LA and ultrasound Flashcards

1
Q

what is the lipophilic portion of a LA

A
  • benzene ring
  • it is necessary for activity
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2
Q

ester chemical structure

A

-CO-

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3
Q

amide chemical structure

A

-NHC-

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4
Q

what is the hydrophilic portion of LA

A
  • quaternary amine
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5
Q

intracellular pH

A

7.0

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6
Q

extracellular pH

A

7.4

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7
Q

s enantiomer

A

left = sinister

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8
Q

r enantiomer

A

right = rectus

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9
Q

what are pure isomers

A
  • they only have one type of enantiomer (s or r)
  • ropivacaine and levobupivacaine (both s)
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10
Q

benefit of s enantiomer

A
  • less neuro and cardio toxic
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11
Q

MOA of LA

A
  • inhibits Na channels by binding to alpha subunit, slowing rate of depolarization not allowing threshold potential to be reached
  • binds in activated and inactivated states
  • binds on internal part of channel
  • weak binding
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12
Q

frequency dependent blockade

A
  • only has access when receptor is open
  • nerves with more activity = faster blockade
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13
Q

what is Cm

A
  • minimum concentration to produce blockade
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14
Q

factors that effect Cm

A
  • larger diameter increases Cm
  • high frequency and higher pH decreases Cm
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15
Q

Cm for motor to sensory

A
  • Cm for motor is twice sensory = sensory block with no motor
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16
Q

Cm epidural vs spinal

A
  • unchanged Cm
  • direct access to nerves = less amount
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17
Q

how many node of Ranvier must be blocked

A
  • at least 2, preferably 3
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18
Q

order of blockade with fibers

A
  1. B fibers (preganglionic SNS fibers)
  2. C and A-delta fibers (pain, temp, touch) (afferent)
  3. A-gamma fibers
  4. A-beta fibers
  5. A-alpha fibers
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19
Q

order of blockade “senses”

A
  • autonomic
  • temp
  • pain
  • touch
  • pressure
  • motor
  • vibration
  • proprioception
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20
Q

what is a weak base pK value

A

7.6 - 8.9

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21
Q

base plus acid =

A
  • more ionized
  • just about physiological pH = >50% ionized
  • locals with pks nearest physiologic pH = faster onset
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22
Q

what form can cross the lipid bylayer

A

un-ionized

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23
Q

what is the weak acid local

A
  • benzocaine
  • pKa of 3.5
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24
Q

pKa of lidocaine

A

7.9

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25
Q

alkalinization

A
  • adding bicarb raises pH closer to pKa = faster onset by 3-5 min
26
Q

distribution of LA

A

1st uptake into lungs
2nd distribution into high perfused areas (heart, brain, kidneys)
3rd low perfused areas (muscle, fat)
- amides are more widely distributed

27
Q

protein binding of LA

A
  • bupivacaine and ropivacaine highly bound
  • lido not as much
  • proteins are to large to cross the placenta
28
Q

why is placental transfer of LA important

A
  • causes ion trapping
  • unionized LA crosses placenta and hits low fetal pH = drug becomes ionized and cant cross back = toxicity in fetus
29
Q

what is potency of LA related to

A
  • lipid solubility
  • more lipid soluble = easier to cross lipid by-layer
30
Q

what is the onset of a LA related to

A
  • state of ionization (most important)
  • lipid solubility
31
Q

DOA is related to

A
  • protein binding & lipid solubility
  • higher affinity to proteins and lipids = stronger attachment = drug remains close to Na channels to act longer
32
Q

metabolism of amides

A
  • mainly hepatic
  • minimal renal
33
Q

amide LA clearance fastest to slowest

A
  • fastest = prilocaine
  • intermediate = lido & mepivicaine
  • slowest = etidocaine, bupivacaine, ropivacaine
34
Q

metabolism of esters LA

A
  • rapid hydrolysis from cholinesterases in plasma and liver
  • cocaine is an exception, in liver
35
Q

ester LA clearance fastest to slowest

A
  • rapid = chloroprocaine
  • intermediate = procaine
  • slow = tatracaine
36
Q

what are the metabolites of ester LA

A
  • paraaminobenzoic acid (PABA) (causes allergies)
37
Q

what local injection site contains little to no cholinesterase enzyme

A
  • CSF
  • must wait until drug goes into systemic circulation
38
Q

plasma cholinesterase is inhibited

A
  • deficiency
  • liver disease
  • increased BUN
  • parturients
  • chemo pts
39
Q

