Excessive Daytime Sleepiness in Chronic Obstructive Pulmonary Disease: DISCUSSION
The data reported in this study do not support the notion of a strong relationship between hypoxemia per se and an objective measure of EDS in a group of patients with chronic daytime and nocturnal hypoxemia. Taken together, this group of patients with COPD did not reveal any evidence of subjective or objective EDS as assessed by a reliable physiologic measure of sleepiness. Furthermore, Guilleminault et al, in a recent study, also found no relationship between hypoxemia and mean sleep onset latencies with MSLT defined mild vs severe sleepiness in patients with OSAS.
It seems clear from these data that severe hypoxemia can exist without producing either objective or subjective evidence of pathologic daytime sleepiness. Can one infer from this that there is no relationship between nocturnal hypoxemia and consequent excessive daytime sleepiness? These data would suggest that hypoxemia in and of itself does not invariably lead to objective daytime sleepiness as measured by decreased sleep onset latencies. This is despite the fact that, as a group, these patients exhibited short total sleep time and fragmented sleep. These facts could easily explain the occurrence of at least one very short latency nap (less than five minutes) in eight of the 14 patients. Viagra Professional
Since it seems clear from these data that hypoxemia does not lead to the invariable consequence of objective daytime sleepiness, does this necessarily imply that hypoxemia is not a pathogenetic factor in patients with nocturnal respiratory disturbances and complaints of EDS? Certainly, one can note a number of differences in the respiratory disturbances, and thus the nature of the hypoxemia in patients with OSAS. In the recent study by Guilleminault et al, the number of obstructive apneic events was noted to be far in excess of those found in our study group; and therefore, the number of discrete events of hypoxemia is appreciably greater. However, arousal reponses in their “sleepy” group (x sleep latency of 4.5 minutes) were similar to our study group (47.1 vs 49.9), yet the COPD mean sleep latency is notably longer (4.5 minutes vs 11.0 minutes). This would suggest that “fragmented” or “poor” sleep alone is not sufficient to account for the differences in MSLT results. Furthermore, since the obstructive apnea group of Guilleminault et al did not have waking hypoxemia, and our group clearly did, it can be concluded that the degree of waking hypoxemia does not appear to be a major contributing factor to the level of daytime sleepiness as defined by the mean sleep onset latency. However, since patients with OSAS are not normally hypoxemic in the waking state, the actual change in oxyhemoglobin saturation from waking to sleep would be considerably greater. In our previous study, the drop in Pa02 from waking to the lowest noted during sleep was not significantly different in the asymptomatic patients without cornplaints of EDS. However, the decrease in oxyhemoglobin saturation was significantly greater in the group with EDS. It would appear likely that it is this factor (ie, the acute decrease in oxyhemoglobin saturation) rather than the absolute level of daytime or nocturnal hypoxemia that could be linked to the presence of complaints of excessive daytime sleepiness. In future studies, therefore, it would seem prudent to make a distinction between measuring sleepiness subjectively and/or objectively and to describe more carefully the pattern (both qualitatively and quantitatively) of nocturnal hypoxemia.