Sonoclot凝血和血小板功能分析仪监测肝移植术中凝血功能变化的应用

目的 探讨肝移植术中凝血功能的变化和Sonoclot凝血及血小板功能分析仪(sonoct coagution & piatelet function analgzer,SCA)在肝移植术中的应用.方法 24例择期肝移植手术患者全部采用原位经典非转流手术方法.于麻醉诱导前(TO)、手术开始后60 min(T1),无肝期30 min(T2)、新肝期30 min(T3)、新肝期120 min(T4)和术毕(T5)时分别采集桡动脉血检测,硅燥土激活的全血血栓弹性描记图(thrombelastography,TEG),指标包括R值、K值、Alpha角和MA值;玻璃珠激活的全血SCA,指标包括ACT、CR和PF值;常规凝血指标包括PT、APTT、INR、Fbg和Plt.结果 (1)SCA和TEG诊断凝血因子缺乏、纤维蛋白凝胶形成速度和血小板功能(都正常或者都异常)的Kappa值分别是0.371(P<0.05)、0.363(P<0.05)、0.438(P<0.05).gbACT与R、CR与α角、PF与MA呈正相关(r=0.790,P<0.05;r=0.766,P<0.05;r=0.502,P<0.05),CR与K呈负相关(r=-0.588,P<0.05).(2)与T0时比较,T3～T5时PT、INR、gbACT及R延长和FBG、CR、α及MA降低(P<0.05),T1～T5时APTT、T3时K延长(P<0.05),T2～T4时PF降低.结论SCA能够准确地监测肝移植术中凝血功能的变化.     

止血环酸在心肺转流术中对凝血功能的影响

目的 应用sonoclot分析仪(SCT)观察止血环酸在心脏手术中的血液保护效果。方法36例心脏手术患者分成工组(抑肽酶,n=12)、Ⅱ组(止血环酸,n=12)和Ⅲ组(非用药组,n=12)。Ⅰ、Ⅱ组在心肺转流(CPB)下完成心脏手术,Ⅲ组则为非CPB下的冠脉搭桥手术。应用SCT观察切皮前和鱼精蛋白中和肝素后的凝血和血小板(Plt)功能的变化。结果 sonACT在T_1时点Ⅲ组为(123.21±18.58)s,明显高于Ⅰ组的(110.36±24.72)s和Ⅱ组的(106.09±13.91)s(P均<0.05);纤维蛋白凝集率(clot rate)、Plt功能在T_1与T_2时点三组之间均无显著差异。Plt在T_2时点Ⅲ组则明显高于Ⅰ、Ⅱ组。Ⅰ、Ⅱ组在T_2时点的Plt较T_1下降非常显著(P<0.01),Ⅲ组则无明显改变。结论 止血环酸对CPB下心脏手术患者凝血与Plt功能的影响与抑肽酶相似,非CPB下冠状动脉搭桥术对血液系统的影响明显减轻。     

心脏手术中凝血及血小板功能的变化

目的应用Sonoclot凝血及血小板功能分析仪(SCT)检测风心病和冠心病患者心脏手术中凝血与血小板功能的变化.方法ASAⅡ～Ⅲ级心脏手术患者30例,其中瓣膜置换术15例(瓣膜组),冠脉搭桥术15例(CABG组).采用静吸复合全身麻醉.分别于麻醉前(T1)、诱导后(T2)、肝素化后(3mg/kg)(T3)、CPB结束鱼精蛋白拮抗后5min(T4)抽血,检测激活全血凝固时间(sonACT)、凝血速率和血小板功能,并在T1和T4行血小板计数.结果与T1相比,T2的凝血速率明显升高(P＜0.05);T3的sonACT明显延长(P＜0.01),凝结率和血小板功能显著下降(P＜0.01);T4的sonACT明显延长、血小板功能明显升高(P＜0.01),血小板计数显著降低(P＜0.01).另外,瓣膜组T3的sonACT明显长于CABG组(P＜0.05);CABG组T1的凝血速率(30.32±3.07凝血信号/min)明显高于瓣膜组(24.15±4.13凝血信号/min)(P＜0.05).CABG组T4的血小板功能(2.83±0.90)明显高于瓣膜组(2.00±0.81)(P＜0.05).结论心脏手术中监测凝血及血小板功能具有一定价值,尤其在CPB结束后.瓣膜组患者的凝血及血小板功能虽在正常范围内但均低于冠心病患者.     

