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APEX Pharmacology > PHARMACOLOGY-local anesthetics > Flashcards

PHARMACOLOGY-local anesthetics Flashcards

1
Q 
What is the function of the following nerve types
A alpha
A delta
B
C
A

A alpha = motor
A delta = fast pain (dolor)
B = preganglionic SNS
C = Slow pain

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2
Q

What neuronal factors increase conduction velocity

A

Myelination

Wider axonal diameter

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3
Q

How are peripheral nerves subdivided

What are the different subdivisions

A

Subdivided by their diameter and myelination

Subdivisions = A, B, C

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4
Q

What is the order of LA inhibition of peripheral nerves from first to last

A
  1. B fiber
  2. C fibers
  3. Small diameter A fibers (delta, gamma)
  4. Large diameter A fiber (alpha, beta)
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5
Q

How does regression of a peripheral blockade occur (order nerves from first to last)

A

Opposite order of initial onset

  1. large diameter A fibers
  2. Small diameter A fibers
  3. C fibers
  4. B fibers
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6
Q

Order the peripheral nerves by their conduction velocity, from greatest to least

A
  1. A alpha, beta
  2. A gamma, delta
  3. B
  4. C
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7
Q

Order the peripheral nerves by their diameter from biggest to smallest

A
  1. A alpha, beta
  2. A gamma, delta
  3. B
  4. C
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8
Q

Which peripheral nerve senses temperature, touch, and fast pain

A

A delta

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9
Q

Which peripheral nerve senses slow pain, temperature, and touch

A

C

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10
Q 
Describe the function of the following peripheral A nerve types
alpha
beta
gamma
delta
A 
alpha = skeletal muscle (motor), proprioception
beta = touch, pressure
gamma = skeletal muscle tone
delta = fast pain, temp, touch
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11
Q

Which peripheral nerve functions at the preganglionic ANS fibers

A

B

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12
Q

Define minimum effective concentration related to LA

A

Cm is a unit of measure that quantifies the concentration of LA that is required to block conduction

analogous to ED50/MAC

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13
Q

Describe the minimum effective concentration for peripheral fibers that are more easily blocked vs more resistant to block

A

Cm is lower in fibers that are easily blocked

Cm is higher in fibers that are more resistant to LA block

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14
Q

Describe the minimum effective concentration (Cm) required for the following peripheral nerve variables
Wider diameter=
Higher tissue pH=
Greater nerve stimulation=

A

Wider diameter= Higher Cm
Higher tissue pH= Reduced Cm
Greater nerve stimulation= Reduced Cm

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15
Q

What type of channels are affected by local anesthetics

A

Voltage-gated sodium channels

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16
Q

How do local anesthetics affect voltage-gated sodium channels

A

They reversibly bond to the alpha subunit of the channel

This blocks the channel and reduces Na+ conductance

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17
Q

What 3 states can sodium channels exist

A
  1. Resting (nonconducting)
  2. Active (conducting)
  3. Inactive (nonconducting)
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18
Q

During what state does LA bind to the voltage-gated sodium channels

A

Active (open)

Inactive (closed refractory)

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19
Q

When are local anesthetics unable to bind to voltage-gated Na+ channels

A

During the channels resting state

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20
Q

What are the resting membrane potential and threshold potential of peripheral nerves

A 
RMP = -70 mV
TP = -55 mV
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21
Q

How is the resting membrane potential maintained in peripheral nerves

A

By K+

After polarization, K+ conductance restores RMP via the Na/K-ATPase pumps

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22
Q

What ion is the primary determinant of threshold potential of a peripheral nerve

A

Ca++

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23
Q

What effect do local anesthetics have on resting membrane potential or threshold potential

A

No effect

LA only inhibits the ability to initiate an AP

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24
Q

Are local anesthetics acids or bases

A

They are weak bases

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25
Q

What occurs to the local anesthetic structure when it is injected

A

Dissociation into an uncharged base and an ionized conjugate acid

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26
Q

With a pKa >7.4, what percent of the local anesthetic exist in the charged state

A

> 50% exists as ionized, conjugate acid

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27
Q

How does local anesthetic diffuse through peripheral neurons

What occurs once the LA is in the neuron and why

A

non-ionized LA diffuse through lipid-rich axolemma

In the neuron, LA dissociated according to a new equilibrium d/t slightly more acidic environment inside the neuron

