A G Rocco1, J H Philip, R A Boas, D Scott. 1. Harvard Medical School, Department of Anesthesia, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Abstract
BACKGROUND AND OBJECTIVES: The origin and the presence of negative pressure 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 course, the pressure at the needle tip was continuously measured as it traversed the interspinous ligament and the ligamentum flavum. METHODS: In a group of 22 patients, fluid was infused under gravity, and in a second group of 25 patients, boluses of fluid were administered at controlled infusion rates and under gravity. The volume-pressure-flow relationship was thus measured in one of two ways, either with a manual syringe and pressure transducer or with a pressure-monitoring-computer-controlled volumetric infusion pump. RESULTS: Natural pressure, (i.e., pressure in the epidural space before instrumentation is applied) could be approached when the space was first entered before fluid was infused (initial pressure); or after fluid had been infused (residual pressure). Epidural pressure could be extrapolated from the upsweep of the volume-pressure-flow relationship by projecting it back to just before the 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 lifted to a certain height, at which flow began and continued at a perceptible rate, with very little or no further increase in height required to maintain flow. The pressure at which flow began was the critical opening pressure, a characteristic of a Starling resistor. Furthermore, resistance to inflow of fluid was related to the presence or absence of natural or surgical disease in the epidural space. Resistance was significantly higher in the diseased than in the surgical group, at 114 (range, 22-226) mm Hg/L/h versus 46 (range, 8-86) mm Hg/L/h. Three phases were seen in the pressure-time recordings. CONCLUSIONS: Volume-pressure-flow relationships in the epidural space can be explained by a model in which epidural and subarachnoid pressures are inextricably related with the Starling pressure, dependent on the subarachnoid pressure. This model suggests reasons why spread of anesthetics might be difficult to predict.
BACKGROUND AND OBJECTIVES: The origin and the presence of negative pressure 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 course, the pressure at the needle tip was continuously measured as it traversed the interspinous ligament and the ligamentum flavum. METHODS: In a group of 22 patients, fluid was infused under gravity, and in a second group of 25 patients, boluses of fluid were administered at controlled infusion rates and under gravity. The volume-pressure-flow relationship was thus measured in one of two ways, either with a manual syringe and pressure transducer or with a pressure-monitoring-computer-controlled volumetric infusion pump. RESULTS: Natural pressure, (i.e., pressure in the epidural space before instrumentation is applied) could be approached when the space was first entered before fluid was infused (initial pressure); or after fluid had been infused (residual pressure). Epidural pressure could be extrapolated from the upsweep of the volume-pressure-flow relationship by projecting it back to just before the 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 lifted to a certain height, at which flow began and continued at a perceptible rate, with very little or no further increase in height required to maintain flow. The pressure at which flow began was the critical opening pressure, a characteristic of a Starling resistor. Furthermore, resistance to inflow of fluid was related to the presence or absence of natural or surgical disease in the epidural space. Resistance was significantly higher in the diseased than in the surgical group, at 114 (range, 22-226) mm Hg/L/h versus 46 (range, 8-86) mm Hg/L/h. Three phases were seen in the pressure-time recordings. CONCLUSIONS: Volume-pressure-flow relationships in the epidural space can be explained by a model in which epidural and subarachnoid pressures are inextricably related with the Starling pressure, dependent on the subarachnoid pressure. This model suggests reasons why spread of anesthetics might be difficult to predict.