non-cardiogenic pulmonary edema

Please register or login

Welcome to ScubaBoard, the world's largest scuba diving community. Registration is not required to read the forums, but we encourage you to join. Joining has its benefits and enables you to participate in the discussions.

Benefits of registering include

  • Ability to post and comment on topics and discussions.
  • A Free photo gallery to share your dive photos with the world.
  • You can make this box go away

Joining is quick and easy. Log in or Register now!

Interesting results, DDM. If they remain consistent, it would seem to me that people who have had IPE ought to be warned against further diving.

That's the way we're leaning. It's not consistent even in people who are susceptible, so we can't even recommend conditions under which they're ok to dive.



That's what Dr. Moon is trying to get to the bottom of right now. There appears to be a genetic link but there's nothing concrete yet.

In layman's terms, what other tests results indicate a genetic predisposition when you have only had 2 test subjects? How has consistency been established?
With all due respect, it is easy to sit in a doctor's chair across from a patient and tell someone not to dive anymore when you have so few answers as to the cause. That is like telling someone who got hit by a bus while crossing the street not to walk anymore.
 
When I arrived at the hospital 7/4/2010 my bp was in the 140's/90's(which sounds like a common theme with cases I have read about). One of the findings in my case was an elevated thyroid level which was attributed to armour thyroid medicine I was prescribed from another doctor which was considered unnecessary by the Endocrinologist that saw me and was discontinued(My thyroid had been checked every 3 months since then and has been fine). Although I was fully tested for heart disease with ekgs, echo, heart cath, I tried to understand the link between the pulmonary artery and IPE and my cardiologist just told me that had nothing to do with what happened to me. The cardiologist prescribed lisinopril 5mg before releasing me. After my 6 week check up, he released me with no further instructions to follow up on my bp. I went to an internal medicine doctor locally and my bp was fine but she just wrote me another prescription for the lisinopril. I took it upon myself to visit 2 pulmonary doctors and was tested with no findings. They both suggested I quit diving because they had no idea why it happened to me. I had to bring literature with me to their offices because they had never heard of IPE and one was recommended by DAN. The one recommended by DAN suggested I take up another adrenaline sport like he was doing, something along the lines of hang gliding.
I contacted Dr. Moon about a month after my occurrence. I received the following email:

Ms. Goldman:The study is indeed still being conducted. Regarding your case it is possible that your mild hypertension contributed. Are you still taking lisinopril or other blood pressure medication? Can you tell me your age?

Many thanks for your interest. Please let me know your dive profile, and I would also need to review your medical records. 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

From this, it sounded as if it would be written off to mild hypertension so I did not pursue further testing. I would not mind going through the tests if I felt like I could get some concrete answers that I have not already received from all the testing I was put through, but a vague genetic predisposition would tell me nothing.
 
On another side note, taking the bp medicine makes me feel like crap.I have fatigue, dizzy upon standing and weakness. My bp now runs what it did when I was in my teens 110/70 (sometimes less) and my heart rate averages 70. My primary physician also added coreg cr 10 mg when I went to him for a check up about a month ago because he said it was just good for your heart, that he took it himself.

The reason I agreed to continue on the coreg even though it is making me feel tired, etc, is this:

"Two placebo-controlled studies compared the acute hemodynamic effects of COREG to baseline measurements in 59 and 49 patients with NYHA class II-IV heart failure receiving diuretics, ACE inhibitors, and digitalis. There were significant reductions in systemic blood pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and heart rate. Initial effects on cardiac output, stroke volume index, and systemic vascular resistance were small and variable."

In my layman's mind, it sounded like it would help with IPE because of the reduction in pulmonary artery pressure and PCWP? I did my AN/DECO and first dives of my Adv Rec Trimix a few weeks ago a week after beginning coreg cr. We had 3 intense days of diving and I felt awesome. The dive to 160ffw felt no different than 20ffw on my breathing rate. (And yes, I received a doctor's release to do the class.)
 
Last edited:
I'm not sure I am understanding this. What is the difference in negative pressure pulmonary edema and IPE?

Hi Denise,

Negative pressure pulmonary edema (NPPE) can occur when an individual endeavors to vigorously inhale against an obstructed upper airway. Such obstruction, which can be either partial or complete, can be the result of foreign body aspiration, growths of various varieties, laryngospasm, strangulation and the like. This action creates a vacuum within the lung and fluid from outside of the lung tissue proper can thereby be drawn into the alveoli. Immersion typically has nothing to do with it. I suppose it could occur in divers given the right set of circumstances, but I am not aware of any documented cases.

Immersion pulmonary edema (IPE) occurs only when immersion in water is involved. It may be related to increased pulmonary artery pressures and/or other factors, but whatever the cause(s) the mechanism almost certainly does not involve negative intrathoracic pressures.

Regards,

DocVikingo

This is educational only and does not constitute or imply a doctor-patient relationship. It is not medical advice to you or any other individual and should not be construed as such.
 
