Sleep Apnea¶

Chapter 308 | Part 7: Disorders of the Respiratory System · Part 7 – Respiratory Disorders · Chapter 308

Key Clinical Points¶

OSA is defined by nocturnal/daytime symptoms plus sleep study findings (AHI ≥5 events/h) OR AHI ≥15 events/h without symptoms.
CSA is less common, associated with heart failure, opioids, or high altitude, and presents with frequent awakenings and fatigue.
CPAP is the standard first-line therapy; adherence is highly variable (average 50–80%) and improves with support.
Oral appliances advance the mandible and work best for mild/moderate OSA or CPAP intolerance.
ASV is contraindicated in patients with even a small amount of CSA and LVEF <45% due to increased mortality risk.
Obesity is a major risk factor; a 10% weight gain is associated with a >30% increase in AHI.
Hypopnea criteria: ≥30% airflow reduction for ≥10s with ≥3% desaturation OR arousal.
Apnea criteria: Cessation of airflow for ≥10s with persistent effort (obstructive) or absence of effort (central).
RERA: Partial obstruction with increasing inspiratory effort punctuated by arousal, without meeting hypopnea criteria.
Women are often underdiagnosed due to lower arousal threshold and different presentation (REM sleep predominance).
CPAP side effects include nasal congestion, claustrophobia, difficulty exhaling, and aerophagia; treatable with humidification or mask changes.
Upper airway neurostimulation is an option for patients who fail CPAP, reducing AHI for at least 5 years.
Vibrotactile positional therapy can reduce AHI by up to 50% in supine-predominant OSA.
OSA is strongly associated with hypertension, cardiovascular disease, and metabolic disorders.
AHI alone does not correlate strongly with degree of sleepiness; residual sleepiness may persist after treatment.

DEFINITION & OVERVIEW¶

• OSA: More common disorder; causes daytime sleepiness, impaired function, hypertension, and cardiovascular disease. • CSA: Less common; may occur alone or as mixed apnea. Associated with heart failure, atrial fibrillation, and increased risk of mortality. • Chronic Hyperventilation: Distinct condition requiring exclusion of acute causes (e.g., DKA, asthma). Confirmed by arterial blood gas showing compensated respiratory alkalosis (low PaCO_2, low bicarbonate). • Diagnosis Criteria (OSA): 1. Presence of symptoms (snoring, snorting, gasping, or breathing pauses) OR AHI ≥15 events/h. 2. Requirement of 5 or more episodes of apnea or hypopnea per hour (AHI ≥5) if symptoms are present. • Event Definitions: - Each episode must involve a reduction in breathing for ≥10 s with either a ≥3% drop in oxygen saturation OR a brain cortical arousal.

Central Sleep Apnea¶

• Pathophysiology: Often caused by increased sensitivity to PCO_2 (unsteady breathing) or prolonged circulation delay (e.g., in heart failure). → Prolonged circulation delay leads to Cheyne-Stokes breathing (crescendo-decrescendo). • Risk Factors: Opioid medications (dose-dependent), hypoxia (high altitude), and blunted chemosensitivity. • Complex Sleep Apnea: Term used when CPAP (especially high pressure) induces central apnea. • Treatment of CSA: 1. Optimization of heart failure therapy. 2. Adaptive servoventilation (ASV): Effective for regularizing breathing; however, contraindicated in patients with CSA and LVEF <45% due to mortality risk. 3. Transvenous phrenic nerve stimulator: Reduces AHI by ≈50% and nearly eliminates central apneas.

EPIDEMIOLOGY¶

• Gender Differences: Prevalence is 2x higher in men due to android obesity and longer pharyngeal length. Women have lower arousal thresholds and more REM-predominant apneas. • Age Factors: Prevalence increases with age (5–15% in middle-aged; >20% in elderly). • Pediatric Peak: 3–8 years old due to lymphoid hypertrophy; prevalence declines as airway grows, then rises again in adolescence/adulthood due to obesity. • Obesity Impact: 1. 40–60% of OSA cases are attributable to excess weight. 2. A 10% weight gain results in a >30% increase in AHI. 3. Obesity reduces chest wall compliance and lung volume, leading to loss of caudal traction on the airway. • Ethnicity: East Asian patients may have OSA at lower BMIs due to craniofacial factors; African Americans are at higher risk than white counterparts.

