Kallioinen Minna, Posti Jussi P, Rahi Melissa, Sharma Deepak, Katila Ari, Grönlund Juha, Vahlberg Tero, Frantzén Janek, Olkkola Klaus T, Saari Teijo I, Takala Riikka
Division of Perioperative Services, Intensive Care Medicine and Pain Management, Turku University Hospital and University of Turku, Turku, Finland.
Department of Anaesthesiology and Intensive Care, University of Turku, Turku, Finland.
Acta Anaesthesiol Scand. 2020 Oct;64(9):1278-1286. doi: 10.1111/aas.13663. Epub 2020 Jul 15.
Cerebral autoregulation is often impaired after aneurysmal subarachnoid haemorrhage (aSAH). Dexmedetomidine is being increasingly used, but its effects on cerebral autoregulation in patients with aSAH have not been studied before. Dexmedetomidine could be a useful sedative in patients with aSAH as it enables neurological assessment during the infusion. The aim of this preliminary study was to compare the effects of dexmedetomidine on dynamic and static cerebral autoregulation with propofol and/or midazolam in patients with aSAH.
Ten patients were recruited. Dynamic and static cerebral autoregulation were assessed using transcranial Doppler ultrasound during propofol and/or midazolam infusion and then during three increasing doses of dexmedetomidine infusion (0.7, 1.0 and 1.4 μg/kg/h). Transient hyperaemic response ratio (THRR) and strength of autoregulation (SA) were calculated to assess dynamic cerebral autoregulation. Static rate of autoregulation (sRoR)% was calculated by using noradrenaline infusion to increase the mean arterial pressure 20 mm Hg above the baseline.
Data from nine patients were analysed. Compared to baseline, we found no statistically significant changes in THRR or sROR%. THRR was (mean ± SD) 1.20 ± 0.14, 1.17 ± 0.13 (P = .93), 1.14 ± 0.09 (P = .72) and 1.19 ± 0.18 (P = 1.0) and sROR% was 150.89 ± 84.37, 75.22 ± 27.75 (P = .08), 128.25 ± 58.35 (P = .84) and 104.82 ± 36.92 (P = .42) at baseline and during 0.7, 1.0 and 1.4 μg/kg/h dexmedetomidine infusion, respectively. Dynamic SA was significantly reduced after 1.0 μg/kg/h dexmedetomidine (P = .02).
Compared to propofol and/or midazolam, dexmedetomidine did not alter static cerebral autoregulation in aSAH patients, whereas a significant change was observed in dynamic SA. Further and larger studies with dexmedetomidine in aSAH patients are warranted.
动脉瘤性蛛网膜下腔出血(aSAH)后,脑自动调节功能常受损。右美托咪定的应用越来越广泛,但此前尚未研究其对aSAH患者脑自动调节功能的影响。右美托咪定可能是aSAH患者有用的镇静剂,因为在输注过程中可进行神经功能评估。本初步研究的目的是比较右美托咪定与丙泊酚和/或咪达唑仑对aSAH患者动态和静态脑自动调节功能的影响。
招募10例患者。在输注丙泊酚和/或咪达唑仑期间,然后在右美托咪定输注剂量逐渐增加的三个阶段(0.7、1.0和1.4μg/kg/h),使用经颅多普勒超声评估动态和静态脑自动调节功能。计算瞬时充血反应率(THRR)和自动调节强度(SA)以评估动态脑自动调节功能。通过输注去甲肾上腺素使平均动脉压比基线升高20mmHg来计算静态自动调节率(sRoR)%。
分析了9例患者的数据。与基线相比,我们发现THRR或sROR%无统计学显著变化。THRR(均值±标准差)在基线时为1.20±0.14,在0.7μg/kg/h右美托咪定输注期间为1.17±0.13(P = 0.93),在1.0μg/kg/h右美托咪定输注期间为1.14±0.09(P = 0.72),在1.4μg/kg/h右美托咪定输注期间为1.19±0.18(P = 1.0);sROR%在基线时为150.89±84.37,在0.7μg/kg/h、1.0μg/kg/h和1.4μg/kg/h右美托咪定输注期间分别为75.22±27.75(P = 0.08)、128.25±58.35(P = 0.84)和104.82±36.92(P = 0.42)。在1.0μg/kg/h右美托咪定输注后,动态SA显著降低(P = 0.02)。
与丙泊酚和/或咪达唑仑相比,右美托咪定未改变aSAH患者的静态脑自动调节功能,而动态SA有显著变化。有必要对aSAH患者进一步开展更大规模的右美托咪定研究。