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Anesthesia > Local Anesthetics > Flashcards

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)

A

300 mg

22
Q

Max dose of Mepivacaine for infiltration

A

300 mg

23
Q

Max dose of prilocaine for infiltration

A

400 mg

24
Q

Max dose of Bupivacaine for infiltration

A

150 mg

25
Q

Max dose of Ropivacaine for infiltration

A

200 mg

26
Q

Max dose of Procaine for infiltration

A

500 mg

27
Q

Max dose of Chlorprocaine for infiltration

A

600 mg

28
Q

Major LA for IV anesthesia

A

Chlorprocaine, Lidocaine, Prilocaine

29
Q

Major LA for local anesthesia

A

All

30
Q

Major LA for peripheral nerve block

A

Procaine, Chlorprocaine, All amides

31
Q

Major LA for epidural anesthesia

A

Chlorprocaine, all amides

32
Q

Major LA for spinal anesthesia

A

Procaine, tetracaine, Bupfivacaine, ropivacaine

33
Q

CNS toxicity symptoms

A

circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech, TC seizures

34
Q

How do LA cause seizures?

A

depression fo cortical inhibitory neurons, letting excitatory pathways rule

35
Q

How can LA seizures propogate LA toxicity?

A

hypoxemia/metabolic acidosis

acidosis propogates LA toxicity

36
Q

Tx for CNS toxicity of LA

A

-Benzos vs Propofol

37
Q

Cardiovasular toxicity of LA effects

A 
profound hypotension (relax arteriolar SM relaxation)
direct myocardial depression
impaired cardiac automaticiy/conduction = prolonged PR, wide QRS
38
Q

LA with highest cardiac toxicity?

A

bupivacaine

39
Q

How do interlipids help reduce toxic events?

A

provide lipid sink that binds to LA and pulls it out of active circulation = diminish toxicity

40
Q

Esters vs amides; more allergic reactions

A

esters = produce PABA metabolites = hypersensitivity

41
Q

Does cross sensitivity between esters and amides for hypersensitivity exist?

A

Esters make PABA (allergen)

some amides contain methylparaben as preservative (cross reacts w/ PABA); it is not the amide itself but the preservative

42
Q

Major use of Tetracaine

A

spinal anesthesia (high risk of TNS)

RARELY used for epidural/PNB (slow onset, profound motor blockade, high toxicity at high conc)

43
Q

Major uses of lidocaine

A

topical, local, IV, PNB, epidural/spinal (restricted 2/2 side effects)

44
Q

What form of lidocaine infusion has highest risk of neurotoxicyt and neural injury?

A

spinal anesthesia (via continuous spinal) = cauda equina syndrome

maldistribution and high does through small gauge catheter

45
Q

What is TNS?

A

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
Q

Factors increasing risk of TNS?

A

lithotomy position

knee arthroscopy positioning

outpatient procedures

47
Q

1st line treatment for TNS

A

NSAIDS

48
Q

How does mepivacaine vary from lidocaine?

A

piperdine ring = less vasodilation = longer duration of action

49
Q

Major limitation of mepivacaine?

A

ineffective as topical anesthetic

50
Q

Major limitation of prilocaine

A

At high doses may result in clinically significant of ortho-toluidine = can convert hgb to methemoglobin

antidote = methylene blue

51
Q

most comonly used LA for epidural anesthesia and post op pain management

A

bupivacaine (long duration, very low motor blockade)

Anesthesia (9 decks)

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