Anaesthtics Flashcards
What are types of anaesthesia
General:
Inhaled/volatile
IV
Local:
Regional
Can be combined
What is conscious sedation
Conscious sedation: use of small amounts of anaesthetic or benzodiazepines
to produce a ‘sleepy-like’ state. (Maintain verbal contact but feel comfortable)
What are the steps which occur during anaesthesi
• Premedication (Hypnotic-benzodiazepine).
• Induction (usually intravenous but may be inhalational) - reasonable dose
• Intraoperative analgesia (usually an opioid) - resp rate becomes depressed so need a tube
• Muscle paralysis-facilitate intubation/ventilation/stillness.
• Maintenance (intravenous and/or inhalational) -initial might be wearing off, switch to volatile typically
• Reversal of muscle paralysis and recovery which includes
postoperative analgesia (opioid/NSAID/paracetamol).
• Provision for PONV.
• POINT: during anaesthesia many (interacting) pharmacological
agents “on board” requiring excellent pharmacological knowledge
and skill to manage.
Describe volatile general anaesthesia
Blow oxygen over top -
anaesthetic goes through a face
mask to patient
What are some classes of volatile GE
N2O, Xe, Isoflurane, Halothane, Fluroxene
What ate some examples of IV GE
Intravenous • Propofol • Barbiturates • Etomidate • Ketamine
What are Guedel’s signs
Stage 1: analgesia and consciousness Stage 2: unconscious, breathing erratic but delirium could occur, leading to an excitement phase. Stage 3: surgical anaesthesia, with four levels describing increasing depth until breathing weak. Stage 4: respiratory paralysis and death.
What is anaesthesia a combination of
Anaesthesia is a combination of; • Analgesia • Hypnosis (loss of consciousness) • Depression of spinal reflexes • Muscle relaxation (insensibility and immobility)
What is mac
Minimum alveolar concentration for
expression of different responses
varies. Memory goes first, then
consciousnesss.
Measure at alveolus the conc of
volatile anaesthetic. The conc that
prevents movement to a surgical
incision in 50% of population = mac
How is the potency of volatile anaestheitcs defined
• What is potency ? (M&R year 1).
• Volatile anaesthetic potency is described by MAC or
Minimum Alveolar Concentration.
– [Alveolar] (at 1atm) at which 50% of subjects fail to move to
surgical stimulus (unpremedicated breathing O2/air)
– At equilibrium [alveolar] = [spinal cord]
– MAC, MAC-BAR (Autonomic Response), MACawake
• Anatomical substrate for MAC is spinal cord
– In animal models if section cord (i.e., remove connection to
the brain) MAC is unchanged.
What afctros affecr induction and recovery
Partition coefficients (solubility)
• 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)
Nt very soluble in blood.- in an out quickly. Exposing the brain very quickly. Not dissolve. When you switch it off - wake up quickly. Unless obese bc more fat. Other thing that .deterines solubility Higher solubility = greather potency.
Wat affects mac
• Age (High in infants lower in elderly) • Hyperthermia (increased); hypothermia (decreased) • Pregnancy (increased) • Alcoholism (increased) • Central stimulants (increased) • Other anaesthetics and sedatives (decreased) • Opioids (decreased)
What are the effects of n2o on mac
Nitrous Oxide is very often added to other volatile agents (reduced dosing).
Typically use isoflurane with some N2O and o2. Adding second gas - reduce conc of first. Ading n20 reduces the mac N2O has good slide effect profile, also good anaesthetic profile, can be mixed with the primary one
What is the role of gaba receptirs in anaesthesia
• GABAA receptors critical target • Major inhibitory transmitter • LGIC (Cl- conductance) • Potentiate GABA activity • Anxiolysis • Sedation • Anaesthesia • With the exception of Xe,N2O and ketamine all anaesthetics potentiate GABAA mediated Cl- conductance to depress CNS activity. • NMDA receptors probable other site
desctibe the areas of the brain targeted by anaesthesia
• Reticular formation (hindbrain, midbrain and thalamus)
depressed. Connectivity lost.