The problem is that (non iatrogenic) pulmonary edema is almost never a condition of total body volume overload -- in fact, a lot of patients with pulmonary edema are volume contracted, but the volume they do have is in the wrong place. My guess is that anyone completing a dive is volume neutral or depleted (depending on whether they are diving a wetsuit or have a p-valve :) ). You'd be better off stocking your kit with nitro tablets!

Well noted :blinking:
 
When I arrived at the hospital 7/4/2010 my bp was in the 140's/90's(which sounds like a common theme with cases I have read about). One of the findings in my case was an elevated thyroid level which was attributed to armour thyroid medicine I was prescribed from another doctor which was considered unnecessary by the Endocrinologist that saw me and was discontinued(My thyroid had been checked every 3 months since then and has been fine). Although I was fully tested for heart disease with ekgs, echo, heart cath, I tried to understand the link between the pulmonary artery and IPE and my cardiologist just told me that had nothing to do with what happened to me. The cardiologist prescribed lisinopril 5mg before releasing me. After my 6 week check up, he released me with no further instructions to follow up on my bp. I went to an internal medicine doctor locally and my bp was fine but she just wrote me another prescription for the lisinopril. I took it upon myself to visit 2 pulmonary doctors and was tested with no findings. They both suggested I quit diving because they had no idea why it happened to me. I had to bring literature with me to their offices because they had never heard of IPE and one was recommended by DAN. The one recommended by DAN suggested I take up another adrenaline sport like he was doing, something along the lines of hang gliding.
I contacted Dr. Moon about a month after my occurrence. I received the following email:

Ms. Goldman:The study is indeed still being conducted. Regarding your case it is possible that your mild hypertension contributed. Are you still taking lisinopril or other blood pressure medication? Can you tell me your age?

Many thanks for your interest. Please let me know your dive profile, and I would also need to review your medical records. 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

From this, it sounded as if it would be written off to mild hypertension so I did not pursue further testing. I would not mind going through the tests if I felt like I could get some concrete answers that I have not already received from all the testing I was put through, but a vague genetic predisposition would tell me nothing.


Denise,
Without testing you it would be impossible to determine exactly what happened. Hypertension and immersion could both easily have been factors. With IPE, a couple of things seem to be at work. First, when the body is immersed in water, the effect of gravity is negated and so blood isn't pulled into the dependent (lower) parts of the body. This causes blood to be distributed more evenly in the body, which increases the amount of blood in the pulmonary arteries. Also, in cold water, the peripheral blood vessels constrict and shunt even more blood into the core and thus into the pulmonary arteries.
Typically, the pulmonary arteries will enlarge to compensate for the greater amount of blood. It appears that some people's pulmonary arteries do not dilate sufficiently, which results in higher pulmonary artery (PA) pressure - if you try to push more fluid through a pipe that doesn't change in size, the pressure in that pipe will increase. Add to this the effects of exercise, and we can see dramatic increases in PA pressure (over 50 systolic, with high normal being 25). This drives fluid out of the capillaries and into the alveolar membrane, and possibly into the alveoli themselves.
Did you ever follow up with Dr. Moon?
 
No, that was our only correspondence. Do you do other heart/lung related testing besides the cold water immersion and exercise immersion? I read the report written by the second participant. I believe he said he needed to exercise, lose weight and get his b/p down before diving again. Are those recommendations from the study or his own observations? Did the use of Viagra work in reducing the effects you describe above? Have you tried other heart medications in the trial to determine whether or not they lessen the impact?
 
I just read about Kat's testing done in Feb 2011. Thank you Eric for the link in your sig line. An excerpt taken from her website:

"Swimming Induced Pulmonary Edema, or SIPE, is an emerging condition that affects athletes in the swim portion of triathlon events. "Symptoms include marked respiratory distress, wet-sounding popping or crackling in the lungs with breathing, a “junky” rattling cough, and the hallmark; coughing up pink, frothy blood-tinged sputum. When it occurs during exercise, one of the first sensations is shortness of breath that is substantially out of proportion to the effort being expended. SIPE is believed to occur from a combination of factors that creates what can be thought of as a “perfect storm” that leads to capillary leak".

With the help and dedication of Dr. Charles C. Miller III - aka 'Trey' - and my cardiologist, we are trying to identify my triggers and work to prevent a recurrence of SIPE. We discovered that I had mild-hypertension so I began taking Atacand (16mg) in Sept. 2007. We think over hydration and lack of a proper warm-up on race morning could also be factors. I have been careful to begin the swim slowly and build my speed and to monitor fluid intake carefully leading up to race day, and on race morning. The wetsuit is another factor that may contribute to SIPE, but don't have any evidence to suggest it is part of the problem since I've raced in the same suit for 3 years now - with and without SIPE."

Well, I guess her having it four times and being a triathlon rules out diet, exercise, losing weight and keeping your b/p under control as ways to prevent it. :(


What is your take on the coreg?
 
