During CPR, therapy focuses primarily on restarting the arrested heart and ensuring cerebral perfusion. For the splanchnic and renal circulation, the period of CPR represents a time of very low perfusion. When vasopressors are given during CPR in order to increase vital organ perfusion, splanchnic and renal blood flow may come close to zero.

Negovsky and Safar have long maintained that selfintoxication from visceral organ ischemia as a result of cardiac arrest delays or prevents full neurologic recovery and may be a secondary cause of neuronal injury. Nevertheless, the effects of visceral organ ischemia and reperfusion (I/R) on the postresucitation syndrome, which is characterized by a systemic inflammatory response similar to that observed in other systemic inflammatory conditions such as sepsis, are not fully understood.

In the non-cardiac arrest setting, the two major directions of research on visceral organ ischemia are the contribution of individual visceral organs to development of secondary organ dysfunction and multiple organ failure; and studies of visceral organ injury, surgery, or transplant-ation resulting in or requiring ischemia. This chapter reviews the mechanisms of ischemia and reperfusion injury of the visceral organs; puts them in the context of cardiac arrest, the period of resuscitation (CPR), and the postresuscitation period; and considers how visceral organ ischemia may contribute to the postresuscitation syndrome.

Splanchnic circulation

Splanchnic circulation refers to the vasculature that brings blood to and from the major abdominal organs including the liver, spleen, stomach, pancreas, and small and large intestine.