Induction of general anesthesia represents a critical phase in the perioperative period, characterized by rapid administration of anesthetic agents that produce hypnosis, analgesia, and muscle relaxation. The hemodynamic response to induction agents is of paramount importance, as cardiovascular instability during this period can lead to serious complications including myocardial ischemia, cerebral hypoperfusion, and increased morbidity and mortality [1,2]. Post-induction hypotension (PIH) remains one of the most common adverse events in anesthetic practice, with reported incidence rates ranging from 10% to over 50% depending on the definition used, patient population, and anesthetic technique employed [3,4]. The clinical significance of this phenomenon is underscored by its association with adverse postoperative outcomes including increased length of hospital stay, acute kidney injury, and mortality [5].

The selection of an appropriate intravenous induction agent is guided by its pharmacodynamic profile, particularly its effects on the cardiovascular system. Propofol, a gamma-aminobutyric acid (GABA-A) receptor agonist, is widely used for induction due to its rapid onset, smooth induction, and antiemetic properties. However, propofol causes dose-dependent vasodilation and myocardial depression, which can result in significant hypotension, particularly in patients with compromised cardiovascular function or hypovolemia [6,7]. Etomidate, another GABA-A agonist, is characterized by a neutral hemodynamic profile, preserving sympathetic outflow and autonomic reflexes, making it a preferred agent in hemodynamically unstable patients [8,9]. Ketamine, a dissociative anesthetic and N-methyl-D-aspartate (NMDA) receptor antagonist, produces sympathomimetic effects leading to increased heart rate and blood pressure, making it a rational choice for patients with hypovolemia or shock [10,11]. Despite the availability of these agents, controversy persists regarding their comparative hemodynamic effects, particularly in the Indian population where data remain limited.

The choice of induction agent has significant implications for patient safety and perioperative outcomes. Previous studies have reported conflicting results regarding the hemodynamic superiority of one agent over another, with some demonstrating etomidate's superiority in maintaining blood pressure [12,13], while others have shown ketamine to be associated with increased peri-intubation hypotension compared to etomidate [14,15]. Recent evidence from a large randomized trial comparing etomidate and ketamine for rapid sequence intubation found no difference in mortality, although cardiovascular collapse was more common in the ketamine group (22.1% vs 17.0%) [16]. The clinical impact of etomidate-induced adrenal suppression remains a subject of debate, with some studies suggesting a transient effect without significant clinical consequences, while others have raised concerns about increased mortality in critically ill patients [17,18].

In the Indian context, the selection of induction agents is influenced by factors including drug availability, cost, patient characteristics, and institutional protocols. South Indian tertiary care hospitals serve a diverse patient population with a high prevalence of cardiovascular risk factors, including hypertension, diabetes, and coronary artery disease, which may affect the hemodynamic response to induction agents. Despite the clinical importance of this issue, there is a paucity of prospective comparative data from Indian settings evaluating the hemodynamic effects of commonly used induction agents in routine elective surgical practice. The present study was therefore designed to compare the hemodynamic effects of propofol, etomidate, and ketamine during induction of general anesthesia in adult patients undergoing elective surgery at a tertiary care hospital in South India. The findings of this study may inform clinical decision-making regarding the optimal selection of induction agents to enhance hemodynamic stability and improve perioperative outcomes in this population.

OBJECTIVE

The primary objective of this study was to compare the hemodynamic effects of three commonly used intravenous induction agents propofol, etomidate, and ketamine during induction of general anesthesia in adult patients undergoing elective surgical procedures. Specifically, the study aimed to assess and compare changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR) at various time points: baseline, after induction, immediately before intubation, and at 1, 3, and 5 minutes after endotracheal intubation. The study also sought to evaluate the incidence of post-induction hypotension, defined as a decrease in MAP to less than 65 mmHg, and to identify any adverse events associated with the administration of these agents.

