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Three clinical investigations together with a combined editorial and review of the cardiovascular physiology of spinal anaesthesia in normal and preeclamptic pregnancy form the basis of a thesis to be submitted for the degree of Doctor of Medicine at the University of St Andrews. First, the longstanding consensus that spinal anaesthesia could cause severe hypotension in severe preeclampsia was examined using three approaches. The doses of ephedrine required to maintain systolic blood pressure above predetermined limits were first compared in spinal versus epidural anaesthesia. The doses of ephedrine required were then similarly studied during spinal anaesthesia in preeclamptic versus normal control subjects. The principal outcome of these studies, that preeclamptic patients were resistant to hypotension after a spinal anaesthetic, was then further investigated by studying pulse transit time (PTT) changes in normal versus preeclamptic pregnancy. PTT was explored both as beat-to-beat monitor of cardiovascular function and also as an indicator of changes in arterial stiffness. The cardiovascular physiology of obstetric spinal anaesthesia was then reviewed in the light of the three clinical investigations, developments in reproductive vascular biology and the regulation of venous capacitance. It is argued that the theory of a role for vena caval compression as the single cause of spinal anaesthetic induced hypotension in obstetrics should be revised.

Spinal anesthesia is an excellent choice as the primary anesthetic for lower abdominal, perineal, and lower extremity procedures. Spinal anesthesia boasts several distinct advantages over general anesthesia. However, it is important to note that spinal anesthesia does not come without risk. The most common adverse reaction of spinal anesthesia is hypotension. Anesthesia providers use several methods to combat the hypotension that is so commonly associated with spinal anesthesia. One emerging trend to prevent spinal anesthesia-induced hypotension (SAIH) is the administration of ondansetron, a serotonin 5-hydroxytryptamine3 antagonist. Evidence has shown that the administration of ondansetron just prior to spinal anesthesia administration may decrease the prevalence of SAIH by blocking the serotonin receptors in the heart, thus preventing the triggering of the Bezold-Jarisch Reflex, a triad of hypotension, bradycardia, and peripheral vasodilation. Despite the mounting evidence supporting the use of ondansetron to prevent this phenomenon, it has not been widely adopted as the standard of care. The purpose of this project was to translate evidence-based anesthesia care of patients undergoing spinal anesthesia into practice by increasing anesthesia provider knowledge regarding the efficacy of pre-spinal anesthetic ondansetron in attenuating SAIH. An educational in-service was delivered to anesthesia providers at a 292 private-bed community hospital in West Virginia regarding the efficacy of ondansetron in the mitigation of SAIH in an attempt to increase provider knowledge about the usefulness of this intervention. Nineteen anesthesia providers took part in the in-service. Pre- and post-intervention Likert surveys were delivered that assessed the providers’ knowledge regarding the intervention, current use of the intervention in his or her practice, and willingness to adopt the intervention if sufficient evidence supports the change. It was concluded that the in-service increased provider knowledge regarding the use of ondansetron in the attenuation of SAIH and influenced an intended change in provider practice. Continuing education should be utilized to inform the evolution of evidence-based practice in anesthesia.