Risk Factors¶

• Anatomical/Genetic: Mandibular retrognathia, micrognathia, and craniofacial morphology. - Retrognathia/micrognathia reduces posterior airway space (most evident in nonobese patients). • Medical Conditions: Diabetes mellitus, hypertension, atrial fibrillation, and endocrine syndromes (acromegaly, hypothyroidism). • Nasal Factors: High nasal resistance (septal deviation, polyps) can trigger mouth opening, breaking the seal between tongue and palate, leading to posterior tongue collapse. • Genetics: Strong familial aggregation; first-degree relatives have ≈2x higher odds of OSA.

ETIOLOGY & PATHOPHYSIOLOGY¶

• Mechanism of Collapse: 1. Inspiration creates negative intraluminal pressure. 2. Pharyngeal dilator muscles provide stability; however, muscle activity drops during sleep. 3. Collapse occurs when muscle activation fails to counteract suction or when the system is over-sensitive/under-sensitive to CO_2. • Arousal Dynamics: 1. Low arousal threshold → premature awakening before pharyngeal muscles can compensate for high CO_2. 2. High arousal threshold → failure to terminate apneas, leading to prolonged duration and severe desaturation.

Anatomical Factors¶

• Sites of Collapse: Soft palate (most common), tongue base, lateral pharyngeal walls, and epiglottis. - Soft tissue enlargement due to fat deposition or lymphoid tissue. - Skeletal structure: Retrognathia/micrognathia reduces posterior airway space. - Nasal Resistance: High resistance leads to mouth opening, breaking the seal between tongue and palate.

Physiological Factors¶

• Ventilatory Control: Pharyngeal muscle activation is linked to ventilatory drive; CO_2 buildup normally activates both diaphragm and pharyngeal muscles. - Over-sensitivity → wide fluctuations in ventilation/arousal. - Under-sensitivity → failure to activate pharyngeal muscles during high CO_2.

CLINICAL FEATURES¶

• Symptoms: 1. Snoring (common, but absence does not rule out OSA). 2. Gasping/Snorting (reflects termination of apneas). 3. Daytime Sleepiness (primary symptom; women often report 'fatigue'). • Physical Findings: 1. Obesity (central/neck circumference) and hypertension. 2. Oropharynx: Small orifice, crowded tongue, low-lying soft palate, bulky uvula, large tonsils. 3. Nasal Cavity: Polyps, septal deviation, allergic rhinitis. 4. Cardiac: Signs of heart failure or cor pulmonale.

Symptoms and History¶

• Sleep History: Obtain from bed partner if possible. - Distinction: Absence of dyspnea helps distinguish OSA from paroxysmal nocturnal dyspnea, asthma, or GERD.

Physical Findings¶

• Craniofacial: Identify retrognathia and micrognathia to guide surgical decisions. - Nasal Assessment: Check for polyps/septal deviation which increase pharyngeal collapse risk.

DIFFERENTIAL DIAGNOSIS¶

• OSA vs. CSA: CSA involves hyperventilation alternating with apnea; often linked to heart failure. • OSA vs. Narcolepsy: Use Multiple Sleep Latency Test (MSLT) or Maintenance of Wakefulness Test (MWT). • OSA vs. Hyperventilation: Rule out acute causes like DKA or asthma before diagnosing chronic hyperventilation. • OSA vs. Nocturnal Asthma/GERD: Absence of dyspnea in OSA helps differentiate from these conditions.

Central Sleep Apnea Differential¶

• Cheyne-Stokes: Characterized by crescendo-decrescendo breathing due to circulation delay in heart failure. - Idiopathic Hypoventilation: Distinguished by waking hypoxemia/hypercarbia suggesting cardiopulmonary disease.

DIAGNOSTIC APPROACH¶

Identify Respiratory Events (Table 1):
Apnea: Cessation of airflow ≥ 10s with either persistent effort (Obstructive) or absent effort (Central).
Hypopnea: ≥30% reduction in airflow for ≥10s with ≥3% desaturation OR an arousal.
RERA: Partial obstruction without meeting hypopnea criteria but showing increased inspirior effort followed by arousal.
Flow-limited breath: Identified by a 'scooped-out' inspiratory flow shape (Figure 2).
Determine Severity (Table 2):
Mild OSAHS: AHI of 5–14 events/h.
Moderate OSAHS: Ahi of 15–29 events/h.
Severe OSAHS: AHI of ≥30 events/h.
Quantify Risk:
RDI (Respiratory Disturbance Index) includes RERAs in the count.

