Dexmedetomidine is a selective a2 receptor agonist administered intravenously as a sedative and analgesic in intensive care and operating room settings. It has a strong preference for a2 receptors and a terminal half-life of 2 hours, but liver impairment can dramatically increase its plasma levels and duration due to decreased metabolism. Its potent binding and short half-life can cause physiological dependence and withdrawal symptoms like tachycardia, hypertension, and anxiety after only a few days of administration. Large intravenous boluses paradoxically cause hypertension with decreased heart rate due to crossover a1 receptor stimulation similar to phenylephrine.
Dexmedetomidine is a selective a2 receptor agonist administered intravenously as a sedative and analgesic in intensive care and operating room settings. It has a strong preference for a2 receptors and a terminal half-life of 2 hours, but liver impairment can dramatically increase its plasma levels and duration due to decreased metabolism. Its potent binding and short half-life can cause physiological dependence and withdrawal symptoms like tachycardia, hypertension, and anxiety after only a few days of administration. Large intravenous boluses paradoxically cause hypertension with decreased heart rate due to crossover a1 receptor stimulation similar to phenylephrine.
Dexmedetomidine is a selective a2 receptor agonist administered intravenously as a sedative and analgesic in intensive care and operating room settings. It has a strong preference for a2 receptors and a terminal half-life of 2 hours, but liver impairment can dramatically increase its plasma levels and duration due to decreased metabolism. Its potent binding and short half-life can cause physiological dependence and withdrawal symptoms like tachycardia, hypertension, and anxiety after only a few days of administration. Large intravenous boluses paradoxically cause hypertension with decreased heart rate due to crossover a1 receptor stimulation similar to phenylephrine.
Dexmedetomidine is a selective a2 agonist with a 1,600:1 preference for a2 receptors. It is intravenously
administered as an infusion from 0.1 to 1.5 g/kg/minute with a terminal elimination half-life of 2 hours. Most often, this a2 agonist is used in the intensive care and operating room settings as a sedative and analgesic due to its central sympatholytic effects. Dexmedetomidine undergoes extensive biotransformation in the liver and is excreted mostly in the urine; liver impairment can dramatically increase plasma levels and duration of action due to signifiantly decreased metabolism during infusion. It’s potent binding and short half-life can induce physiologic dependence and result in the aforementioned withdrawal phenomenon after only days of administration resulting in tachycardia, hypertension, and anxiety. Interestingly, large intravenous boluses (0.25 to 1 g/kg over 3 to 5 minutes) result in a paradoxical hypertension with a decrease in heart rate and resembles phenylephrine and is the resultant effect of crossover a1 stimulation.
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