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LOCALS Flashcards

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1
Q

LAs reversibly block

A

AFFERENT nerve transmission

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2
Q

Order of blockade observed

A
  1. autonomic blockade
  2. somatic sensory blockade
  3. somatic motor blockade
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3
Q

Myelination in PNS is done by

A

Schwann cells

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4
Q

LA cannot easily penetrate myelin so it acts at

A

nodes of ranvier

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5
Q

You need enough LA concentration to block

A

three nodes of ranvier to effectively block a nerve

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6
Q

Pain fibers

A

A-delta, pain/temperature = FAST pain

C - dull pain/temperature = SLOW pain

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7
Q

A-alpha fibers are

A

motor and propioception

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8
Q

A-beta fibers are

A

motor, touch, and pressure.

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9
Q

A-gamma fibers are

A

motor/muscle tone, muscle spindle

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10
Q

A-delta fibers are

A

pain, temperature, touch, FAST pain

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11
Q

B fibers are

A

PREganglionic, myelinated, autonomic

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12
Q

C fibers are

A

dull pain, temperature, touch, POST ganglionic, autonomic, no myelin, SLOW pain

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13
Q

when using LA we typically don’t fully block or block

A

A-alpha or A-beta

A-alpha : motor / proprioception
A-beta : motor, touch, pressure

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14
Q

preganglionic fibers are

A

more readily blocked than any other fiber, even though they’re myelinated

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15
Q

the sensitivity of a peripheral nerve to LA is inversely

A

related to its size (clinically / in-vivo)

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16
Q

unmyelinated fibers are usually at the

A

mantle [[superficial]] part of nerve fibers

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17
Q

clinical sequence of anesthesia with LAs

A

1st. sympathetic block -> C fibers
2nd. loss of pain and temperature, sensation -A delta
3rd. loss of proprioception - a gamma

4th loss of touch and pressure if you have dense enough block - a beta

5th motor blockade A-alphpa (not intentional)

