Local Anesthesia Flashcards
What was the original local anesthetic?
Cocaine
What properties would you want for the ideal local anesthetic?
Reversible blockade that is lipo and hydrophilic, lot toxicity, quick acting, and active topically, IV, and IM. Safe, simple, and cheap.
What’s the MOA of local anesthetics?
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)
What form of the voltage gated Na channels do the local anesthetics bind?
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
Describe the differential effect local anesthetics have on nerves
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)
Which fibers are anesthetized first? Last?
B fibers are first to go, then Aδ and C fibers (Pain). Motor axons are the last to be anesthetized.
Why is Henderson Hasselbach important?
B/c they have to cross the membrane in the un-‐ionized state. Most are weak bases with pkA of 8
What percentage of the drug crosses the membrane at an extraneural pH of 9?
90%
What percentage of the drug crosses the membrane at an extra neural pH of 7?
10%
How does inflammation affect the drug’s ability to cross the membrane?
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
What groups of drugs are used as local anesthetics?
Amides and esters. Both are topical only and almost all have benzene ring.
How are amides metabolized and eliminated?
Hepatic metabolism and affected by CV, Liver dz, pregnancy, cimetidine, βBlockers, and volatile anesthetics. Renally eliminated
What’s lidocaine’s onset and duration of action?
Fast onset medium duration.
What’s mepivicaine’s onset and duration of action?
Slow onset medium duration. Low potency.
What’s prilocaine’s onset and duration of action?
Fast onset medium duration. Low potency. Methemoglbinemia (give methylene blue).
What’s bupivacaine’s onset and duration of action?
Slow onset long duration. High potency. Most cardiotoxic.
What’s ropivacaine onset and duration of action?
Slow onset long duration. High potency. Less cardiotoxic
What’s articaine’s onset and duration of action?
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.
What’s the metabolism and elimination of esters?
Non-Hepatic Metabolism & affected by Liver dz, pregnancy, chemo, and enzyme polymorphism. Renally eliminated. Not
metabolized in the CSF.
What’s procaine’s duration?
Slow onset short duration.
What’s chlorprocaine’s duration of action?
Fast onset short duration
What’s tetracaine’s duration of action?
Slow onset long duration. High potency.
What’s a natural ester derivative?
Cocaine
What ADE’s are associated with local anesthetics?
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.
