How Sleep Apnea Works: Types, Symptoms, Diagnosis, and CPAP Therapy

This article is for informational purposes only. Consult a qualified healthcare professional for medical advice, diagnosis, or treatment.

What Is Sleep Apnea?

Sleep apnea is a common but serious sleep disorder characterized by repeated interruptions of breathing during sleep. Each cessation of airflow lasting at least 10 seconds is called an apnea; a reduction in airflow of ≥30% accompanied by oxygen desaturation or arousal is called a hypopnea. These events fragment sleep architecture, prevent restorative deep sleep, and cause intermittent hypoxemia (low blood oxygen) and hypercapnia (elevated carbon dioxide) with repeated arousals. The result is excessive daytime sleepiness, impaired cognition, and, in the long term, serious cardiovascular and metabolic consequences. Sleep apnea is estimated to affect approximately 936 million adults worldwide in its mild-to-severe form, making it one of the most prevalent chronic conditions globally, yet a majority of cases remain undiagnosed.

Types of Sleep Apnea

Obstructive Sleep Apnea: The Mechanism

OSA results from repetitive collapse of the pharyngeal airway (throat) during sleep. The upper airway is a collapsible tube held open by approximately 20 pharyngeal dilator muscles, of which the genioglossus (tongue muscle) is most important. During wakefulness, neural drive to these muscles keeps the airway patent. During sleep — particularly REM sleep — this neuromuscular activity falls. In individuals with anatomical predispositions (smaller upper airway, retrognathia, macroglossia, excess soft tissue, enlarged tonsils), the drop in muscle tone allows the airway to narrow or completely collapse.

When airflow ceases, blood oxygen saturation falls and carbon dioxide accumulates. This hypoxic and hypercapnic drive eventually triggers a cortical arousal — a brief awakening, often too brief to be remembered — that restores muscle tone and reopens the airway, producing the characteristic gasping or snorting sound. The cycle then repeats, sometimes hundreds of times per night. Importantly, the sleeper typically has no conscious awareness of these events.

Central Sleep Apnea

In central sleep apnea, the breathing pauses are caused by a lack of respiratory effort rather than physical obstruction. The brainstem's respiratory rhythm generators (pre-Bötzinger complex in the medulla) fail to maintain adequate drive. CSA subtypes include:

• Cheyne-Stokes breathing: Cyclical waxing and waning of tidal volume with central apneas; associated with heart failure, stroke, and high altitude
• Idiopathic central sleep apnea: No identifiable cause
• Treatment-emergent CSA (complex sleep apnea): Central apneas that emerge when OSA is treated with CPAP, likely due to hypocapnia (over-ventilation lowers CO₂ below the apneic threshold)
• Opioid-induced CSA: Opioid medications suppress the pre-Bötzinger complex, disrupting respiratory rhythm

Risk Factors

• Obesity: The strongest modifiable risk factor; each 10% increase in body weight increases OSA risk ~6-fold. Fat deposition in the tongue, soft palate, and parapharyngeal walls narrows the airway.
• Male sex: Men are 2–3 times more likely to have OSA; women's risk increases significantly after menopause, narrowing the gap
• Age: Prevalence increases with age due to declining muscle tone and anatomical changes
• Anatomical factors: Retrognathia (recessed chin), micrognathia, enlarged tonsils/adenoids, deviated nasal septum
• Family history: OSA has 40% heritability; genes influencing craniofacial morphology and ventilatory control are implicated
• Alcohol and sedatives: Reduce pharyngeal muscle tone, worsening OSA
• Smoking: Increases upper airway inflammation and OSA risk

Symptoms and Consequences

Diagnosis

The Apnea-Hypopnea Index (AHI) — the average number of apneas and hypopneas per hour of sleep — is the primary diagnostic metric:

• AHI 5–14: Mild OSA
• AHI 15–29: Moderate OSA
• AHI ≥30: Severe OSA

Diagnosis requires overnight sleep testing:

• In-laboratory polysomnography (PSG): Gold standard. Monitors electroencephalography (EEG), electrooculography (EOG), electromyography (EMG), electrocardiography (ECG), airflow, respiratory effort, oxygen saturation, and body position simultaneously. Staged by a sleep technologist.
• Home sleep apnea testing (HSAT): Portable devices measuring airflow, respiratory effort, and SpO₂. Less comprehensive but sufficient to diagnose moderate-to-severe OSA. Not adequate for suspected CSA, parasomnias, or significant comorbidities.

Treatment

Continuous Positive Airway Pressure (CPAP)

CPAP is the first-line and most effective treatment for moderate-to-severe OSA. A machine delivers a continuous stream of pressurized air through a mask worn over the nose (or nose and mouth), acting as a pneumatic splint to keep the upper airway open throughout the night. CPAP eliminates apneas and hypopneas in >95% of patients when used consistently. Benefits include: resolution of daytime sleepiness, improved cognitive function, blood pressure reduction (average -2–3 mmHg systolic), reduced atrial fibrillation recurrence, and improved quality of life. The main challenge is adherence — only 50–60% of patients use CPAP >4 hours per night, largely due to mask discomfort, claustrophobia, and pressure intolerance.

Alternative Treatments

• Mandibular advancement devices (MADs): Custom oral appliances that protrude the lower jaw, enlarging the retroglossal airway. Effective for mild-moderate OSA; less effective than CPAP for severe OSA but often better tolerated.
• Positional therapy: Avoiding supine sleep (OSA is typically 2× worse in the supine position) using positional pillows or vibrating devices.
• Surgical options: Uvulopalatopharyngoplasty (UPPP), tonsillectomy, maxillomandibular advancement (MMA) — most effective surgery with up to 86% success rate.
• Hypoglossal nerve stimulation (Inspire): An implantable device that stimulates the hypoglossal nerve to advance the tongue during inspiration, approved for CPAP-intolerant moderate-to-severe OSA patients.
• Weight loss: Bariatric surgery can dramatically reduce AHI in severely obese patients; a 10% weight loss reduces AHI by approximately 26%.