Cerebral hemodynamics after cardiac arrest: implications for clinical management.

Abstract

Following resuscitation from cardiac arrest, hypoxic ischemic brain injury (HIBI) ensues, which is the primary determinant of adverse outcome. The pathophysiology of HIBI can be compartmentalized into primary and secondary injury, resulting from cerebral ischemia during cardiac arrest and reperfusion following successful resuscitation, respectively. During the secondary injury phase, increased attention has been directed towards the optimization of cerebral oxygen delivery to prevent additive injury to the brain. During this phase, cerebral hemodynamics are characterized by early hyperemia following resuscitation and then a protracted phase of cerebral hypoperfusion termed "no-reflow" during which additional hypoxic-ischemic injury can occur. As such, identification of therapeutic strategies to optimize cerebral delivery of oxygen is at the forefront of HIBI research. Unfortunately, randomized control trials investigating the manipulation of arterial carbon dioxide tension and mean arterial pressure augmentation as methods to potentially improve cerebral oxygen delivery have shown no impact on clinical outcomes. Emerging literature suggests differential patient-specific phenotypes may exist in patients with HIBI. The potential to personalize therapeutic strategies in the critical care setting based upon patient-specific pathophysiology presents an attractive strategy to improve HIBI outcomes. Herein, we review the cerebral hemodynamic pathophysiology of HIBI, discuss patient phenotypes as it pertains to personalizing care, as well as suggest future directions.