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Original Research

Influence of body mass on predicted values of static hyperinflation in COPD

, , , &
Pages 2551-2555 | Published online: 23 Aug 2018
 

Abstract

Introduction

For interpretation of body plethysmographic static hyperinflation, reference values are of crucial importance. Earliest reference values have been published by the European Coal and Steel Community (ECSC) and are based on sex, body height and age as predictors. As obesity can lead to a reduction of functional residual capacity (FRC) in lung-healthy subjects, more recent approaches included body weight or body surface area. This raises the question whether these models are appropriate in patients with COPD-induced hyperinflation.

Method

Several FRC prediction models and their relation to body weight were analyzed in 1513 patients with stable COPD (mean [SD] age: 64.5 [8.2] years; GOLD grades 1–4: 219/722/484/88), a subset of the multicenter COPD and Systemic Consequences – Comorbidities Network cohort.

Results

Absolute values of FRC were inversely related to body mass index (p<0.001). Applying the ECSC equations to calculate predicted values, this pattern was maintained (p<0.001). By contrast, an inverted, ie, positive, relation occurred when using equations that include body weight or surface area (p<0.001). The present analysis confirmed the inverse relation of body mass and FRC in COPD, resulting from a restrictive ventilatory pattern by diaphragm elevation and decreased chest wall compliance in obesity. The weight influence in the prediction models, as obtained from lung-healthy controls, appears to lead to an overcorrection and consequently to an inappropriate overestimation of hyperinflation as indicated by FRC %predicted in COPD.

Conclusion

It is concluded that models not including body weight as predictor, like the classical ECSC equations, could be superior in the interpretation of FRC in COPD.

Acknowledgments

This work was supported by the German Federal Ministry of Education and Research (BMBF) Competence Network Asthma and COPD (ASCONET) and performed in collaboration with the German Center for Lung Research (DZL). The project was funded by the BMBF with grant number 01 GI 0881 and was supported by unrestricted grants from AstraZeneca GmbH, Bayer Schering Pharma AG, Boehringer Ingelheim Pharma GmbH & Co. KG, Chiesi GmbH, Glaxo-SmithKline, Grifols Deutschland GmbH, MSD Sharp & Dohme GmbH, Mundipharma GmbH, Novartis Deutschland GmbH, Pfizer Pharma GmbH, Takeda Pharma Vertrieb GmbH & Co. KG and TEVA GmbH for patient investigations and laboratory measurements. The funding bodies had no involvement in the design of the study, or the collection, analysis or interpretation of the data.

Disclosure

The authors report no conflicts of interest in this work.