Original Research Article Open Access

Dexmedetomidine Versus Propofol Infusion During Monitored Anaesthesia

Care for Endoscopic Retrograde Cholangiopancreatography: A Prospective

Randomised Double-Blind Study

Ritika Godara

*, Kamlesh K. Shekhawat

, Ketki Jangid

, Amit Kumar

¹ Postgraduate Resident (3rd Year), Department of Anaesthesiology, Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

² Professor and Head, Department of Anaesthesiology, Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

³ Senior Resident, Department of Anaesthesiology, Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

⁴ Associate Professor, Department of Anaesthesiology, Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

Corresponding Author: Dr. Ritika Godara, Postgraduate Resident (3rd Year), Department of Anaesthesiology, Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India. Email:

ritika.godara786@gmail.com

A R T I C L E I N F O

Article type:

Original Research Article

Corresponding author:

Dr. Ritika Godara

Email:

ritika.godara786@gmail.com

Keywords:

dexmedetomidine; propofol; monitored anaesthesia care; ERCP;

Ramsay Sedation Scale; recovery time; haemodynamic stability

A B S T R A C T

Background: Monitored anaesthesia care for endoscopic retrograde cholangiopancreatography (ERCP) requires agents that bal‐

ance rapid induction, procedural comfort, and cardiorespiratory safety. Dexmedetomidine and propofol differ pharmacologically

in their onset, recovery, and haemodynamic profiles. This study compared their sedation efficacy and safety in adult patients un‐

dergoing ERCP.

Methods: A single-centre, hospital-based, double-blind, randomised, active-controlled prospective study was conducted at Pa‐

cific Institute of Medical Sciences, Udaipur (IEC No. STU/IEC/2024/36, dated 16.05.2024). A total of 120 adult patients under‐

going elective ERCP were equally randomised to Group D (dexmedetomidine: loading 1μg/kg over 10 minutes, maintenance

0.2–0.7μg/kg/hour) and Group P (propofol: loading 0.5mg/kg, maintenance 25–75μg/kg/min). Onset time to Ramsay Sedation

Scale (RSS) score 4, recovery time to RSS 1, haemodynamic and respiratory parameters, total rescue fentanyl dose, and adverse

events were compared.

Results: Baseline characteristics were comparable between groups (all p>0.05). Propofol achieved faster onset (9.18 vs 12.0

minutes; p<0.001). Dexmedetomidine showed significantly shorter recovery (7.95 vs 22.6 minutes; p<0.0001). Mean arterial

pressure was significantly better maintained with dexmedetomidine from 15 minutes onwards (p<0.001). Heart rate was signi‐

ficantly higher in the dexmedetomidine group from 45 minutes onwards. Oxygen saturation and respiratory rate were signific‐

antly better preserved with dexmedetomidine during the procedure. Rescue fentanyl requirement was higher with dexme‐

detomidine (118 vs 64.4μg; p<0.0001). No major adverse events occurred in either group.

Conclusion: Propofol offers faster onset while dexmedetomidine provides quicker recovery with superior haemodynamic and

respiratory stability. Dexmedetomidine is preferred when cardiorespiratory safety is the priority; propofol when rapid induction

is required. Both agents are safe for ERCP sedation without major adverse events.

Keywords: dexmedetomidine; propofol; monitored anaesthesia care; ERCP; Ramsay Sedation Scale; recovery time; haemody‐

namic stability

INTRODUCTION

Endoscopic retrograde cholangiopancreatography (ERCP) is a complex therapeutic

endoscopic procedure used in the management of pancreaticobiliary disease, includ‐

ing choledocholithiasis, biliary strictures, and chronic pancreatitis. It demands pro‐

longed patient cooperation in the prone position, which limits airway access, and is

associated with significant discomfort from biliary instrumentation, contrast injection,

and sphincterotomy.

[1,2]

These factors collectively necessitate reliable sedation that

achieves both procedural comfort and safety, and that supports timely recovery given

the typical high procedural throughput of endoscopy units.

