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At least 289 records · Page 16Linked to original sources
PubMed2000

Sevoflurane-fentanyl versus etomidate-fentanyl for anesthetic induction in coronary artery bypass graft surgery patients.

OBJECTIVE: To compare the hemodynamic effects of sevoflurane-fentanyl with etomidate-fentanyl during anesthetic induction in patients with coronary artery disease with good left ventricular function. DESIGN: A prospective randomized trial. SETTING: University hospital. PARTICIPANTS: Twenty patients scheduled for elective coronary artery bypass graft surgery. INTERVENTIONS: Patients were allocated randomly to receive either 4% sevoflurane/nitrous oxide 67%/oxygen 33% (sevoflurane group) or etomidate, 0.2 mg/kg, for induction (intravenous group). Both techniques were supplemented by 10 microg/kg of fentanyl and muscle relaxation with pancuronium. Anesthesia was maintained in both groups with 2% sevoflurane/nitrous oxide 67%/oxygen 33%. MEASUREMENTS AND MAIN RESULTS: Time to loss of consciousness and airway complications during induction were assessed. Hemodynamics were recorded at 1-minute intervals during the induction period up to 5 minutes postintubation. Induction of anesthesia was significantly faster in patients given etomidate compared with patients who received sevoflurane; loss of eyelid reflex was 45 seconds (standard deviation 17 seconds) versus 97 seconds (standard deviation 20 seconds). None of the patients who received sevoflurane had airway complications during the induction period. Both anesthetic induction techniques provided cardiostability with little change in cardiac index (2%). The decrease in mean arterial blood pressure was greater in the patients who received sevoflurane induction (maximal decrease 28% v 14%). The heart rate and filling pressure changes were insignificant. CONCLUSION: Sevoflurane inhalation induction produced minimal changes in cardiac index and no airway complications in patients with coronary artery disease with good left ventricular function. Induction was faster with etomidate, however, and blood pressure remained higher.

Anesthesia, General↗
PubMed1985

[Effect of an introductory dose of etomidate, methohexital and midazolam on adrenal cortex function before and after ACTH-stimulation].

The adrenocortical function after induction of anaesthesia using either etomidate, methohexital or midazolam was examined in 30 patients undergoing open heart surgery (ACVB). Midazolam and methohexital did not suppress the typical stress response assessed from the magnitude of the ACTH, cortisol and aldosterone levels. The ACTH-test was also normal. In contrast, induction of anaesthesia using etomidate led to a progressive fall in cortisol and aldosterone accompanied by an increase in ACTH. The ACTH-test resulted in only a minor increase in adrenocortical hormones. Thus an induction dose of etomidate, in contrast to methohexital and midazolam, markedly alters the normal function of the adrenal cortex. This side-effect of etomidate lasts for at least 4 hours but is no longer detectable after 24 hours.

Adrenal Cortex↗
PubMed1989

Effects of thiopentone and etomidate on median nerve somatosensory evoked responses.

Somatosensory evoked potentials (SEP) after median nerve stimulation were recorded in 40 patients during infusion of either 15 mg/kg bw thiopentone or 1 mg/kg bw etomidate (n = 10) within 15 min and after 0.3 mg/kg bw etomidate (n = 20). Marked alterations of SEP waveforms and changes in latencies were observed in all patients. Central conduction time (CCT) was significantly correlated to plasma thiopentone concentration. Infusion of high doses of thiopentone and etomidate was followed by a complete loss of middle and long latency components. Amplitude of the primary cortical SEP N20 was found to be unchanged after thiopentone and to be increased after etomidate, indicating the synchronizing properties of this drug. A pronounced increase in SEP latencies and CCT and waveform alterations have to be considered during hypnotic drug administration in intensive care medicine and intraoperatively.

Adult↗
PubMedDate not supplied

Regional EMS experience with etomidate for facilitated intubation.

