Exploring the depths of immersion pulmonary edema

Richard T. Mahon

J Appl Physiol 110:589-590, 2011. First published 13 January 2011;

doi:10.1152/japplphysiol.00019.2011
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J Appl Physiol 110: 589590, 2011;

doi:10.1152/japplphysiol.00019.2011.

Invited Editorial

Exploring the depths of immersion pulmonary edema

Richard T. Mahon
Undersea Medicine Department, Naval Medical Research Center, Silver Spring, Maryland

Address for reprint requests and other correspondence: R. T. Mahon,

Undersea Medicine Dept., Naval Medical Research Center, 503 Robert Grant
Ave., Silver Spring, MD 20910-7500 (e-mail: Richard.Mahon@med.navy.
mil).
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only thermal protection did not attenuate the rise in pulmonary artery pressure.
The techniques described in that first study were then applied to the hyperbaric environment [4.7 atmospheres absolute
(ATA)]. Peacher et al. (3) studied the exercising diver in
thermoneutral water and explored any potential benefits of
breathing oxygen enriched air. To my knowledge this publication represents the most in-depth study of pulmonary and
vascular physiology in diving environments and brings a tear to
the eye of anyone who fondly recalls the halcyon years of basic
whole human diving physiology.
In those studies, the overall increase in pulmonary artery
pressure was observed, but with quite a range of variability,
supporting the notion of individual IPE susceptibility. The
pulmonary hypertension Peachers group noted in thermoneutral hyperbaric exercising divers was attenuated with oxygenenriched air and approached the values seen in simple surface
(1 ATA) immersion. Interestingly, the pulmonary capillary
wedge pressure was unaffected by oxygen tension. These
observations support elevated pulmonary vascular pressures as
the cause of IPE but leave open the question as to whether
susceptible individuals may have an excessive rise in pulmonary artery pressure caused by exaggerated peripheral venoconstriction or nonhomogeneous pulmonary vasoconstriction,
as has been suggested for HAPE.
This work presented by lead author Fraser reporting the third
study in this series describes a lack of protection provided by
oxygen-enriched air in preventing immersion-related pulmonary hypertension in cold water at 4.7 ATA (1). In addition to
the generous scientific value, their work provides practical
insight as well. In summing up their body of work with an eye
to application, if IPE is a concern the first goal should be to
stay warm and consider an oxygen-enriched breathing mixture.
And if you are unable to stay warm, the enriched oxygen is not
so helpful. This certainly has direct implication for operational
divers, especially those in the military.
Beyond delivering an elegant method for testing the pulmonary vascular system in diving and answering some basic
whole human physiology questions, these studies also deliver
the goods on expanding our questions. And after all, isnt that
the hallmark of good research?
So then, where are we and where do we go from here? What
is the cause of the pulmonary vascular variability? Does the
variability itself provide insights into other pathological processes in much the same way that research in hypoxic pulmonary vasoconstriction has enlightened the overall field of pulmonary vascular hypertension? What is the mechanism of
cold-related pulmonary hypertension and why is that not improved with oxygen enrichment? What other modalities can be
examined and tested for decreasing pulmonary pressures in
diving? And last but far from least, do actual patients with IPE
have an exuberant increase in pulmonary arterial pressures
with immersion?
589

