Immersion Pulmonary Edema

[cutlass]

Interesting . . . reading the papers in the Rubicon archives on this issue, it appears that most patients get treated with diuresis, although the few where invasive monitoring took place had normal wedges. There is also a suggestion that lowered intraalveolar pressures due to higher inspiratory effort on a regulator may play a role in transudation of fluid. Putting all this together, I wonder if the first intervention in such patients ought to be afterload reduction and BIPAP?

This comment reminds me of HAPE (high-altitude pulmonary edema). HAPE also has a bias to younger, male populations. Of course, the significant difference between IPE and HAPE are the oxygen partial pressures involved; hypoxia is widely regarded as key to HAPE. But I'm wondering if another mechanism besides PO2 is involved; e.g. a similar response to reduced breathing resistance at high altitude and reduced mechanical effort for lungs now buoyant from immersion.

 

[o2fill]

The key to IPE is exertion in cold water, and can happen to young healthy divers. It resolves rapidly once out of water. However, what you describe is unlikely IPE but an organic heart disease.

With respect, I would differ with this analysis and conclusion. I experienced IPE in warm water without any exertion. There was no evidence of cardiac involvement and this was confirmed by a stress test shortly after the incident. BP was normal. As for resolving quickly, I was forced to remain on O2 for 24 hours and absent significant quantities on our dive boat I might well have succumbed to hypoxia or, at the very least, experienced longer term consequences of oxygen deprivation.

The latest research indicates that there are two distinct variants of IPE. One appears to be exertion induced (military and triathlon swimmers). A second category involves divers and is at this point unexplained. However, what is known is that once experienced, IPE appears to have a reoccurrance rate as high as 30%.

Dive safely,

Phil