急性心肌梗死反复室颤一例护理体会

2007年7月，我院成功抢救1例急性心肌梗死反复室颤患者，现将护理体会报告如下。     

急性心肌梗死室颤与QTc离散度的关系分析

目的　探讨校正QTc离散度 (QTcd)与急性心肌梗死 (AMI)发生室颤的关系 ,比较 41例AMI与 45例非心肌梗死者 ,住院期间不同时期心电图QTcd。结果　AMI者室颤组 (AⅠ 组 )在室颤发生前的QTcd(73 .2 5± 9.45 )ms显著延长 ,此AMI之非室颤组 (AⅡ 组 )及非心梗之对照组 (B组 )有非常显著的差异 (4 2 .75± 7.2 4)ms、(3 0 .42± 9.19)ms,P <0 .0 1。认为QTcd对AMI室颤发生有预示作用     

电针及人参对慢性心肌梗死大鼠室颤阈（VFT）的影响

目的：探讨中药人参及针刺对心肌梗死诱发心律失常的良性调整作用,方法：采用结扎大鼠左冠状动脉前降支的慢性心肌梗死模型,用室颤阈（VFT）为观察指标,共选用SD纯种成年大鼠90只,体重200－250g,雌雄不限,随机分为正常组,假手术组,假手术电针组,结扎组,结扎＋电针组,结扎＋人参治疗组,电针组取“内关”“灵道”穴每天电针30分钟治疗2周,人参组以及人参水煎剂每日一次（1g/ml)喂养2周,结果：电针治疗组及人参治疗组慢性心梗大鼠室颤阈均显著高于未治疗组,并能改变缺血心肌对异丙肾上腺素的致颤敏感性,结论：电针及人参治疗能提高缺血心肌的室颤阈,降低其易颤性,及其对致颤药敏感性。     

胺碘酮抢救急性心肌梗死并室颤发作1例

患者男,46岁。因突发胸痛,大汗1h余急诊入院。入院时体检：T36．7℃、P85次／min、R19次／min、BP130／100mmHg。全身皮肤湿润,无黄染及出血点,瞳孔大小正常,对光反射灵敏。口唇微绀,颈静脉无怒张,颈软。双肺呼吸浅快,可闻及少量湿罗音,心率85次／min,律不齐,心音低钝、遥远、无杂音。腹软、肝脾不大,无病理反射。既往有胸痛、胸闷发作史,近年发作较频繁。入院时心电图示：①窦性     

一例急性心肌梗死并反复室颤患者的抢救体会

急性心肌梗死(AMI)第一个24小时常发生严重的并发症及猝死，严密观察病情，及时采取应对措施，是提高治愈率的关键。2003年10月我科收治一例急性广泛前壁心肌梗死患者，入院5分钟后反复出现室颤，经积极抢救，病人转危为安。现将抢救体会报告如下。     

老年大鼠急性心肌梗死模型的制备

目的:建立一种稳定可重复的老年大鼠急性心肌梗死动物模型。方法:老年Wistar雄性大鼠乌拉坦麻醉后,气管切开插管,连通呼吸机,左侧3、4肋间开胸后结扎左冠状动脉前降支,收紧结扎线当时出现前降支支配区域心肌变苍白或发绀,心电图ST段抬高≥0.2 mV或T波高耸形成单峰融合波,提示结扎成功。结果:60只老年大鼠,死亡6只,成功制备54只,模型制备成功率90%,22只出现心室纤颤(室颤),其中3只死亡,室颤发生率36.7%,室颤死亡占总死亡的50%。结论:正确使用麻醉药、顺利气管插管、准确结扎冠状动脉及减少术中出血与肺损伤是制模成功的基础,本文建立的方法简单、有效,为研究老年急性心肌梗死提供了新的手段。     

抑郁对急性心肌梗死大鼠血清炎性因子及内皮功能的影响

目的 探讨抑郁对急性心肌梗死大鼠血清炎性因子及内皮功能的影响机制.方法 实验大鼠46只,随机分为假手术组10只,梗死模型组、抑郁模型组、路优泰组各12只.给药4 w后用Open-field法观察各组大鼠行为学变化,测定血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6、内皮素(ET)-1、一氧化氮(NO)的浓度,以及心肌梗死面积、电镜下心肌超微结构的改变.结果 与假手术组相比,抑郁模型组水平穿越格数、竖立次数、理毛时间均减少,中央格停留时间、粪便粒数均增加(P＜0.01);与抑郁模型组相比,梗死模型组、路优泰组水平穿越格数、竖立次数、理毛时间明显增加,中央格停留时间、粪便粒数明显减少(P＜0.05,P＜0.01).抑郁组大鼠4 w后,TNF-α、IL-6、ET-1浓度明显高于各组,NO浓度低于各组(P＜0.05,P＜0.01).抑郁组大鼠心肌梗死面积最大且电镜下心肌细胞损伤最为严重.结论 抑郁可增加血清TNF-α、IL-6、ET浓度及减少NO浓度,从而加重心肌梗死后心肌细胞的损害.     

