Azathioprine-Induced Multisystem Organ Failure and Cardiogenic Shock

Azathioprine is administered to treat increasing numbers of disorders over a wide range of organ systems. The potential for the drug to cause widespread organ dysfunction is not fully appreciated. In fact, azathioprine can cause multisystem organ dysfunction involving the kidneys, liver, and cardiovascular system. The discovery of global cardiac dysfunction as one component of this complication may indicate a mechanism of hypotension. Clinicians must be aware of the potential for azathioprine to cause such toxicities to facilitate appropriate patient management.     

心脏术后低心输出量综合征的体外膜肺氧合技术疗效观察

近年来,随着心脏直视手术数量的增长,手术技术、心肌保护技术及围术期管理技术都得到显著改善,但仍有2%～6%的患者术后出现低心输出量综合征(low cardiac output syndrom,LCOS)而难以脱离体外循环(extracorporeal circulation,ECC),需要对心脏进行机械性辅助(mechanical circulatory support,MCS)。体外膜肺氧合技术(extracorporeal membrane oxygenation,ECMO)可为心脏术后出现LCOS的患者提供心功能恢复时间,为其脱离ECC提供了一个手段[1]。但迄     

主动脉球囊反搏术(IABP)治疗心源性休克的护理体会

本文总结了主动脉球囊反搏治疗7例心源性休克患者的应用情况,术前、术中、术后及并发症的护理体会。提出应严密监测病情变化,预防并发症,恰当护理可提高主动脉球囊反搏成功率。     

急性心肌梗死合并心源性休克预后分析

目的探讨急性心肌梗死合并心源性休克不同治疗的预后及生存率。方法对36例急性心肌梗死合并心源性休克患者的临床资料进行回顾性分析。结果36例患者中经相关治疗痊愈31例（86.1%）,死亡5例（13.8%）。结论早期的溶栓及PC I术使梗死相关血管恢复再灌注是避免急性心肌梗死合并心源性休克的重要手段。     

Vasopressin During Cardiopulmonary Resuscitation and Different Shock States

Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time.     

急性心肌梗死合并心源性休克的诊治分析

目的探讨急性心肌梗死合并心源性休克的临床治疗效果。方法对张家港市第一人民医院急诊科收治的25例急性心肌梗死合并心源性休克患者的临床资料进行回顾性的分析和总结。结果经应用溶栓治疗、机械通气、应用血管活性药物、抗凝药物等相关治疗和处理后,19例患者抢救成功,抢救成功率为76%。结论急性心肌梗死合并心源性休克病死率高,早期诊断,积极预防和治疗,可降低心源性休克的病死率。     

异丙酚对大鼠失血性休克复苏后肠道的保护作用

目的:探讨短时间内异丙酚对失血性休克复苏后肠道的保护作用。方法:将大鼠随机分为假手术组(C组)、失血性休克复苏组(HS-R组)和异丙酚组(P组),每组8只。建立失血性休克复苏动物模型,HS-R组、P组分别在复苏后采用微量泵持续泵入生理盐水1mL·kg-1·h-1、异丙酚1mL·kg-1·h-1,维持2h,测血浆中二胺氧化酶(DAO)水平;开腹取小肠组织约5cm,3cm匀浆后分别采用黄嘌呤氧化酶法、硫代巴比妥酸比色法测超氧化物歧化酶(SOD)和丙二醛(MDA)水平,2cm做病理组织切片HE染色,观察肠道组织病理学改变。结果:HS-R组及P组的MDA及DAO水平均较C组升高,P组较HS-R组有所降低(均P<0.05);HS-R组及P组的SOD水平较C组降低,P组较HS-R组有所升高(均P<0.05);肠道组织病理学评分P组及HS-R组均高于C组,但P组较HS-R组低(均P<0.05)。结论:失血性休克复苏后肠道组织出现明显的损伤,短时间内异丙酚可通过抗氧自由基作用减轻此损伤。     

参麦注射液在低血容量性休克早期液体复苏中的应用

目的 观察参麦注射液对低血容量性休克患者早期液体复苏时的临床应用.方法将2010年5月-2013年1月在泉州解放军180医院急诊科急救的68例低血容量性休克随机分为治疗组和对照组,每组34例,对照组按照抗休克常规治疗,治疗组在对照组基础上加用参麦注射液60 ml,0.5 h内静脉滴注完.检测部分常规、生化、凝血指标.结果 经抗休克治疗后,两组部分常规、生化、凝血指标与治疗前相比差异均有统计学意义（P＜0.05）,且治疗组指标较对照组改善更为明显,差异具有统计学意义（P＜0.05）.两组收缩压在治疗0.5,1,2,6,12和24 h时间点的差异具有统计学意义（P＜0.05）.结论 在低血容量性休克的早期液体复苏中,使用参麦注射液配合常规液体复苏有助于改善患者临床症状,为下一步治疗争取宝贵机会.     

