手术病人急性等容血液稀释时血流动力学的变化

目的:研究手术病人行急性等容血液稀释(ANHD)时血流动力学的代偿性变化及可能机制,为临床手术病人术中应用ANHD奠定基础。方法:随机选择临床大中型非心脏外科手术40例,全麻后行ANHD,人为放血和手术失血造成三个不同的HD水平,HCT分别为(29.16±1.31)%、(25.34±1.58)%、(23.02±1.93)%。测定各水平的血流动力学参数及动脉血乳酸等。结果:心输出量CO(心脏指数CI)随着血液不断稀释而升高,到了HD3时不再升高,反而降低,与其相邻两组比有差异(P<0.05),与HD前比无差异(P>0.05)。回输血后CO(CI)再次明显升高。同时心脏每搏搏血量SV,心搏指数SVI,左室每搏作功指数LVSWI,右室每搏作功指数RVSWI在各阶段的变化与CO(CI)相似。总外周阻力SVR,肺循环阻力PVR均随血液不断稀释而呈降低趋势。血乳酸在HD1和HD2时均明显低于HD前(P<0.01),而在HD3时,血乳酸明显升高,与HD前及HD1、HD2比均有明显差异(P<0.01)。结论:临床非心脏外科手术病人行ANHD时,主要通过心输出量的升高进行代偿。HCT为(23.02±1.93)%时心脏失代偿。CO的升高是通过增加心脏射血量(SV)而不是增加HR来实现的。总外周阻力及肺血管阻力不断下降与血粘度降低和血管扩张有关。

Cardiovascular response to Acute Normovolemic Hemodilution in surgery patients

Objective Acute Normovolemic Hemodilution(ANHD) as a method to conserve blood and derease transfusion requirements is currently used in many major surgical procedures. To investigate the effects of ANHD on sysytemic hemodynamic and look for the acceptable limit of ANHD.Methods Forty adults, ASA class Ⅰ-Ⅱ patients undergoing non-cardiac surgery were administered a standard anesthetic with FiO_ 2 >80%,P_ ET CO_ 2 4～5 kpa and controlled ventilation. At normal body temperiture, ANHD was accomplished by exchanged whole blood for 4% Gelofusine. Further HD was achieved due to intraoperative blood loss which was salvaged by 4% Gelofusine. Different HD levels were produced by different operative blood loss, and then three different HD levels was produced:HD_ 1 , HD_ 2 and HD_ 3 . The HCT levels of HD was obtained from (39.14±4.09)% to (29.16±1.31)% (HD_ 1 ), (25.34±1.58)% (HD_ 2 ) and (23.02±1.93)% (HD_ 3 ). Plasma lactate (LA) and hemodynamic variables were measured prior to HD and 30mins after every step of HD as well as 15mins after reinfusion.Results CI(CO) was increased by 10% and 24% during the HD_ 1 and HD_ 2 ;CI(CO) did not increase but decrease to approximately initial level during HD_ 3 ;SVR and PVR decreased gradully during HD. LA decreased during HD_ 1 and HD_ 2 , But increased during HD_ 3 (P<0.01).After reinfusion, CI(CO) increased and LA decreased to approximately initial level.The variety of SV,SVI,LVSWI,RVSWI was similar to that of CI(CO).Conclusion The primary compensatory mechanisms induced by ANHD is increase in CI(CO). The increase in CO may be accounted for increase in stroke volume (SV), the heart rate remains constant. In patients who was not able to increase cardiac output can not adapt to ANHD.The changes of SVR and PVR were associated with the vasodilution and the decrease of blood viscocity.