Anes- Neuromuscular blocking agents

kelseyfmeyer's version from 2015-11-30 13:46


Question Answer
most common reason you'd want to use them on a patient?Ophthalmologic procedures (eye should NOT MOVE AT ALL when you are doing a procedure on it- could be detrimental)
which benzo is NOT IM?diazepam
why is using a NMBA blocker on the eye for eye sx so awesome?extraocular muscles paralysed, centralisation and immobilisation of the globe
5 good indications for using a neuromuscular blocking agent?(1) intraocular sx (2) ET intubation (humans, pigs) (3) thoracotomy (4) fracture retraction (5) laparotomy
why is NMBA good for fracture retraction?the mm might be very contracted
if you are using NMBAs systemically, or for a thoracotomy, what must you do?provide mechanical ventilation
If you need to get a dog to relax during a procedure, you have options. what are they? (4)(1) Deep level of anaesthesia (lots of CV depression tho) (2) Local anaesthesia (may or may not be good to the specific sx-- might be fine for fx repair, but not really for a celeotomy.) (3) Centrally acting muscle relaxants (eg benzodiazepines, α2-agonists, guaifenesin) (4) Peripherally acting muscle relaxants (NMBA= neuromuscular blocking agents; provide “paralysis”)
explain the Physiology of normal neuromuscular contractionMotor nerve action potential--> release of ACh--> ACh receptor binding--> activation of ligand-gated channels--> mm contraction
What is acetylcholine? where is it stored? what triggers its release?Neurotransmitter, stored within the nerve terminal in vesicles. AP reaches nerve terminal, ACh storage vesicles release ACh into the junctional cleft
Once ACh is released into the junctional cleft, what does it do and how does it do it?ACh crosses the cleft to bind to the postjunctional receptors, and 2 ACh molecules are necessary to activate opening of ion channel (Hydrolyzed by acetylcholinesterasis)
what is the structure of the Postsynaptic ACh-receptors? how does ACh affect it, and a successful activation leads to what?Pentrameric protein structure (5 diff areas basically, 2 alphas, a beta, a gamma, and a delta). ACh needs to react with both α-units (so need 2 ACh's), and when both alpha units are bound, there is a conformational change which results in the channel opening (~Na++ goes IN, and Ca++ in, and K+ OUT)
what are the two types of NMBAs?(1) depolarizing relaxants (2) non-depolarizing relaxants
what is the drugs which is the NMBA depolarizing relaxant?Suxamethonium (aka Succinylcholine)
explain the "depolarizing" vs "non-depolarizing" conceptdepolarizing is that it makes the synapse release all the ACh FIRST, and THEN the receptor is blocked. Whereas non-depolarizing just block the receptor and don't allow any depolarization to occur
what are the 4 main drugs which are NMBA non-depolarizing relaxants?Atracurium, Rocuronium, Vecuronium, Mivacurium
how would you describe the Succinylcholine structure? how does it act with the receptor?it looks like two AChs back to back. It binds non-competitively
Succinylcholine--> how does it act on the receptor? how long does it act? how long does it take to work?It's a NON-competitive, short onset, short acting NMBA depolarizing relaxant
because Succinylcholine is a depolarizing relaxant, what are some signs you might seen when you first administer?Initial muscle fasciculation (non-depolarizings don't have this)
how is succinylcholine degraded?pseudocholinesterasis (NOT like the other ones which is acetylcholine esterases)
what are the 4 major side effects of Succinylcholine?(1) cardiovascular (bradycardia or tachycardia, hypertension, arrythmias) (2) trigger malignant hyperthermia (3) hyperkalaemia (4) INC intraocular pressure (IOP)
which NMBA is not good for eye sx and why?succinylcholine, because it inc intraocular pressure
which NMBA causes hyperkalemia?succinylcholine (bc depol is inc K+ out side of cell)
which NMBA causes malig hyperthermia?succinylcholine (causes mm fasciculations and such, inc activity/heat)
which is used more often... depolarizing, or Non-depolarising NMBAs?non-depol
which NMBA drug category CAN you antagonize?you can antagonize the non-depolarizing ones, because they work COMPETITIVELY (the depol ones are not competitive so you can't antagonize)
how do Non-depolarising NMBAs work?They bind to ACh-receptors COMPETITIVELY and work as an ion channel blockade. Because of this they do NOT induce a AP which is why they do not cause mm fasciculations
Non-depolarising NMBAs can be classified as what two groups?(1) benzylisoquinolines (2) aminosteroids
Nondepolarizing---> Benzylisoquinolines--> what are the three drugs in this category?Atracurium, cis-atracurium, Mivacurium (Where MI CIS AT, BEN??)
