European Journal of Cardiovascular Medicine

Direct laryngoscopy and endotracheal intubation can activate sympathetic and sympathoadrenal pathways, causing transient increases in heart rate (HR), systolic and diastolic blood pressure, and mean arterial pressure (MAP). These changes usually peak within the first few minutes after intubation. Although brief in many healthy adults, marked haemodynamic fluctuations may increase myocardial oxygen demand and can be undesirable in patients with limited cardiovascular reserve. The magnitude of the response is influenced by factors such as airway stimulation, duration and number of laryngoscopy attempts, depth of anaesthesia, and the drugs used during induction.

Dexmedetomidine is a selective α₂-adrenergic agonist with sedative, analgesic, and sympatholytic effects. By reducing central sympathetic outflow and norepinephrine release, it may blunt the cardiovascular response to airway manipulation. Its use before induction has been studied at several doses and by different administration schedules. However, the dose that offers useful attenuation while limiting bradycardia, hypotension, and excessive sedation remains a clinical consideration.

Sebastian et al. compared intravenous dexmedetomidine doses with placebo and reported attenuation of haemodynamic responses, while also examining the balance between dose and adverse effects [1]. Sharma et al. found that 0.5 and 1.0 µg/kg doses both blunted the response in their trial, with fewer adverse effects reported with the lower dose [2]. In a study of patients undergoing cardiac surgery, Silpa et al. found that 1.0 µg/kg provided greater suppression of the post-intubation response than 0.5 µg/kg [3]. A meta-analysis by De Cassai et al. supported the haemodynamic efficacy of intravenous dexmedetomidine compared with no dexmedetomidine, while considering adverse events such as bradycardia and hypotension [4]. More recent work by Singh et al. also assessed intravenous dexmedetomidine and haemodynamic outcomes around laryngoscopy and intubation [5]. Findings across studies may differ with patient population, anaesthetic technique, dose, infusion timing, and outcome measurement.

A direct comparison of intravenous dexmedetomidine 0.5 µg/kg and 1.0 µg/kg in patients undergoing elective surgery can help clarify their relative effects on HR and blood pressure, as well as their safety profiles. This prospective comparative study evaluated both doses using standardized anaesthesia, serial haemodynamic measurements, and monitoring for adverse events and sedation.

AIM

To compare the efficacy and safety of intravenous dexmedetomidine 0.5 µg/kg versus 1.0 µg/kg in attenuating haemodynamic responses to laryngoscopy and endotracheal intubation.

OBJECTIVES

1. To compare serial heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure between the two dose groups.
2. To compare the incidence of adverse events, including bradycardia, hypotension, hypertension, and arrhythmias.
3. To compare the level of sedation achieved with each dose using the Ramsay Sedation Score.

Source of Data

Data were obtained from adult patients undergoing elective surgery under general anaesthesia with endotracheal intubation in the Department of Anaesthesiology. After institutional ethics committee approval, eligible patients who provided written informed consent were enrolled. The attached thesis identifies the study institution as PCMC’s PGI YCM Hospital, Pimpri, Pune, and describes a 12-month study period.

Study Design

The study was conducted as a prospective, randomized, double-blind, parallel-group comparative study. Participants were allocated to receive intravenous dexmedetomidine 0.5 µg/kg or 1.0 µg/kg before induction of general anaesthesia.

Study Location

The study was conducted in the Department of Anaesthesiology, PCMC’s Postgraduate Institute and YCM Hospital, Pimpri, Pune.

Study Duration

The study was conducted over 12 months following approval by the institutional ethics committee.

Sample Size

The sample size was rounded up to 32 participants per group, giving a total sample size of 64 participants.

Inclusion Criteria

Patients were included if they:

• Were 18–65 years of age and of either sex.
• Had American Society of Anesthesiologists (ASA) physical status I or II.
• Were scheduled for elective surgery under general anaesthesia requiring endotracheal intubation.
• Provided written informed consent.

Exclusion Criteria

Patients were excluded if they had:

• ASA physical status III or higher.
• Known cardiovascular disease, clinically significant arrhythmia, conduction abnormality, or baseline bradycardia.
• Known allergy or contraindication to dexmedetomidine or study medications.
• Significant hepatic, renal, neurological, or respiratory disease.
• Current use of beta-blockers, calcium-channel blockers, ACE inhibitors, or other drugs likely to alter the haemodynamic response.
• Emergency surgery, a full stomach, pregnancy, or an anticipated difficult airway.
• Failed, traumatic, prolonged, or multiple-attempt intubation.

