Postoperative Stroke in Patients After Spinal Anesthesia and Disparate Response Patterns of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

Spinal anesthesia is generally accepted as an effective and safe practice. Three rare incidents of postoperative cerebral infarction after surgery under spinal anesthesia with bupivacaine prompted us to assess whether spinal bupivacaine may impact carotid or cerebral blood flow and baroreflex functionality. We found that all three patients shared common pathology of stenosis or atheromatous lesions in the carotid or middle cerebral artery. In a companion animal study, we further observed that subarachnoid application of bupivacaine that reached low thoracic spinal cord in male Sprague‐Dawley rats elicited an initial (Phase I) reduction in mean arterial pressure (MAP), carotid blood flow (CBF) and baroreflexmediated sympathetic vasomotor tone, all of which returned to baseline in Phase II. Whereas heart rate (HR) exhibited sustained reduction, cardiac vagal baroreflex, baroreflex efficiency index (BEI) and tissue perfusion and oxygen in cerebral cortex supplied by middle cerebral artery remained unaltered during both phases. However, in one‐third of animals studied, Phase II gave way to a Phase III characterized by secondary hypotension and depressed baroreflex‐mediated sympathetic vasomotor tone, along with continuous decline in HR, sustained cardiac vagal baroreflex, decreased BEI, and reduction in CBF and tissue perfusion or oxygen in cerebral cortex. We conclude that carotid and cerebral blood flow can be compromised after spinal anesthesia, and impaired baroreflex‐mediated sympathetic vasomotor tone that leads to hypotension plays a contributory role.