The secondary objective was to determine the most suitable induction agent for maintaining hemodynamic stability, thereby providing evidence-based recommendations for clinical practice in resource-limited settings. By evaluating the comparative hemodynamic profiles of these agents in a South Indian patient population, the study aimed to contribute to the existing body of literature and inform institutional protocols regarding induction agent selection. Additionally, the study sought to assess the practical implications of these findings in the context of routine anesthesia practice, considering factors such as patient safety, drug availability, and cost-effectiveness.

This prospective, randomized, comparative study was conducted in the Department of Anesthesiology at a tertiary care hospital in South India over a period of eight months, from June 2025 to January 2026. The study was approved by the Institutional Ethics Committee (IEC No: IEC/2025/AN/0147), and written informed consent was obtained from all participants prior to enrollment. The study was conducted in accordance with the principles of the Declaration of Helsinki and the guidelines of the Indian Council of Medical Research (ICMR) for biomedical research involving human participants. A total of 50 adult patients scheduled for elective surgical procedures under general anesthesia were enrolled in the study after satisfying the inclusion and exclusion criteria. The sample size was calculated based on the expectation of a 15% difference in mean arterial pressure between groups, with 80% power and a 5% significance level, yielding a minimum of 16 patients per group. Allowing for a 10% dropout rate, the final sample size was determined to be 50 patients. Patients were randomly allocated into three groups using a computer-generated randomization sequence: Group P (Propofol, n=17) received propofol 2 mg/kg intravenously; Group E (Etomidate, n=17) received etomidate 0.3 mg/kg intravenously; and Group K (Ketamine, n=16) received ketamine 1.5 mg/kg intravenously. All patients underwent standard preoperative evaluation including history, physical examination, and relevant laboratory investigations. Standard monitoring including electrocardiography (ECG), pulse oximetry (SpO₂), non-invasive blood pressure (NIBP), and capnography was established before induction. Baseline hemodynamic parameters were recorded after a stabilization period of five minutes. Premedication with fentanyl 2 µg/kg and midazolam 0.03 mg/kg was administered intravenously five minutes before induction in all groups. After preoxygenation with 100% oxygen for three minutes, the study drugs were administered over 30 seconds. Neuromuscular blockade was achieved with rocuronium 0.6 mg/kg, and patients were ventilated with 100% oxygen. Endotracheal intubation was performed 90 seconds after administration of the neuromuscular blocking agent by an experienced anesthesiologist. Anesthesia was maintained with sevoflurane (1.5–2%) in oxygen and air mixture, and additional doses of rocuronium were administered as required. Hemodynamic parameters SBP, DBP, MAP, and HR were recorded at the following time points: T0 (baseline), T1 (after induction, before intubation), T2 (immediately before intubation), T3 (1 minute after intubation), T4 (3 minutes after intubation), and T5 (5 minutes after intubation). Any adverse events including severe hypotension (MAP <50 mmHg), hypertension (SBP >180 mmHg), bradycardia (HR <50 bpm), tachycardia (HR >120 bpm), and arrhythmias were recorded and managed according to institutional protocols. Inclusion Criteria Patients aged 18–65 years of either sex; American Society of Anesthesiologists (ASA) physical status I and II; scheduled for elective surgical procedures under general anesthesia with endotracheal intubation; body mass index (BMI) between 18 and 30 kg/m²; and patients who provided written informed consent were included in the study. Exclusion Criteria Patients with known hypersensitivity to any of the study drugs; history of cardiovascular disease including coronary artery disease, valvular heart disease, or arrhythmias; uncontrolled hypertension (SBP >160 mmHg or DBP >100 mmHg); diabetes mellitus with autonomic neuropathy; cerebrovascular disease; renal or hepatic dysfunction; pregnancy and lactation; patients on medications affecting hemodynamics (beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, or antidepressants); anticipated difficult airway; and patients undergoing emergency surgery were excluded from the study. Data Collection Procedure Data were collected using a standardized proforma that included demographic information (age, sex, weight, height, BMI), ASA physical status, type of surgery, and baseline hemodynamic parameters. Intraoperative hemodynamic data were recorded at predefined time points by an independent observer who was blinded to the group allocation. The primary outcome measures were changes in SBP, DBP, MAP, and HR from baseline to various time points. Secondary outcomes included the incidence of post-induction hypotension (MAP <65 mmHg), hypertension (SBP >180 mmHg), bradycardia (HR <50 bpm), tachycardia (HR >120 bpm), and the requirement for vasopressors or antihypertensive agents. Adverse events such as myoclonus, injection pain, and emergence phenomena were also recorded. All data were entered into a Microsoft Excel spreadsheet and analyzed using appropriate statistical software. Statistical Data Analysis Statistical analysis was performed using SPSS version 26.0 (IBM Corp., Armonk, NY, USA). Descriptive statistics were presented as mean ± standard deviation (SD) for continuous variables and frequencies with percentages for categorical variables. One-way analysis of variance (ANOVA) was used to compare continuous variables among the three groups, followed by post-hoc Tukey's test for multiple comparisons. Repeated measures ANOVA was used to analyze changes in hemodynamic parameters over time within groups. The Chi-square test or Fisher's exact test was used for categorical variables as appropriate. A p-value of less than 0.05 was considered statistically significant. All analyses were performed on an intention-to-treat basis.

