• Phenol alcohol
• General anaesthetic

• Aqueous 1% emulsion containing soya oil and egg lecithin
• Supports the growth of bacteria
• Nutritionally rich: 1kcal/ml

• Half-life 2-3minutes
• Metabolised by the liver; inactive metabolites.
• Extensive distribution into fat and protein (98% protein bound)
• Half life of redistribution = 2 to 8 minutes
• Terminal elimination = 3 to 20 hours

• GABA agonist

• Thought to be a GABA agonist;
• Increases inhibitory neurotransmission

• Sedation (rapid onset)
• Anaesthesia
• Rapid induction of anaesthesia (eg. for intubation)
• Decrease of cerebral metabolic demand

• Short half life
• Decreases cerebral metabolic demand, thus decreasing ICP
• Decreases seziure activity

• Hypotension may exacerbate secondary brain injury

• Loss of airway reflexes
• Hypotension
• Hyperlipidemia
• Propofol infusion syndrome

• Benzodiazepine

• Half-life 90 minutes;
• Metabolised by the liver;
• Active metabolites are renally excreted
• Extensive distribution into fat and protein (97% protein bound)

• GABA agonist

• Allosteric modulator of GABA neurotransmission; increases the rate of opening of GABA channels

• Sedation (slower onset)
• Anaesthesia
• Anxiolytic
• Decrease of cerebral metabolic demand

• Decreases cerebral metabolic demand, thus decreasing ICP
• Decreases seziure activity

• Slow waking; context-sensitive half-life becomes prolonged
• Sudden withdrawal may precipitate seizures
• Prolonged effect in renal or hepatic impairment

• Loss of airway reflexes
• Prolonged sedation may be undesirable
• Slow onset of maximal effect (up to 30min) results in unnecessarily large doses being given by impatient staff
• Tolerance and dependence develops
• Benzodiazepines in general (not just midazolam) are associated with an increased risk of delirium, particularly among the elderly

• Sedative dissociative

• IV administration
• Initial rapid redistribution (6 minutes)
• Prolonged elimination phase half life =  2 hrs.
• 94% protein bound.
• Volume of distribution 1.5 L/kg
• Hepatic metabolism into inactive metabolites
   

• Centrally acting alpha-2 receptor agonist

• Acts on presynaptic alpha-2 receptors to decrease the release of synaptic noradrenaline in the central nervous system, thereby decreasing sympathetic outflow.

• Sedation (slower in onset compared to propofol)
• Analgesia: synergy with opiates
• Management of agitation in both intubated and non-intubated patients

• Less delirium than with benzodiazepines

• No effect on cerebral metabolic demand

• Reduces opiate requirements
• Effective co-analgesic
• Effective for procedural analgesia and sedation
• Additional benefit of sedation without respiratory depression

• Bradycardia
• Hypotension

• Dissociative anaesthetic

• Multiple possible routes of administration
• Half life 0.5-2hrs
• 50% protein bound
• Volume of distribution 1.8 L/kg
• Hepatic metabolism into weakly active metabolites, which are cleared renally

• NMDA receptor antagonist

• Competitive antagonism of glutamate neurotransmission at the NMDA receptor

• Sedation for procedures
• Co-analgesia with opiates
• Induction of anaesthesia of patients whose haemodynamic stability is only assured by their sympathetic excitation

• Can be used in trauma patients who are haemodynamically stable

• Will probably increase ntracraial pressure

• Reduces opiate requirements
• Effective co-analgesic
• Effective for procedural analgesia and sedation

• Confusion
• Delirium
• Bronchorrhoea
• Sialorrhoea
• Sympathetic stimulation

• Opiate

• Multiple possible routes of administration
• Half-life 4-9 hours, however has a rapid initial redistribution.
• Hepatic metabolicm into active metabolites, which are cleared renally

• opiate mu- receptor agonist

• Activates opioid receptors, which activate numerous intracellular signalling pathways including decreasing the intracellular cAMP levels and closing voltage-sentitive calcium channels, overall leading to decreased neuronal excitability

• Strong analgesic
• Decreases sympathetic responses to pain
• Decreases sedation requiremens
• Improves tolerance of uncomfortable features of ICU stay (eg. ETT, central lines)

• Confusion
• Delirium
• Hypotension
• Euphoria/Dysphoria
• Respiratory depression
• Constipation

• Barbiturate

• Half life ~ 9 hours; rapid redistribution decreases the duration of effect.
• Extensive distribution into fat

• GABA receptors

• Allosteric modulator of GABA neurotransmission; increases the duration of opening of GABA channels

• Rapid sequence induction
• Decrease of cerebral metabolic demand

• Decreases cerebral metabolic demand, thus decreasing ICP
• Decreases seziure activity (very potent antiepileptic)
• Well tolerated in hemodynamic instability

• Very slow waking; as drug redistributes from tissue compartment

• May precipitate acute porphyria
• May have a immunosuppressant effect by enhancing porphyrin synthesis.

Features

Tramadol

Celecoxib

Ketamine

Class/mechanism

Partial opioid receptor agonist;
Serotonin receptor agonist

NSAID (selctive for COX-2)

Anaesthetic;
NMDA receptor antagonist

Advantages

Synergistic with other analgesics

Less respiratory depression than with other opiates

Low toxicity
Synergy with opioids

Dissociative sedation
Opioid-sparing effect

Disadvantages

Weak opioid effect
Lowers seziure threshold
Slow onset
Interacts with SSRIs

May cause renal impairment
May cause platelet dysfunction
Slow onset
Weak analgesic

Confusion, delirium
Emergeance phenomena
Requires speialist staff to be present