Flashcards in Neuromuscular Blockers Deck (26)
Which chemical do all NMBs resemble?
Name the only depolarizing NMB on the market. What enzyme degrades it? Is this enzyme found in the synaptic cleft?
Succinylcholine. Degraded by pseudocholinesterase aka butyrylcholinesterase. Not found in the cleft in high amounts.
Which type of NMB competes with Ach for the receptor?
Non-depolarizing NMBs are competitive.
What are the two types of non-depolarizing NMBs?
Amino steroid derivatives and benzylisoquinoline derivatives
Name the three amino steroid derivatives and the two benzylisoquinoline derivatives.
Amino steroids: pancuronium, rocuronium, vecuronium.
Benzylisoquinoline derivatives: atracurium, cistracurium.
NMBs work on ________ Ach receptors.
Briefly describe the mechanism of action of non-depolarizing NMBs.
They competitively block nicotinic Ach receptors to prevent Ach from binding, causing flaccid paralysis.
___% blockage of Ach nicotinic receptors is needed for paralysis from non-depolarizing NMBs.
Depolarizing NMBs cause _______ paralysis during phase 1 and _______ paralysis during phase 2.
spastic during phase 1 and flaccid during phase 2
What is the primary clinical use for depolarizing NMBs? Why?
For intubation because they are fast acting and wear off fast
Which two non-depolarizing NMBs are cleared organ-independently?
Is succinylcholine metabolized in an organ independent manner?
Atracurium and cistracurium are metabolized organ-independently.
Succinylcholine is organ-independent, too.
Describe the sequence of paralysis for NMBs.
Small muscles first, large muscles last
What type of NMBs are often used during hypothermia protocol?
Which NMB is the longest acting?
Amino-steroid derivative NMBs are dependent on these two organs for metabolism.
Which NMBs are deactivated via spontaneous Hofmann elimination reactions in vivo?
What type of NMBs have the following AEs: Bradycardia, Masseter muscle rigidity, hyperkalemia, malignant hyperthermia, muscle pain, anaphylaxis, increased intragastric pressure, increased intra-ocular pressure.
Butyrylcholinesterase deficiency would be a contraindication to using which specific NMB?
Name the medication, when taken concomitantly, increases risk for acute quadriplegic myopathy syndrome.
Name four drugs that increase (potentiate) NMB blockade.
1. General (inhaled) anesthetics
3. Calcium channel blockers
4. Local anesthetics
What train-of-four values are "ideal" for surgical procedures and what percentage of receptors blocked correspond to each value?
2/4 twitches = 85% blocked
1/4 twitches = 90% blocked
this is ideal
How are non-depolarizing NMBs reversed clinically?
How are depolarizing NMBs reversed clinically?
Acetylcholinesterase inhibitors are given for non-depolarizing NMBs.
Depolarizing NMBs cannot be reversed clinically right now.
Name an AE that pancuronium and some rocuroniums may cause.
Tachycardia, which leads to hypertension.
Name two AEs that atracurium might cause.
1. Histamine release and all the garbo that comes along with that.
2. Tachycardia and seizure-like activity from the metabolite laudanosine.
What is Acute Quadriplegic Myopathy Snydrome (AQMS)? What NMBs can cause it? Concomitant use of which drugs increase risk for this?
Residual and prolonged paralysis from the NMB lasting days to weeks. Non-depolarizing NMBs can cause it. Higher risk with concomitant steroid use.