Background: Laryngoscopy, tracheal intubation, and pneumoperitoneum during laparoscopic surgery provoke significant sympathetic stimulation, resulting in tachycardia and hypertension. Pharmacological attenuation of this hemodynamic stress response is essential to improve perioperative stability. This study compared dexmedetomidine and fentanyl for their effectiveness in controlling hemodynamic responses during these critical periods. Material and methods: This prospective, randomized, double-blind study included 100 adult patients of ASA physical status I and II undergoing elective laparoscopic surgery under general anaesthesia. Patients were randomly allocated into two groups (n = 50 each). Group D received dexmedetomidine (1 µg/kg loading dose followed by 0.2 µg/kg/h infusion), while Group F received fentanyl in an equivalent dosing regimen. Heart rate, systolic, diastolic, and mean arterial blood pressure, and oxygen saturation were recorded at baseline, during airway manipulation, throughout pneumoperitoneum, at extubation, and during the postoperative period up to 6 hours. Demographic variables were also compared. Results: Baseline demographic characteristics and initial hemodynamic parameters were comparable between the two groups. Dexmedetomidine produced a significantly greater attenuation of heart rate and blood pressure responses following the loading dose, during laryngoscopy and intubation, throughout pneumoperitoneum, and at extubation compared with fentanyl. The differences were most pronounced during periods of maximal surgical stress. Hemodynamic parameters gradually returned toward baseline values in both groups during late postoperative monitoring, with no significant intergroup differences at 3 and 6 hours. Oxygen saturation remained stable and comparable between the groups at all time points. Conclusion: Dexmedetomidine provides superior control of hemodynamic stress responses compared with fentanyl during laparoscopic surgery, without compromising oxygenation. Its use contributes to improved perioperative hemodynamic stability during airway manipulation and pneumoperitoneum
Laparoscopic surgery has become increasingly prevalent due to its advantages of reduced postoperative pain, shorter hospital stays, and faster recovery compared with open procedures. However, the creation of pneumoperitoneum and airway manipulation during anaesthesia can elicit significant hemodynamic stress responses, characterized by elevations in heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) due to sympathetic stimulation. These responses can increase perioperative morbidity, particularly in patients with cardiovascular comorbidities, making their attenuation a key goal in anaesthetic management [1].
Direct laryngoscopy and tracheal intubation are well documented to provoke a surge in catecholamine release, leading to transient but clinically relevant increases in HR and blood pressure [2]. Similarly, pneumoperitoneum-induced increases in intra-abdominal pressure can further augment cardiovascular responses through neurohumoral activation and mechanical effects on venous return [3]. Effective modulation of these physiological responses is essential to ensure hemodynamic stability during laparoscopic surgery.
Fentanyl, a potent synthetic opioid, is frequently used in anaesthetic practice for its analgesic properties and its ability to blunt the sympathoadrenal response to noxious stimuli. Intravenous fentanyl has been shown to attenuate the pressor response to laryngoscopy and intubation in a dose-dependent manner [4]. Nevertheless, its use may be limited by side effects such as respiratory depression and potential for postoperative nausea.
Dexmedetomidine, a highly selective α2-adrenergic agonist, exerts sedative, analgesic, and sympatholytic effects without significant respiratory depression. It has gained attention in perioperative medicine due to its ability to provide more stable hemodynamic control through central inhibition of sympathetic outflow, thereby attenuating stress responses to both intubation and pneumoperitoneum [5,6]. Several clinical studies suggest that dexmedetomidine may offer superior modulation of perioperative hemodynamic changes compared with traditional agents like fentanyl in laparoscopic surgery [7].
Given this context, the present study was designed to compare the effects of dexmedetomidine and fentanyl on hemodynamic stress responses during laryngoscopy, pneumoperitoneum, and the perioperative period in patients undergoing elective laparoscopic procedures
After obtaining approval from the Institutional Ethics Committee (IEC No. IEC/RESCH/01/2020) and written informed consent from all participants, this prospective, randomized, double-blind study was conducted in the Department of Anaesthesiology, Gujarat Adani Institute of Medical Sciences, Bhuj, between April 2020 and July 2021.
