Ludwig H C, Klingler M, Timmermann A, Weyland W, Mursch K, Reparon C, Markakis E
Department of Neurosurgery, Georg-August University, Göttingen, Germany.
Anasthesiol Intensivmed Notfallmed Schmerzther. 2000 Mar;35(3):141-5. doi: 10.1055/s-2000-13008.
Due to the exponential shape of the intracranial volume-pressure relation, simple measurement of epidural, parenchymal or intraventricular intracranial pressure (ICP) in traumatic brain injury (TBI) often fails to early recognize patients with a fulminant development of intracranial hypertension even during recently available methods of tissue PO2 and microdialysis measurements. One approach to this problem could be repetitive intracranial volume provocations to evaluate a trend of the intracranial elastance. Several previously published methods use invasive volume challenge through access to the cerebrospinal fluid (CSF). This pilot study describes changes in intracranial pressure due to variations of airway pressure with BIPAP ventilation maneuvers.
Ten patients with severe TBI were enrolled and completed the study. The inclusion was based on radiologic signs due to TBI in the first CT-scan and the clinical indication for insertion of an ICP monitoring device. Patients with elevated ICP above 20 mm Hg were excluded. The epidural ICP response together with haemodynamic parameters in relation to defined airway pressure changes (delta PAW) was detected. The influence of the duration of delta PAW was evaluated additionally. Data of central venous pressure (CVP), ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), airway pressure (PAW) and blood flow velocity of the middle cerebral artery (VMCA) were analyzed on the basis of differences between the maximum (inspiration) and minimum PAW values (expiration).
Elevations of PAW in the range of 20 to 35 cm H2O resulted in changes of the ICPmean from 4.1 to 6.0 mm Hg (r = 0.9, p < 0.05). A correlation was estimated for the changes of systolic arterial pressure (Part) and CPPmean due to PAW variations which ranged between 4.5 and 11.6 mm Hg (r = 0.99, p < 0.05). Concerning the transcranial doppler measurements the data of changes of the blood flow velocity of the middle cerebral artery (VMCA) revealed a positive correlation to PAW with a r = 0.99, p < 0.05.
Elevation of the venous outflow resistance and a transient increase in cardiac output have to be considered as mechanisms for transduction of transthoracic pressure changes to intracranial pressure variations. We conclude, that trends of changes in elastance can be derived from intermittent airway pressure variations. This can be useful in easy and on line dynamic monitoring of ICP in traumatic brain injury.
由于颅内体积 - 压力关系呈指数形式,在创伤性脑损伤(TBI)中,简单测量硬膜外、脑实质或脑室内颅内压(ICP)往往无法早期识别出即使在最近可用的组织PO2和微透析测量方法下仍会迅速发展为颅内高压的患者。解决这个问题的一种方法可能是反复进行颅内体积激发试验以评估颅内弹性的变化趋势。此前发表的几种方法通过获取脑脊液(CSF)进行有创体积挑战。这项初步研究描述了双水平气道正压通气(BIPAP)操作引起的气道压力变化导致的颅内压变化。
招募了10例重度TBI患者并完成了研究。纳入标准基于首次CT扫描中TBI的放射学征象以及插入ICP监测装置的临床指征。排除ICP高于20 mmHg的患者。检测硬膜外ICP反应以及与确定的气道压力变化(ΔPAW)相关的血流动力学参数。另外评估了ΔPAW持续时间的影响。基于最大(吸气)和最小PAW值(呼气)之间的差异,分析中心静脉压(CVP)、ICP、平均动脉压(MAP)、脑灌注压(CPP)、气道压力(PAW)和大脑中动脉血流速度(VMCA)的数据。
PAW升高至20至35 cm H2O范围导致ICPmean从4.1 mmHg变化至6.0 mmHg(r = 0.9,p < 0.05)。估计了由于PAW变化导致的收缩压(Part)和CPPmean变化之间的相关性,其范围在4.5至11.6 mmHg之间(r = 0.99,p < 0.05)。关于经颅多普勒测量,大脑中动脉血流速度(VMCA)变化的数据显示与PAW呈正相关,r = 0.99,p < 0.05。
必须将静脉流出阻力升高和心输出量短暂增加视为将胸内压力变化传导至颅内压变化的机制。我们得出结论,弹性变化趋势可从间歇性气道压力变化中得出。这对于创伤性脑损伤中ICP的简便在线动态监测可能有用。