Requirement for Discharge in the Care of a Responsible Adult in Procedural Sedation in the Emergency Department: Necessity or Potential Barrier to Health Equity?

BACKGROUND: Procedural sedation is commonly practiced by emergency physicians to facilitate patient care in the emergency department (ED). Although various guidelines have modernized our approach to procedural sedation, many procedural sedation guidelines and practices still often require that patients be discharged into the care of a responsible adult. DISCUSSION: Such requirement for discharge often cannot be met by underserved and undomiciled patients. Benzodiazepines, opioids, propofol, ketamine, "ketofol," etomidate, and methohexital have all been utilized for procedural sedation in the ED. For patients who may require discharge without the presence of an accompanying responsible adult, ketamine, propofol, methohexital, "ketofol," and etomidate are ideal agents for procedural sedation given rapid onsets, short durations of action, and rapid recovery times in patients without renal or hepatic impairment. Proper pre- and postprocedure protocols should be utilized when performing procedural sedation to ensure patient safety. Through the use of appropriate medications and observation protocols, patients can safely be discharged 2 to 4 h postprocedure. CONCLUSION: There is no pharmacodynamic or pharmacokinetic basis to require discharge in the care of a responsible adult after procedural sedation. Thoughtful medication selection and the use of evidence-based pre- and postprocedure protocols in the ED can help circumvent this requirement, which likely disproportionally impacts patients who are of low socioeconomic status or undomiciled.

Echocardiographic Assessment of the Alterations in Pulmonary Blood Flow Associated with Ketamine and Etomidate Administration in Children with Tetralogy of Fallot.

BACKGROUND: Despite widespread uses of ketamine, the clinical studies determining its effect on pulmonary blood flow in children with tetralogy of Fallot (TOF) are lacking. Furthermore, the quantification of pulmonary blood flow is not possible in these patients, because pulmonary artery catheter is contraindicated. Therefore, the purpose of this study was to evaluate the changes in pulmonary blood flow by intra-operative transesophageal echocardiography after ketamine or etomidate administration in children with TOF. METHODS: Eleven children each in the two clinical variants of TOF (group A-moderate to severe cyanosis; group B-mild to minimal cyanosis) undergoing intracardiac repair were prospectively studied after endotracheal intubation. A single bolus dose of ketamine (2 mg/kg) and etomidate (0.3 mg/kg) was administered in a random order after 15 minute interval. Hemodynamic, arterial blood gas, and echocardiographic measurements were obtained at 7 consecutive times (T) points (baseline, 1, 2, 4, 6, 8, and 15 minutes after drug administration). RESULTS: Ketamine produced a significant reduction in VTI-T (velocity time integrals total of left upper pulmonary vein), RVOT-PG (right ventricular outflow tract peak gradient), and MG (mean gradient) in group A while those in group B had a significant increase in VTI-T, RVOT-PG, and RVOT-MG at time (T1, T2, T4, and T6; P = 0.00). This divergent behavior, however, was not observed with etomidate. CONCLUSION: Etomidate does not change pulmonary blood flow. However, ketamine produces divergent effects; it increases pulmonary blood flow in children with minimal cyanosis and decreases pulmonary blood flow in children with moderate to severe cyanosis.

Assessment of the effect of etomidate on voltage-gated sodium channels and action potentials in rat primary sensory cortex pyramidal neurons.

Although it is known that general anesthetics can suppress cortical neurons׳ activity, the underlying mechanisms are still poorly understood, especially the kinetic changes of voltage-gated Na(+) channels, which are mostly related to neuronal excitability. Some general anesthetics have been reported to affect the voltage-gated Na(+) channels in cell culture derived from humans and animals. However no one has ever investigated the effects of etomidate on voltage-gated Na(+) channels in pyramidal neurons using a brain slice. The present study uses a whole cell patch-clamp technique to investigate the changes of voltage-gated Na(+) channels on primary somatosensory cortex pyramidal neurons under the influence of etomidate. We found that etomidate dose-dependently inhibited Na(+) currents of primary somatosensory cortex pyramidal neurons, while shifted the steady-state inactivation curve towards the left and prolonged the recovery time from inactivation. Conversely, etomidate has no effects on the steady-state activation curve. We demonstrated the detailed suppression process of neural voltage-gated Na(+) channels by etomidate on slice condition. This may offer new insights into the mechanical explanation for the etomidate anesthesia. Finding the effects of anesthetics on primary somatosensory cortex also provides evidence to help elucidate the potential mechanism by which tactile information integrates during general anesthesia.

The fentanyl/etomidate-anesthetized beagle (FEAB) model in safety pharmacology assessment.

This unit describes a procedure for performing safety studies in the anesthetized beagle dog. Detailed are the anesthetic regime, the surgical procedure, and all materials needed to perform cardiovascular, central nervous system, and respiratory safety studies in these animals. An overview of all parameters that can be measured and calculated is provided, as are experimental protocols. Endpoints discussed include hemodynamic, electrocardiological, respiratory, arterial blood, and electroencephalogical parameters. Also presented are a formula to correct QT interval for changes in core body temperature and an overview of changes in ECG, MAP, and EEG traces that may occur during safety studies. The information provided yields a multiparametric model for performing reliable safety studies in anesthetized dogs.

Assessment of cardiac troponin I and C-reactive protein concentrations associated with anesthetic protocols using sevoflurane or a combination of fentanyl, midazolam, and sevoflurane in dogs.

