Local Anesthetics - Test 1 Flashcards
if the same dose of an LA is given to the same person via both tracheal and epidural routes, at which site will the block wear off fastest?
why?
tracheal block will be shorter d/t higher rate of blood flow and higher rate of uptake
goals for regional anesthesia (3)
already know I’m gonna read this twice, put 5/5 and move on 4ever
- understanding peripheral nerve anatomy
- understanding LAs, US equipment, and nerve block techniques
- practice
vertebrae that correlates with the xiphoid
T9
which is more likely to cause an allergic reaction - ester or amide?
why?
esters
metabolite: PABA
nerve fibers that carry reflexes
Aγ fibers
what is the best (but most complicated) method to sustain a patient with cardiac toxicity from LA?
cardiac bypass
onset and duration of ropivacaine
slow onset
duration 180-600 min (long)
amides bind the lipid side of the chain with ____
NHC
max dose of bupivacaine
why is it especially important to pay attention to max dose with this drug?
2.5 mg/kg
bupivacaine is particularly cardiotoxic and is very lipophilic - so it’s long-lasting and its effect doesn’t “wear off” quickly
effect of epinephrine on LA & why
potentiates effects
- causes vasoconstriction = decreased blood flow = decreased circulatory uptake = decreased metabolism
- increased duration of action, potency, and reduction of absorption into tissue
why is 5% lidocaine not used much anymore for subarachnoid blocks?
neurotoxicity
(specifically cauda equina syndrome when catheters were used to continuously infuse; TNS has been reported from single injections)
function of Aα nerve fibers
motor signals and proprioception
nerves that form the sciatic nerve
tibial (L4-S3) & common peroneal (L4-S2)
treatments for LA CNS toxicity
which is most common and why?
benzos and propofol
benzos most common - caution use with propofol d/t myocardial depression (pt may also have CV toxicity)
nerve fibers that have subgroups of alpha, beta, gamma, and delta fibers
A fibers
the lateral and medial cords form which nerve?
median nerve
what are transient neurologic symptoms (TNS)?
what specific LA techniques have been associated with TNS?
resolvable syndromes with s/s simular to cauda equina syndrome
subarachnoid catheters, particularly with 5% lidocaine
3 factors that determine the longevity of LA action
- dose to start
- tissue distribution & lipid solubility
- drug metabolism
max dose of ropivacaine
3 mg/kg
LA with metabolite that is a precursor for methemoglobin
what is the metabolite?
there’s two
prilocaine
o-toluidine
and benzocaine
max dose of prilocaine
8 mg/kg
2 main concerns of bupivacaine use
- particular propensity to cause cardiac effects
- prolonged duration may be concerning because it doesn’t “wear off”
onset and duration of lidocaine
fast onset
duration 90-120 min (medium)
How many pairs of spinal nerves are there?
What are the groups of spinal nerves?
31 pairs:
- 8 cervical
- 12 thoracic
- 5 lumbar
- 5 sacral
- 1 coccygeal
functional unit of the peripheral nerve
axon
MOA of local anesthetics
- interrupt Na+ current in the nerve
- prevents depolarization
- (Stoelting - bind to voltage-gated Na+ channels, inhibiting passage of Na+ ions and preventing transmission of nerve impulses)
which form of the LA binds to the Na+ receptor - ionized or nonionized?
is this its water or lipid-soluble form?
ionized
water soluble
how does tissue distribution (blood flow to tissues) affect LAs?
the higher the blood flow to the tissue LA is injected into, the faster the LA will enter the bloodstream to be metabolized
(increased blood flow = increased entry into bloodstream = increased metabolism = decreased effect on nerve)
effect of clonidine on LAs & why
increases potency and duration of blocks by delaying repolarization
(has alpha 2 agonist properties)
effect of opioids on LA block
increased potency (sometimes recognized as increased speed of onset)
density of block/total duration of action won’t change
He said that it probably doesnt really speed onset, but instead juast makes for a less spotty block because other receptors are covered with opioids
function of B nerve fibers
difference vs. A fibers
carry autonomic signals
less myelination
how are nerve fiber sizes classified?
