化学物品中毒现场急救课件.ppt

1、Contents Background General introduction Acute Organophosphate poisoning Acute carbon monoxide poisoning Acute sedatives-hypnotics poisoning Alcohol Intoxication/WithdrawalBackground There are about 9000000 kinds of chemicla People have many opportunity to touch with poisonBackgroundThere are 175147

2、6 poisoning pts in USA in 1993Poison control center(PCC)is established in Chicago 1953。Major duty:ponent of poison;4.information2.Dangerous 5.toxicology3.first aid 6.general knowledge of preservationBackground Countryside city。Countryside-pesticide intoxication。City-food-poisoning,carbon monoxide po

3、isoning,Hypnotic intoxication。Establish PCC in Beijing,Shanghai,Shenyang What is poison?A poison is anything someone eats(ingestion),breathes(inhalation),gets in the eyes(ocular exposure),or on the skin(dermal exposure),that can cause sickness or death if it gets into body or on the body.Poison can

4、be found in four forms:solid,liquid,spray and gas.General introduction toxic substance:drug,chemical,bad food and so on.Acute poisoning：short time，large dose Chronic poisoning：long time、small doseEtiopathogenisis and pathogenesy Cause of a poisoning Occupational poisoning Life poisoningnAccidental p

5、oisoning,nSuicidalnAbuse，addication ,homicdalPathogenesy-Absorption By mouth;inhalation（Powder dust、smoke、steam）,skin mucosa,muscle or intravenous injection Rectum、urinary canal、female sheath vagina、bladder、peritoneum、eye Insect stings or bitePathogenesis-metabolism spread all over body by blood liv

6、er metabolismPoisonousnessPoisonousnessOxidation,deoxidize,hydrolyse,bondingPathogenesis-Eliminate breathe out by respiratory tract（gas，volatile matter）Discharge by kidney Discharge by alimentary tract Skin Milk 1.Local effect强酸、强碱强酸、强碱吸收组织水分吸收组织水分与蛋白质脂肪结合与蛋白质脂肪结合组织细胞变性坏死组织细胞变性坏死2.Hypoxia 1)Inhibiti

7、on respiratory function：2)Change blood constituent3)Inhibition cells respiratory：cyanide，hydrogen sulfide4)Destroy Cardiovascular function1)1)破坏酶蛋白质部分的金属或活性中心破坏酶蛋白质部分的金属或活性中心氰化物抑制细胞色素氧化酶氰化物抑制细胞色素氧化酶FeFe+；一一氧化碳抑制细胞色素氧化酶氧化碳抑制细胞色素氧化酶FeFe+从而破从而破坏酶蛋白质分子中的金属，使细胞发生坏酶蛋白质分子中的金属，使细胞发生窒息窒息2)2)毒物与基质竞争同一种酶而产生抑制作

8、毒物与基质竞争同一种酶而产生抑制作用用,丙二酸结构与琥珀酸相似，抑制三丙二酸结构与琥珀酸相似，抑制三羟酸循环中琥珀酸脱氢酶羟酸循环中琥珀酸脱氢酶3.Inhibitory enzyme activity3)3)与酶的活性剂作用：与酶的活性剂作用：氟化物与氟化物与MgMg+形成复合物，使形成复合物，使MgMg+失去激活磷酸葡萄失去激活磷酸葡萄糖变为酶的作用糖变为酶的作用4)4)去除辅酶：去除辅酶：铅中毒时，造成烟酸的铅中毒时，造成烟酸的消耗增多，使辅酶消耗增多，使辅酶I I和辅酶和辅酶IIII减少，抑减少，抑制了脱氢酶的作用制了脱氢酶的作用5)5)与基质直接作用：与基质直接作用：氟乙酸直接与柠氟乙

