心源性休克体外膜肺氧合治疗的临床研究
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摘要
研究目的
总结2004年12月至2010年12月阜外医院149例患者接受体外膜肺氧合(ECMO)治疗的临床经验,并尝试确定院内死亡的预测因子。
研究方法
记录149例接受ECMO治疗患者基本资料,ECMO系统建立时的临床特征,并发症及院内死亡率。按是否发生院内死亡将患者分为两组,比较两组之间在ECMO前U一般情况、ECMO治疗期间的血流动力学参数、心肌酶谱、呼吸机设置、血气代谢、肝肾功能等指标以及并发症发生上的差异,同时以逻辑回归计算院内死亡的预测因子。因为成人和小儿某些生理指标本身存在差异,故将患者分为成人及小儿组,比较这方面指标在成人及小儿中的异同。并对出院患者进行电话随访。
研究结果
98名为男性,51名女性,其中成人91名。71例手术室内建立ECMO,45例外科ICU建立ECMO,16例内科病房或急诊室建立ECMO。40例ECMO前发生心脏骤停并行常规心肺复苏。12例患者同时接受IABP治疗。平均ECMO时间为128.9±83.6小时(12-504小时)。104例脱机,83例存活出院,总存活率57%。21例撤机后院内死亡,死亡的原因主要是感染及多器官功能衰竭,41例因多种原因不能脱机或放弃治疗。与死亡组比较,存活患者体重高于死亡患者(P=0.003)；存活患者ECMO前行心肺复苏比例较低(P=0.002)；在手术室建立ECMO的患者存活率较高(P=0.030)。与采用中心插管比较,采用外周插管建立ECMO的患者存活率较高(P=0.015)。ECMO支持期间,ECMO建立4小时,存活组辅助流量较死亡组高(P=0.029)。死亡患者ECMO建立前动脉收缩压和平均动脉压较存活组低(P<0.05),且在ECMO建立24小时和撤机前的正性肌力药物剂量较存活组高(P<0.05)。存活组在ECMO建立时的混合静脉血氧饱和度较死亡组高(P=0.010),血乳酸水平在ECMO建立时、ECMO建立24小时和撤机前均低于死亡组(P<0.05)。另外存活组的ALP在ECMO建立第5天较低(P=0.020), DBil在ECMO建立第3天较低(p=0.044), Crea水平在ECMO建立的第3天和第5天较低(P<0.05)。单因素分析表明婴幼儿、中心插管、ECMO前及期间前高乳酸血症、ECMO前CPR、ECMO期间感染、溶血、下肢缺血、更换氧合器、急性肾衰、DIC及消化道出血与院内死亡相关,经逻辑回归计算,ECMO前CPR、急性肾衰、感染及ECMO期间发生并发症为院内死亡的预测因子。83例出院患者电话随访至2011年1月1日,其中12例由于无法联系而失访,随访率为85.5%；其余71例患者中11例死亡余60例患者存活,占全部出院患者的84.3%。
研究结论
ECMO是一种有效的循环呼吸衰竭辅助支持疗法,使用时机非常重要,尽早及时建立,为临床治疗创造机会,可减少并发症和多器官功能衰竭的发生。ECMO前CPR、ECMO支持治疗期间肾功能损害、感染、严重并发症是患者院内死亡的危险因素。远期随访结果表明患者有较高的远期生存率。
研究目的
总结心肺功能衰竭患者接受体外膜式氧合(ECMO)治疗的临床经验,评价Medtronic系统和Quadrox PLS系统在临床的应用疗效和生物相容性。
研究方法
分析2004年12月至2009年12月北京阜外心血管病医院收治的121例心肺功能衰竭患者接受ECMO治疗的临床资料,根据采用的ECMO支持系统不同,将121例患者分为两组,M组：65例,男41例,女24例,年龄26.60±25.90岁,使用Medtronic Carmeda heparin-bonded系统行ECMO支持治疗；Q组：56例,男39例,女17例,年龄32.40±23.90岁,使用Quadrox PLS系统行ECMO支持治疗。
通过对比两组治疗期间氧合器跨膜压差、凝血抗凝水平、血液破坏程度、血浆渗漏、器官功能、并发症及院内病死率,同时扫描电镜观察两组系统使用后人工表面的形态学表现,评价两种支持系统的临床疗效和生物相容性。
研究结果
ECMO期间Q组各时点氧合器跨膜压差较M组低(ECMO建立时15.00±6.00mmHg vs.28.00±5.00 mmHg, P<0.001; ECMO建立24h 16.00±5.00 mmHg vs. 30.00±7.00 mmHg, P=0.000); Q组系统血栓(7.14% vs.23.08%,P=0.027)、血浆渗漏(0%vs.50.77%,P=0.000)、溶血发生率(14.29%vs.29.23%,P=0.040)较M组降低；而两组撤机率、并发症发生率和院内病死率比较差异无统计学意义(P>0.05)。
研究结论
两种ECMO系统临床上均可提供安全有效的心肺支持,Quadrox PLS系统膜肺跨膜压差较低,且避免了血浆渗漏,对凝血系统干扰小,具有较高的生物相容度。
研究目的
作为体外生命支持技术,休外膜肺(ECMO)是对有效地提高了严重心肺功能衰竭患者的救治成功率,但是疗中也存在一些问题。本研究观察体外膜肺治疗对人血液系统的影响,揭示ECMO期间血常规,炎性介质及凝血指标的变化规律。
研究方法
连续27例成人ECMO患者,分别于ECMO建立时,建立24小时及撤机前抽静脉血检测血常规。另外分别在ECMO建立前,ECMO建立1小时,6小时、24小时、48小时、72小时、撤机前分别采中心静脉血标本,分离血浆冻存测定各时点炎性介质、全血激活凝血时间、凝血酶原时间、活化部分凝血酶原时间及纤维蛋白原等指标,观察其变化情况。同时按是否发生院内死亡将患者分为两组,比较二者各时点上述指标的差异。
研究结果
ECMO建立后,血红蛋白各时点浓度没有明显变化。在ECMO期间白细胞和中性粒细胞总体逐渐升高趋势,存活组白细胞和中性粒细胞计数在ECMO建立时较死亡组低,差异有显著性(P<0.01)。淋巴细胞在ECMO辅助24小时较建立时降低,撤机前上升达峰值,组间未见显著性差异。血小板数量在ECMO期间进行性下降,组间未见显著性差异。PT、APTT与ECMO前相比均明显延长(P<0.05),纤维蛋白原在ECMO建立后一过性降低,6小时后逐渐升高,撤机前达峰值。存活组TNF-α、IL-2和IL-6水平在ECMO治疗24小时后逐渐下降,撤机前较死亡组低(P<0.05)。
研究结论
心脏术后心源性休克患者ECMO前已存在凝血功能紊乱和炎性反应。ECMO激活白细胞及血小板,激活内外源性凝血系统；同时导致全身炎性反应。存活组炎性反应强度随病情改善逐渐下降。
研究目的
本研究观察体外膜肺治疗对人内分泌系统的影响,揭示ECMO期间甲状腺激素、血管紧张素醛固酮系统、皮质醇及BNP的变化规律。
研究方法
连续27例成人ECMO患者,分别在ECMO建立前,ECMO建立1小时,6小时、24小时、48小时、72小时、撤机前分别采中心静脉血标本,分离血浆冻存测定各时点游离四碘甲腺原氨酸(FT4)、游离三碘甲腺原氨酸(FT3)、促甲状腺激素(TSH)、皮质醇、血管紧张素(AGⅡ)、醛固酮(ALD)、脑钠肽(BNP)和S100蛋白等指标。同时按是否发生院内死亡将患者分为两组,比较二者各时点上述指标的差异。
研究结果
ECMO前及ECMO期间各甲状腺激素水平均低于正常值。ECMO早期FT3呈下降趋势,在ECMO建立24小时显著低于ECMO建立时的水平(P<0.05),此后后逐渐上升,至停机前接近ECMO建立前水平。ECMO期间FT4持续维持在较低水平。ECMO建立后TSH进行性下降,组内比较,各时点较ECMO建立前显著降低(P<0.05),存活组在ECMO建立48小时后上升,至撤机前,TSH水平较死亡组显著高(P<0.05)。ECMO前及ECMO期间AGⅡ和ALD高于正常值。存活组AGⅡ在ECMO建立早期轻度上升,24小时后逐渐下降,至72小时和撤机前较死亡组差异显著(P<0.05)。存活组ALD在ECMO建立6小时后逐渐下降,至72小时和撤机前较死亡组差异显著(P<0.05)。皮质醇在ECMO建立前就高于正常值,ECMO早期,继续上升,至24小时后,逐渐下降。ECMO早期BNP水平轻度上升,至48小时后开始下降,存活组撤机前BNP低于死亡组,差异有显著性(P<0.05)。ECMO期间S100蛋白高于正常值,且呈进行性上升趋势。
研究结论
心脏术后心源性休克患者ECMO前已存在凝血功能紊乱和炎性反应。ECMO激活白细胞及血小板,激活内外源性凝血系统；同时导致全身炎性反应。存活组炎性反应强度随病情改善逐渐下降。
Objective
This report reviews our experience in venoarterial extracorporeal membrane oxygenation (ECMO) support treatment in cardiogenic shock patients, as well as look for predictors of in-hospital mortality after ECMO.
Methods
Reviewed the clinical data and protocols of 149 consecutive extracorporeal membrane oxygenation(ECMO) cases performed in Fuwai Hospital from Dec.2004 to Dec.2010, they were divided into two groups accoding to hospital survival. The clinical data therapeutic parameters before and during ECMO were compared between the two groups. Stepwise logistic regression identified predictors of in-hospital mortality. All discharged patients were followed up by telephone.
