Local Anesthetics and Neuromuscular Blockers B&B

Question 1

what are the 2 classes of local anesthetics?

Answer 1

1. amides - lidocaine, mepivacaine, bupivacaine
2. esters - procaine, cocaine, benzocaine, tetracaine

Question 2

all local anesthetics are weak ____

how does this contribute to their mechanism?

Answer 2

weak bases!

1. unprotonated/uncharged form is able to cross membranes
2. inside cell, binds H+ and becomes protonated/charged and is trapped within cell
3. from inside, blocks Na+ channels to exert anesthetic effect

therefore, acidic environments require more drug for effect!

Question 3

why is epinephrine sometimes given with local anesthetics? (2 reasons)

Answer 3

epi causes vasoconstriction —>

1. less bleeding during procedures
2. less washout = more local effect

Question 4

which types of nerve fibers are more readily blocked by local anesthetics and why?

Answer 4

small fibers > large fibers (ok this makes sense)

myelinated > unmyelinated (ok why?)

why: myelinated fibers are v dependent on nodes of Ranvier for saltatory conduction - just blocking a couple of these wipes the nerve out

Question 5

which sensory modalities are lost first vs last (4 total) with local anesthetics and why?

Answer 5

local anesthetics work best on small, myelinated fibers and worst on large, unmyelinated fibers

so…

pain is lost first, followed by temperature, touch, and lastly pressure

Question 6

which local anesthetic is considered most cardiotoxic?

Answer 6

[generally pretty safe but if you had to choose]

bupivacaine is most cardiotoxic

Question 7

what is the cardiovascular effect of MOST local anesthetics and which is the exception to this?

Answer 7

most can cause hypotension, arrhythmia, bradycardia, heart block

however, cocaine is exception - can cause HTN, vasoconstriction

Question 8

which 3 drugs can cause acquired methemoglobinemia, and how is this treated?

Answer 8

1. local anesthetics (benzocaine)
2. nitric oxide
3. dapsone (antibiotic)

tx: methylene blue

[recall Fe3+ = methemoglobin, cannot bind O2 and also prevents remaining Fe2+ from releasing O2]

Question 9

After an endoscopy procedure, a patient experiences SOB. Their O2 sat is 88, but their PaO2 is normal. Blood draw appears “chocolate brown.” What do you think is going on?

Answer 9

methemoglobinemia - can be caused by benzocaine (local anesthetic used for throat analgesia), NO, and dapsone (antibiotic)

Fe3+ cannot bind O2, turns blood chocolate brown! O2 sat will be variable because methemoglobin interferes with device function

Question 10

what kind of drugs are succinylcholine, tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium? which of these is different in mechanism?

Answer 10

neuromuscular blockers (paralytics)

all block depolarizing EXCEPT for succinylcholine which is a depolarizing agent (sustained depolarization prevents muscle contraction)

Question 11

describe the MOA of succinylcholine

Answer 11

depolarizing neuromuscular blocker - basically 2 ACh stuck together, very strong nicotinic agonist

sustained depolarization prevents muscle contraction (NOT metabolized by AChE)

Phase 1: depolarization, muscle fasciculation
Phase 2: desensitization, muscle does not respond to ACh

Question 12

what are the main side effects of succinylcholine? (2)

Answer 12

depolarizing neuromuscular blocker (sustained depolarization prevents muscle contraction)

1. hyperkalemia - caution in burn patients, dialysis patients (already have high K+, can send into cardiac arrest!)
2. malignant hyperthermia

Question 13

how do non-depolarizing neuromuscular blocking agents (NMBA) work?

ex: tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

Answer 13

competitive antagonists of nicotinic ACh receptors —> paralysis

note - may cause marked histamine release (hypotension —> compensatory tachycardia)

can be reversed with AChE inhibitors (physostigmine, neostigmine, pyridostigmine, edrophonium), causing ACh to flood the synapse (overcome competitive inhibition)

Question 14

what is the main side effect of non-depolarizing neuromuscular blocking agents (NMBA)?

ex: tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

Answer 14

[competitive antagonists of nicotinic ACh receptors —> paralysis]

marked histamine release causes hypotension —> compensatory tachycardia

Question 15

code blue =

what procedure will be done? which 2 drugs are required?

Answer 15

code blue = respiratory distress

response is rapid sequence intubation: standard practice for emergent intubation, using etomidate (sedation) + succinylcholine (flaccid - rapid onset/offset neuromuscular blocker)