Neuromuscular Blocking agent factoids Flashcards
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?
No
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
