File:Dexmedetomidine skeletal.svg
Systematic (IUPAC) name
Clinical data
Trade names Precedex, Dexdor
AHFS/ monograph
  • US: C (Risk not ruled out)
Intravenous infusion only
Pharmacokinetic data
Protein binding 94%
Metabolism Near complete hepatic metabolism to inactive metabolites
Half-life 2 hours
Excretion Urinary
113775-47-6 7pxY
PubChem CID 68602
DrugBank DB00633 7pxY
ChemSpider 4470605 7pxY
KEGG D00514 7pxY
ChEBI CHEBI:4466 7pxY
Chemical data
Formula C13H16N2
200.28 g/mol
 14pxY (what is this?)  (verify)

Dexmedetomidine (trade names Precedex [US market], Dexdor [European market], Dexdomitor) is a sedative medication used by intensive care units and anesthesiologists. It is relatively unusual in its ability to provide sedation without causing respiratory depression. Like clonidine, it is an agonist of α2-adrenergic receptors in certain parts of the brain.[1] It is the S-enantiomer of medetomidine,[2] used in veterinary medicine. Dexmedetomidine hydrochloride is also used in veterinary medicine for dogs and cats.[3] The drug was developed by Orion Pharma.[4]


Dexmedetomidine is indicated for sedation of critically ill or injured patients in an intensive care unit setting. Its indication in the US was recently expanded to include nonintubated patient requiring sedation for surgery or procedures short-term. It is also useful as an adjunct for sedation and general anesthesia in the setting of certain operations and invasive medical procedures, such as colonoscopy. There are no absolute contraindications to the use of dexmedetomidine. Limiting its usefulness is the caution that the drug cannot be bolused due to concerns about peripheral α2-receptor stimulation with resulting hypotension and bradycardia, combined with its current high cost relative to generic medications such as propofol, fentanyl and midazolam which can achieve similar clinical effects.

Intensive care unit sedation

Compared to midazolam, dexmedetomidine was similarly effective for sedation, but shortened the time to extubation. It was associated with less delirium, fast heart rates and low blood pressures, but more slowed heart rates.[5] It also seemed to be superior to lorazepam for ventilated patients in the intensive care unit.[6] Compared to midazolam, dexmedetomidine is superior due to reduced intensive care costs. The reduced costs are due to a reduction in intensive care unit stay as well as reduced mechanical ventilation.[7]

Procedural sedation

Dexmedetomidine has sedative, analgesic, sympatholytic, and anxiolytic effects that blunt many of the cardiovascular responses in the perioperative period. It reduces the requirements for volatile anesthetics, sedatives and analgesics without causing significant respiratory depression.[8] Dexmedetomidine has also been used for procedural sedation in children.[9]


Dexmedetomidine may be useful for the treatment of the deleterious cardiovascular effects of acute amphetamines and cocaine intoxication and overdose.[10][11] Dexmedetomidine may also offer a new paradigm in the pharmacologic treatment of symptoms of distress (intractable pain, agitation, or delirium) at the end of life. Recently, an investigator initiated IND was approved by the FDA to examine the use of dexmedetomidine in treating cancer patients at the end of life who are suffering from intractable pain, agitation, or delirium.[12]

Dosage and administration

Intravenous infusion of dexmedetomidine is commonly initiated with a 1 µg/kg loading dose, administered over 10 minutes, followed by a maintenance infusion of 0.2–1.0 µg/kg/hour. There may be great individual variability in the hemodynamic effects (especially on heart rate and blood pressure), as well as the sedative effects of this drug. For this reason, the dose must be carefully adjusted to achieve the desired clinical effect.[13]

Veterinary use

Dexmedetomidine (trade name Dexdomitor) is commonly used as a sedative, anxiolytic, and anesthetic adjunct in dogs and cats. It is formulated in a much higher concentration (500 µg/ml) and given at a much higher dose in small animals than in humans. As a stand alone agent, it is labeled at 375 µg/m2 IV or 500 µg/m2 IM in dogs (10-20x higher than human loading dose, depending on weight of dog). The effective dose can be markedly decreased with the concurrent administration of an opioid (2-10 µg/kg given with morphine equivalent of 0.2-1 mg/kg when given IV). It can also be used combined with an equal volume (0.05 to 0.3 ml total of each, depending on level of sedation desired and weight of cat) of ketamine and opioid (butorphanol, buprenorphine, morphine, or hydromorphone) to provide profound sedation as an IM injection in cats (known in veterinary circles as "Kitty Magic"). As an anxiolytic agent, it is typically given at a 0.5-2 µg/kg bolus followed by a continuous infusion at 0.5-2 µg/kg/h. It is most often used for this purpose post-operatively. It is also used at this dose for maintenance of sedation in patients being mechanically ventilated.