Procedure and Methodology

After preoperative assessment, fasting status and eligibility were confirmed, and written informed consent was obtained. Patients were assigned to one of two groups using a computer-generated randomization sequence. Allocation was concealed in sequentially numbered, opaque envelopes. A clinician not involved in patient monitoring prepared the study medication in identical syringes labelled with the participant’s study code, maintaining blinding of the patient and outcome assessor.

Group A received dexmedetomidine 0.5 µg/kg intravenously, and Group B received dexmedetomidine 1.0 µg/kg intravenously. Each dose was diluted with normal saline to the same volume and infused over 10 minutes, with the infusion completed 5 minutes before induction. No routine anticholinergic premedication was administered, to avoid its potential effect on heart rate.

After securing intravenous access, standard monitoring was instituted, including electrocardiography, non-invasive blood pressure, pulse oximetry, and capnography. Baseline heart rate, systolic blood pressure, diastolic blood pressure, MAP, and oxygen saturation were recorded after the patient had rested supine. The same anaesthetic protocol was followed in both groups. Anaesthesia was induced with intravenous fentanyl and propofol, followed by a non-depolarizing neuromuscular blocking agent. Direct laryngoscopy was performed by an experienced anaesthesiologist, and endotracheal intubation was attempted once adequate neuromuscular blockade was achieved. The duration of laryngoscopy and number of attempts were recorded.

Heart rate, systolic blood pressure, diastolic blood pressure, and MAP were recorded at baseline, after study-drug infusion, after induction and before intubation, immediately after intubation, and at 1, 3, 5, and 10 minutes after intubation. The primary outcome was the between-group difference in heart rate at 5 minutes after intubation. Changes in the other haemodynamic variables over time were assessed as secondary outcomes. Sedation was evaluated using the Ramsay Sedation Score before study-drug administration and after infusion. Hypotension, hypertension, bradycardia, tachycardia, arrhythmias, and any requirement for rescue treatment were documented and managed according to a predefined institutional protocol.

Sample Processing

No blood, tissue, or other biological samples were collected for laboratory analysis. Physiological measurements were recorded directly from the patient monitors at the predefined time points. The case record forms were checked for completeness, coded, and entered into the study database before analysis.

Statistical Methods

Data were entered into Microsoft Excel and analysed using IBM SPSS Statistics version 26. Continuous variables were summarized as mean and standard deviation or median and interquartile range, as appropriate. Categorical variables were summarized as frequency and percentage. Distribution of continuous variables was assessed using the Shapiro–Wilk test.

Between-group comparisons were performed using the independent-samples t test for normally distributed continuous variables and the Mann–Whitney U test for non-normally distributed variables. Repeated haemodynamic measurements were analysed using repeated-measures analysis of variance or a linear mixed-effects model, as appropriate. Categorical outcomes were compared using the chi-square test or Fisher’s exact test. Results were reported with effect estimates and 95% confidence intervals where applicable. A two-sided p value <0.05 was considered statistically significant.

Data Collection

A structured case record form was used to collect demographic details, ASA physical status, medical and medication history, preoperative assessment findings, type of surgery, anaesthetic and intubation details, study-drug dose and timing, serial haemodynamic values, sedation scores, and adverse events. Each participant was assigned a unique study code, and identifying information was kept separate from the analysis dataset.

Table 1: Baseline demographic and procedural characteristics

The study included 31 patients in each dose group. Baseline demographic and procedural characteristics were comparable. Mean age was 35.82±6.10 years in the 0.5 µg/kg group and 37.75±6.95 years in the 1.0 µg/kg group (p=0.250). The groups had similar sex distributions, body weight, height, ASA physical status, and duration of laryngoscopy; none of the between-group differences was statistically significant (all p>0.05). These findings indicate that the groups were similar in the measured baseline characteristics.

