Comparison of Intravenous Lignocaine and Dexmedetomidine in Attenuating the Haemodynamic Response to Laryngoscopy and Intubation: A Randomised Double-blind Clinical Study

1. Associate Professor, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India. 2. Associate Professor, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India. 3. Junior Resident, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India. 4. Associate Professor, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India. 5. Professor, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India. 6. Professor, Department of Anaesthesiology, Pt. B.D. Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India.

Abstract

Introduction: Endotracheal intubation often triggers a sympathetic response, leading to an increase in Heart Rate (HR) and blood pressure. Dexmedetomidine (DEX) and lignocaine have shown the potential to mitigate cardiovascular changes secondary to intubation.

Aim: To compare the efficacy of 0.25 mcg/kg and 0.5 mcg/kg DEX with 1.5 mg/kg lignocaine in attenuating haemodynamic responses during the peri-intubation period.

Materials and Methods: This randomised double-blind study included 90 patients classified as American Society of Anaesthesiologists (ASA) I and II, aged 16-65 years. Patients were divided into three groups: Group A received lignocaine (1.5 mg/kg); Group B received DEX (0.25 mcg/kg); and Group C received DEX (0.5 mcg/kg). Haemodynamic parameters were recorded at various intervals before and after laryngoscopy. Data were checked for normality before statistical analysis using the Shapiro-Wilk test. Normally distributed continuous variables were compared using Analysis of Variance (ANOVA), while categorical variables were analysed using the Chi-square test. For all statistical tests, a p-value of less than 0.05 was considered indicative of a significant difference.

Results: All groups were found to be comparable in terms of age, weight, and gender distribution. The mean age in Group A was 36.10±12.60 years, in Group B was 36.10±13.47 years, and in Group C was 37.37±11.49 years. Inter-group comparisons between Group A and Group C showed statistically significant lower HR values in Group C (79.23±10.37 vs. 90.7±17.68) at T0 as well as T1 (90.07±14.65 vs. 99.93±17.02, p-value 0.019). The comparison between Groups A and C revealed significantly lower Systolic Blood Pressure (SBP) values in Group C at T0, T1, T3, and T5. Inter-group comparisons between Groups A and B showed that Diastolic Blood Pressure (DBP) values were significantly lower at T5 in Group B (69.33±10.09 vs. 62.33±9.11, p-value 0.006). Between Groups A and C, significant differences were noted at T0, T1, T3, and T5 in Mean Arterial Pressure (MAP).

Conclusion: DEX at a dose of 0.5 mcg/kg appears to be a more effective option for managing haemodynamic responses compared to lignocaine. Nevertheless, the haemodynamic stability achieved with 0.25 mcg/kg of DEX is nearly equivalent to that observed with both 0.5 mcg/kg of DEX and 1.5 mg/kg of lignocaine.

Adrenergic alpha-2 receptor agonist, Airway management, Blood pressure, General anaesthesia, Heart rate, Sympathetic nervous system

Endotracheal intubation is a common procedure in operating rooms to establish a secure airway. However, it often triggers a sympathetic response, leading to undesirable effects like increased HR and elevated blood pressure. DEX, an alpha-2 adrenergic agonist, is shorter-acting than clonidine and has a higher selectivity for alpha-2 receptors. It produces sedation by acting on these receptors, resulting in decreased sympathetic nervous system activity and reduced levels of arousal. Due to its sympatholytic effect, DEX has demonstrated potential in mitigating the cardiovascular changes associated with intubation (1),(2),(3).

Lignocaine is an amide local anaesthetic that is also used to control ventricular tachyarrhythmias by blocking sodium channels. It has been demonstrated to attenuate the haemodynamic response to laryngoscopy (4),(5),(6). While existing studies have explored varying doses of DEX, ranging from 0.5 micrograms/kg to 1 microgram/kg (1),(2),(3),(7),(8),(9),(10),(11),(12),(13),(14), there is a notable knowledge gap regarding a direct comparison between lower doses of DEX (0.25 mcg/kg and 0.5 mcg/kg) and lignocaine. This randomised controlled trial aims to bridge this gap by providing insights into the comparative efficacy of these medications in managing haemodynamic responses during the crucial peri-intubation period.

