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*Pharmacology > Apex- Local Anesthetics > Flashcards

Apex- Local Anesthetics Flashcards

1
Q

Local anesthetics inhibit peripheral nerves (speed of onset) in what order?

-A fibers (a,b,d,g); B fibers; C fibers

A
  1. B
  2. C
  3. A gamma
  4. A delta
  5. A beta
  6. A. Alpha
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2
Q

Conduction velocity is increased by what 2 things

A

degree of myleination and a wider axon diameter

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3
Q

Mylin insulates the axon and allows the electrical current to skip along the uninsulated regions, known as :

What is this process called?

A

Nodes of Ranvier

-saltatory conduction

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4
Q

What measure for local anesthetics is analogous to ED50 for IV drugs and MAC for volatile anesthetics?

A

Cm - Minimum effective Concentration

-quantifies the concentretion of a local anesthetic that is required to block conduction

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5
Q

What is a good example of a differential blockade and why?

A

Epidural BPV

  • in low concentrations it provides analgesia and spares motor function
  • as concentration is increased, it anesthetizes resistant nerves that control motor function and proprioception
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6
Q

label from top to bottom

A
  • Epineurum
  • Perineurium
  • Endoneurium
  • Mylin sheath
  • Axon
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7
Q

Which type of nerve fibers mediate skeletal muscle tone?

A

A-gamma

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8
Q

Which peripheral nerve fibers mediate touch and pressure?

A

A- Beta

(touch and pressure - oh Baby)

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9
Q

Local anesthetics can bind to the voltage-gated sodium channel when it is in the

  1. Resting and active states
  2. Resting and inactive states
  3. Active and inactive states
  4. Active state only
A
  1. Active and inactive states
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10
Q

Local anesthetics preferentially bind to what subunit of the sodium channel

A

alpha subunit

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11
Q

The guarded receptor hypothesis states that local anesthetics can’t bind when a receptor is in which state?

A

resting state

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12
Q

What 3 states can the sodium channel exist in? (what mV are each)

A

Resting

  • -70mV
  • Closed (able to be open)

Active:

  • -70- +35mV
  • When TP is reached, channel opens and NA+ follows it’s concentration gradient (inside to outside)

Inactive:

  • +35- -70mV
  • Channel is closed
  • Inactivation gate plugs the channel until RMP is restablished
    • Restoration of RMP converts the channel from the inactive state to the resting state, at which point the nerve can be stimulated again
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13
Q

T/F: Local anesthetics have no effect on TP or RMP

A

True!

-When a cricial number of sodium channels are blocked by a local anesthetic, sodium is unable to enter the neuron in sufficent quantity

>cell can’t depolarize

>action potential can’t be propagated

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14
Q

What electrolyte regulates RMP vs TP

A

RMP- K

TP- CA

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15
Q

What is the RMP and TP in the peripheral nerves?

A

RMP = -70mV

TP = -55mV

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16
Q
  • Decreased serum K = RMP becomes more (negative postive)
  • Increased serum K = RMP becomes more (negative/positive)
A
  • decreased serum K = RMP more negative (more K leaking out)
  • increased serum K = RMP more positive (less K leaking out)

Think gradients

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17
Q
  • Decreased serum CA++ - TP becomes more (negative/positive)
  • increased serum CA++ - TP becomes more (negative/positive)
A

decreased serum Ca- TP becomes more negative (think you give CA to raise the TP)

-increased serum CA - TP becomes more positive

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18
Q

T/F- local anestheetics bind to the alpha-subunit on the outside of the sodium channel

A

false- inside of the sodium channel (when in the active or inactive state)

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19
Q

Select the true statement regarding the primary MOA of local anesthetics:

A. The conjugate acid binds to the extracellular portion of the sodium channel

B. The conjugate acid binds to the intracellular portion of the sodium channel

C. The uncharged base binds to the extracellular portion of the sodium channel

D. The unchanged base binds to the intracellular portion of the sodium channel.

A

B. The conjugate acid binds to the intracellular portion of the sodium channel

-local anesthetics are weak bases; when placed into a soultion, they dissociate into an unchanged base and its conjugate acid

-the uncharged base from is required to gain entry into the cell; however, it’s actually the conjugate acid that binds to the sodium channel

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20
Q

Are local anesthetics weak acids or weak bases

A

weak bases

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21
Q

What happens after you inject a local anesthetic around a nerve?

A

It rapidly dissociates into an uncharged/non-ionized base (LA) and an ionized conjucate acid (LA+)

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22
Q

What is the primary determinant of a local anesthetics onset?

