Induction of anaethesia Flashcards
Describe the pharmacokinetics of propofol: absorption, solubility, distribution, metabolism, elimination
Absorption: Given IV as not effective if given orally (extensively metabolised in gut + liver)
Solubility: lipophilic
Distribution: 98% protein bound (distributes rapidly to brain => fast induction
Metabolism: metabolised by glucuronidation in liver
Elimination: renal
Describe the mechanism of action of propofol and alfaxalone
GABA beta subunit:
- enhances GABA-A receptor activity
- opens Cl- channel => Cl- influx => hyperpolarisation
=> sedation, hypnosis and anaesthesia
Describe the induction of anaesthesia via propofol
Rapid onset of action
rapid uptake by CNS
5-8 mins unconsciousness (induction, not maintenance) - good for ‘top ups’ or TIVA
What is the route of administration of propofol?
slow IV - cats and dogs
What chemical is propofol?
Milky alkyl phenol
Describe the pharmacodynamics of propofol: CNS, Respiratory and Cardiovascular effects
CNS Effects:
Anaesthesia only (no analgesia)
↓ CMRO₂ (brain O₂ consumption)
Respiratory Effects:
Respiratory depression
Cardiovascular Effects:
Depressed cardiovascular reflexes
Sympathetic depression causes:
- Stable cardiac output
- ↓ Heart rate (blunted baroreceptor reflex)
- ↓ MAP, SVR, CVP
Describe the pharmacokinetics of alfaxalone: absorption, solubility, distribution, metabolism, elimination
Absorption - good systemic absorption when given IV or IM
Solubility - soluble in water => improves IM absorption and stability
Distribution - 30-50% protein bound
Metabolism - hepatic (Rapid), lungs and kidneys
Elimination - renal, and small % bile
Describe the pharmacodynamics of alfaxalone
Anaesthesia (no analgesia)
respiratory and cardiovascular depression (less than propofol)
decreased CMRO2 (brain O2 consumption)
Haemodynamic effects minimal
- Stable cardiac output
- Stable heart rate
- Stable MAP, SVR, CVP
Describe the recovery from alfaxalone
Rapid and smooth if premedicated
Should not be disturbed during recovery as excitement can occur
What type of drug is alfaxalone?
Clear, colourless neuroactive steroid
What is the route of administration of alfaxalone?
slow IV (or IM, not licensed) - good for ‘top ups’ or TIVA
For dogs, cats, rabbits
Describe the use of alfaxolone and propofol in unhealthy animals
Dose is reduced in unhealthy animals (ASA II-V)
Describe how alfaxolone/propofol is used
Inject either drug slowly to effect over 60 seconds
Animal will become sedated and then unconscious
In most cases the next step will be securing the airway
Always feel for a pulse following induction
Oxygen can be delivered before and during induction for compromised animals
In the event of apnoea, intubate and ventilate the animal
Occasional rigidity and twitching is observed post and during induction
What is ketamine licensed for?
cats
dogs
ruminants
rodents
rabbits
primates
horses
Describe the use of ketamine on its own
Dissociative anaesthesia - increased muscle tone, salivation and animals that did not really appear to be unconscious
Good analgesia
Combined with other drugs
What is the route of administration of ketamine?
IV or IM (can sting)
Describe the pharmacodynamics of ketamine
Dissociative anaesthesia
increased CMRO2
Haemodynamic effects minimal:
-Stable cardiac output
- Increased heart rate
- Increased MAP, SVR, CVP
Describe the pharmacokinetics of ketamine
Absorption, solubility, distribution, metabolism, excretion
Absorption - good bioavailability => well absorbed via multiple routes
Solubility - soluble in water
Distribution - 12% protein bound => large proportion remains free and active => rapid CNS penetration
Metabolism - liver converts to norketamine (still active, less potent)
Elimination - renal, and small % bile
Describe the mechanism of action of ketamine
Primary Mechanism:
- Non-competitive NMDA receptor antagonist.
- Blocks NMDA receptor Ca²⁺ channel pores.
- Reduces presynaptic glutamate release.
Other Mechanisms:
Opioid receptor interaction:
- Weak affinity for mu and kappa receptors.
- Naloxone (opioid antagonist) does not antagonize ketamine’s analgesic effects
Antagonistic interactions:
- Monoaminergic, muscarinic, and nicotinic receptors.
- Produces anticholinergic effects (e.g., tachycardia, bronchodilation).
Local anaesthetic properties:
- Inhibits neuronal sodium channels at high doses.
What is drawback of ketamine?
Rocky recovery
What is a volatile agent?
Inhalation agents e.g., isoflurane, sevoflurane
What is the use of volatile agents?
Maintenance (can be used for induction)
What is the drawback of using volatile agents as an induction agent?
stress
What is the mechanism of action of volatile agents
potentiation of GABA receptors
Inhibition at NMDA receptors