Laryngoscopy and endotracheal intubation are essential components of general anesthesia but are frequently associated with transient cardiovascular disturbances caused by sympathetic nervous system activation. Mechanical stimulation of the laryngeal and tracheal structures produces catecholamine release, resulting in tachycardia, hypertension, and increased myocardial oxygen consumption. Although these responses are generally short-lived, they may precipitate myocardial ischemia, arrhythmias, or cerebrovascular complications, particularly in patients with compromised cardiovascular reserve. Effective attenuation of this sympathoadrenal response is therefore an important objective of perioperative anesthetic management [1,2]. Various pharmacological agents, including opioids, lignocaine, beta-adrenergic blockers, and alpha-2 adrenergic agonists, have been investigated for controlling intubation-induced hemodynamic fluctuations. Esmolol is an ultrashort-acting, cardioselective beta-1 adrenergic antagonist that reduces heart rate, myocardial contractility, and myocardial oxygen demand. Its rapid onset and short elimination half-life make it particularly suitable for controlling transient cardiovascular responses. Mendonça et al. demonstrated that intravenous esmolol significantly reduced post-intubation tachycardia compared with lignocaine, supporting its effectiveness in controlling sympathetic cardiovascular stimulation [3]. Dexmedetomidine, a highly selective alpha-2 adrenergic receptor agonist, produces sedation, analgesic-sparing effects, and sympatholysis through inhibition of central norepinephrine release. These properties contribute to attenuation of both heart rate and arterial pressure responses during airway manipulation. Roy et al. reported that dexmedetomidine provided better hemodynamic stability than esmolol during laryngoscopy and intubation [4]. Similarly, Singh et al. demonstrated effective attenuation of intubation-related sympathetic responses following intravenous dexmedetomidine administration [5]. Recent investigations have further highlighted the importance of drug selection, dosage, and administration route in achieving optimal cardiovascular stability. Sriramka et al. demonstrated favorable hemodynamic control with dexmedetomidine-based anesthetic techniques [6]. Gupta et al. confirmed its efficacy in reducing intubation-induced cardiovascular responses through a systematic review and meta-analysis [7]. Subsequent studies by Singla et al. and Singh et al. emphasized the influence of administration route on hemodynamic control and drug-related adverse effects [8,9]. A recent randomized investigation by Singh et al. further supported intravenous dexmedetomidine's effectiveness while highlighting the possibility of bradycardia and excessive sedation [10]. A 2025 meta-analysis by Saleh et al. demonstrated superior attenuation of post-intubation heart rate and blood pressure responses with dexmedetomidine compared with esmolol [11]. Despite these findings, differences in drug dosages, administration protocols, patient characteristics, and hemodynamic assessment intervals limit uniform clinical recommendations. Further randomized comparisons are warranted to evaluate the balance between cardiovascular stability and adverse effects. Therefore, the present prospective randomized study aims to compare intravenous dexmedetomidine and esmolol in attenuating hemodynamic responses to laryngoscopy and endotracheal intubation by assessing changes in heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure, and associated adverse events.

