CAJ | 학술논문

目的分析脓毒性心肌病(SIC)的发生、发展是否与左室动脉偶联有关.方法回顾2012年12月至2014年1月北京协和医院重症医学科感染性休克合并SIC 46例患者,分生存组和死亡组,记录血流动力学参数、乳酸,分析心脏弹性(Ees)、动脉弹性(Ea)及心室动脉偶联(Ea/Ees)、心脏做功及其效率,比较两组心室动脉偶联状态.结果 Ea/Ees与对外做功、做功效率和每搏量相关,与组织灌注相关;SIC前24 h和SIC后12h外周血管阻力指数(SVRI)与Ea正相关,SIC 24 h后动脉顺应性增加;如果12 h Ees下降10.3％,平均动脉压(MAP) 85 mmHg(1 mmHg=0.133 kPa)比95 mmHg好;发生SIC时Ea和Ea/Ees均增加,Ees下降,Ea与SVRI有关;SIC后6 h Ees下降到最低,SIC后12 h Ees才开始增加;SIC后24、36 h后Ea和Ea/Ees均明显降低,48 h Ees才明显升高;死亡组患者SIC 30 h后Ea持续降低,Ees降低,治疗后Ea/Ees无改善.结论 SIC发生、转归同时受Ees和Ea影响,并与Ea/Ees密切联系,治疗脓毒性心肌病目标是改Ea/Ees,SIC 36 h内应降低Ea,48 h后应提高Ees.
목적 분석농독성심기병(SIC)적발생、발전시부여좌실동맥우련유관.방법 회고2012년12월지2014년1월북경협화의원중증의학과감염성휴극합병SIC 46례환자,분생존조화사망조,기록혈류동역학삼수、유산,분석심장탄성(Ees)、동맥탄성(Ea)급심실동맥우련(Ea/Ees)、심장주공급기효솔,비교량조심실동맥우련상태.결과 Ea/Ees여대외주공、주공효솔화매박량상관,여조직관주상관;SIC전24 h화SIC후12h외주혈관조력지수(SVRI)여Ea정상관,SIC 24 h후동맥순응성증가;여과12 h Ees하강10.3％,평균동맥압(MAP) 85 mmHg(1 mmHg=0.133 kPa)비95 mmHg호;발생SIC시Ea화Ea/Ees균증가,Ees하강,Ea여SVRI유관;SIC후6 h Ees하강도최저,SIC후12 h Ees재개시증가;SIC후24、36 h후Ea화Ea/Ees균명현강저,48 h Ees재명현승고;사망조환자SIC 30 h후Ea지속강저,Ees강저,치료후Ea/Ees무개선.결론 SIC발생、전귀동시수Ees화Ea영향,병여Ea/Ees밀절련계,치료농독성심기병목표시개Ea/Ees,SIC 36 h내응강저Ea,48 h후응제고Ees.
Objective To explore the occurrence and development of sepsis-induced cardiomyopathy (SIC) and its correlation with left ventricular arterial coupling.Methods A total of 46 SIC patients were recruited and divided into non-survival and survival groups.And hemodynamics parameters, lactate, cardiac elastance (Ees), arterial elastance (Ea) and ventricular-arterial coupling (Ea/Ees), stroke work (SW), total mechanical work (PVA) and cardiac work efficiency (SW/PVA) were recorded before and after an onset of SIC.Results The occurrence and development of SIC had close correlations with left ventricular arterial coupling.Heart and arterial elastance affected the occurrence and outcome of SIC.The former was a underlying cause while the latter a precipitating factor;the primary treatment goal of SIC was improving ventricular-arterial coupling.And the short-term objective was reducing arterial elastance and longterm strategy improving cardiac elastance;Ea declined initially when SIC recovered.And it was consistent with ventricular-arterial coupling improvement.Ees recovery was delayed;before and after SIC, low peripheral vascular resistance within 36 h could reduce arterial elastance Ea;ventricular artery coupling affected cardiac external work, work efficiency and stroke volume and was associated with tissue perfusion.Conclusion The occurrence and outcome of SIC are simultaneously influenced by Ees and Ea and are closely correlated with Ea/Ees.Treatment goal of SIC is improving ventricular-arterial coupling.Ea should be reduced within 36 h and Ees should be boosted after 48 h.