心肺转流围术期血浆肝素浓度的变化

目的　心肺转流 (CPB)围术期血浆肝素浓度的变化及其与抗凝监测、肝素中和及肝素反跳的关系。方法　 10例成人CPB心脏手术病人 ,于麻醉后肝素前、肝素 1、2、3、4、5、10min、CPB前、CPB后 5、10、30min、停机、中和 1∶0 5、1∶0 75、1∶1、中和结束及术后 1～ 6h采血。分别测定血浆肝素浓度 (应用发色底物抗Xa方法 ) ,激活部分凝血致活酶时间 (APTT)、凝血酶时间 (TT)及激活全血凝固时间 (ACT)。结果　静注肝素 (4 0 0U/kg)后 1min血浆浓度达高峰为 (6 4 6± 1 0 5 )U/ml,到CPB开始时为 (4 2 8± 0 30 )U/ml,停机时为 (2 82± 0 4 1)U/ml。CPB前血浆肝素浓度与ACT显著相关 (r =0 896 ,P <0 0 1)。首次中和 (比值为 1∶0 5 )后肝素浓度为 (0 12± 0 10 )U/ml。术后 3～ 4h肝素浓度重新升高 (与基础值相比P <0 0 1) ,但与ACT、APTT及TT均无相关性 (P >0 0 5 )。结论　CPB前ACT能可靠监测肝素抗凝 ;CPB后鱼精蛋白首次按 1∶0 5已基本能中和游离的肝素 ;总比例 1∶1 5后 ,无肝素反跳     

体外循环后凝血系统的变化

体外循环(CPB)对凝血系统有多方面影响。本文旨在通过测定APTT、PT和ACT等指标来了解CPB后凝血系统的变化,对防治心内直视手术后出血可能有一定的临床意义。资料与方法择期心脏瓣膜替换病人33例,术前没有抗凝治疗,出凝血检查和肝肾功能正常。麻醉采用静脉芬太尼和安氟醚吸入,CPB用Sarns机,膜式氧合器。预充液为乳酸林格氏液1500ml、706代血浆500ml和各种电解质,肝素化剂量400U/kg,CPB中ACT>480秒,其它资料见     

舒芬太尼和芬太尼复合麻醉下体外循环先天性心脏病手术患儿应激反应的比较

目的 比较舒芬太尼和芬太尼复合麻醉下体外循环(CPB)先天性心脏病手术患儿的应激反应.方法 择期拟在体外循环下行先天性心脏病手术患儿24例,年龄2～6岁,随机分为2组(n=12):舒芬太尼复合麻醉组(S组)和芬太尼复合麻醉组(F组).静脉注射咪达唑仑0.1 mg/kg,维库溴铵0.15 mg/kg,舒芬太尼0.7μg/kg(S组)或芬太尼5μg/kg(F组),气管插管后机械通气,切皮前两组静脉注射维库溴铵0.08 mg/kg、咪达唑仑0.05 mg/kg、舒芬太尼0.7μg/kg(S组)或芬太尼5μg/kg(F组),劈胸骨前静脉注射舒芬太尼1.5μg/kg(S组)或芬太尼10 μg/kg(F组),劈胸骨后静脉输注异丙酚6～9 mg·kg~(-1)·h~(-1),按需间断静脉注射维库溴铵0.08 mg/kg维持麻醉.转流前体外循环机内加入眯达唑仑0.1 mg/kg,S组静脉注射舒芬太尼1.5 μg/kg,F组静脉注射芬太尼10 μg/kg.于入室(T_1)、麻醉诱导前即刻(T_2)、气管插管后1 min(T_3)、5 min(T_4)、10 min(T_5)、切皮后1 min(T_6)、劈胸骨后1 min(T_7)时记录MAP、HR.于T_1、T_3、T_7、复温即刻(T_8)、停CPB后10 min(T_9)、术后24 h(T_10)时抽取桡动脉血样5 ml,测定血浆促肾上腺皮质激素、皮质醇、胰高血糖素、乳酸、血糖浓度.结果 两组MAP和HR均在正常范围内.与F组比较,S组血浆促肾上腺皮质激素、皮质醇、胰高血糖素和乳酸浓度降低(P<0.05或0.01),血糖浓度差异无统计学意义(P>0.05).与T_1时比较,两组T_(7,9,10)时血浆促肾上腺皮质激素、胰高血糖素和血糖浓度升高,T_(7,9,10)时皮质醇浓度升高,T_(8～10)时乳酸浓度升高(P<0.05).结论 与芬太尼复合麻醉相比,舒芬太尼复合麻醉可更有效地抑制体外循环先天性心脏病手术患儿应激反应.     