Monitored anaesthesia care (MAC) has become the preferred approach for ERCP sed‐

ation, allowing titration of sedative agents to achieve deep, controllable sedation while

maintaining spontaneous ventilation. The prone position, which is standard in most

ERCP suites, amplifies the consequences of sedation-related respiratory compromise

by restricting chest wall movement, impairing airway access, and delaying recogni‐

tion of early desaturation.

[3]

Drug selection for MAC in ERCP must therefore balance

rapid induction — which reduces procedural delay — against cardiorespiratory stabil‐

ity, recovery profile, and opioid requirement.

Propofol is a highly lipophilic intravenous hypnotic agent that potentiates GABA-A

receptor-mediated neuronal inhibition, producing rapid onset of sedation within

seconds of administration. Its pharmacokinetic profile, characterised by rapid redistri‐

bution and efficient hepatic metabolism, supports a short context-sensitive half-time

and predictable recovery.

[4]

However, it lacks intrinsic analgesic activity and causes

dose-dependent respiratory depression and systemic vasodilatation, which may trans‐

late into hypotension particularly in patients with limited cardiorespiratory reserve.

[5]

Dexmedetomidine is a highly selective α2-adrenergic receptor agonist that produces

sedation by reducing sympathetic outflow from the locus coeruleus, inducing a state

resembling physiological non-REM sleep. Unlike propofol, its sedation is arousable, it

possesses intrinsic analgesic properties that may reduce opioid requirement, and its ef‐

fect on respiratory drive is minimal even at deeper sedation levels, making it pharma‐

cologically attractive for procedures with limited airway access.

[6,7]

However, its on‐

set is slower due to the need for a loading infusion to avoid abrupt haemodynamic

shifts, and its sympatholytic properties may cause bradycardia.

Despite growing use of both agents in ERCP, comparative data from standardised ran‐

domised trials remain limited, particularly from Indian centres, where patient popula‐

tions and procedural protocols may differ from those in high-income settings. The

present study was designed to directly compare dexmedetomidine and propofol in

terms of onset of sedation, recovery time, haemodynamic and respiratory stability,

rescue analgesic requirement, and adverse events during monitored anaesthesia care

for ERCP.

AIM

To compare dexmedetomidine and propofol infusions in terms of onset of sedation,

recovery time, haemodynamic and respiratory parameters, rescue analgesic require‐

ment, and adverse effects during monitored anaesthesia care for endoscopic retrograde

cholangiopancreatography.

MATERIAL AND METHODS

This was a single-centre, hospital-based, double-blind, randomised, active-controlled

prospective study. The study was conducted in the Department of Anaesthesiology at

Pacific Institute of Medical Sciences, Udaipur, Rajasthan — a tertiary care teaching

hospital. The study duration was 18 months, with 12 months dedicated to participant

recruitment and data collection. Ethical approval was obtained from the Institutional

Ethics Committee of Pacific Institute of Medical Sciences, Udaipur, under approval

number STU/IEC/2024/36, dated 16th May 2024. The study was conducted in accord‐

ance with the Declaration of Helsinki. Written informed consent was obtained from all

participants before allocation to study groups. The primary outcomes were onset time

to achieve a Ramsay Sedation Scale (RSS) score of 4 and recovery time from proced‐

ure completion to RSS score of 1. Secondary outcomes were intra-procedural haemo‐

dynamic stability (heart rate, mean arterial pressure), respiratory parameters (respirat‐

ory rate, SpO₂), total cumulative rescue fentanyl dose, and the occurrence of postoper‐

ative nausea and vomiting. Sedation-related adverse events — defined as hypoxaemia

(SpO₂ <90% for >10 seconds), respiratory depression (RR <10 breaths/min), hypoten‐

sion (MAP <65 mmHg), and bradycardia (HR <45 bpm) — were recorded and man‐

aged per institutional protocol.

