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N929 Pharmacology II > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Local anesthetics are used to treat

A

chronic and acute pain; major component of clinical anesthesia

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2
Q

Local anesthetics are drugs that

A

reversibly block conduction of electrical impulses along nerve fibers

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3
Q

Schwann cells act to

A

support and insulate each axon

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4
Q

In unmyelinated nerves,

A

single Schwann cells cover several axons

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5
Q

In myelinated nerves,

A

the Schwann cell covers only one axon and has several concentric layers of myelin

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6
Q

To block impulses in myelinated fibers

A

it is necessary for local anesthetic to inhibit channels in three successive nodes

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7
Q

Fasciculi are

A

bundles of axons

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8
Q

The three connective tissues of fasciculi include

A

endoneurium, perineurium, and epineurium

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9
Q

The endoneurium is

A

a thin, delicate collage that embeds the axon in the fascicule

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10
Q

The perineurium consists of

A

layers of flattened cells that binds groups of fascicules together

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11
Q

The epineurium surrounds

A

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

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12
Q

The intracellular ratio of potassium is

A

30:1

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13
Q

The Nernst equation is

A

the potential to cause a reaction

expresses the charged created by K+ concentration gradient

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14
Q

The local anesthetic site of action is

A

specific sites on the Na+ channel
preferential to open and inactive states
to a lesser extent it also blocks K+ channels, Ca2+ channels and GPCRs

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15
Q

The mechanism of action of local anesthetics is to

A

block transmission of nerve impulses

LAs do not alter the resting transmembrane potential or threshold potential

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16
Q

The frequency-dependent blockade is

A

the use of a “use-dependent” or “phasic block”

the resting nerve is less sensitive to LA than one repeatedly stimulated

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17
Q

The modulated receptor hypothesis of LA action is

A

preference to attach during active or inactive states

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18
Q

Describe the mechanism of action of local anesthetics

A

diffusion of an unionized base across the nerve membrane
re-equilibrium between the base and cationic forms
binding of the cation to a receptor inside the sodium channel resulting in its blockade and inhibition of Na_ conduction

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19
Q

All local anesthetics are considered to be

A

weak bases

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20
Q

Nerves have different sensitivity to LAs based on

A

small diameter and lack of myelin (both enhance sensitivity)

larger nerves conduct impulses faster and are harder to block

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21
Q

Describe which nerve fibers are blocked first

A

preganglionic are blocked with low concentrations followed by small C fiber and small A fibers resulting in a loss of pain and temperature

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22
Q

The first thing that will be seen if a block is working is

A

vasodilation; an engorged arm

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23
Q

Type B fibers are

A

small in diameter <3
lightly myelinated
preganglionic autonomic vasomotor
have early block onset

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24
Q

Type C fibers are

A

found in the sympathetic and dorsal root
function as postganglionic vasomotor and pain, warm and cold temperatures, and touch
have no myelination
moderate diameter and early block onset

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25
Q

Type A fibers are

A

blocked last
heavily myelinated
large diameter

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26
Q

The chemical structure of local anesthetics includes

A

an aromatic ring system
tertiary amine
either an ester or amide linkage

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27
Q

Local anesthetics that are esters include

A

procaine, chloroprocaine, tetracaine, cocaine, benzocaine

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28
Q

Local anesthetics that are amides include

A

lidocaine, mepivacaine, prilocaine, bupivacaine, ropivacaine, articaine

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29
Q

The ester or amide linkage is relevant clinically because

A

it has implications for metabolism, duration, and allergic potential
affects drug potency, speed of onset, duration of action, and differential block potential

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30
Q

Key differences about esters include

A

ester metabolism is through plasma, occurs throughout the body and is rapid
esters have a higher potential for allergy- cross reactivity among esters
tend to have shorter acting due to ready metabolism

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31
Q

Key differences about amides include

A 
allergy is extremely rare- no cross allergy among the class or between ester and amide agents
metabolized in the liver
longer acting because they are more liphophilic and protein bound
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32
Q

The minimum effective concentration of LA is

A

necessary to produce conduction blockade of a nerve impulse
min. concentration of motor fibers approx. twice that of sensory fibers
less LA is needed for intrathecal vs. epidural anesthesia

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33
Q

An important distinction between LA and other medications is

A

agents are meant to remain localized in the area of injection- the higher the concentration injected, the faster the onset
systemic absorption results in termination of the drug

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34
Q

Absorption influences

A

drug termination and toxicity- the slower a LA is absorbed, the less likely toxicity

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35
Q

Lipid solubility correlates with

A

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

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36
Q

A strong relationship exists between potency and

A

lipid solubility

larger lipid-soluble LA are water insoluble and highly protein bound

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37
Q

LAs bind to

A

alpha 1 acid glycoprotein

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38
Q

These factors affect duration of action:

A

injection site

relationship between protein binding and lipid solubility- drug tends to remain in vicinity of Na+ channel

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39
Q

lidocaine, bupivacaine, and tetracaine onset and duration of action

A

lidocaine: fast, duration is 90-120 minutes
bupivacaine: slow, duration of action 180-600 minutes
tetracaine: slow; duration 180-600 minutes

