Guided learning- Anaesthetics Flashcards
3 a’s of conciousness?
- alertness -> upper brainstem reticular formation
- awareness -> cerebral cortex
- attention -> limbic system frontoparietal association areas
definitions:
normal
fully orientated time place and person
define sedation
allows patients to tolerate unpleasant diagnostic or surgical procedures
relieves anxiety and discomfort
verbal contact can be maintained
define coma
state of extreme unresponsiveness
individual exhibits no voluntary movement or behaviour
define anaesthesia
no concious awareness
patient without feeling or sensation
enters a drug induced and predictably reversible coma
define : concious sedation
patient relaxed and calm
able to undergo minor surgical procedures w/out too much discomfort
can maintain verbal contact
3 levels of sedation and effects
- minimal sedation
- airway unaffected
- CV function unaffected
- normal responsiveness
- spontaenous ventilation unaffected
- reduced anxiety
- moderate sedation / concious sedation
- no airway intervention
- CV usually maintained
- responsive to verbal and tactile stimulation
- sponatenous ventilation is adequate
- Deep sedation (anaesthesia in UK)
- Airway intervention may be required
- CV function usually maintained
- responsive to purposeful repeated or pain stimulation
- spontaenous ventilation may be inadequate
3 scales of sedation?
- Ramsay (6 point)
- richmond sedation agitation scale (10 point)
- Riker sedation agitation scale (7 point)
Ramsay scale
aim?
levels
- aim for level 2 -> cooperative, oriented, calm
- 1 = agitated
- 2 = aim 3 = Response to verbal
- 4 and 5 = brisk / sluggish response to glabellar tap or loud auditory stimulus -> elicit blink reflex
- 6= unresponsive
- note unvalidated atm
Richmond scale
aim?
levels
- 10 point scale with -5 being unarousable and +4 being combatitive/ violent to staff.
- Aim for between 0 and -2:
- -2 = light sedation, briefly awaken with eye contact to voice under 10 s
- -1 = drowsy, not fully alert but sustained eye contact to voice more than 10 s
- 0 = alert and calm
Riker sedation agitation scale
aim?
levels
- 7 point scale
- Aim : level 4 -> calm, coopertive, easily arousable, follows commands
- 7 = dangerous agitation
- 1 = unarousable
What is the aim in anaesthesia?
- always aim for calm and relaxed
- allows procedure to be performed
- reduces agitation
- if too sedated prolongs recovery and longer procedure time
Normal pupil sizes in light and dark ?
Pupillary responses during anaesthesia?
What is always checked for in the anaesthetised patient?
- Light -> 2 -4 mm
- dark -> 4-8 mm
- Overdose -> FULL DILATION
- Deep surgical anaesthesia (stages 2 - 4 ) -> 6-8 mm DILATED
- brainstem function reduced
- diaphragmatic respiration
- eye and resp reflexes reduced
- Light surgical anaesthesia (stage 3) -> MIOSIS, CONSTRICTED
- PNS takes over
- reflexes dampened
- Analgesia (stage 1) -> 2-4 mm NORMAL
- conciusness not sig. affected
- Always check for pupillary light reflex and corneal blink reflex
What drugs are used for sedation
- SEDATION = BOrED
- Benzodiazepines
- Opiates
- Entonox
- Dexmedetomidine
Name the benzodiazepines used in sedation
What is the MOA
- Midazolam
- Lorazepam
- Diazepam
- Temazepam
MOA: Binds Y subunit of GABAa receptor, PAM
increase affinity for GABA and freq of channel opening
increase Cl- conductance into cell
HYPERPOLARISES cell reduce AP firing
Benzodiazepines:
USES
SE’s?
- Sedatives, muscle relaxants (hyperkinetic disorder)
- anxiolytic and panic disorder
- epilepsy
- chronic insomnia
SE’s:
- memory loss
- no analgesia
- decrease cog. function on recovery from sedation
- prolonged use can result in tolerance and dependency
- avoid in patients with heart/ resp/ liver problems or depressive / -ve sx.
Benzodiazepines:
reversal agent?
Flumazenil
(Shoo Benzo or ill give ya the FLU)
OPIATES:
name 3 short acting used in sedation
MOA?
