关键词： 心脏直视手术   心脏瓣膜病   复苏   温血灌注  

摘要： 目的:总结10例重症瓣膜置换患者心脏复苏困难的成功处理经验,尝试心肌保护新方法。方法:对经多次除颤不能复苏的重症瓣膜置换患者,采用重新阻断升主动脉,行4∶1半钾或全钾温冷血停搏液诱停加纯温血持续灌注,待心脏完全静止后再开放升主动脉的方法。结果:10例重症瓣膜置换患者心脏复苏困难均自动复苏。结论:再次阻断升主动脉,行4∶1半钾或全钾温冷血停搏液诱停加纯温血(不含停搏液)持续灌注的处理,对于复苏困难的心脏具有较好的临床效果。

关键词： cardiac arrest   ventricular defibrillation   nitric oxide synthase inhibitor   ROSC   FREE-RADICAL CONCENTRATION   FOCAL CEREBRAL-ISCHEMIA   MYOCARDIAL-ISCHEMIA   INFARCT SIZE   REPERFUSION   INHIBITION   GENERATION   PERFUSION   BIOLOGY   INJURY  

摘要： Background: We have demonstrated previously that the nitric oxide synthase (NOS) inhibitor N-G-nitro-(L)-arginine ((L)-NNA) decreases free radical generation and nitrosative injury via peroxynitrite formation after epicardial dc shocks. Objective: Our purpose was to explore the effects of NOS inhibition and NOS donation on cardiopulmonary resuscitation (CPR) success after cardiac arrest of variable duration. We used the non-selective NOS inhibitor (L)-NNA and the selective neuronal NOS inhibitor ARR-17477, the NOS donor S-nitroso-N-acetylpenicillamine (SNAP) and the vasodilator Enalaprilat, which lowers arterial pressure via a non-NO mechanism. Methods: Part I: 17 pigs undergoing 4 min supported (i.e. with closed-chest compression and ventilation) ventricular fibrillation (VF) were divided into two groups: a no-(L)-NNA group (n = 8) receiving IV saline and all L-NNA group (n = 9) receiving IV (L)-NNA (5 mg/kg) for 8 min before VF was induced. Part II: 35 pigs undergoing 6-8 min VF were randomized to three groups: a no-(L)-NNA group (n = 13) receiving IV saline, an (L)-NNA group (n = 11) receiving IV L-NNA (5 mg/kg) and an ARR17477 group (n = 11) receiving IV ARR17477 (5 mg/kg) before VF. All animals in Part II underwent unsupported VF (no chest compression or ventilation) for 6 min (n = 13) or 8 min (17 = 22); closed-chest compression, ventilation and epinephrine (adrenaline) were employed after defibrillation. Part III: 12 swine were divided into two groups: control (n = 6) receiving saline and an (L)NNA group (n = 6) receiving IV (L)NNA (5 mg/kg). Swine underwent 6 min unsupported VF and 2 min supported VF before defibrillation. Part IV: 25 animals were studied to determine the effect of the NO donor SNAP and the angiotensin-converting enzyme inhibitor Enalaprilat on coronary perfusion pressure (CPP). Results: In Part I, after defibrillation, with continued ventilation, chest compression and epinephrine, 8/9 (L)-NNA pigs achieved ROSC versus 4/8 control pigs (p = 0.11). After 60 s of CPR, 7/9 pigs in the (L)-NN

关键词： active compression-decompression   cardiac arrest   LUCAS-CPR   out-of-hospital CPR   return of spontaneous circulation   THERAPEUTIC HYPOTHERMIA   CHEST COMPRESSIONS   TIME   CPR  

摘要： Lund University Cardiopulmonary Assist System (LUCAS) is a new gas-driven CPR device providing automatic chest compression and active decompression. This is a report of the first 100 consecutive cases treated with LUCAS due to out-of-hospital cardiac arrest (58% asystole, 42% ventricular fibrillation (VF)). Safety aspects were also investigated and it was found that LUCAS can be used safely regarding noise levels and oxygen concentrations within the ambulance. A crash test (10 G) showed no displacement of the device from the manikin. Of the 71 patients with witnessed cardiac arrest, 39% received bystander CPR. In those 28 patients where LUCAS-CPR was initiated more than 15 min after the ambulance alarm and in the 29 unwitnessed cases. none survived for 30 days. Of the 43 witnessed cases treated with LUCAS within 15 min, 24 had VF and 15 (63%) of these cases achieved a stable return of spontaneous circulation (ROSC) and 6 (25%) of them survived with a good neurological recovery after 30 days; 5 (26%) of the 19 patients with asystole achieved ROSC and 1 (5%) survived for over 30 days. One patient where ROSC could not be achieved was transported with on-going LUCAS-CPR to the catheter laboratory and after PCI for an occluded LAD a stable ROSC occurred, but the patient never regained consciousness and died 15 days later. To conclude, establishment of an adequate cerebral circulation as quickly as possible after cardiac arrest is mandatory for a good outcome. In this report patients with a witnessed cardiac arrest receiving LUCAS-CPR within 15 min from the ambulance call had a 30-day survival of 25% in VF and 5% in asystole, but if the interval was more than 15 min, there were no 30-day survivors. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

