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Chem/Phys > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

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1
Q

Local anesthetics reversibly block _____ nerve transmission to produce analgesia and anesthesia without loss of consciouness.

A

Afferent

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2
Q

What is the order of blockade for LA?

A

1) Autonomic blockade
2) Somatic sensory blockade
3) Somatic motor blockade

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3
Q

How are local anesthetics used?

A
  • Infiltrated around nerve
  • Applies topically to skin/mucous membrane
  • Injected into blood vessels (after first exsanguinated BV)
  • Subarachnoid and epidurla spaces
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4
Q

How are impulses propagated in unmyelinated fibers?

A

Impulses travel along length of fiber in a continuous fashion

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5
Q

How are impulses propagated in myelinated fibers?

A

Conduction is “saltatory” (50x) faster that it appears as if impulses leap from one node of Ranvier to the next

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6
Q

The velocity an impulse travels is ____ proportional to diameter of fiber.

A

Directly. Larger diameter, higher conduction velocity

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7
Q

What is the average size of A fibers?

A

1-22 microns

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8
Q

What is average size B fibers?

A

1-3 micrometers

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9
Q

What is average size of C fibers?

A

0.1-2.5 micrometers

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10
Q

What do a-alpha fibers control?

A

Motor and proprioception

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11
Q

What do a-beta fibers control?

A

Motor, touch pressure

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12
Q

What do a-gamma fibers control?

A

Motor/muscle tone (muscle spindle)

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13
Q

What do A-delta fibers control?

A

Pain, temperature, touch

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14
Q

What do B-fibers control?

A

Preganglionic autonomic

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15
Q

What do C-fibers control?

A

Dull pain, temperature, touch. Postganglionic autonomic (no myelin)

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16
Q

What is order of size of A fibers?

A

alpha, beta, gamma, delta

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17
Q

Which fibers are we aiming to block with anesthesia?

A

A-delta

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18
Q

Which fibers are challenging to block with LA?

A

A-alpha and A-beta

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19
Q

Large fibers have the _____ conduction velocity and the ____ lowest threshold for excitability.

A

Highest; Lowest

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20
Q

What is the difference seen in sensitivity of peripheral nerve to LA clinically vs in a lab?

A

Clinically, we saw sensitivity of p.n. to LA is inversely related to size (why we see autonomic first, sensory second, motor thirt) HOWEVER, in lab, the larger fibers (motor) are actually MORE sensitive to LA than C fibers (unmyelinated and small)

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21
Q

What might account for difference in clinical vs lab observation?

A
  • Larger nerves are found deep in nerve bundles-are therefore harder for LA to reach
  • -Variable activity for different nerves (pain fibers fire at high requency)
  • -variable ion channel mechanisms
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22
Q

Outer surface of peripheral nerve is known as _____

A

Mantle

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23
Q

Inner surface of peripheral nerve is known as ___

A

core

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24
Q

What does the sequence of onset and recovery from local anesthetic block rely on?

A

Where it is located

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25
Q

What is the clinical sequence of anesthesia?

A

1) Sympathetic block (vasodilation, warm skin)
2) Loss pain and temperature sensation
3) Loss of proprioception
4) Loss of touch and pressure
5) Motor blockade

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26
Q

What is nerve blockade caused by?

A

Prevention of voltage dependent increase in Na conductance

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27
Q

Voltage gated sodium channels in ______ ____ serve as receptors for local anesthetics molecules

A

Inactivated-closed state

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28
Q

Where do local anesthetics bind?

A

Internal H gate of channel and physically obstruct the external openings of channels

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29
Q

How do local anesthetics prevent passage of sodium ions through these channels?

A

By bindign and stabilizing them in the inactivated-closed conformational state

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30
Q

Do local anesthetics alter the membrane potential or threshold at all?

A

No, simply makes depolarization less likely to happen by blocking influx of Na

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31
Q

When do LA access the nerve cell?

A

Activated-open state

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32
Q

When to LA easily bind to the nerve cell?

A

Inactivated-closed state

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33
Q

When does the blockade occur more rapidly?

A

When nerve is frequently cycled through action potential

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34
Q

A resting nerve is ___ sensitive to block than a repetitively stimulated nerve. Why?

A

less

-Lipid solubility determines the abiilty to achieve block since LA has to diffuse through axonal membrane instead of through Na channel

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35
Q

What contributes to differential nerve block?

