Sleep hypoventilation and daytime hypercapnia in stable chronic obstructive pulmonary disease
Authors Holmedahl N, Ãverland B, Fondenes O, Ellingsen I, Hardie JA
Received 14 November 2013
Accepted for publication 16 December 2013
Published 27 February 2014 Volume 2014:9(1) Pages 265—275
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Nils Henrik Holmedahl,1 Britt Øverland,2 Ove Fondenes,3 Ivar Ellingsen,1 Jon Andrew Hardie4
1Glittreklinikken LHL Helse as, Hakadal, Norway; 2Lovisenberg Diakonale Hospital, ENT Department, Oslo, Norway; 3Norwegian National Centre of Excellence in Home Mechanical Ventilation, Haukeland University Hospital, Bergen, Norway; 4Department of Clinical Science, University of Bergen, Norway
Purpose: To explore the associations between sleep hypoventilation (SH) and daytime arterial pressures of carbon dioxide (PaCO2), sleep stages, and sleep apneas/hypopneas (AHI) in subjects with chronic obstructive pulmonary disease (COPD). SH has previously been found in COPD-subjects with chronic hypercapnic respiratory failure (CHRF) using supplementary oxygen (LTOT), and has been proposed as a possible predictor for CHRF.
Patients and methods: A prospectively designed observational study in a pulmonary rehabilitation hospital of 100 (39 male) stable COPD inpatients with a mean forced expiratory volume in 1 second (FEV1) of 1.1 L (42% of predicted) and a mean age of 64 years, using polysomnography with transcutaneous measurement of carbon dioxide pressure increase (ΔPtcCO2).
Results: SH as defined by the American Academy of Sleep Medicine (AASM) was found in 15 of the subjects, seven of whom used LTOT. However, six had SH despite being normocapnic during the daytime (only one on LTOT). Subjects with SH had a greater ΔPtcCO2 increase from nonrapid eye movement (NREM) to rapid eye movement (REM) sleep stages compared to non-SH subjects (mean [standard deviation] between-groups difference =0.23(0.20) kPa, P<0.0005). Subjects with apnea/hypopnea index ≥15 (overlap, N=27) did not differ from those with COPD alone (AHI <5, N=25) in sleep ΔPtcCO2 or daytime PaCO2. A regression model with the variables FEV1, LTOT, and sleep maximum ΔPtcCO2 explained 56% of the variance in daytime PaCO2 (F(3, 94) =40.37, P<0.001).
Conclusion: In stable COPD, SH as defined by the AASM was found both in normocapnic, non-LTOT subjects and in hypercapnic, LTOT-using subjects. Between-sleep-stage increase in ΔPtcCO2 was higher in subjects with SH. Overlap subjects did not differ from simple COPD subjects in sleep ΔPtcCO2 or daytime PaCO2.
Keywords: blood gas analysis, etiology, physiopathology, carbon dioxide, polysomnography
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