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Pulmonary Gas Exchange Abnormalities in Mild Chronic Obstructive Pulmonary Disease. Implications for Dyspnea and Exercise Intole

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Pulmonary Gas Exchange Abnormalities in Mild Chronic Obstructive Pulmonary Disease. Implications for Dyspnea and Exercise Intole &get_box_var;ORIGINAL ARTICLE Pulmonary Gas Exchange Abnormalities in Mild Chronic Obstructive Pulmonary Disease Implications for Dyspnea and Exercise Intolerance Amany F. Elbehairy1,2, Casey E. Ciavaglia1, Katherine A. Webb1, Jordan A. Guenette3, Dennis Jensen4, Sahar M. Mourad2, J. Alberto Neder1, and Denis E. O’Donnell1; on behalf of the Canadian Respiratory Research Network 1Respiratory Investigation Unit, Department of Medicine, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada; 2Department of Chest Diseases, Faculty of Medicine, Alexandria University, Alexandria, Egypt; 3Department of Physical Therapy and Centre for Heart Lung Innovation, University of British Columbia and St. Paul’s Hospital, Vancouver, British Columbia, Canada; and 4Department of Kinesiology and Physical Education, McGill University, Montreal, Quebec, Canada – Abstract subjects throughout exercise. The alveolar arterial O2 tension gradient: was: elevated at rest and throughout exercise in COPD (P , Rationale: Several studies in mild chronic obstructive pulmonary 0.05). VE/VCO2, dead space to tidal volume ratio (VD/VT), and arterial P , disease (COPD) have shown a higher: : than normal ventilatory to end-tidal CO2 difference were all higher ( 0.05) in patients with equivalent for carbon dioxide (VE/VCO2) during exercise. Our COPD than in control subjects during exercise. In patients with objective was to examine pulmonary: : gas exchange abnormalities COPD versus control subjects, there was significant dynamic fl P , and the mechanisms of high VE/VCO2 in mild COPD and its impact hyperin ation and greater tidal volume constraints ( 0.05). on dyspnea and exercise intolerance. Standardized dyspnea intensity ratings were also higher (P , 0.05) in patients with COPD versus control subjects in association with higher Methods: Twenty-two subjects (11 patients with GOLD [Global ventilatory: : requirements. Within all subjects, VD/VT correlated with the Initiative for Chronic Obstructive Lung Disease] grade 1B COPD, VE/VCO ratio during submaximal exercise (r = 0.780, P , 0.001). 11 age-matched healthy control subjects) undertook physiological 2 testing and a symptom-limited incremental cycle exercise test with Conclusions: High VD/VT was the most consistent gas exchange arterial blood gas collection. abnormality in smokers with only mild spirometric abnormalities. Compensatory increases in minute ventilation during exercise Measurements and Main Results: Patients (post-bronchodilator 6 6 maintained alveolar ventilation and arterial blood gas homeostasis FEV1:94 10% predicted; mean SD) had evidence of peripheral but at the expense of earlier dynamic mechanical constraints, greater airway dysfunction and reduced peak oxygen uptake compared with dyspnea, and exercise intolerance in mild COPD. control subjects (80 6 18 vs. 113 6 24% predicted; P , 0.05). Arterial blood gases were within the normal range and effective Keywords: mild chronic obstructive pulmonary disease; exercise; alveolar ventilation was not significantly different from control ventilatory inefficiency; gas exchange; dyspnea (Received in original form January 26, 2015; accepted in final form March 27, 2015 ) Supported by the Ontario Thoracic Society; William Spear/Richard Start Endowment Fund, Queen’s University; and the Canadian Respiratory Research Network (CRRN). The CRRN is supported by grants from the Canadian Institutes of Health Research (CIHR)–Institute of Circulatory and Respiratory Health; Canadian Lung Association (CLA)/Canadian Thoracic Society (CTS); British Columbia Lung Association; and Industry Partners Boehringer-Ingelheim Canada Ltd., AstraZeneca Canada Inc., and Novartis Canada Ltd. Financial support to A.F.E. was provided by an Egyptian Ministry of Higher Education and Scientific Research Scholarship. J.A.G. was supported by a Scholar Award from the Michael Smith Foundation for Health Research. D.J. was supported by a Chercheurs-Boursiers Junior 1 salary award from the Fonds de Recherche du Quebec-Sant ´ e ´ and by a William Dawson Research Scholar Award. The funders had no role in the study design, data collection and analysis, or preparation of the manuscript. Author Contributions: All authors played a role in the content and writing of the manuscript. In addition: D.E.O’D. was the principal investigator and contributed the original idea for the study; D.E.O’D., A.F.E., and K.A.W. had input into the study design and conduct of study; A.F.E. and C.E.C. collected the data; and A.F.E. performed data analysis and prepared it for presentation. Correspondence and requests for reprints should be addressed