A

Distance between nodes of ranvier in myelinated fibers

-Larger fiber, harder to bind, harder to block

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36
Q

Internodal distance ____ with fiber diameter

A

Increases

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37
Q

How many nodes of ranvier need to be blocked to blcok nerve?

A

3 (1cm)

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38
Q

What is a differential nerve block?

A

Sensory block with incomplete motor block

  • Pain conducting fibers (A delta, C fibers) blocked
  • Aalpha, beta and gamma fibers not completely blocked.
  • Patient will feel pressure but not pain
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39
Q

What are the 2 classifications of LA?

A

Aminoamides

Aminoesters

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40
Q

What do LA molecules consist of?

A
  • Lipophilic head (aromatic ring),
  • Intermediate chain (either amid(NH), or Ester (COO-)) group.
  • Hydrophilic tail (tertiary amine)
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41
Q

Which part of molecule allows molecule to penetrate membrane?

A

Lipophilic head

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42
Q

Which part of molecule allows LA to form bond?

A

Hydophilic

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43
Q

How can amides be identified?

A

have an “i” in drug name before -caine part

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44
Q

What effects biotransformation of molecule?

A

Intermediate chain (ester vs amide)

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45
Q

How are ester linkages metabolized?

A

Readily hydrolyzed by non-specific esterases in plasma and tissue (mostly liver)

VERY rapid metabolization

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46
Q

How are amide linkages metabolized?

A

In liver (takes longer, increases toxicity risk)

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47
Q

Highly lipid-soluble anesthetics are _____potent and have a _____ duration of action than water-soluble.

A

More; longer

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48
Q

Increasing length of intermediate chain ___ the potency and toxicity and alters metabolism rate and DOA

A

Increases

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49
Q

Increase in length of terminal group located on tertiary amine and aromatic ring ____ potency and toxicity

A

increase

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50
Q

Enantiomers of chiral drug vary in terms of ___, ___ and ___.

A

Pharmacokinetics, pharmacodynamics, and toxicity

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51
Q

What is Cm?

A

Minimal blocking concentration

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52
Q

How does nerve fiber influence Cm?

A

Increase diameter= increase Cm

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53
Q

How does motor nerve vs sensory nerve affect Cm?

A

Motor nerve is high Cm than sensory

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54
Q

How does tissue pH affect Cm?

A

Higher pH= Decrease in Cm

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55
Q

How does nerve stimulation influence Cm?

A

More nerve stimulation, Decrease in Cm

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56
Q

What is exparel?

A

Bupivicaine liposome that allows for prolonged DOA and theoretical decrease in toxicity

Dose: depends on sx site

Max dose: 266 mg or 20 mL

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57
Q

What is absorption governed by?

A

Physiochemical characteristics or drug

Physiologic conditions at site of deposit

Volume of solution or vehicle used

Concentration of LA

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58
Q

What are physiochemical factors?

A

pKa, pH, lipid solubitliy

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59
Q

What are physiologic conditions?

A
  • Tissue pH
  • Co2
  • temperature
  • patient characteristics
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60
Q

Absoprtion by type of block? High to low.

A
  • Intravenous
  • Tracheal
  • Intercostal
  • Caudal
  • Paracervical
  • Epidrual
  • Brachial Plexus
  • Subarachnoid
  • Subcutaneous
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61
Q

Do ionized or non-ionized dugs cross a lipid membrane?

A

Non-ionized

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62
Q

Why is ionization important for LA?

A

Unionized diffuses across nerve sheath and membrane BUT once inside cell, molecules re-equilibrate and IONIZED version binds to receptor in Na channel

63
Q

Ionized form is favored when…

A

Acidic in basic environment

Basic drug in acidic environment

64
Q

Non-ionized favored when

A

Acidic drug in relatively acidic environment

Basic drug in relatively basic environment

65
Q

All local anesthetics act as what?

A

Weak bases with pka 7.5-9

66
Q

Why are local anesthetics packaged in acidic formulations?

A

Improves solubility and stability in vial and is often to preserve epinephrine

67
Q

What is ideal pKa for LA?

A

7.4. We want 50% ionization, 50% nonionized

68
Q

In areas of high/normal pH values, rate and amount of abosprtion is ____

A

higher

69
Q

At lower pH, rate and amount of absoprtion are

A

lower

70
Q

Which drug does not have onset that reflects pka?

