Chest

Chest

Volume 120, Issue 5, November 2001, Pages 1686-1694
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Pulmonary Edema Associated With Scuba Diving: Case Reports and Review

https://doi.org/10.1378/chest.120.5.1686Get rights and content

Acute pulmonary edema has been associated with cold-water immersion in swimmers and divers. We report on eight divers using a self-contained underwater breathing apparatus (scuba) who developed acute pulmonary edema manifested by dyspnea, hypoxemia, and characteristic chest radiographic findings. All cases occurred in cold water. All scuba divers were treated with complete resolution, and three have returned to diving without further episodes. Mechanisms that would contribute to a raised capillary transmural pressure or to a reduced blood-gas barrier function or integrity are discussed. Pulmonary edema in scuba divers is multifactorial, and constitutional factors may play a role. Physicians should be aware of this potential, likely underreported, problem in scuba divers.

Section snippets

Materials and Methods

Information was collected on scuba divers from 1986 to 1999, who were referred to the Pacific Grove Hyperbaric Facility in Monterey, CA, the John Muir Medical Center in Walnut Creek, CA, or Doctors Medical Center in San Pablo, CA, for the evaluation of pulmonary edema that developed during diving. Data regarding patient diving history, details of incident dives, medications, medical history including prior episodes, laboratory and radiograph evaluations, treatments, and outcomes were reviewed

Discussion

The pathophysiologic mechanisms for the development of acute pulmonary edema in apparently otherwise healthy scuba divers are not clear. In most divers, the pulmonary edema occurs without an obvious precipitating cause, can occur in shallow or deep dives and in cold or warm water, and has been reported in swimmers.234 Patients may have arterial blood gas findings of acidosis and hypoxemia, chest radiographic abnormalities, rarely have evidence of heart failure, and survivors respond completely

Pulmonary Edema

The development of pulmonary edema represents a pathophysiologic spectrum. On one end of this spectrum is the pure cardiogenic origin of pulmonary edema (as in congestive heart failure) due to increased pulmonary capillary hydrostatic pressure that produces edema fluid with a relatively low protein content. At the other end is a more severe, noncardiogenic form caused by increased capillary permeability, as in patients with ARDS. In patients with ARDS, the edema arises from lung cell injury

Immersion Effects

Immersion causes the central pooling of blood by facilitation of the venous return, which increases the preload. This physical shift of blood centrally during immersion is further aided by the high density of water, which diminishes or eliminates the usual pooling of blood in the peripheral veins that occurs in air (in this respect, immersion is analogous to a gravity-free state).24 Blood redistribution during immersion in thermoneutral water (ie, 91.4 to 95°F) and in cool water corresponds to

Negative-Pressure Effects

Clinically silent negative-pressure pulmonary edema as a consequence of acute airway obstruction or vigorous attempts to breathe against a high resistance to flow has been described.3233 Factors that could contribute to pulmonary edema in scuba divers include scuba valve failure (rare), low tank air pressure with certain types of regulators, a tank not turned completely on, the use of a breathing apparatus with a high inspiratory resistance, and panic associated with an increased effort of

Neurogenic Pulmonary Edema

Pulmonary edema develops in several clinical conditions that have both cardiogenic and noncardiogenic (permeability) components. Although the pathogenesis of nervous system-induced pulmonary edema remains incompletely understood, the two major mechanisms are elevated intravascular pressure and pulmonary capillary leak. Intracranial hypertension causes a massive centrally mediated sympathetic discharge, which increases systemic and pulmonary vascular resistance and leads to high transmural

HAPE

Although not directly relevant to divers and swimmers, a discussion of HAPE may help to clarify the pathophysiology of pulmonary edema. HAPE is associated with high pulmonary arterial pressures, normal wedge pressures, and reduced barrier function of the pulmonary vascular wall. HAPE-prone mountaineers had significant (p < 0.01) elevations of plasma endothelin-1 levels compared to HAPE-resistant control subjects. This potent pulmonary vasoconstrictor peptide causes an exaggerated pulmonary

Peak Exercise and Pulmonary Edema

There have been several published case reports4647484950 of pulmonary edema in athletes during peak exercise and during bicycle ergometry,51 and it is well-known to occur in racehorses.5253 Increased cardiac output during exercise rarely would be expected to raise pulmonary capillary pressure to the point of microvascular rupture in humans. However, combined with the pulmonary mechanics of effort associated with extreme exertion, capillary tolerance could be exceeded. A role for the activation

Pulmonary Barotrauma

Breath-hold diving has been reported to result in intra-alveolar hemorrhaging54 and death from diffuse bilateral pulmonary vascular injury.6 Pulmonary barotrauma due to lung overinflation usually is associated with a rapid or uncontrolled ascent while breathing from a compressed air source and can lead to air embolism.55 This serious condition may be second only to drowning as a cause of death among recreational scuba divers. Neither condition seems to play a role in our cases.

Conclusion

There are > 3 million scuba divers in the United States alone. Physicians will increasingly be asked to evaluate and treat scuba diving-related problems and to assess individuals for fitness to dive. Factors potentially contributing to the development of pulmonary edema in the diver or swimmer include poor physical condition, underlying cardiovascular dysfunction, hypertension, asthma, anxiety, and strenuous exertion before, during, or after diving. External factors contributing to the

Acknowledgment

We acknowledge the assistance of John B. West, MD, PhD, Claude A. Piantadosi, MD, and Anthony Woolf, MD, for their thorough reviews of the manuscript and invaluable suggestions. We also thank James L. Caruso, MD, for his assistance in providing case information from the Divers Alert Network files.

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    Copyright © 2001 The American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.