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 ISI Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Koike, A.
Right arrow Articles by Fu, L. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koike, A.
Right arrow Articles by Fu, L. T.
(Chest. 2004;125:182-190.)
© 2004 American College of Chest Physicians

Cerebral Oxygenation During Exercise in Cardiac Patients*

Akira Koike, MD; Haruki Itoh, MD; Reiko Oohara, BS; Masayo Hoshimoto; Akihiko Tajima, BS; Tadanori Aizawa, MD and Long Tai Fu, MD

* From The Cardiovascular Institute, Tokyo, Japan.

Correspondence to: Akira Koike, MD, The Cardiovascular Institute, 3-10, Roppongi 7-chome, Minato-ku, Tokyo 106-0032, Japan;e-mail: koike{at}cepp.ne.jp

Background: Until recently, compensatory mechanisms have been believed to regulate adequately cerebral blood flow in humans. However, this has been called into question by a series of new investigations suggesting that patients with left ventricular dysfunction suffer from cerebral hypoperfusion. We compared cerebral oxygenation during incremental exercise between patients with valvular heart disease and normal subjects.

Methods: Thirty-three patients with valvular disease and 33 normal subjects performed a symptom-limited incremental exercise test using a cycle ergometer. Oxyhemoglobin at the forehead was continuously monitored during exercise using near-infrared spectroscopy. Respiratory gas measurements were performed on a breath-by-breath basis.

Results: The increase in oxyhemoglobin during exercise was significantly lower in the patients with valvular disease than in normal subjects. The change in oxyhemoglobin during exercise ({Delta}O2Hb) at the forehead was negatively correlated with the slope of the increase in minute ventilation to the increase in carbon dioxide output ({Delta}E/{Delta}CO2), and positively correlated with the peak oxygen uptake (O2), gas exchange threshold (GET), and slope of the increase in O2 to the increase in the work rate ({Delta}O2/{Delta}WR). Among the patients with valvular disease, 15 patients showed a decrease in oxyhemoglobin at the forehead during exercise. When compared with the patients with increased oxyhemoglobin, those with decreased levels exhibited a higher {Delta}E/{Delta}CO2 and a lower peak O2, GET, and {Delta}O2/{Delta}WR.

Conclusions: The present findings strongly suggest that cerebral oxygenation during exercise is dependent on the cardiovascular and pulmonary systems. The study also indicated the presence of cerebral hypoperfusion during exercise in cardiac patients whose cardiac output fails to increase normally.

Key Words: brain • cerebrovascular circulation • exercise






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American College of Chest Physicians.