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November 25, 2025
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Brand Name :
Precedex, Igalmi
Synonyms :
dexmedetomidine
Class :
Sedatives
Brand Name :
Precedex, Igalmi
Synonyms :
dexmedetomidine
Class :
Sedatives
Dosage Forms & StrengthsÂ
injectable solutionÂ
Glass vial with a single dosage of 200mcg/2mL (100mcg/mL). Â
Further dilution is required before administrationÂ
Sublingual filmÂ
180mgÂ
120mgÂ
injectable solution ready-to-useÂ
0.9% NaCl 1000mcg/250mL (4mcg/mL)Â
0.9% NaCl 400mcg/100mL (4mcg/mL)Â
0.9% NaCl 200mcg/50mL (4mcg/mL)Â
0.9% NaCl 80mcg/20mL (4mcg/mL)Â
Loading dose: 1 mcg/kg Intravenous over 10 mins
Maintenance dose: 0.6 mcg/kg/hr Intravenous titrate to effect (generally 0.2 to 1 mcg/kg/hr)
fiberoptic intubation while Awake
Loading dose: 1 mcg/kg Intravenous over 10 mins
Maintenance dose: 0.7 mcg/kg/hr Intravenous till endotracheal tube is secured
Mild/moderate
120 mcg Sublingual or buccal initially
If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 240 mcg/day
Severe
180 mcg Sublingual or buccal initially
If the agitation continues, administer 90 mcg in two doses at least 2 hours apart; do not exceed more than 360 mcg/day
Dose Adjustments
Dosage Modifications
Intravenous:
Consider lowering the dosage in individuals with hepatic impairment and those over 65 yrs of age; clearance declines with increasing severity of the hepatic impairment
Renal impairment: Dose adjustment is not required
Sublingual or buccal:
Renal impairment
dose adjustment is not necessary
Hepatic impairment
Mild/moderate (Child-Pugh score A or B)
Mild/moderate agitation: 90 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 210 mcg/day
Severe agitation: 120 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 240 mcg/day
Severe (Child-Pugh score C)
Mild/moderate agitation: 60 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 180 mcg/day
Severe agitation: 90 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 210 mcg/day
Dosage Forms & StrengthsÂ
injectable solutionÂ
Glass vial with a single dosage of 200mcg/2mL (100mcg/mL). Â
Further dilution is required before administrationÂ
Sublingual filmÂ
180mgÂ
120mgÂ
injectable solution ready-to-useÂ
0.9% NaCl 1000mcg/250mL (4mcg/mL)Â
0.9% NaCl 400mcg/100mL (4mcg/mL)Â
0.9% NaCl 200mcg/50mL (4mcg/mL)Â
0.9% NaCl 80mcg/20mL (4mcg/mL)Â
Less than 1 month: Safety & efficacy were not established
Sedation is initiated during non-invasive procedures
1 month to less than 2 yrs: 1.5 mcg/kg intravenous loading infusion; infuse for 10 minutes
2 yrs to less than 18 yrs: 2 mcg/kg intravenous loading infusion; infuse for 10 minutes
if clinically indicated, Consider lowering dose
Sedation should be maintained throughout non-invasive procedures
1 month to less than 18 yrs: 1.5 mcg/kg/hr intravenous initially; titrate inorder to achieve a desired clinical effect within a dose range of about 0.5 to 1.5 mcg/kg/hr
Dosage Forms & StrengthsÂ
injectable solutionÂ
Glass vial with a single dosage of 200mcg/2mL (100mcg/mL). Â
Further dilution is required before administrationÂ
Sublingual filmÂ
180mgÂ
120mgÂ
injectable solution ready-to-useÂ
0.9% NaCl 1000mcg/250mL (4mcg/mL)Â
0.9% NaCl 400mcg/100mL (4mcg/mL)Â
0.9% NaCl 200mcg/50mL (4mcg/mL)Â
0.9% NaCl 80mcg/20mL (4mcg/mL)Â
Loading dose: 1 mcg/kg Intravenous over 10 mins
Maintenance dose: 0.6 mcg/kg/hr Intravenous titrate to effect (generally 0.2 to 1 mcg/kg/hr)
fiberoptic intubation while Awake
Loading dose: 1 mcg/kg Intravenous over 10 mins
Maintenance dose: 0.7 mcg/kg/hr Intravenous till endotracheal tube is secured
Mild/moderate
120 mcg Sublingual or buccal initially
If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 240 mcg/day
Dose Adjustments
Dosage Modifications
Intravenous:
Consider lowering the dosage in individuals with hepatic impairment and those over 65 yrs of age; clearance declines with increasing severity of the hepatic impairment
