Confused on AGE; holding breath OK if lungs are near-empty?

[Gelirfella]

Yeah, it's a confusion. When I took OW in the mid-eighties, there wasn't even such a thing as arterial gas embolisms. Just exploding lungs and fizzing blood, depending on your mistake.

When I read the AGE description in my OW materials I was so perplexed by the description. My medical training could not reconcile what I was reading. So I immediately went to the literature and that’s where I found the microbubble overload theory and was finally able to make peace with air embolism. I sort of doubted its existence outside of iatrogenic causes based on what I read in the text. But the hyperbaric guys have some good thoughts on it. I think it would just require more physiology education than is reasonable so they stick with “lung blows up into the artery.”

There could be something I’m missing though.

 

[John C. Ratliff]

When I read the AGE description in my OW materials I was so perplexed by the description. My medical training could not reconcile what I was reading. So I immediately went to the literature and that’s where I found the microbubble overload theory and was finally able to make peace with air embolism. I sort of doubted its existence outside of iatrogenic causes based on what I read in the text. But the hyperbaric guys have some good thoughts on it. I think it would just require more physiology education than is reasonable so they stick with “lung blows up into the artery.”

There could be something I’m missing though.

Yes, you’re missing something; that something is that there is only two cell walls thickness between the capillaries and the alveoli. The pressure difference is huge too. A tear in the alveoli will result in a subsequent tear in the capillary, with transfer to the blood stream of the air. We don’t have to run any experiments, as actual life-and-death accidents have happened, and been diagnosed, sometimes during autopsy. This isn’t happening on the micro level, but on the macro level.

Diagnosis of arterial gas embolism in SCUBA diving: modification suggestion of autopsy techniques and experience in eight cases - Forensic Science, Medicine and Pathology

The purpose of this study was to suggest modifications of autopsy techniques in order to improve post-mortem diagnosis of arterial gas embolism (AGE) based on multidisciplinary investigation of SCUBA diving fatalities. Five adult human cadavers from the voluntary donation program of the Human...

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Diagnosis of arterial gas embolism in SCUBA diving: modification suggestion of autopsy techniques and experience in eight cases

Josep M. Casadesús, Fernando Aguirre, Ana Carrera, Pere Boadas-Vaello, Maria T. Serrando & Francisco Reina
Forensic Science, Medicine and Pathology volume 14, pages 18–25 (2018)Cite this article

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Abstract
The purpose of this study was to suggest modifications of autopsy techniques in order to improve post-mortem diagnosis of arterial gas embolism (AGE) based on multidisciplinary investigation of SCUBA diving fatalities. Five adult human cadavers from the voluntary donation program of the Human Anatomy Laboratory, and eight judicial autopsied bodies of SCUBA divers from the Forensic Pathology Service were assessed. Before performing any autopsies, we accessed the diving plan and the divers’ profiles for each case. We then introduced a new dissection procedure that included identification, isolation, and manipulation of carotid, vertebral and thoracic arterial systems. The dissected vascular structures that allowed optimall isolation of the systemic arterial circulation were identified and ligated. In three of the eight judicial cases, we had a strongly suggestive history of arterial gas embolism following pulmonary barotrauma (PBt/AGE). In these cases, the additional arterial dissection allowed us to clearly diagnose AGE in one of them. The autopsy of the rest of the cases showed other causes of death such as asphyxia by drowning and heart attack. In all cases we were able to reject decompression sickness, and in some of them we showed the presence of artefacts secondary to decomposition and resuscitation maneuvers. These results allow us to suggest a specific autopsy technique divided into four steps, aimed at confirming or excluding some evidence of dysbaric disorders according to a re-enactment of the incident. We have demonstrated the presence of large volumes of intravascular air, which is typical of PBt/AGE.

SeaRat

 

[Gelirfella]

Yes, you’re missing something; that something is that there is only two cell walls thickness between the arterials and the alveoli. The pressure difference is huge too. A tear in the alveoli will result in a subsequent tear in the capillary, with transfer to the blood stream of the air. We don’t have to run any experiments, as actual life-and-death accidents have happened, and been diagnosed. This isn’t happening on the micro level, but on the macro level.

SeaRat

I assure you I understand the anatomy of the lung. You can’t see an injury on the arterial side of a capillary without a microscope. Any injury at the level of 2 cell layers is not seen on grossly. You’re saying there are path reports that show injury to the capillary bed, probably true. Though I’d be interested to read the path report from an Autopsy on a AGE death. But doesn’t take much to injure a capillary bed. Sure pressure differential is large. But if the pressure differential is large enough to force air into the arterial system, why isn’t it large enough to rupture the wall of the alveolus and allow the pressure to escape into the pleural space? I don’t actually know the answer to this. What is the pressure tolerance of the wall of the alveolus/visceral pleura relative to the pressure required to force air into the arterial system at the level of the capillary? Resistance is huge in vessels that small.

