Anaesthesia in Research Flashcards
What are the subgroups of neuromuscular blocking agents?
Non-Depolarising blockers (nicotinic antagonists)
Depolarising blockers (nicotinic agonists)
What is curare?
An example of a non-depolarising neuromuscular blocker used by indigenous South Americans to paralyse prey
What are neuromuscular blocking agents?
Drugs that act on the neuromuscular junction (at the muscle itself) rather than through the CNS
How can using neuromuscular blockers reduce damage to muscle in surgery?
It makes muscles lose all tone, there is less damage because the muscle was not rigid when it was manipulated
What type of receptor are nAChRs and what is their purpose?
ION channel receptors - purpose is to bring in Sodium ions
How do non-depolarising neuromuscular blockers work?
They block nAChRs, therefore no influx of sodium ions, therefore no depolarising to threshold for voltage gated calcium channels, insufficient calcium liberated from SR, no contraction.
What kind of antagonists are non-depolarising neuromuscular blockers?
Competitive antagonists
What are the antidotes for non-depolarising neuromuscular blockers and how do they work?
Acetylcholinesterase inhibitor - less AChE, more ACh in the synapse which outcompetes the blocker.
New antidote is 4-aminopyridine - makes lots of ACh get released from presynaptic neutron, so there is enough to outcompete
What are the side effects of administering AChE inhibitors as an non-depolarising NMB antidote, and how can this be managed?
Increase in parasympathetic signalling (mucous, tears, stomach acid, bladder contraction etc). Managed by administering directly to muscle to avoid it going systemic
Why is atracurium unique as a non-depolarising neuromuscular blocker?
It is broken down chemically, not enzymatically, so it doesn’t need to get to a source of enzymes to get broken down.
Why do we have many different non-depolarising NM blocker drugs?
Because they also have a range of “other effects” that need to be considered like some induce histamine release, some drop BP etc
How does depolarising NM blocker work?
nAChR agonist.
PHASE I -
1. Small muscle jerks/contractions
2. Desensitisation of receptor due to ongoing “noise”(~30sec)
PHASE II -
- Drug is metabolised, and the metabolite succinylmonocholine is itself an ANTAGONIST therefore acts like non-depolarising NM blocker
- Blocks Na influx
- No threshold for Ca channels
- No Ca to open SR
- No contration
What is the antidote for Succinylcholine, and what is important to remember about it?
Pseudcholinesterase. However 1 in 2000 people have an enzyme variant. That means the paralysis lasts hours instead of minutes
What are risks associated with depolarising neuromuscular blockers?
- muscle pain during induction
- can cause hyperkalaemia
- can cause malignant hyperthermia
Why is it necessary to intubate any patients with neuromuscular blockers?
Neuromuscular blockers paralyse skeletal muscles, respiratory muscles are skeletal muscles, patient must be intubated or will asphyxiate