Nondepolarizing---> Aminosteroids--> what are the three drugs in this category?Vecuronium, Pancuronium, Rocuronium
(said in class) which non-depol agent is best in sheep?Mivacurium (which is a Benzylisoquinoline) (Sheep says "mivac the grass up with my mouth")
(said in class) which non-depol agent is best in horses?Atracurium (which is a benzylisoquinoline) (horse are near A-TRAC)
(said in class) shortest acting non-depol agent?Rocuronium (R for rapid)
What properties do NMBAs lack?are neither anaesthetic nor analgesic. ---> if not used right can be paralyzed and funny conscious (horrible). this must be avoided at all costs by closely monitoring the adequacy of anaesthesia
how do you go about Monitoring the neuromuscular blockade?you can use a peripheral nerve stimulator
explain how a peripheral nerve stimulator works (what do you use it for?)(used to monitor the NM blockade) small electric current through a pair of electrodes attached to the skin over a nerve. Usually use the ulnar, peroneal, or facial nerve. Give current, and then measure for speed of contraction.
how do you know when the patient is ready to be done with anesthesia, based on the peripheral nerve stimulator?she said "wait till 4 twitches come back" until you can turn off the iso (look at slide 22 for "train of four" diagram) Machine gives you percentage: 90% makes sure pt is able to breathe again
% on peripheral nerve stimulator which indicates that they pt can breath on its own?90%
peripheral nerve simulator--> what is a Train-of-four?four stimuli of 0.5-msec duration over a period of 1.5 sec
what is the train of four ratio today which means it is acceptable time for recovery?0.9 (if %, 90%)
if the TOF ratio (train of four) is <0.7, what do you think it means?there is a dec hypoxic ventilory response (so don't stop breathing for them)
what are conditions the pt might have which cause the NMBA to last longer, thus requiring more time for recovery?Renal or liver diseases, volatile anaesthestics, acidosis, hypokalaemia, hypothermia
which organs, if diseased, will cause NMBA to last longer?kidney/liver
how do anesthetics affect NMBA?cause them to last longer
how does body pH affect NMBAs? body temp?ACIDOSIS causes them to last longer (acid takes a long time to wear off). Hypothermia also extends their effects
how does K+ levels affect NMBAs?low K means they will last LONGER (think about it like how mm stuff and need k to repol so if low K then this is just a super long refractory period)
if you want to use the peripheral nerve stimulator to monitor recovery, what should you think about and do beforehand?FIRST measure twitches before you give NMBA so you can compare to recovery response
Signs of inadequate anaesthesia during muscle relaxant use? (6)Increase in HR, Increase in BP, Salivation, Lacrimation, Increase in ETCO2, Muscle twitching, esp around the head
****MAKE SURE ANESTHESIA IS ADEQUATE WITH NMBASunacceptable to have paralysis in conscious pt
what are the two ways a pt can recovery from NMBA?(1) spontaneous recovery (it wears off) (2) Antagonism of NMB with anticholinesterase agent
what category of drugs can you use to reverse NMBAs? two examples!(DONT FORGET only can reverse non-depolarizing agents because they work COMPETITIVELY) you use ANTICHOLINESTERASES like neostigmine and edrophonium (THE NEWEST antagonist is sugammadex, but it's basically too expensive right now). You want an anti-cholinesterase because cholinesterase is what breaks down ACh, so if there is more ACh in the synapse, then it can compete with the NMBA for the binding site
explain what can happen when you antagonize a non-depol NMBA, and how you deal with these consequencesWhen you antagonize, you are antagonizing the enzyme that breaks down ACh (acetylcholine esterase) which means there is MORE ACH in the synapse to compete with the competitive non-depol NMBA. However, this leads to SIDE EFFECTS of too much ACH (Which activates the PARASYMP system) so side effects are bradycardia, arrythmias, bronchoconstriction, and salivation. You can combat these side effects with ATROPINE or GLYCOPYRROLATE (these are ANTICHOLINERGIC) which means they antagonize the muscarinic (parasymp) receptors causing the side effects
summary: what DO NMBAs provide and what DON'T they provide?DO provide paralysis, DON'T provide anesthesia or analgesia (so you need to provide it for them)
when is a situation where you should not use a NMBA?if no ventilator is avail, don't do it
which NMBAs can be antagonized?The non-depolarizing (because they are competitive for the binding site)

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