Pathophysiologic Consideration

The field of medicine related to cardiopulmonary resuscitation deals with a hypoxic-ischemic process that involves the entire body. Although the inciting factors that lead to CA can be varied (e.g., primary ventricular fibrillation or asphyxiation), total circulatory failure with CA injures both brain and extracerebral organs. The injury stimulates complex adaptive and maladaptive responses at the levels of cells, tissues, organs, and, ultimately, the organism. The primary injury in specific organs causes secondary effects on other organs, which can worsen injury to the brain and heart. A common example of such an injury is disruption of the gastrointestinal barrier caused by ischemia, leading to bacterial toxin leakage into the bloodstream (11,12) . Ischemic injury can also disrupt blood vessels, releasing a variety of mediators that potentially injure otherwise unaffected tissues and cells (13,14). This complex interplay between the heart, brain, vasculature, gastrointestinal tract, muscle, inflammatory system, coagulation system, and other organs requires intervention by a multidisciplinary team that can address multiorgan injury. Although the focus of this chapter is the management of brain injury after CA, some discussions will address the systemic injury in relation to the neurologic injury and recovery. A detailed discussion of the cellular and molecular pathophysiologic mechanisms of post cardiac arrest, ischemic brain injury, and their relevance to neuroprotective therapies is provided in Chapters 25 and 29.

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