JUGULAR LIGATION DOES NOT INCREASE INTRACRANIAL-PRESSURE BUT DOES INCREASE BIHEMISPHERIC CEREBRAL BLOOD-FLOW AND METABOLISM

Objectives: To answer the following questions: a) Does jugular venous ligation (simulating venovenous extracorporeal life support) alter pro ximal jugular venous pressure, intracranial pressure, hemispheric cere bral blood flow, or cerebral metabolism? b) Does release of ligation r everse these effects? and c) What are the comparative effects of venou s ligation alone vs. venous ligation in combination with arterial liga tion? Design: Prospective, randomized, laboratory investigation. Setti ng: Multidisciplinary laboratory setting. Subjects: Sixteen swine, wei ghing 8.1 to 12.1 kg, 3 to 4 wks of age. Interventions: Sixteen swine were randomly assigned to two groups, utilizing a random sequence of v essel ligation. Nine swine underwent occlusion of the right internal a nd external jugular veins alone (venovenous ligation) followed by rele ase of the occlusion and then occlusion of the right common carotid ar tery and the right internal and external jugular veins together (venoa rterial ligation). The remaining seven swine underwent venoarterial li gation, followed by release of the occlusion and then venovenous ligat ion. In the experimental group in which venovenous ligation was perfor med first, the 5, and 30-min release periods after ligation were taken to represent the effects of draining the right jugular vein during ve novenous extracorporeal life support. Measurements and Main Results: D ata were obtained at baseline, 5, and 30 mins after each ligation/rele ase period. Intracranial pressure, right and left internal jugular pre ssures/flow rates, and cerebral sinus lactate concentrations were meas ured. Cerebral blood flow was determined using Xe-133 clearance method ology, and the cerebral metabolic rate was calculated. There were no s ignificant differences between the ipsilateral internal jugular pressu re or extracorporeal life support at 5 or 30 mins after venovenous or venoarterial ligation compared with baseline values or compared with t he release of the ligation at 5 or 30 mins. There was a significant in crease in right-side (44.7 +/- 2.0 vs. 38.8 +/- 2.4 mL/kg/min; p < .05 ) and left-side (42.9 +/- 2.3 vs. 38.7 +/- 1.9 mL/ kg/min; p < .05) ce rebral blood flow 5 mins after venovenous ligation when compared with baseline values. Similarly, after venoarterial ligation, there was a s ignificant increase in right-side (44.6 +/- 2.2 vs. 38.8 +/- 2.4 mL/ k g/min; p < .05) and left-side (43.9 +/- 1.5 vs. 38.7 +/- 1.9 mL/kg/min ; p < .05) cerebral blood flow. Cerebral oxygen consumption was signif icantly increased after venovenous (2.7 +/- 0.2 to 3.2 +/- 0.2 mL/kg/m in; p < .05) and venoarterial (2.7 +/- 0.2 to 3.1 +/- 0.2 mL/kg/min; p < .05) ligation at 5 mins after ligation, This increase persisted at the 30-min period and after release of ligation. Conclusions: Ligation of the right jugular veins alone (venovenous ligation) or jugular vei ns and right carotid artery (venoarterial ligation) does not increase jugular venous pressures or intracranial pressure, However, this proce dure does increase cerebral blood flow and cerebral oxygen consumption . These findings demonstrate that there is adequate decompression of t he venous system by the cerebrovascular system and retrograde decompre ssion during extracorporeal life support appears unwarranted.