七氟烷对体外循环冠状动脉旁路移植术患者左心室功能的影响

目的 评价七氟烷对体外循环(CPB)冠状动脉旁路移植术(CABG)患者左心室功能的影响.方法 择期CPB下行CABG的冠心病患者35例,男性30例,女性5例,年龄53～75岁,身高150～183 cm,体重46～100 kg,AsAⅡ或Ⅲ级,七氟烷分为冠脉搭桥前后2个阶段给药,分别为气管插管后至锯胸骨前和关闭胸腔至手术结束前,CPB期间停止吸入七氟烷.七氟烷呼气末浓度相当于1 MAC.围术期行食管超声心动图(TEE)检查,于锯胸骨前未吸入七氟烷(T_1)、吸入5 min(T_2)、15 min(T_3)、关闭胸腔后未吸入七氟烷(T_4)、吸入5 min(T_5)、15 min(T_6)时记录平均动脉压(MAP)和TEE监测指标:E波、A波、S波.D波和AR波的峰值、心指数(CI)、左室短轴缩短率(FS)、左室射血分数(LVEF),左心室舒张早期血流播散速度(Vp),计算E波与A波峰值比(E/A)、S波与D波峰值比(S/D) 和E波与Vp的比值(E/Vp).结果 与T_1时比较,T_(2,3)时MAP降低,T_3时LVEF、FS和CI降低,T_4时HR、LVEF、FS、CI升高,.E波:A波、S波、D波和AR波的峰值升高(P<0.05或0.01);与T_4时比较,T_(5,6)时MAP降低,T_6时LVEF、FS和CI降低(P<0.05或0.01).结论 呼气末浓度相当于1 MAc的七氟烷可明显抑制CPB下CABG患者左心室收缩功能,但对舒张功能无明显影响.     

无肝素化体外循环转流及早期炎性因子的表达

目的探讨采用鱼精蛋白-琼脂糖凝胶进行无肝素化体外循环(CPB)的可行性。方法选择健康成年家犬12只,犬龄2～3岁,雌雄不限,体重20～28(23.3±3.7)kg。按随机数字表法将12只犬分为两组,每组6只,肝素化组:行常规CPB;非肝素化组:采用鱼精蛋白-琼脂糖凝胶吸附血浆凝血因子,即行无肝素化CPB。于CPB开始时和CPB1 h、2 h、3 h采用酶联免疫吸附法(ELISA)测定动脉血中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和白细胞介素8(IL-8)的浓度,并进行比较。结果非肝素化组和肝素化组犬在CPB过程中肉眼观察膜肺内均未见血栓形成,全血激活凝血时间(ACT)始终>480 s,生命体征均平稳。两组血浆TNF-α、IL-6和IL-8浓度在CPB开始时差异无统计学意义,非肝素化组血浆TNF-α和IL-8于CPB 1 h、CPB 2 h和CPB 3 h时均高于肝素化组[CPB3 h TNF-α:(156.48±16.65)ng/L vs.(115.87±15.63)ng/L,t=4.356,P=0.001;CPB 3 h IL-8:(365.38±46.18)ng/L vs.(299.29±34.50)ng/L,t=2.808,P=0.019],而两组IL-6浓度差异无统计学意义(P>0.05)。结论依靠鱼精蛋白-琼脂糖凝胶对凝血因子进行吸附,以进行无肝素化CPB效果明确,但具有一定的促进全身炎症反应效应。     

用激活全血凝固时间估计最短肝素化时间

选择连续实施CPB心脏手术病人50例,肝素化前取血2ml,经中心静脉测压管注入肝素300 IU/kg。用40ml注射器连接中心静脉测压管,以10ml/min速率持续抽取上腔静脉血并经三通取血2ml,取血时间为注入肝素后1,2,3,4,5及10min,每次取血时间为12s。取血后立即测ACT(Hemochoron801)。肝素化指标定为ACT值大于400s。     

