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Sleep induces profound changes on the respiratory system (Chapter 100), especially in patients with underlying cardiopulmonary or neuromuscular disorders. Sleep-related hypoventilation syndromes have in common an abnormal increase in partial pressure of carbon dioxide (PaCO2) and/or a decrease in PaO2 during sleep. A rather arbitrary threshold was chosen aiming to standardize definitions and facilitate research; in 1999 the American Academy of Sleep Medicine (AASM) included an arterial PaCO2 >45 mm Hg during wakefulness and a greater than 10 mm Hg increase in PaCO2 during sleep from awake supine values in the definition of sleep hypoventilation syndromes.1 Similarly, the International Classification of Sleep Disorders (ICSD-3) incorporated a PaCO2 during sleep greater than 45 mm Hg or, more vaguely than the AASM definition, a disproportionate increase relative to levels during wakefulness in the diagnostic criteria for sleep-related hypoxemia/hypoventilation syndromes.2 The AASM Sleep Apnea Definitions Task Force revised scoring of sleep hypoventilation in 2012 to include a PaCO2 increase >55 mm Hg for ≥10 min or a ≥10-mm Hg increase in PaCO2 during sleep in comparison to awake supine values to a value exceeding 50 mm Hg for ≥10 minutes.3 These definitions are clearly subjective. While based on data that normal individuals rarely have a PaCO2 >55 mm Hg during sleep, the precise PaCO2 demarcating the transition from physiologic hypercapnia to pathologic hypoventilation remains unclear. The duration of 10 min chosen by the AASM Task Force was arbitrary and based on consensus with a lack of normative data on the amount of total sleep time at different values of PaCO2 in sleeping adults.3 The measurement of fluctuations in PaCO2 during sleep is rather impractical and probably unattainable outside of a research setting. The determination of surrogate variables, such as end-tidal CO2 (ETCO2) or transcutaneous CO2 (PtcCO2) are more suitable for routine medical practice. However, these measurement methods are susceptible to imprecision when correlated with PaCO2 either due to sensor drifting (PtcCO2) or due to altered underlying ventilatory physiology (underestimation of PaCO2 by ETCO2 in the setting of increased dead-space ventilation), or because of technical inaccuracies.

Sleep is associated with stage-specific changes in ventilation covered in Chapter 100. Loss of the wakefulness drive to breathe, altered ventilatory response to hypoxia and hypercapnia, and increased upper airway resistance result in a decrease in ventilation in both non–rapid eye movement (NREM) and rapid eye movement (REM) sleep when compared with wakefulness. Consequently, there is a small normal physiologic increase in the PaCO2, usually no larger than 6 mm Hg during sleep.

The small decrease in ventilation and increase in PaCO2 during sleep is usually of little clinical consequence in normal individuals. However, in ...

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