A

Chloroprocaine. It is not a very potent drug, so we have to give a LOT of chloroprocaine for effect. This causes the effect to be fast

71
Q

General rule for onset and pka?

A

pKa closer to 7.4 means higher percent unionized and therefore quicker onset

72
Q

How can anesthetist influence ph/pka relationship to speed onset?

A
  • Adding bicarb increases onset, enhances block depth and increases spread of block
  • Infected tissues will not absorb LA
  • Ion trapping in pregnancy
  • Decreasing temperature reduces systemic drug absorption
73
Q

What is most important factor in potency?

A

Lipid solubility

Eitdocaine, bupivicaine, tetracaine are HIGHLY potent and lipid soluble

74
Q

Duration of action is ____ related to time LA is in contact with nerve fiber.

A

Directly

75
Q

How does tissue blood flow influence DOA?

A

More blood flow, more opportunity for drug to be carried away

76
Q

How does addition of vasoconstrictors affect DOA?

A

Decrease blood flow, LA stays where it is

77
Q

How does lipid solubility affect DOA?

A

More fat, LA wants to stay in tissue

78
Q

How does protein binding affect DOA?

A

1 effect of DOA

79
Q

What is intrinsic vasodilator activity?

A

Lidocaine causes local blood vessels to dilate.

80
Q

Why do we add vasoconstricTors to LA?

A

1) Inhibition of systemic absorption of LA
2) Prolongation of the LA effect
3) Detection of TV injection

81
Q

What is most important factor for DOA?

A

Protein binding Keep LA bound to local proteins

82
Q

What determines lipid concentration LA in blood?

A
  • Concentration LA administered
  • Tissue blood flow
83
Q

How are esters metabolized?

A
  • Primarily hydrolyzed by pseudocholinesterase enzymes in plasma (lesser extent- the liver) (<5% excreted unchanged in urine)
  • This is very fast metabolization
  • EXCEPTION COCAINE
    • sig. metabolized in liver with 10-12% excreted unchanged in urine
84
Q

What metabolite forms with metabolization of esters?

A

Para-aminobenzoic acid (PABA)

  • Has been known to ellicit allergic reaction
85
Q

How are amides metabolized?

A
  • Liver
    • microsomal enzymes (cytochrome p450)
    • More complex and slower than esters
    • aromatic hydroxylation, n-dealkylation, amide hydrolysis
  • This means systemic toxicity and cumulative effects are very possible
86
Q

Potency is most influenced by ______

A

lipid solubility

87
Q

Duration of action is most influenced by ___ _____

A

Protein binding

88
Q

Onset is most influenced by ____

A

pka

89
Q

Max dose bupivicaine?

A

2.5 mg/kg

90
Q

What is max dose ropivicaine without epinephrine?

A

3 mg/kg

91
Q

What is max dose ropivicaine with epinephrine?

A

3.5 mg/kg

92
Q

Max dose etidocaine?

A

4 mg/kg

93
Q

Max dose lidocaine without epi? With epi?

A

4 mg/kg without epi

7 mg/kg with epi

94
Q

Max dose mepivacaine without epi? With epi?

A

4 mg/kg without epi

7 mg/kg with epi

95
Q

What is max dose chloroprocaine?

A

12 mg/kg

96
Q

Max dose cocaine?

A

3 mg/kg

97
Q

Max dose tetracaine?

A

3mg/kg

98
Q

Which LA can we mix with epinephrine?

A

Ropivicaine

Lidocaine

Mepivacaine

99
Q

CNS signs of local anesthetic toxicity?

A
  • Circumoral/tongue numbness
  • Tinnitus
  • vision changes
  • dizziness
  • slurred speech
  • restlessness
  • Muscle twitching, especially in face then extremities indicates IMMINENT onset of seizure
  • Seizure collowed by CNS depression, apnea, hypotension
100
Q

What are toxicity signs for cocaine?

A

Restlessness

Tremors

Seizures

euphoria

101
Q

What are local anesthetic toxicity effects on cardiovascular system?

A
  • CVS is more resistant to toxicity compared to CNS
  • Hypotension
  • Myocardial depression
  • AV conduction block
    • reduced SVR, CO, widened PRi and QRS, VT–> CV collapse
102
Q

Which drug is most CV toxic?

