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Pharmacology 2 > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Local anesthetics cause a loss of sensation in a discrete region of the body (regional anesthesia), how is this done?

A

Local anesthetics cause a loss of sensation in a discrete region of the body (regional anesthesia)

caused by inability of nervous impulses to be transmitted to the brain*

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2
Q

Local anesthetics cause a loss of sensation in a discrete region of the body (regional anesthesia), what can mimic the LA?

A

may be mimicked by anoxia, trauma, hypothermia, or chemicals irritants (such as alcohol or phenol)

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3
Q

RMP (resting membrane potential) determined by what electrolyte concentration, will differential across nerve cell membrane (neurolemma)*

A

RMP (resting membrane potential) determined by K + concentration differential across nerve cell membrane (neurolemma)*

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4
Q

What is the resting membrane potential voltage inside the cell?

A

Inside of cell is -70mv relative to outside

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5
Q

If the neuron is stimulated, what happens? in terms of electrophysiology.

A

If neuron is stimulated (depolarized) (Na channels open, Na goes in the cell while K goes out)

  • action potential is triggered
  • Negative wave moves along outer cell membrane
  • -Membrane becomes permeable to Na +
  • This depolarizes the neurolemma
  • -Na+ permeability gets turned off and K+ gets turned on to turn off depolarization (turns off to reset the RMP)
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6
Q

How fast can a nerve conduction happen?

A

One millisecond has elapsed (this happens quickly) during an actionpotential

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7
Q

Local anesthetics are poorly soluble in what solution?

A

Local anesthetics are poorly soluble in water.

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8
Q

Generally, local anesthetics with a chiral center, which enantiomers is less toxic?

A

Generally, local anesthetics with a chiral center, the S (Left) enantiomers are less toxic than the R.

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9
Q

What three chemical structures do local anesthetics consist of?

A

Aromatic residue:
Intermediate chain:
Amino group:

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10
Q

What is the Aromatic residue in the Local Anesthetics?

A

Aromatic residue: benzoic acid derivative; lipophilic*

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11
Q

What is the intermediate chain in the local anesthetics?

A

Intermediate chain: contains ester OR amide bond (this connects the the aromatic residue and the amino group)

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12
Q

What is the amino group in the local anesthetics?

A

Amino group: secondary or tertiary amine; hydrophilic*

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13
Q

What part of the local anesthetic chemical structure is hydrophilic?

A

Amino group: secondary or tertiary amine; hydrophilic*

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14
Q

What part of the local anesthetic chemical structure is lipophilic?

A

Aromatic residue: benzoic acid derivative; lipophilic*

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15
Q

What is the mechanism of action for local anesthetics?

A

Inhibits voltage-gated sodium channels*

Reversible blockade of neural tissue

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16
Q

Do local anesthetics work inside or outside the cell?

A

Must be delivered to inside of cell membrane to be effective* (non-ionized reaction will pass through membrane)
Un-charged base is needed to penetrate neurolemma
Charged salt is needed to bind to receptor site (from the inside)

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17
Q

How can local anesthetics block potassium channels??

A

Local anesthetics Can also block K+ channels (need to give a lot for this), higher concentrations needed to do so (we don’t go near this)

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18
Q

How are Local Anesthetics classified as?

A

Aminoesters (COO) or aminoamides (NHCO)

  • -weakly basic compound
  • -different metabolic pathways
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19
Q

What plasma proteins do local anesthetics bind to?

A

Bind to plasma proteins (a1-acid glycoprotein and serum albumin)

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20
Q

In marketed epi-containing solutions, the pH is even where? and almost no molecules exist in what form?

A

In marketed epi-containing solutions, the pH is even lower, and almost no molecules exist in the un-ionized form (the pH is even lower to preserve the epinephrine)

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21
Q

How does charged and uncharged portions of local anesthetics interact with cell membranes?

A

Uncharged species penetrates lipid membrane

Charged species interacts with receptor

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22
Q

Which chemical substitution will increase the the lipid solubility and potency of local anesthetics?

A

Increasing alkyl substitution increases lipid solubility and potency*
on aromatic ring or tertiary amine
lengthening chain increases potency and toxicity*

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23
Q

What determines the onset of a local anesthetics?

A

Onset is pKa (the more non-ionized the faster the onset)

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24
Q

What determines the potency of a local anesthetic?

A

Potency is length of chain and Lipophilicity (the longer the chain the more potent the drug, will also increase the toxicity)

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25
Q

What determines the duration of a local anesthetic?

A

Duration is Protein Binding (the more protein bond the longer it will last or the more it will hang around)

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26
Q

Compounds with asymmetrical carbons (chiral) have optical isomers (enantiomers), will this have a different properties than a racemic mixture?

