Anesthesia - Neuromuscular blocking agents

pbhati17's version from 2017-03-06 15:56


Question Answer
Most common reason you'd want to use them on a PTx?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 paralyzed, centralization & immobilization 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 much 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 anesthesia (lots of CV depression tho)
(2) Local anesthesia (may or may not be good to the specific Sx-might be fine for fox 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 w/in 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 & how does it do it?ACh crosses the cleft to bind to the post junctional receptors & 2 ACh molecules are necessary to activate opening of ion channel (Hydrolyzed by acetylcholinesterases)
What is the structure of the Postsynaptic ACh-receptors? How does ACh affect it & a successful activation leads to what?Pentrameric protein structure (5 diff areas basically, 2 alphas, a beta, a gamma & a delta). ACh needs to react w/ both α-units (so need 2 ACh's) & when both α units are bound, there is a conformational change which results in the channel opening (~Na++ goes IN & Ca++ in & K+ OUT)
What are the 2 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 & THEN the receptor is blocked. Whereas non-depolarizing just block the receptor & don't allow any depolarization to occur
What are the 4 main drugs which are NMBA non-depolarizing relaxants?Atracurium
How would you describe the Succinylcholine structure? How does it act w/ the receptor?It looks like 2 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
Bc Succinylcholine is a depolarizing relaxant, what are some signs you might seen when you 1st administer?Initial muscle fasciculation (non-depolarizing 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, arrhythmias)
(2) Trigger malignant hyperthermia
(3) Hyperkalemia
(4) ↑ intraocular pressure (IOP)
Which NMBA is not good for eye Sx & why?Succinylcholine, bc it ↑ intraocular pressure
Which NMBA czs hyperkalemia?Succinylcholine (bc depol is ↑ K+ outside of cell)


Question Answer
Which NMBA czs malig hyperthermia?Succinylcholine (czs mm fasciculations & such, ↑ activity/heat)
Which is used more often... depolarizing, or Non-depolarizing NMBAs?Non-depol
Which NMBA drug category CAN you antagonize?You can antagonize the non-depolarizing ones, bc they work COMPETITIVELY (the depol ones are not competitive so you can't antagonize)
How do Non-depolarizing NMBAs work?They bind to ACh-receptors COMPETITIVELY & work as an ion channel blockade. Bc of this they do NOT induce an AP which is why they do not cz mm fasciculations
Non-depolarizing NMBAs can be classified as what 2 groups?(1) Benzylisoquinolines
(2) Aminosteroids
Nondepolarizing → Benzylisoquinolines → what are the 3 drugs in this category?Atracurium
Nondepolarizing → Aminosteroids → what are the 3 drugs in this category?Vecuronium
(Said in class) Which non-depol agent is best in sheep?Mivacurium (which is a Benzylisoquinoline) (Sheep says "mivac the grass up w/ 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 anesthetic nor analgesic. → if not used right can be paralyzed & funny conscious (horrible). This must be avoided at all costs by closely monitoring the adequacy of anesthesia
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 & then measure for speed of contraction.
How do you know when the PTx is ready to be done w/ 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 4" diagram) Machine gives you percentage: 90% makes sure PTx is able to breathe again
% on peripheral nerve stimulator which indicates that they PTx can breathe on its own?90%
Peripheral nerve simulator → what is a Train-of-4?4 stimuli of 0.5-msec duration over a period of 1.5 sec
What is the train of 4 ratio today which means it is acceptable time for recovery?0.9 (if %, 90%)
If the TOF ratio (train of 4) is <0.7, what do you think it means?There is a ↓ hypoxic ventilory response (so don't stop breathing for them)
What are conditions the PTx might have which cz the NMBA to last longer, thus requiring more time for recovery?Renal or liver dzs
Volatile anesthetics
Which organs, if dzd, will cz NMBA to last longer?Kidney/liver
How do anesthetics affect NMBA?Cz them to last longer
How does body pH affect NMBAs? Body temp?ACIDOSIS czs them to last longer (acid takes a long time to wear off). Hypothermia also extends their effects


Question Answer
If you want to use the peripheral nerve stimulator to monitor recovery, what should you think about & do beforehand?1st measure twitches before you give NMBA so you can compare to recovery response
Signs of inadequate anesthesia during muscle relaxant use? (6)↑ in HR
↑ in BP
↑ in ETCO2
Muscle twitching
esp around the head
****MAKE SURE ANESTHESIA IS ADEQUATE w/ NMBASUnacceptable to have paralysis in conscious PTx
What are the 2 ways a PTx can recovery from NMBA?(1) Spontaneous recovery (it wears off)
(2) Antagonism of NMB w/ anticholinesterase agent
What category of drugs can you use to reverse NMBAs? 2 examples!(DONT FORGET only can reverse non-depolarizing agents bc they work COMPETITIVELY) You use ANTICHOLINESTERASES like Neostigmine & Edrophonium (THE NEWEST antagonist is Sugammadex, but it's basically too expensive right now). You want an anti-cholinesterase bc cholinesterase is what breaks down ACh, so if there is more ACh in the synapse, then it can compete w/ the NMBA for the binding site
Explain what can happen when you antagonize a non-depol NMBA & how you deal w/ 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 w/ 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, arrhythmias, bronchoconstriction & salivation. You can combat these side effects w/ ATROPINE or GLYCOPYRROLATE (these are ANTICHOLINERGIC) which means they antagonize the muscarinic (parasymp) receptors causing the side effects
Summary: what DO NMBAs provide & 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 (bc they are competitive for the binding site)