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1.
目的 探讨应用亚低温治疗心肺复苏患者脑复苏的临床疗效及护理方法.方法 选取2007年1月至2011年12月我科收治的心脏骤停患者40例,经心肺复苏(CPR)达到基础生命支持后随机分为常规治疗组与亚低温治疗组各20例.随访3个月观察其临床疗效及并发症发生率.结果 亚低温治疗组治愈率显著高予常规治疗组;亚低温治疗组的致残率显著低于常规治疗组;2组并发症发生率比较差异无统计学意义.结论 对心脏骤停后CPR患者实行亚低温治疗是一种安全有效、切实可行的治疗方法.正确使用电脑降温毯及专科护理等是降低亚低温治疗脑复苏并发症的关键护理措施.  相似文献   

2.
亚低温联合生脉注射液在心肺脑复苏中的应用   总被引:8,自引:1,他引:8  
目的:探讨亚低温联合生脉注射液在心肺脑复苏(CPCR)救治中的可行性及疗效。方法:选择本院急诊科收治心搏骤停行心肺复苏成功患者80例,采用随机数字表法分为亚低温组(43例)和对照组(37例)。两组患者给予复苏兴奋药物、降颅压、激素等基础复苏药;亚低温组同时联用大剂量生脉注射液。两组患者均在复苏即刻以及复苏后1、3和7 d进行格拉斯哥昏迷评分(GCS),同时抽取静脉血3 m l,检测血浆丙二醛(M DA)含量及尿酸(UA)浓度。结果:与治疗前比较,亚低温组治疗后GCS明显升高(P<0.05或P<0.01),M DA含量和UA浓度则均明显降低(P<0.05或P<0.01);而对照组治疗前后GCS、M DA和UA均无明显变化(P均>0.05)。结论:亚低温联合大剂量生脉注射液能明显改善CPCR患者的神经功能,是安全、有效、易于推广的CPCR途径。  相似文献   

3.
亚低温治疗在临床上又称冬眠疗法或人工冬眠,它利用对中枢神经系统具有抑制作用的镇静药物,使病人进入睡眠状态.冉配合物理降温,使病人体温处于一种可控性的低温状态,中枢神经系统处于抑制状态。亚低温治疗常用于心肺复苏(CPR)后、颅脑损伤及重型颅脑手术后、低温麻醉、高热惊厥或超高热、感染巾毒性休克早期及颅内感染等患者。  相似文献   

4.
目的:探讨亚低温技术在心肺复苏后对患者神经功能预后的影响。方法:回顾性分析我院2001-03-2008-05急诊抢救室收治的30例心肺复苏患者的临床资料,根据是否采用亚低温技术,患者随机分为两组:常温组与亚低温组,每组各15例。对复苏后患者的平均脑部温度、血氧饱和度(SaO2)、血酸碱值(pH)、平均动脉压(MAP)、意识障碍评分(GCS)等指标进行分析,3个月后对两组病人神经功能预后进行评定。结果:常温组与亚低温组患者复苏时平均脑部温度分为(36.7±1.3)℃和(33.5±1.1)℃(P<0.05),血氧饱和度(SaO2)、血酸碱值(pH)、平均动脉压(MAP)、意识障碍评分(GCS)等基本相近(P>0.05);3个月后两组神经功能转归良好率分别为40%和73%(P<0.05),其中亚低温6h内实施者优于6h后实施者;神经功能缺损评分(nerve functional in-sufficent,NFI)分别18.7±4.3和14.9±3.7(P<0.05),修改后的Barthel指数(modified Barthel index,MBI)分别为69.5±3.6和74.4±4.5(P<0.05)。结论:亚低温技术在心肺复苏后患者的脑复苏中具有显著的神经功能保护作用,可改善心肺复苏后患者的神经功能状况,实施降温越早,对脑复苏越有利。  相似文献   

5.
目的:分析亚低温对自主循环恢复(ROSC)后的心肺复苏患者预后和脑功能的影响。方法:按照随机分配原则对66例心肺复苏后获得ROSC的患者进行分组,根据是否用亚低温治疗以及ROSC后不同时间予低温治疗分为常温组和低温A、B组。比较低温两组和常温组中第1、3、7、28天的GCS评分、SOFA评分和28 d的生存率和CPC评分。结果:各组ROSC率、28 d生存率和第1、3、7天SOFA评分比较差异无显著性,第7天GCS评分和第28天的CPC评分常温组与低温两组比较差异有显著性,两低温组之间比较差异无显著性。结论:亚低温对心肺复苏患者ROSC的28 d生存率影响不大,但对ROSC患者的脑功能恢复有明显益处,值得临床上推广应用,在ROSC后1 h内进行亚低温治疗患者开始时机对生存率和CPC影响不大。  相似文献   