参附注射液对兔体外循环时胰岛素抵抗的影响

目的 探讨参附注射液SFI对兔CPB时胰岛素抵抗的影响.方法 健康成年新西兰大白兔30只,雌雄不拘,体重2.2～2.5 kg,随机分为3组(n=10),假手术组(S组)和CPB组腹腔注射等容量生理盐水,SFI组于CPB前2 d、1 d及麻醉诱导前30 min时腹腔注射SFI 10 ml/kg.于麻醉诱导后5 min(T_1)、主动脉阻断即刻(T_2)、主动脉开放5 min(T_3)、主动脉开放35 min(T_4)和主动脉开放75 min (T_5)时采集动脉血样,测定血糖及胰岛素水平,并计算胰岛素抵抗指数(HOMA-IR).于CPB 150 min时取右后肢股四头肌组织,测定骨骼肌胰岛素受体底物-1(IRS-1)、磷脂酰肌醇3激酶p85亚单位(P13Kp85)、葡萄糖转运蛋白(GLUT)4的表达水平.结果 与T_1时比较,3组T_(2～5)时血糖、胰岛素水平及HOMA-IR均升高(P<0.05);与S组比较,CPB组和SFI组T_(2～5)时血糖、胰岛素水平及HOMA-IR均升高,P13Kp85及GLUT4表达下调(P<0.05);与CPB组比较,SFI组T_(2～5)时血糖水平及HOMA-IR降低,胰岛素水平升高,P13Kp85及GLUT4表达上调(P<0.05).结论 SFI可改善CPB诱导的兔胰岛素抵抗,其机制可能与上调骨骼肌胰岛素信号转导分子的表达有关.     

The effect of temperature and aprotinin during cardiopulmonary bypass on three different methods of activated clotting time measurement

The activated clotting time (ACT) is used frequently for monitoring blood anticoagulant response with heparin before, during, and after cardiopulmonary bypass (CPB). Many cardiac procedures involving CPB require reduction of the patient's blood temperature and use of the serine protease inhibitor, aprotinin. Three different methods of ACT measurement were compared to show the effects of different CPB temperatures and the presence of aprotinin. A total of 42 patients were included in the study: 14 received CPB at 28 degrees C, 14 received CPB at 32 degrees C, and 14 normothermic (37 degrees C) CPB. Within each temperature group, seven received aprotinin. The ACT in each group of patients was measured by a celite activator (C-ACT), a kaolin activator (K-ACT), and a celite, kaolin and glass activator (MAX-ACT). All three methods of ACT measurement showed significant increases (p < .05) in clotting times at hypothermic CPB compared with normothermic groups. During heparinization the C-ACT was significantly increased (p < .05) in the presence of aprotinin. Comparability between the 3 ACT measurement methods showed a very high correlation between C-ACT and K-ACT clotting times (R2 = .8962), and slightly lower correlation between MAX-ACT and C-ACT (R2 = .7780), and MAX-ACT and K-ACT (R2 = .7827). All ACT measurements are affected by changes in blood temperature. The C-ACT measurement is prolonged with aprotinin, whereas the MAX-ACT and K-ACT method of measurement in the presence of aprotinin are not significantly altered. It appears that the MAX-ACT produces lower values and may necessitate additional heparin therapy for ACT target values considered safe during CPB. Further study is required from these additional findings.     

瑞芬太尼预处理对冠状动脉旁路移植术患者体外循环期间的脑保护作用

目的 探讨瑞芬太尼预处理对冠状动脉旁路移植术患者体外循环期间的脑保护作用.方法 择期行体外循环(CPB)冠状动脉旁路移植术的患者40例,ASA Ⅱ或Ⅲ级,随机分为4组(n=10):对照组(C组)和不同剂量瑞芬太尼预处理组(R_(1～3)组).R_(1～3)组于麻醉诱导后30 min时分别静脉输注瑞芬太尼0.6、1.2和1.8 μg·kg~(-1)min~(-1),输注时间5 min,重复3次,间隔5 min;C组以生理盐水代替瑞芬太尼.于麻醉诱导前(T_0)、CPB开始前(T_1)、CPB 30 min(T_2)、CPB结束(T_3)时取颈内静脉血样3 ml,采用ELISA法测定血浆S-100β蛋白浓度,采用比色法测定血浆超氧化物歧化酶(SOD)活性和丙二醛(MDA)浓度.结果 与T_0时比较,T_(1～3)时各组血浆S-100β蛋白和MDA浓度升高,SOD活性降低(P<0.05或0.01);与C组比较,R_3组T_(2,3)时血浆S-100β蛋折和MDA浓度降低,SOD活性升高(P<0.05),R_1组和R_2组上述指标差异无统计学意义(P>0.05).结论 瑞芬太尼(1.8μg·kg~(-1)min~(-1))预处理可减轻冠状动脉旁路移植术患者CPB诱发脑损伤,其机制可能与抑制脑脂质过氧化反应有关.     