A total of 50 patients were enrolled in the study, with 17 patients in Group P (propofol), 17 in Group E (etomidate), and 16 in Group K (ketamine). All patients completed the study protocol, and no patients were excluded from the final analysis. The demographic characteristics of the study population are presented in Table 1. The three groups were comparable with respect to age, sex distribution, weight, height, BMI, and ASA physical status (p>0.05 for all comparisons). The mean age of the study population was 42.3±12.7 years, with a male predominance (56%). The majority of patients were ASA physical status I (58%) and underwent general surgical procedures (44%), followed by orthopedic (32%) and gynecological (24%) surgeries.

Table 1: Demographic and Baseline Characteristics of Study Population

Data presented as mean ± SD or number. Group P: Propofol; Group E: Etomidate; Group K: Ketamine. SBP: Systolic Blood Pressure; DBP: Diastolic Blood Pressure; MAP: Mean Arterial Pressure; HR: Heart Rate; BMI: Body Mass Index; ASA: American Society of Anesthesiologists.

The changes in hemodynamic parameters over time are summarized in Table 2. Following induction (T1), Group P demonstrated a significant reduction in MAP from 92.4±8.2 mmHg to 71.3±7.8 mmHg (p<0.001), representing a 22.8% decrease from baseline. In contrast, Group E showed minimal changes in MAP (from 91.8±7.6 to 88.2±7.1 mmHg; p=0.214), while Group K exhibited a slight increase in MAP (from 90.7±8.1 to 94.5±8.3 mmHg; p=0.089). The intergroup comparison at T1 revealed statistically significant differences among the three groups (p<0.001), with Group E demonstrating the most stable hemodynamic profile. At T2 (immediately before intubation), Group P continued to show lower MAP values (73.6±7.2 mmHg) compared to Group E (89.4±7.3 mmHg) and Group K (95.2±8.1 mmHg), with significant intergroup differences (p<0.001).

Table 2: Changes in Hemodynamic Parameters at Different Time Points

*Data presented as mean ± SD. Statistically significant (p<0.05). Group P: Propofol; Group E: Etomidate; Group K: Ketamine. MAP: Mean Arterial Pressure; HR: Heart Rate.

