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local anesthetics Flashcards

1
Q

which LA is manufactured as a single enantiomer

A

ropivicaine (pure S enantiomer), less neuro toxicity and cardio toxicity than its racemic mixture

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2
Q

which LA is manufactured as a single enantiomer

A

ropivicaine (pure S enantiomer), less neuro toxicity and cardio toxicity than its racemic mixture

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3
Q

where is
epineurium
perineurium
endoneurium

A
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4
Q

ID parts of the axon

A
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5
Q

a alpha
myelination
function
diameter
velocity
block onset

A

myelination: heavy
function: skeletal muscle- motor proprioception
diameter: 12-20
velocity: +++++
block onset: 4th

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6
Q

a beta
myelination
function
diameter
velocity
block onset

A

myelination: heavy
function: touch, pressure
diameter: 5-12
velocity: ++++
block onset: 4th

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7
Q

a gamma
myelination
function
diameter
velocity
block onset

A

myelination: medium
function: skeletal muscle- tone
diameter: 3-6
velocity: +++
block onset: 3rd

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8
Q

a delta
myelination
function
diameter
velocity
block onset

A

myelination: medium
function: fast pain, temperature, touch
diameter: 2-5
velocity: +++
block onset: 3rd

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9
Q

b fibers
myelination
function
diameter
velocity
block onset

A

myelination: light
function: preganglionic ANS fibers
diameter: 3
velocity: ++
block onset: 1st

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10
Q

C sympathetic
myelination
function
diameter
velocity
block onset

A

myelination: none
function: post ganglionic ANS fibers
diameter: 0.3-1.3
velocity: +
block onset: 2nd

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11
Q

C dorsal root
myelination
function
diameter
velocity
block onset

A

myelination: none
function: slow pain, temperature, touch
diameter: 0.4-1.2
velocity: +
block onset: 2nd

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12
Q

LA’s inhibit peripheral nerves in the following order

A

B fibers > C fibers > small diameter A fibers > large diameter A fibers

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13
Q

LA’s can bind to VG channels in which states

A

active and inactive states

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14
Q

LA’s bind to which subunit on VgNa channel

A

alpha

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15
Q

describe resting state

A

-70mV, channel is closed

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16
Q

describe active state

A

-70 to +35mV
when threshold potential is reached, channel opens
open channel allows Na to follow concentration gradient (outside to inside)

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17
Q

describe inactive state

A

channel is closed
inactivation gate plugs channel until RMP is re established
restoration of RMP converts channel from inactive state to resting state. at this point, the nerve is ready to be stimulated again

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18
Q

what do LA’s do to RMP and TP

A

have no effect on TP and RMP

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19
Q

3 things that influence RMP

A
  1. chemical force (concentration gradient)
  2. electrostatic counter force
  3. Na/K/ATPase (3 Na out for every 2 K in)
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20
Q

what does decreased serum K do to RMP

A

becomes more negative

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21
Q

what does increased serum K do to RMP

A

becomes more positive

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22
Q

TP and primary electrolyte

A

-55, Ca2+

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23
Q

repolarization

A

occurs when K leaves the cell or Cl- enters the cells
cell is resistant to subsequent depolarization during during refractory period because Na channels are in the closed inactive state

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24
Q

henderson hasslebach equation

A
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25
Q

primary determinant of onset of LA

A

pKa
-if the pKa is further away from pH of blood, less lipophilic availability and therefore longer OOA

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26
Q

primary determinant of potency of LA

A

lipophilicity (via aromatic ring)
-easier time diffusing through epineurium
-more lipophilic means more potent and longer DOA

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27
Q

does the ionized or non ionized species of LA bind to VgNa channel

A

ionized

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28
Q

what do vasoconstrictors do to LA activity

A

prolong effect by decreasing uptake

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29
Q

are LA’s acids or bases?
is the pH low or high

A

weak base with low pH to guard against precipitation

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30
Q

why can we predict that >50% of LA will exist in ionized state when it enters the blood stream

A

weak based with pKa > physiologic pH so a greater fraction will exist in the ionized state

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31
Q

what 3 paths can a LA travel after its injected near a peripheral nerve?

