Role of respiratory drive in hyperoxia-induced hypercapnia in ready-to-wean subjects with COPD

Abstract

BACKGROUND: Hyperoxia-induced hypercapnia in subjects with COPD is mainly explained by alterations in the ventilation/perfusion ratio. However, it is unclear why respiratory drive does not prevent CO2 retention. Some authors have highlighted the importance of respiratory drive in CO2 increases during hyperoxia. The aim of the study was to examine the effects of hyperoxia on respiratory drive in subjects with COPD. METHODS: Fourteen intubated, ready-to-wean subjects with COPD were studied during normoxia and hyperoxia. A CO2 response test was then performed with the rebreathing method to measure the hypercapnic drive response, defined as the ratio of change in airway-occlusion pressure 0.1 s after the start of inspiratory flow (ΔP0.1) to change in PaCO2 (ΔPaCO2), and the hypercapnic ventilatory response, defined as the ratio of change in minute volume (ΔVE) to ΔPaCO2. RESULTS: Hyperoxia produced a significant increase in PaCO2 (55 ± 9 vs 58 ± 10 mm Hg, P =.02) and a decrease in pH (7.41 ± 0.05 vs 7.38 ± 0.05, P =.01) compared with normoxia, with a non-significant decrease in VE (9.9 ± 2.9 vs 9.1 ± 2.3 L/min, P =.16) and no changes in P0.1 (2.85 ± 1.40 vs 2.82 ± 1.16 cm H2O, P =.97) The correlation between hyperoxia-induced changes in VE and PaCO2 was r2 = 0.38 (P =.02). Median ΔP0.1/ΔPaCO2 and ΔVE/ΔPaCO2 did not show significant differences between normoxia and hyperoxia: 0.22 (0.12– 0.49) cm H2O/mm Hg versus 0.25 (0.14–0.34) cm H2O/mm Hg (P =.30) and 0.37 (0.12– 0.54) L/min/mm Hg versus 0.35 (0.12– 0.96) L/min/mm Hg (P =.20), respectively. CONCLUSIONS: In ready-to-wean subjects with COPD exacerbations, hyperoxia is followed by an increase in PaCO2, but it does not significantly modify the respiratory drive or the ventilatory response to hypercapnia.