Maintenance of blood heparin concentration rather than activated clotting time better preserves the coagulation system in hypothermic cardiopulmonary bypass

In cardiopulmonary bypass (CPB), despite heparin regimens in which the activated clotting time (ACT) is kept at more than 400 s, there is biochemical evidence of thrombin generation indicating activation of the coagulation system and increased fibrinolytic activity. Therefore, to reduce the coagulant activation has been one of the main issues in the improvement of CPB. The purpose of this study was to compare the heparin concentration with the ACT and to evaluate the effect of keeping higher heparin concentration on the coagulation and fibrinolytic systems during hypothermic CPB, employing moderate hypothermia (MHT) or deep hypothermic circulatory arrest (DHT). Heparin was either administered to maintain an ACT >400 s (ACT group) or to maintain a whole blood heparin concentration of 3 mg/kg (heparin group). At the lowest core temperature during CPB, the ACT and the heparinase ACT (unrelated to heparin concentration) were increased the most whereas the whole blood heparin concentration was less than half the initial concentration in both ACT groups of MHT and DHT. The thrombin-antithrombin III (TAT) content just after CPB in both MHT and DHT was significantly lower in the heparin group than in the ACT group. In conclusion, ACT does not reflect the whole blood heparin concentration during hypothermic CPB. Furthermore, maintenance of the higher heparin concentration during hypothermic CPB may suppress the activation of the coagulation system via thrombin inhibition. That effect was more remarkable in deep hypothermic CPB. Therefore, we believe that anticoagulation management during hypothermic CPB should be based on the maintenance of the higher blood heparin concentration.     

The treatment of heparin resistance with Antithrombin III in cardiac surgery

PURPOSE: To report three patients who developed heparin resistance during cardiac surgery which was successfully managed with 1000 U Antithrombin III (AT III). CLINICAL FEATURES: We observed heparin resistance prior to cardiopulmonary bypass (CPB) in one patient and during the CPB in two patients. In the first patient who was scheduled for mitral valve replacement, although heparin was administered sequentially up to 500 U x kg(-1) prior the CPB, the ACT value was 354 sec. After 1,000 U ATIII were administered the ACT was 395 sec and CPB was initiated. The ACT remained between 496 and 599 sec throughout CPB and a total of 260 mg protamine sulfate was given. In the other two patients following 300 U x kg(-1) heparin, the ACT was up to 400 sec and CPB was initiated. During CPB, ACT were decreased 360 sec and 295 sec in patients II and III respectively. Although heparin was added 1,500 U, ACT increased to > or = 400 sec could not be achieved. In the second patient ATIII activity was found 10%. After the administration of 1,000 U ATIII, ATIII activity was found to be 67% 40 min later and ACT were increased up to 400 sec. There was no thrombosis within the extracorporeal circuit, additional heparin was not required, less protamine was administered (< or = 3 mg x kg(-1)) and no excessive postoperative bleeding was observed in all patients. CONCLUSION: We recommend that AT III supplementation should be considered to manage heparin resistance prior or during CPB in patients undergoing open heart surgery.     

Heparin-coated Cardiopulmonary Bypass Circuits in Coronary Bypass Surgery

Abstract: Cardiopulmonary bypass (CPB) is a nonphysiologic environment for an organism. The damage of blood components may also lead to organ dysfunction, sometimes recognized as postperfusion syndrome. One possible way to diminish the risk of these complications would be to reduce the thorombogenicity and to improve the biocompatibility of the artificial surfaces by using a heparin-coated CPB circuit. In this study, we compared a heparin-coated CPB circuit with a noncoated CPB circuit in terms of biocompatibility in 20 patients undergoing elective coronary bypass surgery. We employed a Dura-flo II (n = 10) as a heparin-coated CPB circuit and a Univox IC (n = 10) as control subjects. Ten patients (Group C) were operated on using the heparin-coated CPB circuit. A total of 10 patients were given heparin in a reduced dose (2.0 mg/kg), and additional heparin was given if the activated clotting time (ACT) was below 400 s. The control group also included 10 patients (Group NC), who were operated on with noncoated devices. They received 2.5 mg/kg of heparin, and additional heparin was given if the ACT was below 450 s. All patients had normal coagulation parameters and did not receive blood transfusion. We measured complement activation levels (C3a, C4a), platelet count, thrombin-antithrombin III complex levels, D-dimer levels, and ACT during CPB and respiratory index postoperatively. The concentration of C3a in group NC was significantly higher than that in group C. Platelet reduction in group NC was significantly greater than that in group C. There were no significant differences in the remaining parameters between the 2 groups. We concluded that heparin-coated CPB circuits improved biocompatibility by reducing complement activation and platelet consumption and enabled us to reduce the dose of heparin required for systemic heparinization.     

