Comparison between intravenous and nebulised lignocaine for haemodynamic response to laryngoscopy and intubation

Several studies have been made in order to attenuate thesehaemodynamic response to laryngoscopy and intubation. Many drugs also have beenused for the same purpose [3]. The techniques include topical anaesthesia oforopharynx (viscous lignocaine) laryngotracheal instillation of lignocaine justprior to intubation, intravenous lignocaine, adrenergic blocking drugs, (eitheralpha or beta blockers) vasodilators like hydrallazine, sodium nitroprusside,nitroglycerine, deep inhalational anaesthesia, intravenous opioids etc., Nosingle agent has been established as the most Anaesthesia Section appropriatefor this purpose. Among the recommended procedures, intravenous lidocaine orfentanyl appear to best fulfill the above mentioned criteria [2]. Lignocaine isa amide (-NHCO-) synthetic local anaesthetic. The use of lignocaine is wellknown in treatment of patients with ventricular dysarrthmias and as prophylaxisin treatment of ventricular tachyarrthmias especially in connection withmyocardial infarction and mechanical irritation of cardia. The principalmetabolic pathway of lignocaine is oxidative dealkalysation in the liver tomonoethylglylcinexylidide followed by hydrolysis of this metabolite to xylidide.Monoethylglycinexylidide has approximately 80% of the activity of lignocainefor protection against cardiac dysarrythmias. Lignocaine prevents transmissionof nerve impulse (conduction blockade) by inhibiting passage of sodium ionsthrough ion selective sodium channels in nerve membrane [4]. The sodium channelitself 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 syntheticopioid agonist which is popularly used as intravenous analgesic supplement,component of inhalation anaesthesia, balanced anaesthesia and neuroleptanalgesia and also as a sole anaesthetic. It is 75 to 125 times more potentthan morphine as an analgesic [5]. After intravenous administration, onset ofeffect is 1-2 minutes, and the duration is 1 hour. Consequently it has provedideal for control of the short lived haemodynamic sequelae, associated withlaryngoscopy and intubation.

Some studies note a response of intravenous lignocaine inblunt-ing rises in pulse, blood pressure, intracranial and intraocularpressure. Studies have discussed the possible mechanisms to account for theseobservations with IV lignocaine. These include a direct myocardial depressanteffect, a peripheral vasodilating effect and finally an effect on synaptictransmission [8]. A review on “Prophylactic lidocaine use preintubationâ€. Theysaid that a dose of prophylactic lidocaine of 1.5 mg/kg given intravenously 3minutes before intubation is optimal. No studies document any harmful effectsof prophylactic lidocaine given preintubation [15]. Wang et al., [16] reportedmost optimal time of administration of intravenous lidocaine to attenuate theincrease of intraocular pressure seemed to be the space between 1-3 minutesbefore laryngoscopy and tracheal intubation. Wilson et al., [17] showed thatirrespective of the timing of administration of injection of lignocaine 2, 3 or4 minutes before tracheal intubation, there was a significant increase in heartrate of 21-26% in all groups. There was no significant increase in mean artrialpressure (MAP) in response to intubation in any group of patients givenlignocaine before intubation, but in the placebo group, MAP increased by 19%compared to baseline values. Mollick et al., [18] observed that intravenouslignocaine with pethidine did attenuate the sympathetic responses tolaryngoscopy and endotracheal intubation which came down to base line before 5minute after intubation. But the group of patients which was treated only withlignocaine, their sympathetic responses did not come down to base line at 5minute after laryngoscopy and endotracheal intubation. Similar to ourobservation Bachofen M [2] too reported that fentanyl showed a significantpressure-lowering action persisting over the whole observation period in allpatients while no significant effect of lidocaine on the pressure responsecould be observed. Malde and Sarode [19] concluded that “ given 5 minutes priorto intubation, lignocaine (1.5 mg/kg) and fentanyl (2 µg/kg) both attenuatedthe rise in pulse rate, though fentanyl was better.