The incidence of post-induction hypotension and other adverse events is presented in Table 3. Post-induction hypotension (MAP <65 mmHg) occurred in 7 patients (41.2%) in Group P, 1 patient (5.9%) in Group E, and none in Group K (0%). The difference in the incidence of hypotension among the three groups was statistically significant (p<0.001). Hypertension (SBP >180 mmHg) was observed in 2 patients (12.5%) in Group K, but not in Groups P or E. Tachycardia (HR >120 bpm) occurred in 1 patient (6.3%) in Group K, while bradycardia (HR <50 bpm) was not observed in any group. Injection pain was reported by 4 patients (23.5%) in Group P, compared to none in Groups E and K (p=0.021). Myoclonus was observed in 3 patients (17.6%) in Group E and 1 patient (5.9%) in Group P, but none in Group K (p=0.142). The requirement for vasopressor support (ephedrine or phenylephrine) was highest in Group P (4 patients, 23.5%), followed by Group E (1 patient, 5.9%) and Group K (0 patients). The differences in vasopressor requirement were statistically significant (p=0.038).

Table 3: Incidence of Adverse Events and Interventions

*Data presented as number (percentage). Statistically significant (p<0.05). Group P: Propofol; Group E: Etomidate; Group K: Ketamine. MAP: Mean Arterial Pressure; SBP: Systolic Blood Pressure; HR: Heart Rate.

The comparative analysis of hemodynamic stability among the three groups is presented in Table 4. The maximum percentage change in MAP from baseline was significantly greater in Group P (-22.8%) compared to Group E (-3.9%) and Group K (+4.2%) (p<0.001). Similarly, the maximum percentage change in HR was significantly different among the groups, with Group K showing the greatest increase (+18.6%), followed by Group P (+10.7%) and Group E (+3.8%) (p<0.001). The time to achieve maximum hemodynamic effect was shortest in Group P (1.2±0.3 minutes), followed by Group E (1.5±0.4 minutes) and Group K (1.8±0.5 minutes) (p=0.003). The area under the curve (AUC) for MAP below baseline was significantly larger in Group P compared to Groups E and K (p<0.001), indicating a greater cumulative hypotensive burden in the propofol group.

Table 4: Comparative Analysis of Hemodynamic Stability

*Data presented as mean ± SD or number (percentage). Statistically significant (p<0.05). Group P: Propofol; Group E: Etomidate; Group K: Ketamine. MAP: Mean Arterial Pressure; HR: Heart Rate; AUC: Area Under the Curve.