Study population: A total of 100 adult patients scheduled for elective laparoscopic surgery under general anaesthesia were enrolled. Patients aged 18–50 years, weighing 40–80 kg, and belonging to American Society of Anesthesiologists (ASA) physical status I or II were included. Patients who refused consent, had ASA grade III or higher, anticipated difficult airway (Mallampati grade IV with mouth opening <2 fingers), significant cardiovascular, respiratory, neurological, metabolic disorders, severe hypotension, pregnancy, or those receiving beta-blockers or having documented coronary artery disease or left ventricular dysfunction were excluded.
Randomization and study groups: Eligible patients were randomly allocated into two equal groups of 50 each using a randomization method, ensuring double blinding of both the patient and the investigator recording data.
Preoperative assessment and monitoring: All patients underwent a detailed pre-anaesthetic evaluation one day prior to surgery, including history, physical examination, airway assessment, and routine investigations. On the day of surgery, baseline vital parameters were recorded in the pre-operative area. After shifting to the operating room, standard monitoring was instituted, including electrocardiography, non-invasive blood pressure monitoring, and pulse oximetry.
Baseline heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and peripheral oxygen saturation (SpO₂) were recorded before administration of the study drug.
Anaesthetic technique: All patients were premedicated intravenously with glycopyrrolate (4 µg/kg), ondansetron (80 µg/kg), and midazolam (10 µg/kg). Following preoxygenation with 100% oxygen for 5 minutes, induction of anaesthesia was achieved with propofol (2.5 mg/kg IV) and succinylcholine (2 mg/kg IV) to facilitate tracheal intubation. Anaesthesia was maintained with a mixture of oxygen and nitrous oxide (50:50), atracurium for neuromuscular blockade, controlled ventilation, and inhalational agents (isoflurane or sevoflurane) as required.
Data collection: Hemodynamic parameters—HR, SBP, DBP, MAP—and SpO₂ were recorded at predefined time intervals corresponding to the peri-intubation period, pneumoperitoneum, extubation, and postoperative recovery. These included baseline (before study drug administration), after loading dose, during laryngoscopy and intubation, at various intervals during pneumoperitoneum, at extubation, and during the postoperative period up to 6 hours.
Statistical analysis: Data were compiled and analyzed using GraphPad statistical software. Continuous variables were expressed as mean ± standard deviation. Intergroup comparisons were performed using the unpaired Student’s t-test. A p value <0.05 was considered statistically significant.
The two study groups were comparable with respect to baseline demographic and clinical characteristics. There were no statistically significant differences between Group D and Group F in terms of age, body weight, sex distribution, or ASA physical status, indicating adequate matching and minimizing confounding due to baseline variables (Table 1).
Baseline heart rate was similar between the groups. Following administration of the study drugs, Group D demonstrated a sustained attenuation of heart rate compared with Group F across most intraoperative time points. This difference became evident after the loading dose and persisted during laryngoscopy, tracheal intubation, and throughout pneumoperitoneum. The divergence in heart rate response remained significant during extubation and the early post-extubation period. However, heart rate values converged between the two groups during late postoperative follow-up, with no significant differences observed at 3 and 6 hours (Table 2). These findings suggest superior suppression of sympathoadrenal responses with dexmedetomidine during periods of maximal surgical stress.
Both groups had comparable baseline systolic blood pressure. From 10 minutes after the loading dose onward, Group D consistently exhibited lower systolic blood pressure compared with Group F during laryngoscopy, intubation, and the entire duration of pneumoperitoneum. This trend continued through extubation and the immediate postoperative phase. Similar to heart rate, systolic blood pressure values equalized during the later postoperative period, with no significant intergroup differences at 3 and 6 hours (Table 3).