关键词： 心脏骤停   心肺复苏   胺碘酮   护理  

摘要： 目的观察应用静脉负荷量胺碘酮在心脏骤停复苏中的疗效和护理的作用。方法2001年1月～2002年11月我院急诊科收治的81例心脏骤停患者。经心电图或心电示波证实为心室颤动(室颤)、心室扑动(室扑)时,即刻进行标准的心肺复苏(CPR)。当200J或300J1～2次体外非同步直流电击除颤不成功时,立即给予胺碘酮300mg,生理盐水稀释至10ml,1～2min内静脉注射完毕,再行直流电击除颤(300～360J),并继以胺碘酮1000μg/min速度静脉滴注。在CPR过程中除胺碘酮外不再应用其他抗心律失常药,但肾上腺素、阿托品、多巴胺等常规抢救药均可应用。选择1998～2000年我急救中心77例年龄、性别与之相匹配的心脏骤停患者作为对照组。对照组CPR方法同上,主要药物除胺碘酮外亦基本同治疗组,抗心律失常药主要为利多卡因。结果治疗组显效18例(22.2%),对照组6例(7.8%),P<0.05。治疗组有效37例(45.7%),对照组32例(41.6%),P>0.05。总有效率(显效+有效)治疗组67.9%(55例),对照组49.4%(38例),P<0.05。结论快速静脉负荷量胺碘酮在心脏骤停复苏中复苏成功率高,较肾上腺素或/和利多卡因可以明显增加复苏成功住院率及生存率。护士的反应能力和急救技能在一定程度上增加了复苏成功率。

关键词： 猝死,心脏性   心肺复苏   心律转复   持续心肺复苏   心脏性猝死   复苏成功   急性心肌梗死(AMI)   救治   呼吸骤停  

摘要： 2005年1月12日,经过125 min持续心肺复苏(CPR)成功救治1例急性心肌梗死(AMI)致心搏、呼吸骤停患者,并完全康复出院,报告如下。

关键词： 心血管急救   心脏急症   心肺复苏   救治   讲座   高级生命支持   美国心脏协会   心脏骤停   40岁以下   中毒治疗   工作组   毒理学   指南  

摘要： 中毒引起心脏骤停相对少见，但确是40岁以下人群发生心脏骤停的主要原因。在标准的心血管急救指南不够理想或适用时．大多数人认同的指南是由美国心脏协会(AHA)毒理学工作组对高级生命支持方案(ACLS)进行了修改，作为严重中毒治疗的指南。

关键词： 心脏骤停   心脏复苏   呼吸复苏  

摘要： 目的:总结呼吸循环骤停复苏操作技术的经验。方法:对38例心脏骤停者进行人工呼吸、心脏按压、电除颤及药物应用。结果:心肺复苏成功32例,心肺脑复苏成功20例。结论:尽早进行心肺复苏是挽救心脏骤停患者生命的关键,是脑功能完全恢复的基础。

关键词： cardiac arrest   ischaemia   nitric oxide   reperfusion   UNFOLDED PROTEIN RESPONSE   INITIATION-FACTOR EIF-2-ALPHA   OXIDE-INDUCED APOPTOSIS   GLOBAL BRAIN ISCHEMIA   NITRIC-OXIDE   ENDOPLASMIC-RETICULUM   CARDIOPULMONARY-RESUSCITATION   TRANSLATIONAL CONTROL   CEREBRAL-ISCHEMIA   BLOOD-FLOW  