A

pKa

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23
Q

What is the primary determinant of potency?

A

Lipophilicity

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24
Q

What is added to some local anesthetics to reduce the rate of vascular uptake in order to prolong the duration of action?

A

Vasoconstrictors / Epi

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25
Q

What is pKa

A

The pH where 50% of the drug exisits as uncharged/nonionized form and 50% charged/conjugate acid

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26
Q

What 3 places can the local anesthetic travel after injected near a peripheral nerve?

A
  1. into the nerve
  2. surrounding tissues & bind proteins
  3. systemic circulation
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27
Q

T/F- local anesthetics are packaged as salts in aqueous solutions

A

true

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28
Q

T/F- the vial soluations are aciditc to help prevent preciptiation

A

True

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29
Q

3 main components of the local anesthetic molecule

A
  1. Benzene ring (lipophilic- permits diffusion thru lipid bilayers)
  2. Intermediate side chain (determines class- ester or amide; metabolism, and allergic potential)
  3. Tertiary amine (hydrophilic, accepts proton, makes molecule a weak base)
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30
Q

What determines the local anesthetics drug glass (ester/amide)

A

The intermediate side chain

  • blue = ester
  • orange = amide
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31
Q

What is the blue thing and what purpose does it serve

A

Benzene ring

-lipophilic - permits diffusion thru lipid bi-layers

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32
Q

What is the yellow structure

blue vs orange

what purpose does it serve

A

intermediate side chain

-determines the drug class

blue = ester

orange = amide

-determins how it will be metabolized (ester = esterases, amide = p450)

& allergic potential

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33
Q

What structure determins allergic potential

A

the intermediate chain (yellow)

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34
Q

What is the pink structure and what puprose properites does it have (3)

A

teriary amine

  • hydrophillic
  • accepts proton
  • makes molecule a weak base
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35
Q

Which structure makes a molecule a weak base?

A

The tertiary amine (pink)

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36
Q

Two classes of local anesthetics

A

Esters and Amides

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37
Q

Which local anesthetic undergoes both hydrolysis by pseudocholinesterase and P450 metabolism?

A

Cocaine

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38
Q

T/F- a patient with liver disease should receive a reduce dose of single shot amide local anesthetic

A

False

however, dose should be reduced by 10-50% if repeat injections or a continuous infusion are planned

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39
Q

What is the allergic potential of a local anesthetic governed by?

A

The intermediate chain

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40
Q

T/F- true local anesthetic allergy is more likely with an amide compared to an ester

A

false

ester > amide

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41
Q

Why are esters more likely to cause a true local anesthetic allergy

A

because of the PABA metabolite

(Para-aminobenzoic acid) - immunogenic molecule capable of causing an allergic reaction

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42
Q

Which local anesthetic class has cross-sensitivity within the class

A

esters

  • if allergic to one ester, avoid the rest and give an amide instead
  • if allergic to one amide, can use another amide without issue (no PABA)
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43
Q

Ester or Amide:

-COO-

A

Ester

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44
Q

Ester or Amide:

-NHCO-

A

Amide

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45
Q

Which characteristics correlate BEST with a local anesthetic duration of action

  1. Protein binding
  2. Lipid solubility
  3. pKa
  4. Concentration
A

1. Protein binding

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46
Q

Match:

onset of action:

potency:

duration of action:

Primary variables: lipid solubility, protein binding, pka

Secondary variables: intrinsic vasodilating effect, lipid solubility, dose, addition of vasoconstrictors, concentration

A

onset of action: pKa

  • dose, concentration

potency: lipid solubility

  • intrinsic vasodilating effects

duration of action: protein binding

  • lipid solublity, intrinsic vasodilating effect, addition of vasoconstrictors
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47
Q
A
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48
Q

If the pKa of a LA is (close/further) from the pH of the blood, there will be (more/less) molecules available to the penetrate the membrane leading to a (faster/slower) onset of action

A

pKa closer to pH:

  • more (lipid soluble, unchanged) molecules to penetrate membrane
  • faster onset of action

pKa further from pH:

  • fewer lipid solubalbe uncharged molecules to penetrate the membrane (more ionized)
  • slower onset of action
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49
Q

If chloroprocaine has a high pKa why does it have a rapid onset of action?

A

bc it isn’t very potent so a larger doses is needed

>giving more molecules creates a mass effect that accounts for the rapid onset of action despite a high pKa

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50
Q

Which has a faster onset and why:

0.75% bpv or 0.25% bpv

A

0.75% = faster onset bc more molecules are given

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51
Q

What happens when there is an alkyl group substiution on the amide group and benzene ring?

