The Brain After Cardiac Arrest

Jonathan Elmer, MD, MS; Clifton W. Callaway, MD, PhD

Disclosures

Semin Neurol. 2017;37(1):019-024. 

In This Article

Abstract and Introduction

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.

Introduction

Cardiac arrest (CA) is the most common cause of death in the developed world, claiming over 17 million lives annually.[1–3] Despite advances in care, the majority of patients who are treated after the return of spontaneous circulation (ROSC) will succumb to the sequelae of hypoxic-ischemic brain injury before hospital discharge. Similar to traumatic brain injury, hypoxic-ischemic brain injury after CA results in both primary and secondary injuries, with distinct mechanisms and treatment strategies (Fig. 1). High-quality cardiopulmonary resuscitation (CPR) initiated as soon as possible after collapse, and early defibrillation to rapidly restore normal perfusion, are the most important interventions to reduce the severity of primary brain injury.[4] It remains unclear whether care provided after ROSC can reduce the severity of primary brain injury or if therapies after CPR improve outcomes only by reducing the risk of secondary brain injury. Evidence-based therapies in the hours to days after ROSC that improve neurologic outcomes include targeted temperature management; early coronary revascularization; delayed, multimodal neurologic prognostication; and postacute care rehabilitation.[5] In this review, we provide an overview of the mechanisms and consequences of postarrest brain injury as an introduction to the many specific therapies that are reviewed in depth elsewhere in this issue.

Figure 1.

Conceptual map of brain injury after cardiac arrest. ASA, aspirin; BBB, blood–brain barrier; ROS, reactive oxygen species.

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