The present study aimed to determine whether using a lower dose of DEX (0.25 mcg/kg) can provide the same stability as the standard 0.5 mcg/kg dose or 1.5 mg/kg of lignocaine during intubation. This exploration could help optimise drug dosages for better patient care. The primary objective is to compare the effects of intravenous lignocaine with two different doses of DEX on HR, SBP, DBP, and MAP during laryngoscopy and intubation. The secondary objective is to compare the side effects of both drugs.

Material and Methods

This randomised double-blind study was conducted in the Department of Anaesthesiology and Critical Care at Pt. BD Sharma PGIMS, Rohtak, Haryana, India, from September 2021 to August 2022.

Sample size calculation: The sample size was determined using the mean and standard deviation values of HR from the study conducted by Gulabani M et al., (7).

The mean values used were 83.20 and 74.63, while the standard deviation values were 12.46 (rounded to 12.5) and 7.78 (rounded to 7.8). The pooled standard deviation was calculated to be 10.42.

N= 2 (Zα+ Zβ)² (s)²/Δ²

Where,

N: sample size
Zα: 1.96
Zβ: 0.84
S²: 10.42=108.57
Δ²: Difference between means: 83.20-74.63= (8.57)²

Where, Zα is the z variate of alpha error i.e., a constant with a value of 1.96, Zβ is the z variate of beta error i.e., a constant with a value of 0.84.

Approximate estimates: 80% power, Type I error to be 5%, Type II error to be 20%,

Substituting the values,

N= 2 (1.96+0.84)² (108.57)/73.44
= 2 (2.8)² (108.57)/73.44
=23.18

Approximately, 23 subjects/patients per group.

Considering the drop rate/attrition, the authors included 30 patients in each group, resulting in a total sample size of 90 patients, with 30 patients in each group. Ethical clearance was obtained from the Institutional Ethical Committee (BREC/Th/20/Anaesth./23). The study was registered with the Central Trial Registry of India (CTRI number: CTRI/2022/04/041867). Informed written consent was obtained from all participants.

Inclusion criteria: Patients classified as ASA I and II of either sex, aged between 16 and 65 years, who were scheduled for surgery under general anaesthesia, were included in the study.

Exclusion criteria: Patients with anticipated difficult intubation, those with oropharyngeal pathology, or a history of cardiovascular problems (e.g., ischemic heart disease, cerebrovascular accident)were excluded from the study.

Out of the 100 patients assessed, 90 patients were included, while 10 patients (8 did not meet the criteria and 2 declined participation) were excluded from the study (Table/Fig 1).

Procedure

After taking the medical history, all patients were subjected to a general physical and systemic examination during the pre-operative visit, which took place the day before surgery. Routine relevant investigations were carried out.

All patients enrolled in the study were advised to fast for six hours for solids and two hours for clear liquids before the scheduled time of surgery. They were pre-medicated with a tablet of alprazolam 0.25 mg and a tablet of pantoprazole 40 mg, taken orally the night before surgery. Upon arrival in the operating room, routine monitors, including HR, Electrocardiography (ECG), pulse oximetry (SpO₂), Non Invasive Blood Pressure (NIBP), and End-Tidal CO₂ (EtCO₂), were established, and baseline readings of vital parameters (B1) were recorded. An intravenous line was secured.

Patients were randomly allocated into three groups of 30 patients each using a computer-generated random number table (Table/Fig 1). Participants were not informed about the medications they were receiving to ensure blinding. Each group received the following medications intravenously:

Group A (n=30): Received 10 mL of normal saline via an infusion pump over 10 minutes before induction, followed by a bolus of 1.5 mg/kg lignocaine diluted to 5 mL of normal saline, administered 90 seconds before direct laryngoscopy.

Group B (n=30): Received DEX 0.25 mcg/kg diluted to 10 mL in normal saline via an infusion pump 10 minutes before induction of general anaesthesia, followed by a bolus of 5 mL of normal saline, administered 90 seconds before direct laryngoscopy.

Group C (n=30): Received DEX 0.5 mcg/kg diluted to 10 mL in normal saline via an infusion pump 10 minutes before induction of general anaesthesia, followed by a bolus of 5 mL of normal saline, administered 90 seconds before direct laryngoscopy.

Anaesthesiologists involved in the intraoperative management were not part of the data collection and processing.

