Influence of carbon monoxide, hypoxic hypoxia or potassium cyanide pretreatment on acute carbon monoxide and hypoxic hypoxia lethality.

Pre-exposure of mice to 500 or 1000 ppm of carbon monoxide (CO) for 4 hours resulted in a significant decrease in lethality induced by exposure to 2500 ppm of CO 24 hours later. Pre-exposure to CO had no effect on lethality induced by hypoxic hypoxia (low inspired O2 tension) or potassium cyanide (KCN). Pre-exposure to 10% O2 for 4 hours significantly decreased lethality induced 24 hours later by CO or 7% O2 exposures lethality induced 24 hours later by CO or 7% O2 exposures but had no effect on KCN-induced lethality. Pretreatment with a nonlethal dose of KCN had no significant effect on lethality induced 24 hours later by exposure to CO (2500 ppm), 7% O2 or KCN. The alterations in CO lethality were not associated with alterations in carboxyhemoglobin levels. Studies of oxygen consumption and indicators of oxygen delivery to tissues (P50 and red blood cell 2,3-diphosphoglycerate) failed to provide any evidence of pretreatment alteration. Examination of blood lactate, pyruvate and lactate/pyruvate ratios in control and pre-exposed mice after a short exposure to 2500 ppm of CO showed significantly lower lactate and lactate/pyruvate ratios in the pre-exposed mice as compared to controls. These data suggest that animals pre-exposed to 1000 ppm of CO and 10% O2 are less hypoxic than non-pre-exposed animals even through their oxygen delivery system is unchanged.     

Acute carbon monoxide poisoning during pregnancy

The course of a pregnant patient at term who was acutely exposed to carbon monoxide is described. A review of the fetal-maternal carboxyhemoglobin relationships and the differences in fetal oxyhemoglobin physiology are used to explain the recommendation that pregnant women with carbon monoxide poisoning should receive 100% oxygen therapy for up to five times longer than is otherwise necessary. The role of hyperbaric oxygen therapy is considered.     

急性一氧化碳中毒后的迟发性脑病

目的：分析急性一氧化碳中毒导致迟发性脑病的发生机制和临床表现，探讨其综合治疗的方法和预后的影响因素。资料来源：应用计算机检索中国期刊全文数据库1983—01／2000—10和CBMdise相关文章。 检索词“急性、一氧化碳中毒、迟发性、脑病”．限定文章语言种类为中文。 资料选择：对资料进行初审．选取有关急性一氧化碳的发病机制、临床表现、治疗和预后的相关文章。纳入标准：①随机对照临床研究。②不限定盲法。排除标准、重复的同一研究。 资料提炼：共收集到240篇关手急性一氧化碳中毒导致脑病的相关文献，24篇符合纳入标准。 资料综合：急性一氧化碳中毒导致脑病的发病机制较为复杂．临床表现从症状、体征、脑电图、脑CT、磁共振方面来加深对该病的认识。治疗方法常采用：①神经细胞活化剂、血管扩张剂、抗凝剂及维生素。②高压氧。②紫外线照射充氧自血回输疗法。④针刺疗法。影响急性一氧化碳中毒后迟发性脑病预后的因素常与年龄、中毒程度、并发症及其救治的时间有关。 结论：急性一氧化碳中毒可以导致脑病的发生，是多种机制共同作用的结果。目前尚无特异性的治疗方法，应采取综合治疗．但治疗效果不理想，可遗留不同程度的智力及肢体功能障碍，长期存在睁眼昏迷。     

急性一氧化碳中毒的临床表现与MRI分析

目的评价MRI对急性CO 中毒的诊断价值.方法分析59例经临床确诊的急性CO中毒患者的头颅MRI资料.结果 MRI异常表现为苍白球变性坏死,双侧大脑白质区脑水肿,以脑室周围为主的长T 1长T2信号,后期出现脑萎缩征象,海马区及脑干的改变.结论本病的诊断主要依靠病史、临床表现和影像检查,头颅MRI对本病的诊断、鉴别诊断及判断预后有价值.     

急性一氧化碳中毒后的迟发性脑病

目的:分析急性一氧化碳中毒导致迟发性脑病的发生机制和临床表现,探讨其综合治疗的方法和预后的影响因素。资料来源:应用计算机检索中国期刊全文数据库1983-01/2000-10和CBMdise相关文章。检索词“急性、一氧化碳中毒、迟发性、脑病”,限定文章语言种类为中文。资料选择:对资料进行初审,选取有关急性一氧化碳的发病机制、临床表现、治疗和预后的相关文章。纳入标准:①随机对照临床研究。②不限定盲法。排除标准:重复的同一研究。资料提炼:共收集到240篇关于急性一氧化碳中毒导致脑病的相关文献,24篇符合纳入标准。资料综合:急性一氧化碳中毒导致脑病的发病机制较为复杂,临床表现从症状、体征、脑电图、脑CT、磁共振方面来加深对该病的认识。治疗方法常采用:①神经细胞活化剂、血管扩张剂、抗凝剂及维生素。②高压氧。③紫外线照射充氧自血回输疗法。④针刺疗法。影响急性一氧化碳中毒后迟发性脑病预后的因素常与年龄、中毒程度、并发症及其救治的时间有关。结论:急性一氧化碳中毒可以导致脑病的发生,是多种机制共同作用的结果。目前尚无特异性的治疗方法,应采取综合治疗,但治疗效果不理想,可遗留不同程度的智力及肢体功能障碍,长期存在睁眼昏迷。     

A human factors analysis of an EMS crew's exposure to carbon monoxide

The safety of personnel and resources is considered to be a cornerstone of prehospital Emergency Medical Services (EMS) operations and practice. However, barriers exist that limit the comprehensive reporting of EMS safety data. To overcome these barriers, many high risk industries utilize a technique called Human Factors Analysis (HFA) as a means of error reduction. The goal of this approach is to analyze processes for the purposes of making an environment safer for patients and providers. This report describes an application of this approach to safety incident analysis following a situation during which a paramedic ambulance crew was exposed to high levels of carbon monoxide.