Local Anesthesia

Question 1

What was the original local anesthetic?

Answer 1

Cocaine

Question 2

What properties would you want for the ideal local anesthetic?

Answer 2

Reversible blockade that is lipo and hydrophilic, lot toxicity, quick acting, and active topically, IV, and IM. Safe, simple, and cheap.

Question 3

What’s the MOA of local anesthetics?

Answer 3

Blockade of voltage gated Na channels. 2 ways: Lipophilic= passes through the membrane and binds to the inside of the channel. Hydrophilic= dissolves in the membrane and affects the channel in the membrane. Prevent that area from firing APs (below threshold)

Question 4

What form of the voltage gated Na channels do the local anesthetics bind?

Answer 4

These drugs preferentially bind to the activated and inactivated Na channels. Not the closed (deactivated), b/c the closed channel prevents the drug from blocking it

Question 5

Describe the differential effect local anesthetics have on nerves

Answer 5

Larger fibers take more drug and longer time. Myelinated fibers take more drug over more area. Fibers in the center of the nerve are anesthetized last (distal fibers). These are the last to be anesthetized (proximal to distal) and return to normal fxn last (proximal to distal). Also depends on electrolyte balance of the pt (Na and K)

Question 6

Which fibers are anesthetized first? Last?

Answer 6

B fibers are first to go, then Aδ and C fibers (Pain). Motor axons are the last to be anesthetized.

Question 7

Why is Henderson Hasselbach important?

Answer 7

B/c they have to cross the membrane in the un-­‐ionized state. Most are weak bases with pkA of 8

Question 8

What percentage of the drug crosses the membrane at an extraneural pH of 9?

Answer 8

90%

Question 9

What percentage of the drug crosses the membrane at an extra neural pH of 7?

Answer 9

10%

Question 10

How does inflammation affect the drug’s ability to cross the membrane?

Answer 10

In areas of inflammation, the pH is typically acidic, around 6, so 99% of the drug doesn’t go into the nerve. Can be toxic

Question 11

What groups of drugs are used as local anesthetics?

Answer 11

Amides and esters. Both are topical only and almost all have benzene ring.

Question 12

How are amides metabolized and eliminated?

Answer 12

Hepatic metabolism and affected by CV, Liver dz, pregnancy, cimetidine, βBlockers, and volatile anesthetics. Renally eliminated

Question 13

What’s lidocaine’s onset and duration of action?

Answer 13

Fast onset medium duration.

Question 14

What’s mepivicaine’s onset and duration of action?

Answer 14

Slow onset medium duration. Low potency.

Question 15

What’s prilocaine’s onset and duration of action?

Answer 15

Fast onset medium duration. Low potency. Methemoglbinemia (give methylene blue).

Question 16

What’s bupivacaine’s onset and duration of action?

Answer 16

Slow onset long duration. High potency. Most cardiotoxic.

Question 17

What’s ropivacaine onset and duration of action?

Answer 17

Slow onset long duration. High potency. Less cardiotoxic

Question 18

What’s articaine’s onset and duration of action?

Answer 18

Weird one because it’s ester and amide and has thiophene ring (only one without a benzene!) Fast onset medium duration. Used in dental work. Better penetration into bone.

Question 19

What’s the metabolism and elimination of esters?

Answer 19

Non-­Hepatic Metabolism & affected by Liver dz, pregnancy, chemo, and enzyme polymorphism. Renally eliminated. Not
metabolized in the CSF.

Question 20

What’s procaine’s duration?

Answer 20

Slow onset short duration.

Question 21

What’s chlorprocaine’s duration of action?

Answer 21

Fast onset short duration

Question 22

What’s tetracaine’s duration of action?

Answer 22

Slow onset long duration. High potency.

Question 23

What’s a natural ester derivative?

Answer 23

Cocaine

Question 24

What ADE’s are associated with local anesthetics?

Answer 24

With systematization near max dose: Ringing in ears, metallic taste, numbing of lips/tongue (STOP injection if this happens). Can also cause seizures (give diazepam or succinylcholine). Little chance of allergic rxn (except for esters), no cross reactivity b/w groups. Preservatives in the preps are also allergenic.

Question 25

What can vasoconstrictors be used for?

Answer 25

Constrictors like epi, phenylephrine, and oxymetazoline (α agonists) keep the drug where you inject it and also stop minor bleeding at wound site

Question 26

What can be used to increase blood flow and reverse anesthesia?

Answer 26

Phentolamine (α1 block)

Question 27

What causes ADEs with vasoconstrictors?

Answer 27

Injection anxiety with increased SNS

Question 28

What ADEs are seen with Epi use?

Answer 28

Drug interaction w/ BBlockers, TCAs, Halothane and Worsen CV dz and Cerebrovascular dz.

Question 29

Which local anesthetics can be applied to all surfaces?

Answer 29

Benzocaine and dyclonine

Question 30

Which anesthetics cannot be applied to mucus membranes?

Answer 30

Dibucaine and pramoxine

Question 31

What’s EMLA?

Answer 31

Lidocaine and prilocaine cream.

Question 32

What compounded drug’s are in LET?

Answer 32

Lidocaine, epi, tetracaine liquid. Used for peds pts before stitches.

Question 33

When would you use lidocaine and oxymetazoline?

Answer 33

Used by ENT to decrease engorgement and provide anesthesia

Question 34

What factors affect CSF density?

Answer 34

Dosing, [Drug], Temperature, Drug volume, and the pts position.

Question 35

What does adding dextrose to the CSF do?

Answer 35

Makes the drug hyperbaric, spec. gravity higher than CSF so it sinks

Question 36

What does adding water to the CSF do?

Answer 36

It decreases the specific gravity so it floats

Question 37

What injection techniques should you use when applying local anesthetics?

Answer 37

Use the smallest needle, inject into subQ before raising wheal and neutralize acidic solutions w/ Na bicarb