Endotracheal administration of lidocaine inhibits isoflurane-induced tachycardia

Rapid increase in inspired isoflurane concentration increases heart rate and arterial blood pressure. To investigate whether the responses to isoflurane were elicited from stimulation of lower airway and/or lungs, haemodynamic responses to isoflurane administered after tracheal intubation were measured with or without endotracheal or intravenous administration of lidocaine.

Seventy-two ASA physical status 1 patients, aged 21-50 yr, were randomly allocated to one of four groups. After tracheal intubation, anaesthesia was maintained with oxygen 100% and isoflurane 1.0% with controlled ventilation. After stabilization for 15 min, the isoflurane concentration was rapidly increased to 3.0% in three groups. An endotracheal lidocaine group received pretreatment with endotracheal 0.4 ml lidocaine 8% spray, an intravenous lidocaine group received pretreatment of 32 mg lidocaine i.v., and an isoflurane 3% group received not pre- treatment. In a control group, inspired isoflurane concentration was maintained at 1.0%. Heart rate, systolic blood pressure and end-tidal isoflurane concentration were measured every minute for 10 min.

The rapid increase in isoflurane concentration increased heart rate (25 +/- 12% increase from baseline; P < 0.05) but the increase was reduced by endotracheal lidocaine (9 +/- 9%), but not by intravenous lidocaine (22 +/- 13%). The plasma concentration of lidocaine was lower in the endotracheal lidocaine group (0.4 +/- 0.3 microgram.ml-1) than in the i.v. lidocaine group (1.5 +/- 0.2 micrograms.ml-1).

The isoflurane-induced tachycardia is reduced by pre-treatment with endotracheal lidocaine.