急性一氧化碳中毒致心肌损伤的临床观察

目的通过观测一氧化碳（CO）中毒患者早期血清心肌酶与心电图变化,判断急性一氧化碳中毒致心肌损伤与预后的关系。方法对50例急性一氧化碳中毒患者治疗过程中心肌酶谱与心电图变化进行观察。结果急性一氧化碳中毒患者心肌酶水平均有不同程度升高,心电图有不同程度改变,不同程度一氧化碳（CO）中毒者血清心肌酶检测差异有统计学意义（P〈0．01）,中毒程度与血清心肌酶呈正相关。结论一氧化碳中毒患者早期血清心肌酶显著增高,心电图有不同程度改变。通过观察一氧化碳中毒患者心肌酶与心电图改变有助于了解心肌损害程度及损伤是否继续存在,对指导制定抢救措施意义重大,并可作为药物治疗的观察指标,为判断疗效和预后提供可靠依据。     

急性一氧化碳中毒心肌损害68例临床分析

目的评价急性一氧化碳（CO）中毒时心肌酶变化及心电图的改变对心肌损害的诊断价值。方法回顾性分析2004年10月-2008年3月急诊入院的急性CO中毒患者68例,分为轻度、中度和重度中毒组。同时在健康体检中随机选取60例健康人为对照组。68例患者入院24h内采静脉血,对照组清晨抽空腹静脉血,测定心肌酶并完成12导联心电图描记。结果急性CO中毒患者中有23例（占33．8％）血清心肌酶谱改变。中、重度中毒者多有不同程度的心肌酶升高,与健康对照组相比,差异有统计学意义（P〈0．01）,中、重度中毒与轻度中毒相比,差异亦有统计学意义（P〈0．01）。心电图异常改变有52例（占76．5％）。经治疗68例患者均康复出院,在CO中毒纠正后,心肌酶和心电图均恢复正常。结论心肌酶升高是预测急性CO中毒心肌损害的理想指标。     

急性一氧化碳中毒118例心肌损害分析

目的 观察急性一氧化碳中毒(ACOP)对心肌的损害,使该中毒患者得到更加全面的治疗.方法 对ACOP患者118例血清心肌酶谱、心肌肌钙蛋白 I(cTnI)的变化及心电图检查指标作回顾性分析.结果 ACOP患者118例有心电图改变的91例(77.1%),其中ST-T改变的有85例(72.0%);有103例(87.3%)出现心肌损害,其中72例(61.9%)血清心肌酶谱及cTnI在急性期变化明显,中重度一氧化碳中毒组较轻度中毒组心肌酶谱指标和cTnI水平明显升高,组间差异有统计学意义(P<0.01).结论 ACOP患者有较高的心肌损害发生率,中毒越重,心肌酶、cTnI升高越显著,心电图ST-T改变越明显,心肌损害越明显,需要相应的治疗.     

急性一氧化碳中毒对心肌损害的临床观察

目的探讨急性一氧化碳中毒对心脏的损害,使急性CO中毒患者得到更全面的治疗。方法观察70例急性一氧化碳中毒患者的心电图及心肌酶改变。结果发现48例出现心肌酶改变（68．6％）,40例出现心电图改变（57．1％）,其中,ST-T改变20例（28．6％）,窦性心动过速24例（34．3％）,快速房颤7例（10％）,室性早搏4例（5．71％）,心电图正常15例（21．4％）。结论急性一氧化碳中毒患者大部分心肌酶有不同程度升高,心电图有相应改变,心肌酶的改变明显优于心电图,前者更有临床意义,需要引起重视。     

