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A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
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A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
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A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients

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A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients
Journal Article

A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients

2000
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Overview
To avoid ischaemic secondary insults after severe head injury (SHI) it would be helpful to know the relationship between cerebral perfusion pressure (CPP) and intracranial pressure (ICP). Static cerebrovascular autoregulation (AR) was tested in 14 patients after SHI. Mean arterial pressure (MAP) was varied to detect changes in intracranial pressure (ICP) indicative of intact AR. Three types of responses were observed: (1) MAP elevation causes an increase in ICP; (2) MAP elevation has no or very little effect on ICP; (3) MAP elevation lowers ICP; Changes between types 1/2 and type 3 suggests AR breakpoints. Varying response types and breakpoints were observed between and within patients. Lower AR breakpoints were seen from 60 to 80 mmHg CPP, upper breakpoints were as high as 112. CPP monitoring achieves a two-fold utility in targeted therapy: (1) defining the range of intact AR; and (2) lower AR breakpoint assessment to avoid secondary insults. Although the precise relationship between pAR breakpoints and the adequacy of cerebral perfusion to meet metabolic needs remains unclear, a technique such as described here is simple and has much to offer in targeting therapy toward specific pathophysiological processes in traumatic brain injury.