European Journal of Cardiovascular Medicine

Laparoscopic surgery(1) also known as minimally invasive surgery has become the standard approach for many abdominal procedures owing to its advantages over open surgery which includes reduced surgical trauma, less postoperative pain, shorter hospital stay, and faster recovery. However, the creation of carbon dioxide (CO₂) pneumoperitoneum and airway manipulation during general anaesthesia are associated with significant hemodynamic disturbances, which remain a concern for anaesthesiologists.

CO₂ pneumoperitoneum increases intra-abdominal pressure, leading to reduced venous return, reduced cardiac output, decreased lung compliance, impaired ventilation and increased systemic vascular resistance. These changes, compounded by CO₂ absorption and hypercarbia, result in sympathetic activation manifested as tachycardia and hypertension. In addition, laryngoscopy and endotracheal intubation provoke an acute stress response due to stimulation of the laryngeal and tracheal structures, causing abrupt increases in heart rate and arterial blood pressure. Such hemodynamic fluctuations may be detrimental, particularly in patients with limited cardiovascular reserve.

Dexmedetomidine, a highly selective presynaptic α₂-adrenergic agonist, is increasingly used as an anaesthetic adjunct because of its sedative, analgesic, and sympatholytic properties. By reducing central sympathetic outflow and attenuating catecholamine release, dexmedetomidine effectively blunts the pressor response to laryngoscopy and intubation.(2)(3) Its favourable effects on cardiovascular stability during CO₂ pneumoperitoneum, along with preservation of respiratory function, make it a promising agent in laparoscopic surgeries.

Although several studies have evaluated the role of dexmedetomidine in attenuating perioperative hemodynamic responses, evidence remains variable with respect to dosing regimens and timing of administration. Therefore, this randomised controlled study was undertaken to assess the efficacy of dexmedetomidine in attenuating hemodynamic responses to laryngoscopy, endotracheal intubation, and CO₂ pneumoperitoneum in patients undergoing laparoscopic surgery under general anaesthesia.

Study Design and Setting: This prospective, randomised, double-blind controlled trial was conducted in the Department of Anaesthesiology, GMERS Medical College and Hospital, Sola, Ahmedabad, from July 2022 to June 2024. The study protocol was approved by the Institutional Ethics Committee, and written informed consent was obtained from all participants prior to enrolment. Study Population: Patients aged 18–50 years with American Society of Anesthesiologists (ASA) physical status I and II, scheduled for elective laparoscopic cholecystectomy, laparoscopic appendicectomy, laparoscopic hernioplasty, or laparoscopic hysterectomy under general anaesthesia were included in the study. Inclusion Criteria: • Age between 18 and 50 years • ASA physical status I and II • Patients scheduled for elective laparoscopic surgeries Exclusion Criteria: • ASA physical status III and IV • Age <18 years or >50 years • Emergency surgeries • Patient refusal to participate Sample Size Calculation: The sample size was calculated to detect a clinically significant difference in hemodynamic parameters between the two groups. Assuming a type I error (α) of 0.01 and a power of 99% (type II error β of 0.01), with an expected difference in means of 7.5 and standard deviations of 7.68 and 6.16 in the two groups, the calculated sample size was 44 patients per group. To compensate for potential dropouts, a total of 90 patients were enrolled, with 45 patients allocated to each group. Randomization and Blinding: Patients were randomly allocated into two groups (45 each) using computer-generated random numbers: • Group D: Dexmedetomidine group • Group C: Control (0.9% normal saline) group Allocation concealment was achieved using a sealed envelope technique. The study was double-blinded, the study drug was prepared by an anaesthesiologist not involved in patient management or data collection, using identical syringes containing either dexmedetomidine or normal saline. Both the patients and the investigators recording observations were blinded to group allocation. Anesthetic Technique and Intervention: After written informed consent and thorough examination all patients received standardized balanced general anaesthesia. Group D received dexmedetomidine at a loading dose of 1 µg/kg infused over 10 minutes before induction, followed by a maintenance infusion of 0.5 µg/kg/h throughout the surgery. Group C received an equivalent volume of 0.9% normal saline at the same infusion rate. Premedication consisted of intravenous glycopyrrolate (0.2 mg), fentanyl (2mcg/kg), and ondansetron (4mg). Anaesthesia was induced with intravenous propofol (2.5 – 3 mg/kg) following lignocaine (2%) (1.5 mg/kg) administration. Endotracheal intubation was facilitated with intravenous succinylcholine (2 mg/kg), and neuromuscular blockade was maintained with intermittent boluses of atracurium (0.1 mg/kg). Anaesthesia was maintained with sevoflurane in oxygen and air. Intraoperative Monitoring: Standard monitoring included electrocardiography, non-invasive blood pressure, end tidal carbon dioxide levels and pulse oximetry. Hemodynamic parameters were recorded at baseline, after administration of the loading dose, post-intubation, during pneumoperitoneum, at 15-minute intervals intraoperatively, at deflation of pneumoperitoneum, after cessation of infusion, post-extubation and at the 2nd and 4th postoperative hour. Postoperative Assessment: Postoperatively, patients were monitored in the recovery room for 4 hours. Pain was assessed using a 10-point Visual Analogue Scale (VAS) on which 0 indicated no pain and 10 indicated worst pain imaginable. Tramadol 100 mg intravenously was given if VAS > 3 and ondansetron 4 mg intravenously was used to treat emesis. The degree of sedation was evaluated using the 6 point Ramsay Sedation Scale. 1 = Anxious or agitated and restless or both. 2 = Cooperative, oriented and tranquil. 3 = Drowsy but responds to commands. 4 = Asleep, brisk response to light glabellar tap or loud auditory stimulus. 5 = Asleep, sluggish response to light glabellar tap or loud auditory stimulus. 6 = Asleep and unarousable. Sedation score >3 is considered an undue sedation. Hemodynamic stability and adverse effects were also recorded. Outcome Measures: The primary outcome was the efficacy and safety of dexmedetomidine in attenuating perioperative hemodynamic responses. Secondary outcomes included duration of postoperative analgesia and sedation, and intraoperative requirement of additional anaesthetic agents. Statistical Analysis: Data were analysed using appropriate descriptive and inferential statistical methods. Continuous variables were expressed as mean ± standard deviation, and categorical variables as numbers and percentages. The statistical analysis was done using OPENEPI software by independent t-test for quantitative data and chi-square test for qualitative data. Significance of P value was suggested as follows: ‘P’ Value >0.05: insignificant. ‘P’ Value ≤0.05: significant ‘P’ Value< 0.001: highly significant.

