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ORIGINAL ARTICLE
Year : 2015  |  Volume : 4  |  Issue : 2  |  Page : 86-90

Comparison of intravenous lignocaine and intravenous dexmedetomidine for attenuation of hemodynamic stress response to laryngoscopy and endotracheal intubation


Department of Anaesthesiology and Critical Care, Kurnool Medical College and Government General Hospital, Kurnool, Andhra Pradesh, India

Date of Web Publication12-Jun-2015

Correspondence Address:
Dr. Saya Raghavendra Prasad
Department of Anaesthesiology and Critical Care, Kurnool Medical College and Government General Hospital, Kurnool - 518 002, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2277-8632.158579

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  Abstract 

Context: Direct laryngoscopy and endotracheal intubation following induction of anesthesia is almost always associated with hemodynamic stress response due to reflex sympathoadrenal discharge.
Aim: Aim of our study was to compare the efficacy of lignocaine and dexmedetomidine in attenuating the hemodynamic response to laryngoscopy and intubation.
Settings and Design: The present prospective randomized study was carried out in a tertiary care teaching hospital. A total of 100 American Society of Anesthesiologist physical status I and II patients posted for elective surgery under general anesthesia were enrolled in the study. Patients were randomly divided into two groups, group L (lignocaine group) and group D (dexmedetomidine group) with 50 patients in each group.
Materials and Methods: Group L received 1.5 mg/kg of lignocaine intravenous (IV) and group D received 1 mcg/kg of dexmedetomidine as IV infusion. Thiopentone was given until eyelash reflex disappeared, and intubation was facilitated with succinylcholine. Anesthesia was maintained with 33:66 oxygen: Nitrous oxide, isoflurane, and vecuronium. Hemodynamic parameters were recorded during the basal period, preinduction, after induction, during intubation, 1 min, 3 min, 5 min, and 10 min after intubation.
Statistical Analysis Used: Data were analyzed using Graphpad Prism Software version 6.03 (Graphpad Software Inc., USA). P < 0.05 was considered as statistically significant.
Results: Maximum increase in heart rate was around 38% in group L and 10% in group D (P = 0.000). Maximum increase in mean arterial pressure was 22% in group L and 6% in group D (P = 0.000). Thiopentone dose requirement was 19% less in group D compared to group L (P < 0.001).
Conclusion: Dexmedetomidine attenuates the hemodynamic stress response to laryngoscopy and intubation more effectively compared with lignocaine without any deleterious effects. Furthermore, dexmedetomidine decreases dose of thiopentone for induction of anesthesia.

Keywords: Dexmedetomidine, hemodynamic stress response, intubation, laryngoscopy, lignocaine


How to cite this article:
Prasad SR, Matam UM, Ojili GP. Comparison of intravenous lignocaine and intravenous dexmedetomidine for attenuation of hemodynamic stress response to laryngoscopy and endotracheal intubation. J NTR Univ Health Sci 2015;4:86-90

How to cite this URL:
Prasad SR, Matam UM, Ojili GP. Comparison of intravenous lignocaine and intravenous dexmedetomidine for attenuation of hemodynamic stress response to laryngoscopy and endotracheal intubation. J NTR Univ Health Sci [serial online] 2015 [cited 2019 Oct 21];4:86-90. Available from: http://www.jdrntruhs.org/text.asp?2015/4/2/86/158579


  Introduction Top


Direct laryngoscopy and endotracheal intubation following induction of anesthesia is almost always associated with hemodynamic changes due to reflex sympathetic discharge. This increased sympathoadrenal activity may result in hypertension, tachycardia, and arrhythmias. [1],[2],[3] Transitory hypertension and tachycardia may predispose to the development of pulmonary edema, [4] and myocardial insufficiency. Various agents such as opioids, [5] beta adrenergic blockers, [6],[7] calcium channel antagonists, [8] and clonidine [9] have been used to blunt the hemodynamic response to laryngoscopy and intubation, but they all had limitations.

Intravenous (IV) lignocaine is one of the oldest, cheapest and most easily available drug used for attenuation of hemodynamic response to laryngoscopy and intubation. [10],[11],[12],[13],[14],[15]

Dexmedetomidine is a new alpha-2 adrenergic agonist having 8-times more affinity for alpha-2 adrenoceptors as compared with clonidine. Pretreatment with dexmedetomidine attenuates hemodynamic response to laryngoscopy and intubation. [16],[17],[18],[19],[20],[21]

The present study was undertaken to compare the efficacy of 1.5 mg/kg of IV lignocaine and 1 mcg/kg of dexmedetomidine IV infusion in attenuating the hemodynamic response to laryngoscopy and intubation.


