心肺脑复苏(CPCR)成功11例体会

心跳呼吸骤停是临床急救医学最紧急而又困难并具有挑战意义的问题之一。如何提高心肺脑复苏（CPCR）的成功率,是临床急救医务人员所关注的问题。我院按照2005版国际心肺复苏指南的要求进行抢救的11例心跳呼吸骤停患者收到一定的效果,现报告如下。     

经支气管镜气管插管与常规气管插管救治呼吸衰竭对比分析

目的：回顾性分析呼吸机辅助呼吸救治危重呼吸衰竭患者气管插管方式对于救治成功率的影响。方法：我科收治的各种呼吸衰竭患者94例,回顾分析插管方式对于救治成功率、引发心跳骤停及其对心肺复苏效果的影响。结果：经纤维支气管镜经口气管插管（35例）与经直接喉镜经口（59例）引发心跳骤停有明显统计学差异（X^2=11．5,v=1,t〈0．001）。经直接喉镜经口气管插管在术前用药与否对引发心跳骤停并无统计学意义,但是对于引发心跳骤停后心肺复苏成功率确有明显统计学意义。结论：经纤维支气管镜气管插管具有较高的安全性,在经直接喉镜气管插管是选择镇静药或浅麻醉药物应慎重,尽力避免心跳骤停和心肺复苏失败。     

可视喉镜气管插管对心跳骤停抢救患者血流动力学及心肺复苏质量的影响

摘要 目的：探讨可视喉镜气管插管对心跳骤停抢救患者血流动力学及心肺复苏质量的影响。方法：选取联勤保障部队第九四〇医院于2020年4月~2022年5月期间收治的98例心跳骤停抢救患者为研究对象,根据插管方式将患者分为B组（可视喉镜气管插管,n=50）、A组（传统直接喉镜气管插管,n=48）。对比两组插管次数、声门暴露时间、插管时间、气道与牙齿损伤、心肺复苏质量及血流动力学指标变化情况,观察两组不良反应发生情况。结果：B组的插管次数少于A组,声门暴露时间、插管时间短于A组,气道与牙齿损伤比例少于A组（P<0.05）。B组的插管成功率、心肺复苏（CPR）成功率、存活率均高于A组（P<0.05）。B组插管后15 min的收缩压（SBP）、舒张压（DBP）、平均动脉压（MAP）及心率（HR）均低于A组同期（P<0.05）。B组的不良反应发生率低于A组（P<0.05）。结论：相比于传统直接喉镜气管插管用于心跳骤停抢救患者,可视喉镜气管插管可维持血流动力学稳定,提高插管成功率和心肺复苏质量,安全性较好。     

在小鼠心跳骤停期间应用中度低温对复苏后抗氧化物酶活性的影响

目的：低温在许多小鼠心跳骤停后复苏模型的研究中被证实是有效的。心跳骤停后释放的氧自由基是产生继发性损伤的一个重要机制。本研究旨在探索心跳骤停期间应用中度低温对复苏后抗氧化物酶活性的影响。方法：用氯化钾诱导8min心跳骤停。此实验分为常温心跳骤停组（NCA）、低温心跳骤停组（HCA）TL对照组。HCA组在心跳骤停5min后开始降温使核心温度维持在（30．0±1．0）℃。应用胸部按压和肾上腺素来复苏。在心跳骤停两组各选择三个时间点：复苏后1h、4h和24h。测量超氧化物歧化酶（SOD）和过氧化氢酶（CAT）在心脏和肝脏的活性。结果：实验动物在HCA组比常NCA组生存率高。HCA组比NCA组复苏时间明显延长。与NCA组相比,HCA组复苏后24h的SOD活性在肝脏表达明显降低。与NCA组相比,HCA组复苏后4h的CAT活性在肝脏表达显著增高。结论：在心跳骤停过程中,与正常体温相比,应用中度低温能够提高生存率。与正常体温相比较,在心跳骤停中期间应用中度低温不影响心脏的SOD与CAT活性,应用中度低温在肝脏可延迟性抑制SOD的活性并且短暂提高CAT活性。     

