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N929: Advanced Pharmacology > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

What is the axolemma?

A

cell membrane of

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2
Q

What do schwann cells do in unmyelinated nerves?

A

one single schwann cell will cover multiple axons.

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3
Q

What do schwann cells do in myelinated nerves?

A

in larger nerves, one schwann cell covers only one axon and has several concentric layers of myelin

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4
Q

What are the breaks in the myelin sheath called?

A

Nodes of Ravier

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5
Q

What level of nerves/neurons do we block?

A

primarily first order

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6
Q

Will unmyelinated or myelinated nerves be blocked faster?

A

unmyelinated

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7
Q

Where are VG Na channels located along the axon?

A

at/in the Nodes of Ranvier

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8
Q

To block a myelinated axon, how much must be blocked?

A

At least 3 nodes of ranvier in a row

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9
Q

What is a fasciculi?

A

bundle of axons

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10
Q

How many layers cover a fasciculi?

A

3;
Endoneurium
Perineurium
Epineurium

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11
Q

What is the endoneurium?

A

thin delicate collagen that embeds the axon in the fascicule

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12
Q

What is the perineurium?

A

layers of flattened cells that binds groups of fascicles together

  • bundles of fascicles
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13
Q

What is the epineurium?

A

surrounds the perineurium and is composed of connective tissue that holds fascicles together to perform a peripheral nerve

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14
Q

Injecting into the perineurium does what?

A

separates the nerves

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15
Q

injecting into the perineurium injecting into he endoneurium will be good or bad?

A

direct nerve injury

  • needle trauma
  • local anesthetic volume will cause pressure
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16
Q

injecting into the perineurium injecting into he endoneurium will be good or bad?

A

direct nerve injury

  • needle trauma
  • local anesthetic volume will cause pressure
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17
Q

What is the normal neuron RMP?

A

-70 to -90mV

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18
Q

What is the most important pump in the axolemma?

A

Na+/K+ ATPase pump?

2K in
3Na out

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19
Q

What is the intracellular K:Na concentration?

A

30:1

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20
Q

What does the Nernst equation express?

A

the charge created by the K concentration gradient

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21
Q

In the axoplasm, is there excess anions or cations?

A

anions

negatively charged ions

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22
Q

What causes a nerve cell depolarization (what ion movement?)

A

VG na channels open, Na rushes INTO the cell

[overrides the K that is maintaining the potential]

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23
Q

When do the VG Na channels reach an inactive state?

A

+20mV

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24
Q

What phases of the Na channel opening do LA act on?

A

open and inactive

NOT closed

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25
Q

What phases of the Na channel opening do LA act on [preferentially]?

A

open and inactive

NOT closed

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26
Q

What confirmation is the Na channel in during repolarization?

A

inactive

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27
Q

Will LA bind to the VG Na channels when in the closed state?
open state?
inactive state?

A

closed- no
open- yes
inactive- yes

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28
Q

Will LA bind to the VG Na channels when in the closed state?
open state?
inactive state?

A

closed- no
open- yes
inactive- yes

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29
Q

LA act on which channels?

A

Na (preferentially)
K
Ca
G-protein coupled receptors

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30
Q

LA prevents movement of what ion and in which direction?

A

binds to VG Na channel;

Na cannot rush in, no action potential

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31
Q

How to LA affect the action potential?

A

LA block the transmission of the AP;

do not change the RMP

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32
Q

How do LA affect the RMP?

A

they don’t alter the RMP, only AP transmission

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33
Q

What is “frequency-dependent blockade”?

A

resting nerve is less sensitive to LA

a stimulated nerve will be affected more by the LA

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34
Q

What is “use-dependent” block?

A

resting nerve is less sensitive to LA

a stimulated nerve will be affected more by the LA

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35
Q

What is “phasic block”?

A

resting nerve is less sensitive to LA

a stimulated nerve will be affected more by the LA

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36
Q

What is the LA MOA?

A
  1. UNionized drug crosses nerve sheath & cell membrane
  2. Re-equilibrium drug binds with H+ ion inside the cell (inside the bi-phospholipid layer)
  3. drugH binds to open or inactive Na channel producing BLOCK
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37
Q

ALL local anesthetics are acids or bases?

