Effect of Central Venous Pressure on Spinal Cord Oxygenation

To analyze the effect of central venous pressure on cerebrospinal fluid oxygen tension and intrathecal pressure, multiparameter sensors were introduced into the intrathecal space for continuous monitoring of cerebrospinal fluid Po(2), Pco(2), and intrathecal pressure in 15 pigs. After 20 min of aortic clamping, hypervolemia was established for 20 min, followed by normovolemia. The animals were divided into 3 groups: in group 1, cerebrospinal fluid Po(2) = 0% at some time during crossclamping; in group 2, cerebrospinal fluid Po(2) was <50%; and in group 3, cerebrospinal fluid Po(2) remained > or = 50%. Mean decreases in cerebrospinal fluid Po(2) during the initial 20 min of crossclamping were 82%, 57%, and 15% in groups 1, 2, and 3, respectively. Following induction of hypervolemia, central venous and cerebrospinal fluid pressures increased simultaneously; this caused a significant decrease in cerebrospinal fluid Po(2) in group 2 only. In this model, aortic clamping did not increase cerebrospinal fluid pressure if central venous pressure was not elevated. The detrimental effect of elevated intrathecal pressure on cerebrospinal fluid oxygenation was seen only in animals with an intermediate degree of spinal cord ischemia. This might have important implications for the prevention of paraplegia during thoracoabdominal aortic replacement.