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28
Q

How do local anesthetics bind to the voltage-gated sodium channel

A

The ionized portion (conjugate acid) bonds to the alpha subunit

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29
Q

What 3 key components make up local anesthetic molecular structure

A
  1. Benzene ring
  2. Intermediate side chain
  3. Tertiary amine
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30
Q

What portion of the local anesthetic molecular structure determines the drug class

A

The intermediate side chain

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31
Q

What are the 2 types of local anesthetic drug classes

A
  1. Ester

2. Amide

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32
Q

How do the 2 types of local anesthetic classes differ

A
  1. Ester = metabolized in plasma by pseudocholinesterase

2. Amide = metabolized in the liver by P450 system

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33
Q

List the ester-type local anesthetics

A 
Benzocaine
Cocaine
Chloroprocaine
Procaine
Tetracaine
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34
Q

List the amide-type local anesthetics

A 
Bupivicaine
Dibucaine
Lidocaine
Mepivacaine
Ropivacaine
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35
Q

Allergic reactions to local anesthetics occur more commonly with which type of LA and why

A

More common with esters due to PABA (para-aminobenzoic acid)

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36
Q

If a patient has an allergy to an ester local anesthetic can they receive an amide? Why

A

Yes if it is preservative-free

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37
Q

What properties does the benzene ring have in the local anesthetic structure

A

Lipophilic

Permits diffusion through lipid bilayers

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38
Q

What properties does the intermediate chain have in the local anesthetic structure

A

Determines the class of the LA (ester v amide)
Metabolism
Allergic potential

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39
Q

What properties does the tertiary amine have in the local anesthetic structure

A

Hydrophilic
Accepts proton
Makes molecule a weak base

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40
Q

What properties determine the following for local anesthetics
Onset
Potency
Duration of action

A

Onset = pKa
Potency = Lipid solubility
Duration of action = protein binding

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41
Q

What PK/PD factors do the following variables of local anesthetics have
pKa
Lipid solubility
Protein binding

A

pKa = onset of action
Lipid solubility = potency
Protein binding = duration of action

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42
Q

Explain how pKa affects onset of action for local anesthetics

A

if the pKa is closer to the pH of blood, a larger fraction will be non-ionized (lipid soluble) allowing for diffusion into neuron

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43
Q

What effect does local anesthetic concentration have on onset

A

Higher concentration can increase onset

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44
Q

How does lipid solubility affect the potency of local anesthetics

A

More lipid soluble LA = more diffusion of LA into neuron = more bound receptors

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45
Q

What local anesthetic property affects vascular uptake

How is this effect countered

A

Vasodilatory property

Countered with the coadministration of epinephrine for vasoconstriction

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46
Q

What factors prolong local anesthetic duration of action

A

Protein binding
Lipid solubility
Coadministration of epinephrine

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47
Q

Which local anesthetic has no intrinsic vasodilating effect

A

Cocaine

It inhibits NE reuptake causing vasoconstriction

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48
Q

What 2 factors determine ionization of a local anesthetic

A

pH of a solution

pKa of the drug

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49
Q 
Compare the pKa for the following local anesthetics from least to greatest
Ropivacaine
Prilocaine
Lidocaine
Mepivacaine
Levobupivacaine
Bupivacaine
A

Mepivacaine < prilocaine < lidocaine < ropivacaine < levobupivacaine < bupivacaine

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50
Q

How does the pKa of ester LAs compare to amide LAs

A

Ester pKa is higher than amide

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51
Q

How does benzocaine differ from other local anesthetics (3)

A

The pKa is much lower (3.5)

It is non-ionized at physiologic pH but still produces anesthesia
Methemoglobinemia is a significant risk

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52
Q

How do pharmacokinetics for local anesthetics differ from typical systemic administration

