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Local Anesthetics Flashcards

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1
Q

What two things affect nerve conduction velocity

A

myelin
diameter (^diameter > ^ conduction velocity)

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2
Q

order of block onset in nerve types

A
  1. B fibers
  2. C fibers
  3. Alpha Gamma and delta fibers
  4. Alpha alpha and beta
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3
Q

what is nerve resting membrane potential and it’s primary determinant?

A

-70mv and K is the primary determinant

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4
Q

what is nerve typical threshold potential? and it’s primary determinant?

A

-55mv and Ca++ is the principal determinant

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5
Q

LA mech of action

A

reversibly bind alpha subunit inside the voltage gated sodium channels.

can only bind channels in the open/active or close/inactive state. cannot bind channels in the resting state

After injection the lipid soluble uncharged base portion diffused through the nerve. a new equilibrium is established and the conjugate acid is what actually bind the sodium channel.

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6
Q

what are the three main compents of LA chemical structure? which ones determines LA class?

A

benzene ring
intermediate side chain - determines ester vs amide class
tertiary amine

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7
Q

Name the Ester LAs

A

benzocaine
cocaine
procaine
tetracaine
Chloroprocaine

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8
Q

name the amide LAs

A

“two is”
bupivicaine
dibucaine
lidocaine
mepivicaine
ropivicaine

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9
Q

how are amide LAs metabolized?

A

P450 system

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10
Q

how are ester LA metabolized?

A

pusdocholinesterase

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11
Q

which LA class exhibits cross sensitivity throughout the class?

A

ester types

if allergy to ester LA don’t use any ester LAs

if allergy to one amide LA okay to use another amide LA but make sure it is preservative free

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12
Q

allergy to which class of LA is more common? what causes the allergic reaction?

A

more common to esters

Ester LA are derivatives of para-aminobenzoic acid, which is typically what causes the allergic reaction

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13
Q

why must you avoid LAs with preservatives is a pt has any allergy to ANY LA?

A

methylparaben is a preservative and is similar to PABA so it could also cause an allergic reaction.

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14
Q

What are primary and secondary determinants of LA onset of action?

A

primary is Pka

seconday: dose and concentration

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15
Q

what are primary and secondary determinants of LA potency?

A

primary: lipid solubility
secondary: intrinsic vasodilating activity

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16
Q

primary and secondary determinants of LA duration of action?

A

primary: protein binding
secondary: lipid solubility, intrinsic vasodilating capabilities, addition of vasoconstrcitors

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17
Q

describe LA vasoconstrictive/vasodilating properties

A

in small doses (sub clinical use) LA cause vasoconstrcition.

in larger doses (clinical use dose) LAs cause vasodilation. Some cause more than other

Cocaine: exception, intense vasoconstricting properties

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18
Q

cocaine mech of action

A

inhibits re-uptake of NE

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18
Q

which two LA have no intrinsic vasodilating properites according to some texts?

A

ropivicaine
chloroprocaine

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19
Q

which LA has zero protein binding?

A

chloroprocaine

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20
Q

how does the Pka of ester LA compare to amide LAs?

A

Pka of all ester LAs is higher than Pka of amide LAs

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21
Q

which two factors affect drug ionization?

A

pH of solution
pKa of the drug

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22
Q

when is ionziation greatest in relation to pH and Pka?

A

greatest ionization when Pka is far from pH

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23
Q

how is onset affected by Pka and pH? what is the exception?

A

the closer Pka is to pH the faster the onset.

Exception: chloroproaine becuase it is so concentrated still has a fast onset even though pKa is not close to pH.