Results
There were 98 male patients. The mean was 29.7±24.8 years (age range 3 days～76 years.The mean weight was 43.6±28.6kg (range 3.2-100 kg). The mean ECMO duration was 128.9±83.6 hrs (range 12～504 hrs).71 patients had ECMO initiated in the operating room because of the inability to wean from cardiopulmonary bypass,45 patients instituted in the intensive care unit, and 16 patients instituted in the word or emergency room. There are 40 patients who suffered from cardiac arrest prior to ECMO. 12 patients received IABP and ECMO at the same time.The mean ECMO duration was 128.9±83.6hrs.104 patients weaned off successfully from ECMO.83 of them were discharged and 21 died of post-operative complications.41 patients could not wean off from ECMO. Weights and CPR pre-ECMO were also differ between the survival and the dead(p=0.003 and 0.002 separately). The in-hospital mortality was significantly lower in the patients that ECMO initiated in operating room (P=0.030). Lactic acid concentration of artery blood before ECMO in survived patients were significantly lower than that of dead patients before and during ECMO period(P=0.005). SBP and MAP before ECMO in survived patients was significantly higher than that of dead patients(P< 0.05). The dosages of inotropics were higher in the dead group during ECMO(.P< 0.05). The plasma alkaline phosphatase (ALP)、Direct bilirubin (DBil) and Creantine were lower in the survivors during ECMO(P<0.05). Bleeding, renal failure, hemolysis, infection, lower limb ischemia, MSOF, DIC, Oxygenator plasma leakage were the complications significantly related to the dead. The follow up study that used telephone interviews found that 12 case missing and 11 patients died, while other patients alive after discharged.
Conclusions
ECMO is an effective mechanical assistant therapy method for cardiogenic shock. Earlier usage of ECMO for heart failure patient and avoiding the main organs from un-recovery trauma are still the key point of success of ECMO.
Objective
To summarize the clinical experiences of performing extracorporeal membrane oxygenation (ECMO) on patients with respiratory failure and compare the clinical outcomes of Medtronic system and Quadrox PLS system.
Methods
We retrospectively analyzed the clinical data of 121 respiratory failure patients who underwent ECMO in Fuwai Hospital from December 2004 to December 2009. Based on the different systems used, the patients were divided into two groups. In group M, there were 65 patients including 41 males and 24 females, with an average age of 26.6±25.9 years old; and they accepted Medtronic ECMO system treatment. In group Q, there were 56 patients including 40 males and 17 females, with an average age of 32.4±23.9 years old and they underwent Quadrox PLS ECMO system therapy. The evaluation of the clinical outcomes of these two different systems was based on the comparison of trans-membrane pressure drop (TMPD), anticoagulation, hemolysis, plasma leakage, organ function, complication and hospital mortality between the two groups.
Results
Compared with group M, ECMO with Quadrox PLS system was associated with lower TMPD (at the beginning of ECMO:15.00±6.00 mmHg vs.28.00±5.00 mmHg, P<0.001; 24 hours later:16.00±5.00 mmHg vs.30.00±7.00 mmHg, P=0.000) and and less thrombus formation (7.14%vs.23.08%, P=0.027), plasma leakage (0%vs.50.77%, P=0.000), less hemolysis (14.29%vs.29.23%, P=0.040). There were no significant differences between the two groups in other aspects like support duration, complication rate and hospital mortality.
Conclusion
Both devices have similar effects for safe clinical application, but Quadrox PLS ECMO system has a relatively high biocompatibility with lower TMPD, less plasma leakage and thrombus formation.
Objective
Extracorporeal membrane oxygenation (ECMO) is a life-saving support system used for severe cardiogenic shock cases in our center. Although ECMO has reduced mortality in these critically ill patients, almost all patients treated with ECMO develop a systemic inflammatory response syndrome (SIRS) characterized by a cytokine storm, leukocyte activation, and multisystem organ dysfunction.