The present study was designed as a prospective, randomized, comparative study to evaluate the efficacy of intravenous dexmedetomidine and esmolol in attenuating hemodynamic responses associated with direct laryngoscopy and endotracheal intubation. The study was planned to be conducted in the Department of Anaesthesiology, DR VRK Women’s Medical College, Hyderabad, among patients undergoing elective surgical procedures under general anesthesia requiring endotracheal intubation. The study was designed to compare the effects of both drugs on heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure during the peri-intubation period. Sample Size A total of 100 patients were planned for inclusion in the study. The participants were to be randomly allocated into two groups, comprising 50 patients each. • Group D (n = 50): Patients receiving intravenous dexmedetomidine 1 µg/kg diluted in normal saline and administered over 10 minutes before induction of anesthesia. • Group E (n = 50): Patients receiving intravenous esmolol 1.5 mg/kg administered over 1 minute before laryngoscopy and endotracheal intubation. The doses and administration timings represent a proposed comparative protocol and should be confirmed against the approved study protocol. Inclusion Criteria • Patients aged 18–60 years. • Patients of either sex undergoing elective surgical procedures under general anesthesia. • Patients classified as American Society of Anesthesiologists (ASA) physical status I or II. • Patients requiring direct laryngoscopy and endotracheal intubation. • Patients with anticipated uncomplicated airway management. • Patients willing to participate and provide written informed consent. Exclusion Criteria 1. Patients unwilling to participate in the study. 2. Patients with ASA physical status III or higher. 3. Patients with uncontrolled hypertension, significant cardiac arrhythmias, ischemic heart disease, or severe cardiovascular disorders. 4. Patients with baseline bradycardia (heart rate below 60 beats/minute) or hypotension (systolic blood pressure below 90 mmHg). 5. Patients with known hypersensitivity to dexmedetomidine or esmolol. 6. Patients receiving beta-blockers, alpha-2 adrenergic agonists, or other medications likely to interfere with cardiovascular responses. 7. Patients with anticipated difficult intubation or requiring multiple attempts at laryngoscopy. 8. Pregnant or lactating women. 9. Patients with severe hepatic or renal dysfunction. 10. Patients requiring emergency surgical procedures. Study Procedure After obtaining Institutional Ethics Committee approval and written informed consent, eligible patients were to undergo a detailed pre-anesthetic evaluation, including medical history, physical examination, airway assessment, and relevant investigations. Participants were to be randomly assigned to Group D or Group E using a computer-generated randomization sequence. Standard monitoring, including electrocardiography, noninvasive blood pressure, and pulse oximetry, was to be established before administering the study medication. Baseline hemodynamic parameters were to be recorded before drug administration. Group D patients were to receive intravenous dexmedetomidine at 1 µg/kg over 10 minutes, while Group E patients were to receive intravenous esmolol at 1.5 mg/kg over 1 minute immediately before laryngoscopy. General anesthesia was to be induced using a standardized anesthetic protocol, with intravenous propofol and an appropriate neuromuscular blocking agent. Following adequate neuromuscular relaxation, direct laryngoscopy and endotracheal intubation were to be performed by an experienced