OBJECTIVE: To report the preliminary experience of the Central New York emergency medical services (EMS) region with etomidate for prehospital facilitated intubation. METHODS: Prospective recording of all intubations (facilitated and nonfacilitated) was completed during the first six months of the etomidate protocol, from January 1 to June 30, 2000. These results were compared with retrospective comparison data obtained for an 18-month period from stored documented prehospital care reports (PCRs), a period when diazepam was used for facilitated intubation. RESULTS: During the study period, 343 (84%) of 409 attempted intubations were successful. Of these, 24 facilitated intubations (using etomidate) were attempted (all on breathing, agitated patients), and 19 (79%, CI 63%-95%) were successful. Eighteen of these (95%) were intubated successfully on the first attempt. The median age of the patients requiring intubation was 70 years (range 14-90), and 60% were female. There were no reported incidences of vomiting, broken teeth, or bleeding. The region's prior 18-month experience using diazepam for facilitated intubation resulted in ten (23%, CI 1%-36%) successful intubations of 43 facilitated intubation attempts. CONCLUSIONS: Preliminary data suggest increased rates of success for facilitated intubation using etomidate, when compared with diazepam, with most intubations successful on the first attempt. Limitations of this study include a small sample size and self-reporting of airway data by paramedics.

Adolescent↗
PubMed1978

An investigation of the centrally and peripherally mediated cardiovascular effects of etomidate in the rabbit.

In the decerebrate rabbit etomidate caused dose-related decreases in mean arterial pressure and preganglionic sympathetic nerve activity. There were no significant alterations in heart rate. Etomidate was found to have no effect on the baroreceptor reflex. In pithed animals the effects of etomidate were of short duration and of a lesser magnitude than in the decerebrate animal. It was concluded that the additional effects in the decerebrate rabbit were a result of depression of central cardiovascular control. It was found that etomidate was largely without effect on the cardiovascular system at normal anaesthetic doses (0.5-1 mg-kg-1). However, larger doses (2-8 mg kg-1) produced marked depression of central cardiovascular control, the myocardium and the peripheral vasculature.

Animals↗
PubMed1982

Plasma concentration and E.E.G. after various regimens of etomidate.

Etomidate was injected i.v. within 10 or 60 s at various doses. After etomidate 0.3 mg kg-1 the plasma concentration was 1.6 micrograms ml-1 at 1 min after the end of injection. For about 7 min a good hypnotic effect (stages C0-D2) was observed on the e.e.g. recording. For surgical procedures, however, a combination with analgesic drugs appeared to be necessary. When the dose of etomidate was increased (0.1-0.4 mg kg-1) a linear increase in plasma concentration and slow e.e.g. activity was observed concomitantly. Anaesthesia could be prolonged with additional injections or with continuous infusion. Each additional injection produced a steep increase in concentration of short duration with marked deepening of hypnosis. The infusion induced only a moderate increase in plasma concentration, whereas the depth of sleep during the period of infusion remained nearly the same. E.e.g. changes induced by etomidate are similar to those after barbiturates and other i.v. anaesthetics.

Adult↗
PubMed1992

Does etomidate cause haemolysis?

Etomidate is currently presented as a solution with propylene glycol as solvent. This organic solvent has an extremely high osmolality and is probably responsible for some of the side effects of this drug. In order to detect haemolysis, an indication for cell damage, we have measured serum haptoglobin concentrations in 12 healthy male volunteers after administration of etomidate 0.3 mg kg-1. Six subjects received etomidate in propylene glycol (EtoPG) with an osmolality of 4965 mosmol kg-1 and six received etomidate in lipid emulsion (EtoLip, 400 mosmol kg-1). Haptoglobin concentrations in the EtoPG group decreased by 44% and 43% from baseline values at 2 and 4 h after administration, respectively, and were significantly smaller than after administration of EtoLip. After 24 h, haptoglobin concentrations had not reached baseline values.