OBJECTIVE: To report serum cardiac troponin I (cTnI) and C-reactive protein (CRP) concentrations in dogs anesthetized for elective surgery using two anesthetic protocols. STUDY DESIGN: Prospective, randomized clinical study. ANIMALS: Twenty client-owned dogs presenting for elective ovariohysterectomy or castration. METHODS: The dogs were randomized into two groups. All dogs were premedicated with glycopyrrolate (0.011 mg kg(-1)) and hydromorphone (0.1 mg kg(-1)) i.m. approximately 30 minutes prior to induction of anesthesia. Anesthesia in dogs in group 1 was induced with propofol (6 mg kg(-1)) i.v. to effect and in dogs in group 2 with diazepam (0.2 mg kg(-1)) i.v. followed by etomidate (2 mg kg(-1)) i.v. to effect. For maintenance of anesthesia, group 1 received sevoflurane (adjustable vaporizer setting 0.5-4%) and group 2 received a combination of fentanyl (0.8 microg kg(-1) minute(-1)) and midazolam (8.0 microg kg(-1) minute(-1)) i.v. plus sevoflurane (adjustable vaporizer setting 0.5-4%) to maintain anesthesia. Serum cTnI and CRP concentrations were measured at baseline and 6, 18, and 24 hours post-anesthetic induction. Biochemical analysis was performed at baseline. Lactate was obtained at baseline and 6 hours post-anesthetic induction. Heart rate and mean arterial blood pressure were measured intra-operatively. RESULTS: Baseline serum cTnI and CRP concentrations were comparable between groups. A significant difference in serum cTnI or CRP concentrations was not detected post-operatively between groups at any time point. Serum CRP concentrations were significantly increased post-anesthetic induction in both groups, which was attributed to surgical trauma. CONCLUSIONS AND CLINICAL RELEVANCE: There was no significant difference in serum cTnI and CRP concentrations between anesthetic protocols. Further investigation in a larger number of dogs is necessary to confirm the current findings.

An assessment of the cerebral protective effects of etomidate in a model of incomplete forebrain ischemia in the rat.

The cerebral protective effects of etomidate were evaluated in a model of incomplete forebrain ischemia. Fourteen Wistar-Kyoto rats were anesthetized with halothane. After preparation, the rats were alloted to either the control group (halothane anesthesia, n = 7) or the etomidate group (n = 7). In the etomidate group, immediately before and during the period of ischemia, the animals received etomidate in sufficient concentration to achieve electroencephalogram burst suppression (loading dose, 7.5 mg/kg; infusion, 0.3-0.5 mg/kg/min). Both groups were subjected to a 10-minute ischemic insult accomplished by bilateral carotid artery occlusion and simultaneous hypotension (mean arterial pressure, 35 mm Hg). Histological evaluation of the brain was performed after a 4-day recovery period. Injury was evaluated in coronal brain sections in five structures: neocortex, striatum, reticular nucleus of the thalamus, and the CA1 and CA3 areas of the hippocampus. The location of the sections in the rostral-caudal axis was chosen to encompass anterior areas within the core of the ischemic territory as well as more posterior regions within the anticipated "watershed" zone between the occluded anterior and the intact posterior circulations. In the animals that received etomidate, statistically significant (P less than 0.05) reduction in the severity of the ischemic injury was observed in the CA3 area and in the ventral portion of the CA1 area of the hippocampus in the more posterior sections. There was an apparent trend toward protection in other structures in both rostral and caudal sections, but these changes were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic assessment of the haemodynamic effects of propofol: a comparison with etomidate and thiopentone.

The haemodynamic effects of propofol (2 mg/kg), etomidate (0.2 mg/kg) and thiopentone (4 mg/kg) were studied in 30 ASA 1 and 2 patients in whom anaesthesia had been induced with midazolam 0.1 mg/kg, fentanyl 5 micrograms/kg, vecuronium 0.1 mg/kg and atropine 10 micrograms/kg, and maintained with nitrous oxide in oxygen. Arterial pressure was measured directly and left ventricular diameters were determined by transoesophageal echocardiography. Systolic blood pressure after propofol and thiopentone and the end-systolic quotient (systolic pressure/end-systolic diameter), a measure of inotropy, decreased. Fractional shortening (end-diastolic-end-systolic diameter/end-diastolic diameter) decreased only in the thiopentone group. Diastolic blood pressure and end-diastolic diameter (a measure of preload) did not change in any of the groups, and the etomidate group showed no changes in the haemodynamic variables measured. Propofol shows simultaneous negative inotropy and afterload reduction, while thiopentone is exclusively negatively inotropic.

Clinical assessment of etomidate for outpatient general anesthesia: a preliminary evaluation.

Etomidate, a nonnarcotic, nonbarbiturate hypnotic agent, was assessed in a group of 20 patients requiring general anesthesia for outpatient oral surgical procedures. Changes in mean blood pressure, heart rate, and transcutaneous oxygen tension (PtcO2) were examined following the intravenous administration of etomidate for the induction and maintenance of general anesthesia. Clinical evidence of pain on injection, myoclonic muscle activity, apnea, nausea, and emesis were documented. A postoperative questionnaire evaluated levels of amnesia and acceptance of the drug by the patient and surgeon. No significant (P less than 0.05) change in PtcO2 occurred during etomidate infusion; however, a statistically significant but clinically insignificant change did occur in mean blood pressure and heart rate. Although myoclonic muscle activity, pain on injection, and nausea and vomiting were documented, the subjective evaluation of this agent by patient and surgeon was favorable.