week 2 regional & locals 4 of 4 Flashcards

1
Q

amides are metabolized by

A

P450 enzymes in the liver

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2
Q

greatest to least metabolism of amides

A

prilocaine>lidocaine>mepivacaine>ropivacaine>bupivacaine

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3
Q

comparing amid metabolism to ester metabolsim

A

amid metabolism is consistently slower than ester

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4
Q

abnormal liver function or decrease blood flow to liver results in what concerns with amides

A

toxicity

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5
Q

T/F

amides are excreted by the kidneys very little

A

True!

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6
Q

what two locals are metabolized to PABA and associated with anaphylaxis

A

procaine and benzocaine

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7
Q

what metabolizes ester local anesthetics

3 names for this one thing

A

plasma pseudocholinesterase (plasma cholinesterase or butyrylcholinesterase)

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8
Q

why do esters not accumulate in blood

A

ester hydrolysis is very rapid in the blood stream (excreted in the urine)

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9
Q

esters are derived from

A

benzoic acid

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10
Q

what is important about CSF and the termination of action of local anesthetics

A

The CSF lacks esterase enzymes, so termination of action of LA intrathecally depends on redistribution into the bloodstream as it does for all other nerve blocks

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11
Q

as soon as you stick someone for a local what is the absolute first thing you do
what is the second thing you do

A

ALWAYS ASPIRATE

second- test dose- check HR, numbness around lips, tinnitus

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12
Q

what two drugs can cause methemoglobinemia- and many hospitals/ facilities do not permit use

A

Prilocaine: causes methemoglobinemia (generally not used)

Benzocaine (common ingredient in topical LA sprays) can cause

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13
Q

treatment for methemoglobinemia

A

IV methylene blue (1-2 mg/kg of a 1% solution over 5 minutes)

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14
Q

what does methylene blue do to the FE

A

FE3-FE2

ferric to ferrous

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15
Q

LA toxicity-
Neurological:
Early symptoms:

A

Circumoral numbness, tongue paresthesia, dizziness, tinnitus, blurred vision

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16
Q

LA Toxicity

Neurological:
Excitatory signs:

A

Restlessness, agitation, nervousness, feeling of “impending doom”,
Muscle twitching may preceded “tonic-clonic” seizures
Higher blood concentrations (toxicity) may produce CNS depression- coma, respiratory arrest

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17
Q

Seizures:

prevention-

A

benzodiazepines & hyperventilation (raise seizure threshold)
Propofol (0.5-2 mg/kg) –quickly terminates seizure activity after onset (careful with airway/hypotension etc… )
Benzodiazepines and barbiturates may terminate seizure as well

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18
Q

what is the concern with respiratory and metabolic acidosis as it relates to seizures

A

it will decrease (lower) seizure threshold

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19
Q

Cocaine toxicity: patient presentation

A

Restlessness, emesis, tremors, convulsions, arrhythmias, respiratory failure, cardiac arrest

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20
Q

Unintentional injection of large volumes of chloroprocaine in SA space (intended for epidural space: resulting in)

A

Total spinal

Prolonged neurological deficits (direct neurotoxicity and/or preservative– now prepared preservative free)

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21
Q

total spinal occurs when what spinal level is reached

A

T4-cardiocelerators

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22
Q

what block did we talk about last semester that patients can end of with a total spinal

A

retrobulbar block

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23
Q

patient is having an emergency C section which local anesthetic will you administer and why?

