Define sedation. Allows patients to tolerate unpleasant
diagnostic or surgical procedures and to relieve anxiety and
discomfort. Verbal contact can be maintained. Define coma. A state
of extreme unresponsiveness, in which an individual exhibits no
voluntary movement or behaviour. Define anaesthesia. If GA then
drug induced and predictably reversible coma.
Slide 3
What is anaesthesia? Analgesia Amnesia Muscle relaxation
Amnesia induced by intra-venous anaesthetic agents and then
maintained by using inhalational anaesthetic agents. Analgesia
provided by various analgesic drugs or by regional/peripheral nerve
blocks. Muscle relaxation not required in all patients or surgical
procedures. Muscle relaxants are used to facilitate tracheal
intubation, mechanical ventilation or surgical procedure. 1.General
2.Regional (e.g. spinal, brachial plexus block, femoral nerve
block) 3.Local
Slide 4
GA: Inhalational vs. IV? Volatile Intravenous Onset Offset
Specific Drugs Metabolism Principle side effects Notes Slow
Alveolar gas exchange Rapid Dependent on Cardiac Output One
arm-brain circulation time Alveolar gas
exchangeRedistribution/metabolism Nitrous Oxide Isoflurane
Sevoflurane Thiopentone Propofol Ketamine Almost noneLiver Cardiac
suppression Respiratory depression Cardiac suppression Respiratory
Depression Malignant Hyperpyrexia (ethers) Bone marrow suppression
(N2O) Anaphylaxis (any)
Slide 5
GA Scoring systems What is the difference between general
anaesthesia and moderate sedation? (American Society of
anaesthesiologists) General anaesthesia: Unrousable even with
painful stimulus. Moderate sedation: Purposeful response to
verbal/tactile stimulation. (usually referred to as conscious
sedation) RAMSAY RICHMOND AGITATION SCALE
Slide 6
To understand muscle relaxants, we need to understand the
neuromuscular junction. Order these steps at the NMJ Action
potential arrives at motor nerve terminal Voltage-gated Ca2+
channels open allowing Ca2+ influx Increase in intracellular [Ca2+]
causes fusion of presynaptic vesicles to cell membrane and release
of Acetylcholine by exocytosis Ach diffuses across the synaptic
cleft and binds to nAChR on postsynaptic membrane. nAChR is a
Na+/K+ channel it opens and there is Na+ influx Na+ influx
generates action potential in the motor endplate called an endplate
potential (EPP) Upon reaching threshold an AP occurs in the muscle
Acetylchloinesterase hydrolyses Ach to choline and acetate, which
are recycled General anaesthesia: muscle relaxation
Slide 7
1. Action potential arrives at motor nerve terminal 2.
Voltage-gated Ca2+ channels open allowing Ca2+ influx 3. Increase
in intracellular [Ca2+] causes fusion of presynaptic vesicles to
cell membrane and release of ACh by exocytosis 4. ACh diffuses
across the synaptic cleft and binds to nAChR on postsynaptic
membrane. nAChR is a Na+/K+ channel. It opens and there is Na+
influx 5. Na+ influx generates action potential in the motor
endplate called an endplate potential (EPP) 6. Upon reaching
threshold an AP occurs in the muscle 7. Acetylchloinesterase
hydrolyses ACh to choline and acetate, which are recycled General
anaesthesia: muscle relaxation
Slide 8
When would you need to give drugs for muscle relaxation?
Intubation (insertion of tube into trachea) Surgery requires
muscles relaxed e.g. abdominal surgery How does a depolarising
muscle relaxant work? Similar structure to Ach so binds to nAChR at
NMJ Example? Side-effects Fasciculations K+ efflux can lead to
hyperkalemia Suxamethonium Important points about suxamethonium:
Cannot be reversed wait for it to wear off in 3-5mins Wears off as
broken down by pseudocholinesterase. People deficient in this
enzyme get suxamethonium apnoea and stop breathing for up to 2hrs
What are the TWO categories of muscle relaxant? Depolarising
Non-depolarising General anaesthesia: muscle relaxation
Slide 9
THREE examples? How does a non-depolarising muscle relaxant
work? Competes with ACh and blocks nAChR Atracurium Rocuronium
Vecuronium Hoffman degradation not dependent on liver/kidneys pH
and temperature dependent. Why might you need to reverse muscle
relaxation? End of operation to allow patient to breathe on their
own Failed intubation wake patient up, let them breathe on their
own Reversal agents: Atracurium: anticholinesterases e.g.
neostigmine and pyridostigmine. Inhibit acetylecholinesterase which
breaksdown Ach, thus more Ach available to compete with muscle
relaxant Rocuronium and vecuronium: drug called sugammadex
(expensive) General anaesthesia: muscle relaxation
Slide 10
How do local anaesthetics work? Block Na channels Examples?
Lidocaine (still pronounced lig-no-caine) Bupivicaine slower onset,
longer lasting Why can local anaesthetics give a mobile block (loss
of sensation, motor function retained)? Larger diameter, myelinated
motor fibres less sensitive to anaesthetic than sensory fibres
Local anaesthetics Diffusion gradient Fibre size Myelination What 3
factors can determine the effect of LA?
Slide 11
How can local anaesthetic toxicity occur? Intravascular
injection Signs and symptoms? Paraesthesia of tongue and lips CNS
Drowsiness Seizures Muscle twitching CVS Hypotension Bradycardia
Cardiac arrest Related to Na channel blocking action Local
anaesthetics Remember! Local anaesthetic is less effective in
acidic tissues (becomes ionised), so will not be used for certain
procedures, such as abcess I&D.