Baseline diastolic blood pressure did not differ significantly between the groups. Group D showed a significantly attenuated diastolic blood pressure response during laryngoscopy, intubation, and pneumoperitoneum when compared with Group F. The difference was also evident during extubation and early recovery. By 60 minutes post-extubation and during subsequent follow-up, diastolic blood pressure values were comparable between the groups (Table 4).
Mean arterial pressure followed a pattern similar to systolic and diastolic pressures. After the loading dose, Group D maintained lower mean arterial pressure during airway manipulation, pneumoperitoneum, and extubation, reflecting better control of hemodynamic stress responses. The intergroup differences diminished over time, with no significant variation observed during late postoperative measurements (Table 5).
Peripheral oxygen saturation remained within normal limits throughout the study period in both groups. No clinically or statistically significant differences were observed at any intraoperative or postoperative time point, indicating that neither drug adversely affected oxygenation (Table 6)..
Table 1. Demographic Data
|
Variable |
Group D (n = 50) |
Group F (n = 50) |
P value |
|
Age (years) |
35.7 ± 7.41 |
36.9 ± 8.42 |
0.4486 |
|
Weight (kg) |
59.5 ± 9.1 |
57.3 ± 7.66 |
0.4255 |
|
Sex (M : F) |
28 : 22 |
26 : 24 |
0.8662 |
|
ASA (I / II) |
31 / 19 |
29 / 21 |
0.6831 |
Table 2. Intraoperative Heart Rate (beats/min)
|
Time Point / Variable |
Group D (n = 50) |
Group F (n = 50) |
P value |
|
Baseline |
91.7 ± 3.79 |
89.3 ± 8.19 |
0.063 |
|
5 min after loading dose |
78.0 ± 3.21 |
86.9 ± 7.20 |
<0.0001 |
|
10 min after loading dose |
73.6 ± 2.78 |
84.1 ± 6.94 |
<0.0001 |
|
During laryngoscopy |
84.2 ± 3.61 |
87.9 ± 6.14 |
0.0004 |
|
1 min after intubation |
81.2 ± 4.43 |
87.1 ± 5.46 |
<0.0001 |
|
3 min after intubation |
79.1 ± 5.75 |
86.1 ± 5.30 |
<0.0001 |
|
5 min after intubation |
78.3 ± 5.56 |
85.0 ± 4.98 |
<0.0001 |
|
Pre-pneumoperitoneum |
76.4 ± 6.56 |
84.2 ± 5.34 |
<0.0001 |
|
Pneumoperitoneum – 5 min |
74.1 ± 6.62 |
87.5 ± 6.32 |
<0.0001 |
|
Pneumoperitoneum – 15 min |
72.2 ± 6.71 |
85.9 ± 5.92 |
<0.0001 |
|
Pneumoperitoneum – 30 min |
68.9 ± 5.41 |
84.1 ± 5.98 |
<0.0001 |
|
Pneumoperitoneum – 45 min |
67.4 ± 5.00 |
83.1 ± 6.50 |
<0.0001 |
|
Pneumoperitoneum – 60 min |
67.0 ± 4.68 |
83.5 ± 6.45 |
<0.0001 |
|
At extubation |
75.3 ± 5.76 |
90.6 ± 4.46 |
<0.0001 |
|
Post-extubation – 15 min |
77.3 ± 3.02 |
87.6 ± 5.02 |
<0.0001 |
|
Post-extubation – 30 min |
79.9 ± 3.55 |
87.2 ± 6.15 |
<0.0001 |
|
Post-extubation – 60 min |
82.8 ± 3.44 |
88.1 ± 6.97 |
<0.0001 |
|
3 hour |
87.9 ± 4.60 |
88.4 ± 7.24 |
0.6604 |
|
6 hour |
91.5 ± 3.52 |
90.1 ± 7.74 |
