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Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors

¹ Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia, ² Faculty of Medicine, Flinders University of South Australia, South Australia, ³ Faculty of Health Sciences, University of Sydney, New South Wales, ⁴ Centre for Respiratory Failure and Sleep Disorders and Institute of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, and ⁵ Institute for Breathing and Sleep, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia

CORRESPONDENCE: F.J. O'Donoghue, Institute for Breathing and Sleep, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia. Fax: 61 394965124. E-mail: fods66@iprimus.com.au

Keywords: chronic obstructive pulmonary disease, hypercapnia, sleep hypoventilation

Received: July 24, 2002
Accepted January 15, 2003

This study was funded by grants from the Australian National Health and Medical Research Council and Air Liquide Australia.

Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity.

Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (P_t,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (P_a,CO2) for in vivo calibration and to correct for drift in the sensor.

Of the patients, 43% spent 20% of sleep time with P_t,CO2 >1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline P_a,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. P_a,CO2 increased mean±sd 0.70±0.65 kPa (5.29±4.92 mmHg) from night to morning, and this change was highly significant. The change in P_a,CO2 was strongly correlated with severity of SH.

Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.

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