Table 2: Serial haemodynamic measurements

Haemodynamic values were similar between groups at baseline for heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure. After intubation, the 1.0 µg/kg group had lower mean systolic blood pressure immediately after intubation (T3: 121.5±6.8 vs 127.7±6.4 mmHg; p=0.001) and at 3 minutes (T4: 115.3±6.6 vs 120.2±6.5 mmHg; p=0.005). Diastolic blood pressure was lower in the 1.0 µg/kg group immediately after intubation (68.1±5.8 vs 72.5±6.1 mmHg; p=0.005), while the differences at 3 and 5 minutes were not statistically significant. Heart rate differed significantly only at 3 minutes, when it was lower in the 1.0 µg/kg group (66.4±7.0 vs 70.7±9.3 beats/min; p=0.044). Mean arterial pressure did not differ significantly between groups at any measured time point.

Table 3: Adverse events and complications

Adverse events were uncommon in both groups, and no statistically significant between-group differences were observed. Hypotension occurred in one patient (3.2%) in the 1.0 µg/kg group and none in the 0.5 µg/kg group (p=1.000). Bradycardia occurred in two patients (6.5%) receiving 0.5 µg/kg and one patient (3.2%) receiving 1.0 µg/kg (p=1.000). No nausea, vomiting, or respiratory depression was reported in either group. Hypertension and arrhythmia counts were not reported separately in the source results, so their occurrence cannot be determined from this table.

Table 4: Ramsay Sedation Score distribution

Ramsay Sedation Scores showed a shift toward deeper sedation in the 1.0 µg/kg group. Scores of 2 or 3 were more frequent in the 0.5 µg/kg group, whereas scores of 4 to 6 were more frequent in the 1.0 µg/kg group. The overall ordinal score distribution differed between groups (Mann–Whitney U=251; approximate p=0.001). A score of 4 or higher was recorded in 19/31 patients (61.3%) receiving 1.0 µg/kg, compared with 7/31 (22.6%) receiving 0.5 µg/kg; the difference was 38.7 percentage points (95% CI 14.2 to 57.4; p=0.004).

Table 1. Baseline demographic and procedural characteristics

The two groups were comparable in the measured baseline variables. There were no statistically significant differences in age, sex distribution, weight, height, ASA physical status, or laryngoscopy duration; all reported p values exceeded 0.05. The mean age difference was small (−1.93 years; 95% CI −5.25 to 1.39), as was the difference in laryngoscopy duration (+0.60 seconds; 95% CI −1.28 to 2.48). This comparability is consistent with dose-comparison trials by Jarineshin et al. (2015)[1], Kakkar et al. (2016)[3], Sebastian et al. (2017)[5], Sharma et al. (2018)[8], and Jain et al. (2023)[19], which enrolled similar elective-surgery populations and reported comparable baseline characteristics. Comparable groups make the haemodynamic comparisons easier to interpret, although they do not rule out confounding from factors not shown here, such as anaesthetic depth, premedication, or intubation technique.

Table 2. Serial haemodynamic measurements

At baseline, the two groups had similar heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP). The between-group differences were statistically significant at only a few post-induction time points: SBP was lower in the 1.0 µg/kg group immediately after intubation and at 3 minutes; DBP was lower immediately after intubation; and heart rate was lower at 3 minutes. MAP did not differ significantly at any measured time point. Thus, the results suggest some additional suppression of SBP and DBP with 1.0 µg/kg, but do not show a consistent difference across all haemodynamic measures and time points.

Previous direct dose-comparison trials have reported mixed results. Gulabani et al. (2015)[2] and Jain et al. (2023)[19] reported stronger haemodynamic suppression with the higher dose, which is consistent with the lower post-intubation SBP in the present table. Silpa et al. (2020)[12] also found 1.0 µg/kg more effective than 0.5 µg/kg in elective cardiac surgery. In contrast, Jarineshin et al. (2015)[1] and Sharma and Mehta (2018)[8] reported broadly similar attenuation with the two doses; Sebastian et al. (2017)[5] found that an intermediate dose could provide effective attenuation. Differences in patient risk, drug infusion time, anaesthetic technique, and outcome timing may help explain this variation. Other studies of dexmedetomidine—including those comparing it with active drugs or alternative administration routes—support its ability to blunt parts of the intubation response, while also showing that the measured effect varies by parameter and protocol [3,4,7,9–11,13,14,16,18].

