ArticleNeurotrauma reports2020
The Impact of Vasopressor and Sedative Agents on Cerebrovascular Reactivity and Compensatory Reserve in Traumatic Brain Injury: An Exploratory Analysis.
Article in Neurotrauma reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 59 citations in OpenAlex.
- A novel algorithm for the continuous determination of individualized intracranial pressure (iICP) thresholds using a multi-window weighted approach.BMC medical informatics and decision making · 2026Article
- Early Autonomic Dysfunction Following Severe TBI and Impact on Cerebral Hemodynamics: A Narrative Review.Journal of clinical medicine · 2026Review
- Optimal cerebrovascular reactivity thresholds for the determination of individualized intracranial pressure thresholds in traumatic brain injury: a CAHR-TBI cohort study.Critical care (London, England) · 2025Article
- Commercial NIRS May Not Detect Hemispheric Regional Disparity in Continuously Measured COx/COx-a: An Exploratory Healthy and Cranial Trauma Time-Series Analysis.Bioengineering (Basel, Switzerland) · 2025Article
- Continuous personalized cerebrovascular reactivity-based physiologic metrics in neurocritical care: a narrative review of the current landscape, limitations, and future directions.Frontiers in physiology · 2025Review
- High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury.Neurotrauma reports · 2025Article
- Association Between Clinical Measures of Depth of Sedation and Multimodal Cerebral Physiology in Acute Traumatic Neural Injury.Neurotrauma reports · 2024Article
- Statistical properties of cerebral near infrared and intracranial pressure-based cerebrovascular reactivity metrics in moderate and severe neural injury: a machine learning and time-series analysis.Intensive care medicine experimental · 2023Article
- The impact of sedative and vasopressor agents on cerebrovascular reactivity in severe traumatic brain injury.Intensive care medicine experimental · 2023Article
- Temporal relationship between vasopressor and sedative administration and cerebrovascular response in traumatic brain injury: a time-series analysis.Intensive care medicine experimental · 2023Article
- Cerebrovascular Reactivity Is Not Associated With Therapeutic Intensity in Adult Traumatic Brain Injury: A Validation Study.Neurotrauma reports · 2023Article
- Case report: Continuous spinal cord physiologic monitoring following traumatic spinal cord injury-A report from the Winnipeg Intraspinal Pressure Study (WISP).Frontiers in neurology · 2023Article
- Intracranial Pressure Monitoring and Treatment Thresholds in Acute Neural Injury: A Narrative Review of the Historical Achievements, Current State, and Future Perspectives.Neurotrauma reports · 2023Article
- Discrete Fourier Transform Windowing Techniques for Cerebral Physiological Research in Neural Injury: A Practical Demonstration.Neurotrauma reports · 2023Article
- Association between cerebrovascular reactivity in adult traumatic brain injury and improvement in patient outcome over time: an exploratory analysis.Acta neurochirurgica · 2022Article
- Optimal bispectral index level of sedation and cerebral oximetry in traumatic brain injury: a non-invasive individualized approach in critical care?Intensive care medicine experimental · 2022Article
- Automated Pupillometry as an Assessment Tool for Intracranial Hemodynamics in Septic Patients.Cells · 2022Observational
- Continuous Determination of the Optimal Bispectral Index Value Based on Cerebrovascular Reactivity in Moderate/Severe Traumatic Brain Injury: A Retrospective Observational Cohort Study of a Novel Individualized Sedation Target.Critical care explorations · 2022Article
- Intracranial Pressure-Derived Cerebrovascular Reactivity Indices, Chronological Age, and Biological Sex in Traumatic Brain Injury: A Scoping Review.Neurotrauma reports · 2022Article
- Dynamic Temporal Relationship Between Autonomic Function and Cerebrovascular Reactivity in Moderate/Severe Traumatic Brain Injury.Frontiers in network physiology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impact of vasopressor and sedative drugs on cerebrovascular reactivity in traumatic brain injury (TBI) remains unclear. The aim of this study was to evaluate the impact of changes of doses of commonly administered sedation (i.e., propofol, fentanyl, and ketamine) and vasopressor agents (i.e., norepinephrine [NE], phenylephrine [PE], and vasopressin[VSP]) on cerebrovascular reactivity and compensatory reserve in patients with moderate/severe TBI. Using the Winnipeg Acute TBI Database, we identified 38 patients with more than 1000 distinct changes of infusion rates and more than 500 h of paired drug infusion/physiology data. Cerebrovascular reactivity was assessed using pressure reactivity index (PRx) and cerebral compensatory reserve was assessed using RAP (the correlation [R] between pulse amplitude of intracranial pressure [ICP; A] and ICP [P]). We evaluated the data in two phases. First, we assessed the relationship between mean hourly dose of medication and its relation to both mean hourly index values, and time spent above a given index threshold. Second, we evaluated time-series data for each individual dose change per medication, assessing for a statistically significant change in PRx and RAP metrics. The results of the analysis confirmed that, overall, the mean hourly dose of sedative (propofol, fentanyl, and ketamine) and vasopressor (NE, PE, and VSP) agents does not impact hourly cerebrovascular reactivity or compensatory reserve measures. Similarly, incremental dose changes in these medications in general do not lead to significant changes in cerebrovascular reactivity or compensatory reserve. For propofol with incremental dose increases, in situations where PRx is intact (i.e., PRx <0 prior), a statistically significant increase in PRx was seen. However, this may not indicate deteriorating cerebrovascular reactivity as the final PRx (∼0.05) may still be considered to be intact cerebrovascular reactivity. As such, this finding with regards to propofol remains "weak." This study indicates that commonly administered sedative and vasopressor agents with incremental dosing changes have no clinically significant influence on cerebrovascular reactivity or compensatory reserve in TBI. These results should be considered preliminary, requiring further investigation.
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