Methods
27 consecutive extracorporeal membrane oxygenation (ECMO) cases performed in Fuwai hospital were included in this study. They were divided into two groups according to hospital survival. Blood samples were taken from jugular vein to assay blood routine test at ECMO established,24 hours established and before ECMO wean. The plasma concentration of coagulant factors and cytokines were mearured at different time points as following:before ECMO, 1hr,6hrs,24hrs,48hrs,72hrs after ECMO and ECMO wean.
Results
White blood cell and neutriophil counts were rosed during ECMO, and compared to the death group, the vales were lower in the survivors (P<0.01). Lymphcytes decreased significantly at 24hrs after ECMO established and increased later in both groups. Platelet counts drop down gradually significantly after ECMO set up. Prothrombin time (PT) and Activated partial thromboplastin time (aPTT) prolonged obviously after ECMO set up (P<0.01). Plasma frinogen concentration drop down after ECMO initiated, and rose gradually after 6 hrs. The plasma concentrations of tumor necrosis factor-alpha (TNF-a) and interleukin-6 declined after 24 hours ECMO initiated in the survivors, but remained unchanged in the died group.
Conclusion
ECMO develop a systemic inflammatory response syndrome characterized by leukocyte coagulation system and cytokine system activation. And as the patients'condition improved, the response is relieved and limited.
Objective
Neuroendocrine system hameostasis among patients receiving mechanical support is largely unknown. To obtain information on neuroendocrine system homeostasis during adult extracorporeal membrane oxygenation (ECMO), renin Angiotensin Aldosterone system (RAAS) and thyroid gland function, B-type natriuretic peptide(BNP) and S100 protein were studied during ECMO period.
Methods
Twenty seven patients with cardiogenic shock who were supported by extracorporeal membrane oxygenation (ECMO) were evaluated. They were divided into two groups according to hospital survival. Serial determinations of plasma free thyroxine (FT4), free triiodothyronine (T3), thyroid-stimulating hormone (TSH), plasma AngiotensionⅡ(AngⅡ),aldosterone (Aldo),BNP and S100 protein at different time points as following:before ECMO, lhr,6hrs, 24hrs,48hrs,72hrs after ECMO and ECMO wean.
Results
Plasma FT3 and TSH were decreased after ECMO set up till 48 hours, and then increased in the survivors, the TSH level was significantly higher compared with the dead group when ECMO wean(p< 0.05). The plasma FT4 remained low level during ECMO therapy. The plasma AngⅡand aldosterone elevated during ECMO, after 24 hrs to 48 hrs support, decreased gradually in the survivors, and significantly lower at the time when ECMO wean (p< 0.05). The plasma cortisol, BNP and S100 protein level were elvated during ECMO. The plasma BNP and S100 level were elevated during ECMO period in both groups, and which were significantly lower in the survivors after 72 hrs after ECMO established (p< 0.05), but remained increasing in the dead group. The plasma cortisol remained high level during ECMO, and began to slightly drop down after 24 hrs support in both group, no significant difference between the survivors and dead groups.
Conclusion
Our results revealed neuroendocrine system changes in the patients receiving mechanical support. The thyroid function decreased during ECMO, and the plasma concentration of FT3, FT4 and TSH were remained lower level. The renin angiotensin adosterone system (RAAS) was activated during ECMO, the plasma concentration of angiotensin and adosterone keeped on higher level during support. The BNP and S100 protein were elevated during ECMO period. In brief, compared with the dead group, the neuroendocrine system hemostasis recovered partially in the survors group.
总结2004年12月至2010年12月阜外医院149例患者接受体外膜肺氧合(ECMO)治疗的临床经验,并尝试确定院内死亡的预测因子。
研究方法
记录149例接受ECMO治疗患者基本资料,ECMO系统建立时的临床特征,并发症及院内死亡率。按是否发生院内死亡将患者分为两组,比较两组之间在ECMO前U一般情况、ECMO治疗期间的血流动力学参数、心肌酶谱、呼吸机设置、血气代谢、肝肾功能等指标以及并发症发生上的差异,同时以逻辑回归计算院内死亡的预测因子。因为成人和小儿某些生理指标本身存在差异,故将患者分为成人及小儿组,比较这方面指标在成人及小儿中的异同。并对出院患者进行电话随访。
