Hydration Revisited – Myths Versus Facts

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... It looks like you're saying that breathing dry air is a risk factor for IPE. Can you expand on that?

Just the opposite, actually. I should write with greater care. :)

In a controlled physics experiment in glassware, dry moving air is a great transport for picking up water and carrying it away. I expect that something similar happens in my lungs.

The fact that we are not quickly stricken down by low humidity suggests to me that there must be some compensatory mechanism.

I was marveling at how well "some compensatory mechanism" works to prevent pulmonary edema, even under challenging conditions where we could expect continuous, extraordinary evacuation of water vapor from the alveolar environment.

I was not trying to suggest that breathing dry air and getting PE are strongly and positively correlated. In fact, I would expect none, or a weakly negative correlation between getting PE and breathing partial pressures of water vapor slightly below what we normally encounter. If the air is a bit drier than usual, with all other things being equal, I would expect to see less PE, not more.

In environments with very low (near zero) partial pressures of water vapor, I think things get interesting.

Earlier, I was trying to express how curious and fascinating I find it that some imagined protective "drying effect" of breathing a gas with very little water vapor could only rarely be overwhelmed.

Immersion edema occasionally happens while breathing a dry gas. Similar edema occurs every so often when mountaineers breathe dry air at high altitude (HAPE). I would expect the low partial pressure of water vapor in the thinner air to effectively remove moisture from the lungs, and maybe it does, most of the time.

But some force can overwhelm that evaporation, leading to unchecked pooling of fluids. I wonder what that something-force is?

Perhaps more to your point, but tangential to mine: does the failure of "some compensatory mechanism" strongly correlate with pulmonary edema, or perhaps even define it?

In the specific case of immersion pulmonary edema, I think overhydration is a compelling story. I think Dr Roussos' article and advice make this case nicely. I learned quite a bit from them, and expect to happily cite them in the future.

 
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Water which is ingested moves very quickly from the gut into the intravascular space. Movement out of the intravascular into the extravascular space is a little slower, because it is dependent on perfusion as well as diffusion. Repletion of the intracellular space is definitely slower, but this space does not become depleted until volume loss is either pretty severe or fairly prolonged. The average recreational diver, who has not developed Montezuma's revenge and has not looked at the bottom of the tequila bottle the night before, is highly unlikely to have any significant intracellular volume deficits. Sweating and insensible loss (skin and respiration) will primarily deplete the intravascular space, which is pretty quick to tank up with drinking.
 
As regards, "I can never be too hydrated," that is largely correct. One can over-hydrate and develop water intoxication from the extreme washout of blood sodium, but this typically occurs only under unusual circumstances, such as in marathon runners who overdo the hydration thing. However, IPE is not the result of over-hydration and very likely is little affected by such. IPE appears to be a clearly pathological condition caused by an as yet not fully understood mechanism(s) that results in capillaries leaking fluid into interstitial spaces of the lung.

Regards,

DocVikingo

I have to disagree with you and I think Duke Dive Medicine is, as well: "We are finding that overhydration is definitely correlated with increased risk of IPE in susceptible individuals."

Best,

CR
 
We are finding that overhydration is definitely correlated with increased risk of IPE in susceptible individuals.
DDM

Hey DDM,

Care to share what you have regarding the typical rec diver, e.g., otherwise healthy, not enging in rapid onset extreme exercise?

Thanks,

DocV
 
DocV,

it appears that the development of IPE may occur even at rest without having to engage in "extreme exercise". In patients without any other pathophysiology, the primary cause is thought to be the patient's inability to vasodilate pulmonary vasculature to accommodate the increased blood flow from immersion. Once critically increased hydrostatic pressure is reached inside the pulmonary vasculature, fluid will transudate into the alveoli causing pulmonary edema. Considering this context, it stands to reason that by avoiding over hydration, less volume gets shunted, less hydrostatic pressure is generated and thus the threshold of transudation may not be reached.

If interested, you can find various articles on this topic on Page 33: http://addhelium.com/site/wp-content/uploads/2014/11/AddHeliumResourceLibrary.pdf

Regards,
 
It appears that the development of IPE may occur even at rest without having to engage in "extreme exercise".

I was unable to find the terminology "extreme exercise" anywhere in my prior post. While I did mention marathon runners, this was in regard to water intoxication, not IPE, although of course they can sustain it.

In any event, I was unable to find any research in your reference list to support your assertion above, "even at rest". All of the articles I read stated or implicated that exertion was involved in IPE to varying degrees. And, when IPE did develop "at rest," it was preceded by a period of exertion of some type.

Did I miss something?

Regards,

DocVikingo
 
Excessive hydration increases intravascular volume, at least transiently. That increased volume, coupled with the fluid redistribution from immersion and in-water exercise, can result in increased pulmonary artery pressure. Preliminary (unpublished as of this writing) research indicates that IPE can be reliably induced in susceptible individuals by giving them a large amount of PO fluid and then having them exercise in the water.

Best regards,
DDM

---------- Post added December 5th, 2014 at 11:55 AM ----------

DocV,

it appears that the development of IPE may occur even at rest without having to engage in "extreme exercise". In patients without any other pathophysiology...

That would be very unusual. Exercise is an important component of "pure" IPE. If an individual suffered from IPE simply by immersing himself/herself in water I would suspect that there would be some other contributing factor.

Best regards,
DDM
 
I was unable to find the terminology "extreme exercise" anywhere in my prior post. While I did mention marathon runners, this was in regard to water intoxication, not IPE, although of course they can sustain it.

In any event, I was unable to find any research in your reference list to support your assertion above, "even at rest". All of the articles I read stated or implicated that exertion was involved in IPE to varying degrees. And, when IPE did develop "at rest," it was preceded by a period of exertion of some type.

Did I miss something?

Regards,

DocVikingo


Hello DocVikingo:

I was quoting you from here:

Hey DDM,

Care to share what you have regarding the typical rec diver, e.g., otherwise healthy, not enging in rapid onset extreme exercise?

Thanks,

DocV


You are correct: None of the report cited included the development of IPE at rest (it was an anecdotal conversation I had and thus should not have be used), however, IPE did develop in snorkelers and I am presuming those were not engaging in "extremes" of exercise. The two personally known cases were not involving exertion - one was myself. I was diving without current, without exertion, swimming slowly through the Spiegel Grove.

My apologies for the confusion.
 
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