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Significance of End-Tidal PCO₂ Response to Exercise and Its Relation to Functional Capacity in Patients With Chronic Heart Failure^*

^* From the Department of Internal Medicine, Niigata Prefectural Shibata Hospital, Shibata, Japan.

Correspondence to: Yasuhiko Tanabe, MD, Niigata Prefectural Shibata Hospital, Ohtemachi 4–5-48, Shibata City, Niigata, 957-8588 Japan

Objectives: The value of end-tidal PCO₂ monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO₂ 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 O₂ uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO₂ output (E-CO₂), 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 PO₂ or PCO₂ values at rest and during exercise were not different among the four groups. However, end-tidal PCO₂ was significantly lower, and arterial to end-tidal PCO₂ difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO₂ 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 PCO₂ during exercise was significantly correlated with peak O₂ uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to E-CO₂ (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001).

Conclusions: The decreased end-tidal PCO₂ 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 PCO₂ during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.

Key Words: cardiac output • cardiomyopathy • exercise • heart failure • ventilation

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