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Obstructive Sleep Apnea (OSA) - Complete 15-Mark Answer

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DEFINITION AND CLASSIFICATION

• Apnea: A drop in peak respiratory signal of ≥90% from baseline, lasting ≥10 seconds; classified as:
  • Obstructive: No airflow despite continued respiratory effort
  • Central: No airflow and no respiratory effort
  • Mixed: Begins central, becomes obstructive in latter portion
• Hypopnea: Drop in peak respiratory signal ≥30% from baseline, lasting ≥10 seconds, with either ≥3% oxygen desaturation or a microarousal
• RERA (Respiratory Effort-Related Arousal): Upper airway narrowing causing airflow flattening that terminates in microarousal, not qualifying as a hypopnea

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EPIDEMIOLOGY

• Overall prevalence of OSA is 5% or higher in the general adult population, depending on definitions and population studied
• Men:women ratio = 2-3:1; postmenopausal women have ~3-fold higher risk vs. premenopausal women (due to loss of protective effect of progesterone and estrogen)
• Ethnic variation: Asians have similar or higher OSA prevalence despite lower BMI due to craniofacial anatomy; Hispanics are 2.14 times more likely to have severe SDB vs. Whites; young Blacks (<25 years) have higher prevalence than other groups
• Pregnancy: Prevalence of gestational OSA ~3.6% in early pregnancy, rising to ~8.3% in mid-pregnancy
• Aging: Prevalence increases with age, peaking in the 6th-7th decade
• OSA is a global "bottleneck" problem; demand for sleep medicine services far exceeds capacity worldwide

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PATHOGENESIS

1. Upper Airway Anatomy

• Nasopharynx (nares to hard palate)
• Retropalatal oropharynx (hard palate to caudal soft palate)
• Retroglossal oropharynx (caudal soft palate to epiglottis base) - most common site of obstruction
• Hypopharynx (tongue base to larynx)

2. Critical Closing Pressure (Pcrit) Model

• Normal (Pcrit < -10 cm H₂O) - non-collapsible
• Non-apneic snoring: Pcrit = -10 to -5 cm H₂O
• Obstructive hypopnea: Pcrit = -5 to 0 cm H₂O
• Obstructive apnea: Pcrit > 0 cm H₂O (airway collapses passively)

3. Neuromuscular Factors

• Myoadaptive changes: Loading of upper airway dilators causes fiber type shifts - contractility preserved but muscles become more fatigable
• Muscle injury: In severe OSA, reduced contractility may occur
• Connective tissue alterations: Impair mechanical coupling
• Denervation: Sensory and motor - from repeated snoring trauma
• Upper airway inflammation: Edema from snoring increases wall thickness

4. Anatomic Risk Factors Predisposing to OSA

• Small retrognathic mandible or retropositioned maxilla (bony restriction)
• Enlarged soft tissue volumes: tongue hypertrophy, tonsillar enlargement, elongated soft palate
• Increased lateral pharyngeal wall thickness and parapharyngeal fat pad volume
• Increased airway length (predisposes to collapse)
• Reduced lung volume (recumbency reduces tracheal traction, narrowing the upper airway)

5. Fluid Shift Mechanism

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RISK FACTORS

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CLINICAL FEATURES

Nocturnal Symptoms

• Heavy, habitual snoring (most common presenting complaint; not specific for OSA)
• Witnessed apneas by bed partner (most specific symptom)
• Nocturnal choking/gasping
• Restless sleep, frequent awakenings
• Nocturia (due to increased ANP release from right atrial stretch)
• Diaphoresis, palpitations
• Gastroesophageal reflux
• Morning headache (hypercapnia-mediated)
• Erectile dysfunction

Daytime Symptoms

• Excessive daytime sleepiness (EDS) - cardinal daytime symptom; defined as propensity to fall asleep in unwanted situations during waking hours
• Unrefreshing sleep
• Cognitive impairment: poor attention, memory, executive function
• Irritability, mood disturbance, depression
• Fatigue, lightheadedness
• Increased motor vehicle accident risk (2-7x higher risk of crashes)

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DIAGNOSIS

Screening Questionnaires

• STOP: Snoring, Tiredness, Observed apnea, high blood Pressure
• BANG: BMI >35, Age >50, Neck circumference >40 cm, Gender (male)
• Score ≥3: high risk for OSA

Gold Standard: Polysomnography (PSG)

• EEG (sleep staging)
• EOG (eye movements - REM identification)
• EMG (muscle activity)
• Oronasal thermistor + nasal pressure cannula (airflow)
• Thoracic/abdominal respiratory inductance plethysmography bands (respiratory effort - shows paradoxical thoracoabdominal motion in obstructive events)
• Pulse oximetry (SpO₂)
• ECG
• Leg EMG (periodic limb movements)

Home Sleep Apnea Testing (HSAT)

• Limited-channel portable monitors (at minimum: airflow, effort, oximetry)
• Appropriate for patients with high pretest probability of moderate-severe OSA without significant comorbidities (COPD, heart failure, central apnea, neuromuscular disease)
• HSAT underestimates AHI (divides events by total recording time, not sleep time); if negative in high-suspicion patient, in-lab PSG is required

