Neural respiratory drive in chronic thromboembolic pulmonary hypertension: Effect of balloon pulmonary angioplasty.

Excessive ventilation (V̇E) during exercise, ascribed to heightened neural ventilatory drive and/or to increased "wasted" ventilation, is a feature of chronic thromboembolic pulmonary hypertension (CTEPH). In selected CTEPH patients, balloon pulmonary angioplasty (BPA) allows near-normalization of resting haemodynamic parameters but does not allow excess exercise hyperventilation to normalize. Neural ventilatory drive can be estimated by studying how arterial PCO2 (PaCO2), end-tidal PCO2 (PETCO2), V̇E and CO2 output (V̇CO2) change across the exercise-to-recovery transition during a cardiopulmonary exercise test. Increased "wasted" ventilation can be quantified by the physiological dead space fraction of tidal volume (VD/VT) calculated with the Enghoff simplification of the Bohr equation. These measurements were made before and after BPA in 22 CTEPH patients without significant cardiac and/or pulmonary comorbidities. Our observations suggest that before BPA, excessive hyperventilation was secondary to both heightened neural ventilatory drive and increased "wasted" ventilation; after BPA, measurements made across the exercise-to-recovery transition suggest that heightened neural ventilatory drive was no longer present.

Exercise hyperventilation and pulmonary gas exchange in chronic thromboembolic pulmonary hypertension: Effects of balloon pulmonary angioplasty.

BACKGROUND: Excessive ventilation (V̇E) and abnormal gas exchange during exercise are features of chronic thromboembolic pulmonary hypertension (CTEPH). In selected CTEPH patients, balloon pulmonary angioplasty (BPA) improves symptoms and exercise capacity. How BPA affects exercise hyperventilation and gas exchange is poorly understood. METHODS: In this longitudinal observational study, symptom-limited cardiopulmonary exercise tests and carbon monoxide lung diffusion (DLCO) were performed before and after BPA (interval, mean (SD): 3.1 (2.4) months) in 36 CTEPH patients without significant cardiac and/or pulmonary comorbidities. RESULTS: Peak work rate improved by 20% after BPA whilst V̇E at peak did not change despite improved ventilatory efficiency (lower V̇E with respect to CO2 output [V̇CO2]). At the highest identical work rate pre- and post-BPA (75 (30) watts), V̇E and alveolar-arterial oxygen gradient (P(Ai-a)O2) decreased by 17% and 19% after BPA, respectively. The physiological dead space fraction of tidal volume (VD/VT), calculated from measurements of arterial and mixed expired CO2, decreased by 20%. In the meantime, DLCO did not change. The best correlates of P(Ai-a)O2 measured at peak exercise were physiological VD/VT before BPA and DLCO after BPA. CONCLUSIONS: Ventilatory efficiency, physiological VD/VT, and pulmonary gas exchange improved after BPA. The fact that DLCO did not change suggests that the pulmonary capillary blood volume and probably the true alveolar dead space were unaffected by BPA. The correlation between DLCO measured before BPA and P(Ai-a)O2 measured after BPA suggests that DLCO may provide an easily accessible marker to predict the response to BPA in terms of pulmonary gas exchange.