心肺复苏后脑复苏的研究进展

在过去的10年里,美国心脏学会进行了大量的基础和临床研究,于2010年10月颁布了《2010美国心脏协会心肺复苏及心血管急救指南》［1］。新指南强调了早期心脏按压的重要性,简化了心肺复苏的流程,对心脏按压的质量提出了新的要求。随着医疗技术的发展,近年来心脏骤停后自主循环恢复的成功率虽然已经有了一定的提高,但是患者长时间存活率并未提高,仍有25％~50％的心跳骤停患者虽然恢复了自主循环,但仅有2％～10％的患者不出现神经功能缺陷［2］。临床上心肺复苏后脑功能完全恢复非常少见。     

规范化心肺复苏的急救护理体会

目的:为了探究不同的急救措施对心脏骤停者心肺复苏的影响,并对如何改善急救时护理的方法来提高急救的成功率。方法:对从2013年6月至2014年6月1年中在我市某医院急救的84例心跳骤停者分为死亡组、有效组合存活组3组,并回顾和分析了84例患者的CPR时间(TC)、患者心脏骤停发生的时间和除颤开始时间。结果分析:在急救的84例患者中,死亡的52例,复苏成功的有32例患者。结论分析:在对患者进行心肺复苏急救的过程中,早期的复苏及其熟练的配合抢救是心肺复苏的关键要素。     

谷氨酸在心肺脑复苏中的影响

心跳呼吸骤停及心肺脑复苏(CPCR)的过程均导致机体发生缺血/再灌注损伤(I瓜)等复杂的病理生理变化.脑的缺血再灌注损伤是一个快速的级联反应,包括能量代谢障碍、氧自由基的生成增多、兴奋性氨基酸释放增加、炎性细胞因子释放增加等.这些环节紧密连接,互为因果,形成恶性循环,最终导致神经元的凋亡或坏死.谷氨酸是大脑中一种关键的兴奋性神经递质,它的过多释放在神经元损伤发展过程中起着重要作用.随着细胞外高浓度谷氨酸的结合,N-甲基-D-天冬氨酸受体(NMDAR)开放,大量Ca2+内流,导致细胞内钙超载,是引起脑损伤的共同通路.本文就神经兴奋毒性的研究进行综述.     

1007型THUMPER心肺复苏机在急诊心肺复苏中的临床观察

目的观察1007型THUMPER心肺复苏机（萨勃机）在急诊心肺复苏中的临床效果。方法将114例心肺骤停患者分为萨勃机组59例和徒手心肺复苏组55例,两组患者均使用电除颤和药物治疗,比较两种方法在心肺复苏中的有效率。结果萨勃机组在心肺复苏中的有效率明显高于徒手心肺复苏组,差异有统计学意义（P〈0.05）,但对患者的存活率无明显优势（P〉0.05）。结论 1007型THUMPER心肺复苏机在心肺复苏抢救中有效率得到提高,值得临床推广。     

心肺复苏后大鼠神经元氧自由基的变化及卡尼汀的干预作用

目的:研究心肺复苏后大鼠脑细胞氧自由基的改变及卡尼汀的干预作用。方法:本实验采用窒息合并冰氯化钾停跳液致大鼠心跳骤停5min后开始心肺复苏的动物模型,SD大鼠88只,随机分为11组:对照组(假手术组)、复苏后3、12、24、48、72h组(每组8只),复苏后卡尼汀干预3、12、24、48、72h组(每组8只)。各组抽静脉血测定血液中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力。结果:心跳骤停/心肺复苏后各组大鼠血清中MDA含量较对照组显著升高(p<0.05),SOD活力显著降低(P<0.05)。使用卡尼汀干预后,血清MDA含量显著降低(P<0.05),SOD活力基本正常(P<0.05)。结论:心肺复苏后大鼠氧自由基产生增多,清除减少;卡尼汀干预后,氧自由基产生减少。卡尼汀对心肺复苏后大鼠具有保护作用。     

