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what do local anesthetics do?
provide REVERSIBLE conduction block of both central and peripheral nerve impulses
- -autonomic, sensory, and motor block occur with increasing amounts of local anesthetic in the affected area
- -not all blocked at the same time and with the same amount of local anesthetic
how do local anesthetics work?
- -block the propagation of electrical potential (action potential) in electrically excitable tissues
- -supress excitation in different tissues
Uses of local anesthetics
- -neuraxial block (spinal or epidural)
- -regional block (UE or LE)
- -local infiltration
- -IV regional (Bier block)
- -cardiac arrhythmias
- -surrounds the axon
- -made up of connective tissue, capillaries, and fibroblasts
- -surrounds individual fibers that are gathered into fascicles
- -made up of dense connective tissue
- -encases entire peripheral nerve
- -made up of even denser connective tissue
Which fiber types are myelinated?
- A- heavy myelination
- B- light myelination
Which fiber types are unmyelinated?
- -increases conduction velocity
- -makes nerve susceptible to LA induced conduction blockade (block only needed at nodes of Ranvier)
nodes of Ranvier
breaks in myelin
what 2 aspects affect susceptibility to LA blockade?
- 1) fiber size
- 2) presence or absence of myelin
Clinically where does blockade usually occur first?
type A delta fibers as they have a small diameter and are heavily myelinated
What effect do the 3 connective tissue layers have on penetration?
they form a barrier to penetration of local anesthetics
In what order does peripheral nerve blockade usually progress (sensory, autonomic, and motor)?
- 1st autonomic
- 2nd sensory
- 3rd motor
What sensations typically get blocked first? Last?
- 1st- pain and temp sensation
- Last- pressure or touch
Will patients feel touch or pressure after local infiltration?
Yes, and we should tell them this so they expect it. However, they should not feel sharp pain.
Local anesthetics MOA
- -blocks the Na+ channels!!!
- -slows the rate of depolarization
- -threshold is not reached
- -result is conduction blockade
How do the local anesthetics affect the sodium channels?
- -bind to the Na+ channels in the inactive state (inactivation gate is closed)
- -block inner and outer Na+ gates
- -Na+ channel activation and depolarization is prevented and threshold is not reached
Are the local anesthetics acid or basic drugs?
Explain how both the ionized and nonionized forms of the local anesthetics are at work in causing their effect.
- -Nonionized form passes thru the membrane
- -Becomes ionized
- -Ionized form plugs the Na+ channel
Frequency dependent blockade
- -during onset or recovery from local anesthetic blockade, the block is incomplete
- -blockade will be enhanced by repetitive stimulation causing a use dependent binding to the Na+ channels
- -ex: might ask a pt to engage neuromuscular transmission by opening and closing their fist
local anesthetics basic structure
- -all esters or amides
- -have a lipophilic and hydrophilic portion that's joined by an ester or an amide
What in the local anesthetic chemical structure tells you it's a base?
-the N has a lone pair of electrons and could accept an H+ ion
How can you differentiate btw an amide and an ester?
-All amides have 2 i's in the name
Bupivicaine max dose
3 mg / kg
Lido max dose (with epi and without)?
- without 4.5 mg / kg
- with dpi 7 mg / kg
Max dose ropivicaine
3 mg / kg
chloroprocaine max dose
12 mg /kg
cocaine max dose
3 mg / kg
procaine max dose
12 mg / kg
tetracaine max dose
3 mg / kg
What benefits do levobupivicaine and ropivicaine have over bupivicaine?
They are both less potent than bupivicaine so there's less toxicity.
Rank the following drugs from most lipid soluble to least: lido, rovipicaine, bupivicaine, chloroprocaine, procaine, tetracaine)
- tetracaine 5,822
- bupivicaine 3,420
- chloroprocaine 810
- rovipicaine 775
- lido 366
- procaine 100
What pharmacologic parameter is associated with onset? with duration?
- Onset- pKa
- Duration- protein binding
Will a higher or lower pKa lead to a faster onset?
lower pKa agents will have more nonionized fraction and thus a faster onset
Why does chloroprocaine have a fast onset even though it have a high degree of ionization?
It has a low toxicity and hence is used in higher concentrations. The rapid onset is from mass diffusion or concentration effect.
What happens to local anesthetics in an acidic environment? Why?