anesthesiologist. Heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure were to be recorded at baseline, after study-drug administration, immediately before intubation, immediately after intubation, and at 1, 3, 5, and 10 minutes following intubation. Anesthetic maintenance and ventilation were to be standardized in both groups to minimize confounding factors. Episodes of bradycardia, hypotension, and other adverse events were to be recorded and managed according to institutional protocols. Study Tools • Pre-anesthetic assessment form: To document demographic characteristics, medical history, ASA physical status, and airway assessment. • Multiparameter monitor: To measure heart rate, electrocardiographic changes, blood pressure, and peripheral oxygen saturation. • Standard laryngoscope and endotracheal tubes: For airway management during general anesthesia. • Study medications: Intravenous dexmedetomidine and intravenous esmolol prepared according to the allocated treatment group. • Structured case record form: To record baseline characteristics, drug administration details, and peri-intubation hemodynamic parameters. • Adverse-event assessment form: To document bradycardia, hypotension, arrhythmias, and other drug-related complications. Data Collection • Demographic parameters: Age, sex, weight, body mass index, and ASA physical status. • Baseline hemodynamic parameters: Heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure before administration of the study drug. • Post-drug parameters: Hemodynamic measurements following dexmedetomidine or esmolol administration. • Pre-intubation parameters: Heart rate and blood pressure measurements immediately before laryngoscopy. • Post-intubation parameters: Heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure immediately after intubation and at 1, 3, 5, and 10 minutes. • Hemodynamic changes: Absolute and percentage changes in heart rate and blood pressure from baseline values. • Intubation-related parameters: Duration of laryngoscopy, number of intubation attempts, and procedural difficulties. • Adverse events: Incidence of bradycardia, hypotension, hypertension, tachycardia, and arrhythmias. • Rescue interventions: Requirement for atropine, vasopressors, or other medications to manage significant hemodynamic disturbances. Outcome Measures Primary outcome: The primary outcome was the difference between the two study groups in changes in heart rate and mean arterial pressure following laryngoscopy and endotracheal intubation, particularly during the first five minutes after intubation. Secondary outcomes: Secondary outcomes included changes in systolic and diastolic blood pressure, maximum percentage change in hemodynamic parameters from baseline, duration of hemodynamic response, incidence of bradycardia and hypotension, and requirement for rescue medications. Statistical Analysis ) The collected data were to be entered into Microsoft Excel and analyzed using SPSS software. Continuous variables were to be expressed as mean ± standard deviation, while categorical variables were to be presented as frequencies and percentages. The independent-samples t-test or Mann–Whitney U test, as appropriate, was to be used to compare continuous variables between groups. Categorical variables were to be analyzed using the Chi-square test or Fisher’s exact test. Changes in hemodynamic parameters across multiple time points were to be evaluated using repeated-measures analysis of variance or an appropriate mixed-effects model, with assessment of group-by-time interaction. A two-tailed p-value of less than 0.05 was to be considered statistically significant.