急性一氧化碳中毒患者心肌损伤状况分析

目的 探讨急性一氧化碳中毒患者心肌损伤的状况并对其进行分析.方法 对2011年9月-2013年1月本院收治的75例急性一氧化碳中毒并导致心肌损伤患者治疗过程中的心电图变化和心肌酶检测结果进行观察分析.结果 75例急性患者中,有71例治愈,总治愈率为94.67%,有4人死亡,病死率为5.33%;患者心电图改变正常的有22例,占29.33%,异常的有53例,占70.67%;所有患者的心肌酶检测结果都偏高.结论 急性一氧化碳中毒的患者在初期会出现血清心肌酶明显地增高,心电图不同程度改变的现象,急诊室通过对一氧化碳中毒患者心肌酶与心电图改变的观察,有助于确定心肌损伤是否存在并了解损伤程度,对急诊医生抢救患者并根据患者状况制定急救措施具有非常重要的意义,并且可以作为用药指标来指导患者用药和疗效判断的依据.     

急性一氧化碳中毒致心肌损害的临床研究

急性一氧化碳（CO）中毒病死率居各种中毒的首位。血液丰富的大脑和心脏受累最为明显。对急性CO中毒，临床上很重视有无脑组织损害，常常忽略心肌损害。对近年来收治的130例急性CO中毒患者的心肌酶和心电图进行分析，旨在探讨其对心脏损害的影响。报告如下：     

急性毒鼠强中毒患者血清心肌酶谱改变的临床意义

目的探讨急性毒鼠强中毒患者血清心肌酶谱改变的临床意义.方法采用速率法对32例急性毒鼠强中毒患者血清心肌酶谱进行检测,同时每位患者行心电图检查,分析心肌酶值与轻、重度分型的关系及改变的原因.结果22例轻度中毒无抽搐的患者与10例重度中毒有抽搐的患者心肌酶值进行比较,ck、ck-MB、a-HBD、LDH均P＜0.01,有统计学意义;28例心电图正常,仅4例有轻度改变.结论急性毒鼠强中毒患者,特别是重度中毒患者骨骼肌抽搐是引起心肌酶升高的主要原因,而非心脏损害.     

急性一氧化碳中毒心肌损害的临床诊治

目的:探讨急性一氧化碳(CO)中毒对心肌细胞损害的临床诊治。方法:对1999年8月～2007年12月间抢救治疗的CO中毒305例临床资料进行回顾性分析。结果:305例患者中,并发心肌损害者117例,占38.3%。结论:急性CO中毒心肌损害的确诊应符合4个基本条件:(1)CO中毒的明确病史,和(或)血COHb定量10%以上;(2)心肌受损的临床症状和体征;(3)心肌酶学的改变;(4)心电图的改变。治疗上必须加强对心肌损害的严密观察,及时给予心肌保护药物,早期应用激素及高压氧可预防和治疗心肌损害。     

急性一氧化碳中毒致心肌损害临床研究

目的探讨急性一氧化碳中毒（acute carbon monoxide poisoning,ACOP）患者血清心肌酶及心电图变化,了解对心肌损害情况。方法对44例ACOP患者（轻度中毒组17例、中度中毒组9例、重度中毒18例）入院后24h内抽取空腹静脉血测定肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）、α-羟丁酸脱氢酶（HBDH）、天门冬氨酸氨基转移酶（AST）,并常规描记体表心电图。结果轻度ACOP患者血清心肌酶与正常对照组比较,差异无统计学意义（P〉0.05）;中、重度ACOP患者较轻度中毒患者明显增高（P〈0.05）,且中毒程度越重心肌酶越高;ACOP可致心电图出现ST-T和各种心律失常改变。结论中、重度ACOP患者存在心肌损害,中毒程度越深,心肌损害越重;CO中毒可致不同类型心电图改变。     

急性有机磷中毒患者并发心肌损害55例临床分析

目的探讨急性有机磷中毒患者并发心肌损害的心电图及心肌酶学的变化情况。方法对我院1999年1月-2009年1月所收治55例急性有机磷中毒致心肌损害患者的情况进行回顾性分析。结果当心率分别为60～120次/min、120～140次/min、〉150次/min时,中重度中毒患者的心率改变比轻度患者变化明显（P〈0.05）;所有患者中心电图异常17例（30.91%）,心肌酶学均有不同程度的升高。结论有机磷中毒患者,尤其是重症患者,密切观察心肌的损害及损害程度,早期保护心脏功能,将有助于降低病死率。     

高压氧治疗一氧化碳中毒头颅CT动态变化的临床分析

目的探讨高压氧（HBO）治疗急性一氧化碳（CO）中毒头颅cT的动态表现与临床关系,选择合理的治疗方案。方法选取85例急性CO中毒患者,按临床表现分为轻、中、重度3组,均给予HBO及常规治疗,分别于发病12h内、1周、1个月行头颅CT检查,6个月后随访。结果85例患者首次头颅CT检查有31例（36．5％）阳性;1周时复查44例（51．8％）阳性,阳性率较首次检查明显增加（P〈0．05）;治疗后1个月复查CT阳性患者降至29例（34．1％）,较1周时明显下降（P〈0．05）。CO中毒后迟发性脑病（DEACMP）患者1周时头颅CT阳性率（88．5％）明显高于无DEACMP患者（35．6％）（P〈0．05）。HBO治疗急性CO中毒总有效率为96．5％,显效率无DEACMP组（98．3％）明显高于DEACMP组（61．5％）（P〈0．05）。结论CO中毒后动态头颅CT检查有助于判断中毒程度及脑损伤程度,早期判断预后,指导临床治疗;HBO治疗CO中毒疗效显著。     

急性一氧化碳中毒患者心肌肌钙蛋白I测定的临床意义

目的探讨急性一氧化碳中毒(ACOP)患者心肌肌钙蛋白I(TnI)的变化及临床意义。方法测定156例ACOP患者的TnI水平,按其结果分为TnI阳性组76例和TnI阴性组80例,分析ACOP患者TnI与心肌损伤发生率、机械通气发生率和EICU住院时间的关系。结果TnI阳性组中有42例患者有心脏事件(心绞痛、心律失常)的发生,发生率为55.3%,TnI阴性组有11例,发生率为13.8%,明显低于阳性组(P<0.01),TnI阳性组机械通气的发生率为(52.6%),比TnI阴性组(23.8%)高,差异具有显著性(P<0.05),TnI阳性组EICU住院时间(6.51±1.59)d明显高于TnI阴性组(4.96±1.49)d,差异具有显著性(P<0.05)。结论TnI对诊断微小心肌损伤具有高度敏感性和特异性,ACOP患者TnI升高,表明心脏事件的发生率和机械通气的发生率增高,EICU住院时间延长,TnI可作为反映病情严重程度和评估预后的一项参考指标。     

急性一氧化碳中毒后发生急性肺损伤的相关危险因素分析

目的 探讨急性一氧化碳中毒后发生急性肺损伤的相关危险因素.方法 整理2007年1月至2009年12月于哈尔滨市第一医院就诊,诊断为“急性一氧化碳中毒”患者180例的临床资料,分为发生急性肺损伤组和未发生急性肺损伤组,收集了指标:年龄、性别、中毒媒介、有无误吸、中毒程度、入院时动脉血氧分压、动脉血乳酸;入院时血常规白细胞计数;入院时生化肌酸激酶浓度.进行了单因素分析、Logistic回归分析,筛选出急性一氧化碳中毒后发生急性肺损伤的相关危险因素.结果 该研究总例数180例,男86例,女94例,年龄(42.90±18.99)岁.发生急性肺损伤患者38例,患病率21.11％.通过单因素分析显示年龄、性别、入院时血氧分压发生急性肺损伤组和未发生急性肺损伤组比较差异无统计学意义(P＞0.05).有无误吸;中毒媒介;中毒程度;昏迷时间;入院时动脉血乳酸、入院时血常规白细胞计数、入院时生化肌酸激酶浓度,两组比较差异有统计学意义(P＜0.05).对单因素分析差异有统计学意义的指标进行二项logistic回归分析,显示误吸、重度中毒、煤烟中毒、血动脉乳酸升高的OR值分别为3.06、4.80、2.00、1.20;均是急性一氧化碳中毒后发生急性急性肺损伤的相关危险因素(P＜0.05).结论 误吸、重度中毒、煤烟中毒、血乳酸升高均是急性一氧化碳中毒后发生急性急性肺损伤的危险因素.     

急性CO中毒死亡患者临床特征分析

目的 了解东莞地区急性一氧化碳(CO)中毒死亡患者的临床特征,探讨急性CO中毒的防治策略.方法 对1998年1月-2010年12月期间急诊科接诊和收治的急性CO中毒死亡患者进行系统的回顾性分析研究.结果 13年间共接诊和收治急性CO中毒死亡患者47例,男女比例为1∶1.94;平均年龄(26.76±10.41)岁,高发年...     

早期大剂量纳洛酮治疗急性CO中毒临床观察

目的：探讨院前早期应用大剂量纳洛酮治疗急性CO中毒的疗效与安全性。方法：以随机对照设计对145例急性CO中毒昏迷患者进行临床研究．对照组采用常规治疗方案，治疗组在对照组的基础上接受院前早期应用大剂量纳洛酮。观察两组病例在治疗期间的Glascow评分变化、平均意识觉醒时间以及发病2个月时迟发性脑病的发生率的差异。结果：两组病例在治疗期间的Glascow评分、平均意识觉醒时间以及发病2个月时迟发性脑病的发生率等情况的差异显著。结论：院前早期廊用大剂量纳洛酮治疗急性CO中毒疗效显著．安全性高。     

Acute carbon monoxide poisoning in an animal model: the effects of altered glucose on morbidity and mortality

An animal in model which the common carotid artery and the jugular vein serving one side of the brain are occluded by indwelling catheters has been used during the past few years to investigate acute carbon monoxide (CO) poisoning. This article reviews the recent research examining the pattern of changes in blood glucose concentration which results from CO exposure, and the manner in which altered glucose concentration alters neurologic outcome and mortality. At present it appears that either greatly depressed glucose or greatly elevated glucose during and/or after CO exposure increases morbidity and mortality. Cyanide (CN) poisoning, in contrast to CO, produces a different pattern of changes in blood glucose and lactate, and unlike CO, fails to slow cardiac AV conduction and ventricular repolarization. Through the use of magnetic resonance imaging and spectroscopic techniques, cerebral cortical edema and the changes in brain phosphagens have been assessed following CO poisoning in the rat. The published results as well as data from recent pilot studies are discussed in the light of our current understanding of CO toxicology.     

Serum Levels of NT-ProBNP as an Early Cardiac Marker of Carbon Monoxide Poisoning

Acute carbon monoxide (CO) poisoning may cause cardiotoxicity. The natriuretic peptides, including atrial natriuretic peptide, brain natriuretic peptide (BNP), N-BNP, and NT-proBNP (N-terminal pro brain natriuretic peptide), are endogenous cardiac hormones that may be secreted upon myocardial stress. The aim of this study was to assess the plasma NT-proBNP level in acute CO poisoning and to compare it with healthy control. After approval by the ethical committee, 15 healthy controls and 15 patients admitted to the Gaziantep University Hospital (Gaziantep, Turkey) between January 2005 and July 2005 with the diagnosis of carbon monoxide poisoning were studied. Echocardiography was performed to all patients. Serum NT-proBNP, creatine kinase (CK), creatine kinase-MB (CK-MB), and troponin-T were also analyzed, along with the carboxyhemoglobin (COHb) level. The correlation between serum NT-proBNP and COHb level was investigated. Electrocardiography (ECG) was performed to all patients and healthy controls, and the results were compared. Differences in troponin, CK, and CK-MB levels were not statistically significant between groups (p > 0.05). The level of NT-proBNP and COHb were found to be increased in the study group. There was a positive correlation between the COHb and the NT-proBNP (r = 0.829, p < 0.01), and between the COHb and the CK (r = 0.394, p < 0.01). There was no difference between groups in other parameters, all of which were within normal range. Thus, in this sudy we showed that the plasma NT-proBNP level may contribute to the early diagnosis of cardiotoxicity in patients with carbon monoxide poisoning.     

Serum levels of NT-ProBNP as an early cardiac marker of carbon monoxide poisoning

Acute carbon monoxide (CO) poisoning may cause cardiotoxicity. The natriuretic peptides, including atrial natriuretic peptide, brain natriuretic peptide (BNP), N-BNP, and NT-proBNP (N-terminal pro brain natriuretic peptide), are endogenous cardiac hormones that may be secreted upon myocardial stress. The aim of this study was to assess the plasma NT-proBNP level in acute CO poisoning and to compare it with healthy control. After approval by the ethical committee, 15 healthy controls and 15 patients admitted to the Gaziantep University Hospital (Gaziantep, Turkey) between January 2005 and July 2005 with the diagnosis of carbon monoxide poisoning were studied. Echocardiography was performed to all patients. Serum NT-proBNP, creatine kinase (CK), creatine kinase-MB (CK-MB), and troponin-T were also analyzed, along with the carboxyhemoglobin (COHb) level. The correlation between serum NT-proBNP and COHb level was investigated. Electrocardiography (ECG) was performed to all patients and healthy controls, and the results were compared. Differences in troponin, CK, and CK-MB levels were not statistically significant between groups (p > 0.05). The level of NT-proBNP and COHb were found to be increased in the study group. There was a positive correlation between the COHb and the NT-proBNP (r = 0.829, p < 0.01), and between the COHb and the CK (r = 0.394, p < 0.01). There was no difference between groups in other parameters, all of which were within normal range. Thus, in this study we showed that the plasma NT-proBNP level may contribute to the early diagnosis of cardiotoxicity in patients with carbon monoxide poisoning.     

Epidemiology of acute carbon monoxide poisoning in a Spanish region

BACKGROUND: In Spain, as in most of the world, the incidence of acute carbon monoxide poisoning is probably underestimated. METHODS: During an eighteen-month period we studied, by means of a standardized data collection form, all the cases of acute carbon monoxide poisoning that were diagnosed in 2 university hospitals. RESULTS: During the study, 154 patients were diagnosed with carbon monoxide poisoning. The mean age was 32.2+/-15.5 years. The two principal exposure sites were the kitchen (43%) and bathroom (23%). The majority of the cases related to malfunction of the water heater (30%) and of the central heating (23%) and 68% occurred in the home. Improper combustion of butane (31%), propane (13%), and natural gas (12%) were most frequent. The most prevalent clinical manifestations were headache (94%), dizziness (56%), nausea (45%), loss of consciousness (38%), and weakness (34%). Five patients died. In 14.4%, symptoms suggested delayed neurological syndrome. The largest number of cases of poisoning occurred during the months of December and January. CONCLUSIONS: Compared with previous Spanish series or with the antecedent year, acute carbon monoxide poisoning has a high prevalence in our region. Two factors appear to be essential to the accurate diagnosis of acute carbon monoxide poisoning: 1) the ability of emergency room physicians to recognize the clinical symptoms of carbon monoxide poisoning and 2) access to a carbon monoxide-oximeter.     

急性一氧化碳中毒患者高压氧治疗及护理探讨

目的 通过对急性一氧化碳(CO)中毒患者的高压氧临床治疗及护理策略的探讨,提高广大群众对一氧化碳中毒的认识和自我保护能力.方法 采用对照组和实验组分别对不同程度急性CO中毒患者行高压氧治疗及采取相应的护理措施,观察其疗效并进行对比.结果 高压氧对急性CO中毒治疗疗效显著,效率及治愈率高.实验组治愈率为32.7％,显效率为55.6％,对照组治愈率为10％.结论 将高压氧用于急性CO中毒患者的临床治疗及护理过程之中,其临床效果显著,患者生存质量得以较大程度提高与改善,值得在临床治疗急性CO中毒患者之中进行推广并应用.