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    Obstructive Sleep ApneaCauses, Consequences, Cures

    Peter K Franklin MD ABSMEssentia HealthSleep Medicine

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    Discussion today

    A littl b k d i l h i l A little background in sleep physiology Introduction to sleep center/laboratory The meaning of excessive daytime sleepiness Obstructive Sleep Apnea

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    Why Do We Sleep?

    Restores body/brain deficits caused by waking activity no supporting evidenceactivity no supporting evidence

    Energy conservation limit activity/energy expense (esp. warm blooded animals)

    Immobilization/protection from predators

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    Laying down memory tracks is important in learning

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    Sleep Physiology Sleep was once considered passive; however, EEG

    development proves it is active and complex.

    There are two kinds of sleep:

    1. Non REM2. REM (rapid eye movement)

    Non REM is classified as: Stage 1 (transitional)

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    g ( )Stage 2Slow wave (delta)

    Sleep Physiology

    Stage 1 (transition between waking and sleep)30 7 i t ~30 sec 7minutes

    Reactivity to outside stimuli

    Short dreams

    People feel they are awake if asked

    Disconjugate rolling eye movements

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    Sleep Physiology

    Stage 2 About 50% of total sleep time About 50% of total sleep time Spindles/K complexes

    Delta Sleep (slow wave) EMG activity low Physiologically stable heart rate/respiration slow

    and regularand regular Arousal difficult 10-20% of total sleep time

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    REM Sleep

    EEG resembles stage 1/waking trace

    EMG lowest activity (paralysis)

    Rapid conjugate eye movements

    Dreaming usually reported

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    REM Sleep

    Physiologic instability elevated and irregular heart rate respiratory rate and blood pressureheart rate, respiratory rate and blood pressure

    Erections in males

    About 20% of normal sleep time

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    Sleep Architecture

    Normally we cycle through all stages every 70-120 minutes70 120 minutes

    Most slow wave sleep is early in the night, most REM towards morning

    Age differences are prominent sleep in the elderly is fragmented / many stage changes / little slow wave sleeplittle slow wave sleep

    Optimum sleep may be at age 10-12 sound sleep, easy onset/wakening, fully alert, circadian rhythms well entrained

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    Sleep Studies

    Nocturnal polysomnogram monitors:EEG EEG

    EOG (oculogram) EMG (chin and leg) Respiratory effort and airflow EKG Oximetry Videotape

    Sleep Apnea Syndrome

    Incidence:4 t 6% f A i h Sl 4 to 6% of American men have Sleep apnea

    Female more UAA Female OSA usually post menopausal Ratio evens out post menopausal

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    Sleep Study Procedure: Outpatient 8:00PM to 8:00AM

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    The great sleep divide



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    Who Needs A Sleep Study?

    Loud snorers, witnessed apneas, marked daytime somnolencedaytime somnolence

    Lifelong sleepiness despite adequate sleep,

    RLS / PLMS /movement disorders/noc seizures

    In other words..the DOESIn other words..the DOES

    Clinically Significant E.D.S.

    Persistent and unremitting

    Increasing sleep time may not fix the sleepiness

    Patient may c/o sleep loss consequences, i.e., loss of energy, memory loss or fatigue

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    E.D.S.: A Serious Problem

    50% report M.V.A.

    50% report occupational accidents

    May have lost jobs

    Disrupts family life

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    p y

    Excessive Daytime Sleepiness DDX

    1.Sleep apnea syndromes

    2.Neurologic conditionsg Narcolepsy Idiopathic CNS hypersomnolence Sleeping Sickness (African Trypanosomiasis) Klein-Levine syndrome

    3.Chronically insufficient sleep

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    y p

    4.Circadian rhythm abnormality

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    Excessive Daytime Sleepiness DDX continued

    5. Disturbed nocturnal sleep Periodic leg movementg Central sleep apnea

    CHF/exaggerated Cheyne-StokesCNSAltitude

    Medical Disordersasthma,angina, CHF, chronic pain syndrome, e.g. RA, reflux

    6. Drugs7. Depression 10% with major depression

    Four General Causes of E.D.S.

