Non-Depolarizing Muscle Relaxants (3) Flashcards
How do we decide which NDMB to use?
influenced by differences in
* Onset
* Duration of action
* Rate of recovery
* Metabolism
usually base choice on DOA and comorbidities of the pt
What is the MOA of NDMB?
- Act at pre-junctional sites to block Ach release
- Competitive inhibitors for alpha subunits on nACHRs
- Bind and do not cause conformation change
What are characteristics of NDMB associated with nerve stimulation and reversals?
- Decreased twitch response to a single stimulus
- Unsustained response (fade) to continuous stimulus
- TOF ratio < 0.7
- Post-tetanic potentiation
- Potentiation of other non-depolarizing drugs
- Antagonism by anticholinesterase drugs
- No fasciculations during onset
What does the “fade” with NDMB suggest?
Some fibers are contracting while some are blocked
- some are more susceptible to NMBD
What are adverse side effects to NDMB?
- Cardiovascular effects
- Critical illness myopathy
- Altered responses
What causes cardiovascular effects associated with NDMBs?
- release of histamine
- effects at cardiac muscarinic receptors
- effects on nAchRs at autonomic ganglia
What are the cardiovascular effects associated with NDMBs?
- Varies between patient d/t underlying disease and preop meds
- rarely clinically significant
What is a autonomic margin of safety?
Difference between dose that produces blockade (ED95) and dose that creates circulatory effects
What is the autonomic margin of safety for pancuronium?
Same as the normal dose
What is critical illness myopathy?
Skeletal muscle weakness
When can critical illness myopathy occur?
- Weeks to months after NMBD discontinued
- patient with multiorgan fx vent >6 days
- usually from aminosteroid blocker
What potentially enhances risk of critical illness myopathy?
Large dose glucocorticoids prior to NMBD
What is the MOA of critical illness myopathy?
unknown
Why do you want to stick with the same NDMB once you pick one?
If you switch to another one to redose then they compound on each other and it will be hard to get pt reversed
How do volatiles affect NMBs?
Dose dependent enhancement of muscle relaxation with onset as early as 30 minutes
Des>Sevo>Iso
What are some drugs that enhance or antagonize blockade and what is the MOA?
Diuretics, Corticosteroids, Metoclopromide, LA
- increase Ach release
- depression of cholinesterase activity
- depression of nerve conduction
Magnesium ________ blockade of NMBs
enhances
What is MOA of magnesium increasing non depolarizing NMBs?
- decreases prejunctional release of Ach
- decreases sensitivity to postjunctional membranes
What does giving ephedrine prior to non-depolarizing NMBs cause?
Decrease onset time from increase in CO and skeletal muscle flow
How does esmolol prior to induction affect non-depolarizing NMBs?
delays onset of the paralytic
Why is it important to prevent hypothermia in patients?
Even mild hypothermia double duration of vec and pancuronium through slowing of hepatic enzyme activity
Which NDMB are somewhat temperature dependent on metabolism?
Atracurium and Cisatracurium
- hoffman elimination and ester hydrolysis (need to have pretty close to normal body temp or the drugs action will be prolonged)
What changes in potassium are associated with NMBDs?
Acute hypokalemia
- hyperpolarize the cell
- resistance to depolarizing NMBDs
- increased sensitivity to non depolarizing NMBD
Acute hyperkalemia
- decreases Vrm (partial depolarizes cell)
- increases effects of depolarizing NMB
- resistance to non-depolarizing NMBs
When do burn patients have increased resistance to non-depolarizing NMBs?
10 -60 days post injury → need more of drug to have the same effect