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40
Q

Local anesthetic is absorbed the quickest via

A

intravenous, tracheal, caudal, paracervical, epidural, brachial, sciatic, subcutaneous

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41
Q

The speed of absorption has implications to

A

toxicity

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42
Q

LA cause relaxation of

A 
smooth muscle (lidocaine, ropivacaine, and cocaine are exceptions)
relaxation causes vasodilation that decreases duration of action, increases plasma concentration and potential toxicity
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43
Q

Additives include

A

clonidine, dexmedetomidine, epinephrine, opioids, sodium bicarbonate, ketorolac, dexamethasone, hyaluronidase

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44
Q

Epinephrine is a

A

vasoconstrictor that reduces the rate of vascular absorption- increased duration and potency of block while decreasing risk of systemic toxicity

45
Q

Epinephrine is unique in that it does not

A

prolong the block for all LA to same extent
lidocaine, mepivacaine, and procaine- local infiltration, peripheral nerve block and epidural
prilocaine and bupivacaine- prolonged with peripheral but not epidural

46
Q

Sodium bicarbonate is used as an additive because

A

it raises the pH of the LA solution resulting in more drug in the nonionized state
commonly used in epidurals
may result in less pain on injection
major limitation is the precipitation that can occur

47
Q

The absorption or injection of LA into systemic circulation results in

A

rapid redistribution

with esters broken down in blood and amides free floating

48
Q

Which organs receive the most local anesthetic first?

A

brain, heart, and lungs receive most initially because they are highly perfused- can be concerning because of toxic levels to brain and heart

49
Q

Renal dysfunction affects clearance

A

far less than hepatic failure

hepatic failure affects protein binding to both A1AG and albumin

50
Q

Pregnancy causes

A

mechanical changes that result in reduction in epidural space
hormonal changes that progesterone levels affect sensitivity to LA

51
Q

LAST is

A

local anesthetic systemic toxicity and is a serious but rare event during regional anesthesia

52
Q

LAST most commonly occurs from

A

an inadvertent intravascular injection- initial blocking of inhibitory neurons thought to cause seizures
blocking of cardiac ion channels results in bradycardia- Vfib is most serious complication

53
Q

Shorter acting drugs are thought to be

A

less cardiotoxic

more potent agents have higher lipid solubility and protein binding

54
Q

LAST is most common in

A

epidurals, axillary, and interscalene

very uncommon

55
Q

The classic clinical presentation of LAST:

A

rapid onset and includes agitation tinnitus, circumoral numbness, blurred vision, and metallic taste
followed by muscle twitching, unconsciousness, and seizures
very high levels can result in cardiac and respiratory arrest

56
Q

Prevention strategies for LAST include

A

test dosing, incremental injection with aspiration, use of pharmacologic markers, and ultrasound

57
Q

Treatment for LAST includes

A

prompt recognition and diagnosis
airway management priority followed by seizure suppression, prevent hypoxia and acidosis
lipid emulsion therapy
Vasopressors (no vasopressin)

58
Q

The lipid emulsion therapy mechanism of action is

A
  1. capture local anesthetic in blood (lipid sink)
  2. increased fatty acid uptake by mitochondria
  3. interference of Na+ channel binding
  4. Promotion of calcium entry
  5. accelerated shunting
59
Q

Max dose of lidocaine is

A

4 mg/kg; 7 mg/kg with epi

60
Q

Max dose of mepivacaine is

A

4 mg/kg; 7 mg/kg with epi

61
Q

max dose of bupivacaine is

A

3 mg/kg

62
Q

Max dose of ropivacaine is

A

3 mg/kg

63
Q

Max dose of procaine is

A

12 mg/kg

64
Q

Max dose of chloroprocaine is

A

11 mg/kg, 14 mg/kg with epi

65
Q

Max dose of prilocaine is

A

7 mg/kg; 8.5 mg/kg with epi

66
Q

Max dose of tetracaine is

A

3 mg/kg

67
Q

Esters are metabolized to and derivates of

A

para aminobenzoic acid (PABA)

68
Q

Side effects of local anesthetics include

A

methemoglobinemia- Fe2+ converted to ferric hemoglobin Fe3+ causing reduced oxygen carrying capability and tissue hypoxia
presents as decreasing oxygen saturation not responsive to therapy

69
Q

Prilocaine can cause methemoglobinemia because

A

one of its metabolites is ortho-toluidine
dosing should not exceed 2.5 mg/kg
should be avoided in children under 6, pregnant women, patients taking other oxidizing drugs

70
Q

Treatment of methemoglobinemia includes

A

methylene blue, transfusion, or dialysis

71
Q

Cauda equina syndrome

A

manifests as bowel and bladder dysfunction with lower extremity weakness and sensory impairment related to cord ischemia
risk factors include supernormal doses of LA or maldistribution of LA within intrathecal space

72
Q

Transient neurologic symptoms are associated with

A

intrathecal lidocaine and can present as burning, aching, cramp like pain in the low back and radiating down the thighs
other risk factors include lithotomy position and outpatient surgery

