M5 Muscle Relaxants Flashcards
What is phase 1 va phase 2 block?
Both terms referee to succ
Phase 1; continues end plate depolarization & ms relaxation
Phase 2; is a prolonged depolarization of prejunctional muscle endplate result in conformational changes to Ach-Rec such that resume NDNMB (Caused by increased activity of Na-K Atpase puking K in and Na out restoring ms function and rec not responding appropriately to succ)
Medications concomitant use with succinylcholine that prolongs it’s duration?
Common one is Ecothiophate (cholenistrase inhibitor drops used for glucoma)
Others; esmolol, pancuronium, cyclophosphamide, phenelzine).
Psudocholeniterase/Butyrylcholinesterase deficiency types?
1- heterozygous results in ~ 30 min block
2- homozygous results in 4-8 hours block after succinylcholine
What test used to differentiate types of cholinesterase enzyme deficiency?
Dibucaine
It inhibits choleinasterase enzyme and then measuring the % of the enzymes remained uninhibited in blood.
40-60% heterozygous
20 or less homozygous
Highest risk timing of hyperkalaemic cardiac arrest following succ is …
Between 7-10 days following denervation.
Most likely to result from NS. Fasciculation following succ
Increased ICP and Abdominal pressure.
Myalgia is not 100% strongly associated.
Muscle relaxant most likely cause histamine release?
Mivacurium & atracurium
The benzylisoquinolone NMB
Which muscles first to recover after NMB?
Most resistance to NMB,
Diaphragm/larynx Abdomen > then oculi/ geniohyoid/adductor pollicis.
Because adductor pollicis more sensitive to NMB it’s recovery a better indicator of all other muscles are recovered.
Mention the common situation that potentiate NMB?
Volatiles, Mg (as in OB), hypoCa, hypoK, acidosis, hypothermia.
Extreme ages (neonates and adults),
Will patients with CP & SLE be resistant or sensitive to NMB?
Some degree of resistance to NDNMB and normal response with succinylcholine.
For SLE, it will be sensitive to NDNMB & succinylcholine (in general, autoimmune dis have hypersensitivity to all ma relaxation)
Just memorize this
3 Hot points about cisatracurium
1) Hoffmann process is slowed with hypothermia
2) metabolized by liver and excerpted by kidney
3) Laudanosine is breakdown product and it can stimulate CNS at extremely high levels (esp with atracurium because it’s less potent then cis and therefore need greater dose)
A 2 NMB that metabolized by psudocholinesterase and relaxation could be prolonged in atypical psudocholinesterase ptn’s?
Micacurium & succinylcholine
Which is better for long term gtt in ICU patient?
Which NMB has active metabolite should be avoided in long gtt?
Cisatricurium.
Vecuronium led to prolonged polyneuropathy with weakness and therefore its C/I for long gtt, esp in setting of steroid use
Which NDNMB is entirely devoid of metabolism (do not undergo metabolism at all, instead get excreted out as it is)?
Rocuronim
Out of all other NDNMB. Therefore, in setting of liver dysfunction with poor bile excretion, Roc is not metabolized and not decreased, prolonging it’s blockade.
What is a new parameter included in extubation criteria?
RSBI (rapid shallow breathing index) which is RR/TV and should be <105
It means ptn ventilating, with good lung compliance and strong which indirect indicator of strength.
