Westermaier Thomas, Stetter Christian, Kunze Ekkehard, Willner Nadine, Holzmeier Judith, Kilgenstein Christian, Lee Jin-Yul, Ernestus Ralf-Ingo, Roewer Norbert, Muellenbach Ralf Michael
Departments of Neurosurgery and.
J Neurosurg. 2014 Nov;121(5):1056-62. doi: 10.3171/2014.7.JNS132611. Epub 2014 Aug 22.
The authors undertook this study to investigate whether the physiological mechanism of cerebral blood flow (CBF) regulation by alteration of the arterial partial pressure of carbon dioxide (PaCO₂) can be used to increase CBF after aneurysmal subarachnoid hemorrhage (aSAH).
In 6 mechanically ventilated patients with poor-grade aSAH, the PaCO₂ was first decreased to 30 mm Hg by modification of the respiratory rate, then gradually increased to 40, 50 and 60 mm Hg for 15 minutes each setting. Thereafter, the respirator settings were returned to baseline parameters. Intracerebral CBF measurement and brain tissue oxygen saturation (StiO₂), measured by near-infrared spectroscopy (NIRS), were the primary and secondary end points. Intracranial pressure (ICP) was controlled by external ventricular drainage.
A total of 60 interventions were performed in 6 patients. CBF decreased to 77% of baseline at a PaCO₂ of 30 mm Hg and increased to 98%, 124%, and 143% at PaCO₂ values of 40, 50, and 60 mm Hg, respectively. Simultaneously, StiO₂ decreased to 94%, then increased to 99%, 105%, and 111% of baseline. A slightly elevated delivery rate of cerebrospinal fluid was noticed under continuous drainage. ICP remained constant. After returning to baseline respirator settings, both CBF and StiO₂ remained elevated and only gradually returned to pre-hypercapnia values without a rebound effect. None of the patients developed secondary cerebral infarction.
Gradual hypercapnia was well tolerated by poor-grade SAH patients. Both CBF and StiO₂ reacted with a sustained elevation upon hypercapnia; this elevation outlasted the period of hypercapnia and only slowly returned to normal without a rebound effect. Elevations of ICP were well compensated by continuous CSF drainage. Hypercapnia may yield a therapeutic potential in this state of critical brain perfusion. Clinical trial registration no.: NCT01799525 ( ClinicalTrials.gov ).
作者开展本研究以调查通过改变动脉血二氧化碳分压（PaCO₂）来调节脑血流量（CBF）的生理机制是否可用于增加动脉瘤性蛛网膜下腔出血（aSAH）后的脑血流量。
对6例病情分级较差的aSAH且接受机械通气的患者，首先通过调整呼吸频率将PaCO₂降至30 mmHg，然后分别将其逐渐升至40、50和60 mmHg，每个设定值维持15分钟。此后，将呼吸机设置恢复至基线参数。通过近红外光谱（NIRS）测量的脑内CBF和脑组织氧饱和度（StiO₂）分别作为主要和次要终点。通过外部脑室引流控制颅内压（ICP）。
6例患者共进行了60次干预。在PaCO₂为30 mmHg时，CBF降至基线的77%，而在PaCO₂值为40、50和60 mmHg时，分别升至98%、124%和143%。同时，StiO₂降至基线的94%，然后升至99%、105%和111%。持续引流时发现脑脊液引流率略有升高。ICP保持恒定。恢复至基线呼吸机设置后，CBF和StiO₂均保持升高，且仅逐渐恢复至高碳酸血症前的值，无反弹效应。所有患者均未发生继发性脑梗死。
病情分级较差的SAH患者对逐渐升高的二氧化碳分压耐受性良好。高碳酸血症时CBF和StiO₂均持续升高；这种升高在高碳酸血症期后仍持续存在，且仅缓慢恢复正常，无反弹效应。持续的脑脊液引流可很好地代偿ICP的升高。在这种严重脑灌注状态下，高碳酸血症可能具有治疗潜力。临床试验注册号：NCT01799525（ClinicalTrials.gov）。