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24
List area from most to least vascular uptake
Iced Tittis In Igloos Can Exacerbate Boners for some Suckers IV tracheal intrapleural intercostal caudal epidural brachial plexus femoral sciatic subcutaneous
25
Exparel max dose
266mg
26
what can exparel be mixed with?
LR, NS, or bupivicane
27
when is exparel contra indicated?
paracervical use in obsetric population
28
when/where is exparel use not reccomended?
epidural, intrathecal, intrarticular, or during pregnancy
29
what happens if exparel is mixed with LA other than bupiviane?
will disrupt liposomal structure and can cause immediate release of bupivicane
30
rules of exparel use with lidocaine and bupivicane?
after lidocaine infiltration must wait 20min before exparel admin after exparel infiltration: no bupivicane in any form for at least 96hrs
31
Amide LA max doses
levobupi. 2mg/kg or 150mg bupivicane 2.5mg/kg or 175mg bupi with epi. 3mg/kg or 200mg ropi 3mg/kg or 200mg lidocaine. 4.5mg/kg or 300mg mepivicaine 7mg/kg. or 400mg lido with epi 7mg/kg or 500mg prilocaine. 8mg/kg. or 500mg < 70kg and 600mg > 70kg
32
Ester LA max doses
procaine 7mg/kg or 350-600mg chloroprocaine 11mg/kg or 800mg chloroprocaine w epi. 14mg/kg or 1,000mg
33
what is abnormal about benzocaine? what is a significant risk with its use?
Pka is 3.5 so it is totally non-ionized at physiologic pH. all other LA work by the conjugate acid binding the sodium channel. methemoglobinemia is a significant risk
34
most common cause of LAST?
intravascular injection during regional
35
36
what is the most frequent, as well as the first symptom of last? waht is the exception?
seizure exception: first symptom of last with bupivicaine is cardiac arrest
37
38
is last more common with PNBs or epidurals?
PNBs
39
symptoms of plasma Lidocaine concentration 1-5mcg/ml
analgesia
40
symptoms of plasma Lidocaine concentration 5-10mcg/ml
Neuro: tinnitus skeletal m. twitching perioral numbness restlessness vertigo blurred vision CV: hypotension myocardial depression
41
symptoms of plasma Lidocaine concentration 10-15mcg/ml
seizure loss of consciousness
42
symptoms of plasma Lidocaine concentration 15-25mcg/ml
coma resp arrest
43
symptoms of plasma Lidocaine concentration >25mcg/ml
CV collapse
44
what 3 things increase risk of CNS toxicity from LAs and why?
1. hypercarbia 2. hyperkalemia 3. metabolic acidosis 1. increases cerebral blood flow so ^ drug delivery to the brain. Also decreases protein binding so there is more free fraction of drug available to enter brain 2. increases resting membrane potential and neurons are more likely to depolarize 3. decreases conduction threshold and favors ion trapping in the brain
45
what three things decrease risk of CNS toxicity for LAs?
1. hypocarbia 2. hpokalmeia 3. CNS depressants - raise seizure threshold
46
which two things affect LA ability to cause CV toxicity?
1. affinity for voltage gated Na chanels in active and inactive states 2. rate of dissociate form receptors during diastole
47
why does bupi have a higher risk of CV toxicity than lidocaine?
bupi has a greater affinity for receptors and a slower rate of disocciation during diastole
48
list the LAs in order from most to least difficult to resuscitate following CV toxicity
bupi>levobupi>ropi>lidocaine
49
what is the main risk of Cocaine toxicity?
SNS stimulation
50
what drugs warrant avoidance of cocaine?
MAOIs TCAs sympathomimetic drugs
51
how to treat cocaine toxicity?
alpha blockers before beta blockers
52
cocaine dose
1.5-3mg/kg or < 150-200mg
53
LAST tx
1. manage airway 2. tx seizure 3. ACLS with modification 4. Intralipid (20% lipid emulsion)
54
how should you manage airway during last?
100% FiO2 because hypoxia worsens symptoms
55
how to treat seizures from last
give benzo, dont give propofol if benzos are ineffective can give small dose sux or roc. this will decrease muscle contraction and associate increase in oxygen consumption avoiding hypoxemia and acidosis. this won't stop seizure activity in the brain though
56
ACLS modifications for LAST
avoid epi, it hinders effectiveness of intralipid. if you must give, keep dose <1mcg/kg avoid: vaso, lidocaine, procanamide, BB, and CCB amio is agent of choice for vent dysrhythmias if ACLS is unsuccessful prep for cardiac bypass.
