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 (microHbO(2)) are unclear. At the splanchnic level, reduction of sympathetic tone may promote vasodilation and increase microHbO(2). However, these splanchnic effects are counteracted by systemic effects of TEA (e.g., decreased cardiac output (CO) and mean arterial pressure (MAP)), thus making the net effect on microHbO(2) difficult to predict. In this respect, effects of TEA on microHbO(2) may differ between physiological and compromised circulatory conditions, and additionally may depend on adequate fluid resuscitation. Furthermore, TEA may alter the relationship between regional microHbO(2) and systemic oxygen-transport (DO(2)). METHODS Chronically instrumented dogs (flow probes for CO measurement) were anaesthetized, their lungs ventilated and randomly received TEA with lidocaine (n=6) or epidural saline (controls, n=6). Animals were studied under physiological and compromised circulatory conditions (PEEP 10 cm H(2)O), both with and without fluid resuscitation. We measured gastric mucosal microHbO(2) by reflectance spectrophotometry, systemic DO(2), and systemic haemodynamics (CO, MAP). RESULTS Under physiological conditions, TEA preserved microHbO(2) (47 (3)% and 49 (5)%, mean (sem)) despite significantly decreasing DO(2) (11.3 (0.8) to 10.0 (0.7) ml kg(-1) min(-1)) and MAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatory conditions, TEA aggravated the reduction in microHbO(2) (to 32 (1)%), DO(2) (to 6.7 (0.8) ml kg(-1) min(-1)) and MAP (to 52 (4) mm Hg), compared with controls. During TEA, fluid resuscitation completely restored these variables. TEA preserved the correlation between microHbO(2) and DO(2), compared with controls. CONCLUSIONS TEA maintains microHbO(2) under physiological conditions, but aggravates the reduction of microHbO(2) induced by cardiocirculatory depression, thereby preserving the relationship between gastric mucosal and systemic oxygenation.

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