Neuromuscular blockers

Question 1

What are clinical indicators of residual NMB?

Answer 1

TOF 0.9 = less risk. Sustained head lift (5s), Vital capacity >5ml/kg, grip strength, eye opening, Generation of a negative pressure breath

Question 2

Potentiates both DNMB and NDNMB

Answer 2

antibiotics, antidysrhytmics, local anesthetics (even those given in the field), inhaled anesthetics and lithium, Diuretics (hypokalemia)

Question 3

Potentiates Succlynilcholine

Answer 3

Neostigmine

Question 4

potentiates NDNMB

Answer 4

Dantroline, ketamine

Question 5

Prolongs NMB, especially intermediate NDNMB

Answer 5

Hypothermia

Question 6

decreased pH does what to atricurium?

Answer 6

Prolongs DOA by inhibiting Hoffman elimination

Question 7

Primary elimination of all LONG acting NMB

Answer 7

Renal elimination - can have prolonged block in renal patients

Question 8

Fasciculation increase the risk of….

Answer 8

Hyperkalemia, Myalgias, increased intragastric pressure and aspiration

Question 9

Often times a defasiculating dose is give to this specific population

Answer 9

Head trauma, to offset the risk of increased ICP

Question 10

The defasiculating dose of rocuronium and vecuronium

Answer 10

1/10 of intubating dose, roc=0.06mg/kg and vec=0.01mg/kg

Question 11

DOC for sever liver and renal disease

Answer 11

Cicatricurium - eliminated by Hoffman elimination

Question 12

Which NMB will last longer in liver disease patients?

Answer 12

SCh, and steroidal NMB “oniums” Rocuronium, vecuronium,

Question 13

When is there a detectble NMB with PNS?

Answer 13

when 75-85% of receptors are blocked

Question 14

when is paralysis complete?

Answer 14

90-95% recepros blocked

Question 15

what is the range of adequate muscle blockade for surgery?

Answer 15

85-90% receptor blockade (one to two twitches)

Question 16

When should PNS start?

Answer 16

Prior to the administration of NMB but after induction of anesthesia

Question 17

What are the most used sites for PNS monitoring

Answer 17

Ulnar nerve - adductor pollicis(lesslikelyhood of direct muscle stimulation, Facial nerve and paroneal nerve- dorsiflexion

Question 18

Succs MOA?

Answer 18

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

Question 19

What is the reversal of succs?

Answer 19

There isn’t one! Sucks block is terminated by diffusion of succs away from the NMJ

Question 20

What is the black box warning of succs having to do with pediatric administration?

Answer 20

May result in profound bradycardia or asystole

Question 21

What is a dibucaine number? What does it indicate? What does this have to do with succs?

Answer 21

Indicates genetic make-up of a person with regard to pseudocholinesterase If you have a low dibucaine number, succs will act longer

Question 22

Which NMBs release histamine?

Answer 22

D-tubo - moderate amount Mivacurium - small amount Atracurium - small amount Succs- small amount

Question 23

Which NMBs cause increase/decrease in BP?

Answer 23

Decrease- mivacurium, D-tubo, succs Increase- pancuronium

Question 24

Which NMBs cause increase/decrease in HR?

Answer 24

Decrease- succs Increase- mivacurium, atracurium, D-tubo, pancuronium (None- roc, vec)

Question 25

What drugs have an effect on depolarizer or non-depolarizer NMBs

Answer 25

Antibiotics Cholinesterase inhibitor (succs only) Antidysrhythmics Dantrolene, ketamine (NDMRs only, not sure about succs) Inhalational agents Locals

Question 26

What is the priming principle? (AKA the defasciculating dose)

Answer 26

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

Question 27

What class of drugs will reverse nondepolarizing NMBs? How does it work?

Answer 27

Anticholinesterases, they competitively binds to and inhibits AChE in the NMJ, increasing availability of ACh

Question 28

Which NMB reversal is most reliable in a deep block (over 90% receptors)

Answer 28

Neostigmine Note: Nothing can block a profound block (100%)

Question 29

What anticholinergic has a similar onset and duration to Neostigmine, and is mixed together to decrease side effects? It is also used with pyridostigmine.

Answer 29

Glycopyrrolate

Question 30

Due to similar onset times, which anticholinergic is endrophonium administered with?

Answer 30

Atropine

Question 31

Side effects of anticholinesterases?

Answer 31

Bradycardia Bronchospasm N/V Increased secretions and peristalsis

Question 32

Which would you use succhs for, a bronchospasm or laryngospasm?

Answer 32

Laryngospasm Succs can actually make the bronchospasm worse Note: use more gas or ketamine to break the bronchospasm

Question 33

In order to reverse the patient, they must have how many twitches present, if any?

Answer 33

One twitch at least

Question 34

What are clinical signs of adequate reversal?

Answer 34

Head lift, cough, swallow Spontaneous ventilation Open eyes, protrude tongue

Question 35

What does physostigmine reverse?

Answer 35

Reverses confusion/disorientation following atropine/scopalamine Reverses somnolence with opioids/valium/versed/IA/ketamine Usually only used bc provider error

Question 36

Which drug is the only organophosphate anticholinesterase drug used clinically, lowers IOP, useful in treating glaucoma, and may prolong DOA of succs?

Answer 36

Echothiopate

Question 37

What is the preferred nerve and correlating muscle used for peripheral nerve stimulation (PNS) to detect twitches?

Answer 37

Ulnar nerve Adductor pollicis muscle