Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Overview

Journal Neurocrit Care

Specialty Critical Care

Date 2012 Apr 6

PMID 22477613

Citations 51

Authors

Marcel J H Aries

Marek Czosnyka

Karol P Budohoski

Angelos G Kolias

Danila K Radolovich

Andrea Lavinio

John D Pickard

Peter Smielewski

Affiliations

Soon will be listed here.

Abstract

Background: Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP.

Methods: A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003-2009) with continuous ABP and ICP monitoring.

Results: PAx was worse in patients who died compared to those who survived (-0.04 ± 0.15 vs. -0.16 ± 0.15, χ2 = 28, p < 0.001). In contrast to PRx, PAx was able to differentiate between fatal and non-fatal outcome in a group of 120 patients with ICP levels below 15 mmHg (-0.04 ± 0.16 vs. -0.14 ± 0.16, χ2 = 6, p = 0.01).

Conclusions: PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.

Citing Articles

Does Targeting CPP at CPPopt Actually Improve Cerebrovascular Reactivity? A Secondary Analysis of the COGiTATE Randomized Controlled Trial.

Beqiri E, Tas J, Czosnyka M, van Kaam R, Donnelly J, Haeren R Neurocrit Care. 2024; .

PMID: 39623160 DOI: 10.1007/s12028-024-02168-y.

Association Between Clinical Measures of Depth of Sedation and Multimodal Cerebral Physiology in Acute Traumatic Neural Injury.

Park K, Froese L, Bergmann T, Gomez A, Sainbhi A, Vakitbilir N Neurotrauma Rep. 2024; 5(1):916-956.

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The association of acute and chronic phase cerebrovascular reactivity with patient reported quality of life following moderate-to-severe traumatic brain injury.

Gomez A, Marquez I, Froese L, Bergmann T, Sainbhi A, Vakitbilir N Sci Rep. 2024; 14(1):20737.

PMID: 39237683 PMC: 11377742. DOI: 10.1038/s41598-024-71843-z.

Cerebral physiologic insult burden in acute traumatic neural injury: a Canadian High Resolution-TBI (CAHR-TBI) descriptive analysis.

Stein K, Gomez A, Griesdale D, Sekhon M, Bernard F, Gallagher C Crit Care. 2024; 28(1):294.

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Associations Between Intracranial Pressure Extremes and Continuous Metrics of Cerebrovascular Pressure Reactivity in Acute Traumatic Neural Injury: A Scoping Review.

Stein K, Amenta F, Froese L, Gomez A, Sainbhi A, Vakitbilir N Neurotrauma Rep. 2024; 5(1):483-496.

PMID: 39036433 PMC: 11257139. DOI: 10.1089/neur.2023.0115.

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