ArticleAdvances in experimental medicine and biology2024
Evaluating the Status of the Injured Brain: Cerebrovascular Reserve (CVR) Is Not Equivalent to Induced Cerebrovascular Reactivity (iCVRx) and Induced Pressure Reactivity (iPRx) in Defining the Critical Cerebral Perfusion Pressure (CPP).
Article in Advances in experimental medicine and biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Methods evaluating the status of the injured brain have evolved over the past 63 years since Lundberg first reported clinical measurement of intracranial pressure (ICP) to evaluate the status of the injured brain (Lundberg, Acta Psychiatr Scand Suppl. 36:1-193, 1960). Subsequent evaluation involved measurement of the autoregulatory capacity of the brain by measuring cerebral blood flow (CBF) with decreasing mean arterial pressure (MAP) to define the critical CPP where the vasodilatory capacity of the cerebral circulation is exceeded and CBF begins to fall (CPP of 50 mmHg). A seminal advance was made by Marmarou (Marmarou et al., J Neurosurg. 48:332-344, 1978) who measured brain compliance by injecting a bolus of saline into the intracranial catheter while measuring the rise in intracranial pressure (ICP) otherwise known as induced pressure reactivity (iPRx). Seeking to utilise continuous measurement of iPRx in traumatic brain injury (TBI) patients with continuous monitoring of ICP, the ICP response to arterial pulsations was developed to evaluate the optimal CPP patients with raised ICP by the arterial pulsations-based iPRx. A similar approach was made with Doppler measurement of CBF with arterial pulsations for iCVRx to guide optimal CPP (CPPopt). Both iPRx and iCVRx are associated with microvascular shunts (MVS) and can accurately measure the critical CPP, whereas the CBF autoregulation curve by decreasing MAP does not. Sophisticated continuous multimodal monitoring established with ICM+ algorithms successfully identifies CPPopt for ICP control and identifies CBF dysregulation as related to outcome, but does not provide insights into the mechanisms involved in the loss of CBF autoregulation as related to increased ICP and potentially effective treatments (Froese et al., Neurocrit Care. 34:325-335, 2021).
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