A total of 90 adult patients, of either sex, belonging to ASA grade I and II, in age group of 18-50 years, were randomly selected and compared using bolus injection followed by infusion of dexmedetomidine (Group D, n = 45) or normal saline (Group C, n = 45) in laparoscopic surgeries for their efficacy in regard to pressor responses to intubation, extubation, hemodynamic stability and adverse events. Group D received dexmedetomidine at a loading dose of 1 µg/kg infused over 10 minutes before induction, followed by a maintenance infusion of 0.5 µg/kg/h throughout the surgery. Group C received an equivalent volume of 0.9% normal saline at the same infusion rate. All patients completed the study and were included in the final analysis.

Demographic and Baseline Characteristics:

The two groups were comparable with respect to age, sex distribution, body weight, ASA physical status, type of surgery, and duration of surgery (P > 0.05 for all variables). There were no statistically significant differences in baseline heart rate, systolic blood pressure, diastolic blood pressure, or oxygen saturation between the groups (P > 0.05).

Heart Rate

Baseline heart rates were comparable between the two groups (P = 0.689). Following administration of the loading dose, Group D demonstrated a significant reduction in heart rate compared with Group C (P < 0.001). After laryngoscopy and intubation, heart rate increased significantly in Group C, whereas Group D showed effective attenuation of this response (P < 0.001).

During pneumoperitoneum and throughout the intraoperative period, heart rate remained significantly lower and more stable in Group D compared to Group C (P < 0.001). Following extubation, Group C exhibited a significant rise in heart rate, while Group D maintained lower values (P < 0.001). The difference persisted up to 4 hours postoperatively (Table 1).

TABLE-1: MEAN HEART RATE(BEATS/MIN)

Systolic Blood Pressure

Baseline systolic blood pressure (SBP) was comparable between the groups (P = 0.245). After the loading dose of dexmedetomidine, Group D showed a significant reduction in SBP compared to Group C (P < 0.001). Marked attenuation of the pressor response to intubation and pneumoperitoneum was observed in Group D (P < 0.001).

SBP remained significantly lower in Group D during the early intraoperative period and after extubation (P < 0.05). No clinically significant hypotension was observed. SBP values became comparable between the groups by the late intraoperative and postoperative periods (Table 2).