冠脉结扎法大鼠急性心肌梗死的造模

目的 探讨冠脉结扎法制作大鼠急性心肌梗死模型。 方法 40只Sprauge-Dawley大鼠随机分为冠脉结扎组和假手术组,大鼠经麻醉后,气管插管连接小动物呼吸机,打开左侧胸腔,暴露心脏,结扎左冠状动脉前降支,假手术组只用线穿过左前降支而不结 扎,其余步骤同冠脉结扎组。手术前后均行心电图检查,4周后行血流动力学检测,取出心脏,观察其外形变化,行HE染色后于显微镜下观察其病理变化。 结果 冠脉结扎组制作心梗模型成功率为100%,术后存活率为65%,假手术组术后存活率为80%。冠脉结扎组术后4周取出的心脏,左心室较假手术组扩大,缺血区室壁变薄。 结论 冠脉结扎法制作大鼠心肌梗死模型,效果稳定,成功率高,制作方便,经济易推广。     

017急性心肌梗死患者预防性应用利多卡因可以减少原发性室颤的发生[英]／Wyman MG…／／Am J Cardiol

该研究通过对急性心肌梗死患者预防性应用利多卡因，观察是否能减少原发性室颤的发生率和急性心肌梗死患者的死亡率。     

卡维地洛对大鼠急性心肌梗死后心肌重塑的影响

目的:建立大鼠急性心肌梗死(AMI)模型,用组织学的方法,观察AMI后早期卡维地洛处理,心肌重塑相关指标的变化。方法:结扎左冠状动脉前降支复制AMI模型。将大鼠随机分为假手术(S)组、心肌梗死组(I)、高剂量卡维地洛组(H)2mg·kg-1·d-1和低剂量卡维地洛组(L)1mg·kg-1·d-1。实验动物存活2h后,药物组每日口服不同剂量卡维地洛。各组均于用药后2周观察光镜及透视电镜下左心室心肌组织学改变并进行定量分析。结果:药物组心肌梗死面积明显减小(I组、L组和H组分别为0.149±0.010、0.039±0.009和0.028±0.004),与I组比较,P均<0.05,残存心肌纤维断裂及排列紊乱程度减轻;梗死区、非梗死区内心肌细胞退行性改变减轻,心肌细胞线粒体以增生、肿胀为主,线粒体膜完整,细胞核增大。心肌间质中幼稚毛细血管密度增加(I组、L组和H组分别为4.36±0.010,7.22±0.009和9.86±0.004),与I组比较,P均<0.05,上述改变在H组更明显。结论:AMI后卡维地洛早期干预,可改善AMI后心肌重塑水平并具有剂量依赖性。卡维地洛的线粒体保护作用可能是其抑制AMI后心肌重塑、改善AMI患者预后的细胞学机制之一。     

Primary ventricular fibrillation in acute myocardial infarction

Primary ventricular fibrillation is an acute life-threatening event if not treated promptly. The ability to predict this event during the course of an acute myocardial infarction could therefore have an important impact on the mode of treatment and monitoring. In the present study, clinical and laboratory information available at the initial evaluation of patients with an acute myocardial infarction was tested for its ability to predict subsequent primary ventricular fibrillation. Multiple logistic regression analysis was employed to select the predictors. Serum potassium, serum creatinine and no smoking were significant predictors of subsequent ventricular fibrillation. Although the prediction was statistically significant, the clinical value of the prediction is quite limited.     