研究结果
98名为男性,51名女性,其中成人91名。71例手术室内建立ECMO,45例外科ICU建立ECMO,16例内科病房或急诊室建立ECMO。40例ECMO前发生心脏骤停并行常规心肺复苏。12例患者同时接受IABP治疗。平均ECMO时间为128.9±83.6小时(12-504小时)。104例脱机,83例存活出院,总存活率57%。21例撤机后院内死亡,死亡的原因主要是感染及多器官功能衰竭,41例因多种原因不能脱机或放弃治疗。与死亡组比较,存活患者体重高于死亡患者(P=0.003)；存活患者ECMO前行心肺复苏比例较低(P=0.002)；在手术室建立ECMO的患者存活率较高(P=0.030)。与采用中心插管比较,采用外周插管建立ECMO的患者存活率较高(P=0.015)。ECMO支持期间,ECMO建立4小时,存活组辅助流量较死亡组高(P=0.029)。死亡患者ECMO建立前动脉收缩压和平均动脉压较存活组低(P<0.05),且在ECMO建立24小时和撤机前的正性肌力药物剂量较存活组高(P<0.05)。存活组在ECMO建立时的混合静脉血氧饱和度较死亡组高(P=0.010),血乳酸水平在ECMO建立时、ECMO建立24小时和撤机前均低于死亡组(P<0.05)。另外存活组的ALP在ECMO建立第5天较低(P=0.020), DBil在ECMO建立第3天较低(p=0.044), Crea水平在ECMO建立的第3天和第5天较低(P<0.05)。单因素分析表明婴幼儿、中心插管、ECMO前及期间前高乳酸血症、ECMO前CPR、ECMO期间感染、溶血、下肢缺血、更换氧合器、急性肾衰、DIC及消化道出血与院内死亡相关,经逻辑回归计算,ECMO前CPR、急性肾衰、感染及ECMO期间发生并发症为院内死亡的预测因子。83例出院患者电话随访至2011年1月1日,其中12例由于无法联系而失访,随访率为85.5%；其余71例患者中11例死亡余60例患者存活,占全部出院患者的84.3%。
研究结论
ECMO是一种有效的循环呼吸衰竭辅助支持疗法,使用时机非常重要,尽早及时建立,为临床治疗创造机会,可减少并发症和多器官功能衰竭的发生。ECMO前CPR、ECMO支持治疗期间肾功能损害、感染、严重并发症是患者院内死亡的危险因素。远期随访结果表明患者有较高的远期生存率。
研究目的
总结心肺功能衰竭患者接受体外膜式氧合(ECMO)治疗的临床经验,评价Medtronic系统和Quadrox PLS系统在临床的应用疗效和生物相容性。
研究方法
分析2004年12月至2009年12月北京阜外心血管病医院收治的121例心肺功能衰竭患者接受ECMO治疗的临床资料,根据采用的ECMO支持系统不同,将121例患者分为两组,M组：65例,男41例,女24例,年龄26.60±25.90岁,使用Medtronic Carmeda heparin-bonded系统行ECMO支持治疗；Q组：56例,男39例,女17例,年龄32.40±23.90岁,使用Quadrox PLS系统行ECMO支持治疗。
通过对比两组治疗期间氧合器跨膜压差、凝血抗凝水平、血液破坏程度、血浆渗漏、器官功能、并发症及院内病死率,同时扫描电镜观察两组系统使用后人工表面的形态学表现,评价两种支持系统的临床疗效和生物相容性。
研究结果
ECMO期间Q组各时点氧合器跨膜压差较M组低(ECMO建立时15.00±6.00mmHg vs.28.00±5.00 mmHg, P<0.001; ECMO建立24h 16.00±5.00 mmHg vs. 30.00±7.00 mmHg, P=0.000); Q组系统血栓(7.14% vs.23.08%,P=0.027)、血浆渗漏(0%vs.50.77%,P=0.000)、溶血发生率(14.29%vs.29.23%,P=0.040)较M组降低；而两组撤机率、并发症发生率和院内病死率比较差异无统计学意义(P>0.05)。
研究结论
两种ECMO系统临床上均可提供安全有效的心肺支持,Quadrox PLS系统膜肺跨膜压差较低,且避免了血浆渗漏,对凝血系统干扰小,具有较高的生物相容度。
研究目的
作为体外生命支持技术,休外膜肺(ECMO)是对有效地提高了严重心肺功能衰竭患者的救治成功率,但是疗中也存在一些问题。本研究观察体外膜肺治疗对人血液系统的影响,揭示ECMO期间血常规,炎性介质及凝血指标的变化规律。
研究方法
连续27例成人ECMO患者,分别于ECMO建立时,建立24小时及撤机前抽静脉血检测血常规。另外分别在ECMO建立前,ECMO建立1小时,6小时、24小时、48小时、72小时、撤机前分别采中心静脉血标本,分离血浆冻存测定各时点炎性介质、全血激活凝血时间、凝血酶原时间、活化部分凝血酶原时间及纤维蛋白原等指标,观察其变化情况。同时按是否发生院内死亡将患者分为两组,比较二者各时点上述指标的差异。
研究结果
ECMO建立后,血红蛋白各时点浓度没有明显变化。在ECMO期间白细胞和中性粒细胞总体逐渐升高趋势,存活组白细胞和中性粒细胞计数在ECMO建立时较死亡组低,差异有显著性(P<0.01)。淋巴细胞在ECMO辅助24小时较建立时降低,撤机前上升达峰值,组间未见显著性差异。血小板数量在ECMO期间进行性下降,组间未见显著性差异。PT、APTT与ECMO前相比均明显延长(P<0.05),纤维蛋白原在ECMO建立后一过性降低,6小时后逐渐升高,撤机前达峰值。存活组TNF-α、IL-2和IL-6水平在ECMO治疗24小时后逐渐下降,撤机前较死亡组低(P<0.05)。
研究结论
心脏术后心源性休克患者ECMO前已存在凝血功能紊乱和炎性反应。ECMO激活白细胞及血小板,激活内外源性凝血系统；同时导致全身炎性反应。存活组炎性反应强度随病情改善逐渐下降。
研究目的
本研究观察体外膜肺治疗对人内分泌系统的影响,揭示ECMO期间甲状腺激素、血管紧张素醛固酮系统、皮质醇及BNP的变化规律。
研究方法
连续27例成人ECMO患者,分别在ECMO建立前,ECMO建立1小时,6小时、24小时、48小时、72小时、撤机前分别采中心静脉血标本,分离血浆冻存测定各时点游离四碘甲腺原氨酸(FT4)、游离三碘甲腺原氨酸(FT3)、促甲状腺激素(TSH)、皮质醇、血管紧张素(AGⅡ)、醛固酮(ALD)、脑钠肽(BNP)和S100蛋白等指标。同时按是否发生院内死亡将患者分为两组,比较二者各时点上述指标的差异。
研究结果
ECMO前及ECMO期间各甲状腺激素水平均低于正常值。ECMO早期FT3呈下降趋势,在ECMO建立24小时显著低于ECMO建立时的水平(P<0.05),此后后逐渐上升,至停机前接近ECMO建立前水平。ECMO期间FT4持续维持在较低水平。ECMO建立后TSH进行性下降,组内比较,各时点较ECMO建立前显著降低(P<0.05),存活组在ECMO建立48小时后上升,至撤机前,TSH水平较死亡组显著高(P<0.05)。ECMO前及ECMO期间AGⅡ和ALD高于正常值。存活组AGⅡ在ECMO建立早期轻度上升,24小时后逐渐下降,至72小时和撤机前较死亡组差异显著(P<0.05)。存活组ALD在ECMO建立6小时后逐渐下降,至72小时和撤机前较死亡组差异显著(P<0.05)。皮质醇在ECMO建立前就高于正常值,ECMO早期,继续上升,至24小时后,逐渐下降。ECMO早期BNP水平轻度上升,至48小时后开始下降,存活组撤机前BNP低于死亡组,差异有显著性(P<0.05)。ECMO期间S100蛋白高于正常值,且呈进行性上升趋势。
研究结论
心脏术后心源性休克患者ECMO前已存在凝血功能紊乱和炎性反应。ECMO激活白细胞及血小板,激活内外源性凝血系统；同时导致全身炎性反应。存活组炎性反应强度随病情改善逐渐下降。
Objective
This report reviews our experience in venoarterial extracorporeal membrane oxygenation (ECMO) support treatment in cardiogenic shock patients, as well as look for predictors of in-hospital mortality after ECMO.
Methods
Reviewed the clinical data and protocols of 149 consecutive extracorporeal membrane oxygenation(ECMO) cases performed in Fuwai Hospital from Dec.2004 to Dec.2010, they were divided into two groups accoding to hospital survival. The clinical data therapeutic parameters before and during ECMO were compared between the two groups. Stepwise logistic regression identified predictors of in-hospital mortality. All discharged patients were followed up by telephone.
