Sleep Apnea¶
Chapter 308 | Part 7: Disorders of the Respiratory System
KEY CLINICAL POINTS¶
- Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder, characterized by recurrent episodes of partial or complete upper airway obstruction during sleep.
- OSA is strongly associated with obesity, male sex, and older age, with a 2:1 male-to-female prevalence ratio.
- The apnea-hypopnea index (AHI) is the primary diagnostic criterion, defined as ≥ 5 events/hour of sleep (mild), ≥ 15 events/hour (moderate), or ≥ 30 events/hour (severe).
- Continuous positive airway pressure (CPAP) is the gold standard treatment, with adherence rates averaging 50–80%.
- Central sleep apnea (CSA) is less common and often associated with heart failure, opioids, or high altitude, with Cheyne-Stokes breathing as a hallmark pattern.
1. DEFINITION & OVERVIEW¶
Obstructive sleep apnea (OSA) and central sleep apnea (CSA) are classified as sleep-related breathing disorders. OSA involves recurrent episodes of partial or complete upper airway obstruction during sleep, while CSA is characterized by central respiratory instability. Both disorders disrupt sleep and are associated with impaired ventilation, leading to daytime sleepiness, cardiovascular complications, and increased mortality risk.
Table 308-1 Respiratory Event Definitions¶
| Event Type | Definition | Key Features |
|---|---|---|
| Apnea | Cessation of airflow ‡10 s with respiratory effort (obstructive) or absence of effort (central) | Accompanied by arousal or desaturation |
| Hypopnea | ‡30% reduction in airflow ‡10 s with ‡3% desaturation or arousal | Partial obstruction with reduced ventilation |
| Respiratory Effort–Related Arousal (RERA) | Partial obstruction without hypopnea criteria but with increased inspiratory effort | Punctuated by arousal without desaturation |
| Flow-Limited Breath | Partially obstructed breath with flattened inspiratory flow shape | Identified via pleural pressure monitoring |
Table 308-2 Obstructive Sleep Apnea/Hypopnea Syndrome (OSAHS): Quantification and Severity Scale¶
| Parameter | Definition |
|---|---|
| Apnea-Hypopnea Index (AHI) | Number of apneas/hypopneas per hour of sleep |
| Respiratory Disturbance Index (RDI) | AHI + RERAs per hour of sleep |
| Parameter | Definition |
|---|---|
| Mild OSAHS | AHI 5–14 events/hour |
| Moderate OSAHS | AHI 15–29 events/hour |
| Severe OSAHS | AHI ‡30 events/hour |
1.1 Diagnostic Criteria¶
OSA is diagnosed based on clinical symptoms (daytime sleepiness, snoring, witnessed apneas) and sleep study findings. A polysomnogram (PSG) is the gold standard, with an AHI ≥ 5 events/hour. CSA is diagnosed when there is no upper airway obstruction but central respiratory instability is present, often with Cheyne-Stokes breathing patterns.
1.2 Classification¶
OSA severity is classified by AHI: mild (5–14), moderate (15–29), severe ( ≥ 30). CSA is categorized as isolated or mixed (with obstructive events).
2. EPIDEMIOLOGY¶
OSA prevalence is 2–4% in adults, with a 2:1 male-to-female ratio. Obesity is a major risk factor, with 40–60% of cases attributable to excess weight. Prevalence increases with age, from 5–15% in middle-aged adults to >20% in the elderly. CSA is less common, with a higher incidence in patients with heart failure, opioids, or high-altitude exposure.
2.1 Risk Factors¶
Obesity, male sex, older age, craniofacial abnormalities (e.g., retrognathia), sedentary lifestyle, and genetic predisposition. In women, menopause increases risk due to reduced estrogen levels.
2.2 Demographics¶
OSA is more prevalent in men (2:1 ratio) and in individuals with obesity. African Americans and East Asians have higher risk at lower BMI due to craniofacial anatomy. Elderly patients show weaker association with obesity.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
OSA results from upper airway collapse during sleep due to reduced pharyngeal muscle tone, obesity, and anatomical narrowing. CSA arises from central respiratory instability, often linked to heart failure, opioids, or high altitude. Pathophysiology includes sympathetic overactivity, intermittent hypoxemia, and neurohumoral activation.
3.1 OSA Pathogenesis¶
Pharyngeal collapse during sleep due to reduced neuromuscular activation, anatomical narrowing (e.g., enlarged tonsils, fat deposition), and increased collapsibility in REM sleep. Obesity exacerbates airway narrowing and reduces lung volumes.
3.2 CSA Pathogenesis¶
Central respiratory instability from impaired chemoreceptor sensitivity, heart failure, or opioid use. Cheyne-Stokes breathing is a hallmark, with alternating hyperventilation and apnea due to delayed circulatory response.