Other Investigations

• Overnight pulse oximetry: Shows characteristic "sawtooth pattern" of desaturations; useful screening tool but misses apneas/hypopneas without desaturation; limited sensitivity
• Wearable technologies (smartwatches, rings): Growing role but insufficient validation data currently for diagnostic use

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PATHOPHYSIOLOGIC CONSEQUENCES

1. Chronic intermittent hypoxia (CIH) with reoxygenation - oxidative stress
2. Sleep fragmentation - cortical arousal at apnea termination
3. Increased negative intrathoracic pressure - mechanical cardiac effects

A. Neurocognitive Consequences

• Hypoxia-reperfusion injury: increased lipid peroxidation and oxidative stress in neural tissue
• Neurovascular endothelial dysfunction: reduced nitric oxide, impaired vasodilation
• Hypercoagulability and atherosclerosis: risk of vascular dementia
• Increased β-amyloid deposition: linked to Alzheimer disease development
• Functional deficits: attention, memory, vigilance, executive function (motor speed spared; fine motor coordination impaired)

B. Cardiovascular Consequences

C. Metabolic Consequences

• Type 2 Diabetes: CIH impairs insulin sensitivity independently of obesity; disrupts glucose homeostasis
• Metabolic syndrome: OSA is strongly associated
• Increased leptin resistance; dysregulated adipokines

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TREATMENT

Decision to Treat (Fishman, Ch. 98)

• Moderate-severe OSA (AHI ≥15): Treat regardless of symptoms - improves neurobehavioral function, quality of life, BP
• Mild OSA (AHI 5-14) with symptoms or comorbidities: PAP therapy if daytime sleepiness, HTN, ischemic heart disease, or history of stroke
• Nonsleepy patients: Shared decision-making (insufficient evidence to mandate or withhold PAP)

1. Behavioral / Conservative Therapies

• Weight loss: Strongly recommended for overweight/obese patients (10% weight loss → 26% AHI reduction); not sufficient as sole therapy for most
• Sleep position therapy: For positional OSA (AHI in supine ≥2x non-supine position; prevalence 50-70% of OSA patients) - lateral sleep positioning reduces obstruction; tennis ball technique, positional alarm devices
• Avoidance of alcohol/sedatives especially within 2-4 hours of bedtime
• Smoking cessation (airway inflammation reduction)
• Sleep hygiene optimization

2. Positive Airway Pressure (PAP) Therapy - First-Line Treatment

• Delivers fixed continuous pressure throughout inspiration and expiration
• Acts as a pneumatic splint preventing airway collapse during sleep
• Increases airway caliber in retropalatal and retroglossal regions (primarily lateral dimensions)
• Remains the mainstay of therapy for most OSA patients

• Fixed CPAP: Single set pressure; titrated in lab or via auto-titration at home
• Auto-titrating PAP (APAP): Adjusts pressure breath-by-breath; useful for variable OSA
• Bilevel PAP (BPAP): Separate inspiratory (IPAP) and expiratory (EPAP) pressures; useful for patients who cannot tolerate high CPAP pressure, or with significant hypercapnia/OHS
• ASV (Adaptive Servo-Ventilation): For complex and central sleep apnea; contraindicated in heart failure with EF ≤45%

• Nasal pillows, nasal mask, oronasal (full-face) mask - chosen based on patient preference and mouth breathing

3. Oral Appliances

• Protrude the mandible forward, increasing posterior pharyngeal space and raising Pcrit
• Recommended as first-line alternative to CPAP for mild-moderate OSA or primary snoring (AASM/AADSM guidelines)
• Less effective than CPAP at reducing AHI and hypoxemia but comparable improvement in subjective sleepiness and quality of life
• Higher patient adherence than CPAP
• Custom devices by qualified dentists preferred over over-the-counter devices
• Side effects: salivation, tooth pain, gum soreness, myofascial pain, TMJ issues

4. Surgical Treatments

5. Pharmacologic and Adjunctive Therapies

• Nasal corticosteroids + montelukast: improve snoring but not effective for moderate-severe OSA as monotherapy; useful adjuncts to lower CPAP pressure requirements
• Oxygen supplementation: Addresses hypoxemia but does not resolve apneas/hypopneas; may blunt hypoxic arousal response and prolong apnea duration; not recommended as primary OSA therapy
• Stimulant medications (modafinil, armodafinil): Adjunctive for residual EDS despite adequate PAP therapy; do not treat the underlying SDB

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SPECIAL SITUATIONS

Overlap Syndrome (OSA + COPD)

• Combined obstructive physiology during both wakefulness and sleep
• More severe nocturnal hypoxemia and hypercapnia than either condition alone
• Preferentially treated with BPAP (Fishman, Ch. 98 block 30)

OHS with Severe OSA

• Obesity Hypoventilation Syndrome: BMI ≥30 + PaCO₂ >45 mmHg (awake) not explained by other causes
• OSA present in >90% of OHS patients
• BPAP is preferred initial therapy

Perioperative Considerations (Fishman, Ch. 102)

• Anesthesia and surgery alter sleep architecture; postoperative opioids blunt chemosensitivity
• Preoperative screening for OSA is prudent though its value in reducing postoperative complications is not definitively established

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KEY POINTS SUMMARY

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