Am. J. Respir. Crit. Care Med., Vol 155, No. 2, Feb 1997, 609-614.
O2-induced change in ventilation and ventilatory drive in COPD
CR Dick, Z Liu, CS Sassoon, RB Berry and CK Mahutte
Department of Medicine, University of California, Irvine, USA.
We examined the role of respiratory control during O2-induced hypercarbia
in patients with chronic obstructive pulmonary disease (COPD), by comparing
the observed change in ventilation (delta VEobs) with the delta VE
predicted (delta VEpred) from the patients' ventilatory drive and the
O2-induced delta PaCO2 and delta SaO2. Eleven stable hypoxemic COPD
patients (mean +/- SD: FEV1 = 1.00 +/- 0.25 L, FVC = 2.33 +/- 0.38 L; room
air PaCO2 = 52.7 +/- 7.9 mm Hg, SaO2 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 SaO2 = -0.74 +/- 0.31 L/min/%). After breathing 100% O2 for
15 min, the mean delta VEobs was - 0.08 +/- 0.62 (SEM) L/min (p = NS), the
delta SaO2 was 7.6 +/- 3.6% (p < 0.001), and the delta PaCO2 was 6.6 +/-
3.3 mm Hg (p < 0.001). The delta VEpred was expressed as the sum of a
decrease in ventilation due to suppression of hypoxic drive [calculated as
the product (delta VE/SaO2) x delta SaO2] and an increase in ventilation
due to the O2- induced hypercarbia [calculated as the production (delta
VE/delta PCO2) x delta PaCO2]. The mean delta VEpred [-0.96 +/- 0.68 (SEM)]
did not differ significantly from mean delta VEobs. We conclude that the
O2- induced delta VEobs is equal to that expected from the ventilatory
drives and the changes in PaCO2 and SaO2; and that O2-induced hypercarbia
does not indicate a failure of respiratory control mechanisms in the
maintenance of PaCO2 homeostasis.
