OBJECTIVES: The value of end-tidal PCO(2) monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO(2) response to exercise and its relation to functional capacity in patients with chronic heart failure. METHODS AND RESULTS: Maximal upright ergometer exercise with respiratory gas analysis and arterial blood gas analysis were performed in 105 patients with chronic heart failure (34 patients in New York Heart Association [NYHA] class I, 38 patients in NYHA class II, and 33 patients in NYHA class III) and 14 normal control subjects. Peak O(2) uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO(2) output (VE-VCO(2)), and the ratio of physiologic dead space to tidal volume (VD/VT) were determined. Cardiac output was also measured during exercise in 28 patients with chronic heart failure. Arterial PO(2) or PCO(2) values at rest and during exercise were not different among the four groups. However, end-tidal PCO(2) was significantly lower, and arterial to end-tidal PCO(2) difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO(2) during exercise was significantly reduced as the severity of chronic heart failure advanced (45.7 +/- 4.0 mm Hg in normal control subjects, 43.5 +/- 4.8 mm Hg in NYHA class I patients, 39.7 +/- 5.1 mm Hg in NYHA class II patients, and 34.9 +/- 5.3 mm Hg in NYHA class III patients). The maximal end-tidal PCO(2) during exercise was significantly correlated with peak O(2) uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to Ve-VCO(2) (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001). CONCLUSIONS: The decreased end-tidal PCO(2) during exercise, which is caused by high ventilation/perfusion ratio mismatching, reflects both reduced cardiac output response to exercise and increased exercise ventilation due to enlarged physiologic dead space in advanced chronic heart failure. The end-tidal PCO(2) during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.
OBJECTIVES: The value of end-tidal PCO(2) monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO(2) response to exercise and its relation to functional capacity in patients with chronic heart failure. METHODS AND RESULTS: Maximal upright ergometer exercise with respiratory gas analysis and arterial blood gas analysis were performed in 105 patients with chronic heart failure (34 patients in New York Heart Association [NYHA] class I, 38 patients in NYHA class II, and 33 patients in NYHA class III) and 14 normal control subjects. Peak O(2) uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO(2) output (VE-VCO(2)), and the ratio of physiologic dead space to tidal volume (VD/VT) were determined. Cardiac output was also measured during exercise in 28 patients with chronic heart failure. Arterial PO(2) or PCO(2) values at rest and during exercise were not different among the four groups. However, end-tidal PCO(2) was significantly lower, and arterial to end-tidal PCO(2) difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO(2) during exercise was significantly reduced as the severity of chronic heart failure advanced (45.7 +/- 4.0 mm Hg in normal control subjects, 43.5 +/- 4.8 mm Hg in NYHA class I patients, 39.7 +/- 5.1 mm Hg in NYHA class II patients, and 34.9 +/- 5.3 mm Hg in NYHA class III patients). The maximal end-tidal PCO(2) during exercise was significantly correlated with peak O(2) uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to Ve-VCO(2) (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001). CONCLUSIONS: The decreased end-tidal PCO(2) during exercise, which is caused by high ventilation/perfusion ratio mismatching, reflects both reduced cardiac output response to exercise and increased exercise ventilation due to enlarged physiologic dead space in advanced chronic heart failure. The end-tidal PCO(2) during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.
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