Neuromuscular Blocking agent factoids Flashcards Preview

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What are the three reasons we use Neuromuscular blocking agents?

Increase surgical exposure
Facilitate intubation
Assist in mechanical ventilation


Where is the site of action for NMBA's?

The NMJ within the Somatic nervous system


Are NMBA's water or lipid soluble and why?

They are water soluble because they contain quaternary ammonium in their structure.


Do NMBA's cross the BBB?



Which NMBA acts by mimicking the effect of ACh?

Succinylcholine. It is considered an agonist (although antagonistic)


What are the risks of increased, or repeated, or a continuous infusion doses of Succinylcholine?

A phase II block (Membrane repolarizes but receptor is desensitized to the effect of acetylcholine). This will prolong the effect of the NM blockade


What is responsible for the breakdown of Succinylcholine?

Pseudocholine esterase in the plasma


What is a phase I vs phase II block when speaking of Succinylcholine?

Phase I - membrane depolarizes, resulting in an initial discharge that produces transient fasciculations followed by flaccid paralysis.
Phase II- Membrane repolarizes, but receptor is desensitized to the effect of acetylcholine. Prolonged block occurs.


How do non depolarizing NMBA's work?

They competitively antagonize ACh at the post-junctional receptor. Effects depend on *concentration* and affinity for ACh receptor


Which muscle is less susceptible to NMBA's in comparison to peripheral and upper airway muscles (Larynx)?

The diaphragm


If paralysis is observed in a peripheral nerve, does this mean that everything is paralyzed?

No, the periphery is more susceptible to NMBS than the upper airway, which is more susceptible than the diaphragm. However, we generally use the adductor pollicis (thumb twitching muscle) and dosing is recommended off of this.


What differentiates the two main classes of NMBA's?

Whether it is an agonist or an antagonist at the site.


Where do we monitor the nerves on the body?

The ulnar nerve and the facial nerve. This is monitoring peripherally. Can also monitor posterior tibial nerve


What is train of four monitoring?

Stimulation of a nerve to determine the level of paralyzation. It guides decision to dose NMBA's. A series of four twitches at 2 Hz every 1/2 second for 2 sec. Reflects blockade from 70%-100%; useful during onset, maintenance, and emergence/ Train of four ratio is determined by comparing twitch 1 to twitch 4


What will you see for Non-D-NMBA's in terms of train of four?

Fade. The first twitch will be greater than the last twitch. Or nothing if too much is on board.


What will you see for Depol-NMBA's in terms of train of four?

You will see equal amplitude across the board. You will see no twitches at all, or all twitches will be the same.


What is used because train of four twitches can be hard to determine?

Double burst stimulation (two short burst of tetany). It allows tactile detection of small amounts of residual NMB. It is easier to feel. It will be a much more pronounced decrease in amplitude from the first to second. Easier to identify then a change in four twitches.


What is tetanus/post titanic count?

Generally consists of rapid delivery of a 30-, 50-, 100-Hz stimulus for 5 seconds/ Should be used sparingly for deep block assessment; painful.
It floods the NMJ with acetylcholine that will give a larger response to twitches. If you do this, and they still have no twitch, you can be very certain that they are very blocked. However, we do not use this a lot in everyday anesthesia


What is double burst simulation?

Two short bursts of 50 Hz tetanus separated by 0.75 sec. Similar to train of four; useful during onset, maintenance, and emergence; may be easier to detect fade than with train of four.


What is a post-tetanic count and when is it used?

50-Hz tetanus for 5 sec, a 3- sec pause, then single twitches of 1 Hz. Used only when train-of-four and double-burst stimulation is absent; count of less than eight indicates deep block, and prolonged recovery is likely


What is a single-twitch nerve stimulation?

A single supra maximal electrical stimulus ranging from 0.1-1.0 Hz. Requires baseline before drug administration; generally used as a qualitative rather than quantitative assessment.


How do NDNMBA's and DNMBAs differ in terms of twitch monitoring?

Non-depolarizers have fade


The onset of an NMBA is proportional to what?

The dose/concentration at receptor site.


What is inversely related to the onset of the NMBA?

Potency. Because the onset is proportional to the dose. The faster the onset, the less potent the drug, because you give more of it. ***The concentration of the drug available at the receptors is what impacts the onset of the block*** The way to get a large concentration of the drug there is high volume of drug.


