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

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...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 2016-03, Vol.133 (10), p.988-996
Hauptverfasser: 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
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container_end_page 996
container_issue 10
container_start_page 988
container_title Circulation (New York, N.Y.)
container_volume 133
creator 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
description 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.
doi_str_mv 10.1161/CIRCULATIONAHA.115.019464
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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.</description><identifier>ISSN: 0009-7322</identifier><identifier>ISSN: 1524-4539</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.115.019464</identifier><identifier>PMID: 26882910</identifier><language>eng</language><publisher>United States: by the American College of Cardiology Foundation and the American Heart Association, Inc</publisher><subject>Adult ; Cardiac Output - drug effects ; Cardiac Output - physiology ; Cold Temperature - adverse effects ; Exercise Test - drug effects ; Exercise Test - methods ; Female ; Humans ; Male ; Middle Aged ; Oxygen Consumption - drug effects ; Oxygen Consumption - physiology ; Pulmonary Edema - drug therapy ; Pulmonary Edema - etiology ; Pulmonary Edema - physiopathology ; Pulmonary Wedge Pressure - drug effects ; Pulmonary Wedge Pressure - physiology ; Risk Reduction Behavior ; Sildenafil Citrate - pharmacology ; Sildenafil Citrate - therapeutic use ; Swimming - physiology ; Vasodilator Agents - pharmacology ; Vasodilator Agents - therapeutic use</subject><ispartof>Circulation (New York, N.Y.), 2016-03, Vol.133 (10), p.988-996</ispartof><rights>2016 by the American College of Cardiology Foundation and the American Heart Association, Inc.</rights><rights>2016 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4264-e0bc3bd3475c8c3d3689bc703bda964e459b07700a2001ef27a1df1d1a7a60513</citedby><cites>FETCH-LOGICAL-c4264-e0bc3bd3475c8c3d3689bc703bda964e459b07700a2001ef27a1df1d1a7a60513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26882910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moon, Richard E</creatorcontrib><creatorcontrib>Martina, Stefanie D</creatorcontrib><creatorcontrib>Peacher, Dionne F</creatorcontrib><creatorcontrib>Potter, Jennifer F</creatorcontrib><creatorcontrib>Wester, Tracy E</creatorcontrib><creatorcontrib>Cherry, Anne D</creatorcontrib><creatorcontrib>Natoli, Michael J</creatorcontrib><creatorcontrib>Otteni, Claire E</creatorcontrib><creatorcontrib>Kernagis, Dawn N</creatorcontrib><creatorcontrib>White, William D</creatorcontrib><creatorcontrib>Freiberger, John J</creatorcontrib><title>Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>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.</description><subject>Adult</subject><subject>Cardiac Output - drug effects</subject><subject>Cardiac Output - physiology</subject><subject>Cold Temperature - adverse effects</subject><subject>Exercise Test - drug effects</subject><subject>Exercise Test - methods</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Oxygen Consumption - drug effects</subject><subject>Oxygen Consumption - physiology</subject><subject>Pulmonary Edema - drug therapy</subject><subject>Pulmonary Edema - etiology</subject><subject>Pulmonary Edema - physiopathology</subject><subject>Pulmonary Wedge Pressure - drug effects</subject><subject>Pulmonary Wedge Pressure - physiology</subject><subject>Risk Reduction Behavior</subject><subject>Sildenafil Citrate - pharmacology</subject><subject>Sildenafil Citrate - therapeutic use</subject><subject>Swimming - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasodilator Agents - therapeutic use</subject><issn>0009-7322</issn><issn>1524-4539</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUU1rGzEQFaWhcdz-hbK99bKppNWHVWjBmHwYTBMchx6FVtJ61Wgld7Vb438fFSehufU0zJv33gzzAPiE4DlCDH1ZLNeL-9V8s7z5Mb-eZ4yeQyQII2_ABFFMSkIr8RZMIISi5BXGp-AspV-5ZRWn78ApZrMZFghOwOZu77rOhW25DGbU1hS3o-9iUP2huDC2U1-LWzW0cdcekos-bg-FCqZYu_RQrG1WDC6G4qcb2uLOeWODapx_D04a5ZP98FSn4P7yYrO4Llc3V8vFfFVqghkpLax1VZuKcKpnujIVm4lac5gxJRixhIoacg6hwhAi22CukGmQQYorBimqpuD70Xc31p012oahV17uetfl-2VUTr6eBNfKbfwjKcKcCZgNPj8Z9PH3aNMgO5e09V4FG8ckEeeIY4byP6dAHKm6jyn1tnlZg6D8m4p8nUrGqDymkrUf_73zRfkcQyZ8OxL20Q-2Tw9-3Ntetlb5of2PBY-5WJ8e</recordid><startdate>20160308</startdate><enddate>20160308</enddate><creator>Moon, Richard E</creator><creator>Martina, Stefanie D</creator><creator>Peacher, Dionne F</creator><creator>Potter, Jennifer F</creator><creator>Wester, Tracy E</creator><creator>Cherry, Anne D</creator><creator>Natoli, Michael J</creator><creator>Otteni, Claire E</creator><creator>Kernagis, Dawn N</creator><creator>White, William D</creator><creator>Freiberger, John J</creator><general>by the American College of Cardiology Foundation and the American Heart Association, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160308</creationdate><title>Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil</title><author>Moon, Richard E ; 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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.</abstract><cop>United States</cop><pub>by the American College of Cardiology Foundation and the American Heart Association, Inc</pub><pmid>26882910</pmid><doi>10.1161/CIRCULATIONAHA.115.019464</doi><tpages>9</tpages></addata></record>
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source MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete
subjects Adult
Cardiac Output - drug effects
Cardiac Output - physiology
Cold Temperature - adverse effects
Exercise Test - drug effects
Exercise Test - methods
Female
Humans
Male
Middle Aged
Oxygen Consumption - drug effects
Oxygen Consumption - physiology
Pulmonary Edema - drug therapy
Pulmonary Edema - etiology
Pulmonary Edema - physiopathology
Pulmonary Wedge Pressure - drug effects
Pulmonary Wedge Pressure - physiology
Risk Reduction Behavior
Sildenafil Citrate - pharmacology
Sildenafil Citrate - therapeutic use
Swimming - physiology
Vasodilator Agents - pharmacology
Vasodilator Agents - therapeutic use
title Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil
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