OBJECTIVES: The aim of this study was to analyze the relation between ventilation and carbon dioxide production and the control of ventilation in patients with chronic heart failure. BACKGROUND: Patients with chronic heart failure exhibit an increased ventilatory response to exercise. Ventilation is closely linked to carbon dioxide production, producing a high correlation between the two variables. This relation is nonlinear at high levels of exercise. METHODS: The ventilation/carbon dioxide production ratio during exercise was examined in 29 patients with chronic heart failure and 9 normal volunteers. RESULTS: In the patients with heart failure, there were three patterns: in the least severely affected patients, the pattern was similar to that of the normal subjects, with an initial decrease in the ventilation/carbon dioxide production ratio to a plateau maintained during exercise; in more severely affected patients, there was an increase in the ratio at the end of exercise, and in the most severely affected patients, the ratio increased from the outset of exercise. The ventilation/carbon dioxide relation is not adequately described by a straight line relation. CONCLUSIONS: The ventilation/carbon dioxide ratio is not fixed, and the changes that occur in this ratio reflect either a noncarbon dioxide-driven ventilatory stimulus or an increase in ventilation-perfusion mismatch due to increased dead space ventilation. The different patterns of this ratio may provide clues to the pathophysiologic mechanisms of the excessive ventilation and breathlessness seen during exercise in chronic heart failure.
OBJECTIVES: The aim of this study was to analyze the relation between ventilation and carbon dioxide production and the control of ventilation in patients with chronic heart failure. BACKGROUND:Patients with chronic heart failure exhibit an increased ventilatory response to exercise. Ventilation is closely linked to carbon dioxide production, producing a high correlation between the two variables. This relation is nonlinear at high levels of exercise. METHODS: The ventilation/carbon dioxide production ratio during exercise was examined in 29 patients with chronic heart failure and 9 normal volunteers. RESULTS: In the patients with heart failure, there were three patterns: in the least severely affected patients, the pattern was similar to that of the normal subjects, with an initial decrease in the ventilation/carbon dioxide production ratio to a plateau maintained during exercise; in more severely affected patients, there was an increase in the ratio at the end of exercise, and in the most severely affected patients, the ratio increased from the outset of exercise. The ventilation/carbon dioxide relation is not adequately described by a straight line relation. CONCLUSIONS: The ventilation/carbon dioxide ratio is not fixed, and the changes that occur in this ratio reflect either a noncarbon dioxide-driven ventilatory stimulus or an increase in ventilation-perfusion mismatch due to increased dead space ventilation. The different patterns of this ratio may provide clues to the pathophysiologic mechanisms of the excessive ventilation and breathlessness seen during exercise in chronic heart failure.