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 [6, 7].
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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