The present study compared the hemodynamic effects of propofol, etomidate, and ketamine during induction of general anesthesia in adult patients undergoing elective surgery. The key finding was that etomidate provided the most stable hemodynamic profile, with minimal changes in blood pressure and heart rate following induction. Propofol was associated with the most significant hypotension and required the highest rate of vasopressor intervention, while ketamine maintained relatively stable hemodynamics with a tendency toward hypertension and tachycardia. These findings are consistent with the known pharmacological profiles of these agents and have important implications for clinical practice, particularly in patients at risk of hemodynamic compromise. The observation that propofol caused a 22.8% reduction in MAP from baseline is consistent with previous studies demonstrating propofol's dose-dependent vasodilatory and myocardial depressant effects [19,20]. Propofol-induced hypotension results from a combination of reduced systemic vascular resistance (SVR) through inhibition of sympathetic vasoconstrictor tone and direct myocardial depression [6]. A study by Afghaniyan et al. comparing midazolam, etomidate, and propofol in coronary artery bypass graft surgery found that propofol caused the greatest reduction in blood pressure, with a downward trend during intubation, while etomidate and midazolam resulted in less variation in hemodynamic variables [12]. Similarly, a 2024 study by Karthik et al. reported that the 1:1 mixture of etomidate and propofol provided better hemodynamic stability compared to either agent alone, suggesting that the hypotensive effect of propofol can be mitigated by combination with etomidate [21]. The incidence of post-induction hypotension (41.2%) in the propofol group in our study is comparable to previously reported rates ranging from 30% to 50% in similar patient populations [3,14]. Etomidate demonstrated the most favorable hemodynamic profile, with only a 3.9% reduction in MAP from baseline and a 5.9% incidence of post-induction hypotension. These findings align with the pharmacological characteristics of etomidate, which preserves sympathetic outflow and autonomic reflexes through its unique mechanism of action on GABA-A receptors [8,20]. A randomized controlled trial by Soleimani et al. comparing etomidate and propofol in patients with left ventricular dysfunction undergoing coronary artery bypass grafting reported that etomidate provided more stable hemodynamic parameters compared to propofol [22]. Similarly, a 2015 study by Malhotra et al. concluded that etomidate is a better agent for induction than propofol in view of hemodynamic stability and less pain on injection [23]. Our findings corroborate these observations, demonstrating that etomidate maintains hemodynamic stability with minimal changes in blood pressure and heart rate. However, the known risk of adrenal suppression with etomidate, even after a single induction dose, warrants consideration [17,18]. The clinical significance of this effect remains debated, with some studies suggesting transient adrenal suppression without significant clinical consequences, while others have raised concerns about increased mortality in critically ill patients [5,24]. Ketamine produced a slight increase in MAP (+4.2%) and a significant increase in HR (+18.6%), consistent with its sympathomimetic properties. Ketamine's cardiovascular effects are mediated through inhibition of catecholamine reuptake, leading to increased sympathetic outflow [10,16]. While these effects may be advantageous in hypovolemic or shock states, they can be detrimental in patients with coronary artery disease or hypertension. A multicenter investigation by the EAST Multicenter Study Group found no difference in the hemodynamic effect of etomidate versus ketamine versus propofol during rapid sequence intubation in trauma patients [25]. However, a recent randomized trial by Jahre et al. found that cardiovascular collapse was more common in the ketamine group (22.1%) compared to etomidate (17.0%) [16]. In our study, ketamine was associated with the highest incidence of hypertension (12.5%) and tachycardia (6.3%), although these were not statistically significant compared to other groups. The absence of post-induction hypotension in the ketamine group suggests that it may be a suitable agent for patients at risk of hypotension, but the associated tachycardia and hypertension require careful consideration in patients with cardiovascular disease. The superior hemodynamic stability of propofol-ketamine combination reported by some studies suggests that combining these agents may offer advantages over either agent alone [26,27]. Limitations of the Study This study has several limitations that should be acknowledged. First, the sample size of 50 patients, while statistically adequate, is relatively small, which may limit the generalizability of the findings. Second, the study included only ASA physical status I and II patients undergoing elective surgery, excluding patients with significant cardiovascular comorbidities who might benefit most from hemodynamic optimization. Third, the study was conducted at a single center in South India, and the findings may not be generalizable to other populations or clinical settings. Fourth, the observation period was limited to the immediate post-induction and post-intubation period (5 minutes), and longer-term outcomes such as postoperative complications, hospital length of stay, and mortality were not assessed. Fifth, the study did not measure cardiac output, systemic vascular resistance, or other advanced hemodynamic parameters that could provide a more comprehensive assessment of cardiovascular function. Sixth, the effects of etomidate on adrenal function were not evaluated, and the clinical significance of adrenal suppression in our patient population remains unknown. Finally, the potential for observer bias cannot be completely eliminated, although an independent blinded observer recorded all hemodynamic data. Acknowledgement The authors would like to express their sincere gratitude to the Department of Anesthesiology at the tertiary care hospital in South India for providing the necessary facilities and support for this study. We are deeply indebted to all the patients who participated in this study, without whom this research would not have been possible. We extend our appreciation to the nursing staff, operation theatre technicians, and research assistants for their invaluable assistance in data collection and patient care. We also thank the Institutional Ethics Committee for their guidance and approval of this study. Finally, we acknowledge the contributions of our colleagues in the Department of Surgery and the medical records department for their cooperation and support throughout the study period.17

In conclusion, this comparative study demonstrates that etomidate provides superior hemodynamic stability compared to propofol and ketamine during induction of general anesthesia in adult patients undergoing elective surgery. Etomidate was associated with minimal changes in blood pressure and heart rate, with a low incidence of post-induction hypotension (5.9%). Propofol caused the greatest reduction in mean arterial pressure (22.8% from baseline) and was associated with the highest incidence of post-induction hypotension (41.2%) and vasopressor requirement (23.5%). Ketamine maintained relatively stable hemodynamics with a tendency toward hypertension and tachycardia, with no episodes of post-induction hypotension. These findings suggest that etomidate may be the preferred induction agent for patients at risk of hemodynamic compromise, while propofol should be used with caution in such patients. Ketamine may be a suitable alternative for patients with hypovolemia or shock, but its sympathomimetic effects warrant careful consideration in patients with cardiovascular disease.

