Etomidate is an intravenous hypnotic agent that has played a notable role in the history of modern anesthesia. Introduced in the 1970s, it was initially embraced for its rapid onset, short duration of action, and remarkable cardiovascular stability. Over time, however, concerns regarding its effects on adrenal steroid synthesis led to a significant decline in routine use. Despite this reduction, etomidate continues to occupy an important niche in modern anesthetic practice due to its benefits for patients for whom hemodynamic stability is a critical priority and for whom other anesthetic agents may be contraindicated.
One of the clinical benefits of etomidate that preserves its role in modern anesthesia is its minimal impact on cardiovascular function. Unlike many other induction agents, such as propofol or thiopental, etomidate produces little to no depression of myocardial contractility and causes minimal changes in heart rate, systemic vascular resistance, or blood pressure. This makes it particularly valuable in patients with limited cardiac reserve, severe coronary artery disease, cardiomyopathy, or critical valvular pathology. In these settings, even modest reductions in blood pressure can lead to myocardial ischemia or end-organ hypoperfusion, and the stability it offers can be a decisive advantage.
Etomidate also has a favorable respiratory profile during induction. While it can cause brief apnea, the overall degree of respiratory depression is generally less pronounced than with other commonly used induction agents. Its rapid onset of hypnosis, typically within one circulation time, allows for predictable and efficient airway control. These characteristics have contributed to its continued use in emergency airway management, including rapid sequence induction in critically ill or hemodynamically unstable patients.
The primary factor responsible for the decline in etomidate use is its effect on adrenal function. Etomidate inhibits 11β-hydroxylase, a key enzyme in cortisol and aldosterone synthesis. Even a single induction dose can result in transient adrenal suppression that lasts up to 24 hours. In critically ill patients, particularly those with sepsis or septic shock, adequate cortisol production is essential for maintaining vascular tone and responding to physiologic stress. Studies suggesting an association between etomidate use and increased mortality in septic patients prompted widespread caution and led many clinicians to favor alternative agents.
As a consequence of these findings, etomidate is now used far more selectively than in previous decades. Safer alternatives with fewer endocrine effects are readily available for routine elective cases. Propofol, for example, has become the dominant induction agent in stable patients due to its favorable recovery profile and antiemetic properties, despite its tendency to cause hypotension.
Nevertheless, etomidate remains an important tool in specific clinical situations. In patients with severe hemodynamic instability, such as those experiencing trauma, acute hemorrhage, or cardiogenic shock, the immediate benefit of cardiovascular stability may outweigh the risks of transient adrenal suppression. In such cases, a single dose of etomidate may reduce the need for vasopressors or fluid boluses during induction, thereby preventing further physiological compromise. Its use may also be considered in patients with intracranial pathology, as it reduces cerebral metabolic rate and intracranial pressure while preserving cerebral perfusion pressure.
In modern anesthesia, etomidate is no longer a first-line agent for routine use but has instead become a specialized option for high-risk scenarios with specific clinical benefits. The evolution of etomidate’s role reflects a broader trend in anesthetic practice toward individualized agent selection that balances short-term physiological needs against potential downstream effects to achieve the safest possible outcome for each patient.
