Pulmonary Gas Exchange Abnormalities in Mild COPD: Implications for Dyspnea and Exercise Intolerance (original) (raw)
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Physiological and clinical relevance of exercise ventilatory efficiency in COPD
The European respiratory journal, 2017
Exercise ventilation (V'E) relative to carbon dioxide output (V'CO2 ) is particularly relevant to patients limited by the respiratory system, e.g. those with chronic obstructive pulmonary disease (COPD). High V'E-V'CO2 (poor ventilatory efficiency) has been found to be a key physiological abnormality in symptomatic patients with largely preserved forced expiratory volume in 1 s (FEV1). Establishing an association between high V'E-V'CO2 and exertional dyspnoea in mild COPD provides evidence that exercise intolerance is not a mere consequence of detraining. As the disease evolves, poor ventilatory efficiency might help explaining "out-of-proportion" breathlessness (to FEV1 impairment). Regardless, disease severity, cardiocirculatory co-morbidities such as heart failure and pulmonary hypertension have been found to increase V'E-V'CO2 In fact, a high V'E-V'CO2 has been found to be a powerful predictor of poor outcome in lung resection su...
COPD: Journal of Chronic Obstructive Pulmonary Disease, 2014
The difference between total lung capacity (TLC) by body plethysmography and alveolar volume (VA) from the single-breath lung diffusing capacity measurement provides an index of ventilation distribution inequalities in COPD. The relevance of these abnormalities to dyspnea and exercise intolerance across the continuum of disease severity remains unknown. Two-hundred and seventy-six COPD patients distributed across GOLD grades 1 to 4 and 67 healthy controls were evaluated. The "poorly communicating fraction" (PCF) of the TLC was estimated as the ratio (%) of TLC to VA. Healthy subjects showed signifi cantly lower PCF values compared to GOLD grades 1 to 4 (10 ± 3% vs. 17 ± 8% vs. 27 ± 10% vs. 37 ± 10% vs. 56 ± 11%, respectively; p < 0.05). Pulmonary gas exchange impairment, mechanical ventilatory constraints and ventilation-corrected dyspnea scores worsened across PCF tertiles (p < 0.05). Of note, GOLD grades 1 and 2 patients with the highest PCF values had pronounced exercise ventilatory ineffi ciency and dyspnea as a limiting symptom. In fact, dyspnea was a signifi cant contributor to exercise limitation only in those with "moderate" or "extensive" PCF (p < 0.05). A receiver operating characteristics curve analysis revealed that PCF was a better predictor of severely reduced maximal exercise capacity than traditional pulmonary function indexes including FEV 1 (area under the curve (95% confi dence interval) = 0.85 (0.81-0.89), best cutoff = 33.4 %; p < 0.01). In conclusion, PCF is a readily available functional marker of gas exchange and mechanical abnormalities relevant to dyspnea and exercise intolerance across the COPD grades. COPD, 00:1
Ventilatory and Cardiocirculatory Exercise Profiles in COPD
CHEST Journal, 2012
The impact of PH on exercise tolerance is largely unknown. We evaluated and compared the circulatory and ventilatory profi les during exercise in patients with COPD without PH, with moderate PH, and with severe PH. Methods: Forty-seven patients, GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages II to IV, underwent cardiopulmonary exercise testing and right-sided heart catheterization at rest and during exercise. Patients were divided into three groups based on mean pulmonary artery pressure (mPAP) at rest: no PH (mPAP, , 25 mm Hg), moderate PH (mPAP, 25-39 mm Hg), and severe PH (mPAP, Ն 40 mm Hg). Mixed venous oxygen saturation (S VO 2 ) was used for evaluating the circulatory reserve. Pa CO 2 and the calculated breathing reserve were used for evaluation of the ventilatory reserve. Results: Patients without PH (n 5 24) had an end-exercise S VO 2 of 48% Ϯ 9%, an increasing Pa CO 2 with exercise, and a breathing reserve of 22% Ϯ 20%. Patients with moderate PH (n 5 14) had an exercise S VO 2 of 40% Ϯ 8%, an increasing Pa CO 2 , and a breathing reserve of 26% Ϯ 15%. Patients with severe PH (n 5 9) had a signifi cantly lower end-exercise S VO 2 (30% Ϯ 6%), a breathing reserve of 37% Ϯ 11%, and an absence of Pa CO 2 accumulation. Conclusion: Patients with severe PH showed an exhausted circulatory reserve at the end of exercise. A profi le of circulatory reserve in combination with ventilatory impairments was found in patients with COPD and moderate or no PH. The results suggest that pulmonary vasodilation might only improve exercise tolerance in patients with COPD and severe PH.
Effect of exercise mode on oxygen uptake and blood gases in COPD patients
Respiratory Medicine, 2004
Patients with chronic obstructive pulmonary disease (COPD) are characterised by decreased exercise tolerance, and, more variably, exercise induced hypoxaemia (EIH). Evaluation of physical work capacity and physiological responses to exercise may be performed by various procedures, but there are diverging opinions as to which exercise test should be preferred. In the current study, oxygen uptake and arterial blood gases in COPD patients have been compared during submaximal and maximal exercise on treadmill and ergometer bicycle.