Epi as an additive

A
  • marker for intravascular injection
  • 1:200,000 or 5mcg/ml
  • limits systemic absorption (decrease toxicity)
  • no effect to onset, prolongs DOA
40
Q

which 2 LA have no vasodilator activity

A
  • cocaine
  • ropivacaine
41
Q

pH of lido 2%

A

6.5

42
Q

pH of lido 2% w/epi

A

4.5

43
Q

what are the effects of mixing locals

A

effects are additive not synergistic
faster onset and longer DOA

44
Q

max dose of bupivacaine

A

plain = 175 mg (2.5 mg/kg)
w/epi = 225 mg (3 mg/kg)

45
Q

max dose of etidocaine

A

plain = 300 mg (4mg/kg)
w/epi = 400 mg (5mg/kg)

46
Q

max dose of lidocaine

A

plain = 300 mg (4.5 mg/kg)
w/ epi = 500 mg (7mg/kg)

47
Q

max dose of mepivacaine

A

plain = 300 mg (4.5 mg/kg)
w/ epi = 500 mg (7mg/kg)

48
Q

max dose of prilocaine

A

plain = 500 mg (6 mg/kg)
w/epi = 600 mg (9mg/kg)

49
Q

max dose with ropivacaine

A

plain = 200 (2.5mg/kg)
w/epi = 200 (2.5 mg/kg)

50
Q

max dose of chloroprocaine

A

plain = 800 (12mg/kg)
w/epi = 1000 (15mg/kg)

51
Q

max dose of cocaine

A

plain (3 mg/kg)

52
Q

max dose of procaine

A

plain = 500 (7 mg/kg)
w/epi = 600 (8 mg/kg)

53
Q

max dose of tetracaine

A

plain = 100 (1.5 mg/kg)
w/epi = 200 (2.5 mg/kg)

54
Q

Hadzic’s progression

A
  • signs from toxic effects of LA
  • vertigo
  • tinnitus
  • ominous feelings
  • circumoral numbness
  • garrulousness
  • tremors
  • myoclonic jerks
  • convulsions
  • coma
  • CV collapse
55
Q

systemic levels are related to BF of tissues (fastest to slowest)

A
  • IV
  • tracheal
  • intercostal
  • caudal
  • paracervical
  • epidural
  • brachial plexus
  • subarachnoid
  • subcutaneous
    (in time i can please everyone but suzi and sally
56
Q

transient neurological symptoms (TNS)

A
  • pain in lower back, buttocks, and posterior thighs
  • sign of neurotoxicity
  • highest risk with intrathecal lido
57
Q

cauda equina syndrome

A
  • diffuse injury across lumbosacral plexus
  • bowel and bladder sphincter dysfunction
  • paraplegia
  • related to lido
58
Q

anterior spinal artery syndrome

A
  • lower extremity paresis and variable sensory deficit
59
Q

cardiotoxicity w LA

A
  • more resistant that CNS (3x blood concentration than seizures)
  • profound hypotension
  • bupivacaine may see CV before CNS @ (8-10 mcg/ml)
60
Q

treatment of LA toxicity

A
  • 100% fiO2
  • benzos
  • avoid propofol, vasopressin, CCB, BB, LA
  • decrease epi to <1 mcg/kg
  • lipid emulsion 20%
61
Q

lipid emulsion dosing

A

-1.5 ml/kg LBW
- infusion @ .25 ml/kg/min, double rate if CV still unstable
- upper limit: 10ml/kg over first 30 min

62
Q

methemoglobinemia

A
  • hemoglobin oxidized to methemoglobin (cant carry O2)
  • treatment = methylene blue 1-2mg/kg IV over 5 min, do not exceed 7.8 mg/kg