57
Lipid Emulsion dosing for LAST
>70kg 100ml bolus over 2/3 min 250ml infusion over 15-20min <70kg 1.5ml/kg bolus over 2-3min 0.25ml/kg infusion if pt remains unstable repeat bolus and double the infusion continue for 15min after CV stability
58
lipid emulsion recommended max dose?
12ml/kg
59
lipid emulsion mech of action
lipid sink impairs LA binding to voltage gated Na channels
60
is lipid emulsion therapy safe in pregancy?
yes
61
what is a theoretical concern with intralipid use?
pacreatitis 2ndary to hyperlipidemia and hypermylasemia (amylase)
62
most common cause of death from liposuction?
PE
63
why is tumescent anesthesia used during liposuction?
for patient comfort
64
what is tumescent lidocaine made up of?
NS lidocaine bicarb epi
65
Tumescent lidocaine max dose
55mg/kg
66
with liposuction serum lidocaine levels seldom get higher than?
1.5mcg/ml
67
when doe plasma concentrations peak from tumescent lidocaine and when is it totally eliminated from the body?
peak 12 hours elminiated at 36hours
68
when should tumescent lidocaine dose me reduced?
when taking any medications that inhibit CYP 3A4 or CYP1A2
69
when can you do MAC vs GA for lipsuction?
if tumescent volume small MAC is okay if volume >2-3L GA is reccommended
70
what are two complications that can occur from tumescent lidocaine?
fluid overload and pulm edema
71
How is methemoglobin formed?
when iron molecule (Fe+2) on hgb is oxidized to ferrous form Fe+3
72
what two ways does methemoglobinemia decrease O2 carrying capacity?
1. methgb can't bind O2 2. shifts oxy-hgb diss curve to the left
73
drugs than can cause methgb?
benzocaine cetacaine prilocaine EMLA cream phenytoin nipride nitro
74
s/s of methgbemia
hypoxia not fixed by ^ FiO2 cyanosis chocolate colored blood tachycardia tachypnea changes is LOC
75
spo2 reading with methemoglobinemia
85%
76
what do you need to diagnois methgbemia?
co-oximieter
77
cyanosis in the presence of normal to high PaCO2 suggests what?
methgbemia
78
methgbemia tx
methyleme blue 1-2mg/kg over 5min max dose is 7-8mg/kg
79
how does methylene blue treat methgbemia?
reduces methgb back to hgb
80
when will methyele blue be ineffective in treating methgbemia? how do you treat in this situation?
pt with glucose-6phosphate reductase deficiency. treat with exchange transfusion
81
patient population that is at higher risk for methgbemia and why?
neonates because they are relatively deficient in methgb reductase
82
What is EMLA cream made of?
50% lidocaine 50% prilocaine
83
EMLA cream can provide analgesia how quickly? and peaks when?
analgesia within 1hr and peaks in 2-3hours
84
what skin conditions increase risk of toxicity from EMLA cream?
psoriasis, eczema, and skin wounds can increase risk of toxicity
85
how can EMLA cream cause methgbemia?
prilocaine is metabolized to 0-toluidine which oxidzes hgb to methgb
86
who are more likely to become toxic form emla cream?
infants and small children
87
where can you apply EMLA cream?
only to intact skin and never to mucous membranes
88
EMLA dosing
0-3mo or < 5kg 1g 3-12mo & > 5kg. 2g 1-6yrs & >10kg. 10g 7-12yrs & > 20kg. 20g
89
EMLA max area of application
0-3mo or < 5kg 10cm square 3-12mo & > 5kg. 20cm sqaured 1-6yrs & >10kg. 100 cm squared 7-12yrs & > 20kg. 200 cm squared
90
which additive increase DOA of LAs
epi decadron dextran
91
how does dextran increase DOA?
it decreases systemic uptake just like epi
92
what additive increase onset of LA
sodium bicarb
93
which additive provide supplemental analgesia with LAs?
clonidine epi opioids (neuraxial only)
94
which additives ^ LA diffusion through tissue?
hyaluronidase
95
Epis ability to increase DOA is more effective with LAs with intermediate or long DOA?
intermediate i.e extends lidocaine better than bupivicane
96
how does decadron increase LA duration of action? how much does it increase DOA and of which blocks?
glucocorticoid activity > decreaesd uptake of LA. can extend BP block by up to 50%
97
which LA decreases effectivness of opiods in the epidural space?
chloroprocaine
98
how does bicarb speed onset of LAs? how do you actually add bicarb to LA and how much do you add?
it increases number of lipid soluble molecules. add 1ml 8.4% sodium bicarb to 10ml LA if you add more it will precipitate

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