In the publications relating to the cardiovascular effects of etomidate, you are surprised by an enormous disagreement. Some report a slight decrease in blood pressure and heart rate, others the reverse. The explanation is simple: performing anaesthesia on a patient who is not intubated and by no means offered other stimulation will always reduce haemodynamics. Confirming other experiences, Weiss-Bloom and Reich [30] showed that if the haemodynamic response to intubation was to be blunted by a combination of etomidate and fentanyl, a dose of 5-10 mg/kg of the latter would be needed. The recognitions made in the older studies [31-49] reflect a broad agreement which has now been established: etomidate is the least inotropic acting hypnotic. Also in a newer study on induction in elderly patients for cataract surgery [50], the etomidate group reacted with an av. increase in BP of 19% compared to an occasionally drop in BP of av. 42% after propofol. The findings of propofol causing more serious cardiac depression may leave the sentiments cool what day-case patients are concerned, since this is well tolerated by cardially healthy patients. Nevertheless, all anaesthetists are occasionally dealing with patients who were also seriously ill before they started working with them, and for these ‘risk-patients’ another induction drug is required. That it still is possible also to meet serious complications in etomidate anaesthesia was shown in two case-reports by van den Hurk and Teijen [51].

Newer studies generally focuses on more specific parameters. Ebert et al. [52] compared the sympathetic response to anaesthetic induction with propofol and etomidate. They found that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains haemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes. Tassani et al. [53] did not find any significant change in the systemic vascular resistance when eltanolone, thiopental and etomidate were given during extracorporal circulation. The stronger haemodynamic depression produced by eltanolone compared with etomidate and thiopental [54] thus appears to relate to a negative inotropic effect. An experimental study [55] showed that etomidate, in contrast to thiopental, was inert to cardiac muscle cells.Jellish et al. [56] titrated the dosage of etomidate to burst suppression, for which they needed 0.5-1.7 mg/kg. Thereby, they found more stable haemodynamics during laryngoscopy and intubation as compared with lower dose (0.4-0.6 mg/kg guided by EEG) of etomidate or thiopental 3-6 mg/kg. Using the same principle, Shapiro et al. found a need for vasopressor support in half of the patients [57] – but this finding must be relativized by the anaesthetic action of etomidate, which does not invite for burst suppression monitoring as a guidance; accordingly, the authors needed a mean induction dosage of 0.73 mg/kg and 48 mg/kg/min. Reichl et al. [226] found that “To avoid severe hypotension, alternatives to propofol anesthetic induction (e.g., etomidate) should be considered in patients older than 50 yr of age with ASA physical status >3.” They concluded that it is advisable to avoid propofol induction in patients who present with baseline MAP <70 mm Hg.” Dhawan et al. [288] found by each 25 children with right-to-left or left-to-right shunt that etomidate at 0.3 mg/kg produced only minimal changes in hemodynamic parameters and shunt fraction in children with congenital shunt lesions.

A possible explanation to the beneficial haemodynamic effects was demonstrated in an animal study. Etomidate shows some structural similarities with -adrenoceptor agonists and in mice, Paris et al. [202] found that etomidate exerted a clear agonistic effect on this receptor, responsible for cardiovascular stability or, in case of very rapid injection, even an overshooting hypertensive response.