Skip Navigation

European Heart Journal 1995 16(1):1886-1891;
Copyright © 1995 by the European Society of Cardiology.
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by ANDREAS, S.
Right arrow Articles by FIGULLA, H. R.
Right arrow Search for Related Content
PubMed
Right arrow Articles by ANDREAS, S.
Right arrow Articles by FIGULLA, H. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1995 The European Society of Cardiology

Ventilation and dyspnoea during exercise in patients with heart failure

S. ANDREAS, S. VONHOF, H. KREUZER and H. R. FIGULLA

Department of Cardiology and Pneumology, Georg August University Göttingen, Germany

revised 10 March 1995; accepted 4 April 1995.

Correspondence: S. Andreas, MD, Abteilung Kardiologie und Pneumologie, Universitätsklinikum, Robert-Koch-Str. 40, W-37075 Göttinen, Germany

Abstract

Patients with chronic heart failure have an increased ventilation/carbon dioxide production ratio (VE/Vco2) during exercise. Recently it was discussed whether the cause of this increase was a ventilatory stimulus driven other than by CO2 Dyspnoea during exercise is thought to be related to impaired respiratory function. However, clinical confirmation is scarce. Ninety-two patients (age 51 ± 9 years) with heart failure due to idiopathic dilated cardiomyopathy exercised on a bicycle ergometer to exhaustion, and measurement of ventilatory gases and Swan-Ganz catheterization were performed. The maximal oxygen consumption corrected for body weight (Vo2max kg–1) was 16·6 ± 5·5 ml x min–1 x kg–1 The increase in (VE/Vco2 during exercise was related to an increase in respiratory rate (r=0·43; P<0·00001) but not to an increase in cardiac index or capillary wedge pressure. Nineteen patients stopped exercising because of dyspnoea. Their maximal tidal volume and Vo2max kg–1 were lower than the 67 patients who stopped exercise because of fatigue (P<0·001 and P<0·00001 respectively). Other variables showed no significant difference.

In conclusion, the increase in VE/Vco2 during exercise may reflect a non-CO2 driven ventilatory stimulus as it cannot be attributed to increased pulmonary vascular pressures or an insufficient increase in cardiac output leading to a ventilation-perfusion mismatch. Low oxygen uptake is a prominent finding in patients with chronic heart failure who experienced dyspnoea during exercise, and dyspnoea is in part related to impaired respiratory function.

Key Words: Heart failure—congestive • exercise • ventilation


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.