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18
Q

LAs bind at the

A

internal H gate of the VG sodium ion channel at the INACTIVE-closed state

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19
Q

LA easily ACCESS VGNC

A

when they are activated-open

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20
Q

LA easily BINDS to VGNC when

A

they are in inactivated-closed

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21
Q

a resting nerve is less sensitive

A

to LA than a repetitively stimulated one

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22
Q

_____ determines how sensitive the nerve is to an LA in a resting nerve

A

LIPID SOLUBILITY

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23
Q

the cationic charged form of LA interacts preferentially with

A

inactivated state of the Na channel

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24
Q

inter nodal distance of nodes of ranvier increases with

A

fiber diameter

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25
Distance between nodes of ranvier in myelinated fibers contributes to
DIFFERENTIAL nerve block / why? cause big somatic neurons are gonna take a lot of LA to block , so youre alble to block function of pain before getting to the point where you actually block motor
26
Organic Chemistry Components of an LA
lipophilic head (aromatic ring) , intermediate chain * (either an ester or amide) and a hydrophilic tail (tertiary amine)
27
esters have less of a
toxicity risk because they are metabolized faster [[ester hydrolysis]]
28
increase in the length of the intermediate chain (increase in number of carbons) increases
potency and toxicity and alters metabolism rate and DOA - cause you've made the drugs more lipid soluble - intermediate chain here alters DOA and metabolism cause you could potentially change the amide or ester group
29
increase in length of tertiary amine chain increases
potency and toxicity - more lipid soluble
30
Minimum Blocking Concentration =
minimum concentration at a nerve required to block it
31
fiber diameter and minimum concentration
directly related
32
minimum concentration and tissue ph
If acidic, require too much LA
33
Potency and minimum concentration
more potent drug = lower minimum concentration, because less molecules of the drug will be needed to block the nerve
34
increased tissue pH or high frequency of nerve stimulation =
[alkalosis] or more excitable nerve = decreases minimum concentration cause frequency dependent block and increase degree of NONionized molecules
35
the more vascular the region
the higher the risk of systemic absorption and the higher the risk of plasma toxicity.
36
Top 3 sites of vascular systemic uptake
IV Trachel intercostal
37
least vascular region
subQ , so lowest risk of toxicity
38
All LAs are
weak bases pKa 7.5 - 9 *one exception
39
LAs are packaged in an acidic form to
improve solubility and stability, so they don't precipitate out. Also to preserve epinephrine
40
Adding bicarb increases
the onset, enhances the block depth, and increases the spread of the block
41
deceasing temperature reduces
drug absorption across the nerve membrane, could delay onset.
42
LAs for labor
1. Ester, cause rapid metabolism | 2. Amide that is HIGHLY Protein bound because it will stay local
43
DOA is effected by
blood flow (affects uptake) lipid solubility protein binding
44
potency in LAs =
lipid solubility, this is an inherent property of the drug, depends on chemical structure
45
Most important factor for DOA =
protein binding. binds to local proteins with great affinity = stay there for a while.
46
Use of vasoconstrictor with LA serves three purposes
1. inhibition of systemic absorption (decreases uptake) 2. prolongation of the LA effect 3. detection of IV injection *
47
determinants of of concentration of LA in systemic blood
``` tissue blood flow concentration of LA used Pulmonary first pass metabolism of drug vasoconstrictor? ```
48
when people are allergic to esters they are responding to
PABA (metabolite)
49
Esters are metabolized by
pseudocholinesterase in the plasma and some in the liver less than 5% unchanged in kidneys
50
Cocaine metabolism
significantly metabolized in liver (therefore longer DOA) and 10-12% excreted unchanged in urine
51
metabolism of amides is effected by
liver disease! cYP450 = liver decreased hepatic blood flow, drugs that interfere with cyp450
52
after systemic absorption, amide LA are
more widely distributed in tissues than ester LA
53
muscle twitching especially in face and then extremities indicates
imminent onset of seizures, r/t CNS toxicity
54
How to treat seizures in CNS toxicity
bicarb/benzo 100%fio2 ventilation
55
SE of cocaine with CNS toxicity include
euphoria, restlessness, tremors, seizures excessive norepinephrine and dopa + CNS
56
Toxic systemic affects are more likely with
AMIDES over esters
57
In CNS toxicity seizures are followed by
CNS depression
58
CV more resistant to
LA toxicity than CNS
59
LA toxicity on heart =
hypotension, AV conduction block, myocardial depression, reduced SVR (HYPOTENSION), reduced CO (myocardial depression) widened PRi and QRS (AV conduction block) CV collapse
60
most CV toxic =
bupivocaine
61
cocaine overdose =
massive sympathetic outflow coronary vasospasm MI
62
Increased risk of CVS effects =
pregnancy | have already received other CV modulating drugs
63
treatment of CV collapse with overdose
1. crack chest/ cpr 2. modified ACLS, no amio no lidocaine, 3. INTRALIPID 20%
64
Intralipid is more beneficial for drugs that are
very lipid soluble
65
TNS
Transient neurological symptoms neuroinflammatory symptoms causes pain I lower back, buttocks, posterior thighs. presents 6-36 Hours after recovery from block, lasts about a week.
66
Cauda equina is associated with
lidocaine 5%, tetracaine, and chloroprocaine
67
Anterior Spinal Artery Syndrome
LE paralysis with +/- sensory deficit | unknown cause, vasoconstrictors/PVD/advanced age may increase it
68
allergic reactions are more common with
ESTERS -> PABA
69
pseudocholinesterase inhibitors will prolong
the actions of ESTERS
70
cimetidine and propanolol
decreased hepatic blood flow, decrease clearance of amide LAs and COCAINE
71
Fentanyl, clonoidine, epi ->
synergistic effects when added to LA
72
fibers that are more easily blocked have a lower
Cm
73
There is a greater fraction of the ionized drug
inside the cell rather than outside the cell. ICF = slightly more acidic than ECF
74
Onset of 0.75% bupivacaine will be faster than 0.2% bupivacaine because
higher concentration = more molecules = quicker onset why chloroprocaine is fast onset despite high pKa
75
Cardiac arrest can occur before seizure with
bupivacaine
76
Toxicity is more common with
PNB than with epidural anesthesia
77
Factors that increase risk for CNS toxicity
hypercarbia, hyperkalemia, metabolic acidosis
78
hypercarbia increases risk for CNS toxicity because
hypercarbia / acidosis -> leads to vasodilation in cebereal blood flow leads to increased drug in brain Hypercarbia also decreases protein binding
79
difficulty of cardiac resuscitation in order
bupivacaine > levobupivacaine > ropivacaine > lidocaine
80
EMLA cream is made of
50% Lido and 50% prilocaine, therefore risk for methomglobienemia from prilocaine
81
epidural doses per segment
1.25 to 1.6 mL/segmente desired block

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