Tracheal intubation following laryngoscopy is associated with a sympathetic surge due to noxious stimulation, resulting in tachycardia and hypertension, which may be detrimental, especially in patients with cardiovascular or cerebrovascular comorbidities¹. Various pharmacological agents such as opioids, beta-blockers, and calcium channel blockers have been employed to mitigate these responses, but their effectiveness varies, and they are often associated with side effects².

Dexmedetomidine, a selective α2-adrenoceptor agonist, has gained attention for its sedative, analgesic, and sympatholytic properties³. By reducing central sympathetic outflow and enhancing vagal activity, dexmedetomidine can blunt cardiovascular responses to noxious stimuli without significant respiratory depression⁴. Its use in anesthesia induction and perioperative care has expanded in recent years⁵.

Previous studies have investigated the effectiveness of dexmedetomidine in attenuating haemodynamic changes during laryngoscopy and intubation⁶. Most of these studies have employed a dose of 1 μg/kg, administered over 10 minutes prior to induction, and have shown favorable outcomes in terms of stability of heart rate and blood pressure⁷. However, higher doses may also be associated with adverse effects such as bradycardia and hypotension⁸. Thus, there is growing interest in exploring lower doses that might achieve adequate haemodynamic control while minimizing side effects⁹.

In this context, we designed a comparative study to evaluate the efficacy of two different doses of dexmedetomidine—0.5 μg/kg and 1 μg/kg—for attenuating the haemodynamic response to laryngoscopy and tracheal intubation. We hypothesized that both doses would blunt the sympathetic response, but the higher dose might offer more profound attenuation. The primary endpoints included changes in heart rate, systolic and diastolic blood pressure, and mean arterial pressure at various peri-intubation time points.

This study aims to contribute to the optimization of dexmedetomidine dosing strategies in general anesthesia, particularly in settings requiring blunting of laryngoscopy-induced sympathetic responses.

This prospective, randomized, double-blind comparative study was conducted in the Department of Anesthesiology at a tertiary care hospital over six months.

Study Population:

Sixty adult patients aged 18–60 years of ASA physical status I or II, scheduled for elective surgeries under general anesthesia requiring endotracheal intubation, were enrolled.

Inclusion Criteria:

• Age 18–60 years
• ASA I or II
• Elective surgery under general anesthesia
• Informed consent provided

Exclusion Criteria:

• History of cardiovascular, renal, or hepatic disease
• Use of β-blockers, sedatives, or antihypertensives
• Anticipated difficult airway
• Allergy to study drug
• Pregnancy or lactation

Randomization and Grouping:

Patients were randomly allocated into two groups (n=30 each) using a computer-generated randomization table:

• Group A: Received dexmedetomidine 0.5 μg/kg diluted in 50 mL NS over 10 minutes
• Group B: Received dexmedetomidine 1 μg/kg in 50 mL NS over 10 minutes

Both groups received standard premedication and monitoring.

Anesthesia Protocol:

All patients received glycopyrrolate 0.2 mg IV and fentanyl 2 μg/kg IV before induction. Induction was with propofol 2 mg/kg and vecuronium 0.1 mg/kg. Intubation was performed 3 minutes after muscle relaxant administration.

Monitoring and Data Collection:

Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were recorded at:

• Baseline (T0)
• Post-drug infusion (T1)
• Immediately post-intubation (T2)
• 1 min (T3), 3 min (T4), 5 min (T5), and 10 min (T6) post-intubation

Statistical Analysis:

Data were analyzed using SPSS v22. Quantitative variables were compared using Student’s t-test, and categorical variables using Chi-square test. A p-value <0.05 was considered statistically significant

Table 1: Baseline Demographics

In table 1, Comparable Age between Group A (38.3 ± 8.2 years) and Group B (36.9 ± 7.5 years), p = 0.52. Distribution of Sex beteen Group A = 16 males, 14 females; Group B = 17 males, 13 females, p = 0.80. Whereas, Weight between Group A = 64.2 ± 6.1 kg; Group B = 63.5 ± 5.9 kg, p = 0.65.