0.2390 |
Table 3. Systolic Blood Pressure (mmHg)
|
Time Point |
Group D (n = 50) |
Group F (n = 50) |
p value |
|
Baseline |
132.8 ± 9.23 |
130.7 ± 10.61 |
0.3077 |
|
5 min after loading dose |
128.4 ± 7.87 |
127.1 ± 6.11 |
0.3709 |
|
10 min after loading dose |
117.4 ± 7.62 |
121.3 ± 4.96 |
0.0034 |
|
During laryngoscopy |
121.4 ± 7.06 |
132.4 ± 5.42 |
<0.0001 |
|
1 min after intubation |
120.3 ± 7.69 |
129.2 ± 4.09 |
<0.0001 |
|
3 min after intubation |
118.6 ± 7.39 |
126.1 ± 2.37 |
<0.0001 |
|
5 min after intubation |
117.8 ± 6.26 |
127.0 ± 2.92 |
<0.0001 |
|
Pre-pneumoperitoneum |
117.1 ± 6.18 |
126.1 ± 4.28 |
<0.0001 |
|
Pneumoperitoneum – 5 min |
119.2 ± 6.68 |
129.7 ± 3.40 |
<0.0001 |
|
Pneumoperitoneum – 15 min |
115.1 ± 9.25 |
126.1 ± 4.26 |
<0.0001 |
|
Pneumoperitoneum – 30 min |
112.6 ± 5.76 |
125.2 ± 4.18 |
<0.0001 |
|
Pneumoperitoneum – 45 min |
110.2 ± 6.73 |
127.1 ± 5.57 |
<0.0001 |
|
Pneumoperitoneum – 60 min |
112.1 ± 6.91 |
127.8 ± 4.41 |
<0.0001 |
|
At extubation |
119.6 ± 3.28 |
132.3 ± 4.19 |
<0.0001 |
|
Post-extubation – 15 min |
118.8 ± 3.71 |
131.7 ± 5.06 |
<0.0001 |
|
Post-extubation – 30 min |
122.9 ± 3.82 |
131.3 ± 4.43 |
<0.0001 |
|
Post-extubation – 60 min |
126.5 ± 3.50 |
130.1 ± 3.50 |
<0.0001 |
|
3 hour |
126.7 ± 4.57 |
127.1 ± 3.11 |
0.6137 |
|
6 hour |
128.3 ± 7.85 |
129.4 ± 6.08 |
0.4485 |
Table 4. Diastolic Blood Pressure (mmHg)
|
Time Point |
Group D (n = 50) Mean ± SD |
Group F (n = 50) Mean ± SD |
p value |
|
Baseline |
82.2 ± 7.81 |
81.8 ± 6.03 |
0.8209 |
|
5 min after loading dose |
79.1 ± 7.63 |
80.8 ± 5.36 |
0.1944 |
|
10 min after loading dose |
75.1 ± 6.50 |
78.4 ± 5.07 |
0.0061 |
|
During laryngoscopy |
79.9 ± 6.00 |
83.9 ± 5.05 |
0.0006 |
|
1 min after intubation |
78.5 ± 5.19 |
81.8 ± 5.54 |
0.0035 |
|
3 min after intubation |
75.6 ± 7.40 |
80.2 ± 5.73 |
0.0009 |
|
5 min after intubation |
75.5 ± 7.64 |
79.1 ± 5.64 |
0.0093 |
|
Pre-pneumoperitoneum |
74.4 ± 8.15 |
77.5 ± 5.12 |
0.0264 |
|
Pneumoperitoneum – 5 min |
75.7 ± 7.47 |
78.9 ± 4.52 |
0.0123 |
|
Pneumoperitoneum – 15 min |
74.1 ± 6.73 |
77.9 ± 5.01 |
0.0017 |
|
Pneumoperitoneum – 30 min |
73.8 ± 6.11 |
77.4 ± 5.89 |
0.0037 |
|
Pneumoperitoneum – 45 min |
74.2 ± 6.82 |
78.1 ± 6.03 |
0.0041 |
|
Pneumoperitoneum – 60 min |
75.2 ± 5.78 |
78.2 ± 3.81 |
0.0031 |
|
At extubation |
78.8 ± 6.10 |
84.2 ± 4.54 |
0.0001 |
|
Post-extubation – 15 min |
76.7 ± 4.49 |
83.1 ± 3.51 |
0.0001 |
|
Post-extubation – 30 min |
78.9 ± 5.09 |
81.1 ± 4.13 |
0.0246 |
|
Post-extubation – 60 min |
80.6 ± 7.65 |
80.9 ± 3.99 |
0.8021 |
|
3 hour |
81.9 ± 8.26 |
82.6 ± 3.86 |
0.5710 |
|
6 hour |
81.7 ± 7.52 |
81.5 ± 4.36 |
0.8850 |
Table 5. Mean Blood Pressure (mmHg)
|
Time Point |
Group D (n = 50) |
Group F (n = 50) |
p value |
|