H2S对心跳骤停复苏大鼠脑血流动力学及神经功能的影响

目的:探讨吸入外源性H_2S对心跳骤停复苏大鼠脑血流动力学及神经功能的影响。方法:选择成年雄性SD大鼠18只,随机分为假手术组(sham,n=6)、窒息导致心跳骤停复苏组(CA,n=6)、心跳骤停复苏+H_2S组(H_2S,n=6),观察H_2S对心跳骤停复苏大鼠脑血流的影响。选择成年雄性SD大鼠45只,随机分为sham组(n=5)、CA(n=20)和H_2S组(n=20),观察H_2S对心跳骤停复苏大鼠神经功能和存活率的影响。结果:CA组与H_2S组在ROSC后MAP和CPP均快速上升,远高于基础值(P0.05);而后两组MAP和CPP均缓慢下降,实验结束时,明显低于基础值(P0.05)。两组间比较差异无统计学意义(P0.05)。CA组与H_2S组CBF曲线在ROSC后上升至峰值,随后逐渐下降,两组在峰值无明显差异,但H_2S组CBF减少量显著少于CA组(P0.05)。而在CVR曲线,在实验最后,CA组CVR值仍明显高于基础值(P0.05),而H_2S组基本降至基础值,明显低于CA组(P0.05)。H_2S组的14天存活率(80%)明显高于CA组(50%,P0.05)。在胶带移除实验(tape removal test,TRT)所需时间上,CA组与H_2S组在第1天、第3天及第14天都存在显著差异(P0.05)。H_2S组第14天海马CA1区神经元存活数(33±8)明显多于CA组(20±6,P0.05),但仍较假手术组少(53±10,P0.05)。结论:外源性H_2S吸入对大鼠心跳骤停复苏后MAP及CPP无明显影响。外源性H_2S通过降低CVR,改善CBF,从而改善大鼠心跳骤停复苏后的脑循环。外源性H_2S能明显提高心跳骤停复苏后大鼠的存活率,降低TRT所需时间,同时显著增加海马CA1区神经元的存活,改善大鼠心跳骤停复苏后神经功能转归。     

Protein Phosphatases but not Reactive Oxygen Species Play Functional Role in Acute Amphetamine-Mediated Dopamine Release

Drug abuse-induced neurodegeneration can be triggered by elevated production of reactive oxygen species (ROS). Involvement of oxidative stress in acute amphetamine (AMPH)-mediated dopamine (DA) release, however, has not been completely understood yet. In order to elucidate the dopaminergic response of PC12 cells to a single dose of 10 μM AMPH, ROS production was measured as related to the extracellular DA level. Due to the spontaneous oxidation of peroxide-sensitive fluorophore 2′,7′-dichlorofluorescin diacetate (DCFH-DA) to 2′,7′-dichlorofluorescein (DCF), the increase in fluorescence could not be unambiguously attributed to AMPH-triggered ROS production. Based on Amplex Red fluorescence, no ROS production was detected after acute AMPH application. Our data strongly suggest that ROS development was not the main triggering factor for immediate DA release after acute AMPH treatment. On the other hand, AMPH-induced elevation of DA levels in rat brain striatal slices was quenched by the water soluble antioxidant, N-acetylcysteine (NAC) at 10 mM. In this study, we also investigated the contribution of protein phosphatases to the AMPH-induced rat brain striatal dopaminergic response. The experimental protocol, double AMPH challenge was applied for screening the effect of NAC and cantharidin on AMPH-mediated DA release. Here we show that AMPH-mediated DA release increased nearly twofold in striatal rat brain slices pretreated for 30 min with 1000 μM cantharidin, a selective PP1 and PP2A inhibitor. These findings prove the lack of ROS inhibitory action on protein phosphatase activity in acute AMPH-mediated DA efflux.     

Mixed Venous Oxygen Saturation in Relation to Cardiac Output in Myocardial Infarction

Mixed venous oxygen saturations derived from measurement of mixed venous oxygen tension were compared with dye dilution cardiac output determinations in 26 patients with acute myocardial infarction. Mixed venous oxygen saturation was greatly reduced in patients with shock or failure complicating myocardial infarction. The level of oxygen saturation correlated with cardiac output determinations. The measurement of mixed venous oxygen saturation, which is relatively simple and does not require elaborate equipment, should be an important aid to the rational treatment of patients with low output states complicating acute myocardial infarction.     

