1Respiratory Investigation Unit and Laboratory of Clinical Exercise Physiology, Queen's University and Kingston General Hospital, Kingston, Ontario, Canada2Division of Respiratory Medicine, Federal University of Rio Grande do Sul, Porto Alegre, Brazil3Laboratory of Respiratory Pathophysiology, Respiratory Division, Department of Medicine, Federal University of Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil4Department of Chest Diseases, Faculty of Medicine, Alexandria University, Alexandria, Egypt5Respiratory Division, Pulmonary Function and Clinical Exercise Physiology, Federal University of Sao Paulo, Sao Paulo, Brazil; and6Department of Public Health and Infectious Diseases, Sapienza University of Rome, Rome, Italy
Checking for direct PDF access through Ovid
Exertional dyspnea is present across the spectrum of chronic obstructive pulmonary disease (COPD) severity. However, without realizing it themselves, patients may decrease daily physical activity to avoid distressing respiratory sensations. Dyspnea also may be associated with deconditioning. Cardiopulmonary exercise testing can uncover exertional dyspnea and its physiological determinants in patients with preserved or only mildly reduced FEV1. Dyspnea in mild COPD can largely be explained by increased “wasted” ventilation in the physiological dead space, which heightens the drive to breathe and worsens the inspiratory mechanical constraints. During incremental exercise testing, this is readily identified as an excessive ventilation-to-metabolic demand, that is, a high ventilation (Symbole) to carbon dioxide output (Symbolco2) relationship. Linking increases in Symbole/Symbolco2 to exertional dyspnea may provide objective evidence that a patient's poor exercise tolerance is not just a consequence of deconditioning. This information should prompt a proactive therapeutic approach to increase the available ventilatory reserve by, for example, giving inhaled bronchodilators. Considering that the structural determinants of ventilatory inefficiency (early emphysema, ventilation-perfusion mismatching, and microvascular disease) may progress despite only modest changes in FEV1, serial Symbole/Symbolco2 measurements might also prove valuable to track disease progression in these symptomatic patients.