Etomidate Opioids

Answer This feature of bradycardia is typical of patients who take (3-blockers, which should be continued so they result ultimately in better anesthetic management. The drugs given could have been modified (i.e., etomidate instead of propofol, which does not raise or may cause a slower heart rate). The potent opioids in the fentanyl family all cause vagal transmitted bradycardia. The muscle relaxant vecuronium (norcuron) has no effect on heart rate and could have been replaced by pancuronium, which has a vagolytic effect and will counter bradycardia in the usual induction bolus doses. 

Onset of unconsciousness is rapid but it is associated with a high incidence of excitatory effects, comparable to methohexitone, but these can be reduced by prior administration of an opioid. Analogous to the barbiturates, etomidate decreases CMR02, CBF and ICP but the haemodynamic stability of the drug will maintain CPP. Its well-known inhibition of adrenocortical function limits its clinical usefulness for long-term control of elevated ICP. While etomidate can produce convulsion-like EEC potentials in the absence of apparent convulsions, it has been used to terminate status epilepticus. 

Opioids, such as morphine and fentanyl, are safe, whereas there is insufficient data on some other analgesics to be sure of their position. All muscle relaxants are probably safe, although there are insufficient data about most to be completely sure atropine and neostigmine are safe. Drugs which are unsafe or probably unsafe include barbiturates, etomidate, enflurane, alcuronium, mepivacaine, pentazocine, some benzodiazepines (temazepam is safe, other benzodiazepines less certain), calcium channel blockers and aminophylline. 

Etomidate is a carboxylated imidazole that can be used for induction of anesthesia in patients with limited cardiovascular reserve. Its major advantage over other intravenous anesthetics is that it causes minimal cardiovascular and respiratory depression. Etomidate produces a rapid loss of consciousness, with minimal hypotension even in elderly patients with poor cardiovascular reserve. The heart rate is usually unchanged, and the incidence of apnea is low. The drug has no analgesic effects, and coadministration of opioid analgesics is required to decrease cardiac responses during tracheal intubation and to lessen spontaneous muscle movements. Following an induction dose, initial recovery from etomidate is less rapid (< 10 minutes) compared with recovery from propofol. 

Several drugs are used intravenously, alone or in combination with other drugs, to achieve an anesthetic state (as components of balanced anesthesia) or to sedate patients in intensive care units who must be mechanically ventilated. These drugs include the following (1) barbiturates (thiopental, methohexital) (2) benzodiazepines (midazolam, diazepam) (3) opioid analgesics (morphine, fentanyl, sufentanil, alfentanil, remifentanil) (4) propofol (5) ketamine and (6) miscellaneous drugs (droperidol, etomidate, dexmedetomidine). Figure 25-2 shows the structures of... 

The anesthetic effect of (+)-etomidate subsides within a few minutes owing to redistribution of the drug. Etomidate can provoke myoclonic movements that can be prevented by premedication with a benzodiazepine or an opioid. Because it has little effect on the autonomic nervous system, it is suitable for induction in combination anesthesia. Etomidate inhibits cortisol synthesis in subanesthetic doses and can therefore be used in the long-term treatment of adrenocortical overactivity (Cushing disease). 

Usually intravenous pre-oxygenation followed by a small dose of an opioid, e.g., fentanyl or alfentanil to provide analgesia and sedation, followed by propofol or, less commonly, thiopental or etomidate to induce anaesthesia. Airway patency is maintained with an oral airway and face-mask, a laryngeal mask airway (LMA), or a tracheal tube. Insertion of a tracheal tube usually requires paralysis with a neuromuscular blocker and is undertaken if there is a risk of pulmonary aspiration from regurgitated gastric contents or from blood. 

Etomidate, maprotiline, metoclopramide, opioids (intrathecally), physostigmine... 

The main adverse effects with etomidate are pain on injection and muscle twitching during induction, both of which can be reduced by using an opioid analgesic. It also causes suppression of the adrenal cortex. 

Bradycardia occurring during anaesthetic induction with vecuronium and etomidate, or to a iesser extent thiopental, has also been reported, particularly in patients also receiving fentanyl, see also Neuromuscular blockers + Opioids , p.l30. 

The respiratoiy depressant effects of ketamine and morphine may be additive. The dose requirements of desflurane, etomidate, propofol and thiopental may be lower after opioid use. Opisthotonos or grand mal seizures have rarely been associated with the use of propofol with alfentanil and/or fentanyl. The effects of in-halational anaesthetics may be enhanced by opioid analgesics. 

The manufaeturer of etomidate recommends that the dose of etomidate should be redueed in patients who have already received opioids. ... 

Myoclonus is observed in 50-80% of patients receiving induction of anesthesia with etomidate and is associated with postoperative discomfort. Pretreatment with an opioid, a benzodiazepine, and magnesium sulfate reduces the incidence of myoclonus but does not completely prevent it. The effect of pretreatment with dexmede-tomidine or sodium thiopental on etomidate-related myoclonus has been studied in 90 ASA I-II patients undergoing elective surgery, who were randomized to 0.9% saline (n=30), dexmedetomidine 0.5 micrograms/kg ( =30), or sodium thiopental 1 mg/kg ( =30) administered by infusion over 10 minutes and followed 1 minute later by etomidate 0.3 mg/kg over 60 seconds [24. There were fewer cases of myoclonus in those who received dexmedetomidine or sodium thiopental (68% and 64% versus 36% of controls). 

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