Drug Protocols and Target Sedation: Group D (dexmedetomidine): loading infusion

of 1μg/kg administered over 10 minutes, followed by maintenance infusion at 0.2–

0.7μg/kg/hour. Group P (propofol): induction bolus of 0.5mg/kg, followed by main‐

tenance infusion at 25–75μg/kg/min. The target sedation level for both groups was a

Ramsay Sedation Scale score of 4. Intravenous fentanyl 0.5μg/kg was administered

as rescue medication if the target sedation level was not achieved or if the patient

showed intolerance to the procedure.

[17-42]

STUDY PARTICIPANTS, INCLUSION AND EXCLUSION CRITERIA

INCLUSION CRITERIA:

1. Adult patients aged 31–70 years scheduled for elective ERCP.

2. ASA physical status I, II, or III.

3. Written informed consent obtained.

EXCLUSION CRITERIA:

1. Known allergy to dexmedetomidine, propofol, or fentanyl.

2. Pre-existing bradycardia defined as heart rate less than 60 beats per minute.

3. Significant cardiovascular disease, arrhythmia, or haemodynamic instability.

4. Severe hepatic, renal, or pulmonary disease.

5. Active substance abuse or chronic opioid use.

6. Pregnancy or lactation.

7. Emergency or unplanned ERCP.

Sample Size and Randomisation:Sample size was calculated based on expected dif‐

ferences in onset and recovery time between the two agents. The minimum required

sample was 120 patients, 60 per group. Randomisation was performed using a com‐

puter-generated random number sequence; allocation was concealed using sealed

Godara R. et al. Current Trends in Medicine & Clinical Research

Curr. Trends Med. Clin. Res. 2026; Vol.2 July-Sept 2026

Current Trends in Medicine and Clinical Research

ISSN: 3108-1223

Correspondence: Dr. Ritika Godara | Email: ritika.godara786@gmail.com

Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

opaque envelopes opened sequentially at the time of assignment. Double blinding was

maintained: the drug was prepared by a pharmacist not involved in data collection,

and participants and the data-recording anaesthesiologist were blinded to group alloc‐

ation.

Data Collection Procedure: Standard monitoring — non-invasive blood pressure,

continuous ECG, and pulse oximetry — was applied to all participants. Baseline val‐

ues (T0) of heart rate, MAP, respiratory rate, SpO₂, and RSS were recorded before

drug administration. The study drug was prepared and administered by a separate

pharmacist. The time from initiation of infusion to achievement of RSS 4 was recor‐

ded as onset time. Parameters were then recorded at 5-minute intervals from T1 to T8

(up to 60 minutes), and in the post-procedure recovery area at 0, 10, 20, and 30

minutes. Recovery time was defined as time from infusion discontinuation to RSS 1.

PONV was assessed clinically at 30 minutes post-procedure. Any sedation-related ad‐

verse event was recorded and managed immediately per protocol.

Statistical Analysis: Data were analysed using Stata version 17.0. Continuous vari‐

ables were expressed as mean±SD and compared using independent t-test or Mann–

Whitney U test. Categorical variables were expressed as frequencies and percentages

and compared using Pearson chi-square test. A p-value of <0.05 was considered stat‐

istically significant.

RESULTS

A total of 120 participants were enrolled and randomised, with 60 in each group. No

participant was lost to follow-up and all completed the study. Detailed findings are

presented below.

Table 1: Baseline Characteristics

Characteristic Group D (n=60) n /

Mean

Group D

Group P (n=60) n /

Mean

Group P % | P-

value

Age Group (years)

31–40 11 18.3 11 18.3 | 0.957

41–50 17 28.3 15 25.0

51–60 20 33.3 22 36.7

61–70 12 20.0 12 20.0

Mean age (years) 51.0 51.7 P=0.689

Gender

Male 46 76.7 38 63.3 | 0.112

Female 14 23.3 22 36.7

ASA Physical

Status

ASA I 13 21.7 23 38.3 | 0.063

ASA II 23 38.3 24 40.0

ASA III 24 40.0 13 21.7

Indication for

ERCP

Choledocholithiasis 8 13.3 16 26.7 | 0.354

Biliary stricture 17 28.3 14 23.3

Chronic pancreatitis 19 31.7 15 25.0

Diagnostic 16 26.7 15 25.0

Mean body weight

(kg)