  Materials and Methods Top


After obtaining institutional review board approval and informed written consent from the patients, the present prospective randomized study was carried out in a tertiary care teaching hospital. A total of 100 American Society of Anesthesiologists (ASA) physical status I and II patients aged between 18 and 60 years undergoing elective surgery were enrolled in the study. Patients with hypertension, cardiac, coronary, renal, hepatic, cerebral diseases, and peripheral vascular diseases, bradycardia, obese patients, anticipated difficult airway, pregnant, and nursing women, history suggestive of sensitivity to drugs used during the study and in whom intubation attempts lasted longer than 15 s were excluded from the study.

Patients were randomly divided into two groups with the help of computer-generated coded envelopes, group L (lignocaine group) and group D (dexmedetomidine group) with 50 patients in each group. All patients included in the study were premedicated with tablet alprazolam 0.5 mg and tablet ranitidine 150 mg orally at bedtime the night before surgery. They were kept nil orally 10 pm onwards on the previous night.

On arrival of the patient in the operating room baseline parameters such as heart rate (HR), mean arterial pressure (MAP), respiratory rate, and oxygen saturation (SpO 2 ) were recorded. All patients were prehydrated with 500 ml of Ringer's lactate solution.

Group L received 100 ml of normal saline 20 min preoperatively over a period of 10 min, and the infusion was completed 10 min before induction and 1.5 mg/kg of lignocaine was administered IV 3 min before intubation. Group D received dexmedetomidine 1 mcg/kg diluted in 100 ml of normal saline IV over a period of 10 min, and the infusion was completed 10 min before induction.

All the patients were premedicated with injection glycopyrrolate 0.004 mg/kg IV, injection ondansetron 0.08 mg/kg IV, injection midazolam 0.02 mg/kg IV, and injection tramadol 1 mg/kg IV before preoxygenation. Ramsay sedation scale score was employed for assessing the sedation before induction of anesthesia in both the groups (1 = anxious, agitated and restless, 2 = awake, cooperative, tranquil and oriented, 3 = responds to verbal commands, 4 = brisk response to loud noise, 5 = sluggish response to loud noise, 6 = no response to loud noise).

After preoxygenation, all patients were induced with injection thiopentone as 2.5% solution IV till loss of the eye lash reflex occurred. Endotracheal intubation was facilitated with 2 mg/kg of succinylcholine given IV 1 min prior to laryngoscopy and intubation. Laryngoscopy was performed using Macintosh laryngoscope, trachea intubated with appropriate size endotracheal tube, and connected to closed circuit. After confirmation of bilateral equal air entry, endotracheal tube was fixed.

No surgical or any other stimulus was applied during 10 min of study period and vecuronium was the only additional drug given during this period. Anesthesia was maintained using 33% oxygen and 66% nitrous oxide with isoflurane and vecuronium. At the end of the procedure, patients were reversed with an injection neostigmine 0.05 mg/kg IV and injection glycopyrolate 0.08 mg/kg IV. Patients were extubated when they regained reflexes and consciousness.

Hemodynamic parameters were recorded during the basal period, preinduction, after induction, during intubation, 1 min, 3 min, 5 min, and 10 min after intubation.

Statistical analysis

Data were analyzed using Graphpad Prism Software version 6.03 (Graphpad Software Inc., USA). Quantitative data was analyzed using Student's t-test and qualitative data were analyzed using Fisher's exact test. P < 0.05 was considered as statistically significant and P < 0.001 was considered to be statistically highly significant.


  Results Top


All the data was expressed as mean and standard deviation for continuous data and number and percent for categorical data. The two groups were comparable in patient characteristics with respect to age, weight, gender, and ASA physical status (P > 0.05) [Table 1]. Surgical procedures in which the study was carried are shown in [Table 1].
Table 1: Demographic Data and Type of Surgeries

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Preinduction changes in HR and MAP were insignificant in group L. Infusion of dexmedetomidine was well tolerated in all patients in group D. Ten minutes after infusion of dexmedetomidine, there was around 11% fall in HR and 9% fall in MAP when compared to baseline. Compared to group L, fall in HR and MAP was highly significant in group D (P = 0.000) [Table 2] and [Table 3]. None of the patients in our study had respiratory depression, fall in SpO 2 or bradycardia.
Table 2: Comparison of Mean HR (Beats/Min) In Both Groups at Various Intervals

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Table 3: Comparison of Mean Map (MMHG) In Both Groups at Various Intervals

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About 100% of patients in group L were awake, calm, cooperative and tranquil (sedation score 2), while in group D 96% of patients were arousable to verbal commands (sedation score 3) and 4% of patients responded briskly to loud noise (sedation score 4) [Table 4]. The mean induction dose of injection thiopentone in group L was 283.4 ± 22.6 mg, while it was 229 ± 22.02 mg in group D. The decrease in the dose requirement was by 19% in group D as compared to group L (P < 0.001) [Figure 1].
Table 4: Ramsay Sedation Scale Score

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Figure 1: Mean induction dose of injection thiopentone (mg) in group L and group D

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Increase in HR and MAP with laryngoscopy and intubation was observed in both the groups. Increase in HR and MAP was maximum immediately after intubation in both the groups when compared to baseline. Maximum increase in HR was around 38% in group L and 10% in group D when compared to baseline, and the difference was statistically highly significant (P = 0.000) [Table 2]. Maximum increase in MAP was 22% in group L and 6% in group D when compared to baseline, and the difference was statistically highly significant (P = 0.000) [Table 3].


