Asphyxial Cardiac Arrest

Sudden cardiac arrest is a significant source of morbidity and mortality, with neurological injury affecting the majority of persons who initially have restoration of pulses. The rat asphyxial cardiac arrest is an established model for neurological injury after cardiac arrest. This model reproduces many aspects of neurological injury observed in humans – transient coma, evolving motor deficits and persistent sensorimotor deficits – as well as the systemic metabolic disruptions that attend the clinical disease. Rats are anesthetized, intubated and placed on mechanical ventilation. After establishing femoral arterial and venous access, rats are chemically paralyzed, and the ventilator turned off. Hypoxemia leads to highly reproducible bradyasystolic circulatory arrest. Cardiac arrest is reversed after 8 min by resuming mechanical ventilation, chest compressions and intravenous administration of epinephrine. After restoring circulation, rats are supported on the ventilator for 1–2 h and then extubated. After extubation, rats require fluid supplementation for several days until they are able to resume feeding. Temperature during the first day of recovery strongly influences outcome, making control of temperature essential during experiments. Neurological deficits can be measured clinically, and histological damage to the brain becomes clear after several days.