A, B, and C
A is the largest
C is the smallest
vertebrae that is the most prominent cervical level (“vertebral prominens”)
C7
why can CNS effects be seen with LA toxicity?
crossing blood-brain barrier & depression of inhibitory neurons
uses of liposomal bupivacaine (Exparel)
long-acting pain relief for ortho surgeries
peripheral nerve blocks
given as a single injection
rates of LA uptake from fastest to slowest
tracheal > intercostal > caudal > epidural > brachial plexus > femoral/sciatic
(aka- highest to lowest bloodflow)
what characteristics of a nerve fiber make it harder to block with LAs?
the larger and more myelinated, the harder to block
components of PNS order of physical size
afferent and efferent fibers > fascicles (bundles of axons) > individual nerve fibers (axons)
typical timing of systemic toxicity
why does this occur?
occurrence is usually rapid
most often in < 1 min, majority < 5 min from time of injection
d/t direct injection of LA intravascularly rather than into tissue
max dose of procaine
12 mg/kg
How is ropivacaine similar to bupivacaine?
How is it different?
similar: onset, time, duration
different: less cardiotoxic effects, generally less pronounced motor block potency
esters bind the lipid side of the chain with ____
CO
nerve roots that form the radial nerve
C5-T1
onset and duration of chloroprocaine
fast onset
short duration (30-60 min)
how does clonidine improve LA blockade duration and potency?
inhibits peripheral nerve signal conduction in A and C fibers
key to classifying types of local anesthetics
the link between the lipophilic ring and the hydrocarbon
hallmark s/s of both cauda equina syndrome and TNS
deficits of:
- bowel
- bladder
- lower extremity motor
- lower extremity sensory
what is dibucaine?
what do the following mean:
dibucaine no. 80
dibucaine no. 20
dibucaine is an LA that inhibits plasma cholinesterase
dibucaine no 80 - plasmacholinesterase is 80% inhibited when exposed to dibucaine (normal)
dibucaine no 20 - plasmacholinesterase only 20% inhibited when exposed to dibucaine (expect longer recovery from ester LAs, ~3 hrs)
LA used to evaluate for the presence of normal enzyme function
In normal patients, how much pseudocholinesterase is inhibited by this LA?
dibucaine - exposing a patient’s pseudocholinesterase to dibucaine should inhibit the action of the enzyme
normal pts - 80% (Dibucaine no. 80)
direction of spinous processes at cervical vs. lumbar levels
cervical - caudad
lumbar - straight
what organ removes a large portion of the LA, especially lidocaine?
lungs
brand new info- thought lidocaine was metabolized by ur lil liver
metabolism of esters vs. amides
which is generally faster?
- esters: pseudocholinesterases
- amides: liver
- generally faster: esterases
vertebrae that is the plane of Ludwig
what does this correlate?
T4
carina and angle of Louis
onset and duration of tetracaine
slow onset
long duration
3 states of sodium channel
in which state/states can a LA block?
- activated open
- inactivated closed
- rested closed
LAs can block in channels 1&2 only
primary mediator for influx of Na+ into peripheral nerves
voltage-gated sodium channels
LAs associated with methemoglobinemia
How is methemoglobinemia treated?
prilocaine & benzocaine
1-2 mg/kg methylene blue IV
CNS communication to the body occurs via the __________.
is this motor or sensory?
ventral root from ventrolateral aspect of the cord
motor (efferent)
acute and significant uptake of LA may result in what adverse effect?
hypoventilation, respiratory arrest
MOA of 20% lipid solution for LAST
lipids absorb the LA, which accelerates its removal from cardiac receptors
how does the dose of LA impact systemic absorption?
larger doses increase concentration gradient of the LA
vertebrae that correlates with the umbilicus
T10- dermatome
L4- vertbrae
function of Aδ nerve fibers
fast pain, temperature, and touch
part of LA chemical structure that is lipophilic
aromatic benzene ring
where does the spinal cord terminate in most adults?
what does it transition into?
