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Intracardiac Shunting across a Patent Foramen Ovale May Exacerbate Hypoxemia in High-Altitude Pulmonary Edema

Benjamin D. Levine, MD; Paul A. Grayburn, MD; Wyatt F. Voyles, MD; E. Richard Greene, PhD; Robert C. Roach; and Peter H. Hackett, MD
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Grant Support: By a grant from the William O. Moseley Foundation, Boston, Massachusetts; National Heart, Lung, and Blood Institute training grant HL 07360; and National Institutes of Health area grant R15HL4047601.

Requests for Reprints: Benjamin D. Levine: Division of Cardiology, H8.116, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9034.

Current Author Addresses: Dr. Levine: Division of Cardiology, H8.116, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9034.

Dr. Grayburn: Veterans Administration Medical Center (111A), 4500 South Lancaster Road, Dallas, TX 75216.

Dr. Greene and Mr. Roach: Biomedical Research Division, Lovelace Medical Foundation, 2425 Ridgecrest Drive, Southeast, Albuquerque, NM 87108.

Dr. Voyles: 2031 Shadow Court, Loveland, CO 80538. Dr. Hackett: Denali Medical Research Project, 742 K Street, Anchorage, AK 99501.

Ann Intern Med. 1991;114(7):569-570. doi:10.7326/0003-4819-114-7-569
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This excerpt has been provided in the absence of an abstract.

Rapid ascent to altitude in susceptible persons may result in severe hypoxemia, pulmonary hypertension, and even pulmonary edema. This life-threatening syndrome affects approximately 1% of climbers who rapidly ascend to more than 3000 m (1). The underlying mechanisms for this problem have yet to be determined. We used bubble contrast and Doppler echocardiography on 12 climbers at 4200 m on Mount McKinley, Alaska, to test the hypothesis that a patent foramen ovale may provide an avenue for right-to-left shunting during high-altitude-induced hypoxia and pulmonary hypertension, resulting in disproportionate hypoxemia and contributing to the development of high-altitude pulmonary edema.

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