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but more risk. Recent FDA approval of hypoglossal nerve stimulator. Septoplasty is not a Rx for OSA, but can improve CPAP compliance.
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Sleep Medicine
Sleep Medicine
Matt T. Bianchi
Karim Awad
SLEEP PHYSIOLOGY
SLEEP-RELATED BREATHING DISORDERS
QUANTIFYING RESPIRATORY EVENTS
Physiological monitoring (in-lab polysomnography or at-home w/limited channels)
Apnea → cessation of nasal/oral airflow for ≥ 10 s. Obstructive apnea → respiratory effort persists during apnea. Central apnea → no respiratory effort. Hypopnea → ↓ airflow by ≥30% w/desat of ≥4% for ≥10 s (some Defs use 3%). Apnea-hypopnea index (AHI) → number of apnea/hypopnea per hour of sleep.
Severity: determined by AHI (0-5 normal, 5-15 mild, 15-30 moderate, >30 severe), medical risk is proportional if untreated. Oxygen desaturation nadir can also be considered. Upper airway resistance syndrome is a mild form w/AHI<5 but occurrence of respiratory arousals (requires esophageal manometry).
OBSTRUCTIVE SLEEP APNEA [OSA]
Intro: 2/2 upper airway obstruction (usu. retropalatal & retrolingual). 10%-20% adult prevalence (defined by AHI>5). Risk factors: Male, ↑age/BMI, smoking, EtOH, airway anatomy, FH, comorbidities (DM, HTN, CAD, stroke). Consequences: ↑mortality, HTN (BMJ 2000;320:479), CAD, CHF, Stroke, GERD, insulin resistance. Anatomic factors: Neck circumference > 17(men) >16 (women); retrognathia; deviated septum, small oropharynx size, macroglossia; large uvula, low-lying soft palate, large tonsils/adenoids.
Clinical features/dx: Daytime sleepiness not always present, even in severe cases; snoring, witnessed apneas & awakenings w/gasping/choking also variable. Lab PSG: Gold standard for dx; home test kits w/limited respiration channels are growing alternative, but not for routine screening. Apneas & hypopneas often more prominent in REM & while supine. EEG arousals often follow each apnea/hypopnea. Adjunctive evaluation if surgery considered (nasopharynx endoscopy, face/neck imaging).
Rx: General measures: wt loss (if 20-50 lb lost, repeat PSG), positional therapy (e.g.: if OSA worse in supine, reduce supine position → anti-snore shirt, elevated head/trunk to 30 degrees), quit smoking, ↓ EtOH. CPAP: For symptomatic pts w/AHI ≥ 5/h, & any w/AHI>15. Improves sxs & nulls consequences of OSA. Only 50%-60% pts adhere long-term. Insurance requires at least 4 hrs/night on >70% of nights. Oral devices: Pushes mandible & tongue forward. Requires dental specialist to fit. Best for mild-mod OSA, especially for those who don’t tolerate CPAP. Provent valves are adhesive patches on each nare, provide equivalent of low-pressure CPAP w/o a machine by redirecting nasal expiration back to posterior pharynx. Upper airway surgery: Palate reduction surgery has mixed results. Maxillo-mandibular advancement better results
but more risk. Recent FDA approval of hypoglossal nerve stimulator. Septoplasty is not a Rx for OSA, but can improve CPAP compliance.
but more risk. Recent FDA approval of hypoglossal nerve stimulator. Septoplasty is not a Rx for OSA, but can improve CPAP compliance.
Positive airway pressure (PAP) machines & monitoring: CPAP (continuous pressure), BiPAP (2-level), auto-PAP (machine adjusts w/in pre-set range according to detected apneas/hypopneas), backup rate (used w/BiPAP for select pts w/central apnea or neuromuscular weakness), adaptive servoventilation (ASV; for complex apnea). All machines collect usage data (compliance), as well as mask leak & respiratory event rates while on the mask (i.e., efficacy). Effectiveness may be less than efficacy, if PAP use is less than 100% of total sleep time (as is commonly the case).
