Sleep Apnea: Mechanisms, Prevalence, and Health Consequences
Obstructive sleep apnea affects 26% of adults aged 30–70; AHI >30 events/hour is severe; each apnea event causes 10–90s hypoxia, arousal, and sympathetic surge; CPAP reduces CVD risk and blood pressure.
| Measure | Value | Unit | Notes |
|---|---|---|---|
| OSA prevalence (adults 30–70) | 26 | % of adults | Peppard 2013; AHI ≥5 with symptoms; significantly higher than previous estimates |
| Apnea definition | ≥10 | seconds airflow cessation | AASM definition; accompanied by ≥4% oxygen desaturation or arousal |
| AHI severity thresholds | 5–14 mild, 15–29 moderate, ≥30 severe | events/hour | AHI = Apnea-Hypopnea Index |
| Oxygen desaturation during events | 5–30 | % SpO2 drop | Severe OSA can drop O2 to 70–80% from 98% baseline |
| CPAP BP reduction | 2–4 | mmHg reduction | Cochrane review; 24-hour ambulatory BP; larger in severe, non-dipping patients |
Mechanism of Obstructive Sleep Apnea
During obstructive sleep apnea, the upper airway — typically at the level of the oropharynx, behind the tongue and soft palate — repeatedly collapses or narrows during sleep. This occurs because:
- Sleep reduces pharyngeal muscle tone (particularly during REM)
- Anatomical factors (excess tissue, reduced airway caliber, retrognathia) further narrow the airway
- The sleeping brain fails to maintain adequate neuromuscular activation of the genioglossus and other pharyngeal dilators
- Airway collapses → airflow stops → CO₂ rises, O₂ falls → arousal center (amygdala/locus coeruleus) detects hypercapnia → brief arousal → airway reopens → cycle repeats
Each cycle fragments sleep, preventing sustained slow-wave sleep and REM sleep, and generates a sympathetic surge that spikes blood pressure by 20–40 mmHg.
Prevalence and Demographics
The Wisconsin Sleep Cohort (Young et al., 2004; Peppard et al., 2013) provides the most robust prevalence data:
- AHI ≥5 with symptoms: 26% of men and 9% of women aged 30–70
- AHI ≥15 (moderate-severe): 14% of men, 5% of women
- Prevalence has increased ~14–55% over 20 years, tracking obesity epidemic
Risk factors: obesity (most important modifiable factor), male sex, age, retrognathia, large neck circumference (>40cm), nasal obstruction, family history.
Central vs Obstructive Sleep Apnea
| Feature | Obstructive | Central |
|---|---|---|
| Airflow | Absent | Absent |
| Respiratory effort | Present (struggles) | Absent |
| Mechanism | Airway collapse | Brainstem respiratory control failure |
| Common cause | Obesity, anatomy | Heart failure, altitude, brainstem lesion |
| Treatment | CPAP, positional, surgery | ASV therapy, treat underlying cause |
Consequences and Treatment
Severe untreated OSA (AHI >30):
- 3× higher all-cause mortality (Young 2008, 18-year follow-up)
- 2× higher cardiovascular mortality
- Increased atrial fibrillation, stroke, heart failure
- Impaired glucose metabolism, insulin resistance
CPAP (Continuous Positive Airway Pressure) is the primary treatment. It pneumatically splints the airway open with pressurized air (typically 6–14 cm H₂O), eliminating apneas and restoring sleep architecture. Adherent CPAP use (>4h/night) reduces:
- Blood pressure by 2–4 mmHg
- Cardiovascular event risk (in moderate-severe OSA)
- Excessive daytime sleepiness (largest patient-reported improvement)
Related Pages
Sources
- Peppard PE et al. — Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol (2013)
- Young T et al. — Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep (2008)
- Punjabi NM — The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc (2008)
- Giles TL et al. — Continuous positive airway pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev (2006)
Frequently Asked Questions
What is obstructive sleep apnea?
Obstructive sleep apnea (OSA) is a disorder characterized by repeated episodes of partial or complete upper airway obstruction during sleep. Each event (apnea = complete cessation; hypopnea = partial reduction) lasts ≥10 seconds, causes oxygen desaturation, and typically ends with a brief arousal as the brain forces the airway open. This fragmentation of sleep and repeated hypoxia causes excessive daytime sleepiness, cardiovascular stress, and metabolic disruption.
How is sleep apnea diagnosed?
The gold standard diagnosis is polysomnography (PSG) in a sleep lab, measuring airflow, effort, oxygen saturation, EEG, EMG, and ECG simultaneously. Home sleep apnea testing (HSAT) devices measure simpler metrics (airflow, effort, SpO2) and are appropriate for uncomplicated suspected OSA. Diagnosis requires AHI ≥5 events/hour with symptoms, or AHI ≥15 regardless of symptoms.