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      Cardiovascular and respiratory dysfunction in chronic obstructive pulmonary disease complicated by impaired peripheral oxygenation

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          Abstract

          Background

          Impaired peripheral oxygenation (IPO)-related variables readily achieved with cardiopulmonary exercise testing (CPET) represent cardiovascular dysfunction. These variables include peak oxygen uptake ( ( V ˙ O 2 ) < 85 % predicted, anaerobic threshold < 40 % V ˙ O 2 max predicted, V ˙ O 2 - work rate slope <8.6 mL/watt, oxygen pulse <80% predicted, and ventilatory equivalents for O 2 and CO 2 at nadir of >31 and >34, respectively. Some of these six variables may be normal while the others are abnormal in patients with chronic obstructive pulmonary disease (COPD). This may result in confusion when using the interpretation algorithm for diagnostic purposes. We therefore hypothesized that patients found to have abnormal values for all six variables would have worse cardiovascular function than patients with abnormal values for none or some of these variables.

          Methods

          In this cross-sectional comparative study, 58 COPD patients attending a university teaching hospital underwent symptom-limited CPET with multiple lactate measurements. Patients with abnormal values in all six IPO-related variables were assigned to an IPO group while those who did not meet the requirements for the IPO group were assigned to a non-IPO group. Cardiovascular function was measured by two-dimensional echocardiography and Δ lactate / Δ V ˙ O 2 , and respiratory dynamics were compared between the two groups.

          Results

          Fourteen IPO and 43 non-IPO patients were entered into the study. Both groups were similar with regard to left ventricular ejection fraction and right ventricular morphology ( P>0.05 for both). At peak exercise, both groups reached a similar heart rate level and Δ lactate / Δ V ˙ O 2 . The IPO patients had an unfavorable dead space to tidal volume ratio, mean inspiratory tidal flow, and shallow breathing ( P<0.05– P<0.001).

          Conclusion

          Our IPO and non-IPO patients with COPD had similar cardiovascular performance at rest and at peak exercise, indicating that IPO variables are non-specific for cardiovascular function in these patients. COPD patients with full IPO variables have more deranged ventilatory function.

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          Most cited references 30

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          Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease.

          This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator. In a randomised double-blind crossover study, 23 patients with COPD (mean +/- SEM forced expiratory volume in one second 42 +/- 3% of the predicted value) inhaled salmeterol 50 microg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate. After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175 +/- 52%, inspiratory capacity (IC) increased by 11 +/- 2% pred and functional residual capacity decreased by 11 +/- 3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (VO2) and carbon dioxide output. Salmeterol increased peak exercise endurance, VO2 and ventilation by 58 +/- 19, 8 +/- 3 and 12 +/- 3%, respectively. Improvements in peak VO2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT. Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance.
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            Respiratory muscle and cardiopulmonary function during exercise in very severe COPD.

            Chronic obstructive pulmonary disease (COPD) is thought to limit exercise capacity through a decreased ventilatory reserve, with cardiovascular factors playing a minimal role. We assessed respiratory muscle (RM) and cardiopulmonary function during exercise in very severe COPD (FEV1 0.79 +/- 0.17 L). We determined minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), heart rate (HR), respiratory rate (RR), and O2 pulse with a metabolic cart. RM function was assessed from esophageal and gastric pressures. Dyspnea was assessed with a visual analog scale (VAS). Exercise capacity (peak VO2 = 36 +/- 31%), ventilatory reserve (VE/maximum voluntary ventilation [MW] = 89 +/- 31%), HR = 76 +/- 15%, and O2 pulse (O2Pmax = 45 +/- 15%) were abnormal. Peak VO2 correlated with O2Pmax(r = 0.82), the change in end-inspiratory pleural pressure (deltaPpli) (r = -0.74), maximal transdiaphragmatic pressure (Pdimax) (r = 0.68), and VEmax (r = 0.58). There were similar correlations with exercise endurance time. Multiple regression analysis revealed O2Pmax to be the best predictor of peak VO2. Thereafter, only VEmax and deltaPpli remained significant (r2 = 0.87). O2Pmax correlated with inspiratory muscle function (Pplimax, r = -0.58; Pdimax, r = 0.53; deltaPpli, r = -0.47; and PImax, r = -0.47). By multiple regression analysis, the predictors of O2Pmax were Pplimax and deltaPpli (r2 = 0.47). In very severe COPD, the impressive swings in intrathoracic pressure resulting from deranged ventilatory mechanics are the most likely cause of exercise limitation and reduced O2 pulse. The contributions of factors such as deconditioning, hypoxemia, and concurrent heart disease remain unknown.
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              Ventilatory and cardiocirculatory exercise profiles in COPD: the role of pulmonary hypertension.

              Pulmonary hypertension (PH) is a well-recognized complication of COPD. The impact of PH on exercise tolerance is largely unknown. We evaluated and compared the circulatory and ventilatory profiles during exercise in patients with COPD without PH, with moderate PH, and with severe PH.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                11 February 2015
                : 10
                : 329-337
                Affiliations
                [1 ]Division of Pulmonary Medicine and Department of Critical Care Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, Republic of China
                [2 ]School of Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, Republic of China
                [3 ]Division of Cardiology and Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, Republic of China
                Author notes
                Correspondence: Ming-Lung Chuang, Division of Pulmonary Medicine and Department of Critical Care Medicine, Chung Shan Medical University Hospital, #110, Section 1, Chien-Kuo North Road, South District, Taichung 40201, Taiwan, Republic of China, Tel +88 64 2473 9595 Ext 34718, Fax +88 64 2473 9220, Email yuan1007@ 123456ms36.hinet.net
                Article
                copd-10-329
                10.2147/COPD.S76209
                4334300
                © 2015 Chuang et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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