2: Anaesthetic Drugs Flashcards
what are the different types of anaesthetic techniques
general - inhalation and intravenous
local - regional
give some practical uses of anaesthesia
premedication
induction
- IV maintenance
- IV and/or inhalation
give 4 examples of intravenous anesthetics
propofol (rapid)
barbituates (rapid)
etomidate
ketamine (slower)
what is conscious sedation
is the use of small amounts of anaesthetic or benzodiazepines to produce a sleep like state
describe the process of administering anaesthesia in 7 steps
- premedication
- induction - Iv/inhalation
- intraoperative analgesia
- muscle paralysis
- maintenance
- reversal of muscle paralysis
- provision for PONV
what are the stages of Guedel’s signs for anaesthesia
stage 1 : analgesia and consciousness
stage 2 : unconscious, breathing erratic, excitement phase
stage 3 : surgical anaesthesia, increasing depth until breathing weak
stage 4 : respiratory paralysis and death
what is anaesthesia a combination of (4 - DAHM!)
- Depression of spinal reflexes
- Analgesia
- Hypnosis
- Muscle paralysis
how do you determine the volatile anaesthetic potency
minimum alveolar concentration
what is the anatomical substrate for MAC
spinal cord
What is MAC (minimum alveolar concentration)
[alveolar] at 1 atm at which 50% of subjects fail to move to surgical stimulus (unpremediated breathing air)
at equilibrium [alveolar] = [spinal cord]
explain how partition coefficients (solubility) affect the induction and recovery of general anaesthesia
- blood : gas partition (in the blood) - low value fast induction and recovery e.g. desflurane
- oil : gas partition (in fat) - determines potency and slow accumulation due to partition into fat e.g. halothane
- greater ability to travel in fat, the higher the potency but the anaesthetic can accumulate in fat so can take patient a long time to wake up
give 5 factors that would increase MAC
age (high in infants low in elderly)
hyperthermia
pregnancy
alcoholism
central stimulants
give 3 factors that would decrease MAC
age
other anaesthetics and sedatives
opioids
give 4 examples of inhalational anaesthetics
nitrous oxide
xenon
chloroform
cyclopropane
what is the role of GABA receptors in general anaesthesia
GABAa receptors are a critical target and act as a major inhibitory transmitter for CL- conductance via LGIC
- all anaesthetics (except for Xe, N20 and ketamine) potentiate GABAa mediated Cl- conductance to depress CNS activity
what is the relationship between anaesthetic potency, lipid solubility and GABAa activity
potency correlates with lipid solubility and GABAa activity
which 3 anaesthetics do not potentiate GABAa as their mode of action
Xe
N2O
ketamine
what are the 3 main effects from anaesthetics potentiating GABA
anxiolysis
sedation
anaesthesia
how do anaesthetics modulate the consciousness of the brain
modulate the balance between excitation (glutamate) and inhibition (GABA)
what are the effects of general anaesthesia on the brain circuity
- reticular formation (hindbrain, midbrain and thalamus) depressed and connectivity lost
- hippocampus depressed (memory)
- brainstem depressed (resp and CVS)
- spinal cord - depress dorsal horn (analgesia) and motor neuronal activity (MAC)
what can be used as a sole anaesthetic in TIVA (total intravenous anaesthesia)
propofol (rapid)
barbituates (rapid)
ketamine (slower)
what is involved in regional anaesthesia
involves selectively anaesthetising a part of the body
- blocks a nerve and hence the patient remains awake
- uses local anaesthetic or an opioid
- extradural/intrathecal/combined (labour)
give 4 examples of local anesthetics
- lidocaine
- bupivacaine
- ropivacaine
- procaine
what is the lipid solubility of local anasthetics
higher
- greater potency
what is the dissociation constant characteristic of local anaesthetics
lower pKa (more unionised) = faster onset
what is the chemical link and protein binding duration for local anaesthetics
- metabolism higher
- protein binding - higher for longer duration
give 4 examples of nerves blocked in regional anaesthesia in the upper extemitiy
- interscalene nerve
- supraclavicular nerve
- infraclavicular nerve
- axillary nerve
give 4 examples of nerves blocked in the regional anaesthesia in the lower extremity
femoral nerve
sciatic nerve
popliteal
saphenous
which local anaesthetic is used for wound analgesia
bupivacaine
what is the mechanism of action of wound analgesia
block small myelinated (afferent) nerves in preference hence nociceptive and symp block
- cocaine archetypal
- esters - short acting
- amides - longer acting
- adrenaline inc duration
