Intracranial Pressure

Peter Smielewski, Luzius Steiner, Corina Puppo, Karol Budohoski, Georgios V. Varsos, Marek Czosnyka, Smielewski, Peter, Steiner, Luzius, Puppo, Corina, Budohoski, Karol, Varsos, Georgios V., Czosnyka, Marek

Brain arterial critical closing pressure (CrCP) has been studied in several diseases such as traumatic brain injury (TBI), subarachnoid haemorrhage, hydrocephalus, and in various physiological scenarios: intracranial hypertension, decreased cerebral perfusion pressure, hypercapnia, etc. Little or nothing so far has been demonstrated to characterise change in CrCP during mild hypocapnia. We retrospectively analysed recordings of intracranial pressure (ICP), arterial blood pressure (ABP) and blood flow velocity from 27 severe TBI patients (mean 39.5 ± 3.4 years, 6 women) in whom a ventilation increase (20% increase in respiratory minute volume) was performed over 50 min as part of a standard clinical CO2reactivity test. CrCP was calculated using the Windkessel model of cerebral arterial flow. Arteriolar wall tension (WT) was calculated as a difference between CrCP and ICP. The compartmental compliances arterial (Ca) and cerebrospinal fluid space (Ci) were also evaluated. During hypocapnia, ICP decreased from 17±6.8 to 13.2±6.6 mmHg (p < 0.000001). Wall tension increased from 14.5 ± 9.9 to 21.7±9.1 mmHg (p < 0.0002). CrCP, being a sum of WT + ICP, changed significantly from 31.5 ± 11.9 mmHg to 34.9±11.1 mmHg (p < 0.002), and the closing margin (ABP-CrCP) remained constant at an average value of 60 mmHg. Cadecreased significantly during hypocapnia by 30% (p < 0.00001) and Ciincreased by 26% (p < 0.003). During hypocapnia in TBI patients, ICP decreases and WT increases. CrCP increases slightly as the rise in wall tension outweighs the decrease in ICP. The closing margin remained unchanged, suggesting that the risk of hypocapnia-induced ischemia might not be increased.