Small changes in lung function in runners with marathon‐induced interstitial lung edema
نویسندگان
چکیده
The purpose of this study was to assess lung function in runners with marathon-induced lung edema. Thirty-six (24 males) healthy subjects, 34 (SD 9) years old, body mass index 23.7 (2.6) kg/m(2) had posterior/anterior (PA) radiographs taken 1 day before and 21 (6) minutes post marathon finish. Pulmonary function was performed 1-3 weeks before and 73 (27) minutes post finish. The PA radiographs were viewed together, as a set, and evaluated by two experienced readers separately who were blinded as to time the images were obtained. Radiographs were scored for edema based on four different radiological characteristics such that the summed scores for any runner could range from 0 (no edema) to a maximum of 8 (severe interstitial edema). Overall, the mean edema score increased significantly from 0.2 to 1.0 units (P < 0.01), and from 0.0 to 2.9 units post exercise in the six subjects that were edema positive (P = 0.03). Despite a 2% decrease in forced vital capacity (FVC, P = 0.024) and a 12% decrease in alveolar-membrane diffusing capacity for carbon monoxide (DmCO, P = 0.01), there was no relation between the change in the edema score and the change in DmCO or FVC. In conclusion, (1) mild pulmonary edema occurs in at least 17% of subjects and that changes in pulmonary function cannot predict the occurrence or severity of edema, (2) lung edema is of minimal physiological significance as marathon performance is unaffected, exercise-induced arterial hypoxemia is unlikely, and postexercise pulmonary function changes are mild.
منابع مشابه
Lung Changes in Shock
In the very beginning stage of the lung changes are Perivascular, capillary wall edema, thickening of the interstitial, lymph and vascular dilatation. In the late stage of the shock the following changes will occuree Microthromboses of the lung capillary, polynulcear infiltration into the interstitial, the existence of polynuclear in the alveoli, proliferation of interstitial mesenchyma,...
متن کاملMathematical Modelling of Pulmonary Edema
The excess accumulation of water in lung interstitial or alveolar is called pulmonary edema which is caused by factors that upset the normal Starling balance in micro-circulation. Pulmonary edema disturbs the alveolar gas exchanges which are normally regulated by the respiratory system. Mathematical modelling of pulmonary edema may help to predict the lung conditions and the mechanisms involved...
متن کاملMathematical Modelling of Pulmonary Edema
The excess accumulation of water in lung interstitial or alveolar is called pulmonary edema which is caused by factors that upset the normal Starling balance in micro-circulation. Pulmonary edema disturbs the alveolar gas exchanges which are normally regulated by the respiratory system. Mathematical modelling of pulmonary edema may help to predict the lung conditions and the mechanisms involved...
متن کاملThe Assessment of Health-Related Quality of Life in Scleroderma-Interstitial Lung Disease
Introduction: Pulmonary involvement is the most common cause of mortality and disability in patients with systemic sclerosis and it significantly affects the quality of life in these patients. Therefore, early diagnosis and treatment of pulmonary involvement seems necessary in patients with SSc. In this study, we aimed to assess the health-related quality of life (HRQoL) in patients with Sclero...
متن کاملA Case Report of Small Cell Lung Carcinoma in a Patient with Progressive Diffuse Sclerosis
Connective tissue diseases, including scleroderma, may be associated with an increased risk of lung cancer. The most common type of lung cancer associated with systemic sclerosis is adenocarcinoma or bronchoalveolar carcinoma, and small cell carcinoma is rare. This reports presents a 54-year-old non-smoker woman with a history of scleroderma who was examined due to aggravation of shortness of ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 2 شماره
صفحات -
تاریخ انتشار 2014