EPIDURAL SPACE AS A STARLING RESISTOR AND ELEVATION OF INFLOW RESISTANCE IN A DISEASED EPIDURAL SPACE

Citation
Ag. Rocco et al., EPIDURAL SPACE AS A STARLING RESISTOR AND ELEVATION OF INFLOW RESISTANCE IN A DISEASED EPIDURAL SPACE, Regional anesthesia, 22(2), 1997, pp. 167-177
Citations number
41
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
0146521X
Volume
22
Issue
2
Year of publication
1997
Pages
167 - 177
Database
ISI
SICI code
0146-521X(1997)22:2<167:ESAASR>2.0.ZU;2-G
Abstract
Background and Objectives. The origin and the presence of negative pre ssure in the epidural space as well as the relationship of the extent of epidural anesthesia to epidural pressure has long been a subject of controversy. To further elucidate epidural pressure and its time cour se, the pressure at the needle tip was continuously measured as it tra versed the interspinous ligament and the ligamentum flavum. Methods. I n a group of 22 patients, fluid was infused under gravity, and in a se cond group of 25 patients, boluses of fluid were administered at contr olled infusion rates and under gravity. The volume-pressure-now relati onship was thus measured in one of two ways, either with a manual syri nge and pressure transducer or with a pressure-monitoring-computer-con trolled volumetric infusion pump. Results. Natural pressure, (i.e., pr essure in the epidural space before instrumentation is applied) could be approached when the space was first entered before fluid was infuse d (initial pressure); or after fluid had been infused (residual pressu re). Epidural pressure could be extrapolated from the upsweep of the v olume-pressure-now relationship by projecting it back to just before t he first injection. The extrapolated pressure lay between the initial and residual pressures. Medicinal solution placed in the barrel of the syringe did not infuse under gravity until the syringe barrel was lif ted to a certain height, at which now began and continued at a percept ible rate, with very little or no further increase in height required to maintain now. The pressure at which now began was the critical open ing pressure, a characteristic of a Starling resistor. Furthermore, re sistance to inflow of fluid was related to the presence or absence of natural or surgical disease in the epidural space. Resistance was sign ificantly higher in the diseased than in the surgical group, at 114 (r ange, 22-226) mm Hg/L/h versus 46 (range, 8-86) mm Hg/L/h. Three phase s were seen in the pressure-time recordings. Conclusions. Volume-press ure-flow relationships in the epidural space can be explained by a mod el in which epidural and subarachnoid pressures are inextricably relat ed with the Starling pressure, dependent on the subarachinoid pressure . This model suggests reasons why spread of anesthetics might be diffi cult to predict.