一次性力竭运动对大鼠PHB1表达及线粒体功能的影响

目的：观察一次性力竭运动后大鼠脑、心、骨骼肌组织和线粒体中PHB1含量的变化及对大鼠线粒体功能的影响,探寻PHB1与线粒体功能和能量代谢的关系。方法：健康雄性SD大鼠40只,随机分为2组（n=20）：对照组和一次性力竭运动组,大鼠进行一次性急性跑台运动建立力竭运动模型。收集各组大鼠的心、脑和骨骼肌组织样品并提取线粒体,检测其呼吸功能和ROS的变化。用Western blot方法检测组织和线粒体中PHB1蛋白表达水平;用分光光度计检测各器官中ATP含量以及线粒体中复合体V活性（ATP合酶活性）。结果：①一次性力竭运动后脑、心肌、骨骼肌中ATP含量显著性降低;②一次性力竭运动后脑、心肌、骨骼肌线粒体中复合体V活性、RCR、ROS显著性降低,ST4均显著性升高,ST3无显著性差异。③一次性力竭运动后心、脑、骨骼肌线粒体中PHB1的表达显著性减少。④通过相关性分析得出：一次性力竭运动后心、脑、骨骼肌中ATP含量与心、脑、骨骼肌中复合体V活性呈正相关;心、脑、骨骼肌中ATP含量和心、脑骨骼肌中PHB1的表达呈正相关。结论：一次性力竭运动后,降低线粒体氧化磷酸化功能,使大鼠脑、骨骼肌线粒体内ROS生成增加,PHB1的表达、ATP含量和复合体V活性均下降。一次性力竭运动使得大鼠线粒体内PHB1表达降低,线粒体功能减弱,机体能量代谢降低。     

Coupled pacing improves cardiac efficiency during acute atrial fibrillation with or without cardiac dysfunction

Coupled pacing (CP), a method for controlling ventricular rate during atrial fibrillation (AF), consists of a single electrical stimulation applied to the ventricles after each spontaneous activation. CP results in a mechanical contraction rate approximately one-half the rate during AF. Paired stimulation in which two electrical stimuli are delivered to the ventricles has also been proposed as a therapy for heart failure. Although paired stimulation enhances contractility, it greatly increases energy consumption. The primary hypothesis of the present study is that CP improves cardiac function during acute AF without a similar increase in energy consumption because of the reduced rate of ventricular contractions. In a canine model, CP was applied during four stages: sinus rhythm (SR), acute AF, cardiac dysfunction (CD), and AF in the presence of cardiac dysfunction. The rate of ventricular contraction decreased in all four stages as the result of CP. In addition, we determined the changes in external cardiac work, myocardial oxygen consumption, and myocardial efficiency in the each of four stages. CP partially reversed the effects of AF and CD on external cardiac work, whereas myocardial oxygen consumption increased only moderately. In all stages but SR, CP increased myocardial efficiency because of the marked increases in cardiac work compared with the moderate increases in total energy consumed. Thus this pacing therapy may be a viable therapy for patients with concurrent atrial fibrillation and heart failure.     

Hypoxia divergently regulates production of reactive oxygen species in human pulmonary and coronary artery smooth muscle cells

Acute hypoxia causes pulmonary vasoconstriction and coronary vasodilation. The divergent effects of hypoxia on pulmonary and coronary vascular smooth muscle cells suggest that the mechanisms involved in oxygen sensing and downstream effectors are different in these two types of cells. Since production of reactive oxygen species (ROS) is regulated by oxygen tension, ROS have been hypothesized to be a signaling mechanism in hypoxia-induced pulmonary vasoconstriction and vascular remodeling. Furthermore, an increased ROS production is also implicated in arteriosclerosis. In this study, we determined and compared the effects of hypoxia on ROS levels in human pulmonary arterial smooth muscle cells (PASMC) and coronary arterial smooth muscle cells (CASMC). Our results indicated that acute exposure to hypoxia (Po(2) = 25-30 mmHg for 5-10 min) significantly and rapidly decreased ROS levels in both PASMC and CASMC. However, chronic exposure to hypoxia (Po(2) = 30 mmHg for 48 h) markedly increased ROS levels in PASMC, but decreased ROS production in CASMC. Furthermore, chronic treatment with endothelin-1, a potent vasoconstrictor and mitogen, caused a significant increase in ROS production in both PASMC and CASMC. The inhibitory effect of acute hypoxia on ROS production in PASMC was also accelerated in cells chronically treated with endothelin-1. While the decreased ROS in PASMC and CASMC after acute exposure to hypoxia may reflect the lower level of oxygen substrate available for ROS production, the increased ROS production in PASMC during chronic hypoxia may reflect a pathophysiological response unique to the pulmonary vasculature that contributes to the development of pulmonary vascular remodeling in patients with hypoxia-associated pulmonary hypertension.     

Layer-specific differences in reactive oxygen species levels after oxygen-glucose deprivation in acute hippocampal slices

The major role of reactive oxygen species (ROS) in the pathomechanism of ischemia have been widely recognized. Still, measurements of the precise time course and regional distribution of ischemia-induced ROS level changes in acute brain slices have been missing. By using acute hippocampal slices and the fluorescent dye CM-H2DCFDA, we showed that reoxygenation after in vitro ischemia (oxygen-glucose deprivation; OGD) increased ROS levels in the hippocampal CA1 layers vulnerable to ischemia but did not have significant effects in the resistant stratum granulosum in the dentate gyrus (DG). Production of ROS started during OGD, but, contrary to reoxygenation, it manifested as a ROS level increase exclusively in the presence of catalase and glutathione peroxidase inhibition. The mechanism of ROS production involves the activation of NMDA receptors and nitric oxide synthases. The inhibition of ROS response by either AP-5 or L-NAME together with the ROS sensitivity profile of the dye suggest that peroxynitrite, the reaction product of superoxide and nitric oxide, plays a role in the response. Direct visualization of layer-specific effects of ROS production and its scavenging, shown for the first time in acute hippocampal slices, suggests that distinct ROS homeostasis may underlie the different ischemic vulnerability of CA1 and DG.     

无创机械通气治疗急性心肌梗死低氧血症的护理体会

目的:探讨Bi PAP无创呼吸机辅助呼吸治疗急性心肌梗死低氧血症的临床疗效和护理措施。方法:选取我院2013年8月至2014年12月抢救中心急性心肌梗死伴低氧血症患者,在常规治疗及高流量吸氧后,末梢血氧饱和度(SPO2)90%者40例,采用无创呼吸机辅助治疗并加强护理,观察治疗后血气指标SPO2、Pa O2和Pa CO2的变化。结果:所有患者在无创通气30 min后SPO2均升至90%以上,而PO2升至正常低限,1 h后Pa O2恢复正常。结论:无创呼吸机辅助治疗是治疗急性心肌梗死低氧血症的有效方法。     

The effect of permeability transition pore opening on reactive oxygen species production in rat brain mitochondria

The influence of mitochondrial permeability transition pore (MPTP) opening on reactive oxygen species (ROS) production in the rat brain mitochondria was studied. It was shown that ROS production is regulated differently by the rate of oxygen consumption and membrane potential, dependent on steady-state or non-equilibrium conditions. Under steady-state conditions, at constant rate of Ca2+-cycling and oxygen consumption, ROS production is potential-dependent and decreases with the inhibition of respiration and mitochondrial depolarization. The constant rate of ROS release is in accord with proportional dependence of the rate of ROS formation on that of oxygen consumption. On the contrary, transition to non-equilibrium state, due to the release of cytochrome c from mitochondria and progressive respiration inhibition, results in the loss of proportionality in the rate of ROS production on the rate of respiration and an exponential rise of ROS production with time, independent of membrane potential. Independent of steady-state or non-equilibrium conditions, the rate of ROS formation is controlled by the rate of potential-dependent uptake of Ca2+ which is the rate-limiting step in ROS production. It was shown that MPTP opening differently regulates ROS production, dependent on Ca2+ concentration. At low calcium MPTP opening results in the decrease in ROS production because of partial mitochondrial depolarization, in spite of sustained increase in oxygen consumption rate by a cyclosporine A-sensitive component due to simultaneous work of Ca2+-uniporter and MPTP as Ca2+-influx and efflux pathways. The effect of MPTP opening at low Ca2+ concentrations is similar to that of Ca2+-ionophore, A-23187. At high calcium MPTP opening results in the increase of ROS release due to the rapid transition to non-equilibrium state because of cytochrome c loss and progressive gating of electron flow in respiratory chain. Thus, under physiological conditions MPTP opening at low intracellular calcium could attenuate oxidative damage and the impairment of neuronal functions by diminishing ROS formation in mitochondria.     

