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Clinical Investigations: CARDIOLOGY |

Significance of End-Tidal Pco2 Response to Exercise and Its Relation to Functional Capacity in Patients With Chronic Heart Failure*

Yasuhiko Tanabe, MD; Yukio Hosaka, MD; Masahiro Ito, MD; Eiichi Ito, MD; Kaoru Suzuki, MD
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*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



Chest. 2001;119(3):811-817. doi:10.1378/chest.119.3.811
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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 (V̇e-V̇co2), 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 V̇e-V̇co2 (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.

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