A

Absorption into systemic circulation removes (eliminates) the drug from the site, eliminating its effects

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53
Q

What are 5 factors that influence vascular uptake and plasma concentration

A
  1. Site of injection
  2. Tissue blood flow
  3. Physiochemical properties of local anesthetic
  4. Metabolism
  5. Addition of vasoconstrictor
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54
Q

What injection sites are at increased risk for LAST

list from greatest to least

A 
IV
Tracheal
Interpleural
Intercostal
Caudal
Epidural
Brachial plexus
Femoral
Sciatic
Subcutaneous
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55
Q

What determines the final plasma concentration of a local anesthetic

A

The total dose of anesthetic (NOT its concentration or speed of injection)

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56
Q

What protein do local anesthetics preferential bind to

A

alpha 1-acid glycoprotein

also albumin

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57
Q

How are amide and ester local anesthetics metabolized

A 
Amides = P450 enzyme in liver
Esters = pseudocholinesterase in plasma
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58
Q

How is cocaine metabolized

A

By pseudo cholinesterase in plasma and hepatic P450 enzymes

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59
Q

What effect does the addition of a vasoconstrictor with local anesthetic have at the injection site

A

Decreases systemic absorption by up to one-third

Prolongs duration

Greater effect with LA that have greater dilating properties

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60
Q

Describe the formulation of exparel allowing it to be long-acting

A

Aqueous droplets of bupivacaine are housed in liposomal suspension
As lipid membrane of suspension erodes bupivacaine is release

61
Q

What are the benefits of exparel

A

Duration of up to several days

Reduction in opioid consumption

62
Q

What is the maximum Exparel dose

A

266 mg

63
Q

What type of block is Exparel contraindicated

A

Paracervical block
Epidural
Intrathecal
Intraarticular

64
Q 
Site the maximum dose (mg/kg) for amide local anesthetics (plain)
Levobupivacaine
Bupivacaine
Ropivacaine
Lidocaine
Mepivacaine
Prilocaine
A 
Levobupivacaine = 2 mg/kg
Bupivacaine = 2.5 mg/kg
Ropivacaine = 3 mg/kg
Lidocaine = 4.5 mg/kg
Mepivacaine = 7 mg/kg
Prilocaine = 8 mg/kg
65
Q

Site the maximum dose (mg/kg) of local anesthetic with epi
Bupivacaine + epi
Lidocaine + epi

A

Bupivacaine + epi = 3 mg/kg

Lidocaine + epi = 7 mg/kg

66
Q

Site the maximum dose (mg/kg) for ester local anesthetics
Procaine
Chloroprocaine
Chloroprocaine + epi

A

Procaine = 7 - 10 mg/kg
Chloroprocaine = 11 mg/kg
Chloroprocaine + epi = 14 mg/kg

67
Q 
What is the max TOTAL dose for
Levobupivacaine
Bupivacaine
Ropivacaine
Lidocaine
Mepivacaine
Prilocaine
A 
Levobupivacaine = 150 mg
Bupivacaine = 175 mg
Ropivacaine = 200 mg
Lidocaine = 300 mg
Mepivacaine = 400 mg
Prilocaine = 500 mg<70 kg; 600 > 70 kg
68
Q

What is the max TOTAL dose for
Bupivacaine + epi
Lidocaine + epi

A

Bupivacaine + epi = 200

Lidocaine + epi = 500

69
Q

What is the max TOTAL dose for
Procaine
Chloroprocaine
Chloroprocaine + epi

A

Procaine = 350 - 600 mg
Chloroprocaine = 800 mg
Chloroprocaine + epi = 1,000 mg

70
Q

What is the most common cause of toxic plasma concentration

A

Inadvertent intravascular injection during peripheral regional anesthesia

71
Q

What is the most frequent symptom of LA system toxicity

A

Seizure

72
Q

What is the most frequent symptom of bupivacaine toxicity

A

Cardiac arrest BEFORE seizure

73
Q

What CNS effects are present with lidocaine plasma concentration of 5 - 10 mcg/mL

