Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, CA, USA.
Anaesthesia. 2013 Jul;68(7):736-41. doi: 10.1111/anae.12254. Epub 2013 Apr 24.
There is currently no consensus regarding how to intervene in anaesthetic-induced hypotension. Whether or not the balance between cerebral oxygen supply and demand is maintained lacks adequate elucidation. It is thus intriguing to explore how cerebral tissue oxygen saturation is affected by anaesthetic-induced hypotension. Thirty-three patients scheduled for elective non-neurosurgical procedures were included in this study. Physiological measurements were performed immediately before induction with propofol and fentanyl and after tracheal intubation. Mean (SD) Bispectral index decreased from 84.3 (9.3) to 24.4 (8.0) (p<0.001). Mean arterial pressure decreased from 84.4 (10.6) mmHg to 53.6 (11.4) mmHg (p<0.001). However, cerebral tissue oxygen saturation remained stable (67.0 (9.4) % vs 67.5 (7.8) %, p=0.6). These results imply that the fine balance between cerebral oxygen supply and demand is not disrupted by anaesthetic-induced hypotension. An interpretation based on neurovascular coupling and cerebral autoregulation is proposed.
目前对于如何干预麻醉诱导性低血压尚没有共识。脑氧供需平衡是否得到维持缺乏充分的阐述。因此,探讨麻醉诱导性低血压对脑组织氧饱和度的影响是很有趣的。本研究纳入了 33 例择期非神经外科手术患者。在使用丙泊酚和芬太尼诱导前和气管插管后立即进行生理测量。平均(标准差)脑电双频指数从 84.3(9.3)降至 24.4(8.0)(p<0.001)。平均动脉压从 84.4(10.6)mmHg 降至 53.6(11.4)mmHg(p<0.001)。然而,脑组织氧饱和度保持稳定(67.0(9.4)% vs 67.5(7.8)%,p=0.6)。这些结果表明,脑氧供与需求之间的精细平衡并未被麻醉诱导性低血压所打破。提出了一种基于神经血管耦合和脑自动调节的解释。