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Thursday, 2 September 2021

 


Monitoring and modifying brain oxygenation in patients at risk of hypoxic ischaemic brain injury after cardiac arrest

 

by Markus Benedikt Skrifvars, Mypinder Sekhon and Erik Anders Åneman 

Critical Care volume 25, Article number: 312 (2021) Published: 31 August 2021

The majority of adverse clinical outcomes following successful resuscitation from cardiac arrest, are attributable to hypoxic ischemic brain injury [1]. The cornerstone of hypoxic ischemic brain injury management has traditionally focused on preventing secondary ischemic injury, following the return of spontaneous circulation (ROSC) [2]. Among the various mechanisms implicated in the pathophysiology of secondary injury, post-resuscitation cerebral ischemia is linked to central physiologic variables that may be modifiable [3]. Observational data demonstrate associations between perturbations in physiologic variables known to reduce cerebral blood flow (CBF)—such as arterial hypotension [4] and hypocapnia [5]—and adverse clinical outcome. This adds credence to the importance of optimizing cerebral oxygen delivery, to mitigate secondary ischemic injury. Recently, sentinel randomized controlled trials (RCTs) aimed at augmenting mean arterial pressure (MAP)—a key physiologic determinant of cerebral oxygen delivery—have yielded important insights into the importance of mitigating secondary cerebral ischemia [67]. Although it did not establish a definitive link to improved neurological outcome, the COMACARE study demonstrated reduced levels of neurofilament light, a biomarker of brain injury, in patients undergoing an augmented MAP strategy following ROSC [8]. Patients may continue to experience episodes of brain hypoxia following cardiac arrest, despite goal-directed therapy and augmented MAP, with considerable heterogeneity in the underlying cerebrovascular hemodynamics in individual patients [9]. Thus, a targeted approach to the individualized management of hypoxic ischemic brain injury in the post-resuscitation phase requires the longitudinal monitoring of brain oxygenation—providing clinicians with real time physiologic data points to optimize cerebral oxygen delivery, similar to that applied in patients with traumatic brain injury (TBI) [10]. Near infrared spectroscopy (NIRS) provides an easily implemented and virtually complication-free way to monitor regional cerebral oxygen saturation (rSO2) in critically ill patients. The insertion of oxygen sensing catheters provides a real time assessment of the partial pressure of oxygen in brain tissue (PbtO2). This approach has gained widespread use following neurotrauma.

In this narrative review, we discuss the available means for monitoring the occurrence of brain ischemia in patients at risk of hypoxic ischemic brain injury. Specifically, we decided to review the evidence for non-invasive monitoring, using NIRS and invasive monitoring via the insertion of tissue oxygen monitors and jugular bulb catheters. These two approaches to monitoring brain oxygenation have different advantages and limitations (Fig. 1). We also discuss ways to modify cerebral oxygenation, with a special focus on MAP and blood carbon dioxide and oxygen levels.

 

 

 

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