Plasma Concentrations of Epinephrine Need to Be Monitored in Study of Incidence of Hypotensive/Bradycardic Events

To the Editor: I read with interest the article by Sia et al. (1) about the effect of epinephrine-containing anesthetic solutions on the incidence of hypotensive/bradycardic events (HBE) during shoulder surgery in the sitting position under interscalene brachial plexus block (ISB). I agree with the authors that preventive measures need to be assessed because of the large frequency (13%–28%) of this acute and life threatening complication. The most likely cause of these events is the activation of the Bezold-Jarisch reflex (BJR). Beta-blocking drugs have been proven to prevent this phenomenon by decreasing the sympathetic tone (2,3). Sedation could also decrease endogenous catecholamine level and protect from HBE, but this remains to be demonstrated in a prospective manner (4).The hypothesis that exogenous epinephrine (via local anesthetic solutions or arthroscopic irrigating solutions) could increase the incidence of HBE has been proposed by Kinsella but never been proven (5). In their article, Sia et al. report a reduction of the incidence of HBE from 29% to 11% by withdrawing epinephrine from the lidocaine-bupivacaine mixture (1). I would like to make some comments about this work. As it is mentioned in their Discussion section, the use of a vasodilating drug like urapidil to improve the visualization of the surgical field is a very important concern. The understanding of the paper could have been made clearer if the 30 patients who had received urapidil or metoprolol had been excluded from the analysis. Instead of focusing on the effects of epinephrine, the authors define a new entity called “urapidil or non-urapidil induced HBE” that makes the reading of their study rather difficult. Furthermore, it is obvious that the injection of a vasodilator increases venous pooling in lower limbs and may induce an experimental BJR. However, even when they consider only the 85 patients who did not receive urapidil or metoprolol, the authors find that the incidence of HBE is more frequent in the epinephrine group (29% vs 4%). I think that the consequences of such a very small dose of epinephrine added to an anesthetic solution and administered in a plexus sheath are surprising. If we believe the authors’ statements, in this setting, epinephrine withdrawal from the local anesthetic solution could decrease blood pressure and heart rate enough to reduce the bleeding in the surgical field, the urapidil use, and above all the incidence of HBE (<5%). Does that mean that HBE occurring during shoulder surgery in the sitting position under ISB is no more a clinical concern? We regret that plasma concentrations of epinephrine have not been monitored. In a study about the hemodynamic responses to epinephrine-containing perianal lidocaine, Barber et al. (6) have compared lidocaine 0.5% with or without 1:200,000 epinephrine. They have shown that despite increasing plasma concentrations, there were no changes in blood pressure, heart rate, or plasma norepinephrine levels. I do not understand why the same doses of epinephrine injected in the interscalene space could produce more hemodynamic effects than in the perianal region.