Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil.
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BACKGROUND: Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise than in the general population and are reduced by sildenafil. METHODS AND RESULTS: Ten study subjects with a history of SIPE (mean age, 41.6 years) and 20 control subjects (mean age, 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6 to 7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptible subjects. Average o2 and cardiac output in controls and SIPE-susceptible subjects were: o2 2.42 L·min(-1) versus 1.95 L·min(-1), P=0.2; and cardiac output 17.9 L·min(-1) versus 13.8 L·min(-1), P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min(-1) was 22.5 mm Hg in controls versus 34.0 mm Hg in SIPE-susceptible subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18.8 mm Hg (P=0.028). After sildenafil, there were no statistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible subjects and controls. CONCLUSIONS: These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00815646.
Pulmonary Wedge Pressure
Risk Reduction Behavior
Published Version (Please cite this version)10.1161/CIRCULATIONAHA.115.019464
Publication InfoMoon, Richard E; Martina, Stefanie D; Peacher, Dionne F; Potter, Jennifer F; Wester, Tracy E; Cherry, Anne D; ... Freiberger, John J (2016). Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation, 133(10). pp. 988-996. 10.1161/CIRCULATIONAHA.115.019464. Retrieved from https://hdl.handle.net/10161/14796.
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Assistant Professor of Anesthesiology
Adjunct Associate Professor in the Department of Anethesiology
Dr Freiberger works on the translation of basic science research on reactive oxygen species signaling into clinical practice involving hyperbaric oxygen (HBO). He has performed animal experiments in the use of HBO for ischemic preconditioning and he is currently funded to conduct a randomized controlled trial of the use of HBO for the treatment of bisphosphonate-induced osteonecrosis of the jaw. The mechanisms of action for HBO in the treatment of: diabetic wounds, bony and soft tissue rad
Professor of Anesthesiology
Research interests include the study of cardiorespiratory function in humans exposed to environmental conditions ranging from 200 feet of seawater depth to high altitude, gas exchange during diving, the pathophysiology of high altitude pulmonary edema, the effect of anesthesia and postoperative analgesia on pulmonary function and monitoring of tissue oxygenation. Ongoing human studies include mechanisms of immersion pulmonary edema and the effect of chemosensitivity on postoperative ventilation
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