Renal impairment: Dose adjustment is not required
Sublingual or buccal:
Renal impairment
dose adjustment is not necessary
Hepatic impairment
Mild/moderate (Child-Pugh score A or B)
Mild/moderate agitation: 90 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 210 mcg/day
Severe agitation: 120 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 240 mcg/day
Severe (Child-Pugh score C)
Mild/moderate agitation: 60 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 180 mcg/day
Severe agitation: 90 mcg Sublingual initially; If the agitation continues, administer 60 mcg in two doses at least 2 hours apart; do not exceed more than 210 mcg/day
may enhance the CNS depressant effect
may enhance the CNS depressant effect
may enhance the CNS depressant effect
may enhance the CNS depressant effect
may enhance the CNS depressant effect
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased CNS depressant effect when combined with dexmedetomidine
may have an increased AV-blocking effect when combined with beta-blockers
dexmedetomidine: they may increase the CNS depressant effect of CNS stimulants
dexmedetomidine: they may increase the CNS depressant effect of CNS stimulants
dexmedetomidine: they may increase the CNS depressant effect of CNS stimulants
beta
beta
may enhance the CNS depressant effect
may increase the CNS depressant effect
may increase the CNS depressant effect
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
acrivastine and pseudoephedrineÂ
may increase the CNS depressant effect of CNS depressants
may increase the AV-blocking effect of beta blockers
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
promethazine/dextromethorphanÂ
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
may increase the CNS depressant effect of CNS Depressants
buprenorphine,long-acting injectionÂ
may increase the CNS depressant effect of CNS Depressants
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
It may decrease the diagnostic effect when combined with Alpha-/Beta-Agonists
may increase the CNS depressant effect of CNS Depressants
acetaminophen/doxylamine/dextromethorphanÂ
may increase the CNS depressant effect CNS Depressants
may decrease the antihypertensive effect when combined with alpha2-agonists
may increase the vasoconstricting effect of Ergot Derivatives
mirtazapine: it may decrease the antihypertensive effect of Alpha2-Agonists
bromocriptine: they may increase the hypertensive effect of Alpha2-Agonists
esketamine: they may increase the hypertensive effect of Alpha2-Agonists
may increase the adverse effect of Monoamine Oxidase Inhibitors
It may increase the hypertensive effect when combined with Alpha-/Beta-Agonists
mianserin: it may decrease the therapeutic effect of Alpha2-Agonists
may enhance the AV-blocking effect of beta-blockers
may enhance the AV-blocking effect of beta-blockers
may enhance the AV-blocking effect of beta-blockers
may enhance the AV-blocking effect of beta-blockers
may enhance the AV-blocking effect of beta-blockers
may increase the effect of beta-blockers
may increase the effect of beta-blockers
may increase the effect of beta-blockers
may increase the effect of beta-blockers
may increase the effect of beta-blockers
may increase the effect of beta-blockers
may increase the AV-blocking effect
may increase the AV-blocking effect
may increase the AV-blocking effect
may increase the AV-blocking effect
may increase the AV-blocking effect
It may enhance the risk of nephrotoxicity when combined with phenylbutazone
When encainide is used together with dexmedetomidine, this leads to a reduction in the encainide’s metabolism
When ponesimod is used together with dexmedetomidine, this leads to enhanced risk or seriousness of bradycardia
may enhance the risk or severity of hypertension when combined
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
It may increase the hypertensive effect when combined with Alpha-/Beta-Agonists