Adult↗
PubMed1992

Changes in cardiac index and estimated systemic vascular resistance during induction of anaesthesia with thiopentone, methohexitone, propofol and etomidate.

Changes in cardiac index (CI) and estimated systemic vascular resistance (ESVR) were assessed non-invasively using pulsed Doppler ultrasound during induction of anaesthesia. Ninety-six ASA I patients were allocated randomly to one of four groups to receive alfentanil 8 micrograms kg-1 followed by a dose of thiopentone, methohexitone, propofol or etomidate sufficient to obtund the eyelash reflex. CI increased significantly by 8% 1 min after administration of both methohexitone (P < 0.05) and propofol (P < 0.05), returning to pre-induction values thereafter. CI increased after thiopentone but the increase was not statistically significant. There was a significant decrease in CI of 16% after induction with etomidate (P < 0.001). ESVR decreased significantly from pre-induction values by 18% after methohexitone (P < 0.001) and 23% after propofol (P < 0.001). ESVR in the thiopentone group decreased, but this was not statistically significant. ESVR increased significantly by 12% 1 min after induction of anaesthesia with etomidate (P < 0.05) and then decreased towards pre-induction values. The results suggest that the cardiostability of etomidate may not be as complete in all groups of patients as previous studies have suggested.

Blood Flow Velocity↗
PubMed1997

Haemolysis after etomidate: comparison of propylene glycol and lipid formulations.

We sought to determine if the solvent in the formulation of etomidate is responsible for haemolysis in patients. In a randomized, prospective, double-blind study of 49 patients undergoing otolaryngological surgery, patients received etomidate dissolved in propylene glycol or in lipid emulsion. Concentrations of free haemoglobin and haptoglobin were measured before and for up to 360 min after injection of etomidate. Free haemoglobin concentrations increased by 216.8 mg litre-1 in patients who received the propylene glycol formulation and by 11.8 mg litre-1 in the lipid emulsion group (P < or = 0.0004). Correspondingly, reductions in haptoglobin concentrations were significantly greater in the propylene glycol group (P < or = 0.002). We conclude that with respect to haemolysis, lipid emulsion is superior to propylene glycol as a solvent for etomidate.

Anesthetics, Intravenous↗
PubMed1999

Solvent for etomidate may cause pain and adverse effects.

We tested the hypothesis that the solvent for etomidate was a factor in the incidence of pain and other side effects after injection, and that these were associated with histamine release. Nine of 10 volunteers who received etomidate in a propylene glycol formulation reported moderate to severe pain on injection; only one of 10 subjects who received a lipid emulsion formulation reported mild pain (P < 0.05). The incidence of venous sequelae in the injected vein over the next 8 days was 50% in the propylene glycol group and 0% in the lipid emulsion group (P < 0.05). In one volunteer in the propylene group, there was a 13-fold increase in histamine concentrations and in one subject a four-fold increase. In the lipid emulsion group, no volunteer had an increase in histamine concentrations > 1 ng ml-1. We conclude that etomidate formulated in propylene glycol may cause direct injury to vascular endothelium resulting in pain and venous sequelae, whereas etomidate in lipid emulsion does not. There was no relationship between pain or venous sequelae and histamine release.

Adult↗
PubMed1995

The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy.

