L21 local anesthetics Flashcards
General mechanism of local anesthetics
Bind to sodium channels in the nerves to block nerve transmission
differences between myelinated and non-myelinated nerves
myelinated you only need to block about 3 nodes of ranier while unmyelinated the length that must be blocked is longer - they are more difficult to block
Core vs. Mantle fibers block
core is on the inside of a peripheral nerve and mantle fibers surround. Nerves going to peripheral never are more towards the core therefore the anesthetic needs to penetrate deeper to reach them. onset begins proximal and moves distal
Fiber class A
myelinated fibers - larger fibers making them more difficult to block (A alpha is the biggest)
Fiber class B
myelinated fibers- very small - the easiest to block
pre-ganglionic sympathetic
blocked with all anesthetics (sympathetic blockade)
Fiber class C
unmyelinated fibers- more difficult to block
visceral pain - generalized dull slow pain
A alpha fibers do
largest and hardest to block are responsible for motor
A beta fibers
tactile, proprioception, touch
A delta
pain, cold, temperature, smallest easiest of A group
fast, instant pain
order of blockage difficulty
sympathetics>pain>motor
3 states of sodium channels
- resting - M-gate closed, H-gate open
- Open - M-gate and H-gate open
- Inactivated- M-gate open, H-gate closed
where do local anesthesics bind
on the sodium channels on the inside of the cell- must be lipophilic.
frequency dependent blockade
in active nerves (fire more often) will be more quickly blocked by local anesthetic
bind more easily to open or inactivated Na+ channels
2 groups of local anethetics
esters
amides
molecular structure of local anesthetics
all have benzene rings and tertiary amine groups allowing for a lone electron pair that can accept or donate electrons (give a charged and uncharged forms)
most are weak bases (except benzocaine)
% charged depends on pH and pKa
charged molecule bind to the sodium channel better but only the uncharged can cross the lipid bilayer
why add sodium bicarbonate
faster onset time for local anesthetics because increasing the pH around the anesthetic molecules increases the number in the uncharged form which is easier to cross membranes into cells
onset time primary determinants
pH and pKa
higher pH and lower pKa speeds up the onset time bc you get more molecules in the uncharged form
primary determinant of potency
lipid solubility - more soluble = more potent (need less)
protein binding affects
duration (theses are not blood proteins) More binding=longer lasting
anesthetics bind proteins on the nearby tissues creating a sink that can be slowly released to the nerve
why would you add epinephrine to a local anesthetic
for vasoconstriction - reduces blood flow - keeps the anesthetic closer to the nerve
more important for drugs that are not very highly protein bound
also helps confirm that the drug is not being injected into the blood stream (if in blood vessel it will increase HR)
neuraxial anesthesis
sinal and epidural- indications for a surgery chest or below\
do your injection around L4/L5
where does the spinal cord end
adult - L1
infant- L3
spinal vs epidural
spina- inject around the caudal equina (L3-L4) the anesthetic will diffuse up and everything below that point will be blocked
epidural - block at nerve roots, can be done at any level, outside the dural and CSF. some will spread up and down and the nerves around the site will be blocked but there is sparing of the nerves below
respiratory affects with LAs
block of sympathetics lowers BP (arterial and venal dilation) and if it decreases too low than you could have decreased blood to the brain which could lead to a respiratory arrest
CV affects with a local anesthetic
sympathectomy- arterial dilation and venodilation reduces BP
bradycardia- unopposed vagal stimulation of heart
order of absorption
intercostal>caudal>epidural
must be very careful with intercostal bc there is the greatest change of overdose
highly protein bound or lipophilic can become sequestered decreasing absorption
pt caracteristics
high blood flow affect on local anesthetics
higher blood flow = more absorption
Elimination of esters
metabolized in the plasma by plasma cholinesterase (same as succ)
amides elimination
metabolized in the liver
max recommended dose of bupivacaine
3mg/kg in adults and 2.5 mg/kg in infants
max recommended dose of lidocaine
5 mg/kg plain
7 mg/kg with epi
bc epinephrine vasoconstricts to increase absorption of drugs that are not highly protein bound
neurotoxicity
excitatory lightheadedness, numbness can lead to seizures worsened by acidosis (less protein binding and more blood flow to brain)
Cardiovascular toxicity
usually happens after neurotoxicy (4X-2X the concentration) (or too large of a load given so both happen at the same time)
the heart has the same voltage gated sodium channels as the nerves
direct vasodilation
inhibition of normal sympathetic nervous symptom responses
cocaine- arrhythmias
heart block, slurred QRS,
ways to prevent CV toxicity
aspirate on needle before injection to make sure not in a blood vesicle
inject with epi
if CV toxicity occurs
ABCs
no lidocaine
stop seizures
specific antidote– intralipid (very lipophilic can absorb anesthetics out of the blood stream)
posterior puncture headaches
common complication
worse standing than laying
do a blood patch
esters
Cocaine HCl
Procaine HCl
Tetracaine HCl
Benzocaine (only one that is not a weak base)
Amides
Lidocaine HCl (only one that can be given IV)
Mepivacaine HCl
Bupivacaine HCl
Ropivacaine