    1. Sleep at night quantity quality

    2. Circadian rhythm

    3. Drugs

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    4. CNS pathology

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    Sleep at Night

    QuantitySleepiness directly related to the amount of sleep:Sleepiness directly related to the amount of sleep:

    Sleep requirement is individual Sleep deprivation is accumulative

    QualitySleep fragmentation produces a functional sleep loss

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    Circadian Rhythm

    Correlates with body temperature

    Nadirs0500 a.m.1400

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    Drugs Tranquilizers (i.e., benzodiazepines) Antihistamines

    A tid t Antidepressants Antipsychotics Antihypertensives (-blockers) ETOH noc time dose:

    s sleep latency

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    worsens underlying sleep pathfragments sleep

    CNS Pathology


    Idiopathic CNS hypersomnolence

    Central apneas


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    Case: 47-year-old-male

    Loud snorerwitnessed apneasexcessive daytime sleepiness

    PMHx:chronic low back pain after MVA 7 years ago

    ROSA.M. headaches50# weight gain since his accident

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    50# weight gain since his accidentnocturia 2-3 times per night

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    Case: 47 year-old-male

    Exam:AVSS AVSS

    511, 278# HEENT: Classic thick uvula and redundant

    soft palatal tissue Neck: Stout

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    Abd: Obese

    Case: 47-year-old male

    Overnight Polysomnography Apnea/hypopnea index 66/hr (longest duration 46

    seconds; lowest 02 saturation 72%)seconds; lowest 02 saturation 72%)

    Sleep architectureStage 1 8%Stage 2 56%Stage SWS 16%Stage REM 20%

    t 12% d l h i t i

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    comment: 12% scored as alpha intrusion

    Nasal C-PAP applied and titrated to 11 cm with REM rebound

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    47 year-old-male

    Impression:S b t ti lSevere obstructive sleep apneaAlpha intrusion

    Plan:Setup on 11 cm N-CPAPFollow up in 2 months

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    Follow-up in 2 months

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    47 year-old-male

    Follow-up visit: Wife thrilled with the quietWife thrilled with the quiet

    Pt. initially felt betterNo a.m. headachesNo nocturiaSome improvement in the daytime sleepiness

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    Increased back painSleep less restorative

    47 year-old-male

    ImpressionS OSA ll t ll d 11 N CPAP Severe OSA well controlled on 11 N-CPAP

    Alpha intrusion secondary to chronic pain syndrome unmasked by successful treatment of his OSA


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    Elavil 25 mg at h.s.

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    47-year-old male

    Two major points:

    1. DDx of excessive daytime sleepiness.

    2. There may be more than one underlying disorder. Follow-up is very important.

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    Obstructive Sleep Apnea

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    Sleep Apnea Syndrome

    When a person, especially advanced in years, is lying on his back in heavy sleep and snoring loudly, it very commonly happens that inspiration fails to overcome thecommonly happens that inspiration fails to overcome the resistance in the pharynx, of which stridor or snoring is the audible sign, and there will be perfect silence through 2, 3 or 4 respiratory cycles in which there are ineffectual

    movements; finally, air enters with a loud snort, after which there are severald i i ti deep inspirations.

    W. H. Broadbent 1877

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    Sleep Apnea Symptoms

    Excessive daytime sleepiness after adequate sleep time

    Loud snoring with silent pauses - witnessed apnea Irritability, Memory Loss Morning headaches - Hypoxemia, Hypercapnia Interfering with daily life

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    Snoring a Sleep Disorder?

    Laugh and the world laughs with you Snore and you sleep alone

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    Sleep Apnea Syndrome

    Incidence 1-5% of population Male to female ratio is 6:1 Female (usually post menopausal) Ratio evens out post menopausal

    Sleep Apnea Syndrome

    Hypersomnolence 80 90% 80-90% disrupts daily life differential diagnosis

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    Sleep Apnea Syndrome

    Personality change and intellectual deterioration: 50% Inability to concentrate

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    Sleep Apnea Syndrome

    Morning headaches Hypoxemia Hypoxemia Hypercapnia

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    Sleep Apnea Syndrome

    Impotence 50% treatable

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    Physical Exam

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    Physical Exam:

    General Inspection: Is there any doubt ?

    Facial Inspection:

    Facial reconstruction Down Syndrome

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    Nose Inspection

    Prior broken nose Severe rosacea, rhinophyma


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