L2
transitions into collection of nerves called cauda equina
component of amides that can cause an allergic reaction
which amide is most likely to cause an allergic reaction?
preservatives such as methylparaben
prilocaine
nerve roots that form the brachial plexus
where does the brachial plexus emerge?
C5-T1
between the anterior and middle scalene muscles
conditions that increase risk of toxicity with use of esters vs. amides
- esters: plasma cholinesterase deficiency
- amides: liver dysfunction
MOA of cardiotoxicity seen with LAs
blockade of excitatory neurons resulting in cardiac dysrhythmias and arrest
CNS communication from the body is via the _____________.
is this motor or sensory?
dorsolateral aspect of the cord
sensory
what is pKa?
what is the effect of pH lower than the pKa of the drug?
pH at which half of the drug is nonionized and the other half is ionized
if pH of patient is lower than pKa of the drug, the LA becomes more ionized and less able to enter the nerve
onset and duration of procaine
slow onset
duration 60-90 min (short, I think?)
non-nerve blockade uses of LAs (4)
- inhibition of ventricular dysrhytmias
- reduced CBF (for high ICP during intubation)
- pain management
- use of lidocaine to blunt respiratory stimulation (via smooth muscle relaxation)
what is the max dose of mepivacaine
does the max dose change if epinephrine is added?
4.5 mg/kg
yup, with epi max is 7 mg/kg
onset and duration of mepivacaine
onset: fast
duration: 120-240 min (medium)
vertebrae that correlates with superior angle of the scapula and sternal notch
T2
vertebrae that correlates with the superior iliac crest, L4-5 disc space, and the umbilicus
L4
nerve fiber recovery from LA
heavy myelinated fibers
A delta fibers
C fibers
B fibers
function of Aβ fibers
touch and pressure recognition
max dose of chloroprocaine
12 mg/kg
how does lipophilicity of LA impact its potency and duration of action?
increased lipophilicity = increased potency & longer duration of action
where are the cervical spinal nerves in relation to the vertebral bodies?
lying above the like-named vertebral body
T/F - liposomal bupivacaine (Exparel) must be given via indwelling catheter
false - single injection can be used for same effect d/t long duration of
feel free to reword
general order of nerve fiber blockade
B fibers
C fibers
A delta fibers
heavily myelinated fibers
LA components that increase cardiotoxicity
which LA is particularly associated with CV tox?
likely r/t high protein binding, more assoc. with longer-acting drugs
bupivicaine
keys to prevent LAST (5)
- aspiration
- incremental dosing
- use of US
- test dosing
- knowledge of toxic levels
which LA class names have 2 i’s
amides
ex - lidocaine, mepavicaine, bupivicaine, prilocaine, ropivicaine
active LA in “hurricaine spray”
benzocaine
sustained-release LA
what explains its prolonged duration of action?
how long does the block last?
liposomal bupivacaine (Exparel)
prolonged duration presumably from delayed uptake
allegedly lasts 24-48 hours
myelinated vs. unmyelinated fibers
(size, speed, function)
myelinated:
- larger
- faster conduction
- assoc. with motor and sensory function
unmyelinated:
- slower conduction
- transmit pain, temperature, and autonomic impulses
LA with particular propensity to cause cardiac effects more than others
bupivicaine
where are nerve Na+ channels located?