Baseline |
99.0 ± 6.17 |
98.1 ± 4.61 |
0.4072 |
|
5 min after loading dose |
95.5 ± 5.69 |
96.3 ± 3.89 |
0.4485 |
|
10 min after loading dose |
89.2 ± 4.88 |
92.7 ± 3.58 |
0.0001 |
|
During laryngoscopy |
93.7 ± 4.16 |
100.0 ± 3.67 |
<0.0001 |
|
1 min after intubation |
92.5 ± 4.19 |
97.6 ± 3.63 |
<0.0001 |
|
3 min after intubation |
90.0 ± 5.13 |
95.5 ± 3.92 |
<0.0001 |
|
5 min after intubation |
89.6 ± 5.36 |
95.1 ± 3.94 |
<0.0001 |
|
Pre-pneumoperitoneum |
88.6 ± 5.74 |
93.7 ± 3.63 |
<0.0001 |
|
Pneumoperitoneum – 5 min |
90.2 ± 5.16 |
95.8 ± 3.41 |
<0.0001 |
|
Pneumoperitoneum – 15 min |
87.7 ± 5.32 |
94.0 ± 3.58 |
<0.0001 |
|
Pneumoperitoneum – 30 min |
86.7 ± 4.42 |
93.3 ± 4.25 |
<0.0001 |
|
Pneumoperitoneum – 45 min |
86.2 ± 5.07 |
94.4 ± 4.36 |
<0.0001 |
|
Pneumoperitoneum – 60 min |
87.5 ± 4.10 |
94.7 ± 3.13 |
<0.0001 |
|
At extubation |
92.4 ± 4.16 |
100.0 ± 3.16 |
<0.0001 |
|
Post-extubation – 15 min |
90.8 ± 3.07 |
99.3 ± 3.10 |
<0.0001 |
|
Post-extubation – 30 min |
93.6 ± 3.62 |
97.8 ± 3.15 |
<0.0001 |
|
Post-extubation – 60 min |
95.9 ± 5.09 |
97.3 ± 2.79 |
0.099 |
|
3 hour |
96.8 ± 5.92 |
97.4 ± 2.55 |
0.519 |
|
6 hour |
97.3 ± 5.19 |
97.5 ± 3.51 |
0.791 |
Table 6. SpO₂ (%)
|
Time Point |
Group D (n = 50) |
Group F (n = 50) |
p value |
|
Baseline |
99.6 ± 0.85 |
99.5 ± 0.42 |
0.420 |
|
5 min after loading dose |
99.82 ± 0.58 |
99.6 ± 0.081 |
0.081 |
|
10 min after loading dose |
100 |
100 |
– |
|
During laryngoscopy |
100 |
100 |
– |
|
1 min after intubation |
100 |
100 |
– |
|
3 min after intubation |
100 |
100 |
– |
|
5 min after intubation |
100 |
100 |
– |
|
Pre-pneumoperitoneum |
100 |
100 |
– |
|
Pneumoperitoneum – 5 min |
100 |
100 |
– |
|
Pneumoperitoneum – 15 min |
100 |
100 |
– |
|
Pneumoperitoneum – 30 min |
100 |
100 |
– |
|
Pneumoperitoneum – 45 min |
100 |
100 |
– |
|
Pneumoperitoneum – 60 min |
100 |
100 |
– |
|
At extubation |
99.7 ± 0.64 |
99.4 ± 1.07 |
0.080 |
|
Post-extubation – 15 min |
99.7 ± 0.64 |
99.5 ± 0.85 |
0.300 |
|
Post-extubation – 30 min |
99.6 ± 0.69 |
99.5 ± 0.75 |
0.580 |
|
Post-extubation – 60 min |
99.8 ± 0.47 |
99.8 ± 0.46 |
0.830 |
|
3 hour |
99.5 ± 0.83 |
99.7 ± 0.62 |
0.280 |
|
6 hour |
99.7 ± 0.59 |
99.7 ± 0.56 |
1.000 |
In the present study, dexmedetomidine demonstrated a markedly greater attenuation of perioperative hemodynamic stress responses than fentanyl, as evidenced by significantly lower heart rate and blood pressure at key time points during airway manipulation, pneumoperitoneum, and extubation. These findings are consistent with previous clinical observations that dexmedetomidine effectively modulates sympathetic activity, leading to more stable intraoperative hemodynamics in laparoscopic procedures [8,9]. Specifically, studies comparing dexmedetomidine and fentanyl in laparoscopic settings have reported similar trends of reduced HR, SBP, DBP, and MAP with dexmedetomidine, reinforcing the results observed in our cohorts [10].
