OP
LOL. Snorkeling is an excellent idea. 
Denisegg's incident and near miss at Jackson Blue
- Thread starter denisegg
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Maybe try just snorkeling.....as a first step........But after reading about you for a year now, have someone tie a rope to you so you don't make a break for the bottom when you spot something cool....
Quick, someone confiscate all her weights!!! :lol:
OP
.....
Cruisin Home
Contributor
My thoughts here as a medical scientist and engineer who is fascinated with solving medical mysteries (inventor of medical imaging systems).
1) I suffered PE twice in life. Once due to inhalstion of fumes from an adhesive I was using. Very scary, quick onset, dialed 911 and almost couldnt speak, couldnt get a breathe. Second was on a deep wreck dive. More mild than the adhesive insident but remember really troubled breathing. I was tired that day (had done many dives the previous days) and a little stuffy. Never had problem repeat with over 1000 dives since.
2) The cousin of IPE is HAPE (high altitude Pulmonary Edema). Occurs to very healthy subjects with no real precursor symptoms or warnings. Read a bit on the mountain climber in Everest and you will see it is a very scary problem and doesnt mean that because you had it once that you will ever have again.
3) Another more deadly cousin is Cerebral Edema, also HACE (high altitude). One thing in common with the PEs is that once Edema of the organ is brought on, it seems to beget more edema, and that begets more, creating a vicious death spiral that is hard to get out of. You are lucky in that yopu broke free before the point of no return. This death spiral of EDema may be brought on by the bodies immune system. Some examples of this in the lung are "cytokine storms" which are brought about by strong viral or bacterial infections. Essentially the immune system goes into overdrive and ends up loading the lung with fluid. Sometimes steroid treatment shows positive result. I have personally witness children in ICU setting on ECMO (extra corpeal membran oxygenation : fancy word for a machine breathing for you).
My opinion: We dont know what causes these activity related edema, maybe someday. My own opinions of things that may contritube is fatigue (you had sveral days of diving), i believe it contributed to my own incident. Second is the breathing of a very dry gas, particularly at depth when one has to "work" for it a little more than ususal. Our sinues I believe are a humidifier for our lungs and during regulator breathing they dont get a chance to perform this function. My opinion is you may and probably never have another episode. Possible link with a hypo active thyroid, can be related to fatigue. Again; these are just my opinions.
I think what is more important than Why is the What to do? You survived on your basic instincts and training, and also the blessing of being around good people/buddy. there is no substitue for that. I believe you have brought about an awareness that we deep divers should understand and know the onset of symptoms of IPE and what to do. High altitude climbers are way ahead of us in this aspect. Maybe your experience and this message board will do that! congrats.
And boy there is nothing worse than the feeling of not being able to get a breathe. I hope it never happens to me (or you) again.
1) I suffered PE twice in life. Once due to inhalstion of fumes from an adhesive I was using. Very scary, quick onset, dialed 911 and almost couldnt speak, couldnt get a breathe. Second was on a deep wreck dive. More mild than the adhesive insident but remember really troubled breathing. I was tired that day (had done many dives the previous days) and a little stuffy. Never had problem repeat with over 1000 dives since.
2) The cousin of IPE is HAPE (high altitude Pulmonary Edema). Occurs to very healthy subjects with no real precursor symptoms or warnings. Read a bit on the mountain climber in Everest and you will see it is a very scary problem and doesnt mean that because you had it once that you will ever have again.
3) Another more deadly cousin is Cerebral Edema, also HACE (high altitude). One thing in common with the PEs is that once Edema of the organ is brought on, it seems to beget more edema, and that begets more, creating a vicious death spiral that is hard to get out of. You are lucky in that yopu broke free before the point of no return. This death spiral of EDema may be brought on by the bodies immune system. Some examples of this in the lung are "cytokine storms" which are brought about by strong viral or bacterial infections. Essentially the immune system goes into overdrive and ends up loading the lung with fluid. Sometimes steroid treatment shows positive result. I have personally witness children in ICU setting on ECMO (extra corpeal membran oxygenation : fancy word for a machine breathing for you).