- FENTANYL -> Short acting and strong
- AFENTANIL
- REMIFENTANIL
MOA:
Binds mu opiod R , GPCR (Gi/ Go)
Promotes opening Katp and Kir channels, inhibits opening VGCC and inhibit NT release via exocytosis block.
HYPERPOLARISATION via K+ efflux, and decreased NT release
Decrease neuronal transmission
OPIODS:
1) cardinal signs of OD
2) reversal agent?
3) Adv’s?
4) adjunct to what?
- Pinpoint pupils (miosis)
- Respiratory depression
- Coma
Reversal -> Naloxone (shorter acting antagonist) (Naltrexone longer acting)
Adv: good sedatives, analgesics, SM relaxants ,
adjunct to anaesthesia:
- counteracts increase in CV and RR during invasive treatment
- decrease dose of anaesthetic required as sedative effect
- fast acting used as adjunct to prevent resp depression and OD
SEDATIVES:
Name inhaled sedative
MOA
onset
adv’s
disadv’s
ENTONOX = Nitrous oxide 50: 50 mix O2 and N2O
Onset 2- 3 mins
MOA: unclear modulates range of R may induce opiod release
Adv’s: sweet smelling, non airway irritant, good analgesic
Disadv : potential teratogen, increase ear and lung pressures
SEDATIVES:
Name sedative used in ICU
Moa?
Dexmedetomidine
Used in ICU for procedures when patient needs to maintain verbal contact
MOA: selective alpha2 adrenoR AGONIST
Binds presynaptic adrenoR to inhibit NA release and terminate pain signals
postsynaptically inhibits SNS -> reduce BP and HR
3 main effects of anaesthetics?
Two main groups?
Unconciousness (Reticular formation and reticular activating system)
Loss of reflexes
Analgesia
Two main groups : 1) Local 2) General
Name 3 local anaesthetics
Two groups and metabolism T 1/2
MOA?
- LIDOCAINE (amide)
- BUPVICAINE (amide)
- LEVOBUPVICAINE (amide)
Two groups :
1) Amino Amides metabolism in LIVER, longer T 1/2 (3 Hrs)
2) Amino Esters metabolism in PLASMA, T 1/2 3 mins
MOA -> inhibit VG Na channel, dampends neuronal activity by inhibiting depolarisation, reduced sensory transmission to the cortex
Enter channel when open and by crossing PM and binding from the inside.
uses and duration of:
Lidocaine
Bupvicaine
Levobupvicaine
Lidocaine: Nerve block, dental and topical procedures
duration 1-2 hours
Bupvicaine: regional IV anaesthesia, peripheral nerve block, epidural and SNS nerve block
Duration 1- 3 hours
Levobupvicaine: same as Bupvicaine (regional IV anaesthesia, peripheral nerve block, epidural and SNS nerve block)
Duration 1-3 hours
+ Less cardiotoxic than bupvicaine (would not used bupvicaine in HF patient)
Local anaesthetics:
administration?
advantages?
side effects?
properties?
Limitations?
Admin : low dose and only affect small localised region
Adv: flexible, good recovery and few SE’s
SE’s: can get local irritation at site of admin, local ischaemia and traumatic admin can cause tissue damage
Properties: works best in small un or lightly myelinated neurons (Adelta or C fibres)
Limited by: Inflammatory soup, which is acidic. Leads to ionisation of basic and pH dependent LA drugs and inability to cross PM to bind to VG Na channel.
Considerations w Local anaesthetics?
systemic effects w OD?
Agent with low irritant effect and toxicity
Half life adequate for procedure (amide in liver therefore longer T1/2, esters in plasma therefore T1/2 only mins).
Rapid onset of action
systemic effects OD: CV and CNS changes (cardiotoxicity and decreased conciousness/ sedation), anaphylaxis with esters
Actions of General Anaesthetics?
reversible block nerve conduction
loss of sensation affecting whole body
loss of conciousness
Two groups of GA?
List the GA’s
- Inhalation and intravenous
PINKS
Propofol (IV because your veins are proper full)
Isoflurane
Nitrous oxide (entonox)
Ketamine (NMDA antagonist)
Sevoflurane
Name the inhaled GA’s?
Adv’s?
Compared by what value?
Smoking is a SIN
Sevoflurane
Isoflurance
Nitrous oxide (entonox)
Adv’s: All have low solubility therefore rapid induction and few lingering effects.
