Optimal Cerebral Perfusion Pressure and Brain Tissue Oxygen in Aneurysmal Subarachnoid Hemorrhage

Author:

Megjhani Murad12ORCID,Weiss Miriam34ORCID,Ford Jenna1ORCID,Terilli Kalijah12ORCID,Kastenholz Nick3,Nametz Daniel12,Kwon Soon Bin12ORCID,Velazquez Angela1,Agarwal Sachin1,Roh David J.1,Conzen-Dilger Catharina3ORCID,Albanna Walid3,Veldeman Michael3ORCID,Connolly E. Sander5,Claassen Jan1,Aries Marcel67ORCID,Schubert Gerrit A.34ORCID,Park Soojin182ORCID

Affiliation:

1. Department of Neurology (M.M., K.T., D.N., S.B.K., J.F., A.V., S.A., D.J.R., J.C., S.P.), Columbia University, NY.

2. Program in Hospital and Intensive Care Informatics of Department of Neurology (M.M., K.T., D.N., S.B.K., S.P.), Columbia University, NY.

3. Department of Neurosurgery, RWTH Aachen University, Germany (M.W., N.C.K., C.C.-D., W.A., M.V., G.A.S.).

4. Department of Neurosurgery, Kantonsspital Aarau, Switzerland (M.W., G.A.S.).

5. Department of Neurosurgery (E.S.C.), Columbia University, NY.

6. Department of Intensive Care, Maastricht University Medical Center, Maastricht University, the Netherlands (M.A.).

7. School for Mental Health and Neuroscience (MHeNS), Maastricht University Medical Center, the Netherlands (M.A.).

8. Department of Biomedical Informatics (S.P.), Columbia University, NY.

Abstract

Background: Targeting a cerebral perfusion pressure optimal for cerebral autoregulation (CPPopt) has been gaining more attention to prevent secondary damage after acute neurological injury. Brain tissue oxygenation (PbtO 2 ) can identify insufficient cerebral blood flow and secondary brain injury. Defining the relationship between CPPopt and PbtO 2 after aneurysmal subarachnoid hemorrhage may result in (1) mechanistic insights into whether and how CPPopt-based strategies might be beneficial and (2) establishing support for the use of PbtO 2 as an adjunctive monitor for adequate or optimal local perfusion. Methods: We performed a retrospective analysis of a prospectively collected 2-center dataset of patients with aneurysmal subarachnoid hemorrhage with or without later diagnosis of delayed cerebral ischemia (DCI). CPPopt was calculated as the cerebral perfusion pressure (CPP) value corresponding to the lowest pressure reactivity index (moving correlation coefficient of mean arterial and intracranial pressure). The relationship of (hourly) deltaCPP (CPP−CPPopt) and PbtO 2 was investigated using natural spline regression analysis. Data after DCI diagnosis were excluded. Brain tissue hypoxia was defined as PbtO 2 <20 mmHg. Results: One hundred thirty-one patients were included with a median of 44.0 (interquartile range, 20.8–78.3) hourly CPPopt/PbtO2 datapoints. The regression plot revealed a nonlinear relationship between PbtO 2 and deltaCPP ( P <0.001) with PbtO 2 decrease with deltaCPP <0 mmHg and stable PbtO 2 with deltaCPP ≥0mmHg, although there was substantial individual variation. Brain tissue hypoxia (34.6% of all measurements) was more frequent with deltaCPP <0 mmHg. These dynamics were similar in patients with or without DCI. Conclusions: We found a nonlinear relationship between PbtO 2 and deviation of patients’ CPP from CPPopt in aneurysmal subarachnoid hemorrhage patients in the pre-DCI period. CPP values below calculated CPPopt were associated with lower PbtO 2 . Nevertheless, the nature of PbtO 2 measurements is complex, and the variability is high. Combined multimodality monitoring with CPP/CPPopt and PbtO 2 should be recommended to redefine individual pressure targets (CPP/CPPopt) and retain the option to detect local perfusion deficits during DCI (PbtO 2 ), which cannot be fulfilled by both measurements interchangeably.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Advanced and Specialized Nursing,Cardiology and Cardiovascular Medicine,Neurology (clinical)

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