Local Anesthetics

Question 1

Local Anesthetics MOA

Answer 1

Produce reversible blockade of conduction of electrical impulses along nerve fibers

Causes reversible and transient loss of sensation (analgesia) in a portion of the body without a loss of consciousness

Question 2

Local Anesthetic Site of Action

Answer 2

Reversibly block voltage-gated sodium channels in neurons

Question 3

Local Anesthetic Sequence of Action

Answer 3

First

Pain
Temperature
Touch
Pressure
Motor

Last

Question 4

Local Anesthetic Classes

Answer 4

Amides and Esters (depends on intermediate linkage between aromatic ring and tertiary amine)

Question 5

Local Anesthetic Normal pH

Answer 5

Weak Bases

Question 6

Amide Local Anesthetic Metabolism

Answer 6

Metabolized in the liver by CYP1A2 and CYP3A4 can result in significant systemic levels with rapid absorption, increases potential for toxicity

Question 7

Ester Local Anesthetic Metabolism

Answer 7

Metabolism catalyzed by plasma and tissue cholinesterase via hydrolysis rapid and occurs throughout body, reduces potential for toxicity

Question 8

Amide Local Anesthetic Excretion

Answer 8

Kidneys

Question 9

Ester Local Anesthetic Excretion

Answer 9

Results in water soluble metabolites that are excreted in urine

Question 10

Inherent effect of Local Anesthetics on Vasculature

Answer 10

Vasodilation (increases risk for systemic absorption and toxicity)

Question 11

Effect of Epinephrine on Local Anesthetics

Answer 11

Adding vasoconstrictor keeps LA at action site

Question 12

Local Anesthetics Allergic Reactions

Answer 12

More common with Esters due to being derivatives of PABA

Less common with Amide

Question 13

Local Anesthetic Toxicity

Answer 13

LAST (Local Anesthetic Systemic Toxicity)

Goes from circumoral numbness and blurred vision. All the way to cardiac failure, respiratory failure, and CNS depression

Question 14

Treatment for LAST

Answer 14

Lipid emulsion 20% infusion

Question 15

Local Anesthetic Metabolic Complication

Answer 15

Acquired Methemoglobinemia

LA metabolites include o-toluidine derivatives, which are responsible for inducing hemoglobin oxidation

Metabolite causes iron atom in hemoglobin to be oxidized from a ferrous form (Fe2+) ferric form (Fe3+) (conversion of hemoglobin to methemoglobin)

Question 16

Treatment for Acquired Methemoglobinemia caused by LA

Answer 16

Methylene Blue 1-2 mg/kg over 5 min

Question 17

Lidocaine Dosing withOUT Epi

Answer 17

5 mg/kg

Max Dose= 350 mg

Question 18

Lidocaine Dosing WITH Epi

Answer 18

7 mg/kg

Max Dose= 500 mg

Question 19

Bupivacaine withOUT Epi

Answer 19

2 mg/kg

Max Dose= 175 mg

Question 20

Bupivacaine WITH Epi

Answer 20

3 mg/kg

Max Dose= 225 mg

Question 21

Chloroprocaine withOUT Epi

Answer 21

11 mg/kg

Max Dose= 800 mg

Question 22

Chloroprocaine WITH Epi

Answer 22

14 mg/kg

Max Dose= 1000 mg

Question 23

Chloroprocaine Potency, Onset, and Duration

Answer 23

Potency= Low
Onset= Fast
Duration= Short

Question 24

Bupivacaine Potency, Onset, and Duration

Answer 24

Potency= High
Onset= Slow
Duration= Long; Longer with Epi

Question 25

Lidocaine Potency, Onset, and Duration

Answer 25

Potency= Intermediate
Onset= Fast
Duration= Intermediate; Long with Epi

Question 26

Chloroprocaine Injection Concentrations

Answer 26

1, 2, and 3%

Question 27

Lidocaine Injection Concentrations

Answer 27

0.5, 1, 1.5, 2%

Question 28

Bupivacaine Injection Concentrations

Answer 28

0.25, 0.5, 0.75%