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 Background Arterial CO 2 tension (PaCO 2 ) and physiological dead space (V D ) are not routinely measured during clinical cardiopulmonary exercise testing (CPET). Abnormal changes in PaCO 2 accompanied by increased V D 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 PaCO 2 and V D prediction models using ‘ideal’ alveolar air equations and basic ventilation and gas-exchangegas exchange measurements during CPET in HF. Methods Forty-seven NYHA class II/III HF (LVEF=21±7%; age=55±9years; male=89%; BMI=28±5kg/m 2 ) performed step-wise cycle ergometry CPET to volitional fatigue. Breath-by-breath ventilation and gas exchange were measured continuously. Steady-state PaCO 2 was measured at rest and peak exercise via radial arterial catheterization. Criterion V D was calculated via ‘ideal’ alveolar equations, whereas PaCO 2 or V D models were based on end-tidal CO 2 tension (P ET CO 2 ), tidal volume (V T ), and/or weight. Results Criterion measurements of PaCO 2 (38±5 vs. 33±5mmHg, P D (0.26±0.07 vs. 0.41±0.15L, P ET CO 2 −0.0021×V T , was the strongest predictor of PaCO 2 at rest and peak exercise (bias±95%LOA=−3.24±6.63 and −0.98±5.76mmHg; R 2 = 0.57 and 0.75, P D at rest and peak exercise (bias±95%LOA=−0.03±0.06 and −0.02±0.13L; R 2 = 0.86 and 0.83, P Conclusions These data suggest predicted PaCO 2 and V D 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 PaCO 2 and V D can be used to improve interpretability of exercise ventilatory responses in HF.
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