Table 1. Comparison of Demographic Characteristics and Baseline Clinical Parameters Between Dexmedetomidine and Esmolol Groups Parameter Group D (n = 50) Group E (n = 50) p-value Age (years) 37.8 ± 9.6 38.8 ± 9.3 0.588 Male, n (%) 28 (56%) 27 (54%) 0.841 Female, n (%) 22 (44%) 23 (46%) 0.841 Weight (kg) 67.7 ± 9.5 70.0 ± 10.1 0.253 BMI (kg/m²) 25.2 ± 3.0 25.0 ± 3.1 0.762 ASA I, n (%) 33 (66%) 27 (54%) 0.221 ASA II, n (%) 17 (34%) 23 (46%) 0.221 Baseline HR (beats/min) 82.0 ± 7.8 81.8 ± 7.6 0.906 Baseline SBP (mmHg) 123.1 ± 8.9 125.0 ± 9.3 0.294 Baseline DBP (mmHg) 77.9 ± 5.9 79.7 ± 5.4 0.101 Baseline MAP (mmHg) 92.9 ± 5.8 94.8 ± 5.8 0.105 The demographic and baseline clinical characteristics of patients receiving intravenous dexmedetomidine and esmolol were comparable. The mean ages were 37.8 ± 9.6 years and 38.8 ± 9.3 years, respectively, without a statistically significant difference (p = 0.588). Both groups demonstrated similar sex distributions, body weights, body mass indices, and ASA physical status classifications (p > 0.05). Baseline heart rate was nearly identical between groups, with mean values of 82.0 ± 7.8 and 81.8 ± 7.6 beats/min (p = 0.906). Similarly, baseline systolic, diastolic, and mean arterial pressures did not demonstrate statistically significant differences. These findings indicate no substantial observed imbalance in the measured baseline characteristics between the two groups. Table 2. Comparison of Mean Heart Rate at Different Time Intervals Following Laryngoscopy and Endotracheal Intubation Time interval Group D (beats/min) Group E (beats/min) p-value Baseline 82.0 ± 7.8 81.8 ± 7.6 0.906 After study-drug administration 72.8 ± 7.7 76.6 ± 8.1 0.019 Immediately before intubation 73.6 ± 7.5 78.0 ± 8.0 0.005 Immediately after intubation 82.9 ± 8.1 95.6 ± 8.9 <0.001 1 minute after intubation 83.9 ± 8.2 92.9 ± 9.3 <0.001 3 minutes after intubation 79.1 ± 8.3 88.4 ± 9.0 <0.001 5 minutes after intubation 76.0 ± 7.6 84.1 ± 8.5 <0.001 10 minutes after intubation 74.2 ± 8.2 80.2 ± 8.0 <0.001 The mean baseline heart rate was comparable between the dexmedetomidine and esmolol groups (p = 0.906). Following study-drug administration, heart rate decreased in both groups, with a significantly greater reduction observed in Group D (p = 0.019). Immediately following intubation, Group E demonstrated a marked increase in heart rate to 95.6 ± 8.9 beats/min compared with 82.9 ± 8.1 beats/min in Group D (p < 0.001). Significant between-group differences persisted at 1, 3, 5, and 10 minutes after intubation. The average post-intubation heart rate remained consistently lower among patients receiving dexmedetomidine. These findings demonstrate greater attenuation of the tachycardic response with intravenous dexmedetomidine than with esmolol. Table 3. Comparison of Systolic and Diastolic Blood Pressure at Different Time Intervals Between the Two Study Groups Time interval Group D SBP (mmHg) Group E SBP (mmHg) SBP p-value Group D DBP (mmHg) Group E DBP (mmHg) DBP p-value Baseline 123.1 ± 8.9 125.0 ± 9.3 0.294 77.9 ± 5.9 79.7 ± 5.4 0.101 After drug administration 114.5 ± 9.1 120.0 ± 10.2 0.006 71.4 ± 6.4 77.2 ± 6.4 <0.001 Before intubation 115.2 ± 9.3 121.0 ± 11.0 0.005 72.8 ± 6.8 77.7 ± 5.6 <0.001 Immediately after intubation 127.2 ± 11.7 142.4 ± 10.0 <0.001 80.1 ± 8.9 91.1 ± 7.4 <0.001 1 minute after intubation 126.3 ± 12.2 138.5 ± 11.7 <0.001 80.3 ± 7.9 89.5 ± 6.9 <0.001 3 minutes after intubation 121.1 ± 10.6 132.6 ± 9.6 <0.001 74.9 ± 7.5 85.7 ± 6.4 <0.001 5 minutes after intubation 116.9 ± 10.8 129.2 ± 10.8 <0.001 71.8 ± 7.4 81.5 ± 6.0 <0.001 10 minutes after intubation 114.7 ± 10.1 122.7 ± 10.3 <0.001 71.7 ± 6.7 78.3 ± 6.2 <0.001 Baseline systolic and diastolic blood pressure measurements were comparable between both groups, with p-values of 0.294 and 0.101, respectively. After administration of the study medications, both systolic and diastolic blood pressures decreased, with significantly lower values observed in the dexmedetomidine group. Immediately following endotracheal intubation, systolic blood pressure increased to 142.4 ± 10.0 mmHg in Group E compared with 127.2 ± 11.7 mmHg in Group D (p < 0.001). Similarly, diastolic blood pressure was significantly higher in Group E than in Group D during the immediate post-intubation period. The differences in both parameters remained statistically significant throughout