to Denis E. O’Donnell, M.D., 102 Stuart Street, Kingston, ON, K7L 2V6 Canada. E-mail: [email protected] This article has an online supplement, which is accessible from this issue’s table of contents online at www.atsjournals.org Am J Respir Crit Care Med Vol 191, Iss 12, pp 1384–1394, Jun 15, 2015 Copyright © 2015 by the American Thoracic Society Originally Published in Press as DOI: 10.1164/rccm.201501-0157OC on March 13, 2015 Internet address: www.atsjournals.org 1384 American Journal of Respiratory and Critical Care Medicine Volume 191 Number 12 | June 15 2015 ORIGINAL ARTICLE The current study extends the previous Given the evidence of increased lung At a Glance Commentary work by primarily examining the compliance, early airway closure, extensive abnormalities of pulmonary gas exchange peripheral airway dysfunction, and Scientific Knowledge on the that drive the increased total (minute) maldistribution of ventilation in smokers Subject: Heterogeneous mechanical ventilation during exercise (14–19). with nearly preserved spirometry (17, 22, and pulmonary gas exchange A seminal study by Barbera and 23), it is not surprising that an increased: : impairment can exist in smokers with colleagues showed that in patients proportion of lung units with low VA/Q only minor spirometric abnormalities, with mild-to-moderate COPD, the ratios is thought to be the dominant gas but their precise clinical relevance alveolar–arterial oxygen tension gradient exchange abnormality in mild COPD (21). – remains unknown. The presence of (A aPO2) was increased at rest and during However, several exercise studies in mild a high ventilatory equivalent for CO2, exercise (20). The investigators further COPD point to consistent abnormalities of suggesting reduced ventilatory demonstrated that arterial oxygenation surrogate measures of ventilatory: : efficiency – efficiency, has consistently been improved at a standardized submaximal derived from analysis of VE VCO2: : – – reported in several exercise studies in exercise work rate as a result of increased relationships (15 19). Thus, the VE VCO2 mild chronic obstructive pulmonary and improved distribution of ventilation. slope and nadir of the ventilatory: : disease, but the underlying In that study, comparison with a healthy equivalent for carbon dioxide (VE/VCO2) mechanisms and consequences for control group was not undertaken to during submaximal exercise were exercise tolerance are poorly account for the established effects of aging consistently higher than in age-matched understood. on pulmonary gas exchange. Moreover, healthy control subjects (15–19). This is the potential role of increased wasted compatible with an increased dead space to What This Study Adds to the ventilation and its interaction with dynamic tidal volume ratio (VD/VT), alterations in Field: Increased physiological dead respiratory mechanics and dyspnea were the set point for PaCO2, or both (24). space and wasted ventilation were not formally examined (20). More recently, The clinical importance of ventilatory the most consistent pulmonary gas Rodr´ıguez-Roisin and colleagues confirmed inefficiency during exercise is increasingly – exchange abnormalities during exercise widened A aPO2 during resting breathing recognized in various cardiopulmonary in the patients with mild chronic and predominance of lung: : units with low diseases (25–28). In this context, studies obstructive pulmonary disease. ventilation–perfusion (VA/Q) ratios in have shown that, in contrast to the situation Although effective alveolar ventilation the majority of a subsample (n = 15) of in congestive heart failure, the usefulness of and arterial blood gas homeostasis patients with Global Initiative for Chronic surrogate measures: of ventilatory: efficiency – were adequately preserved by Obstructive Lung Disease (GOLD) stage 1 derived from the VE VCO2 slope is limited compensatory increases in minute mild COPD (21). as mechanical constraints increase with ventilation, this forced earlier dynamic respiratory mechanical constraints, greater dyspnea, and exercise Table 1. Subject Characteristics intolerance in these patients despite a largely preserved FEV1. Mild COPD Healthy Male:female, n 6:5 5:6 Chronic obstructive pulmonary disease Age, yr 64.0 6 11 64.1 6 10 (COPD) is increasing in prevalence Height, cm 167 6 11 169 6 8 worldwide, and the vast majority of Body mass, kg 77.1 6 15.9 78.9 6 11.7 patients have mild airway obstruction by BMI, kg/m2 27.2 6 3.4 27.5 6 3.3 6 6 spirometric criteria (1–5). Such patients Smoking history, pack-years 35.6 14.9* 1.5 3.2 Smoking status, % current smokers 45%* 0% have increased all-cause mortality and BDI focal score, 0–12 8.0 6 1.2* 11.8 6 0.6 reduced health-related quality of life, Modified MRC dyspnea scale, 0–4 2.0 6 0.4* 0.3 6 0.5 exercise capacity, and habitual physical CAT score, 0–40 15.6 6 7.7* 2.9 6 1.9 activity (6–10). Moreover, a subset Oxygen cost
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