Lecture 14 (Exam 3 Nondepolarizing NMBD) Flashcards
Selection of Non-depolarizing NMBD is influenced by what factors?
Onset
Duration of action
Rate of Recovery
Metabolism
What is the MOA of Non-depolarizing NMBD?
Act at pre-junctional sites to block ACh release.
Also acts on BOTH alpha subunits of the post-junctional nAChR.
No conformational change.
Characteristics of Non-depolarizer Blockade.
-Decrease twitch response to _________.
-__________ response to a continuous stimulus.
- TOF ratio _________
-Decrease twitch response to single twitch.
- Unsustained (fade) response to a continuous stimulus.
- TOF ratio <0.7
Characteristics of Non-depolarizer Blockade.
Post-tetanic potentiation
Potentiation of other ___________.
Antagonism by ___________
No _________ during onset.
Potentiation of other non-depolarizing drugs.
Antagonism by anticholinesterase
No fasciculations during onset.
Why is there a fade in twitch response with non-depolarizing NMBD?
Fade suggest some fibers are contracting while some are blocked. Some receptors are more susceptible to NMBD than others.
What happens if you intubate with Vecuronium and you give Rocuronium for maintenance?
The two non-depolarizing NMBDs can potentiate each other and prolong the duration of the recovery period.
The cardiovascular effects of non-depolarizing NMBD are due to what factors?
Release of histamine
Effects on cardiac muscarinic receptors
Effects on nAChRs at autonomic ganglia
Cardiovascular effects from non-depolarizing NMBD are __________ clinically significant.
rarely
The patient often is already on drugs to counter the cardiovascular effects. Fentanyl to counter the tachycardic effects of histamine or pressors to treat the hypotension.
Most NMBDs have a __________ autonomic margin of safety.
Wide
Vec, Roc, Cis
What non-depolarizing NMBD has the same dose for ED95 and autonomic nervous system stimulation?
What is the side effect of this drug?
Pancuronium (sympathomimetic) will result in tachycardia at the ED95 dose. This can be offset by giving a narcotic.
Be mindful in administering pancuronium in patients with coronary artery disease, aortic stenosis, cardiac issues, etc…
What is critical illness myopathy?
Skeletal muscle weakness occurs weeks to months after the NMBD drip is discontinued.
Factors that contribute to critical illness myopathy included:
Patients with __________ who were ventilated for six days.
__________ prior to NMBD may enhance risk.
_________ (chemical classification) blocker
Multi-System Organ Failure
Glucocorticoids
Aminosteroid Blocker
If patients have predosing factors leading to critical illness myopathy, what actions must be taken?
Nerve monitoring (continuous)
More Sedation
More Analgesia
Small Doses of NMBD
What is the altered response if a non-depolarizing NMBD and a volatile anesthetics are concurrently used?
What is the MOA?
There will be a dose-dependent enhancement to the NMBD.
(Desflurane will have the most enhancement > Sevo > Iso)
MOA: Dose-dependent inhibition nAChR
What is the altered response if a non-depolarizing NMBD was given concurrently with loop diuretics, corticosteroids, metoclopramide, and local anesthetics? (3)
Enhance or prolong the blockade d/t depression of cholinesterase activity. Most of these drugs also decrease ACh release. Cause depression of nerve conduction
______ is dosed on ACTUAL body weight.
______ is dosed on IDEAL body weight.
Succinylcholine (Depolarizing NMBD)
Non-depolarizing NMBD
What is the altered response if a non-depolarizing NMBD is given with magnesium?
MOA?
The blockade will be enhanced.
MOA: Decreases prejunctional release of ACh and decreases sensitivity to the postjunctional membrane.
What is the altered response if a non-depolarizing NMBD is given with ephedrine (SNS drug)?
What is the altered response if esmolol is given before induction with a non-depolarizing NMBD?
Faster onset time d/t increased CO and skeletal muscle flow.
If esmolol is given before induction, there will be a delayed onset.
What altered response in non-depolarizing NMBD if there is hypothermia?
MOA? Hint * hepatic
Even with mild hypothermia, Vec and Pancuronium will double in duration.
MOA: Temperature slows down hepatic enzyme activity.
Which non-depolarizing NMBD is not metabolized by the liver but is pH and temperature dependent?
What is the MOA?
Atracurium and Cisatracurium
MOA: temperature-dependent elimination process through Hoffman elimination (need normal temperature and pH) and ester hydrolysis
Acute hypokalemia with NMBD
________ cell membrane.
Resistance to ___________
Increased sensitivity to _________
Acute hypokalemia with NMBD
Hyperpolarize cell membrane.
Resistance to depolarizing NMBD
Increased sensitivity to non-depolarizing NMBD
Hypokalemia will increase the concentration gradient of the K+, and caused more K+ to move out of the cell, increasing resting membrane potential (making the resting membrane potential more negative). This will make the cell harder to depolarize, which is why there is resistance to depolarizing NMBD.
Acute hyperkalemia with NMBD.
There will be a partially ___________ cell membrane.
Increases effect of __________
Resistance to ___________
Acute hyperkalemia with NMBD.
There will be a partially depolarized cell membrane.
Increases effect of depolarizing NMBD
Resistance to non-depolarizing NMBD
Burns are resistant to non-depolarizing NMBD ______ days post-injury.
When does the resistance go away?
What non-depolarizing drug is the exception to burns, and what is the dose?
Ten days
Resistance goes away in 60 days.
Rocuronium 1.2mg/kg