6.
目的 探讨亚低温治疗对心搏骤停后心肺复苏患者的临床疗效,寻找一种切实可行的亚低温治疗的监测指标.方法 选取2005年1月至2010年2月中国医科大学附属盛京医院急诊科收治的心搏骤停患者40例,经心肺复苏(PCR)达到自主循环恢复后随机分为常规治疗组与亚低温治疗组各20例.随访3个月观察其临床疗效,同时监测局部脑组织的氧饱和度(rSO2)在亚低温治疗各时点的变化.结果 亚低温治疗组治愈率显著高于常规治疗组;亚低温治疗组的致残率显著低于常规治疗组.亚低温治疗12 h后rS02明显上升,24 h后rSO2持续维持在稳定状态,与对照组相比差异具有统计学意义(P<0.01).结论 对心搏骤停后心肺复苏患者实行亚低温治疗能减轻脑组织氧代谢紊乱,改善预后.无创持续监测rSO2对亚低温治疗具有指导意义.  相似文献   

7.
亚低温疗法用于脑复苏的国内外研究概况   总被引:2,自引:0,他引:2  
傅一明 《临床荟萃》2000,15(12):569-570
随着心肺复苏技术的发展,心脏骤停后心肺复苏水平已有明显提高,但由于脑组织对缺血的耐受性较差,易引起不可逆损害,导致脑复苏失败而影响了心脏骤停后整个心肺脑复苏水平。减少脑缺血对脑组织的损害,提高脑复苏水平已成为现代急救的关键所在。近10多年,国内外学者对脑复苏的研究越来越多,改进脑复苏方法主要包括[1]:①加压再灌注。②紧急心肺旁路。③药物(如钙离子拮抗剂等)。④低温疗法。中度低温效果确切,但因其在应用中难于管理和引起的并发症而受到限制[2],其中亚低温对脑组织具有明显的保护作用,而对心血管等其他系统无不利影响,是脑复…  相似文献   

8.
Objective To study clinical effect of moderate hypothennia treatment in patients with cardiac arrest survivors and search a practical monitoring way during moderate hypothennia treatment. Method A total of 40 patients of CPR following the restoration of spontaneous circulation were randomly divided into the hypothermia therapy group ( n= 20) and the routine therapy group ( n= 20), the clinical effect on patient followed for three months is evaluated. At the same time regional cerebral oxygen saturation (rSO2) was detected at different times after moderate hypothennia treatment in two groups. Results The recovery rate were higher and the mutilation rate was lower in hypothermia therapy group than that of the routine therapy group. rSO2 obviously increased after 12 hours of hypothermic treatment, and continuing kept stable level after 24 hours of hypothermic treatment, but it was also higher than routine therapy group (P<0.01). Conclusions Moderate hypothermia can alleviate the metabolic disorder of the brain tissue and improve the prognosis in patients with cardiac arrest survivors. Noninvasire continuously monitoring of rSO2 has important significance for instructing moderate hypothermia treatment in clinic.  相似文献   

9.
目的:探讨颅脑降温监护治疗仪在心肺脑复苏(CPCR)中的应用时机及护理方法。方法:将确定心跳和呼吸停止时间在6 min内、经心肺复苏(CPR)术后自主循环恢复并能维持24 h以上的68名复苏患者随机分为A组和B组各34例,A组患者在实施常规CPR同时,2 min内即用颅脑降温监护仪进行亚低温治疗;B组患者经CPR、在自主循环恢复后再用颅脑降温监护治疗仪进行亚低温治疗。两组均在2~4 h内使体表温度降至32~34℃,持续12~24 h。比较两组自主呼吸恢复情况、意识恢复(GCS评分)情况。结果:两组患者自主呼吸恢复人数及恢复时间比较,差异有统计学意义(P<0.05);24 h、48 h时、72 h内意识恢复(GCS评分)情况比较,差异有统计学意义(P<0.05)。结论:颅脑降温监护治疗仪实施越早越好,最好在实施常规基础生命支持(BLS)和高级生命支持(ACLS)同时开始,并配合高质量CPCR技术及精心护理,可有效提高脑复苏成功率。  相似文献   