Results
There were 98 male patients. The mean was 29.7±24.8 years (age range 3 days～76 years.The mean weight was 43.6±28.6kg (range 3.2-100 kg). The mean ECMO duration was 128.9±83.6 hrs (range 12～504 hrs).71 patients had ECMO initiated in the operating room because of the inability to wean from cardiopulmonary bypass,45 patients instituted in the intensive care unit, and 16 patients instituted in the word or emergency room. There are 40 patients who suffered from cardiac arrest prior to ECMO. 12 patients received IABP and ECMO at the same time.The mean ECMO duration was 128.9±83.6hrs.104 patients weaned off successfully from ECMO.83 of them were discharged and 21 died of post-operative complications.41 patients could not wean off from ECMO. Weights and CPR pre-ECMO were also differ between the survival and the dead(p=0.003 and 0.002 separately). The in-hospital mortality was significantly lower in the patients that ECMO initiated in operating room (P=0.030). Lactic acid concentration of artery blood before ECMO in survived patients were significantly lower than that of dead patients before and during ECMO period(P=0.005). SBP and MAP before ECMO in survived patients was significantly higher than that of dead patients(P< 0.05). The dosages of inotropics were higher in the dead group during ECMO(.P< 0.05). The plasma alkaline phosphatase (ALP)、Direct bilirubin (DBil) and Creantine were lower in the survivors during ECMO(P<0.05). Bleeding, renal failure, hemolysis, infection, lower limb ischemia, MSOF, DIC, Oxygenator plasma leakage were the complications significantly related to the dead. The follow up study that used telephone interviews found that 12 case missing and 11 patients died, while other patients alive after discharged.
Conclusions
ECMO is an effective mechanical assistant therapy method for cardiogenic shock. Earlier usage of ECMO for heart failure patient and avoiding the main organs from un-recovery trauma are still the key point of success of ECMO.
Objective
To summarize the clinical experiences of performing extracorporeal membrane oxygenation (ECMO) on patients with respiratory failure and compare the clinical outcomes of Medtronic system and Quadrox PLS system.
Methods
We retrospectively analyzed the clinical data of 121 respiratory failure patients who underwent ECMO in Fuwai Hospital from December 2004 to December 2009. Based on the different systems used, the patients were divided into two groups. In group M, there were 65 patients including 41 males and 24 females, with an average age of 26.6±25.9 years old; and they accepted Medtronic ECMO system treatment. In group Q, there were 56 patients including 40 males and 17 females, with an average age of 32.4±23.9 years old and they underwent Quadrox PLS ECMO system therapy. The evaluation of the clinical outcomes of these two different systems was based on the comparison of trans-membrane pressure drop (TMPD), anticoagulation, hemolysis, plasma leakage, organ function, complication and hospital mortality between the two groups.
Results
Compared with group M, ECMO with Quadrox PLS system was associated with lower TMPD (at the beginning of ECMO:15.00±6.00 mmHg vs.28.00±5.00 mmHg, P<0.001; 24 hours later:16.00±5.00 mmHg vs.30.00±7.00 mmHg, P=0.000) and and less thrombus formation (7.14%vs.23.08%, P=0.027), plasma leakage (0%vs.50.77%, P=0.000), less hemolysis (14.29%vs.29.23%, P=0.040). There were no significant differences between the two groups in other aspects like support duration, complication rate and hospital mortality.
Conclusion
Both devices have similar effects for safe clinical application, but Quadrox PLS ECMO system has a relatively high biocompatibility with lower TMPD, less plasma leakage and thrombus formation.
Objective
Extracorporeal membrane oxygenation (ECMO) is a life-saving support system used for severe cardiogenic shock cases in our center. Although ECMO has reduced mortality in these critically ill patients, almost all patients treated with ECMO develop a systemic inflammatory response syndrome (SIRS) characterized by a cytokine storm, leukocyte activation, and multisystem organ dysfunction.
Methods
27 consecutive extracorporeal membrane oxygenation (ECMO) cases performed in Fuwai hospital were included in this study. They were divided into two groups according to hospital survival. Blood samples were taken from jugular vein to assay blood routine test at ECMO established,24 hours established and before ECMO wean. The plasma concentration of coagulant factors and cytokines were mearured at different time points as following:before ECMO, 1hr,6hrs,24hrs,48hrs,72hrs after ECMO and ECMO wean.
Results
White blood cell and neutriophil counts were rosed during ECMO, and compared to the death group, the vales were lower in the survivors (P<0.01). Lymphcytes decreased significantly at 24hrs after ECMO established and increased later in both groups. Platelet counts drop down gradually significantly after ECMO set up. Prothrombin time (PT) and Activated partial thromboplastin time (aPTT) prolonged obviously after ECMO set up (P<0.01). Plasma frinogen concentration drop down after ECMO initiated, and rose gradually after 6 hrs. The plasma concentrations of tumor necrosis factor-alpha (TNF-a) and interleukin-6 declined after 24 hours ECMO initiated in the survivors, but remained unchanged in the died group.
Conclusion
ECMO develop a systemic inflammatory response syndrome characterized by leukocyte coagulation system and cytokine system activation. And as the patients'condition improved, the response is relieved and limited.
Objective
Neuroendocrine system hameostasis among patients receiving mechanical support is largely unknown. To obtain information on neuroendocrine system homeostasis during adult extracorporeal membrane oxygenation (ECMO), renin Angiotensin Aldosterone system (RAAS) and thyroid gland function, B-type natriuretic peptide(BNP) and S100 protein were studied during ECMO period.
Methods
Twenty seven patients with cardiogenic shock who were supported by extracorporeal membrane oxygenation (ECMO) were evaluated. They were divided into two groups according to hospital survival. Serial determinations of plasma free thyroxine (FT4), free triiodothyronine (T3), thyroid-stimulating hormone (TSH), plasma AngiotensionⅡ(AngⅡ),aldosterone (Aldo),BNP and S100 protein at different time points as following:before ECMO, lhr,6hrs, 24hrs,48hrs,72hrs after ECMO and ECMO wean.
Results
Plasma FT3 and TSH were decreased after ECMO set up till 48 hours, and then increased in the survivors, the TSH level was significantly higher compared with the dead group when ECMO wean(p< 0.05). The plasma FT4 remained low level during ECMO therapy. The plasma AngⅡand aldosterone elevated during ECMO, after 24 hrs to 48 hrs support, decreased gradually in the survivors, and significantly lower at the time when ECMO wean (p< 0.05). The plasma cortisol, BNP and S100 protein level were elvated during ECMO. The plasma BNP and S100 level were elevated during ECMO period in both groups, and which were significantly lower in the survivors after 72 hrs after ECMO established (p< 0.05), but remained increasing in the dead group. The plasma cortisol remained high level during ECMO, and began to slightly drop down after 24 hrs support in both group, no significant difference between the survivors and dead groups.
Conclusion
Our results revealed neuroendocrine system changes in the patients receiving mechanical support. The thyroid function decreased during ECMO, and the plasma concentration of FT3, FT4 and TSH were remained lower level. The renin angiotensin adosterone system (RAAS) was activated during ECMO, the plasma concentration of angiotensin and adosterone keeped on higher level during support. The BNP and S100 protein were elevated during ECMO period. In brief, compared with the dead group, the neuroendocrine system hemostasis recovered partially in the survors group.
引文
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15. Risnes I, Wagner K, Ueland T, et al. Interleukin-6 may predict survival in extracorporeal membrane oxygenation treatment [J]. Perfusion,2008,23:173-178.