A 
Tinnitus
Muscle twitching
Numb lip and tongues
Restlessness
Vertigo
Blurred vision
74
Q

What CNS effects are present with lidocaine plasma concentration of 10 - 15 mcg/mL

A

Seizures

Loss of consciousness

75
Q

What CNS effects are present with lidocaine plasma concentration of 15 - 25 mcg/mL

A

Coma

76
Q

What CV effects are present with lidocaine plasma concentration of 5 - 10 mcg/mL

A

HoTN

Myocardial depression

77
Q

What cardiopulmonary effects are present with lidocaine plasma concentration of 15 - 25 mcg/mL

A

Respiratory arrest

78
Q

What CNS effects are present with lidocaine plasma concentration of >25 mcg/mL

A

CV collapse

79
Q

What abnormal physiology increases risk of CNS toxicity with local anesthetics

A
  1. Hypercarbia
  2. Hyperkalemia
  3. Metabolic acidosis
80
Q

How does hypercarbia increase the risk for CNS toxicity from local anesthetics

A
  1. It increases cerebral BF and delivery of drug to brain

2. It decreases protein binding which increases free fraction of LA available

81
Q

how does hyperkalemia increase the risk for CNS toxicity from local anesthetics

A

It raises the resting membrane potential, making neurons more likely to depolarizes.

82
Q

How does metabolic acidosis increase the risk for CNS toxicity from local anesthetics

A
  1. Decreased convulsion threshold

2. Favors ion trapping in brain

83
Q

How does systemic acidosis affect LA

A

Increases the fraction of conjugate acid (ionized) and decreases the amount of uncharged base (non-ionized)

84
Q

What are 3 factors that decrease the risk for CNS toxicity d/t local anesthetics

A
  1. Hypocarbia
  2. Hypokalemia
  3. CNS depressants
85
Q

How does hypocarbia decrease the risk for CNS toxicity from local anesthetics
Name an intervention to accomplish the above

A

It decreases cerebral BF and reduces drug delivery to the brain

intervention = hyperventilation

86
Q

How does hypokalemia decrease the risk for CNS toxicity from local anesthetics

A

Makes the resting membrane potential more negative (lowers it). The neuron requires a larger stimulus for depolarization

87
Q

How do CNS depressants decrease the risk for local anesthetic induced CNS toxicity
Examples

A

The seizure threshold is raised

Ex: benzos, barbiturates

88
Q

How do local anesthetics disrupt hemodynamics (3)

A
  1. Alter cardiac action potential
  2. Alter myocardial performance
  3. Alter vascular resistance
89
Q

How does local anesthetic toxicity affect cardiac action potential (4 factors)

A

Decreases automaticity, conduction velocity, action potential duration and effective refractory period

90
Q

How does local anesthetic toxicity affect myocardial performance

A

By impairing intracellular calcium regulation

91
Q

How does local anesthetic toxicity affect vascular resistance (low vs high concentrations)

A

Low concentration = vasoconstriction

High concentration = vasodilation, decreased SVR

92
Q

What 2 factors determine the extent of cardiotoxicity from local anesthetics

A
  1. Affinity for the voltage-gated Na+ channels in the active and inactive states
  2. Rate of dissociation from the receptor during diastole
93
Q

How does receptor affinity and dissociation compare between lidocaine and bupivacaine

A

Bupivacaine has a greater affinity for VG Na+ channels and a slower rate of dissociation from the receptor during diastole

More bupivacaine remains at the receptor for longer

94
Q

Co-administration of which drugs can increase bupivacaine toxicity (3)

A

Beta-blockers
CCBs
Digitalis

95
Q

What is the primary risk of cocaine toxicity and why

A

Excessive SNS stimulation

D/t vasocontrictive properties from inhibition of NE uptake in the presynaptic nerve terminal (more NE at the nerve)

96
Q

What effect do beta-blockers have in an acute cocaine overdose

A

Could cause unopposed alpha-1 stimulation

  • High SVR (from alpha-1 stim)
  • Reduced inotropy (beta-1 antagonism)