A

WEAK BASE

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38
Q

Are big or small nerves easier to block?

A

small, unmyelinated

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39
Q

What will be seen first, before loss of sensation or movement? Why?

A

vasodilation d/t blockage of small preganglionic (controls SNS) fibers first

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40
Q

What type of nerves are harder to block?

A

big, myelinated

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41
Q

What will you see first when a nerve is blocked?

A

vasodilation/flushing d/t blocking of small preganglionic neurons (SNS)

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42
Q

Why do pregnant women complain of nausea after getting a spinal?

A

vasodilation distal to the block resulting in hypotension =

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43
Q

is sensation or motor lost first?

A

sensation - smaller block = loss of sensation not motor

Be careful d/t unintended injury

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44
Q

If motor is blocked, what does that tell us?

A

preganglionic & sensory nerves should be blocked

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45
Q

Who is Karl Koller?

A

introduced cocaine in 1884

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46
Q

Who first began using a drug as a local anesthetic?

A

Karl Koller

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47
Q

When was a drug first used as a local anesthetic?

A

1884

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48
Q

What are the 3 specific portion of the chemical structure of local anesthetics?

A 
aromatic ring (makes it lipophilic)
tertiary ring (hydorphilic)
ester OR amide linkage
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49
Q

Why can local anesthetics get through the axon?

A

aromatic ring

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50
Q

What are 3 characteristics that differentiate ester vs amide local anesthetics?

A
  1. metabolism
  2. duration of action
  3. allergic potential
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51
Q

How to know what kind a local anesthetic is?

A

ester (one i)

amide (two i)

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52
Q

How are amides metabolized?

A

by the liver

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53
Q

Which type of local anesthetics will have more allergies?

A

esters

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54
Q

What is a metabolite that increases the risk of an allergic reaction?

A

PABA
para-amino benzoic acid

is made from ester local anesthetics

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55
Q

What is a metabolite that increases the risk of an allergic reaction?

A

PABA
para-amino benzoic acid

is made from ester local anesthetics

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56
Q

When does the affect of the LA wear off?

A

when it goes somewhere else in the body

more volume can last longer b/c it takes longer to go elsewhere in the body

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57
Q

What is C(m)

A

minimum concentration of LA necessary to produce conduction blockade of a nerve impulse

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58
Q

How does the C(m) of sensory fibers differ from the C(m) of motor fibers?

A

C(m) of motor fibers is approximately TWICE that of sensory fibers

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59
Q

Does intrathecal or spinal anesthesia require more local anesthetic?

A

epidural

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60
Q

When injecting an epidural (labor) what is the concentration/volume like?

A

lower concentration, higher volume

NEVER entering into the dura; hoping to get the nerve roots as they exit

large volume will spread

To allow sensation of contraction & assist

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61
Q

Spinal is where?

A

intrathecal; compromising the dura

injecting onto the nerve

FANTASTIC BLOCK

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62
Q

Where does the spinal cord end?

A

L1-L2?

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63
Q

Where does the dural sac end?

A

sacrum

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64
Q

After L1 what is present in the spinal cord?

A

3 nerves (sacral roots)

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65
Q

What is the ligament that attaches the spinal cord to the sacrum?

A

Coccygeal ligament

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66
Q

How will increasing the concentration affect the onset?

A

increased concentration = faster onset

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67
Q

How will increasing the concentration affect the onset?

A

increased concentration = faster onset

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68
Q

Never inject more than __ mL of a drug

A

5mL

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69
Q

ALWAYS ___ before you inject

70
Q

Local anesthetics have a strong relationship between potency and ___

A

lipid solubility

71
Q

What types of local anesthetics are water insoluble?

A

larger lipid-soluble

72
Q

What type of local anesthetics are highly protein bound?

A

larger lipid soluble

73
Q

What does lipid solubility of local anesthetics correlate with? (5)

A

protein binding
increased potency
longer duration of action
tendency for severe cardiac toxicity

74
Q

Potent local anesthetics will produce what?

A

good, strong, block

BAD if injected into the wrong place

75
Q

What type of local anesthetics (E or A) are lipophilic & protein bound?

76
Q

What kind of local anesthetics have more cardio toxicity?