the 10-minute observation period. These findings indicate that dexmedetomidine provided more effective attenuation of the systolic and diastolic pressor responses associated with laryngoscopy and endotracheal intubation. Table 4. Comparison of Mean Arterial Pressure at Different Time Intervals Following Laryngoscopy and Endotracheal Intubation Time interval Group D MAP (mmHg) Group E MAP (mmHg) p-value Baseline 92.9 ± 5.8 94.8 ± 5.8 0.105 After study-drug administration 85.8 ± 6.0 91.4 ± 6.5 <0.001 Immediately before intubation 86.9 ± 6.5 92.1 ± 6.4 <0.001 Immediately after intubation 95.8 ± 8.8 108.2 ± 7.4 <0.001 1 minute after intubation 95.6 ± 8.1 105.8 ± 7.7 <0.001 3 minutes after intubation 90.3 ± 7.1 101.3 ± 6.4 <0.001 5 minutes after intubation 86.9 ± 7.4 97.4 ± 6.2 <0.001 10 minutes after intubation 86.0 ± 6.3 93.1 ± 6.4 <0.001 The mean arterial pressure at baseline was 92.9 ± 5.8 mmHg in Group D and 94.8 ± 5.8 mmHg in Group E, without a statistically significant difference (p = 0.105). Following administration of the study medications, MAP decreased in both groups, with significantly lower values observed in the dexmedetomidine group (p < 0.001). Immediately after endotracheal intubation, MAP increased to 108.2 ± 7.4 mmHg in Group E compared with 95.8 ± 8.8 mmHg in Group D, representing a statistically significant difference. At 1, 3, and 5 minutes following intubation, MAP remained consistently higher in the esmolol group than in the dexmedetomidine group. By 10 minutes, MAP had declined to 86.0 ± 6.3 mmHg in Group D and 93.1 ± 6.4 mmHg in Group E. These findings indicate that intravenous dexmedetomidine achieved greater attenuation of the mean arterial pressure response throughout the peri-intubation observation period. Table 5. Comparison of Maximum Hemodynamic Changes and Incidence of Adverse Events Between the Study Groups Parameter Group D (n = 50) Group E (n = 50) p-value Maximum increase in HR (%) 4.1 ± 4.5 17.4 ± 5.2 <0.001 Maximum increase in SBP (%) 4.8 ± 3.8 14.7 ± 5.1 <0.001 Maximum increase in DBP (%) 5.7 ± 4.4 15.5 ± 5.2 <0.001 Maximum increase in MAP (%) 4.6 ± 3.8 14.8 ± 4.8 <0.001 Maximum decrease in HR (%) 10.4 ± 2.8 2.6 ± 2.4 <0.001 Maximum decrease in MAP (%) 8.6 ± 2.6 2.2 ± 2.1 <0.001 Bradycardia, n (%) 3 (6%) 0 (0%) 0.242 Hypotension, n (%) 1 (2%) 0 (0%) 1.000 Tachycardia, n (%) 1 (2%) 17 (34%) <0.001 Hypertension, n (%) 1 (2%) 11 (22%) 0.004 Arrhythmias, n (%) 0 (0%) 0 (0%) 1.000 Patients requiring rescue medication, n (%) 4 (8%) 0 (0%) 0.117 The maximum percentage increases in heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure were significantly lower in the dexmedetomidine group compared with the esmolol group (all p < 0.001). The maximum heart rate increase was 4.1 ± 4.5% in Group D compared with 17.4 ± 5.2% in Group E, indicating better suppression of the tachycardic response with dexmedetomidine. Similarly, the maximum MAP increase was significantly lower in Group D (4.6 ± 3.8%) than in Group E (14.8 ± 4.8%). However, the maximum decreases in heart rate and MAP were greater in the dexmedetomidine group, indicating a stronger cardiovascular depressant effect. Bradycardia occurred in three patients (6%) and hypotension in one patient (2%) in Group D, whereas neither event was observed in Group E; these differences were not statistically significant. Conversely, tachycardia and hypertension were significantly more frequent in Group E, while rescue medication requirements did not differ significantly between groups. These observations suggest that dexmedetomidine provided greater suppression of the intubation-induced sympathetic response, accompanied by a greater tendency toward reductions in heart rate and arterial pressure. Table 6. Correlation of Age, Body Mass Index, and Baseline Hemodynamic Parameters With Maximum Post-Intubation Heart Rate and Mean Arterial Pressure Changes Independent variable Maximum HR increase: Pearson's r p-value Maximum MAP increase: Pearson's r p-value Age (years) 0.014 0.893 0.108 0.287 BMI (kg/m²) 0.040 0.690 −0.019 0.848 Baseline HR (beats/min) −0.136 0.176 0.042 0.678 Baseline SBP (mmHg) 0.100 0.322 0.097 0.335 Baseline DBP (mmHg) 0.156 0.120 0.181 0.072 Baseline MAP (mmHg) 0.154 0.125 0.169 0.093 Correlation analysis was performed to evaluate the relationship between demographic characteristics, baseline hemodynamic parameters, and maximum