My opinion: We dont know what causes these activity related edema, maybe someday. My own opinions of things that may contritube is fatigue (you had sveral days of diving), i believe it contributed to my own incident. Second is the breathing of a very dry gas, particularly at depth when one has to "work" for it a little more than ususal. Our sinues I believe are a humidifier for our lungs and during regulator breathing they dont get a chance to perform this function. My opinion is you may and probably never have another episode. Possible link with a hypo active thyroid, can be related to fatigue. Again; these are just my opinions.
I think what is more important than Why is the What to do? You survived on your basic instincts and training, and also the blessing of being around good people/buddy. there is no substitue for that. I believe you have brought about an awareness that we deep divers should understand and know the onset of symptoms of IPE and what to do. High altitude climbers are way ahead of us in this aspect. Maybe your experience and this message board will do that! congrats.
And boy there is nothing worse than the feeling of not being able to get a breathe. I hope it never happens to me (or you) again.
Cruisin Home
Contributor
Did the pulmonogist or cardiologist ever mention "patent Foramen Ovale" PFO? Laymen terms it is a hole in the heart that is present in fetus but sometimes does not close in some people. Can produce no symtoms in life but does give more risk of certain vasular injuries such as stroke and pulmonary embolism.
Why I ask is a high altitude study showed a link between climbers susceptible to HA pulmonary edema and PFO.
Study
The key features of HAPE are exaggerated pulmonary hypertension and arterial hypoxemia at high altitude. The mechanisms underlying the condition are not fully understood, but there is evidence that a PFO may worsen the hypoxemia seen.
In the current study, Dr. Yves Allemann, from the Swiss Cardiovascular Center in Bern, and colleagues used transesophageal echocardiography to look for PFOs in 16 HAPE-susceptible mountaineers and in 19 mountaineers resistant to HAPE. Pulmonary artery pressure was estimated with Doppler echocardiography and pulse oximetry was used to determine oxygen saturation. All measurements were taken at high and low altitudes.
At low altitude, the PFO rates were 56% and 11% in HAPE-sensitive and -resistant subjects, respectively (p = 0.004). Similarly, at high altitude, the corresponding rates were 69% and 16%.
Prior to the onset of pulmonary edema at high altitude, HAPE-susceptible subjects had an oxygen saturation of 73%, significantly lower than the 83% noted in controls (p = 0.001). In HAPE-susceptible subjects, a large PFO was associated with a mean oxygen saturation of 65%, whereas with smaller or no PFO the saturation was 77%.
"We speculate that at high altitude, a large PFO may contribute to exaggerated arterial hypoxemia and facilitate HAPE," the investigators conclude.
The key features of HAPE are exaggerated pulmonary hypertension and arterial hypoxemia at high altitude. The mechanisms underlying the condition are not fully understood, but there is evidence that a PFO may worsen the hypoxemia seen.
In the current study, Dr. Yves Allemann, from the Swiss Cardiovascular Center in Bern, and colleagues used transesophageal echocardiography to look for PFOs in 16 HAPE-susceptible mountaineers and in 19 mountaineers resistant to HAPE. Pulmonary artery pressure was estimated with Doppler echocardiography and pulse oximetry was used to determine oxygen saturation. All measurements were taken at high and low altitudes.
At low altitude, the PFO rates were 56% and 11% in HAPE-sensitive and -resistant subjects, respectively (p = 0.004). Similarly, at high altitude, the corresponding rates were 69% and 16%.
Prior to the onset of pulmonary edema at high altitude, HAPE-susceptible subjects had an oxygen saturation of 73%, significantly lower than the 83% noted in controls (p = 0.001). In HAPE-susceptible subjects, a large PFO was associated with a mean oxygen saturation of 65%, whereas with smaller or no PFO the saturation was 77%.
"We speculate that at high altitude, a large PFO may contribute to exaggerated arterial hypoxemia and facilitate HAPE," the investigators conclude.
Why I ask is a high altitude study showed a link between climbers susceptible to HA pulmonary edema and PFO.
