The hemodynamic responses to laryngoscopy and endotracheal intubation have been recognized since 1951.1In patients ranked ASA 1, laryngoscopy and intubation lead to an average increase in blood pressure of 40 to 50%, and a 20% increase in heart rate. These changes, which are greatest one minute after intubation, last for 5 to 10 min. They are due to sympathetic and adrenal stimulation, which may also result in some arrhythmias.2No single drug or technique is 100% efficient.3Since clonidine and lignocaine have been known to blunt sympathetic responses to laryngoscopy and endotracheal intubation, their efficacy has been compared.

Institutional ethical committee approval was taken for this prospective , randomised, double blind study. Written informed consent was obtained from the patients. The study was conducted in 60 subjects aged between 15–65 years, ASA I and II patients undergoing elective surgeries under General Anaesthesia. Patients with Diabetes, Hypertension, Cardiovascular, respiratory, or neurological disorders and patients on beta-blockers or calcium channel blockers were excluded.

All the patients included in the study was given tab. Alprazolam 0.5 mg and Tab. Pantoprazole 40 mg orally, on the night before surgery and was kept nil per oral 6 hours for solids and 2 hours for clear fluids before induction. On arrival to the operation theatre (O.T), intravenous(IV) access was taken using 18G intravenous cannula on the non-dominant hand and an infusion of normal saline was started. The patient was connected with the multi-parameter monitor, which records heart rate (HR), non- invasive measurements of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial presuure (MAP), continuous ECG monitoring and oxygen saturation (SpO2). The baseline systolic blood pressure, diastolic blood pressure, mean arterial pressure, heart rate and oxygen saturation were recorded. All the patient were pre-oxygenated with 100% oxygen for 3 minutes and pre-medicated with Inj. Midazolam (0.02 mg/kg body weight), Inj. Glycolpyrrolate (0.01 mg/kg bodyweight), Inj. fentanyl (1.5 mcg/kg body weight), Inj. Ondansetron (0.1mg/kg body weight) three minutes before induction. Group 1 was given intravenous Clonidine (2 microgram per kilogram) ten minutes before induction. Group 2 was given intravenous Lignocaine (1.5 milligram per kilogram) three minutes before intubation. Induction of general anaesthesia for all patients was done with Injection propofol 2mg/kg. This will be followed by an intubating dose of injection vecuronium bromide 0.1mg/kg. Patients then were bag and mask ventilated for three minutes. Endotracheal intubation was done using appropriate endotracheal tube cuffed. After confirming bilateral equal air entry, cuff inflated, tube fixed, connected to circuit and positive pressure ventilation will be continued. Recordings of HR, SBP, DBP, MAP and SPO2 were taken at basal (before premedication), after induction, at laryngoscopy and intubation and at 1 min, 5min, and 10 min post intubation.Anaesthesia was maintained with Oxygen (33%) + Nitrous oxide (66%) + volatile anesthetic (sevoflurane or isoflurane) and further neuromuscular blockade was maintained by vecuronium bromide at dose of 0.01mg/kg and IPPV. Adequacy of ventilation was monitored clinically and SpO2 monitoring

Table 1- Demography of the patients

Table 1 shows demographic data – age, BMI, gender and ASA grade which were comparable between Group 1 and Group 2.

Table 2: Comparison of heart rate

The patients in group 2 showed rise in HR at the time of intubation to 10 minutes after intubation. The highest HR recorded at the time of intubation was 87.80±13.60 in group 1 and 106.2±15.6 in group 2. There was a statistically significant difference (p value<0.05) in the heart rate from intubation to 10 minutes after intubation.

Table 3: Comparison of SBP

The baseline SBP in group 1 was 120.7±11.2 mm Hg, which dropped to102.1±21.4 mm Hg with induction and later increased to 115.2±17.6 mm Hg at intubation and was the maximum SBP recorded following which there was gradual fall and remained lesser than baseline even after 10 minutes. In group 2, baseline SBP was 117.9±9.6 mm Hg which dropped to 108.8±10.5 mm Hg with induction and increased at intubation to 133.1±16.2 mm Hg which was the maximum SBP recorded and gradually decreased to 107.8±12.6 mm Hg after 10 minutes. The rise in SBP in group 1 were less as compared to group 2 and was statistically significant from the time of intubation till 10 minutes after intubation.

Table 4:  Comparison of DBP

The baseline DBP in group 1 was 81±9 mm Hg, which dropped to 70±12 mm Hg with induction and later increased to 80±15 mm Hg at intubation and was the maximum SBP recorded following which there was gradual fall and remained lesser than baseline even after 10 minutes. In group 2, baseline DBP was 78±8 mm Hg which dropped to 74±11 mm Hg with induction and increased at intubation to 95±17 mm Hg which was the maximum DBP recorded and gradually decreased to 73.3±13.0 mm Hg after 10 minutes. Diastolic pressures were less elevated in group 1 compared to group 2 from time of intubation to 10 minutes after intubation and it was statistically significant

Table 5: Comparison of MAP

The baseline MAP in group 1 was 94±10 mm Hg and decreased at induction to 81±15 mm Hg. With intubation it rose to 92±16 mm Hg and gradually decreased and at 10 minutes it was 77±11 mm Hg. In group 2, baseline MAP was 91±8 mm Hg and it decreased with induction to 85±11 mm Hg and increased at intubation to 108±16 mm Hg and finally settled down to 85±13 mm Hg.Mean arterial pressure too was better controlled in group 2 compared to group 1 from the time of intubation to 10 minutes after intubation. The difference in MAP between the two groups was statistically significant from the time of intubation till 10 minutes after intubation (p value<0.05).