I am aware there are real world cases of air embolism. I’m saying I’m not convinced of the mechanism. Just saying over and over, this is the mechanism isn’t very convincing though it is a sound rhetorical practice. An H and E stained slide from a lung with alveolar disruption and capillary injury in a patient with an AGE is not anything like definitive evidence of mechanism. That diver experienced a rapid ascent and it is equally if not more plausible that a larger than normal burden of micro bubbles existed in their blood at the time of said ascent. So many that the capillary bed was unable to adequately filter the gas leading to a substantially larger than normal microbubble burden in the arterial system which could the. Coalesce into a lethal gas bubble. If you can point to the study that proves the mechanism is mechanical disruption of the capillary bed and gas forced into the arterial system by high pressure feel free. But note, I said study not paper that suggests a mechanism without evidence. I’ll gladly admit that I’m wrong. But I believe, based on my current reading of the literature, that there is room for debate on the mechanism here. And if microbubble load is the primary driver, all it does is reinforce the importance of a slow ascent.

 

[johndiver999]

I don't pretend to understand what you are discussing above, but it sounds to me like you are saying that the damage is associated with micro bubbles in the blood around the lungs - so wouldn't that take some time (at depth) for the diver to develop that load of gas?

If that is the case, then it would seem to be hard to explain AGE's that result from very short dives of 60 seconds or something?

 

[John C. Ratliff]

I assure you I understand the anatomy of the lung. You can’t see an injury on the arterial side of a capillary without a microscope. Any injury at the level of 2 cell layers is not seen on grossly. You’re saying there are path reports that show injury to the capillary bed, probably true. Though I’d be interested to read the path report from an Autopsy on a AGE death. But doesn’t take much to injure a capillary bed. Sure pressure differential is large. But if the pressure differential is large enough to force air into the arterial system, why isn’t it large enough to rupture the wall of the alveolus and allow the pressure to escape into the pleural space? I don’t actually know the answer to this. What is the pressure tolerance of the wall of the alveolus/visceral pleura relative to the pressure required to force air into the arterial system at the level of the capillary? Resistance is huge in vessels that small.

I am aware there are real world cases of air embolism. I’m saying I’m not convinced of the mechanism. Just saying over and over, this is the mechanism isn’t very convincing though it is a sound rhetorical practice. An H and E stained slide from a lung with alveolar disruption and capillary injury in a patient with an AGE is not anything like definitive evidence of mechanism. That diver experienced a rapid ascent and it is equally if not more plausible that a larger than normal burden of micro bubbles existed in their blood at the time of said ascent. So many that the capillary bed was unable to adequately filter the gas leading to a substantially larger than normal microbubble burden in the arterial system which could the. Coalesce into a lethal gas bubble. If you can point to the study that proves the mechanism is mechanical disruption of the capillary bed and gas forced into the arterial system by high pressure feel free. But note, I said study not paper that suggests a mechanism without evidence. I’ll gladly admit that I’m wrong. But I believe, based on my current reading of the literature, that there is room for debate on the mechanism here. And if microbubble load is the primary driver, all it does is reinforce the importance of a slow ascent.

I think one thing that might prove definitive is if air, rather than nitrogen, is what’s in the arterial system. Your microbubble theory would realistically result in nitrogen bubbles, not air bubbles. But from what I’ve heard over the years, it is air that is found in the arterial system. A couple of other things, a short review of the literature shows that the micro bubbles are detected in the venous system, whereas air emboli are found in the arterial system. How do you account for this?

Now, I gave you a study, and assume that you can get the actual study and not just the abstract. It seems that you have some resources (college or hospital) that I don’t have, so maybe you could take this to the next level yourself.

SeaRat

This study may help validate some of your assumptions, but seems to show gas in the arterial system on autopsy. Take a look.

https://www.ceskpatol.cz/docs/558-s-fulltext.pdf

 

[Gelirfella]

I think one thing that might prove definitive is if air, rather than nitrogen, is what’s in the arterial system. Your microbubble theory would realistically result in nitrogen bubbles, not air bubbles. But from what I’ve heard over the years, it is air that is found in the arterial system. A couple of other things, a short review of the literature shows that the micro bubbles are detected in the venous system, whereas air emboli are found in the arterial system. How do you account for this?

Now, I gave you a study, and assume that you can get the actual study and not just the abstract. It seems that you have some resources (college or hospital) that I don’t have, so maybe you could take this to the next level yourself.

