Sleep Apnea

Obstructive Sleep Apnea (OSA)

OSA is the most common form of sleep apnea, affecting approximately 15-30% of men and 10-15% of women. It results from recurrent collapse of the upper airway during sleep.

Pathophysiology

During sleep, muscle tone decreases throughout the body, including the muscles that maintain upper airway patency (the genioglossus, tensor palatini, and others). In susceptible individuals, this normal decrease in muscle tone results in pharyngeal collapse, typically at the level of the soft palate and/or tongue base.

Airway collapse causes:

• Apneas—complete cessation of airflow for ≥10 seconds despite continued respiratory effort
• Hypopneas—partial reduction in airflow (typically ≥30%) associated with oxygen desaturation (≥3-4%) or arousal
• Respiratory effort-related arousals (RERAs)—increased respiratory effort leading to arousal without meeting criteria for apnea or hypopnea

These events trigger brief arousals (often not consciously perceived) that restore airway muscle tone and breathing. This pattern repeats dozens to hundreds of times per night.

Risk Factors

• Obesity (particularly neck circumference >17 inches in men, >16 inches in women)
• Male sex (though post-menopausal women have increased risk)
• Age (prevalence increases with age)
• Anatomical factors: retrognathia, enlarged tonsils, macroglossia, deviated septum, nasal polyps
• Neuromuscular conditions affecting airway tone
• Genetic predisposition
• Alcohol and sedative use (worsen airway collapsibility)

Clinical Presentation and Symptoms

Nocturnal Symptoms

• Loud, chronic snoring—often reported by bed partners, frequently punctuated by gasps or choking sounds
• Witnessed apneas—bed partner observes breathing cessation during sleep
• Nocturnal awakenings with gasping or choking sensation
• Nocturia—frequent nighttime urination (caused by increased atrial natriuretic peptide release from intrathoracic pressure changes)
• Sleep fragmentation—restless, unrefreshing sleep

Daytime Symptoms

• Excessive daytime sleepiness—difficulty staying awake during passive activities, inappropriate sleep episodes
• Morning headaches—caused by nocturnal hypercapnia and vasodilation
• Cognitive impairment—difficulties with attention, concentration, memory, executive function
• Mood disturbances—irritability, depression, anxiety
• Decreased libido or erectile dysfunction
• Fatigue and reduced quality of life

Diagnosis

The gold standard for diagnosing OSA is polysomnography (PSG), but home sleep apnea testing (HSAT) is appropriate for many patients.

Polysomnography (In-Lab Sleep Study)

PSG provides comprehensive monitoring including EEG (sleep staging), EOG (eye movements), EMG (muscle tone, leg movements), airflow sensors, respiratory effort belts, pulse oximetry, ECG, body position sensor, and snoring microphone. If you have an upcoming sleep study, read What to Expect at Your Sleep Study. After your study, our guide to Understanding Your Sleep Study Results can help you interpret the report.

PSG is indicated when:

• HSAT is technically inadequate or fails to establish diagnosis despite high clinical suspicion
• Patient has significant comorbidities (heart failure, COPD, neuromuscular disease)
• Suspected comorbid sleep disorders (periodic limb movements, parasomnias, narcolepsy)
• CPAP titration is needed

Home Sleep Apnea Testing (HSAT)

HSAT is a simplified portable monitor typically recording airflow, respiratory effort, oxygen saturation, and heart rate. It's appropriate for patients with high pretest probability of moderate-to-severe OSA without significant comorbidities. HSAT may underestimate severity since it doesn't measure sleep directly.

Apnea-Hypopnea Index (AHI)

OSA severity is classified by the AHI (number of apneas and hypopneas per hour of sleep):

• Normal: AHI <5
• Mild OSA: AHI 5-14
• Moderate OSA: AHI 15-29
• Severe OSA: AHI ≥30

However, treatment decisions should incorporate symptoms, oxygen desaturation severity, and comorbidities—not AHI alone.

