McCulloch T J, Visco E, Lam A M
Departments of Anesthesiology and Neurological Surgery, University of Washington School of Medicine, Seattle, Washington 98104, USA.
Anesthesiology. 2000 Nov;93(5):1205-9. doi: 10.1097/00000542-200011000-00012.
Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia.
Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation.
The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg.
Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.
高碳酸血症会破坏脑自动调节功能,但关于全身麻醉期间高碳酸血症与自动调节之间的相互作用知之甚少。在正常碳酸血症状态下,七氟醚(浓度高达1.5倍最低肺泡浓度)和丙泊酚不会损害脑自动调节功能。本研究旨在确定在丙泊酚或七氟醚麻醉期间损害脑自动调节功能所需的高碳酸血症水平。
在一项随机交叉研究中,8名健康受试者接受瑞芬太尼输注,并分别用丙泊酚(140微克·千克⁻¹·分钟⁻¹)和七氟醚(呼气末浓度1.0 - 1.1%)进行麻醉。调整通气以实现动脉血二氧化碳分压(Paco2)的逐步升高,直至自动调节功能受损。通过用去氧肾上腺素将平均动脉压(MAP)从80 mmHg升高到100 mmHg来测试脑自动调节功能,同时用经颅多普勒测量大脑中动脉血流速度。计算自动调节指数,其值范围为0至1,代表自动调节功能从无到完美,自动调节指数为0.4或更低表示自动调节功能明显受损。
显著损害脑自动调节功能的Paco2阈值范围为50至66 mmHg。七氟醚麻醉期间阈值平均为56 ± 4 mmHg(平均值 ± 标准差),丙泊酚麻醉期间为61 ± 4 mmHg(P = 0.03)。在MAP为100 mmHg时测得的二氧化碳反应性比MAP为80 mmHg时高30%。
即使是轻度高碳酸血症在全身麻醉期间也会显著损害脑自动调节功能。在高碳酸血症对脑自动调节功能的影响方面,丙泊酚麻醉和七氟醚麻醉之间存在显著差异。这种差异出现在临床相关的Paco2水平。当诱发高碳酸血症时,二氧化碳反应性受MAP的显著影响。