Chest
Volume 142, Issue 5, November 2012, Pages 1166-1174
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Original Research
Pulmonary Vascular Disease
Ventilatory and Cardiocirculatory Exercise Profiles in COPD: The Role of Pulmonary Hypertension

https://doi.org/10.1378/chest.11-2798Get rights and content

Background

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.

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, ≥ 40 mm Hg). Mixed venous oxygen saturation (Svo2) was used for evaluating the circulatory reserve. Paco2 and the calculated breathing reserve were used for evaluation of the ventilatory reserve.

Results

Patients without PH (n = 24) had an end-exercise Svo2 of 48% ± 9%, an increasing Paco2 with exercise, and a breathing reserve of 22% ± 20%. Patients with moderate PH (n = 14) had an exercise Svo2 of 40% ± 8%, an increasing Paco2, and a breathing reserve of 26% ± 15%. Patients with severe PH (n = 9) had a significantly lower end-exercise Svo2 (30% ± 6%), a breathing reserve of 37% ± 11%, and an absence of Paco2 accumulation.

Conclusion

Patients with severe PH showed an exhausted circulatory reserve at the end of exercise. A profile 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.

Section snippets

Patients

Subjects were either recruited from the local outpatient clinic or referred by other hospitals for the evaluation of PH. Subjects were diagnosed with moderate to very severe COPD according to American Thoracic Society/European Respiratory Society criteria.15 Exclusion criteria were (1) a history of left-sided cardiac failure, (2) left ventricular dysfunction and/or valvular disease on Doppler echocardiography, (3) atrial fibrillation, (4) neuromuscular disorders, or (5) an acute exacerbation of

Study Population

Forty-seven patients with COPD (25 men, 22 women; mean age, 65 y) were included. Twenty-four patients had no PH, 14 patients had moderate PH, and nine patients had severe PH. Demographic data, pulmonary function, and resting hemodynamics are summarized in Table 1.

Incremental Cardiopulmonary Exercise Test

The characteristics of the three groups are presented in Table 2 and Figure 1. The subjects had a severe impaired exercise capacity, as evidenced by peak work rates and

o2s that were, on average, < 50% predicted and < 15 mL/kg/min,

Discussion

In this study, we used CPET data combined with invasive hemodynamic measurements at rest and during maximal exercise to evaluate whether PH contributes to exercise intolerance in COPD. Only in patients with COPD and severe PH did the Svo2 at end-exercise decrease to a level usually found in healthy subjects,27, 28 which is consistent with reaching a circulatory limitation. From this, together with the finding of a low CO/

o2 slope, we can conclude that these patients had exhausted their

Conclusions

The current study shows a PH-induced circulatory limitation to exercise in patients with COPD and an mPAP of ≥ 40 mm Hg. In patients with COPD without or with moderate PH, the exercise profile indicates a circulatory reserve and a predominantly ventilatory limitation to exercise.

Acknowledgments

Author contributions: Dr Vonk-Noordegraaf serves as guarantor and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Boerrigter: contributed to the concept and design of the study, acquisition of data, analysis or interpretation of data, drafting of the manuscript, and final approval of the version of the manuscript to be published.

Dr Bogaard: contributed to the analysis or interpretation of data, drafting of the manuscript, and final approval of the

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    Funding/Support: Dr Vonk-Noordegraaf was supported by the Netherlands Organisation for Scientific Research-VIDI [Project No. 917.96.306].

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

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