急性一氧化碳中毒心肌损害的临床分析

目的探讨急性一氧化碳中毒对心肌的损害情况。方法采用回顾性调查方法分析152例急性一氧化碳中毒患者,分为轻度、中度、重度3组,分析其血清心肌酶值差异和心电图改变。结果血清心肌酶异常率轻度组、中度组、重度组间差异有统计学意义(P<0.05)。有心电图改变者以ST-T改变为主,中毒越重,心电图改变越明显。结论中度、重度一氧化碳中毒患者有较高的心肌损害发生率,中毒越重,心肌损害越明显。     

急性一氧化碳中毒性心肌损害72例临床资料分析

目的探讨急性一氧化碳中毒病人心肌损害时心肌酶变化及可能的发病机制。方法回顾性分析72例急性一氧化碳中毒心肌损害的临床资料。结果72例病人中,治愈68例,总治愈率94.44%。死亡4例,死亡原因分别为急性心肌梗死2例,急性左心衰竭和心室颤动各1例。结论心肌酶升高是预测急性一氧化碳中毒心肌损害的理想指标。     

急性一氧化碳中毒对心肌损害的分析

目的 分析急性一氧化碳(CO)中毒对心肌的损害.方法 选取我院2008年3月至2010年4月急诊入院的急性一氧化碳中毒患者68例,进行心电图、心肌酶临床观察,并做回顾性分析.结果 一氧化碳中毒患者的心电图异常46例(67.6％),其中ST-T改变32例(52.9％),窦性心动过速12例(8.8％),窦性心动过缓4例(2...     

急性一氧化碳中毒性心肌损害66例临床分析

急性一氧化碳中毒 (ＡＣＯＰ)在临床上甚为常见 ,而ＡＣＯＰ性心肌损害也屡见不鲜。我们回顾性分析我院急诊科在1981年 1月至 2 0 0 0年 12月期间 ,共救治的ＡＣＯＰ 486例 ,其中有ＡＣＯＰ性心肌损害者 66例 ,现作一简要临床分析。一、资料与方法1 对象 :ＡＣＯＰ性心肌损害 66例中 ,男 48例 ,女 18例。年龄 6～ 84岁 ,平均年龄 (47± 15 )岁。属生产性ＡＣＯＰ性心表 1　486例ＣＯ中毒发生心肌损害相关因素分析检查项目总例数 心肌损害例数率 (% ) χ2 检查项目总例数 心肌损害例数率 (% ) χ2ＡＣＯＰ程度 (ＨｂＣＯ)中毒后就诊时间 (ｈ)…     

102例急性一氧化碳中毒患者的心电图分析

目的探讨急性一氧化碳中毒（ACOP）者对心肌的损害及心肌损害时的心电图（ECG）变化,阐述引起心电图改变的机制。方法分析102例ACOP者心肌损害的临床资料。结果 102例中97例出现ECG异常,占95.1%,且与中毒程度成正相关。结论 ACOP可致心肌损害,应及早应用保护心脏的药物。     

急性一氧化碳中毒致心肌损害的临床研究

目的观测一氧化碳（CO）中毒病人早期血清心肌酶与心电图变化，判断其与预后的关系。方法对44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CO中毒者血清心肌酶检测差异非常显著（P〈0.01），中毒程度越重血清心肌酶越高。结论一氧化碳中毒病人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及判断疗效和预后的依据。     

急性有机磷中毒致心肌损害27例报告

1998年 2月至 2 0 0 0年 5月 ,我院收治急性有机磷中毒患者 3 4例 ,其中 2 7例出现不同程度的心肌损害 ,现报告如下。临床资料 :本组男 6例 ,女 2 1例 ;年龄 18～ 41岁。患者均为口服中毒 ,农药种类为 DDV、160 5、乐果、10 5 9。中毒轻度 10例 ,中度 12例 ,重度 5例。患者均于入院次日凌晨抽空腹血测定心肌酶 ,包括肌酸磷酸激酶 (CPK)及其同功酶 (CPK- MB)、谷草转氨酶 (AST)、乳酸脱氢酶 (L DH)。心肌酶活力升高达正常值上限 2倍以上为阳性。结果 :本组心肌酶升高 15例 (占 5 5 .5 6% ) ,其中死亡 3例均为重度者 ,其心肌酶 CPK均 …     

