急性甲胺磷中毒致心脏骤停56分钟复苏成功1例报告

1　病例简介患者 ,男 ,31岁 ,自服甲胺磷 4 5 0ｍＬ ,2 0ｍｉｎ后送入我科。查 :Ｐ 10 8次 /ｍｉｎ ,ＢＰ 12 2 / 76ｍｍＨｇ ,深昏迷 ,全身大汗 ,呼吸道有大量分泌物 ,二便失禁 ,双侧瞳孔针尖大小 ,双肺满布湿性罗音 ,呼出气味为大蒜味 ,心律齐 ,腹软 ,四肢肌张力弱 ,间有四肢抽搐。血胆碱脂酶 :6 0Ｕ/Ｌ。初步诊断 :急性重度有机磷(甲胺磷 )中毒。立即大量清水洗胃 ,洗出大量白色沫状胃内容物并留置胃管 ,每 30ｍｉｎ洗胃 2 0 0 0ｍＬ ,同时留置静脉套管针输液 ,阿托品 2 0ｍｇ ,每 15～ 2 0ｍｉｎ静注 1次 ,至阿托品化后 ,用量减为 5～ …     

急性心肌梗死合并心脏骤停复苏17例分析

目的:探讨抢救急性心肌梗死(AMI)合并心脏骤停的有效方法。方法:回顾分析AMI合并心脏骤停17例心肺复苏资料。结果:即刻电除颤10例,均恢复窦性心律,其中9例痊愈出院;6例在10分钟后电除颤,1例未除颤,均死亡。结论:AMI出现心脏骤停时,立即行电除颤应为首要抢救手段。     

急性心肌梗死心脏骤停16例临床分析

心脏骤停是临床最紧急，最危险的急症，急性心肌梗死导致的原发性心脏骤停，若经过及时有效的治疗，心肺复苏的机会较多，抢救成功率较高。1999年1月～2003年6月，我们抢救16例急性心肌梗死心脏骤停患者，就有关复苏的若干问题进行探讨。     

1例卵巢癌术中急性肺栓塞致心脏骤停患者的护理

回顾性分析本院1例卵巢癌术中急性肺栓塞致心脏骤停患者应用体外膜氧合(extracorporeal membrane oxygenation, ECMO)技术进行抢救的护理,总结其护理急救及护理配合要点,包括术中急性肺栓塞急救小组的组织及配合、使用ECMO期间的病情监测、并发症的观察及有效的护理配合。     

急性左心衰肺水肿致心脏骤停成功进行心肺复苏1例

急性左心衰肺水肿是一种危及生命的心血管病急症，而其导致心脏骤停后再能够成功进行CPR的病例则更为少见。2006—04—27我科对1例急性左心衰肺水肿导致心脏骤停的患者成功地进行了心肺复苏（CPR），现报道如下。     

心脏骤停后综合征相关急性胃肠损伤的研究进展

我国心脏骤停(cardia arrest,CA)现状严峻,每年约有54.4万人发生心源性猝死,由心脏骤停导致的猝死人数高居世界之首,严重危害国民健康[1]。近年来,尽管心肺复苏(cardiopulmonary resuscitation,CPR)领域相关理论和技术取得了巨大进步,有效改善了自主循环恢复率,但是并未改善患者长期生存率[2];在美国,CA出院生存率仅有10.6%[3],而我国院前心脏骤停的生存率甚至不到1%[4]。     

急性脑卒中致吞咽障碍的早期康复训练

吞咽障碍是脑卒中常见的症状，常由球麻痹或假性球麻痹引起，轻者只有吞咽不畅感或者出现误咽，重者出现水和营养的摄取困难。若得不到及时有效的康复治疗，患者可因吞咽障碍易出现误吸，发生吸入性肺炎，严重者可因窒息而危及生命。因此，在脑卒中早期有计划地根据病情对意识清楚的吞咽障碍患者进行康复治疗，使患者及时得到足够的营养补充，增强机体抵抗力，对疾病的康复有着重要的意义。近年来，随着医学的不断发展，对急性脑卒中吞咽障碍患者实施以吞咽障碍功能训练为主的早期康复护理措施，取得较好的效果，现将其综述如下。     

急性脑卒中继发急性心肌梗死11例临床分析

急性脑卒中时,由于脑血液循环障碍对心血管系统尤其是心肌有一定的影响,可引起心脏活动的改变,甚至继发急性心肌梗死,可成为患者死亡的直接原因.现将我院1998年2月至2005年9月收治的急性脑卒中继发急性心肌梗死（AMI）11例患者的临床资料分析如下 。     

