中国心脏起搏与心电生理杂志
中國心髒起搏與心電生理雜誌
중국심장기박여심전생리잡지
CHINESE JOURNAL OF CARDIAC PACING AND ELECOPHYSIOLOGY
2001年
2期
113-115
,共3页
高蕴雅%龚镇楠%朱伯良%张觉先%孙友法%方祖祥%石镭%戚文航%王志刚
高蘊雅%龔鎮楠%硃伯良%張覺先%孫友法%方祖祥%石鐳%慼文航%王誌剛
고온아%공진남%주백량%장각선%손우법%방조상%석뢰%척문항%왕지강
心脏除颤,低能量%心肌损伤%病理检查%心电图记录%心肌酶
心髒除顫,低能量%心肌損傷%病理檢查%心電圖記錄%心肌酶
심장제전,저능량%심기손상%병리검사%심전도기록%심기매
在13只犬的低能量心脏除颤实验中,应用病理检查、除颤心电图记录以及除颤前后肌酸磷酸激酶及其同工酶(CPK和CPK-MB)测定三种方法探测心肌损伤。肉眼观察和显微镜检查见到5只犬(除颤7~21次,能量10~40 J)电极处心脏轻度充血,2只犬(除颤9~20次,能量20~50 J)心肌苍白、心内膜附有血栓,6只犬(除颤7~29次,能量10~60 J)心内膜水肿、血栓形成、局部心肌断裂和退行性变、心肌间质出血等病理变化。记录到4只犬(除颤8~24次,能量20~50 J)除颤放电后ST段压低或ST段抬高心电图波形。测得2只犬(除颤10~19次,能量5~40J)除颤后CPK和CPK-MB有轻度升高(1只CPK由104升至110 IU,另1只CPK-MB由47.1升至60.9 IU)。本实验提示:低能量心脏除颤可导致心肌损伤;损伤可能由热和电等因素造成;损伤程度与除颤能量和除颤脉冲间隔时间等因素有关;损伤范围为局灶性且可能愈合。
在13隻犬的低能量心髒除顫實驗中,應用病理檢查、除顫心電圖記錄以及除顫前後肌痠燐痠激酶及其同工酶(CPK和CPK-MB)測定三種方法探測心肌損傷。肉眼觀察和顯微鏡檢查見到5隻犬(除顫7~21次,能量10~40 J)電極處心髒輕度充血,2隻犬(除顫9~20次,能量20~50 J)心肌蒼白、心內膜附有血栓,6隻犬(除顫7~29次,能量10~60 J)心內膜水腫、血栓形成、跼部心肌斷裂和退行性變、心肌間質齣血等病理變化。記錄到4隻犬(除顫8~24次,能量20~50 J)除顫放電後ST段壓低或ST段抬高心電圖波形。測得2隻犬(除顫10~19次,能量5~40J)除顫後CPK和CPK-MB有輕度升高(1隻CPK由104升至110 IU,另1隻CPK-MB由47.1升至60.9 IU)。本實驗提示:低能量心髒除顫可導緻心肌損傷;損傷可能由熱和電等因素造成;損傷程度與除顫能量和除顫脈遲間隔時間等因素有關;損傷範圍為跼竈性且可能愈閤。
재13지견적저능량심장제전실험중,응용병리검사、제전심전도기록이급제전전후기산린산격매급기동공매(CPK화CPK-MB)측정삼충방법탐측심기손상。육안관찰화현미경검사견도5지견(제전7~21차,능량10~40 J)전겁처심장경도충혈,2지견(제전9~20차,능량20~50 J)심기창백、심내막부유혈전,6지견(제전7~29차,능량10~60 J)심내막수종、혈전형성、국부심기단렬화퇴행성변、심기간질출혈등병리변화。기록도4지견(제전8~24차,능량20~50 J)제전방전후ST단압저혹ST단태고심전도파형。측득2지견(제전10~19차,능량5~40J)제전후CPK화CPK-MB유경도승고(1지CPK유104승지110 IU,령1지CPK-MB유47.1승지60.9 IU)。본실험제시:저능량심장제전가도치심기손상;손상가능유열화전등인소조성;손상정도여제전능량화제전맥충간격시간등인소유관;손상범위위국조성차가능유합。
During low energy defibrillation experiments in 13 dogs,three methods for the detection of myocardial injury were used:pathologic examination,defibrillation electrocardiogram recording,and creatine phosphokinase (CPK) and CPK-MB determination before and after defibrillation.In visual observation and microscopic examination,5 dogs (7~21 shocks,10~40 J) showed slight hyperemia in the area around electrodes,2 dogs (9~20 shocks,20~50 J) showed pale myocardium,and endocardium with thrombi.Also,pathologic changes including endocardial edema,thrombosis,localized fragmentation of myocardium and retrograde changes,and myocardial interstitial hemorrhage were found in 6 dogs (7~29 shocks,10~60 J).ST-T segment changes in electrocardiographic patterns were recorded after defibrillation charges in 4 dogs(8~24 shocks,20~50 J).CPK and CPK-MB showed slight elevation in 2 dogs (10~19 shocks ,5~40 J) after receiving defibrillation shocks,with CPK elevated from 104 to 110 IU in one,and CPK-MB from 47.1 to 60.9 IU in the other.This study suggests the following:low energy defibrillation may cause myocardial injury,with heat and electricity as possible causative factors;the degree of injury is related to the energy used for defibrillation and the time intervals between shocks;the injury is localized,and may heal.