A
  1. can diffuse into nerve
  2. can diffuse into surrounding tissue and bind to neighboring proteins
  3. can diffuse into systemic circulation
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32
Q

basic structure (3 parts) of a LA molecule includes what and what is their significance

A
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33
Q

true allergy is more likely with

A

esters because of para amino benzoic acid (PABA) metabolite

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34
Q

is there cross sensitivity in the amide group

A

no, not like the ester group

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35
Q

COO

A

ester

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36
Q

NHCO

A

amide

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37
Q

does the ionized or non ionized species bind to the alpha subunit of the inside of the VgNa channel

A

the non ionized

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38
Q

explain why chlorprocaine has a fast onset

A

the pKa is high which means its further from the blood pH and less ionized species are available which would make you think the OOA is increased. However, because it it not potent it is given in large doses and the more molecules creates a mass effect which explains why it still has a rapid onset

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39
Q

why does .75% bupiv have a faster OOA than .25% bupiv

A

more molecules

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40
Q

what happens to a LA with more intrinsic vasodilating ability

A

increase rate of uptake and shorten DOA by up to 1/3

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41
Q

acid does what to a proton

A

donates
HA–> H+ + A-

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42
Q

base does what to a proton

A

accepts
B+ + H- = BH+

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43
Q

ionization is dependent on 2 factors

A

pKa of drug
pH of solution

44
Q

in an acidic solution, weak bases are

A

more ionized and water soluble

45
Q

in an acidic solution, weak acids are

A

more nonionized and lipid soluble

46
Q

in a basic solution, weak bases are

A

more non ionized and lipid soluble

47
Q

in a basic solution, weak acids are

A

more ionized and water soluble

48
Q

amide type, pKa, ionization at 7.4%, protein binding (%) for
bupivicaine
levobupivicaine
ropivicaine
lidocaine
prilocaine
mepivicaine

A
49
Q

ester type, pKa, ionization at 7.4%, protein binding (%) for
procaine
chlorprocaine
tetracaine

A
50
Q

which LA’s have higher pKa values in general

A

esters (8.5-8.9) over amides (8.1 is the highest)

51
Q

benzocaine pKa

A

3.5. “odd man out”
-non ionized at physiologic pH
-metHGBemia is significant risk

52
Q

factors that influence vascular uptake and plasma clearance of LA’s

A

site of injection
tissue BF
physiochemical properties of LA
metabolism
addition of vasoconstrictor

53
Q

site of LA injection and highest to lowest plasma concentration (Cp) and pneumonic

A

I think I can push each bolus super slowly for safety
IV, tracheal, intercostal, caudal, paracervical, epidural, brachial plexus, subarachnoid/sciatic, femoral, SQ

54
Q

LA’s preferentially bind to which protein

A

alpha 1 acid glycoproteins (but will also bind to albumin)

55
Q

what does the addition of precedes do to a brachial plexus block

A

extends DOA

56
Q

max dose of exparel and how it is dispensed

A

266mg
133mg in 10mL or
266mg in 20mL

57
Q

rules for giving exparel (and lidocaine) to a patient

A

after infiltrating lidocaine, no liposomal bupiv for at least 20m
after infiltrating liposomal bupiv, no lidocaine (in any form) for 96h

58
Q

levobupivicaine max dose in mg and mg/kg

A

2mg/kg or 150mg

59
Q

bupivicaine max dose in mg and mg/kg

A

2.5mg/kg or 175mg

60
Q

bupivicaine and epinephrine max dose in mg and mg/kg

A

3mg/kg or 200mg

61
Q

ropivicaine max dose in mg and mg/kg

A

3mg/kg or 200mg

62
Q

lidocaine max dose in mg and mg/kg

A

4.5mg/kg or 300mg

63
Q

mepivicaine max dose in mg and mg/kg

A

7mg/kg or 400mg

64
Q

lidocaine and epinephrine max dose in mg and mg/kg

A

7mg/kg or 500mg

65
Q

prilocaine max dose in mg and mg/kg

A

8mg/kg or if <70kg, 500mg. if >70kg, 600mg

66
Q

procaine max dose in mg and mg/kg

A

7mg/kg or 350-600mg

67
Q

chlorprocaine max dose in mg and mg/kg

A

11mg/kg or 800mg

68
Q

chlorprocaine and epi max dose in mg and mg/kg

A

14mg/kg or 1000mg

69
Q

most frequent sx of LA toxicity and exception

A

seizure
bupiv is exception, cardiac arrest before seizure

70
Q

what to expect with 1-5mcg/kg Cp of lidocaine

A

analgesia

71
Q

what to expect with 5-10mcg/kg Cp of lidocaine

A

tinnitus, skeletal muscle twitching, numbness of lips and tongue, restlessness, vertigo, blurred vision, HoTN, myocardial depression

72
Q

what to expect with 10-15 mcg/kg Cp of lidocaine

A

seizures, loss of consciousness

73
Q

what to expect with 15-25mcg/kg Cp of lidocaine

A

coma, resp arrest

74
Q

what to expect with >25mcg/kg Cp of lidocaine

A

CV collapse

75
Q

factors that increase risk of LA CNS toxicity (3)

A

hypercarbia (increases CBF and drug delivery to brain, decreases protein binding and increases free fraction of LA)
hyperkalemia (raises RMP making neurons more likely to depol)
metabolic acidosis (decreases convulsion threshold and favors ion trapping inside the brain)