Prediction of in-hospital ventricular fibrillation from admission data in acute myocardial infarction

We studied retrospectively 26 readily obtainable clinical and electrocardiographic variables in 22 consecutive patients who experienced primary ventricular fibrillation in association with an episode of acute myocardial infarction. Twenty-eight consecutive patients who had an uncomplicated course after acute myocardial infarction served as controls. The clinical profile of the two groups was similar except that patients who had primary ventricular fibrillation smoked more and had a higher peak creatinine phosphokinase level at the time of infarction. The data was evaluated using univariate and stepwise logistic regression analysis. This analysis demonstrated that patients who developed primary ventricular fibrillation had, on admission (1) more evidence of congestive heart failure (Killip classification), (2) a lower diastolic blood pressure, (3) greater ST-segment elevation, (4) a longer QTc interval, and (5) a less distinguishable J point on the electrocardiogram. This method of logistic analysis that utilizes easily obtainable hospital admission data serves as a preliminary model for prediction of the relative risk of primary ventricular fibrillation in a patient with acute myocardial infarction. The ability to identify patients at risk has important therapeutic implications.     

Electrocardiographic features at onset of ventricular fibrillation in acute myocardial infarction: Relation to intraventricular conduction defects, configuration of initiating QRS complex, preceding heart rate and initiating coupling interval

In prospectively collected consecutive patient data from twocoronary care units (CCU), 32 patients with acute myocardialinfarction (AMI) developed primary or complicating ventricularfibrillation (VF). A I2-lead ECG on the day of admission wasavailable in 30 patients, and was compared to similar ECGs froma control group of 90 consecutive AMI patients without VF. Leftanterior hemiblock (LAH) occurred in 33% of the VF patientsand in 11% of the controls; the difference is statisticallysignificant. In 20 of the 32 patients the VF occurred duringcontinuous ECG registration. The QRS complex initiating theVF was as frequently of left as it was of right bundle branchblock configuration. When compared with a second control group of 77 consecutiveAMI patients under continuous ECG recording who did not developVF, the heart rate in the VF patients was significantly higherjust prior to the development of this arrhythmia. The VF initiatingcoupling interval was shorter than the upper normal limit ofthe Q T interval in 40% of the VFs. In primary VF and in patientsnot treated with antiarrhyth-mic drugs the coupling intervalswere close to the upper normal limit of the QT interval. Incomplicating VF and particularly when antiarrhythmic therapywas used the coupling intervals showed a wider variation.     

Refractory ventricular fibrillation complicating acute myocardial infarction terminated by intracoronary stenting

We report on a case of intractable recurrent ventricular fibrillation that responded poorly to antiarrhythmic medication and balloon angioplasty, but resolved instantaneously following intracoronary stenting. © 1996 Wiley-Liss, Inc.     

急性心肌梗死后不同时期心房颤动发生的临床机制

目的 探讨急性心肌梗死(AMI)后不同时间发生心房颤动(Af)的临床意义及机制。方法 按AMI后12h内和大于12h发生Af者,将106例有Af的AMI患者分为早期组(48例)和后期组(58例),回顾性分析急性心肌梗死后不同时期心房颤动发生者的超声心动图、冠状动脉造影(CAG),急诊经皮腔内冠动脉成形术(PTCA)和静脉溶栓的临床资料。结果 统计学显示两组的年龄(65.7±12.6岁vs 68.1±10.2岁)、左心房内径(38.1±3.26mm vs 39.O±4.35mm)无显著性差别(P>O.05)。早期组的左心室射血分数(O.58±O.12 vs O.40±O.10,P相似文献   

Risk factors for primary ventricular fibrillation during acute myocardial infarction: a systematic review and meta-analysis.

AIMS: To evaluate potential risk factors for primary ventricular fibrillation (PVF) during acute myocardial infarction (AMI) by a systematic review and meta-analyses. METHODS AND RESULTS: We searched PubMed for English articles on 'humans' published between 1964 and January 2006 using a validated combination of MESH terms. Twenty-one cohort studies describing 57 158 patients with AMI were analysed. Patients with validated PVF (n=2316) were characterized by an earlier admission (weighted mean difference -2.62 h), male gender [odds ratio (OR 1.27)], smoking (OR 1.26), absence of history of angina (OR for history of angina 0.84), lower heart rate at admission (weighted mean difference -4.02 b.p.m.), ST-segment elevation on admission ECG (OR 3.35), AV conduction block before PVF (OR 2.02), and lower serum potassium at admission (weighted mean difference -0.27 meq/L). Patients with validated PVF developed a larger enzymatic infarct size (standardized mean difference 0.74, P<0.00001). PVF was not associated with a history of myocardial infarction or hypertension. CONCLUSION: Patients who developed a validated PVF presented with characteristics of both abrupt coronary occlusion and early hospital admission. This review provides no evidence for risk factors for PVF other than ST-elevation and time from onset of symptoms. To find new risk factors, studies should compare validated PVF patients with non-PVF patients who have no signs of heart failure and comparable time delay between onset of symptoms and medical attendance.     