9、酸直接与柠檬酸相结合形成氟柠檬酸，阻止三羧酸檬酸相结合形成氟柠檬酸，阻止三羧酸循环的继续进行循环的继续进行 Organophosphate poisoning，可抑制体内的，可抑制体内的胆碱酯酶，使组织中乙酰胆碱过量积蓄，引胆碱酯酶，使组织中乙酰胆碱过量积蓄，引起一系列以乙酰胆碱为传导介质的神经处于起一系列以乙酰胆碱为传导介质的神经处于过度兴奋状态，最后则转为抑制过度兴奋状态，最后则转为抑制Carbon tetrachloride poisoning，首先作用于，首先作用于CNSCNS，使之产生交感神经冲动，体内产生大量，使之产生交感神经冲动，体内产生大量单胺类物质，使内脏血管收缩引起供血不足

10、，单胺类物质，使内脏血管收缩引起供血不足，中毒数小时后可出现肝、肾损害中毒数小时后可出现肝、肾损害 4.Dromotropism medium1.一氧化碳与氧竞争血红蛋白，而一氧化碳与氧竞争血红蛋白，而形成碳氧血红蛋白，破坏了正常的形成碳氧血红蛋白，破坏了正常的输氧功能输氧功能2.2.异烟肼与维生素异烟肼与维生素B B及烟酸的结构相及烟酸的结构相似，因此，异烟肼在体内可与维生似，因此，异烟肼在体内可与维生素素B B竞争，而取代其作用，因而引竞争，而取代其作用，因而引起中毒起中毒5.Competition receptor6.Interfere cell or organella physiol

11、ogic function carbon tetrachloride（CCl4）CHCl3（trichlormethane)肝细胞膜中的肝细胞膜中的unsaturated fatty acidlipid peroxidationmitochondria(线粒体线粒体)、endoplasmic reticulum(内质网内质网)变性变性hepatocyte(肝细胞肝细胞)death Phenols(酚类酚类)线粒体内线粒体内oxidative phosphorylation(氧化磷酸化氧化磷酸化)uncoupling(解偶解偶联联)inhibiting adenosine triphosphat

12、e(三磷三磷酸腺苷酸腺苷)synthesis(合成合成)、store(贮存贮存)。The factor of influence toxic action Physico-chemical property of poison fine particle,solubility,evaporability Susceptibility of individual sex,age,nutrition,health status,living habit Diagnosis poisoning History Sign and symptom conscious state breathing he

13、art rate blood pressure pupil,skin,mucosaLaboratory examination Detection of poison:blood,gastric juice and urine Blood,urine examinationTherapeutic principleCPRGet rid of the environmentDecrease AbsorptionSpecific antidotes Cleaning poison in gastrointestinal tractHeteropathyPrevent ComplicationEme

14、rgent management Breathing support Circulation support Treatment coma Treatment convulsionSPECIFIC ANTIDOTESOrgnaophosphorus-Pralidoxime Iodide，AtropineBenzodiazepinesFlumazenilPain-killerNaloxoneIsoniazidvitamin B6Eliminate poison Emetic Gastric lavage Activated carbon adsorption Catharsis Whole-bo

15、wel irrigationEmetic压舌板、刺激咽后壁压舌板、刺激咽后壁饮温水饮温水200-300ml200-300ml吐根糖浆吐根糖浆+200ml+200ml水水休克、意识不清休克、意识不清禁用禁用摄入腐蚀性毒物摄入腐蚀性毒物-禁用禁用Purpose of Gastric lavageEliminate poison in gastric,prevent absorbPreparation for operation or some examinationIndication and contraindication Indication Non-corrosive poison Con

16、traindication Corrosive poisonstrong acid,baseesophageal varix,aneurysm of aortaSevere heart disease，upper gastrointestinal bleeding，gastric perforationPrinciple of gastric lavage一般毒物的洗胃原则一般毒物的洗胃原则 一次性彻底洗胃一次性彻底洗胃（10000-20000ml）、）、停止洗胃标准为无色无味。停止洗胃标准为无色无味。有机磷中毒的洗胃原则有机磷中毒的洗胃原则 首次足量首次足量 20000-30000ml 持续

17、胃肠减压持续胃肠减压 留置胃管接胃肠减压器留置胃管接胃肠减压器 反复少量洗胃反复少量洗胃 2000-5000ml/1-2h洗胃的操作步骤洗胃的操作步骤洗胃步骤：洗胃步骤：1.先将胃内容物尽量抽尽先将胃内容物尽量抽尽 2.灌入灌入300-500ml洗胃液洗胃液 3.再排出灌入液体再排出灌入液体 4.反复灌洗直到洗胃液纯清无味反复灌洗直到洗胃液纯清无味 注意事项注意事项:1.洗胃液每次进入不宜过多，进出要平衡。洗胃液每次进入不宜过多，进出要平衡。2.洗胃液性质尽可能视毒物而定，液温洗胃液性质尽可能视毒物而定，液温37 3.掌握适应症与禁忌症掌握适应症与禁忌症 洗胃要注意和观察的几个问题洗胃要注意和

18、观察的几个问题 洗胃与胃出血的关系洗胃与胃出血的关系 少量可给保护胃少量可给保护胃粘膜药，大量停止洗胃、持续胃肠减压粘膜药，大量停止洗胃、持续胃肠减压观察出血情况观察出血情况 洗胃时要密切观察生命体征、腹部情况、洗胃时要密切观察生命体征、腹部情况、洗出液的性质洗出液的性质Catharsis and Whole-bowel irrigation 硫酸钠硫酸钠-15-20+水水200口服口服 硫酸镁硫酸镁-15-20+水水200口服（引起高血镁）口服（引起高血镁）20%甘露醇甘露醇250胃管内灌入胃管内灌入-1小时腹泻、小时腹泻、3小时排空。小时排空。1%盐水、肥皂水盐水、肥皂水5000-高位连续

19、灌肠清高位连续灌肠清洗洗 活性炭加入灌肠液，促进毒物吸附排出活性炭加入灌肠液，促进毒物吸附排出 Eliminate poison Forced diuresis 强化利尿强化利尿 Blood purification（血液净化）（血液净化）hemodialysis HD（血液透析）（血液透析）hemoperfusion,HP（血液灌流）（血液灌流）plasma exchange PE（血浆置换）（血浆置换）High pressure oxygen 高压氧高压氧Hemodialysis HD血液透析血液透析 机理：血液经体外循环进入透析器，通过透析机理：血液经体外循环进入透析器，通过透析膜和透析

20、液之间形成的膜和透析液之间形成的溶液浓度梯度溶液浓度梯度，促使血，促使血液内液内溶质弥散溶质弥散至透析液内。至透析液内。可透析毒物的性质：可透析毒物的性质：water-solubility水溶性、水溶性、heavy metals,生物性毒物。生物性毒物。种类：蛇毒、鱼胆、利眠宁、种类：蛇毒、鱼胆、利眠宁、diamorphine海海洛因洛因、扑热息痛、扑热息痛、Isoniazid异烟肼异烟肼、aminoglycosides氨基糖甙类、氨基糖甙类、arsenic砷、砷、mercury汞等。汞等。Hemoperfusion HP血液灌流血液灌流 机理：血液流经灌流器，血液中的毒物机理：血液流经灌流器

21、，血液中的毒物被吸附到具有广大表面积的吸附剂上。被吸附到具有广大表面积的吸附剂上。吸附剂：活性炭、合成树脂吸附剂：活性炭、合成树脂 毒物性质：脂溶性、大分子化合物、易毒物性质：脂溶性、大分子化合物、易与血浆蛋白结合的药物、毒物。与血浆蛋白结合的药物、毒物。种类：安定类、苯巴比妥类、抗抑郁类、种类：安定类、苯巴比妥类、抗抑郁类、有机磷类、伴有肝衰竭、肾衰竭者。有机磷类、伴有肝衰竭、肾衰竭者。plasma exchange PE血浆置换血浆置换 机理：将血液引入血浆分离器中，使血机理：将血液引入血浆分离器中，使血细胞与血浆分离，弃去全部血浆，注入细胞与血浆分离，弃去全部血浆，注入新鲜血浆和平衡液。

22、新鲜血浆和平衡液。毒物性质：与血浆蛋白结合率高（大于毒物性质：与血浆蛋白结合率高（大于60%）Acute Organophosphate poisoningAcute Organophosphate poisoning Feature：毒性大、起病快毒性大、起病快;发病迅速；发病迅速；中毒途径多；诊断要快、准确；抢救及中毒途径多；诊断要快、准确；抢救及时。时。Classify 分类：分类：剧毒、高毒、中毒、低毒剧毒、高毒、中毒、低毒 Acute Organophosphate poisoning Etiopathogenisis：Accidental suicide Pathogenesis：

23、Poison metabolism mechanism acute poisoning;chronic poisoningOrganophosphate Absorption:readily Distribution:blood brain barrier Metabolism:in the liver Elimination:primarily in the urine Half-life:4 hoursMechanism 体内胆碱能神经的化学介质体内胆碱能神经的化学介质-乙酰胆碱乙酰胆碱 交感、副交感神经节前纤维交感、副交感神经节前纤维 副交感神经节后纤维副交感神经节后纤维 横纹肌的运动神

24、经横纹肌的运动神经-肌肉接头肌肉接头 交感神经节后纤维（交感神经节后纤维（支配泪腺、血管平滑支配泪腺、血管平滑肌）肌）中枢神经系统中枢神经系统胆碱能神经末梢胆碱能神经末梢-胆碱酯酶胆碱酯酶CENTRAL NERVOUS SYSTEMACh(nic)Skeletal MuscleACh(nic)ACh(nic)ACh(nic)ACh(nic)NA ACh(mus)ACh(mus)Blood vessels etcSweat GlandsAdrenal medullaSalivary glandsetcPara-sympathetic systemCholine receptor Muscarin

25、ic receptor（M-R）毒蕈碱 n heart:restrainnblood vessel：dilatationn smooth muscle：contractnsphincter pupillae muscle:contractncontractglandular organ:secrete Nicotinic receptor（N-R）烟碱N1-R：gangliocyte;ganglioneureexcited N2-R：skeletal musclecontract急性有机磷中毒急性有机磷中毒-机理机理 有机磷毒物与有机磷毒物与胆碱酯酶胆碱酯酶acetylcholinestera

26、se(AchE)结合，形结合，形成磷酰化胆碱酯酶，失去水解活性，成磷酰化胆碱酯酶，失去水解活性，造成造成乙酰胆碱乙酰胆碱acetylcholine蓄积蓄积产生产生毒蕈碱毒蕈碱（M）样、）样、烟碱烟碱（N）样症状）样症状和和中枢神经中枢神经系统的症状。系统的症状。The organophosphates are powerful inhibitors of carboxylic ester hydrolases,including acetylcholinesterase(found in nervous tissues and erythrocytes)and butyrylcholinest

27、erase(plasma or pseudocholinesterase).As a result of this enzyme inhibition,the substrate acetylcholine accumulates急性有机磷中毒急性有机磷中毒-机理机理 中枢神经系统：脑内中枢神经系统：脑内Ach含量增高含量增高-大脑大脑多部位先兴奋后抑制。多部位先兴奋后抑制。惊厥、呼吸中枢惊厥、呼吸中枢抑制。抑制。神经神经-肌肉接头：神经肌肉接头：神经-肌肉接头的传递肌肉接头的传递阻断，导致肌无力和肌麻痹。阻断，导致肌无力和肌麻痹。呼吸系统：呼吸肌麻痹、气道分泌物阻呼吸系统：呼吸肌麻痹、气道分

28、泌物阻塞。塞。急性有机磷中毒急性有机磷中毒-机理机理 循环系统：循环系统：*对心脏直接毒性对心脏直接毒性：心动过缓、心肌收缩力：心动过缓、心肌收缩力降低、各种心律失常降低、各种心律失常 *抑制交感心血管中枢抑制交感心血管中枢：外周血管扩张、血：外周血管扩张、血压下降。压下降。*兴奋心血管迷走中枢：兴奋心血管迷走中枢：心动过缓、心肌收心动过缓、心肌收缩力降低、血压下降。缩力降低、血压下降。神经节、腺体、平滑肌：腺体分泌增加、肠蠕神经节、腺体、平滑肌：腺体分泌增加、肠蠕动增加。动增加。中毒途径及特点中毒途径及特点 呼吸道吸收：呼吸道吸收：有机磷沸点低、易挥发，有机磷沸点低、易挥发，易从呼吸道吸收易

29、从呼吸道吸收,30min发病。发病。消化道吸收：消化道吸收：吸收快、吸收快、10min2h发病。发病。皮肤黏膜吸收：皮肤黏膜吸收：有机磷是脂溶性，能透有机磷是脂溶性，能透过皮肤黏膜入血，潜伏期长、过皮肤黏膜入血，潜伏期长、26h发病。发病。主要致死因素：呼吸衰竭主要致死因素：呼吸衰竭Symptoms and Signs Muscarinic:SLUDGE,bronchorrhea,bradycardia and miosis.Nicotinic:muscle weakness,fasciculation or paralysis tarchycardia,bronchodilation,myd

30、riasis.CNS:restless,drowsy,confusion,tremor,ataxia,delirium,seizure,coma.Muscarinic effects 毒蕈碱毒蕈碱（M）UrinationMiosisBronchospasmEmesisLacrimationSalivationBradycardia hypotension尿频、尿失禁尿频、尿失禁缩瞳，视力模糊缩瞳，视力模糊气管痉挛，分泌增加气管痉挛，分泌增加呕吐、腹泻、腹痛呕吐、腹泻、腹痛流泪、流汗、流口水流泪、流汗、流口水肺水肿肺水肿心跳减慢，心跳减慢，血压下降血压下降nicotinic manifestat

31、ions.muscular twitching,fasciculation,tachycardia,hypertension central nervous system manifestations:Headache头痛头痛,Drowsiness 昏睡昏睡,Confusion 意识混乱意识混乱,Slurred speech言语不清言语不清,Emotional lability 情感不稳情感不稳,Ataxia 共济失调共济失调,Tremor 震颤震颤,Delirium 精神错乱精神错乱,Seizure 癫痫癫痫.Restrain center of breath and circulatede

32、gree Slight ：ChE 50-70%。Muscarinic symptom and sign;Midrange：ChE 30-50%,Muscarinic symptom and sign,nicotinic effects Heavy：ChE 30%,Muscarinic,nicotinic，central nervous system symptom and signDelayed neuropathy 急性中毒症状消失后急性中毒症状消失后2-3周周 motoriusthe lower limbs palsy麻痹麻痹,amyotrophy肌萎缩肌萎缩 Nerve fibrofat

33、ty degeneration,nerve cell demyelinate脱髓鞘脱髓鞘 有机磷有机磷抑制抑制神经病靶酯酶（神经病靶酯酶（neuropathy target esterase，NTE)Delayed neuropathy stages Progression：sense neuropathy Stable phase：sensory disability last 312 month：618 month motor function partly or complete recovery，spasm,motor nerve functional disturbance。Inte

34、rmediate syndrome 发生在急性中毒恢复后发生在急性中毒恢复后14天天 瘫痪（颈屈肌、脑神经支配的肌肉、肢瘫痪（颈屈肌、脑神经支配的肌肉、肢体近侧肌、呼吸肌）体近侧肌、呼吸肌）418天缓解天缓解 严重者呼吸衰竭严重者呼吸衰竭 神经肌肉接头处突触后功能障碍神经肌肉接头处突触后功能障碍Laboratory examination serum cholinesterase Organophosphate metabolic product othersDiagnosis History garlic-like odor蒜臭味蒜臭味 typical symptom：Pupil size

35、small,胃胃肠肠道道 症状、症状、coma。Laboratory examination：serum cholinesterase,Organophosphate metabolic product。Atropine test：1-2mg-atropinizationDifferential diagnosis Muscarinic poison globe fish poison acute gastroenteritis;AGE Heatstroke Hypnotic intoxication Pesticide intoxicationTherapeutic principleGet

36、 rid of the environment Cannot use the hot waterEliminate the poison queasy、gastric lavageSpecific antidotes Atropine、PAMHeteropathy Oxygen therapy、diuresisEmergency Management Airway Breathing Cardiopulmonary resuscitation;CPR CNS：convulsion use valium and phenobarbital，forbid use Succinylcholine o

37、r Morphine。Cerebral edema：mannitol、glucocorticosteroid pneumonedema：Atropine，aminophylline and morphine cant be useSpecific antidotes Cholinesterase resurrecter胆碱酯酶复活胆碱酯酶复活剂剂N样症状效果好样症状效果好 碘解磷定碘解磷定(pyraloxime methoiodide)氯磷定（氯磷定（pyraldoxime methylchloride）Atropine,block muscarinic receptors,causing i

38、nhibition of all muscarinic functions.Early,enough,association,repetitions阿托品类生物碱阿托品类生物碱-莨 菪 碱颠茄曼佗罗The effect of Atropine atropine poisoning1.BLURRED VISION2.CONFUSIONa;5.CONSTIPATION6.URINARY7.RETENTION atropinization1.mydriasis2.Tachycardia3.Blushing4.Skin and mucousdry 5.dry6.crackles disappearSy

39、mptomatic treatment keeping Water-Electrolyte and acid-base balance Prevention and cure pulmonary infection make use of sedative Plasmapheresis Prevention and cure intermediate syndromeAcute carbon monoxide poisoningAcute carbon monoxide poisoning 无色、无臭、不溶于水的窒息性气体无色、无臭、不溶于水的窒息性气体 比重：比重：0.967 含碳物质不完全

40、燃烧产生的气体含碳物质不完全燃烧产生的气体 空气中最高允许浓度空气中最高允许浓度0.05%或或30mg/m3 吸入过量可发生急性中毒吸入过量可发生急性中毒Acute carbon monoxide poisoning浓度，浓度，暴露时间，暴露时间，min 症状症状0.0005 100 无明显症状无明显症状0.003 360 对中枢神经有害对中枢神经有害0.04-0.05短时间短时间 呼吸困难呼吸困难0.05-0.1短时间短时间 头痛、晕眩头痛、晕眩0.1-0.2 短时间短时间 短时间内死亡短时间内死亡1 短时间短时间 立即死亡立即死亡Acute carbon monoxide poisonin

41、g Etiology livingpoisoning burn coalwater-heateroccupational poisoningmisoperationNo protectionAccidental poisonincoal mineaccidentSuicidalhomicdalMechanismCO+Hb COHbCO+Fe+restraint cell respirationCant carrying oxygenhypoxiaCO+HbO2+Hb=260CO-HbO2-Hb=36001Clinical manifestation Slight：HbCO10-20%，头痛、眩

42、晕、心悸、恶心、呕吐、短暂晕厥。吸空气可好转。Midrange：HbCO30-40%，昏迷、虚脱。皮肤樱桃红。吸空气或高压氧可很快清醒，数日恢复，不留后遗症。Heavy：HbCO50%，深昏迷、各种反射消失、瞳孔散大、血压下降呼吸抑制。严重者昏迷数天出现脏器功能障碍。临床表现-迟发脑病 意识障碍恢复后 经过2-60天的“假愈期”3%-10%病人出现脑病：神经意识障碍：痴呆、谵妄、去皮层状态。锥体外系神经障碍：震颤麻痹综合征。锥体系神经损害：偏瘫、病理反射（+）大脑皮层局灶性功能障碍：失语、失明、继发癫痫。Laboratory examination 血血COHb测定：特异性、判断严重程度测定：

43、特异性、判断严重程度 动脉血气分析动脉血气分析 脑电图：弥漫性低波幅慢波脑电图：弥漫性低波幅慢波 头部头部CT：具有鉴别诊断意义：具有鉴别诊断意义诊断和鉴别诊断诊断和鉴别诊断 有吸入有吸入CO病史病史 典型临床表现典型临床表现 实验室检查：定性或定量阳性、心肌酶实验室检查：定性或定量阳性、心肌酶增高增高 其他：心电图、头颅其他：心电图、头颅CT、脑电图、脑电图 除外：安眠药中毒，其他有毒气体中毒、除外：安眠药中毒，其他有毒气体中毒、脑血管意外、糖尿病酮症酸中毒脑血管意外、糖尿病酮症酸中毒Emergency treatmentGet rid of the environmentOxygen th

44、erapy：Hyperbaric oxygen treatment only after severe carbon monoxide poisoning in otherwise stable patients respiratory failure：mechanical ventilationexchange blood,blood transfusionDiuresis:prevention and cure brain edema promote recovery of function：sugar、vitaminATP、coenzymeA、cytochromeC。acute seda

45、tives-hypnotics poisoningBackground Sedative-hypnotics are a group of drugs that cause CNS depression.Benzodiazepines(BZD)barbiturates nonbarbiturate nonbenzodiazepine sedative-hypnotics(NBNB)the most commonly used agents Background acute sedative-hypnotics poisoning withdrawal syndromeEtiologyBenzo

46、diazepines(BZD)Long acting(half life 30h):chlordiazepoxide(利眠宁利眠宁)diazepam（地西泮、安定）（地西泮、安定）flurazepam（氟安定）（氟安定）Short acting(half life 6-30h):alprazolam(阿普唑仑阿普唑仑)Ultrashort acting:triazolam(三唑仑三唑仑)Etiology Barbiturates Ultrashort acting Methohexital(Brevital甲己炔巴比妥甲己炔巴比妥)thiopental(Pentothal硫喷妥那硫喷妥那)Sh

47、ort acting pentobarbital(Nembutal戊巴比妥戊巴比妥)secobarbital(Seconal司可巴比妥司可巴比妥)Intermediate acting Amobarbital(Amytal异戊巴比妥异戊巴比妥)butalbital(Fioricet,Fiorinal异丁巴比妥异丁巴比妥)Long acting Phenobarbital(Luminal鲁米那鲁米那)Nonbarbiturate,nonbenzodiazepine sedative-hypnotics(NBNB)Chloral hydrate(水合氯醛)Ethchlorvynol(乙氯维诺)Gl

48、utethimide(导眠能)Methyprylon(甲乙哌酮)Meprobamate(眠尔通)Etiology一、Pharmacokinetics：Pharmacokinetics of the BZD Most BZD are extensively metabolized by the liver.Some are metabolized to products which are active and may have a much longer half life than the parent drug.The major route of metabolism is N-deme

49、thylation.in the elderly Cimetidine PathogenesisPathogenesis2、Pharmacokinetics of Barbiturates Barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys.ie phenobarbital（苯巴比妥）.Barbiturates with high lipid solubility are metabolized to more polar compounds in the liver

50、before being excreted via the kidneys.ie thiopental（硫喷妥）.3、Pharmacokinetics of NBNB Most NBNB are extensively metabolized by the liverPathogenesisw BZD In the CNS,benzodiazepines exert their clinical effect by enhancing the activity of the inhibitory neurotransmitter GABA.(The clinical effects of GA