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  • AutorenbildMichael Mutter

The fate of arterial gas embolism and its consequences

If arterial gas emboli occur, this does not necessarily mean decompression sickness; on the contrary, usually nothing happens at all. Why is this so?

courtesy Patrick Rhyner and Karin Aggeler, Tauchschule H20

Arterial gas embolism (AGE) is a cause of decompression illness (DCI). Gas bubbles enter the arterial circulation after dives from the venous circulation bypassing the pulmonary filter via cardiac (e.g. PFO = patent foramen ovale) or pulmonary (intrapulmonary arteriovenous anastomoses, IPAVA) right-left shunts, where they may cause dramatic consequences in a terminal organ (e.g. brain, kidney, etc.) by clogging small vessels (e.g. stroke). For this reason, diving behavior is aimed at preventing gas bubbles from forming in the first place, primarily by adhering to decompression limits, but also by following other rules of "low bubble diving" as recommended by SUHMS.

However, if AGE occurs, end-organ damage is very rare. Why this is so is explained by a study from last year, which specifically deals with the decompression syndrome of the inner ear, but gives very basic insights into the behavior of AGE.

The fate of arterial gas emboli

The article uses gas kinetic models to explain how gas bubbles behave in the arterial circulation. This is where it gets really interesting. When a gas bubble enters the arterial blood, it encounters an environment that is not supersaturated by inert gas, but undersaturated. Why? Inert gas is removed from venous blood during the decompression phase by exhaling in the lungs. For this reason, the arterial blood is low in inert gas. As a result, the partial pressure of inert gas in the gas bubble, which is in the arterial circulation and came from the venous system, is higher than the partial pressure of inert gas in the surrounding arterial blood. Therefore, inert gas diffuses out of the bubble into the blood and for this reason the bubble begins to shrink as soon as it enters the arterial circulation. If the way to a terminal organ (e.g., brain, inner ear) is long enough, there is sufficient time for the AGE to shrink to the point where it no longer causes damage.

If a gas bubble enters the arterial blood, it shrinks rapidly.

How long does it take a gas bubble to reach the inner ear or the brain? It depends on how it gets there. It takes the least time if it passes a PFO on its way to the inner ear. Then it is exposed to arterial conditions for about 3 s, when passing an IPAVA it is 5.5 s and when passing pulmonary capillaries (succeeds only very small bubbles) it is about 8 s. As mentioned, the bubble shrinks during this transit as the inert gas diffuses across the concentration gradient from inside to outside the bubble.

The dependence of diving depth

The higher the pressure or the deeper and longer the dive, the more densely concentrated the gas is inside a bubble. Consequently, bubbles of the same diameter shrink more slowly at high pressure (i.e., after long, deep dives) and have a longer lifetime than after shallow, short dives. The current estimated lifespan of bubbles small enough to cross the pulmonary capillary bed suggests that they are unlikely to survive transport to the inner ear or brain, even during deep dives. This, along with the lung filter, is one of the main reasons why detection of VGE correlates so poorly with the occurrence of DCI.

Survival of arterial gas bubbles, modified after "Advances in Decompression Theory and Practice", David Doolette, RF4.

The situation is different in the case of crossover via a PFO or an IPAVA. If the bubble is large enough and the inert gas pressure in the bubble is high enough, the time to reach the end organ (e.g., the brain or inner ear) is not sufficient for the bubble to shrink sufficiently. It cloggs a capillary and causes tissue damage. The risk is greater with a cardiac right-to-left shunt (e.g., PFO) than with a pulmonary one (IPAVA) because the transit time is shorter in the former (3 s vs. 5.5 s, compare left graph in the figure). In his presentation at Rebreather Forum 4 (RF4), David Doolette, one of the authors of the study, showed that even then, recreational diving is unlikely to manifest AGE; simply because the pressure in an arterialized bladder is relatively low and by the time it reaches the brain, it shrinks too much to do any damage. However, the deeper the dive, the higher the risk that an AGE will reach the brain or inner ear to cause symptoms, because there is not enough time for sufficient shrinkage due to the higher inert gas pressure inside the bubble.

Bad news for tech divers

If recreational divers are hardly affected by this, the risk increases significantly from about 60 m diving depth. Some relief can be achieved by switching to a decogas with hyperbaric oxygen, since the environment of the gas bubble is further optimized by minimizing the inert gas pressure (ideally practically zero with 100% oxygen breathing) and thus the bubble is induced to shrink even more (cf. figure, right graph). The effect is not very large, however, because the time for the bubble to shrink does not change and is only short. Therefore, especially in technical diving, provoking AGE must be avoided at all costs. For this reason, maneuvers that open a PFO should be avoided at all costs. (Once again, the PFO, because it is a very direct shortcut to the brain, is a major risk factor for manifest AGE). Therefore, for example, DSMBs should not be inflated by mouth, which has already been pointed out in this blog.

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