A

Chloroprocaine- fast onset

TEST

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24
Q

lidocaine neurological toxicity

A

Neurotoxicity (cauda equine syndrome/transient neurological symptoms)

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25
Respiratory effects from lidocaine toxicity
Lidocaine depresses hypoxic drive (the ventilator response to low PaO2) Apnea can result Most often as result of high/total spinal
26
what do all local anesthetics do to the cardiovascular system
All LA depress myocardial automaticity (spontaneous phase IV depolarization) Depress myocardial contractility & conduction velocity
27
all LA except cocaine at high levels produce:
smooth muscle relaxation (arteriolar vasodilation)
28
why do LA produce direct cardiac muscle membrane changes
cardiac NA channel blockade
29
arrhythmias, heart block, depression of ventricular contractility, hypotension- cardiac arrest / cv collapse occur from
LA toxicity
30
what are the presenting signs of cardiovascular toxicity during general anesthesia
arrhythmias or CV collapse
31
what are the presenting sings in an awake patient of cardiovascular LA toxocity
CV stimulation (tachycardia & hypertension) with CNS excitation
32
lipid emulsion therapy dose- this is done why?
1.5mg/kg | bupivacaine induced cardiac toxicity- of note very difficult to resuscitate
33
which medication can produce SEVERE CV toxicity when unintended intravascular injection occurs
(left ventricular depression, A-V heart block, VT/V-fib)***
34
what are predisposing risk factors for LA toxicity
Pregnancy, hypoxemia, respiratory acidosis and young children are predisposing risk factors
35
treatment of cocaine induced arrhythmias
Adrenergic antagonists | Calcium channel antagonists
36
Cocaine CV toxicity: unlike those of any other LA
Adrenergic nerve terminals normally reabsorb norepi after its release– cocaine inhibits this Potentiated adrenergic stimulation HTN & ventricular ectop
37
lidocaine 5mcg/ml manifestations
circumoral and tongue numbness | lightheadedness and tinnitus
38
lidocaine 6mcg/ml manifestations
visual disturbances
39
lidocaine 8mcg/ml
muscle twitching
40
lidocaine 10mcg/ml
unconsciousness
41
lidocaine 12 mcg/ml
convulsions
42
lidocaine 15 mcg/ml
coma
43
lidocaine 20mcg/ml
respiratory arrest
44
lidocaine 26 mcg/ml
cardiovascular collapse
45
what are sings of anaphylaxis
...
46
how do you treat anaphylaxis
...
47
immunological/hypersensitivity of amides occur with what substance
Amides prepared with a preservative called“methylparaben” (which has a chemical structure similar to PABA)
48
which type of LA has induced hypersensitivity reactions more often
Esters induce hypersensitivity reactions more often than amides (IgG or IgE)
49
therapeutic lab value:
look for the presence effectiveness of specific drugs in the blood
50
normal lab value
The range of results expected from lab tests without influence from a therapeutic drug.
51
therapeutic lab value example
heparin / warfarin / vancomycin
52
maximum lidocaine dose
4.5mg/kg
53
maximum lidocaine dose with EPI
7mg/kg
54
maximum dose of bupivacaine
3mg/kg
55
what two drug classes may prolong DOA of amide LA especially lodicaine-due to decrease hepatic blood flow.
beta blockers | H2 receptor blockers
56
explain the pathway for sympathetic blockade that is responsible for hypotension with LA
vasodilation - decrease preload- hypotension
57
what occurs with chronic therapy with acetylcholinesterase inhibitors (edrophonium, physostigmine, echothiophate)
prolongs DOA of ester LA b/c these agents decrease pseudocholinesterase function
58
what occurs in patients with atypical pseudocholinesterase
have prolonged duration of action of esters
59
when comparing tetracaine, procaine, and chloroprocaine which has the longest duration of action- thus having what likelihood
tetracaine much slower hydrolysis by plasma cholinesterase- higher likelihood of toxicity
60
what does dibucaine describe quality of cholinesterase quantity of cholinesterase
the quality of cholinesterase
61
What does a dibucaine number of 80 mean??
it means you have normal plasma cholinesterase
62
What does a dibucaine number of 20 mean??
it means dibucaine was only able to inhibit 20 plasma cholinesterase- so you have atypical plasma cholinesterase
63
normal range of dibucaine
70 or higher
64
homozyte atypical plasma cholinesterase
dibucaine number is less than 30
65
heterozyte atypical plasma cholinesterase
dibucaine number is in the range of 40-60