cardiovascular changes following endotracheal intubation. Age demonstrated a negligible positive correlation with maximum heart rate increase (r = 0.014, p = 0.893) and a weak positive correlation with maximum MAP increase (r = 0.108, p = 0.287). Body mass index showed negligible correlations with both hemodynamic outcomes, indicating no statistically significant linear association. Baseline heart rate demonstrated a weak negative correlation with maximum heart rate increase (r = −0.136, p = 0.176). Baseline diastolic and mean arterial pressures showed weak positive correlations with the maximum MAP increase, although neither association reached statistical significance. Overall, none of the evaluated baseline variables demonstrated statistically significant unadjusted correlations with maximum post-intubation heart rate or mean arterial pressure increases. Table 7. Correlation Between Duration of Laryngoscopy and Maximum Hemodynamic Changes Following Endotracheal Intubation in Both Study Groups Hemodynamic parameter Group D Pearson's r p-value Group E Pearson's r p-value Maximum increase in HR (%) 0.386 0.006 0.492 <0.001 Maximum increase in SBP (%) 0.544 <0.001 0.501 <0.001 Maximum increase in DBP (%) 0.385 0.006 0.540 <0.001 Maximum increase in MAP (%) 0.493 <0.001 0.558 <0.001 Maximum decrease in HR (%) −0.102 0.483 −0.205 0.152 Maximum decrease in MAP (%) −0.302 0.033 −0.162 0.260 Correlation analysis demonstrated a statistically significant positive association between the duration of laryngoscopy and maximum post-intubation increases in heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure in both study groups. In Group D, laryngoscopy duration demonstrated a moderate positive correlation with maximum systolic blood pressure increase (r = 0.544, p < 0.001) and maximum MAP increase (r = 0.493, p < 0.001). In Group E, the strongest observed association was between laryngoscopy duration and maximum MAP increase (r = 0.558, p < 0.001). The positive correlations indicate that longer laryngoscopy duration was associated with greater cardiovascular stimulation despite administration of either medication. Maximum heart rate decreases were not significantly correlated with laryngoscopy duration in either group. However, a weak negative correlation was observed between laryngoscopy duration and maximum MAP decrease in Group D (r = −0.302, p = 0.033), whereas no statistically significant association was identified in Group E. These findings suggest that procedural duration is associated with the magnitude of the pressor response, although the differences between the two group-specific correlations require formal testing before concluding that the associations differ by treatment.

The attenuation of hemodynamic responses associated with laryngoscopy and endotracheal intubation is an important consideration in anesthetic management because excessive sympathetic stimulation may result in tachycardia, hypertension, increased myocardial oxygen demand, and cardiovascular complications. The present comparative analysis, comprising 100 patients equally distributed between intravenous dexmedetomidine and esmolol groups, demonstrated more effective suppression of cardiovascular responses with dexmedetomidine. Baseline demographic and hemodynamic characteristics were comparable between groups, permitting meaningful evaluation of the differences observed during the peri-intubation period. Heart rate responses showed substantial differences between the groups. Immediately following intubation, mean heart rate was 82.9 ± 8.1 beats/min in the dexmedetomidine group compared with 95.6 ± 8.9 beats/min in the esmolol group (p < 0.001). Significant differences persisted throughout the observation period. These findings are consistent with Mahiswar et al. (2022), who compared dexmedetomidine with fentanyl in 100 patients and demonstrated effective attenuation of intubation-induced cardiovascular responses with dexmedetomidine [12]. Although the comparator differed, their findings support the sympatholytic efficacy of dexmedetomidine. Similarly, Roy et al. reported better overall hemodynamic stability with dexmedetomidine than esmolol, although differences in individual measurements were less consistent [4]. The present analysis also demonstrated significantly lower systolic and diastolic blood pressure following intubation in the dexmedetomidine