Brain Tissue Oxygenation, Cardiac Complications, and Haemodynamic Interactions After Aneurysmal Subarachnoid Haemorrhage: A Systematic Review

Brain tissue oxygen tension (PbtO₂) monitoring is increasingly used as a component of multimodal neuromonitoring in patients with poor-grade aneurysmal subarachnoid haemorrhage (aSAH).However, it remains uncertain whether PbtO₂ abnormalities predict early cardiac complications and how systemic haemodynamic and cardiorespiratory factors influence regional cerebral oxygenation.This systematic review aimed to determine whether invasively measured PbtO₂ is associated with subsequent early cardiac complications or haemodynamic instability of cardiovascular origin after aSAH and to synthesise evidence on the effects of systemic haemodynamic and selected cardiorespiratory variables and interventions on PbtO₂.PubMed/MEDLINE, Web of Science, Scopus, CENTRAL, Europe PMC, and ClinicalTrials.govwere searched, together with backward citation searching, to identify studies of adults with aSAH who underwent invasive PbtO₂ monitoring.No restrictions on publication date or language were applied.The review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020, and methodological quality was appraised using design-specific Joanna Briggs Institute critical appraisal tools.Owing to substantial clinical and methodological heterogeneity, findings were synthesised narratively.The searches identified 961 records, of which 21 publication reports published between 2005 and 2026 met the eligibility criteria.None directly evaluated whether antecedent PbtO₂ abnormalities or cumulative hypoxic burden predicted subsequent early cardiac complications.The available evidence predominantly addressed the reverse relationship, examining how systemic physiological variables and therapeutic interventions affected regional brain tissue oxygenation.Lower mean arterial pressure or cerebral perfusion pressure was frequently associated with lower PbtO₂, whereas controlled arterial pressure augmentation often improved oxygenation.Responses were heterogeneous and appeared to depend on baseline oxygenation, cerebrovascular autoregulatory status, probe location, and local cerebral pathology.Fluid administration produced larger increases in PbtO₂ when accompanied by an increase in cardiac index.Respiratory, pharmacological, and osmotic interventions had variable effects, reflecting their combined systemic, cerebral, and intracranial consequences.Lower PbtO₂ or impaired oxygen reactivity was associated in some reports with metabolic crisis, delayed cerebral infarction, spreading depolarisation, mortality, or unfavourable neurological outcome.However, independent prognostic value was not consistently demonstrated.Meta-analysis was not appropriate because of heterogeneity in study designs, interventions, physiological thresholds, analytical methods, repeated observations, and potentially overlapping cohorts.Current evidence does not establish PbtO₂ as a predictor of early cardiac complications after aSAH.PbtO₂ is a regional and context-dependent physiological measure influenced by interacting systemic, cerebral, respiratory, and intracranial factors.It should therefore be interpreted as part of multimodal neuromonitoring rather than according to a universal haemodynamic or oxygen threshold.Prospective multicentre studies incorporating synchronised PbtO₂ and cardiac monitoring, standardised hypoxicburden metrics, and temporally adjudicated cardiac outcomes are required.