60.9 62.4 P=0.468

Table 1 confirms comparable baseline characteristics between both groups. Age distri‐

bution, mean age (51 vs 51.7 years; p=0.689), gender distribution (p=0.112), ASA

status (p=0.063), ERCP indication (p=0.354), and body weight (60.9 vs 62.4kg;

p=0.468) were all statistically comparable, confirming adequate baseline equivalence

between the groups.

Table 2: Onset Time, Recovery Time, and Rescue Fentanyl Requirement

Outcome Group D

Mean

Group D

Range

Group P

Mean

Group P Range | P-

value

Onset time to RSS 4

(minutes)

12.0 ± 2.03 9 – 15 9.18 ± 1.59 6 – 11 | < 0.001

Recovery time to RSS 1

(minutes)

7.95 ± 2.57 4 – 12 22.6 ± 4.7 15 – 30 | < 0.0001

Total rescue fentanyl (μg) 118 61 – 180 64.4 26 – 100 | < 0.0001

Table 2 shows the primary and key secondary efficacy outcomes. Propofol achieved

the target sedation level significantly faster (9.18 vs 12.0 minutes; p<0.001). Dexme‐

detomidine demonstrated markedly shorter recovery (7.95 vs 22.6 minutes;

p<0.0001), a difference of nearly 15 minutes representing a clinically and operation‐

ally meaningful advantage. Total rescue fentanyl requirement was significantly higher

in the dexmedetomidine group (118 vs 64.4μg; p<0.0001), reflecting the absence of

intrinsic analgesic activity in propofol relative to the need to supplement dexme‐

detomidine’s own analgesic effect in this procedure.

Table 3: Heart Rate Across All Time Points

Time Point Group D

Mean HR

(bpm)

Group P

Mean HR

(bpm)

Dif‐

fer‐

ence

P-

value

Baseline (T0) 84.8 86.3 −1.5 0.44

(NS)

5 min (T1) 84.8 86.0 −1.2 0.53

(NS)

15 min (T3) 85.0 84.0 +1.0 0.62

(NS)

30 min (T6) 85.1 81.0 +4.1 0.06

(NS)

45 min (T7)* 85.2 80.5 +4.7 0.03*

60 min (T8)* 84.9 79.2 +5.7 0.01*

Post-op 0 min (T9)* 86.0 80.3 +5.7 0.01*

Post-op 10 min (T10)* 86.9 81.2 +5.7 0.01*

Post-op 20 min (T11)* 87.9 82.2 +5.7 0.01*

Post-op 30 min (T12)* 88.7 83.3 +5.4 0.02*

* Statistically significant (p < 0.05). HR remained

stable with dexmedetomidine; propofol group showed

a progressive intra-procedural decline.

Table 3 shows heart rate trends. Groups were comparable at baseline and during the

first 30 minutes of the procedure. From 45 minutes onwards (T7) and throughout the

recovery period, heart rate was significantly higher in the dexmedetomidine group

than in the propofol group (p=0.03 to 0.01). The propofol group showed a consistent

intra-procedural decline in heart rate, while dexmedetomidine maintained a stable rate

throughout the procedure and early recovery.

