Central alpha2 agonist
Greater selectivity for A2 than clonidine

D-stereoisomer

Lipid soluble (rapid distribution)

95%

2l/kg (steady state)

Hepatic via CYP and glucuronidation
inactive metabolites

Large variation in CSHT with infusion length (T1/2 5 minutes after 10 minutes IV, T1/2 240 minutes after 8 hour IV)

Central Antihypertensive

-

1. Sedation
2. Analgesia
3. Delirium prevention and management
4. Withdrawal syndromes
5. Perioperative sympatholytic

Clear, colourless solution
IV only in Aus (PO overseas)
Comparitively expensive

Specific alpha-2 agonist acting primarily in the locus coeruleus to increase conductance through K+ channels. 8 times more selective than clonidine. Acts on all 3 subtypes of alpha-2R (A, B, C)

CNS
- Decreased sympathetic activity
- Decreased agitation
- Induces state resembling non-REM sleep without impairment of cognitive function. Easily roused but sedated.
- Analgesia produced in the posterior horns of the spinal cord, reduces need for opioid analgesia
- Decreases circulating cerebral catecholamines
- Decreases CBF/CMRO2/Mild decrease in ICP
- Decreases shivering

CVS: Decreased MAP and HR

Resp: Clinically insignificant increase in PaCO2 and decrease in RR

- Transient hypertension (due to peripheral smooth muscle α2B agonism) -> reflex bradycardia
Later, hypotension and bradycardia.
Rebound HTN on ceasing dose
- Dry mouth
- nausea

Without loading dose (commonly not used because of bradycardia), 30 minutes to reach effective concentration

Inactive metabolites
Excreted in urine

IV Infusion
Dose: 0.3-1mcg/kg/min

Sedative / Hypnotic

Level 1

Short term sedation
Adjunct sedative when ventilator weaning in delirious and agitated patients

Clear, colourless solution
IV only in Aus (PO overseas)
Comparitively expensive, D-stereoisomer

Selective central α2 agonism
Inhibition of noradrenaline release in locus ceruleus
Peripherally at higher doses

CNS: sedation: REM sleep-like state,min respiratory depression
Analgesia without as much confusion or disorientation as benzos. Pts easily aroused.
Spinal cord analgesia Decreases cerebral VO2, blood flow and ICP No antiemesis
CVS: Higher doses cause peripheral α2 effects – vasoconstriction,
followed by hypotension and bradycardia (Decreased sympathetic output)
Resp: Minimal Resp depression

Transient hypertension (due to peripheral smooth muscle α2B agonism) -> reflex bradycardia
Later, hypotension and bradycardia.
Rebound HTN on ceasing dose
Dry mouth, nausea

A: Without loading dose (commonly not used because of bradycardia), 30 minutes to reach effective concentration

Excreted in urine

0.3-1mcg/kg/hr