Effect of intravenous lidocaine infusion on arterial baroreflex
Yoneda, I.
Masui. Japanese Journal of Anesthesiology 42(5): 652-663
1993
ISSN/ISBN: 0021-4892 PMID: 8515540 Document Number: 411016
The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg cntdot kg-1 bolus + 100 mu-g cntdot kg-1 cntdot min-1, 3 mg cntdot kg-1 bolus + 200 mu-g cntdot kg-1 cntdot min-1, 6 mg cntdot kg-1 bolus + 400 mu-g cntdot kg-1 cntdot min-1 and 12 mg cntdot kg-1 bolus + 800 mu-g cntdot kg-1 cntdot min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 mu-g cntdot kg-1) and phenylephrine (2-4 mu-g cntdot kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine ( lt 5 mu-g cntdot ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels ( gt 10 mu-g cntdot ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg cntdot kg-1 + 100 mu-g cntdot kg-1 cntdot min-1). Respiratory acidosis (Pa-CO-2: 65.6+-3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.