脑卒中残损评价表评定急性脑卒中患者的有效性分析

目的 初步探讨脑卒中残损评价表（SIAS）评估急性脑卒中患者的有效性。方法 对42例急性脑卒中患者用SIAS，Brunnstrom运动功能评定，Fugl-Meyer运动功能评定以及功能独立性测量（FIM）4种量表进行评定，将SIAS运动项目部分与Brunnstrom运动功能评定和Fugl-Meyer运动功能评定结果。SIAS总分与FIM总分进行相关和回归分析。结果 SIAS运动项目部分得分与Brunnstrom运动功能评定分级，Fugl-Meyer运动功能评定得分之间显著相关（r=0.7440-0.9426)。SIAS总分与Fugl-Meyer运动功能得分间，SIAS总分与FIM总分间可建立回归方程。结论 SIAS评定急性脑卒中患者显示出良好的效度，可在临床推广应用。     

Kinetics and characteristics of an acute phase response following cardiac arrest

Objective: Inflammation and hypoxia are frequently associated, but their interaction is poorly understood. In vitro studies have shown that hypoxia stimulates the genes of acute phase proteins (APP) and cytokines known to induce APP. We decided to determine kinetics and potential determinants of an acute phase response after cardiac arrest and to assess whether isolated moderate hypoxia can induce APP in humans in vivo. Design: Prospective, observational study in patients and human experiment. Setting: Tertiary care university hospital. Patients and participants: 22 patients after primarily successful cardiopulmonary resuscitation (CPR) and 7 healthy volunteers. Interventions: None in patients; exposure of volunteers to simulated altitude (460 torr/6 h). Results: Following CPR, type-1 APP (C-reactive protein, α₁-acidglycoprotein, serum amyloid A) and type-2 APP (haptoglobin, α₁-antitrypsin) increased consistently within 1–2 days and the ’negative' APP transferrin was downregulated. This APP response occurred irrespective of the cause of arrest, the estimated time of anoxia, clinical course or patient outcome and was not different in patients with and without infectious complications. Exposure of healthy volunteers to less severe but more prolonged hypoxia did not induce APP, although a time dependent increase of serum erythropoietin (EPO) was measurable under these conditions, indicating the activation of oxygen dependent gene expression. Conclusions: (i) A marked acute phase response occurs regularly after cardiac arrest, but within the complexity of this situation the severity of hypoxia is not a predominant determinant of this response. (ii) Despite in vitro evidence for similarities in the oxygen dependent regulation of APP and EPO production, the oxygen sensitivity of these proteins in vivo is different. (iii) Measurements of APP are not revealing regarding infectious complications in the early phase after CPR. Received: 28 March 1999 Final revision received: 10 June 1999 Accepted: 1 September 1999     

Ventricular fibrillation induced by transoesophageal cardiac pacing: a new model of cardiac arrest in rats

OBJECTIVE: To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. METHODS: A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. RESULTS: A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. CONCLUSIONS: Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.     

The development and implementation of cardiac arrest centers

In the last decade, many regionalized centers for the care of post-cardiac arrest patients (cardiac arrest centers) have all independently developed with a common goal of providing multi-disciplinary and organized care plans for this patient population. The American Heart Association recently issued support for regionalized and organized comprehensive care for post-arrest patients through a position paper as well as the 2010 American Heart Association BLS/ACLS guidelines. This paper outlines the formation, structure, and implementation of four cardiac arrest centers, and also discusses a statewide model of post-arrest center care. This paper may assist other potential clinical sites that are considering or actively developing cardiac arrest centers of their own.     

经皮电刺激心外膜建立大鼠心搏骤停模型

目的 通过经皮电刺激心外膜的方法建立大鼠心搏骤停(cardiac arrest,CA)模型.方法 实验地点在中山大学卫生部辅助循环重点实验室,选择20只雄性Sprague-Dawley大鼠,两根经皮刺人心外膜的细针作为电极与刺激器相连,持续刺激3 min而诱发CA,无干预观察6 min后进行心肺复苏(cardiopulmonary resuscitation,CPR).结果 刺激电流强度1 mA时诱发CA成功12只,2 mA时全部诱发成功.从有效电刺激开始到成功诱发CA的时间为(5.10±2.81)s.电刺激结束时表现为室颤的18只,无脉性电活动2只.CPR用时(207.4±148.8)s,自主循环恢复率为20/20,CA后4 h内的死亡率为5/25,72 h时存活率为10/20.有2只大鼠分别并发轻微肌肉收缩和轻度肺叶损伤.结论 经皮电刺激心外膜诱发大鼠CA具有模型稳定、操作简单、所需刺激电流强度小、并发症少的优点.     