Ten minutes before the induction of anaesthesia, patients received the respective infusions of drugs as per their allocated group. All patients were pre-oxygenated for three minutes. A standard anaesthetic technique was used in all three groups. Anaesthesia induction was performed with injection (inj.) fentanyl 2 mcg/kg and inj. thiopentone sodium 5 mg/kg. The ability to mask ventilate the patient was confirmed before administering inj. vecuronium 0.1 mg/kg intravenously. All patients were manually ventilated for three minutes. Ninety seconds before laryngoscopy, the patients received the respective drugs according to their allocated group. Laryngoscopy and orotracheal intubation using an appropriately sized cuffed Endotracheal Tube (ETT) were performed. The time taken for laryngoscopy and intubation was noted in seconds, measuring the time from picking up the laryngoscope to obtaining an EtCO₂ tracing on the monitor to confirm successful intubation.

Thereafter, anaesthesia was maintained with nitrous oxide in oxygen (50:50) and sevoflurane titrated to 1 MAC. Additional doses of muscle relaxant were administered as required to maintain adequate neuromuscular blockade. At the end of the surgery, anaesthesia was discontinued, and after observing spontaneous respiratory efforts, residual neuromuscular blockade was reversed with inj. glycopyrrolate and inj. neostigmine (0.05 mg/kg), and the patient was extubated. Once fully awake, the patients were shifted to the post-anaesthesia care unit and observed for any side effects like bradycardia, hypotension, and post-operative Nausea and Vomiting (PONV) for one hour at 15-minute intervals.

The following parameters were recorded: haemodynamic parameters like HR in beats per minute (bpm), SBP in mmHg, DBP in mmHg, MAP in mmHg, and oxygen saturation (SpO₂) in percentage (%). These parameters were recorded using an automatic multi-parameter monitor at the following intervals: before administering the study drug (B1), just before laryngoscopy (B2), just after intubation (T0), and after intubation at one minute, three minutes, and five minutes (T1, T3, T5).

Any side effects, including bradycardia, hypotension, PONV, and dysrhythmias, were noted. Hypotension (defined as SBP <25% below baseline) was treated in a stepwise manner with intravenous fluids and inj. mephentermine 3 mg. Bradycardia (defined as HR <40/min) was treated with inj. atropine 0.6 mg i.v. increments until the desired effect was achieved.

Statistical Analysis

Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS) program for Windows, version 28.0. Continuous variables are presented as mean±SD, and categorical variables are presented as absolute numbers and percentages. Data were checked for normality before statistical analysis using the Shapiro-Wilk test. Normally distributed continuous variables were compared using Analysis of Variance (ANOVA). If the F value was significant and variance was homogeneous, the Tukey multiple comparison test was used to assess the differences between the individual groups. Categorical variables were analysed using the Chi-square test. For haemodynamic variables, values from baseline to various time points were analysed using paired t-tests for each group, respectively, and mean percentage change±SD was reported. For all statistical tests, a p-value of less than 0.05 was considered indicative of a significant difference.

Results

All three groups were found to be similar in terms of age distribution, gender distribution, and American Society of Anaesthesiologists (ASA) class, with no statistically significant differences (Table/Fig 2). The mean age in Group A was 36.10±12.60 years, in Group B was 36.10±13.47 years, and in Group C was 37.37±11.49 years. The mean weight was 61.37±13.40 kg in Group A, 59.97±12.69 kg in Group B, and 59.33±13.37 kg in Group C. In Group A, 43.3% of the patients were female, while 56.7% were male; in Group B, 40.0% of the patients were female, while 60.0% were male. In Group C, 53.3% of the patients were female, while 46.7% were male. The time taken for laryngoscopy and intubation was also found to be similar in all three groups (Table/Fig 2).

The mean HR in Group A increased significantly at T1; however, the values returned to below baseline at T5. Group B patients did not show any significant change in HR values when compared to baseline. Patients in Group C showed statistically significant lower HR values at B2 and T0 (Table/Fig 3). There was no significant difference in HR values between Groups A and B. However, inter-group comparison between Groups A and C showed statistically significant lower HR values in Group C at T0 as well as T1. An inter-group comparison between Groups B and C showed a statistically significant difference at T0 only (Table/Fig 4).

