Neuromuscular blockers Flashcards Preview

Summer Pharm (2016) ** > Neuromuscular blockers > Flashcards

Flashcards in Neuromuscular blockers Deck (37):
1

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

2

Potentiates both DNMB and NDNMB

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

3

Potentiates Succlynilcholine

Neostigmine

4

potentiates NDNMB

Dantroline, ketamine

5

Prolongs NMB, especially intermediate NDNMB

Hypothermia

6

decreased pH does what to atricurium?

Prolongs DOA by inhibiting Hoffman elimination

7

Primary elimination of all LONG acting NMB

Renal elimination - can have prolonged block in renal patients

8

Fasciculation increase the risk of....

Hyperkalemia, Myalgias, increased intragastric pressure and aspiration

9

Often times a defasiculating dose is give to this specific population

Head trauma, to offset the risk of increased ICP

10

The defasiculating dose of rocuronium and vecuronium

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

11

DOC for sever liver and renal disease

Cicatricurium - eliminated by Hoffman elimination

12

Which NMB will last longer in liver disease patients?

SCh, and steroidal NMB "oniums" Rocuronium, vecuronium,

13

When is there a detectble NMB with PNS?

when 75-85% of receptors are blocked

14

when is paralysis complete?

90-95% recepros blocked

15

what is the range of adequate muscle blockade for surgery?

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

16

When should PNS start?

Prior to the administration of NMB but after induction of anesthesia

17

What are the most used sites for PNS monitoring

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

18

Succs MOA?

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

19

What is the reversal of succs?

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

20

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

May result in profound bradycardia or asystole

21

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

22

Which NMBs release histamine?

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

23

Which NMBs cause increase/decrease in BP?

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

24

Which NMBs cause increase/decrease in HR?

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

25

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

26

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

27

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

28

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

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

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.

Glycopyrrolate

30

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

Atropine

31

Side effects of anticholinesterases?

Bradycardia Bronchospasm N/V Increased secretions and peristalsis

32

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

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

33

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

One twitch at least

34

What are clinical signs of adequate reversal?

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

35

What does physostigmine reverse?

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

36

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

Echothiopate

37

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

Ulnar nerve Adductor pollicis muscle