姚晨玲-镇静催眠药中毒课件

Toxicity,Sedative-Hypnotics

中山急诊姚晨玲Background

Sedative-hypnoticsareagroupofdrugsthatcauseCNSdepression.Benzodiazepines(BZD)barbituratesnonbarbituratenonbenzodiazepinesedative-hypnotics(NBNB)themostcommonlyusedagentsBackgroundacutesedative-hypnoticspoisoningwithdrawalsyndromeEtiologyBarbiturates

UltrashortactingMethohexital(Brevital甲己炔巴比妥)thiopental(Pentothal硫喷妥那)Shortactingpentobarbital(Nembutal戊巴比妥)secobarbital(Seconal司可巴比妥)IntermediateactingAmobarbital(Amytal异戊巴比妥)butalbital(Fioricet,Fiorinal异丁巴比妥) LongactingPhenobarbital(Luminal鲁米那)Nonbarbiturate,nonbenzodiazepinesedative-hypnotics(NBNB) Chloralhydrate(水合氯醛) Ethchlorvynol(乙氯维诺) Glutethimide(导眠能) Methyprylon(甲乙哌酮) Meprobamate(眠尔通)Etiology一、Pharmacokinetics

：1、PharmacokineticsoftheBZDMostBZDareextensivelymetabolizedbytheliver.Somearemetabolizedtoproductswhichareactiveandmayhaveamuchlongerhalflifethantheparentdrug.ThemajorrouteofmetabolismisN-demethylation. intheelderly

Cimetidine

PathogenesisPathogenesis2、PharmacokineticsofBarbituratesBarbiturateswithlowlipidsolubilityareexcretedintheunchangedformbythekidneys.iephenobarbital（苯巴比妥）.Barbiturateswithhighlipidsolubilityaremetabolizedtomorepolarcompoundsintheliverbeforebeingexcretedviathekidneys.iethiopental（硫喷妥）.

BZD IntheCNS,benzodiazepinesexerttheirclinicaleffectbyenhancingtheactivityoftheinhibitoryneurotransmitterGABA. (TheclinicaleffectsofGABAreleaseandGABA-gatedchloridechannelsincludesleepinductionandexcitementinhibition)Barbiturates inprolongationofthedurationofopeningofGABA-gatedchloridechannels,leadingtohyperpolarizationofthemembraneandsuppressionofneurotransmission.。NBNB similartotheactionofBarbiturates二、ThemechanismofactionPathogenesisClinicalBenzodiazepineblurredvision,dizziness,confusion,drowsiness,anxiety,agitation,andunresponsivenessorcoma.BZDoverdoseinitselfisremarkablysafe.mostpatientswithbenzodiazepineoverdosecanbemanagedintheEDandreleasedhomeafterappropriatecare.Whencombinedwithothersedatives(mostfrequentlyalcohol),patientswithbenzodiazepineoverdosecanpresentwithprofoundlydepressedlevelsofconsciousness..

ChloralhydrateMildintoxicationischaracterizedbyataxia,lethargySeverepoisoningleadsto

stupor,coma,pinpointpupils,hypotension,sloworrapidandshallowrespiration,hypothermia,areflexia,andmuscleflaccidity.ArrhythmiasClinicalClinicalGlutethimide(Doriden)LossofbrainstemreflexesFlaccidityAnticholinergiceffectsDelayedgastricemptyingMaycausehyperthermiaorheatstrokeMethaqualone(Quaalude)ResemblesbarbituratepoisoningHasmorepronouncedmotorproblems(eg,ataxia)andisknownaswallbangerbecauseofthisphenomenon.CanleadtoseveremuscularhypertonicityandseizuresClinicalLabStudies

Obtainacompletebloodcount(CBC),arterialbloodgas(ABG),glucose,chemistry,ImagingStudies:

Obtainanabdominalx-ray.Chloralhydrateisradiopaque.OtherTests:Obtainanelectrocardiogram(ECG);Co-ingesteddrugsmayhavedirectcardiaceffects(eg,tricyclicantidepressants).

QuantitativeserumdrugconcentrationsarerecommendedforpatientswithserioustoxicityBarbiturates:Forshort-actingdrugs,thelethaldoseis3goraserumconcentrationhigherthan3.5mg/dL.Forlong-actingdrugs,thelethaldoseis5-10goraconcentrationhigherthan8mg/dL.Chloralhydrate:Thelethaldoseis10gandaconcentrationhigherthan100mg/mListoxicLabStudies

DifferentialsToxicity,AlcoholsHypoglycemiaDiabeticKetoacidosisNeoplasms,BrainTreatmentEmergencyDepartmentCareEstablishABCs,obtainIVaccess,provideoxygenEnsureadequateairwayandventilation.Doendotrachealintubationifnecessary.Fluidresuscitationandanti-shockNaloxoneisrecommendedtothepatientswithcomma.EliminationenhancementAlkalinediuresisenhanceseliminationofphenobarbitalandotherlong-actingbarbiturates.Itisrecommendedforallsymptomaticpatientswithlong-actingbarbituratetoxicity.Con