Types of polysomnography (PSG): diagnostic vs. split night (if meets OSA severity criteria in first half of night → start CPAP). If first night is diagnostic only, can return for second night of CPAP titration, or try auto-PAP at home (if more than mild OSA found). One night may not reflect variability of home sleep; try to mimic home, i.e., no abrupt discontinuation of meds. Multiple sleep latency test (MSLT): Following overnight PSG (to r/o OSA & PLMS), pt has 5 nap opportunities q2h the following day; instructed to try to sleep; measure latency & whether REM occurs. If looking for REM (i.e., narcolepsy), must be off SSRI/TCA, which suppress REM (false negative), & stimulants for 2-4 wks (to avoid rebound sleepiness false positives). Maintenance of wakefulness test (MWT): Different from MSLT b/c instructed to stay awake; less commonly used; uncertain validity for assessing work safety such as drowsy driving risk.
CENTRAL SLEEP APNEA [CSA]
Introduction: Apneic episodes w/o vent. effort. Accounts for 15% of sleep-related breathing d/o. More in middle-aged men. Features: Like OSA. Can be idiopathic/primary or secondary (e.g., CHF: 50% have CSA; chronic opiate use). Pathophys: Respiratory drive → metabolic & voluntary systems. In NREM, only metabolic (hypercapneic ventilatory drive) system working. In CSA, CO2 ventilatory drive↓, i.e., more CO2 must accumulate before ventilation stimulated. PSG: CSA usu. during sleep onset & NREM stage 1/2. Awake PaCO2: nl.
Rx: Treat underlying cause of CSA. CPAP may worsen central apnea. If CPAP not effective, adaptive servoventilation (ASV). Adjunctive therapy: Supplemental O2 for select pts. Acetazolamide: Causes metabolic acidosis thus ↑respiratory drive. Theophylline/medroxyprogesterone: Stimulates ventilation. Hypnotics: reduce transitional instability via arousals.
COMPLEX APNEA
Introduction: Some pts w/OSA have paradoxical response to PAP: emergence of central apnea. Risk factors include opiates, CHF, CNS dz. Pathophys: Chemoreceptor sensitivity, such that PAP drives CO2 below apnea threshold (greater risk w/higher pressures, or w/BIPAP). PSG: obstructive pattern before PAP applied, then mixed/central events on PAP.
Rx: In half of pts showing this pattern, it resolves spontaneously on standard PAP; other half it persists, & thus need ASV or adjunctive therapy (see section on central apnea).
EXCESSIVE SLEEPINESS
Introduction: Sleepiness leading to ↓ alertness; interferes w/daily activity. 5% of general population. Most common causes: OSA, insufficient sleep. Treated like narcolepsy (naps, stimulants) after ensuring adequate sleep duration & quality, & ruling out 1°/treatable causes.
NARCOLEPSY
Introduction: 0.05% of population, onset usu. teens/early adult. Excessive sleepiness w/REM intrusions into wakefulness (cataplexy, sleep paralysis, hypnagogic hallucinations). Only ˜15% have all four symptoms. Most cases sporadic, but familial pattern in up to 1/3.
Pathophysiology: a/w HLA, DR2, & DQ1. Narcolepsy can be 2/2 medical dz (brainstem or hypothalamic lesion, encephalitis, head trauma, PD). Hypocretin deficiency: Secreted by lateral hypothalamus, wake promoting. ↓ levels of CSF hypocretin & (postmortem) ↓hypocretin neurons → cause of narcolepsy w/cataplexy (but not w/o cataplexy). CSF hypocretin ≤ 110 pg/mL: highly specific (˜99%) & sensitive (˜90%) for narcolepsy w/cataplexy (JNNP 2003;74:1667); not sensitive for pts w/atypical, mild, or w/o cataplexy.
