Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (15)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yasunobu, Y.
Right arrow Articles by Wasserman, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yasunobu, Y.
Right arrow Articles by Wasserman, K.
(Chest. 2005;127:1637-1646.)
© 2005 American College of Chest Physicians

End-tidal PCO2 Abnormality and Exercise Limitation in Patients With Primary Pulmonary Hypertension*

Yuji Yasunobu, MD; Ronald J. Oudiz, MD; Xing-Guo Sun, MD; James E. Hansen, MD, FCCP and Karlman Wasserman, MD, PhD, FCCP

* From the Department of Medicine, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, Torrance, CA.

Correspondence to: Karlman Wasserman, MD, PhD, FCCP, Department of Medicine, Harbor-UCLA Medical Center, 1000 W Carson St, Box 405, Torrance, CA 90509-2910; e-mail: kwasserman{at}rei.edu

Objectives: Primary pulmonary hypertension (PPH) is a pulmonary vasculopathy resulting in exercise intolerance, usually due to dyspnea. We hypothesized that ventilation is increased during exercise in PPH relative to normal because the ventilated lung is underperfused, cardiac output increase is restricted, and arterial hypoxemia may develop. Our aim was to determine the size of the reduction in end-tidal PCO2 (PETCO2) as a reflection of the abnormality in ventilatory efficiency and ventilatory drive in PPH patients.

Methods: We performed cardiopulmonary exercise testing (CPET) in 52 PPH patients. All had hemodynamic measurements to confirm the diagnosis of PPH. A subgroup of 29 patients who underwent right-heart catheterization within 50 days of CPET were studied to compare their CPET responses to resting hemodynamics. Nine healthy volunteers matched for age and gender served as CPET control subjects.

Results: In PPH patients, the percentage of predicted peak oxygen uptake (O2) correlated significantly with mean pulmonary artery pressure (mPAP) [r = – 0.59, p = 0.0007, n = 29]. PETCO2 values at rest, anaerobic threshold (AT), and peak O2 were proportionately reduced as percentage of predicted peak O2 decreased (r = 0.66 to 0.72, p < 0.0001, n = 52). PETCO2 values at rest, AT, and peak O2 were also reduced as mPAP increased (r = – 0.51 to – 0.53, p < 0.005, n = 29). In contrast to normal subjects in whom PETCO2 increased from rest to AT, PETCO2 decreased in PPH patients, except for two patients with mild PPH in whom there was no change. Also, PETCO2 increased rather than decreased further at the start of recovery, in contrast to normal. Although usually normal at rest, oxyhemoglobin saturation decreased during exercise in most PPH patients.

Conclusions: In patients with PPH, PETCO2 at rest and exercise is significantly reduced in proportion to physiologic disease severity. The range of values is unusually low. Furthermore, the directional changes of PETCO2 during exercise and early recovery are in the opposite direction of normal.

Key Words: anaerobic threshold • end-tidal CO2 • mean pulmonary artery pressure • peak oxygen uptake • primary pulmonary hypertension • ventilatory equivalent for CO2




This article has been cited by other articles:


Home page
ChestHome page
J. E. Hansen, G. Ulubay, B. F. Chow, X.-G. Sun, and K. Wasserman
Mixed-Expired and End-Tidal CO2 Distinguish Between Ventilation and Perfusion Defects During Exercise Testing in Patients With Lung and Heart Diseases
Chest, September 1, 2007; 132(3): 977 - 983.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American College of Chest Physicians.