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Original Research: Pulmonary Vascular Disease |

Ventilatory and Cardiocirculatory Exercise Profiles in COPDExercise Profiles in COPD-Pulmonary Hypertension: The Role of Pulmonary Hypertension

Bart G. Boerrigter, MD; Harm J. Bogaard, MD, PhD; Pia Trip, MD; Herman Groepenhoff, MSc; Heleen Rietema, MD; Sebastiaan Holverda, PhD; Anco Boonstra, MD, PhD; Pieter E. Postmus, MD, PhD, FCCP; Nico Westerhof, PhD; Anton Vonk-Noordegraaf, MD, PhD, FCCP
Author and Funding Information

From the Department of Pulmonary Diseases (Drs Boerrigter, Bogaard, Trip, Rietema, Holverda, Boonstra, Postmus, Westerhof, and Vonk-Noordegraaf and Mr Groepenhoff) and the Department of Physiology (Dr Westerhof), Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.

Correspondence to: Anton Vonk-Noordegraaf, MD, PhD, VU University Medical Center, Department of Pulmonary Diseases, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands; e-mail: a.vonk@vumc.nl


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.


Chest. 2012;142(5):1166-1174. doi:10.1378/chest.11-2798
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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.

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