The intravenous anesthetics which are commonly used for electroconvulsive therapy (ECT) possess dose-dependent anticonvulsant properties. Since the clinical efficacy of ECT depends on the induction of a seizure of adequate duration, it is important to determine the optimal dose of the hypnotic for use during ECT. We compared the duration of seizure activity and cognitive recovery profiles after different doses of methohexital, propofol, and etomidate administered to induce hypnosis prior to ECT. Ten outpatients with major depressive disorders receiving maintenance ECT participated in this prospective, randomized, cross-over study. Patients were premedicated with glycopyrrolate, 0.2 mg intravenously (i.v.), and labetalol, 20-30 mg i.v., and hypnosis was induced with an i.v. bolus injection of methohexital or propofol (0.75, 1.0, and 1.5 mg/kg), or etomidate (0.15, 0.2, and 0.3 mg/kg), administered over 10-15 s. Adequate muscle paralysis was achieved with succinylcholine, 1.0-1.4 mg/kg i.v. Each patient's seizure threshold was determined prior to enrollment in the study and the electrical stimulus variables were kept constant throughout the study period. After delivery of a bilateral electrical stimulus, the duration of the resulting electroencephalographic (EEG) and motor seizures were recorded. A total of 90 ECT treatments were evaluated. The durations of EEG and motor seizures were longest after etomidate and shortest after propofol. There were no significant dose-related differences in motor and EEG seizure durations (means +/- SD) after the low, intermediate, and high doses of etomidate of 44 +/- 11 and 77 +/- 19, 43 +/- 10 and 76 +/- 34, 42 +/- 16 and 78 +/- 56 s, respectively. Conversely, both methohexital and propofol, 0.75, 1.0, and 1.5 mg/kg, produced dose-dependent decreases in motor and EEG seizure durations (i.e., 37 +/- 10 and 58 +/- 12, 36 +/- 8 and 62 +/- 24, and 29 +/- 13 and 48 +/- 20 for methohexital; 34 +/- 15 and 56 +/- 29, 31 +/- 8 and 50 +/- 17, and 20 +/- 6 and 33 +/- 12 for propofol, respectively). The awakening times were similar, regardless of the hypnotic or dose administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of thiopental, fentanyl, and etomidate on upper extremity somatosensory evoked potentials in humans.

The effects of three anesthetic induction agents on somatosensory evoked potentials (SEP) were assessed in unpremedicated patients who were without neurologic abnormality of the upper extremities. SEP was assessed by stimulation of the nondominant median nerve and responses were recorded over Erbs point (N10), second cervical vertebra (N14), and the contralateral cortex (P15, N20, P23 latencies, and P15-N20 and N20-P23 amplitudes). Nine patients received thipental (4 mg/kg, iv bolus), nine patients received fentanyl (25 micrograms/kg, iv bolus), and nine patients received etomidate (0.4 mg/kg, iv bolus). SEP was assessed before and after drug administration at motor threshold stimulus intensity. Thiopental increased the latency of N10, N14, and N20. The amplitudes of N10-, N14-, and scalp-recorded waves were not altered by thiopental. Fentanyl increased N20 and P23 latency and decreased the amplitude of P15-N20. Etomidate increased latency of N20 and P23 without alteration of latencies of N10 or N14 and increased the amplitude of P15-N20 and N20-P23, while the amplitude of N10 was unchanged and the amplitude of N14 was decreased. It is concluded that thiopental or fentanyl causes only modest alterations in early waves of upper extremity SEP, whereas etomidate increases the amplitude of scalp-recorded waves. The effect of etomidate on SEP may make diagnosis of neurologic injury more difficult because of the changing waveform.

Adult↗
PubMed1988

Dose-related changes in the rate of cerebrospinal fluid formation and resistance to reabsorption of cerebrospinal fluid following administration of thiopental, midazolam, and etomidate in dogs.

The rate of cerebrospinal fluid (CSF) formation (Vf) and resistance to reabsorption of CSF (Ra) were determined in dogs at four doses of thiopental (6, 12, 18, and 24 mg.kg-1.h-1), midazolam (0.5, 1.0, 1.5, and 2.0 mg.kg-1.h-1), and etomidate (0.86, 1.72, 2.58, and 3.44 mg.kg-1.h-1). Results were compared within and between groups and to previously reported normal values for Vf (0.030-0.054 ml/min) and Ra (220-240 cmH2O.ml-1.min) in dogs. At the two lower doses of thiopental, midazolam, or etomidate Vf was not significantly different than previously reported normal values. At the two higher doses of each drug Vf was 0.019-0.024 ml/min, significantly reduced compared to Vf at the two lower doses of each drug. The pattern of Ra data was more varied. With thiopental Ra was elevated at the lowest dose, (354 +/- 17 cmH2O.ml-1.min, mean +/- SD) reduced at the highest dose (156 +/- 19 cmH2O.ml-1.min), and not significantly different than previously reported normal values at the two intermediate doses. With midazolam Ra was elevated at the lowest and highest doses (332 +/- 25 and 378 +/- 18 cmH2O.ml-1.min) and normal at the two intermediate doses. With etomidate Ra was normal at the three lower doses and reduced at the highest dose (187 +/- 13 cmH2O.ml-1.min). It is concluded that CSF volume may be increased and the CSF pressure at which CSF volume contracts may be increased by doses of thiopental or midazolam that increase Ra, but not increased by etomidate.

