Obst Sleep Apnea Slides 060515

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    MAY 15, 2006

    Obstructive Sleep Apnea

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    Consequences of OSA

    Subjective complaints: snoring, sleepiness

    Neuropsychological sequelae

    Metabolic Derangements

    ypertensioneart an! "ascular Disease

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    Neurobehavioral #ffects

    Sleepiness$ten!ency to fall asleep #p%orth Sleepiness Scale is commonly use! subjective test of

    sleepiness &he MS'& is a polysomnographic test of sleep ten!ency requiring

    subjects to try to fall asleep !uring !aytime nap opportunities lasting() min or less* &he latency from lights out to sleep onset is theprincipal outcome measure* +atients %ith severe OSA often havemean sleep onset latencies in the pathological range of minutes orless, some ( SD belo% normal mean values of -(*

    M.& an! OS'#/ testing also !elineate !egree of sleepiness in pts

    %ith OSA

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    Neurobehavioral #ffects

    Si0able effect of OSA on the ability to sustain attention overtime, particularly on the quality of the performance ratherthan simple reaction time

    Mo!erate to severe OSA negatively impacts memory an!

    e1ecutive performance2although presence an! !egree of!eficit in these categories is controversial

    3O' stu!ies in!icate that pts %ith OSA have significantlyimpaire! 3O' an! social functioning an! a high prevalenceof minor psychiatric morbi!ity

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    Neurobehavioral #ffects an! &reatment

    4mprovements in both subjective an! objective tests ofsleepinessare seen %ith C+A+ therapy for OSA* &heseimprovements are mo!erate to large* Subjective scoresimprove to a larger !egree than objective scores*

    #valuation of attention5base! cognitive outcomes, there isa much more mo!est improvement of functioning %ithC+A+

    QOL: the large impairments in sleepiness an! energyrelate! 3O' scores sho% substantial improvement %ith

    C+A+2those %ith the most severe OSA reap the mostbenefit

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    Metabolic #ffects

    Insulin Resistance: hyperglycemia resultingfrom both an impaire! insulin secretory responseto glucose an! !ecrease! insulin effectiveness in

    stimulating glucose upta6e by s6eletal muscle an!in restraining hepatic glucose pro!uction

    Metabolic Syndroe: hyperinsulinemia,glucose intolerance, !yslipi!emia, central obesity

    an! hypertension7 all ris6 factors for vascular!isease

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    OSA an! 4mpaire! 8lucose Metabolism

    Meslier et al 200! 9 male patients referre! for

    polysomnography un!er%ent a (hour oral glucose tolerance test*

    9 pts ha! OSAS ;A4 < -)= >asting an! postloa! bloo! glucose

    increase! %ith severity of sleepapnea

    4nsulin sensitivity !ecrease! %ithincreasing severity of sleep apnea

    ?M4, age an! A4 are all have anin!epen!ent effect on bloo!glucose an! insulin sensitivity

    Ip et al 2002 -@ pts %ith OSAS ;A4

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    Mechanism of 4nsulin /esistance

    Altere! a!renergic function

    Direct effects of hypo1emia on glucose regulation

    /elease of proinflammatory cyto6ines that affect

    metabolism

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    #ffect of C+A+

    abu et al 2005 ( pts %ith DM type 44,

    obesity ;mean ?M4 (*=,an! OSA ;mean A4 B=%ere evaluate! before an!after a 9) !ay trial of C+A+

    &here %ere significantre!uctions in postpran!ialglucose values

    Conclu!e! that OSA ispathophysiologically relate!to impaire! glucose

    homeostasis an! that C+A+is an important therapy forpts %ith DM type 44 an! OSA

    (arsc* et al 200! >orty patients %ith A4

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    ypertension

    isconsin Sleepo*ort Study 4ncrease! ris6 for

    !evelopment of &N in pts%ith OSA over a to @ year

    follo% up perio! Severity of OSA increase!

    ris6 for !evelopment of &Nin!epen!ent of baseline&N status, age, gen!er,?M4, alcohol an! cigarette

    use

    Sleep (eart (ealt*Study 'arge cross5sectional stu!y

    ;B-( participants= #levate! ris6 for &N foun!

    in subjects %ith SD? aftera!justing for !emographics,?M4, alcohol consumptionan! smo6ing

    Association bet%een SD?an! &N %as seenregar!less of age, gen!er,ethnicity, ?M4

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    Mechanism

    4n!ivi!ual episo!es of sleep apnea cause acutesurges in / an! ?+ at apnea termination !rivenby (Y"O3IA

    #pi!emiologic evi!ence an! physiologic stu!ies inhumans an! animals support the i!ea that chronice1posure to repeate! apneas may lea! to asustaine! !iurnal &N via increase!