• Reticular system often called “activating system” due to
ability to increase arousal.
• Thalamus transmits and modifies sensory information.
• Hippocampus depressed (memory).
• Brainstem depressed (respiratory and some CVS).
• Spinal cord-depress dorsal horn (analgesia) and motor
neuronal activity (MAC).
what are the main iv anaesthetivs
• Propofol (rapid), Barbiturates (rapid), Ketamine
(slower).
• Given intravenously for ‘induction’.
• Can be used as sole anaesthetic in TIVA (Total
IntraVenous Anaesthesia).
• Target sites as for inhalational.
• With exception of Ketamine (NMDA) all potentiate
GABAA.
• Systems target as for inhalational.
How Do We Describe Intravenous
Anaesthetic Potency?
• Plasma concentration to achieve a specific end
point (loss of eyelash reflex or a BIS value or…..).
• For induction in mixed anaesthesia – Bolus to end
point then switch to volatile.
• TIVA uses a defined PK based algorithm to infuse
at a rate to maintain set point. Pre-ceeded by a
bolus. Electrodes
In which situations are local and recional anaestehtic sued
Dentistry Obstetrics Regional surgery (patient awake) Post-op (wound pain) Chronic pain management (PHN)
What are some egs of local anestehtics and what are
Lidocaine,
Bupivacaine, Ropivacaine and Procaine.
Wat are the charactersistsic of local anaesthetics
Characteristics • Lipid solubility – potency (higher greater potency) • Dissociation constant (pKa) – time of onset. Lower pKa faster onset • Chemical link – metabolism • Protein binding – duration (higher for longer duration)
Whats the diffreence between an ester and amide link
If ester - esterases will chop it up. Very short acting. Aside link - longer acting.
Can predict degree to Chico will block a response based on the chemistry o
these molecules. Lipid solubility determines potency.
Describe bupivacqaine infiltration for wound analgesia
• Cocaine archetypal • Esters-shorter acting • Amides-longer acting • Block is USE Dependent • Block small myelinated (afferent) nerves in preferance hence nociceptive and symp block • Adrenaline ↑ duration Bupivacaine an amide so more stable-longer lasting. Slow onset (pKa 8.2).
Block voltage Na Chanels. Use depended blocks. Dont want it to bock non-firing neurones. Want to switch off pain fibres and nothing
else. Pain - they fire - selective black of pain fibres. Goes into memb, loses charge, sucked into inside of Na Handel. It blocks the
channel. Ap is then stopped. The degree it goes in is proportial to the degree to which the nerve is firing . Can potentiate effects by
adding adrenaline
Compare lidocaine, bipivaxaine, ropivacains ancd procaine
ss
What is regional anesthsia
• As the name suggests selectively anaesthetising a part
of the body.
• Often described as a ‘block’ of a nerve and hence the
patient remains awake.
• Uses local anaesthetic and or an opioid.
• Upper extremity (e.g.,); interscalene, supraclavicular,
infraclavicular, axillary.
• Lower extremity (e.g.,) ; femoral, sciatic, popliteal,
saphenous.
• Extradural / Intrathecal / Combined (labour).
Local into nerve root thats supplying a region - booking outflow and inflow from that area.
What are the main anaesthtic side effects
• Too many agent specific effects to list and remember
polypharmacology !
• General anaesthesia
– PONV (opioids)
– CVS – hypotension
– POCD (increases with increasing age)
– Chest infection
• Local and regional
– Depends on the agent used and usually result from systemic spread (Locals are Na+
channel blockers so cardiovascular toxicity)
• Increased general concern re: allergic reactions/anaphylaxis
If they vomited ast time, they will again. F they are particularly sensitive
to a particular anaesthetic or opioid, use a different one. Cvs unstable
patients - anaesthetic might be too much, think abt local instead. Post
operative cognitive dysfunction - use a different, low exposure, dont put
to sleep for example. if it ends up in vascular compartment- wills top
heart.
