Propofol benzodiazepines

Emergence delirium with restlessness, disorientation and unpleasant dreams or hallucinations may occur for up 24 hours following ketamine administration. Their incidence is reduced by psychological preparation of the patient, avoidance of verbal and tactile stimulation during the recovery period, or by concomitant administration of opioids, benzodiazepines, propofol or physostigmine. However, unpleasant dreams may persist. 

Mice lacking the 8 subunit, which is mainly expressed in cerebellum and thalamus, display an attenuation of ssatrighting reflex time following the administration of the neurosteroids, alphaxalone and pregnanolone, while the responses to propofol, etomindate, ketamine and the benzodiazepine midazolam were unaffected. This demonstrates the role of GABAa receptors containing the 8 subunit for neurosteroid action. 

Adequate pain control (i.e., morphine) and sedative use (i.e., propofol, benzodiazepine)... 

The GABA-gated chloride ion channel is modulated by several classes of drugs that bind to allosteric sites on the receptor complex the benzodiazepines, barbiturates and related intravenous general anesthetics such as etomidate and propofol, as well as anesthetic steroids and endogenous neurosteroids. It appears that some types of GABAa receptor are directly enhanced by ethanol and volatile general anesthetics (Fig. 16-2) [7,8,20]. 

The following agents may be affected by theophylline Benzodiazepines, -agonists, halothane, ketamine, lithium, nondepolarizing muscle relaxants, propofol, ranitidine, and tetracyclines. Probenecid may increase the effects of dyphylline. 

Opioids play an important role in anesthetic practice. Opioid analgesics potentiate the efficacy of anesthetics. They can be given as part of the premedication as well as during the operation. Examples of short acting agents with high potency are fentanyl, sufentanyl, alfentanil and remifentanil. Because of their hemodynamic stability these agents can be used for patients with compromised myocardial function. Respiration must be maintained artificially and may be depressed into the postoperative period. They are usually supplemented with inhalation anesthetic, benzodiazepines or propofol. 

Refractory status epilepticus that has failed to respond to one of these treatments, and has continued for more than 20-30 min, requires urgent action. The accepted strategy is to paralyze and ventilate the patient and administer an antiepileptic drug in sufficient dosage to suppress EEG evidence of seizure activity. The barbiturate anaesthetic thiopental (thiopentone), the benzodiazepine midazolam, and the anaesthetic propofol have all been used. What little comparative evidence there is remains inconclusive. Such treatment can only be carried out with facilities for artificial ventilation and intensive care, and effects can only be monitored by EEG recording. 

Barbiturates may precipitate episodes of acute intermittent porphyria (AIP) and their use is contraindicated in patients who are predisposed to this condition. Some animal models indicate that ketamine, etomidate, and the benzodiazepines may be porphyrinogenic and propofol is considered to be the intravenous anaesthetic of choice in AlP-prone patients. 

Ketamine has been traditionally contraindicated in patients with increased ICP or reduced cerebral compliance because it increases CMR02, CBF and ICP. These deleterious effects can be antagonised by the concomitant administration of propofol, or thiopentone, and benzodiazepines. Furthermore, ketamine is an antagonist at the NMDA receptor. Nevertheless, ketamine can adversely affect neurological outcome in the presence of brain ischaemia. 

Recovery is sufficiently rapid with most intravenous drugs to permit their use for short ambulatory (outpatient) surgical procedures. In the case of propofol, recovery times are similar to those seen with sevoflurane and desflurane. Although most intravenous anesthetics lack antinociceptive (analgesic) properties, their potency is adequate for short superficial surgical procedures when combined with nitrous oxide or local anesthetics, or both. Adjunctive use of potent opioids (eg, fentanyl, sufentanil or remifentanil see Chapter 31) contributes to improved cardiovascular stability, enhanced sedation, and perioperative analgesia. However, opioid compounds also enhance the ventilatory depressant effects of the intravenous agents and increase postoperative emesis. Benzodiazepines (eg, midazolam, diazepam) have a slower onset and slower recovery than the barbiturates or propofol and are rarely used for induction of anesthesia. However, preanesthetic administration of benzodiazepines (eg, midazolam) can be used to provide anxiolysis, sedation, and amnesia when used as part of an inhalational, intravenous, or balanced anesthetic technique. 

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... 

Recovery after propofol or midazolam has been compared in two studies (36,37). Memory was significantly impaired by midazolam, an effect that was reminiscent of the problems experienced with short-acting oral benzodiazepine hypnotics, such as triazolam. 

Benzodiazepines can be used to control agitation. Avoid phenothiazines due to possible hypotension. Animals may need to be heavily sedated so they do not injure themselves or others. Control seizures with a benzodiazepine, pheno-barbital, or propofol. Rhabdomyolysis can occur if agitation or seizures are not controlled. 

Avoid imnecessary stimulation, which may induce rigidity and spasms. The primary treatment for spasms and rigidity is sedation with a benzodiazepine, such as midazolam or diazepam. Additional sedation may be provided with propofol or a phenothiazine, usually chlorpromazine. In severe disease prolonged spasms and respiratory dys-fimction will necessitate tracheal intubation and mechanical ventilation will be required. If the patient has been intubated and sedation alone is inadequate to control spasms, a neuromuscular blocking drug, e.g., intermittent doses of pancuronium or a continuous infusion of atracurium, will be required. 

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