A.G.E. Questions and answers

[Diver Dennis]

Here is a link...

http://www.scuba-doc.com/gasemb.pdf

 

[lamont]

here's the GI3 article on bounce diving:

http://www.wkpp.org/articles/Decompression/why_we_do_not_bounce_dive_after_diving.htm

basically his claim is that if you're offgassing in bubble form after a dive, that if you go back down and collect some bottles that you can compress bubbles enough to get through the lungs and then expand them on the arterial side -- do-it-yourself PFO.

 

[Azza]

Catherine, I will try to explain the answer to what I think you are asking. I will simplify this for some on the board who may not have too much background on this, so please don't feel I am telling you how to suck eggs.

Sometimes I have trouble spitting out what I am trying to say as well but anyway here goes.

As we descend, and spend time at depth, we uptake Inert Gasses due to increased Partial Pressures.

As we ascend this uptake of the Inert gasses must now flow out of wherever they have accumulated.

We must ascend at a slow rate, so these Inert Gasses don't come out of "solution" and become bubbles. However some bubbles do occur and generally don't cause us any harm.

As the Inert gasses come out of our body they flow into the Veinous system where they are pumped into the right side of the heart, then get pumped from there through the Pulmonery Artery to the lungs, where the lungs act like filter beds and filter out the Inert gasses before returning the blood to the left side of the heart, via the Pulmonery Vein, to be redistributed through out the body.

The danger can be if you have too many bubbles, the lungs may not filter out all of the excess Inert Gasses, then send them through to the left side of the heart to be distributed through out the body. As they are not being filtered out, they grow as the ambient pressure decreases (I.E. you ascend) and can become lodged in vital capillaries depriving the tissues, brain, spine etc of vital blood. This is an Aterial Gas Embolism.

In the case of a PFO, which is a "hole" between the left and ride side of the heart (we are all born with them however in some people they do not close after birth) the gas can shunt directly from the veinous system (Right side of the heart) into the arterial system (left side of the heart) causing AGE. Some divers with PFO have dived for years with the PFO and never had a problem. However you may be doing a little deco, have a coughing fit, and this could be enough to shunt gas through the PFO.

Is this what you were asking?

Sorry if this is really simplified but I am typing in a rush as I have to be somewhere shortly.

If anyone needs any expansion on any of this please feel free to ask.

 

[Wildcard]

So you just tried to explain super basic pathiophysolgy to a critical care flight nurse? Ummm? ya....
Let me try to reask your question c. If the bubbles aint coming from the normal pathways that cause AGE, where are they coming from?
This is a question for Dr Deco!

 

[Azza]

So you just tried to explain super basic pathiophysolgy to a critical care flight nurse? Ummm? ya....

No need to be sarcastic... I had no idea C was a nurse. You may have also missed the bit where I said

I will simplify this for some on the board who may not have too much background on this, so please don't feel I am telling you how to suck eggs.

I took the question;

I want to know when a diver takes a gas bubble hit in the arterial bed, and it did not come from an overexpansion injury....where is the orgin most likely?

and gave what I think is the most likely scenario;

The danger can be if you have too many bubbles, the lungs may not effectively filter out all of the excess Inert Gasses, then send them through to the left side of the heart to be distributed through out the body. As they are not being filtered out, they grow as the ambient pressure decreases (I.E. you ascend) and can become lodged in vital capillaries depriving the tissues, brain, spine etc of vital blood.

I.E. a shunt from excess bubbles that the lungs couldnt cope with.

Let me try to reask your question c. If the bubbles aint coming from the normal pathways that cause AGE, where are they coming from?
This is a question for Dr Deco!

AFAIK inert gasses don't offgas into the arterial system, and if they do I have never seen it documented anywhere. It could be that the gas being ongassed bubbled due to a very fast ascent. There is also the possibility of it not even being a diving condition, such as a blod clot, that was aggravated by diving.
I am interested in Dr Deco answer as well. I wanna know if I am right...