Table 2: Heart Rate (beats/min)

In table 2, Group B (1 µg/kg) had a markedly lower rise in heart rate post-intubation. The sympathetic surge seen in Group A was significantly attenuated in Group B, suggesting a stronger sympatholytic effect at the higher dose.

Table 3: Systolic Blood Pressure (mmHg)

Table 4: Diastolic Blood Pressure (mmHg)

Table 5: Mean Arterial Pressure (MAP) (mmHg)

In table 5, MAP, a key indicator of perfusion, increased significantly post-intubation in Group A. Group B maintained lower and more stable MAP, affirming that 1 µg/kg is the more effective dose for pressor response suppression.

Table 6: Sedation Score (Ramsay Sedation Scale)

Endotracheal intubation following laryngoscopy provokes a pronounced sympathetic response, manifesting as tachycardia and hypertension. While transient in healthy individuals, these haemodynamic surges can be detrimental in patients with cardiovascular disease, leading to myocardial ischemia, arrhythmias, or cerebrovascular accidents¹¹⁻¹². Consequently, blunting this reflex sympathetic activity has been a long-standing goal in anesthetic practice.

Dexmedetomidine, a selective α2-adrenergic agonist, offers a promising pharmacologic profile with sedative, anxiolytic, and sympatholytic properties, making it ideal for this purpose¹³. Its mechanism of action involves activation of central α2-receptors in the locus coeruleus, reducing norepinephrine release and sympathetic outflow¹⁴. The present study evaluates and compares two dosing regimens of dexmedetomidine—0.5 µg/kg and 1 µg/kg—in blunting the haemodynamic response to laryngoscopy and intubation.

Our results show that while both doses attenuate the haemodynamic responses, 1 µg/kg dexmedetomidine was significantly more effective. Group B (1 µg/kg) consistently showed lower heart rates and blood pressure readings at all post-intubation time points when compared with Group A (0.5 µg/kg), with statistical significance (p < 0.001). This is in concordance with the findings of Scheinin et al., who observed effective suppression of catecholamine release and cardiovascular responses at the 1 µg/kg dose¹⁵.

In a study by Talke et al., the dose-dependent suppression of sympathetic tone with dexmedetomidine was well-demonstrated¹⁶. Similar findings were also reported by Bajwa et al., who highlighted that 1 µg/kg dexmedetomidine not only attenuated the stress response but also reduced the requirement for other anesthetic agents during induction¹⁷. Our study reinforces these findings by showing that the higher dose better mitigates sympathetic activation without leading to serious bradycardia or hypotension.

Rao et al. compared 0.5 and 1 µg/kg dexmedetomidine in elective surgeries and found that although both doses attenuated HR and MAP, the 1 µg/kg dose provided more stable haemodynamics throughout the peri-intubation period¹⁸. Similarly, our results indicate that 1 µg/kg achieves a more favorable balance of sympathetic suppression and clinical safety.

An additional finding in our study was a higher Ramsay sedation score in Group B. This deeper sedation may contribute indirectly to reduced sympathetic tone. However, the sedation was not excessive and did not delay recovery or cause respiratory depression. This aligns with the findings of Ebert et al., who showed that dexmedetomidine offers cooperative sedation without significant respiratory compromise¹⁹.

A major strength of our study lies in its double-blind, randomized design and standardized anesthesia protocol, minimizing potential bias. However, the relatively small sample size and exclusion of high-risk patients (e.g., ASA III/IV, elderly) are limitations. Future studies with larger, more diverse populations and additional variables like stress hormone levels (cortisol, catecholamines) could offer deeper mechanistic insights.

Dexmedetomidine at a dose of 1 μg/kg is significantly more effective than 0.5 μg/kg in attenuating the haemodynamic response to laryngoscopy and intubation. It maintains stable heart rate and blood pressure post-intubation, with an acceptable sedation profile. This supports its use as a safe pre-induction adjunct in anesthesia practice. The superior efficacy, acceptable sedation, and lack of significant adverse effects make it a valuable adjunct to modern anesthetic practice.