Table 4: Mean Arterial Pressure Across All Time Points

Time Point Group D

Mean MAP

(mmHg)

Group P Mean

MAP (mmHg)

Dif‐

fer‐

ence

P-

value

Baseline (T0) 93.8 93.8 0 1.00

(NS)

5 min (T1) 93.9 93.9 0 1.00

(NS)

10 min (T2) 93.6 93.7 −0.1 0.95

(NS)

15 min (T3)* 93.7 89.5 +4.2 0.02*

20 min (T4)* 93.4 85.6 +7.8 <

0.001*

30 min (T6)* 93.2 85.8 +7.4 <

0.001*

45 min (T7)* 93.3 85.8 +7.5 <

0.001*

60 min (T8)* 93.3 85.9 +7.4 <

0.001*

Post-op 0 min (T9)* 95.2 87.8 +7.4 <

0.001*

Post-op 30 min (T12)* 100.0 93.8 +6.2 <

0.001*

* Statistically significant (p < 0.05). Dexme‐

detomidine maintained stable MAP throughout;

propofol showed significant decline from 15

minutes.

Table 4 shows MAP trends. Both groups had identical baseline MAP (93.8 mmHg).

From 15 minutes onwards, MAP in the propofol group declined significantly com‐

pared to the dexmedetomidine group (89.5 vs 93.7 at 15 min; p=0.02). From 20

minutes through the entire intra-procedural phase and recovery (T4–T12), MAP dif‐

ferences were highly significant (p<0.001). The dexmedetomidine group maintained

MAP within a narrow stable range throughout, while propofol caused a sustained re‐

duction of approximately 7–8 mmHg from baseline during the procedure.

Table 5: Respiratory Rate and Oxygen Saturation Across Time Points

Godara R. et al. Current Trends in Medicine & Clinical Research

Curr. Trends Med. Clin. Res. 2026; Vol.2 July-Sept 2026

Current Trends in Medicine and Clinical Research

ISSN: 3108-1223

Correspondence: Dr. Ritika Godara | Email: ritika.godara786@gmail.com

Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Time Point D

SpO₂

SpO₂ P D

RR P

Baseline (T0) 99.7 99.8 0.07 17 18 0.06

10 min (T2) 99.3 98.7 <0.001* 17 17 0.92

20 min (T4) 99.0 97.7 <0.001* 17 16 0.11

30 min (T6) 98.6 97.6 <0.001* 17 15 0.01*

45 min (T7) 98.5 97.3 <0.001* 17 15 0.003*

60 min (T8) 98.4 97.3 <0.001* 17 15 0.002*

Post-op 0 min (T9) 98.5 97.7 0.006* 17 16 0.12

Post-op 30 min (T12) 98.2 98.6 0.21 19 17 0.01*

D = dexmedetomidine; P = propofol; * significant (p <

0.05). SpO₂ and RR were better preserved with dexme‐

detomidine intra-procedurally and converged post-pro‐

cedure.

Table 5 presents SpO₂ and RR data. SpO₂ was comparable at baseline but diverged

significantly from 10 minutes onwards (p<0.001 for T2–T9), with dexmedetomidine

maintaining higher saturation values throughout the procedure. The groups converged

at post-procedure 10 and 20 minutes. Respiratory rate similarly remained stable at 17

breaths/min throughout the intra-procedural phase with dexmedetomidine, while

propofol was associated with a significant decline to 15 breaths/min from 30 minutes

onwards (p=0.01–0.002).

Table 6: Postoperative Nausea and Vomiting and Adverse Events

Outcome Group D n Group D % Group P n Group P % P

PONV: No 51 85.0 47 78.3 0.345

PONV: Yes 9 15.0 13 21.7 (NS)

Hypoxaemia (SpO₂ <90%) 0 0 0 0 —

Respiratory depression (RR <10) 0 0 0 0 —

Bradycardia (HR <45 bpm) 0 0 0 0 —

Serious adverse events 0 0 0 0 —

Table 6 shows PONV and safety data. PONV occurred in 15% of the dexme‐

detomidine group and 21.7% of the propofol group, with no statistically significant

difference (p=0.345). No predefined adverse events — hypoxaemia, respiratory de‐

pression, bradycardia, or serious adverse events — occurred in either group, confirm‐

ing the safety of both regimens at the doses used.

