Gas Exchange and Ventilatory Efficiency During Exercise in Pulmonary Vascular Diseases.

BACKGROUND AND OBJECTIVE

Ventilatory inefficiency (high V'/V'CO) and resting hypocapnia are common in pulmonary vascular disease and are associated with poor prognosis. Low resting PaCO suggests increased chemosensitivity or an altered PaCO set-point. We aimed to determine the relationships between exercise gas exchange variables reflecting the PaCO set-point, exercise capacity, hemodynamics and V'/V'CO.

METHODS

Pulmonary 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 PaCO: hypocapnic (PaCO ≤34mmHg) or normocapnic (PaCO 35-45mmHg). The PaCO set-point was estimated by the maximal value of end-tidal PCO (maximal PCO) between the anaerobic threshold and respiratory compensation point.

RESULTS

The hypocapnic group (n=39) had lower resting cardiac index (3.1±0.8 vs. 3.7±0.7L/min/m, p<0.01), lower peak V'O (15.8±3.5 vs. 20.7±4.3mL/kg/min, p<0.01), and higher V'/V'CO slope (60.6±17.6 vs. 38.2±8.0, p<0.01). At peak exercise, hypocapic patients had lower PaO, higher V/V and higher PCO. Maximal PCO (r=0.59) and V/V (r=-0.59) were more related to cardiac index than PaO or PaCO at rest or peak exercise. Maximal PCO was the strongest correlate of V'/V'CO slope (r=-0.86), peak V'O (r=0.64) and peak work rate (r=0.49).

CONCLUSIONS

Resting hypocapnia is associated with worse cardiac function, more ventilatory inefficiency and reduced exercise capacity. This could be explained by elevated chemosensitivity and lower PaCO set-point. Maximal PCO may be a useful non-invasive marker of PaCO setpoint and disease severity even with submaximal effort.