(Exam 3) - Non-depolarizing Muscle Relaxants Flashcards
What is the only Short-Acting non-depolarizing NMBD (that is not used anymore)?
Mivacurium (Mivacron)
(slide 37)
Which receptor do Non-Depolarizing muscle relaxants work on?
Nicotinic Acetylcholine Receptors
Slide 3
What is Mivacurium(Mivacron):
Intubating dose:
Onset:
DOA:
With it’s DOA, what has to be considered?
0.15mg/kg
2-3 min
12-20min
Since its DOA is so short, may have to give supplemental doses.
(slide 37)
True or False:
Non-depolarizing drugs only bind to one alpha-subunit
False - They compete for both alpha-subunits. 💁🏻♀️
Slide 3
Since there is no conformational change in the nicotinic acetylcholine receptor, there are no shifts in which electrolytes?
Sodium and Potassium
Slide 3
TOF ratio of _________ is indicative of a successful Non-Depolarizing NMBA block.
< 0.7
Slide 4
What is the only Long-acting NMBD that we have to know/use?
What class of drug is it considered?
What properties does it have?
Induction dose:
Onset:
Duration:
Pancuronium (Pavulon)
Class: Bisquaternary aminosteroid
Properties: Vagolytic (inhibits actions of the vagus nerve)
Induction dose: 0.1 mg/kg
Onset: 3-5 mins
Duration: 60-90 mins
(slide 20)
How many stereoisomers does Mivacurium (Mivacron) have and what are they? Which ones actually have neruomuscular blocking activity?
3 stereoisomers:
Cis-cis
*Cis-trans
*Trans-trans
*NM blocking ability
(slide 38)
You give your patient Rocuronium for intubation, which drug should you give to maintain the paralysis?
Rocuronium - non-depolarizing drugs potentiate the action of other non-depolarizing drugs so both duration and recovery are long if you give a different drug
Slide 4
How is Mivacurium(Mivacron) cleared?
by plasma cholinesterase, but not the same on as succ
(slide 38)
Does Mivacurium (Mivacron) release histamine?
And what additional detail or symptoms are seen about your answer?
Yes it can.
But only at doses that are >3X ED95 (this is never done- almost OD)
Would see:
- Transient MAP drop
- More common with rapid, large doses
- MAP drop more in HTN pts than non-HTN pts
(slide 39)
Pancuronium majorily is eliminated how?
By how much percent?
80% eliminated unchanged in the urine
(slide 21)
CV adverse effects are due to what three things?
- Release of histamine
- Effects on cardiac muscarinic receptors
- Effects on nACh-Rs at autonomic ganglia
Slide 7
Skeletal muscle weakness that occurs weeks to months after NMBDs are discontinued…
Critical Illness Myopathy
Slide 8
Giving what drugs prior to NMBD may enhance risk for critical illness myopathy?
Glucocorticoids
Slide 8
In the presence of LIVER DX, what would we expect when considering the administration of Pavulon?
_________ volume distribution
______ initial dose needed
Prolonged ___________ ___ time
D/t deficient protein production, fluid leaks out grossly throughout the body, thereby causing the following:
⬆️ VD
Larger initial dose is needed
Prolonged elimination 1/2 time
(slide 21)
What class of drug normally causes critical illness myopathy?
Aminosteroid blocker (roc, vec, panc)
Slide 8
Would 75-year-old Pee-paw be a good candidate for receiving Pancuronium?
Why or why not?
No!
Pee-paw has seen more moons than most and thus has a ⬇️ plasma clearance d/t ⬇️ renal function.
(slide 21)
You give Pavulon to your pt undergoing a sloppabotomy (i.e., irrelevant procedure). What cardiovascular effects would you expect to see?
Why?
Where does this medication affect most often?
Will the BP ⬆️ or ⬇️?
⬆️ in HR, MAP, and CO
d/t vagal blockade (remember it’s a vagolytic)
occurs mostly at the SA node
BP increases d/t HR
(slide 22)
CV effects of Pavulon continued.
Why else might we see an ⬆️ in HR, MAP, and CO? (we already said vagal blockade in a prev card)
What does that mean?
Does this mean we’ll have changes in the SVR or inotropy?
d/t SNS activation
This means that we’ll have release of NE presynaptically AND a simultaneous blockade of NE reuptake
No, there will not be changes in SVR or inotropy
(slide 22)
T/F: Pancuronium will cause histamine release
False
(slide 22)
When comparing Intermediate-acting NMBDs with Long-acting NMBDs, we would see a similar _____ of maximum ________.
Intermediate NMBDs would also have a _____ of the duration of Long-acting NMBDs.
Would CV effects be minimal or profound with Intermediate NMBDs?
What type of drugs could antagonize the intermediate NMBDs?
How long before this drug-mediated antagonism would take place?
onset; blockade
1/3
minimal/absent CV effects with Intermediate NMBDs
Anticholinesterase drugs would antagonize Intermediate NMBDs
would take ~20 mins after giving a full induction/intubation dose before antagonism would occur
(slide 24)
List the 4 Intermediate-acting NMBDs.
Vecuronium
Rocuronium
Cisatracurium
Atracurium
(slide 23)
How does acute hypokalemia alter response to NMBD?
- Acute hypokalemia hyperpolarizes cell membrane (increased transmembrane potential)
- Resistance to depolarizing NMBDs.
- ↑ sensitivity to non-depolarizing NMBDs.
Slide 14
How does acute hyperkalemia alter the response to NMBD?
- Acute hyperkalemia decreases membrane potential (partially depolarizes cell membrane)
- ↑ effects of depolarizing NMBDs.
- Resistance to non-depolarizing NMBDs.
Slide 14