窒息法与室颤法心肺复苏动物模型的比较研究

目的 对比窒息法与室颤法心搏骤停动物模型在心肺复苏过程中生理指标的变化特点及其在顶测自主循环恢复(restoration of spontaneous circulation,ROSC)率、24 h生存率中的作用.方法 60只SD大鼠随机(随机数字法)制作窒息法与室颤法心肺复苏大鼠动物(n=30)模型,持续监测呼气末二氧化碳(PETCO2)、主动脉压、左室压、肢体Ⅱ导联心电图,对比分析这两种模型中以上监测指标在复苏前、按压10 s、按压1 min、按压3 min、ROSC 1 h、ROSC 2 h的变化及其与ROSC率及24 h存活率的关系.结果 PETCO2、主动脉压、左室压及心电图在两种复苏动物模型各有其变化规律.室颤组ROSC大鼠在复苏前、按压1 min与按压3 min时的PETCO2高于Non-ROSC大鼠(P＜0.05),24 h存活大鼠在ROSC 1 h与ROSC 2 h的PETCO2高于24 h死亡大鼠(P＜0.05).而窒息组ROSC及24 h存活大鼠在各时间点的PETCO2与Non-ROSC及24 h死亡大鼠比较差异无统计学意义.室颤组在ROSC 1 h,ROSC2h的dp/dt40与-dp/dt40均低于窒息组(P＜0.05).结论 窒息法与室颤法复苏动物模型各有特点,PETCO2在室颤法心搏骤停模型有助于预判ROSC及24 h生存率.研究者应根据自身的实验目的 以及模拟的不同临床状况对所需的动物模型作出选择.

Abstract：

Objective To compare the changes of physiological parameters after cardiac arrest caused by asphyxia with that of cardiac arrest induced by ventricular fibrillation in rats and assess the values of the parameters on predicting ROSC and 24 h survival rate. Method Two groups of Sprague-Dwaley rats, which randomly (ramdom number) included 30 animals in each group, were investigated. Cardiac arrest were induced by asphyxia (AS group) or ventricular fibrillation(VF group). PETCO2, aortic pressure, left ventricular pressure and ECG of limb lead Ⅱ were recorded continuously, dP/dt4o was calculated with the windaq software. The parameters were compared between the two groups at baseline, precordial compression(PC) 10 s, PC 1 min, PC 3 min, ROSC 1 h and ROSC 2 h. The relations were explored between the parameters and ROSC/24 h survival rate. Results PETCO2,aortic pressure, left ventricular pressure and ECG have distinctive changes in the two groups. In group VF, PETCO2 of ROSC rats at BL, PC 1 min and PC 3 min were higher than those of Non-ROSC rats (P ＜ 0.05); PETCO2of 24 h survival rats at ROSC 1 h and ROSC 2 h were higher than those of 24 h death rats (P ＜ 0.05), which were not observed in the group AS. dP/dt40 and - dP/dt40 at ROSC 1 h and ROSC 2 h in group VF were higher than those in group AS (P ＜ 0.05). Conclusions Physiological parameters after cardiac arrest caused by asphyxia or that of cardiac arrest induced by ventricular fibrillation in rats have unique features respectively. PETCO2 in cardiac arrest caused by ventricular fibrillation may predict ROSC and 24 h survival rate. Researchers have to select the appropriate cardiac arrest model according their research purposes and clinical requirments.     

Out-of-hospital cardiac arrest

Myocardial disease and death from cardiac arrest remain significant public health problems. Sudden death events and out-of-hospital cardiac arrests (OHCA) are encountered frequently by emergency medical services. Despite more than 30 years of research, survival rates remain extremely low. This article reviews access and presentations, demographics, OHCA outcomes, and response systems and processes in treatment of patients with arrest in this setting.     

Evolution of somatosensory evoked potentials after cardiac arrest induced hypoxic-ischemic injury

Aim

We tested the hypothesis that early recovery of cortical SEP would be associated with milder hypoxic-ischemic injury and better outcome after resuscitation from CA.

Methods

Sixteen adult male Wistar rats were subjected to asphyxial cardiac arrest. Half underwent 7 min of asphyxia (Group CA7) and half underwent 9 min (Group CA9). Continuous SEPs from median nerve stimulation were recorded from these rats for 4 h immediately following CA, and at 24, 48, and 72 h. Clinical recovery was evaluated using the Neurologic Deficit Scale.

Results

All rats in group CA7 survived to 72 h, while only 50% of rats in group CA9 survived to that time. Mean NDS values in the CA7 group at 24, 48, and 72 h after CA were significantly higher than those of CA9. The N10 (first negative potential at 10 ms) amplitude was significantly lower within 1 h after CA in rats that suffered longer CA durations. SEPs were also analyzed by separating the rats into good (NDS ≥ 50) vs. bad (NDS < 50) outcomes at 72 h, again showing significant difference in N10 and peak-to-peak amplitudes between the two groups. In addition, a smaller N7 potential was consistently observed to recover earlier in all rats.

