Bb Neuromuscular Blockade

Front 1

what are the characteristics of a depolarizing phase-1 block?

Back 1

no fade to tetanus or twitch, TOF ratio of 1, sustained tetanus, no post-tetanic potentiation, no reversal from anticholinesterase drugs, fasciculations

Front 2

What is the priming principle?

Back 2

method to shorten time to maximal relaxation for RSI by pretreatment with a small dose of a nondepolarizer, give nondepolarizer 5 min before depolarizer, it should be given in 1/10th the intubating dose

Front 3

What is the typical dose of narcan?

Back 3

0.01mg/kg

Front 4

In what conditions do you see reduced cholinesterase activity?

Back 4

BLOMP: burns, liver disease, organophosphates, echothiophate, malnutrition, pregnancy

Front 5

What are causes of prolonged paralysis after administration of neuromuscular blockers?

Back 5

phase 2 block, atypical pseudocholinesterase, reduced cholinesterase activity, inadequate reversal of nondepolarizer

Front 6

What drugs and conditions can cause inadequate reversal of nondepolarizers?

Back 6

SEDH: Systemic disease(MG, MD), Electrolytes(increasd mag, lithium, na, low K, ca), Drugs(antibiotics, volatile and local anesthetics, cardiovascular drugs, ketamine, lasix), Hypothermia

Front 7

What is the difference in the dose of atropine given with edrophonium and neostigmine?

Back 7

edroponium give 10ug/kg, neostigmine give 15ug/kg

Front 8

How do muscarinic side effects of edrophonium compare with neostigmine and pyridostigmine?

Back 8

muscarinic side effects with edrophonium are less

Front 9

How much time should you allow for anticholinesterases to antagonize the block?

Back 9

15-30min

Front 10

What can happen when giving doses of neostigmine larger than 5mg?

Back 10

may potentiate the block

Front 11

What happens to the duration of action of neostigmine in renal failure?

Back 11

lasts longer(should reduce dose by 50-75%)

Front 12

What are causes of resistance to nondepolarizers?

Back 12

burns, increased K or ca, paralyzed extremity

Front 13

What are the effects of pancuronium and dTC on the cardiovascular system?

Back 13

pancuronium: anti-vagal and sympathomimetic, it is preferred when hypotension and bradycardia are present; d-TC: releases histamine

Front 14

When should you extubate a patient who has had a neuromuscular block?

Back 14

awake and alert with stable vital signs, and stable circulatory status, good blood gas of 40%(PaO2>80 and PaCO2<50 with normal pH, MIF more negative than -20, VC>15cc/kg, strong grip and head lift for 10s(after being reversed)

Front 15

How is pancuronium metabolized and eliminated?

Back 15

metabolized in the liver; 80% excreted in urine

Front 16

How is d-TC metabolized and eliminated?

Back 16

minimal hepatic metabolism(good in renal failure), 10% eliminated in bile and the rest is eliminated renally

Front 17

How is vecuronium metabolized and eliminated?

Back 17

hepatic metabolism with mainly biliary excretion, effect of renal failure on vecuronium is minimal

Front 18

How is the onset and duration of mivacurium different in children versus adults?

Back 18

faster onset and shorter duration of action in children, intubating dose is larger(0.2mg/kg versus 0.15mg/kg in adults)

Front 19

What are the adverse effects of mivacurium?

Back 19

most frequent is transient flushing; higher doses can cause histamine release and hypotension, bronchospasm is rare, longer block in renal or liver disease

Front 20

What is the onset, duration and type of elimination of rocuronium?

Back 20

onset 60-90s, duration 30min, biliary excretion(up to 30% renal excretion,

Front 21

How should you alter dosing in renal or liver failure for rocuronium?

Back 21

dosing should be decreased for both, but there should be a larger dose decrease in liver failure

Front 22

What drugs inhibit pseudocholinesterase?

Back 22

Echotiophate, anticholinesterase, trimethaphan, pancuronium

Front 23

How does magnesium affect neuromuscular blockade?

Back 23

decreases the release of ACh from the nerve terminal, decreases the sensitivity of the end-plate to the effects of ACh; potentiates the effects of SCh and nondepolarizers

Front 24

What can potentiate the NM blockade?

Back 24

anesthetics, CV drugs, lasix, ketamine and increased Li, Na, mag, abx, botulism, procaine, decreased ca, K, hypothermia, respiratory acidosis, alkalosis, hepatic dysfxn

Front 25

Which antibiotics do not potentiate neuromuscular blockade?

Back 25

Penecillins, cephalosporins

Front 26

How is the action of SCh terminated?

Back 26

diffusion away from the motor endplate(little or no pseudocholinesterase at NMJ)

Front 27

What is dibucaine?

Back 27

amide local anesthetic that inhibits pseudocholinesterase

Front 28

In the presence of atypical homozygous pseudocholinesterase how is SCh broken down and how long does it take?

Back 28

nonenzymatic hydrolysis; 1-3hrs

Front 29

What is the characteristics of the electrical current applied with a train of four stimulation?

Back 29

4 2hz stimulations over 2s

Front 30

How is the action of ACh terminated?

Back 30

acetylcholinesterase

Front 31

Why can't nondepolarizers and SCh easily cross lipid membranes?

Back 31

nondepolarizers: too large
SCh: too highly ionized

Front 32

What antibiotics potentiate neuromuscular blockade?

Back 32

tetracyclines, aminoglycosides, lincosamide, polymixins,

Front 33

What is the average clinical duration of cisatracurium?

Back 33

around 1hr

Front 34

What muscles groups are the most, and least sensitive to neuromuscular blocking drugs?

Back 34

diaphragm is most resistant, respiratory ,facial and upper airway are intermediate, extremity and abdominal muscles are the most sensitive

Front 35

Disappearance of the fourth, third, second twitch correspond to how much residual block?

Back 35

2nd-90%, 3rd-80%, 4th-75%