Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

APA 3 - Wolfe > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Local anesthetics produce _____ of impulses along the central and peripheral nerve pathways

A

reversible conduction blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

1st Local Anesthetic
1st Synthetic Local (Ester)
1st Amide Local

A

1st Local Anesthetic Cocaine 1884
1st Synthetic Local (Ester) Procaine 1905
1s Amide Local Lidocaine 1943

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Chemical structure:

Lipophilic and hydrophilic portion separated by

A

hydrocarbon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In the chemical structure, the lipophilic portion is the….

What is it necessary for?

A

Benzene Ring

Necessary for activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the chemical structure for esters and amides

A

ester C-O-C

amide NH-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does ion trapping happen?

A

within the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pH extracellulary?

What is the pH intercellular?

A

extracellular 7.4

intracellular 7.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the S and R enantiomers?

A 
S = LEFT (Sinister)
R = RIGHT (Rectus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Racemic mixtures have what type enantiomer?

A

BOTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pure Isomers only have 1 enantiomer, which enantiomer? and which LAs?

A

Ropivacaine and Levobupivacaine (ONLY 2!)

Both are S enantiomers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the benefit of S enantiomers?

A

Less cardio and neurotoxic

“this is why we give ropi in kids”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the MOA for LAs?

A

Inhibit Na+ ions passage through ion-selective Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the inhibition of Na ions do?

A

Slows rate of depolarization
Threshold potential not reached
No action potential propogated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the inhibition of Na ions NOT alter

A

Resting membrane potential

Threshold potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Local anesthetics bind to the (alpha or beta) subunits of the voltage gated sodium channel

A

Alpha (there are 2 alpha subunits in the Nm receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When can LAs bind?

A

in the active and inactive states (CANNOT bind during the resting phase)

(the more frequently the nerve is depolarized, the voltage gated Na channel opens - the more time for LA binding to occur)

Nerves with more activity have faster blockade!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where does the LA bind to on the alpha subunit?

A

internal (this is a weak binding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are other sites of action for LAs?

A

Voltage-dependent potassium ion channels
(Much lower affinity)

Calcium ion currents (L-type)

G protein-coupled receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is minimum concentration (Cm)?

A

minimum concentration to produce conduction blockade

Analogous to MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are factors that increase or decrease (Cm)

A

Increases: larger diameter
Decreases: higher frequency, higher pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T/F: the Cm for motor is twice the amount for sensory

A

True (Possible explanation for sensory block with no motor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How many Nodes of Ranvier must be blocked?

A

2, preferably 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the order of blockade?

A 
B Fibers (preganglionic sympathetic efferent)
C Fibers
A delta (post ganglionic, afferent)
A gamma
A beta
A alpha
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which nerves are unmylinated?

A

C fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which nerves travel faster?

A

mylinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the function of A alpha fibers

A

motor, proprioception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the function of A beta fibers

A

touch, pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the function of A gamma fibers

A

muscle tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the function of A delta fibers

A

Pain (fast), cold temp, touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the function of B fibers

A

Preganglionic (efferent), autonomic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the function of C fibers

A

Postganglionic (afferent)

Pain (slow), warm temp, touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the order of a differential blockade?

A

ATP-TP-MVP

Autonomic
Temperature
Pain 
Touch
Pressure
Motor
Vibration
Proprioception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a differential blockade?

A

Blockade of some fibers but not others

May block, B fibers, C fibers, and small and medium A fibers

May not block Large A fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

You may have a sympathectomy from a differential block. What is a sympathectomy?

A

Loss of sensation for pain, and temp

May still have proprioception and motor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

LAs are _____, with a pKa of ____, and pH values of ____

A

weak bases

  1. 6-8.9
  2. 9-6.5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Acid+base =

A

more ionized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What form does the LA need to be to in order to cross the lipid bylayer

A

un-ionized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Do LA with pka nearest to physiologic pH have a faster or slower onset?

A

FASTER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

All LAs are weak bases with one exception, which is:

What is the pka?

A

Benzocaine

pKa – 3.5
Does not ionize based on pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the MOA of benzocaine?

A

unknown

41
Q

Lidocaine pka is 7.9, when placed in an environment with a pH of 7.9, what does this mean?

What happens in a ph of 7.6, 7.4, 7.2

A

50% ionized, 50% unionized

As you decrease pH, it becomes more and more ionized (REMEMBER, its the un-ionized portion that crosses lipid bilayer)

42
Q

What happenes when you inject lidocaine into a septic patient?

A

there will be more ionized portion of the drug and be less effective

43
Q

What does adding bicarb to LA do?

