Sleep Medicine


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    • Ask about sleepiness during the day (meetings, reading, watching TV)
    • Distinguish between Excessive Daytime Sleepiness (EDS) and Fatigue
    • Different from exhaustion (not enough energy for mental activity)
      • Fatigue is rarely due to sleep disorder.
      • Fatigue is due to:
        • Chronic infections
        • Malignancy
        • Autoimmune
        • Endocrinopathies
        • Neurological (Mesthenia gravis, MS, parkinson's)
        • Psych disease (mood etc..)
        • Chronic Fatigue syndrome
    • Categorize poor sleep as:
      • Extrinsic (circumstantial)
      • Intrinsic (disease related)
    • Extrinsic and Intrinsic Causes of Excessive Sleepiness

      Extrinsic Causes

      *** MOST COMMON*** Insufficient sleep duration (or inadequate opportunity for sleep)

      Circadian rhythm disturbance (shift work sleep disorder, jet lag)

      Drug-, substance-, or medical condition–related hypersomnia

      Environmental sleep disorder (ambient noise, pets)

      Intrinsic Causes

      Sleep-disordered breathing syndromes, such as obstructive sleep apnea and central sleep apnea


      Idiopathic hypersomnia

      Restless legs syndrome and periodic limb movement disorder

      Circadian rhythm sleep disorders



    • Always include thorough sleep schedule in history.
      • Sleep diary for 1-2 weeks is a good idea!
    • Actigraph (wrist-watch shaped device measures movement and ambient light over 1-2w.
    • Subjective questionnaires (Epworth Sleepiness Scale) - quantifying EDS (Excessive daytime sleepiness)
    • Polysomnography
      • Useful if primary sleep disorder (such as sleep disordered bleathing is suggested in history).
    • Mean Sleep Latency Testing. (MSLT) - measures time to sleep of breath naps.
      • Helpful in narcolepsy and idiopathic hypersomnia.
      • Helpful for patients not responding to therapy (i.e. OSA + CPAP = still poor sleep).
      • MSLT >15m = normal.
      • MSLT < 5m is pathologic sleepiness.


    Excessive Daytime Sleepiness Therapy

    • Regardless of cause, should always:
      • Counseling to maintain firm sleep-wake schedule allowing for 8hrs of sleep.
    • Specific tx:
      • CPAP for OSA.
      • Stimulants for narcolepsy
      • Naps, caffeinated beverages (for short term therapy).
      • Counsel to avoid driving if drowsy.


    Jet Lag

    • Results when internal circadian clock is out of phase.
      • (following air travel across time zones, usually >5 zones).
    • Symptoms proportional to distance traveled (insomnia, EDS, impairment etc..).
    • Self limited, takes several days to realign internal clock.
    • Management:
      • Avoid sleep depravation and dehydration before travel.
      • Hypnotic medication during flight.
      • Naps, caffeinated beverages, or stimulants after flight.
      • Specific interventions: bright light, melatonin at specific times (depending on time traveled).

    Shift Work Disorder

    • 1/5 Americans have shift schedule.
    • Increased risk of MVA.
    • Shift Work Sleep Disorder (SWSD) associated with night shift, mechanistically similar to jet lag.
    • Management:
      • Bright light treatment before night shift.
      • Caffeinated beverages during shift.
      • Planned napping during work hours.
      • Bright light avoidance +/- hypnotic medications in AM to sleep.

    Obstructive Sleep Apnea

    • Narrowing of the upper airways during sleep --> no air flow --> hypoxia.
      • Drive to breathe --> snoring. 
      • Men 30-60yo --> 24% will have OSA
      • Women 30-60yo --> 9% will have OSA
      • Occurs in younger and slender patients.
    • Upper airway obstruction causes "apneas" complete sessation of air flow, or hypopneas (reduction in flow).
      • Known as "Disordered breathing events".
    • Severity measured by AHI (Apnea-Hypopnea Index)
      • Represents sum of apneas and hypopneas per hour.
      • Obtained only through formal sleep study (overnight oximetry not adequate).
      • Apnea-Hypopnea Index

          5 - 15 = Mild (may not need treatment)