Regulation of mitochondrial uncoupling respiration during exercise in rat heart: role of reactive oxygen species (ROS) and uncoupling protein 2

The physiological significance of cardiac mitochondrial uncoupling protein 2 (UCP2)-mediated uncoupling respiration in exercise is unknown. In the current study, mitochondrial respiratory function, UCP2 mRNA level, UCP2-mediated respiration (UCR), and reactive oxygen species (ROS) generation, as well as manganese superoxide dismutase (MnSOD) activity were determined in rat heart with or without endurance training after an acute bout of exercise of different duration. In the untrained rats, state 4 respiration and UCR-independent respiration rates were progressively increased with exercise time and were 64 and 70% higher, respectively, than resting rate at 150 min, whereas UCR was elevated by 86% with no significant change in state 3 respiration. UCP2 mRNA level showed a 5- and 4-fold increase, respectively, after 45 and 90 min of exercise, but returned to resting level at 120 and 150 min. Mitochondrial ROS production and membrane potential (Deltapsi) increased progressively until 120 min, followed by a decrease to the resting level at 150 min. MnSOD mRNA abundance showed a 2-fold increase at 120 min but MnSOD activity did not change with exercise. Training significantly increased mitochondrial ATP synthetase activity, ADP to oxygen consumption (P/O) ratio, respiratory control ratio, and MnSOD activity, whereas exercise-induced state 4 respiration, UCR, ROS production, and Deltapsi were attenuated in the trained rats. We conclude that (1) UCP2 mRNA expression and activity in rat heart can be upregulated during prolonged exercise, which may reduce cross-membrane Deltapsi and thus ROS production; and (2) endurance training can blunt exercise-induced UCP2 and UCR, and improve mitochondrial efficiency of oxidative phosphorylation due to increased removal of ROS.     

Suitable Concentrations of Uric Acid Can Reduce Cell Death in Models of OGD and Cerebral Ischemia–Reperfusion Injury

Cerebral infarction (CI) is a common clinical cerebrovascular disease, and to explore the pathophysiological mechanisms and seek effective treatment means are the hotspot and difficult point in medical research nowadays. Numerous studies have confirmed that uric acid plays an important role in CI, but the mechanism has not yet been clarified. When treating HT22 and BV-2 cells with different concentrations of uric acid, uric acid below 450 μM does not have significant effect on cell viability, but uric acid more than 500 μM can significantly inhibit cell viability. After establishing models of OGD (oxygen-glucose deprivation) with HT22 and BV-2 cells, uric acid at a low concentration (50 μM) cannot improve cell viability and apoptosis, and Reactive oxygen species (ROS) levels during OGD/reoxygenation; a suitable concentration (300 μM) of uric acid can significantly improve cell viability and apoptosis, and reduce ROS production during OGD/reoxygenation; but a high concentration (1000 μM) of uric acid can further reduce cell viability and enhance ROS production. After establishing middle cerebral artery occlusion of male rats with suture method, damage and increase of ROS production in brain tissue could be seen, and after adding suitable concentration of uric acid, the degree of brain damage and ROS production was reduced. Therefore, different concentrations of uric acid should have different effect, and suitable concentrations of uric acid have neuroprotective effect, and this finding may provide guidance for study on the clinical curative effect of uric acid.