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Clinical Investigations: SLEEP AND BREATHING |

Underestimation of Nocturnal Hypoxemia Due to Monitoring Conditions in Patients With COPD*

Folkert Brijker, MD; Frank J. J. van den Elshout, MD, PhD; Yvonne F. Heijdra, MD, PhD; Hans Th. M. Folgering, MD, PhD
Author and Funding Information

*From the Department of Pulmonology (Drs. Brijker and van den Elshout), Rijnstate Hospital, Arnhem, The Netherlands; and the Department of Pulmonology (Drs. Heijdra and Folgering), Dekkerswald, University of Nijmegen, The Netherlands.

Correspondence to: Folkert Brijker, MD, Department of Pulmonary Diseases, Rijnstate Hospital, PO Box 9555, 6800 TA Arnhem, The Netherlands; e-mail: zonnebloem@compuserve.com



Chest. 2001;119(6):1820-1826. doi:10.1378/chest.119.6.1820
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Study objectives: COPD patients run a risk of developing nocturnal oxygen desaturation. When evaluating patients with nocturnal hypoxemia, an unfamiliar hospital environment and the monitoring equipment may cause sleep disturbances. It was hypothesized that increased sleep disruption will lead to fewer 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; and PSG in the hospital.

Setting: Department of Pulmonology, Rijnstate Hospital Arnhem, The Netherlands.

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% predicted) participated in the study. All subjects had significant instances of nocturnal 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 (Sao2) level was higher during PSG monitoring at home (89.7%; range, 77 to 93%) than during oximetry monitoring (88.5%; range, 80 to 92%) [p < 0.025]. The fraction of time spent in hypoxemia (ie, Sao2< 90%) was lower during PSG monitoring at home (40.8%; range, 5 to 100%) than during oximetry monitoring (59.9%; range, 6 to 100%)[ p < 0.01]. Desaturation time (ΔSao2> 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 monitoring reduced the differences between PSG monitoring at home and oximetry monitoring, although a difference in the desaturation time remained (PSG monitoring at home, 31.9% [range, 2 to 75%]; oximetry monitoring, 50.4% [range, 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], but no differences in Sao2 levels were found between PSG monitoring at home and PSG monitoring in the hospital.

Conclusion: The artifacts due to sleep-monitoring equipment may cause an underestimation of the degree of nocturnal hypoxemia in COPD patients. The addition of an unfamiliar environment causes more sleep disruption, but this does not affect nocturnal Sao2 levels further.

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