10.
肾上腺素在心肺脑复苏中的应用   总被引:1,自引:0,他引:1  
决定心搏骤停复苏成功的一个重要因素是冠状动脉灌注压,即主动脉舒张压和右房舒张压之差。实验证明右房舒张压很低,与正常窦性心律相比,在胸外按压时变化也较小,但是,正常心律时平均主动脉压舒张压约100mmHg,心搏骤停10分钟后复苏时约10~15mmHg,因此复苏时增加主动脉舒张压,亦即增加冠状动脉灌注压,可以提高复功苏成率。  相似文献   

11.
不同降温方法对大鼠心肺脑复苏的作用   总被引:2,自引:0,他引:2  
目的研究亚低温脑复苏时不同降温方法的效果及对大鼠脑的保护作用。方法建立心肺复苏模型,SD大鼠45只,分成对照组、常温复苏组及低温复苏A组(体表降温)、低温复苏B组(0.5ml·kg^-1·min^-1静注4℃ NS)、低温复苏C组(0.5ml·kg^-1·min^-1静注4℃NS结合体表降温)、低温复苏D组(1ml·kg^-1·min^-1静注4℃NS)和低温复苏E组(1ml·kg-^1·min^-1静注4℃NS结合体表降温),分别观察各组血清及大脑皮质SOD、MDA、NO、Na^+ K^+ -ATP酶及P53、Bax、Bcl-2表达和脑组织含水量比。结果低温复苏各组均能达到亚低温状态,特别是低温复苏D、E组达到亚低温状态仅需(26.71±4.65)min及(10.00±2.52)min。低温复苏D组脑组织含水量比、MDA、NO、P53和Bax光密度值分别为(79.58±0.40)%、(14.16±2.36)nmol/gprot、(35.28±4.94)μmol/gprot、(0.0136±0.0001)和(0.0304±0.0019),低温复苏E组分别为(79.46±0.30)%、(10.30±3.16)nmol/gprot、(33.18±4.93)μmol/gpmt、(0.0134±0.0040)和(0.0323±0.0029).均较常温复苏组明显下降(P〈0.05)。低温复苏D组脑组织SOD、Na^+ K^+ -ATP酶分别为(114.45±3.07)U/mgprot、(30.50±2.06)μmolpi/(mgpnt·hour),低温复苏E组分别为(114.45±8.11)U/mgprot、(28.10±5.67)μmolpi/(mgpnt·hour),均较常温复苏组明显升高(P〈0.05)。结论静脉快速灌注冷生理盐水或同时结合体表降温均能在较短的时间内达到理想的亚低温状态并产生良好的脑保护效果。  相似文献   

12.
亚低温对心肺复苏后患者神经功能状况及生活质量的影响   总被引:9,自引:2,他引:9  
目的 探讨亚低温对心肺复苏后患者神经功能状况及生活质量的影响及其机制。方法 采用格拉斯哥昏迷评分 (GCS)、神经功能缺损评分 (NFI)、Barthel指数 (MBI)及生活质量评分 (QOL)对心肺复苏后患者的神经功能状况及生活质量进行评定 ,并观察亚低温对他们的影响。结果 在心肺复苏后第7d ,亚低温组GCS评分明显比常规治疗组高 (P <0 0 5 ) ;在复苏后第 12周和 2 4周 ,亚低温组NFI评分及QOL评分均明显较常规治疗组低 (P <0 0 5 ) ,MBI评分明显较常规治疗组高 (P <0 0 1)。结论 亚低温可改善心肺复苏后患者的神经功能状况 ,提高患者的生活质量  相似文献   

13.
目的 探究护理干预对全身亚低温治疗心肺复苏后患者神经系统预后的改善作用。 方法 将2012年12月-2015年9月收治的50例心肺复苏后行全身亚低温治疗患者随机分为对照组和观察组,对照组实施常规护理,观察组实施针对性护理干预。观察2组患者神经系统改善情况、日常生活能力、神经复苏预后、并发症发生率、护理满意度。 结果 观察组神经功能缺损评分显著低于对照组,日常生活活动能力评分显著高于对照组,神经系统预后明显好于对照组,并发症发生率低于对照组,护理满意度高于对照组。 结论 心肺复苏后患者行亚低温治疗过程中,对患者实施有效护理干预,可以降低患者神经功能缺损程度评分,提高患者神经复苏预后,同时降低并发症的发生,提高患者的生存质量,有效提高患者的护理满意度。  相似文献   