The sympatholytic properties of dexmedetomidine are attributable to its high affinity for central α2-adrenergic receptors, which inhibit norepinephrine release and blunt catecholaminergic responses to surgical stressors. Such mechanisms likely underlie the significantly attenuated HR and blood pressure elevations observed in our dexmedetomidine group during intubation and pneumoperitoneum, compared with fentanyl [11]. These effects contribute to improved hemodynamic stability during phases of significant sympathetic activation, aligning with the preferred anesthetic goal of minimizing perioperative cardiac workload.
While fentanyl has been traditionally used for stress response attenuation due to its potent analgesic effect, its influence on hemodynamic parameters appears less consistent in the context of laparoscopic surgery. Some studies have shown that fentanyl provides adequate suppression of pressor responses to laryngoscopy and intubation when administered in specific doses, but may not sustain hemodynamic control throughout prolonged surgical stimuli such as pneumoperitoneum [12]. In contrast, our results suggest that dexmedetomidine’s continuous sympatholytic action yields more consistent attenuation across various intraoperative stressors.
Importantly, both agents maintained adequate oxygenation without clinically significant differences in SpO₂. This affirms that the enhanced hemodynamic control observed with dexmedetomidine did not compromise respiratory function, a concern often associated with opioid use.
Overall, the hemodynamic profile observed with dexmedetomidine supports its use as a superior agent for controlling perioperative stress responses in laparoscopic surgery, potentially enhancing cardiovascular safety and reducing the need for additional vasoactive medications.
Dexmedetomidine was more effective than fentanyl in attenuating the hemodynamic stress responses associated with laryngoscopy, tracheal intubation, pneumoperitoneum, and extubation in patients undergoing elective laparoscopic surgery under general anaesthesia. Patients receiving dexmedetomidine demonstrated better control of heart rate and arterial blood pressure across intraoperative and early postoperative periods, reflecting superior modulation of sympathetic responses. Both drugs maintained stable oxygen saturation without clinically significant respiratory compromise. These findings support the use of dexmedetomidine as a preferable agent over fentanyl for achieving perioperative hemodynamic stability during laparoscopic procedures