A

Compounds with asymmetrical carbons (chiral) have optical isomers (enantiomers), MAY have different properties than racemic mixture
D(+) isomer has greater CV toxicity, prefer the S (Left) isomer**

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27
Q

State dependent blockade: block depends on the state of the sodium channel receptor, What are the three states in which the receptor can be in?

A

State dependent blockade: block depends on the state of the sodium channel receptor: resting vs. activated vs. inactivated

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28
Q

Frequency and voltage-dependence of Na-channel block, when do local anesthetic have a
higher affinity when channels are (what state) or which state of the cell (in terms of voltage)?

A

Frequency and voltage-dependence of Na-channel block

higher affinity when channels are inactivated or when cell is hyper-polarized

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29
Q

Degree of blockade by local anesthetic depends upon how much the nerve has been stimulated, what state of the nerve will have a less sensitive to a block?

A

resting nerve less sensitive to blockade than one repeatedly stimulated

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30
Q

Degree of blockade by local anesthetic depends upon how much the nerve has been stimulated, what does a higher frequency of stimulation mean in terms the degree of blockade?

A

higher frequency stimulation = greater degree of blockade

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31
Q

What are the 5 things the LA block depends on in terms of susceptibility?

A
  1. Length of nerve fiber exposed to LA
    1. Presence of myelin (makes the block better)
    2. Size of fiber
    3. Position of fiber in nerve bundle (we inject outside the bundle) (the center of the bundle will take longer to block)
    4. Specific LA (onset)
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32
Q

What are the types of afferent fibers, in order, that will get block first from a local anesthetic?

A
  • —(first) B: pre-ganglionic myelinated, vasocontriction, skin temp (when you block this, you will have vasodilation and feel hot)
  • –(2nd) C: post-ganglionic un-myelinated. Nociceptors of paleo-spinothalamic tract (slow pain).
  • –(third) A-delta (Aδ): free nerve endings of touch and pressure. Cold thermoreceptors. Nociceptors of neo-spinothalamic tract (fast pain).
  • —A-gamma (Ay) fibers (pressure?)
  • -Aβ: cutaneous mechanorecptors
  • -Aα: muscle spindle (also motor)
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33
Q

Toxicity (meaning this has to hit the blood stream) is based on dose and rate of absorption (depends where you put it, if you put it IV its going to be the fastest), this can be decreased by what?

A

Toxicity (meaning this has to hit the blood stream) is based on dose and rate of absorption (depends where you put it, if you put it IV its going to be the fastest)
decreased by vasoconstrictors (slow down absorption)

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34
Q

Toxicity for a local anesthetic is related to non-bound or bound drug???

A

Toxicity of a local anesthetic is related to non-bound drug concentration (unbond drug is what will cause effect)

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35
Q

Esters hydrolyzed by?

A

Esters hydrolyzed by plasma esterases, probably cholinesterase

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36
Q

Local anesthetics are bound by what two things?

A

Bound by plasma proteins and lung tissue

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37
Q

Amide-linked local anesthetics are degraded by what organs?

A

Amide-linked local anesthetics are degraded by hepatic endoplasmic reticulum

  • –N-dealkylation and hydrolysis (makes more water soluble)
  • –lung uptake may also be important
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38
Q

Amide-linked local anesthetics are

bound extensively to plasma protein?

A

Amide-linked local anesthetics are

bound extensively to a1-acid glycoprotein (binds to weak bases)

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39
Q

LA’s decrease electrical activity of all excitable tissues (including cardiac) At low doses LA’s are effective at what?

A

LA’s decrease electrical activity of all excitable tissues (including cardiac), At low doses LA’s are effective anticonvulsants by raising the seizure threshold (B/C it blocks Na channel)

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40
Q

As plasma levels rise, local anesthetics cause what? (in terms of toxicity s/s)

A

As plasma levels rise, local anesthetics cause light-headedness, dizziness, paresthesias (usually get ringing in the ears), Further increase cause disorientation, LOC, and tonic-clonic seizures

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41
Q

LA’s depress electrical conduction in myocardial tissues

greater affinity for sodium channels when channel is in what position?

A

LA’s depress electrical conduction in myocardial tissues
greater affinity for sodium channels when channel is in open position (frequency dependent blockade) tachycardia potentiates cardiac toxicity*

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42
Q

What kind of kinetics does Bupivacaine display?

A

Bupivacaine displays fast-in slow-out kinetics (this is not good)

  • -compared with lidocaine
  • -potentiated by hyperkalemia
  • -Progesterone may increase susceptibility (pregnancy makes it worst)
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43
Q

What is the name of the preservative that local anesthetics contain?