14.
Full cerebral recovery after cardiopulmonary resuscitation is still a rare event. Unfortunately, up to now, no specific and outcome-improving therapy was available after such events. From several cases it is known that low body and brain temperature during a cardiocirculatory arrest improves the neurological outcome following these events. As it is not possible in acute events to induce hypothermia beforehand, whether cooling after the insult could also be protective was evaluated. After animal studies in the 1990s and first clinical pilot trials of mild therapeutic and induced hypothermia, two randomized trials of hypothermic therapy after successful resuscitation after cardiac arrest were conducted. These studies demonstrated that hypothermia after cardiac arrest could improve neurological outcome as well as overall mortality.  相似文献   

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16.
亚低温治疗是指通过控制性降低患者核心温度以保护器官免受损伤影响。至今,亚低温治疗作为一种脑保护方法已经用于多种脑损伤疾病中。并且逐渐发现在其他器官损伤时也可能具有一定的保护作用。本文述评了亚低温治疗的应用范围、目前的临床研究证据以及国内的应用现状。讨论将来研究及临床使用亚低温治疗以改善器官损伤预后的注意事项。  相似文献   

17.
目的基于超高效液相色谱-飞行时间质谱(UPLC-QTOF-MS)技术寻找CA后大鼠心肌损伤的潜在生物标志物,初步揭示亚低温对心肌保护作用的机制。方法建立窒息性CA模型,将20只自主循环恢复后的SD大鼠随机分为常温组、亚低温组,ROSC后24h收集心肌组织样本进行代谢组学检测,采用SIMCA-P 14.1和MetaboAnalyst 4.0对预处理后的数据进行代谢轮廓分析,筛选差异代谢物,将内源性代谢物进行代谢通路分析。结果成功制作了大鼠窒息性CA模型,心肌HE染色显示,常温组大鼠心肌结构紊乱,心肌纤维断裂,间质充血,细胞核染色不均匀,亚低温治疗后改善了心肌损伤程度;代谢组学检测结果显示,常温组和亚低温组心肌代谢指纹不同,共筛选出20种差异代谢物,代谢通路分析提示嘌呤代谢、缬氨酸/亮氨酸/异亮氨酸代谢在亚低温干预后显著改变。结论亚低温治疗在一定程度上减轻CA后心肌损伤程度,嘌呤代谢和氨基酸代谢参与了亚低温对心肌的保护。  相似文献   

