Sedation is a critical component in various medical procedures, ranging from diagnostic interventions to surgical operations and intensive care management. The choice of sedative agent plays a pivotal role in ensuring patient safety, procedural success, and overall clinical outcomes. Two commonly used sedative agents, Dexmedetomidine and Propofol, have garnered significant attention in anesthetic practice due to their distinct pharmacological profiles and hemodynamic effects.

Dexmedetomidine is a highly selective α2-adrenergic receptor agonist with sedative, anxiolytic, and analgesic properties. It exerts its effects by decreasing sympathetic activity and norepinephrine release, leading to sedation that closely resembles natural sleep without causing significant respiratory depression. Its unique action on central α2 receptors allows for cooperative sedation, where patients remain arousable and maintain airway reflexes, making it favorable in many clinical settings [1]. The hemodynamic effects of dexmedetomidine include bradycardia and hypotension due to sympatholysis, but these are generally well-tolerated and predictable.

In contrast, Propofol is a short-acting intravenous anesthetic agent widely used for induction and maintenance of sedation. It acts primarily on GABA_A receptors, enhancing inhibitory neurotransmission. Propofol provides rapid onset and offset of sedation, allowing precise control over sedation depth. However, propofol is associated with dose-dependent hypotension and respiratory depression, which can pose challenges in hemodynamically unstable patients or those with compromised respiratory function [2].

The hemodynamic stability during sedation is crucial, especially in critically ill patients or those undergoing procedures requiring sedation outside the operating room, such as endoscopy, radiological interventions, or in intensive care units. Unstable hemodynamics can increase perioperative morbidity and mortality. Therefore, understanding the comparative hemodynamic effects of these agents is essential to tailor sedation regimens appropriately.

Several studies have investigated the hemodynamic profiles of dexmedetomidine and propofol in various clinical contexts. Dexmedetomidine is noted for providing sedation with minimal respiratory depression but can cause bradycardia and hypotension. Propofol offers the advantage of rapid recovery but may induce significant hypotension and respiratory compromise, especially at higher doses or in vulnerable populations [3]. While each agent has its own merits and limitations, the choice often depends on the patient's baseline cardiovascular status, the required depth of sedation, and the anticipated duration of sedation.

A comparative evaluation of dexmedetomidine and propofol's hemodynamic effects during sedation can help clinicians optimize patient safety and improve outcomes. Moreover, the nuanced understanding of their cardiovascular profiles may inform guidelines for sedative use in specific patient populations.

Aim

To compare the hemodynamic effects of dexmedetomidine versus propofol for sedation in adult patients undergoing elective procedures.

Objectives

1. To evaluate and compare changes in heart rate and blood pressure during sedation with dexmedetomidine and propofol.
2. To assess the incidence of adverse hemodynamic events such as hypotension and bradycardia in both groups.
3. To compare recovery profiles and overall sedation quality between dexmedetomidine and propofol.

Source of Data

The study data were collected from adult patients scheduled for elective diagnostic or therapeutic procedures requiring sedation at [Hospital/Institution Name]. Data included demographic parameters, baseline vital signs, intraoperative hemodynamic parameters, sedation details, and recovery profiles.

Study Design

This was a prospective, randomized, comparative clinical study.

Study Location

The study was conducted in the Department of Anesthesiology at tertiary care teaching hospital.

Study Duration

The study was carried out over a period of 12 months.

Sample Size

A total of 200 patients were enrolled in the study, with 100 patients allocated to the dexmedetomidine group and 100 patients to the propofol group.

Inclusion Criteria

• Adult patients aged 18 to 65 years.
• ASA physical status I and II.
• Patients scheduled for elective procedures requiring sedation.
• Patients who provided informed written consent.

Exclusion Criteria

• Patients with known allergy or hypersensitivity to dexmedetomidine or propofol.
• Patients with significant cardiovascular disease (e.g., severe arrhythmias, uncontrolled hypertension, heart failure).
• Patients with respiratory insufficiency or obstructive sleep apnea.
• Pregnant or lactating women.
• Patients on beta-blockers or other drugs affecting heart rate or blood pressure.
• Patients with neurological or psychiatric disorders that may interfere with sedation assessment.

Procedure and Methodology

After obtaining ethical committee approval and informed consent, patients were randomized into two groups using computer-generated random numbers. Patients were kept fasting as per standard guidelines and monitored continuously throughout the procedure.

Standard monitoring included ECG, non-invasive blood pressure, pulse oximetry, and respiratory rate. Baseline hemodynamic parameters (heart rate, systolic, diastolic, and mean arterial pressure) were recorded.

