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An investigation of extravascular lung water during exercise in those individuals susceptible to immersion pulmonary edema or high altitude pulmonary edema

University of British Columbia

Introduction: High altitude pulmonary edema (HAPE) is caused by hypoxic vasoconstriction, leading to increased pulmonary artery pressure (PPA). Increased PPA results in extravasation of fluid from the pulmonary capillaries to the interstitial space and inhibition of gas exchange. Immersion pulmonary edema (IPE) is likely the result of increased hydrostatic pressure due to water immersion combined with cold and physical exertion, further elevating PPA. During maximal exercise, some humans develop pulmonary edema independent of hypoxia or immersion; this is a possible cause of exercise-induced arterial hypoxemia (EIAH). Purpose: The purpose of this study was to 1) investigate the common mechanisms that are responsible for the development of HAPE, IPE, and EIAH; and 2) investigate the factors that determine an individual’s susceptibility to HAPE/IPE. Hypotheses: We hypothesize that 1) individuals susceptible to HAPE/IPE will develop increased extravascular lung water (EVLW) following exercise; and 2) these changes will not occur in HAPE/IPE-resistant controls. Methods: This study included 9 healthy fit participants who previously experienced HAPE or IPE. Participants performed a 45-minute maximal exercise task on a cycle ergometer. A matched control group of 9 participants with experience at altitude or immersion and no history of HAPE/IPE also performed the task. Diffusion capacity of CO (DLco) was measured before and after exercise. Computed tomography was used to confirm EVLW following exercise. Results: Both groups showed a significant reduction in lung density post-exercise (p=0.013). Participants susceptible to HAPE/IPE had a significantly lower density compared to resistant participants (p=0.037). DLco decreased significantly after exercise (p<0.001), without difference in the change between groups (p=0.77). Discussion: Because of the post-exercise increase in volume, the decrease in lung density should be considered to represent no change in EVLW. The decrease in DLco was consistent with results found in other studies. Lower lung density in HAPE/IPE-susceptible participants could be the result of damage caused by HAPE/IPE, increased vascular reactivity, or decreased lymphatics. Conclusion: Susceptibility to HAPE/IPE does not increase risk of developing EVLW during maximal exercise. Participants susceptible to HAPE/IPE displayed a significantly lower lung density that necessitates further research.

Text

2011-08-17

Attribution-NonCommercial-NoDerivs 3.0 Unported

http://hdl.handle.net/2429/36739

Kinesiology

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/3.0/