Abstract
Episodes of prolonged hypercarbia frequently occur during treatment of respiratory distress in preterm infants and may induce redistribution of cardiac output similar to the redistribution seen during hypoxia. This hypothesis was tested by exposing 7 newborn piglets to four hours of hypercarbia (8,5 - 10 Kpa) followed by return to normocarbia. Cardiac output and organ blood flow (micropheres) were measured during baseline, 1/2, 2 and 4 hours of hypercarbia and 15 and 45 min. following return to normocarbia.Prolonged hypercarbia resulted in redistribution of cardiac output with increments distributed to the brain and diafragm and reductions to the liver (hepatic artery), small intestine and kidneys. The reduction in cardiac output distribution to the splanchic circulation persisted following return to normocarbia. Thus: episodes of prolonged PaCO2 elevation in the neonate may compromise splanchnic blood flow.
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