Study
The key features of HAPE are exaggerated pulmonary hypertension and arterial hypoxemia at high altitude. The mechanisms underlying the condition are not fully understood, but there is evidence that a PFO may worsen the hypoxemia seen.
In the current study, Dr. Yves Allemann, from the Swiss Cardiovascular Center in Bern, and colleagues used transesophageal echocardiography to look for PFOs in 16 HAPE-susceptible mountaineers and in 19 mountaineers resistant to HAPE. Pulmonary artery pressure was estimated with Doppler echocardiography and pulse oximetry was used to determine oxygen saturation. All measurements were taken at high and low altitudes.
At low altitude, the PFO rates were 56% and 11% in HAPE-sensitive and -resistant subjects, respectively (p = 0.004). Similarly, at high altitude, the corresponding rates were 69% and 16%.
Prior to the onset of pulmonary edema at high altitude, HAPE-susceptible subjects had an oxygen saturation of 73%, significantly lower than the 83% noted in controls (p = 0.001). In HAPE-susceptible subjects, a large PFO was associated with a mean oxygen saturation of 65%, whereas with smaller or no PFO the saturation was 77%.
"We speculate that at high altitude, a large PFO may contribute to exaggerated arterial hypoxemia and facilitate HAPE," the investigators conclude.
The key features of HAPE are exaggerated pulmonary hypertension and arterial hypoxemia at high altitude. The mechanisms underlying the condition are not fully understood, but there is evidence that a PFO may worsen the hypoxemia seen.
In the current study, Dr. Yves Allemann, from the Swiss Cardiovascular Center in Bern, and colleagues used transesophageal echocardiography to look for PFOs in 16 HAPE-susceptible mountaineers and in 19 mountaineers resistant to HAPE. Pulmonary artery pressure was estimated with Doppler echocardiography and pulse oximetry was used to determine oxygen saturation. All measurements were taken at high and low altitudes.
At low altitude, the PFO rates were 56% and 11% in HAPE-sensitive and -resistant subjects, respectively (p = 0.004). Similarly, at high altitude, the corresponding rates were 69% and 16%.
Prior to the onset of pulmonary edema at high altitude, HAPE-susceptible subjects had an oxygen saturation of 73%, significantly lower than the 83% noted in controls (p = 0.001). In HAPE-susceptible subjects, a large PFO was associated with a mean oxygen saturation of 65%, whereas with smaller or no PFO the saturation was 77%.
"We speculate that at high altitude, a large PFO may contribute to exaggerated arterial hypoxemia and facilitate HAPE," the investigators conclude.
OP
Amen to that!! Thank you so much for all the awesome information. It is my understanding that I was checked for PFO and nothing was found.
Thank you for sharing with me that IPE happened to you and that you were able to continue to dive and have not had a recurrence. I know that is not a guarantee, but it gives much hope and reassurance.
OP
Someone from SB who knows Dr. Moon at Duke that is running the current study funded by the Navy and DAN on IPE contacted me and got me in touch with Dr. Moon. I am currently getting Dr. Moon the information he requested on my case so that he can review it and he asked me to share this:
If any other individuals have contacted you about their experience with IPE please pass on to them that we are still interested in doing studies.
Richard Moon, MD
Professor of Anesthesiology
Professor of Medicine
Chief, Division of General, Vascular and Transplant Anesthesia
Medical Director, Center for Hyperbaric Medicine & Environmental Physiology
Duke University Medical Center
Durham, NC 27710
Tel: (919) 684-8762
Fax: (919) 681-4698
If any other individuals have contacted you about their experience with IPE please pass on to them that we are still interested in doing studies.
Richard Moon, MD
Professor of Anesthesiology
Professor of Medicine
Chief, Division of General, Vascular and Transplant Anesthesia
Medical Director, Center for Hyperbaric Medicine & Environmental Physiology
Duke University Medical Center
Durham, NC 27710
Tel: (919) 684-8762
Fax: (919) 681-4698
OP
I have to say it has been fascinating how many people have reached out not only to me but to each other in sharing all the information that is available about IPE to raise awareness and search together for answers.
Great news Denise.. and you certainly deserve the best of care.. thanks for continuing to share here
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