TABLE-2: MEAN SYSTOLIC BLOOD PRESSURE (mm hg)

Diastolic Blood Pressure

Baseline diastolic blood pressure (DBP) was similar in both groups (P = 0.074). Following the loading dose, Group D demonstrated a significant reduction in DBP compared to Group C (P < 0.001). The rise in DBP associated with intubation and pneumoperitoneum was significantly attenuated in Group D (P < 0.001).

During extubation and early postoperative hours, DBP remained significantly lower in Group D compared to Group C (P < 0.001). DBP values were comparable between the groups at later postoperative time points (Table 3).

TABLE-3: MEAN DIASTOLIC BLOOD PRESSURE (mmhg)

Oxygen Saturation

Oxygen saturation (SpO₂) remained comparable between the two groups at all measured time points throughout the perioperative period (P > 0.05). No episodes of clinically significant desaturation were observed in either group.

Post-operative Pain (VAS)

VAS scores were significantly lower in Group D compared to Group C at 0, 2, and 4 hours postoperatively (P < 0.05). Patients receiving dexmedetomidine experienced better postoperative analgesia during the early recovery period (Table 4).

TABLE-4: MEAN VISUAL ANALOGUE SCORE (VAS)

Sedation (Ramsay Sedation Score)

Immediately postoperatively, Group D exhibited slightly higher sedation scores compared to Group C (P = 0.01). Sedation scores were comparable at 2 hours postoperatively (P = 0.874). By 4 hours, Group D had significantly lower sedation scores than Group C, indicating faster recovery without excessive sedation (P < 0.001) (Table 5).

TABLE-5: MEAN RAMSAY SEDATION SCORE (RSS)

In the present randomized double-blind controlled study, we demonstrated that perioperative administration of dexmedetomidine as a loading dose of 1mcg/kg over 10 minutes followed by continuous intraoperative infusion of 0.5 mcg/kg/hr significantly attenuated the hemodynamic responses to various noxious stimuli associated with laryngoscopy-intubation, laparoscopic surgeries. Patients receiving dexmedetomidine (Group D) exhibited significantly lower heart rate, systolic blood pressure, and diastolic blood pressure compared to the control group – normal saline group (Group C) at most perioperative time points, particularly following laryngoscopy, endotracheal intubation, creation of pneumoperitoneum, and during emergence from anaesthesia (P < 0.001).

Hemodynamic Responses during laparoscopic surgery and airway manipulation

Laparoscopic surgery(1) is associated with characteristic hemodynamic alterations resulting from the combined effects of pneumoperitoneum and carbon dioxide absorption which is exaggerated by anesthetic agents, patient positioning. Among these, pneumoperitoneum-induced elevation of intra-abdominal pressure (IAP) remains the principal determinant of cardiovascular changes. An increase in IAP beyond 10–12 mm Hg leads to a reduction in venous return secondary to inferior vena cava compression and increased intrathoracic pressure, resulting in a decrease in cardiac output by approximately 10–30%. Despite this reduction in preload, central venous pressure and pulmonary capillary wedge pressure often increase paradoxically due to external mechanical compression rather than true volume expansion.

Pneumoperitoneum also induces a rise in systemic and pulmonary vascular resistance, mediated by mechanical vascular compression and activation of neurohumoral pathways, including catecholamine and vasopressin release. The consequent increase in afterload manifests as elevated mean arterial pressure and may precipitate pulmonary hypertension. These effects are accentuated in the Reverse-Trendelenburg position, where gravitational pooling further compromises venous return. Although cardiac index frequently declines during the initial phase of insufflation, it generally stabilizes within 10 minutes in healthy individuals; however, the magnitude of decline correlates directly with IAP and may be poorly tolerated in patients with compromised cardiac reserve.

In addition to pneumoperitoneum, laryngoscopy and

endotracheal intubation evoke a pronounced sympathetic response due to stimulation of oropharyngeal and laryngeal mechanoreceptors. This results in catecholamine release, leading to tachycardia, increased systemic vascular resistance, and elevated arterial pressure, thereby increasing myocardial oxygen demand. Such responses may be detrimental in patients with coronary artery disease, hypertension, or cerebrovascular pathology, predisposing them to myocardial ischemia, arrhythmias, or intracranial hemorrhage.