A

Increased lipid solublity (potency)

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52
Q

Why does lidocaine undergo a faster rate of vascular uptake?

A

because it has a greater degree of intrinsic vasodilating properties

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53
Q

If a LA is highly protein bound does it decrease or increase the duration of action?

A

extends duration of action bc the molecules that bind to the plasma proteins serve as a tissue resovior

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54
Q

T/F- a higher degree of lipid solublity correlates with a longer duration of action

A

true

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55
Q

Which local anesthetic doesn’t possess any intrinsic vasodilating activity?

A

Cocaine

-it inhibits NE reuptake and causes vasoconstriction

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56
Q

Which substance donates vs accepts a proton (acid vs base)

A

acid- donates a proton [HA+ > H+ + A]

base- accepts a proton [B- + H+ >BH]

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57
Q

What happens when you put a strong acid or base in water?

A

it dissociates completely

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58
Q

What happen when you put a weak acid or base in water?

A

A fraction of it will ionize and the remaining fraction will be unionized

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59
Q

What does ionization depend on?

A

The pH of a solution and the pKa of a drug

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60
Q

When a basic drug (such as lidocaine) is placed into a relatively more acidic enviornment (like the blood), the Hendereson-Hasselbalch equation predicts that the (ionized/unionized) fraction will predominate.

A

the ionized fraction (conjugate acid)

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61
Q

In an (acidic/basic) solution, weak bases are more (ionized/un-ionized) and (water/lipid soluble)

A

Weak base

Acidic solution

  • more ionized
  • water-soluble

Basic solution

  • more non-ionized
    • lipid-soluble
62
Q

In an (acidic/basic) solution, weak ACIDS are more (ionized/un-ionized) and (water/lipid soluble)

A

Weak acid

Basic solution

  • more ionized
  • water-soluble

Acidic solution

  • more non-ionized
  • lipid-soluble
63
Q

Which local anesthetic does not undergo protein binding?

A

Chloroprocaine

64
Q

Which 3 locals have a PKA of 8.1

A

BPV, Levo-BPV, Ropi

65
Q

PKA of lidocaine

What other LA has the same pKa?

A

7.9

Priolocaine

66
Q

pKa of Mepivacaine

A

7.6

67
Q

PkA’s of:

Procaine -

Chloroprocaine-

Tetracaine-

A

Procaine - 8.9

Chloroprocaine- 8.7

Tetracaine- 8.5

68
Q

Local anesthetic with the highest pKa

A

Procaine (8.9)

69
Q

What LA is the only one with a pKa well below physiologic pH?

Why?

A

Benzocaine (3.5pKa)

-it is non-ionized at physiologic pH but still possesses anesthetic activity

70
Q

Why are local anesthetics unique in their action?

A

Because we usually administer them directly to their site of action instead of relying on the bloodstream to do it for us .

71
Q

Lowest protein bound amide- anesthetic

A

Prilocaine 55%

72
Q

Protein binding of mepivacaine

A

78%

73
Q

Which LA is only 6% protein bound?

A

Procaine

74
Q

Which ester-anesthetic is the most protein bound?

A

Tetracaine- 76%

75
Q

Mneumonic for Most vascular areas for local anesthetic uptake

A

I Think Illogical Imbiciles Can’t Educate but Fabulous Schools Should

I-IV

T-Tracheal

I- Interpleural

I-Intercostal

  • Caudal
  • Epidural
  • Brachial plexus
  • Femoral
  • Sciatic
  • Subq

(spinal)

76
Q

Someone asks you for 100mg of BPV; how much would you draw up if you had :

  1. 25% BPV:
  2. 5% BPV:
A
  1. 25% - 40 mls (2.5mg x 40mls - 100mg)
  2. 5% - 20 mls (5mg x 20mls = 100mg)
77
Q
A
78
Q

What kinds of proteins do local anesthetics preferentially bind to?

A

Alpha-1 Acid Glycoprotein

Increased in:

  • surgical stress
  • MI
  • chronic pain
  • RA
  • elderly

Decreased in:

-pregnancy and neonates

79
Q

What acts as a reservoir for local anesthetics that can help remove the LA from the circulation, limiting plasma concentration?

A

the lungs

80
Q

What does the addition of dexamethasone do?

