Postoperative Stroke after Spinal Anesthesia and Responses of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

Abstract

Spinal anesthesia is generally accepted as an effective and safe practice. Three rare incidents of postoperative cerebral infarction after surgery under spinal anesthesia prompted us to assess whether spinal bupivacaine may compromise carotid or cerebral blood flow. Postoperative examination after the stroke incident revealed that all three patients shared a common pathology of stenosis or atheromatosis in the carotid or middle cerebral artery. In a companion study using 69 Sprague-Dawley rats, subarachnoid application of bupivacaine elicited an initial (Phase I) reduction in the mean arterial pressure, carotid blood flow (CBF) and baroreflex-mediated sympathetic vasomotor tone, all of which subsequently returned to baseline (Phase II). Whereas heart rate (HR) exhibited sustained reduction, cardiac vagal baroreflex, baroreflex efficiency index (BEI) and tissue perfusion and oxygen in the cerebral cortex remained unaltered. However, in one-third of the rats studied, Phase II gave way to Phase III characterized by secondary hypotension and depressed baroreflex-mediated sympathetic vasomotor tone, along with declined HR, sustained cardiac vagal baroreflex, decreased BEI, reduced CBF and waning tissue perfusion or oxygen in the cerebral cortex. We concluded that carotid and cerebral blood flow can indeed be compromised after spinal anesthesia, and an impaired baroreflex-mediated sympathetic vasomotor tone, which leads to hypotension, plays a contributory role.

Effect of phenylephrine rescue injection on hypotension after spinal anaesthesia for caesarean delivery when guided by both heart rate and SBP during an early warning window

“…Heart rate-guided phenylephrine after spinal anaesthesia 427 However, some studies have shown that spinal anaesthesia below T4 has no negative effect on baroreflex sensitivity, and the Bezold-Jarisch reflex, which may cause bradycardia, is uncommon. 16,17 In theory, blockade of the sympathetic nerve fibres would be several dermatomes above the level of loss of pinprick sensation, thus loss of pinprick sensation to T4 and above may block the cardiac sympathetic nerves. However, the block level does not reach T4 immediately after spinal injection.…”

“…The difference between hypotension after spinal anaesthesia and pathological shock is that spinal anaesthesia may inhibit the cardiac sympathetic nerves and thus impair the baroreflex compensatory increase in HR. However, some studies have shown that spinal anaesthesia below T4 has no negative effect on baroreflex sensitivity, and the Bezold–Jarisch reflex, which may cause bradycardia, is uncommon 16,17 . In theory, blockade of the sympathetic nerve fibres would be several dermatomes above the level of loss of pinprick sensation, thus loss of pinprick sensation to T4 and above may block the cardiac sympathetic nerves.…”