Gormley W P, Murray J M, Trinick T R
Department of *Anaesthesia, Ulster, Hospital Trust, Dundonald, Belfast, Northern Ireland.
Anesth Analg. 1996 Feb;82(2):358-61. doi: 10.1097/00000539-199602000-00025.
This study was designed to investigate the effect of intravenous lidocaine on the sympathetic activity after a rapid increase in desflurane concentration. Twenty ASA grade I and II patients, were allocated randomly to a control group (C) and a lidocaine group (L). After induction of anesthesia with intravenous propofol 2 mg/kg and muscle relaxation with intravenous vecuronium 0.1 mg/kg, desflurane was given to achieve an end-tidal minimum alveolar anesthetic concentration (MAC) of 0.7 Group L received 1.5 mg/kg lidocaine intravenously, while Group C received an equal volume of 0.9% sodium chloride solution intravenously. These solutions were prepared and coded by a colleague who took no further part in the study. The concentration of desflurane was then abruptly increased to 1.5 MAC. Heart rate and mean arterial pressure were noted every half minute. Blood samples were taken for plasma catecholamines at rest, 0.7 MAC, and at 1-min intervals for 5 min after the increase in desflurane concentration. There was a significant increase in heart rate and mean arterial pressure in both groups. The increase in heart rate was significantly less in Group L from 0.5 until 2.5 min (P < 0.05). There was no difference in mean arterial pressure between the groups except at 4.5 and 5.0 min (P < 0.05). Plasma catecholamines were not significantly different between the groups. Intravenous lidocaine did not attenuate the sympathetic response to a rapid increase in desflurane concentration. It is unlikely that airway irritation is the cause of this phenomenon.
