Effects of thoracic epidural anaesthesia on microvascular gastric mucosal oxygenation in physiological and compromised circulatory conditions in dogs

Background. The effects of thoracic epidural anaesthesia (TEA)on gastric mucosal microvascular haemoglobin oxygenation (µHbO₂)are unclear. At the splanchnic level, reduction of sympathetictone may promote vasodilation and increase µHbO₂. However,these splanchnic effects are counteracted by systemic effectsof TEA (e.g., decreased cardiac output (CO) and mean arterialpressure (MAP)), thus making the net effect on µHbO₂ difficultto predict. In this respect, effects of TEA on µHbO₂ maydiffer between physiological and compromised circulatory conditions,and additionally may depend on adequate fluid resuscitation.Furthermore, TEA may alter the relationship between regionalµHbO₂ and systemic oxygen-transport (DO₂). Methods. Chronically instrumented dogs (flow probes for CO measurement)were anaesthetized, their lungs ventilated and randomly receivedTEA with lidocaine (n=6) or epidural saline (controls, n=6).Animals were studied under physiological and compromised circulatoryconditions (PEEP 10 cm H₂O), both with and without fluid resuscitation.We measured gastric mucosal µHbO₂ by reflectance spectrophotometry,systemic DO₂, and systemic haemodynamics (CO, MAP). Results. Under physiological conditions, TEA preserved µHbO₂(47 (3)% and 49 (5)%, mean (SEM)) despite significantly decreasingDO₂ (11.3 (0.8) to 10.0 (0.7) ml kg^–1 min^–1) andMAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatoryconditions, TEA aggravated the reduction in µHbO₂ (to32 (1)%), DO₂ (to 6.7 (0.8) ml kg^–1 min^–1) and MAP(to 52 (4) mm Hg), compared with controls. During TEA, fluidresuscitation completely restored these variables. TEA preservedthe correlation between µHbO₂ and DO₂, compared with controls. Conclusions. TEA maintains µHbO₂ under physiological conditions,but aggravates the reduction of µHbO₂ induced by cardiocirculatorydepression, thereby preserving the relationship between gastricmucosal and systemic oxygenation. Presented in part at the German Anaesthesia Congress 2003 (April9–12, Munich, Germany) and the European Society of IntensiveCare Congress 2003 (October 5–8, Amsterdam, The Netherlands).