© 2005 European Society of Cardiology
Exercise hyperventilation in chronic heart failure is not caused by systemic lactic acidosis
a National Heart and Lung Institute, Imperial College of Science, Technology and Medicine London, UK
b Medizinische Klinik II, Klinikum der Universität Regensburg Franz-Josef-Strauß-Allee 11, 93042, Regensburg, Germany
c Medizinische Klinik II, Johannes Gutenberg Universität Mainz Germany
d Universitätsklinik (Charité, Campus Virchow) der Humboldt-Universität zu Berlin Germany
e Faculty of Medicine, University of Sydney Australia
* Corresponding author. Medizinische Klinik II, Klinikum der Universität Regensburg, Franz-Josef-Strauß-Allee 11, 93042, Regensburg, Germany. Tel.: +49 941 9447264; fax: +49 941 9447213. E-mail address: roland.wensel{at}klinik.uni-regensburg.de
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Abstract |
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Background: Patients with heart failure have an abnormally high ventilatory response to exercise associated with gas exchange defects and reduced arterial pCO2.
Aims: We examined the possibility of lactic acidosis as the stimulus to this increased ventilation that abnormally depresses pCO2 during exercise in heart failure.
Method and results: We studied 18 patients with chronic heart failure. We measured VE/VCO2 slope during exercise, arterial blood gases and lactate concentrations during cardiopulmonary exercise testing (rest, peak exercise and one minute after the end of exercise). Neither VE/VCO2 slope nor arterial pCO2 were related to arterial lactate concentrations at peak exercise (r=–0.16, p=0.65 and r=–0.15, p=0.6). During early recovery, patients with a high VE/VCO2 slope had a particularly pronounced rise in arterial lactate and hydrogen ion concentrations (r=0.57, p<0.05 and r=0.84, p<0.0001) and yet their arterial pCO2 rose rather than fell (r=0.79, p<0.001). The rise in arterial pCO2 correlated with the increase in arterial hydrogen concentration (r=0.78, p<0.001) and with arterial pCO2 at peak exercise (r=–0.76, p<0.001).
Conclusions: In heart failure VE/VCO2 slope and low arterial pCO2 at peak exercise are not related to the degree of systemic lactic acidosis. Lactic acidosis is therefore not a plausible mechanism of exercise induced hyperventilation.
Key Words: Heart failure • Exercise • Ventilation
Received July 29, 2004; Revised September 24, 2004; Accepted December 20, 2004
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