Abstract

BackgroundIn traumatic brain injury (TBI) the patterns of intracranial pressure (ICP) waveforms may reflect pathological processes that ultimately lead to unfavorable outcome. In particular, ICP slow waves (sw) (0.005–0.05 Hz) magnitude and complexity have been shown to have positive association with favorable outcome. Mild-moderate hypocapnia is currently used for short periods to treat critical elevations in ICP. Our goals were to assess changes in the ICP sw activity occurring following sudden onset of mild-moderate hypocapnia and to examine the relationship between changes in ICP sw activity and other physiological variables during the hypocapnic challenge.MethodsICP, arterial blood pressure (ABP), and bilateral middle cerebral artery blood flow velocity (FV), were prospectively collected in 29 adult severe TBI patients requiring ICP monitoring and mechanical ventilation in whom a minute volume ventilation increase (15–20% increase in respiratory minute volume) was performed as part of a clinical CO2-reactivity test. The time series were first treated using FFT filter (pass-band set to 0.005–0.05 Hz). Power spectral density analysis was performed. We calculated the following: mean value, standard deviation, variance and coefficient of variation in the time domain; total power and frequency centroid in the frequency domain; cerebrospinal compliance (Ci) and compensatory reserve index (RAP).ResultsHypocapnia led to a decrease in power and increase in frequency centroid and entropy of slow waves in ICP and FV (not ABP). In a multiple linear regression model, RAP at the baseline was the strongest predictor for the decrease in the power of ICP slow waves (p < 0.001).ConclusionIn severe TBI patients, a sudden mild-moderate hypocapnia induces a decrease in mean ICP and FV, but also in slow waves power of both signals. At the same time, it increases their higher frequency content and their morphological complexity. The difference in power of the ICP slow waves between the baseline and the hypocapnia period depends on the baseline cerebrospinal compensatory reserve as measured by RAP.

Highlights

  • In traumatic brain injury (TBI) the mean value of intracranial pressure (ICP) might not be sufficient to help fully interpret the clinical status of the patient, while ICP waveforms contain information about the nature of the cerebrospinal circulation pathophysiology

  • These vascular changes are responsible for alterations in cerebral blood volume (CBV) and subsequently contribute to the oscillations observed in the cerebral blood flow velocity (FV) measured at the middle cerebral artery (MCA) [25]

  • We present a retrospective analysis of waveform recordings of ICP, arterial blood pressure (ABP), and bilateral MCA blood flow velocity, prospectively collected during CO2-reactivity studies in adult severe TBI patients requiring ICP monitoring and mechanical ventilation admitted in the Neurocritical Care Unit (NCCU) at Addenbrooke’s Hospital, Cambridge, from March 2001 to February 2002

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Summary

Introduction

In traumatic brain injury (TBI) the mean value of intracranial pressure (ICP) might not be sufficient to help fully interpret the clinical status of the patient, while ICP waveforms contain information about the nature of the cerebrospinal circulation pathophysiology. Rhythmic oscillations in diameter of cerebral vessels can be triggered by fluctuations in mean arterial blood pressure (ABP) and/or by local neurochemical mechanisms [20, 16] These vascular changes are responsible for alterations in CBV and subsequently contribute to the oscillations observed in the cerebral blood flow velocity (FV) measured at the middle cerebral artery (MCA) [25]. Methods ICP, arterial blood pressure (ABP), and bilateral middle cerebral artery blood flow velocity (FV), were prospectively collected in 29 adult severe TBI patients requiring ICP monitoring and mechanical ventilation in whom a minute volume ventilation increase (15–20% increase in respiratory minute volume) was performed as part of a clinical CO2-reactivity test. Conclusion In severe TBI patients, a sudden mild-moderate hypocapnia induces a decrease in mean ICP and FV, and in slow waves power of both signals.

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