Cardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers

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TitreCardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers
Type de publicationJournal Article
Year of Publication2017
AuteursCastagna O, Gempp E, Poyet R, Schmid B, Desruelle A-V, Crunel V, Maurin A, Choppard R, MacIver DH
JournalAMERICAN JOURNAL OF CARDIOLOGY
Volume119
Pagination929-932
Date PublishedMAR 15
Type of ArticleArticle
ISSN0002-9149
Résumé

This study assessed the relation between altered cardiac function and the development of interstitial pulmonary edema in scuba divers. Fifteen healthy men performed a 30-minute scuba dive in open sea. They were instructed to fin for 30 minutes and were wearing wet suits. Before and immediately after immersion, cardiac indexes and extravascular lung water were measured using echocardiography and lung ultrasound, respectively. The mean ultrasound lung comet score increased from 0 to 4.6 +/- 3.4. The diameter of the inferior caval vein increased by 47 5.2%, systolic pulmonary artery pressure by 105 +/- 8.6%, left atrial volume by 18.0 +/- 3.3%, and left ventricle end-diastolic volume by 10 +/- 2.4% suggesting that both right and left ventricular (LV) filling pressures were elevated. Doppler studies showed an increased mitral E peak (+2.5 +/- 0.3%) and E/A ratio (+22.5 3.4%) with a decreased mitral A peak (-16.4 2.7%), E peak deceleration time (14.5 +/- 2.4%) consistent with rapid early LV filling but without a change in LV stroke volume. There was an increase in right/left ventricle diameter ratio (+33.6 +/- 4.8%) suggesting a relative increase in eight sided heart output compared with the left. Furthermore, the lung comet score correlated significantly with inferior caval vein diameter, systolic pulmonary artery pressure, right/left ventricle diameter ratio, and E-wave deceleration time. In conclusion, the altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema. Our findings have important implications for the pathogenesis of cardiogenic pulmonary edema. (C) 2016 Elsevier Inc. All rights reserved.

DOI10.1016/j.amjcard.2016.11.050