        16 - 30 = Moderate

              >30 = Severe

      • Mild AHI
        • May not need treatment.
        • Sleep on side, lose weight, don't drink EtOH before bed.
        • Decrease drugs that decrease upper airway tone: EtOH, sedatives, narcotics.
      • Moderate / Severe AHI  -> require treatment.
    • Risk Factors:
      • Obesity, esp in trunk adipose tissue.
      • M>F (similar following menopause)
      • Alcohol and sedative drug use.
      • Tonsillar hypertrophy
      • Macroglossia
      • Retrognathia / Micrognathia.
      • Upper airway mass lesions.
      • STOP-BANG Score

        • Snoring?
        • Tired (fatigued during day?)
        • Observed (Anyone observe you stop breathing?)
        • Pressure (Hypertension?)
        • -
        • BMI >35
        • Age >50 years
        • Neck circumference > 16in (>40 cm)
        • Gender (Male)


        Score 5-8 = HIGH risk for OSA

        Score 3-4 = INTERMEDIATE risk for OSA

        Score 0-2 = LOW risk for OSA


    • Clinical Features
      • Bed Partner: Loud snoring, gasping, breathing pauses
      • Patient: Frequent awakenings, snorting, non-restorative sleep.  (AM headaches are non-specific)
      • EDS is consequence of OSA, does not occur in all OSA
      • Complications:
        • Mood alterations, difficulty concentrating, problems completing tasks at school/workplace.
        • Often picked up post-anesthesia after OR or narcotic anelgesia.
    • Diagnosis:
      • GOLD STD: Polysomnography
      • Multichannel portable home monitoring
        • Considered, cheaper, easier, more available, not yet widely used (2014).
      • Ovenight oximetry: not sensitive or specific in pts with mod-to-high OSA risk.
        • Normal may help rule out OSA in pts with low pretest probability.
    • Treatment:
      • Conservative measures:
        • Weight loss (even small reductions, can be significant in AHI).
        • No EtOH at bedtime
        • Avoid supine if OSA is position dependent (i.e. strap tennis ball on back of head).
      • First line: CPAP
        • Acts as a pneumanic splint -> eliminates upper airway flow limitation.
        • Used esp if symptomatic (daytime sleepiness, when driving, talking to people).
        • Improves quality of sleep, QOL, energy level, alertness.  Patients feel better.
          • Effectiveness depends on compliance (variable).
          • Side Effects:
            • rhinitis, nasal congestion, heated humidification, nasal saline or steroids can be used, but not studied.
            • Claustrophobia: managed by proper mask fitting, and desentiziation program (gradually increase mask time while awake).
        • Pressure titrated in sleep lab, but alternative is "Auto-CPAP" that detects upper airway narrowing and responds to airway pressure.
      • Oral Devices
        • "Mandibular Advancement Devices" - hold mandible forward.
        • If not tolerating CPAP or refuse to use CPAP.
        • Used only in patients for mild-to-moderate OSA. (often need repeat testing to see response)
      • Upper Airway Surgery
        • Soft pallatal procedures (UPPP - uveo-palatal-pharyngeal-plasty) result in modest reduction in AHI.
        • Only if surgically correctable condition.  (Nasal polyps, septal deviation, enlarged tonsils, retrognathia).
          • Often try CPAP first.
      • Others:
        • Nocturnal oxygen -> helps with nocturnal desaturations (does not help open airway), does not help OSA, not recommended as primary therapy.
        • BiPAP (Bi-Level inspiratory and expiratory positive pressure)
          • Used in:  hypoventilation syndrome (improves alveolar ventilation) or if constant pressure of CPAP not tolerable.
          • Efficacy of BiPAP vs. CPAP in OSA has not been established.
        • NEW!  Nasal-End-Spiratory-Pressure
          • Applied to nasal opening by adhesive, generates pressure on exhalation (reduces AHI).
          • Insufficient evidence that more effective than CPAP, or better compliance.
      • Admitted Patients with OSA
        • Overnight oximetry
        • Elevate head of bed 30°
        • Minimize use of opioids and benzos
        • CPAP only if desaturating or apneic episoes (Anesthesiology society guideline)
          • Study: CPAP for all inpatients with OSA = No change in complications or length of stay.