Exercise ventilatory inefficiency in mild to end-stage COPD
The European respiratory journal, 2014
Ventilatory inefficiency during exercise is a key pathophysiological feature of chronic obstructive pulmonary disease. Currently, it is unknown how this physiological marker relates to clinically relevant outcomes as resting ventilatory impairment progresses across disease stages. Slope and intercept of the linear region of the ventilation-carbon dioxide output relationship and the ratio between these variables, at the lowest point (nadir), were contrasted in 316 patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1-4 (forced expiratory volume in 1 s, ranging from 148% pred to 12% pred) and 69 aged- and gender-matched controls, Compared to controls, slope and intercept were higher in GOLD stages 1 and 2, leading to higher nadirs (p<0.05). Despite even larger intercepts in GOLD stages 3 and 4, slopes diminished as disease evolved (from mean±sd 35±6 in GOLD stage 1 to 24±5 in GOLD stage 3, p<0.05). As a result, there were no significant differences...
Ventilatory Inefficiency as a Limiting Factor for Exercise in Patients With COPD
Respiratory Care, 2012
BACKGROUND: Ventilatory inefficiency increases ventilatory demand; corresponds to an abnormal increase in the ratio of minute ventilation (V E) to CO 2 production (V CO 2); represents increased dead space, deregulation of respiratory control, and early lactic threshold; and is associated with expiratory flow limitation that enhances dynamic hyperinflation and may limit exercise capacity. OBJECTIVE: To evaluate the influence of ventilatory inefficiency over exercise capacity in COPD patients. METHODS: Prospective study of 35 COPD subjects with different levels of severity, in whom cardiopulmonary stress test was performed. Ventilatory inefficiency was represented by the V E /V CO 2 relation. Its influence over maximal oxygen consumption (V O 2 max), power (W), and ventilatory threshold was evaluated. Surrogate parameters of cardiac function, like oxygen pulse (V O 2 /heart rate) and circulatory power (%V O 2 max ؋ peak systolic pressure), were also evaluated. RESULTS: Cardiopulmonary stress test was stopped due to dyspnea with elevated V E and marked reduction of breathing reserve. A severe increase in V E /V CO 2 (mean ؎ SD 35.9 ؎ 5.6), a decrease of V O 2 max (mean ؎ SD 75.2 ؎ 20%), and a decrease of W (mean ؎ SD 68.6 ؎ 23.3%) were demonstrated. Twenty-eight patients presented dynamic hyperinflation. Linear regression showed a reduction of 2.04% on V O 2 max (P < .001), 2.6% on W (P < .001), 1% on V O 2 /heart rate (P ؍ .049), and 322.7 units on circulatory power (P ؍ .02) per each unit of increment in V E /V CO 2 , respectively. CONCLUSIONS: Ventilatory inefficiency correlates with a reduction in exercise capacity in COPD patients. Including this parameter in the evaluation of exercise limitation in this patient population may mean a contribution toward the understanding of its pathophysiology.
Evolution of Dyspnea during Exercise in COPD: Impact of Critical Volume Constraints
Rationale: Patients with chronic obstructive pulmonary disease (COPD) primarily describe their exertional dyspnea using descriptors alluding to increased effort or work of breathing and unsatisfied inspiration or inspiratory difficulty. Objectives: The purpose of this study was to examine the impact of changes in dynamic respiratory mechanics during incremental (INCR) and high-intensity constant work-rate (CWR) cycle exercise on the evolution of dyspnea intensity and its major qualitative dimensions in patients with moderate-to-severe COPD. Methods: Sixteen subjects with COPD performed symptom-limited INCR and CWR cycle exercise tests. Measurements included dyspnea intensity and qualitative descriptors, breathing pattern, operating lung volumes, and esophageal pressure (Pes). Measurements and Main Results: During both exercise tests, there was an inflection in the relation between tidal volume (VT) and ventilation. This inflection occurred significantly earlier in time during CWR versus INCR exercise but at a similar ventilation, VT, and tidal Pes swing. Beyond this inflection, there was no further change in VT despite a continued increase in ventilation and tidal Pes. During both tests, "work and effort" was the dominant dyspnea descriptor selected up to the inflection point, whereas after this point dyspnea intensity and the selection frequency of "unsatisfied inspiration" rose sharply. Conclusions: Regardless of the exercise test protocol, the inflection (or plateau) in the VT response marked the point where dyspnea intensity rose abruptly and there was a transition in the dominant qualitative descriptor choice from "work and effort" to "unsatisfied inspiration." Intensity and quality of dyspnea evolve separately and are strongly influenced by mechanical constraints on VT expansion during exercise in COPD. Supported by the William Spear/Richard Start Endowment Fund, Queen's University. Pierantonio Laveneziana received a