It may decrease the vasoconstricting effect when combined with Alpha-/Beta-Agonists
It may increase the hypertensive effect when combined with Alpha-/Beta-Agonists
It may decrease the therapeutic effect when combined with Alpha-/Beta-Agonists
may increase the effects of pharmacodynamic synergism
monoamine oxidase inhibitor: they may increase the hypertensive effect of Alpha2-Agonists
monoamine oxidase inhibitor: they may increase the hypertensive effect of Alpha2-Agonists
monoamine oxidase inhibitor: they may increase the hypertensive effect of Alpha2-Agonists
monoamine oxidase inhibitor: they may increase the hypertensive effect of Alpha2-Agonists
monoamine oxidase inhibitor: they may increase the hypertensive effect of Alpha2-Agonists
doxofylline: they may increase the hypertensive effect of Alpha2-Agonists
tedizolid: they may increase the hypertensive effect of Alpha2-Agonists
decongestant: they may increase the hypertensive effect of Alpha 2-Agonists
acetaminophen/dextromethorphan/pseudoephedrine/guaifenesin
decongestant: they may increase the hypertensive effect of Alpha 2-Agonists
brompheniramine, dextromethorphan and phenylephrine
decongestant: they may increase the hypertensive effect of Alpha 2-Agonists
decongestant: they may increase the hypertensive effect of Alpha 2-Agonists
sympathomimetics: they may increase the hypertensive effect of Alpha 2-Agonists
sympathomimetics: they may increase the hypertensive effect of Alpha 2-Agonists
sympathomimetics: they may increase the hypertensive effect of Alpha 2-Agonists
sympathomimetics: they may increase the hypertensive effect of Alpha 2-Agonists
sympathomimetics: they may increase the hypertensive effect of Alpha 2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
may decrease the therapeutic effect when combined with Alpha2-Agonists
When dexmedetomidine is aided by hesperetin, it reduces hesperetin’s metabolism
it increases the effect of CNS depressants
Actions and spectrum:Â
dexmedetomidine is a selective alpha-2 adrenergic agonist with a wide range of actions and a spectrum of effects. Its primary action is to stimulate alpha-2 receptors in brain and spinal cord, leading to sedation and analgesia. It also has sympatholytic properties, reducing sympathetic outflow and resulting in decreased blood pressure and heart rate.
dexmedetomidine has anxiolytic effects and can induce a state of calm and relaxation in patients. Additionally, it has been shown to have neuroprotective and anti-inflammatory properties. Its spectrum of effects includes sedation, analgesia, anxiolysis, sympatholysis, and neuroprotection.Â
Frequency definedÂ
1-10%Â
Pyrexia (4-5%)Â
Dry mouth (3-4%)Â
Hypoxia (2-4%)Â
Atelectasis (3%)Â
Postprocedural hemorrhage (2-3%)Â
Agitation (2%)Â
Pain (2%)Â
Chills or rigors (2%)Â
Oliguria (2%)
Acidosis (1-2%)Â
Pulmonary edema (1%)Â
decreased Urine output (1%)Â
Bradycardia (5-7%)Â
Atrial fibrillation (4%)Â
Vomiting (3-4%)Â
Hypovolemia (3%)Â
Tachycardia (2-3%)Â
Anemia (2-3%)Â
Hyperthermia (2%)Â
Hyperglycemia (2%)Â
Thirst (2%)Â
Pleural effusion (1-2%)Â
Hypocalcemia (1%)Â
Sinus tachycardia (1%)Â Â
>10%Â
Hypertension (12-16%)Â
Hypotension (25-28%)Â
Nausea (9-11%)Â Â
<1%Â
WheezingÂ
Ventricular tachycardiaÂ
Peripheral edema Â
Post marketing ReportsÂ
Cardiac disorders: atrial fibrillation, bradycardia, cardiac disorder, myocardial infarction, tachycardia, ventricular tachycardia, Arrhythmia, atrioventricular block, cardiac arrest, extrasystoles, supraventricular tachycardia, ventricular arrhythmiaÂ
Gastrointestinal disorders: diarrhea, vomiting, Abdominal pain, nauseaÂ
Investigations: increased blood alkaline phosphatase, EKG T wave inversion, QT prolonged, increased AST/ALT, increased blood urea, increased GGTÂ
Nutrition and Metabolism disorders: hyperkalemia, hypovolemia, Acidosis, hypoglycemia, hypernatremiaÂ
Psychiatric disorders: confusional state, hallucination, Agitation, delirium, illusionÂ