Consequences of Untreated OSA

Cardiovascular Complications

OSA independently increases risk of:

• Hypertension—present in 50-60% of OSA patients; OSA causes nocturnal and daytime BP elevation via sympathetic activation and endothelial dysfunction
• Atrial fibrillation—risk increases 2-4 fold; untreated OSA increases AF recurrence after cardioversion or ablation
• Coronary artery disease—intermittent hypoxemia promotes atherosclerosis and plaque instability
• Heart failure—both systolic and diastolic dysfunction; OSA is highly prevalent in heart failure patients
• Stroke—2-3 fold increased risk; OSA worsens stroke outcomes
• Sudden cardiac death—risk is highest during sleep hours in OSA patients (opposite of the general population)

Metabolic and Other Consequences

• Insulin resistance and type 2 diabetes—OSA impairs glucose metabolism independent of obesity
• Dyslipidemia and non-alcoholic fatty liver disease
• Cognitive impairment affecting memory, attention, executive function
• Increased risk of depression and anxiety
• Possible increased risk of dementia and mild cognitive impairment
• Motor vehicle accidents—2-7 fold increased risk due to sleepiness
• Perioperative complications—increased anesthesia risk and postoperative respiratory complications

Treatment Options

Continuous Positive Airway Pressure (CPAP)

CPAP is the first-line treatment for moderate-to-severe OSA. It delivers pressurized room air via a nasal or oronasal mask, creating a pneumatic splint that prevents airway collapse. For a detailed walkthrough of getting started, see our complete CPAP patient guide.

Mechanism: CPAP maintains positive pressure throughout the respiratory cycle, keeping the pharyngeal airway patent. Optimal pressure is typically determined by titration during sleep study or via auto-titrating CPAP (APAP).

Efficacy: CPAP is highly effective when used consistently. It eliminates respiratory events, improves sleep quality, reduces daytime sleepiness, lowers blood pressure, and improves quality of life. Cardiovascular benefits require consistent nightly use (≥4 hours/night, preferably 6-7 hours).

Adherence challenges: Up to 30-40% of patients struggle with CPAP adherence. Strategies to improve adherence include:

• Comprehensive patient education and expectation-setting
• Mask fitting and adjustment
• Humidification
• Treating nasal congestion (nasal steroids, saline rinses)
• Pressure relief settings (EPR, C-Flex)
• Behavioral support and follow-up

Oral Appliances

Mandibular advancement devices (MADs) reposition the lower jaw forward, increasing upper airway caliber. They're appropriate for mild-to-moderate OSA or patients who cannot tolerate CPAP. Custom-fitted devices are more effective than over-the-counter options. Side effects may include temporomandibular joint discomfort and dental changes. Efficacy should be confirmed with follow-up sleep testing.

Surgical Options

Surgery may be considered for anatomically-based obstruction or CPAP intolerance:

• Uvulopalatopharyngoplasty (UPPP): Removes excess palatal tissue; variable efficacy
• Maxillomandibular advancement (MMA): Most effective surgical option for appropriately selected patients
• Hypoglossal nerve stimulation: Implanted device stimulates tongue protrusor muscles; FDA-approved for moderate-to-severe OSA meeting specific criteria
• Nasal surgery: Addresses structural nasal obstruction; typically adjunctive therapy

Lifestyle Modifications

• Weight loss: Even modest weight reduction (10%) can improve AHI significantly in overweight/obese patients
• Avoid alcohol and sedatives: These worsen airway collapsibility
• Smoking cessation: Smoking increases upper airway inflammation
• Positional therapy: Avoid supine position if positional OSA is documented — see our comprehensive guide to positional therapy

Central Sleep Apnea

Central sleep apnea (CSA) results from instability in respiratory control, with absent or reduced respiratory effort during apneic events. Unlike OSA, the problem is not mechanical obstruction but rather neurological respiratory control.

Types of CSA

• Cheyne-Stokes respiration: Crescendo-decrescendo breathing pattern with central apneas; commonly seen in heart failure and stroke
• CSA due to medications/substances: Particularly chronic opioid use
• High-altitude periodic breathing: Occurs at elevations >8,000 feet
• Primary CSA (idiopathic): Rare, diagnosis of exclusion
• Treatment-emergent CSA: Develops during CPAP treatment of OSA (often resolves with continued therapy)

Treatment

Treatment depends on the underlying cause:

• Optimize heart failure management (if Cheyne-Stokes)
• Reduce or discontinue opioids if possible
• CPAP, BiPAP, or adaptive servo-ventilation (ASV) depending on specific diagnosis
• Oxygen therapy in selected cases
• Acetazolamide for high-altitude periodic breathing