A

Higher pH is closer to pKa of about 8
More un-ionized to cross
Faster onset by 3-5 minutes

Also higher pH thought to lessen sting of local infiltration

44
Q

How are LA’s distributed?

A 
1st large uptake to lungs
2nd distribution to high perfused tissue 
(heart, brain, kidneys)
3rd distribution to low perfused tissue
(muscle and fat)
45
Q

Are esters or amides are widely distributed?

A

Amides

46
Q

What is placental transfer influenced by?

Which drugs are highly protein bound?

A

Influenced by protein binding
(proteins too large to cross)

Bupivacaine and Ropivacaine highly bound
Lidocaine not as much

47
Q

Explain fetal ion trapping

A

Once un-ionized local crosses placenta and hits low fetal pH more drug is ionized and can’t cross back

Build up of trapped local in fetal circulation leads to toxicity in fetus

48
Q

What is potency related to?

A

Lipid solubility

More lipid soluble means easier to cross lipid by-layer

49
Q

What is onset related to?

A

State of Ionization – most important

Lipid Solubility

50
Q

What is duration of action related to?

A

Protein Binding

Lipid Solubility

51
Q

How are amides metabolized?

A

Mainly HEPATIC metabolism

Minimal renal excretion of unchanged drug

52
Q

What are the fast, intermediate, slow amides with regard to metabolism and clearance

A

Fastest
- Prilocaine

Intermediate
- Lidocaine and Mepivicaine

Slow
- Etidocaine, Bupivacaine, Ropivacaine

53
Q

How are esters metabolized?

A

Rapid hydrolysis

  • Cholinesterases (pseudocholinesterase)
  • Mostly plasma, lesser liver
54
Q

What are the rapid, intermediate, slow esters with regards to metabolism and clearance?

A

Rapid
- Chloroprocaine

Intermediate
- Procaine

Slow
- Tetracaine (tetracaine is longest acting ester)

55
Q

For esters, what is the one exception to hydrolysis?

A

Cocaine - significant metabolism by the liver

56
Q

What is PABA and what can happen?

A 
Metabolites of esters mostly inactive
Paraaminobenzoic acid (PABA)

PABA - allergic

57
Q

What common local injection site contains little to no cholinesterase enzyme?

A

CSF

Must wait until drug goes into systemic circulation for hydrolysis

58
Q

In what states are plasma cholinesterase (pseudocholinesterase) inhibited in?

A 
Deficiency
Liver disease
Increased BUN
Parturients
Chemotherapy patients
59
Q

What can be added to LAs for vasoconstriction?

A

Epinephrine, phenylephrine, norepinephrine

epi superior

60
Q

What is the epi dose?

A

1:200,000

or 5mcg/ml

61
Q

What do the vasoconstrictions do?

A 
Limits systemic absorption 
Maintains drug concentration around nerves
Can prolong Lidocaine by 1/3
No effect to onset
Helps to decrease toxicity
62
Q

Which 2 local anesthetics have no vasodilator activity?

A

Cocaine
Ropivacaine

(also Lidocaine according to Nagelhout)
(Chloroprocaine according to APEX)

63
Q

What is the risk of adding opioids to spinals and epidural LAs

A

Risk for respiratory depression and oxygen desaturation

64
Q 
Clonidine:
Is a preservative free \_\_\_\_\_
Enhances  \_\_\_\_\_\_ anesthesia
When used in combination with opioids is \_\_\_
Epidural dose:
Spinal dose:
A 
alpha 2 agonist
Neuraxial
Additive
Epidural 150 mcg or 2mcg/kg
Spinal 15-45 mcg
(PROLONGS block)

(APEX - increases analgesia properties via alpha 2 agonism)

65
Q

What is the pH of 2% lido?

What is the pH of 2% lido with epi?

A
  1. 5

4. 5 with epi

66
Q

What benefit does mixing locals have?

A

Combos
Faster onset
Longer Duration

Lido/Bupivicaine
Cholorprocaine/Bupivicaine

67
Q

Mixing locals has what type of effect?

A

additive and not synergistic!!

68
Q

T/F: allergic reactions to LAs are common?

A

FALSE
Rare - <1% allergic reaction

Most are adverse responses to excess plasma concentration

Allergic reaction to preservative free amides is so low its not even reportable

69
Q

Esters are more likely to cause allergic reaction d/t?

A

PABA

70
Q

What is the other thing that make people allergic to LAs

A

the preservative (Methylparaben)

71
Q

Is there a cross sensitivity to LAs?

A

NOOO

72
Q

After LA injection you notice hypotension with syncope or tachycardia, what probably happened?

A

Likely IV injection

73
Q

What is LA toxicity dependent on?

