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      Assessing Exercise Limitation Using Cardiopulmonary Exercise Testing

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          Abstract

          The cardiopulmonary exercise test (CPET) is an important physiological investigation that can aid clinicians in their evaluation of exercise intolerance and dyspnea. Maximal oxygen consumption ( V ˙ O 2max ) is the gold-standard measure of aerobic fitness and is determined by the variables that define oxygen delivery in the Fick equation ( V ˙ O 2 = cardiac output × arterial-venous O 2 content difference). In healthy subjects, of the variables involved in oxygen delivery, it is the limitations of the cardiovascular system that are most responsible for limiting exercise, as ventilation and gas exchange are sufficient to maintain arterial O 2 content up to peak exercise. Patients with lung disease can develop a pulmonary limitation to exercise which can contribute to exercise intolerance and dyspnea. In these patients, ventilation may be insufficient for metabolic demand, as demonstrated by an inadequate breathing reserve, expiratory flow limitation, dynamic hyperinflation, and/or retention of arterial CO 2. Lung disease patients can also develop gas exchange impairments with exercise as demonstrated by an increased alveolar-to-arterial O 2 pressure difference. CPET testing data, when combined with other clinical/investigation studies, can provide the clinician with an objective method to evaluate cardiopulmonary physiology and determination of exercise intolerance.

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          Most cited references87

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          Exercise pathophysiology in patients with primary pulmonary hypertension.

          Patients with primary pulmonary hypertension (PPH) have a pulmonary vasculopathy that leads to exercise intolerance due to dyspnea and fatigue. To better understand the basis of the exercise limitation in patients with PPH, cardiopulmonary exercise testing (CPET) with gas exchange measurements, New York Heart Association (NYHA) symptom class, and resting pulmonary hemodynamics were studied. We retrospectively evaluated 53 PPH patients who had right heart catheterization and cycle ergometer CPET studies to maximum tolerance as part of their clinical workups. No adverse events occurred during CPET. Reductions in peak O(2) uptake (VO(2)), anaerobic threshold, peak O(2) pulse, rate of increase in VO(2), and ventilatory efficiency were consistently found. NYHA class correlated well with the above parameters of aerobic function and ventilatory efficiency but less well with resting pulmonary hemodynamics. Patients with PPH can safely undergo noninvasive cycle ergometer CPET to their maximal tolerance. The CPET abnormalities were consistent and characteristic and correlated well with NYHA class.
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            ACC/AHA Guidelines for Exercise Testing. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing).

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              Exercise-induced arterial hypoxemia.

              Exercise-induced arterial hypoxemia (EIAH) at or near sea level is now recognized to occur in a significant number of fit, healthy subjects of both genders and of varying ages. Our review aims to define EIAH and to critically analyze what we currently understand, and do not understand, about its underlying mechanisms and its consequences to exercise performance. Based on the effects on maximal O(2) uptake of preventing EIAH, we suggest that mild EIAH be defined as an arterial O(2) saturation of 93-95% (or 3-4% 25-30 Torr) and inadequate compensatory hyperventilation (arterial PCO(2) >35 Torr) commonly contribute to EIAH, as do acid- and temperature-induced shifts in O(2) dissociation at any given arterial PO(2). In turn, expiratory flow limitation presents a significant mechanical constraint to exercise hyperpnea, whereas ventilation-perfusion ratio maldistribution and diffusion limitation contribute about equally to the excessive A-a DO(2). Exactly how diffusion limitation is incurred or how ventilation-perfusion ratio becomes maldistributed with heavy exercise remains unknown and controversial. Hypotheses linked to extravascular lung water accumulation or inflammatory changes in the "silent" zone of the lung's peripheral airways are in the early stages of exploration. Indirect evidence suggests that an inadequate hyperventilatory response is attributable to feedback inhibition triggered by mechanical constraints and/or reduced sensitivity to existing stimuli; but these mechanisms cannot be verified without a sensitive measure of central neural respiratory motor output. Finally, EIAH has detrimental effects on maximal O(2) uptake, but we have not yet determined the cause or even precisely identified which organ system, involved directly or indirectly with O(2) transport to muscle, is responsible for this limitation.
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                Author and article information

                Journal
                Pulm Med
                Pulm Med
                PM
                Pulmonary Medicine
                Hindawi Publishing Corporation
                2090-1836
                2090-1844
                2012
                19 November 2012
                : 2012
                : 824091
                Affiliations
                1Pulmonary Division, Department of Medicine, 8334B Aberhart Centre, University of Alberta, Edmonton, AB, Canada T6G 2B7
                2Centre for Lung Health, Covenant Health, Edmonton, AB, Canada
                3School of Physical Therapy, University of Saskatchewan, Saskatoon, SK, Canada
                4Division of Respiratory, Critical Care and Sleep Medicine and Airways Research Group, University of Saskatchewan, Saskatoon, SK, Canada
                Author notes

                Academic Editor: Denis O'Donnell

                Article
                10.1155/2012/824091
                3506917
                23213518
                e4c19328-c693-40bf-8799-57e217545393
                Copyright © 2012 Michael K. Stickland et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 June 2012
                : 26 September 2012
                Categories
                Review Article

                Respiratory medicine
                Respiratory medicine

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