Neuromuscular Agents Flashcards
What are neuromuscular agents?
NB used in isolation?
Drugs that paralyse patients that are undergoing surgery or need venitlation and act at the neuromuscular junction.
They are not sedatives, amnesic or analgesics.
Not used in isolation, part of balanced anaethesia
What is the clinical use of NMBA’s?
- Facilitate intubation of the trachea (intra operative ventilation)
- Facilitate surgical exposure (e.g abdomen relaxed)
- Prevent deleterious movement during surgery
- Intensive Care: ventilation, decrease O2 consumption etc
What two enzyme will NMNA’s act on primarily?
Nicotinic acetylcholine receptors. @ bind to alpha 1 subunits.
Acetylcholinesterase on basal lamina made by muscle cells.
Mechanism of action and example of depolarising NMBA
Succinylcholine (SCh).
Mimics ACh acts as an agonist. 1 molecule binds to both alpha subunits.
Biphasic response. Causes contractions followed by relaxation. Is not broken down by AChE.
Acts until kidney elimination or broken down
What are some features of Succinylcholine?
Fast(est) acting (<60s)
Duration of action short
broken down by pseudocholinesterase
Side effects/ Disadvantages of Succinylcholine
Cannot be reversed
Fasciculations can cause postop muscle pain
cardiac dysryhtmias
Mechanism of non depolarising NMBA’s
NB benzylisoquinolones and aminosteroids
They are positively charged ammonium compounds that attach to 1 or both alpha subunits of the AChR.
Competitive interaction between NMBA and ACh.
Block acquired when 70% receptors occupied.
Atracurium: onset; excretion; CV effects; Acting
Onset: 3-5 mins
Excretion indepenedent of liver and kidney
CV effects: transient skinrash, hypotension
Acting: Intermediate (25-45 mins)
Mivacurium: Potency; onset; Acting; degradation
Potency: 3 times that of atracurium
Onset: 3-4 mins
Acting: Short acting (20-25mins)
Degradation: pseudocholinesterase (irreversible?)
Rocuronium: Onset: Acting; potency
Onset: fast due to large dose (low potency)
Acting: Intermedate 40
Vecuronium: onset; acting; excretion;
Onset: slower onset
Acting: intermediate acting
Excretion: kidney
Pancuronium: potency; onset; acting; CV effects; excretion
Potency: high Onset: slow Long Acting 1.5-2 hours (good for long cardiac surgeries) increases BP and HR Excretion liver and kidneys
How can we reverse NMBA’s note only for non depolarising
Titrate perfectly
Accelerate reversal- increase ACh at NMJ or decrease plasma NMBA
What are some drugs that causes reversals?
Anticholinesterases, to stop ACh breakdown. Tilts competiton for AChR
Eg Neostigmine/ pryidostigmine
What is the problem with NMBA’s reversers?
How are these combatted?
Act at all cholinergic receptors causing side effects.
Parasympathetic activity altered causing bradycardias, ssalviations.
Combat: combined with atropine or an antimucarinic drug to stop this
Sugammadex
Binds to rocuronium and take sit into the plasma where it is excreted. Expensive
What is a TOF?
fade?
Train of four is 4 stimuli done on a peripheral nerve every 0.5s.
TOF count is number of twitches seen.
TOFR is ratio of the 4th twitch to the 1st twitch. Complete NM block has a ratio of 0 and count of 0
Fade shows deficiency of NM transmission
Use adductor pollicis as surrogate, diaphragm less senstive.
What is the danger of a residual block from NMBA’s?
When will a reversal drug given?
The ventilatory response to hypoxia is impaired until a TOFR of 0.9. Hard to measure this. Pharyngeal muscles at 0.8
When count is at 4 to prevent reparalysis
