The procedure of anesthetic induction is essential for maintaining stable blood pressure in patients who have heart problems undergoing surgery without heart involvement. Medical professionals select etomidate or propofol for anesthetic purposes because these induction agents produce different cardiovascular consequences within the patient population at risk. Propofol works as an intravenous anesthetic commonly used in practice yet causes substantial blood pressure drops because it dilates blood vessels and limits sympathetic activation (1,2). The choice of etomidate over other anesthetic agents remains strong since it preserves cardiovascular stability by avoiding harmful impacts on myocardial function and vessel receptors (3,4).

Patients suffering from cardiac disease need to consider anesthetic agent hemodynamic effects because blood pressure rate changes could trigger myocardial ischemia and arrhythmias and lead to hemodynamic collapse (5). Various investigations demonstrate that propofol administration leads to substantial drops in systolic blood pressure (SBP) alongside mean arterial pressure (MAP) levels which may need supplementary vasopressor treatment to keep stable hemodynamics (6,7). The drug etomidate provides better control of systolic blood pressure and mean arterial pressure however adrenal suppression risks have restricted its clinical application (8,9). Medical professionals continue to debate how these drugs affect cardiac patient hemodynamics when used during non-cardiac surgery procedures.

The research explores the circulating blood pressure changes during induction between etomidate and propofol when used with patients who have heart diseases undergoing non-cardiac surgical procedures. Measuring SBP together with DBP and CO and HR before and after the induction process stands as the main study goal. Research findings from this study will have value for determining the best anesthetics for patients with cardiac risks during non-cardiac surgical procedures while streamlining cardiac management during the perioperative period.

The researchers conducted this study as a randomized controlled prospective design within a tertiary care hospital framework. Institutional ethics committee approval enabled the research while all participants needed to sign consent forms before clinical participation.

The research selected 100 patients who had heart disease before surgery required for non-cardiac procedures. Adult patients (aged 40–80 years) with cardiovascular disease either due to hypertension or ischemic heart disease or heart failure and categorized as ASA (American Society of Anesthesiologists) II or III were considered for the study. The research excluded patients with known adrenal insufficiency together with severe valvular disease and pregnancy or drug allergies to study medications.

Based on a computer-generated randomized sequence patients were organized into two equal groups of fifty members. The patients within Group P received propofol at a dosage of 2 mg/kg for their induction yet the patients within Group E obtained etomidate at a dosage of 0.3 mg/kg. The substance administrator who delivered the medications was not aware of the research procedures.

The patient evaluation consisted of standard measures and required baseline measurements of their hemodynamic state. Standard operating room monitoring consisting of electrocardiography and non-invasive blood pressure measurement with pulse oximetry began after the patient arrived. The patients underwent three minutes of preoxygenation treatment using 100% oxygen right before the induction sequence.

• Group P: Received intravenous (IV) propofol (2 mg/kg) over 30 seconds.
• Group E: Received IV etomidate (0.3 mg/kg) over 30 seconds.

Fentanyl and rocuronium delivered in a specific dosage enabled professionals to perform tracheal intubation after patients received induction. The patients received anesthesia care consisting of sevoflurane combined with intermittent fentanyl boluses while breathing in a 50% oxygen-air mixture.

The research team measured theseodynamic parameters: systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) at the following moments:

• Baseline (before induction)
• Immediately after induction
• 1 minute post-induction
• 3 minutes post-induction
• 5 minutes post-induction

Any substantial alteration in blood pressure that dropped MAP by more than 20% received IV fluid and vasopressor medical intervention when necessary. The analysis of data occurred through SPSS version 25 which IBM Corp. based at Armonk, NY delivered

The research enrolled 100 patients who were divided between receiving etomidate treatment as one group and propofol treatment as the other group. Table 1 shows the baseline characteristics which remained equal between groups (p > 0.05). Age, gender balance, BMI measurements as well as hypertension and diabetes mellitus statistics did not demonstrate statistical differences (p > 0.05). The groups displayed equivalent measures of both initial systolic blood pressure (SBP) and diastolic blood pressure (DBP) and heart rate (HR) values before anesthesia was initiated.

The participants in the propofol group demonstrated a substantial decline in SBP level to 110 ± 7 mmHg right after induction when compared to the etomidate group with 125 ± 8 mmHg (p < 0.001). The propofol-treated patients experienced a sustained decrease of blood pressure after induction because their systolic pressure measured 98 ± 4 mmHg at five minutes post-administration while the etomidate-treated patients maintained stable SBP levels at 120 ± 5 mmHg (p < 0.001) (Table 2).