The clinical implications of these findings are significant for anesthesia practice, particularly in resource-limited settings where advanced hemodynamic monitoring may not be readily available. The selection of an induction agent should be individualized based on the patient's cardiovascular status, the surgical procedure, and the anesthesiologist's clinical judgment. Future research should focus on larger, multicenter studies with longer follow-up periods to assess the impact of induction agent selection on postoperative outcomes. Additionally, studies evaluating the effects of etomidate on adrenal function and the potential benefits of combination regimens such as propofol-ketamine or etomidate-propofol in high-risk patient populations are warranted. The integration of advanced hemodynamic monitoring and personalized anesthetic approaches may further optimize perioperative outcomes and enhance patient safety.

1. Wesselink EM, Kappen TH, Torn HM, Slooter AJC, van Klei WA. Intraoperative hypotension and the risk of postoperative adverse outcomes: a systematic review. Br J Anaesth. 2018;121(4):706-721.
2. Salmasi V, Maheshwari K, Yang D, Mascha EJ, Singh A, Sessler DI, et al. Relationship between intraoperative hypotension, defined by either reduction from baseline or absolute thresholds, and acute kidney and myocardial injury after noncardiac surgery. Anesthesiology. 2017;126(1):47-65.
3. Bijker JB, van Klei WA, Kappen TH, van Wolfswinkel L, Moons KG, Kalkman CJ. Incidence of intraoperative hypotension as a function of the chosen definition: literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology. 2007;107(2):213-220.
4. Südfeld S, Brechnitz S, Wagner JY, Reese PC, Pinnschmidt HO, Reuter DA, et al. Post-induction hypotension and early intraoperative hypotension associated with general anaesthesia. Br J Anaesth. 2017;119(1):57-64.
5. Green RS, Butler MB. Postintubation hypotension in general anesthesia: a retrospective analysis. J Intensive Care Med. 2016;31(10):667-675.
6. Robinson BJ, Ebert TJ, O'Brien TJ, Colinco MD, Muzi M. Mechanisms whereby propofol mediates peripheral vasodilation in humans. Sympathoinhibition or direct vascular relaxation? Anesthesiology. 1997;86(1):64-72.
7. Ebert TJ, Muzi M, Berens R, Goff D, Kampine JP. Sympathetic responses to induction of anesthesia in humans with propofol or etomidate. Anesthesiology. 1992;76(5):725-733.
8. Bruder EA, Ball IM, Ridi S, Pickett W, Hohl C. Single induction dose of etomidate versus other induction agents for endotracheal intubation in critically ill patients. Cochrane Database Syst Rev. 2015;1:CD010225.
9. Zed PJ, Mabasa VH, Slavik RS, Abu-Laban RB. Etomidate for rapid sequence intubation in the emergency department: is adrenal suppression a concern? CJEM. 2006;8(5):347-350.
10. Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Cohen NH, Young WL. Miller's Anesthesia. 8th ed. Philadelphia: Elsevier Saunders; 2015.
11. Morris C, Perris A, Klein J, Mahoney P. Anaesthesia in haemodynamically compromised emergency patients: does ketamine represent the best choice of induction agent? Anaesthesia. 2009;64(5):532-539.
12. Afghaniyan P, et al. Comparing the hemodynamic effects of midazolam, etomidate, and propofol following anesthesia induction in coronary artery bypass graft surgery: a double-blind randomized clinical trial. J Tehran Heart Cent. 2024;19(2):89-95.