MANAGEMENT & TREATMENT¶

CPAP Therapy (First-line):
Standard treatment for OSA.
Side Effects (Table 3) and Management:
Nasal congestion → Provide heated humidification, administer saline/steroid nasal sprays.
Difficulty exhaling → Temporarily reduce pressure, provide bilevel positive airway pressure.
Aerophagia → Administer antacids.
Oral Appliances:
Action: Advance the mandible.
Use Case: Best for mild/moderate OSA or patients with CPAP intolerance.
Surgical/Interventional Options:
Upper airway neurostimulation (for CPAP failure; reduces AHI for ≥5 years).
Transvenous phrenic nerve stimulator (for moderate to severe CSA; ≈50% reduction in AHI).
Positional Therapy:
Vibrotactile positional therapy: Reduces AHI by up to 50% in supine-predominant OSA.

PROGNOSIS & COMPLICATIONS¶

• Cardiovascular: Strong association with hypertension, heart failure, and atrial fibrillation. • Metabolic: Associated with metabolic disorders. • Pediatric: Associated with behavioral problems in children.

SPECIAL CONSIDERATIONS¶

• Pediatric: Peak incidence at 3–8 years due to lymphoid hypertrophy; risk increases again in adolescence/adulthood with obesity. - Ethnic: East Asian patients may have OSA at lower BMI due to craniofacial factors; African Americans are at higher risk than white counterparts. - Gender: Women are often underdiagnosed and present with more fatigue than sleepiness.

KEY PEARLS & CLINICAL TRAPS¶

• Diagnostic Clues: 1. Snoring is common but not required for diagnosis. 2. Gasping/snorting indicates termination of apneas. 3. Absence of dyspnea helps rule out asthma or heart failure as the primary cause of breathing issues. • Exclusion Criteria: 1. Rule out acute hyperventilation (DKA, asthma) before diagnosing chronic hyperventilation. 2. ASV is strictly contraindicated in CSA patients with LVEF <45%. 3. AHI alone does not correlate perfectly with sleepiness; residual fatigue may persist after treatment.

Reference Tables¶

TABLE 308-1 Respiratory Event Definitions • • Persistent respiratory effort (obstructive apneas, Fig. 308-2 A ), or •…¶

Harrison's 22e, p.2279

• Apnea: Cessation of airflow for ≥10 s during sleep, accompanied by:
• Persistent respiratory effort (obstructive apneas, Fig. 308-2A), or
• Absence of respiratory effort (central apneas, Fig. 308-2B)
• Hypopnea: A ≥30% reduction in airflow for at least 10 s during sleep that is
accompanied by either a ≥3% desaturation or an arousal (Fig. 308-2C)
• Respiratory effort–related arousal (RERA): Partial obstruction that does not
meet the criteria for hypopnea but provides evidence of increasing inspiratory
effort (usually through pleural pressure monitoring) punctuated by an arousal
(Fig. 308-2D)
• Flow-limited breath: A partially obstructed breath, typically within a hypopnea
or RERA, identified by a flattened or “scooped-out” inspiratory flow shape
(Fig. 308-3)

TABLE 308-2 Obstructive Sleep Apnea/Hypopnea Syndrome (OSAHS): Quantification and Severity Scale • Apnea-hypopnea index…¶

Harrison's 22e, p.2280

• Apnea-hypopnea index (AHI)a: Number of apneas plus hypopneas per hour of
sleep
• Respiratory disturbance index (RDI): Number of apneas plus hypopneas plus
RERAs per hour of sleep
• Mild OSAHS: AHI of 5–14 events/h
• Moderate OSAHS: AHI of 15–29 events/h
• Severe OSAHS: AHI of ≥30 events/h

TABLE 308-3 Side Effects of Continuous Positive Airway Pressure (CPAP) and Their Treatments¶

Harrison's 22e, p.2281

SIDE EFFECT	TREATMENT
Nasal congestion	Provide heated humidification, administer saline/steroid nasal sprays
Difficulty exhaling	Temporarily reduce pressure, provide bilevel positive airway pressure
Aerophagia	Administer antacids