NMB an Reversals Flashcards
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)
Potentiates Succlynilcholine
Neostigmine
potentiates NDNMB
Dantroline, ketamine
Prolongs NMB, especially intermediate NDNMB
Hypothermia
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)