Unlike in human patients, dexmedetomidine tends to cause initial hypertension in small animals. It is considered contra-indicated in dogs with mitral-insufficiency and dilated cardiomyopathy due to concerns over its transient increase in afterload and bradycardia both of which could contribute to acute decompensation. In cats with hypertrophic cardiomyopathy, however, it is considered by some to be particularly useful when sedation is required as the resultant bradycardia may be of benefit in states where diastolic function is compromised. Dexmedetomidine is also considered to be contraindicated in hypotensive and/or hypovolemic patients, hyperkalemic patients (such as cats who have had prolonged urethral obstruction or other conditions causing acute renal failure) and should be used with extreme caution in geriatric patients.

Also unlike in human patients, a reversal agent, atipamazole (trade name Antisedan) is commonly used to reverse the effects of dexmedtomidine after sedation is no longer needed. It is given IM in an equal volume to the Dexdomitor solution used. This makes dexmeditomine particularly useful for outpatient procedures as sedative effects can be completely (or almost completely) resolved within 30 minutes of the end of a procedure (especially if a short acting opioid such as fentanyl is used as part of the sedative protocol).

Pricing and patent life

Template:Outdated section Dexmedetomidine is currently more expensive than off-patent sedatives, such as propofol and midazolam (median per-patient drug acquisition cost was reported as $75 for dexmedetomidine vs $60 for midazolam in one study).[14] Dexmedetomidine is expected to lose patent protection in the United States in 2013 at which time the acquisition cost of this drug will likely decrease.[15]

See also


  1. ^ Cormack JR, Orme RM, Costello TG (2005). "The role of alpha2-agonists in neurosurgery". Journal of Clinical Neuroscience 12 (4): 375–8. PMID 15925765. doi:10.1016/j.jocn.2004.06.008. 
  2. ^ a b PubChem 5311068
  3. ^
  4. ^
  5. ^ Riker RR, Shehabi Y, Bokesch PM, Ceraso D, Wisemandle W, Koura F, Whitten P, Margolis BD, Byrne DW, Ely EW, Rocha MG (2009). "Dexmedetomidine vs Midazolam for Sedation of Critically Ill Patients: A Randomized Trial". JAMA 301 (5): 489–99. PMID 19188334. doi:10.1001/jama.2009.56. 
  6. ^ Pandharipande, PP; Pun, BT; Herr, DL; Maze, M; Girard, TD; Miller, RR; Shintani, AK; Thompson, JL et al. (2007). "Effect of sedation with dexmedetomidine vs lorazepam on acute brain dysfunction in mechanically ventilated patients: the MENDS randomized controlled trial". JAMA 298 (22): 2644–53. PMID 18073360. doi:10.1001/jama.298.22.2644. 
  7. ^ O'Connor, M; Bucknall, T; Manias, E (2009). "Sedation Management in Australian and New Zealand Intensive Care Units: Doctors' and Nurses' Practices and Opinions". Am J Crit Care 19 (3): 285–95. PMID 19770414. doi:10.4037/ajcc2009541. 
  8. ^ Paris A, Tonner PH (2005). "Dexmedetomidine in anaesthesia". Current Opinion in Anaesthesiology 18 (4): 412–8. PMID 16534267. doi:10.1097/ 
  9. ^ Ahmed, S. S.; Unland, T; Slaven, J. E.; Nitu, M. E.; Rigby, M. R. (2014). "Successful use of intravenous dexmedetomidine for magnetic resonance imaging sedation in autistic children". Southern Medical Journal 107 (9): 559–64. PMID 25188619. doi:10.14423/SMJ.0000000000000160.  edit
  10. ^ Menon DV, Wang Z, Fadel PJ, Arbique D, Leonard D, Li JL, Victor RG, Vongpatanasin W (2007). "Central sympatholysis as a novel countermeasure for cocaine-induced sympathetic activation and vasoconstriction in humans". J Am Coll Cardiol 50 (7): 626–33. PMID 17692748. doi:10.1016/j.jacc.2007.03.060. 
  11. ^ John R. Richards , Timothy E. Albertson , Robert W. Derlet , Richard A. Lange , Kent R. Olson , B. Zane Horowitz (February 2015). "Treatment of toxicity from amphetamines, related derivatives, and analogues: A systematic clinical review.". Drug & Alcohol Dependence. doi:10.1016/j.drugalcdep.2015.01.040. 
  12. ^ Jackson KC, Wang Z, Wohlt P, Fine PG (2006). "Dexmedetomidine a novel analgesic with palliative medicine potential". J Pain and Palliative Care Pharmacotherapy 20 (2): 23–7. PMID 16702133. doi:10.1080/J354v20n02_05. 
  13. ^ "Dosing Guidelines for Precedex" (PDF). Retrieved 2010-11-21. 
  14. ^ Dasta JF, Kane-Gill SL, Pencina M et al. (2010). "A cost-minimization analysis of dexmedetomidine compared with midazolam for long-term sedation in the intensive care unit". Crit Care Med 38 (2): 497–503. PMID 19789442. doi:10.1097/CCM.0b013e3181bc81c9. 
  15. ^ Wunsch H (2011). "Weighing the Costs and Benefits of a Sedative". JAMA 307 (11): 1195–1197. doi:10.1001/jama.2012.319. 

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