A

BUPIVICAINE

77
Q

What kind of protein do local anesthetics bind to preferentially?

A

alpha1-acid glycoprotein

78
Q

What affects the duration of action of a local anesthetic?

A
  1. lipid solubility
  2. protein binding [↑ protein binding = longer DOA]
  3. injection site [is it vascular?]
79
Q

For weak bases, closer to what pH means more ionized drug?

A

7.4

cannot cross membrane when ionized

80
Q

Local anesthetics with a pKa closer to 7.4 will be slower or faster?

A

faster; LESS ionized drug

81
Q

What are the 3 local anesthetics that do not cause vasodilation? (or the least)

A

lidocaine, ropivacaine, cocaine

82
Q

How does vasodilation affect the PK of local anesthetics?

A
  1. decreases the duration of action

2. increases plasma concentration [potential toxicity]

83
Q

What determines the plasma level of local anesthetics?

A

the total dose given,

not volume or concentration

84
Q

What tissue/location results in the highest blood concentration of local anesthetics?

A

more vascular..

intravenous
tracheal
caudal
paracervical

85
Q

What tissue/location results in the lowest blood concentration of local anesthetics?

A

less vascular.. (less to more)

subcutaneous
sciatic
brachial
epidural
paracervical
86
Q

What are the 2 most common additives to local anesthetics?

A
  1. epinephrine

2. sodium bicarbonate

87
Q

What are 6 other less common additives to local anesthetics?

A 
clonidine
dexmedetomidine
opioids
ketorolac
dexamethasone
hyaluronidase
88
Q

Why is epinephrine added to local anesthetics?

A

it is a vasoconstrictor that reduces the rate of vascular absorption

89
Q

How does epinephrine change the PK/PD of a local anesthetic? (3)

A
  1. increased duration
  2. increased potency
  3. decreased risk of toxicity
90
Q

What is the benefit of adding bicarb to the local anesthetic?

A
  1. adding bicarb will increase the pH of the solution, resulting in more unionized drug
  2. may result in less pain on injection
91
Q

What is a limitation that can occur when bicarbonate is added to the local anesthetic solution?

A

precipitation;

do not add with an solution containing epi

92
Q

Which class of local anesthetic is metabolized quicker if absorbed into the systemic circulation?

A

esters (plasma esterases hydrolyze med)

93
Q

What class of local anesthetic is metabolized slower in the systemic circulation?

A

amides (metabolized by CYP450 in the liver)

94
Q

How will hepatic disease effect local anesthetics?

A

it will prolong the metabolism of amides (via CYP450), and patient might have low serum protein levels

95
Q

What patient population might be more sensitive to local anesthetics and why?

A
  1. elderly d/t ↓hepatic or renal function & low serum protein = less protein binding and more free drug
  2. pregnant women.
    epidural space will be mechanically compressed. Same volume of medication will have a greater spread up or down when injected.
    AND
    there is some suggestion that progesterone increases sensitivity to local anesthetics
96
Q

What is the plasma half-life of procaine and chloroprocaine?

A

less than one minute

97
Q

Which local anesthetics have a serum half-life of less than one minute?

A

procaine & chloroprocaine

98
Q

What is LAST?

A

Local Anesthetic Systemic Toxicity

99
Q

What is the most common cause of LAST?

A

the inadvertent injection of local anesthetic intravascularly

100
Q

In LAST, what causes bradycardia?

A

the blocking of CARDIAC Na channels

101
Q

What is the most serious cardiac sequalae of LAST?

A

ventricular fibrillation

102
Q

In LAST, what mechanism is thought to be the cause of seizures?

A

blocking inhibitory neurons in the brain

103
Q

In LAST, which drugs are the least cardiotoxic?

A

the shortest acting

104
Q

Do more or less potent local anesthetics have higher lipid solubility & protein binding?

A

more potent agents have higher lipid solubility & protein binding

105
Q

What local anesthetic is the most protein bound?

A

Bupivacaine

106
Q

When does LAST present?

A

rapid onset, within 1 minute

107
Q

What are the first s/s of LAST?

A 
agitation
tinnitus
circumoral numbness
blurred vision
metallic taste
108
Q

What are s/s LAST is progressing?