A

Bupivicaine- cardiac arrest may occur at lower levels of toxic doses (inadvertant IV injection)

103
Q

What increases risk of toxicity?

A
  • Pregnancy
  • Hypoxia
  • pH abnormalities
  • CV modulating drugs
104
Q

What does cocaine overdose manifest as in CV system?

A
  • Massive sympathetic outflow
  • coronary vasospasm
  • MI
  • dysrhythmia including v-fib
  • dopamine, epi, surge
105
Q

How come lidocaine doesn’t interfere with normal cardiac conduction at normal levels?

A

Lidocaine molecule pops on and off receptor so it doesn’t interfere with normal conduction pathways

106
Q

Treatment of CV collapse from local anesthetic toxicity?

A
  • Resuscitation often fails
  • Prevention is ideal
    • incremental fractionated dosing
    • aspirate before EVERY injection
    • watch ECG for early signs
  • Basic CPR (2.5 hours minimum)
  • Modified ACLS (no lidocaine)
  • Intralipid
  • CPB
107
Q

What is intralipid dose for LA toxicity?

A

Intralipid 20% 1.5 mL/kg rapidbolus immediately

Infusion of 0.25 mL/kg/min x 10minutes

108
Q

What are transient neurologic symptoms?

A
  • AKA Transient radicular irritation
  • Neuro-inflmmatory process that causes pain in:
    • lower back
    • buttocks
    • posterior thighs
  • Occurs 6-36 hours after full recovery from SAB–> about a week
109
Q

What is cauda equina syndrom?

A
  • Diffuse lumbosacral injury
  • numbness in LE
  • loss of bowel and bladder control
  • paraplegia
  • Lidocaine 5%, tetracaine, chloroprocaine implicated
110
Q

What is anterior spinal artery syndrome?

A
  • LE paralysis with +/- sensory deficit
  • Unknown cause
  • Vasoconstrictors? PVD, advanced age have increased risk
111
Q

What might cause allergic reaction from LA?

A
  • True incidence <1%
  • High plasma concentration vs allergy?
    • look for reactions causing touble breathing, hives, third spacing
  • Esters are more implicated than amids (PABA?)
  • Preservative reaction? (methylparaben) implicated in cauda equina
  • NOT MH triggers
112
Q

What are drug interactions with LA?

A
  • Pseudocholinesterase inhibitors may prolong duration of ester anesthetics (used in alzheimer patients)
  • Cimetidine and propranolol decrease hepatic blood flow–> decrease clearance of amide LA and cocaine
113
Q

How do you select LA agent?

A
  • Type of surgery
  • Spreadability
  • Onset
  • Potency
  • Duration
  • Toxicity risk
  • Site of metabolism
114
Q

Other uses of lidocine?

A
  • Cough suppression
  • Attenuate ICP elevation and BP elevation durign laryngoscopy
  • Attenuate reflex bronchospasm with airway instrumentation
  • suppression ventricular dysrhythmias
115
Q

What is unique about cocaine?

A
  • Unique ester
  • Blocks NE and dopamine reuptake
    • unique side effect profile
      • CNS: euphoria
      • CV: stimulation, sympathomimetic
  • Different metabolism; liver and plasma esterases
  • Currently used ENT sx
116
Q

Procaine:

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Ester prototype
  • Used in spinal anesthesia prior to devleopment of lidocaine
    • not current favorite
  • Pka= 8.9 3% unionized SLOW ONSET
  • Low lipid solubiltiy (1%) and protein binding (5%) SHORT DOA
  • Issues
    • hypersensitivity
    • higher nausea incidence
    • higher incidence CNS s/e
    • metabolite interferes with efficacy of sulfonamide antibiotics
117
Q

Tetracaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Ester
  • pka 8.5, 7% unionized (SLOW ONSET)
  • 80% lipid solubility; 85% protein binding- LONG ACTING
  • Max 3mg/kg
  • Primarily used in spinal and corneal anesthesia
    • long DOA for an ESTER (esp with epi, can be 6 hours)
  • High incidence of TNS
  • Not popular for epidural or PNB
    • slow onset
    • profound motor block
    • toxicity risk w lg doses
118
Q

Chloroprocaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Ester
  • pKa 8.7; 2% unionized- FAST onset (outlier!!)
  • 1% lipid solubility; 7% protein binding- SHORT DOA
  • Max 12mg/kg
  • Popular in OB epidural anesthesia
    • ULTRA rapid serum hydrolysis has very low toxicity risk to mom and fetus
    • epidural and PNB when short duration desired
  • Spinal still being reinvestigated; off label use
119
Q

Lidocaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Amide
  • Very popular
  • pka- 7.9 24% unionized FAST
  • 4% lipid solubility
  • 65% protein binding- MOD DOA
  • Concentrations Topical 4%, regional (0;25-0.5%), pnb 1-2%; spinal (1.5-5%); epidural (1.5-2%)
  • 2 active metabolites
    • monoethylglycinexylidide 80% activity & xylididde 10% activity
  • Spinal use controversial- linked to cauda equina syndrome
120
Q

Mepivicaine?

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Class: amide
  • pKa- 7.6: 39% unionized FAST ONSET
  • 1 lipid solubility
  • 75% protein bound- MODERATE DOA
  • Max 4mg/kg, 7 mg/kg with epi
  • Structurally similar to bupivicaine
  • CLINCIALLY similar to lidocaine
    • rapid onset
    • less vasodilation= longer DOA
      • Use when vasconstrictor contraindicated )
      • Use in fingers, toes, nose and hoe’s
    • Serum e 1/2t ~ 2 hours
    • Slightly more CNS toxicity compared to lidocaine
    • cannot use topically
121
Q

Prilocaine

Class?

pka? unionized %?

Anything special?

A
  • Amide
  • 7.9 pka; 24% unionized
  • Rapid metabolism leads to less CNS toxciity than lidocaine
  • Toxic metabolite
    • ortho-toludine
      • avoid in OB
      • Doses >600 mg= conversion of hgb to methemoglobin
122
Q

What other LA can trigger methemoglobinemia besides prilocaine? Treatment?

A

Benzocaine- topical preparations

Treatment with metylene blue 1-2mg/kg IV over 5 minutes

123
Q

Etidocaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Class: amide
  • pKa 7.7 33% unionized FAST ONSET
  • 140 lipid solubility
  • 95% protein binding- LONG DOA
  • Used for infiltration/PNB (0.5-1%) and epidural anesthesia (1-1.5%)
  • Prominent frequency-dependent blockade
  • not used frequently
124
Q

Bupivicaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Class: amide
  • pKa 8.1; 17% non-ionized MODERATE ONSET
  • 30 Lipid solubility
  • 95% protein binding LONG DOA
  • Longer DOA nad longer onset compared to lidocaine
  • Popular for differential nerve block
    • sensory>motor
    • great choice postop pain, labor epidural
  • Concentrations
    • spinal (0.5-0.75%)
    • epidraul (0.0625-0.5%)
    • PNB(0.25-0.5%)
  • Highly protein bound to alpha 1 glycoprotein
  • S/E PRO: low incidence neuro complications
  • S/e con: very cardio toxic (use 0.5% or lower conc for epidural, pnb)
    • serum e 1/2t is 2.5 hours
125
Q

Ropivicaine

Class?

pka? unionized %?

lipid solubility/protein binding?

Anything special?

A
  • Class: amide
  • Pka- 8.1; 17% non-ionized: SLOW onset ( from book)
  • 94% protein bound LONG DOA
  • S(-) or levo enantiomer of homolog of bupivicaine with a propyl tail on piperidine ring
  • Good for differential blockade
  • Less cardiotoxic
  • More vasoconstriction
  • 2 active metabolites:
    • shoter serum e 1/2t (~2hours) compared to bupi
  • More expensive, use when larger doses needed
126
Q

Levobupivacaine

A

S(-) enantiomer bupivacaine

  • less cardiotoxic
  • serum E 1/2 t= 2.6 hours
  • More expensive… reserve for cases where larger LA doses required
127
Q

Dosing in PNB?

A
  • Volume dictated by type of block
  • choose concentration based on limitations of max dose balanced with density of blockade desired
128
Q

Epidural dosing main points?

A
  • Volume dictated to what level of block desired
    • 1.25 mL-1.6mL per segment desired
  • Choose concentration based on density of block desired (labor vs sx epidural)
129
Q

Duration action Chloroprocaine

A

50-70 min 2 seg regression

130
Q

Segement regression time lidocaine?

A

90-130 min

1.5-2ish hours

131
Q

2 segment regression mepivacaine?

A

90-150 min

1.5-2.5ish hours

132
Q

2 segment regression prilocaine

A

120-160 min

133
Q

2 seg regression bupivacaine?

