The influence of airway pressure changes on intracranial pressure (ICP) and the blood flow velocity in the middle cerebral artery (V-MCA)

Objective: 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. Patients and methods: 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 P-AW) was detected. The influence of the duration of Delta P-AW was evaluated additionally. Data of central venous pressure (CVP), ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), airway pressure (P-AW) and blood flow velocity of the middle cerebral artery (V-MCA) were analyzed on the basis of differences between the maximum (inspiration) and minimum P-AW values (expiration). Results: Elevations of P-AW 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 (P-art) and CPPmean due to P-AW 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 (V-MCA) revealed a positive correlation to P-AW with a r = 0.99, p < 0.05. Conclusions: 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.