A

It extends the duration of a brachial plexus block

81
Q

Explain how Exparel works

A

It’s essentially droplets of BPV that are housed in an lipid emulsion that slowly erodes over time, releasing a constant supply of BPV over several days

82
Q

Max dose of Exparel

A

226mg

83
Q

What local anesthetic is contraindicated for paracervical block in the obstetric population?

A

Exparel

84
Q

If lidocaine is to be infiltrated at the surgical site, it must be administered a minimum of ____minutes (before/after) exparel injection.

A

20 minutes BEFORE exparel

-if given after exparel, it can disrupt the liposmal supsension causing the immediate release of BPV (and poss toxicity i would assume?)

85
Q

BPV in any form may not be administered within ____ hours following exparel administration.

A

96 hours

86
Q

Match the Max doses of LAs

Lidocaine:

Ropi:

BPV:

Mepivacaine:

400mg, 300mg, 200mg, 175mg

A

Lidocaine: 300mg

Ropi: 200mg

BPV: 175mg

Mepivacaine: 400mg

87
Q

Max dose mg/kg

LevoBPV:

BPV:

BPV with Epi:

Ropi:

Lido

Lido with Epi:

Mepivacaine:

Priolocaine:

Procaine:

Chloroprocaine:

Chloroprocaine + Epi:

A

LevoBPV: 2mg/kg

BPV: 2.5mg/kg

BPV with Epi: 3mg/kg

Ropi: 3mg/kg

Lido: 4.5mg/kg

Lido with Epi: 7mg/kg

Mepivacaine: 7mg/kg

Priolocaine: 8mg/kg

Procaine: 7-10mg/kg

Chloroprocaine: 11mg/kg

Chloroprocaine + Epi: 14mg/kg

88
Q

If there is different rate of vascular uptake with different sites, how do clinicians typically determine the max doses?

A

adults- they will just stay under the total max dose

peds- they will weight base

89
Q

Ropi max dose

mg/kg

total

A

3mg/kg

200mg

90
Q

Max dose of chloroprocaine

mg/kg

total

A

11mg/kg

800mg

91
Q

chloroprocaine with epi max

mg/kg

total

A

14mg/kg

total = 1,000

think it’s double lido and epi

92
Q

Cocaine max dose

mg/kg

total

A

1.5-3mg/kg

150-200mg total

93
Q

What’s the most common cause of LAST

A

inadvertent intravascular injection during regional anesthesia

94
Q

T/F- last is more common with epdiural anesthesia than with peripheral nerve blocks

A

false

PNB > epidural

95
Q

with LAST, do CNS or cardaic complications usually present first

A

CNS

(except BPV)

96
Q

Treatment of cocaine toxicity

A

Vasodilator or mixed alpha/beta agonist such as labetalol

97
Q

Lidocaine Cp mcg/ml

CNS vs Cardiopulmonary effects

>25

15-25

10-15

5-10

1-5

A
98
Q

3 factors that increase risk of LAST

A

1. Hypercarbia

  • Increased CBF > increased drug delivery to the brain
  • Decreases protein binding + increases free fx to enter brain

2. Hyperkalemia

  • Raises RMP, making neurons more likely to depolarize

3. Metabolic acidosis

  • Decreases convulsion threshold and favors ion trapping in the brain

*acidosis increases the free fraction of the ionized portion and decreases unionized - so technically that should decrease the amount that can pass through the BBB, but it’s not enough to decrease the risk of CNS toxicity .

99
Q

Why would hyperventilating a patient with suspected LAST be good?

A
  • hypocarbia decreases CBF and reduces drug delivery to the brain

+ can lower serum K, which would lower RMP, requiring a larger stimulus to depolarize the nerve

100
Q

Why would you give a benzo with someone with LAST

A

to raise the seizure threshold

101
Q

Why does BPV have a higher morbidity with LAST? (2)

A
  1. it has a greater affinity for the voltage-gated sodium channel &
  2. a slower rate of dissociation from the receptor during diastole

(so it remains at the receptor for a longer time)

102
Q

Rank difficulty of cardiac resussitation from LAST from most to least difficult:

ropi, levoBPV, BPV, lido

A

BPV > LevoBPV > Ropi > Lido

103
Q

What 4 things increase the risk of BVP toxicity

A
  1. pregnancy
  2. beta blockers
  3. calcium channel blockers
  4. digitalis
104
Q

What 2 drug classes would see a patient on and be like yo dont give cocaine as your anesthetic to a doc lol

A

MAOIs and TCA’s - both increase the amount of NE and cocaine inhibits reuptake of NE into the presynaptic terminal and would result in excessive SNS stimulation

105
Q

Best drugs to manage HTN in cocaine OD

A
  1. Vasodilator such as nitro
  2. Labetaolol (mixed alpha and beta)
    - if you give a pure beta blocker, you have unapposed alpha stimulation (from the cocaine) + reduced inotropy (from the beta blocker) setting you up for chf and cardiovascular collapse
106
Q

One mintue folowing an interscalene block, a 62kg patient has a seizure; how much 20% lipid emulsion should you administer?

