恶性高热 2017.ppt
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1、恶性高热(Malignant Hyperthermia,MH)概述恶性高热(Malignant Hyperthermia,MH)是一个基因性临床病理综合征,患者平时无异常表现,在全麻过程中接触挥发性吸入麻醉药和去极化肌松药(琥珀酰胆碱)后出现骨骼肌强直性收缩,产生大量能量,导致体温持续快速增高,在没有特异性治疗药物的情况下,一般的临床降温措施难以控制体温的增高,最终可导致患者死亡。在一般人群中,预计MH发作的发生率为每100,000次麻醉剂给予1例Exposure of an individual who has a genetic susceptibility(ryanodine recep
2、tor RYR1 or dihydropyridine receptor DHP mutation)to an anesthetic triggering agent(ie,volatile inhalational anesthetic agent,succinylcholine,or both)may result in malignant hyperthermia.This reaction is caused by an altered calcium balance between the lumen of the sarcoplasmic reticulum(SR)and the
3、sarcoplasm.Normally,muscle cell depolarization is sensed by the DHP receptor,which is thought to signal RYR1 opening by a direct physical connection.In malignant hyperthermia,accumulation of abnormally high levels of calcium in the sarcoplasm causes uncontrolled anaerobic and aerobic metabolism and
4、sustained muscle cell contraction.This results in the clinical manifestations of respiratory acidosis,metabolic acidosis,muscle rigidity,and hyperthermia.If the process continues unabated,adenosine triphosphate(ATP)depletion eventually causes widespread muscle fiber hypoxia(cell death,rhabdomyolysis
5、),which manifests clinically as hyperkalemia and myoglobinuria and an increase in creatine kinase.Dantrolene sodium binds to RYR1,causing it to favor the closed state,thereby reversing the uninhibited flow of calcium into the sarcoplasm.Larach MG,Gronert GA,Allen GC,et al.Clinical presentation,treat
6、ment,and complications of malignant hyperthermia in North America from 1987 to 2006.Anesth Analg 2010;110:498.发病机制骨骼肌细胞膜发育缺陷诱发药物肌细胞浆内钙离子浓度迅速增高,使肌肉挛缩产热急剧增加,体温迅速升高酸中毒高血钾低血氧心律失常死亡(MOF,DIC)诱发药物吸入麻醉药:乙醚、氟烷、安氟烷、异氟烷、地氟烷和七氟烷。去极化肌松药:琥珀胆碱其它有过报道的药物:氯胺酮、利多卡因和氟哌啶醇。Typical order of appearance of clinical signs Ty
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