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Regional Anesthesia > Local Anesthetics - Pharmacology > Flashcards

Local Anesthetics - Pharmacology Flashcards

1
Q

local anesthetics result in

A

spontaneous, complete return of nerve conduction as Rx is cleared from site of action

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2
Q

Are LAs toxic to nerves?

A

No

-possibly at extreme doses/prolonged use

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3
Q

Site of action for LAs

A

Sodium channel

  1. inhibit influx of sodium ions
  2. prevent Na channels from assuming “open/active” state
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4
Q

Importance of lipid solubility of LAs

A

Lipid solubility associated w/ potency

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5
Q

components of LAs

A
  1. aromatic ring (potency/lipid solubility)
  2. amine/ester intermediate
  3. terminal amine
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6
Q

LAs are stored as

A

Acids (combined with HCl salts to maintain stability)

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7
Q

pH of LAs

A

All LAs are bases

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8
Q

LAs are ______ in solutions with greater alkalinity relative to drugs pK

A

non-ionized

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9
Q

Time for onset of LA

A

dependent on proportion of molecules in tertiary/lipid-soluble structure when exposed to physiologic pH
(Drugs pKa)

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10
Q

Non-ionized form of LAs

A

lipid soluble, tertiary

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11
Q

Ionized form of LAs

A

water soluble, quaternary (ionized)

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12
Q

LA injected into pt with acidic tissue, what will occur?

A

Less potent d/t less molecules in non-ionized form, more in ionized form

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13
Q

LA injected into pt who has been hyperventilated, what will occur?

A

LA = more potent in alkaline pt

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14
Q

Which form of LA crosses cellular membrane?

A

non-ionized

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15
Q

Which form of LA blocks Na+ channel?

A

ionized (active)

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16
Q

Where does LA block Na+ channel?

A

intracellularly

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17
Q

More lipophilic LA is, _____

A 
More potent (stronger)
and faster (time of onset)
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18
Q

LA + NaHCO3 would result in

A

increased speed + potency of LA

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19
Q

maximum amount of bicarb you can add

A

1mEq (mL) per 10 mL Lido/Mepiv

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20
Q

Consequence of using too much bicarb

A

crystallization

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21
Q

Which anesthetics should not be given with bicarb?

A

Bupivicaine

Ropivicaine

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22
Q

LA of choice for labor epidurals

A

Chloroprocaine

d/t rapid hydrolysis in plasma

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23
Q

Ester LAs

A

contain 1 “i” in name

-tetracaine, procaine, chlorprocaine

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24
Q

Amide LAs

A

contain 2 “i”s in name

-Lidocaine, Bupivicaine, Prilocaine

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25
Q

intracellularly which is the active form of LA?

A

ionized

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26
Q

LAs bind to receptor in what form

A

binds to inactive, closed sodium channel

PREVENTS open/active form

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27
Q

Which nerve is blocked faster: thicker or thinner?

A

thinner

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28
Q

Which nerve is blocked faster: myelinated or unmyelinated?

A

myelinated

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29
Q

Which nerve is blocked faster: inner or outer?

A

Outer nerve

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30
Q

Cm

A

Minimal concentration

-concentration of LA reqd to produce conduction blockade of nerve impulses

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31
Q

At low concentrations of LA, ______ blockade will result

A

autonomic blockade

“sympathectomy”

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32
Q

At low-medium concentrations of LA, _____ blockade will result

A

sensory

-pain + temperature

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33
Q

At high concentrations of LA, ____ blockade will result

A

motor

34
Q

Approximate dose of motor blockade

A

2 x Cm (of sensory blockade)

35
Q

According to diffusion, which part of axon will be blocked first?

A

Mantle (proximal/outer portion)

–> core bundle (distal) is inner portion, blocked last

36
Q

At what portion of nerve (location) is required to cause block?

A

Na+ channels at Nodes of Ranvier

37
Q

What is required to produce a blockade in the nerve?