Conclusions

The diminished recovery of N10 is associated with longer CA times in rats. Higher N10 and peak-to-peak amplitudes during early recovery are associated with better neurologic outcomes. N7, which may represent thalamic activity, recovers much earlier than cortical responses (N10), suggesting failure of thalamocortical conduction during early recovery.     

Hypocalcemia following resuscitation from cardiac arrest revisited

Objective

Hypocalcemia associated with cardiac arrest has been reported. However, mechanistic hypotheses for the decrease in ionized calcium (iCa) vary and its importance unknown. The objective of this study was to assess the relationships of iCa, pH, base excess (BE), and lactate in two porcine cardiac arrest models, and to determine the effect of exogenous calcium administration on post-resuscitation hemodynamics.

Methods

Swine were instrumented and VF was induced either electrically (EVF, n = 65) or spontaneously, ischemically induced (IVF) with balloon occlusion of the LAD (n = 37). Animals were resuscitated after 7 min of VF. BE, iCa, and pH, were determined prearrest and at 15, 30, 60, 90, 120 min after ROSC. Lactate was also measured in 26 animals in the EVF group. Twelve EVF animals were randomized to receive 1 g of CaCl₂ infused over 20 min after ROSC or normal saline.

Results

iCa, BE, and pH declined significantly over the 60 min following ROSC, regardless of VF type, with the lowest levels observed at the nadir of left ventricular stroke work post-resuscitation. Lactate was strongly correlated with BE (r = −0.89, p < 0.0001) and iCa (r = −0.40, p < 0.0001). In a multivariate generalized linear mixed model, iCa was 0.005 mg/dL higher for every one unit increase in BE (95% CI 0.003-0.007, p < 0.0001), while controlling for type of induced VF. While there was a univariate correlation between iCa and BE, when BE was included in the regression analysis with lactate, only lactate showed a statistically significant relationship with iCa (p = 0.02). Post-resuscitation CaCl₂ infusion improved post-ROSC hemodynamics when compared to saline infusion (LV stroke work control 8 ± 5 g m vs 23 ± 4, p = 0.014, at 30 min) with no significant difference in tau between groups.

Conclusions

Ionized hypocalcemia occurs following ROSC. CaCl₂ improves post-ROSC hemodynamics suggesting that hypocalcemia may play a role in early post-resuscitation myocardial dysfunction.     

急性心肌梗死心肺复苏后紧急介入治疗的作用

目的探讨紧急介入治疗能否改善急性心肌梗死心肺复苏后患者的预后。方法回顾性分析院前及急诊室发生心脏骤停的急性心肌梗死患者32例,分为在心肺复苏后同时进行紧急介入治疗组(n= 12)和保守治疗组(n=20)．比较两组的住院期间病死率、严重心律失常、心力衰竭、心原性休克和严重出血的发生率。结果介入组住院期间死亡2例(17%),保守组死亡14例(70%),p＜0．01;心肺复苏后发生心力衰竭者两组分别为3例(25%)和16例(80%),P＜0．01;两组的严重心律失常、心原性休克和严重出血发生率差异无统计学意义(P＞0．05);Logistic回归分析表明,急诊介入治疗能显著降低病死率,而心肺复苏时间＞20min,将增加病死率。结论早期紧急介入治疗能显著改善急性心肌梗死心肺复苏患者的预后。     

Inconsistencies in cardiac arrest reporting

Data relating to survival from in-hospital cardiac arrest are used to audit staff performance and to help to determine whether new resuscitation techniques are effective. Individual studies into outcome from cardiac arrest have defined inclusion and exclusion criteria, but no such national criteria have been published to enable constant auditing of cardiac arrests. The aim of this survey was to investigate the consistency with which in-hospital cardiac arrests are recorded throughout the United Kingdom. Such data are, almost universally, collected by Resuscitation Officers (RO). A questionnaire was sent to ROs across the UK asking them to state how they would interpret and categorise hypothetical, but nonetheless typical, clinical situations involving a cardiac arrest team being called. These included an event where the patient had regained consciousness prior to the arrival of the cardiac team and also an event where rigor mortis was already present and the resuscitation promptly abandoned upon the arrival of the cardiac arrest team. The percentage survival to discharge of adult cardiac arrests for each hospital was also requested. This identified whether inclusion or exclusion of certain clinical events may have influenced cardiac arrest survival figures for that hospital. It is clear from this study that in-hospital clinical events when a cardiac arrest team is called are audited with a great deal of inconsistency. Some events, such as a patient who has rigor mortis, are excluded as a false or inappropriate call in some hospitals and included as an unsuccessful resuscitation in others. There is a need for guidance on the inclusion and exclusion criteria for auditing of cardiac arrests so that meaningful data can be obtained from across the UK and useful conclusions drawn. The situation at present will result in data being audited that are of limited use. In the era of evidence-based medicine, it seems vital to obtain accurate cardiac arrest survival figures in order to have any hope of improving them.