3种晶体液复苏对失血性休克大鼠的影响

目的 探讨不同晶体液复苏对失血性休克大鼠的影响.方法 雄性SD大鼠40只,随机分为对照组、休克组、生理盐水组、乳酸林格液组和醋酸林格液组,每组8只.生理盐水组、乳酸林格液组和醋酸林格液组放血至平均动脉压(MAP)30~40 mmHg后维持60 min,分别给予3倍失血量的晶体液进行复苏60 min.记录5组大鼠生理指标直至复苏结束.分别于基础阶段(0 min)、失血阶段(10 min)、休克阶段(70 min)和复苏阶段(130 min)行血气和生化检测,记录各组生存情况.结果 休克组和3个液体复苏组失血和休克阶段MAP、pH、红细胞比容(Hct)、碱剩余(BE)低于对照组,休克指数(SI)和乳酸(Lac)高于对照组(P<0.05).复苏阶段3个液体复苏组MAP低于对照组,高于休克组,SI高于对照组,低于休克组(P<0.05);休克组pH和BE均低于对照组,3个液体复苏组均高于休克组(P<0.05);休克组和3个液体复苏组Hct低于对照组,且3个液体复苏组低于休克组(P<0.05);休克组和乳酸林格液组Lac高于对照组、生理盐水组和醋酸林格液组(P<0.05).失血阶段休克组和3个液体复苏组丙氨酸转氨酶(ALT)均较对照组升高(P<0.05).休克阶段和复苏阶段休克组和3个液体复苏组生化指标均较对照组升高(P<0.05);复苏阶段3个液体复苏组生化指标低于休克组,乳酸林格液组乳酸脱氢酶(LDH)高于醋酸林格液组,生理盐水组肌酸激酶(CK)高于醋酸林格液组,乳酸林格液组ALT高于生理盐水组和醋酸林格液组(P<0.05).3个液体复苏组生存时间均长于休克组(P<0.05),醋酸林格液组生存时间长于生理盐水组和乳酸林格液组,但差异无统计学意义(P>0.05).结论 对于失血性休克进行晶体液复苏时,醋酸林格液相对于生理盐水和乳酸林格液在改善代谢情况、减缓脏器损伤和延长生存时间等方面具有一定优势.     

限制性液体复苏在产科失血性休克治疗中的应用

目的 分析对产科失血性休克患者限制性液体复苏的优势与效果.方法 选取2013年12月至2014年12月我院产科收治的92例失血性休克患者,根据复苏方式不同分为限制组与积极组,对比两组的治疗效果、并发症以及患者满意率.结果 治疗后积极组的血压值以及血气剩余碱较限制组明显更高,而PT时间明显更低;限制组患者治疗后输液量、出血量、DIC发生率以及ARDS发生率均显著低于积极组;限制组患者对复苏方式满意人数以及满意率均显著大于积极组.结论 限制性液体复苏治疗产科失血性休克具有显著效果,能够减少再次出血,降低死亡率和致残率,值得应用.     

脂肪乳对罗哌卡因致大鼠心脏停搏的复苏作用

目的探讨脂肪乳对罗哌卡因致大鼠心脏停搏的复苏作用。方法 44只大鼠随机分为2组,脂肪乳组(A组,n=22)和对照组(B组,n=22)。大鼠静脉注射罗哌卡因20mg/kg,观察到心跳停止1min时行胸外心脏按压,2min时静脉注射20%脂肪乳注射液5 mL/kg(A组)或生理盐水5 mL/kg(B组),复苏药物和肾上腺素20μg/kg,5%碳酸氢钠2 mL/kg,继续心脏按压,直到恢复自主心率,恢复自主循环。记录基础的心率、血压,大鼠恢复心跳的时间,大鼠恢复自主循环的时间。大鼠的复苏成功率。记录两组使用肾上腺素的剂量。结果实验组心脏停搏后30min有2只大鼠死亡,对照组有1只大鼠死亡。A组恢复自主循环时间是(258.3±11.5)s,B组恢复自主循环时间是(268.7±12.7)s。两组的差异无统计学意义。两组所用的肾上腺素的量无显著性差异。结论脂肪乳剂对罗哌卡因所致的心脏停跳无明显的复苏效果。     

Two Cases of Refractory Cardiogenic Shock Secondary to Bupropion Successfully Treated with Veno-Arterial Extracorporeal Membrane Oxygenation

Bupropion inhibits the uptake of dopamine and norepinephrine. Clinical effects in overdose include seizure, status epilepticus, tachycardia, arrhythmias, and cardiogenic shock. We report two cases of severe bupropion toxicity resulting in refractory cardiogenic shock, cardiac arrest, and repeated seizures treated successfully. Patients with cardiovascular failure related to poisoning may particularly benefit from extracorporeal membrane oxygenation (ECMO). These are the first cases of bupropion toxicity treated with veno-arterial EMCO (VA-ECMO) in which bupropion toxicity is supported by confirmatory testing. Both cases demonstrate the effectiveness of VA-ECMO in poisoned patients with severe cardiogenic shock or cardiopulmonary failure.     