A

2-3 Nodes of Ranvier

38
Q

absorption + circulation take LA ____ from site of action

A

away

39
Q

absorption depends on

A

vascularity of tissue (blood flow)

40
Q

Blood flow is dependent on

A
  1. site of injection
  2. addition of vasoconstrictor
  3. LA agent used
41
Q

Site of injection: order of vascularity mneumonic

A

ITICPEBSS

I think I can please everyone but susan + sally

42
Q

Site of injection: order of vascularity (high to low)

A

IV, Tracheal, Intercostal, Caudal, Paracervical, Epidural, Brachial Plexus, Sciatic-femoral, Subcutaneous

43
Q

only drug with intrinsic vasoconstrictor properties

A

cocaine

44
Q

LA DOA is proportional to

A

the time the drug is in contact with nerve fiber

45
Q

Addition of epi will cause

A

increased DOA of LA

46
Q

vasoconstrictors do not affect

A

speed of onset

47
Q

A/Es of Epi in LAs

A
  • cardiac irritability in presence of VAs

- avoid in tissues supplied by end-arteries (fingers, ears, nose, penis)

48
Q

In an awake patient, where will LA toxicity be seen first?

A

neuro system

49
Q

If pt under GA has LA toxicity, what could be presenting sign?

A

CV collapse

50
Q

LAST treatment

A

Intra-lipid 20%

  1. bolus 1.5mL/kg
  2. infusion .25mL/kg/min
51
Q

LAST - ACLS

A

Different: decrease epi bolus to 1 mcg/kg

52
Q

tx for LAST if remains unstable after 1st intvn

A

rebolus 1-2x, 2x infusion rate

53
Q

Max dose intralipid

A

12mL/kg

54
Q

Do not administer LA without what?

A

Knowing where intralipid is

55
Q

LA effects on immune system

A

allergic response - rare
increased risk w/ esters (PABA)
amides: methylparaben similar to PABA structure
*decreases inflammatory response generally

56
Q

LA effects on musculoskeletal system

A

myotoxicity if injected into muscle

57
Q

role of LA in pain management

A

infusion decreases amount of opioids req

-assoc. w/ shortened LOS after surgery

58
Q

1% Lidocaine=

A

10 mg/mL

59
Q

1:100,000 epi =

A

10mcg/mL
or
.01 mg/mL

60
Q

LAs administered together have

A

additive effects

61
Q

LAs potentiate ______

A

NMDRs

62
Q

In what type of patients should you avoid certain LAs?

A

known plasma cholinesterase deficiency: avoid esters

63
Q

only LA with intrinsic vasoconstriction

A

cocaine

64
Q

cocaine is used for what type of procedures

A

ENT

65
Q

cocaine type of metabolism

A

hepatic

66
Q

1st synthetic LA

A

procaine

67
Q

Procaine

A
  • *ester**
  • fast onset
  • low toxicity
  • metabolized to PABA
  • pk = 8.9
68
Q

Chlorprocaine

A
  • *ester**
  • rapid onset
  • low potency/toxicity
  • pk=9.1
  • used in labor/parturients
69
Q

Tetracaine

A
  • *ester**
  • slow onset
  • long DOA
  • moderate toxicity
  • pK=8.6
70
Q

Metabolism of Amides - fastest to slowest

A

Prilocaine > Lidocaine > Mepivicaine > Ropi > Bupi

71
Q

How is metabolism related to toxicity?

A

As metabolism slows, risk of toxicity increases

Ropi/Bupi > Prilocaine

72
Q

Lidocaine

A

amide
-most versatile LA
-rapid onset
-moderate DOA/potency/toxicity
-used for everything*
-Hepatic metabolism, 1st pass pulm uptake
-Good for bronchospasm
AEs: increased risk for cauda equina (esp > 5%), TNS
pK: 7.7

73
Q

Mepivicaine

A

amide
Moderate onset/duration/potency/toxicity
pK: 7.6

74
Q

Bupivicaine

A

amide
-slow onset
-LONG doa
-high potency/toxicity
-cardiac toxicity: resistant to Tx (R-isomer)
1st pass pulm uptake - propranolol impairs this
pK: 8.1

75
Q

Etidocaine

A

amide
-rapid onset
-long DOA
-high potency
pK: 7.7

76
Q

Prilocaine

A

amide
1st pass pulm uptake
**metabolite: o-tulidine (risk of methemoglobinemia)
**fastest metabolism

77
Q

Treatment for Methemoglobinemia

A

Methylene Blue

1mg/kg over 5min

78
Q

Ropivicaine

A

amide
similar to Bupivicaine
except: Less cardiotoxic
pK: 8.1

79
Q

Max dose: procaine

A

7mg/kg

+epi = 12 mg/kg

80
Q

Max dose: chloroprocaine

A

9mg/kg

+epi = 12 mg/kg

81
Q

Max dose: Lidocaine

A

5mg/kg

+epi = 7mg/kg

82
Q

Max dose: Bupi/Ropi

A

2.5mg/kg

+epi = 3mg/kg

Regional Anesthesia (4 decks)

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