Epidemiology
Etiology
Pathophysiology
- Obstruction of the upper airways → apnea → ↓ partial pressure of oxygen in arterial blood (PaO2), ↑ partial pressure of carbon dioxide in arterial blood (PaCO2, also known as hypercapnia), which leads to:
- ↑ Hypoxic pulmonary vasoconstriction → ↑ pulmonary hypertension → cor pulmonale
- ↑ Sympathetic activity → secondary hypertension
- Respiratory acidosis → renal compensation → increased HCO3− retention and decreased chloride reabsorption
Clinical features
- Pulmonary hypertension and cor pulmonale
- edema
Diagnostics
Tip
In OSA, hypercapnia is usually absent when the patient is awake. This fact explains why arterial blood gases would be mostly normal in a patient with OSA. Therefore, this test is not useful for diagnosis.
Treatment
- First-Line:
- Continuous Positive Airway Pressure (CPAP): Most effective treatment. Acts as a pneumatic splint to maintain airway patency.
- Lifestyle Modifications: Weight loss (most effective non-device intervention), avoidance of alcohol/sedatives, positional therapy (avoiding supine position).
- Second-Line/Alternative:
- Oral appliances: Mandibular advancement devices for mild-to-moderate OSA or patients intolerant of CPAP.
- Surgery: Uvulopalatopharyngoplasty (UPPP) or hypoglossal nerve stimulation in select cases.
Upper airway modification
- Description: surgical dilatation of the upper airway or neurostimulation of upper airway muscles
- Procedures
- Uvulopalatopharyngoplasty: resection of the uvula and redundant retrolingual, soft palate, and tonsillar tissue
- Other procedures include hypoglossal nerve stimulation, radiofrequency ablation of tongue and/or soft palate tissue, and palatal implants.