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

•Patients with chronic thromboembolic hypertension have excess exercise hyperventilation.•Excess hyperventilation is ascribed partly to heightened ventilatory neural drive.•Balloon pulmonary angioplasty near-normalizes patients’ resting haemodynamics.•Although less, patients still have excess exercise hyperventilation after angioplasty.•Ventilatory neural drive seems no longer heightened after 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.