A

Methylparaben

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44
Q

What is the purpose of the preservative in local anesthetics?

A

Methylparaben is used to inhibit microbial growth

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45
Q

What is one side effect of methylparaben?

A

Methylparaben can be a potent allergen

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46
Q

Preseverative containing local anesthetics should not be used for which type of blocks?

A

Preservative containing local anesthetics should NOT be used for neuraxial blockade (spinal, epidural or caudal)*

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47
Q

What does Procaine get rapidly metabolized into? why is this bad?

A

Rapidly metabolized to PABA (this is an allergenic agent?), prob by plasma cholinesterase

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48
Q

What is the concentration of 2-chloroprocaine?

A

2-3%

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49
Q

What is the onset of 2-chloroprocaine?

A

5-15min

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50
Q

What is the duration of 2-chloroprocaine?

A

30-45-min

30-90 w/ Epi

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51
Q

What is the maximum dosage of 2-chloroprocaine?

A

800mg

1000mg w/ Epi

52
Q

What is the potency and toxicity of 2-chloroprocaine?

A

potency is low

toxicity is low

53
Q

How is 2-chloroprocaine made?

A

Produced by chloride substitution of the aromatic ring, this increases susceptibility of ester ring to hydrolysis and allows for a rapid onset and short duration

54
Q

When 2-chloroprocaine is in plasma, the t1/2b is 21 seconds, what does this mean?

A
  • –Can use high concentrations with decreased risk of toxicity
  • –Increased toxicity with plasma cholinesterase deficiency
55
Q

What is 3% 2-chloroprocaine used for?

A

3% solution used for epidural blockade

56
Q

What is 2% 2-chloroprocaine used for?

A

2% for peripheral neural block (onset really quick)

57
Q

What are the two preservatives that are issues with 2-chloroprocaine?

A

Preservative problems
—sodium bisulfite (this is an irritant)
neural irritation following SAB
—-ethylenediaminetetracetic acid (EDTA) (need this in the drug, but this is reason why you cant use it for a spinal) (it causes->)
back pain/spasms

58
Q

What is tetracaine used for?

A

–Excellent topical anesthetic (2%)
–Highly lipophilic - rapidly absorbed into bloodstream
(eyedrops)
–Available in lyophilized form (frozen and dehydrated), or a 1% solution for SAB
—-reconstituted with 10% dextrose, CSF or sterile water for SAB
—-2-3 minute half life in plasma

59
Q

How would you use tetracaine for spinal anethesia?

A
  • Used for spinal anesthesia: 1% solution
  • Usual dose: 5-15mg
  • Usually mixed with D10W in equal parts (this makes it dense)
  • Epinephrine use with SAB increases duration by 25%
60
Q

What toxicity property will cocaine relate to?

A

–Toxicity related to vasoconstrictive properties and actions on catecholamine metabolism
–Can cause hypertension and coronary vasospasm
resulting in ischemia and infarction

61
Q

Cocaine Blocks catecholamine uptake centrally and peripherally, by blocking what neurotransmitter reuptake is likely cause of euphoric effect

A

Blocks catecholamine uptake centrally and peripherally

blocking dopamine reuptake is likely cause of euphoric effect* (this is the high)

62
Q

what is cocaine hydrolyzed by?

A

Hydrolyzed by esterases

  • —Between 1% & 10% excreted unchanged in urine
  • –Safer alternatives: lidocaine and neosynephrine
  • –Do not use in liver failure patients
63
Q

Lidocaine is metabolized by what?

A

Metabolized by mixed-function oxidases and amidases

  • –De-ethylation of the amino nitrogen leads to monoethylglycine xylidide (MEGX) and glycine xylidide
  • —-MEGX may be seizuregenic* (only if you give this in a high dose?)
64
Q

With Lidocaine, acidosis increase toxicity because?

A

Acidosis increases toxicity (because it)

Decreases plasma protein binding

65
Q

Do we use lidocaine for SAB?

A

Use of hyperbaric (denser than spinal fluid) lidocaine for SAB (subarachnoid block) is controversial***
—“Not for spinal anesthesia”

66
Q

what is the dose and how do we use lidocaine for regional anesthesia?

A

IV regional anesthesia (UE) (upper extremity) : 50 cc of 0.5% preservative free and NO epi

67
Q

What is the concentration of lidocaine?

A

0.5-2%

68
Q

What is the onset of lidocaine?

A

15min

69
Q

What is the duration of lidocaine?

A

30-120min

120-360min w/ Epi

70
Q

What is the maximum dosage of lidocaine?

