Anesthetics and Anesthetic Adjuncts Analgesics [ Opiates, fentanyl (Sublimaze)] General depressants a. Benzodiazepines [benzodiazepines midazolam (Versed)] b. Barbiturates [secobarbital] Neuroleptics [ droperidol (Inapsine)]
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Midazolam is used for conscious sedation, anxiolysis, and amnesia during minor surgical or diagnostic procedures.
Midazolam is used as an inducing agent, and as an adjunct to regional anesthesia.
Midazolam, as other benzodiazepines (BDZs) act at limbic, thalamic, and hypothalamic structures producing a dose dependant CNS depression including sedation, hypnosis, skeletal muscle relaxation, and anticonvulsant activity.
BDZs act by potentiating the action of GABA at GABAA receptors. Benzodiazepines cause allosteric modulation of GABAA receptor complex, but do not activate the channel.
Unlike barbiturates which augment GABA responses by increasing the length of time that chloride channels remain open, BDZs enhance GABA efficacy by increasing the affinity of GABA to its binding site on the GABAA receptor.
Fentanyl is a strong agonist at µ- and kappa- opiate receptors.
Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (µ and delta receptor agonist) resulting in hyperpolarization and reduced neuronal excitability.
Analgesia is mediated through changes in the perception of pain at spinal cord (µ2-, delta-, kappa-receptors) and brain (µ1- and kappa3 receptors).
Opiate receptors are G-protein coupled receptors. Opioid-G-protein systems include cAMP and PLC-intositol triphosphate.
The emotional response to pain is altered. Opiates do not alter the pain threshold of afferent nerve endings to noxious stimuli.
Opioids can modulate the endocrine and immune systems inhibiting release of vasopressin, somatostatin, insulin and glucagons.
Stimulatory effects of opioids are the result of "disinhibition" as the release of inhibitory neurotransmitters such as GABA is blocked.
Clinically, stimulation of µ-receptors produces analgesia, euphoria, respiratory depression, miosis, decreased gastrointestinal motility, and physical dependence.
Kappa-receptor stimulation produces analgesia, miosis, respiratory depression, as well as, dysphoria and some psychomimetic effects (i.e., disorientation and/or depersonalization).
Miosis is produced by excitatory action on the autonomic segment of the nucleus of the oculomotor nerve.
Opiate-induced respiratory depression is caused by direct action on brain stem. respiratory centers while bradycardia is due to depression of the medullary vasomotor center and vagal nucleus stimulation.
Opiate agonists action on the GI tract results in constipation and delayed digestion, while urinary smooth muscle tone is increased by opiate agonists, sometimes causes urinary retention.