Alveolar Air and O₂ Uptake During Exercise in Patients With Heart Failure

Peak exercise pulmonary oxygen uptake (V̇O₂) is a primary marker of prognosis in heart failure (HF). The pathophysiology of impaired peak V̇O₂ is unclear in patients. To what extent alveolar airway function affects V̇O₂ during cardiopulmonary exercise testing (CPET) has not been fully elucidated. This study aimed to describe how changes in alveolar ventilation (V̇_A), volume (V_A), and related parameters couple with exercise V̇O₂ in HF.

A total of 35 patients with HF (left ventricular ejection fraction 20 ± 6%, age 53 ± 7 y) participated in CPET with breath-to-breath measurements of ventilation and gas exchange. At rest, 20 W, and peak exercise, arterial CO₂ tension was measured via radial arterial catheterization and used in alveolar equations to derive V̇_A and V_A. Resting lung diffusion capacity for carbon monoxide (DL_CO) was assessed and indexed to V_A for each time point. Resting R² between V̇O₂ and V̇_A, V_A, DL_CO, and DL_CO/V_A was 0.68, 0.18, 0.20, and 0.07, respectively (all P < .05 except DL_CO/V_A). 20 W R² between V̇O₂ and V̇_A, V_A, DL_CO, and DL_CO/V_A was 0.64, 0.32, 0.07, and 0.18 (all P < .05 except DL_CO). Peak exercise R² between V̇O₂ and V̇_A, V_A, DL_CO, and DL_CO/V_A was 0.55, 0.31, 0.34, and 0.06 (all P < .05 except DL_CO/V_A).

These data suggest that alveolar airway function that is not exclusively related to effects caused by localized lung diffusivity affects exercise V̇O₂ in moderate-to-severe HF.