EVOLUTION OF NOCTURNAL OXYHEMOGLOBIN DESATURATION IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE AND A DAYTIME PAO2 ABOVE 60-MM HG

We studied 31 clinically stable chronic obstructive pulmonary disease (COPD) patients with a Pa(O2) greater-than-or-equal-to 60 mm Hg using polysomnographic sleep study at baseline (between 1983 and 1986) and at a mean follow-up time of 42.5 months to examine the evolution of rapid-eye-movement (REM) sleep nocturnal oxyhemoglobin desaturation (NOD). Arterial blood gases and spirometry measured at baseline and follow-up were compared with mean nocturnal Sa(O2) and to other REM sleep Sa(O2) parameters. We postulated that the onset of NOD would be seen most frequently in those patients with marked derangements of lung mechanics and greater longitudinal deterioration in arterial blood gases. Eight of the subjects developed REM-NOD on follow-up polysomnography. The appearance of REM-NOD was not related, or only minimally so, to initial Pa(O2), Pa(CO2), or mean nocturnal Sa(O2). Upon follow-up, however, the onset of NOD was always associated with deterioration of daytime Pa(O2) and Pa(CO2), mainly in those patients with the most severe baseline derangement of spirometry (lung mechanics). On the other hand, one group showed equivalent deterioration in daytime Pa(O2) and a stable Pa(CO2) but had less severely deranged baseline mechanics and demonstrated a fall in mean nocturnal Sa(O2) only. The findings in this latter group indicate that the development of NOD is not purely a result of decreasing daytime Pa(O2). We conclude that the onset of REM-NOD is mainly related to a severe derangement of lung mechanics with deterioration of resting awake gas exchange (progressive hypoxemia, hypercarbia, and worsening airflow). The onset of REM-NOD over time in some patients with a Pa(O2) > 60 mm Hg is a sign of progression of the underlying disease process.