中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2010年
1期
29-32
,共4页
韩光炜%余守章%王兆民%李士通%邬子林
韓光煒%餘守章%王兆民%李士通%鄔子林
한광위%여수장%왕조민%리사통%오자림
靶控输注%脑电双频谱指数%丙泊酚%瑞芬太尼%半数有效浓度
靶控輸註%腦電雙頻譜指數%丙泊酚%瑞芬太尼%半數有效濃度
파공수주%뇌전쌍빈보지수%병박분%서분태니%반수유효농도
Target-controlled infusion%Bispectral index%Propofol%Remifentanil%Medium effective concentration
目的 测定抑制喉罩通气道LMA-Fastrach、LMA-Proseal置管和气管插管心血管反应的瑞芬太尼半数有效浓度以及比较置管期间相应脑电双频谱指数(BIS)的变化.方法 择期全麻下行胆囊切除术患者63例,美国麻醉医师协会(ASA)I～II级,按置管类型的不同随机均分为T、F、P 3组,每组21例.4 mg/L启动并调整丙泊酚靶控,使得BIS稳定于45～55,之后按Minto药代模式设置并启动瑞芬太尼效应室靶控,5 min后给0.6 mg/kg罗库溴铵,2 min后置管:T组气管插管,F组LMA-Fastrach置管,P组放置LMA-Proseal.比较患者麻醉诱导前、诱导后平均动脉压(MAP)、心率(HR)值及置管前后的BIS变化.记录置管前1、2min及置管后5min内的MAP、HR值以判定患者有无心血管反应.应用Dixon-Mood序贯法计算抑制3种置管心血管反应的瑞芬太尼的半数有效浓度(EC50).结果 与麻醉诱导前相比,3组麻醉诱导后MAP、HR均明显下降[MAP:T、F、P组麻醉诱导前后分别为(87.9+10.5)mmHg比(71.6+9.0)mm Hg,(91.8+8.8)mm Hg比(73.5±9.9)mm Hg,(87.2±10.2)mm Hg比(70.9+8.6)am Hg,HR:T、F、P组麻醉诱导前后分别为(78.8±11.6)次/min比(68.7+8.5)次/min,(74.8±10.3)次/min比(64.1±6.7)次/min,(76.7±8.2)次/min比(67.3±8.3)次/min,1 mm Hg=0.133 kPa,P<0.05],而置管前后的BIS值则无变化(P>0.05).瑞芬太尼抑制3组置管心血管反应的半数有效浓度依次为T组4.47 μg/L、F组4.78 μg/L、P组2.05 μg/L.结论 Minto模式靶控测得瑞芬太尼抑制3种置管心血管反应的EC50 LMA-Fastrach置管略高于气管插管,LMA-Proseal置管则最低.
目的 測定抑製喉罩通氣道LMA-Fastrach、LMA-Proseal置管和氣管插管心血管反應的瑞芬太尼半數有效濃度以及比較置管期間相應腦電雙頻譜指數(BIS)的變化.方法 擇期全痳下行膽囊切除術患者63例,美國痳醉醫師協會(ASA)I～II級,按置管類型的不同隨機均分為T、F、P 3組,每組21例.4 mg/L啟動併調整丙泊酚靶控,使得BIS穩定于45～55,之後按Minto藥代模式設置併啟動瑞芬太尼效應室靶控,5 min後給0.6 mg/kg囉庫溴銨,2 min後置管:T組氣管插管,F組LMA-Fastrach置管,P組放置LMA-Proseal.比較患者痳醉誘導前、誘導後平均動脈壓(MAP)、心率(HR)值及置管前後的BIS變化.記錄置管前1、2min及置管後5min內的MAP、HR值以判定患者有無心血管反應.應用Dixon-Mood序貫法計算抑製3種置管心血管反應的瑞芬太尼的半數有效濃度(EC50).結果 與痳醉誘導前相比,3組痳醉誘導後MAP、HR均明顯下降[MAP:T、F、P組痳醉誘導前後分彆為(87.9+10.5)mmHg比(71.6+9.0)mm Hg,(91.8+8.8)mm Hg比(73.5±9.9)mm Hg,(87.2±10.2)mm Hg比(70.9+8.6)am Hg,HR:T、F、P組痳醉誘導前後分彆為(78.8±11.6)次/min比(68.7+8.5)次/min,(74.8±10.3)次/min比(64.1±6.7)次/min,(76.7±8.2)次/min比(67.3±8.3)次/min,1 mm Hg=0.133 kPa,P<0.05],而置管前後的BIS值則無變化(P>0.05).瑞芬太尼抑製3組置管心血管反應的半數有效濃度依次為T組4.47 μg/L、F組4.78 μg/L、P組2.05 μg/L.結論 Minto模式靶控測得瑞芬太尼抑製3種置管心血管反應的EC50 LMA-Fastrach置管略高于氣管插管,LMA-Proseal置管則最低.