SeaRat

This study may help validate some of your assumptions, but seems to show gas in the arterial system on autopsy. Take a look.

https://www.ceskpatol.cz/docs/558-s-fulltext.pdf

That’s a good case report. Thanks for providing it. It isn’t a study so much as a description of events but it is helpful. Even here the uncertainty in mechanism comes through in their description of the various mechanisms of passage of air into the arterial circulation. I remain suspicious about the proposed mechanism of arterial wall rupture and air passage that way. Not sure how anyone concludes that happens aside from the presence of large volumes of gas in the arterial system and the concomitant presence of obvious over expansion injury. But that’s correlation not causation and the microbubble burden makes more sense to me. Perhaps complete failure of the lungs ability to filter micro bubbles occurs in an ascent like this.

If that is the case, then it would seem to be hard to explain AGE's that result from very short dives of 60 seconds or something?

Not really. Time is one variable, but another factor related to microbubble formation is change in pressure. The solubility of a gas in solution is dictated by primarily pressure and temperature aside from the qualities of the solution and the gas itself. So even in a relatively short dive more gas dissolves in the blood at depth than at the surface regardless of degree of tissue saturation. A rapid change in pressure will result in gas bubbling out of solution. This is why as time has evolved we’ve come to realize that every diver experiences microbubble formation basically every time they dive. It’s not about presence or absence of micro bubbles but rather the degree of the microbubble burden. That’s where the microbubble model came from as far as I understand it (which is not very far). This may even be a phenomenon occuring in something as benign as diving to the bottom of a 10 foot pool and coming back up immediately. However, as the burden is low and the lung’s ability to compensate is high no ill effects are experienced. But go to 60 feet and rocket to the surface in 3 seconds and the story may be different.

 

[tridacna]

Where is @Dr Simon Mitchell when you need him?

 

[Gelirfella]

I think one thing that might prove definitive is if air, rather than nitrogen, is what’s in the arterial system. Your microbubble theory would realistically result in nitrogen bubbles, not air bubbles. But from what I’ve heard over the years, it is air that is found in the arterial system. A couple of other things, a short review of the literature shows that the micro bubbles are detected in the venous system, whereas air emboli are found in the arterial system. How do you account for this?

Sorry. Did not respond to this. I’d be curious to know if anyone has sampled the gas in the arterial system to find out. That would be I imagine logistically difficult. It would require locating the gas bubble with imaging and sampling with a needle so as not to contaminate the gas with air. Probably possible. Maybe demonstrated in a mouse model. Not sure how likely this is to have occurred to a human. But this is a good point and would be a good way to examine mechanism if it were feasible.

In terms of cross over from venous to arterial system. This is discussed in the case report you mention. Several methods exist. The microbubble theory woild argue that in the absence of a PFO the micro bubbles fail to diffuse out of the capillaries into the alveoli in adequate volume because of the shear volume of them. In “normAl” ascents the lungs can keep up. It’s probable that some small amount of bubbles normally pass into the arterial system, but they are small enough in number and size that they have no clinical significance. However, if that burden becomes too high the volume passing through the capillary bed without diffusion may rise to the point of substantial clinical significance. Other factors may be at play as well. For instance the rising pressure in the alveoli may actually impair diffusion increasing the risk.

 

[johndiver999]

Not really. Time is one variable, but another factor related to microbubble formation is change in pressure. The solubility of a gas in solution is dictated by primarily pressure and temperature aside from the qualities of the solution and the gas itself. So even in a relatively short dive more gas dissolves in the blood at depth than at the surface regardless of degree of tissue saturation. A rapid change in pressure will result in gas bubbling out of solution. This is why as time has evolved we’ve come to realize that every diver experiences microbubble formation basically every time they dive. It’s not about presence or absence of micro bubbles but rather the degree of the microbubble burden. That’s where the microbubble model came from as far as I understand it (which is not very far). This may even be a phenomenon occuring in something as benign as diving to the bottom of a 10 foot pool and coming back up immediately. However, as the burden is low and the lung’s ability to compensate is high no ill effects are experienced. But go to 60 feet and rocket to the surface in 3 seconds and the story may be different.

Nope, NOT buying it now. Freedivers go down way over 100 or 200 feet and then shoot to the surface and don't get it, but a scuba diver goes to 15 feet for 20 seconds is going to get all these bubbles? Makes zero sense.

 

[The Chairman]

in the mid-eighties, there wasn't even such a thing as arterial gas embolisms.

Oh, they were there.

I know of an Instructor candidate in South Florida who tried to prove he could hold his breath and ascend from the bottom of a 12 ft pool. He went into a coma and died.

Keep your airway open. You don't have to exhale... just keep your glottis open. The air will come out naturally as you ascend and you don't have to incur an injury.