A

300mg

500mg w/ Epi

71
Q

What is the potency and toxicity of lidocaine?

A

potency is moderate

toxicity is moderate

72
Q

What kind of structure is Mepivacaine?

A

Dual ring structure

73
Q

Which medication is Mepivacaine similar too?

A

Local anesthetic properties similar to lidocaine

  • –slightly less toxic
  • —“MPF”: methyl-paraben free
  • –Less vasodilation than lidocaine*
74
Q

What patient population do we not use mepivacaine for?

A

Not for OB use* (because of), Prolonged half life in fetus, the fetus is unable to metabolize double ring structure

75
Q

What is the concentration of Mepivicaine?

A

1-2%

76
Q

What is the onset of Mepivicaine?

A

15min

77
Q

What is the duration of Mepivicaine?

A

60-140min

140-200 min w/ Epo

78
Q

What is the maxmum dosage of Mepivicaine?

A

400mg

500mg w/ Epi

79
Q

What is the potency and toxicity f Mepivicaine?

A

Potency is moderate

Toxicity is moderate

80
Q

Prilocaine is an analog of which Local anesthetic?

A

it is a Lidocaine analog which has a Similar onset and duration

81
Q

Why is Prilocaine not widely used?

A

Not widely used because of association with methemoglobinemia**

  • –metabolic product is 3- and 5- hydroxytoluidine
  • –potent oxidants of hemoglobin
82
Q

What is the treatment of Methemoglobinemia?

A

Methylene blue

83
Q

What is EMLA cream?

A

EMLA cream used as topical anesthetic

  • —Eutectic mixture local anesthetic: melting point of cream (18 deg C) is less than individual components
  • —Lidocaine 2.5% and prilocaine 2.5%
84
Q

What are some characteristics of Bupivacaine?

A
  • -Potent, longer-acting LA
  • -High pKa limits placental transfer
  • -Longer latency to onset
  • -Differential blockade*
  • —-Often good sensory blockade with minimal motor blockade
85
Q

What makes Bupivacaine different from other LA in terms of CNS toxicity?

A

No aura of CNS toxicity prior to cardiovascular collapse (you don’t see any mental symptoms, you just see the cardiovascular collapse) this has a Fast-in, slow out kinetics in myocardial tissue (not good)

86
Q

Which concentration of Bupivacaine is banned for OB anesthesia?

A

0.75% banned by FDA for use in OB anesthesia (use it for spinals, not epiduals)

87
Q

Is Bupivacaine used for IV regional anesthesia?

A

Not for IV regional anesthesia

88
Q

What is the concentration for Bupivicaine?

A

0.25-0.75%

89
Q

What is the onset of Bupivicaine?

A

10-20min

90
Q

What is the duration of Bupivicaine?

A

120-240min

180-240min w/ Epi

91
Q

What is the maximum dosage for Bupivicaine?

A

175mg

225mg w/ Epi

92
Q

What is the potency and toxicity of Bupivicaine?

A

potency is high

Toxicity is high

93
Q

Ropivacaine is chemically similar to which two local anesthetics?

A

Chemically similar to bupivacaine and mepivacaine
Wanted long acting LA like bupivacaine (with motor sparing) and lower toxicity similar to mepivacaine

Arrhythmogenicity intermediate between mepivacaine and bupivacaine

94
Q

What is Ropivacaine used for?

A

Not marketed for spinal anesthesia

  • –Used extensively for epidural anesthesia
  • –(great for blocks, has a better margin of safety)
95
Q

What is the concentration of Ropivicaine?

A

0.5-1%

96
Q

What is the onset of Ropivicaine?

A

15 min

97
Q

What is the duration of Ropivicaine?

A

2-6hr

98
Q

What is the Maximum dosage of Ropivicaine?

A

200mg

99
Q

What is the potency and toxicity of Ropivicaine?

A

Potency is moderate

Toxicity is low

100
Q

What kind of concentration do you need to block thicker nerves?

A

Higher concentration to block thicker nerves e.g., sacral nerve roots and sciatic nerve

101
Q

What two things can you do with a local anesthetic if you want to block a highly vascular area?

A

Need more drug to block highly vascular area, or use epi containing solutions*

102
Q

What physical properties determine the onset and duration of a local anesthetic?

A

Axonal length and diameter have an impact on onset and duration

103
Q

what environment are local anesthetics less effective in?

A

Local anesthetics are less effective in infected (acidotic) tissues

104
Q

How can you create a more intense analgesia with a SAB and Epidural anesthetic?

