Larsen F S, Ejlersen E, Hansen B A, Knudsen G M, Tygstrup N, Secher N H
Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark.
J Hepatol. 1995 Aug;23(2):212-7. doi: 10.1016/0168-8278(95)80338-6.
In management of patients with fulminant hepatic failure, it is recommended that mean arterial pressure should be raised if cerebral perfusion pressure is lower than 50 mmHg, but the influence of such therapy on cerebral blood flow is unknown. We examined cerebral blood flow autoregulation in seven consecutive patients with fulminant hepatic failure during treatment of imminent insufficient cerebral perfusion pressure. Cerebral perfusion was evaluated by transcranial Doppler assessed mean flow velocity in the middle cerebral artery and by the arterio-venous difference for oxygen. Intracranial pressure was recorded by a subdural transducer and cerebral perfusion pressure calculated as the difference between mean arterial pressure and intracranial pressure. After 20 (range 10 to 43) min, mean arterial pressure was raised from 74 (43-80) to 94 (76-114) mmHg by i.v. noradrenaline, cerebral perfusion pressure increased from 49 (26-75) to 82 (50-108) mmHg (p < 0.01) as the intracranial pressure remained unchanged at 26 (3-35) mmHg. The mean flow veolocity increased from 68 (30-134) to 108 (48-168) cm s-1 and the arterio-venous difference for oxygen by 46 (10-82)% (p < 0.05). Both mean flow velocity (r = 0.63) and arterio-venous difference for oxygen (r = 0.71) were correlated to mean arterial pressure (p < 0.001), and a lower blood pressure limit of autoregulation could not be identified in any of the patients. These data suggest that the cerebral blood flow is not autoregulated in patients with fulminant hepatic failure and therefore cerebral blood flow should be "clamped" within the normal physiologic range by manipulation of arterial blood pressure in order to avoid cerebral hypoxia and/or hypertensive induced cerebral oedema.
在暴发性肝衰竭患者的管理中，建议如果脑灌注压低于50mmHg，应提高平均动脉压，但这种治疗对脑血流量的影响尚不清楚。我们在7例连续的暴发性肝衰竭患者即将出现脑灌注不足时进行治疗期间，检测了脑血流自动调节功能。通过经颅多普勒评估大脑中动脉的平均流速以及氧的动静脉差值来评估脑灌注。通过硬膜下传感器记录颅内压，并将脑灌注压计算为平均动脉压与颅内压之差。20（范围10至43）分钟后，通过静脉注射去甲肾上腺素将平均动脉压从74（43 - 80）mmHg提高到94（76 - 114）mmHg，颅内压在26（3 - 35）mmHg保持不变，脑灌注压从49（26 - 75）mmHg增加到82（50 - 108）mmHg（p < 0.01）。平均流速从68（30 - 134）cm s-1增加到108（48 - 168）cm s-1，氧的动静脉差值增加46（10 - 82）%（p < 0.05）。平均流速（r = 0.63）和氧的动静脉差值（r = 0.71）均与平均动脉压相关（p < 0.001），且在任何患者中均未确定自动调节的较低血压界限。这些数据表明，暴发性肝衰竭患者的脑血流不受自动调节，因此应通过控制动脉血压将脑血流“钳制”在正常生理范围内，以避免脑缺氧和/或高血压性脑水肿。