Increases risk for CHF and CV collapse

97
Q

Which beta-blocker is best in the setting of acute cocaine toxicity

A

Labetalol - because it’s a mixed alpha/beta antagonist

98
Q

Dosing for cocaine use as topical vasoconstrictor

A

1.5 - 3.0 mg/kg

Total dose = 150 - 200 mg

99
Q

2 Measures for decreasing the risk of LAST

A
  1. Test dose

2. Incremental dosing with period aspiration

100
Q

What are the treatments for LAST (first to last)

A
  1. Airway (100% FiO2)
  2. Treat Sz with benzos
  3. ACLS (low dose epi, no lidocaine)
  4. Lipid emulsion
  5. Avoid beta-blockers
101
Q

What medications can be used if benzodiazepines are ineffective in a patient seizing from LAST
Why

A

Succinylcholine or nondepolarizer to stop muscle contractions
Stopping sz minimizes O2 consumption, hypoxemia, and acidosis

102
Q

Why is propofol avoided in a patient with LAST

A

Because it augments myocardial depression that is already present

103
Q

What modifications are made to ACLS interventions for a patient with LAST

A
  1. Minimal epinephrine doses (<1 mcg/kg)
    - epi reduces effectiveness of lipid emulsion
  2. Avoid vasopressin
  3. Avoid lidocaine and procainamide
104
Q

What is the drug of choice for ventricular dysrhythmias in patients with LAST

A

Amiodarone

105
Q

What is the initial bolus dose for lipid emulsion therapy

A

20% of dose

1.5 mL/kg (lean body mass)

106
Q

What is the infusion dose for lipid emulsion therapy

A

0.25 mL/kg/min

107
Q

What intervention is taken if the symptoms of LAST are slow to resolve following initiation of lipid therapy

A

Repeat bolus dose up to 2 more times

Increase infusion to 0.5 mL/kg/min

108
Q

How long should the lipid infusion run for a patient with LAST

A

Continue infusion 10 min after achieving hemodynamic stability

109
Q

What is the maximum recommended dose of lipid emulsion in patients with LAST

A

10 mL/kg in the first 30 min

110
Q

What is lipid emulsion mechanism of action

A
  1. Lipids act as an intravascular reservoir sequestering LA and decreasing plasma concentrations
111
Q

What effect does lipid emulsion have on myocardial metabolism

A

Enhanced myocardial fatty acid metabolism

112
Q

What 2 inotropic effect does lipid emulsion have on cardiac inotropy

A
  1. Increases Ca++ influx

2. Increased intracellular Ca++ concentration

113
Q

What effect occurs at the cell membrane with lipid emulsion administration for LAST

A

Impaired local anesthetic binding to VG Na+ channels

114
Q

Why is return of hemodynamic instability a concern following lipid emulsion

A

It may reoccur due to local anesthetic duration exceeding that of the lipid emulsion

115
Q

If a patient with LAST is unresponsive to lipid emulsion, what is the treatment of last resort

A

Cardiopulmonary bypass

116
Q

What medications makeup tumescent anesthetic

A

Sodium chloride
Lidocaine
Epinephrine
Bicarbonate

117
Q

What is tumescent anesthesia

A

Dilute solution of NaCl, lidocaine, epi, and HCO3 injected into the adipose tissue during liposuction

118
Q

What is the maximum dose of lidocaine for tumescent anesthesia

A

55 mg/kg

119
Q

When does serum lidocaine concentration peak following tumescent anesthesia

A

12 hours

120
Q

When is lidocaine completely eliminated following tumescent anesthesia

A

36 hours

121
Q

When is general anesthesia recommended for patients receiving tumescent injection

A

When >2 - 3 L of tumescent is injected

122
Q

When does methemoglobin form

A

When the iron molecule on Hgb (Fe2+) is oxidized to its ferric form (F3+)

123
Q

What effect does methemoglobinemia have on oxygenation (3)

A
  1. Reduces O2-carrying capacity
  2. MethHgb can’t bind to O2
  3. LEFT SHIFT of Oxyhgb dissociation curve
124
Q