A significant decrease in mean SBP was noted in Group A at B2, followed by an increase at T1. However, the SBP values persistently decreased thereafter at T3 and T5. A highly significant drop in blood pressure was observed in Group B at B2 and T5 when compared to baseline. The mean SBP baseline in Group C was 130.83±14.23 mm of Hg. There was a statistically significant decrease in SBP readings at all time points in the study for Group C (Table/Fig 5). Inter-group comparison between Groups A and B showed that the mean values were insignificantly different, except at T5. However, the comparison between Groups A and C revealed significantly lower blood pressure values in Group C at T0, T1, T3, and T5. Among Groups B and C, no statistically significant differences were noted (Table/Fig 6).

A statistically significant decrease in DBP was observed at B2 and T1, while a highly significant decrease was noted at T5 in Group A. Patients in Group C experienced a consistent decline in DBP, except at T1. A significant decrease in DBP was recorded at B2, T0, T3, and T5 in Group C (Table/Fig 7). Inter-group comparisons between Group A and Group B revealed that diastolic values were significantly lower at T5 in Group B. A significant difference between Group A and Group C was observed at T1, T3, and T5, as shown in (Table/Fig 8). However, no significant differences were found when comparing Group B and Group C at B1, B2, T1, T3, and T5.

A significant decrease in mean blood pressure was noted at B2 and T1 in Group A. Patients in Group B exhibited significantly lower blood pressure at B2, T3, and T5 (Table/Fig 9). When comparing Group A to Group B, a statistically significant difference was observed at T5. Significant differences between Group A and Group C were noted at T0, T1, T3, and T5. Consistent with the findings regarding diastolic blood pressure, inter-group comparisons between Group B and Group C did not reveal any significant differences in mean blood pressure (Table/Fig 10).

No episodes of bradycardia, hypotension, PONV were observed during the postoperative observation period. A comparison of oxygen saturation among the three groups showed no significant differences (Table/Fig 11). Additionally, no abnormalities were noted in the ECG for any of the groups.

Discussion

Endotracheal intubation is a routine procedure in operating theatres for establishing a secure airway. However, it often elicits a sympathetic response, resulting in undesired effects such as tachycardia and hypertension. Notably, the elevation in arterial pressure parallels an increase in plasma noradrenaline concentration, implying a notable surge in sympathetic nerve activity associated with the process of intubation (12). An anaesthesiologist's dual objective during laryngoscopy is to secure the airway effectively and mitigate the associated haemodynamic perturbations. Various pharmacological agents have been employed to dampen the haemodynamic response to laryngoscopy, and among them, DEX, an alpha-2 adrenergic agonist, has shown promise in reducing these cardiovascular changes. While some researchers have investigated the use of DEX in doses of 0.5 mcg/kg (2),(7),(8),(9),(10),(15),(16), 0.75 mcg/kg (13), 1 mcg/kg (1),(3),(7),(10),(11),(15),(16),(17), 0.2 mcg/kg/hr, and 0.4 mcg/kg/hr (18) to attenuate the haemodynamic responses associated with laryngoscopy, the efficacy of a lower dose, specifically 0.25 mcg/kg, remains unexplored in this context.

As a highly selective alpha-2 receptor agonist, DEX exhibits eight times greater selectivity for alpha-2 receptors compared to clonidine. DEX acts by inhibiting the release of noradrenaline at the locus coeruleus in the pons. The cardiovascular effects of DEX follow a biphasic pattern: initially causing hypertension through the activation of alpha-2B receptors on vascular smooth muscle, and subsequently leading to hypotension due to reduced central noradrenaline release (19).

Heart Rate (HR): The present study elucidates the significant impact of DEX dosage on HR values during intubation procedures. Specifically, the administration of DEX at 0.5 mcg/kg emerged as a key determinant in achieving the lowest HR values compared to both lignocaine and a lower DEX dose (0.25 mcg/kg). When examining lignocaine in comparison to lower doses of DEX, the authors did not observe any statistically significant difference in HR values. This finding suggests that within the spectrum of lower DEX dosages, lignocaine may not exhibit a distinct advantage in modulating HR responses during the intubation process.

The comparison between the lower dose (0.25 mcg/kg) and the higher dose (0.5 mcg/kg) of DEX reveals a dose-dependent relationship in the attenuation of HR. Notably, the higher dose of DEX resulted in lower HR values during intubation. In summary, present findings highlight the dosage-dependent influence of DEX on HR responses during intubation. While lignocaine may not demonstrate a statistical advantage over lower doses of DEX, the impact of a higher DEX dose emphasises the importance of dosage precision in achieving desired haemodynamic outcomes.