목적 측정억제후조통기도LMA-Fastrach、LMA-Proseal치관화기관삽관심혈관반응적서분태니반수유효농도이급비교치관기간상응뇌전쌍빈보지수(BIS)적변화.방법 택기전마하행담낭절제술환자63례,미국마취의사협회(ASA)I～II급,안치관류형적불동수궤균분위T、F、P 3조,매조21례.4 mg/L계동병조정병박분파공,사득BIS은정우45～55,지후안Minto약대모식설치병계동서분태니효응실파공,5 min후급0.6 mg/kg라고추안,2 min후치관:T조기관삽관,F조LMA-Fastrach치관,P조방치LMA-Proseal.비교환자마취유도전、유도후평균동맥압(MAP)、심솔(HR)치급치관전후적BIS변화.기록치관전1、2min급치관후5min내적MAP、HR치이판정환자유무심혈관반응.응용Dixon-Mood서관법계산억제3충치관심혈관반응적서분태니적반수유효농도(EC50).결과 여마취유도전상비,3조마취유도후MAP、HR균명현하강[MAP:T、F、P조마취유도전후분별위(87.9+10.5)mmHg비(71.6+9.0)mm Hg,(91.8+8.8)mm Hg비(73.5±9.9)mm Hg,(87.2±10.2)mm Hg비(70.9+8.6)am Hg,HR:T、F、P조마취유도전후분별위(78.8±11.6)차/min비(68.7+8.5)차/min,(74.8±10.3)차/min비(64.1±6.7)차/min,(76.7±8.2)차/min비(67.3±8.3)차/min,1 mm Hg=0.133 kPa,P<0.05],이치관전후적BIS치칙무변화(P>0.05).서분태니억제3조치관심혈관반응적반수유효농도의차위T조4.47 μg/L、F조4.78 μg/L、P조2.05 μg/L.결론 Minto모식파공측득서분태니억제3충치관심혈관반응적EC50 LMA-Fastrach치관략고우기관삽관,LMA-Proseal치관칙최저.
Objective To measure the medium effective concentration (EC50) of remifentanil for blunting cardiovascular response to placement of LMA-Fastrach, LMA-Proseal and tracheal intubation, and to compare the change of brain bispectral index (BIS) during these procedures. Methods Sixty-three patients (ASA I-II) scheduled for cholecystectomy under general anesthesia were enrolled. According to different options of intubation, all the patients were randomly allocated into three groups (n=21 each): group T by laryngoscope and tracheal intubation, group F by LMA-Fastrach and group P by LMA-Proseal.Initially, a target plasma concentration of 4 mg/L propofol was chosen, and was adjusted to maintain BIS between 45 and 55. Then, the effect-site concentration of remifentanil was started at designed concentration according to Minto's pharmacokinetic model. Five minutes later, 0.6 mg/kg (2 ED95) rocuronium was given, and intubation was performed 2 min after rocuronium administration. The pre- and post-induction mean arterial pressure (MAP), heart rate (HR) and BIS were compared among these groups. MAP and HR at 1 and 2 min pre-intubation and at 5 min post-intubation were also recorded to evaluate whether there was a cardiovascular response in these patients. Subsequently, the EC50 of remifentanil for blunting the cardiovascular response to 3 options of intubation was calculated using the Dixon-Mood up- and down- sequence. Results Compared with pre-induction, all the patients in 3 groups experienced significantly lower post-inductive MAP and HR [MAP of pre- and post-induction in T, F, P groups were (87.9±10.5) mm Hg vs (71.6±9.0) mm Hg, (91.8±8.8)mm Hg vs (73.5±9.9) mm Hg, (87.2±10.2) mm Hg vs (70.9±8.6) mm Hg, HR of pre- and post-induction in T, F, P groups were (78.8±11.6) min-1 vs (68.7±8.5) min-1,(74.8±10.3) min-1 vs (64.1±6.7) min-1, (76.7±8.2) min-1 vs (67.3±8.3) min-1,1 mm Hg=0.133 kPa, P<0.05] but BIS unchanged basically (P>0.05). The EC50 of remifentail for blunting cardiovascular response to intubation was 4.47 μg/L for group T, 4.78 μg/L for group F and 2.05 μg/L for group P, respectively. Conclusion EC50 of remifentail for blunting cardiovascular responses to intubation as shown by Minto's model appears slightly higher in LMA-Fastrach than that in tracheal intubation, and the lowest is in LMA-Proseal intubation.