A

200-260

3-4

134
Q

2 seg regression ropivacaine?

A

160-200min

135
Q

Amount mL per segment block for epidural?

A

1.25-1.6 mL

136
Q

Lidocaine spinal usual concentration? volume? dose? baricity?

A

Concentration: 1.5% , 5%

Volume: 1-2 mL

Dose 30-100 mg

Hyperbaric

137
Q

Mepivacaine spinal usual conc? usual volume? total dose/70kg?

A

Concentration: 4%

  • Volume 1-2mL
  • total dose 40-80 mg

Cocentration 0.25-1%

  • volume 1-4 mL
  • Dose 5-20 mg

both hyperbaric

138
Q

Tetracaine spinal conc, volume, dose?

A

Concentration 0.25

  • Vol: 2-6 mL
  • dose 5-20 mg

Concentration 1%

  • vol 1-2 mL
  • dose 5-20 mg

Concentration 0.25%??

  • vol 1-2 mL
  • dose 2.5-5 mg
139
Q

Bupivacaine spinal conc, volume, dose?

A

Concentration 0.75%

  • Vol: 2-3 mL
  • Dose 15-20 mg

Concentration 0.5%

  • Vol 3-4
  • dose 15-20 mg
140
Q

Levobupivicaine spinal dose?

A

Concentration 0.75%

  • Volume: 2-3 mL
  • drug 15-20

Concentration 0.5%

  • volume 3-4 mL
  • drug 15-20 mg
141
Q

Ropivicaine spinal conc, volume total drug?

A

Concentration 0.75%

  • Volume 2-3
  • drug 15-20 mg
142
Q

Main issues with procaine administration?

A
  • Hypersensitivity
  • higher nausea incidence
  • higher incidence CNS s/e
  • metabolite interferes with efficacy of sulfonamide antibiotics
143
Q

What is main use of tetracaine?

Biggest S/E?

What is tetracaine not as popular for?

A
  • Main use inspinal/corneal anesthesia
    • long DOA for ester
  • Higher incidence of Transient Neurologic Syndrome (TNS)
  • Not as popular for epidural/PNB
    • slow onset
    • profound botor block
    • toxicity risk with large doses
144
Q

What is chloroprocaines most popular use?

A

Popular in OB epidrual anesthesia (spinal still being reinvestigated)

  • Since it’s an ester, super fast metabolism from hydrolysis so veyr low toxicity risk to mom and fetus
  • Good in PNB when quick DOA desired
145
Q

What are the concentrations of lidocaine available? For which purposes?

A
  • 4%- Topical
  • 0.25-0.5%- Regional
  • 1-2%= PNB
  • 1.5-5%= Spinal (spinal use still controversial)
  • 1.5-2%= epidural
146
Q

2 active metabolites of lidocaine?

A
  • Monoethylglycinexylidide
    • 80% activity of lidocaine
  • Xylidide
    • 10% activity
147
Q

What is mepivicaine clinically similar to? Structurally similar to?

A

STRUCTUALLY similar to bupivicaine

CLINICALLY similar to lidocaine

  • rapid onset
  • Less vasodilation= longer DOA c/t lidocaine
  • use when vasoconstrictors contraindicated
    • fingers, toes, nose, and hoe’s

Slightly MORE CNS toxic compared to lidocaine

148
Q

What is toxic metabolite in prilocaine?

A
  • Ortho-toludine
    • avoid in OB
    • Doses >600 mg can cause conversion of Hgb to methemoglobin
149
Q

What is bupivicaine popular for?

A

Differential blockade (sensory >motor) great for postop block and epidural

150
Q

Concentrations bupivicaine?

(Spinal, epidural, PNB dose)

A

Spinal (0.5-0.75%)

Epidural 0.0625-0.5 %

PNB (0.25-0.5%)

151
Q

s/e pro and con with bupivicaine?

A

S/E PRO

  • Less neuro complications

S/E CON

  • More CV s/e
    • use 0.5% or lower for conc for epidural, PNB
    • serum 1/2t e 2.5 hours
152
Q

Meds good for differential blockade?

A

Bupivicaine

Ropivicaine

153
Q

What is ropivicaines cardiotoxic likelihood?

A

Less cardiotoxic than bupivicaine

154
Q
A

Chem/Phys (9 decks)

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