Several studies have been made in order to attenuate these haemodynamic response to laryngoscopy and intubation. Many drugs also have been used for the same purpose [3]. The techniques include topical anaesthesia of oropharynx (viscous lignocaine) laryngotracheal instillation of lignocaine just prior to intubation, intravenous lignocaine, adrenergic blocking drugs, (either alpha or beta blockers) vasodilators like hydrallazine, sodium nitroprusside, nitroglycerine, deep inhalational anaesthesia, intravenous opioids etc., No single agent has been established as the most Anaesthesia Section appropriate for this purpose. Among the recommended procedures, intravenous lidocaine or fentanyl appear to best fulfill the above mentioned criteria [2]. Lignocaine is a amide (-NHCO-) synthetic local anaesthetic. The use of lignocaine is well known in treatment of patients with ventricular dysarrthmias and as prophylaxis in treatment of ventricular tachyarrthmias especially in connection with myocardial infarction and mechanical irritation of cardia. The principal metabolic pathway of lignocaine is oxidative dealkalysation in the liver to monoethylglylcinexylidide followed by hydrolysis of this metabolite to xylidide. Monoethylglycinexylidide has approximately 80% of the activity of lignocaine for protection against cardiac dysarrythmias. Lignocaine prevents transmission of nerve impulse (conduction blockade) by inhibiting passage of sodium ions through ion selective sodium channels in nerve membrane [4]. The sodium channel itself is a specific receptor to lignocaine molecule. Fentanyl is a potent, synthetic narcotic analgesic with a rapid onset and short duration of action. It is extremely lipid soluble, has a low molecular weight and is a synthetic opioid agonist which is popularly used as intravenous analgesic supplement, component of inhalation anaesthesia, balanced anaesthesia and neurolept analgesia and also as a sole anaesthetic. It is 75 to 125 times more potent than morphine as an analgesic [5]. After intravenous administration, onset of effect is 1-2 minutes, and the duration is 1 hour. Consequently it has proved ideal for control of the short lived haemodynamic sequelae, associated with laryngoscopy and intubation.

Some studies note a response of intravenous lignocaine in blunt-ing rises in pulse, blood pressure, intracranial and intraocular pressure. Studies have discussed the possible mechanisms to account for these observations with IV lignocaine. These include a direct myocardial depressant effect, a peripheral vasodilating effect and finally an effect on synaptic transmission [8]. A review on “Prophylactic lidocaine use preintubation”. They said that a dose of prophylactic lidocaine of 1.5 mg/kg given intravenously 3 minutes before intubation is optimal. No studies document any harmful effects of prophylactic lidocaine given preintubation [15]. Wang et al., [16] reported most optimal time of administration of intravenous lidocaine to attenuate the increase of intraocular pressure seemed to be the space between 1-3 minutes before laryngoscopy and tracheal intubation. Wilson et al., [17] showed that irrespective of the timing of administration of injection of lignocaine 2, 3 or 4 minutes before tracheal intubation, there was a significant increase in heart rate of 21-26% in all groups. There was no significant increase in mean artrial pressure (MAP) in response to intubation in any group of patients given lignocaine before intubation, but in the placebo group, MAP increased by 19% compared to baseline values. Mollick et al., [18] observed that intravenous lignocaine with pethidine did attenuate the sympathetic responses to laryngoscopy and endotracheal intubation which came down to base line before 5 minute after intubation. But the group of patients which was treated only with lignocaine, their sympathetic responses did not come down to base line at 5 minute after laryngoscopy and endotracheal intubation. Similar to our observation Bachofen M [2] too reported that fentanyl showed a significant pressure-lowering action persisting over the whole observation period in all patients while no significant effect of lidocaine on the pressure response could be observed. Malde and Sarode [19] concluded that “ given 5 minutes prior to intubation, lignocaine (1.5 mg/kg) and fentanyl (2 µg/kg) both attenuated the rise in pulse rate, though fentanyl was better.