what are the side effects of general anaesthesia (4)
PONV - post operative nausea + vomiting (opioids)
CVS - hypotension
POCD (post operative cognitive dysfunction )
chest infection
identify 5 examples of where local and regional anaesthesia are used
dentistry
obstetrics
regional surgery (patient awake)
post-op (wound pain)
chronic pain management
what are the side effects of local and regional anaesthesia
depends on the agent used and usually result from systemic spread
- locals are Na+ channel blockers so cardiovascular toxicity
what is intravenous anaesthetic potency
plasma concentration to achieve a specific end point (e.g. loss of eyelash reflex)
- for induction in mixed anaesthesia - bolus til end point then swtich to volatile
- TIVA uses a defined PK based algorithm to infuse at a rate to maintain set point but pre-ceded by a bolus
why are nitrous oxides often added to other volatile agents
reduced dosing
what is the meyer-overton hypothesis
anaesthetic potency correlates to its lipid solubility and GABAa activity
what are the molecular-cellular targets of general anaesthesia
GABAa and NMDA glutamate receptors
what are the target sites of main IV anaesthetics
- ketamine NMDA
- barbituates and propfol GABAa
compare the potecy, speed, metabolism and duration of local anaesthetics
- compared to procaine, bupivacaine is more potent with a longer duration of action
- procaine is ester metabolised and has a slower onset time but not much in it
what are the phases of general anaesthesia
- pre-assessment
- preparation
- induction
- maintenance
- emergence
- recovery
- follow-up
give an examples of a depolarising muscle relaxant
succinylcholine - used in rapid sequence inductions
- binds to NAChR resulting in persistent depolarisation of the motor end plate
give an example of a non-depolarising muscle relaxant
atracurium, rocuronium
- competitive antagonist of nAChR
compare when endotracheal vs laryngeal airways are used
- endotracheal usually for emergencies and pt w ‘full stomach’, major surgery, long duration surgery
- laryngeal mask/iGel used for elective, well fasted pt, short duration surgery
what are the components of maintenance of GA (4)
- IV (TIVA e.g. propofol), inhalational (volatiles)
- fluid management
- other essential drugs e.g. abx, insulin, etc
- drugs to prevent PONV, post op pain, etc
what are the different ways in which a patient is ‘woken up’ after GA (5)
- wears off: e.g. suxamethonium, mivacurium which is metabolised by enzymes in our body after one-off use
- withdraw: stops maintenance IV drugs and volatiles
- reverse: antagonising non-depolarising muscle relaxants e.g. neostigmine+glycopyrrolate
- antagonise: e.g. opiates, BZDs use antagonists e.g. flumazenil, naloxone
- stimulate: not used often but resp stimulants e.g. doxapram
what are the components of recovery of a pt following anaesthesia
■ Monitoring- (EWS chart, fluid balance, etc.)
■ Airway (ability to maintain airway without support)
■ Side effects of GA drugs
- Sedation
- PONV
- Shivering
■ Side effects of Regional anaesthesia
- Monitoring sensory and motor block levels
- Hypotension
■ Observing for Surgical complications
- Bleeding
- Vascular supply
■ Post operative pain management
■ “fit for ward” tests.
what are the advantages of using ketamine to induce anaesthesia
- good choice for haemodynamically unstable patients
- preserves BP and does not cause cardiosuppression
what alterations need to be made for a patient taking prednisolone before surgery
hydrocortisone supplementation
- needed to prevent Addisonian crisis as long term steroids cause the adrenals to be suppressed and not produce enough cortisol
when are neuromuscular blocking drugs used
as adjuncts to anaesthetic agents as they cause muscle paralysis which is a necessary prerequisite for mechanical ventilation
in what conditions are non-depolarising anaesthetic agents contraindicated and why
myasthenia gravis
- pt w this conditions have fewer nicotinic receptors due to autoimmune mediated destruction so they are more sensitive to non-depolarising blockade which is how these agents work
give a contraindication of succinylcholine
penetrating eye injuries or acute angle glaucoma as ↑ intraocular pressure
why is thiopental useful
lowers intracranial pressure so useful in head trauma
what might the use of the non depolarising neuromuscular blocker cause and how is this reversed
- generalised histamine release on administration may produce facial flushing, tachycardia and hypotension
- reversed by Neostigmine
*Neostigmine also reverses Vecuronium, Pancuronium
