Use of 'ideal' alveolar air equations and corrected end-tidal PCO2 to estimate arterial PCO2 and physiological dead space during exercise in patients with heart failure.

Abstract

Arterial CO2 tension (PaCO2) and physiological dead space (VD) are not routinely measured during clinical cardiopulmonary exercise testing (CPET). Abnormal changes in PaCO2 accompanied by increased VD directly contribute to impaired exercise ventilatory function in heart failure (HF). Because arterial catheterization is not standard practice during CPET, this study tested the construct validity of PaCO2 and VD prediction models using 'ideal' alveolar air equations and basic ventilation and gas-exchangegas exchange measurements during CPET in HF. Forty-seven NYHA class II/III HF (LVEF=21±7%; age=55±9years; male=89%; BMI=28±5kg/m2) performed step-wise cycle ergometry CPET to volitional fatigue. Breath-by-breath ventilation and gas exchange were measured continuously. Steady-state PaCO2 was measured at rest and peak exercise via radial arterial catheterization. Criterion VD was calculated via 'ideal' alveolar equations, whereas PaCO2 or VD models were based on end-tidal CO2 tension (PETCO2), tidal volume (VT), and/or weight. Criterion measurements of PaCO2 (38±5 vs. 33±5mmHg, P<0.01) and VD (0.26±0.07 vs. 0.41±0.15L, P<0.01) differed at rest vs. peak exercise, respectively. The equation, 5.5+0.90×PETCO2-0.0021×VT, was the strongest predictor of PaCO2 at rest and peak exercise (bias±95%LOA=-3.24±6.63 and -0.98±5.76mmHg; R2=0.57 and 0.75, P<0.001, respectively). This equation closely predicted VD at rest and peak exercise (bias±95%LOA=-0.03±0.06 and -0.02±0.13L; R2=0.86 and 0.83, P<0.001, respectively). These data suggest predicted PaCO2 and VD based on breath-by-breath gas exchange and ventilatory responses demonstrate acceptable agreement with criterion measurements at peak exercise in HF patients. Routine assessment of PaCO2 and VD can be used to improve interpretability of exercise ventilatory responses in HF.