A

93mls

(20% lipid emulsion - 1.5ml/kg of lean body mass/1 minute)

107
Q

Steps in treating Last 1-4

A

1. Manage airway

  • 100% Fio2
  • Hypoxia and acidosis will worsen LAST

2. Benzos

  • Raise the seizure threshold
  • If ineffective, give a small dose of sux or NDMR to stop muscle contraction
    • This minimizes o2 consumption, hypoxemia and acidosis but will not stop seizure activity in the brain
  • Avoid propofol (cardiac depression)

3. ACLS with specific modifications

  • Epi can hinder LAST resusitation and also reduces effectiveness of lipid emulsion therapy
    • If given, should be given in doses of < 1mcg/kg
  • Avoid vasopressin
  • Amio is agent of choice for ventricular dysthryhmias
    • avoid lidocaine and procainamide

4. Lipid emulsion therapy

  • 20% 1.5ml/kg (lean body mass) over 1 minute
  • Infusion = 0.25ml/kg/min
  • Can repeat bolus up to 2 more times and increase gtt to 0.5ml/kg/min
  • Continue gtt for 10 mins after acheiving hemodynamic stability
  • Max dose is 10ml/kg in the first 30 mins

*Avoid beta blockers and caclcium channel blockers which will enhance LA induced cardiac disturbances

-if unresponsive to modified ACLS and lipipd emulsion therpay, prepare for Cardiopulmonary bypasss.

108
Q

LAST: what can you do if benzos are ineffective for seizure control

A

smal ldose of sux or NDMR

  • will minimize o2 consumption, hypoxemia, and acidosis
  • won’t stop seizure activity in the brain
109
Q

why should you be cautious with Epi in LAST

A

it can hinder resusitation and reduce the effectivenss of lipid emulsion therapy

-if used , keep doses < 1mcg/kg

110
Q

Safe or unsafe in LAST:

Propofol

A

unsafe

111
Q

Safe or unsafe in LAST:

Benzos

A
112
Q

Safe or unsafe in LAST:

Betablockers

A

unsafe

113
Q

Safe or unsafe in LAST:

CCBs

A

unsafe

114
Q

Safe or unsafe in LAST:

Vasopressin

A

unsafe

115
Q

20% lipid emulsion:

Bolus dose:

Infusion:

if sx are slow to resolve:

max dose:

A

Bolus dose: 1.5ml/kg (LBW) over 1 minute

Infusion: 0.25ml/kg/min

if sx are slow to resolve:

  • can repeat bolus dose up to 2 more times &
  • increase rate to 0.5ml/kg/min

max dose:

  • 10ml/kg in 1st 30 minutes
116
Q

T/F: lipid emulsion therpay is safe in pregnancy

A

True

117
Q

How long should lipid emulsion therapy be maintained after restoration of hemodynamic stability

A

10 minutes

118
Q

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

A

Amio

119
Q

What is the maximum recommended dose for lidocaine during tumescent anesthesia?

  • 5mg/kg
  • 7mg/kg
  • 55mg/kg
  • 75mg/kg
A

-55mg/kg

120
Q

the plasma concentration of lidocaine peaks at ___hrs and is completely eliminated by ____hrs

A

peak: 12 hours
gone: 36 hours

121
Q

The decision to use MAC or GA is influenced by the amount of tumescent to be injected; GA is recommended if > _____ L of tumescent is planned.

why?

A

>2-3L = General

Bc of risk for fluid shifts

122
Q

Why is fluid management essential in patients getting tumescent ?

A

bc fluid overload and pulmonary edema may occur as a result of intravascular volume expansion

123
Q

Purpose of large volume tumescent anesthesia during liposuction

purpose of added lidocaine

pupose of added epi

A
  • the large volume injected into the adipose tissue makes it firm and increases the ease of removal

lidocaine- prevents discomfort

epi- minimizes vascular uptake of both the local anesthetic and large volume solution

124
Q

What is the most common cause of death with liposuction?

A

PE

125
Q

When is methemoglobin formed?

