very small if you limit yourself to shallow dives, breathe a 32% or 36% mix and not get anywhere close to NDL limits. Would the benefit be "measurable"? If a properly controlled study were conducted, then the number of subjects included would probably have to be very high in order to have sufficient power to reveal a significant difference in DCI incidence. Practically speaking, I don't think any research entity would ever spend the money, time, or effort to do such a study. There is very little DCI risk when doing dives with a max depth of 35 fsw...even if you choose to breathe air. Furthermore, with shallow dives, proper diving technique and lung health are probably more important factors preventing AGE than minimizing nitrogen load per se.

My advice is to go out there and enjoy the sport of diving. Dive conservatively. Manage your gas supply appropriately, i.e., don't run out of gas. Follow prescribed guidelines (recommended ascent rates, NDL tables or computer-derived NDLs, safety stops, etc.) and stay physically fit.

 

[JonKranhouse]

Oxygen metabolizes and nitrogen bubbles. To minimize any risk of nitrogen coming out of tissues, perhaps via an undiagnosed PFO after very long exposure at depth (albeit just 35'), a high O2% will be safer - as long as you stay far far away from maximizing your CNS and pulmonary "clocks."

Some people insist on buying a car with a 5-star crash test rating, others buy a "reasonably" safe 3-star car because they like the style. Even if there's insufficient research to answer your question definitively, my philosophy is if it can't hurt, and it might help (e.g. prevent brain / bone lesions), then absolutely, positively, go for a high O2%. And follow Bubbletrubble's advice:

Dive conservatively. Manage your gas supply appropriately, i.e., don't run out of gas. Follow prescribed guidelines (recommended ascent rates, NDL tables or computer-derived NDLs, safety stops, etc.) and stay physically fit.

 

[Plane Trouble]

K roger that... I will probably plan on upgrading to Nitrox diver this summer... It wouldn't hurt me to learn some new stuff anyway...

 

[Dr Deco]

Hello Readers :

​

I have been away for several weeks [east coast] and have not been able to read the mail. This thread seems to have gathered several topics. I will add my piece to them.

The PFO Question

Many posters over the years have noted the poor relationship between the occurrence of PFOs and the risk of DCS. It is necessary that several occurrences converge for DCS to appear. Clearly, there must be bubbles in the venous system in the first place. Granting that this happens to some degree, something else must play a role. A part of this, I believe, is the ability of the brain vasculature to allow the bubbles to pass through. What luck!

Decades ago, I investigated this with Doppler ultrasound probes with sheep as the test subjects [ref 1,2]. A probe was surgically implanted on the carotid artery [big artery to the brain] and another over the sagittal sinus [the big vein draining a large portion of the brain]. Following chamber dives that produced very substantial dissolved nitrogen loads, bubbles were produced and carried to the heart and lungs. This could be verified by precordial ultrasound probes. In some cases, bubble loads exceeded the ability of the lungs to filter them. Bubbles could be heard flowing in the carotid artery to the brain. After a few heart beats, the bubbles could be heard exiting the brain and flowing through the sagittal sinus. While I could not make any quantitative determination, the number of exiting bubbles seemed large. The sheep did not display any neurological residuals, although subtle changes would be difficult to see. They are sheep, after all. Studies indicate that small bubble volumes in the brain capillaries are not held and trapped [ref 3].

Another study indicated that arterialization with saline injection [recumbent subject] did not result in arterialization with decompression in an erect subject [ref 4]. This is probably a matter of flow hemodynamics positioning the flow from the inferior vena cava with respect to the PFO. [This is both portioning effects and the Coanda effect.]

References

1. MR Powell and MP Spencer. The Pathophysiology of Decompression Sickness and Doppler-detectable Gas Bubbles. Final Technical Report, O.N.R., Contract #N00014-73-C-0094, (1980).

2. MR Powell, MP Spencer, and O von Ramm. Ultrasonic Surveillance of Decompression. In: The Physiology and Medicine of Diving, 3rd Edition, [P. Bennett, D. Elliott, eds.] pp. 404-434, Baillière Tindall, London (1982).

3. Gorman, D. F. and D. M. Browning (1986). Cerebral vasoreactivity and arterial gas embolism. Undersea Biomed. Res., 13, (3), 317.

4. Powell, M. R., K. V. Kumar, W. Norfleet, and J. Waligora, B. Butler (1995). Patent foramen ovale and hypobaric decompression. Aviat Space Environ Med. 66(3):273-5

Deco Programs

There are always hopes that deco programs become more sophisticated. However, for simple dives, we basically have the No-D limits and that will not change. [Deep dives with decompression are a different story.] You will not get around the laws of nature on that one.

There is another aspect, however, and that involves the fact that you do not form bubbles upon pressure reduction. The microbubbles are already present. If they were absent, you could ascend to the surface from possibly hundreds of feet. It is not known how to modify the nuclei concentration, and no one is working on this question. I had an interest in this question, but I have retired.

Activity Post Dive

The one aspect that can be demonstrated to change bubble formation during depress is physical activity. You do not need a hundred subjects to achieve some degree of statistical validity. You can see it with ten subjects and a few dives. Physical activity is a microbubble producer and activity postdive should be minimized.
References

Powell, MR, J Waligora, W Norfleet, KV Kumar. Project ARGO - Gas Phase Formation In Simulated Microgravity. NASA Tech Memorandum 104762, pp. 87, (1993).

Waligora, J, Powell, MR, and W Norfleet. The abaroferic hypothesis: a mechanism for the reduction of decompression sickness in microgravity, Aviat. Space Environ. Med., 64, 421, (1993).

Powell, MR, W. Norfleet, J Waligora, KV Kumar, R. Robinson, and B. D. Butler. Modifications of physiological processes concerning extravehicular activity in microgravity. Inter. Cong. Environ. Systems, SAE Technical Paper Series, (1994).

Powell, MR, J Waligora, KV Kumar. Hypobaric decompression in simulated null gravity; a model using chair-rest adynamia. Undersea Biomed. Res., 22 (Suppl), 67, (1995).

Powell, MR, J Waligora, and KV Kumar. Decompression gas phase formation in simulated null gravity. 25th International Conference on Environmental Systems. SAE Technical Paper Series 951590, (1995).

Loftin K.C., J. Conkin, MR Powell. Modeling the effects of exercise during 100% oxygen prebreathe on the risk of hypobaric decompression sickness. Aviat. Space and Environ. Med. 68, 199 - 204, (1997).

Dervay, J, MR Powell, and CE Fife Effective lifetimes of tissue micronuclei generated by musculoskeletal stress. Aviat. Space and Environ. Med., 68 (Suppl), A12. (1997).

Dr Deco :doctor: