Ho Loretta, Lau Lawrence, Churilov Leonid, Riedel Bernhard, McNicol Larry, Hahn Robert G, Weinberg Laurence
*Department of Anaesthesia, Austin Hospital, University of Melbourne, Heidelberg, Victoria, Australia †Department of Surgery, Austin Hospital, University of Melbourne, Heidelberg, Victoria, Australia ‡The Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, Melbourne, Victoria, Australia §Department of Anaesthesia, Peter MacCallum Cancer Centre, University of Melbourne, Melbourne, Victoria, Australia ||Department of Anaesthesia, Austin Hospital, Heidelberg, Victoria, Australia ¶Department of Surgery and Anaesthesia Perioperative Pain Medicine Unit, University of Melbourne, Melbourne, Victoria, Australia **Södertälje Hospital, Linköping University, Linköping, Sweden ††Karolinska Institutet, Stockholm, Sweden ‡‡Department of Anaesthesia, Austin Hospital, Heidelberg, Victoria, Australia §§Department of Surgery and Anaesthesia Perioperative Pain Medicine Unit, University of Melbourne, Melbourne, Victoria, Australia.
Shock. 2016 Aug;46(2):149-57. doi: 10.1097/SHK.0000000000000610.
The most effective rate of fluid resuscitation in haemorrhagic shock is unknown.
We performed a randomized crossover pilot study in a healthy volunteer model of compensated haemorrhagic shock. Following venesection of 15 mL/kg of blood, participants were randomized to 20 mL/kg of crystalloid over 10 min (FAST treatment) or 30 min (SLOW treatment). The primary end point was oxygen delivery (DO2). Secondary end points included pressure and flow-based haemodynamic variables, blood volume expansion, and clinical biochemistry.
Nine normotensive healthy adult volunteers participated. No significant differences were observed in DO2 and biochemical variables between the SLOW and FAST groups. Blood volume was reduced by 16% following venesection, with a corresponding 5% reduction in cardiac index (CI) (P < 0.001). Immediately following resuscitation the increase in blood volume corresponded to 54% of the infused volume under FAST treatment and 69% of the infused volume under SLOW treatment (P = 0.03). This blood volume expansion attenuated with time to 24% and 25% of the infused volume 30 min postinfusion. During fluid resuscitation, blood pressure was higher under FAST treatment. However, CI paradoxically decreased in most participants during the resuscitation phase; a finding not observed under SLOW treatment.
FAST or SLOW fluid resuscitation had no significant impact on DO2 between treatment groups. In both groups, changes in CI and blood pressure did not reflect the magnitude of intravascular blood volume deficit. Crystalloid resuscitation expanded intravascular blood volume by approximately 25%.
失血性休克中最有效的液体复苏速率尚不清楚。
我们在代偿性失血性休克的健康志愿者模型中进行了一项随机交叉试验性研究。在抽取15毫升/千克血液后,参与者被随机分为在10分钟内输注20毫升/千克晶体液(快速治疗)或30分钟内输注(缓慢治疗)。主要终点是氧输送(DO2)。次要终点包括基于压力和流量的血流动力学变量、血容量扩充和临床生物化学指标。
九名血压正常的健康成年志愿者参与了研究。缓慢组和快速组在DO2和生化指标方面未观察到显著差异。放血后血容量减少了16%,心指数(CI)相应降低了5%(P<0.001)。复苏后即刻,快速治疗组血容量增加相当于输注量的54%,缓慢治疗组为69%(P=0.03)。输注30分钟后,这种血容量扩充随时间减弱至输注量的24%和25%。液体复苏期间,快速治疗组的血压较高。然而,大多数参与者在复苏阶段CI反而下降;缓慢治疗组未观察到这一现象。
快速或缓慢液体复苏对治疗组间的DO2无显著影响。在两组中,CI和血压的变化均未反映血管内血容量不足的程度。晶体液复苏使血管内血容量扩充了约25%。