Mechanisms of injury in hypoxic-ischemic encephalopathy: implications to therapy.
Cardiac arrest survivors commonly suffer ischemic brain injury, and understanding the mechanisms of injury is essential to providing insight for effective therapies for brain protection. Injury can occur at the time of the cardiac arrest and is dependent not only on the duration but also the degree of impaired circulation. Injury can be ongoing even after the return of spontaneous circulation, giving the clinician an additional window of opportunity to treat and protect the injured brain. This section will review the molecular basis of injury with cardiac arrest and will elucidate the different mechanisms of injury between cardiac arrest, pure respiratory arrest, and arrest secondary to toxins (e.g., carbon monoxide). The rationale for multiple postarrest therapies, such as hypothermia and induced hypertension, will also be reviewed.
Greer
David M
DM
Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology*; D002249:Carbon Monoxide Poisoning / Q000150:complications / Q000503:physiopathology; D006323:Heart Arrest / Q000150:complications*; D006801:Humans; D007036:Hypothermia, Induced / Q000639:trends; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology* / Q000503:physiopathology* / Q000628:therapy; D018696:Neuroprotective Agents / Q000627:therapeutic use; D012131:Respiratory Insufficiency / Q000150:complications; D015912:Thrombolytic Therapy / Q000639:trends; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D018696:Neuroprotective Agents; D014662:Vasoconstrictor Agents