    SYM"A4(4I 4Oan! activation of theRI-A7IO4SI SYS4M

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    &reatment

    &reatment of OSAS !oes appear to lo%er bloo! pressurealthough the literature is inconsistent

    A recent ran!omi0e!, !ouble5blin!, placebo5controlle!stu!y compare! the effects of ( %ee6s of C+A+ versus

    sham5C+A+ versus supplemental nocturnal o1ygen on (5hour ambulatory bloo! pressure in B patients %ithmo!erate5severe OSA C+A+ therapy resulte! in a significant re!uction in !aytime mean

    arterial an! !iastolic bloo! pressure an! nighttime systolic, mean,

    an! !iastolic bloo! pressure Nocturnal supplemental o1ygen therapy improve! o1yhemoglobin

    saturation, it !i! not affect bloo! pressure*

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    eart an! "ascular Disease

    Marinet al publishe! results of-) year observational stu!y of primary snorers ) pt %ith untreate! mil! to

    mo!erate OSA ( pts %ith severe OSA %ho

    refuse! treatment ( pts %ith OSA treate! %ith

    C+A+ (B healthy pts

    &he en!points Emyocar!ialinfarction, stro6e, or acutecoronary insufficiency requiring

    invasive management, !eath ofmyocar!ial infarction or stro6eF%ere times as high in pts %ithuntreate! severe apnea as in thehealthy control in!ivi!uals

    Milleronet al prospectivelymonitore! patients %ith bothCAD ;

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    OSA an! Car!iovascular Disease Abnoralities associated &it* OSA ay be interediary ec*aniss t*atcontribute to t*e initiation and pro)ression o+ cardiac and %ascularpat*olo)y Sypat*etic acti%ation

    8ascoconstriction 4ac*ycardia Increased catec*olaines

    ndot*elial dys+unction Increased le%els o+ endot*elin ay contribute to sustained

    %asoconstriction 8ascular oidati%e stress

    "roduction o+ +ree radicals and %ascular &all isc*eia-reper+usionin#ury

    In+laation Increased R"

    Increased coa)ulation Metabolic dysre)ulation

    Insulin resistance

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    Conclusions

    OSA is implicate! in neuropsychological changesthat affect 3O'7 these changes can be mo!ifie!%ith treatment

    OSA has been i!entifie! as an in!epen!ent ris6factor for &N an! insulin resistance7 both ofthese outcomes appear to be mo!ifie! by treatment

    OSA is in!irectly implicate! in car!iac an!

    vascular !isease

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    3uestions

    Shoul! %i!er OSA screening be !one for patients%ith evi!ence of car!iovascular !iseaseJ

    .hat are the long term effects of OSA treatment in

    terms of car!iovascular morbi!ity an! mortalityJ.hich interventions for OSA yiel! the highest

    benefit for the patient at the lo%est costJ

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    3ui0 K-

    #p%orth scale A* /efers to an objective measure of !aytime somnolence

    ?* /efers to a subjective measure of !aytime somnolence

    C* 4s a scale use! to measure cognitive !ysfunction associate!%ith OSA

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    3ui0 K(

    4nsulin resistance: A* is relate! to obesity

    ?* is relate! to OSA

    C* is relate! to obesity an!, to a lesser e1tent, OSA

    D* is relate! to OSA an!, to a lesser e1tent, obesity

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    3ui0 K

    4nsulin sensitivity A* as been sho%n to mar6e!ly improve in pts %ith OSA only

    after several months of C+A+ use ?* as not been sho%n to mar6e!ly improve in pts %ith OSA

    C* as been sho%n to mar6e!ly improve in pts %ith OSA after( !ays of therapy %ith C+A+