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Review
. 2017 Feb;37(1):19-24.
doi: 10.1055/s-0036-1597833. Epub 2017 Feb 1.

The Brain After Cardiac Arrest

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Free PMC article
Review

The Brain After Cardiac Arrest

Jonathan Elmer et al. Semin Neurol. .
Free PMC article

Abstract

Cardiac arrest is common and deadly. Most patients who are treated in the hospital after achieving return of spontaneous circulation still go on to die from the sequelae of anoxic brain injury. In this review, the authors provide an overview of the mechanisms and consequences of postarrest brain injury. Special attention is paid to potentially modifiable mechanisms of secondary brain injury including seizures, hyperpyrexia, cerebral hypoxia and hypoperfusion, oxidative injury, and the development of cerebral edema. Finally, the authors discuss the outcomes of cardiac arrest survivors with a focus on commonly observed patterns of injury as well as the scales used to measure patient outcome and their limitations.

Figures

Fig. 1
Fig. 1
Conceptual map of brain injury after cardiac arrest. ASA, aspirin; BBB, blood–brain barrier; ROS, reactive oxygen species.
Fig. 2
Fig. 2
Direct monitoring of brain tissue oxygenation or cerebral blood flow in two patients after cardiac arrest reveals significant between-patient variation in the necessary mean arterial pressure (MAP) to maintain adequate brain oxygenation. In the left panel, brain tissue hypoxia at a threshold of 20 mmHg (red line) is present despite intact autoregulation at blood MAPs below ~110 mmHg, but can be overcome by increasing MAP >110 mmHg. In the right panel, autoregulation is mostly intact and brain oxygenation is adequate across a range of MAPs.
Fig. 3
Fig. 3
Cerebral edema may develop early after cardiac arrest or during rewarming. In this patient, baseline computed tomography (CT) scan shortly after cardiac arrest was unremarkable (left). Just at the time of the second CT scan, the patient showed clinical signs of herniation, prompting empiric therapy with hypertonic saline. Basilar and quadrigeminal cisterns were collapsed (center, arrows). After 24 hours, the subject had recovery of brainstem reflexes and improved appearance on CT scan (right). Ultimately, this patient had no recovery of cortical function.

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