SleepApneaSyndromeHealthsleepGoodsleephygieneiscriticalforone’soverallphysicalandmentalhealth.Normallyitshouldtakeabout10-15minutestofallasleepaftergoingtobed.Ifyouareasleepinlessthan5minutes,thatcouldbeasignofexcessivesleepiness.SleepStagesLightSleep.-Stage14-5%oftotalsleeptimeisconsiderednormalincreasesto15%byage70RestfulSleep.-Stage245-55%oftotaltimeDeepSleep.-DeltaorSlowWaveSleepcomposedofStages3and4-Rangeoftotalsleep:10-20%decreaseswithage-about40-50%inchildren-tototalabsencebyage40-50REM.-RapidEyeMovementsleep-20-25%totaltimegetbodyparalysis-atoniamindveryactiveveryvividhallucinatoryimageryordreamingDeltawavesSleepstage11secondSleepstage4Sleepstage2Spindlers(burstsofactivity)StagesofSleepIntroduction

1.Definition

It’sadisordercharacterizedbyrepetitiveepisodesofapneaand/orhypoventilationduringsleepwithaconstellationofsymptomsandsignsrelatedtosleepfragmentationandhypoxicexposure.

SAandSAS

Sleepapnea:anintermittentcessationofairflowatthenoseandmouthduringsleep.

apneas:atleast10s;most：20-30s;or2-3min.Apnea:completeairflowcessation>10s

(2respiratorycycles)

Hypopnea:airflowreduction>50%

(2respiratorycycles)Sleepapneasyndrome1.aclinicaldisorderthatarisesfromrecurrentapneasduringsleep.2.Sleepapneamorethan30timesduring7hsleeporAHI>5measuredbyovernightmonitoringAHI:apnoea/hypopnoeaindex.AHI=apnoea+hypopnoea/h,normal<5.3.itisoneoftheleadingcausesofexcessivedaytimesleepinessandcontributestoimportantcardiovasculardisorders.

2.Epidemiology

prevalenceofSASinpopulationofover40,UnitedStates:2%to4%Spain:1.2%to3.9%,Australia:6.5%,Japan:1.3%to4.2%ShanghaiChina:3.6%.Theprevalenceishigherinelderlyandpredominantinmale.

3.Classificationofsleepapnea

1)Centralsleepapnea2)Obstructivesleepapnea:thecommon3)Mixedsleepapnea4.GradeAHIMild5～15moderate15～30severe>30CentralSleepApneaSyndrome(CSAS)PureCSAS

isuncommon;maybeanisolatedfindingormayoccurinpatientswithprimaryalveolarhypoventilationorwithlesionsofthebrainstem.Thepathogenesismayinvolvethefollowingmechanisms:(1)Suppressionofrespiratorycenter.(2)Reducedresponsetohypoxemiaandhypercapnia.(3)Abnormaltransitionofexpirationtoinspiration.Obstructivesleepapneasyndrome

(OSAS)DefinitionCessationofairflowatthenoseandmouthduringsleepdespitecontinuingrespiratoryandabdominaldrive.Itisacommonconditioncharacterizedbyrepetitiveepisodesofpartialorcompleteupperairwayobstructionduringsleep.

I.EtiologyOducingsympatheticnervoussystemactivationandsleepfragmentationwithadverseeffectsonbothdaytimefunctioningandcardiovascularoutcomes.OSAsyndrome(OSAS):AnAHIof>5associatedwithdaytimesymptoms

Ⅱ.Epidemiology

.

Prevalence:OSAS:1-3%Primarysnoring(PS):3-12%twothirdsareobeseGender:

M/Fratio3:1(Adults:malepredominance)

Age:(children)FromneonatestoadolescentsCommonestinpreschoolchildren(2-5y)(Peakincidenceofadenotonsillarhypertrophy)Race:

MorecommoninAfrican-American??

Ⅲ.Pathogenesisandpredisposingfactors

1.Obesity(astrongriskfactor)

a.FatdepositionaroundtheUAcausenarrowingandabnormalcompliance,predisposingtoUAclosure.

b.Abdominalobesityreducelungvolume,furtherreducingUAsize.

NarrowingorcollapseofUAduringsleepistheprimaryabnormalityinOSAS.Ⅲ.Pathogenesisandpredisposingfactors2.Craniofacial/inheritedfeatures

micrognathia,retrognathia.3Gender-higherinmen(2-3-fold):

1)effectsofandrogenontheUA2)centralfatdepositioninmales

3)differencesinairwayshape(pharyngealairways:menlonger).

Ⅲ.Pathogenesisandpredisposingfactors

4.Reducedmuscletone

alcohol:reducesUAmuscletone,increasesobstructive,reducesarousalresponsesapneawithgreateroxygendesaturation.5.Nasalobstruction

Rhinitis,adeviatedseptumleadstoincreasedapnea,hypopnoeaandarousal.

Nasalcongestionisalsostronglyassociatedwithsnoring.

