Details

Autor(en) / Beteiligte

• Moon, Richard E
• Martina, Stefanie D
• Peacher, Dionne F
• Potter, Jennifer F
• Wester, Tracy E
• Cherry, Anne D
• Natoli, Michael J
• Otteni, Claire E
• Kernagis, Dawn N
• White, William D
• Freiberger, John J

Titel

Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil

Ist Teil von

• Circulation (New York, N.Y.), 2016-03, Vol.133 (10), p.988-996

Ort / Verlag

United States: by the American College of Cardiology Foundation and the American Heart Association, Inc

Erscheinungsjahr

2016

Quelle

MEDLINE

Beschreibungen/Notizen

• 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 (Equation is included in full-text article.)O2 and cardiac output in controls and SIPE-susceptible subjects were(Equation is included in full-text article.)O2 2.42 L·min versus 1.95 L·min, P=0.2; and cardiac output 17.9 L·min versus 13.8 L·min, P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min 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—URLhttp://www.clinicaltrials.gov. Unique identifierNCT00815646.