Sleep apnea

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Sleep Apnea

Definition

Sleep apnea is a disorder of recurrent episodes of absent (apnea) or attenuated (hypopnea) airflow lasting at least 10 seconds during sleep. Episodes may occur 300-500 times per night in severe cases and lead to cyclical hypoxemia, hypercapnia, sleep fragmentation, and systemic consequences. - Guyton and Hall Textbook of Medical Physiology

Types

1. Obstructive Sleep Apnea (OSA) - Most Common

Caused by repetitive partial or complete collapse of the upper airway (especially the pharynx) during sleep despite continued ventilatory effort. During sleep, pharyngeal muscle tone falls - in susceptible individuals, the airway closes entirely. This produces a characteristic sequence: loud snoring → silence (apnea) → gasping/snorting → resumption of breathing. - Guyton and Hall

2. Central Sleep Apnea (CSA)

The CNS drive to respiratory muscles transiently ceases without airway obstruction. Common in heart failure (Cheyne-Stokes respiration), after stroke, or with opioid use. The ventilatory response to CO2 becomes unstable, causing oscillation between central apnea and hyperpnea. Patients are extremely sensitive to sedatives and narcotics. - Goldman-Cecil Medicine

3. Sleep-Related Hypoventilation

Sustained elevation of arterial PCO2 (>55 mm Hg, or ≥10 mm Hg above awake values) during sleep, often in obesity hypoventilation syndrome, without necessarily discrete apnea events. - Goldman-Cecil Medicine

Epidemiology

Affects approximately 1 billion people worldwide; 425 million adults aged 30-69 have moderate-to-severe OSA
In the US: up to 30% of men and 17% of women meet diagnostic criteria
>80% of cases are undiagnosed, disproportionately so in women, racial/ethnic minorities, and low-income communities
Prevalence of sleep-disordered breathing (without symptoms): up to 9% in women and 24% in men aged 30-60
Among surgical patients: OSA rates of 45-75%; bariatric surgery patients up to 77.5% - Miller's Anesthesia

Risk Factors

Obesity - fat deposition in pharyngeal soft tissues; neck circumference >40 cm
Male sex (though women are significantly under-recognized)
Age - prevalence increases with age
Anatomic factors: large tongue, enlarged tonsils/adenoids, retrognathia, specific palate shapes
Nasal obstruction
Alcohol and sedative use (reduce pharyngeal muscle tone)
Heart failure (for central type - Cheyne-Stokes)
Neurological disorders (stroke, brainstem lesions - for central type)

Pathophysiology

With each obstructive event, the combination of progressive asphyxia, increasingly negative intrathoracic pressure, and autonomic arousal produces:

Increased afterload of both ventricles
Decreased left ventricular compliance
Increased pulmonary artery pressure
Decreased coronary artery blood flow
Increased myocardial oxygen demand
On arousal: peripheral vasoconstriction, heart rate surge, blood pressure spike (up to 240/130 mmHg at end of apneic episodes)

This repeated hemodynamic stress drives OSA's cardiovascular consequences. - Goldman-Cecil Medicine

Clinical Features

Nocturnal symptoms:

Loud, chronic snoring
Witnessed apneas, choking, or gasping
Restless sleep, night sweats
Nocturia (mediated via atrial natriuretic peptide)
Confusional parasomnias (sleepwalking, sleep talking - from N3 arousals)

Daytime symptoms:

Excessive daytime somnolence (in ~50% of OSA patients)
Morning headache
Morning dry mouth
Mood disturbances: depression, irritability
Impaired visual and working memory
Insomnia

The Epworth Sleepiness Scale is used to quantify daytime sleepiness across 8 scenarios, scored 0-3 each (max 24). - Goldman-Cecil Medicine

Severity - Apnea-Hypopnea Index (AHI)

The AHI = number of apneas + hypopneas per hour of sleep. It is the standard metric for OSA severity:

Severity	AHI (events/hour)
No sleep apnea	< 5
Mild	5 to < 15 *
Moderate	15 to < 30
Severe	≥ 30

*Mild OSA is only diagnosed if comorbidities (hypertension, atrial fibrillation, daytime sleepiness) are present. - Miller's Anesthesia

Diagnosis

Gold standard: Polysomnography (PSG)

Can be done in-lab or at home. In-lab PSG monitors:

Electroencephalography (EEG) - sleep staging
Electro-oculography (EOG) - REM detection
Electrocardiography (ECG)
Leg and chin EMG
Airflow, respiratory effort, oxygen saturation, body position

Home sleep testing is acceptable for high-pretest-probability uncomplicated OSA but misses central apneas and can underestimate severity.