  Discussion Top


Laryngoscopy and endotracheal intubation are considered as the most critical events during general anesthesia as they provoke transient but marked sympathoadrenal response manifesting as hypertension and tachycardia. [1],[2],[3] Many drugs have been tried by various authors for blunting hemodynamic responses to laryngoscopy and intubation [6],[7],[8],[9] but all such maneuvers had their own limitations.

Lignocaine was used in several studies for attenuation of the stress response. [10],[11],[12],[13],[14],[15] Lignocaine is one of the cheapest and safest drugs used in many centers to attenuate stress response to intubation.

Alpha-2 adrenergic drugs, such as clonidine or dexmedetomidine, attenuate these potentially harmful cardiovascular reactions during laryngoscopy and intubation. Dexmedetomidine is the new alpha-2 agonist having 8-times more affinity for alpha-2 adrenoceptors as compared with clonidine. Dexmedetomidine offers a unique pharmacological profile with sedation, sympatholysis, analgesia, opioid and anesthetic sparing effect, cardiovascular stability and with great advantage to avoid respiratory depression. [22],[23],[24],[25],[26]

The dose of lignocaine used in our study was 1.5 mg/kg IV given 3 min before intubation. Several authors [10],[11],[15] have concluded that 1.5 mg/kg of lignocaine suppresses stress response to intubation when given 3 min before intubation.

The dose of dexmedetomidine used in our study was 1 mcg/kg diluted in 100 ml of normal saline and infused over 10 min. Several authors [16],[17],[18],[19],[20],[21] have used 0.5-1 mcg/kg of dexmedetomidine to attenuate stress response to intubation.

Following infusion of dexmedetomidine, there was 11% reduction in HR and 9% reduction in MAP and the observations are similar to the observations of other studies and can be explained on the basis of decreased central nervous system sympathetic activity. [16],[17],[20],[27] Few authors [18],[21] noted a significant fall in HR in the dexmedetomidine group and an insignificant fall in MAP.

All patients in group L had sedation score 2 in preinduction period. This was due to injection midazolam and injection tramadol used as premedication. Most of the patients in group D had sedation score 3 (responding to verbal commands). None of the patients in group D had respiratory depression or fall in SpO2 . Several authors [17],[20],[22],[28] have reported that dexmedetomine infusion produces sedation which mimics normal sleep, patients are arousable to verbal commands, and it lacks respiratory depression. These properties make dexmedetomidine a better choice of sedation for awake fibreoptic intubation, intensive care unit, postanesthesia care unit, magnetic resonance imaging and awake craniotomy. [25]

The dose of thiopentone required for induction of anesthesia was significantly lower in group D compared to group L. Keniya et al., [17] Scheinin et al., [19] and Bajwa et al. [20] reported decreased thiopentone requirement for induction of anesthesia in the dexmedetomidine group.

Lignocaine did not effectively attenuate hemodynamic response to laryngoscopy and intubation. Few authors [12],[14] reported that the lignocaine fails to attenuate hemodynamic response, and our observations are in accordance with them.

Compared to lignocaine, dexmedetomidine at a dose of 1 mcg/kg significantly attenuated hemodynamic response to laryngoscopy and intubation but could not obtund it completely. Several authors [16],[17],[18],[19],[20],[21] reported that dexmedetomidine at a dose of 0.5-1 μg/kg significantly attenuated hemodynamic response to intubation but did not obtund it completely, and our observations are in accordance with them.

None of the patients had bradycardia or hypotension requiring intervention in group D. Dexmedetomidine was administered as an infusion over 10 min to prevent bradycardia and hypotension associated with a bolus dose. [26]

Limitation of our study was that the effect was not seen in hypertensive and cardiac patients. It will be more useful to study in high-risk hypertensive and cardiac patients which we could not study as we did not have invasive blood pressure monitoring and advanced cardiac setup in our institute. Also plasma catecholamine levels, which is an objective means of measuring hemodynamic stress response was not measured in our study.


  Conclusion Top


Dexmedetomidine 1 mcg/kg IV as 10 min infusion attenuates the hemodynamic stress response to laryngoscopy and intubation more effectively compared to lignocaine 1.5 mg/kg IV without any deleterious effects. Furthermore, dexmedetomidine decreases dose of thiopentone for induction of anesthesia.

 
  References Top

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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