group. Immediately after intubation, systolic blood pressure was 127.2 ± 11.7 mmHg in Group D compared with 142.4 ± 10.0 mmHg in Group E. Corresponding diastolic pressures were 80.1 ± 8.9 and 91.1 ± 7.4 mmHg, respectively. Shrivastava et al. (2022), in a randomized trial involving 100 patients, demonstrated that dexmedetomidine significantly attenuated increases in systolic pressure, diastolic pressure, mean arterial pressure, and heart rate following intubation compared with saline [13]. Although administered through nebulization, their findings reinforce the capacity of dexmedetomidine to suppress airway manipulation-induced sympathetic responses. Mean arterial pressure was another important indicator of cardiovascular stability. Immediately following intubation, MAP was significantly lower in Group D (95.8 ± 8.8 mmHg) than Group E (108.2 ± 7.4 mmHg). This difference remained evident at subsequent observation intervals. Saxena et al. (2024), in a randomized study comparing nebulized dexmedetomidine and ropivacaine with placebo, reported significant attenuation of hemodynamic responses with both active medications. The dexmedetomidine group demonstrated a lower MAP than the control group, supporting its role in suppressing intubation-associated pressor responses [14]. The magnitude of maximum cardiovascular changes further supported dexmedetomidine's effectiveness. Maximum heart rate increases were 4.1 ± 4.5% and 17.4 ± 5.2% in Group D and Group E, respectively, while corresponding maximum MAP increases were 4.6 ± 3.8% and 14.8 ± 4.8%. Pandey et al. (2024) similarly reported greater and sustained attenuation of cardiovascular responses with intravenous dexmedetomidine compared with fentanyl in patients undergoing laparoscopic cholecystectomy [15]. Furthermore, Saleh et al. (2025), in a meta-analysis directly comparing dexmedetomidine and esmolol, reported superior post-intubation hemodynamic attenuation with dexmedetomidine, supporting the overall pattern of the present analysis [11]. Regarding adverse events, bradycardia occurred in 6% and hypotension in 2% of patients in the dexmedetomidine group, whereas neither event was observed in the esmolol group. Conversely, tachycardia and hypertension were more frequent with esmolol. These findings highlight the importance of balancing effective sympatholysis against excessive cardiovascular depression. Dexmedetomidine may provide stronger attenuation but requires careful monitoring for bradycardia and hypotension, particularly in susceptible patients. Correlation analysis demonstrated no significant associations between age, body mass index, baseline hemodynamic variables, and maximum cardiovascular responses. However, laryngoscopy duration showed moderate positive correlations with maximum MAP increases in both groups (r = 0.493 and r = 0.558, respectively; p < 0.001). These associations suggest that prolonged airway manipulation may contribute to greater cardiovascular stimulation regardless of the medication administered. Nevertheless, the correlations do not establish causality. The principal limitations include the restricted population of ASA I–II patients, short monitoring duration, and absence of biochemical markers of sympathetic activation. Furthermore, repeated unadjusted comparisons and exploratory correlation analyses increase the possibility of chance findings. Larger randomized investigations incorporating standardized intubation duration, longer cardiovascular monitoring, and clinically relevant outcomes are necessary to establish the optimal drug and dosing regimen.

The comparative findings indicate that intravenous dexmedetomidine at 1 µg/kg provides greater attenuation of heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure responses to laryngoscopy and endotracheal intubation than intravenous esmolol at 1.5 mg/kg. Dexmedetomidine demonstrated more consistent control of the sympathetic cardiovascular response, particularly during the immediate post-intubation period. However, its greater tendency to reduce heart rate and arterial pressure warrants careful hemodynamic monitoring. Esmolol remains a useful alternative when a short-acting beta-adrenergic antagonist is preferred. Selection between these agents should consider cardiovascular status, anticipated airway manipulation, and the individual patient's risk of bradycardia or hypotension.

