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KM (Spring 2024) Anesthesia Pharm ** > Local Anesthetics III (Exam IV) > Flashcards

Local Anesthetics III (Exam IV) Flashcards

1
Q

How rare are local anesthetic reactions?

A

< 1% occurrence

Attributed to manifestations of excess plasma levels

S6

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2
Q

What local anesthetic class is responsible for more allergic reactions?

A

Esters (due to PABA metabolite)

S6

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3
Q

What preservative commonly used for amide local anesthetics is usually responsible for allergies?

A

Methylparaben (broken down into PABA)

Use preservative free

S6

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4
Q

Is there a cross-sensitivity between esters and amides?

A

No

S6

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5
Q

How can one be tested for local anesthetic allergy?

A

Intradermal testing using preservative free LA

S6

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6
Q

What are presentations of allergic reactions to local anesthetics?

A
  • Rash
  • urticaria
  • laryngeal edema w/ or w/o hypotension & bronchospasm

S6

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7
Q

What is the most serious complication of allergies to local anesthetics?

A

IgE anaphylaxis

S6

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8
Q

What is LAST?

A

Local Anesthetic Systemic Toxicity

S8

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9
Q

What causes LAST syndrome?

A

Excess plasma concentration of LA from:

  • Accidental IV injection
  • Systemic absorption from tissue redistribution and clearance metabolism.

S8

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10
Q

What are other factors that can affect systemic toxicity?

A
  • Patient co-morbidities
  • medications
  • location & technique of block
  • type of LA used & dose

S8

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11
Q

What factors affect the magnitude of systemic absorption of local anesthetic?

A
  • Dose
  • Vascularity of site
  • Concurrent Epi use
  • Properties of the drug itself

S9

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12
Q

Would local anesthetic administered via the trachea have a higher or lower chance of systemic absorption than local anesthetic delivered brachially?

A

Trachea has higher chance of systemic absorption.

S9

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13
Q

Compare and contrast the different areas of local anesthetic administration based on resultant blood concentrations.

A

S9

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14
Q

What serum electrolyte condition will exacerbate local anesthetic toxicity?
Why?

A

Hyperkalemia (lowers seizure threshold)

S10

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15
Q

What CNS s/s will forebode local anesthetic induced seizures?

A

Drowsiness and facial twitching

S10

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16
Q

What s/s would be seen with a plasma lidocaine concentration of 1-5 mcg/ml?

A

Analgesia

S10

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17
Q

What s/s would be seen with a plasma lidocaine concentration of 5-10 mcg/ml?

A
  • Mouth numbness
  • Tinnitus
  • Muscle twitching
  • ↓BP
  • Myocardial depression
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18
Q

What s/s would be seen with a plasma lidocaine concentration of 10-15 mcg/ml?

A
  • Seizures
  • Unconsciousness
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19
Q

What s/s would be seen with a plasma lidocaine concentration of 15-25 mcg/ml?

A
  • Apnea
  • Coma
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20
Q

What s/s would be seen with a plasma lidocaine concentration of >25 mcg/ml?

A

Cardiovascular Depression

S11S12

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21
Q

How does lidocaine affect EKGs?
How does it do this?

A
  • Prolongation of PR interval and QRS widening.
  • Blockade of Na⁺ channels

S11

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22
Q

What can occur if Bupivacaine is given intravenously?

A
  • Significant ↓BP
  • Cardiac Dysrhythmias
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23
Q
A

Arterial hypoxemia, acidosis, or hypercarbia (in animals

S12

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24
Q

What drugs will predispose patients to cardiovascular effects for LA systemic toxicity?

A
  • β-blockers, CCBs, digoxin
  • Epi and Phenylephrine

S12

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25
Q

Why does pregnancy predispose one to cardiovascular toxicity from LA’s?

A

Pregnancy = ↓ plasma cholinesterases

S12

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26
Q

Which three drugs are most responsible for cardiac adverse effects when reaching toxic levels systemically?

A

Bupivacaine > Ropivacaine > Lidocaine

S12

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27
Q

Which two factors predispose our OB population to local anesthetic toxicity?

A
  • ↓ plasma esterases
  • ↓ plasma proteins

S12

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28
Q

Slide 14

A

S14

29
Q

Slide 15

A
30
Q

Should a local anesthetic toxicity patient be hyperventilated or hypoventilated?

A

Hyperventilation = ↓ CO₂ = ↓ acidosis

S15

31
Q

Why is 100% O₂ given for LA toxicity?

A

To inhibit hypoxemia and metabolic acidosis

S15

32
Q

What drugs are used to treat LA induced seizures?

A
  • Supplemental oxygen
  • Benzodiazepine
  • Propofol
  • Muscle relaxant
  • Intralipid: lipid emulsion

S16

33
Q

How does Lipid Emulsion rescue work?

A

Lipid creates lipid compartment
(encapsulate the local anesthetic and transport it away from cardiac and CNS tissue)

Also provides fat for myocardial metabolism.