1. Bhana N, McClellan KJ. Dexmedetomidine: a review of its pharmacology and clinical applications. CNS Drugs. 2000;14(2):111-24.
2. Arain SR, Ruehlow RM, Uhrich TD, Ebert TJ. The efficacy of dexmedetomidine versus morphine for postoperative analgesia after major inpatient surgery. Anesth Analg. 2004;98(1):153-8.
3. Kamibayashi T, Maze M. Clinical uses of alpha2-adrenergic agonists. Anesthesiology. 2000;93(5):1345-9.
4. Paris A, Tonner PH. Dexmedetomidine in anaesthesia. Curr Opin Anaesthesiol. 2005;18(4):412-8.
5. Venn RM, Bryant A, Hall GM, Grounds RM. Effects of dexmedetomidine on cardiovascular stability after coronary artery bypass surgery. Crit Care. 2000;4(5):302-8.
6. Gupta K, Bansal P, Gupta PK, Singh A. Dexmedetomidine as an adjunct in general anesthesia: A review. J Anaesthesiol Clin Pharmacol. 2011;27(3):339-42.
7. Chrysostomou C, Schulman SR, Herrera Castellanos M, Cofer BE, Mitra S, Hossain MM, et al. A phase II/III multicenter, safety, efficacy, and pharmacokinetic study of dexmedetomidine in pediatric patients. Anesth Analg. 2008;107(2):393-402.
8. Keniya VM, Ladi SD, Naphade RW. Dexmedetomidine attenuates sympathoadrenal response to tracheal intubation and reduces the requirement of thiopentone and opioids. Indian J Anaesth. 2011;55(4):347-52.
9. Tufanogullari B, White PF, Peixoto MP, Adams DJ, LaMantia J, Huber PJ. Dexmedetomidine infusion during laparoscopic bariatric surgery: the effect on recovery outcome variables. Anesth Analg. 2008;106(6):1741-8.
10. Venn RM, Hell J, Grounds RM. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care. 2000;4(5):302-8.
11. Hall JE, Uhrich TD, Ebert TJ. Sedative, amnestic, and analgesic properties of dexmedetomidine infusions. Anesth Analg. 2000;90(2):434-8.
12. Menda F, Köner O, Sayin M, Türe H, Imer P, Aykac B. Dexmedetomidine as an adjunct to anesthetic induction to attenuate hemodynamic response to endotracheal intubation in patients undergoing fast-track CABG. Ann Card Anaesth. 2010;13(1):16-21.
13. Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg. 2000;90(3):699-705.
14. Bhana N, Goa KL, McClellan KJ. Dexmedetomidine. Drugs. 2000;59(2):263-8.
15. Scheinin B, Lindgren L, Randell T, Scheinin M, Scheinin H. Dexmedetomidine attenuates sympathoadrenal responses to tracheal intubation and reduces the need for thiopentone and preoperative fentanyl. Br J Anaesth. 1992;68(2):126-31.
16. Talke P, Chen R, Thomas B, Aggarwall A, Gottlieb A, Thorborg P. The hemodynamic and adrenergic effects of perioperative dexmedetomidine infusion after vascular surgery. Anesth Analg. 2000;90(4):834-9.
17. Bajwa SJ, Kaur J, Singh A, Parmar SS, Singh G, Kulshrestha A. Attenuation of pressor response and dose sparing of opioids and anaesthetics with pre-operative dexmedetomidine. Indian J Anaesth. 2012;56(2):123-8.
18. Rao B, Gopalakrishna K, Naik V, Kumar V, Narayana G. Comparative study of two doses of dexmedetomidine for attenuation of hemodynamic responses to laryngoscopy and intubation. J Clin Diagn Res. 2014;8(2):114-7.
19. Ebert TJ, Hall JE, Barney JA, Uhrich TD, Colinco MD. The effects of increasing plasma concentrations of dexmedetomidine in humans. Anesthesiology. 2000;93(2):382-94.