Nodes of Ranvier
what is EMLA cream?
when should it be applied?
equal parts lidocaine & prilocaine for topical use
apply 1 hour in advance (lol we always went with 20-30 min in the ER)
3 factors that affect systemic LA absorption
- site of injection
- dose
- properties of specific drug
what is toxicity?
what is the MOA of LA toxicity?
a dose that enters circulation and brain faster than it can be cleared (not necessarily just a large dose)
LA toxicity results from blocking inhibitory neurons, leaving excitatory neurons “unchecked”, or unopposed
nerve roots that form the ulnar nerve
C8 & T1
if CV toxicity is seen with LA use, ACLS guidelines are used with what exception?
use smaller doses of epi
ex. 100 mcg vs. 1000 mcg
LA most commonly used in aerosolized form for topical use in airway anesthesia
benzocaine
1% lidocaine = _____ mg/mL
10
onset and duration of bupivacaine
slow onset
180-600 min duration (long)
hallmark symptoms of LA CNS toxicity
what other s/s normally follow?
seizures, hyperexcitation
followed by ringing ears, circumoral numbness, tongue numbness
effect of adding bicarbonate to LA
addition of an alkalinizing agent increases the nonionized portion of the drug to allow access to the nerve
this improves pain of injection & onset of block
part of LA chemical structure that is hydrophilic
tertiary amine
preferred method of long-acting pain relief for orthopedic surgery
liposomal bupivacaine (Exparel)
CV effects seen with LA toxicity with typical vs. high concentrations
what is the MOA?
typical - decreased contractility and conductivity
high - smooth muscle relaxation (hypotension)
MOA - same inhibitory mechanism of action on Na+ channels
effect of opioids on LAs
potentiate LA
increase intensity & speed of onset for blocks
what does eutectic mean?
which LA has this property?
has a lower melting point
ex) EMLA cream
why is benzocaine primarily used topically?
it is permanently nonionized (stays lipid-soluble) - crosses into cell and attaches to Na+ channel directly
how does blood flow to tissues affect an LA’s risk of toxicity?
a site with higher blood flow will have increased circulatory uptake and increased risk of toxicity
how do patients with infections respond differently to LAs?
less effect of the drug when injected
onset is slower & less dense
(d/t decreased patient pH)
in which form does the LA enter the nerve - ionized or nonionized?
is this in its water-soluble or lipid-soluble form?
nonionized
lipid soluble
vertebrae that correlates with the inferior angle of the scapulae
T7
how does the addition of epinephrine to LA solution improve the margin of safety?
epinephrine reduces circulatory uptake/metabolism of LA, leading to reduced toxicity
RMP of peripheral nerves
-60 to -90 mV
effect of adding decadron to LA
which route is best - IV or perineural?
increases duration of action
trick question - studies say effects are similar either way
max dose of procaine
12 mg/kg
Does adding sodium bicarbonate improve the potency or duration of LA?
nope - only improves speed of onset and reduces pain of injection
what is cauda equina syndrome?
what can cause this?
toxicity in the intrathecal space
can be caused by LA in prolonged exposure, infection, compression/hematoma, or structural changes
max dose of lidocaine
max dose of lidocaine w/ epi
4.5 mg/kg
w/ epi - 7 mg/kg
esters are metabolized by pseudocholinesterases. what is the exception to this?
cocaine - metabolized by liver
what is the cauda equina?
the terminal end of the spinal cord - fibrous strands in the subarachnoid space
which nerve fibers are not myelinated?
C fibers
location of thoracic, lumbar, sacral, and coccygeal spinal nerves in relation to respective vertebral bodies
below vertebral body
factors that increase risk of LAST (LA systemic toxicity)
- unintended uptake into circulation (fastest - ex. vascular injection)
- fast uptake from highly perfused areas
- higher potency = more toxicity
interspaced among the axon at spaces that are not myelinated
nodes of Ranvier
max dose of tetracaine
3 mg/kg
which nerve fibers are the smallest and are unmyelinated?
what is the function of these fibers?
C fibers
carry pain and temperature signals (C - dorsal root)
vertebrae that correlates with cricoid cartilage
C6
nerve fibers from largest to smallest (7)
- Aα
- Aβ
- Aγ
- Aδ
- B
- C - dorsal root
- C - sympathetic
rank the nerve fibers’ conduction velocity from fastest to slowest (7)
- Aα
- Aβ
- Aγ
- Aδ
- B
- C - dorsal root
- C - sympathetic
PTL that this is the same order as size biggest to smallest
