EFFECT OF CEREBRAL VENOUS CONGESTION ON THE PRESSURE VOLUME INDEX IN THE EVALUATION OF INTRACRANIAL-PRESSURE DYNAMICS

Translocation of cerebrospinal fluid (CSF) between the intracranial an d spinal subarachnoid space was blocked by ligating the cervical spina l core in eight cats under pentobarbital and nitrous oxide anesthesia, and the effects of cerebral venous congestion on the pressure-volume index (PVI), a measure relating the change in intracranial volume, and the logarithm of intracranial pressure (ICP) were evaluated. The chan ges in the volume-pressure response (VPR), a measure of intracranial e lastance, were calculated simultaneously. Cerebral venous congestion w as induced by lowering the head relative to the level of the heart by tilting the trunk of the animals to 20-degrees below horizontal. The p resence of venous congestion was confirmed by an increase in the sagit tal sinus pressure (SSP). The body position was shifted from horizonta l prone (H-1 group) to head-down tilt (D1 group) in four animals (grou p 1) and from head-down tilt (D2 group) to horizontal prone (H-2 group ) in the other four animals (group 2), and PVI and VPR were determined in each group. The changes in ICP and SSP with change of body positio n in group 1 were not significantly different from those in group 2, w ith both pressures changing by 7-8 mm Hg. PVI showed no significant di fferences between the H-1 group and H-2 group or between the D1 group and D2 group. The mean (+/-SEM) PVI for all measurements in the head-d own tilt position (D1 and D2 groups) was significantly higher (0.50 +/ - 0.02 ml; p < 0.01) than in the horizontal position (H-1 and H-2 grou ps; 0.35 +/- 0.02 ml). In contrast, VPR showed a positive linear relat ionship with ICP in both the horizontal and head-down tilt positions. These results show that, when ICP is increased due to cerebral venous congestion, VPR correctly indicates increased intracranial elastance; however, PVI paradoxically indicates an increase in the pressure-buffe ring ability as ICP is increased. The authors conclude that PVI is gre atly affected by the cerebral venous volume and must be interpreted ca utiously.