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SUM'20 - Regional > week 2 regional & locals 4 of 4 > Flashcards

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
Q

Respiratory effects from lidocaine toxicity

A

Lidocaine depresses hypoxic drive (the ventilator response to low PaO2)
Apnea can result
Most often as result of high/total spinal

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26
Q

what do all local anesthetics do to the cardiovascular system

A

All LA depress myocardial automaticity (spontaneous phase IV depolarization)
Depress myocardial contractility & conduction velocity

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27
Q

all LA except cocaine at high levels produce:

A

smooth muscle relaxation (arteriolar vasodilation)

28
Q

why do LA produce direct cardiac muscle membrane changes

A

cardiac NA channel blockade

29
Q

arrhythmias, heart block, depression of ventricular contractility, hypotension- cardiac arrest / cv collapse occur from

A

LA toxicity

30
Q

what are the presenting signs of cardiovascular toxicity during general anesthesia

A

arrhythmias or CV collapse

31
Q

what are the presenting sings in an awake patient of cardiovascular LA toxocity

A

CV stimulation (tachycardia & hypertension) with CNS excitation

32
Q

lipid emulsion therapy dose- this is done why?

A

1.5mg/kg

bupivacaine induced cardiac toxicity- of note very difficult to resuscitate

33
Q

which medication can produce SEVERE CV toxicity when unintended intravascular injection occurs

A

(left ventricular depression, A-V heart block, VT/V-fib)***

34
Q

what are predisposing risk factors for LA toxicity

A

Pregnancy, hypoxemia, respiratory acidosis and young children are predisposing risk factors

35
Q

treatment of cocaine induced arrhythmias

A

Adrenergic antagonists

Calcium channel antagonists

36
Q

Cocaine CV toxicity: unlike those of any other LA

A

Adrenergic nerve terminals normally reabsorb norepi after its release– cocaine inhibits this
Potentiated adrenergic stimulation
HTN & ventricular ectop

37
Q

lidocaine 5mcg/ml manifestations

A

circumoral and tongue numbness

lightheadedness and tinnitus

38
Q

lidocaine 6mcg/ml manifestations

A

visual disturbances

39
Q

lidocaine 8mcg/ml

A

muscle twitching

40
Q

lidocaine 10mcg/ml

A

unconsciousness

41
Q

lidocaine 12 mcg/ml

A

convulsions

42
Q

lidocaine 15 mcg/ml

A

coma

43
Q

lidocaine 20mcg/ml

A

respiratory arrest

44
Q

lidocaine 26 mcg/ml

A

cardiovascular collapse

45
Q

what are sings of anaphylaxis

A

…

46
Q

how do you treat anaphylaxis

A

…

47
Q

immunological/hypersensitivity of amides occur with what substance

A

Amides prepared with a preservative called“methylparaben” (which has a chemical structure similar to PABA)

48
Q

which type of LA has induced hypersensitivity reactions more often

A

Esters induce hypersensitivity reactions more often than amides (IgG or IgE)

49
Q

therapeutic lab value:

A

look for the presence effectiveness of specific drugs in the blood

50
Q

normal lab value

A

The range of results expected from lab tests without influence from a therapeutic drug.

51
Q

therapeutic lab value example

A

heparin / warfarin / vancomycin

52
Q

maximum lidocaine dose

A

4.5mg/kg

53
Q

maximum lidocaine dose with EPI

A

7mg/kg

54
Q

maximum dose of bupivacaine

A

3mg/kg

55
Q

what two drug classes may prolong DOA of amide LA especially lodicaine-due to decrease hepatic blood flow.

A

beta blockers

H2 receptor blockers

56
Q

explain the pathway for sympathetic blockade that is responsible for hypotension with LA

A

vasodilation - decrease preload- hypotension

57
Q

what occurs with chronic therapy with acetylcholinesterase inhibitors (edrophonium, physostigmine, echothiophate)

A

prolongs DOA of ester LA b/c these agents decrease pseudocholinesterase function

58
Q

what occurs in patients with atypical pseudocholinesterase

A

have prolonged duration of action of esters

59
Q

when comparing tetracaine, procaine, and chloroprocaine which has the longest duration of action- thus having what likelihood

A

tetracaine much slower hydrolysis by plasma cholinesterase- higher likelihood of toxicity

60
Q

what does dibucaine describe
quality of cholinesterase
quantity of cholinesterase

A

the quality of cholinesterase

61
Q

What does a dibucaine number of 80 mean??

A

it means you have normal plasma cholinesterase

62
Q

What does a dibucaine number of 20 mean??

A

it means dibucaine was only able to inhibit 20 plasma cholinesterase- so you have atypical plasma cholinesterase

63
Q

normal range of dibucaine

A

70 or higher

64
Q

homozyte atypical plasma cholinesterase

A

dibucaine number is less than 30

65
Q

heterozyte atypical plasma cholinesterase

A

dibucaine number is in the range of 40-60

SUM'20 - Regional (17 decks)

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