T/F Concerning NMBA's, the speed of onset is related to the speed of recovery?

True. Because of compartment equilibration.


What is the priming dose for a NMBA?

Used to accelerate the onset of the drug when being used for intubation. Give 10% of the drug a few minutes prior to inducing anesthesia which will "prime" the receptor.


When would you not want to use a priming dose of NMBA prior to induction?

If you know the case is going to be prolonged. The patient may then exhibit the "floppy fish syndrome."


What is a de-fasciculating dose?

Giving a little ND-NMBA prior to Succinylcholine to eliminate painful fasciculations. Maybe 5 mg of roc. This is different action than a priming dose where you are looking to "prime" some receptors. You have to give increased dose of succ if de-fasciculating because receptors are now blocked and succs is an agonist to ACh


What is the ED95 of Succinylcholine? How much for intubation?

0.3 - 0.6 mg/kg (low potency). In general we say the patient should receive twice the amount for intubation. (Induction dose is 1-1.5 mg/gk)


What NMBA has the fastest onset of action?

Succinylcholine. A dose of 1 mg/kg will cause complete block in less than 1 minute and recovery to a twitch height of 90% in approx 13 minutes.


What is the advantage of the quick nature of Succinylcholine?

RSI. If you need rapid airway control. Facial trauma and struggling to breath. You may also need to control someone who is wild. Break larygospasms (sub-therapeutic dose. - but kids become hypoxic and bradycardia)


What are the adverse effects of Succinylcholine?

Increases intracranial pressure (muscle contraction in neck), increases intraoccular pressure, can cause hyperkalemia (raise by 0.5), has many cardiovascular effects (due to stimulation of cholinergic autonomic receptors)
In regards to SNS, know that adults have much better developed than children, which will become bradycardic.
Also causes myalgia, fasciculations, malignant hyperthermia.
A high dose and repeated dose will cause brady in the adult


How can genetic variants affect NMBA's, specifically Succinylcholine?

A mutation of the BCHE (Butyrylcholinesterase-synthesizes the pseudocholinesterase) gene can cause a deficiency of psudocholinesterase, leading to increased sensitivity and prolonged drug effects.


What is a dibucaine number?

It measures the amount of butyrylcholine that remains unchanged in the blood after the administration of a standard dose of dibucaine ( a local anesthetic). It can tell you if a patient will have trouble breaking down NMBA like succs.


What are the intermediate and long acting NDNMBA's?

Intermediate- Cisatracurium, Atracurium, Vecuronium, Rocuronium
Long- Pancuronium


What are the two NMBA Benzylosoquinolium compounds?

Atracurium and Cisatracurium, both intermediate acting agents


What is Hoffman Elimination and which NMBA's apply to this?

It is a non-enzymatic chemical reaction that involves heat, and it produces alkenes from quaternary amonia salts. It changes the active form of drug to inactive form, then it is eliminated. Atracurium and Cisatracurium


What slows and increases the rate of Hoffman elimination?

DECREASED temp and pH decreases Hoffman elimination, INCREASED temp and pH increase Hoffman elimination
***It is independent of enzymatic activity****


Which ND-NMBA causes histamine release?

Atracurium. It is therefor limited as an intubating drug.


What is the ED95 of Atracurium?

0.2-0.25 mg/kg. Can intubate in 2.5 minutes if you give twice the ED95


How long is the duration of Atracurium and how is it eliminated?

A return to 10% of baseline (1 twitch) in 40 minutes, with complete return in 60 minutes. Undergoes hoffman elimination 60%. It is considered relatively potent


What is Cisatracuriums relationship to Atracurium?

It is a stereoisomer of Atracurium, but does not cause histamine release.


What is the potency and ED95 of Cisatracurium?

It is more potent than Atracurium, and the ED95 is 0.05, **Doses 3-5 times higher are recommended for intubation***


What is Cisatracuriums duration of action?

45 minutes when given twice the ED95, and 68 minutes when given 4x ED95


What is the elimination for Cisatracurium?

It undergoes hoffman elimination, and slightly relies on the kidney as well.


What patient population commonly uses Cisatracurium?

Renal disease, because it is mostly eliminated through hoffman.


Which ND-NMBA do you not see as much because it needs to be refrigerated?



What are the ND-NMBA's that are steroidal compounds?