Heparin-coated cardiopulmonary bypass circuits reduce blood cell trauma. Experiments in the pig

Blood cell trauma and postoperative bleeding remain important problems in cardiopulmonary bypass (CPB). We compared heparin-coated with non-coated circuits in the pig. Twenty animals were perfused for 2 h at normothermia using membrane oxygenators (Bentley Bos 50). Two groups were studied. In the non-coated group (NC, n = 11) the CPB circuits used were without a heparin coating. This group had systemic heparinization of 400 IU/kg to maintain an ACT (activated clotting time) of over 400 s during CPB. In the coated group (C, n = 9), all surfaces exposed to blood in the CPB circuits were heparin-coated. This group had the heparin dose reduced to 25% (100 IU/kg) without further administration regardless of ACT. During CPB, group C displayed shorter ACT (per definition), higher platelet count, platelet adhesion and lower fibrinolysis and haemolysis (P less than 0.05) as compared to group NC. No thromboembolic events were detected during CPB. Three animals in group NC and 4 animals in group C were weaned from CPB and protaminized. Four hours postoperatively, the leucocyte consumption was two-fold greater and blood loss about four-fold greater in group NC as compared with group C (P less than 0.05). Perfusion with heparin-coated surfaces reduces blood cell trauma. The decreased postoperative blood loss observed in group C is probably explained by the reduced dosages of heparin and protamine.     

Effects of heparin, haemodilution and aprotinin on kaolin-based activated clotting time: in vitro comparison of two different point of care devices

BACKGROUND: During cardiopulmonary bypass (CPB), measurement of kaolin-based activated clotting time (kACT) is a standard practice in monitoring heparin-induced anticoagulation. Despite the fact that the kACT test from the Sonoclot Analyzer (SkACT) has been commercially available for several years, no published data on the performance of SkACT are available. Thus, the aim of this in vitro study was to compare SkACT with an established kACT from Hemochron (HkACT). METHODS: Blood was withdrawn from 25 patients before elective cardiac surgery. SkACT and HkACT were measured in duplicate after in vitro administration of heparin (0, 1, 2 and 3 U/ml), calcium-free lactated Ringer's solution (25% and 50% haemodilution) and aprotinin (200 kIU/ml). RESULTS: A total of 600 duplicate kACT measurements were obtained from 25 cardiac surgery patients. Overall, mean bias +/- SD between SkACT and HkACT was 7 +/- 70 s (1.3% +/- 14.1%). Administration of heparin, haemodilution and aprotinin induced a comparable effect on both activated clotting time (ACT) tests. Mean bias ranged from -4 +/- 39 s (-1.7% +/- 12.9%) to 4 +/- 78 s (3.2% +/- 15.6%) for heparinzed blood samples after haemodilution or aprotinin application and increased after combined aprotinin administration and haemodilution. After haemodilution and administration of aprotinin, both ACT tests were less reliable for values >480 s in heparinized blood samples. CONCLUSION: Accuracy and performance of SkACT and HkACT were comparable after in vitro administration of heparin, aprotinin and haemodilution. Both ACT tests were considerably affected by aprotinin and haemodilution.     

