Direct laryngoscopy and tracheal intubation are routinely performed during general anesthesia but are often accompanied by marked hemodynamic disturbances due to reflex sympathetic activation [1]. These responses manifest as tachycardia, hypertension, and arrhythmias, which may lead to complications such as myocardial ischemia, pulmonary edema, or stroke in at-risk individuals [1]. Several pharmacological agents, including opioids, calcium channel blockers, lignocaine, α-agonists, and β-blockers, have been evaluated to mitigate this response, each with inherent limitations [2]. Esmolol, an ultra-short acting, cardioselective β1-adrenergic blocker, is frequently used to control tachycardia during intubation due to its rapid onset and short duration of action [3,4]. In contrast, Dexmedetomidine, a highly selective α2-adrenergic agonist, exerts sympatholytic, sedative, and analgesic effects, attenuating cardiovascular responses without significant respiratory depression [5,6]. Studies have indicated its efficacy in reducing perioperative hemodynamic fluctuations [7]. Given the limited comparative evidence on the relative efficacy of Esmolol and Dexmedetomidine, this study aims to evaluate and compare their ability to blunt the pressor response to laryngoscopy and endotracheal intubation, while also assessing adverse events such as hypotension and bradycardia.

Study Design and Setting This prospective, randomized, interventional study was conducted in the Department of Anesthesiology at Nayati Medicity, Mathura, and Paras Hospital, Gurugram, from December 2019 to May 2021. Sample Size and Randomization Eighty ASA I–II patients (18–65 years) undergoing elective non-cardiac surgery were randomized into two groups (n=40 each) using sealed envelopes: • Group D: Dexmedetomidine 0.75 μg/kg infused over 10 minutes, 2 minutes prior to induction. • Group E: Esmolol 1 mg/kg infused over 10 minutes, 2 minutes prior to induction. Sample size was calculated for 80% power and 5% significance to detect a 20% reduction in hemodynamic response, based on pilot data and prior studies [47,48]. Inclusion/Exclusion Criteria Inclusion: ASA I–II, elective surgery, age 18–65 years. Exclusion: Patient refusal, anticipated difficult airway, intubation >30s/multiple attempts, baseline HR <60 bpm, drug allergy, reactive airway disease, or vasopressor use. Anesthesia Protocol Patients were premedicated with oral alprazolam (0.5 mg) and ranitidine (150 mg). Baseline vitals (T1) were recorded. IV midazolam (0.05 mg/kg) and glycopyrrolate (0.2 mg) were given 30 minutes pre-induction. Preloading with 10 mL/kg normal saline was done. Induction included propofol 2 mg/kg, fentanyl 1.5 μg/kg, and atracurium 0.6 mg/kg, followed by 3 minutes of mask ventilation with 100% oxygen. Laryngoscopy was performed using a Macintosh blade, and anesthesia was maintained with nitrous oxide (66%) and oxygen (33%). Hemodynamic Monitoring HR, SAP, DAP, and MAP were recorded: • Before drug administration (T2), • Pre-laryngoscopy (T3), • During laryngoscopy/intubation (T4), • At 1 (T5), 3 (T6), and 5 (T7) minutes post-intubation. Adverse Events Hypotension was defined as MAP decrease >20% from baseline; bradycardia as HR <60/min. Statistical Analysis Data were analyzed using SPSS v20. Continuous variables were expressed as mean ± SD, and comparisons were performed using Student’s t-test, paired t-test, or Chi-square test. A p value <0.05 was considered significant.

