O-2-induced change in ventilation and ventilatory drive in COPD

We examined the role of respiratory control during O-2-induced hypercarbia in patients with chronic obstructive pulmonary disease (COPD), by comparing the observed change in ventilation (Delta VE(obs)) with the Delta VE predicted (Delta VE(pred)) from the patients' ventilatory drive and the O-2-induced Delta Pa-CO2 and Delta Sa(O2). Eleven stable hypoxemic COPD patients (mean +/- SD: FEV(1) = 1.00 +/- 0.25 L, FVC = 2.33 +/- 0.38 L; room air Pa-CO2 = 52.7 +/- 7.9 mm Hg, Sa(O2) 87.7 +/- 5.1%) were studied. Using standard rebreathing methods, we measured the ventilatory responses to hypercapnia (Delta VE/PCO2 = 0.76 +/- 0.55 L/min/mm Hg) and to hypoxia (Delta VE/Delta Sa(O2) = -0.74 +/- 0.31 L/min/%). After breathing 100% O-2 for 15 min, the mean Delta VE(obs) was -0.08 +/- 0.62 (SEM) L/min (p = NS), the Delta Sa(O2) was 7.6 +/- 3.6% (p < 0.001), and the Delta Pa-CO2 was 6.6 +/- 3.3 mm Hg (p < 0.001). The Delta VE(pred) was expressed as the sum of a decrease in ventilation due to suppression of hypoxic drive [calculated as the product (Delta VE/Sa(O2)).Delta Sa(O2)] and an increase in ventilation due to the O-2-induced hypercarbia [calculated as the production (Delta VE/Delta PCO2).Delta Pa-CO2]. The mean Delta VE(ped) [-0.96 +/- 0.68 (SEM)] did not differ significantly from mean Delta VE(obs). We conclude that the O-2-induced Delta VE(obs) is equal to that expected from the ventilatory drives and the changes in Pa-CO2 and Sa(O2); and that O-2-induced hypercarbia does not indicate a failure of respiratory control mechanisms in the maintenance of Pa-CO2 homeostasis.