16. Dempsey PW, Doyle SE, He JQ, Cheng G. The signaling adaptors and pathways activated by TNF superfamily [J]. Cytokine Growth Factor Rev,2003,14(3):193-209.
17. Cha-Molstad H, Young DP, Kushner I, Samols D. The interaction of C-Rel with C/EBPbeta enhances C/EBPbeta binding to the C-reactive protein gene promoter [J]. Mol Immunol, 2007,44(11):2933-2942.
18. Hocker JR, Wellhausen SR, Ward RA, Simpson PM, Cook LN. Effect of extracorporeal membrane oxygenation on leukocyte function in neonates [J]. Artif Organs,1991,15 (1):23-28.
19. Khoshbin E, Dux AE, Killer H, Sosnowski AW, Firmin RK, Peek GJ. A comparison of radiographic signs of pulmonary inflammation during ECMO between silicon and poly-methyl pentene oxygenators [J]. Perfusion,2007,22(1):15-21.
1. Rune Eggum, Thor Ueland, Tom E. Mollnese, et al. Congenital Perfusion temperature, thyroid hormones and inflammation during pediatric cardiac surgery[J]. Interactive CardioVascular and Thoracic Surgery,2009,10:76-80.
2. Klemperer JD. Thyroid hormone and cardiac surgery [J]. Thyroid,2002,12:517-521.
3. Plumpton K, Nikolaus AH. Identifying infants at risk of marked thyroid suppression post-cardiopulmonary bypass [J]. Intensive Care Med,2005,31:581-587.
4. Nikolaus AH, Camphausen CK, Kececioglu D. Clinical review:thyroid hormone replacement in children after cardiac surgery is it worth a try [J]? Crit Care Med,2006,10: 213-227.
5. Vohra HA, Bapu D, Bahrami T, Gaer JA, Satur CM. Does perioperative administration of thyroid hormones improve outcome following coronary artery bypass grafting [J]. J Card Surg,2008,23:92-96.
6. Bettendorf M, Schmidt KG, Grulich-Henn J, Ulmer HE, Heinrich UE. Triiodothyronine treatment in children after cardiac surgery:a doubleblind, randomized, placebo-controlled study[J]. Lancet 2000;356:529-534.
7. Weise K, Zaritsky A. Endocrine manifestations of critical illness in the child[J]. Pediatr Clin North Am 1987;34:119-130.
8. Semmekrot BA, Pesman GJ, Span PN, et al. Serial plasma concentrations of atrial natriuretic peptide,plasma renin activity, al-dosterone, and antidiuretic hormone in neonates on extracorporeal membrane oxygenation[J]. ASAIO J 2002;48:26-33
9.武婷,文其祥.体外循环对内分泌系统的影响[J].中国体外循环杂志,2008,6(2)：122-125
10. Eggum R, Ueland T, Mollnes TE, Videm V, Aukrust P, Fiane AE, Lindberg HL. Effect of perfusion temperature on the inflammatory response during pediatric cardiac surgery[J]. Ann Thorac Surg2008;85:611-617.
11. Omland T. Advances in congestive heart failure management in the intensive care unit: B-type natriuretic peptides in evaluation of acute heart failure[J]. Crit Care Med,2008, 36:S17-S27.
12. Shu Chien Huang, En-Ting Wu, Wen-Je,et al.Clinical Implication of Blood Levels of B-Type Natriuretic Peptide in Pediatric Patients on Mechanical Circulatory Support[J].Ann Thorac Surg,2006,81:2267-72.
13. Zaccaria Ricci, Cristiana Garisto, Stefano Morelli, et al. pediatric patients Brain natriuretic peptide is removed by continuous veno-venous hemofiltration[J]. Interact CardioVasc Thorac Surg,2009,9:33-36.
14. Georgiadis D. BergerA, Kowatschev E. etal. Predictive value of S100 β and neuron specific enolase levels for adverse neurologic outcome alter cardiac surgery[J]. J Thorac Cardiovasc Surg 2000,119(1):138-147.
15. Scallan mJ. Cerebral injury during paediatric heart surgery:perfusion issues[J]. Perfusion, 2004,; 19(4):221-228.
1.沈洪.现代心肺复苏概念的辨析.中华急诊医学杂志,2002,11(6)：365—366.
2.李春盛.目前心肺复苏存在的问题及对策.中华急诊医学杂志,2005,14(5)：362—363.
3. Abella BS, Alvarado JP, Myklebust H, Edelson DP, Barry A, O'Hearn N,Vanden Hoek TL, Becker LB. Quality of cardiopulmonary resuscitationduring in-hospital cardiac arrest. JAMA.2005;293:305-310.
4. International Liaison Committee on Resuscitation.2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation.2005;112:Ⅲ-1-Ⅲ-136.
5. HerlitzJ, Bang A, GunnarssonJ, etal. Factors associated with survival to hospital dischange among patients hopitalised alive after out of hospital cardiac arrest:change in outcome over 20 years in community of Goteborg. Sweden Heart,2003,89(1):25-30.
6.万健,李国民.3796例院内心肺复苏患者的回顾性分析·中华急诊医学杂志,2005,14(9)：746-749
7. Abella BS, Sandbo N, Vassilatos P, Alvarado JP, O'Hearn N, Wigder HN,Hoffman P, Tynus K, Vanden Hoek TL, Becker LB. Chest compression rates during cardiopulmonary resuscitation are suboptimal:a prospective study during in-hospital cardiac arrest. Circulation.2005; 111:428-434.
8. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest:a 3-phase time-sensitive model. JAMA.2002;288:3035-3038.
9. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen MP. Estimating effectiveness of cardiac arrest interventions:a logistic regression survival model. Circulation.1997;96:3308-3313.
10. Zaritsky A, Morley P.2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2005;112:Ⅲ-128-Ⅲ-130.
11. Manole MD, Kochanek PM, Fink EL, Clark RS. Postcardiac arrest syndrome:focus on the brain. Curr Opin Pediatr.2009 Dec;21(6):745-50.
12. Peberdy MA, Kaye W, Ornato JP, Larkin GL, Nadkarni V, Mancini ME, Berg RA, Nichol G, Lane-Trultt T. Cardiopulmonary resuscitation of adults in the hospital:a report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation. 2003;58:297-308.
13. Marcelo G, Cardarelli, Andrew J,Young, Bartley G.Use of Extracorporeal Membrane Oxygenation for Adults in Cardiac Arrest (E-CPR):A Meta-Analysis of Observational Studies.ASAIO Journal 2009; 55:581-586.
14. Krumnikl JJ, Toller WG, Prenner G, Metzler H. Beneficial outcome after prostaglandin induced post-partum cardiac arrest using levosimendan and extracorporeal membrane oxygenation.Acta Anaesthesiol Scand 50:768-770,2006.