A total of 80 patients were randomized into two groups: Group D (Dexmedetomidine, n=40) and Group E (Esmolol, n=40). The age of participants ranged from 30 to 60 years, and both sexes were equally represented. No adverse effects or complications were observed in either group throughout the study. The demographic characteristics and baseline hemodynamic parameters (HR, SAP, DAP, and MAP) were comparable between the two groups, with no statistically significant differences (P>0.05). Baseline Parameters Table 1: Baseline Parameters of Both Groups Parameters Group Mean Std. Deviation t value P value HR D 79.60 7.76 0.128 0.899 E 79.40 6.17 SAP D 123.40 11.20 -0.323 0.748 E 124.18 10.24 DAP D 77.90 8.80 -0.477 0.635 E 78.80 8.07 MAP D 92.99 9.11 -0.441 0.661 E 93.83 7.93 Unpaired‘t’ test applied. P<0.05 was considered statistically significant. The baseline HR, SAP, DAP, and MAP values were statistically similar between Group D and Group E, confirming the comparability of both groups prior to intervention. Heart Rate (HR) Changes Table 2: Heart Rate at Different Time Intervals in Esmolol Group (E) Time Interval Mean SD t value P value Baseline 79.40 6.17 Before study drug 84.28 8.65 -5.544, df=39 0.001* Pre-laryngoscopy 82.15 6.60 -3.931, df=39 0.001* During laryngoscopy & intub. 92.05 8.69 -9.414, df=39 0.001* 1 min after intubation 98.98 10.46 -12.262, df=39 0.001* 3 min after intubation 99.25 12.41 -9.583, df=39 0.001* 5 min after intubation 99.80 9.63 -12.746, df=39 0.001* In Group E, HR increased significantly during and after intubation, peaking at 99.80 ± 9.63 at 5 minutes compared to baseline (P<0.05). Table 3: Heart Rate at Different Time Intervals in Dexmedetomidine Group (D) Time Interval Mean SD t value P value Baseline 79.60 7.76 Before study drug 81.40 8.43 -1.313, df=39 0.197, NS Pre-laryngoscopy 77.28 7.90 1.515, df=39 0.138, NS During laryngoscopy & intub. 84.35 11.09 -2.113, df=39 0.041* 1 min after intubation 88.33 11.80 -3.489, df=39 0.001* 3 min after intubation 84.10 11.30 -1.904, df=39 0.064, NS 5 min after intubation 82.75 10.86 -1.367, df=39 0.179, NS In Group D, HR peaked at 1 minute post-intubation (88.33 ± 11.80) but returned to near-baseline values within 3–5 minutes (P>0.05 for later time points). Systolic Arterial Pressure (SAP) Changes Table 4: SAP at Different Time Intervals in Esmolol Group (E) Time Interval Mean SD t value P value Baseline 124.18 10.24 Before study drug 128.10 11.34 -4.698, df=39 0.001* Pre-laryngoscopy 124.13 9.66 0.032, df=39 0.974, NS During laryngoscopy & intub. 126.65 12.58 -1.029, df=39 0.310, NS 1 min after intubation 142.28 17.00 -6.479, df=39 0.001* 3 min after intubation 143.03 17.10 -4.803, df=39 0.001* 5 min after intubation 144.25 15.66 -5.518, df=39 0.001* Group E demonstrated a sharp rise in SAP after intubation, peaking at 144.25 ± 15.66 mmHg at 5 minutes (P<0.05). Table 5: SAP at Different Time Intervals in Dexmedetomidine Group (D) Time Interval Mean SD t value P value Baseline 123.40 11.19 Before study drug 123.93 10.59 -0.785, df=39 0.437, NS Pre-laryngoscopy 122.18 15.11 0.641, df=39 0.525, NS During laryngoscopy & intub. 124.05 16.86 -0.246, df=39 0.807, NS 1 min after intubation 129.35 14.89 -2.421, df=39 0.020* 3 min after intubation 130.13 13.18 -2.886, df=39 0.006* 5 min after intubation 130.28 14.07 -2.796, df=39 0.008* Diastolic Arterial Pressure (DAP) Changes Table 6: DAP at Different Time Intervals in Esmolol Group (E) Time Interval Mean SD t value P value Baseline 78.80 8.07 Before study drug 80.10 9.58 -1.960, df=39 0.057, NS Pre-laryngoscopy 80.93 9.36 -0.185, df=39 0.854, NS During laryngoscopy & intub. 85.45 12.20 -2.840, df=39 0.007* 1 min after intubation 93.30 12.80 -5.598, df=39 0.001* 3 min after intubation 94.20 12.64 -4.509, df=39 0.001* 5 min after intubation 94.80 13.70 -5.229, df=39 0.001* Table 7: DAP at Different Time Intervals in Dexmedetomidine Group (D) Time Interval Mean SD t value P value Baseline 77.90 8.80 Before study drug 78.35 8.49 -0.637, df=39 0.528, NS Pre-laryngoscopy 80.18 9.23 1.028, df=39 0.310, NS During laryngoscopy & intub. 81.10 14.34 -1.374, df=39 0.177, NS 1 min after intubation 84.15 14.94 -3.009, df=39 0.005* 3 min after intubation 84.53 13.82 -2.826, df=39 0.007* 5 min after intubation 85.13 14.88 -2.833, df=39 0.007* Mean Arterial Pressure (MAP) Changes Table 8: MAP at Different Time Intervals in Esmolol Group (E) Time Interval Mean SD t value P value Baseline 93.83 7.93 Before study drug 96.55 9.24 -2.611, df=39 0.013* Pre-laryngoscopy 94.09 8.50 -0.110, df=39 0.913, NS During laryngoscopy & intub. 99.18 11.97 -2.407, df=39 0.021* 1 min after intubation 109.63 13.87 -6.146, df=39 0.001* 3 min after intubation 109.71 14.64 -4.807, df=39 0.001* 5 min after intubation 109.92 13.64 -5.563, df=39 0.001* Group E (Esmolol) exhibited significant and sustained increases in HR, SAP, DAP, and MAP during and after intubation. Group D (Dexmedetomidine) showed smaller hemodynamic surges, with values returning near baseline within 3–5 minutes. No adverse events were reported in either group.

