Mild carbon monoxide poisoning impairs left ventricular diastolic function

Rationale:

Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. In mild CO poisoning in which cardiovascular life support is not required, the effects of CO on left and right ventricular functions are unknown in patients without cardiac failure.

Objectives:

Echocardiography was used to determine whether or not mild CO poisoning impairs ventricular function. Twenty otherwise healthy patients with CO poisoning and 20 age- and gender-matched controls were studied. Echocardiographic examinations were performed at the time of admission and 1 week after poisoning.

Results:

The impairment observed in the left and right ventricular diastolic function at the time of admission was greater than the impairment 1 week after poisoning. Mild CO poisoning did not have a significant effect on systolic function. Carboxyhemoglobin levels were positively correlated with left ventricular diastolic dysfunction, whereas the levels were not correlated with right ventricular diastolic function.

Conclusions:

In CO intoxication, the development of left and right ventricular diastolic dysfunction precedes systolic abnormality. Patients with mild CO poisoning do not manifest cardiovascular symptoms; however, it should be borne in mind that most of these patients have myocardial involvement.     

Association between early arterial blood gas tensions and neurological outcome in adult patients following in-hospital cardiac arrest

ObjectiveThe early partial pressures of arterial O₂ (PaO₂) and CO₂ (PaCO₂) have been found in animal studies to be correlated with neurological outcome after brain injury. However, the relationship of early PaO₂ and PaCO₂ to the neurological outcomes of resuscitated patients after cardiac arrest was still not clear.MethodsThis was a retrospective observational cohort study in a single medical center. Adult patients who had in-hospital cardiac arrest between 2006 and 2012 and achieved sustained return of spontaneous circulation (ROSC) (ROSC > 20 min without resumption of chest compression) were included. Multivariable logistic regression analysis was used to identify factors associated with favorable neurological outcome at hospital discharge. The first PaO₂ and PaCO₂ values measured after first sustained ROSC were used for analysis.ResultsOf the 550 included patients, 154 (28%) survived to hospital discharge and 74 (13.5%) achieved favorable neurological outcome. The mean time from sustained ROSC to the measurement of PaO₂ and PaCO₂ was 136.8 min. The mean PaO₂ and PaCO₂ were 167.4 mmHg and 40.3 mmHg, respectively. PaO₂ between 70 and 240 mmHg (odds ratio [OR] 1.96, 95% confidence interval [CI] 1.08–3.64) and PaCO₂ levels (OR 0.98, 95% CI 0.95–0.99) were positively and inversely associated with favorable neurological outcome, respectively.ConclusionsThe early PaO₂ and PaCO₂ levels obtained after ROSC might be correlated with neurological outcome of patients with in-hospital cardiac arrest. However, because of the inherent limitations of the retrospective design, these results should be further validated in future studies.     

不同细胞构筑在高压氧治疗迟发型脑病中的功能研究

目的：通过研究高压氧（ HBO）治疗急性CO中毒大鼠皮层不同细胞构筑在神经细胞凋亡中的差别,探讨HBO治疗急性CO中毒的机制及靶向定位。方法利用雄性SD大鼠,建立急性CO中毒模型。应用免疫组织化学以及免疫荧光的方法,测定在CO中毒和HBO治疗1 d、3 d、7 d、14 d和21 d后Caspase－3、NeuN和MMP－9的表达变化。结果急性CO中毒后,皮层神经细胞凋亡随中毒后时间延长而加重;不同细胞构筑发生凋亡程度不同,内颗粒层和内锥体细胞层最明显;Caspase－3与MMP－9在内颗粒层与内锥体细胞层变化最明显,在1 d开始增多,3 d达到最大值,7 d开始减少;HBO治疗后,MMP－9和Caspase－3降低,尤其以内颗粒层与内锥体细胞层最明显;且HBO治疗7 d后,降低最明显。结论急性CO中毒后,皮层各层神经细胞均发生凋亡现象,内颗粒层和内锥体细胞层最明显;凋亡可能与MMP－9降解神经细胞周围的基质, Caspase－3促进凋亡有关;HBO治疗可能是通过调控复杂的蛋白表达机制,调节MMP－9以及Caspase－3的表达水平,最终抑制神经细胞的凋亡;HBO治疗7 d对凋亡的作用最明显。     

Serum bilirubin value predicts hospital admission in carbon monoxide-poisoned patients. Active player or simple bystander?

OBJECTIVES:

Although carbon monoxide poisoning is a major medical emergency, the armamentarium of recognized prognostic biomarkers displays unsatisfactory diagnostic performance for predicting cumulative endpoints.

METHODS:

We performed a retrospective and observational study to identify all patients admitted for carbon monoxide poisoning during a 2-year period. Complete demographical and clinical information, along with the laboratory data regarding arterial carboxyhemoglobin, hemoglobin, blood lactate and total serum bilirubin, was retrieved.

RESULTS:

The study population consisted of 38 poisoned patients (23 females and 15 males; mean age 39±21 years). Compared with discharged subjects, hospitalized patients displayed significantly higher values for blood lactate and total serum bilirubin, whereas arterial carboxyhemoglobin and hemoglobin did not differ. In a univariate analysis, hospitalization was significantly associated with blood lactate and total serum bilirubin, but not with age, sex, hemoglobin or carboxyhemoglobin. The diagnostic performance obtained after combining the blood lactate and total serum bilirubin results (area under the curve, 0.90; 95% CI, 0.81-0.99; p<0.001) was better than that obtained for either parameter alone.

CONCLUSION:

Although it remains unclear whether total serum bilirubin acts as an active player or a bystander, we conclude that the systematic assessment of bilirubin may, alongside lactate levels, provide useful information for clinical decision making regarding carbon monoxide poisoning.     

二氧化碳冷冻法在结核性胸膜炎中的临床运用

目的观察经支气管镜代替胸腔镜二氧化碳冻切法在结核性胸膜炎中的运用价值.方法将98例结核性胸膜炎导致胸腔包裹性积液患者随机分为对照组和观察组,每组49例,对照组采用放置中心静脉导管引流充分后于胸腔内注入尿激酶10万U,隔天注射1次,观察组采用支气管镜代替胸腔镜二氧化碳冻切治疗.比较2组胸腔积液吸收情况、胸膜厚度、临床症状、肺功能等变化.结果对照组显效16例(32.6%),有效25例(51.0%),无效8例(16.4%),总有效率83.6%.观察组经治疗后患者胸腔积液吸收较快、症状明显改善,胸膜无明显增厚,肺功能改善明显,显效25例(51.0%),有效24例(49.0%),总有效率100.0%.结论经支气管镜代替胸腔镜能在直视下发现胸膜腔内纤维粘连包裹,二氧化碳冻切法可以对病变进行清除,有效减少胸膜肥厚粘连的发生.     

轻度二氧化碳潴留慢性阻塞性肺疾病肺功能和CT的特征

目的探讨轻度CO₂潴留慢性阻塞性肺疾病人群的肺功及影像特征,为监测和治疗提供依据。 方法选择147例慢性阻塞性肺疾病急性加重期患者,分为非CO₂潴留组61例PaCO₂＝40～44.9 mmHg;轻度CO₂潴留组48例PaCO₂＝45～50 mmHg;呼吸衰竭组38例PaCO₂>50 mmHg,比较3组在肺功能和容积CT参数的异同。 结果轻度潴留组在肺功能参数如一秒率(FEV₁%pred)等和肺气肿参数如肺气肿平均密度(MED)、肺密度分布直方图中第15百分位点所对应的CT值(PD15)等,与呼吸衰竭组存在明显差异(P<0.05),与非潴留组无统计学差异(P>0.05)。spearman相关分析显示PaCO₂与FEV₁%Pred、FVC%pred呈中度负相关(r分别是-0.536,-0.576,P<0.001),与PD15和MED存在弱负相关(r＝-0.325,P＝0.002)。 结论轻度CO₂潴留COPD肺结构和功能特征与非潴留COPD相似;呼吸衰竭组COPD具有更严重的病理和肺功能损害;CO₂轻度潴留向Ⅱ型呼吸衰竭进展中,FEV₁%pred等肺功能指标联合PD15和MED影像参数从功能和结构上能更好地反应病情。     

食管病变内镜黏膜剥离术中灌注二氧化碳对术后恢复的影响

目的探讨在全麻状态下行食管病变内镜黏膜剥离术术中灌注二氧化碳对术后机体恢复的影响。方法 2011年10月至2012年12月,对我院收治的接受食管黏膜剥离术治疗的患者72例,随机分成二氧化碳观察组和空气对照组。记录每个患者的手术时间,术后纵隔气肿或皮下气肿的发生例数以及气肿消退时间,术后住院时间。结果二氧化碳组和空气组的平均手术时间分别是(85±52)min和(87±55)min(P0.05),纵膈气肿(CT提示)或皮下气肿的发生率分别是31%和33%(P0.05)。二氧化碳组中发生气肿的患者术后气肿消退时间少于空气组,分别是(4.82±1.54)d和(5.83±1.8)d(P0.05)。二氧化碳组术后平均住院天数少于空气组,分别是(6.1±1.3)d和(7.0±1.8)d(P0.05)。结论食管病变的内镜黏膜剥离术中灌注二氧化碳气体能缩短术后恢复时间,提高术后恢复的质量。     

Hepatoprotective effects of Lycium chinense Miller fruit and its constituent betaine in CCl4-induced hepatic damage in rats

The hepatoprotective activities of Lycium chinense Miller (LC) fruit extract and its component betaine were investigated under carbon tetrachloride (CCl₄)-induced hepatotoxicity in rats. The treatment of LC fruit extract significantly suppressed the increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the sera of CCl₄ injured rats, and restored the decreased levels of anti-oxidant enzymes such as total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and suppressed the expression of inflammatory mediators including inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-1 and -2. To visualize the potential activity of betaine, a component of LC fruit, betaine was substituted for LC extract in CCl₄ injured rats. The biochemical profile in CCl₄ injured rats co-treated with betaine matched those of LC fruit treated CCl₄ injured rats. The ameliorative effects of LC extract, as well as betaine, were also confirmed by histopathological examination. Collectively, the present findings imply that LC fruit, via its component betaine, mitigate CCl₄-induced hepatic injury by increasing antioxidative activity and decreasing inflammatory mediators including iNOS and COX-1/COX-2.     

Carbon monoxide: Anticoagulant or procoagulant?

Within the past decade there have been several investigations attempting to define the impact of exogenous and endogenous carbon monoxide exposure on hemostasis. Critically, two bodies of literature have emerged, with carbon monoxide mediated platelet inhibition cited as a cause of in vitro human and in vitro/in vivo rodent anticoagulation. In contrast, interaction with heme groups associated with fibrinogen, α₂-antiplasmin and plasmin by carbon monoxide has resulted in enhanced coagulation and decreased fibrinolysis in vitro in human and other species, and in vivo in rabbits. Of interest, the ultrastructure of platelet rich plasma thrombi demonstrates an abnormal increase in fine fiber formation and matting that are obtained from humans exposed to carbon monoxide. Further, thrombi obtained from humans and rabbits have very similar ultrastructures, whereas mice and rats have more fine fibers and matting present. In sum, there may be species specific differences with regard to hemostatic response to carbon monoxide. Carbon monoxide may be a Janus-faced molecule, with potential to attenuate or exacerbate thrombophilic disease.