Sleep apnea is a breathing disorder in which the airway repeatedly closes or the brain briefly stops signaling breaths during sleep, fragmenting rest and dropping oxygen levels dozens to hundreds of times each night. The obstructive form (OSA) affects an estimated 936 million adults aged 30-69 worldwide, with 425 million in the moderate-to-severe range (Benjafield 2019).
Sleep apnea (ICD-10: G47.33 obstructive sleep apnea, adult pediatric; G47.31 central sleep apnea) is a sleep-related breathing disorder defined by repetitive complete (apnea) or partial (hypopnea) reductions in airflow during sleep, each lasting at least 10 seconds and typically ending in a brief cortical arousal or oxygen desaturation of 3% or more. Severity is quantified by the apnea-hypopnea index (AHI), the number of these events per hour of sleep: mild 5-15, moderate 15-30, severe >30 by AASM 2017 scoring criteria. Obstructive sleep apnea (OSA) accounts for over 90% of cases and results from collapse of the upper airway at the level of the soft palate, tongue base, or lateral pharyngeal walls when pharyngeal dilator muscle tone falls during sleep. Central sleep apnea (CSA, G47.31) is far less common and reflects a transient loss of respiratory drive from the brainstem, often in the context of heart failure, opioid use, high-altitude exposure, or stroke.
The key symptoms of Sleep Apnea are: Loud habitual snoring most nights, often reported by a bed partner long before the patient seeks care; present in roughly 90% of moderate-to-severe OSA., Witnessed pauses in breathing during sleep followed by a gasp, snort, or choking arousal — the single most specific symptom for OSA., Excessive daytime sleepiness with Epworth Sleepiness Scale score ≥10, falling asleep while reading, watching TV, or stopped in traffic., Non-restorative sleep — waking unrefreshed despite seven or more hours in bed, often with morning grogginess that takes an hour to clear., Morning headaches, typically frontal and dull, that fade over 1-2 hours after waking (driven by overnight CO2 retention and vascular dilation)., Nocturia — waking two or more times nightly to urinate, caused by atrial natriuretic peptide release during apneic events; often misattributed to prostate or bladder issues., Dry mouth or sore throat on waking, reflecting mouth breathing and airway turbulence..
Diagnosis of sleep apnea combines a focused history, validated questionnaires, and an objective sleep study. The history targets snoring, witnessed apneas, gasping arousals, daytime sleepiness (Epworth Sleepiness Scale), nocturia, morning headaches, and bed-partner observations. Screening tools include the STOP-BANG questionnaire (Snoring, Tiredness, Observed apnea, blood Pressure, BMI >35, Age >50, Neck >40 cm, Gender male) — a score of 3 or more is sensitive for OSA and a score of 5-8 strongly predicts moderate-to-severe disease. Examination notes BMI, neck circumference, retrognathia, dental crowding, modified Mallampati score, tonsil size, and nasal patency. The definitive diagnostic test is a sleep study. The American Academy of Sleep Medicine 2017 guidelines support two pathways: in-laboratory polysomnography (PSG, the gold standard) for patients with significant comorbidities, suspected central apnea, complex sleep complaints, or non-diagnostic home testing; and home sleep apnea testing (HSAT) for adults with a high pre-test probability of moderate-to-severe uncomplicated OSA. A negative or inconclusive HSAT in a symptomatic patient should be followed by in-lab PSG rather than treated as a normal result. Severity is graded by AHI: mild 5-15, moderate 15-30, severe >30 events per hour, with attention also to the oxygen desaturation index (ODI) and the lowest nadir SpO2. In treatment-resistant disease, drug-induced sleep endoscopy (DISE) helps localize the level of upper airway collapse and informs surgical or hypoglossal nerve stimulation selection. Comorbid conditions warrant parallel work-up: morning blood pressure, fasting glucose, lipid panel, and an ECG are reasonable when OSA is confirmed.
With consistent therapy at four or more hours nightly, prognosis is excellent. Daytime sleepiness improves within days to weeks, blood pressure falls modestly within 1-3 months, mood and quality of life improve over 3-6 months, and the long-term cardiovascular trajectory bends toward that of age-matched non-OSA peers. Untreated moderate-to-severe OSA, by contrast, raises the long-term risk of incident hypertension, atrial fibrillation, stroke, myocardial infarction, type 2 diabetes, and motor vehicle crashes by approximately 2-3 fold (Sleep Heart Health Study and other longitudinal cohorts). All-cause mortality is elevated in severe untreated disease, with the excess concentrated in cardiovascular events. The strongest prognostic factor is adherence — patients using PAP at least 6 hours per night derive substantially greater symptomatic and cardiovascular benefit than those using it less. For patients matched well to surgical or device therapy, durable response at 5 years is achievable in 60-80% of selected cases.
A sleep medicine physician should be involved when home testing is negative but symptoms persist, when central or complex apnea is suspected, when CPAP fails or is rejected, when surgical or hypoglossal nerve stimulation is being considered, when severe hypoxia or hypoventilation is present, or when sleep apnea coexists with heart failure, refractory hypertension, or stroke. Many adults with high pre-test probability and uncomplicated OSA can be evaluated and started on therapy by a trained primary care or pulmonary clinician with access to home sleep testing.
Find specialists →Sleep apnea is a chronic condition rather than an episode that recovers. With PAP therapy started, snoring stops on the first night, witnessed apneas resolve within nights, daytime sleepiness typically improves over 2-4 weeks, and mood and concentration gains accumulate over 2-3 months. Blood pressure improvements appear within 1-3 months. After surgical treatment (UPPP, MMA, Inspire implantation), post-operative recovery runs 2-6 weeks, with full assessment of therapeutic response on a repeat sleep study at 3-6 months. Weight-loss strategies (tirzepatide, bariatric surgery) produce progressive AHI improvement over 6-18 months as body composition changes.
Aim for 150 minutes per week of moderate aerobic activity (brisk walking, cycling, swimming) plus 2 sessions of resistance training. Regular exercise reduces AHI independently of weight loss in randomized trials, improves daytime alertness, and lowers blood pressure. Patients with severe untreated OSA should avoid extreme exertion or competitive driving sports until treatment is established and daytime sleepiness has improved.
Look for board certification in sleep medicine (often via pulmonology, neurology, ENT, or internal medicine), affiliation with an AASM-accredited sleep center, access to both in-lab PSG and home sleep apnea testing, and a clinic with structured CPAP setup and follow-up (mask fitting, downloaded adherence data, telehealth check-ins). For surgical or hypoglossal nerve stimulation evaluation, an ENT/otolaryngologist trained in DISE and Inspire implantation is the right referral. Continuity of care matters — sleep apnea management is a multi-year relationship and adherence support is the strongest predictor of long-term success.
Medically reviewed by AIHealz Medical Editorial Board · May 12, 2026
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