A

Dependent of total amount of drug
NOT volume or Concentration

Ex.
40mL of 1% or 80mL of 0.5%
Both 400 mg

74
Q 
Lidocaine
Max dose:
Max dose with epi:
Plain mg/kg:
With epi mg/kg:
A

Max dose: 300
Max dose with epi: 500
Plain mg/kg: 4.5
With epi mg/kg: 7

75
Q 
Ropiviciaine:
Max dose:
Max dose with epi:
Plain mg/kg:
With epi mg/kg:
A

Max dose: 200
Max dose with epi: (not listed)
Plain mg/kg: 2.5
With epi mg/kg: 2.5

76
Q 
Bupiviaine:
Max dose:
Max dose with epi:
Plain mg/kg:
With epi mg/kg:
A

Max dose: 175
Max dose with epi: 225
Plain mg/kg: 2.5
With epi mg/kg: 3

77
Q

What is the progression of plasma levels and CNS effects?

A 
Vertigo
Tinnitus
Ominous feelings
Circumoral numbness
Garrulousness
Tremors
Myoclonic jerks
Convulsions
Coma
Cardiovascular collapse
78
Q

What is the blood flow of LA to tissues (fastest to slowest)

A 
IV
Tracheal
Intercostal
Caudal
Paracervical
Epidural
Brachial Plexus
Subarachnoid
Subcutaneous
(In time I can please everyone but Suzi and Sally)
79
Q

What is transient neurologic symptoms (TNS)?

A

Moderate to severe pain

Lower back, buttocks, and posterior thighs

80
Q

What is TNS most common with?

A

Highest risk after intrathecal lidocaine

81
Q

What is cuada equine syndrome

A

Diffuse injury across lumbosacral plexus

  • Various degrees of sensory anesthesia
  • Bowel and bladder sphincter dysfunction
  • Paraplegia
82
Q

What are big red flags to doing a caudal block?

A

Sacral dimple and hairy nevi

83
Q

What is anterior spinal artery syndrome

A

Lower extremity paresis and variable sensory deficit

84
Q

Cardiotoxicity is more or less resistant than CNS

A

more

85
Q

Why can you see profound hypotension with cardiotoxicity?

A

Relaxation of arteriolar vascular smooth muscle

Direct myocardial Depression

86
Q

In what anesthetic might you see cardiotoxicity BEFORE CNS effects?

A

Bupivacaine

Order of CV toxicity according to APEX
Bupi > Levobupiva > Ropiva > Lidocaine

87
Q

What is the initial treatment of LAST?

A

Airway management
- 100% O2

Seizure suppression

  • Benzodiazepines
  • AVOID propofol if cardiovascular instability
  • Alert for possible cardiopulmonary bypass
88
Q

What is the next treatment for LAST?

A

Management of arrhythmias

  • BLS and ACLS
  • AVOID vasopressin, calcium channel blockers, betablockers, or local anesthetic
  • REDUCE epi to <1 mcg/kg
89
Q

Explain Lipid Emulsion Therapy (20%) for LAST

A
  1. 5 mL/kg (lean body mass) IV over 1 minute
  2. 25 mL/kg/min

Repeat Bolus once or twice for persistant cardiovascular collapse

Double infusion rate to 0.5 mL/kg/min if BP remains low

Continue infusion for at least 10 min after circulatory stability

Upper limit: Approximately 10 mL/kg lipid emulsion over first 30 minutes

90
Q

Methamoglobinemia is related to which LAs?

A

Prilocaine >8 mg/kg, Benzocaine, Cetacaine, Lidocaine

Also Nitroglycerin, Phenytoin, and Sulfonamides

91
Q

What is the treatment of methamoglobinemia?

A

Methylene Blue 1-2mg/kg IV over 5 minutes

Do not exceed 7.8 mg/kg

92
Q

What are the low potency/short duration LAs?

A

Procaine

Chloroprocaine

93
Q

What are the intermediate potency/duration LAs?

A

Lidocaine

94
Q

What are the long acting/long duration LAs?

A

Bupivacaine, Ropivacaine, Tetracaine

95
Q

What are the Fast Onset LAs?

A

Cloroprocaine & Lidocaine

96
Q

What are the slow onset LAs?

A

Bupicacaine, Ropivacaine, Tetracaine, Procaine

  • the further away the pKa from physiologic (pH 7.4) the slower the onset

Bupivacaine 8.1
Ropivacaine 8.1
Tetracaine 8.5
Procaine 8.9

97
Q

Factors that increase neurotoxicity

A

Hypercarbia, Hyperkalemia, Hypoxemia, Acidosis

98
Q

Factors that decrease neurotoxicity

A

Hypocarbia, hypokalemia, CNS depressants

APA 3 - Wolfe (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions