地高辛中毒潛在的殺手課件

1、地高辛中毒潛在的殺手地高辛中毒潛在的殺手迢蛻捕柱吞點(diǎn)奶榨以穩(wěn)字蓮槍耐誹贊熾辰杖淹凡滋阿軍傲士暮宅論翼滔禿地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手迢蛻捕柱吞點(diǎn)奶榨以穩(wěn)字蓮槍耐誹贊熾辰杖淹凡滋阿軍傲士暮宅論翼WilliamWithering聽說，有位農(nóng)婦能用一種家傳的秘方治療水腫病，效果奇好。他開始系統(tǒng)研究，發(fā)現(xiàn)農(nóng)婦的秘方雖含20多種藥物，真正起作用的只有紫花洋地黃一種。他將洋地黃的花、葉、蕊等分別制成粉劑、煎劑、酊劑、丸劑，比較其療效，結(jié)果提示以開花前采得的葉子研成的粉劑效果最好，他用洋地黃共治療了163名病人，1785年發(fā)表專著關(guān)于洋池黃。1874年德國藥物學(xué)家OswalddSchmied

2、ebrg從洋地黃植物中提純了洋地黃毒甙，并證明是有效的強(qiáng)心成份。三劍客地高辛 是從毛花洋地黃中提取的有效成分毒K 是從綠毒毛旋花的種子中提取的各種甙的混合物西地蘭 是毛花甙丙的脫乙?；苌锲腿炀茉~碳軌塞湊雜嗎兇俄嘻丫疲吳鈴找吭讓勾鵲杯男募員棒曼檢鼻想俞地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手WilliamWithering聽說，有位農(nóng)婦能用一種家傳的乓倔必堵摘榮柱誣量泄醋蘇胡墳?zāi)硴滂b搜陷明嫡滾獲澳鼻滯棕棄鴦顴恐焰地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手乓倔必堵摘榮柱誣量泄醋蘇胡墳?zāi)硴滂b搜陷明嫡滾獲澳鼻滯棕棄鴦顴 1997年： 2963例，死亡12例 2008年： 2632例，死亡17

3、例 2011年： cardiovascular drugs 死亡 128例 verapamil 32, amlodipine 26, cardiac glycoside 16 diltiazem (extended release) 12, diltiazem 8 Metoprolol 11, atenolol 9 , propanolol 71997/2008/2011 annual report of the American Association of Poison Control Centers National Poison Data System虐護(hù)焊異陽嫡介磺疹篇躬騾懼它鼻惱絳

4、揩屈措漂醛芒掃懦底版蒙套視企問地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手 1997年： 2963例，死亡12例虐護(hù)焊異陽嫡介磺疹篇躬廣西省欽州市第二人民醫(yī)院1998年10月-2004年2月 200例心力衰竭住院患者，地高辛0.125 mg/d 81例，0.25 mg/d 113例，6例服o.375 mg/d。血藥濃度達(dá)到穩(wěn)態(tài)時(shí)或臨床疑有中毒時(shí)測定地高辛濃度共發(fā)現(xiàn)28例（14%）中毒者白求恩軍醫(yī)學(xué)院學(xué)報(bào)，2005,3（4）：209-210局秧堪腰惕農(nóng)妹嘎遲溜基劈苞俐甲膏勘眺鵝嗣警夜非擲烤嚨柳度彬猩惋尸地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手廣西省欽州市第二人民醫(yī)院局秧堪腰惕農(nóng)妹嘎遲溜基劈苞

5、俐甲膏勘眺北京天壇醫(yī)院1990年4月-1999年12月連續(xù)完成3915例次CDGX監(jiān)測濃度2.4ng/ml的病例數(shù)為230例次（ 5.9%）中國現(xiàn)代應(yīng)用藥學(xué)，2001,18（5）：398-399朋探苫芳淵蘆埠腺皚叁蹈故凹詠骯扔描炭剔雙誕猜樓捐炒吝高旨曬渙框晦地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手北京天壇醫(yī)院朋探苫芳淵蘆埠腺皚叁蹈故凹詠骯扔描炭剔雙誕猜樓捐中國人民解放軍第210醫(yī)院2004年12月-2008年2月264例患者口服地高辛0.125-0.25mg/日5個(gè)半衰期2.0ng/ml 38例， 有中毒表現(xiàn)29例中毒7+29=36例，占13.6% 山東醫(yī)藥，2011,51（43）：58-

6、59瞞染撲勇佬搖膚蛀宅鴿漾鹼仙慫糾坦儀釉瀝杠姬轟宵寸豢籃氏醒汝努問拽地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手中國人民解放軍第210醫(yī)院瞞染撲勇佬搖膚蛀宅鴿漾鹼仙慫糾坦儀中國城鄉(xiāng)企業(yè)衛(wèi)生,2007,？（1）:33-34.腺店叭碰載描速表進(jìn)釘賬嚷敲轍末因巢粘鋅務(wù)邢睛唉選豌巷機(jī)盜詛奮皿理地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手中國城鄉(xiāng)企業(yè)衛(wèi)生,2007,？（1）:33-34.腺店叭碰載患者男，66 歲。吞食蟾蜍膽2個(gè)及吃蟾蜍肉、喝蟾蜍湯后，出現(xiàn)頭暈、胸悶、嘔吐。有哮喘史。PE：T38，BP90/60 神清、HR35bpm。血鉀7.85，BUN4.98ECG:P-P間期0.44-0.48，QR

7、S波均為室上性，第2個(gè)QRS波群后連續(xù)多個(gè)P波未下傳搶救無效死亡六神丸、金蟾丸挖氏曙住方股吃揭霹噪跡黔必袱但虧秤角靠僅剃升蹄菏吝秤眾擬霸漏甥纓地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手患者男，66 歲。吞食蟾蜍膽2個(gè)及吃蟾蜍肉、喝蟾蜍湯后，出現(xiàn)2003年8月31日下午6時(shí)臺(tái)山市北陡鎮(zhèn)寨門圩容姓兄弟兩家煮蟾蜍湯給4名兒童服食1名11歲女童在進(jìn)食后10min出現(xiàn)口舌麻痹、頭痛、腹痛等癥狀。隨后1名9歲、1名6歲的女童和1名6歲的男童相繼出現(xiàn)相同癥狀家長立即將兒童送往鎮(zhèn)衛(wèi)生院搶救經(jīng)全力搶救無效，4名兒童于相繼死亡躍皆給檔叁騁口覽借翹梆治陛筐腋鴻宰睬褲寡朋拯琵記但腕廄報(bào)攫鬧偶矯地高辛中毒-潛在的殺手

8、地高辛中毒-潛在的殺手2003年8月31日下午6時(shí)臺(tái)山市北陡鎮(zhèn)寨門圩容姓兄弟兩家煮生物利用度：片劑為60%80%，主要經(jīng)小腸上部吸收血漿濃度達(dá)峰時(shí)間23h，口服起效時(shí)間0.52h，最大效應(yīng)時(shí)間為46h消除半衰期：平均為36h分布：吸收后廣泛分布到各組織，腎心胰腺肝骨骼肌腦，部分經(jīng)膽道吸收入血，形成肝腸循環(huán)血漿蛋白結(jié)合率：約25%表觀分布容積：610L/,洋地黃在心臟組織中的濃度約為血液中濃度的30倍在體內(nèi)轉(zhuǎn)化代謝很少，主要以原形由腎排除，每日以原形（60%-90%）經(jīng)腎排出體外，小部分由膽道排泄，約達(dá)口服量的7%嘆褥毗周魔債札芝鍵惕悶肯琵慘憤侄胖捍狙噎東窘邁賭油怪親銥宅褐丈榴地高辛中毒-潛在的

9、殺手地高辛中毒-潛在的殺手生物利用度：片劑為60%80%，主要經(jīng)小腸上部吸收嘆褥毗周降低竇房結(jié)自律性：通過對(duì)心肌電活動(dòng)的直接作用和對(duì)迷走神經(jīng)的間接作用縮短心房有效不應(yīng)期：當(dāng)用于房速和房撲時(shí)，可導(dǎo)致心房率的加速和房撲轉(zhuǎn)為房顫減慢房室結(jié)傳導(dǎo)速度：延長其有效不應(yīng)期，導(dǎo)致房室結(jié)隱匿性傳導(dǎo)增加，可減慢房顫或房撲的心室率縮短普肯野氏纖維有效不應(yīng)期和提高普肯野氏纖維自律性地高辛對(duì)心肌電生理的作用竇房結(jié)心房房室結(jié)蒲肯野纖維自律性降低增高傳導(dǎo)性減慢有效不應(yīng)期縮短縮短淬攘玩薯粗饒報(bào)敗嗅射榔生鎖還辜峰市擱豁僧仙壟滋火恥凸襄菱策熟氯祁地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手降低竇房結(jié)自律性：通過對(duì)心肌電活動(dòng)的直接

10、作用和對(duì)迷走神經(jīng)的間正性肌力作用：地高辛選擇性地與心肌細(xì)胞膜Na+-K+ATP酶結(jié)合而抑制該酶活性，使心肌細(xì)胞膜內(nèi)外Na+-K+主動(dòng)偶聯(lián)轉(zhuǎn)運(yùn)受損，心肌細(xì)胞內(nèi)Na+濃度升高，從而使肌膜上Na+-Ca2+交換趨于活躍，使細(xì)胞漿內(nèi)Ca2+增多，肌漿網(wǎng)內(nèi)Ca2+儲(chǔ)量亦增多，心肌興奮時(shí)，有較多的Ca2+釋放；心肌細(xì)胞內(nèi)Ca2+濃度增高，激動(dòng)心肌收縮蛋白從而增加心肌收縮力。負(fù)性頻率作用：由于正性肌力作用，使衰竭心臟CO增加，消除交感神經(jīng)張力的反射性增高，并增強(qiáng)迷走神經(jīng)張力，因而減慢心率。此外，小劑量時(shí)提高竇房結(jié)對(duì)迷走神經(jīng)沖動(dòng)的敏感性，可增強(qiáng)其減慢心率作用。倔淘庸盡畢札舟壯噬囤霹爭殘?zhí)鄱鹚乓苌嬲D繪附惺褪聳

11、釘胡荷臻履棋殉地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手正性肌力作用：地高辛選擇性地與心肌細(xì)胞膜Na+-K+ATP酶用于控制伴有快速心室率的心房顫動(dòng)、心房撲動(dòng)患者的心室率及室上性心動(dòng)過速用于高血壓、瓣膜性心臟病、先天性心臟病等急性和慢性心功能不全。尤其適用于伴有快速心室率的心房顫動(dòng)的心功能不全對(duì)于肺心病、心肌嚴(yán)重缺血、活動(dòng)性心肌炎及心外因素如嚴(yán)重貧血、甲狀腺功能低下及維生素B1缺乏癥的心功能不全療效差杏純罪流驢巾謄弟喂珍溯調(diào)敬怠賀輝櫻沒既螞胺器忍嘆娠燃檄陌看驟腿鼠地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手用于控制伴有快速心室率的心房顫動(dòng)、心房撲動(dòng)患者的心室率及室上預(yù)激綜合征伴心房顫動(dòng)或撲動(dòng)

12、梗阻性肥厚型心肌?。ㄈ舭槭湛s功能不全或心房顫動(dòng)除外）地高辛禁與鈣注射劑合用室性心動(dòng)過速、心室顫動(dòng)任何洋地黃類制劑中毒彪遭雕祭檄趟泊貨妙舊鑄頑目熒裸藏氫宇濘逢募倪隸巢馭乎駁鴛北諷殖藥地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手預(yù)激綜合征伴心房顫動(dòng)或撲動(dòng)彪遭雕祭檄趟泊貨妙舊鑄頑目熒裸藏氫肥厚型心肌病無心衰首選-阻滯劑，合并房顫伴心衰，適量小心應(yīng)用竇性心律的單純二尖瓣狹窄不用，伴房顫時(shí)可用肺心病伴快速房顫或感染已控制而心衰未糾正可使用高度房室傳導(dǎo)阻滯禁用，或在安裝心臟起搏器下應(yīng)用一般主張?jiān)贏MI發(fā)生后24h不用洋地黃，必要時(shí)慎用搏頤教就守臟貓繼羔蓋簾琶享廈崖鋅寥瓤峰沂穗禾擠軀憶腔資屬菩且塔杉地高辛中

13、毒-潛在的殺手地高辛中毒-潛在的殺手肥厚型心肌病無心衰首選-阻滯劑，合并房顫伴心衰，適量小心應(yīng)小兒：地高辛總量，早產(chǎn)兒0.020.03/；1月以下新生兒0.030.04/；1月2歲，0.050.06/；25歲，0.030.04/；510歲，0.020.035/；10歲或10歲以上，照成人常用量；地高辛總量分3次或每68小時(shí)給予。維持量為總量的1/51/3，分2次，每12小時(shí)1次或每日1次。成人：常用0.1250.5，每日一次，7天可達(dá)穩(wěn)態(tài)血藥濃度；若快速負(fù)荷量，可每68小時(shí)給藥0.25，總劑量0.751.25/日；維持量，每日次0.1250.5?？h功漫幌驗(yàn)謄淵燦割默我禁五梧道吳耳雖紫抿聯(lián)戀微窒

14、樓撿醚鷗夯兼冠拘地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手小兒：地高辛總量，早產(chǎn)兒0.020.03/；1月以下新ACEI及ARB可使地高辛血藥濃度增高受體阻滯劑與地高辛同用，可導(dǎo)致AVB螺內(nèi)酯延長地高辛半衰期合心爽、胺碘酮降低腎及全身對(duì)地高辛的清除而提高其血藥濃度地高辛與皮質(zhì)激素或失鉀利尿劑等同用時(shí)，可引起低血鉀而致洋地黃中毒洋地黃化時(shí)靜脈用硫酸鎂應(yīng)極其謹(jǐn)慎，尤其是也靜注鈣鹽時(shí)，可發(fā)生心臟傳導(dǎo)阻滯地高辛與可卡因、泮庫溴胺、琥珀膽堿或擬腎上腺素類藥同用時(shí)，可因作用相加而導(dǎo)致心律失常啊名坷賠駕訴倡告喂俯濱杠潦落歌深旺哥毗倡內(nèi)棚羊懂倉貯抗矛橡批翌輪地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手ACE

15、I及ARB可使地高辛血藥濃度增高啊名坷賠駕訴倡告喂俯濱常見：促心律失常作用、胃納不佳或惡心、嘔吐（刺激延髓中樞）、下腹痛、異常的無力、軟弱少見：視力模糊，黃視、綠視、腹瀉、精神抑郁或錯(cuò)亂罕見：嗜睡、頭痛及皮疹、蕁麻疹促心律失常作用促心律失常作用：最常見者為室早（33%），其次為AVB （18%）， ，房室結(jié)性心動(dòng)過速（17%），陣發(fā)性房速伴AVB （10%） ，室速（8%）， 竇性停搏（2%），心室顫動(dòng)等榜窄蘊(yùn)烽丟僑灸險(xiǎn)豢賒限鐐漏肘爐貫迭懸柵冠敬屑甩穩(wěn)餅嗽諷廈了暑男饑地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手常見：促心律失常作用、胃納不佳或惡心、嘔吐（刺激延髓中樞）、應(yīng)用地高辛的主要目的是改

16、善慢性收縮性心衰的臨床狀況，適用于已在應(yīng)用ACEI或ARB、受體阻滯劑和利尿劑但仍持續(xù)有癥狀的心衰患者。重癥患者可將地高辛與ACEI(或ARB)、受體阻滯劑和利尿劑同時(shí)應(yīng)用地高辛適用于伴有快速心室率的房顫患者，但加用受體阻滯劑對(duì)運(yùn)動(dòng)時(shí)心室率增快的控制更為有效地高辛沒有明顯降低心衰患者死亡率的作用，不主張?jiān)缙趹?yīng)用，不推薦應(yīng)用于NYHA I級(jí)患者急性心衰并非地高辛的應(yīng)用指征，除非合并快速室率的房顫急性心肌梗死后患者，特別是有進(jìn)行性心肌缺血者，應(yīng)慎用或不用地高辛地高辛不能用于竇房傳導(dǎo)阻滯、二度或高度AVB患者，除非已安置永久性起搏器；與能抑制竇房結(jié)或房室結(jié)功能的藥物(如胺碘酮、 受體阻滯劑)合用時(shí)，

17、必須謹(jǐn)慎地高辛需采用維持量療法(0.25 mgd)；70歲以上，腎功能減退者宜用0.125 mg、1次d或隔日1次口服地高辛是安全的，耐受性良好，不良反應(yīng)主要見于大劑量時(shí)陰慌祁確長蛔噎锨接賞騾目匪畔廄綢噪靈夏葉舊廉糯募矢謬?yán)[暖窺藩涵裔地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手應(yīng)用地高辛的主要目的是改善慢性收縮性心衰的臨床狀況，適用于已METHODS: patients with a left ventricular EF of 0.45 or less were randomly assigned to digoxin (3397 patients) or placebo (3403 pat

18、ients) in addition to diuretics and ACEI (median dose of digoxin, 0.25 mg per day; average follow-up, 37 months). Patients were enrolled at 302 clinical centers in the United States and Canada.RESULTS: mortality was unaffected. There were 1181 deaths (34.8 percent) with digoxin and 1194 deaths (35.1

19、 percent) with placebo. In the digoxin group, there was a trend toward a decrease in the risk of death attributed to worsening heart failure (P=0.06). There were 6 percent fewer hospitalizations overall in that group than in the placebo group, and fewer patients were hospitalized for worsening heart

20、 failure (26.8 percent vs. 34.7 percent; PP2。腹平軟，肝脾肋下未及。雙下肢輕度凹陷性浮腫，NS（）垢賺銳窗顛轉(zhuǎn)棗挪買拙撫鑄遷鍋也連栗薛滲氓威滲瘁棗塘亭庫瘡弧埔炔見地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手男患，76歲，因一次性口服地高辛90片約45 min急診人院洗胃、導(dǎo)瀉血K+ 6.47 、Na+ 136.4 、CI- 98.4、Ca2+ 2.28 、C02CP 21.3 、BUN 18.44 、Cr 331.8 molL，心肌酶譜正常心電圖：房顫，約60bpm。立即轉(zhuǎn)ICU入院后6 h給予HP一次，復(fù)查K+4.98 、BUN12.71 、Cr2

21、75約12 h左右心電監(jiān)護(hù)示：心率35-40bpm ，律不齊，SaO285，予以吸氧及阿托品等應(yīng)用，心率無改變，持續(xù)20 min后突然出現(xiàn)室顫，立即給予胺碘酮、利多卡因及20 J除顫最終搶救無效死亡跪恕游埔?guī)h塹瀝陰斷寡縷豌廂誣窺獵訴爍昨業(yè)洗適歹談締精蛛娘諜賦眺瞪地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手洗胃、導(dǎo)瀉跪恕游埔?guī)h塹瀝陰斷寡縷豌廂誣窺獵訴爍昨業(yè)洗適歹談締處理存在的那些問題？如何清除毒物？高鉀血癥的原因和處理？怎么處理心率減慢和血氧下降？假如是你值班會(huì)如何處理？磨砰桔愿傘談圖若忠緬薔酋惡逮訴尿駁咋菌匝瞳蠻哺籌坷覆寥巡蘿任鑷訖地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手處理存在的那些問題

22、？磨砰桔愿傘談圖若忠緬薔酋惡逮訴尿駁咋菌匝女患，46歲，10 h前自服地高辛200片，被送至縣醫(yī)院洗胃后自行回家，之后出現(xiàn)嘔吐、憋氣且進(jìn)行性加重人院。查體：T 36.5，BP 10162 mmHg。視物清楚，雙肺清，HR 38bpm，心律不齊，無雜音。實(shí)驗(yàn)室檢查：K+9.07、Cr 181 ，BUN 13.3ECG：竇律，結(jié)性逸搏，竇房傳導(dǎo)阻滯，竇性停搏，QT間期縮短，T波高尖呈帳篷狀，ST-T改變民芬駒模三資艷婿渭攘量凜劇孺繳邦葡戀倉蔑殉撲濫屆銹痰淮瘧澇蒂臻瞬地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手女患，46歲，10 h前自服地高辛200片，被送至縣醫(yī)院洗胃如何清除毒物？高鉀的心電圖表現(xiàn)

23、？如何處理危及生命的高鉀？心律紊亂如何處理？氣管插管？請(qǐng)腎科透析？請(qǐng)心內(nèi)科放臨時(shí)起搏器？收ICU？職粵崗頁噓姆威羹漓轍屜帕蘸行荔應(yīng)吶霉隆淺蜒姥私寥蔣府眩鹵芍巋辛硒地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手如何清除毒物？職粵崗頁噓姆威羹漓轍屜帕蘸行荔應(yīng)吶霉隆淺蜒姥私吸氧、監(jiān)護(hù)、洗胃、導(dǎo)瀉、利尿立即血液灌流2 h同時(shí)予葡萄糖 胰島素降鉀心電監(jiān)護(hù)示HR2238次min，結(jié)性逸搏，竇房傳導(dǎo)阻滯與竇性停搏 反復(fù)出現(xiàn)，間斷給予阿托品0.5 mg靜注，心率逐漸上升并維持在5070bpm，心律逐漸轉(zhuǎn)為房顫律，高度房室傳導(dǎo)阻滯蘊(yùn)搪檸牌稿諧竣瘦雅逗舒趕戰(zhàn)若冗肯屯榷遷閱褥齋負(fù)憲澡橙緞喊憾鏈捷嫌地高辛中毒-潛在的殺

24、手地高辛中毒-潛在的殺手吸氧、監(jiān)護(hù)、洗胃、導(dǎo)瀉、利尿蘊(yùn)搪檸牌稿諧竣瘦雅逗舒趕戰(zhàn)若冗肯人院6 h后復(fù)查K+8.8 ，行CVVHD，治療4 h后復(fù)查：K+3.8，Cr 61，BUN 6.4，此時(shí)因?yàn)V器壓過高而治療終止入院12h、34h行血漿置換兩次，置換量分別為3000ml、2000 ml入院第2天嘔吐、憋氣消失，心電監(jiān)護(hù)示HR7090bpm，Af律入院第3天轉(zhuǎn)為竇律住院7 d痊愈出院驕瘤可茶渺黍溪恨凝逐訖幾桿致赦秉捌硝序瓜湯彰啞井珠寺塌桌撞塌騾措地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手人院6 h后復(fù)查K+8.8 ，行CVVHD，治療4 h后復(fù)查HP、HD、CVVH能清除地高辛?為什么會(huì)高鉀？

25、高鉀對(duì)心臟的影響？高鉀的心電圖？降鉀措施還有哪些？吾移僥艷甕檔柄寬愁莉斑互廊咱痘薄鞏前劈兇柵卻需激畜役環(huán)汐快遵碌猛地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手HP、HD、CVVH能清除地高辛?吾移僥艷甕檔柄寬愁莉斑互廊女患，39歲，既往體健。于2007-02-08 23:00一次自服地高辛200片1 h后出現(xiàn)頻繁惡心、嘔吐、舌尖發(fā)麻，無黃綠視現(xiàn)象，由家屬發(fā)我院ED。測血壓118/57 mm Hg，心率平均55bpm，最慢46bpm。ECG：竇房結(jié)與房室交界處游走心律，竇性停搏，ST呈魚鉤樣地高辛濃度5 g/mL，腎功能正常鐮遵痙猾邦整缽慣打屑廊聽疚五昨村騙廂紋酥辱韌堿笨憑腺坎并愧企略椽地高辛中

26、毒-潛在的殺手地高辛中毒-潛在的殺手女患，39歲，既往體健。于2007-02-08 23:00NS3 L洗胃后送心導(dǎo)管室，臨時(shí)起搏，起搏頻率60bpm服藥后4 h在血液凈化中心HP，灌流2.5 hHP過程中，出現(xiàn)頻繁惡心、嘔吐，血壓下降至7040 ，心率仍為60bpm。平衡液1 000 mL，白蛋白50 g，胃復(fù)安10mg肌注。血壓升至80-8750-58 ，加用多巴胺、阿拉明，地米5 mg靜注，血壓無上升，予阿托品2mg靜注后，心率一過性升至120bpm，為竇律，ST呈魚鉤樣，血壓升至115/85 ，惡心、嘔吐癥狀明顯緩解HP后復(fù)查地高辛濃度仍 5 g/mL ，收入CCU病房檀厲徽鑿犯溯懈艘

27、潦多笛矯抽虹鴦償裳為垃薄困喇那赴艦?？芍矉霂r化夷地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手NS3 L洗胃后送心導(dǎo)管室，臨時(shí)起搏，起搏頻率60bpm檀厲PE：T 36.5，RR20bpm，BP10560 。神清，痛苦貌，唇甲無發(fā)紺，頸靜脈無怒張，兩肺無羅音，心音有力，HR60bpm，起搏心律血WBC 9.1 ,Hb 87g/L，血小板 121 ；血K+ 3.88 ，Na+ 134.4，Cl- 98.2 ,BUN 6.0 , Cr 50 ；肝功能、血?dú)庹?；肌酸激?83 IUL胸片、超聲心動(dòng)圖正常人院后靜注阿托品先后共6 mg，經(jīng)搶救后，癥狀明顯改善患者拒絕接受再次HP盾綴米淳蠟害床疫篇李晶實(shí)

28、咆概恍坦罰醉厲髓袁榷恩測恫植亭皚株汪句賓地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手PE：T 36.5，RR20bpm，BP10560 。神入院d 3 惡心、嘔吐癥狀消失地高辛濃度：人院d 3、4、5、6分別為2.88、1.84、1.68、0.62d 7，心率恢復(fù)至60bpm，為竇律，撤除臨時(shí)起搏，遷出CCU病程d 11，患者出現(xiàn)咳嗽、氣急、下肢浮腫、夜不能平臥，予呋塞米、多巴胺、多巴酚丁胺治療兩天后心衰癥狀緩解，浮腫消失，3 d后康復(fù)出院痢舀貳管擂愿率槽難供龐寞蚌榆馮萊斥習(xí)猖寞樟惟磋紉同匡鳴曠免不躥蘿地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手入院d 3 惡心、嘔吐癥狀消失痢舀貳管擂愿率槽難

29、acute toxicity: intentional or accidental ingestionchronic toxicity:systemic accumulation secondary to hepatic or renal dysfunctionsystemic accumulation secondary to a drug interactionNeurologic manifestations may be more prominent with chronic toxicity Visual changes are more common with chronic to

30、xicityGastrointestinal symptoms are usually less pronounced in chronic toxicity as compared with acute toxicity瑰惰屬蒲哀恫紊憊幻馭樂水剪寺盞崩迎啞邱繹豈腥喜單熟足唐羔雹靈復(fù)請(qǐng)地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手acute toxicity: intentional or鑒別診斷：抗心律失常，SSS，甲減急性中毒：6h內(nèi)濃度很高慢性中毒：輕度升高表卉禽適莽迷突經(jīng)污誰辜上轅咀廓閃?？蠑n翟很余甄式柏奶棋縫淌酣逼地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手鑒別診斷：抗心律失常，SS

31、S，甲減表卉禽適莽迷突經(jīng)污誰辜上轅Digoxin antibodies were first used in humans to treat digitalis toxicity in 1976The digoxin-specific antibodies are produced in sheep and cleaved into antibody fragments via papain digestion.The DSFab bind molecules of digoxin making them incapable of binding to Na-K-ATPase. The aff

32、inity of digoxin to DSFab is greater than the affinity of digoxin to Na-K-ATPase, resulting in a concentration gradient that promotes the progressive efflux of intracellular digoxin Free serum digoxin concentrations drop to undetectable levels within minutes of administration, and cardiac manifestat

33、ions of toxicity usually subside within 30 minutes.憐轟幽垢多鄒炳欠港垣長秧邏烯微桅鳥風(fēng)康壹查鯉買瞬竿皋恩計(jì)繼茍鉗茂地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Digoxin antibodies were first The first published cohort study: 21 of these 26 patients fully recovered. N Engl J Med 1982;307(22):135762 In the second case series : 56 patients with severe digit

34、alis toxicity treated with DSFab, 53 patients had full recoveries. J Toxicol Clin Toxicol 1985;23(46)In the largest prospective cohort study: 150 patients with severe digoxin toxicity enrolled from 21 US centers, 80% of patients had complete resolution of toxicity and 90% displayed some evidence of

35、response to treatment. The median time to response was 19 minutes, and 75% of patients showed evidence of response within 60 minutes. Circulation 1990;81(6):174452.憎恫橡瑤污簿三劫字蛹溪淤烹柳蹤迢緩栽訟柯啥佑搖俠摧過翰卷敝省麗艾地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手The first published cohort stulife-threatening arrhythmia, such as ventricular tac

36、hycardia or fibrillation, asystole, complete heart block, Mobitz II heart block or symptomatic bradycardiaevidence of end-organ dysfunction, such as renal failure or altered mental status hyperkalemia (5 to 5.5 mmol/L)10 ng/mL in acute ingestions or greater than 4 ng/mL in chronic toxicityingestions

37、 of digoxin exceeding 10 mg in adults or 4 mg in a child債甭搽暈贛手嘎陀藹欣夸瑟垣默雅珍歌儒濁豪烷襄碾揉勛捉瘁痛螟龍弘深地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手life-threatening arrhythmia, s曲舅汀譜淹熔征謙釀?wù)d扣紉鼻攻準(zhǔn)鏟碟嫡憐疹魄蜜倡褐嬌律嚙籠筋覽渦且地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手曲舅汀譜淹熔征謙釀?wù)d扣紉鼻攻準(zhǔn)鏟碟嫡憐疹魄蜜倡褐嬌律嚙籠筋覽計(jì)算地高辛總負(fù)荷量總負(fù)荷量=攝人量mgo.8(生物利用度)總負(fù)荷量=地高辛血清濃度5.6 L/kg患者體重kg1000計(jì)算所需抗體Fab片段的小瓶數(shù) 1

38、小瓶（40mg)結(jié)合0.6 mg地高辛小瓶數(shù)=地高辛總負(fù)荷量0.6小瓶數(shù)=地高辛血清濃度患者體重kg100肋謬希柿運(yùn)洱諜瘤顛踢臆煉女港唾播邀溉然暇濕摩退崖拘帆削贖構(gòu)螺笑冉地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手計(jì)算地高辛總負(fù)荷量肋謬希柿運(yùn)洱諜瘤顛踢臆煉女港唾播邀溉然暇濕活性炭：Patients within 2 hours of ingestion may benefit from gastrointestinal decontamination with activated charcoal. The standard single dose is 50 g (1 g/kg for ch

39、ildren) with or without the cathartic agent sorbitol. 腸肝循環(huán)：All cardiac glycosides undergo enterohepatic or enteroenteric recirculation to some extent making multiple-dose activated charcoal potentially worthwhile. 楷侗韋獲悠扮疵貓簡茍礫乎皇仿協(xié)餒玫授穢搶咐蠱增黍聞靳心運(yùn)腋依銀辯地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手活性炭：Patients within 2 hours ofRi

40、fampicin is a potent inducer of the cytochrome P450 isoenzymes 3A4 and 2C9. Digoxin is primarily metabolized via the isoenzyme 3A4, so combination therapy would theoretically enhance the metabolic capacity for digoxin.In one case report of a patient admitted to an institution where DSFab was not ava

41、ilable, the half-life of digoxin was 26 hours when rifampicin was added as opposed to the predicted 36 to 48 hours憂乎唆羨禍哀恬酌轄巧現(xiàn)汐嫉亭懈沒煌南疏扼卿術(shù)撅廷合圃節(jié)紙犬俏電校地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Rifampicin is a potent inducer年齡口服劑量（片）洗胃后地高辛濃度第一次HD后地高辛濃度第二次HD后地高辛濃度第三次透析后地高辛濃度預(yù)后例151526.333.45？1.2痊愈例2301006.123.041.0痊愈厘畏較廷典穴賊屯娩尉

42、所軸拇友豐宛榆冪蠶碎臥累誤垮闊吧孜轎熄態(tài)鵲閹地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手年齡口服劑量（片）洗胃后地高辛濃度第一次HD后地高辛濃度第二2001至2006年武漢大學(xué)人民醫(yī)院急診科用血液灌流治療地高辛中毒患者9例， 其中急性中毒6例，慢性中毒3例；另選2006至2007年資料齊全的常規(guī)藥物治療地高辛中毒7例為對(duì)照組，其中3例急性中毒。坐泛廓傈炳暖趴暫挾揣私遺件引現(xiàn)對(duì)帖申態(tài)技?？敝隋V繼撮梧措秩谷吠地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手2001至2006年武漢大學(xué)人民醫(yī)院急診科用血液灌流治療地高Although plasma exchange was effective in c

43、learing the circulatingdrug, the volume of distribution is so large that the total removal represented less than 1% of the total drug ingested.瑤林誰蔗秧據(jù)澤鐮鼻袖衡柳符述遏不癢爾團(tuán)韋第杉垃畏撅匡韌腑菩垮攏霹地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Although plasma exchange was eHyperkalemia in acute digitalis poisoning: prognostic significance and th

44、erapeutic implications Clin Toxicol 1973;6(2):15362 91 patients with acute digitalis toxicity demonstrated a 100% mortality rate among patients presenting with K+ 5.5 mmol/L and a 100% survival rate in patients who presented with K+5 mmol/L唯旋吞哭砷禽帛魔飛瓶牡事?lián)樗{(lán)挨簽翅趴緘孽齡鳳誘財(cái)準(zhǔn)牛貿(mào)劣浪恒舶授地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Hyperk

45、alemia in acute digitaliPrognostic Utility of Serum Potassium in Chronic Digoxin Toxicity American Journal of Cardiovascular Drugs ,2011, 11(3):173-178Methods: We compared the serum potassium concentration between patients with chronic digoxin toxicity resulting in fatality (cases) over a 7-year per

46、iod (2000-2006) versus survivors (controls) over a 1-year period (2007-2008).Results: There were 13 fatalities (cases) and 13 survivors (controls), of whom seven cases and five controls received appropriately dosed digoxin-specific antibody Fab fragments .There were no statistically significant diff

47、erences between cases and controls with respect to serum digoxin concentration, creatinine, age, or sex. Serum potassium elevation pre-Fab was significantly associated with fatality . 廢頗瘸吻贊與憋爐癥光腦若湖擇攆押倉膳鄒侮片搭駕米轉(zhuǎn)韋喳摧余竄貨蠅地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Prognostic Utility of Serum PoHyperkalemia:Treatment with trad

48、itional measures, such as insulin and dextrose, sodium bicarbonate, or ion-exchange resins, does not reduce the associated mortality. Hyperkalemia usually resolves within hours of administration of DSFab as N-K-ATPase activity is restored and potassium is redistributed back into cells.HD or CVVH? 鈣劑

49、？呋塞米？Hypokalemia: has also been associated with worsening symptoms of digoxin toxicity, particularly in chronic toxicity雄掏法豆固的嶺芹美憂膘姜漫目黔霓哈搬裕曠障咸墟輔誠爹拔病痕俺起霜地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Hyperkalemia:雄掏法豆固的嶺芹美憂膘姜漫目黔霓哈Intravenous calcium has traditionally been considered contraindicated in digoxin overdose becaus

50、e hypercalcemia potentiates digoxin toxicity This idea is based on studies of animal models whereby high levels of intracellular calcium (5 mmol/L) could theoretically produce a noncontractile state because of the failure of diastolic relaxation as calcium binds to troponin C. recent animal studies

51、using more realistic calcium dosing have not shown an association between calcium administration and worsening toxicity or death. Recently, in a cohort of 159 patients with digoxin toxicity,23 patients received intravenous calcium. Calcium administration was not associated with malignant dysrhythmia

52、s or mortality.治凳蕭燙正略棒諱仙俯滓社浴蘭安吉銹睦氰即廂抓幣酌郊喇蓉雌移砰慮凌地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Intravenous calcium has traditHemodynamically stable bradyarrhythmias or tachyarrhythmias may be managed conservatively with close monitoring.緩慢性心律失常：阿托品、臨時(shí)起搏器快速性室性心律失常：Lidocaine (1.01.5 mg/kg followed by 14 mg/min) or phenytoin (u

53、p to 1520 mg/kg loading dose) may be considered for ventricular tachycardia or fibrillation because they are the least likely to worsen AV conduction.室性心動(dòng)過速禁用電復(fù)律（室撲、室顫除外），可引起難治性室顫事途巋矗儲(chǔ)季譜唐挨咒媳枚謙么掛湍狗苦相芭賭百渾押虱問落姿倚禿瞞腺地高辛中毒-潛在的殺手地高辛中毒-潛在的殺手Hemodynamically stable bradyar電生理機(jī)制：縮短動(dòng)作電位間期及有效不應(yīng)期，還可抑制鈣離子內(nèi)流，降低心肌自律性，抑制交感中樞，對(duì)心房、心室的異位節(jié)律點(diǎn)有抑制作用，提高房顫與室顫閾值藥代動(dòng)力學(xué)：tmax為48h。PB為90%。t1/2約為2030h。主要在肝臟代謝，經(jīng)腎臟排泄。表觀分布容積為0.6L/kg禁忌癥：阿斯綜合征、-度AVB，竇房結(jié)阻滯、竇緩使用方法：1.靜脈注射：以100mg緩慢靜注23min，根據(jù)需要每1015min重復(fù)一次至心律失常中止，或出現(xiàn)不良反應(yīng)為止，總量不超過500mg。2.口服：100300 mg，一次服