OSA is defined by sleep interruption resulting from repetitive upper airway narrowing or collapse leading to airway occlusion. You need both symptoms and evidence on objective testing to meet the diagnosis.

Leads to apneas (no flow for 10+ seconds) or hypopneas (reductions in flow). These events divided by total sleep time comprise the apnea-hypopnea index (AHI) which is the best composite metric of OSA severity. The degree of sleepiness does not exactly correlate to the AHI.

AHI OSA Severity
5-14 Mild
15-30 Moderate
>30 Severe
# Pathophysiology of OSA
Sleep --> decreased upper airway tone --> decreased patency --> snoring and dynamic upper airway collapse. Worse during REM due to the atonia of pharyngeal muscles.

Brief awakening from sleep due to hypoxia and adrenergic stress --> microarousals --> restored airway patency --> normal ventilation.

Repetitive arousing stimuli and disrupted sleep architecture contribute to excessive daytime sleepiness and neurocognitive symptoms. Desaturations can be profound especially with other lung or heart diseases. The adrenergic stress is causally linked to hypertension, arrhythmias such as atrial fibrillation. OSA is associated with HF, CV death, and diabetes as well.

Risk Factors

  1. Obesity is the number 1 risk factor for OSA (BMI typically > 40)
  2. Increased age, male sex
  3. Alcohol and other sedative medications
  4. Anatomic: tonsillar hypertrophy, macroglossia, retrognathia, micrognathia, upper airway mass lesions, increased neck size, other craniofacial abnormalities

Clinical Features and Diagnosis

History and Physical

Polysomnography (PSG)

Management of OSA

Indications for Treatment

  1. Daytime symptoms of excessive sleepiness (the strongest indication) or impaired sleep-related QoL (such as mood disturbance, etc) --> all patients should be offered treatment
  2. Asymptomatic patients with severe OSA (AHI > 30), critical occupation, or with comorbid HTN or CV disease

Treatment Modalities

  1. Positive airway pressure (PAP) therapy splints the airways open and reduces the AHI towards zero.
    1. Fixed-CPAP or auto-CPAP. There is no role for BPAP unless there is a comorbid hypoventilation syndrome.
    2. Oral appliances for mild to moderate OSA. Higher rates of adherence
  2. Lifestyle changes such as weight loss (pharm, exercise, diet, surgery) should be offered to all.
  3. Surgical referral should be considered for patients with BMI < 40 who are intolerant for PAP (tonsillectomy, uvulopalatopharyngoplasty, maxillomandibular advancement)

Effects of Treatment

Driving and OSA

Severity of OSA alone (i.e. AHI) is not a reliable predictor of collision risk and should not be used in isolation to assess fitness to drive. You need to consider the comorbidities, sleep schedule, and history and awareness of collisions and risk, in addition to the OSA severity.

References

  1. MKSAP 19
  2. 2011 CTS Guidelines on SDB
  3. 2019 AASM Guideline on OSA and PAP
  4. 2019 CMA Driver's Guide
  5. JAMA RCE for PSA