Respiratory responses to CO₂ rebreathing in lung transplant recipients

To evaluate the respiratory responses after lung transplantation, we studied the hypercarbic ventilatory response in 20 patients with severe obstructive pulmonary disease and compared it with that of 10 normal subjects. Eleven patients underwent bilateral lung transplantation and 9 patients had single-lung transplantation. All patients had preoperative hypercapnia (51.3 ± 9.7 mm Hg) and blunted slopes of CO₂ rebreathing curves for minute ventilation (0.39 ± 0.20 L · min^-1 · mm Hg^-1) and inspiratory occlusion pressure (0.35 ± 0.30 s^-1). The hypercapnia and blunted ventilatory responses persisted at the initial postoperative test (5.8 ± 2.0 days) despite unproved pulmonary function (preoperative forced expiratory volume in 1 second [FEV₁L 0.57 ± 0.16 L; initial postoperative FEV₁, 1.83 ± 0.65 L; p < 0.001). By the 15th to 30th postoperative day (21.3 ± 6.0 days), compared with preoperative and initial postoperative values, end-tidal CO₂ had normalized (40.6 ± 6.9 versus 51.3 ± 9.7 and 49.6 ± 10.3 mm Hg; p < 0.005) and was coupled with enhanced ventliatory responses for the rebreathing curve for minute ventilation (1.26 ± 0.7 versus 0.39 ± 0.20 and 0.32 ± 0.32 L · min^-1 · mm Hg^-1; p < 0.005) and the inspiratory occlusion pressure curve (0.98 ± 7.4 versus 0.35 ± 0.30 and 0.41 ± 0.29 s^-1 p < 0.005). These respiratory responses developed without a change in postoperative pulmonary function (initial postoperative FEV₁, 1.83 ± 0.65 L versus last postoperative FEV₁, 1.96 ± 0.66 L; p = not significant). The last postoperative values also were equivalent to tested normals for end-tidal CO₂ (40.6 ± 6.9 versus 39.9 ± 43 mm Hg), for the minute ventilation curve (1.26 ± 0.7 versus 1.59 ± 0.48 L · min^-1 · mm Hg^-1), and for the inspiratory occlusion pressure curve (0.98 ± 0.74 versus 0.86 ± 0.4 s^-1). We conclude that after lung transplantation, patients with severe chronic obstructive pulmonary disease display a restoration of ventilatory responsiveness that likely is caused by a readjustment of the CO₂ threshold at the central chemoreceptor regulatory center.