The HR measurement for patients given propofol showed a considerable spike following induction (baseline: 74 ± 6 bpm; post-induction: 94 ± 6 bpm; p < 0.001). Patients under etomidate showed no significant heart rate changes after the anesthetic induction because their baseline measurement (75 ± 7 bpm) remained similar to their post-induction measurement (79 ± 6 bpm) with a p value of 0.12 (Table 2).

Among the participants, the propofol group exhibited more occurrences of hypotension (SBP < 90 mmHg) at 30% whereas the etomidate group displayed 4% (p < 0.001). Tachycardia emerged as a greater issue in patients receiving propofol since its occurrence reached 36% while etomidate patients reported 6% (p < 0.001). The patients who received propofol needed vasopressor intervention for 40% of the time whereas patients receiving etomidate required support for 10% only (p < 0.001). Use of propofol or etomidate yielded similar rates of bradycardia between both groups according to the results (p = 0.52) (Table 3).

Table 1: Demographic and Baseline Characteristics

Table 2: Hemodynamic Parameters at Different Time Points

Table 3: Incidence of Hemodynamic Instability

The selection process of anesthetic induction drugs becomes vital for cardiac patients due to destabilizing blood pressures that could lead to serious surgery complications. Scientists evaluated how etomidate versus propofol affects the blood pressure readings of patients with pre-existing cardiac disease undergoing non-cardiac procedures. The study results demonstrate that etomidate leads to better hemodynamic stability than propofol through lowered occurrences of hypotension and tachycardia.

The commonly employed drug propofol causes vasodilation that reduces systemic vascular resistance resulting in patient hypotension (1,2). During the study patients receiving propofol anesthesia demonstrated substantial reductions in both SBP and MAP after receiving the anesthetic agent. The literature shows BP levels decrease an average of 20–30% compared to initial values according to previous studies (3,4). Clinically relevant hypotension occurs because propofol both stops sympathetic engine control and blocks baroreceptor reflexes thus decreasing hemodynamic response mechanisms (5,6).

The hemodynamic balance under etomidate medication administration remained stable because this drug produced minimal effects on blood pressure and heart rate. Earlier research has established how etomidate maintains MAP and SBP readings because it has minimal influence on both myocardial contractility and systemic vascular resistance (7,8). The etomidate group exhibited stable HR because this drug does not affect the autonomic nervous system therefore maintaining a normal heart rate without the tachycardia usually seen after propofol causes hypotension (9).

Our study confirmed the known risk of propofol-related tachycardia as a documented side effect after administration. Baroreceptor activation through the sympathetic nervous system most likely causes this compensatory response by responding to the decreased blood pressure (10). Propofol use results in increased tachycardia as well as elevated myocardial oxygen demands in patients leading potentially dangerous consequences for those with coronary artery disease according to studies (11). Among all sedatives tested etomidate proved to be safer for cardiac patient stability because it did not trigger significant tachycardic effects (12).

Etomidate poses a significant drawback through its effects on 11-beta-hydroxylase enzyme which results in blocking cortisol production (13). The use of a single dose of induction etomidate has shown temporary adrenal insufficiency effects but these effects appear insignificant during brief surgical procedures (14). Measurements indicate that critical ill patients using etomidate suffer greater mortality from adrenal suppression but stable surgical patients undergoing elective procedures show no significant changes (15).

An increased need for vasopressor support characterized the propofol-treated patients because 40% needed BP maintenance medications compared to 10% in subjects receiving etomidate. The study results matched past research which demonstrated vasopressors occur more frequently while patients are under propofol anesthesia due to intense vasodilation (16,17). The administration of propofol in vulnerable patients needs continuous observation together with corrective strategies like fluid treatment or vasopressor administration (18).

This study demonstrates that etomidate functions better than other drugs as an induction agent for patients with heart complications requiring non-heart surgery when patients show signs of hypotension or unstable blood pressure. Selecting an anesthetic agent should happen after factoring in both individual patient health characteristics as well as procedural needs and preferred hospital techniques (19,20). Future investigations must explore long-term clinical results because they include postoperative cardiac events and how patients handled under etomidate-based compared to propofol-based induction (21).

The research evidence shows etomidate creates better cardiovascular stability during anesthesia than propofol for patients handling preoperative cardiac risks during surgical procedures that are not heart-related. The administration of etomidate proved to be superior for maintaining systolic blood pressure while also protecting heart rate and producing a significantly reduced rate of hypotension as well as tachycardia. The practice of using propofol for quick and smooth induction requires continuous monitoring together with possible vasopressor administration for patients whose hearts remain weak. Etomidate emerges as the most appropriate choice for this patient group since it produces minimal negative effects on the cardiovascular system which may help achieve better perioperative safety.

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