Zusammenfassung
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 pCO(2) during exercise in heart failure. Method and results: We studied 18 patients with chronic heart failure. ...
Zusammenfassung
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 pCO(2) 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 pCO(2), 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 pCO(2) rose rather than fell (r=0.79, p < 0.001). The rise in arterial pCO(2) correlated with the increase in arterial hydrogen concentration (r=0.78, p < 0.001) and with arterial pCO(2) 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. (c) 2004 European Society of Cardiology. Published by Elsevier B.V All rights reserved.
Altmetric