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InThe Drink
I suffered a case of IPE which I would consider "moderate" in my twenties (now in late 40's). I have never had a relapse. Still to this day I wonder what the cause. I can say that I was deep, suffered from sinus/allergies, and was a cold dive. Luckily noticed problem with breathing and got to surface ok. Felt like I had a chest cold for a few days. At the time I had never heard of IPE and always attributed to my sinus/allergies and possible cold.
Only a few years later I had a 'severe" case of PE at my home, later attributed to exposure to an epoxy that I was working with in my basement shop. My lungs filled up unbelievably fast and very soon I was gasping for air. could barely speak when I called 911. Scary.. Told physcian of my earlier dive experience and that was then I was told about IPE.
Never had problems since but I did have a very successful sinus surgery and treatment for my seasonal allergies.
No cardiac abnormalities of any kind. Was in Triathlete physical shape for both incidents.
My takeaway from my own experience is to be very conscious of my body, my breathing etc. and to abort a dive at the hint of anything wrong. It seems if I read your case right that you were having mild reactions in an earlier dive, maybe an early warning sign.
Should have cardiac checkup, also looking for a congenital abnormality called PFO.
My guess is there are alot more cases of IPE, particularly of the mild or moderate types that are not well reported.
My thought is it could share etiology with High Altitude PE (HAPE).
In the material I've been reading on this topic, it does not appear that many (if any) of the documented cases of IPE have had any major cardiac dysfunction. There does seem to be some association with hypertension, but the dynamic may be more one of increased resistance to forward flow than inability of the cardiac muscle to maintain normal output in the face of normal vascular tone.
The determinants of flow across blood vessel walls (and it's excessive outflow into the alveoli that causes pulmonary edema) are hydrostatic (pressure inside and pressure outside) and osmotic (concentration of solutes inside versus outside). In addition, intact structures (endothelium) are required. If immersion causes centralization of blood volume (which it does) and that increased volume can't flow forward at a rate sufficient to keep the pulmonary capillary pressure from rising, that could lead to hydrostatic transudation of fluid. If breathing from a regulator requires much inhalational effort (as with a poorly adjusted reg) and causes alveolar pressures to fall below ambient, that can also encourage fluid movement into the alveoli. I can't offhand think of any effect that diving should have on the oncotic pressure, but I don't know if anyone has looked at that. And whether breathing compressed gas can or does do anything to the integrity of alveolar walls or pulmonary capillary endothelium I suspect is also not known.
Duke's studying this, but there is just a lot we don't know about this phenomenon.
In the material I've been reading on this topic, it does not appear that many (if any) of the documented cases of IPE have had any major cardiac dysfunction. There does seem to be some association with hypertension, but the dynamic may be more one of increased resistance to forward flow than inability of the cardiac muscle to maintain normal output in the face of normal vascular tone.
The determinants of flow across blood vessel walls (and it's excessive outflow into the alveoli that causes pulmonary edema) are hydrostatic (pressure inside and pressure outside) and osmotic (concentration of solutes inside versus outside). In addition, intact structures (endothelium) are required. If immersion causes centralization of blood volume (which it does) and that increased volume can't flow forward at a rate sufficient to keep the pulmonary capillary pressure from rising, that could lead to hydrostatic transudation of fluid. If breathing from a regulator requires much inhalational effort (as with a poorly adjusted reg) and causes alveolar pressures to fall below ambient, that can also encourage fluid movement into the alveoli. I can't offhand think of any effect that diving should have on the oncotic pressure, but I don't know if anyone has looked at that. And whether breathing compressed gas can or does do anything to the integrity of alveolar walls or pulmonary capillary endothelium I suspect is also not known.
Duke's studying this, but there is just a lot we don't know about this phenomenon.
Hey John, that's great that your ECG and Echocardiogram/Doppler and your Stress Echo went well. Even if you don't have the answers you want yet, at least you know you're in pretty good cardiac health. You also know to abort at the first sign of trouble and to avoid over-exerting yourself. Have you checked the DAN seminar on medications and their affects on diving? Some beta blockers seem to have less effect on diving than others...
Thanks for updating us. This continues to be an interesting phenomenon that is unfolding ever so slowly...