18.
目的 探讨亚低温治疗对兔心肺复苏后凝血异常及脑微循环血流变化的干预作用.方法 本实验在中山大学卫生部辅助循环重点实验室进行.24只成年新西兰大白兔随机(随机数字法)分为常温(normothermic,NT)治疗组和亚低温治疗(therapeutic hypothermia,TH)组,每组12只,采用交流电致颤的方式建立心肺复苏(CPR)模型,自主循环恢复后(ROSC)NT组动物置于室温下观察12 h,TH组动物采用体表降温的方法诱导亚低温,达到目标温度后维持12 h.所有动物CPR前及ROSC后4,8,12 h分别测定PT,APTT,INR,D-D,血小板计数(BPC);测定抗凝血酶Ⅲ活性(AT-Ⅲ)和血浆蛋白C活性(PC);用PERIMED Multichannel Laser Doppler系统监测大脑皮层微循环血流.各组数据依据正态检验结果用单因素方差分析或秩和检验,多重比较用LSD-t检验,两样本均数的比较用成组t检验,相关性采用Pearson相关性分析,以P<0.05为差异具有统计学意义.结果 NT组动物ROSC后PT,APTT,INR逐渐缩短的趋势,ROSC后12 h APTT明显短于基础值(P=0.025),而AT-Ⅲ和PC活性显著下降.和NT组相比,TH组PT,APTT,INR值显著增大,差异具有统计学意义;但AT-Ⅲ,PC活性、D-D浓度,两组差异无统计学意义.CPR前、ROSC后4,8和12 h NT组大脑皮层血流分别(401.60±11.76),(258.86±34.58),(317.59±23.36)和(371.98±5.79)mL/min,TH组为398.18±12.91.336.19±19.27,347.76±13.80和383.78±3.29 mL/min.ROSC后各时间点TH组大脑皮层血流量明显高于NT组(4 h:t=-6.025,df=16,P=0.000;8 h:t=-2.942,df=12,P=0.012;12 h:t=-3.959,df=8,P=0.004).Pearson相关分析显示ROSC后大脑皮层血流和APTT正相关(4 h:R=0.503,P=0.033;8 h:R=0.565,P=0.035;12 h:R=0.774,P=0.009),与其他凝血指标无关.结论 ROSC后亚低温治疗使凝血功能下降的同时伴随脑微循环血流的增加,CPR后亚低温治疗对ROSC后凝血失衡的影响可能是其发挥脑保护作用的机制之一.
Abstract:
Objective To study the effects of mild hypothermia (MH) on blood coagulation and cerebral microcirculation in rabbits after cardiopulmonary resuscitation (CPR). Method A total of 24 New Zealand rabbits were randomly (random number) divided equally into normothermic group (NT) and MH group. CPR model was established by ventricular fibrillation induced by using alternating current. The rabbits of NT group were observed for 12 h in room temperature after restoration of spontaneous circulation (ROSC). The mild hypothermia was induced in the rabbits of group MH by surface cooling after ROSC, and maintained for 12 h after the aimed low temperature reached. The PT (prothrombin time), APTT (activated partial thromboplastin time), INR (international normalized ratio of prothrombin), D-dimmer (DD) , blood platelet count (BPC) , anti-thrombin Ⅲ activity (AT-Ⅲ) and protein C activity (PC) were measured before CPR and 4 h, 8 h and 12 h after ROSC, and at the same time the cerebral microcirculation was measured by using PERIMED Multichannel Laser Doppler system. One-way ANOVA or Mann-Whitney rank was used to determine the statistical significance between two groups. LSD-t test was used for multiple comparisons,t test for comparisons of means between two independent samples, and Pearson correlation test for correlation analysis. Results The PT, APTT and INR showed a trend of gradually shortening during the course. The APTT in 12 h after ROSC was significantly shorter than that before CPR (23.32 ±5.19 vs. 29.53 ±5.10,P = 0.025), and the activity of AT- Ⅲ and PC were decreased significantly. Compared with the group NT,the PT, APTT and INR in group MH were increased significantly, while there were no differences in the activity of AT- Ⅲ, PC and D-D between two groups. The rates of cerebral microcirculation in group NT before CPR and 4 h, 8 h and 12 h after ROSC were 401.60 ± 11.76 mL/min, 258.86 ± 34. 58 mL/min,317.59 ± 23.36 mL/min and 371.98 ± 5.79 mL/min, respectively, and those in group MT were 398.18 ±12.91 mL/min, 336.19 ± 19.27 mL/min, 347.76 ± 13.80 mL/min and 383.78 ± 3.29 mL/min, respectively. There were significant differences between two groups at each interval after ROSC (4 h: t = - 6.025,df=16, P=0.000;8 h: t= -2.942, df=12, P=0.012;12 h: t= -3.959, df=8, P=0.004). The Pearson correlation test showed that the rate of cerebral microcirculation was positive correlated with APTT after ROSC (4 h:R =0.503,P=0.033;8 h:R=0. 565,P=0. 035;12 h:R=0. 774,P=0. 009), and was not correlated with the other blood coagulants. Conclusions The mild hypothermia led to the inhibition of blood coagulation and improved the cerebral microcirculation concomitantly, which may be one of the mechanism of cerebral protection.  相似文献   

19.

Background

Mild induced hypothermia (MIH) was introduced for post cardiac arrest care in Sweden in 2003, based on two clinical trials. This retrospective study evaluated its association with 30-day survival after out-of-hospital cardiac arrest (OHCA) in a Swedish community from 2003 to 2015.

Methods

Out of 3680 patients with OHCA, 1100 were hospitalized after return of spontaneous circulation and 871 patients who remained unconscious were included in the analysis. Prehospital data were extracted from the Swedish Registry of Cardiopulmonary Resuscitation and in-hospital data were extracted from clinical records. Propensity score analysis on complete data sets and multivariable logistic regression with multiple imputations to compensate for missing data were performed.

Results

Unadjusted 30-day survival was 23.5%; 37% in 386/871 (44%) MIH treated and 13% in 485/871 (56%) non-MIH treated patients. Unadjusted odds ratio (OR) for 30-day survival in patients treated with MIH compared to non-MIH treated patients was 3.79 (95% CI 2.71–5.29; p < 0.0001). Using stratified propensity score analysis and in addition adjusting for in-hospital factors, 30-day survival was not significantly different in patients treated with MIH compared to non-MIH treated patients; OR 1.33 (95% CI 0.83–2.15; p = 0.24). Using multiple imputations to handle missing data yielded a similar adjusted OR of 1.40 (95% CI 0.88–2.22; p = 0.15). Good neurologic outcome at hospital discharge was seen in 82% of patients discharged alive.

Conclusion

Treatment with MIH was not significantly associated with increased 30-day survival in patients remaining unconscious after OHCA when adjusting for potential confounders.  相似文献   

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