What are clinical indicators of residual NMB?
TOF 0.9 = less risk. Sustained head lift (5s), Vital capacity >5ml/kg, grip strength, eye opening, Generation of a negative pressure breath
Potentiates both DNMB and NDNMB
antibiotics, antidysrhytmics, local anesthetics (even those given in the field), inhaled anesthetics and lithium, Diuretics (hypokalemia)
Prolongs NMB, especially intermediate NDNMB
decreased pH does what to atricurium?
Prolongs DOA by inhibiting Hoffman elimination
Primary elimination of all LONG acting NMB
Renal elimination - can have prolonged block in renal patients
Fasciculation increase the risk of....
Hyperkalemia, Myalgias, increased intragastric pressure and aspiration
Often times a defasiculating dose is give to this specific population
Head trauma, to offset the risk of increased ICP
The defasiculating dose of rocuronium and vecuronium
1/10 of intubating dose, roc=0.06mg/kg and vec=0.01mg/kg
DOC for sever liver and renal disease
Cicatricurium - eliminated by Hoffman elimination
Which NMB will last longer in liver disease patients?
SCh, and steroidal NMB "oniums" Rocuronium, vecuronium,
When is there a detectble NMB with PNS?
when 75-85% of receptors are blocked
when is paralysis complete?
90-95% recepros blocked
what is the range of adequate muscle blockade for surgery?
85-90% receptor blockade (one to two twitches)
When should PNS start?
Prior to the administration of NMB but after induction of anesthesia
What are the most used sites for PNS monitoring
Ulnar nerve - adductor pollicis(lesslikelyhood of direct muscle stimulation, Facial nerve and paroneal nerve- dorsiflexion
Succs binds to alpha subunit of Ach nicotinic receptors, channel opens, motor endplate depolarizes, one single contraction occurs, channels stay open and another action potential can't be initiated (due to inactivated Na channels) until succs diffuses back into circulation
What is the reversal of succs?
There isn't one! Sucks block is terminated by diffusion of succs away from the NMJ
What is the black box warning of succs having to do with pediatric administration?
May result in profound bradycardia or asystole
What is a dibucaine number? What does it indicate? What does this have to do with succs?
Indicates genetic make-up of a person with regard to pseudocholinesterase If you have a low dibucaine number, succs will act longer
Which NMBs release histamine?
D-tubo - moderate amount Mivacurium - small amount Atracurium - small amount Succs- small amount
Which NMBs cause increase/decrease in BP?
Decrease- mivacurium, D-tubo, succs Increase- pancuronium
Which NMBs cause increase/decrease in HR?
Decrease- succs Increase- mivacurium, atracurium, D-tubo, pancuronium (None- roc, vec)
What drugs have an effect on depolarizer or non-depolarizer NMBs
Antibiotics Cholinesterase inhibitor (succs only) Antidysrhythmics Dantrolene, ketamine (NDMRs only, not sure about succs) Inhalational agents Locals
What is the priming principle? (AKA the defasciculating dose)
Speeds onset of NDMRs; prevents succs-induced fasciculations Give 10% of intubating dose 5 min before induction The initial small dose primes spare receptors without producing paralysis the time
What class of drugs will reverse nondepolarizing NMBs? How does it work?
Anticholinesterases, they competitively binds to and inhibits AChE in the NMJ, increasing availability of ACh
Which NMB reversal is most reliable in a deep block (over 90% receptors)
Neostigmine Note: Nothing can block a profound block (100%)
What anticholinergic has a similar onset and duration to Neostigmine, and is mixed together to decrease side effects? It is also used with pyridostigmine.
Due to similar onset times, which anticholinergic is endrophonium administered with?