Study objectives: COPD patients run a risk of developing nocturnal oxygen d
esaturation. When evaluating patients with nocturnal hypoxemia, an unfamili
ar hospital environment and the monitoring equipment may cause sleep distur
bances. It was hypothesized that increased sleep disruption will lead to fe
wer instances of desaturation during a night of monitoring.
Design:The following forms of monitoring were evaluated prospectively on 3
nights for each patient: oximetry at home; polysomnography (PSG) at home; a
nd PSG in the hospital.
Setting: Department of Pulmonology, Rijnstate Hospital Arnhem, The Netherla
nds.
Patients: Fourteen stable COPD patients (7 men; median age, 71.5 years; age
range, 59 to 81 years; FEV1, 32.5% predicted; FEV1 range, 19 to 70% predic
ted) participated in the study. All subjects had significant instances of n
octurnal arterial oxygen desaturation. Those patients with a sleep-related
breathing disorder or cardiac failure were excluded from the study.
Measurements and results: The mean nocturnal arterial oxygen saturation (Sa
(O2)) level was higher during PSG monitoring at home (89.7%; range, 77 to 9
3%) than during oximetry monitoring (88.5%; range, 80 to 92%) [p < 0.025].
The fraction of time spent in hypoxemia (ie, Sa(O2) < 90%) was lower during
PSC monitoring at home (40.8%; range, 5 to 100%) than during oximetry moni
toring (59.9%; range, 6 to 100%) [p <less than> 0.01]. Desaturation time (D
elta Sa(O2) > 4%) was lower during PSG monitoring at home (22.1%; range, 3
to 63%) during PSG monitoring at home than during oximetry monitoring (50.4
%; range, 4 to 91%) [p < 0.01]. A correction for actual sleep during PSG mo
nitoring reduced the differences between PSG monitoring at home and oximetr
y monitoring, although a difference in the desaturation time remained (PSG
monitoring at home, 31.9% [range, 2 to 75%]; oximetry monitoring, 50.4% [ra
nge, 4 to 91%]) [p = 0,041]. A comparison of sleep architectures for nights
when PSG was being monitored showed a higher arousal index in the hospital
than at home (PSG monitoring in the hospital, 5.6 arousals per hour [range
, 2 to 16 arousals per hour]; PSG monitoring at home, 2.5 arousals per hour
[range, 1 to 6 arousals per hour]) [p < 0.025], hut no differences in Sa(O
2) levels were found between PSG monitoring at home and PSC monitoring in t
he hospital.
Conclusion: The artifacts due to sleep-monitoring equipment may cause an un
derestimation of the degree of nocturnal hypoxemia in COPD patients. The ad
dition of an unfamiliar environment causes more sleep disruption, but this
does not affect nocturnal Sa(O2) levels further.