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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
intracellularly which is the active form of LA?
ionized
26
LAs bind to receptor in what form
binds to inactive, closed sodium channel | PREVENTS open/active form
27
Which nerve is blocked faster: thicker or thinner?
thinner
28
Which nerve is blocked faster: myelinated or unmyelinated?
myelinated
29
Which nerve is blocked faster: inner or outer?
Outer nerve
30
Cm
Minimal concentration | -concentration of LA reqd to produce conduction blockade of nerve impulses
31
At low concentrations of LA, ______ blockade will result
autonomic blockade | "sympathectomy"
32
At low-medium concentrations of LA, _____ blockade will result
sensory | -pain + temperature
33
At high concentrations of LA, ____ blockade will result
motor
34
Approximate dose of motor blockade
2 x Cm (of sensory blockade)
35
According to diffusion, which part of axon will be blocked first?
Mantle (proximal/outer portion) | --> core bundle (distal) is inner portion, blocked last
36
At what portion of nerve (location) is required to cause block?
Na+ channels at Nodes of Ranvier
37
What is required to produce a blockade in the nerve?
2-3 Nodes of Ranvier
38
absorption + circulation take LA ____ from site of action
away
39
absorption depends on
vascularity of tissue (blood flow)
40
Blood flow is dependent on
1. site of injection 2. addition of vasoconstrictor 3. LA agent used
41
Site of injection: order of vascularity mneumonic
ITICPEBSS | I think I can please everyone but susan + sally
42
Site of injection: order of vascularity (high to low)
IV, Tracheal, Intercostal, Caudal, Paracervical, Epidural, Brachial Plexus, Sciatic-femoral, Subcutaneous
43
only drug with intrinsic vasoconstrictor properties
cocaine
44
LA DOA is proportional to
the time the drug is in contact with nerve fiber
45
Addition of epi will cause
increased DOA of LA
46
vasoconstrictors do not affect
speed of onset
47
A/Es of Epi in LAs
- cardiac irritability in presence of VAs | - avoid in tissues supplied by end-arteries (fingers, ears, nose, penis)
48
In an awake patient, where will LA toxicity be seen first?
neuro system
49
If pt under GA has LA toxicity, what could be presenting sign?
CV collapse
50
LAST treatment
Intra-lipid 20% 1. bolus 1.5mL/kg 2. infusion .25mL/kg/min
51
LAST - ACLS
Different: decrease epi bolus to 1 mcg/kg
52
tx for LAST if remains unstable after 1st intvn
rebolus 1-2x, 2x infusion rate
53
Max dose intralipid
12mL/kg
54
Do not administer LA without what?
Knowing where intralipid is
55
LA effects on immune system
allergic response - rare increased risk w/ esters (PABA) amides: methylparaben similar to PABA structure *decreases inflammatory response generally
56
LA effects on musculoskeletal system
myotoxicity if injected into muscle
57
role of LA in pain management
infusion decreases amount of opioids req | -assoc. w/ shortened LOS after surgery
58
1% Lidocaine=
10 mg/mL
59
1:100,000 epi =
10mcg/mL or .01 mg/mL
60
LAs administered together have
additive effects
61
LAs potentiate ______
NMDRs
62
In what type of patients should you avoid certain LAs?
known plasma cholinesterase deficiency: avoid esters
63
only LA with intrinsic vasoconstriction
cocaine
64
cocaine is used for what type of procedures
ENT
65
cocaine type of metabolism
hepatic
66
1st synthetic LA
procaine
67
Procaine
* *ester** - fast onset - low toxicity - metabolized to PABA - pk = 8.9
68
Chlorprocaine
* *ester** - rapid onset - low potency/toxicity - pk=9.1 * used in labor/parturients
69
Tetracaine
* *ester** - slow onset - long DOA - moderate toxicity - pK=8.6
70
Metabolism of Amides - fastest to slowest
Prilocaine > Lidocaine > Mepivicaine > Ropi > Bupi
71
How is metabolism related to toxicity?
As metabolism slows, risk of toxicity increases | Ropi/Bupi > Prilocaine
72
Lidocaine
**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
Mepivicaine
**amide** Moderate onset/duration/potency/toxicity pK: 7.6
74
Bupivicaine
**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
Etidocaine
**amide** -rapid onset -long DOA -high potency pK: 7.7
76
Prilocaine
**amide** 1st pass pulm uptake **metabolite: o-tulidine (risk of methemoglobinemia) **fastest metabolism
77
Treatment for Methemoglobinemia
Methylene Blue | 1mg/kg over 5min
78
Ropivicaine
**amide** similar to Bupivicaine except: Less cardiotoxic pK: 8.1
79
Max dose: procaine
7mg/kg | +epi = 12 mg/kg
80
Max dose: chloroprocaine
9mg/kg | +epi = 12 mg/kg
81
Max dose: Lidocaine
5mg/kg | +epi = 7mg/kg
82
Max dose: Bupi/Ropi
2.5mg/kg | +epi = 3mg/kg

Regional Anesthesia (4 decks)

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