Absorption↗
PubMed1991

Enhancement of somatosensory evoked potentials by etomidate in cats: an investigation of its site of action.

Enhancement of somatosensory evoked potentials by etomidate has been reported in recent clinical studies. This investigation was designed to investigate the central nervous system site of action responsible for this effect. Six adult cats were anesthetized with halothane (0.8-1%) in a mixture of 50% N2O in O2. A recording electrode was placed stereotactically in the ventral posterior lateral nucleus of thalamus (VPL), and a ball electrode was placed over the surface of the hind limb region of primary sensory cortex. Somatosensory evoked potentials in response to stimulation of tibial nerve thus were simultaneously recorded from cerebral cortex and VPL. The effect of two doses (1 and 3 mg.kg-1) of etomidate given 2 h apart on the latency and amplitude of cortical (positive wave at 15 ms) and thalamic (positive deflection at 10 ms, followed by negative deflection at 17 ms) evoked potentials was studied. There was no significant effect of etomidate on either latency or amplitude of early, positive thalamic potentials. Both doses of etomidate caused a significant increase in the latency and amplitude of cortical potentials. The mean latency of cortical potential increased by 1.72 ms (11%) after the 1 mg.kg-1 dose and 2.3 ms (15.9%) after the 3 mg.kg-1 dose. The maximum mean increase in the amplitude of cortical potentials was 14.3 microV (mean increase 78%, range 28-241%) after 1 mg.kg-1 and 19.1 microV (mean increase 112%, range 28-202%) after 3 mg.kg-1. Cortical amplitude remained significantly elevated for 30 min after 1 mg.kg-1 and for the remainder of the study period (60 min) after 3 mg.kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Sympathetic responses to induction of anesthesia in humans with propofol or etomidate.

Anesthetic induction with propofol commonly results in hypotension. This study explored potential mechanisms contributing to hypotension by recording cardiovascular responses including sympathetic neural activity from patients during induction of anesthesia with propofol (2.5 mg.kg-1 plus 200 micrograms.kg-1.min-1) or, for comparison, etomidate (0.3 mg.kg-1 plus 15 micrograms.kg-1.min-1). Twenty-five consenting, nonpremedicated, ASA physical status 1 and 2, surgical patients were evaluated. Measurements of R-R intervals (ECG), blood pressure (radial artery), forearm vascular resistance (plethysmography), and efferent muscle sympathetic nerve activity ([MSNA] microneurography: peroneal nerve) were obtained at rest and during induction of anesthesia. In addition, a sequential bolus of nitroprusside (100 micrograms) followed by phenylephrine (150 micrograms) was used to obtain data to quantitate the baroreflex regulation of cardiac function (R-R interval) and sympathetic outflow (MSNA) in the awake and anesthetized states. Etomidate induction preserved MSNA, forearm vascular resistance, and blood pressure, whereas propofol reduced MSNA by 76 +/- 5% (mean +/- SEM), leading to a reduction in forearm vascular resistance and a significant hypotension. Both cardiac and sympathetic baroslopes were maintained with etomidate but were significantly reduced with propofol, especially in response to hypotension. These findings suggest that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains hemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes.