Predictors of ventricular fibrillation or cardiac arrest in patients hospitalized for acute myocardial infarction

A community-wide study of patients hospitalized with acute myocardial infarction in metropolitan Baltimore was conducted to examine socio-demographic and clinical characteristics in association with ventricular fibrillation and cardiac arrest (VF/CA). Multivariate analyses revealed that variables significantly associated with occurrence of VF/CA included older age (60 years or older), male sex, and a history of cigarette smoking. These factors allow the identification of subgroups of patients hospitalized with acute myocardial infarction at high risk for the subsequent development of VF/CA, in whom prophylactic therapy and close surveillance are especially recommended.     

Assessment of markers of thrombin generation in patients with acute myocardial infarction complicated by ventricular fibrillation

BACKGROUND: In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated. METHODS: We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias. Levels of thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2 (F1 + 2), fibrinopeptide A (FPA), plasmin-antiplasmin complexes (PAP), protein C, antithrombin, activated partial thromboplastin time (aPTT), thromboplastin time, D-Dimer, fibrinogen, and high-sensitivity C-reactive protein (hs-CRP) were measured in plasma samples of all patients. Blood collection was obtained sequentially in two separate settings. Patients were studied at a median of 351 days after the acute coronary event. RESULTS: Higher levels of TAT complexes (13.4 +/- 22.2 vs. 3.03 +/- 4.3 microg/l; p = 0.02), FPA (79.7 +/- 132.3 vs. 24.04 +/- 41.3 ng/ml; p = 0.04), and F1+2 (1.89 +/- 1.3 vs. 1.16 +/- 0.5 nmol/l; p = 0.01) were observed in patients with VF compared with patients without ventricular tachyarrhythmias during the acute phase of MI. D-Dimer levels displayed a trend without reaching statistical significance (0.69 +/- 0.48 vs. 0.48 +/- 0.24 mg/l; p = 0.06). No differences were found in hs-CRP (3.25 +/- 4.5 vs. 4.4 +/- 8.8 mg/l; p = 0.5) and fibrinogen (2.8 +/- 0.9 vs. 2.7 +/- 0.9 g/l; p = 0.6) measurements. Repeat assessment of markers of coagulation activation at a median of 847 days revealed a highly significant decrease in patients with VF. CONCLUSIONS: Markers of thrombin generation are transiently increased in patients with VF during the acute phase of MI. These findings have implications for risk assessment and genetic screening of patients prone to VF during acute myocardial ischemia.     

急性心肌梗死并发心房颤动的临床意义

目的 观察急性心肌梗死并发心房颤动的临床意义。方法 比较急性心肌梗死心房颤动组20例和非心房颤动组132例的心力衰竭发生率及死亡率。结果 急性心肌梗死心房颤动组心力衰竭发生率（90．0％），及死亡率（60．0％）均明显高于非心房颤动组（31．1％，15．1％，P〈0．01）。结论 急性心肌梗死并发心房颤动预后较差。     

Ventricular fibrillation complicating pacemaker insertion in acute myocardial infarction

Temporary transvenous pacing catheters were placed in 101 patients with acute myocardial infarction (Ml) for the management of bradyarrhythmias or conduction disturbances. Fourteen (14%) patients (group A) developed ventricular fibrillation (VF) at the time of pacing catheter manipulation in the right ventricle. Compared to the remaining 87 (86%) patients (group B), the patients in group A were younger (56.1 vs 65.8 yrs, P = 0.007). Thirteen (92.8%) of 14 patients in group A had inferior MI compared to 58 (66.6%) of 87 patients in group B (P = 0.04). All but one patient in group A had pacemaker insertion within 24 h of the onset of symptoms of Ml compared to 55 (63%) of 87 in group B (P = 0.02). In 12 of the 14 patients in group A, following defibrillation and intravenous bolus administration of lidocaine, the pacing catheter was positioned in the right ventricle without further episodes of VF. It is concluded that (1) in patients with acute MI temporary transvenous pacemaker insertion may be complicated by VF; (2) VF is most likely to occur in younger patients with inferior MI infarction when the pacing catheter is inserted within 24 h of the onset of symptoms of infarction; and (3) administration of an intravenous bolus of lidocaine may be effective in preventing the induction of VF by catheter manipulation.