Local Anesthesia

Question 1

2 classes of local anesthetics

Answer 1

1. aminoamide
2. aminoester

*based on whether an ester bond or an amide bond connects the hydrophobic portion to the hydrophilic portion of the anesthetic

Question 2

local anesthetic administration

Answer 2

*perineural (ex. brachial plexus block)
*infiltration
*IV (analgesia, Bier block)
*transcutaneous/topical (EMLA cream for IV placement)
*spinal
*epidural
*inhaled

Question 3

how do local anesthetics work

Answer 3

*block conduction of neural impulses by decreasing the rate of depolarization in response to excitement
*preventing the achievement of a threshold potential

Question 4

2 forms of local anesthetics

Answer 4

1. uncharged base (more hydrophobic; able to cross cell membranes)
2. protonated quaternary amine (charged; more hydrophilic; unable to cross cellular membranes; presumed to be the active form which binds Na channels)

*the uncharged form crosses the membrane into the neuron and then converts to the protonated form

Question 5

pH and local anesthesia

Answer 5

*pH can directly effect the relative concentrations of the neutral (uncharged base) and the charged (quaternary amine) in both extracellular and intracellular compartments
*pKa = pH when at equilibrium

Question 6

the closer the pKa of the local anesthetic to physiologic pH (7.4)…

Answer 6

the FASTER the onset of the effect
(more acidic = less effective)

Question 7

pharmacokinetics of local anesthetics

Answer 7

*local anesthetics in general are deposited near their site of action and systemic absorption competes with drug entry to the nerve
-decreased duration: once local is absorbed into systemic circulation, it no long can reach its effector site
-potential for systemic toxicity - mediated by plasma concentration; higher plasma concentrations result in potential for toxicity

Question 8

differential blocking of different nerves

Answer 8

autonomics > pain/temp > touch/pressure > motor
(in order from fastest to slowest for the nerve to be blocked)

Question 9

metabolism of aminoester local anesthetics

Answer 9

*metabolized by hydrolysis via plasma esterases
*inhibited by quantitative or qualitative deficiency of plasma cholinesterase activity

Question 10

metabolism of aminoamide local anesthetics

Question 11

systemic toxicity & local anesthetics

Answer 11

*caused by excessive plasma concentration of local anesthetic
*most commonly from inadvertent intravascular injection
*rate of systemic absorption outpaces clearance of the local anesthetic

Question 12

local anesthetic vasoactivity

Answer 12

*most local anesthetics are vasodilators = increases systemic absorption (except cocaine)
*relative differences in vasoconstrictive properties may explain differences in duration of effect (more vasoconstriction = less blood flow = less systemic absorption = longer duration = less potential for toxicity)

Question 13

magnitude of systemic absorption of local anesthetics is dependent on:

Answer 13

*dose of local (higher dose = higher plasma level, even when administered appropriately)
*site of injection, from highest to lowest absorption:
1. intercostal block (highest absorption)
2. caudal
3. epidural
4. brachial plexus
5. sciatic/femoral
*use of vasoconstrictor (decreases systemic absorption)
*amount of inadvertent intravascular administration (if any)

Question 14

local anesthetic systemic toxicity - clinical features

Answer 14

1. CNS - circumoral numbness, facial tingling, restlessness, vertigo, tinnitus, slurred speech, tonic-clonic seizure
2. cardiovascular system - arrhythmia, cardiac arrest, hypotension (usually occurs AFTER CNS symptoms)

Question 15

treatment of local anesthetic systemic toxicity - CNS toxicity

Answer 15

*stop administering local anesthetic at first sign of toxicity
*support ventilation/oxygenation (intubate/mask ventilate) to avoid hypoxemia
*administer antiepileptic drug (benzos or propofol) if seizure activity is noted
*ADMINISTER INTRALIPID to prevent progression to cardiac toxicity

Question 16

cardiac toxicity: lidocaine vs bupivacaine

Answer 16

*bupivacaine is much more cardiotoxic than lidocaine

Question 17

treatment of local anesthetic systemic toxicity - cardiac toxicity

Answer 17

*administer Intralipid
*modified ACLS:
-chest compression / supportive airway management
-no lidocaine, amiodarone, calcium channel blockers, beta blockers
-reduced dose of epinephrine (no more than 1 mcg/kg/dose)
*consider cardiopulmonary bypass for cases of cardiac arrest which are resistant to therapy

Question 18

how to avoid local anesthetic systemic toxicity

Answer 18

*avoid administration of dosages that exceed the anticipated toxic dose
*use a vasoconstrictor (epi) to decrease systemic absorption
*utilize an intravascular marker to identify inadvertent IV administration
*aspirate prior to injection to assess for obvious intravascular needle placement

Question 19

how to calculate a toxic dose of a local anesthetic

Answer 19

*there is a dose range with and without epinephrine
*weight x toxic dose = ?; then divide that mg amount by the concentration in mg/cc

0.5% = 5 mg/cc
1% = 10 mg/cc
2% = 20 mg/cc

Question 20

local anesthetics & allergic reactions

Answer 20

*reactions are rare; less than 1% of all local anesthetic related adverse reactions are caused by allergic reactions
*most commonly, a reaction to an additive/preservative or systemic toxicity
*aminoesters are more likely to evoke hypersensitivity reactions than aminoamides

Question 21

how to choose a local anesthetic

Answer 21

*analgesic (loss of sensation of pain) vs. anesthetic concentration (loss of sensation to intense surgical stimulation)
*duration of action (long-acting vs intermediate acting)

Question 22

bupivacaine - onset & duration of action

Answer 22

onset = 20-30 min
duration of action = 6-12 hrs

Question 23

ropivacaine - onset & duration of action

Answer 23

onset = 20-30 min
duration of action = 6-12 hrs

Question 24

lidocaine - onset & duration of action

Answer 24

onset = 10-20 min
duration of action = 2-4 hrs

Question 25

mepivacaine - onset & duration of action

Answer 25

onset = 10-20 min
duration of action = 2-4 hrs