Real time measurement of heparin concentration during cardiopulmonary bypass

BACKGROUND: A heparin/protamine titration system for measurement of heparin levels (Hepcon) is promising for efficient anticoagulation during cardiopulmonary bypass (CPB). METHODS: Fifty-seven patients subjected to CPB were divided into two groups, control (n = 24) and Hepcon groups (n = 33). The Hepcon group was further divided into three subgroups according to perfusion temperature. For the control group, conventional administration of an anticoagulant (300 IU/kg of heparin) and reversal protocol (heparin 1: protamine 1) was performed. For the Hepcon group, a heparin dose-response assay directed the initial dose of heparin. Hepcon also determined the dose of protamine by the titration. The initial dose of heparin in the control group (300 IU/kg) was statistically less than that of Hepcon group (360+/-80 IU/kg). RESULTS: In the Hepcon group, the sensitivity to heparin was correlated with coagulation time (r = -0.78) and antithrombin III levels (r = 0.70), and individual difference of sensitivity resulted in a wide range of dosage (160 to 490 IU/kg). A strong correlation was observed between plasma and whole blood concentration of heparin (r = 0.86). However, they did not correlate with ACT values. Perfusion temperature didn't affect the heparin level, but did the ACT value. In the Hepcon group, the dose of protamine was significantly less and adverse events were rare. CONCLUSIONS: In conclusion, whole blood heparin measurements correlated well with plasma heparin concentration. Protamine titration of heparin reduced the dose of protamine and decreased the chance of adverse reactions.     

Heparinless cardiopulmonary bypass with argatroban in dogs.

OBJECTIVES: Systemic heparinization is usually required for cardiopulmonary bypass (CPB). However, problems such as heparin-induced thrombocytopenia, protamine shock, and antithrombin III deficiency exist related to CPB with heparinization. The aim of this study was to evaluate argatroban (ARG) as a substitute for heparin during CPB. METHODS: In the pilot study, blood samples were sequentially obtained from dogs with continuous infusion of ARG at a dose of 10 (n = 6), 20 (n = 6), or 30 (n = 6) microg/kg per min for 2 h without CPB. In the main study, dogs underwent CPB for 2 h with 10 (n = 6) or 30 (n = 6) microg/kg per min of ARG or with heparin with blood samples obtained sequentially. Thrombogenicity in each group was evaluated by observation of the blood-contacting surfaces of the CPB circuits with scanning electron microscopy (SEM). Evidence of thromboembolism in the dogs was also investigated in histological specimens of the kidney and spleen in addition to microscopic observation at autopsy. RESULTS: In the pilot study, the activated coagulation time (ACT) reached a maximum level dose-dependently after continuous infusion of ARG for 30 min. ACT returned to the baseline value within 60 min after the termination of continuous infusion. In the main study, CPB with 30 microg/kg per min of ARG achieved thrombin-antithrombin III complex (TAT) level similar to that achieved by CPB with heparin. Platelet count with 30 microg/kg per min of ARG tended to be higher than that with heparin or 10 microg/kg per min of ARG. The SEM appearance of blood-contacting surfaces of the CPB circuits after infusion with 30 microg/kg per min of ARG appeared to be similar to that after infusion with heparin. Depositions on the blood-contacting surfaces of the CPB circuits were also frequently observed with 10 microg/kg per min of ARG. CONCLUSIONS: Coagulability related to CPB was controlled by the appropriate ARG dosage without the use of heparin in dogs. ARG may be a substitute for heparin in CPB.     

Heparin management protocol for cardiopulmonary bypass influences postoperative heparin rebound but not bleeding.

A group of 63 adult patients undergoing cardiac surgical procedures requiring cardiopulmonary bypass (CPB) were studied to examine the relationship between heparin doses administered and postoperative bleeding. Patients were randomly assigned either to receive heparin 200 U/kg and additional heparin as needed to reach and maintain an activated clotting time (ACT) greater than 400 s for CPB (group A, n = 30), or to receive heparin 400 U/kg and additional heparin as needed to reach and maintain a whole blood heparin concentration greater than 4.0 U/ml for CPB (group H, n = 33). Groups were compared for the amount of postoperative bleeding, heparin rebound, homologous transfusion requirements, and standard laboratory coagulation tests. In the last 33 patients studied, additional tests of platelet aggregation and plasma levels of beta thromboglobulin (BTG), antithrombin III, and several markers of fibrinolysis were measured and compared by group. The mean heparin dose was 28,000 +/- 4,800 U for group A and 57,000 +/- 10,700 U for group H (P less than 0.05 for group A vs. group H). At 8 and 24 h postoperatively, mediastinal drainage did not differ significantly between groups (mean 24-h drainage +/- SD = 901 +/- 414 ml in group A, 1035 +/- 501 ml in group H), nor did the incidence of transfusion with homologous blood products.(ABSTRACT TRUNCATED AT 250 WORDS)