摘要： Visceral organs display differential sensitivity to ischemia and reperfusion injury, but the cellular mechanisms underlying these differential responses are not completely understood. A significant response to ischemia identified in brain is stress to the endoplasmic reticulum (ER), as indicated by PKR-like endoplasmic reticulum eIF2 alpha kinase (PERK)-mediated phosphorylation of eIF2 alpha. To determine the generality of this response, we evaluated the PERK pathway in brain, G1 tract, heart, liver, lung, kidney, pancreas and skeletal muscle following a clinically relevant, 10 min cardiac arrest-induced whole body ischemia and either 10 or 90 min reperfusion. The potential role of nitric oxide (NO) on PERK activation was investigated by conducting ischemia and reperfusion in the presence and absence of the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME). Organ stress could be ranked with respect to the degree of eIF2a phosphorylation at 10 min reperfusion. Brain, kidney and GI tract were reactive organs, showing 15 to 20-fold increases in eIF2a(P) compared to controls. Moderately reactive organs included liver and heart, showing 15 to 20-fold increases in eIF2 alpha(P). Pancreas, lung and skeletal muscle were nonreactive. Although treatment of cultured neuroblastoma 104 cells with the NO-donor S-nitroso-N-acetyl-peniciliamine (SNAP) activated PERK, administration of L-NAME had no effect on PERK activation or eIF2 alpha phosphorylation in organs following ischemia and reperfusion. Thus, PERK is activated differentially in reperfused organs independent of NO. These results suggest that ER stress may play a role in differential responses of viscera to ischemia and reperfusion. ER stress in viscera may contribute to the pathophysiology of resuscitation from cardiac arrest and during organ transplantation procedures. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

关键词： myocardial infarction   cells   restenosis   HEMATOPOIETIC STEM-CELLS   TRANSPLANTATION   REPAIR  

摘要： Background-Bone marrow CD133-postive (CD133(+)) cells possess high hematopoietic and angiogenic capacity. We tested the feasibility, safety, and functional effects of the use of enriched CD133(+) progenitor cells after intracoronary administration in patients with recent myocardial infarction. Methods and Results-Among 35 patients with acute myocardial infarction treated with stenting, 19 underwent intracoronary administration of CD133(+) progenitor cells (12.6 +/- 2.2X 10(6) cells) 11.6 +/- 1.4 days later (group 1) and 16 did not (group 2). At 4 months, left ventricular ejection fraction increased significantly in group I (from 45.0 +/- 2.6% to 52.1 +/- 3.5%, P < 0.05), but only tended to increase in case-matched group 2 patients (from 44.3 +/- 3.1% to 48.6 +/- 3.6%, P = NS). Likewise, left ventricular regional chordae shortening increased in group 1 (from 11.5 +/- 1.0% to 16.1 +/- 1.3 %, P< 0.05) but remained unchanged in group 2 patients (from 11.1 +/- 1.1% to 12.7 +/- 1.3 %, P = NS). This was paralleled by reduction in the perfusion defect in group 1 (from 2 8.0 +/- 4.1% to 22.5 +/- 4. 1 %, P < 0.05) and no change in group 2 (from 25.0 +/- 3.0% to 22.6 +/- 4.1%, P=NS). In group 1, two patients developed in-stent reocclusion, 7 developed in-stent restenosis, and 2 developed significant de novo lesion of the infarct-related artery. In group 2, four patients showed in-stent restenosis. In group 1 patients without reocclusion, glucose uptake shown by positron emission tomography with (18)fluorodeoxyglucose in the infarct-related territory increased from 51.2 +/- 2.6% to 57.5 +/- 3.5% (P < 0.05). No stem cell-related arrhythmias were noted, either clinically or during programmed stimulation studies at 4 months. Conclusion-In patients with recent myocardial infarction, intracoronary administration of enriched CD133(+) cells is feasible but was associated with increased incidence of coronary events. Nevertheless, it seems to be associated with improved left ventricular performance paralleled with increased myocardia

关键词： cardiopulmonary resuscitation   cerebrovascular circulation   circulation   perfusion   resuscitation   STANDARD CARDIOPULMONARY-RESUSCITATION   IMPEDANCE THRESHOLD VALVE   INSPIRATORY IMPEDANCE   WALL DECOMPRESSION   CARBON-DIOXIDE   CPR   HYPERVENTILATION   TEMPERATURE   CIRCULATION   VENTILATION  

摘要： Background - A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled - 10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard ( STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. Methods and Results - In protocol 1, 20 pigs ( weight, 30 +/- 0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation ( 100% O-2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO2 values were measured ( mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure ( mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman's repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer's exact test was used for survival. Significance was set at P < 0.05. Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour surv