A

When the iron on the hemeglobin molecule becomes oxidized to it’s ferric form (FE+3).

-This reduces oxygen-carrying capacity and shifts the curve to the left

126
Q

What is required to diagnose methemoglobinemia?

A

A co-oximeter

127
Q

Drugs than can produce methemoglobin

( 3 locals)

(1 sz, 2 dilators, 1 abx)

A

Benzocaine

  • Cetacaine

Prilocaine

Lidocaine

Phenytoin

Nitroprusside, Nitroglycerine

Sulfonamides

128
Q

s/s methemoglobinemia

A

hypoxia that isn’t fixed with increasing FiO2

CCCTT

Chocolate colored blood

Cyanosis

Change in LOC

Tachycardia, tachypneia

129
Q

What is cyanosis in the presecnes of a normal or high PaO2 highly suggestive of ?

A

methemoglobinemia

130
Q

A significant concentration of methemoglobin can lea to an erroneous SpO2 reading of ____%

A

85%

131
Q

Treatment and dosing for methemoglobinemia

(max dose)

A

Methylene blue

1-2mg/kg over 5 minutes

max dose 7-8mg/kg

132
Q

Hepatic metabolizm of _____ yields an oxidizing metabolite O-Toluidine, which can lead to ________________-

A

Prilocaine

methemoglobinemia

133
Q

What does EMLA cream consist of?

A

50% Prilocaine

50% Lidocaine

*risk of methemoglobinemia

134
Q

POX emeits 2 constaint light waves

Red- ____nm; absorbed by ________

Infrared light- _____nm; absorbed by ________

A

Red - 660; absorbed by deoxyhemoglobin

  • Think D/Devel 660

Infrared light- 940nm; absorbed by oxyhemoglobin

135
Q
A
136
Q

Patients with what condition should not receive methylene blue

A

Glucose-6 Phosphate reductase deficiency

G6PR deficiency

  • can precipitate hemolytic crisis
137
Q
A
138
Q

How to treat methemoglobinemia in patietns with a G6PR deficiency (glucose-6-phosphate reductase)

A

exchange transfusion

(methylene blue can precipitate hemolytic crisis in these people)

139
Q

Why are neonates at a higher risk for methemoglobinemia?

A

because fetal hemoglobin is deficient in methemoglobin reductase

140
Q

Why can’t a pulseox measure methemoglobinemia correctly?

A

Bc HgbMet absorbs the 660nm and 940nm wavelengths equally.

141
Q

Onset of EMLA cream and max effect

A

onset = 1 hour

max effect after 2-3 hours

142
Q

What should be applied to EMLA cream after topical application

A

An occlusive dressing

143
Q

What can be applied simultaneously with EMLA cream to hasten the absorption?

A

Nitroglycerine

-sounds liek a great idea

144
Q

max dose for what age/weight groups of EMLA cream:

1g max:

2g:

10g:

20g:

(REMEMBER EMLA MAX IS IN G)!!

A

1mg max: 0-3 months or < 5kg

2mg: 3-12 months and > 5kg
10mg: 1-6 years and > 10kg
20mg: 7-12 years and > 20kg

145
Q
A
146
Q
  • each additaive prolongs the duration of local anesthetics EXCEPT:
  • dexamethasone
  • dextran
  • epi
  • hyaluronidase
A
  • hyaluronidase
  • hyaluronic acid is present in the intersistial matrix & basement membrane; it hinders the spread of substances through tissues
  • hyaluronidase hydrolyzes hyaluronic acid which then facilitates diffusion of substances in the tissues
147
Q

How does sodium bicarb affect local anesthetics & how is it mixed?

A

shortens the onset time (debatable)

-mix 1ml of 8.4% sodium bicarb with 10ml of local anesthetic

148
Q

Which local anesthetic reduces the effectiveness of opioids in the epidural space?

A

Chloroprocaine

149
Q

Someone asks you how does sodium bicarb speed the onset of a local anesthetic

A

-it increases the number of lipid-soluble molecules, which speeds up the onset of action.

150
Q

Select the BEST local anesthetic to use for a subarachnoid block in the patient who has a sensitivity to BPV

A. Etidocaine

B. Tetracaine

C. Chloroprocaine

D. Lidocaine

A

B. Tetracaine

-needed to 1. chose and ester and 2. know that chloroprocaine is not used in spinal anesthesa

151
Q

T/F - chloroprocaine is safe for spinal anesthesia

A

false- neurotoxicity

152
Q
A

*Pharmacology (25 decks)

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