Local Anesthetics Flashcards
Esters:
- short duration
- long duration
- surface action
short duration: procaine
long duration: tetracaine
surface action: benzocaine, cocaine
Amides:
- medium duration
- long duration
medium duration: lidocaine, mepivacaine
long duration: bupivacaine, ropivacaine
Local Anesthesia: definition
sensory transmission from a localized area to the CNS is blocked
Local Anesthetics: MOA
- block voltage dependent Na channels of excitable membranes
- reduce influx of Na ions
- prevent depolarization of the membrane
- block conduction of AP
Role of nonionized (uncharged) and ionized (charged) forms in the MOA
nonionized: reaching the receptor site (penetrates the tissue)
ionized: cause the effect (active drug)
What can be added to the local anesthetics to accelerate the onset of action?
sodium bicarbonate (enhances intracellular access)
What can be added to short acting local anesthetics to prolong duration?
alpha agonist sympathomimetic vasoconstrictor (epinephrine)
Why do we add epinephrine to shorter acting local anesthetics?
duration of action is limited unless blood flow to the area is reduced (higher sustained local tissue concentrations)
E will prolong the duration
Where are esters metabolized?
bloodstream by plasma cholinesterases (very rapid)
Where are amides metabolized?
liver (higher risk of toxicity w/ liver dysfunction)
Which fibers are blocked most easily?
small (vs large)
myelinated (vs unmyelinated)
peripheral (vs core)
type B (vs type C)
What are the effects of central neuraxial techniques and their ADEs?
motor paralysis (impaired respiratory activity)
autonomic nerve blockade (hypotension)
What are some cases in which motor paralysis would be disadventageous?
may limit the ability to bear down during delivery (obstetrical labor)
can hamper ability to ambulate w/o assistance –> falls
may interfere w/ bladder function –> urinary retention
Orderly evolution of block components
sympathetic transmission –> temperature –> pain –> light touch –> motor block
What qualifies successful surgical anesthesia?
ablation of pain AND loss of touch
What tissues should we not inject with anesthesia+vasoconstrictor?
fingers nose penis toes earlobes
Which epidural anesthesia was banned by the FDA in obstetrics and why?
What is the antidote?
bupivacaine
ADE: cardiotoxicity
antidote: lipid resuscitation
A alpha nerve fibers
proprioception (muscle sense), motor
A beta nerve fibers
touch, pressure
A delta nerve fibers
pain, temperature
C nerve fibers
pain, temperature, itch
Amides: ADEs
CNS:
- excitation
- seizures
CV:
- vasodilation
- hypotension
- arrhythmias (bupivacaine)
Cocaine: MOA
blocks Na channels
and
intrinsic sympathomimetic actions
Esters: pharmacokinetics
rapid metabolism via plasma esterases – short half lives
Esters: ADEs
CNS:
- excitation
- seizures
Cocaine: ADEs
when abuse:
HTN
seizures
cardiac arrhythmias
What conditions would cause delayed metabolism and decreased elimination of lidocaine?
impaired hepatic blood flow (CHF)
Toxicity (CNS and CV)
CNS: lightheadedness/sedation restlessness nystagmus tonic clonic convulsions
CV: vasodilator heart block arrhythmias hypotension
Prilocaine: unique effect
metabolized to o toluidine (can convert hemoglobin to methemoglobin)
Ester type metabolized products: unique effect
can cause antibody formation
Treatment for Toxicity
no antidote
manage convulsions w/ IV diazepam
EMLA cream:
- what is it
- MOA
- uses
lidocaine + prilocaine
penetrates keratinized layer of skin –> localized numbness
peds venipuncture, IV catheter placement
