Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil.
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2016-03-08
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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.
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Moon, RE, DF Peacher, JF Potter, TE Wester, AD Cherry, M Natoli, CE Otteni, DN Kernagis, et al. (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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Richard Edward Moon
Research interests include the study of cardiorespiratory function in humans during challenging clinical settings including the perioperative period, and exposure to environmental conditions such as diving and high altitude. Studies have included gas exchange during diving, the pathophysiology of high altitude and immersion pulmonary edema, the effect of anesthesia and postoperative analgesia on pulmonary function and monitoring of tissue oxygenation. Ongoing human studies include the effect of respiratory muscle training on chemosensitivity and blood gases during stressful breathing: underwater exercise.
Anne Cherry
John Jacob Freiberger
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 radionecrosis and decompression sickness are also areas of his inquiry. Dr Freiberger also does basic epidemiological research into accidents and injuries associated with diving, high altitude exposure and other adverse conditions associated with extreme environments. Dr. Freiberger directs the fellowship program at the Duke Center for Hyperbaric Medicine and Environmental Physiology.
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