- They are less effective.
- The acidic environment produces more of the BH+ form of the drug.
Why might you add bicarb to a local anesthetic?
- -Shifts the equation towards the B (non ionized form)
- -It speeds onset
- -Decreases pain with injection
Why is the toxic dose of lido with epi higher than for lido alone?
- -Addition of epi decreases absorption
- -Solutions with epi are more acidic
What pharmacokinetic parameter is associated with duration?
protein binding (and other kinetic factors that pertain to absorption and distribution)
What drugs are considered to have a short duration of action?
- procaine (6%)
- chloroprocaine (0%)
% protein bound
What drugs are considered to have an intermediate duration of action?
- lido (64%), mepivicaine (77%), prilocaine (55%)
% protein bound
What drugs are considered to have a long duration of action?
- "BET- you can bet on it"
- bupivicaine (95%), etidocaine (95%), tetracaine (75%)
% protein bound
What does absorption depend on?
Site of injection and vascularity
What sites have the highest degree of absorption?
Are all formulations of local anesthetics approved for all uses (IV, epidural, spinal)?
No, that's why it's important to look at the vial.
What is CM?
- -minimum concentration of LA needed to provide blockade (loss of sensation) in 50% of pts
- -analagous to MAC
What does adding a vasoconstrictor to a local anesthetic do?
- -Decreases absorption (the drug stays where you put it)
- -Increases neuronal uptake
- -Enhances the quality of the block
- -Prolongs DOA
- -Limits the toxic effects (it can't get to the systemic circulation as easily)
In what pts would we avoid using epi with our local anesthetics?
- -unstable angina
- -cardiac dysrhythmias
- -h/o HTN
- -uteroplacental insufficiency
- -peripheral nerve block anesthesia in areas that may lack collateral blood flow (digits or penis)
- -IV regional anesthesia (bier block)
How are the ester local anesthetics metabolized?
- -ester hydrolysis
- -metabolized by pseudocholinesterases
- -occurs quickly
- -metabolites are water soluble
Is someone with a pseudocholinesterase deficiency at greater or lesser risk for toxic SE with the ester local anesthetics?
At greater risk
Are the esters or amides more associated with allergic reactions?
-The esters as PABA is a metabolite
- -Preservative used in esters or amides that may be associated with allergic reactions
- -MABA causes antibody production
- -slower than ester hydrolysis
what is methemoglobinemia?
- -prilocaine and benzocaine metabolites can accumulate following large doses
- -converts Hgb to methemoglobin
- -this form of Hgb can't bind O2
methylene blue, 1-2 mg / kg of 1% solution IV over 5 mins
What SE usually occur first with the local anesthetics?
CV SE of the local anesthetics
- -decreased automaticity of the heart (spontaneous phase 4 depolarization is depressed and the refractory period is decreased in duration)
- -arteriolar vasodilation
- -bradycardia and heart block
Neuro SE from the local anesthetics
- -circumoral numbness
- -excitation: restlessless, seizure activity, CNS depression, drowsiness, LOC
Why does bupivicaine cause more pronounced depolarization changes in the heart than lidocaine?
-It's more lipid soluble and potent, plus it's largely protein bound and hangs around
cauda equina syndrome
- -thought due to the drug pooling around the caudal equine in high concentrations and causing permanent nerve damage
- -associated with repeat doses of 0.5% tetracaine and 5% lidocaine (no longer used) given thru small bore catheters (no longer used) for spinal anesthesia
- -also associated with lithotomy position
transient radicular irritation
- -full recovery usually occurs within 7 days
- -can occur after spinal anesthesia with different agents
- -onset is delayed, occurs 24 hours after d/c of spinal as it takes time for inflammation to get set up
- -burning pain or aching in LE and buttocks
- -lithotomy position adds to risk
respiratory SE of local anesthetics
- -decreased hypoxic drive and response to CO2
- -blocks reflex bronchoconstriction associated with intubation
- -helpful for a pt with a reactive airway
retro-bulbar apnea syndrome
- -retro-bulbar block done with retina surgery
- -LA is injected into the optic nerve sheath and spreads to the CSF
- -CSF is exposed to high levels of LA
- -this causes depression of the medullary center and apnea
- -treatment is supportive (mechanical ventilation)
- -usually resolves in 1 hour