Dexmedetomidine, sold under the brand name Precedex among others, is a medication used for sedation.
Pregnancy category AU: B1
Routes of administration Intravenous, injection, sublingual, buccal
Protein binding 94% (mostly albumin)
Metabolism Near complete hepatic metabolism to inactive metabolites
Elimination half-life 2–4 hours
Excretion Urine
It is also used in humans to treat acute agitation associated with schizophrenia or bipolar disorder.
It is administered as an injection or intravenous solution or as a buccal or sublingual film.
Similar to clonidine, dexmedetomidine is a sympatholytic drug that acts as an agonist of α2-adrenergic receptors in certain parts of the brain.
Studies suggest dexmedetomidine for sedation in mechanically ventilated adults may reduce time to extubation and ICU stay.
Use of dexmedetomidine appears to be associated with less neurocognitive dysfunction compared to other sedatives.
It can also be used for procedural sedation such as during colonoscopy, and as an adjunct with other sedatives like benzodiazepines, opioids, and propofol to enhance sedation and help maintain hemodynamic stability by decreasing the requirement of other sedatives.
Dexmedetomidine is also used for procedural sedation in children, and can be used for sedation required for awake fibreoptic nasal intubation in patients with a difficult airway.
When used as an adjunct infusion during general anesthesia. In this application, it has been shown to decrease post-operative delirium, pain, nausea and opioid use.
Dexmedetomidine may be useful for the treatment of the negative cardiovascular effects of acute amphetamines and cocaine intoxication and overdose.
Dexmedetomidine has also been used as an adjunct to neuroaxial anesthesia for lower limb procedures.
It has been successfully used to treat opioid withdrawal symptoms.
In is approved by the FDA for the treatment of agitation in schizophrenia and bipolar disorder.
There are no known contraindication to the use of dexmedetomidine.
Dexmedetomidine has a biphasic effect on blood pressure with lower readings at lower drug concentrations and higher readings at higher concentrations.
Common side effects include: hypotension, hypertension, with slight decreases in heart rate, arrhythmias, and hypoxia.
With toxic doses first-degree or second-degree atrioventricular block may occur.
Dexmedetomidine may enhance the effects of other sedatives and anesthetics drugs that lower blood pressure and heart rate, such as beta blockers when co-administered.
It is a highly selective α2-adrenergic receptor agonist.
It is 8 times more selective for the α2-adrenergic receptor than the related drug clonidine.
Dexmedetomidine is able to achieve its effects without causing respiratory depression, unlike opioids and other sedatives such as propofol.
Dexmedetomidine induces sedation by decreasing activity of noradrenergic neurons in the locus ceruleus in the brain stem.
Dexmedetomidine increases the downstream activity of inhibitory γ-aminobutyric acid (GABA) neurons in the ventrolateral preoptic nucleus.
Other sedatives like propofol and benzodiazepines directly increase activity of GABAergic neurons.
Dexmedetomidine’s action on the endogenous sleep-promoting pathway the sedation it produces more closely mirrors natural sleep (specifically stage 2 non-rapid eye movement sleep (NREM)), as demonstrated by EEG studies.
Dexmedetomidine provides less amnesia than benzodiazepines.
It has analgesic effects at the spinal cord level and other supraspinal sites.
Intravenous dexmedetomidine has a rapid distribution half-life of approximately 6 minutes in healthy volunteers, and a longer and more variable distribution half-life in ICU patients.
The terminal elimination half-life of intravenous dexmedetomidine ranged 2.1 to 3.1 hours in healthy adults and 2.2 to 3.7 hours in ICU patients.
The plasma protein binding of dexmedetomidine is about 94%, mostly albumin.
Dexmedetomidine is metabolized by the liver, largely by glucuronidation (34%) as well as by oxidation via CYP2A6 and other cytochrome P450
It is used with caution in people with liver disease or hepatic impairment.
The majority of metabolized dexmedetomidine is excreted in the urine (~95%).
Approved it as a short-term sedative and analgesic for critically ill or injured people on mechanical ventilation in the intensive care unit.