急性一氧化碳中毒168例致心肌损害分析

目的: 观察急性一氧化碳(CO)中毒对心肌的损害，探讨临床意义。方法: 观察分析急性CO中毒患者168例的临床表现、心电图及心肌酶改变。选取健康人130例作为健康对照组，并对两组间血清心肌酶的情况进行比较。结果: 急性CO中毒患者168例均有不同程度的意识障碍，昏迷125例（74.4%），出现心力衰竭24例（14.3%），有心电图改变者共132例（78.6%），其中ST-T改变128例(76.2%)。在168例CO中毒患者中101例（60.1%）血清心肌酶谱改变，轻度中毒无心肌酶改变，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显著性(P<0.05)，病情越严重，心肌酶改变越明显，持续时间越长(P<0.05)。结论: 急性CO中毒对心肌造成的损害，需要相应的治疗。     

急性脑血管病并发心肌损害时心肌酶及心电图变化

目的观察急性脑血管病患者并发心肌损害时血清心肌酶、心电图的变化,分析其临床意义。方法用酶速率法测定急性脑血管病88例患者的血清心肌酶谱,包括肌酸激酶(CK)、心肌型肌酸激酶同工酶(CK-MB)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(α-HBDH),同时进行心电图检查,并根据神经功能缺损程度分轻、中、重型组,多组间进行对比分析。结果急性脑血管病(脑梗死与脑出血组)患者血清心肌酶除CK-MB外,AST、CK、LDH、α-HBDH与正常对照组比较具有统计学意义(P0.05或P0.01);脑梗死与脑出血组血清心肌酶比较无统计学意义(P0.05);重型组血清心肌酶明显高于轻型组(P0.01);心电图阳性组与心电图阴性组血清心肌酶比较无统计学意义(P0.05)。结论急性脑血管病患者并发心肌损害,血清心肌酶有明显的改变,其变化与病情轻重有关。检测血清心肌酶有助于判断病情的轻重及预后。     

一氧化碳中毒对心肌损害的探讨

目的探讨一氧化碳中毒对心肌的损害情况。方法2003年12月-2005年3月我院急性一氧化碳中毒住院患者48例分为轻、中、重度中毒3组，分析其血清心肌酶值差异和心电图改变。结果48例一氧化碳中毒患者有32例血清心肌酶值升高，占66．7％，轻、中、重度中毒组间差异有非常显著性意义（P〈0．01）。有心电圈改变者28例，占58.3％，以ST—T改变为主，中毒越重。心电图改变越明显。结论中、重度一氧化碳中毒患者有较高的心肌损害发生率，中毒越重。心肌损害越明显。     

Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases

From January 1978 through March 1984, 115 cases of acute carbon monoxide poisoning were treated with hyperbaric oxygen. Exposure resulted from accidental sources (n = 39), attempted suicide (n = 47), and smoke inhalation (n = 29). Forty-one victims were never unconscious, 30 victims were unconscious at the scene but awoke before arriving at the hospital, and 44 victims were unconscious in the ED. Eleven patients (9.6%) died, and two victims (1.9% of the survivors) experienced major sequelae. All these patients were comatose on arrival. The remaining 102 patients recovered fully. Carboxyhemoglobin levels did not correlate with clinical findings, thereby demonstrating the variability between carbon monoxide exposure and impairment of the cellular cytochrome system. Hyperbaric oxygen therapy facilitates the rapid removal of carbon monoxide from the hemoglobin and cytochrome systems while reoxygenating compromised tissues, and it can be an effective treatment in reducing mortality and morbidity.     

Subacute sequelae of carbon monoxide poisoning

From January 1980 to August 1983, 213 patients with carbon monoxide poisoning were seen; 131 received hyperbaric oxygen and had no sequelae. Eighty-two patients were treated with normobaric oxygen; ten (12.1%) returned with clinically significant sequelae. The specific neurological sequelae included headaches, irritability, personality changes, confusion, and loss of memory. This recurrent symptomatology developed within one to 21 days (mean, 5.7 days) after the initial exposure, although no reexposure occurred. These recurring symptoms resolved rapidly with hyperbaric oxygen therapy. We recommend that hyperbaric oxygen therapy be used whenever CO poisoning symptoms recur.     

急性一氧化碳中毒后迟发性脑病血清SOD活性、MDA水平的检测

目的 探讨急性一氧化碳中毒后迟发性脑病(DEACMP)与自由基的关系。方法 将42例急性一氧化碳中毒后迟发性脑病患者在高压氧及常规治疗前后进行血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平的检测，并与37例健康正常组进行比较。结果 治疗前DEACMP患者血清SOD活性较对照组明显降低，血清MDA水平较对照组显著升高；治疗1月后，血清SoD活性升高、MDA水平虽较治疗前降低，但与对照组比较仍有显著性差异。结论 自由基在DEACMP发病中起着重要作用，对于指导临床治疗及判断预后具有重要意义。     

Cutaneous blisters and carbon monoxide poisoning

We present the cases of three patients with skin blisters following carbon monoxide (CO) poisoning. Their blisters appeared to be related to the severity of the poisoning (HbCO levels of more than 40%). Two of the three patients died despite aggressive initial 100% surface oxygen followed by hyperbaric oxygen therapy. The pathophysiology of this type of blister remains unresolved. It could result from pressure necrosis alone or from a combination of pressure necrosis and direct CO inhibition of tissue oxidative enzymes. Although skin involvement as a result of CO poisoning is less frequently reported today than in the past (perhaps because of misidentified burns or because of more aggressive resuscitation and treatment protocols), the physician should recognize that such blisters may signal severe CO poisoning.     

急性一氧化碳中毒心脏损害的临床分析

目的 :探讨急性一氧化碳 (CO)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 :回顾性分析近年来我院收治的急性CO中毒患者的临床表现、心电图及心肌酶改变。结果 :15 8例急性CO中毒患者中 87.3%出现昏迷 ,12 .7%出现心力衰竭 ,随机将其中 6 5例中毒患者作心电图及心肌酶检查 ,发现 5 6例出现心电图改变 ,4 4例出现心肌酶改变。结论 :急性CO中毒不仅对神经系统造成损害 ,对心脏的损害也很严重 ,需要给予相应的治疗。     

Development of delayed neurologic sequelae in acute carbon monoxide poisoning cases caused by briquette-based kotatsu: A case-control study

Briquette-based kotatsu, a traditional Japanese heating system, is still used in rural areas and has been linked to the development of acute carbon monoxide (CO) poisoning. This study aimed to investigate the occurrence of delayed neurologic sequelae (DNS) in patients with acute CO poisoning caused by briquette-based kotatsu.This retrospective study included 17 patients treated for acute CO poisoning due to briquette-based kotatsu, between April 2017 and March 2020. Patients were divided into either a sequelae group (3 patients) or a non-sequelae group (14 patients) based on the presence or absence, respectively, of DNS. Demographic data, kotatsu characteristics, clinical findings, and therapies were compared between the 2 groups.Significant differences were noted in patient posture during their initial discovery. Specifically, all non-sequelae patients only had their legs under the kotatsu quilt and all sequelae patients had their entire bodies under the kotatsu quilt (P = .001). There were no statistically significant differences in carbon monoxide levels in hemoglobin (CO-Hb) or the creatine-kinase myocardial band (CK-MB), between the 2 groups; however, troponin-I levels were significantly higher in the sequelae group (P = .026). Abnormal head imaging findings were noted in 2 sequelae-group patients, with a significant difference between the groups (P = .025).We speculate that acute CO poisoning, caused by briquette-based kotatsu, may lead to DNS more frequently in patients in who cover their entire body with the kotatsu quilt and are found in this position. Patients should be warned about the dangers of acute CO poisoning when using briquette-based kotatsu.     

Serum NSE and S100B protein levels for evaluating the impaired consciousness in patients with acute carbon monoxide poisoning

The aim of this study was to investigate the associations between the levels of neuron-specific enolase (NSE) and S100B protein and coma duration, and evaluate the optimal cut-off values for prediction coma duration ≥ 72 hours in patients with acute carbon monoxide poisoning (ACOP).A total of 60 patients with ACOP were divided into 3 following groups according to their status of consciousness and coma duration at admission: Awake group [Glasgow Coma Scale score (GCS score) ≥ 13 points], Coma < 72 hours group (GCS score < 13 points and coma duration < 72 h), and Coma ≥ 72 hours group (GCS score < 13 points and coma duration ≥ 72 h). The levels of serum NSE and S100B protein were measured after admission.There were significant differences in GCS score, carbon monoxide (CO) exposure time, NSE, and S100B levels between the Coma ≥ 72 h group and the Awake group, and between the Coma < 72 h group and the Awake group. Significant differences in GCS score, NSE, and S100B levels were also found between Coma ≥ 72 h group and Coma < 72 h group. Correlation analysis showed that NSE and S100B were positively correlated (r_s = 0.590, P < .01); NSE and S100B were negatively correlated with GCS score (r_s = -0.583, r_s = -0.590, respectively, both P < .01). The areas under the curve (AUCs) of NSE, S100B, and GCS score to predict the coma duration ≥ 72 hours were 0.754, 0.791, and 0.785, respectively. Pairwise comparisons did not show differences among the 3 groups (all P > .05). The sensitivity and specificity of NSE prediction with a cut-off value of 13 μg/L were 80% and 64%, respectively, and those of S100B prediction with a cut-off value of 0.43 μg/L were 70% and 88%, respectively.The NSE and S100B protein levels were significantly correlated with the degree of impaired consciousness and had the same clinical value in predicting coma duration of ≥ 72 hours in patients with ACOP.