Local Anesthetics

Question 1

What are some of the methods of local anesthesia?

Answer 1

Topical, Local Infiltration, Nerve Block, Spinal Anesthesia, Epidural

Question 2

What is the MOA of local anesthetics?

Answer 2

Act directly on nerve cells to block their ability to conduct impulses; Bind directly to voltage-dependent sodium channels

Question 3

What are the effects of local anesthetic on the AP?

Answer 3

Slows rate of depolarization, reduces the height of the AP, Reduces the rise of the AP
AND
Slows axonal conduction, prevents propagation of the AP, Increases threshold potent ion
BUT does not change RMP

Question 4

What kind of channel do local anesthetics have higher affinity for?

Answer 4

Inactive over unopened (remember: unactivated –> activated –> inactive)

Question 5

What decreases the efficacy of local anesthetics?

Answer 5

Decreased tissue pH –> such as during infection or inflammation

Question 6

What types of fibers are blocked first?

Answer 6

Autonomic fibers, small non-myelinated C fibers and small myelinated A(delta) fibers BEFORE larger myelinated A(delta), A(beta) and A(alpha) fibers

Question 7

What is the order of block?

Answer 7

1. Pain
2. Cold
3. Warmth
4. Touch
5. Deep pressure
6. Motor
   (Recovery in reverse order)

Question 8

What are some SE of local anesthetics?

Answer 8

Interfere with the function of all organs in which conduction of impulses occurs (CNS, ganglia, NMJ, muscle); CNS toxicity: stimulation first, depression at higher doses –> death; CV toxicity: Depression of CV system after CNS effects develop, decrease BP, decrease rate of conduction, Arteriolar vasodilation; Hypersensitivity: rare, more frequent with ester local anesthetics

Question 9

What does toxicity depend on? And how are ester local an

Answer 9

The balance between the rate of absorption into the systemic circulation and elimination

Question 10

How are ester local anesthetics inactivated? And how amide local anesthetics metabolized?

Answer 10

Esters are inactivated by plasma esterase’s

Amides are metabolized by the liver

Question 11

Local ester anesthetic that also blocks uptake of Norepi; Potent vasoconstrictor; Used for topical anesthetics of the URT

Answer 11

Cocaine

Question 12

Short acting ester; first synthetic local anesthetic; Supplanted by new agents but still used for infiltration; Low potency, slow onset, short duration of action

Answer 12

Procaine

Question 13

Long acting ester local anesthetic; More potent and longer duration of action than procain; widely used in spinal anesthesia and in topical and ophthalmic preparations; not for peripheral nerve block

Answer 13

Tetracaine

Question 14

Ester Anesthetic with low water solubility, therefore too slowly absorbed when applied topically to be toxic; Applied to wounds and ulcerated surfaces where it provides relief for long periods of time

Answer 14

Benzocaine

Question 15

Amide; intermediate duration of action; Produces faster, more intense, longer lasting and more extensive anesthesia compared to Procain; Often used with vasoconstrictors to decrease toxicity; Wide range of clinical uses

Answer 15

Lidocaine

Question 16

Long acting amide local anesthetic; Capable of producing prolonged anesthesia; Provides more sensory than motor block; More cardiotoxic than equi-effective doses of lidocaine;

Answer 16

Bupivicaine

Question 17

Long acting amide local anesthetic; Similar actions to bupivicaine with less cardiotoxicity; Suitable for epidural and regional anesthesia; More motor-sparing than bupivacaine

Answer 17

Ropivacaine