    Central Sleep Apnea

    • Two categories:
      • Retainers of CO2
      • Non-Retainers of CO2
    • Loss of ventilatory output from the central ventilatory center in braim stem
      • Appears on polysomnography as loss of respiratory effort and loss of airflow for ≥10s.
      • During sleep: Increase in arterial pCO2 --> near linear increase in ventilation (weaker influence of pO2)
      • In central sleep apnea, patient hyperventilates, drives down pCO2 level near apneic threshold, followed by apnea.
      • Normal:
        • This can happen in "physiologic" (normal) central apnea when pt transitions awake-->to sleep.
        • "Sleep onset central apnea" is transient until arterial pCO2 rises, and ventilation stabilizes.
      • Abnormal:
        • Pathologic central sleep apnea throughout sleep cycle, even during non-REM sleep.
    • Risk Factors:
      • Heart failure
      • Atrial fibrillation
      • Stroke
      • Brainstem lesions
      • Kidney failure.
      • Opioid Analgesics.
      • Travel to higher altitudes
      • NOTE: Many have no risk factors "primary" or "idiopathic"
    • Small percentage of pts with CPAP for OSA develop central sleep apnea.  "CPAP emergent CSA".
    • Types:
      • Chene-Stokes Breathing often observed:  waxing-waning tidal volume.
      • Often ass'd with heart failure --> exaggerated response to CO2, and may indicate worse survival.
        • Cheyne-StokesRespiration.png
    • Symptoms
      • Frequent awakenings from sleep
      • Insomnia
      • Non-restorative sleep
      • Excessive Daytime Sleepiness(EDS)
      • PND
      • (Mimic OSA, CHF, CNS disease)
      • Many CSA symptoms report no symptoms.
    • Diagnosis:
      • Polysomnography!  
      • Oximetry alone does not reliably descriminate between obstructive and central sleep apnea.
    • Treatment:
      • Treatment only indicated if pt has symptoms
      • Target co-morbid condition
        • Medically optimize comorbid conditions (heart failure, withdraw opioids, etc..)
      • Uncertainty:
        • Uncertain if need further treatment options as a comanagement of these comorbid conditions. 
        • Also uncertain if need to treat asymptomatic CSA --> Very little Evidence (2014)
      • Specific Therapies
        • CPAP
          • --> if coexisting OSA
          • CSA can be made worse with CPAP, use ASV-->
        • Adaptive ServoVentilation (ASV)
          • Timed delivery of pressure support, synchronized to patient's breathing effort.
          • Useful for patients with central sleep apnea (such as Chene Stokes Breathing).
          • (MUST R/O reversible causes like heart failure)
          • No clinical outcomes.
        • Others:
          • Supplemental Oxygen
            • Shown in small studies to attenuate CSA.
          • Supplemental CO2 --> may have benefit.
          • Carbonic Anhydrase Inhibitor (Acetazolamide) --> helpful, esp for patients at higher altitude.
          • Theophyline --> stabilizes ventilatory rhythm, but careful in heart failure (b/c proarrhythmic)

    Sleep Related Hypoventilation Syndromes

    • Documented hypercapnia during sleep is gold standard, but rarely practical.
      • Instead sustained reduction in deoxyhemoglobin concentration in setting of a compatible condition lead to diagnosis to hypoventilation syndrome.
      • (I.e. O2 sat <90% x5min or >30% of sleep time by polysomnography).
      • Obstructive of central breathing issues may be features
      • --> difference between hypoventilation and OSA is: Hypoventilation leads to SUSTAINED decreased O2 sat >5min, while OSA leads to transient desaturations.
    • Most Common Causes: (MOST COMMON TYPES)
      • COPD
      • Obesity Hypoventilation Syndrome (formerly Pickwickian syndrome)
      • Restrictive Lung Diseases (Neuromuscular Disease, Kyphoscoliosis)
        • (Neuromuscular Diseases: Neuromuscular disease, Muscular dystrophy, Amyotrophic lateral sclerosis, Myasthenia gravis, Guillain-Barré syndrome, Phrenic nerve injury, Poliomyelitis, post-polio syndrome, Cervical spine injury)


    • Treatments (varied)
      • COPD

        • Patients with COPD or other lung disease can have desats and increase in pCO2 levels during sleep --> evident during REM sleep when muscle activity is decreased. (can also have overlying OSA)
        • Treatment:
          • Optimize COPD.
          • BiPAP often required to improve ventilation  +/- supplemental O2 (If gas exchange issue is severe).
      • Obesity Hypoventilation Syndrome

        • Often misdiagnosed as asthma or COPD.
        • 1/3 of pts with BMI ≥35, and 50% of pts with BMI ≥50 have sleep-related hypoventilation (OHS)
        • pCO >45 is cardinal sign of OHS (reduced ventilation during sleep and wakefullness).
        • Combination: mechanical load by obesity and attenuation of hypoxic and hypercapnic ventilatory drive.
        • Cardiopulmonary morbidity is very high!  (biventricular heart failure, pulmonary HTN)
        • Treatment:
          • First-Line: Weight loss +/- bariatric surgery.
          • First-Line: CPAP  (b/c OSA almost always co-exists)
          • If resistant hypoventilator / hypoxemia:
            • Second-Line: Supplemental O2 and BiPAP.
      • Neuromuscular Disorders

        • Many have no treatment, assisted breathing devices often used.