15. Tiruvolpati R, Balasubramanian SK, Khoshbin E, et al:Successful use of venovenous extracorporeal membrane oxygenation in accidental hypothermic cardiac arrest. ASAIO J. 2005,51:474-476.
16. Kane DA, Thiagarajan RR, Wypij D, Scheurer MA, Fynn-Thompson F, Emani S, del Nido PJ, Betit P, Laussen PC. Rapid-response extracorporeal membrane oxygenation to support cardiopulmonary resuscitation in children with cardiac disease.Circulation.2010 Sep 14;122(11 Suppl):S241-8.
17. Thiagarajan RR, Brogan TV, Scheurer MA, Laussen PC, Rycus PT, Bratton SL.Extracorporeal membrane oxygenation to support cardiopulmonary resuscitation in adults. Ann Thorac Surg.2009 Mar;87(3):778-85.
18.82:Chen YS, Yu HY, Huang SC, Lin JW, Chi NH, Wang CH, Wang SS, Lin FY, Ko WJ.Extracorporeal membrane oxygenation support can extend the duration of cardiopulmonary resuscitation. Crit Care Med.2008 Sep;36(9):2529-35.
19. Wu ET, Huang SC, Chi NH, Lin MT, Ko WJ, Wang SS, Wang JK, Wu MH.Idioventricular rhythm induced by therapeutic hypothermia. Resuscitation.2008, Mar;76(3):471-473.
20. Arlt M, Philipp A, Zimmermann M, Voelkel S, Amann M, Bein T, Muller T, Foltan M, Schmid C, Graf B, Hilker M. Emergency use of extracorporeal membrane oxygenation in cardiopulmonary failure. Artif Organs.2009 Sep;33(9):696-703.
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4. Huang SC, WuET, ChenYS, etal. Experiencewith extracorporeallife supportin podiatric patients after cardiac surgery[J]. ASAIO J,2005,51(5):517-521.
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7. Ko WJ, Lin CY, Chen RJ, Wang SS, Lin FY, Chen YS. Extracorporea membrane oxygenation support for adult postcardiotomy cardiogenic shock[J]. Ann Thorac Surg, 2002,73(2):538-545.
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13. Khoshbin E, Dux AE, Killer H, Sosnowski AW, Firmin RK, Peek GJ. A comparison of radiographic signs of pulmonary inflammation during ECMO between silicon and polymethyl pentene oxygenators[J]. Perfusion,2007,22(1):15-21.
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19. Zimmermann A K, Weber N, Aebert H,et al. Effect of biopassive and bioactive surface-coatings on the hemocompatibility of membrane oxygenators[J]. J Biomed Mater Res B Appl Biomater,2007,80(2):433-439.
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23. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest:a 3-phase time-sensitive model[J]. JAMA,2002,288:3035-3038.
24. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen MP. Estimating effectiveness of cardiac arrest interventions:a logistic regression survival model [J]. Circulation, 1997,96:3308-3313.
25. Zaritsky A, Morley P.2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care[J]. Circulation, 2005,112:111128-130.
26. Manole MD, Kochanek PM, Fink EL, Clark RS. Postcardiac arrest syndrome:focus on the brain[J]. Curr Opin Pediatr,2009,21(6):745-50.
27. Peberdy MA, Kaye W, Omato JP, Larkin GL, Nadkarni V, Mancini ME, Berg RA, Nichol G, Lane-Trultt T. Cardiopulmonary resuscitation of adults in the hospital:a report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation[J]. Resuscitation,2003,58:297-308.
28. Hermans G, Meemseman W, Wilmer A, etal. Extracorporeal memb rane oxygenation:experience in an aduh medical ICU [J]. Thorac Cardiovesc Surg,2007, 55(4)2:23-228.
29. Shah Salman, Shankar V, Kevin B, et al. Clinical outcomes of 84 children with congenital heart disease managed with extracorporeal membrane oxygenation after cardiac surgery [J]. ASAIO J,2005,51(5):504-507.
30. Mahle WT, Forbess JM, Kirshbom PM, et al. Cost-utility analysis of salvage cardiac extracorporeal membrane oxygenation in children [J]. J Thorac Cardiovasc Surg, 2005,129(5):1084-1090.
31. Hamrick SE, Gremmels DB, Keet CA, et al. Neurodevelopmental outcome of infants supported with extracorporeal membrane oxygenation after cardiac surgery [J]. Pediatrics,2003,111(6 Pt 1):e671-e675.
1. Brown KL, Goldman AP. Neonatal extra-corporeal life support:indications and limitations[J]. Early Hum Dev,2008,84(3):143-148.
2. Schuerer DJ, Kolovos NS, Boyd KV, et al. Extracorporeal membrane oxygenation:current clinical practice, coding, and reimbursement J]. Chest,2008,134(1):179-184.
3. Kind K, Reiss N, Knobl HJ, et al. Introduction of a new oxygenator including a tight fiber for long-term ECMO in infants [J]. ASAIO J,2006,52(2):217-218.
4.柏淑颖,朱德明,王伟.涂层技术在体外循环装置中的应用及意义[J].中国体外循环杂志,2009,7(2)：124-128.
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14. Horton S, Thuys C, Bennett M, et al.Experience with the Jostra Rotaflow and QuadroxD oxygenator for ECMO[J]. Perfusion,2004,19(1):17-23.
15. Formica F, Avalli L, Martino A, et al. Extracorporeal membrane oxygenation with a poly-methylpentene oxygenator (Quadrox D) The experience of a single Italian centre in adult patients with refractorycardiogenic shock[J]. ASAIO J,2008,54(l):89-94.
16. Toomasian JM, Schreiner RJ, Meyer DE, et al. A polymethylpentene fiber gas exchanger for long-term extracorporeal life support[J]. ASAIO J,2005,51 (4):390-397.
1. Nishinaka T, Tatsumi E, Taenaka Y, et al. At least thirty-four days of animal continuous perfusion by a newly developed extracorporeal membrane oxygenation system without systemic anticoagulants [J]. Artif Organs,2002,26(6):548-551.
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4. Britt McILwain, Joseph Timpa, Ashish R et al. Plasma Concentrations of Inflammatory Cytokines Rise Rapidly during ECMO-related SIRS due to the Release of Pre-formed Stores in the Intestine [J].Lab Invest,2010,90(1):128-139.
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9. Levi M, ten Cate H, van der Poll T. Endothelium:interface between coagulation and inflammation[J]. Crit Care Med,2002,30(5 Suppl):s220-224.
10. Mackman N. The role ofthetissuefactor—thrombin pathwayin cardiac ischemia—repefusion injury[J]. Scmin Vase Med,2003,3(2):193-198.
11. Plotz FB, van Oeveren W, Bartlett RH, et al. Blood activation during neonatal extracorporeal life support [J]. J Thorac Cardiovasc Surg,1993,105:823-832.
