Exercise hyperventilation in chronic heart failure is not caused by systemic lactic acidosis

Wensel, Roland, Francis, Darrel P., Georgiadou, Panagiota, Scott, Adam, Genth-Zotz, Sabine, Anker, Stefan D., Coats, Andrew J. S. and Piepoli, Massimo F. (2005) Exercise hyperventilation in chronic heart failure is not caused by systemic lactic acidosis. European Heart Journal, 7 (7). pp. 1105-1111. ISSN 1522-9645

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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.

Item Type: Article
Faculty \ School:
Depositing User: EPrints Services
Date Deposited: 25 Nov 2010 11:13
Last Modified: 11 Jan 2023 15:34
URI: https://ueaeprints.uea.ac.uk/id/eprint/15491
DOI: 10.1016/j.ejheart.2004.12.005

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