Underestimation of nocturnal hypoxemia due to monitoring conditions in patients with COPD

Citation
F. Brijker et al., Underestimation of nocturnal hypoxemia due to monitoring conditions in patients with COPD, CHEST, 119(6), 2001, pp. 1820-1826
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
0012-3692 → ACNP
Volume
119
Issue
6
Year of publication
2001
Pages
1820 - 1826
Database
ISI
SICI code
0012-3692(200106)119:6<1820:UONHDT>2.0.ZU;2-F
Abstract
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.