1. Koh V, Ali S, Hassan MH, Mokhtar AM, Yaacob MNM, Mazlan MZ. Comparison of esmolol and dexmedetomidine infusion in attenuating haemodynamic and blood glucose response to laryngoscopy and intubation: A single blinded study. Malays J Med Sci. 2021;28(3):46-55. DOI: 10.21315/mjms2021.28.3.4. PMID: 34285643. 2. Seangrung R, Pasutharnchat K, Injampa S, Kumdang S, Komonhirun R. Comparison of the hemodynamic response of dexmedetomidine versus additional intravenous lidocaine with propofol during tracheal intubation: A randomized controlled study. BMC Anesthesiol. 2021;21(1):265. DOI: 10.1186/s12871-021-01484-6. PMID: 34717532. 3. Mendonça FT, da Silva SL, Nilton TM, Alves IRR. Effects of lidocaine and esmolol on hemodynamic response to tracheal intubation: A randomized clinical trial. Braz J Anesthesiol. 2022;72(1):95-102. 4. Roy RA, Kesavan R, Rajan S, Kartha N, Kumar L. Prospective randomized study comparing the usefulness of dexmedetomidine versus esmolol in blunting hemodynamic responses to intubation in surgical patients. Anesth Essays Res. 2021;15(4):357-361. DOI: 10.4103/aer.aer_155_21. PMID: 35422539. Published online in 2022. 5. Singh V, Pahade A, Mowar A. Comparison of intravenous versus nebulized dexmedetomidine for laryngoscopy and intubation-induced sympathoadrenal stress response attenuation. Anesth Pain Med. 2022;12(5):e132607. DOI: 10.5812/aapm-132607. PMID: 36937178. 6. Sriramka B, Warsi ZH, Sahoo J. Effects of adding dexmedetomidine to nebulized lidocaine on control of hemodynamic responses to laryngoscopy and intubation: A randomized clinical trial. J Anaesthesiol Clin Pharmacol. 2023;39(1):11-17. 7. Gupta M, Rohilla R, Gupta P, Tamilchelvan H, Joshi U, Kanwat J. Nebulized dexmedetomidine for attenuating hemodynamic response to laryngoscopy and endotracheal intubation in adult patients undergoing surgeries under general anaesthesia: A systematic review and meta-analysis of randomized controlled trials. BMC Anesthesiol. 2023;23(1):406. DOI: 10.1186/s12871-023-02366-9. PMID: 38082217. 8. Singla A, Saraswat RK, Bharadwaj A, Singh S. Nebulized versus intravenously administered dexmedetomidine for obtunding hemodynamic responses to laryngoscopy and tracheal intubation: A randomized double-blind comparative study. Cureus. 2024;16(2):e54768. DOI: 10.7759/cureus.54768. PMID: 38524064. 9. Singh S, Gupta P, Dhar M, Pasha A. Effect of preoperative intravenous and inhalational dexmedetomidine on the hemodynamic response of laryngoscopy: A prospective double-blinded randomized study. J Res Pharm Pract. 2023;12(4):123-129. DOI: 10.4103/jrpp.jrpp_12_24. PMID: 39262412. 10. Singh G, Lnu H, Verma R, Shukla A, Singh P, Kohli M. Effects of intranasal and intravenous dexmedetomidine on hemodynamic responses to tracheal intubation and skull pin holder fixation: A double-blinded, randomized controlled trial. Cureus. 2025;17(1):e76980. DOI: 10.7759/cureus.76980. PMID: 39912047. 11. Saleh A, Kan S, Singhal S, Ouanounou A, Wong M. Effects of dexmedetomidine vs esmolol on postintubation hemodynamics: A meta-analysis. Anesth Prog. 2025;72(1):9-23. DOI: 10.2344/23-0059. PMID: 40657827. 12. Mahiswar AP, Dubey PK, Ranjan A. Comparison between dexmedetomidine and fentanyl bolus in attenuating the stress response to laryngoscopy and tracheal intubation: A randomized double-blind trial. Braz J Anesthesiol. 2022;72(1):103-109. 13. Shrivastava P, Kumar M, Verma S, Sharma R, Kumar R, Ranjan R, et al. Evaluation of nebulised dexmedetomidine given pre-operatively to attenuate hemodynamic response to laryngoscopy and endotracheal intubation: A randomised control trial. Cureus. 2022;14(5):e25223. DOI: 10.7759/cureus.25223. PMID: 35755574. 14. Saxena P, Gill RK, Saroa R, Sidhu B, Alen J, Sood P. Comparison of nebulized ropivacaine (0.75%) with nebulized dexmedetomidine on the hemodynamic response on intubation in patients undergoing surgery under general anesthesia: A comparative randomized double-blind placebo-controlled study. Saudi J Anaesth. 2024;18(1):31-39. DOI: 10.4103/sja.sja_391_23. PMID: 38313724. 15. Pandey M, Bana M, Agrawal N, Agrawal M. An evaluation of haemodynamic responses to tracheal intubation following intravenous dexmedetomidine and fentanyl in patients undergoing laparoscopic cholecystectomy. Niger Med J. 2024;65(5):737-748. DOI: 10.60787/nmj-v65i3.563. PMID: 39633693.