Cerebrovascular pressure reactivity and brain tissue oxygen monitoring provide complementary information regarding the lower and upper limits of cerebral blood flow control in traumatic brain injury: a CAnadian High Resolution-TBI (CAHR-TBI) cohort study

Alwyn Gomez; Mypinder Sekhon; Donald Griesdale; Logan Froese; Eleen Yang; Eric P Thelin; Rahul Raj; Marcel Aries; Clare Gallagher; Francis Bernard; Andreas H Kramer; Frederick A Zeiler

doi:10.1186/s40635-022-00482-3

Cerebrovascular pressure reactivity and brain tissue oxygen monitoring provide complementary information regarding the lower and upper limits of cerebral blood flow control in traumatic brain injury: a CAnadian High Resolution-TBI (CAHR-TBI) cohort study

Intensive Care Med Exp. 2022 Dec 23;10(1):54. doi: 10.1186/s40635-022-00482-3.

Authors

Alwyn Gomez^{1

2}, Mypinder Sekhon^{3

4}, Donald Griesdale³, Logan Froese⁵, Eleen Yang³, Eric P Thelin^{6

7}, Rahul Raj⁸, Marcel Aries^{9

10}, Clare Gallagher^{11

12

13}, Francis Bernard¹⁴, Andreas H Kramer^#^{15

12

13}, Frederick A Zeiler^#^{16

17

5

7

18

19}

Affiliations

¹ Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. gomeza35@myumanitoba.ca.
² Section of Neurosurgery, Department of Surgery, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. gomeza35@myumanitoba.ca.
³ Department of Anesthesiology, Pharmacology & Therapeutics, University of British Columbia, Vancouver, BC, Canada.
⁴ Division of Critical Care, Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
⁵ Biomedical Engineering, Faculty of Engineering, University of Manitoba, Winnipeg, MB, Canada.
⁶ Department of Neurology, Karolinska University Hospital, Stockholm, Sweden.
⁷ Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
⁸ Department of Neurosurgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
⁹ Department of Intensive Care, Maastricht University Medical Center, Maastricht, The Netherlands.
¹⁰ School of Mental Health and Neurosciences, University Maastricht, Maastricht, The Netherlands.
¹¹ Section of Neurosurgery, Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.
¹² Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.
¹³ Hotchkiss Brain Institute, University of Calgary, Calgary, Canada.
¹⁴ Section of Critical Care, Department of Medicine, University of Montreal, Montreal, QC, Canada.
¹⁵ Department of Critical Care Medicine, University of Calgary, Calgary, Canada.
¹⁶ Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada.
¹⁷ Section of Neurosurgery, Department of Surgery, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
¹⁸ Centre On Aging, University of Manitoba, Winnipeg, Canada.
¹⁹ Division of Anaesthesia, Department of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.

^# Contributed equally.

Abstract

Background: Brain tissue oxygen tension (PbtO₂) and cerebrovascular pressure reactivity monitoring have emerged as potential modalities to individualize care in moderate and severe traumatic brain injury (TBI). The relationship between these modalities has had limited exploration. The aim of this study was to examine the relationship between PbtO₂ and cerebral perfusion pressure (CPP) and how this relationship is modified by the state of cerebrovascular pressure reactivity.

Methods: A retrospective multi-institution cohort study utilizing prospectively collected high-resolution physiologic data from the CAnadian High Resolution-TBI (CAHR-TBI) Research Collaborative database collected between 2011 and 2021 was performed. Included in the study were critically ill TBI patients with intracranial pressure (ICP), arterial blood pressure (ABP), and PbtO₂ monitoring treated in any one of three CAHR-TBI affiliated adult intensive care units (ICU). The outcome of interest was how PbtO₂ and CPP are related over a cohort of TBI patients and how this relationship is modified by the state of cerebrovascular reactivity, as determined using the pressure reactivity index (PRx).

Results: A total of 77 patients met the study inclusion criteria with a total of 377,744 min of physiologic data available for the analysis. PbtO₂ produced a triphasic curve when plotted against CPP like previous population-based plots of cerebral blood flow (CBF) versus CPP. The triphasic curve included a plateau region flanked by regions of relative ischemia (hypoxia) and hyperemia (hyperoxia). The plateau region shortened when cerebrovascular pressure reactivity was disrupted compared to when it was intact.

Conclusions: In this exploratory analysis of a multi-institution high-resolution physiology TBI database, PbtO₂ seems to have a triphasic relationship with CPP, over the entire cohort. The CPP range over which the plateau exists is modified by the state of cerebrovascular reactivity. This indicates that in critically ill TBI patients admitted to ICU, PbtO₂ may be reflective of CBF.

Keywords: Brain tissue oxygen tension; Cerebrovascular physiology; Cerebrovascular reactivity; Multi-modal monitoring; Traumatic brain injury.

Abstract

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