        • Assisted breathing devices are first line to alleviate sleep-related symptoms and blood O2 levels (CPAP, BiPAP, etc..)




    • CPAP can be used if OSA present without respiratory pump impairment.
    • BiPAP +/- supplemental O2
      • is usually needed, esp if hypercapnic respiratory failure due to neuromuscular weakness.
      • Especially indicated if:
        • Polycythemia
        • Pulmonary HTN
        • R-sided heart failure
    • Tracheostomy and Home Mechanical Ventilation --> May be appropriate in some pts.
    • Supplemental O2 should not be prescribed without ventilatory support (tracheostomy or NIPPV)
      • can further depress ventilation in pts with respiratory muscle weakness.


    High Altitude

    • Sleep disturbance: high altitude periodic breathing (HAPB) 
      • HAPB is characterized by cyclic central apneas and hyperpnias associated with repetitive arousals from sleep, with paraxysms of dyspnea. 
      • Sleep disturbances and "high altitude periodic breathing" (HAPB) very common at high elevations.
      • Nearly everyone >7500m or >25,000ft will experience high altitude periodic breathing (HAPB)
        • Do not occur <2500 (<8200ft)
      • HAPB
        • Characterized by cyclic central apnea and hyperpnea (repetitive arousals from sleep) paroxysms of dyspnea.
        • Onset coincides with asending, usually first night at elevation. 
      • Mechanism:  Exaggerated ventilatory response to reduced FiO2, "hypobaric hypoxia".
      • Treatment:
        • Gradual ascent (acclimatize).
        • Acetazolamide (accelerates acclimitization) - can be used prophylactically (esp if hx of altitude illness).
        • Supplemented O2 helps disruptive sleep and PND.
    • Acute Mountain Sickness
      • Clincial Dx: Nonspecific (headache, fatigue, nausea, vomiting, poor sleep) in person recent ascended.
      • Wide ranges of susceptibility, usually >6500 ft (2000m)
      • Symptoms delayed 6-12hrs after ascent, resolve in 24hrs if no further ascent.
    • High Altitude Cerebral Edema (HACE)
      • Severe form of Acute Mountain Sickness
      • Encephalopathy (altered mental status), ataxia --> vasogenic edema.
      • High risk of coma and death.
      • Management:
        • DESCENT
        • Dexamethasone, Supplemental O2,, hyperbaric therapy (all temporizing methods).
    • High Altitude Pulmonary Edema (HAPE)
      • Hypoxia --> elevations of pulmonary artery pressures, causing edema.
      • Cough, dyspnea, chest tightness, fatigue, decrease exercise capacity over 2-4 days at altitude.
      • Can be acute onset during sleep.
      • Tachypnea, tachycardic, crackles/wheezing sometimes unilateral, frothy sputum, hemoptysis -->worsening gas exchange. 
      • Treatment:
        • Supplemental O2
        • DESCENT
        • Vasodilators (nifedipine, PDE5 inhibitors like sildenafil)

    Air Travel & Lung Disease

    • Commercial airlines pressurized to: 5000-8200ft (1500-2500m).
    • Lower inspired O2 tension 110-120mmHg (normal 150-160 at sea-level).
    • Persons with underlying lung disease (COPD, pulmonary HTN) can cause substantial reductions in arterial pO2.
    • Screening for travellers:
      • Pulse oximetry at sea level --> O2 <92% indicates need for in-flight supplemental O2.
      • Hypoxia altitude simulation testing indications:
        • Equivocal oxymetry (92-95%) or art. paO2 < 70 AND COPD with hypercapnia on chronic O2, previous in-flight symptoms, or increase in exacerbation.
    • Pts already on supplemental O2 will need increase in flow rates for air travel.
    • Risk of pneumothorax and pneumomediastinum is thought to be low. 
      • Those with bullae, or cystic lung disease--> higher risk, but likely CAN FLY
    • Contraindications to flight:
      • COPD exacerbation
      • Existing pneumothorax (cause air inside pneumothorax to expand --> causing tension).
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