A

muscle twitching, unconsciousness, seizures

followed by

CARDIAC & RESPIRATORY arrest

109
Q

What is the FIRST thing you do if you suspect LAST?

A

CALL FOR HELP

110
Q

What is the SECOND thing you do if you suspect LAST?

A

manage the airway

111
Q

Incidence of LAST

A

0.4 in 10,000

112
Q

LAST is most commonly seen in what 3 regional anesthetics?

A
  1. epidural
  2. axillary blocks
  3. interscalene blocks
113
Q

The brachial plexus is from which nerve roots?

114
Q

Where does the vertebral artery enter the spinal columm?

115
Q

Where does a brachial plexus block target?

A

C5, C6, C7

116
Q

What 2 anatomical structures cause increased risk of LAST during an epidural placement?

A

epidural vein & dura

117
Q

What 2 anatomical structures cause increased risk of LAST during an interscalene block?

A

carotid artery

internal jugular vein

118
Q

What are 4 strategies to prevent LAST?

per Dr. Falyar

A
  1. test dosing
  2. incremental injection with aspiration
  3. use of pharmacologic markers
  4. ultrasound
119
Q

What is the treatment for LAST?

A
  1. recognition
  2. AIRWAY MANAGEMENT
    • Sz suppression with benzo or succinylcholine
    • PREVENT hypoxia & ACIDOSIS (will “trap” medication
  3. LIPID EMULSION THERAPY
  4. VASOPRESSORS
    • EPI <1mg/kg
      • NOT VASOPRESSIN
120
Q

What is the initial bolus dose of lipid emulsion 20% in a patient <70kg?

A

bolus 1.5mg/kg over 2-3 minutes

121
Q

What is the initial bolus dose of lipid emulsion 20% in a patient >70kg?

A

bolus 100mL over 2-3 minutes

122
Q

What is the lipid emulsion 20% infusion dose in a patient <70kg?

A

~0.25mL/kg/min IBW

123
Q

What is the lipid emulsion 20% infusion dose in a patient >70kg?

A

200-250mL over 15-20 minutes

124
Q

What if the patient experiencing LAST is still unstable after bolus and infusion?

A

re-bolus 1 or 2 times.
double infusion rate
**DOSING LIMIT 12ML/KG

125
Q

How long should monitoring continue after LAST event?

A

at least 4-6 hours after event with cardiac involvement

at least 2 hours after limited CNS event

126
Q

What is the maximum dose of lipid emulsion therapy when treating LAST?

127
Q

What medication should be AVOIDED when treating LAST, specifically hypotension?

A

do not give vasopressin

128
Q

Why is it important to make a patient alkalotic when experiencing LAST?

A

increasing the pH will limit the amount of ionized drug = drug is NOT “trapped” in cells

129
Q

What is the MOA of lipid emulsion therapy in the treatment of LAST?
****

A
  1. “capture” local anesthetic in the blood (lipid sink)
  2. increased fatty acid uptake by mitochondria
  3. interference of Na channel binding
  4. promotion of calcium entry
  5. accelerated shunting
130
Q

Allergic reaction is most commonly seen in which type of local anesthetics? Why?

A

ester local anesthetics

esters are metabolized to/derivatives of para-aminobenzoic acid (PABA), which is a known allergen

131
Q

Is there cross reactivity in local anesthetics?

A

Yes, among the esters but NOT with the amides

ie. an allergy to an ESTER does not necessarily mean the patient will be allergic to amides

132
Q

An allergic reaction to an amide local anesthetic is most often caused by what?

A

preservatives

133
Q

When is it necessary to ensure the local anesthetic being administered does not contain preservatives?

A

when doing a spinal or epidural

134
Q

What are 3 preservatives that can sometimes be found in local anesthetic formulations?

A
  1. paraben
  2. methylparaben
  3. metabisulfite
135
Q

What side effect of local anesthetics alters oxygenation?

A

methemoglobinemia

136
Q

What is methemoglobinemia?

A

ferris (Fe2+) form of hemoglobin is converted into ferric (Fe3+) form.

*reduced oxygen carrying capacity = decreased SpO2 that is not responsive to oxygen administration

137
Q

What are 2 local anesthetics most likely to cause methemoglobinemia?

