"Very Few Exercise-Induced Arterialized Gas Bubbles Reach the Cerebral Vasculature"+

[DocVikingo]

[NOTE: Intrapulmonary arterial-venous anastomoses (IPAVAs) are simply connections between two blood vessels within the lungs. These can be between arteries, between veins or between an artery & a vein (arterial-venous). They tend to open during physical activity.]


"Med Sci Sports Exerc. 2015 Jan 26. [Epub ahead of print]

Very Few Exercise-Induced Arterialized Gas Bubbles Reach the Cerebral Vasculature.

Barak OF¹, Madden D, Lovering AT, Lambrechts K, Ljubkovic M, Dujic Z.

Abstract

INTRODUCTION:

Arterialization of venous gas emboli (VGE) formed after surfacing from SCUBA diving can become arterial gas emboli (AGE) through intrapulmonary arterial-venous anastomoses (IPAVAs) that open with exercise.
METHODS:

We recruited twenty PFO negative SCUBA divers and conducted a field and a laboratory study with the aims to investigate the appearance of AGE in intracranial vessels. At the field they performed a single dive to a depth of 18m sea water with a 47 min bottom time and a direct ascent to the surface. Transthoracic echocardiography was used to score VGE and AGE and transcranial Doppler was used to visualize middle (MCA) and posterior cerebral arteries (PCA) with automated objective bubble detection. Observations were conducted for 45 min post-dive at rest and at the laboratory after agitated saline injection at rest and throughout an incremental cycle supine exercise test until exhaustion and for 10 min of recovery.
RESULTS:

After resurfacing all divers presented endogenous VGE and arterialization was present in three divers. Saline contrast injection led to AGE in nine out of 19 subjects at rest. AGE that reached the cerebral arteries post-dive were recorded in 2 divers at 60W, 3 at 90W, 5 at 120W, 6 at 150W and 4 at 180W and in 3, 4, 5, 9 and 9 respectively after saline contrast injection in the lab. All divers had AGE grades of 1 or 2 and only single AGE reached the cerebral vasculature.
CONCLUSION:

These data suggest that few emboli of venous origin reach the brain through exercise-induced IPAVAs but cerebral embolization is not a high risk in the studied population."

Regards,

DocVikingo

 

[doctormike]

Interesting study, thanks for posting!

One of the most difficult questions to answer is what do you do with a diagnosis of PFO once you have it, and you want to continue diving. I'm just a snot doctor, so I'm certainly not qualified to have a real professional opinion about this, but it seems that many of these recommendations are based on gut feelings and educated guessing - things like giving someone a depth limit, etc...

Since any random diver has a 25% chance of having a PFO, and since a symptomatic AGE is a pretty rare occurrence even in technical divers, one might assume that the body can tolerate a certain amount of of gas in the cerebral circulation without neurological injury.

Also, "few" is sort of an arbitrary term. If an AGE in the cerebral vasculature was associated with a significant risk of stroke, then having it occur in 5% (1 out of 20) of PFO negative divers would actually be pretty clinically significant.

So the take home message to me is that even PFO negative people have some right to left shunts. We ALL form venous bubbles on ascent, and therefore some of these will cross over to the arterial circulation. And some patients (based on the size of the PFO? The specifics of their cardiodynamics? Other host factors?) tolerate this better than others. So making a recommendation to dive or not to dive (or to limit profiles) based on the presence of a PFO only is rarely scientifically validated.

Now hopefully one of the smart people on the board (like Lynn or Eric) can tell me why I should shut up and go back to digging out ear wax!

 

[Duke Dive Medicine]

Interesting study Doc, thanks for posting. Mike, I guess you could say that everyone has a potential to shunt through the pulmonary vasculature but only individuals with a PFO can shut through a PFO. Of course there isn't a 1:1 correlation between arterialized bubbles and DCI, or arterialized bubbles and bubbles in the cerebral vasculature as this study demonstrated, but if there are two potential sources of shunting vs. one, it follows that the likelihood of shunting is higher.

Best,
DDM

 

[Kevrumbo]

Nice drawing schematic/overview of anastomoses & capillary beds in the Circulatory System:

http://fce-study.netdna-ssl.com/images/upload-flashcards/928220/726756_m.png

Looks like these Arterio-Venous anastomeses would be the main pathway for gross bubbles causing an AGE in a grave, surfacing-dive accident. . .

