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。     

41例急性毒鼠强中毒患者心电图分析

目的探讨急性毒鼠强中毒对心脏的影响。方法收集1999年至2007年住院的41例急性毒鼠强中毒病人入院时第一次心电图作为分析资料。结粜41例中毒患者中，心电图异常30例，异常率为73．17％。心电图异常主要表现为窦性心动过速，ST－T改变，Q-T间期延长、左心室高电压，并且与中毒程度有一定的关系。结论急性毒鼠强中毒可导致心脏损害。     

急性一氧化碳中毒致急性心肌梗死的临床分析

目的对急性一氧化碳中毒致急性心肌梗死患者的特点进行分析。方法选取2008年1月~2015年12月急性一氧化碳中毒致急性心肌梗死患者15例的临床资料进行分析,探究其临床特点。结果患者接受冠状动脉造影治疗6例,患者不存在动脉粥样斑块3例,患者存在轻度左冠状动脉回旋支以及前降支轻度狭窄的情况1例,患者的左前降支狭窄程度较严重2例,接受支架置入术进行治疗。全部患者经相关治疗之后,死亡2例,其余康复出院。结论急性一氧化碳中毒是导致患者出现心肌梗死的原因之一,同时可在患者原有动脉粥样硬化的基础上导致患者出现心肌梗死。患者在急性一氧化碳中毒之后,其急性心肌梗死症状会被一氧化碳中毒所掩盖,因此,临床应加强急性一氧化碳中毒致心肌梗死患者心肌酶谱、心电图、肌钙蛋白等的检查,避免导致患者出现漏诊的情况。     

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。     

不同程度急性酒精中毒患者心电图变化情况分析

目的探讨不同程度急性酒精中毒患者心电图变化情况。方法选取2012年6月—2013年12月广西柳州钢铁集团公司职工医院收治的急性酒精中毒患者150例作为研究组,其中Ⅰ度酒精中毒45例,Ⅱ度酒精中毒49例,Ⅲ度酒精中毒56例;另选取同期在广西柳州钢铁集团公司职工医院进行体检健康者60例作为对照组。观察两组患者心电图异常情况及不同程度酒精中毒患者心电图异常情况。结果研究组患者窦性心动过速、ST-T变化、期前收缩及心房纤颤发生率高于对照组(P<0.01);Ⅰ度酒精中毒患者窦性心动过速发生率高于Ⅱ度、Ⅲ度酒精中毒患者(P<0.05),Ⅲ度酒精中毒患者ST-T变化、期前收缩、心房纤颤、室上性心动过速发生率高于Ⅰ度、Ⅱ度酒精中毒患者(P<0.05)。结论急性酒精中毒患者心电图变化与酒精中毒程度相关,可根据心电图变化情况判断酒精中毒程度,为治疗提供依据。     

急性一氧化碳中毒心电图改变(附131例分析)

我们对131例一氧化碳中毒患者的心电图进行了动态观察,对其所致的心电图改变进行了分析研究,井对影响心电图改变的因素等进行了分析和探讨。 1 资料与方法 1.1 研究对象 131例急性一氧化碳中毒患者均系我院住院病人,其中男79例,女52例,年龄16～78岁,平均42.4岁。131例患者既往心电图正常,经询问病史,     

58例急性一氧化碳中毒患者的心电图及心肌酶学变化

1998～2002年，我们对58例急性一氧化碳中毒患者行心电图及心肌酶学检查。，现将结果报告如下。资料与方法：本组58例工业性一氧化碳中毒患者，均为男性，年龄18～46岁，平均32．5岁。既往体健．均有急性一氧化碳中毒史及典型的临床表现，血中碳氧血红蛋白测定阳性。轻度11例，中度29例，重度18例。均为急诊入院，入院后全部常规记录心电图，抽血送检心肌酶，治疗后1～2周复查心电图、心肌酶。     

急性砷化氢中毒对心电图及心肌酶影响的研究

目的探讨急性砷化氢中毒对心电图及心肌酶影响,以便早期进行临床诊治,降低死亡率。方法回顾性分析2009年12月至2014年12月62例急性砷化氢中毒患者,按《职业性急性砷化氢中毒诊断标准》分成轻度、中度、重度组,用心电图仪和全自动生化仪检测患者心电图和心肌酶。结果心电图异常48例,发生率为77.42%,其中ST-T改变发生率95.83%,窦性心动过速发生率77.08%,室性早搏发生率60.42%,以上3种异常心电图和其他异常指标相比差异显著(P0.05);心肌酶含量与急性砷化氢中毒程度呈正相关;心电图异常组天冬氨酸氨基转移酶(AST)、肌酸磷酸肌酶(CK)、乳酸脱氢酶(LD)、α-羟丁酸脱氢酶(α-HBD)明显高于心电图正常组(P0.05)。结论心电图和心肌酶可作为急性砷化氢中毒心脏损害的有效指标。     

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。     

Acute respiratory failure after interferon-gamma therapy of end-stage pulmonary fibrosis

Interferon (IFN)-gamma was recently proposed as a treatment for idiopathic pulmonary fibrosis. We report on four patients who developed acute respiratory failure with new alveolar opacities after 2 (two patients), 6, and 35 injections of IFN-gamma-1b. All four patients had advanced idiopathic pulmonary fibrosis (total lung capacity less than 45% predicted or carbon monoxide diffusion capacity less than 30% predicted), and two patients had familial pulmonary fibrosis. No other cause of deterioration was found. Refractory hypoxemia led to death in three cases and to lung transplantation in one case. Pathologic studies in two patients showed diffuse alveolar damage lesions with preexisting usual interstitial pneumonia. These cases suggest that IFN-gamma therapy can induce an acute respiratory failure in patients with end-stage idiopathic pulmonary fibrosis.     

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.     

Transient myocardial dysfunction after smoke inhalation

Acute onset, transient (reversible) myocardial contraction abnormality has been described in patients with acute non-cardiac illness and after acute emotional stress. Such reversible myocardial contraction abnormalities may occur via mechanisms other than reduction in epicardial coronary blood flow. We report a case of acute transient cardiomyopathy after smoke exposure. The patient developed acute heart failure without evidence of carbon monoxide poisoning that resolved within 4 days. An association between brief smoke exposure without carbon monoxide poisoning and acute heart failure has not been previously described.     

Cardiogenic shock complicating acute carbon monoxide poisoning despite neurologic and metabolic recovery

We report the cases of 2 previously healthy young patients with acute carbon monoxide intoxication who deteriorated to cardiogenic shock in the face of apparent metabolic and neurologic recovery. Prolonged exposure to sublethal levels of carbon monoxide (>24 hours, carboxyhemoglobin level of 20.4% and 22.6%) and massive binding of the toxin to myocardial myoglobin and mitochondrial cytochrome chain enzymes might explain their protracted cardiac failure. The good response to inotropic agents and the findings of repeated echocardiographic studies support the probable diagnosis of myocardial stunning. Complete cardiac recovery was observed in both patients.     

Acute elevation of blood carboxyhemoglobin to 6% impairs exercise performance and aggravates symptoms in patients with ischemic heart disease

Acute exposure to carbon monoxide has the potential to impair exercise capacity in patients with ischemic heart disease. The effect of sufficient inhalation of this compound to gradually produce a level of 6% carboxyhemoglobin was studied in 30 nonsmoking patients with obstructive coronary artery disease and evidence of exercise-induced ischemia. After an initial training session, subjects were exposed to air or carbon monoxide on successive days in a randomized double-blind crossover fashion. Cardiac function and exercise capacity were assessed during symptom-limited supine radionuclide ventriculography. On the carbon monoxide day, mean postexposure carboxyhemoglobin was 5.9 +/- 0.1% compared with 1.6 +/- 0.1% (p less than 0.01) after air exposure. The mean duration of exercise was significantly longer after air compared with carbon monoxide exposure (626 +/- 50 s for air versus 585 +/- 49 s for carbon monoxide, p less than 0.05). Actuarial methods suggested that subjects were likely to experience angina earlier during exercise on the day of carbon monoxide exposure (p less than 0.05). Both the level (62 +/- 2.4 versus 60 +/- 2.4%, p = 0.05) and change in left ventricular ejection fraction at submaximal exercise (1.6 +/- 1.6 versus -1.2 +/- 1.6%, p = 0.05) were greater on the air exposure day compared with the carbon monoxide day. The peak exercise left ventricular ejection fraction was not different for the two exposures (57 +/- 2.5% for both). These results demonstrate earlier onset of ventricular dysfunction, angina and poorer exercise performance in patients with ischemic heart disease after acute carbon monoxide exposure sufficient to increase blood carboxyhemoglobin to 6%.     

Mallory–Weiss syndrome in children

The aim of the study was to evaluate the incidence and the etiology of Mallory-Weiss syndrome in children. The study population comprised 2720 children aged 5 months to 18 years who had undergone upper gastrointestinal endoscopy. Mallory-Weiss syndrome was diagnosed in eight (0.3%) of the examined children. Endoscopic examination in five of them revealed linear mucosal tears, mostly above and in one case also below the gastroesophageal junction. In three children a linear scar in the lower portion of the esophagus was seen. No signs of active bleeding were revealed in any of the cases. In four children, Mallory-Weiss syndrome was accompanied by gastritis and duodenitis; two of these children had Helicobacter pylori infection. The concomitant diseases were H. pylori-positive duodenal ulcer (1), bronchial asthma and gastroesophageal reflux disease (1), carbon monoxide poisoning (1). In one case Mallory-Weiss syndrome was diagnosed in early pregnancy. Mallory-Weiss syndrome should be considered, along with others, as a cause of acute upper gastrointestinal bleeding in children. There is a great variety of etiologic factors in Mallory-Weiss syndrome in children.     

Study on changes of heme oxygenase-1 expression in patients with coronary heart disease

BACKGROUND: Heme oxygenase (HO) is a rate-limiting enzyme of endogenetic carbon monoxide (CO) that degrades heme into carbon monoxide, bilirubin, and iron. These products have important physiologic effects: bilirubin is a potent antioxidant that can act against ischemia/reperfusion injury; there is a negative correlation between the content of HO-1 and the incidence of coronary heart disease (CHD). HYPOTHESIS: This study was undertaken to investigate the changes of HO-1 in patients with CHD. METHODS: Thirty-five patients with acute myocardial infarction (AMI), 40 patients with unstable angina pectoris (UAP, diagnosed by coronary angiography), and 30 patients with stable angina pectoris (AP, diagnosed by coronary angiography) were selected for the study; another 30 patients with normal coronary artery (diagnosed by coronary angiography) were selected as controls. The levels of HO-1 protein expression in monocyte and lymphocyte in the subjects were tested by immunohistochemistry and western blot. Computer picture analyzing systems were also used to measure the levels of HO-1 protein expression. RESULTS: Heme oxygenase-1 protein is located in cell plasma. The levels of HO-1 protein expression in patients with CHD were significantly higher than in those without CHD (p < 0.01). There were significant differences of HO-1 expression among the three groups of patients with CHD. The group with AMI was the highest, followed by the group with UAP and finally by the group with AP. CONCLUSIONS: There is a higher expression of HO-1 in patients with CHD. The levels of HO-1 protein are associated with the severity of CHD.     

高压氧联合机械通气治疗重度急性一氧化碳中毒的疗效简

目的 探讨高压氧联合机械通气治疗重度急性一氧化碳中毒的疗效.方法 选取2010年1月～2012年12月于我院MICU进行治疗的28例重度CO中毒患者为研究对象,将其分为对照组（高压氧组）和观察组（高压氧联合机械通气组）各14例,两组患者均同时给予预防感染、防治脑水肿、促进脑细胞代谢等治疗.结果 观察组平均住院时间、昏迷时间短于对照组;迟发性脑病发生率低于对照组;总有效率高于对照组.治疗后6 h,24 h观察组的血氧分压（PaO2） 、碱剩余增加高于对照组,血二氧化碳分压（PaCO2）、CRP、TNF-α、心肌酶谱水平均低于对照组.结论 高压氧联合机械通气治疗重度急性一氧化碳中毒可明显减轻病情,缩短住院时间,改善预后.     

108例急性一氧化碳中毒患者并发心肌损害分析

目的分析急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)时临床心电图表现、心肌酶及肌钙蛋白(cTNT)的改变对心肌损害的临床意义。方法对我院2008年11月～2012年12月收治的108例ACOP患者进行心电图、心肌酶及cTNT定量临床观察,并做回顾性分析。结果 108例ACOP患者均有不同程度意识障碍,昏迷82例,占75.9%;心电图异常80例,占74.1%,其中ST-T改变69例,占63.9%;心肌酶活性升高69例,占63.9%;cTNT活性升高25例,占27.8%。心电图的改变及心肌酶、cTNT的活性升高与年龄呈正比,与中毒程度呈正相关,差异有统计学意义,中、重度中毒与轻度中毒者,重度中毒与中度中毒者比较,差异均有统计学意义(P<0.01)。经治疗,101例患者康复出院,5例因中毒时间长合并多脏器功能衰竭死亡,2例发生一氧化碳中毒迟发性脑病。结论 ACOP可以造成心肌不同程度的损害,需要积极进行相应治疗。