Fig. 5.

Integration of hypoxic–ischaemic brain injury pathophysiology, neuromonitoring, and possible management interventions. Primary injury is characterised by global cerebral ischaemia during the initial cardiac arrest. Thereafter, secondary injury mechanisms take place. The pathophysiologic changes occurring in the oxygen cascade pertaining to oxygen convection, diffusion, and utilisation by mitochondria are central to secondary injury in the post-ROSC setting. Neuromonitoring devices provide physiologic data pertaining to specific stages of the oxygen cascade. Interventions can be compartmentalised based on specific stages of the oxygen cascade at which their physiologic effect is exerted. CBF cerebral blood flow, Hb haemoglobin, HTS hypertonic saline, ICP intracranial pressure, L/P ratio lactate/pyruvate ratio, MAP mean arterial pressure, MCAv middle cerebral artery blood velocity, MMM multi-modal monitoring, NIRS near infrared spectroscopy, PaCO₂ arterial carbon dioxide tension, PbtO₂ brain tissue oxygen tension, rSO₂ regional oxygen saturation, SjvO₂ jugular venous bulb oximetry, TCD transcranial Doppler