Binds primarily to inhibitory G-protein-coupled μ-opioid receptors → inhibits adenylyl cyclase → ↓ cAMP → opens K+ channels and inhibits presynaptic voltage-gated Ca2+ channels → hyperpolarisation and ↓ neurotransmitter release

Binds primarily to inhibitory G-Protein Coupled μ-opioid receptors→ ↑adenylyl cyclase→ ↓cAMP→ hyperpolarization of cell→↓neurotransmitter release

NMDA receptor antagonism
- Inhibits excitatory signaling within CNS
- Also inhibits noradrenaline reuptake in sympathetic nerve terminals

inhibitory action,
modulating the pain response to produce analgesia.

less likely to ppt histamine release
norad& serotonin axn, excitatory centrally

CNS: Causes dissociative anaesthesia
- Hallucinations
- Emergence delirium

CVS: Indirect sympathomimetic
chronotropy, inotrophy and Hypertension
Direct cardiodepressant
 if depletion of NA  hypotension
Resp - Bronchodilation

IV/IM/TD. BA PO 30%SL50%skin>90%
onset IM.: 7-8 mins; IV imm; TD 6 hrs
duration IM:1-2 hrs; IV:0.5-1hr; TD 12hrs

A: 20% oral bioavailability

relative lipid sol 500

Rapid redistribution
pKa 8.4(10% union)

prot bind 80-85%

25%

Mod Vd 4-6L/kg

3l/kg

Slow Hepatic, primarily via CYP3A4clearance

Hepatic metabolism with active
norketamine metabolite

excretion Urine 75%

Renal elimination

half life I.V.: 2-4 hours, prolonged context sensitive half time

T1/2a 15 mins, T1/2b
2~3 hours, CSHT 40mins at 5 hours

Respiratory depression including postoperative recurrence. Bradycardia. Chest-wall rigidity. Nausea and vomiting. Dependence. Decreased gastrointestinal motility.

Similar to other opioids. Differences due to lipid sol.
Does not cause delayed respiratory depression because it rapidly diffuses into and out of the CSF. Raised CSHT prolonged infusion may lead to increased duration of action and SE

Similar. Differences due to lipid sol.
Does not cause delayed respiratory depression because it rapidly diffuses into and out of the CSF. Raised CSHT prolonged infusion may lead to increased duration of action and SE

Increased salivation - Upper airway reflexes intact  laryngospasm - Hypotension if given in shock states - Emergence delirium

Opiate Analgesic

Sedative/hypnotic with non-opioid analgesic properties.

Non-Opiate Analgesic

Sedative / Hypnotic

1. to provide the analgesic component in general anaesthesia
2. in combination with a major tranquillizer to produce neuroleptanalgesia
3. to provide analgesia during labour when regional anaesthesia is not in
use
4. as an agent used for patient-controlled analgesia
5. in premedication and
6. for palliative care

Induction of anaesthesia
- Procedural sedation
- Analgesia
- ?Role in management of depression. - Recreational

Tertiary amine which is a synthetic phenylpiperidine derivative

Phencyclidine (remember the street drug name PCP) derivative that
produces dissociative anesthesia

Level 1

Level 1

μ receptor agonist

colourless solution 50mcg/ml, TDpatch (25mcg-100mcg/hr) and as lozenges

10, 50 or 100mg/ml

Bolus: 1-2 mcg/kg
inf: 1-2 mcg/kg/hr

(relative potency 50-100)

- 1mg/kg induction dose
- 10~20mg analgesia

- Incompatible with thiopental

- Dialysis - unknown