Respiratory, mediastinal, and thoracic disorders: bronchospasm, hypercapnia, hypoxia, respiratory acidosis, Apnea, dyspnea, hypoventilation, pulmonary congestionÂ
Medical and Surgical procedures: Light anesthesiaÂ
Lymphatic system and Blood disorders: AnemiaÂ
Eye disorders: visual impairment, PhotopsiaÂ
General:Â hyperpyrexia, pyrexia, Chills, pain, thirstÂ
Nervous system disorders: dizziness, neuralgia, speech disorder, Convulsion, headache, neuritisÂ
Urinary or Renal disorders: polyuria, OliguriaÂ
Subcutaneous tissue and skin disorders: pruritus, urticaria, Hyperhidrosis, rashÂ
Vascular disorders: hemorrhage, hypotension, Blood pressure fluctuation, hypertensionÂ
Black Box Warning:Â
dexmedetomidine does not have a black box warningÂ
Contraindication/Caution:Â
Contraindication:Â
Caution:Â
Comorbidities:Â
Pregnancy consideration: US FDA pregnancy category: CÂ
Lactation: Excreted into human milk: Unknown Â
Pregnancy category:Â
Pharmacology:Â
dexmedetomidine is the highly selective alpha-2 adrenergic agonist with sedative, analgesic, and anxiolytic properties. It acts primarily on the alpha-2 receptors in the brain, resulting in the inhibition of norepinephrine release and subsequent modulation of the central nervous system activity. The pharmacological effects of dexmedetomidine include sedation, anxiolysis, sympatholysis, and analgesia.Â
dexmedetomidine also has dose-dependent effects on different receptors. At lower doses, it primarily activates alpha-2 receptors, leading to sedation and anxiolysis. At higher doses, it may also activate alpha-1 adrenergic receptors, resulting in vasoconstriction and increased blood pressure. Â
Pharmacodynamics:Â
Pharmacokinetics:Â
AbsorptionÂ
dexmedetomidine can be administered intravenously (IV) or intranasally. When given intravenously, it rapidly and completely enters the systemic circulation, allowing for quick onset of action. Intranasal administration provides a less invasive alternative but may have slower absorption.Â
DistributionÂ
dexmedetomidine has a moderate volume of distribution, indicating extensive distribution throughout the body. It readily crosses the blood-brain barrier and reaches therapeutic concentrations in the central nervous system, contributing to its sedative effects.Â
MetabolismÂ
dexmedetomidine undergoes hepatic metabolism primarily through the cytochrome P450 2A6 (CYP2A6) enzyme pathway. The major metabolite formed is 3-hydroxy-dexmedetomidine, which is pharmacologically inactive. The metabolism of Dexmedetomidine is relatively slow compared to its elimination, resulting in a longer duration of action.Â
Elimination and excretionÂ
dexmedetomidine is primarily eliminated through renal excretion. Approximately 95% of the administered dose is excreted in the urine, with only a small fraction being excreted unchanged. The elimination half-life of dexmedetomidine is around 2 to 3 hours in adults.Â
Administration:Â
dexmedetomidine is primarily administered intravenously (IV) or intranasally. The exact administration method, dose, and duration of treatment will depend on the specific indication and the patient’s individual characteristics.Â
For intravenous administration, dexmedetomidine is typically given as a continuous infusion. It is diluted in an appropriate IV solution and administered using an infusion pump. The infusion rate is carefully adjusted to achieve the desired sedation level, which can range from light to deep sedation.Â
Intranasal administration of dexmedetomidine involves the use of a nasal spray or drops. The drug is administered into one or both nostrils using a suitable device or applicator. The dosage and frequency of intranasal administration may vary depending on the specific formulation and indication.Â
Patient information leafletÂ
Generic Name: dexmedetomidineÂ
Pronounced: (dex-meh-deh-TOE-mi-deen)Â Â
Why do we use dexmedetomidine?Â
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