73
Q

Lidocaine is used for

A

antiarrhythmic, topical, induction, nebulized, multimodal pain management, regional anesthetic

74
Q

lidocaine is used in the ACLS algorithm to

A

depress myocardial automaticity

75
Q

EMLA or Eutetic mixture of local anesthetic is

A

1:1 lidocaine: prilocaine mixture used to numb skin

76
Q

EMLA is contraindicated in

A

mucous membranes, broken skin, infants <1 month, history of methemoglobinemia

77
Q

Lidocaine can be used on induction to

A

decrease pain of Propofol, attenuate CV response to intubation, attenuate increase in ICP in patients with decreased compliance
may also attenuate cough

78
Q

Topical lidocaine can be used to

A

Decrease “emergence phenomenon”- coughing, sore throat, and dysphonia

79
Q

LTA administered at induction has little effect on

A

prevention of coughing during extubation; surgeries <2 hr., reduced coughing by 26%
30 minutes prior to extubation caused significant decrease in coughing

80
Q

The most effective technique to prevent emergence phenomenon is

A

using alkalozied lidocaine in the cuff
needs approximately 60 minutes required to achieve desired effect, low does alkalized lidocaine (40 mg) shown to be more effective

81
Q

The technique used in the alkalized lidocaine cuff is:

A 
achieve correct pressure using air
remove and record amount of air required
add 2 mLs of lidocaine
add 1-2 mLs of sodium bicarbonate
add saline to match cuff volume
82
Q

An airway block is achieved by

A

4% lidocaine applied directly to oropharynx or a transtracheal block of 4% lidocaine injected through the cricothyroid membrane

83
Q

Infusions of lidocaine have been used

A

as part of a multimodal management plan to supplement general anesthesia

84
Q

the mechanism of action of lidocaine infusions

A

relatively unknown
may involve sodium channels
block priming of polymorphonuclear granulocytes

85
Q

Lidocaine infusions are used for

A

reduction of postoperative pain and speed up return of bowel function in open and laparoscopic procedures
decrease pain and improve functional outcomes in prostatectomy, thoracic, and spine procedures

86
Q

Concerns with lidocaine infusion

A

accumulation

87
Q

Lidocaine infusions are considered to be

A

uncertain to the benefits in pain score, GI recovery, PONV, and opioid consumption

88
Q

Peripheral nerve blocks include

A

Bier block

89
Q

Neuraxial anesthesia includes

A

spinal and epidural

90
Q

A bier block is

A

an intravenous regional anesthesia
indicated for short procedures
25-50 mL of 0.5% lidocaine–> onset time 5-10 minutes
tourniquet pain at 20 minutes

91
Q

With epidural anesthesia, we should always

A

aspirate and test dose

can always convert labor epidural to a surgical epidural

92
Q

Effects of lidocaine on organs include:

A

CNS, respiratory, cardiovascular, immunological, musculoskeletal, hematological

93
Q

1-5 mcg/mL of lidocaine in plasma causes

A

analgesia

94
Q

5-10 mcg/mL of lidocaine in plasma causes

A

circumoral numbness, tinnitus, skeletal muscle twitching, systemic hypotension, myocardial depression

95
Q

10-15 mcg/mL of lidocaine in plasma causes

A

seizures, unconsciousness

96
Q

15-25 mcg/mL of lidocaine in plasma causes

A

apnea & coma

97
Q

> 25 mcg/mL of lidocaine in plasma causes

A

cardiovascular depression

98
Q

Treatment for LAST includes:

A

benzodiazepines and hyperventilation- raises seizure threshold
propofol reliably terminates seizure activity
maintain a clear airway
adequate ventilation and oxygenation

99
Q

The administration of 1.5 mg/kg of lidocaine can

A

decrease cerebral blood flow and ICP, block reflex bronchoconstriction on intubation, blunt sympathetic response to intubation

100
Q

Exparel is

A

bupivacaine combined with liposomal agent

101
Q

Exparel is used as

A

part of a multimodal treatment regimen to provide non-opioid pain control
-dose is based on surgical site and volume required to cover the area

102
Q

Exparel should only be administered with

A

bupivacaine, never lidocaine

103
Q

Exparel should be used cautiously in patients with

A

hepatic disease

104
Q

Contraindications to exparel include

A

obstetrical paracervical blockade
Patients <18 years of age
epidural or intrathecal anesthesia
certain peripheral nerve blocks

105
Q

Adverse effects of exparel include

A

> 10% nausea and vomiting

<10% dizziness, tachycardia, headache, somnolence, bradycardia, hypoesthesia, lethargy

106
Q

Cocaine is used primarily

A

topical anesthesia of the nose and throat

107
Q

Cocaine has the ability to

A

block the monoamine transporter in the adrenergic system

blocking reuptake of catecholamines resulting in significant vasoconstriction

108
Q

Cocaine should be used with caution with

A

other epinephrine containing solutions, MOA inhibitors, tricyclics

N929 Pharmacology II (16 decks)

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