neuromuscular blockers Flashcards
Inside of cell is negative or positive at rest? When depolarized?
At rest= negative, depolarized= positive
what type of neurons are motor neurons? where do they orginate?
alpha motor neurons, from anterior horn of spinal cord
steps of AP to ACh channels opening
- AP moves along motor neuron (Nn) towards muscle fiber
- AP voltage opens Ca Channels (allows for ACH vesicles to move to presynpatic terminal)
- ACh is released at motor end plate
steps after ACh release
- some ACh binds to prejunctional receptors on Nn (these mobilize ACh vesicles to move from stockpile to front line)
- ACh molecules bind to acetoylchoine receptors on NMJ motor endplate
- 2 ACh molecules attach to 2 alpha subunits on AChreceptor, allowing Na in
- positive potential coming in opens up voltage gated Na channels, depolarizes muscle membrane
- causes SR to release large amounts of Ca ions
- Ca ions intiate attraction between actin and myosin for contraction
what are the 2 types of AChreceptors
- fetal (lower conductance cation channel with longer opening times - more K release)
- adult
how does muscle contraction terminate
Ach diffuses away or gets removed by acetylcholinesterase
types of NMBs
- depolarizing (agonists)
- non depolarizing (competitive antagonists)
what are the different type of NDNMBs
steriods or benzylquinolones
short acting, intermediate acting, long acting
MOA of Sch
densensitization of Nm receptor
sustained depolarization does not allow for Nm to reset (hyperpolarization)
metabolism of SCh
hydrolyzed by butrylcholinesterase (plasma cholinesterae) … synthesized in liver
needs to diffuse out of NMJ to terminate action
dose of SCh
1-1.5 mg/kg
onset of Sch
30- 60 seconds
duration of Sch
5-10 minutes
side effects of SCh
Fasiculations (Sch only needs to bind to 1 alpha receptor, can bounce from channel to channel, thus they stay open longer), histamine release, cardiac muscarinc binding (SB, JR, Sinus arrest), hyperK, increased intraocular/intragastric/intracrainial pressure, myogolbinura, massesseter spasm
What type of pts have issues with breaking down SCh
-decreased hepatic function
-drug-induced decreases (neo, reglan, chemo)
-chronic diseases
-pregnancy
-obesity (increased activity of plasma cholinesterase)
how can you help treat fasciculations?
pre-dose with small dose NDMR
disease that causes resistance to SCh
MG (less Nm receptors, need more SCh - like 2.0mg/kg)
Which NDMR are steriods and which are quinolones?
Steriods= PVR
pancuronium
vecuronimum
rocuronium
Benzylquinolones= atracurium and cisatracurium
difference between steriod and quinolones?
steroids= eliminated by hepatic mostly (pan= renal)
quinolones= hoffman elimination (cis) or plasma cholinesterase (miv) (spontaneous breakdown at certain pH and temperature)
which drugs release histamine?
SAM
Sch, atracurium, morphine
adverse side effects of NDMRs
Cardiac - effects at cardiac muscariac receptors and autonomic ganglia
pancuronium- blocks vagal response (increases HR & CO, no change in SVR)
conditions that prolong NDMRs
VA, antibiotics (aminoglycosides, tetracyclines and clindaymacin), hypocalcemia, hypermagnesemia, LAs, hypothermia, dantrolene
intubating doses for NDMRs
all are mg/kg
Mivacurium (0.2-0.25)
Rocuronium (0.6-1.2)
Vecuronium (0.1-0.2)
Atracurium (0.5-0.6)
Cisatracrium (0.15-0.2)
Pancuronium (0.08-0.12)
onset of NDMRs
In minutes
Mivacurium (2-3)
Rocuronium (1-3) *
Vecuronium (2-3)
Atracurium (1-3)
Cisatracrium (2-3)
Pancuronium (3-5)
- when Roc given at 1.2 mg/kg onset is the same as Sch, with longer duration
DOA of NDMRs & Sch
In minutes
SCh (6-11)
Mivacurium (15-20)
Rocuronium (50-60)
Vecuronium (40-60)
Atracurium (40-60)
Cisatracrium (40-60)
Pancuronium (90)
what are alternatives is NMBAs are contraindicated?
High dose opioid on induction (I.e. remi 4-5 mcg/kg with propofol)
**should give glycopyrollate at same time (0.2-0.4 mg IV) due to brady
which nondepolarizing NMBA most commonly causes anaphylaxis d/t histamine release? which one most commonly causes anaphylactoid rxn (nonIgE histamine release)?
- roc
- ata
***Note: drugs with single quaternary ammonium group are less likely to cause anaphylaxis than SCh, but cross sensitivity can occur.
*SCh is most common NMB to have anaphylaxis to
what is the mechanism of fade for NDMR vs SCh?
NDMR: Nn ACh receptors are blocked (stops signal to move stockpile SCh to front line.. less ACh available to use after multiple depolarizations) (phase II block)
Sch: stimulates Nn receptors same as ACh… stimulates ACh release repeatedly (phase I block) *
- high dose SCh causes phase II block
explain mechanism of TOF
delivers 4 successive electric stimuli at a frequency of 2 Hz (2 stimulations per second)
if all 4 twitches present= ratio 1
adequate recovery = 0.9
Other names for Cisatricurium, vecuronium, Rocuronium, pancuronium, Sch
Cis-Nimbex
Vec-Nornuron
Pan- pavulon
Roc-Zemuron
Sch- Anectine
disapperance of twitches happens at what % receptor capactiy
- 4th twitch disappears at 75-80% occupancy
- 3rd twitch disappears at 85% occupancy
- 2nd twitch disappears at 85-90% occupancy
- 1st twitch disappears at 90-95% occupancy
explain mechanism of tetantic stimulation
continuous, high frequeuncy 50 or 100 Hz (50 or 100 stimulations per second) causes sustained muscle contraction
explain the sequence of blockade
central muscles blocked before and recover faster than peripheral
best place to measure onset of blockade (intubation conditions)
muscle= orbicularis oculi or corrugator supercilli
nerve= facial nerve
best place to measure recovery
muscle= adductor pollicis
nerve= ulnar nerve
