The pressure reactivity index as a measure of cerebral autoregulation and its application in traumatic brain injury management

Abstract

Severe traumatic brain injury (TBI) is a major cause of morbidity and mortality globally. The Brain Trauma Foundation guidelines advocate for the maintenance of a cerebral perfusion pressure (CPP) between 60 and 70 mmHg following severe TBI. However, such a uniform goal does not account for changes in cerebral autoregulation (CA). CA refers to the complex homeostatic mechanisms by which cerebral blood flow is maintained, despite variations in mean arterial pressure and intracranial pressure. Disruption to CA has become increasingly recognised as a key mediator of secondary brain injury following severe TBI. The pressure reactivity index is calculated as the degree of statistical correlation between the slow wave components of mean arterial pressure and intracranial pressure signals and is a validated dynamic marker of CA status following brain injury. The widespread acceptance of pressure reactivity index has precipitated the consideration of individualised CPP targets or an optimal cerebral perfusion pressure (CPPopt). CPPopt represents an alternative target for cerebral haemodynamic optimisation following severe TBI, and early observational data suggest improved neurological outcomes in patients whose CPP is more proximate to CPPopt. The recent publication of a prospective randomised feasibility study of CPPopt guided therapy in TBI, suggests clinicians caring for such patients should be increasingly familiar with these concepts. In this paper, we present a narrative review of the key landmarks in the development of CPPopt and offer a summary of the evidence for CPPopt-based therapy in comparison to current standards of care.

Keywords: Anaesthesia and Intensive Care; Intensive Care; Trauma; Trauma care delivery; Traumatic brain injury.

Fig. 1

Lassen's original depiction of cerebral autoregulation. In health, CA mechanisms function over a wide range of ABP to maintain appropriate CBF (green). To maintain CBF within this range, afferent cerebral arteries vasodilate as ABP decreases toward the LLA, and vasoconstrict as ABP increases towards the ULA. Following TBI, CA function may become disrupted and manifests as variable narrowing, unflattening, and displacement of the ABP range in which intrinsic mechanisms can stabilise CBF. This change to CA is patient specific (Patient A vs. Patient B) and evolves uniquely with time and the progression of secondary brain injury. ABP: arterial blood pressure; CA: cerebral autoregulation; CBF: cerebral blood flow; CPP: cerebral perfusion pressure; LLA: lower limit of autoregulation; TBI: traumatic brain injury; ULA: upper limit of autoregulation.

Fig. 2

Principles of determination of CPPopt using the PRx. Multimodal neuromonitoring software integrates ABP and ICP data to calculate PRx across the range of observed CPPs in a single patient over time (A–C). PRx <0 indicates well-functioning CA, while PRx>0.25–0.3 is associated with worse neurological outcomes and increased mortality. Curve fitting the CPP against PRx allows for determination of the CPP at which PRx is lowest (D). Note that derivation of this classically described curve is not possible in all patients, nor across all time points in any one patient. This dynamic depiction of CA can be conceptually related to the Lassen curve (E). ABP: arterial blood pressure; CA: cerebral autoregulation; CBF: cerebral blood flow; CPP: cerebral perfusion pressure; CPPopt: Optimal cerebral perfusion pressure; ICP: intracranial pressure; LLA: lower limit of autoregulation; PRx: pressure reactivity index.