• Dexmedetomidine Group (Group D): Patients received a loading dose of dexmedetomidine 1 µg/kg over 10 minutes, followed by a maintenance infusion of 0.2 to 0.7 µg/kg/h titrated to achieve adequate sedation (Ramsay sedation score 3-4).
• Propofol Group (Group P): Patients received an initial bolus dose of propofol 1 mg/kg, followed by a continuous infusion of 25 to 75 µg/kg/min, adjusted to maintain the same sedation target.

Sedation level was assessed using the Ramsay sedation scale at predefined intervals. Hemodynamic parameters were recorded at baseline, during loading, every 5 minutes intraoperatively, and during recovery until discharge criteria were met.

Adverse events such as hypotension (defined as a >20% decrease from baseline mean arterial pressure), bradycardia (heart rate <50 bpm), respiratory depression, and need for intervention were noted.

Sample Processing

No biological samples were collected for laboratory analysis as this was a clinical observational study focusing on hemodynamic monitoring and clinical parameters.

Statistical Methods

Data were entered into Microsoft Excel and analyzed using SPSS version 24.0. Continuous variables were expressed as mean ± standard deviation (SD) and categorical variables as frequencies and percentages.

Comparison between groups for continuous variables was done using Student’s t-test or Mann-Whitney U test based on data normality. Categorical variables were compared using Chi-square or Fisher’s exact test.

A p-value <0.05 was considered statistically significant.

Data Collection

Data were collected on structured proformas designed for the study. Parameters included demographic details, baseline vitals, intraoperative hemodynamic readings, sedation scores, adverse events, and recovery times. Data were collected by anesthesiologists blinded to the group allocation to minimize bias.

Table 1: Baseline Demographic and Clinical Characteristics of Study Participants (n=200)

The baseline demographic and clinical characteristics of the 200 study participants, evenly divided between the dexmedetomidine and propofol groups, were comparable with no statistically significant differences. The mean age was 44.7 ± 11.3 years in the dexmedetomidine group and 45.9 ± 10.7 years in the propofol group (p=0.39). The gender distribution was similar, with males constituting 56.0% and 59.0% of participants, respectively (p=0.67). Additionally, the proportions of patients classified as ASA physical status I were 61.0% and 58.0% (p=0.67), respectively. Both groups had comparable mean weights (68.5 ± 12.7 kg vs. 69.3 ± 13.1 kg, p=0.68), baseline heart rates (78.6 ± 8.9 bpm vs. 77.9 ± 9.2 bpm, p=0.63), and baseline mean arterial pressures (MAP) (92.7 ± 10.1 mmHg vs. 93.4 ± 11.2 mmHg, p=0.68), indicating successful randomization and balanced baseline parameters.

Table 2: Changes in Heart Rate and Blood Pressure during Sedation (n=200)

During sedation, significant differences in hemodynamic changes were observed between the groups. The dexmedetomidine group exhibited a greater maximum decrease in heart rate (18.3 ± 5.7 bpm) compared to the propofol group (10.5 ± 6.1 bpm), with this difference being highly significant (p<0.001). Conversely, propofol caused a more pronounced maximum decrease in MAP (28.9 ± 8.5 mmHg) than dexmedetomidine (22.7 ± 7.3 mmHg), also statistically significant (p<0.001). Furthermore, the time to reach the lowest heart rate and lowest MAP was longer in the dexmedetomidine group (15.2 ± 4.1 and 16.1 ± 3.9 minutes, respectively) compared to the propofol group (10.8 ± 3.5 and 9.9 ± 4.3 minutes), both differences being highly significant (p<0.001). These findings suggest dexmedetomidine induces a more gradual but pronounced bradycardia, while propofol is associated with a quicker and deeper hypotensive effect.

Table 3: Incidence of Adverse Hemodynamic Events (n=200)

*Hypotension defined as MAP decrease >20% from baseline
**Bradycardia defined as HR <50 bpm

Regarding adverse hemodynamic events, the incidence of hypotension was significantly higher in the propofol group (39.0%) compared to the dexmedetomidine group (21.0%, p=0.004). Conversely, bradycardia was more frequent with dexmedetomidine (28.0% vs. 9.0%, p=0.001). Respiratory depression occurred more often in patients receiving propofol (14.0%) than those on dexmedetomidine (5.0%, p=0.03). Similarly, the need for vasoactive drugs to manage hemodynamic instability was significantly greater in the propofol group (25.0%) compared to the dexmedetomidine group (12.0%, p=0.01). These results highlight the distinct hemodynamic safety profiles of the two sedatives.