Dexmedetomidine, a highly selective α2-adrenergic agonist, effectively attenuates these stress responses by inhibiting central sympathetic outflow and reducing norepinephrine release. Its administration results in controlled heart rate reduction, decreased myocardial oxygen consumption, and attenuation of hypertension associated with both intubation and pneumoperitoneum.(2)(3)(4) Additionally, its modest vasodilatory effect counteracts pneumoperitoneum-induced increases in systemic vascular resistance. These findings suggest that dexmedetomidine effectively blunts the sympathetic stress response inherent to laparoscopic procedures and laryngoscopy and intubation. The sedative and analgesic properties of dexmedetomidine, achieved without significant respiratory depression, further contribute to anesthetic stability and reduced intraoperative anesthetic and opioid requirements in laparoscopic surgeries.(5)(6)(7)

In the absence of dexmedetomidine, exaggerated sympathetic responses during airway manipulation and laparoscopic insufflation may necessitate the use of alternative pharmacological agents such as beta-blockers, opioids, vasodilators, or calcium channel blockers. While these agents are effective, their use often requires careful titration and may be associated with variable hemodynamic control and additional adverse effects.

Preventive strategies aimed at minimizing hemodynamic disturbances include maintaining low IAP (≤10–12 mm Hg), slow CO₂ insufflation, adequate depth of anesthesia, judicious fluid administration, and appropriate patient positioning. Pharmacological modulation using agents with sympatholytic and vasodilatory properties remains central to achieving cardiovascular stability during laparoscopic procedures.

The hemodynamic stability observed in the dexmedetomidine group can be attributed to its central sympatholytic action mediated through selective α-2 adrenergic receptor agonism. Dexmedetomidine reduces norepinephrine release by activating presynaptic α-2 receptors in the locus coeruleus and medullary vasomotor center, resulting in decreased sympathetic outflow and enhanced parasympathetic tone. This mechanism explains the consistent reduction in heart rate and blood pressure observed in Group D (P < 0.001) throughout the intraoperative period without compromising oxygen saturation. The preservation of SpO₂ in both groups (P > 0.05) indicates that dexmedetomidine did not cause clinically significant respiratory depression, which is a notable advantage over other sedative-analgesic agents.

Demographic characteristics:

In our study, the demographic characteristics, including age, sex, weight, ASA physical status, type of surgery, and duration of surgery, were comparable between the two groups (P > 0.05), ensuring that observed differences in outcomes were attributable to the pharmacological effects of dexmedetomidine rather than confounding variables. This strengthens the internal validity of our study and aligns with findings from previous randomized controlled trials.

Heart rate:

In the present study, baseline heart rate values were comparable (P > 0.05) between the two groups, confirming similar preoperative autonomic status However, following the administration of dexmedetomidine, a significant and sustained reduction in heart rate was observed in Group D (p < 0.001) at almost all measured intervals, including after intubation, during pneumoperitoneum, and into the postoperative period. This attenuation of tachycardic responses highlights the efficacy of dexmedetomidine in suppressing perioperative sympathetic activation. These findings are consistent with those reported by Kumari et al.(8), Bhattacharjee et al.(9), and Chavan et al.(10) who also observed significant reductions in heart rate with dexmedetomidine during laparoscopic surgeries.

In 2016, Shirishkumar G Chavan et al.(10) conducted a study to assess the effects of dexmedetomidine on perioperative parameters and recovery in laparoscopic cholecystectomy patients. Sixty patients were randomly divided into  two  groups:  Group  A  (n=30):  Patients  received  dexmedetomidine intravenously as a loading dose of 1 μg/kg over 10 minutes, followed by an infusion of 0.2-0.8 μg/kg/hr. Group B (n=30): Patients received normal saline. The study found that dexmedetomidine significantly reduced the stress response to intubation with HR (86.00 ± 5.16 vs. 102.97 ± 7.07/min.), mean BP (95.78 ± 5.35 vs. 110.18 ± 5.35) as compared to the control group (P < 0.05) and after pneumoperitoneum, HR was 85.07 ± 6.23 versus 107.10 ± 4.98, mean BP was 98.98 ± 10.16 versus 118.54 ± 6.27 (P < 0.05) leading to lower heart rate and blood pressure compared to the control group.

Systolic - Diastolic blood pressure:

Similarly, systolic blood pressure remained significantly lower in the dexmedetomidine group during key stress-inducing events such as intubation and pneumoperitoneum. Although the difference became less pronounced at certain later time points and following cessation of infusion, the overall trend favored better blood pressure control in Group D. A transient rise in systolic blood pressure noted at deflation of pneumoperitoneum may be explained by withdrawal of the drug effect and physiological responses to changes in intra-abdominal pressure. Comparable findings have been reported by Sarkar et al.(11), Neil and Patel(12) reinforcing the role of dexmedetomidine in stabilizing systolic blood pressure during laparoscopic procedures.