Vecuronium, Rocuronium and Pancuronium.


What is the only long acting NMBA in the US and what is its potency?

Pancuronium. It is highly potent.


What is the only NMBA that produces tachycardia and mild increase in MAP from vagolytic and indirect sympathomimetic effects?



What is the onset of Pancuronium?

ED95 is 0.075 mg/kg (slow) with an intubation dose of 0.14 mg/kg (4 minutes)


What is the duration of action of Pancuronium? How is it eliminated?

80-110 minutes. Primarily the kidney, which accounts for its long duration of action.


What was the first ND-NMBA with a shorter half-life profile to be introduced?



What are the potency and hemodynamic side effects of Vecuronium?

It has no hemodynamic side effects, and it is potent.


What is the ED95 and intubation dose of Vecuronium?

ED95 is 0.03-0.05 mg/kg, Intuation dose is 0.1 mg/kg - significantly higher doses can be given to speed up induction.


What is the duration of action of Vecuronium?

40 minutes


How is Vecuronium metabolized?

It is a derivative of pancuronium and it is mostly eliminated in the urine unchanged, but does have an active metabolite with renal implications


What is the least potent of the ND-NMBA's?



What are some special characteristics of Rocuronium?

It was designed to be more rapid acting.
It has no CV effects
It is commonly used for fasciculation dosing
It is the least potent


What is the ED95 of Rocuronium?

0.3 mg/kg with an intubation dose of 0.6-1.2 mg/kg


What is the duration of Rocuronium?

30-60 minutes


How is Rocuronium eliminated?

Primarily eliminated unchanged in the bile, some in urine. Not metabolized to to any significant degree


Which two ND-NMBA's can cause Tachycardia?

Atracurium (histamine release), and Pancuronium (vagolytic effect)


Which NDNMBA's was designed for use with RSI? What makes this possible?

Rocuronium. It is possible because of low potency and high doses


What are the reversal agents for NMBA's?

Cholinesterase inhibitors (Neostigmine, Edrophonium)
Edrophonium is fast, but short acting because it does not form a stable bond with AChE
Neostigmine forms a more stronger bond that inactivates the AChE
Anticholinergics (Atropine, Glycopyrolate)


How do cholinesterase inhibitors work?

They inhibit AChE at the NMJ, which increases the available ACh to overcome NMBA-induced competitive block.


Recovery from paralysis is a function of two factors. What are they?

Ongoing spontaneous recovery of the NMJ as the NMBA is eliminated.
Increase in ACh in the NMJ due to decrease in AChE


What anticholinergics do we commonly use?

Atropine and Glycopyrolate


What are the anticholinergics that you can use to reverse Edrophonium and Neostigmine?

Edrophonium = Atropine (both are rapid acting in opposite directions) Neostigmine = Glycopyrolate (slower acting and last a little longer)


Why do you see bradycardia with the reversal of NMBA's?

A cholinergic effect (parasympathetic)


Why can we not reverse DNMBA's?

Because they are agonists. They are not blocking the affect of ACh, they are causing the same effect


What guides the decision of anti-cholinergic when reversing ND-NMBA's?

Onset and action. Fast with fast (eg. Atropine for Edrophonium) Slow with slow (e.g.. Glycopyrolate for Neostigmine.


What action should we see if we stimulate the adductor policies (ulnar nerve)?

Adduction of the thumb


What does the Dibucaine number indicate?

The quality of the butyrylcholinesterase enzyme NOT the quantity.


What action should we see if we stimulate the Orbicularis occult (facial nerve)?

Furrowing of the brows


What are the normal, heterozygous and homozygous Dibucaine numbers?

Normal is about 80%
Heterozygous about 40-60%
Homozygous about 20%


What dose of Neostigmine should be given with TOF with 4 twitches, fade and no fade?

Fade = 0.04 mg/kg
No Fade = 0.015-0.025 mg/kg


What dose of Neostigmine should be given with TOF 1-3 twitches?



Why are anticholinergics given with reversal agents?

Reversal agents will cause the build up of ACh in other tissues as well, and some of the ACh will hit muscarinic receptors and cause a variety of unpleasant symptoms like bronchoconstriction, secretion, etc. So anticholinergics are given to counteract this effect.


What dose of Neostigmine should be given with TOF no twitches?

Delay reversal until TOF count = 2