The differences in this table should be interpreted as selective rather than a uniform advantage of the 1.0 µg/kg dose. In particular, MAP remained statistically similar throughout, and heart-rate differences were significant at only one time point. Multiple unadjusted comparisons were made, so isolated p values near 0.05 should be treated cautiously. The haemodynamic measures had already fallen after drug administration and induction, before intubation; therefore, lower post-intubation readings may reflect the combined effects of dexmedetomidine and the anaesthetic regimen, rather than the intubation response alone. The dose-specific pattern differs across trials, including the BIS-guided trial by Jain et al. (2023)[19], which found lower haemodynamic values with 1.0 µg/kg, and the route-comparison trial by Singh et al. (2024)[20], which found no significant MAP difference between intravenous and inhaled regimens.

Table 3. Adverse events and complications

Adverse events were infrequent, and none of the reported comparisons was statistically significant. Hypotension occurred in one patient receiving 1.0 µg/kg, while bradycardia occurred in two patients receiving 0.5 µg/kg and one patient receiving 1.0 µg/kg. The wide confidence intervals reflect the small number of events and do not establish that the doses have equivalent safety. This is consistent with the uncertainty seen in dexmedetomidine research: the meta-analysis by De Cassai et al. (2021)[15] found haemodynamic attenuation but also identified bradycardia and hypotension as relevant potential adverse effects; later reviews likewise emphasize heterogeneity and the limited power of individual trials to assess uncommon harms [18,21,22]. Studies using lower doses or different routes have also reported variable adverse-event profiles [6,14,16,17].

Hypertension and arrhythmia were not reported separately in the supplied adverse-event table. Their absence from the table cannot be interpreted as zero occurrences. Larger trials and systematic reviews are needed to compare uncommon safety outcomes reliably.

Table 4. Ramsay Sedation Score distribution

Sedation scores shifted toward deeper levels in the 1.0 µg/kg group. A Ramsay score of 4 or higher occurred in 19/31 patients (61.3%) in that group, compared with 7/31 (22.6%) in the 0.5 µg/kg group; the difference was 38.7 percentage points (95% CI 14.2 to 57.4; p=0.004). The overall score distribution also differed (Mann–Whitney U=251; approximate p=0.001). This dose-related increase in sedation is clinically relevant because it accompanies the observed reductions in some haemodynamic measures. Sharma and Mehta (2018)[8] likewise reported fewer adverse effects with the lower dose, while Jain et al. (2023)[19] observed sedation after both doses. Route-comparison work by Niyogi et al. (2019)[11] and Singh et al. (2024)[20] also found that intravenous administration could produce greater sedation than non-intravenous routes. Together, these findings support assessing sedation alongside haemodynamic control when choosing a dose.

Both intravenous dexmedetomidine doses were associated with lower heart rate and blood pressure measurements after study drug administration and induction. Compared with 0.5 µg/kg, the 1.0 µg/kg dose was associated with lower systolic blood pressure immediately after intubation and at 3 minutes, lower diastolic blood pressure immediately after intubation, and lower heart rate at 3 minutes. Mean arterial pressure did not differ significantly between groups at any measured time point. These selective differences suggest a modest advantage of the higher dose for attenuating some post-intubation haemodynamic responses, rather than a consistent effect across all measures and time points.

The 1.0 µg/kg dose produced higher Ramsay Sedation Scores, while the recorded adverse events were uncommon and did not differ significantly between groups. Overall, the higher dose provided greater sedation and some additional haemodynamic attenuation, but the findings should be interpreted alongside the small number of participants, the sparse adverse-event counts, and the time-specific nature of the comparisons.

LIMITATIONS

This study included 62 participants, with 31 in each dose group. The sample may have been insufficient to detect uncommon adverse events or small between-group differences. The findings may also have limited generalisability beyond the population and clinical setting studied.

Haemodynamic measurements were compared separately at each time point using unadjusted tests based on rounded summary data. These comparisons do not account for the correlation between repeated measurements in the same participant or adjust for the number of time-point comparisons. Patient-level data and a repeated-measures analysis would be needed to assess the overall pattern of change more robustly. The statistical values should therefore be checked against the original dataset before final reporting.

Adverse events were infrequent, limiting the precision of comparisons. Hypertension and arrhythmia were not reported separately in the provided results, so their incidence could not be evaluated. The higher Ramsay scores indicate greater sedation, but the available results do not establish whether this difference affected recovery or patient satisfaction. Finally, the study compared two doses only; it cannot determine the optimal dose or compare dexmedetomidine with other strategies

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