Clonidine is a α2 adrenergic agonist, stimulates α2A subtype of α2 adrenergic receptors in the brainstem resulting in a reduction in sympathetic outflow from central nervous system thus causing lowering of arterial pressure by an effect on both cardiac output and peripheral resistance. By its central sympatholytic action, it tends to attenuate the hemodynamic response to any surgical nociceptive stimulus and to improve overall perianesthetic cardiovascular stability.4

Lignocaine is a local anaesthetic of the amino amide type. Tam et al, found that there was complete attenuation (defined as a lack of significant increase) in heart rate and arterial pressure changes when lignocaine 1.5 mg/kg was given 3 minutes before tracheal intubation.5 Advantage of IV lignocaine is that it depresses autonomic nervous system and in addition has anti arrhythmic properties.

In this study, we compared the efficacy of intravenous clonidine and intravenous lignocaine for intubation response attenuation.In our study, the heart rate increased by 2(3%) beats above baseline in group 1 whereas it increased by 15(26.5%) beats in group 2 at intubation. This difference was significant statistically(p value<0.001). Thereafter too, there was statistically significant difference in the heart rate at 1,5 and 10 minutesbetween the two groups and clonidine was better at controlling the heart rate.

 In Group 1, SBP increase during intubation was minimal and did not reach the baseline SBP as well. But in group 2, the rise in SBP at intubation was 12.9 % more than the baseline SBP. This difference was statistically significant too.(p value <0.01).Group 1 had less rise in diastolic blood pressure at intubation and remained much below the baseline DBP whereas group 2 reported an increase of 21.8% above baseline DBP which  was statistically significant(p value<0.01).Mean arterial pressure too was maintained better in group 1 with it being 2.1% lesser than the baseline but in group 2, there was 18.7% increase above baseline (p value<0.01).Even at 1, 5 and 10 minutes, group 1 differed from group 2 showing a sustained attenuation of pressor response with p value<0.05. The SBP, DBP and MAP was well controlled inclonidine group compared to lignocaine group from the time of intubation till 10 minutes after intubation with a p value<0.05.

Similar to our study, Miller et al6, Helfman et al7, Feng et al8 and Singh et al9 found that lignocaine was not very effective in controlling acute hemodynamic response to laryngoscopy and intubation. Clonidine was found to be excellent in attenuating intubation response by Zolunardoet al10 and Batra et al1.

Intravenous Clonidine 1µg/kg given 10 minutes before induction was very effective in attenuating the hemodynamic response following laryngoscopy and intubation compared to intravenous lignocaine 1.5 mg/kg given 3 minutes before intubation.

1. King BD, Harris LC, Greifenstein FE, Elder JD, Dripps RD. Reflex circulatory responses to direct laryngoscopy and tracheal intubation performed during  generalanesthesia. The Journal of the American Society of Anesthesiologists. 1951 Sep 1;12(5):556-66.

2. Bruder N, Ortega D, Granthil C. Consequences and prevention methods of hemodynamic changes during laryngoscopy and intratracheal intubation. InAnnalesfrancaisesd'anesthesieet de reanimation 1992 Jan 1 (Vol. 11, No. 1, pp. 57-71).
3. Vincent JC. Principles of anesthesiology: General and regional anaesthesia. 3^rd Vols I and II. Philadelphia: Lea and Fabiger; 1993.
4. Westfall TC, Westfall DP. Adrenergic agonist and antagonist. In: Bruton LL, Lazo JS, Parker JS, editors. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 11th ed. USA: McGraw-Hill; 2006. p. 255-6.

1. Tam S, Chung F, Campbell M. Intravenous lidocaine: optimal time of injection before tracheal intubation. Anesthesia and Analgesia. 1987 Oct;66(10):1036-8.

6. Miller CD, Warren SJ. Lignocaine fails to attenuate the cardiovascular responses to laryngoscopy and intubation. Br J Anaesth 1990; 65: 216-219.
7. Helfman SM, Gold MI, DeLisser EA, Everard A, Herrinton CA. Which drug prevents tachycardia and hypertension associated with tracheal intubation: Lidocaine, fentanyl, esmolol? AnaesthAnalg 1991Apr; 72(4): 482-6.
8. Feng CK, Chan KH, Liu KN. A comparison of lidocaine, Fentanyl and Esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. ActaAnaesthesiol Sin 1996 Sep; 34(3): 172.
9. Singh H, Viehitvejpaisal P, Gaines GY, White PF. Comparative effects of Lidocaine, Esmolol and Nitroglycerine in modifying the haemodynamic response to laryngoscopy and intubation. J ClinAnaesth 1995 Feb; 7(1): 5-8.
10. Zalunardo MP, Zollinger A. Comparison of intravenous clonidine and esmolol for cardiovascular stress protection during induction of anaesthesia. Der Anaesthesist. 2001 Jan;50(1):21-5.
11. Batra YK, Indu B, Puri GD. Attenuation of pulse rate and Blood pressure response to laryngoscopy and intubation by clonidine. Clin pharmacology. Toxicol.1988 Jul;26(7):360-63.