Diastolic blood pressure followed a similar pattern, with Group D demonstrating significantly lower values than Group C (p < 0.001) during most intraoperative phases, particularly after drug administration, intubation, and pneumoperitoneum. Although the differences diminished after 60 minutes and in the late postoperative period, the overall reduction in diastolic pressure reflects effective modulation of vascular tone by dexmedetomidine. These observations align with studies by Vora et al.(5) of which reported improved diastolic blood pressure control with dexmedetomidine use.

In 2015, Kalpana S. Vora et al.(5) assessed the effects of dexmedetomidine on hemodynamic changes and its role as an anesthetic adjunct in laparoscopic surgeries. The study involved 70 patients who were randomly assigned to receive either dexmedetomidine (Group D) or normal saline (Group S). Group D received a loading dose of 1 µg/kg followed by a maintenance infusion of 0.5 µg/kg/h, while Group S received saline. Results indicated that Group D experienced significantly lower intraoperative heart rates and mean arterial pressures compared to Group S, demonstrating better hemodynamic stability. 

Analgesia:

An important finding of our study was the improved postoperative analgesia observed in the dexmedetomidine group. Patients in Group D consistently reported lower VAS scores at 0, 2, and 4 postoperative hours compared to the control group, with statistically significant differences (p < 0.001). The analgesic effect of dexmedetomidine is mediated through α-2 receptor activation in the dorsal horn of the spinal cord, resulting in inhibition of nociceptive neurotransmission. This opioid-sparing property has been widely documented and was also evident in our study, contributing to improved patient comfort in the early postoperative period. Similar analgesic benefits have been reported in 2012, by Patel et al.(4) who conducted a randomized controlled trial on 60 patients undergoing elective surgeries to assess the effects of dexmedetomidine on perioperative hemodynamics and recovery. Sixty patients were randomly divided into two groups of 30 each. In group A, fentanyl 2 μg/kg and in group B dexmedetomidine were given intravenously as loading dose of 1 μg/kg over 10 min prior to induction. After induction, in group B, dexmedetomidine was given as infusion at a dose of 0.2-0.8 μg/kg. Postoperative analgesia as assessed by VAS, showed significant analgesic effect of dexmedetomidine with a mean score of 5.70±0.60 as compared to 8.13±0.70 of the control group.

Sedation:

Sedation assessment using the Ramsay Sedation Scale revealed that patients receiving dexmedetomidine experienced slightly higher sedation scores (p = 0.01) immediately postoperatively, which gradually normalized over time. By the second postoperative hour, sedation levels were comparable between the two groups, and by the fourth hour, Group D exhibited significantly lower sedation scores than Group C. This finding suggests that dexmedetomidine provides cooperative, easily arousable sedation that resolves predictably without delaying recovery. The sedative effect is attributed to inhibition of neuronal firing in the locus coeruleus, producing a sleep-like state without respiratory compromise. These results are consistent with observations made by Srivastava et al.(13) Notably, oxygen saturation remained stable and comparable between both groups throughout the perioperative and postoperative periods. This confirms that dexmedetomidine, even when administered as a loading dose followed by infusion, does not adversely affect respiratory function. The absence of hypoxia further supports its safety profile as an anesthetic adjuvant.

Limitations

Despite its strengths, our study has certain limitations. The relatively small sample size and single-center design may limit generalizability. Additionally, the exclusion of high-risk patients (ASA III and IV) restricts applicability to broader patient populations. Long-term outcomes such as cognitive recovery and patient satisfaction were not assessed, and future multicenter studies with larger sample sizes are warranted.

In this randomized double-blind controlled trial, dexmedetomidine administered as a loading dose of 1 µg/kg over 10 minutes followed by an infusion of 0.5 µg/kg/h significantly attenuated perioperative hemodynamic responses during laparoscopic surgery. Compared with saline, dexmedetomidine provided superior control of heart rate and arterial pressure during laryngoscopy, endotracheal intubation, pneumoperitoneum, and extubation. Patients receiving dexmedetomidine also demonstrated improved postoperative analgesia with lower Visual Analogue Scale scores and a favorable sedation profile without clinically significant respiratory depression or adverse events. These findings indicate that dexmedetomidine is an effective and safe adjunct to general anesthesia for maintaining hemodynamic stability and enhancing postoperative recovery in elective laparoscopic procedures. Its routine use at the studied doses may improve perioperative cardiovascular control and patient comfort.

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