A

SAB and epidural anesthetics are often combined with opioids for more intense analgesia

105
Q

How can you prolong the duration of action and reduce plasma levels of a local anesthetic?

A

Prolong action and reduce plasma levels by the addition of vasoconstrictors

  • —Lidocaine with epi: 1:100,000; 1:200,000* to see HR
  • –More epi is not better!
  • –Epi serves as a marker of accidental IV injection
106
Q

Which patient population should you be careful with, when using local anesthetics w/ vasoconstrictors? other than obstetrics?

A

Use carefully with patients with cardiovascular disease

  • –unstable angina, hypertension
  • –Peripheral vascular disease, diabetics
107
Q

Local anesthetics w/ vasoconstrictors may be contraindicated in what patient population? other than cardiac?

A

May be contraindicated in obstetric use

uteroplacental insufficiency

108
Q

What makes epi-containing local anesthetic different from non epi-containing? in terms of pH

A

Manufactured epi-containing solutions have a lower pH than non-epi solutions

  • –Therefore: more drug ionization
  • –Anti-oxidant added to solution (sufites) to prevent oxidation of epi
  • —Potential increased for allergic reactions
109
Q

What happens when you inject epi-containing local anesthetic in the artery?

A

Accidental intra-arterial injections can produce intense vasospasm in distal circulation (avoid this)

  • —IA injection can produce CNS toxicity with small drug dose
  • —Do NOT use epi solutions to inject near terminal blood vessels (finger, toes, penis)
110
Q

What will cause more toxicity? bound or unbound drug? in terms of local anesthetics.

A

CNS toxicity is related to available levels of free drug*

—Factors that decrease protein binding can increase the likelihood of achieving toxic levels

111
Q

Why should you be cautious of injections in the head or neck with local anesthetics?

A

Injections in the head and neck can result in rapid onset CNS toxicity (seizures) with minimal intra-arterial injection of LA via retro-grade flow to the brain
—-Reaction to LA in dental office (b/c they inject into vasculature and get a normal response)

112
Q

How can you get a transient CNS toxicity with local anesthetics?

A

Transient CNS toxicity may be seen when the tourniquet is released after IV regional anesthesia (.5% is 5mg/kg, so you essential gave a bolus of lidocaine)

113
Q

What type of local anesthetic class will you more likely get an allergic reaction too?

A

More likely to be allergic to the esters not so much the amides (LA)

114
Q

How can you increase the seizure threshold while using local anesthetics?

A

Concomitant use of benzodiazepines may be helpful in elevating seizure threshold
diazepam, midazolam

115
Q

How do you reduce the risk of getting a toxic level of local anesthetics?

A

Anytime one administers large volumes of LA, potential toxicity is a risk factor

  • —Inject only 5cc at a time
  • —Inject slowly
  • –Carefully aspirate
116
Q

what is the max dose (mg/kg) for lidocaine?

A

4.5mg/kg

7mg/kg w/ epi

117
Q

what is the max dose (mg/kg) for Bupivacaine?

A

2.5mg/kg

3mg/kg w/ epi

118
Q

what is the max dose (mg/kg) for chloroprocaine?

A

10mg/kg

15mg/kg w/ epi

119
Q

What is the duration of lidocaine?

A

120min

240min w/ epi

120
Q

What is the duration of bupivacaine?

A

4h

8h w/ epi

121
Q

What is the duration of chloroprocaine?

A

10min

90min w/ epi

122
Q

What does LAST stand for?

A

LAST (Local Anesthetic Systemic Toxicity) (what happens when you put the wrong stuff in the wrong place)

123
Q

How do you manage LAST?

A
  • –Must have all ASA monitors and resuscitation equipment available as well as 20% lipid emulsion
  • —Administer supplemental O2
  • —Protect the airway from aspiration and provide adequate ventilation
  • —Administer anticonvulsants to terminate seizures if indicated (do not use propofol (b/c of the cardiac depressive properties))
124
Q

How do you administer lipid emulsion for LAST?

A

–Administer 20% lipid emulsion 1-3mg/kg followed by an continuous infusion of .25-.5ml/kg/hr. You can repeat bolus 2 or 3 times ** (know these numbers?) (in real life you open this wide open)
—You must continue chest compressions if indicated until a viable rhythm and vital signs have stabilized.
(keep giving this in icu for at least a day, post arrest)

125
Q

How long will you perform resuscitation for LAST?

A
  • –Normally will perform resuscitation efforts for 1 hour or more (compared to CPR for other causes)
  • –Patient must be monitored post-resuscitation for recurrence of toxicity in an acute care setting.
  • –Usually need a lipid infusion post-resuscitation

Pharmacology 2 (11 decks)

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