Endotracheal administration of lidocaine inhibits isoflurane-induced tachycardia

Purpose: Rapid increase in inspired isoflurane concentration increases hear t rate and arterial blood pressure. To investigate whether the responses to isoflurane were elicited from stimulation of lower airway and/or lungs, ha emodynamic responses to isoflurane administered after tracheal intubation w ere measured with or without endotracheal or intravenous administration of lidocaine. Methods: Seventy-two ASA physical status I patients, aged 21-50 yr, were ra ndomly allocated to one of four groups. After tracheal intubation, anaesthe sia was maintained with oxygen 100% and isoflurane 1.0% with controlled ven tilation. 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 mi lidocaine 8% spray, an intra venous lidocaine group received pretreatment of 32 mg lidocaine iv, and an isoflurane 3% group received not pre-treatment. In a control group, inspire d isoflurane concentration was maintained at 1.0%. Heart rate, systolic blo od pressure and end-tidal isoflurane concentration were measured every minu te for IO min. Results: The rapid increase in isoflurane concentration increased heart rat e (25 +/- 12% increase from baseline; P < 0.05) but the increase was reduce d by endotracheal lidocaine (9 +/- 9%), but not by intravenous lidocaine (2 2 +/- 13%). The plasma concentration of lidocaine was lower in the endotrac heal lidocaine group (0.4 +/- 0.3 mu g.ml(-1)) than in the iv lidocaine gro up (1.5 +/- 0.2 mu g.ml(-1)). Conclusion: The isoflurane-induced tachycardia is reduced by pre-treatment with endotracheal lidocaine.