Sleep-Related Hypoventilation/Hypoxemic Syndromes
||Sleep-Related Hypoventilation/Hypoxemic Syndromes
Upon successful completion of this module, you will be able to:
- Identify the mechanisms of sleep-induced hypoventilation and hypoxemia (SIHH).
- Identify the causes of SIHH.
- Identify and list key elements of congenital central alveolar hypoventilation syndrome.
Sleep-induced hypoventilation is characterized by elevated levels of PaCO2 while asleep, defined in the ICSD-2 as a level > 45 mm Hg or “disproportionately increased relative to levels during wakefulness.” Sleep-induced hypoxemia in the ICSD-2 is defined as “an SpO2 [oxyhemoglobin saturation] during sleep of < 90% for more than five minutes with a nadir of at least 85%” or “> 30% of total sleep time with an SpO2 of < 90%.” Other sources define these gas exchange conditions differently, and the literature is sufficiently controversial in this regard that space limitations prevent any detailed discussion. Nocturnal hypoventilation can be attributed to either decreased ventilatory drive (“won’t breathe”) or worsening mechanics (“can’t breathe”). Nocturnal hypoxemia follows due to the displacement of oxygen in the alveoli from rising carbon dioxide levels, as predicted by the alveolar air equation. Alternatively, arterial hypoxemia alone may be the product of worsening ventilation/perfusion mismatch with greater effective shunt.