Abstract
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 (V̇A), volume (VA), 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 V̇A and VA. Resting lung diffusion capacity for carbon monoxide (DLCO) was assessed and indexed to VA for each time point. Resting R2 between V̇O2 and V̇A, VA, DLCO, and DLCO/VA was 0.68, 0.18, 0.20, and 0.07, respectively (all P < .05 except DLCO/VA). 20 W R2 between V̇O2 and V̇A, VA, DLCO, and DLCO/VA was 0.64, 0.32, 0.07, and 0.18 (all P < .05 except DLCO). Peak exercise R2 between V̇O2 and V̇A, VA, DLCO, and DLCO/VA was 0.55, 0.31, 0.34, and 0.06 (all P < .05 except DLCO/VA). 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.
Highlights
In human heart failure (HF) the pulmonary oxygen uptake
In contrast to what has been observed in healthy adults [10,11,12,13,14], it has not been tested whether O2 transport involving the alveolar airspace and, V
Mean hemoglobin and hematocrit levels were within normal limits, whereas creatinine and brain natriuretic peptide levels were consistent with HF
Summary
O2) response at peak exercise is interpreted as a primary marker of prognosis [1,2,3,4]. HF patients have been observed to demonstrate integrative pathophysiology involving alveoli and O2 transport [5,6,7,8,9], which are features recognized to impact oxidative metabolic capacity. In contrast to what has been observed in healthy adults [10,11,12,13,14], it has not been tested whether O2 transport involving the alveolar airspace and, V. O2 pathophysiology of impaired peak is a primary marker of prognosis in heart V. This study during aimed cardiopulmonary exercise testing (CPET) has not to phenotype how changes in alveolar ventilation been
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