Optimal bispectral index level of sedation and cerebral oximetry in traumatic brain injury: a non-invasive individualized approach in critical care?

Abstract

Background Impaired cerebral autoregulation has been linked with worse outcomes, with literature suggesting that current therapy guidelines fail to significantly impact cerebrovascular reactivity. The cerebral oximetry index (COx_a) is a surrogate measure of cerebrovascular reactivity which can in theory be obtained non-invasively using regional brain tissue oxygen saturation and arterial blood pressure. The goal of this study was to assess the relationship between objectively measured depth of sedation through BIS and autoregulatory capacity measured through COx_a. Methods In a prospectively maintained observational study, we collected continuous regional brain tissue oxygen saturation, intracranial pressure, arterial blood pressure and BIS in traumatic brain injury patients. COx_a was obtained using the Pearson’s correlation between regional brain tissue oxygen saturation and arterial blood pressure and ranges from − 1 to 1 with higher values indicating impairment of cerebrovascular reactivity. Using BIS values and COx_a, a curve-fitting method was applied to determine the minimum value for the COx_a. The associated BIS value with the minimum COx_a is called BISopt. This BISopt was both visually and algorithmically determined, which were compared and assessed over the whole dataset. Results Of the 42 patients, we observed that most had a parabolic relationship between BIS and COx_a. This suggests a potential “optimal” depth of sedation where COx_a is the most intact. Furthermore, when comparing the BISopt algorithm with visual inspection of BISopt, we obtained similar results. Finally, BISopt % yield (determined algorithmically) appeared to be independent from any individual sedative or vasopressor agent, and there was agreement between BISopt found with COx_a and the pressure reactivity index (another surrogate for cerebrovascular reactivity). Conclusions This study suggests that COx_a is capable of detecting disruption in cerebrovascular reactivity which occurs with over-/under-sedation, utilizing a non-invasive measure of determination and assessment. This technique may carry implications for tailoring sedation in patients, focusing on individualized neuroprotection.

The effect of burst suppression on cerebral blood flow and autoregulation: a scoping review of the human and animal literature

“…It is also possible that different depths of sedation have a significant effect on animal and human cerebral autoregulation. For example, previous work looked at the relationship between objectively measured depth of sedation (through the bispectrality index) and cerebrovascular reactivity (surrogate measure of cerebral autoregulation) in patients with TBI ( Froese et al, 2022a ; Froese et al, 2022b ). From this work it was seen in almost all patients that there was a depth of sedation that optimized cerebrovascular reactivity (achieve the most intact cerebral reactivity value), indicating that too much/little sedation results in non-optimal cerebral states.…”

The impact of sedative and vasopressor agents on cerebrovascular reactivity in severe traumatic brain injury

“…First given that cerebrovascular reactivity has a limited impact from currently used guideline-based pharmacological regimens, means that the interest in mediation of cerebrovascular reactivity through other approaches should be explored. Methods like the optimal CPP, individualized ICP and the optimal depth of sedation focus on using physiological (not pharmacological) mediation to attain optimal cerebrovascular reactivity [ 28 , 54 – 58 ]. This focus on pathophysiological mediation may overcome the limitations in current treatments and lead to more personalized targeted treatment.…”

Microvascular Autoregulation in Skeletal Muscle Using Near-Infrared Spectroscopy and Derivation of Optimal Mean Arterial Pressure in the ICU: Pilot Study and Comparison With Cerebral Near-Infrared Spectroscopy

“…Although MAP is a primary determinant of cerebral blood flow, MAP itself is determined by systemic vascular resistance in skeletal muscle. Furthermore, skeletal muscle blood flow control is under a high degree of sympathetic tone (14) and a primary site of action for vasoactive medications, whereas cerebrovascular networks exhibit predominantly myogenic control (44,45) and MA in the brain appears relatively insensitive to changes in vasopressor dosage (46). Furthermore, the role of astrocytes and pericytes in microvascular flow regulation is well-described in the brain (47,48), but corollary cell types and mechanisms in skeletal muscle are either absent or noncontributory.…”