Ševerdija Ervin E, Vranken Nousjka P A, Simons Antoine P, Gommer Erik D, Heijmans John H, Maessen Jos G, Weerwind Patrick W
Departments of Cardiothoracic Surgery.
Departments of Cardiothoracic Surgery.
J Cardiothorac Vasc Anesth. 2015 Oct;29(5):1194-9. doi: 10.1053/j.jvca.2015.03.022. Epub 2015 Apr 2.
To investigate the influence of hemodilution and arterial pCO2 on cerebral autoregulation and cerebral vascular CO2 reactivity.
Prospective interventional study.
University hospital-based single-center study.
Forty adult patients undergoing elective cardiac surgery using normothermic cardiopulmonary bypass.
Blood pressure variations induced by 6/minute metronome-triggered breathing (baseline) and cyclic 6/min changes of indexed pump flow at 3 levels of arterial pCO2.
Based on median hematocrit on bypass, patients were assigned to either a group of a hematocrit ≥28% or<28%. The autoregulation index was calculated from cerebral blood flow velocity and mean arterial blood pressure using transfer function analysis. Cerebral vascular CO2 reactivity was calculated using cerebral tissue oximetry data. Cerebral autoregulation as reflected by autoregulation index (baseline 7.5) was significantly affected by arterial pCO2 (median autoregulation index amounted to 5.7, 4.8, and 2.8 for arterial pCO2 of 4.0, 5.3, and 6.6 kPa, p≤0.002) respectively. Hemodilution resulted in a decreased autoregulation index; however, during hypocapnia and normocapnia, there were no significant differences between the two hematocrit groups. Moreover, the autoregulation index was lowest during hypercapnia when hematocrit was<28% (autoregulation index 3.3 versus 2.6 for hematocrit ≥28% and<28%, respectively, p = 0.014). Cerebral vascular CO2 reactivity during hypocapnia was significantly lower when perioperative hematocrit was<28% (p = 0.018).
Hemodilution down to a hematocrit of<28% combined with hypercapnia negatively affects dynamic cerebral autoregulation, which underlines the importance of tight control of both hematocrit and paCO2 during CPB.
探讨血液稀释和动脉血二氧化碳分压(pCO2)对脑自动调节功能及脑血管二氧化碳反应性的影响。
前瞻性干预性研究。
以大学医院为基础的单中心研究。
40例接受常温体外循环择期心脏手术的成年患者。
通过每分钟6次节拍器触发呼吸(基线)以及在3个动脉pCO2水平下,体外循环泵流量指数每6分钟循环变化一次所引起的血压变化。
根据体外循环期间血细胞比容的中位数,将患者分为血细胞比容≥28%或<28%两组。采用传递函数分析,根据脑血流速度和平均动脉血压计算自动调节指数。利用脑组织血氧饱和度数据计算脑血管二氧化碳反应性。自动调节指数所反映的脑自动调节功能(基线值为7.5)受动脉pCO2显著影响(动脉pCO2为4.0、5.3和6.6 kPa时,自动调节指数中位数分别为5.7、4.8和2.8,p≤0.002)。血液稀释导致自动调节指数降低;然而,在低碳酸血症和正常碳酸血症期间,两组血细胞比容之间无显著差异。此外,当血细胞比容<28%时,高碳酸血症期间自动调节指数最低(血细胞比容≥28%和<28%时,自动调节指数分别为3.3和2.6,p = 0.014)。围手术期血细胞比容<28%时,低碳酸血症期间脑血管二氧化碳反应性显著降低(p = 0.018)。
血细胞比容降至<28%并伴有高碳酸血症会对动态脑自动调节功能产生负面影响,这突出了在体外循环期间严格控制血细胞比容和动脉血二氧化碳分压(PaCO2)的重要性。