Screening PSG is not indicated in asymptomatic patients. Screening questionnaires (STOP-BANG, Berlin, Epworth) can identify high-risk patients but add little beyond careful clinical assessment. - Goldman-Cecil Medicine

Cardiovascular Consequences

Hypertension - most common; OSA is a leading secondary cause
Coronary artery disease
Stroke - 3.5x greater risk of CVD death in untreated women with OSA, reduced to baseline with treatment
Atrial fibrillation
Heart failure exacerbation (and HF causes central-type CSA, creating a vicious cycle)
Increased sympathetic activity, pulmonary hypertension - Braunwald's Heart Disease

Treatment

1. Positive Airway Pressure (PAP) Therapy - First Line

CPAP (Continuous PAP): delivers constant positive pressure to pneumatically splint the airway open - the most effective treatment for OSA of all severities
BiPAP (bilevel PAP): higher inspiratory / lower expiratory pressure - used for CSA, hypoventilation syndromes, or CPAP-intolerant patients
Auto-titrating CPAP (APAP): self-adjusts pressure throughout the night
CPAP dramatically improves sleep architecture and reduces cardiovascular risk - Goldman-Cecil Medicine

2. Oral Appliances

Mandibular advancement devices reposition the lower jaw forward to enlarge the pharyngeal airway. Effective for mild-to-moderate OSA, and in patients who cannot tolerate CPAP.

3. Positional Therapy

For position-dependent OSA (predominantly supine). Lateral sleep positioning can reduce AHI significantly.

4. Lifestyle Modifications

Weight loss - the most impactful intervention; bariatric surgery can result in OSA remission in many obese patients
Alcohol and sedative avoidance (especially at bedtime)
Smoking cessation

5. Surgical Options

Uvulopalatopharyngoplasty (UPPP) - removes excess soft tissue at the back of the throat
Tonsillectomy/adenoidectomy - especially in children
Maxillomandibular advancement
Tracheostomy - bypasses obstructed airway; reserved for severe, refractory cases
Hypoglossal nerve stimulation (Inspire device) - newer therapy for moderate-severe OSA in CPAP-intolerant patients

6. Pharmacotherapy for Residual Sleepiness

For patients who remain sleepy despite adequate PAP therapy:

Modafinil 100-400 mg/day (wake-promoting)
Armodafinil 50-250 mg/day
Solriamfetol (newer dopamine/norepinephrine reuptake inhibitor)
Pitolisant (histamine H3 antagonist)
Goldman-Cecil Medicine

7. Central Sleep Apnea - Specific

Treat underlying cause (optimize heart failure therapy)
CPAP, BiPAP, or Adaptive Servo-Ventilation (ASV) - Note: ASV is contraindicated in HF with EF <45%
Respiratory stimulants (acetazolamide) in some cases

Special Populations

Pregnancy: OSA worsens due to weight gain, mucosal edema, and supine positioning. Associated with pre-eclampsia, gestational hypertension, and adverse fetal outcomes. CPAP remains safe and indicated. - Creasy & Resnik's Maternal-Fetal Medicine

Anesthesia/Surgery: OSA patients have significantly elevated perioperative risk - difficult airway, postoperative respiratory depression (especially with opioids), increased ICU needs. STOP-BANG score is standard preoperative screening. Patients should use their CPAP device perioperatively. - Miller's Anesthesia

Kidney Disease: OSA is common in CKD and ESRD; contributes to hypertension and nocturnal hypoxemia. Fluid redistribution from legs to the pharynx during recumbency is a contributing mechanism. - Brenner and Rector's The Kidney

Summary Table

Feature	Obstructive	Central
Mechanism	Upper airway collapse	Loss of CNS drive
Respiratory effort	Present (increased)	Absent
Common causes	Obesity, anatomy	Heart failure, stroke, opioids
Breathing pattern	Snoring then gasp	Cheyne-Stokes in HF
Treatment	CPAP, surgery, weight loss	Treat cause, CPAP/ASV

Sources: Goldman-Cecil Medicine; Guyton and Hall Textbook of Medical Physiology; Braunwald's Heart Disease; Miller's Anesthesia; Murray & Nadel's Textbook of Respiratory Medicine

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