Local Anesthetics

Question 1

Mechanism of action of local anesthetics?

Answer 1

• Binds to alpha subunit of voltage gated sodium channels on intracellular surface of cell membrane.
• Blocking prevents action potentials from being propagated
• Locals are bases –> best able to cross lipid cell membrane at an uncharged state (NH3 + H+ –> NH4+). A base in an acidic environment will worsen its ability to diffuse.
• Has a higher affinity to the sodium channel in the activated or inactivated state (not the resting state)

Question 2

What is the correct order of systemic absorption for Subcutaneous, IV, intercostal, tracheal, caudal, paracervical, epidural, sciatic, brachial plexus

Answer 2

IV>tracheal>intercostal>caudal>paracervical>epidural>brachial plexus>sciatic>subQ

Question 3

What are the effects of adding 1:200,000 of epinephrine to 2% lidocaine prior to a block?

What about to Bupivicaine or Ropivicaine?

Answer 3

• Causes vasoconstriction –> decreased washout –> increased block duration (50% increase), increased toxic dose
• Increased density of the block –> due to increased neural upatek
• Adding epinephrine to the skin prior to use does not affect the pH
• Does not prolong bupivicaine and ropivicaine as its duration of action is based on protein binding?

Question 4

Which locals are the esters and which are the amides?

Answer 4

Esters = Procaine, benzocaine (One i’s)

Amides = Lidocaine (Two i’s)

Question 5

How are the esters and amide local anesthetics metabolized?

Answer 5

Esters - pseudocholinesterase to PABA (PABA can often cause local reactions that are often incorrectly classified as an allergy)

Amides - Liver

Question 6

After benzocaine topicalization patient has dip in O2 to 85%. What do you do? How is this caused?

Answer 6

Cause: leads to methemoglobinemia –> heme molecules iron ion is oxidezed to 3+ state which leads to left shift of O2-heme dissociation curve and decrease release of O2 to tissues

Tx: Methylene blue corrects ferric ion back to ferrous state and normalized the dissociation curve.

Question 7

What protein is bupivacaine primarily bound to in vivo? What could theoretically happen if you have decreased amounts of that protein?

Answer 7

Alpha 1 acid glycoprotein (AAG): tends to carry more basic drugs

Albumin carries acidic drugs (barbiturates)

If you had decreased amounts of AAG then you would have more biologically active drug that could lead to increased side effects of the drug.

Question 8

What effect does local anesthetics given IV have on muscle block?

Answer 8

-Relaxes bronchial smooth muscle

Question 9

A patient who claims to have an allergic reaction to lidocaine. What is the likely explanation for this?

Answer 9

Actual allergic reaction to methylparaben (presevative)

• Esters (procaine and benzocaine) - metabolized to PABA
• Prilocaine (amine)metabolized to o toluidine –> methemoglobinemia
• Amides –> contiane preservative methylparaben (similar to PABA) which is associated with allergic reactions.

Question 10

What are the neurologic consequences of:

1) Continues infusion of 5% lidocaine
2) Lidocaine spinals
3) chloroprocaine epidurals

Answer 10

1) Cauda Equina syndrome: due to neurotoxicity
2) Transient neurologic symptoms (severe buttocks pain, leg burning, dysethesias)
3) Severe, persistent back pain (due to preservative EDTA)

Question 11

Which local anesthetic is most cardiotoxic?

Answer 11

Bupivacaine

• Very lipid soluble, high degree of protein binding –> long duration of action
• R(+) enantiomer binds avidly to cardiac sodium channel and can cause cardiovascular collapse

Question 12

What is the effect of liposomal bupivacaine vs plain bupivacaine?

Answer 12

Liposomal will increase the half life and extend the block.