 

[TSandM]

The answer to one of Catherine's questions is that bubbles, just like any other emboli, will go where the flow is the greatest. The first major branches off the aortic arch (other than the coronary arteries, which are fairly small) are the vessels headed for the brain. These are large vessels, and the brain has a high flow rate. Therefore, gas emboli are going to have a great tendency to lodge in the central nervous system. In addition, the CNS has the property that interruptions of flow even to small areas are often very visibly symptomatic -- cut off the blood supply to a small part of your biceps muscle for a few minutes and you may not notice it; cut off the blood supply to your speech center and nobody is going to fail to see that.

The mechanism of AGE in someone who did not breath-hold and does not have a PFO is a little harder to come up with. The two things I could postulate would be either an area of air-trapping in the lung (this is why asthma is such a potential danger for divers) or bubbles which made it through the capillary beds in the lunch (or through intraparenchymal shunts) and were then able to expand on the arterial side of the circulation. This is what George is referring to in his article -- the idea that large bubbles are unable to pass the pulmonary filter, but if they are recompressed to become tiny, they can, and will then expand on ascent on the arterial side of the circulation. I don't know if anybody has demonstrated this phenomenon, either in experimental animals or in humans.

 

[DocVikingo]

I know what that is....most babies have it and it closes at birth. My handle on hemodynamics is really pretty okay. (Intraaortic balloon pump, etc)]

Actually, it could stand for a little fine tuning.

All fetuses have an opening between the two upper chambers of the heart (atria) known as the "foramen ovale." Since the fetus' lungs are in a collapsed and essentially non-aerated state, there's no point in the body endeavoring to circulate much blood to them. Only about 5 -10% of the blood in the pulmonary artery enters the lungs in the fetus.

At the moment of birth, the foramen ovale is no longer needed. With aeration of the lungs and increased pulmonary blood flow and pulmonary venous return to the left atrium, the pressure in that chamber becomes higher than in the right atrium. This increased pressure closes the flap valve between the two atria and the tissues eventually grow together over the first year of life.

In somewhere around 20% of persons complete closure does not occur. This is called "patent foramen ovale (PFO)". Depending upon its size and other factors, it may or may not be symptomatic.

Regards,

DocVikingo

 

[Cacia]

The answer to one of Catherine's questions is that bubbles, just like any other emboli, will go where the flow is the greatest. The first major branches off the aortic arch (other than the coronary arteries, which are fairly small) are the vessels headed for the brain. These are large vessels, and the brain has a high flow rate. Therefore, gas emboli are going to have a great tendency to lodge in the central nervous system. In addition, the CNS has the property that interruptions of flow even to small areas are often very visibly symptomatic -- cut off the blood supply to a small part of your biceps muscle for a few minutes and you may not notice it; cut off the blood supply to your speech center and nobody is going to fail to see that.

The mechanism of AGE in someone who did not breath-hold and does not have a PFO is a little harder to come up with. The two things I could postulate would be either an area of air-trapping in the lung (this is why asthma is such a potential danger for divers) or bubbles which made it through the capillary beds in the lunch (or through intraparenchymal shunts) and were then able to expand on the arterial side of the circulation. This is what George is referring to in his article -- the idea that large bubbles are unable to pass the pulmonary filter, but if they are recompressed to become tiny, they can, and will then expand on ascent on the arterial side of the circulation. I don't know if anybody has demonstrated this phenomenon, either in experimental animals or in humans.

TSandsM, thanks...that was exactly what I was asking. I had heard this alluded to, but never really understood the role that flow played. THANKS!

(hey, maybe you should be a doctor!) xoxox

Actually, I love hearing expnations from all vantage points..I find it extremely helpful when trying to peice it together. Lynne always knows what I am asking even when I word it clumsily.

 

[Damselfish]

I had no idea C was a nurse.

Reading peoples profiles is a good thing sometimes.

 

[Cacia]

I am not one anymore, BTW.

Actually, it could stand for a little fine tuning.

I read your answer...is there something I got wrong? I did not get into the PFO physiology because I was really trying to articulate the question about "non-PFO" derived AGE's.

So, Dr V...do you have any theories why a diver would buy an AGE assuming they did a proper bounds profile on a recreational depth dive? Are you curious about this? Is there anything to be gained/understood by us laymen out here?
Lynne?
Actually, insurance implications might make it better form to speak hypothetically...

Another question I have wondered about, is there a way to analyze the gas contents of emboli to determine the origin, or would that be pointless? I was wondering if they have ever been probed, in research.