4. CLINICAL FEATURES¶
OSA presents with daytime sleepiness, snoring, witnessed apneas, morning headaches, and impaired cognition. CSA is associated with frequent arousals, fatigue, and cardiovascular symptoms. Complications include hypertension, cardiovascular disease, and metabolic disorders.
4.1 Symptoms¶
Excessive daytime sleepiness (most common), snoring, gasping, nocturia, dry mouth, and fatigue. Women may report more fatigue than sleepiness.
4.2 Physical Findings¶
Obesity, large neck circumference, enlarged tonsils, uvula, and soft palate. Nasal obstruction (e.g., septal deviation) may contribute to airway collapse.
5. DIFFERENTIAL DIAGNOSIS¶
OSA must be differentiated from other causes of daytime sleepiness (e.g., narcolepsy, depression, hypothyroidism) and respiratory disorders (e.g., asthma, COPD). CSA should be distinguished from OSA and other causes of central hypoventilation.
5.1 Red Flags¶
Unexplained hypertension, nocturnal arrhythmias, or cardiac failure may suggest CSA. Obesity and snoring are strong indicators of OSA.
6. INVESTIGATIONS & DIAGNOSIS¶
Polysomnography (PSG) is the gold standard for diagnosing OSA, measuring airflow, oxygen saturation, and sleep stages. Home sleep tests (HST) are cost-effective for high-risk patients. CSA is diagnosed via PSG with central apneas and absence of obstructive events.
6.1 Diagnostic Tests¶
Polysomnography (PSG) includes EEG, EOG, EMG, airflow, and oximetry. Home sleep tests (HST) measure airflow, oxygen saturation, and respiratory effort. Overnight blood pressure monitoring may reveal nondipping patterns.
6.2 Algorithms¶
- Screen for OSA using STOP-Bang questionnaire. 2. Confirm with PSG or HST. 3. Assess for CSA if central apneas are present. 4. Evaluate for comorbidities (e.g., heart failure, obesity).
7. MANAGEMENT & TREATMENT¶
CPAP is the first-line treatment for OSA, with adherence rates 50–80%. Oral appliances, weight loss, and surgery are alternatives. CSA is managed by addressing underlying causes (e.g., heart failure, opioids) and using adaptive servoventilation (ASV) in select cases.
7.1 Pharmacologic Therapy¶
CPAP remains the gold standard. Adjuncts include sedatives for insomnia, but opioids are contraindicated in CSA. GLP-1 agonists (e.g., liraglutide, tirzepatide) may improve OSA severity.
7.2 Non-Pharmacologic Therapy¶
Weight loss (10% reduction lowers AHI by 30%), positional therapy (vibratory devices for supine OSA), and oral appliances (mandibular advancement).
7.3 Surgical Options¶
Uvulopalatopharyngoplasty (UPPP) for mild OSA, multilevel surgery for severe cases. Upper airway stimulation (hypoglossal nerve stimulation) is approved for refractory OSA.
8. PROGNOSIS & COMPLICATIONS¶
Untreated OSA increases risk of hypertension, cardiovascular disease, stroke, and metabolic disorders. CSA is linked to heart failure and atrial fibrillation. Mortality risk is 3–5 times higher in untreated patients.
8.1 Cardiovascular Impact¶
OSA causes sympathetic overactivity, intermittent hypoxemia, and endothelial dysfunction. CPAP reduces blood pressure by 2–4 mmHg but may not prevent long-term cardiovascular events.
8.2 Complications¶
Daytime sleepiness, cognitive impairment, and increased risk of motor vehicle accidents. OSA is the most common cause of daytime sleepiness, affecting >50% of moderate-to-severe cases.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: OSA may worsen due to weight gain and hormonal changes. Pediatrics: OSA in children is often due to enlarged tonsils and may resolve with growth. Elderly: OSA is less severe but more common, with higher cardiovascular risk.
9.1 Pregnancy¶
OSA risk increases with weight gain and hormonal changes. Untreated OSA is associated with preeclampsia and gestational diabetes.
9.2 Pediatrics¶
Adenotonsillar hypertrophy is a common cause. OSA in children may present with behavioral issues, learning difficulties, and sleep-disordered breathing.
10. KEY POINTS & CLINICAL PEARLS¶
- OSA is the most common sleep disorder, with 40–60% attributable to obesity. 2. CPAP adherence is critical for long-term outcomes. 3. CSA is often associated with heart failure or opioids. 4. Weight loss improves OSA severity. 5. Early diagnosis and treatment reduce cardiovascular risk.