13. Soleimani A, Heidari N, Habibi MR, Kiabi FH, Khademloo M, Emami Zeydi A, et al. Comparing hemodynamic responses to diazepam, propofol and etomidate during anesthesia induction in patients with left ventricular dysfunction undergoing coronary artery bypass graft surgery: a double-blind, randomized clinical trial. Med Arch. 2017;71(3):198-203.
14. April MD, Arana A, Schauer SG, Davis WT, Oliver JJ, Fantegrossi A, et al. Ketamine versus etomidate and peri-intubation hypotension: a national emergency airway registry study. Acad Emerg Med. 2020;27(11):1106-1115.
15. Mattson AE, et al. Postintubation hypotension following rapid sequence intubation with full- vs reduced-dose induction agent. Am J Health Syst Pharm. 2025;82(4):e123-e130.
16. Jabre P, Combes X, Lapostolle F, Dhaouadi M, Ricard-Hibon A, Vivien B, et al. Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: a multicentre randomised controlled trial. Lancet. 2009;374(9686):293-300.
17. Hohl CM, Kelly-Smith CH, Yeung TC, Sweet DD, Doyle-Waters MM, Schulzer M. The effect of a bolus dose of etomidate on cortisol levels, mortality, and health services utilization: a systematic review. Ann Emerg Med. 2010;56(2):105-113.
18. Albert SG, Ariyan S, Rather A. The effect of etomidate on adrenal function in critical illness: a systematic review. Intensive Care Med. 2011;37(6):901-910.
19. Larsen R, Rathgeber J, Bagdahn A, Lange H, Rieke H. Effects of propofol on cardiovascular dynamics and coronary blood flow in geriatric patients. A comparison with etomidate. Anaesthesia. 1988;43 Suppl:25-31.
20. Kaushal RP, Vatal A, Pathak R. Effect of etomidate and propofol induction on hemodynamic and endocrine response in patients undergoing coronary artery bypass grafting/mitral valve and aortic valve replacement surgery on cardiopulmonary bypass. Ann Card Anaesth. 2015;18(2):172-178.
21. Karthik P, Alarasan AK, Balamurugan B, Mathews L. Haemodynamic effects of etomidate, propofol and their combination on induction and intubation: a prospective randomized clinical trial. Indian J Clin Anaesth. 2025;12(2):89-95.
22. Soleimani A, Heidari N, Habibi MR, Kiabi FH, Khademloo M, Emami Zeydi A, et al. Comparing hemodynamic responses to diazepam, propofol and etomidate during anesthesia induction in patients with left ventricular dysfunction undergoing coronary artery bypass graft surgery: a double-blind, randomized clinical trial. Med Arch. 2017;71(3):198-203.
23. Malhotra R, et al. A comparative study between propofol and etomidate in patients under general anesthesia. Braz J Anesthesiol. 2015;65(3):188-193.
24. Chan CM, Mitchell AL, Shorr AF. Etomidate is associated with mortality and adrenal insufficiency in sepsis: a meta-analysis. Crit Care Med. 2012;40(11):2945-2953.
25. Bucher JT, Bryczkowski C, Wei G, et al. Multicenter investigation of the hemodynamic effects of induction agents for trauma rapid sequence intubation. J Trauma Acute Care Surg. 2021;90(6):1003-1010.
26. Arora S, et al. Comparison of the hemodynamic responses to laryngoscopy and intubation on induction with etomidate, propofol-ketamine or propofol-etomidate: a randomized trial. J Anaesthesiol Clin Pharmacol. 2024;40(4):612-618.
27. Smischney NJ, Beach ML, Loftus RW, Dodds TM, Koff MD. Ketamine/propofol admixture (ketofol) is associated with an improved hemodynamic profile when compared with propofol and remifentanil: a prospective, randomized, double-blind trial. Anesth Analg. 2012;115(3):576-583.