Local Anesthetics Flashcards by Stacey Vernon

1st LA

cocaine

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1st synthetic ester

procaine (1905)

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hallmark LA (amide)

lidocaine (1943)

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Progressive shutdown in order

autonomic, somatic sensory, somatic motor

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temporary conduction blockade along peripheral/central nerve pathways

local anesthetics

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Local MOA

block (saltatory) transmission of nerve impulses on axon and dendrites, inhibit passage of Na+ ions through selective Na+ channels in nerve membrane

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Does MOA involve synapse, NMJ, or schwann cell?

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Peripheral nerve wrapped in

epineurium

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Wraps several axon bundles

perineurium

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Wraps axon, has own conducting membrane (axolemma)

endoneurium

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What do schwann cells do

wrap one or more axons, insulate axolemma from e’ment

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Does entire dose of LA get delivered?

No, only 2% reach.. has to penetrate 4-5 layers

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Unidirectional, jumping from nodes of Ranvier, full strength yes or no response

saltatory conduction

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factors of Cm

pH, temp, calcium conc, nerve type, stimulus frequency

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Motor fibers Cm compared to sensory

M is 2X the Cm of sensory

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Peripheral nerves made of

(myelin) A and B fibers and (unmyelin) C fibers

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How many nodes must be exposed for effective blockade

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Most heavily myelinated, largest, fastest

Alpha A fibers

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Alpha A fibers provide ____ and ____ function

motor and proprioception

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Less myelinated preganglionic autonomic nerves

B fibers

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postganglionic sympathetic and afferent sensory

c fibers

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Pain and temp sensation, slowest, tourniquet pain

c fibers

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Receptor theory (MOA)

LAs bind with receptors on INTRACELLULAR side of Na+ channel to prevent depolarization or repolarization (maintain inactive)

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Na+ Channel blockade…

Resting potential not affected
Tonic suppression (local binds while gate is at rest)
Phasic suppression (local binds while gate is open)
Channel stabilizes… an occupied ch will not open

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LAs contain 3 structures:

Unsaturated benzene ring Intermediate chain (amide or ester) Quaternary? amine

Which part of LA structure is lipophilc? hydrophilic?

benzene ring, quat amine

N on end is what? | N in chain is what?

Amine | Amide

pKa + log (ionized/nonionized) =

= pH

pKA think.....

rate of onset

Locals are weak (acid/bases)

bases

Ionized is ? soluble

water soluble

Benzene ring responsible for

anesthetic activity

Site of metabolism

ester or amine (hydrocarbon chain)

The amine end shifts in and out of ionization establishing...

water solubility or membrane permeability

Increased substitutions to either end of molecule will (increase/decrease?) hydrophobicity

increase

Is the pure base form water soluble? will it precipitate?

poorly or non-water soluble, it will precipitate

LAs are shipped as ____, the base ionizes in an acidic carrier and stays water soluble

salts

When/what causes LA to shift to basic form, resulting in lipophilicity?

Injection into tissue

?philic LAs have slow onset

Hydrophilic and highly hydrophobic... moderately hydrophobic have faster onset

?phobic = long activity

hydrophobic

What ties directly to potency?

lipid solubility

Onset of action/diffusion depends on:

chemical structure, lipid solubility, state of ionization (most important)

Higher pKa to get to pH 7.4.. drug becomes more/less? ionized

more ionized

Lower pKa have (slower/faster) onset

rapid

Ropiv/Bupiv ? onset

slower

Duration of action is r/t?

protein binding and lipid solubility

Tetra, bupiv, etido length of action

long acting

Lido, mepiv, prilo length of action

medium

Pro and chloropro length of action

short

All LAs (except cocaine and ropiv) produce ____ of smooth vascular muscle

relaxation

(Increase/decrease) absortpion preferred

decreased

Absorption occurs most rapidly with

intercostal blocks, caudal-lumbar epidurals, brachial plexus, sciatic-femoral, subQ blocks

What determines peak plasma conc?

Total dose (not volume or conc)

1% solution is ?mg/?mL

10mg/mL

Ester metabolism

ester hydrolysis via esterases in plasma/red cells | bloodstream, dont have to go to liver

amides metabolism

liver (P450)

most important differene between esters and amides

site of metabolism

Allergenic byproduct from esters

PABA

Do amides break down to PABA?

no but contain methylparaben (close relative) look for MPF (free) labels

Which class do drugs have i's in names

amides

Toxicities of mixing LAs

ADDITIVE, not independent

Adding bicarb....

to speed onset (carbonation), bu reduced pH?

Topical use LAs...drugs?

apply to mucous membranes, ENT GU cataracts, tetracaine, lidocaine, cocaine

EMLA cream

2.5% lido with 2.5% prilocaine

Topical most rapidly absorbed

tetracaine... then cocaine and lidocaine

cocaine blocks uptake of

epi and NE

Examples of major nerve blocks

brachial plexus, interscalene (require higher conc)

Examples of minor nerve blocks

ulnar, medial (single nerve)

Ankle block is an example of what

infiltration block

Epidural intermediate-acting drugs ? hours

1-2 hours

Epidural long-acting drugs ? hours

3-5 hours

Epidural drugs...

2-chloroprocaine, lidocaine, mepivacaine, bupivicaine, ropivicaine, levobupivi

Indwelling catheter with...

epidural

Effective dosing pattern with epidural

small frequent

Common spinal drugs

bupivi, tetracaine (basically same numbers), lidocaine

varacity...

specific gravity

reactions rarely allergic.. usually..?

toxicity

#1 suspect fo CNS toxicity

lidocaine

#1 suspect for cardiac toxicity

bupivicaine

Prevention of toxicity- pretreat with

benzos.. supplemental 02, 5cc and aspirate

if toxicity occurs... ?ventilation

hyperventilate

2 causes of systemic toxicity

Intravascular injection, too high local dose

resp/metabolic acidosis (increase/decrease) CNS toxicity

increase

sequence of CNS toxicity

metallic taste, lightheaded, tinitus, visual, slurring, muscle twitch, irrational, pass out, seizure, coma, apnea

cardiac toxicity occurs after

CNS toxicity

Lidocaine cardiac tox pattern

hypotension, bradycardia, hypoxia

too much bupivi, what occurs immediately?

resusc resistant left vent dysrhythmias

Locals bind when channels are (open/closed)?

open (systole)

Locals release during which part of cardiac cycle

diastole

CV toxicity

prolong conduction time, increase PR/QRS, CHB, SB, arrest

Treatment of CV toxicity

intralipid 20%

only LA that produced prolonged sensory/motor defecits in spinal/epidural

chloroprocaine

LA that can produce methemoglobin... and what are S&S

prilocaine.. DO NOT USE IN OB | brownish-gray cyanosis, tachypnea, met acid

severe methemoglobinemia

tissue hypoxia, HA, irritability, LOC

have phospholipid bilayers that act as barrier, slow release and prolong duration, decrease toxicity

liposomal preparatiosn

Time release, used for infiltration of surgical site, pain control up to 72 hours

exparel

Examples of liposomal LAs

lidocaine, tetracaine, bupivi

Local Anesthetics Flashcards

(97 cards)