12. Muntean W. Coagulation and antieoagulation in extraeorporeal membrane oxygenation [J]. ArtifOrgans,1999,23(11):979.
13. Mildner RJ, Taub N, Vyas JR, Killer HM, Firmin RK, Field DJ, et al. Cytokine imbalance in infants receiving extracorporeal membrane oxygenation for respiratory failure [J]. Biol Neonate,2005,88(4):321-327.
14. Fortenberry JD, Bhardwaj V, Niemer P, Cornish JD, Wright JA, Bland L. Neutrophil and cytokine activation with neonatal extracorporeal membrane oxygenation [J]. J Pediatr,1996, 128(5 Pt 1):670-678.
15. Risnes I, Wagner K, Ueland T, et al. Interleukin-6 may predict survival in extracorporeal membrane oxygenation treatment [J]. Perfusion,2008,23:173-178.
16. Dempsey PW, Doyle SE, He JQ, Cheng G. The signaling adaptors and pathways activated by TNF superfamily [J]. Cytokine Growth Factor Rev,2003,14(3):193-209.
17. Cha-Molstad H, Young DP, Kushner I, Samols D. The interaction of C-Rel with C/EBPbeta enhances C/EBPbeta binding to the C-reactive protein gene promoter [J]. Mol Immunol, 2007,44(11):2933-2942.
18. Hocker JR, Wellhausen SR, Ward RA, Simpson PM, Cook LN. Effect of extracorporeal membrane oxygenation on leukocyte function in neonates [J]. Artif Organs,1991,15 (1):23-28.
19. Khoshbin E, Dux AE, Killer H, Sosnowski AW, Firmin RK, Peek GJ. A comparison of radiographic signs of pulmonary inflammation during ECMO between silicon and poly-methyl pentene oxygenators [J]. Perfusion,2007,22(1):15-21.
1. Rune Eggum, Thor Ueland, Tom E. Mollnese, et al. Congenital Perfusion temperature, thyroid hormones and inflammation during pediatric cardiac surgery[J]. Interactive CardioVascular and Thoracic Surgery,2009,10:76-80.
2. Klemperer JD. Thyroid hormone and cardiac surgery [J]. Thyroid,2002,12:517-521.
3. Plumpton K, Nikolaus AH. Identifying infants at risk of marked thyroid suppression post-cardiopulmonary bypass [J]. Intensive Care Med,2005,31:581-587.
4. Nikolaus AH, Camphausen CK, Kececioglu D. Clinical review:thyroid hormone replacement in children after cardiac surgery is it worth a try [J]? Crit Care Med,2006,10: 213-227.
5. Vohra HA, Bapu D, Bahrami T, Gaer JA, Satur CM. Does perioperative administration of thyroid hormones improve outcome following coronary artery bypass grafting [J]. J Card Surg,2008,23:92-96.
6. Bettendorf M, Schmidt KG, Grulich-Henn J, Ulmer HE, Heinrich UE. Triiodothyronine treatment in children after cardiac surgery:a doubleblind, randomized, placebo-controlled study[J]. Lancet 2000;356:529-534.
7. Weise K, Zaritsky A. Endocrine manifestations of critical illness in the child[J]. Pediatr Clin North Am 1987;34:119-130.
8. Semmekrot BA, Pesman GJ, Span PN, et al. Serial plasma concentrations of atrial natriuretic peptide,plasma renin activity, al-dosterone, and antidiuretic hormone in neonates on extracorporeal membrane oxygenation[J]. ASAIO J 2002;48:26-33
9.武婷,文其祥.体外循环对内分泌系统的影响[J].中国体外循环杂志,2008,6(2)：122-125
10. Eggum R, Ueland T, Mollnes TE, Videm V, Aukrust P, Fiane AE, Lindberg HL. Effect of perfusion temperature on the inflammatory response during pediatric cardiac surgery[J]. Ann Thorac Surg2008;85:611-617.
11. Omland T. Advances in congestive heart failure management in the intensive care unit: B-type natriuretic peptides in evaluation of acute heart failure[J]. Crit Care Med,2008, 36:S17-S27.
12. Shu Chien Huang, En-Ting Wu, Wen-Je,et al.Clinical Implication of Blood Levels of B-Type Natriuretic Peptide in Pediatric Patients on Mechanical Circulatory Support[J].Ann Thorac Surg,2006,81:2267-72.
13. Zaccaria Ricci, Cristiana Garisto, Stefano Morelli, et al. pediatric patients Brain natriuretic peptide is removed by continuous veno-venous hemofiltration[J]. Interact CardioVasc Thorac Surg,2009,9:33-36.
14. Georgiadis D. BergerA, Kowatschev E. etal. Predictive value of S100 β and neuron specific enolase levels for adverse neurologic outcome alter cardiac surgery[J]. J Thorac Cardiovasc Surg 2000,119(1):138-147.
15. Scallan mJ. Cerebral injury during paediatric heart surgery:perfusion issues[J]. Perfusion, 2004,; 19(4):221-228.
1.沈洪.现代心肺复苏概念的辨析.中华急诊医学杂志,2002,11(6)：365—366.
2.李春盛.目前心肺复苏存在的问题及对策.中华急诊医学杂志,2005,14(5)：362—363.
3. Abella BS, Alvarado JP, Myklebust H, Edelson DP, Barry A, O'Hearn N,Vanden Hoek TL, Becker LB. Quality of cardiopulmonary resuscitationduring in-hospital cardiac arrest. JAMA.2005;293:305-310.
4. International Liaison Committee on Resuscitation.2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation.2005;112:Ⅲ-1-Ⅲ-136.
5. HerlitzJ, Bang A, GunnarssonJ, etal. Factors associated with survival to hospital dischange among patients hopitalised alive after out of hospital cardiac arrest:change in outcome over 20 years in community of Goteborg. Sweden Heart,2003,89(1):25-30.
6.万健,李国民.3796例院内心肺复苏患者的回顾性分析·中华急诊医学杂志,2005,14(9)：746-749
7. Abella BS, Sandbo N, Vassilatos P, Alvarado JP, O'Hearn N, Wigder HN,Hoffman P, Tynus K, Vanden Hoek TL, Becker LB. Chest compression rates during cardiopulmonary resuscitation are suboptimal:a prospective study during in-hospital cardiac arrest. Circulation.2005; 111:428-434.
8. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest:a 3-phase time-sensitive model. JAMA.2002;288:3035-3038.
9. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen MP. Estimating effectiveness of cardiac arrest interventions:a logistic regression survival model. Circulation.1997;96:3308-3313.
10. Zaritsky A, Morley P.2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation.2005;112:Ⅲ-128-Ⅲ-130.
11. Manole MD, Kochanek PM, Fink EL, Clark RS. Postcardiac arrest syndrome:focus on the brain. Curr Opin Pediatr.2009 Dec;21(6):745-50.
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