Pilot Trial of Intravenous Lipid Emulsion Treatment for Severe Nifedipine-Induced Shock

Animal studies and human case reports show promise in using lipid rescue to treat refractory calcium channel antagonist toxicity. However, the majority of research and clinical experience has focused on non-dihydropyridine agents. Thus, we sought to investigate the value of lipid emulsion (ILE) therapy for dihydropyridine-induced shock. This IACUC-approved study utilized seven swine that were sedated with alpha-chloralose, mechanically ventilated, and instrumented for drug delivery and hemodynamic measures. After stabilization and basal measures, nifedipine (0.01875 mg/kg/min) was infused until imminent cardiac arrest (seizure, end tidal CO2 < 10 mmHg, bradydysrhythmia, or pulseless electrical activity). Animals then received a 7 mL/kg bolus of 20% lipid emulsion via central catheter. Lipid circulation was visually confirmed by the presence of fat in peripheral arterial blood. Hemodynamics were continuously monitored until 10 min after lipid bolus. Surviving animals were euthanized. Pre- and post-lipid treatment parameters were analyzed using the Wilxocon signed rank test (p <0.05 significant). Nifedipine toxicity was characterized by vasodilatory hypotension, impaired vascular contractility, and tachycardia with terminal bradycardia. The median time to imminent cardiac arrest from start of nifedipine infusion was 218 min. Lipid treatment did not improve hemodynamics or restore circulation in any animal. There was no benefit from lipid rescue in this model of nifedipine toxicity. Further study of ILE for dihydropyridine toxicity is warranted but initial animal model results are not promising.     

限制性液体复苏在急性上消化道出血所致的失血性休克中的临床应用研究

目的:研究分析限制性液体复苏在急性上消化道出血所致的失血性休克中的临床应用效果。方法:选取2018年11月~2019年11月期间,某院收治的急性上消化道出血所致的失血性休克患者62例,随机分为对照组和试验组各31例。给予对照组患者行常规液体复苏,给予试验组患者行限制性液体复苏。结果:试验组不良反应发生率为6.45%,对照组为25.81%,差异具有统计学意义(P<0.05)。结论:相比于常规液体复苏,在急性上消化道出血所致的失血性休克中,应用限制性液体复苏,血压平稳降低,疗效明确,可使输液量减少,缩短住院时间及凝血酶原时间,安全可靠,值得临床推广及使用。     

羟乙基淀粉早期液体复苏对感染性休克新生兔肝脏的保护作用

目的研究羟乙基淀粉（hydroxyethyl starch,HES）早期液体复苏对感染性休克新生兔肝脏的保护作用。方法接受盲肠结扎穿孔法手术的健康新西兰长耳新生兔60只,随机分为3组,每组20只：①感染性休克组（Ⅰ组,不给予液体）,②HES 10 mL&;#8226;kg 1＋乳酸林格液20 mL&;#8226;kg 1组（Ⅱ组）,③HES 30 mL&;#8226;kg 1（Ⅲ组）。均行左颈总静脉与右颈总动脉置管,通过左颈总静脉置管,用微量输液泵输注规定的液体1 h,经右颈总动脉连续监测平均动脉压（mean artery pressure,MAP）,观察一般情况并测定术后8 h肝脏核因子κB表达情况,苏木精 伊红染色,光镜下观察肝脏改变,检测动脉血气变化。结果与本组0 h比较,Ⅰ组MAP 呈进行性下降,Ⅱ、Ⅲ组血压无明显改变;与Ⅰ组比较, Ⅱ组、Ⅲ组2 h后血压增高,均差异有统计学意义（P＜0.05）。与Ⅰ组比较,Ⅱ、Ⅲ组动脉血氧分压升高,均差异有统计学意义（P＜0.05）。各组间动脉血pH、动脉血二氧化碳分压变化差异无统计学意义。与Ⅰ组比较,Ⅱ、Ⅲ组肝细胞内核因子κB 抗原表达明显降低;与Ⅱ组比较,Ⅲ组肝细胞内核因子κB 抗原表达增高,差异有统计学意义（P＜0.05）。结论采用HES进行早期液体复苏对感染性休克新生兔肝脏有保护作用,10 mL&;#8226;kg 1作用更强。