Table 4: Recovery Profiles and Sedation Quality (n=200)

In terms of recovery and sedation quality, the propofol group demonstrated a significantly shorter mean recovery time (24.3 ± 6.2 minutes) compared to the dexmedetomidine group (32.8 ± 7.5 minutes, p<0.001). Patient satisfaction scores were also higher with dexmedetomidine (8.4 ± 1.1) than propofol (7.9 ± 1.4, p=0.003). Sedation quality was comparable, with good or excellent ratings reported in 91.0% of dexmedetomidine patients and 88.0% of propofol patients (p=0.51). Postoperative nausea was significantly less frequent in the dexmedetomidine group (6.0%) compared to the propofol group (15.0%, p=0.02), suggesting a better side effect profile for dexmedetomidine in this regard.

In this study comparing dexmedetomidine and propofol for sedation in adult patients undergoing elective procedures, baseline demographic and clinical characteristics were well matched between the two groups (Table 1). There were no statistically significant differences in age, gender distribution, ASA physical status, weight, baseline heart rate (HR), or mean arterial pressure (MAP). This similarity ensures that subsequent comparisons of hemodynamic effects and outcomes are not confounded by baseline differences, consistent with previous randomized trials Sheikh TA et al.(2018)[4].

Regarding intraoperative hemodynamics (Table 2), dexmedetomidine caused a significantly greater maximal decrease in HR compared to propofol (18.3 ± 5.7 vs. 10.5 ± 6.1 bpm, p<0.001), which aligns with its known sympatholytic properties mediated by central α2-adrenergic receptor activation [3]. Conversely, propofol produced a larger decrease in MAP than dexmedetomidine (28.9 ± 8.5 vs. 22.7 ± 7.3 mmHg, p<0.001), reflecting its vasodilatory effects and myocardial depression Wu Y et al.(2015)[5]. The time to reach lowest HR and MAP was also significantly longer with dexmedetomidine, indicating a slower onset of hemodynamic changes consistent with other clinical observations Heybati K et al.(2022)[6]. These findings mirror prior studies that highlighted dexmedetomidine’s bradycardic effect and propofol’s propensity to cause more profound hypotension during sedation Bingol Tanriverdi T et al.(2019)[7].

Table 3 shows that adverse hemodynamic events differed between groups. Hypotension occurred more frequently with propofol (39.0%) than dexmedetomidine (21.0%, p=0.004), supporting reports that propofol’s vasodilatory effects can lead to clinically significant hypotension. In contrast, bradycardia was significantly more common with dexmedetomidine (28.0% vs. 9.0%, p=0.001), a recognized side effect due to central sympatholysis Benken S et al.(2020)[8]. Respiratory depression was more frequent in the propofol group (14.0% vs. 5.0%, p=0.03), consistent with propofol’s known respiratory depressant properties versus dexmedetomidine’s minimal impact on respiratory drive Kamali A et al.(2018)[9]. The greater need for vasoactive drugs in the propofol group (25.0% vs. 12.0%, p=0.01) reflects this greater cardiovascular instability, emphasizing the need for careful monitoring with propofol sedation.

Recovery profiles (Table 4) demonstrated a significantly shorter time to recovery with propofol (24.3 ± 6.2 min) compared to dexmedetomidine (32.8 ± 7.5 min, p<0.001), consistent with propofol’s rapid redistribution and clearance Alizadehasl A et al.(2019)[10]. However, patient satisfaction scores were higher with dexmedetomidine (8.4 ± 1.1 vs. 7.9 ± 1.4, p=0.003), likely attributable to dexmedetomidine’s sedative profile resembling natural sleep with less agitation Ahmed SS et al.(2017)[11]. Sedation quality was similar between groups, indicating both agents provide effective sedation. Notably, postoperative nausea was significantly less common with dexmedetomidine (6.0% vs. 15.0%, p=0.02), reinforcing dexmedetomidine’s favorable side effect profile Karanth H et al.(2018)[12].

Dexmedetomidine and propofol are both effective sedative agents, but they differ significantly in their hemodynamic profiles. Dexmedetomidine offers superior hemodynamic stability with less hypotension and respiratory depression but causes more bradycardia and longer recovery times. Propofol facilitates faster recovery but is associated with greater hypotension, respiratory depression, and postoperative nausea. Therefore, dexmedetomidine may be preferable in patients at risk of hemodynamic instability or respiratory compromise, while propofol may be suitable when rapid recovery is prioritized.

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