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Introduction

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Sleep can have profound changes on the respiratory system (see Chapter 96) especially in patients with underlying cardiopulmonary disorders. Sleep-related hypoventilation syndromes are characterized by an abnormal increase in partial pressure of carbon dioxide (PaCO2) and a decrease in PaO2 during sleep. In an attempt to standardize definitions and facilitate research, in 1999 the American Academy of Sleep Medicine (AASM) included an arterial PaCO2 >45 Torr during wakefulness and a greater than 10 Torr increase in PaCO2 during sleep from awake supine values in the definition of sleep hypoventilation syndromes.1 Similarly, the 2005 International Classification of Sleep Disorders (ICSD-2) incorporated a PaCO2 during sleep greater than 45 mm Hg or disproportionately increased relative to levels during wakefulness in the diagnostic criteria for sleep-related hypoxemia/hypoventilation syndromes.2 More recently, the AASM Sleep Apnea Definitions Task Force revised scoring of sleep hypoventilation in 2012 to include a PaCO2 increase >55 mm Hg for ≥10 minutes 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 While based on data that normal individuals rarely have a PaCO2 >55 mm Hg during sleep, the precise PaCO2 level demarcating the transition from physiologic hypercapnia to pathologic hypoventilation remains unclear. The duration of 10 minutes decided 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 PaCO2 values in sleeping adults.3 Sleep is associated with stage-specific changes in ventilation covered in Chapter 96. 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 nonrapid eye movement (NREM) and rapid eye movement (REM) sleep when compared to wakefulness. Consequently there is a small normal physiologic increase in the PaCO2 of 4 to 6 mm Hg during sleep.

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The small decrease in ventilation and increase in PaCO2 during sleep is usually of little clinical consequence in normal individuals but in patients with respiratory muscle weakness, altered respiratory mechanics, impaired gas exchange and/or abnormal ventilatory drive, sleep is a vulnerable time. Nocturnal hypoventilation often precedes chronic daytime hypoventilation but the extent to which sleep can elicit and exacerbate chronic hypoventilation is often under appreciated. A high index of clinical suspicion for nocturnal hypoventilation is necessary especially with the availability of effective treatment, and this chapter aims to review some of the common causes of sleep-related hypoventilation.

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Causes of Sleep-Related Hypoventilation

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The PaCO2 is determined by CO2 production divided by alveolar ventilation (minute ventilation [the product of tidal volume and respiratory rate] minus dead space ventilation). Hypercapnia results when alveolar ...

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