• Mårten Unnerbäck, Johnny T Ottesen, and Peter Reinstrup.
• Department of Clinical Sciences Lund, Intensive Care and Perioperative Medicine, Lund University, Skåne University Hospital, Malmö, Sweden. Marten.Unnerback@med.lu.se.
• Neurocrit Care. 2019 Oct 1; 31 (2): 273-279.

BackgroundThe underlying physiology of the intracranial pressure (ICP) curve morphology is still poorly understood. If this physiology is explained it could be possible to extract clinically relevant information from the ICP curve. The venous outflow from the cranial cavity is pulsatile, and in theory the pulsatile component of venous outflow from the cranial cavity should be attenuated with increasing ICP. In this study, we explored the relationship between ICP and the pulsatility of the venous outflow from the intracranial cavity.MethodsThirty-seven neuro-intensive care patients that had been examined with phase-contrast magnetic resonance imaging regarding cerebral blood flow (CBF) through the internal carotid and vertebral arteries and venous flow in the internal jugular veins were retrospectively included. The pulsatility of the jugular flow was determined by calculating the venous pulsatile index. The results were correlated to clinical data registered in the patient data monitoring system, including ICP and cerebral perfusion pressure (CPP).ResultsCBF was 996 ± 298 ml/min, and the flow in the internal jugular veins equaled 67 ± 17% of the CBF, with a range of 22-97%. The venous pulsatile index correlated negatively to ICP (R = - 0.47 p = 0.003). The lowest flow in the internal jugular veins over the cardiac cycle (Fmin) was not correlated to ICP. Temperature, end-tidal CO2, MAP, and CPP were not correlated to venous pulsatility.ConclusionAn increase in ICP correlates to a lower pulsatility of the venous outflow from the cranial cavity. A lower pulsatility could be due to increased pressure requirements to compress intracranial veins with increasing ICP.

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