What local anesthetics can produce methHgb

A
  1. Benzocaine
  2. Cetacaine
  3. Prilocaine
  4. EMLA cream
125
Q

What non-local anesthetics can produce methHgb

A
  1. Phenytoin
  2. Nitroprusside
  3. NTG
126
Q

What are 6 signs and symptoms of methHgb

A
  1. Hypoxia unchanged by increased FiO2
  2. Cyanosis
  3. Chocolate colored blood
  4. Tachycardia
  5. Tachypnea
  6. Altered LOC
127
Q

What are the 3 physiologic result of methHgb

A
  1. Reduced O2 carrying capacity
  2. Tissue hypoxia
  3. Metabolic acidosis
128
Q

What s/sx are present with 20-50% HgbMet

A
  1. Tachypnea
  2. Tachycardia
  3. Altered mental status
  4. Slate-gray pseudocyanosis
129
Q

What s/sx are present with 50 - 70% HgbMet

A

Dysrhythmias

Coma

130
Q

What symptoms are present with <20% MetHgb

A

Usually none

131
Q

Why is the pulse oximetry altered with HgbMet

A

HgbMet absorbs both 660 nm and 940 nm infrared wavelengths equally, over deoxy and oxygenated blood

132
Q

What is the treatment for HgbMet

A

Methylene blue 1 - 2 mg/kg over 5 minutes

Max = 7 - 8 mg/kg

133
Q

What is the mechanism of action for methylene blue in the presence of HgbMet

A

It is metabolized by methemoglobin reductase forming leucomethylene blue. The metabolite donates and electron which reduces HgbMet back to Hgb

134
Q

What 2 states is methylene blue contraindicated

A
  1. Patients with glucose-6-phosphate reductase deficiency (no methemoglobin reducatase)
  2. Neonates (deficient methemoglobin reductase)
135
Q

What is the makeup of 5% EMLA cream

A
  1. 5% lidocaine

2. 5% prilocaine

136
Q

What is the onset of analgesia and maximum effect following EMLA application

A 
Onset =  1 hour
Max =  2 - 3 hours
137
Q

What skin conditions should be excluded from EMLA application and why

A
  1. Eczema
  2. Psoriasis
  3. Skin wounds

Altered PK can increase risk of toxicity, especially if skin isn’t intact

138
Q

Coadministration of which drug can quicken EMLA absorption

A

NTG

139
Q

Why are infants and small children more susceptible to toxicity from EMLA cream

A

Because the prilocaine oxidizes hgb to MetHgb

140
Q

Adding which medications to local anesthetic injection can improve analgesia (3)

A

Clonidine
Epinephrine
Opioids (neuraxial)

141
Q

The addition of this medication shortens onset of local anesthetic

A

HCO3

142
Q

Which 3 medications can prolong duration of local anesthetic block (3)

A
  1. Epinephrine
  2. Dexamethasone
  3. Dextran
143
Q

What additive improves diffusion of local anesthetic through tissue

A

Hyaluronidase

144
Q

How does epinephrine prolong local anesthetic duration

A

Vasoconstriction d/t alpha-1 agonist effect. Decreases LA systemic uptake

145
Q

How does dexamethasone prolong local anesthetic duration

A
  1. D/t glucocorticoid activity

2. Affects systemic uptake d/t steroid receptor action

146
Q

How do epinephrine and clonidine supplement analgesia with local anesthetic injection

A

The alpha-2 receptor agonism produces analgesia

147
Q

How do opioids affect a chloroprocaine epidural

A

Opioids reduce chloroprocaine effectiveness

148
Q

How does HCO3 shorten onset time of local anesthetic injection

A
  1. Alkalization increases pH and the number of lipid-soluble molecules
  2. Increased non-ionized molecule means higher concentration of LA to pass through membrane
149
Q

How much HCO3 is used to alkalize a local anesthetic injection

A

1 mL of 8.4% HCO3 with 10 mL of LA

APEX Pharmacology (8 decks)

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