ChildrenOSASVastmajorityareassociatedwithadeno-tonsillarhypertrophy(AT-Ht)ObesityinchildrenisariskfactorforOSAS,theseverityisproportionaltothedegreeofobesityDeficitinarousalmechanismsAbnormalcentrallymediatedactivationofUAmusclesAnatomicalFactorsNeuromuscularFactorsadenotonsillarhypertrophynasalobstructionhypothyroidismacromegalyDownsyndromesedativeuseAlcoholSmokingmicrognathiaretrognathiaObesityNeckcircumferencevocalcordparalysisH&NmassesRiskfactorsIV.Clinicalmanifestation

1.commonsymptoms1)heavysnoring–characteristics2)excessivedaytimesleepiness3)witnessedapneas:stopbreathingwhilesleeping-then.snort4)nocturnalgasping5)morningheadaches6)unrefreshingsleep7)moodchanges(irritabilityanddepression).

SituationChanceofdozingSittingandreadingWatchingTVSittinginactiveinapublicplace(e.gatheaterorameeting)AsapassengerinacarforanhourwithoutabreakLyingdowntorestintheafternoonwhencircumstancespermitSittingandtalkingtosomeoneSittingquietlyafteralunchwithoutalcoholInacar,whilestoppedforafewminutesintrafficSleepinessscoreIV.Clinicalmanifestation

2.Respiratorysystem:abnormallungfunction,rightheartfailure3.Cardiacsystem:hypertension,heartfailure4.Othersystem:glycemia,erythrocytosis,cerebraldysfunctiondiabetesrestlesssleeppersonalitychangeimpairedcognitiveskillsPoorjobperformanceweightgainGastroesophagealrefluxHypertensionsmouth-breathing“tired”appearancemorningheadachenocturia/enuresissexualdysfunctionRoadtrafficaccidentsSymptomsofOSASinadults.Snoring.Hyperactivity.Developmentaldelay.Poorconcentration.Bedwetting.Nightmares.NightterrorsSymptomsofOSAinChildrenHeadachesRestlesssleepsObesityLargetonsilsNoisybreathersChronicrunnynosesFrequentUAinfectionsEnuresisADHDattentiondeficit/hyperactivitydisorderIV.Clinicalmanifestation

2.Examination

1).ItshouldincludecarefulinspectionoftheUAforpharyngealcrowding,nasalobstructionandotherpredisposingcraniofacialfeatures.2).AdenotonsillarhypertrophyisimportantinthepathogenesisofOSAinchildrenandadolescents.2.ExaminationHighbloodpressureNasalobstruction-turbinatehypertrophy,polyposis,septaldeviationoralcavityandoropharynxredundantmucosaelongateduvulaMacroglossiaIV.Clinicalmanifestation

3.Investigations:PSGAnovernightsleepstudy(polysomnography,PSG)isthegold-standardinvestigationinOSASandothersleepdisorders.central,obstructive,mixedapneasapnea-cessationofflowfor10shyponea-50%decreaseinfloworEEGarousal

PSGthereportshouldincludemovements.1)thetotalamountofsleep2)theproportionsofdifferentsleepstages3)thenumberofrespiratoryevents(AHI)4)theminimumrecordedoxygensaturation.5)thenumberofEEGarousals6)thepresenceorabsenceofperiodiclegOSAS:PSGscreenChinEMGECGAirflowPeripheralPulseVolumeBPLegMt.OximetryEEGEEGEOGECGsubmentalEMGanteriortibialisEMGnasalandoralairflowrespiratorymuscleeffortoxygensaturationsleeppositionTypeofstudies:FullnightPSGMultiplesleeplatencySplitnightPSGScreeningwithportabledevicesPolysomnographyTheprimarysequenceofevents,physiologicresponses,clinicalfeaturesofOSA

Ⅴ.Differentialdiagnosis1.SimpleSnorerwithoutapnea,hypopneaanddesaturation,PSGnormal.2.UAResistanceSyndromearousalsfromsleepareassociatedwithincreasedairwayresistance,noobstructivehypopneaordesaturationPSG.

3.

Narcolepsyexcessivedaytimesleepinessandcataplexy.PSGandmultiplesleeplatencytest(MSLT).SL<10mininPSG,<8mininMSLT.Ⅴ.TreatmentTreatmentmodalitiesdependson:Severityofthepatient’ssymptoms:daytimesleepiness,sleepfragmentationResultsofthePSG:AHI,oxygendesaturationImpactoncomorbiditydiseasessuchasCHFⅤ.Treatment

1.Weightloss:10-30%reducestheseverity,butimprovementmaynotbelong-term.2.BodyPosition3.Lifestylefactors-alcoholandsedativesavoided.4.orthodonticdevices5.CPAP(Continuouspositiveairwaypressure):themosteffective6.Surgery

orthodonticdevicesTreatment-CPAP100%effectiveifobstructionisexcludedtitratepressurepoorcompliance-50-80%Compliancemayimprovewi