Week 3 - Peripheral Regional Anesthesia Flashcards
What are reasons you would use regional anesthesia?
Improved postop pain relief
Less nausea
Ability to spare anesthetic complications in comorbid conditions
What are the layers of a peripheral nerve?
- Fascicle - injections within are “intrafascicular”
- Perineurium - membrane surrounding each fascicle
- Endonerium - injections within are “intraneural”
- Epineurium - membrane surrounding nerve, loose membrane of connective tissue that easily expands (where you inject the LA)
- Perineural - injection, feel a pop when you enter and there is a lot of pressure behind the syringe – could cause nerve ischemia if injection occurs here
Define Dermatome, Myotome, and Osteotome
Dermatome = area of skin supplied by dorsal root of spinal nerve
Myotome = innervation of skeletal muscle by ventral root
Osteotome = innervation of bones, does not coincide with peripheral structures
**these are a GUIDE.. don’t be fooled by being strict
What is the chemical structure of local anesthetics?
Weak bases with alkaline pKa values that are greater than physiologic pH
Lipophilic aromatic benzene rings joined to a hydrophilic amine or ester link
- Esters: procaine, chloroprocaine, cocaine, tetracaine, benzocaine
- Amides: lidocaine, prilocaine, mepivacaine, bupivacaine, ropivacaine
How are esters and amide LA’s metabolized?
Esters - metabolized by plasma cholinesterases (pseudocholinesterase - if abnormal, risk for LA toxicity)
**there are no cholinesterases in CSF
Amides - metabolized by the liver (slower metabolism than esters)
**hepatic disease may slow clearance and lead to toxicity
What type of LA are people most likely to be allergic to?
Esters
*allergen is PABA, a byproduct of the metabolites of esters
**allergy to amides is usually due to a preservative
What LAs can cause Methemoglobinemia?
Amides
*Prilocaine is most common followed by lidocaine – treat with methylene blue
What is the max dose of chloroprocaine? Typical duration of neural blockade?
Max Dose = 12 mg/kg
Duration = 0.5-1 hour
*used for epidural, infiltration, peripheral nerve block
What is the max dose of cocaine? Typical duration of neural blockade?
Max Dose = 3 mg/kg
Duration = 0.5-1 hr
*topical use
What is the max dose of procaine? Typical duration of neural blockade?
Max Dose = 12 mg/kg
Duration = 0.5-1 hr
*used for spinal, infiltration, peripheral nerve block
What is the max dose of tetracaine? Typical duration of neural blockade?
Max Dose = 3 mg/kg
Duration = 1.5-6 hrs
*Use for spinal and topical
What is the max dose of bupivacaine? Typical duration of neural blockade?
Max Dose = 3 mg/kg
Duration = 1.5-8 hrs
*Used for epidural, spinal, infiltration, peripheral nerve block
What is the max dose of lidocaine? Typical duration of neural blockade?
Max Dose = 4.5 mg/kg (7 mg/kg with epi)
Duration = 0.75-2 hours
*Used for epidural, spinal, infiltration, peripheral nerve block, IV regional, topical
What is the max dose of mepivacaine? Typical duration of neural blockade?
Max Dose = Max Dose = 4.5 mg/kg (7 mg/kg with epi)
Duration = 1-2 hrs
*Used for epidural, infiltration, peripheral nerve block
What is the max dose of prilocaine? Typical duration of neural blockade?
Max Dose = 8 mg/kg
Duration = 0.5-1 hr
*used for peripheral nerve block (dental)
What is the max dose of ropivacaine? Typical duration of neural blockade?
Max Dose = 3 mg/kg
Duration = 1.5-8 hours
*used for epidural, spinal, infiltration, peripheral nerve block
What is the mechanism of action of local anesthetics?
Interrupt conduction of nerve pathway by binding of the drug in ionized form to Na+ channels in the nerve membrane decreasing the action potential
Must be in a nonionized state to cross the membrane – it will become ionized intracellularly and must be in the ionized state to bind to the receptor
Causes differential blockade: sympathetic first affected, then temp, followed by touch, pin-prick and proprioception and finally motor function
How does lipid solubility of the local anesthetic affect potency and duration?
Increased lipid solubility = increased potency and duration
- also increases toxicity of LA – more lipid soluble = more toxic
- Nerves have lipid soluble membranes
What is the site of action of local anesthetics?
Voltage gated Na+ channels
Binds to receptors INTRAcellularly
What are the potency, onset of action, and duration of action of local anesthetics correlated with?
Potency: correlates directly with lipid solubility and molecular weight — more potent agents have a greater affinity for Na Channels
Onset: depends on lipid solubility and relative concentration of nonionized form — closer the pKa to physiologic pH, the greater the nonionized fraction (high pKa = slow onset – exception is chloroprocaine which has high pKa but still a fast onset due to its higher concentration of 3%)
Duration: correlated with lipid solubility and vascularity of area — more lipid soluble, longer DOA (less likely to be cleared by blood flow) – more protein bound, longer DOA (to AAG) and slower elimination
How dose the concentration of local anesthetics affect potency?
Concentration of LA can overcome potency IF concentration is high enough for degree of clinical blockade, but does not affect duration of action (risk toxicity)
*exception is Chloroprocaine – it has high pKa so would normally have slow onset, but we can give such a large percentage that it overcomes its lack of potency
What factors affect LA duration of action?
It is the extent to which the LA stays in the nerve ending vicinity that affects duration of LA
- Lipid solubility
- Vascularity of tissue
- Presence of vasoconstrictors
How factors affect duration and onset of local anesthetics?
pH: onset is faster when LA is closest to the body’s pH
-adding bicarb can improve onset by 1-2 min (minimally clinically practical)
Diffusion: local anesthetics diffuse along gradient from periphery of nerve to interoir
- outer nerves = more proximal structures
- core nerves = motor fibers
- block moves from proximal structures to distal
- smaller amount and concentration of LA block only outer fibers, and the smaller more sensitive fibers
How does nerve fiber prosperities affect duration?
Smaller fiber = shorter length = faster blockade
Myelin = faster block than unmyelin (LA pool by lipid) – why C fibers (smaller diameter) resist block (no myelin on C fibers)
In mixed nerve: motor is usually in large nerve trunk and outer portion of nerve: blocked first – lose motor before sensory