76
Q

LA’s create CV toxicity by

A

decrease automaticity, conduction velocity, AP duration, and effective refractory period
depress myocardium by impairing intracellular calcium regulation
produce a biphasic effect on vascular smooth muscle. low concentration LA causes vasoconstriction while high concentration LA causes vasodilation and a reduction in SVR

77
Q

two features determine extent of cardiotoxicity

A
  1. affinity for VgNa channel in active and inactive states
  2. rate of dissociation from receptor during diastole
78
Q

difficulty of cardiac resuscitation based on LA in order from greatest to least

A

bupiv>levobupiv>ropiv>lido

79
Q

risk off bupiv toxicity is increased with

A

pregnancy, BB’s, CCB’s, digitalis

80
Q

tx of LAST

A
  1. manage aw (100% FiO2, hypoxia and acidosis will worsen sx of LAST)
  2. tx seizures with benzos (avoid prop, can give succ to tx muscle contraction)
  3. ACLS with specific modifications (epi is no bueno, but if you have to then keep dose below 1mcg/kg, avoid vasopressin, amio is agent of choice for ventricular dysrhythmias)
  4. 20% lipid emulsion therapy (if patient is over 70kg, 100mL bolus over 2-3m, infusion 250mL over 15-20m. if patient remains unstable, repeat bolus and/or double infusion. if patient is <70kg, bolus of 1.5mL/kg over 2-3m then .25mL/kg/min infusion. if patient remains unstable, same as above)
81
Q

max recommended dose of 20% lipids

A

12mL/kg

82
Q

proposed MOA of lipid emulsion therapy

A

lipid sink: intravascular reservoir that sequesters LA and reduces plasma concentration of LA
metabolic effect: enhanced myocardial fatty acid metabolism
inotropic effect: increased calcium influx and intracellular calcium concentration
membrane effect: impairs LA binding to VgNa channels

83
Q

dose for 20% lipid emulsion therapy

A

if patient is over 70kg, 100mL bolus over 2-3m, infusion 250mL over 15-20m. if patient remains unstable, repeat bolus and/or double infusion. if patient is <70kg, bolus of 1.5mL/kg over 2-3m then .25mL/kg/min infusion. if patient remains unstable, same as above

84
Q

for tumescent anesthesia, max dose of lidocaine is

A

55mg/kg

85
Q

GA is recommended if ________ of tumescent is used

A

2-3L

86
Q

which LA’s can be responsible for methemoglobinemia

A

benzocaine
prilocaine (O toluidine)
lidocaine
cetacaine
EMLA (50/50 prilocaine, lidocaine)

87
Q

what does methgbemia do to oxyhgb dissociation curve

A

to the left makes it easier for HgbA to bind to O2 but makes it more difficult to release it at the tissue level

88
Q

% methgbemia and sx

A
89
Q

SpO2 and PaO2 for methgbemia

A

SpO2 decreased in setting of normal PaO2

90
Q

dose of methylene blue should not exceed

A

7-8mg/kg

91
Q

glucose 6 phosphate reductase deficiency

A

dont give methyline blue

92
Q

what is required to dx methgbemia

A

co oximeter

93
Q

presentation of methemoglobinemia

A

hypoxia
cyanosis (slate grey pseudo cyanosis)
chocolate colored blood
tachycardia
tachypnea
mental status changes
coma and death

94
Q

how does methylene blue work in the setting of methemoglobinemia

A

it is metabolized by methgb reductase to form leucomethylene blue. this metabolite functions as an electron donor, which reduces metHGB back to HGB

95
Q

population at higher risk for methylene blue toxixity

A

neonates.

96
Q

5% emla cream is

A

50% 2.5 prilocaine and 50% 2.5 lidocaine

97
Q

0-3 months or <5kg and max dose of EMLA, max area of application

A

max dose 1g, max area of application 10cm^2

98
Q

3-12mo and >5kg and max dose of EMLA and max area of application

A

max dose 2g, max area of application 20cm^2

99
Q

1-6y and >10kg max dose of EMLA cream and max area of applicatoin

A

10g, 100cm^2

100
Q

7-12y and >20kg max dose of EMLA cream and max area of application

A

20g, 200cm^2

101
Q

drugs that prolong LA DOA

A

epinephrine
dexamethasone
dextran

102
Q

drugs that provide supplemental analgesia with LA

A

clonidine (100mcg)
epinephrine
opioids (neuraxial only)

103
Q

drugs that shorten onset time of LA

A

sodium bicarb (1mL of 8.4% in 10mL LA)

104
Q

drugs that improve LA diffusion through tissues

A

hyaluronidase

105
Q

causes of methemoglobinemia

A

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