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by Wilmshurst et al. (6) in 1981, immersion pulmonary edema (IPE) has been of more than merely a
casual interest to divers and surface swimmers.
The condition and its consequences are of particular concern
in military diving communities, where IPE imposes not only
significant health risk but also threatens to compromise training
and operations (4).
Despite this interest, the scientific literature addressing this
condition is scant compared with other forms of pulmonary
edema. For example, studies related to high-altitude pulmonary
edema (HAPE) exceed those of IPE by at least an order of
magnitude. Just some of the factors that have hampered IPE
research include the sporadic and currently unpredictable occurrence, its likeliness to manifest in remote locations, and the
inevitable removal of the IPE victim from the insult (immersion) to render medical attention. As such, the majority of work
regarding IPE is limited to case reports or studies performed at
shallow immersion.
The work in this issue of the Journal of Applied Physiology
by Fraser et al. (1) is the third in a series of studies aimed at
confirming ideas about diving physiology as they relate specifically to IPE. The research team should be commended on a
cogent study design that executed complex monitoring in a
unique hyperbaric environment, and their success testifies to an
exceptionally skilled team. At least as worthy of accolades are
the volunteer subjects of the study series for their contributions
toward more thoroughly understanding this condition. By employing the gold standard pulmonary artery catheter in an
immersed hyperbaric environment, the body of work this study
series represents has significantly advanced the understanding
of IPE encountered in diving environments.
Since its initial description, IPE has been considered more
likely to occur in cold water and thought to be associated with
some degree of vascular dysfunction. This hypothesis was
reasonable and sound given that the thoracic blood volume
engorgement seen with immersion has been demonstrated to
increase in cold water. This, coupled with evidence of increased forearm vascular resistance in subjects who had suffered from IPE (especially on exposure to cold), and an
apparent increase in systemic hypertension, lead one to conclude that some engorgement and vascular dysfunction were at
the heart of the issue. Subsequently, there were small studies
that suggested capillary stress failure, further strengthening the
case for pulmonary vascular or cardiovascular dysregulation
(2). However, it wasnt until the first study from this series that
significant progress was made toward understanding the cardiopulmonary vascular physiology in immersed cold-water
exercise. The study demonstrated an increase in pulmonary
artery pressure with exercise in cold water immersion that was
attenuated with thermal body protection (5). However, head
SINCE FIRST DESCRIBED

Invited Editorial
590
Once again, Fraser should be applauded for this effort, the
publication, and the entire group congratulated for the body of
work.

3.

DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the author(s).

4.

REFERENCES
1. Fraser JA, Peacher DF, Freiberger JJ, Natoli MJ, Schinazi EA, Beck
IV, Walker JR, Doar PO, Boso AE, Walker AJ, Kernagis DN, Moon
RE. Risk factors for immersion pulmonary edema: hyperoxia does not
attenuate pulmonary hypertension associated with cold water-immersed
prone exercise at 4.7 ATA. J Appl Physiol (December 9, 2010). doi:
10.1152/japplphysiol.01088.2010.
2. Ludwig BB, Mahon RT, Parrish JS, Lamb C, Kerr S. Pulmonary edema
in combat swimmers: clinical and bronchoalveolar lavage description dem-

5.

6.

onstrating stress failure of the pulmonary capillaries. Undersea Hyperb Med

31, Suppl: 318, 2004.
Peacher DF, Pecorella SRH, Freiberger JJ, Natoli MJ, Schinazi EA,
Doar PO, Boso AE, Walker AJ, Gill M, Kernagis D, Uguccioni D, Moon
RE. Effects of hyperoxia on ventilation and pulmonary hemodynamics
during immersed prone exercise at 4.7 ATA: possible implications for
immersion pulmonary edema. J Appl Physiol 109: 68 78, 2010.
Weiler-Ravell D, Shuypak A, Goldenberg I, Halpern P, Shoshani O,
Hirschhorn G, Margulis A. Pulmonary oedema and haemoptysis induced
by strenuous swimming. BMJ 311: 361362, 1995.
Wester TE, Cherry AD, Pollock NW, Freiberger JJ, Natoli MJ, Schinazi EA, Doar PO, Boso AE, Alford EL, Walker AJ, Uguccioni DM,
Kernagis D, Moon RE. Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA. J Appl Physiol 106: 691700,
2009.
Wilmshurst PT, Nuri M, Crowther A, Betts JC, Webb-Peploe MM.
Forearm vascular responses in subjects who develop recurrent pulmonary
edema when scuba diving: a new syndrome. Br Heart J 45: 349, 1981.

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