Local Anesthetics

Front 1

First local anesthetic?

Back 1

COCAINE!

Front 2

Who is the standard?

Back 2

Lidocaine

Front 3

Other use of lidocaine?

Back 3

Anti-Dysrhythmic

Front 4

Which guys are good for OB?

Back 4

Mepivacaine
Ropivacaine

Front 5

As far as physiology goes, how are K and Na distributed in and around neurons?

Back 5

K is high inside the cell
Na is high outside

Front 6

Mechanism of Local Anesthetics?

Back 6

Prevent increased permeability of nerve membranes to Na (keep it outside)
This slows rate of depolarization
Prevents reaching of Threshold

Front 7

What is the kicker about sodium channels?

Back 7

There are lots of types with different roles

Front 8

Why is it important that there are different types of Na Channels?

Back 8

cause when we block one for pain, we block others with different roles = not optimal.
Sooo research keeps on searching

Front 9

What are the states the Na channels can be in?

Back 9

Rested Closed
Activated Open
Inactivated Closed

Front 10

Which states are good/bad for LA binding?

Back 10

Rested Closed don't like LA's
Inactivated Closed have higher affinity for LA
Activated Open some affinity

Front 11

So what does this mean we do?

Back 11

You have to stimulate the nerve to create the optimum LA binding environment

Front 12

Basic structure of LA's?

Back 12

lipophilic aromatic ring
+
Hydrocarbon Chain
+
hyrdophilic tertiary amine

Front 13

Classification of LA's?

Back 13

Esters

Amides

Front 14

easy way to remember esters and amides?

Back 14

amide has an "i" in it. the amides have an "i" in the prefix of the name ...like lIdocaine

Front 15

Important Physiochemical Properties of LA's

Back 15

Ionization (pKa)
Hydrophobicity (lipid solubility)
Protein Binding
Intrinsic Vasodilator Activity

Front 16

Clinical Properties of LA's?

Back 16

Potency
Concentration
Onset Time
Duration of Action
Toxic Dose
Allergy

Front 17

Why is Ionization of LA's important?

Back 17

Administered as ionized
Body buffers them to non-ionized (free base)
They cross nerve membranes as non-ionized.
They act on Na channels as ionized

Front 18

What is the importance of pKa?

Back 18

it strongly influences onset time
The closer the pKa is to physiologic pH (7.4) the faster it will work

Front 19

Why is Tissue Acidosis a big deal?

Back 19

If there is an infection near site of block, this can lower the pH and cause a longer time of onset

Front 20

How is hydrophobicity measures?

Back 20

Octanol Buffer Partition Coefficient

Front 21

How does this coefficient affect choice of LA?

Back 21

The higher the coefficient, the more Potent the LA

Front 22

What is the most common criteria for choice of drug?

Back 22

Duration of Action

Front 23

What is the most important factor affecting duration?

Back 23

Peripheral Vascular Effects
cause if there is vasoconstriction nearby, the drug can't escape

Front 24

Effect of LA Protein Binding?

Back 24

if they bind, they have a longer duration

Front 25

Who has short duration of action?

Back 25

Procaine
Chloroprocaine

Front 26

Who has a moderate duration?

Back 26

Lidocaine
Mepivacaine
Prilocaine

Front 27

Who are the long duration guys?

Back 27

Bupivacaine
Tetracaine
Etidocaine
Ropivacaine

Front 28

What is meant by Differential Blockade?

Back 28

Blocking sensory, but not Motor Fxn

Front 29

When is this important?

Back 29

LABOR

Front 30

Who is good at differential blockade?

Back 30

Bupivacaine
Ropivacaine

Front 31

Absorption and Distribution affected by???

Back 31

Site of injection
Dosage
Added vasoconstrictor
Inherent vasodilating or vasoconstrictive qualities

Front 32

What effect on toxicity do vasoconstrictors have?

Back 32

Toxic dose is always higher with a vasocontrictor

Front 33

Where is metabolism of LA's?

Back 33

amIdes in the lIver
Esters in the plasma by pseudocholinesterase enz
(cocaine is exception and metabolized in liver)

Front 34

Kicker with amide metabolism?

Back 34

Slower so more likely to cause systemic toxicity than esters
Hepatic disease and CHF decrease rate of metabolism and inc duration of LA action

Front 35

Kicker about ester metabolism?

Back 35

Metabolites are inactive but may resemble PABA which can lead to an allergic rxn

Front 36

What is Cm?

Back 36

Minimum Concentration of LA necessary to completely block nerve

Front 37

Used for?

Back 37

Comparison

Front 38

How is Cm affected by a low pH

Back 38

Cm is higher (cause its farther from pKa)

Front 39

How is Cm affected by a stimulated nerver?

Back 39

Cm is lower

Front 40

How is Cm affected by a myelinated nerve?

Back 40

Cm is lower (b/c you just have to block nodes)

Front 41

How is Cm affected by nerve fiber size?

Back 41

doesn't affect Cm

Front 42

Order of Susceptibility of Fxn of nerves? (easiest to hardest)

Back 42

Pain (needle)
Cold (alcohol swab)
Heat
Touch
Deep Pressure
Motor

Front 43

Who is the additive to remember?

Back 43

Vasoconstrictors!
e.g. epi and phenylephrine

Front 44

What is the reason for most Toxic Rxn's to LA's?

Back 44

Putting the LA in the wrong place (i.e. intraneural, intrathecal, intravenous)

Front 45

CNS Toxicity
Initially vs at high doses?

Back 45

initially its excitation
At higher doses you get CNS depression

Front 46

What is CNS toxicity directly related to?

Back 46

Intrinsic anesthetic potency

Front 47

Which LA is most toxic?

Back 47

cocaine

Front 48

LA's effects on peripheral vasculature?

Back 48

Low doses=vasoconstriction
High doses = vasodilation
but this varies

Front 49

Preventative measures?

Back 49

use a test dose!

Front 50

Rx of toxic rxn

Back 50

stop injection
maintain ABC's
CV monitoring