In the study conducted by Gulabani M et al., the comparison between lignocaine (1.5 mg/kg) and two different doses of DEX (0.5 and 1 mcg/kg) revealed that the higher DEX dose of 1 mcg/kg exhibits a greater reduction in HR values at 1, 3, and 5 minutes after intubation compared to both the 0.5 mcg/kg dose of DEX and lignocaine (7). Additionally, Zhan-Ying G et al., concluded in their comparative evaluation of three different doses of DEX in elderly patients that a dose of 0.25 mcg/kg DEX does not serve as a very useful anaesthesia adjuvant to control haemodynamic stress response to intubation in this population (15). They noted a greater reduction in HR with 1.00 mcg/kg DEX as compared to 0.5 mcg/kg of DEX at the time of intubation (67.2±16.3 vs. 59.1±10.9) as well as five minutes after intubation (63.7±12.5 vs. 59.8±11.6). The authors also noted that 0.50 mcg/kg of DEX was associated with fewer cardiovascular effects but was still sufficient to prevent the tracheal intubation-evoked haemodynamic response in elderly patients (15).

Systolic Blood Pressure (SBP): This research demonstrated that the benefits of 0.5 mcg/kg DEX extended beyond the intubation period. Notably, 0.5 mcg/kg DEX consistently maintained low SBP values not only during intubation but also at one minute, three minutes, and five minutes post-intubation. This sustained effect suggests that DEX at 0.5 mcg/kg may offer prolonged haemodynamic stability during the critical post-intubation period.

In direct comparison to lignocaine, 0.5 mcg/kg of DEX demonstrated a noteworthy advantage, revealing substantially reduced SBP readings during and after intubation. This underscores the superior performance of DEX over lignocaine in mitigating the haemodynamic response, particularly in maintaining lower SBP levels. A significant decline in SBP with both 0.5 and 1 mcg/kg DEX was also reported by Sharma N and Mehta N (16). Kumari K et al., observed a significant difference in blood pressure values in patients who received DEX, with lower SBP noted in the DEX group up to five minutes post-intubation (8).

Diastolic Blood Pressure (DBP): The present findings show that the haemodynamic effects of DEX at a dose of 0.5 mcg/kg also encompass diastolic pressure dynamics. In comparison to lignocaine, DEX at 0.5 mcg/kg exhibited lower diastolic pressure values, with a more pronounced impact observed during the post-intubation period. Interestingly, when contrasted with the lower dose of DEX (0.25 mcg/kg), DBPs were not found to be statistically different, except at the time of intubation. This nuanced understanding of the DBP responses to varying DEX doses adds a layer of complexity to the present findings. While the 0.5 mcg/kg dosage demonstrates a clear advantage over lignocaine in terms of lower diastolic pressure values, the absence of statistically significant differences after intubation when compared to the lower DEX dose suggests that even a lower dose can provide similar haemodynamic stability. Kumari K et al., reported that the maximum percentage increase in DBP was lower in patients who received 0.5 mcg/kg DEX compared to those who received a placebo (19.36% vs. 60.36%) (8).

Administering DEX through an infusion at a loading dose of 0.5 mcg/kg has been found to be as therapeutically effective as a 1.0 mcg/kg dose. This effectiveness extends not only to decreasing the propofol induction dose but also to ensuring favourable intubating conditions and mitigating the haemodynamic response to intubation. Choosing the lower dose was associated with a reduced occurrence of adverse effects, including hypotension and bradycardia (16). The present study results suggest that doses as low as 0.25 mcg/kg could provide similar advantages in controlling the pressor response. As compared to lignocaine (1.5 mg/kg) and fentanyl (2 micrograms/kg), DEX (1 mcg/kg) led to a greater reduction in the SBP and DBP in the 3rd, 5th, and 10th minutes after intubation in the trial conducted by Mahjoubifard M et al., (17).

Mean Arterial Pressure (MAP): The reduction in MAP was also found to be greater in the DEX group than in the two other groups during the 3rd, 5th, and 10th minutes. The present investigation into MAP also revealed statistically significant differences between the lignocaine group and the subset receiving 0.5 mcg/kg of DEX. Notably, consistently lower MAP values were observed with the administration of 0.5 mcg/kg of DEX compared to lignocaine during and after intubation. This finding underscores the potential haemodynamic advantage associated with the 0.5 mcg/kg DEX dosage, suggesting its efficacy in maintaining a more favourable MAP during the observed period. The observed statistical significance between the lignocaine and 0.5 mcg/kg DEX groups indicates a noteworthy clinical impact, supporting the consideration of DEX as a preferred agent for haemodynamic control in specific contexts.