Direct laryngoscopy and endotracheal intubation trigger significant hemodynamic changes due to reflex sympathetic discharge. This heightened sympathoadrenal activity may cause hypertension, tachycardia, and arrhythmias, which in vulnerable patients can result in complications like pulmonary edema, myocardial ischemia, or stroke. Various pharmacologic agents such as opioids, calcium channel antagonists, lignocaine, α-agonists, and β-blockers have been used to attenuate these responses, but their use is limited by adverse effects including sedation, respiratory depression, hypotension, or bradycardia. Dexmedetomidine, an α2-adrenergic agonist, provides sedative, anxiolytic, analgesic, and sympatholytic effects, effectively blunting perioperative cardiovascular responses without significant respiratory depression. Esmolol, a cardioselective β-blocker with a rapid onset and short half-life, is also considered effective in attenuating hemodynamic responses to laryngoscopy and intubation [8,9]. In the present study, 80 patients were randomized into two groups: Group D (Dexmedetomidine, 0.75 mcg/kg) and Group E (Esmolol, 1 mg/kg), both administered 2 minutes prior to induction. The primary objective was to compare the efficacy of these agents in attenuating hemodynamic changes (HR, SAP, DAP, MAP) during and after laryngoscopy and intubation. The results demonstrated that Dexmedetomidine (Group D) provided superior control over heart rate and blood pressure responses compared to Esmolol (Group E), with hemodynamic parameters returning closer to baseline within 5 minutes post-intubation. Both groups were comparable in terms of mean age and gender distribution, with no statistically significant differences. These findings align with previous studies by Li Z et al. [8], Selvaraj et al. [9], and Reddy et al. [10], where demographic characteristics were also matched across groups. A significant difference in HR was observed between the groups, with Group D maintaining lower mean HR from pre-laryngoscopy to the end of the study (P<0.05). Within Group D, HR showed a slight rise during laryngoscopy and at 1-minute post-intubation but returned to baseline by 3–5 minutes. In contrast, Group E exhibited a sustained elevation in HR from drug administration until 5 minutes post-intubation (P<0.05). These findings corroborate the results of Reddy et al. [10], who reported a significantly smaller rise in HR in patients receiving Dexmedetomidine compared to Esmolol. Li Z et al. [8], in a meta-analysis, also found Dexmedetomidine to be more effective in attenuating HR. Kindler et al. [11] observed that Esmolol at 2 mg/kg attenuated HR response but had limited effects on blood pressure, while Miller et al. [12] reported effective HR control with a 100 mg Esmolol bolus. The lower efficacy of Esmolol in our study could be due to the relatively lower dose used (1 mg/kg). Mean SAP was significantly lower in Group D from post-laryngoscopy until 5 minutes post-intubation compared to Group E (P<0.05). Dexmedetomidine maintained better control of SAP, consistent with findings by Reddy et al. [10], Uysal et al. [11], and Selvaraj et al. [9]. Li Z et al. [8] also reported in their meta-analysis that Dexmedetomidine effectively blunts the rise in SAP at all time intervals compared to Esmolol. Group D showed significantly lower DAP at 1-, 3-, and 5-minutes post-intubation compared to Group E (P<0.05). The attenuation of DAP was more consistent with Dexmedetomidine throughout the observation period. Similar results have been documented by Selvaraj et al. [9] and Reddy et al. [10], as well as in Li Z et al.’s [8] meta-analysis.

Administration of Dexmedetomidine at a dose of 0.75 mcg/kg as an infusion given 2 minutes prior to induction of anaesthesia effectively attenuated the hemodynamic response—specifically the rise in heart rate and blood pressure—associated with laryngoscopy and tracheal intubation. In comparison, Esmolol at a dose of 1 mg/kg administered as a bolus 2 minutes before induction was less effective in blunting these cardiovascular responses. These findings suggest that Dexmedetomidine provides superior hemodynamic stability during the critical period of airway manipulation, making it a more reliable agent for preventing the sympathetic surge that commonly follows laryngoscopy and intubation.

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