nocturnal hypoxemia has various pathophysiology


  • hypoxemia can occur in anyone on the steep curve of oxyhemoglobin dissociation curve1
  • overnight oximetry cannot discriminate between different etiologies of hypoxemia
  • use PSG to determine presence of apneas and capnography to determine presence of hypoventilation
  • patients with OSA/CSA have hypoxemia from apnea (using Aa gradient to determine reason for hypoxemia, sleep disordered breathing is characterized by apnea, hyponea, hypoventilation, RERA)
  • in patients with OHS, hypoxia has variety of reasons:
    • hypoventilation
      • presence of OSA or CSA
      • change in O2 sensor from leptin and resultant central hypoventilation
    • V/Q mismatch and increased deadspace ventilation2
      • decreased chest wall and abdominal wall compliance causing restriction
      • increased airway resistance from bronchospasm
      • decreased muscle strength
      • low ERV leads to VQ mismatch that’s worse in supine position. Patients adapt by taking lower tidal volume with higher respiratory rate.
  • in patients with COPD, there’s V/Q mismatch and deadspace from air trapping and emphysema
  • in patients with restrictive lung disease, there’s decreased lung compliance. Hypoxia can also happen with NMS and diaphragmatic paralysis

Footnotes

  1. Murray and Nadel Ch 122 Sleep Disordered Breathing Treatment ↩

  2. https://www-ncbi-nlm-nih-gov.wake.idm.oclc.org/pmc/articles/PMC4444067/ ↩