Interestingly, the present study did not reveal any significant difference in MAP between the groups receiving 0.25 mcg/kg of DEX and 0.5 mcg/kg of DEX. This suggests that, within the parameters of the present investigation, the incremental increase from 0.25 to 0.5 mcg/kg did not yield a discernible difference in MAP. The absence of significant variance in this comparison prompts further exploration into the optimal dosage range of DEX for achieving specific haemodynamic goals without undue fluctuations.

In contrast to present findings, Manne GR et al., observed a different outcome when comparing 0.2 mcg/kg/hr and 0.4 mcg/kg/hr doses of DEX in patients undergoing laparoscopic cholecystectomy (18). They reported that in both DEX groups, there was a significant decrease in MAP in the DEX 0.2 group and a highly significant decrease in the DEX 0.4 group after initiating the infusion. Following intubation and extubation, the pulse rate and MAP increased significantly above the pre-infusion level in the DEX 0.2 group, while in the DEX 0.4 group, they remained below the pre-infusion level. It is worth noting that the difference in findings between our study and that of Manne GR et al., could be attributed to the continuous infusion of DEX used in their study, which was not employed in our investigation (18).

In conclusion, the present findings highlight the significance of dosage precision in the administration of DEX, with the 0.5 mcg/kg dosage demonstrating superiority over lignocaine in maintaining consistently lower MAP values.

Elevated doses of DEX are linked to occurrences of bradycardia and hypotension. In the present study, the authors observed no instances of hypotension or bradycardia when employing doses of 0.25 mcg/kg and 0.5 mcg/kg of DEX. As expected, there was no statistically significant difference in the values of oxygen saturation when comparing lignocaine and DEX. Singh G et al., also reported no side effects in their study comparing 1 mcg/kg of DEX with 1.5 mg/kg of lignocaine (20). However, Mahjoubifard M et al., reported a higher incidence of hypotension and bradycardia with a dose of 1 mcg/kg of DEX (17). The administration of a single dose of 0.5 mcg/kg of DEX leads to a notable reduction in the elevation of HR, SBP, DBP, and MAP lasting up to five minutes after intubation, as indicated by various studies (8),(10),(14). However, the present results demonstrate that even a lower dose of DEX at 0.25 mcg/kg achieves nearly equivalent haemodynamic stability in terms of SBP, MAP, DBP, and HR, except for an increase in DBP and HR at the time of intubation.

Limitation(s)

The study was conducted at a single institute involving ASA 1 and 2 adult patients. As a result, the findings may not be applicable to different settings and cannot be generalised to paediatric, obstetric, or geriatric cohorts. Excluding patients with cardiovascular diseases limits the applicability of the study to high-risk groups. Additionally, the study does not account for genetic differences in drug metabolism, which could influence the findings.

Conducting studies across multiple centres and involving diverse cohorts would improve the generalisability of the results. This approach would provide a more varied patient population, thereby enhancing the understanding of how well the interventions work in different clinical environments. Furthermore, it would be beneficial for future research to focus on the analysis of cost-effectiveness, evaluating the economic implications of incorporating lignocaine or DEX into standard clinical procedures, taking into account both the costs of the drugs and the potential reduction in postoperative complications.

Conclusion

The present study demonstrates the significant haemodynamic advantages of using DEX, particularly at a dose of 0.5 mcg/kg, for managing cardiovascular responses during endotracheal intubation. This dosage not only effectively attenuates HR and blood pressure spikes but also maintains haemodynamic stability in the critical post-intubation period. Compared to lignocaine, DEX at 0.5 mcg/kg shows superior performance in reducing systolic, diastolic, and MAP without the associated risk of hypotension or bradycardia observed with higher doses.

DOI and Others

DOI: 10.7860/JCDR/2024/71081.20252

Date of Submission: Apr 09, 2024
Date of Peer Review: Jun 11, 2024
Date of Acceptance: Aug 02, 2024
Date of Publishing: Nov 01, 2024

Author declaration:
• Financial or Other Competing Interests: None
• Was Ethics Committee Approval obtained for this study? Yes
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. No

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