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RESEARCH PRODUCT

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

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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, pb0.05 and r=0.84, pb0.0001) and yet their arterial pCO2 rose rather than fell (r=0.79, pb0.001). The rise in arterial pCO2 correlated with the increase in arterial hydrogen concentration (r=0.78, pb0.001) and with arterial pCO2 at peak exercise (r=� 0.76, pb0.001). 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. D 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.