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Background <p>Brain tissue hypoxia [brain tissue oxygen tension (PbtO<sub>2</sub>) &lt; 20 mm Hg] and elevated intracranial pressure (ICP) ≥ 22 mm Hg exacerbate hypoxic–ischemic brain injury (HIBI) after cardiac arrest. Multiple pathophysiologic derangements can cause brain tissue hypoxia and/or elevated ICP with impaired intracranial compliance. The mechanisms and severity of these pathophysiologic changes vary both between patients and within patients over time. Clinically distinct phenotypes of HIBI may have different trajectories of PbtO<sub>2</sub> and ICP.</p> Methods <p>We conducted a single-center retrospective study of patients who survived until hospitalization after cardiac arrest and underwent invasive neuromonitoring. We used group-based trajectory modeling to identify distinct trajectories of PbtO<sub>2</sub> and ICP separately over the first 72 h post-arrest and described the clinical characteristics of each trajectory group.</p> Results <p>We included 43 patients who underwent invasive neuromonitoring. We identified three ICP trajectory groups. Group 1 was characterized by normal ICP throughout monitoring, while group 2 demonstrated High–normal ICP during the study period. Group 3 had initially normal ICP, which rapidly increased and remained pathologically elevated thereafter. All ICP trajectory groups had episodically abnormal ICP, PbtO<sub>2</sub>, and cerebral perfusion pressure (CPP) during monitoring. We identified three PbtO<sub>2</sub> trajectory groups. Group 1 had persistent brain tissue hypoxia with more pathological elevations in ICP and inadequate CPP than the other PbtO<sub>2</sub> trajectory groups. Group 2 had mostly normal PbtO<sub>2</sub>, while PbtO2 in group 3 increased linearly over 72 h, though there was a comparable incidence of brain tissue hypoxia, elevated ICP, and low CPP. However, PbtO<sub>2</sub> group 3 had lower survival and more frequently exhibited evidence of severe HIBI.</p> Conclusions <p>We identified distinct PbtO<sub>2</sub> and ICP trajectories after cardiac arrest. Our findings suggest that the physiology of hypoxic–ischemic brain injury is variable, and trajectory groups may represent distinct phenotypes. This work provides a foundation for future studies aimed at disentangling the heterogeneity of hypoxic–ischemic brain injury.</p>

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Intracranial Pressure and Brain Tissue Oxygen Trajectories after Cardiac Arrest

  • 期刊论文

  • 发表日期：

    2026年5月27日

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  • Laura Faiver,
  • Patrick J. Coppler,
  • Cecelia R. Ratay,
  • Jonathan Tam,
  • Lori A. Shutter,
  • Nicholas Case,
  • Jonathan Elmer

摘要

Background

Brain tissue hypoxia [brain tissue oxygen tension (PbtO2) < 20 mm Hg] and elevated intracranial pressure (ICP) ≥ 22 mm Hg exacerbate hypoxic–ischemic brain injury (HIBI) after cardiac arrest. Multiple pathophysiologic derangements can cause brain tissue hypoxia and/or elevated ICP with impaired intracranial compliance. The mechanisms and severity of these pathophysiologic changes vary both between patients and within patients over time. Clinically distinct phenotypes of HIBI may have different trajectories of PbtO2 and ICP.

Methods

We conducted a single-center retrospective study of patients who survived until hospitalization after cardiac arrest and underwent invasive neuromonitoring. We used group-based trajectory modeling to identify distinct trajectories of PbtO2 and ICP separately over the first 72 h post-arrest and described the clinical characteristics of each trajectory group.

Results

We included 43 patients who underwent invasive neuromonitoring. We identified three ICP trajectory groups. Group 1 was characterized by normal ICP throughout monitoring, while group 2 demonstrated High–normal ICP during the study period. Group 3 had initially normal ICP, which rapidly increased and remained pathologically elevated thereafter. All ICP trajectory groups had episodically abnormal ICP, PbtO2, and cerebral perfusion pressure (CPP) during monitoring. We identified three PbtO2 trajectory groups. Group 1 had persistent brain tissue hypoxia with more pathological elevations in ICP and inadequate CPP than the other PbtO2 trajectory groups. Group 2 had mostly normal PbtO2, while PbtO2 in group 3 increased linearly over 72 h, though there was a comparable incidence of brain tissue hypoxia, elevated ICP, and low CPP. However, PbtO2 group 3 had lower survival and more frequently exhibited evidence of severe HIBI.

Conclusions

We identified distinct PbtO2 and ICP trajectories after cardiac arrest. Our findings suggest that the physiology of hypoxic–ischemic brain injury is variable, and trajectory groups may represent distinct phenotypes. This work provides a foundation for future studies aimed at disentangling the heterogeneity of hypoxic–ischemic brain injury.