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Local Anesthetics Flashcards

1
Q

MOA of local ansthetics

A

site- Sodium ion channels

Block conduction of neural transmission by decreasing rate of depolarization in response to excitation (prevent reaching threshold potential)

Does NOT change resting potential, or actual threshold potential value

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2
Q

Describe normal nerve conduction:
resting potential
impulse propogation/excitation

A

Resting potential of neural membrane = -90mV (via Na out, K+ in)

Excitation = increase in permeability to Na = depolarization (more +) = hit threshold = self sustaining influx of Na (massive depolarization)

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3
Q

Form of local anesthetic most helpful for causing activity

A

neutral form = can cross lipophillic membrane to Na channel receptor (ie site of action)

Ionized form inside nerve causes activity

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4
Q

Describe conformations of Na channel, and conformations most helpful for local anesthetic activity

A

Resting-closed : NO ACTIVITY
Activated - Open: ACTIVITY
Inactivated - Closed: ACTIVITY

Repeated depolarization (which cauases activated/inactivated states vs resting) more effective anesthetic binding = enhancement of conduction blockade

USE DEPENDENT / FREQUENCY DEPENDENT BLOCK

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5
Q

Role of pH on LA activity

A

pKa of LA determines proporation of neutral to ionized forms

lower pKa= greater % of unionized (active) drug

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6
Q

Why would you add bicarbonate to LA?

A

Increase pH of environment = more neutral/ionized form (for any given pH)

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7
Q

Why may infected tissue be difficult to anesthetize?

A

infection = low pH

less proportion of neural/ionized form for given pKa of LA

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8
Q

What does the lipid solubility of a LA confer?

A

describes uptake into neural membrane

lipid solubility generally correlates to POTENCY, DURATION OF EFFECT, and sometimes INVERSELY WITH LATENCY/TIME TO ONSET

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9
Q

ETIDOCAINE OR BUPIVUCAINE

more motor blockade?

A

etidocaine

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10
Q

Describe relationship between location of nerve fibers in nerve bundle, and onset of effect.

A

Mantle (external) = 1st = effects proximal structures

Core (internal) = 2nd = effects distal structures

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11
Q

How do lipophilicity and protein binding effect LA uptake into blood stream?

A

higher lipo/PB = slower uptake

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12
Q

LA effect on vasoactivity

A

Vasodilators at clinically relevant concentrations

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13
Q

Why add vasoconstrictors to LA?

A

prolongation of anesthesia by decreased uptake into blood stream

less likelihood of toxicity (uptake is slower than metabolism)

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14
Q

Adding epi to which of the following LA will have greater effect on activity?
Bupivicaine, Tetracaine, Lidocaine

A

TEtracaine

Has vasodilation (greater), so epi will have greater effect on general activity

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15
Q

Esters

A

Cocaine, Procaine, chlorproacaine

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16
Q

Amides

A

lidocaine, bupivicaine, mepivicaine, ropivicaine

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17
Q

Metabolism of esters

A

hydrolysis in plasma

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18
Q

metabolism of amides

A

metabolism by hepatic microsomal enzymes, and lung extraction

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19
Q

Site with highest systemic absorption of LA

A

Intercostal blocks

( > caudal >epidural > brachial plexus) for the most part

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20
Q

LA w/ highest potency (greatest to least)

A

Bupivacaine/Tetracaine > ropivacaine > prilocaine/mepivacaine/lidocaine/chlorprocaine > procaine

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21
Q

Max dose of lidocaine for infiltration (in mg)

22
Q

Max dose of Mepivacaine for infiltration

23
Q

Max dose of prilocaine for infiltration

24
Q

Max dose of Bupivacaine for infiltration

25
Max dose of Ropivacaine for infiltration
200 mg
26
Max dose of Procaine for infiltration
500 mg
27
Max dose of Chlorprocaine for infiltration
600 mg
28
Major LA for IV anesthesia
Chlorprocaine, Lidocaine, Prilocaine
29
Major LA for local anesthesia
All
30
Major LA for peripheral nerve block
Procaine, Chlorprocaine, All amides
31
Major LA for epidural anesthesia
Chlorprocaine, all amides
32
Major LA for spinal anesthesia
Procaine, tetracaine, Bupfivacaine, ropivacaine
33
CNS toxicity symptoms
circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech, TC seizures
34
How do LA cause seizures?
depression fo cortical inhibitory neurons, letting excitatory pathways rule
35
How can LA seizures propogate LA toxicity?
hypoxemia/metabolic acidosis acidosis propogates LA toxicity
36
Tx for CNS toxicity of LA
-Benzos vs Propofol
37
Cardiovasular toxicity of LA effects
``` profound hypotension (relax arteriolar SM relaxation) direct myocardial depression impaired cardiac automaticiy/conduction = prolonged PR, wide QRS ```
38
LA with highest cardiac toxicity?
bupivacaine
39
How do interlipids help reduce toxic events?
provide lipid sink that binds to LA and pulls it out of active circulation = diminish toxicity
40
Esters vs amides; more allergic reactions
esters = produce PABA metabolites = hypersensitivity
41
Does cross sensitivity between esters and amides for hypersensitivity exist?
Esters make PABA (allergen) some amides contain methylparaben as preservative (cross reacts w/ PABA); it is not the amide itself but the preservative
42
Major use of Tetracaine
spinal anesthesia (high risk of TNS) RARELY used for epidural/PNB (slow onset, profound motor blockade, high toxicity at high conc)
43
Major uses of lidocaine
topical, local, IV, PNB, epidural/spinal (restricted 2/2 side effects)
44
What form of lidocaine infusion has highest risk of neurotoxicyt and neural injury?
spinal anesthesia (via continuous spinal) = cauda equina syndrome maldistribution and high does through small gauge catheter
45
What is TNS?
transient neurologic syndrome = pain and dysesthesia following intrathecal doses of lidocaine occurs in up to 1/3 of patients, lasts up to 3 days
46
Factors increasing risk of TNS?
lithotomy position knee arthroscopy positioning outpatient procedures
47
1st line treatment for TNS
NSAIDS
48
How does mepivacaine vary from lidocaine?
piperdine ring = less vasodilation = longer duration of action
49
Major limitation of mepivacaine?
ineffective as topical anesthetic
50
Major limitation of prilocaine
At high doses may result in clinically significant of ortho-toluidine = can convert hgb to methemoglobin antidote = methylene blue
51
most comonly used LA for epidural anesthesia and post op pain management
bupivacaine (long duration, very low motor blockade)

Anesthesia (9 decks)

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