Last edited:
In layman's terms, what other tests results indicate a genetic predisposition when you have only had 2 test subjects? How has consistency been established?
With all due respect, it is easy to sit in a doctor's chair across from a patient and tell someone not to dive anymore when you have so few answers as to the cause. That is like telling someone who got hit by a bus while crossing the street not to walk anymore.

We've already completed a large study sponsored by DAN that looked at pulmonary artery pressure in relation to immersion in cold water and exercise - that's where that correlation comes from. It's theorized that there is a genetic predisposition but nobody's proven it yet; that's what we're working on with the current study, among other things.
I totally empathize with you on your second point. Part of the reason we are cautious with IPE is precisecly because there isn't much known. What we DO know is that certain people are predisposed to it. There's a correlation with cold water and exercise, but it's not 100%, so, it's difficult to predict when it's going to happen. In the eyes of a health care professional, an unpredicatble, potentially fatal condition related to immersion is a contraindication to diving. The last thing we (or anyone else) would want to do is to clear you to dive and then have you suffer a disabling or fatal episode of IPE.

No, that was our only correspondence. Do you do other heart/lung related testing besides the cold water immersion and exercise immersion? Did the use of Viagra work in reducing the effects you describe above? Have you tried other heart medications in the trial to determine whether or not they lessen the impact?

You might consider contacting him again and sending him your medical records. That way, he could determine for sure whether you are a candidate for the study.
The cold water/immersion test is the only one we're doing because those are the known potential triggers of IPE. We haven't tried any other cardiac medications. I can't discuss the efficacy of the sildenafil because we're early in the study and there are no official results published yet (sorry!)

I just read about Kat's testing done in Feb 2011. Thank you for the link in your sig line. An excerpt taken from her website:

"Swimming Induced Pulmonary Edema, or SIPE, is an emerging condition that affects athletes in the swim portion of triathlon events. "Symptoms include marked respiratory distress, wet-sounding popping or crackling in the lungs with breathing, a “junky” rattling cough, and the hallmark; coughing up pink, frothy blood-tinged sputum. When it occurs during exercise, one of the first sensations is shortness of breath that is substantially out of proportion to the effort being expended. SIPE is believed to occur from a combination of factors that creates what can be thought of as a “perfect storm” that leads to capillary leak".

With the help and dedication of Dr. Charles C. Miller III - aka 'Trey' - and my cardiologist, we are trying to identify my triggers and work to prevent a recurrence of SIPE. We discovered that I had mild-hypertension so I began taking Atacand (16mg) in Sept. 2007. We think over hydration and lack of a proper warm-up on race morning could also be factors. I have been careful to begin the swim slowly and build my speed and to monitor fluid intake carefully leading up to race day, and on race morning. The wetsuit is another factor that may contribute to SIPE, but don't have any evidence to suggest it is part of the problem since I've raced in the same suit for 3 years now - with and without SIPE."

Well, I guess her having it four times and being a triathlon rules out diet, exercise, losing weight and keeping your b/p under control as ways to prevent it. :(


What is your take on the coreg?

Kat was our second study subject. She's an amazing woman and it was a pleasure to meet and work with her. For anybody else who's interested: her website, along with her discussion of SIPE, is here:

Endurance Triathletes - Swimming Induced Pulmonary Edema (SIPE) - Immersion Pulmonary Edema (IPE)

As far as the coreg, you might consider discussing the side effects with your PCP and asking him if he thinks you'd do ok without it. Also, if the cardiologist who originally prescribed the lisinopril isn't aware that your PCP prescribed another medication, it might be a good idea to bring him into the loop.
 
Denise, just to try to explain pulmonary edema: In normal circulation, the heart pumps blood forward under pressure, and that pressure causes the blood to flow through vessels which gradually decrease in size. The pressure in the tissue is less than the pressure in the blood vessels, which is what makes the blood keep moving. As a result, there is a pressure gradient across the vessel wall. Vessel walls are permeable to water, but not to the protein molecules that make up plasma, and not to blood cells. The protein molecules thus exert an osmotic pressure that tends to retain water in the blood vessels.

Under normal circumstances, all these forces balance out pretty nicely, so that things diffuse out of and into capillaries, and the net is that fluid doesn't either accumulate in the tissues, or get sucked out of them. But if the balance is upset, one of those things can happen. If the simple hydrostatic pressure in the vessels exceeds the osmotic pressure reclaiming fluid, water will accumulate in the tissues, and this is called edema.

In IPE, it appears that increased hydrostatic pressure is the thing which is out of balance. In negative pressure pulmonary edema, what's happened is that the pressure in the tissues themselves has been dropped (due to the sucking action of trying to inhale against a resistance) so the gradient may be the same as in IPE, but the pressure in the vessels is normal.

When you get an injury or infection and get swelling in the area, it's because the vessels have become leaky due to chemical messengers.

It's all a neat balance of fluid flows, but subject to perturbation. And a swollen knee is one thing, but swollen lungs don't work well.
 
https://www.shearwater.com/products/swift/

Back
Top Bottom