Gas Exchange and Ventilatory Efficiency During Exercise in Pulmonary Vascular Diseases

Abstract

Background and ObjectiveVentilatory inefficiency (high V′E/V′CO2) and resting hypocapnia are common in pulmonary vascular disease and are associated with poor prognosis. Low resting PaCO2 suggests increased chemosensitivity or an altered PaCO2 set-point. We aimed to determine the relationships between exercise gas exchange variables reflecting the PaCO2 set-point, exercise capacity, hemodynamics and V′E/V′CO2. MethodsPulmonary arterial hypertension (n=34), chronic thromboembolic pulmonary hypertension (CTEPH, n=19) and pulmonary veno-occlusive disease (PVOD, n=6) patients underwent rest and peak exercise arterial blood gas measurements during cardiopulmonary exercise testing. Patients were grouped according to resting PaCO2: hypocapnic (PaCO2 ≤34mmHg) or normocapnic (PaCO2 35–45mmHg). The PaCO2 set-point was estimated by the maximal value of end-tidal PCO2 (maximal PETCO2) between the anaerobic threshold and respiratory compensation point. ResultsThe hypocapnic group (n=39) had lower resting cardiac index (3.1±0.8 vs. 3.7±0.7L/min/m2, p<0.01), lower peak V′O2 (15.8±3.5 vs. 20.7±4.3mL/kg/min, p<0.01), and higher V′E/V′CO2 slope (60.6±17.6 vs. 38.2±8.0, p<0.01). At peak exercise, hypocapic patients had lower PaO2, higher VD/VT and higher P(a-ET)CO2. Maximal PETCO2 (r=0.59) and VD/VT (r=−0.59) were more related to cardiac index than PaO2 or PaCO2 at rest or peak exercise. Maximal PETCO2 was the strongest correlate of V′E/V′CO2 slope (r=−0.86), peak V′O2 (r=0.64) and peak work rate (r=0.49). ConclusionsResting hypocapnia is associated with worse cardiac function, more ventilatory inefficiency and reduced exercise capacity. This could be explained by elevated chemosensitivity and lower PaCO2 set-point. Maximal PETCO2 may be a useful non-invasive marker of PaCO2 setpoint and disease severity even with submaximal effort.