DISCUSSION

This double-blind randomised controlled trial enrolled 120 adult patients undergoing

elective ERCP at a tertiary anaesthesiology centre in Udaipur and directly compared

dexmedetomidine and propofol as the primary sedative agents under MAC. Baseline

characteristics were well-matched, ensuring that outcome differences could be attrib‐

uted to the pharmacological properties of the two agents rather than patient-level con‐

founders. The study demonstrated distinct, clinically meaningful differences in seda‐

tion onset, recovery profile, haemodynamic behaviour, respiratory parameters, and an‐

algesic requirement, while both agents proved safe at the doses used.

Propofol achieved the target sedation level (RSS 4) in a mean of 9.18 minutes com‐

pared to 12.0 minutes with dexmedetomidine (p<0.001). This difference arises from

the fundamental pharmacokinetic distinction between the two agents: propofol’s high

lipophilicity enables rapid blood-brain barrier penetration, producing sedation within

seconds to minutes of administration, while dexmedetomidine requires a structured

loading infusion to allow progressive central sympatholytic effect to build without

triggering abrupt haemodynamic instability.

[4,6]

This finding is consistent with

Srivastava U et al. (2021), who reported onset of 7.93 minutes for propofol versus

11.4 minutes for dexmedetomidine in ERCP.

[8]

Zhang N et al. (2024) similarly docu‐

mented faster onset with propofol, while Aqeel N et al. (2024) observed a mean onset

of 11.84 minutes to reach RSS 4 with dexmedetomidine.

[9,10]

The clinical implica‐

tion is that the propofol group was ready for endoscope insertion approximately 3

minutes earlier, which has procedural throughput implications in high-volume units.

However, as the following findings demonstrate, this advantage must be considered

alongside other dimensions of performance.

Dexmedetomidine demonstrated a markedly shorter recovery time (7.95 vs 22.6

minutes; p<0.0001). This nearly three-fold advantage is the most operationally im‐

pactful finding of the present study and is explained by the unique pharmacodynamics

of dexmedetomidine-induced sedation. Unlike propofol, which causes global cortical

depression that must be metabolically cleared, dexmedetomidine induces a state re‐

sembling physiological NREM sleep through which patients can be aroused by gentle

stimulation as soon as the procedural stimulus — endoscope manipulation — ceases.

Recovery is therefore rapid and smooth once the infusion is discontinued. Srivastava

U et al. (2021) reported that 86.67% of dexmedetomidine patients achieved maximum

Modified Aldrete Score within 5 minutes versus 0% in the propofol group.

[8]

Zhang

N et al. (2024) documented recovery durations of 1.6 minutes (dexmedetomidine)

versus 6.9 minutes (propofol),

[9]

and Garg I et al. (2024) found recovery of 7.24

versus 15.2 minutes in dexmedetomidine-propofol versus propofol-ketamine groups.

[11]

The consistent finding across studies is that dexmedetomidine-based regimens

support earlier departure from recovery to ward, which in resource-limited endoscopy

units with multiple parallel lists has direct implications for efficiency.

Dexmedetomidine maintained MAP within a narrow, consistent range throughout the

procedure and recovery. Propofol caused a clinically significant decline in MAP from

15 minutes onwards (89.5 vs 93.7 mmHg; p=0.02), which deepened to a 7–8 mmHg

sustained reduction from 20 minutes through to post-procedure recovery (all

p<0.001). While MAP remained above 85 mmHg in the propofol group — above the

pre-defined hypotension threshold of 65 mmHg — this sustained reduction in a pre‐

dominantly ASA II–III population during prone ERCP is clinically relevant. Propo‐

fol’s hypotensive effect reflects its vasodilatory and mild negative inotropic actions.

Soliman AM et al. (2024) similarly found that dexmedetomidine maintained better

MAP in cancer patients undergoing ERCP.

[12]

Garg I et al. (2024) documented signi‐

ficantly lower MAP in propofol-dexmedetomidine versus propofol-ketamine groups,

the latter attributable to ketamine’s sympathomimetic properties offsetting the dexme‐

detomidine effect.

[11]

Heart rate was stable in the dexmedetomidine group and

showed a modest intra-procedural decline in the propofol group, with significant dif‐

ferences from 45 minutes onwards. No patient in either group met the criteria for

bradycardia (HR <45 bpm), confirming the cardiovascular safety of dexmedetomidine

within the dosing range used.

SpO₂ was significantly better preserved with dexmedetomidine from 10 minutes

through the entire intra-procedural phase (p  <  0.001), consistent with dexme‐

detomidine’s preservation of respiratory drive through its non-GABAergic mechanism

of action. Respiratory rate similarly remained stable at 17 breaths/minute throughout

the procedure with dexmedetomidine, while propofol caused a significant reduction to

15 breaths/min from 30 minutes onwards (p<0.01). No episode of clinical hypox‐

aemia (SpO₂ <90%) or respiratory depression (RR <10) occurred in either group, con‐

sistent with the supplemental oxygen administered and the monitored setting. Soliman

AM et al. (2024) reported a lower incidence of hypoxaemic events with dexme‐

detomidine (14.9% vs 26.7%),

[12]

and Liu Y et al. (2025), in a network meta-analys‐

is, found that dexmedetomidine-fentanyl combinations significantly reduced the pro‐

portion of patients with SpO₂ below 90% compared to propofol-only sedation.

[13]

The present study confirms these protective respiratory properties within a strictly

monitored ERCP setting.

Total rescue fentanyl was significantly higher in the dexmedetomidine group (118 vs

64.4μg; p<0.0001). This finding, while initially appearing counterintuitive given

dexmedetomidine’s intrinsic analgesic effect, reflects the greater depth and quality of

sedation provided by propofol at the doses used. The sedation continuum required for

ERCP, which approaches deep sedation, is readily achievable with propofol’s

GABAergic action, whereas dexmedetomidine’s physiological sleep-like state may

not fully suppress procedural pain from biliary instrumentation without supplemental

opioid. PONV rates were 15% and 21.7% in the dexmedetomidine and propofol

groups respectively, without reaching statistical significance (p=0.345). The lower

rate with dexmedetomidine likely reflects reduced opioid requirement as a driver of

nausea, whereas propofol’s known antiemetic properties may have partially offset the

higher opioid dose in the propofol group.

CONCLUSION

Both dexmedetomidine and propofol are safe and effective sedative agents for mon‐

itored anaesthesia care during ERCP, with no major adverse events in either group.

Propofol achieves the target sedation level significantly faster (9.18 vs 12.0 minutes;

p  <  0.001), which is advantageous when rapid procedural induction is required.

Dexmedetomidine demonstrates markedly shorter recovery (7.95 vs 22.6 minutes;

p<0.0001), superior haemodynamic stability, and better preservation of oxygen sat‐

uration and respiratory rate during the procedure. The higher rescue fentanyl require‐

ment with dexmedetomidine is a recognised trade-off of its mechanism of action in

prolonged pancreaticobiliary intervention. The choice between agents should be

guided by individual patient risk profile: dexmedetomidine is preferred when cardi‐

orespiratory stability and rapid recovery are priorities; propofol when fast induction

and deeper sedation are required. The two agents may also be considered comple‐

mentarily in combination protocols.

Funding: This study received no external funding. All expenses were borne by the in‐

stitute and the principal investigator. Participants received no financial compensation.

IEC No.: STU/IEC/2024/366

Conflict of Interest: The authors declare no conflicts of interest in the design, con‐

duct, analysis, or reporting of this study.

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Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

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Curr. Trends Med. Clin. Res. 2026; Vol.2 July-Sept 2026

Current Trends in Medicine and Clinical Research

ISSN: 3108-1223

Correspondence: Dr. Ritika Godara | Email: ritika.godara786@gmail.com

Pacific Institute of Medical Sciences (PIMS), Umrada, Udaipur, Rajasthan, India.

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.