A

Benzocaine

Prilocaine

138
Q

Why can Prilocaine cause methemoglobinemia?

A

metabolite is o-touidine

139
Q

The dosing of prilocaine should not exceed, what?

140
Q

Is local anesthetic based on TBW or IBW?

141
Q

Prilocaine should be avoided in what 3 patient populations?

A

children under 6yr
pregnant women
patients taking other oxidizing drugs

142
Q

What is the treatment for methemoglobinemia?

A

methylene blue 1-2mg/kg over 3-10 minutes

saturation may drop for ~30 seconds upon administration

143
Q

extremely high levels of methemoglobinemia may require __ or __?

A

dialysis or transfusion

144
Q

What is Cauda Equina Syndrome (CES)?

A

bowel & bladder dysfunction with lower extremity weakness and sensory impairment related to cord ischemia

  • maldistribution of local anesthetic within the intrathecal space
145
Q

What are the risk factors for CES?

cauda equina syndrome

A
  • supranormal doses of local anesthetics
    2-chloroprocaine
    lidocaine
146
Q

What is Transient Neurologic Symptoms (TNS)?

A

burning, aching, cramp like pain in the lower back and radiating down the thighs

  • for up to 5 days post op

most often associated with intrathecal lidocaine

147
Q

What medication is TNS most associated with?

transient neurological symptoms

148
Q

What are 3 risk factors of TNS?

transient neurological symptoms

A
  1. Lidocaine
  2. lithotomy position
    • stretch of nerves in addition to the lidocaine?
  3. outpatient surgery
149
Q

Who discovered Lidocaine & what year?

A

Nils Lofgren

943

150
Q

What list is lidocaine included on?

A

the World Health Organization’s list of essential medications

151
Q

What is EMLA cream?

A

1:1 Lidocaine:Procaine mixture

152
Q

What are the 4 patients or locations EMLA is contraindicated in?

A
  1. open skin
  2. mucous membrane
  3. infants <1 month
  4. Hx methemoglobinemia
153
Q

What is a bier block?

How much medication is used?

A

2 tourniquets

25-50mL of 0.5%Lidocaine
Onset time 5-10 minutes

tourniquet pain is usually at 20 minutes

154
Q

What types of surgery use bier blocks (2)?

A
  1. closed reduction

2. carpal tunnel

155
Q

What are the 2 treatment interventions of LAST?

A
  1. Benzodiazepines

2. hyperventilation (raises seizure threshold)

156
Q

The administration of Lidocaine 1.5mg/kg can (3):

A
  1. decrease CBF & ICP
  2. block reflex bronchoconstriction on intubation
  3. blunt SNS response to intubation
157
Q

What is EXPAREL?

A

new generation of local anesthetic

bupivacaine encapsulated in liposomal agent

158
Q

What can exparel be mixed with?

A

ONLY bupivacaine

159
Q

How long can/does exparel last?

A

up to 72 hours

160
Q

What is the maximum dose of exparel?

A

266mg (20mL) - can be diluted up to 0.89mg/mL 1:14

161
Q

What is the minimum size needle exparel can be administered with into the surgical site?

162
Q

Can Exparel and Lidocaine be mixed?

163
Q

What are 3 situations/patients where exparel should NOT be used?

A
  1. obstetrical paracervical block
  2. patients < 18yr
  3. epidural or intrathecal anesthesia
164
Q

When must exparel be discarded?

A

after 4 hours

165
Q

What is the incidence of N/V with exparel?

166
Q

What type of local anesthetic is cocaine?

A

only naturally occuring

167
Q

What is cocaine made from?

A

Cocoa plant

168
Q

How does cocaine work?

A

blocks the monoamine transporter in the adrenergic system

169
Q

What physiological response is created by cocaine?

A

blocking the reuptake of catecholamines (monoamine transporter block) = more catecholamines = vasoconstriction & SNS stimulation

170
Q

What 3 types of medications should cocaine be used with caution?

A
  1. epinephrine containing medications
  2. MOAIs
  3. tricyclics
171
Q

What is the maximum dose of cocaine?

A

5mL of 5% solution

N929: Advanced Pharmacology (6 decks)

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