Compared by their MAC value: mean alveolar concentration = conc of vapour required in alveoli to prevent motor response in 50% of patients to PAIN stimulus
Potency, onset and recovery, uses of:
Entonox
Sevoflurane
Isoflurane
Entonox: Low potency, moderate recovery, onset 2-3 mins
Sevoflurane: onset and recovery moderate, exhaled and metabolised, day surgery, few SE’s
Isoflurane: Slow onset and recovery, half life from mins- hours, few adverse effects, widely used
IV anaesthesia
induction?
use?
how do they suppress conciousness?
- rapid induction in 30 s
- used to induce generally, maintenance via inhalation or combination
- not used alone due to accumulation and slow redistribution
- suppress conciousness by decreasing CNS activity with inhibitory GABA and inhibiting excitatory Glutamate
Name the IV GA’s?
Mates using KET are Proper Fools
Midazolam
Ketamine
Etomidate
Thiopental
Propofol
Ketamine MOA , uses, SE’s
Midazolam MOA and uses
Thiopental MOA
Ketamine = NMDA glutamate R antagonist -> Blocks Na+/ Ca2+ channels
Uses: Analgesia and IM for short procedures
SE’s: hallucination raised HR/ BP on recovery
Midazolam MOA: Benzodiazepam GABA PAM at Y subunit
Uses: sedative and anxiolytic, short minor procedures w/out loss conciousness
Thiopental MOA: Barbiturate therefore GABA PAM at A/B subunits
Etomidate: MOA, USES
Propofol: MOA, action/ uses
Etomidate:
MOA -> unclear
uses: induction without hangover
Propofol:
MOA -> unclear
Action/ uses -> maintenance, no accumulation therefore can have continous infusion
Drugs for epidurals?
where is the injection (vertebral level) and what layers do you go through?
used for what procedures?
What scale used?
Lidocaine and Bupvicaine
Injection can be done at any vertebral level as entering the EPIDURAL space (between vertebral column and outer meningeal layer surrounding spinal cord) not the SUBARACHNOID space.
Differs from SPINAL anesthesia as spinal anesthesia enters subarachnoid space therefore alway done at L3/L4 to prevent damage to spinal cord.
Epidural goes through 1) skin 2) supraspinous ligament 3) infraspinous ligament 4) ligamentum flavum 4) epidural space
Used for genitourinary procedures/ Obs and Gyn/ Lower limb orthopaedics
Bromage Scale used
What are the bromage scale levels
What does epidural block affect more motor or sensory?
is sensory fully blocked?
- Bromage scale 0-3
- O no block flexes knee and feet
- 1 partial block, partially flexes
- 2 almost complete block, inability to flex knees able to flex feet
- 3 complete block -> unable to move legs or feet
- Epidural affects sensory nerves over motor due lighter myelination and cold and pressure sensation not as affected.
What adjuncts are used in anaesthesia and why?
What two groups are there?
Name them
Used NM blockers (muscle relaxants)
allows relaxation of skeletal muscles, allows relaxation of vocal cords to permit endotracheal tube.
Two groups: 1) Depolarising 2) non depolarising
Nervy anasethetists value Deep sedation nomatterwhat
Non depolarising = Atracurium and Vecuronium
Depolarising = Suxamethonium and Neostigmine
Depolarising NM blockers
MOA
Reversal agents?
Suxamethonium : mimics ACh at NMJ (non competitive), hydrolysis much slower than Ach, prolongs depolarisation and overtime overloads the system -> leads to desensitisation
Neostigmine: Ach esterase inhibitor, prolongs Ach, inital depolarisation followed by desensitisation due to overloading system
reversal agents only exist for non depolarising, depolarising allowed to dissipate naturally.
Non depolarising NMB’s
MOA
reversal agents?
Atracurium and Vecuronium MOA:
Competitively bind to and antagonise the AchR, prevent depolarisation
only takes 3-4 mins to max block, duration 40 mins
widely used due to fast onset
reversible by anticholinesterase (neostigmine) and suggamedex ONLY for Vecuronium. (remember by vencuronlyium w suggamedex).
Reversal agents MOA
Neostigmine -> inhibits anticholinesterase breakdown, increases conc of Ach in cleft to compete with the non depolarising blocker, allow activation of Ach channels again.
Suggamedex -> oligosaccharide that forms a complex w vecuronium, promotes removal from NMJ and into plasma