 

[Saturation]

There are several studies of this type spanning several years usually with Dujic somewhere among the authors. A key concern is exertion at depth, or after the dive during the period of offgassing. This is of high concern for technical divers who have a lot of equipment to be lifted off a dive site during a period of risk. These and other studies suggest that work of a certain METS at depth or immediately post dive can predispose normal people to DCI, risk which rises as the surfacing gas tensions rise.

 

[Duke Dive Medicine]

Nice drawing schematic/overview of anastomoses & capillary beds in the Circulatory System:

http://fce-study.netdna-ssl.com/images/upload-flashcards/928220/726756_m.png

Looks like these Arterio-Venous anastomeses would be the main pathway for gross bubbles causing an AGE in a grave, surfacing-dive accident. . .

Kevin,

The graphic you posted is a great summary but it's a bit of an oversimplification. For shunted bubbles to have central neurological effects, they have to end up in the arteries that supply the brain and spinal cord. The only real way to do that is for them to end up in the arterial circulation in or around the heart, upstream (so to speak) of those arteries. That can happen through the pulmonary vasculature, a PFO or other atrial septal defect, or through circulatory abnormalities like patent ductus arteriosus.

Saturation brought up a great point about exercise at depth, which can lead to increased inert gas uptake and subsequently increase the probability of DCS, whether shunt is present or not.

Best regards,
DDM

 

[dreamdive]

Here is another study:

Madden D, Lozo M, Dujic Z, Ljubkovic M – Exercise after SCUBA diving increases the incidence of arterial gas embolism
J Appl Physiol 2013; 115: 716-722

Exercise after diving increased the incidence of arterialization from 13% at rest to 52%.
[FONT=Helvetica, Arial, sans-serif]What is disturbing is that arterialization can occur during swimming to the boat, going up the ladder, and even handling the tanks. Oxygen administration appears to close the shunts.
Could this mechanism be an explanation of some "undeserved" Type II hits.[/FONT]

 

[Kevrumbo]

Here is another study:

Madden D, Lozo M, Dujic Z, Ljubkovic M – Exercise after SCUBA diving increases the incidence of arterial gas embolism
J Appl Physiol 2013; 115: 716-722

Exercise after diving increased the incidence of arterialization from 13% at rest to 52%.
What is disturbing is that arterialization can occur during swimming to the boat, going up the ladder, and even handling the tanks. Oxygen administration appears to close the shunts.
Could this mechanism be an explanation of some "undeserved" Type II hits.

Interesting . . .now couple that with other pre-disposing factors such as dehydration, insufficient "acclimatization" to a hot/humid tropical environment (thermal stress with opening of these circulatory anatomoses) along with no previous "work-up" deco dives to sensitize the immune system/inflammatory response of the body to inert gas loads & micro-bubbles --and all-day travel the day before to get here to Truk Lagoon from stateside for example.

Jump in for the first dive of the trip on the San Francisco Maru at average depth 51m for an hour bottom time on Air with nearly two more hours of deco time-to-surface; and then post-dive surface recovery of deco cylinders and d'offing backgas double tanks & hauling them aboard . . . and then a twenty minute boat ride back in the 30 deg C tropical sun.

That's your real world recipe for that so-called "undeserved DCS hit". . .

 

[dreamdive]

Interesting . . .now couple that with other pre-disposing factors such as dehydration, insufficient "acclimatization" to a hot/humid tropical environment (thermal stress with opening of these circulatory anatomoses) along with no previous "work-up" deco dives to sensitize the immune system/inflammatory response of the body to inert gas loads & micro-bubbles --and all-day travel the day before to get here to Truk Lagoon from stateside for example.

Jump in for the first dive of the trip on the San Francisco Maru at average depth 51m for an hour bottom time on Air with nearly two more hours of deco time-to-surface; and then post-dive surface recovery of deco cylinders and d'offing backgas double tanks & hauling them aboard . . . and then a twenty minute boat ride back in the 30 deg C tropical sun.

That's your real world recipe for that so-called "undeserved DCS hit". . .

Kevin,

You might enjoy reading "Hydration Revisited - Myths vs. Facts",
Hydration Revisited

Glad I did the SF Maru on CCR trimix ......Truk was awesome! But, you are bringing up some great points.

Claudia

 

[descent]

[-]It's a popular subject! These researchers think there are some drugs that can help close IPAVAs at any inspired pp02 from normoxic to 100%.[/-] (Uh, no, actually, they don't)


Is Diamox safe for hyperbaric use?


[-]Sildenafil, nifedipine and acetazolamide do not allow for blood flow through intrapulmonary arteriovenous anastomoses during exercise while breathing 100% oxygen. ... [/-]