中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2002年
3期
359-363
,共5页
刘品明%高燕%傅向阳%吕俊豪%周瑛%魏向龙%李公信%丁明学%吴宏超%叶文胜%刘映峰%李志樑
劉品明%高燕%傅嚮暘%呂俊豪%週瑛%魏嚮龍%李公信%丁明學%吳宏超%葉文勝%劉映峰%李誌樑
류품명%고연%부향양%려준호%주영%위향룡%리공신%정명학%오굉초%협문성%류영봉%리지량
心脏骤停%心肺复苏%经食管超声心动图%血液动力学
心髒驟停%心肺複囌%經食管超聲心動圖%血液動力學
심장취정%심폐복소%경식관초성심동도%혈액동역학
cardiac arrest%cardiopulmonary resuscitation%transesophageal echocardiography%hemodynamics
目的 对院内心脏骤停患者于心肺复苏期间行经食管超声心动图检查,以进一步探讨心肺复苏时的血液动力学机制.方法 对6例院内心脏骤停患者依照进一步心血管生命支持指南行心肺复苏术.于心肺复苏15 min内,在喉镜指引下,插入多平面食管超声探头,采用二维及脉冲波多普勒超声心动图技术,观察整个心肺复苏过程中二尖瓣、三尖瓣和主动脉瓣的运动状况,左室内径、胸主动脉内径的变化和二尖瓣、主动脉瓣的血流频谱.结果 所有的6例病人,胸按压时,二尖瓣和三尖瓣关闭,同时主动脉瓣开放,前向血流自心室进入体循环和肺循环；发生在胸按压时的主动脉瓣峰值前向血流速度为58.8±11.6?cm/s.而在按压放松时,主动脉瓣关闭伴房室瓣迅速开放,出现心室充盈,二尖瓣峰值前向血流速度为60.6±20.0?cm/s.有5例病人在按压期出现二尖瓣反流,提示存在着室至房的压力阶差.所有的6例病人于胸按压时出现左室内径减小和胸主动脉内径增加,表明直接的心室受压是前向血流产生的机制.结论 上述资料支持心泵理论是人类心肺复苏时产生前向血流的主导性机制.
目的 對院內心髒驟停患者于心肺複囌期間行經食管超聲心動圖檢查,以進一步探討心肺複囌時的血液動力學機製.方法 對6例院內心髒驟停患者依照進一步心血管生命支持指南行心肺複囌術.于心肺複囌15 min內,在喉鏡指引下,插入多平麵食管超聲探頭,採用二維及脈遲波多普勒超聲心動圖技術,觀察整箇心肺複囌過程中二尖瓣、三尖瓣和主動脈瓣的運動狀況,左室內徑、胸主動脈內徑的變化和二尖瓣、主動脈瓣的血流頻譜.結果 所有的6例病人,胸按壓時,二尖瓣和三尖瓣關閉,同時主動脈瓣開放,前嚮血流自心室進入體循環和肺循環；髮生在胸按壓時的主動脈瓣峰值前嚮血流速度為58.8±11.6?cm/s.而在按壓放鬆時,主動脈瓣關閉伴房室瓣迅速開放,齣現心室充盈,二尖瓣峰值前嚮血流速度為60.6±20.0?cm/s.有5例病人在按壓期齣現二尖瓣反流,提示存在著室至房的壓力階差.所有的6例病人于胸按壓時齣現左室內徑減小和胸主動脈內徑增加,錶明直接的心室受壓是前嚮血流產生的機製.結論 上述資料支持心泵理論是人類心肺複囌時產生前嚮血流的主導性機製.
목적 대원내심장취정환자우심폐복소기간행경식관초성심동도검사,이진일보탐토심폐복소시적혈액동역학궤제.방법 대6례원내심장취정환자의조진일보심혈관생명지지지남행심폐복소술.우심폐복소15 min내,재후경지인하,삽입다평면식관초성탐두,채용이유급맥충파다보륵초성심동도기술,관찰정개심폐복소과정중이첨판、삼첨판화주동맥판적운동상황,좌실내경、흉주동맥내경적변화화이첨판、주동맥판적혈류빈보.결과 소유적6례병인,흉안압시,이첨판화삼첨판관폐,동시주동맥판개방,전향혈류자심실진입체순배화폐순배；발생재흉안압시적주동맥판봉치전향혈류속도위58.8±11.6?cm/s.이재안압방송시,주동맥판관폐반방실판신속개방,출현심실충영,이첨판봉치전향혈류속도위60.6±20.0?cm/s.유5례병인재안압기출현이첨판반류,제시존재착실지방적압력계차.소유적6례병인우흉안압시출현좌실내경감소화흉주동맥내경증가,표명직접적심실수압시전향혈유산생적궤제.결론 상술자료지지심빙이론시인류심폐복소시산생전향혈류적주도성궤제.
Objective Transesophageal echocardiography was performed during closed-chest cardiopulmonary resuscitation (CPR) in in-hospital cardiac arrest to further explore the hemodynamic mechanism of CPR. Methods CPR attempts were performed according to advanced cardiovascular life support guidelines in 6 cases of in-hospital cardiac arrest. Multi-plane transesophageal echocardiography was carried out within 15 min of initiation of CPR. Throughout CPR, the motion of the mitral, tricuspid and aortic valves, the changes in the left ventricular cavity size and the thoracic aortic diameter were observed. Trans-mitral and trans-aortic Doppler files of blood flow were also documented. Results A closure of the mitral and tricuspid valves with simultaneous opening of the aortic valve occurred exclusively during chest compression, resulting in forward blood flow in the pulmonary and systemic circulation. Peak forward aortic flow at a velocity of 58.8±11.6?cm/s was recorded during the compression phase. Whereas, a closure of the aortic valve and rapid opening of the atrioventricular valves associated with ventricular filling during relaxation of chest compression was noted in all 6 patients. Peak forward mitral flow at a velocity of 60.6±20.0?cm/s was recorded during the release phase. Mitral regurgitation during the chest compression period was detected in 5 patients, reflecting a positive ventricular-to-atrial pressure gradient. A reduction in the left ventricular chamber and an increase in the thoracic aortic diameter during the compression phase was found in all patients, indicating that direct cardiac compression contributed to forward blood flow. Conclusion These observations favor the cardiac pump theory as the predominant hemodynamic mechanism of forward blood flow during CPR in human beings.