Adult↗
PubMed1996

Etomidate and thiopental inhibit the release of endothelium-derived hyperpolarizing factor in the human renal artery.

BACKGROUND: Endothelium-derived hyperpolarizing factor is thought to be a cytochrome P450-derived arachidonic acid metabolite that hyperpolarizes vascular smooth muscle cells by opening Ca(2+)-activated K+ channels (K+Ca channels). In the rabbit carotid artery both volatile and intravenous anesthetics inhibit the acetylcholine-stimulated release of endothelium-derived hyperpolarizing factor. Because the release of this factor may help to maintain vascular tone in humans under conditions of a failing nitric oxide synthesis, e.g., in atherosclerosis, the effects of two intravenous anesthetics, thiopental and etomidate, on the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine were investigated in human isolated renal artery segments. METHODS: The segments were suspended in Krebs-Henseleit solution (37 degrees C) containing the cyclooxygenase inhibitor diclofenac (1 microM) and preconstricted with norepinephrine (6 microM). Relaxations caused by acetylcholine (1 microM) were compared in the presence and absence of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine (0.1 mM) in control segments and in segments exposed to etomidate or thiopental (0.03-0.3 mM). In addition, the effects of the two anesthetics on the relaxant response to the nitric oxide donors glyceryl trinitrate (3 microM) and sodium nitroprusside (0.1 microM) were examined. RESULTS: The relaxant response to acetylcholine, which was resistant to both nitric oxide synthase and cyclooxygenase blockade, was markedly reduced by the K+Ca channel antagonist tetrabutyl ammonium (3 mM) and the cytochrome P450 inhibitor clotrimazole (30 microM). Both etomidate and thiopental, at a concentration of 0.3 mM, selectively attenuated the relaxant response to acetylcholine in N(G)-nitro-L-arginine-treated segments, but did not affect relaxations elicited by glyceryl trinitrate or sodium nitroprusside. CONCLUSIONS: Etomidate and thiopental inhibit the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine in the human renal artery, an effect that appears to be attributable to the cytochrome P450-inhibiting properties of these anesthetics.

Anesthetics, Intravenous↗
PubMed2006

Ketamine appears associated with better word recall than etomidate after a course of 6 electroconvulsive therapies.

Ten patients treated with electroconvulsive therapy (ECT) for depressive illness received anesthesia with either etomidate or ketamine. Three patients received both etomidate and ketamine anesthesia for ECT during separate episodes of depression. Patients anesthetized with ketamine for ECT had significantly less impairment of short-term memory function than did patients who received ECT with etomidate anesthesia. All patients who received both anesthetics for ECT during 2 different episodes had less memory loss during ECT with ketamine than with etomidate. These results show the importance of studying the effects of all anesthetic agents used during ECT on cognitive functions. The results imply that the effect of ECT on memory may be largely caused by effects mediated by glutamate at N-methyl-d-aspartate receptors and suggest that N-methyl-d-aspartate antagonists may offer protection from memory dysfunction during ECT.

Adult↗
PubMed1979

Plasma potassium, sodium and blood sugar following etomidate and suxamethonium.

Changes in plasma potassium, sodium and blood sugar were studied in Nigerian patients following induction of anaesthesia with etomidate and suxamethonium. Healthy patients presenting for elective surgery as well as psychiatric patients presenting for electroconvulsive therapy were studied. Plasma potasium was essentially unaffected by etomidate administration, but rose significantly when suxamethonium was given. This rise was higher than that observed with thiopentone and suxamethonium in a previous study on a similar group of Nigerians. Blood sugar was not significantly increased by the administration of etomidate but rose significantly after suxamethonium was given. This hyperglycaemic response was greater than when thiopentone was used as the induction agent. Administration of ECT was associated with a further increase in blood sugar. It is concluded that thiopentone is preferable to etomidate in situations where increases in plasma potassium and blood sugar are undesirable following administration of suxamethonium.

Adult↗