S17

34
Q

What is the bolus dose of Lipid Emulsion?

A

1.5 mL/kg of 20% lipid emulsion

S17

35
Q

What is the infusion dose of lipid emulsion?
How long should it be given?

A

0.25 mL/kg/minute for at least 10 minutes

S17

36
Q

What is the max dose for lipid emulsion that should be given?

A

8 mL/kg

???

37
Q

What is the dose for lipid emulsion that should be given in the 1st 30 minutes?

A

3.8 mL/kg

S17

38
Q

What would be the last resort therapy for a patient with severe LAST syndrome in which lipid rescue and ACLS have failed?

A

Cardiopulmonary Bypass

S17

39
Q

Can propofol be used as a substitute for a lipid emulsion?

A

No

S17

40
Q

If cardiac arrest occurs with LAST syndrome, how should our epinephrine dosing change?

A

Small doses (10mcg - 100mcg boluses) are preferred with LAST ACLS.

S17

41
Q

How much vasopressin should be given if a patient is suffering from hypotension from LAST syndrome?

A

Trick question. Vasopression should not be given with LAST syndrome.

42
Q

This card is here just to view the LAST algorithm.

A
43
Q
A

56kg so 1.5mLs x 56kg = 84mLs

20% infusion = 200mgs / 1mL

84mLs x 200mgs = 16,800mgs administered

S22

44
Q

What are the three categories of neural tissue toxicity associated with LA toxicity?

A
  • Transient Neurological Symptoms
  • Cauda Equina Syndrome
  • Anterior Spinal Artery Syndrome

S24

45
Q

What are the s/s of Transient Neurological Symptoms (TNS) ?

A

Moderate to severe pain in the lower back, buttocks, or posterior thighs within 6 - 36 hours post uneventful spinal block.

S25

46
Q

What LA is most often the cause of TNS?

A

Lidocaine or addition of vasoconstrictor?

the patho is still unknown

S25

47
Q

What is the treatment for TNS?

A
  • Trigger point injections
  • NSAIDs

give pain medications!!!

S25

48
Q

How long does TNS typically last?

A

1-7 days

S25

49
Q

What is Cauda Equina Syndrome (CES) ?

A

Diffuse injury @ lumbosacral plexus

S26

50
Q

What are the s/s of CES?

A
  • Varying degrees of sensory anesthesia
  • Bowel & bladder dysfunction
  • Urinary retention

S26

51
Q

What conditions are associated with CES?

A
  • Lumbar disc herniation
  • prolapse or sequestration w/ urinary retention

S26

52
Q

What is the cause of Anterior Spinal Artery Syndrome?

A
  • Thrombosis and/or spasm of the bilateral anterior spinal artery
  • ↓BP
  • Vasoconstrictors
  • PVD
  • Spinal cord compression (hematoma/abscess)

most common sydrome

S27

53
Q

What are the s/s Anterior Spinal Artery Syndrome?

A

Lower extremity paresis w/ variable sensory deficit

S27

54
Q

What is Methemoglobinemia?

A

Life-threatening condition where O₂ carrying capacity is decreased due to MetHgb > 15%

S28

55
Q

Which two LA’s are most often the culprits of methemoglobinemia?

A
  • Prilocaine
  • Benzocaine

S28

56
Q

What is the treatment for methemoglobinemia?

A

Methylene blue 1mg/kg over 5min

S28

57
Q

What is the max dosage of methylene blue?

A

8 mg/kg

S28

58
Q

How long does the reversal from MetHgb (Fe⁺⁺⁺) to Hgb (Fe⁺⁺) typically take?

A

20 - 60 min

S28

59
Q

Lidocaine _________ the ventilatory response to arterial hypoxemia.

What patient population is most susceptible to this?

A

depresses

CO₂ retaining patients (COPD)

S29

60
Q

Continuous or intermittent epidural bupivacaine to treat post-herpetic neuralgia can cause what?

A

Hepatic toxicity

Stopping bupivacaine infusion normalizes LFTs quickly.

S29

61
Q

The most common first intervention when an adverse event is identified is for the anesthesia provider to…

A. Call for help.
B. Administer the antidote
C. Discontinue the causative agent
D. Airway, Breathing, Circulation

A

C first

then A, D, B

S30

62
Q

What is Cocaine’s MOA?

A

Blocks presynaptic re-uptake of NE and Dopamine → Increases postsynaptic levels and ↑SNS.

S31

63
Q

What are CV adverse effects of Cocaine toxicity?

A

HTN, tachycardia, coronary vasospasm, MI (infarction & ischemia), ventricular dysrhythmias (including Vfib).

S31

64
Q

What does parturient mean?

A

Woman in labor

S31

65
Q

What can cocaine do to a parturient patient?

A

↓ uterus blood flow = fetal hypoxia

S31

66
Q

What can hyperpyrexia lead to?

A

seizures

S31

67
Q

What is the algorithm for cocaine-associated chest pain?

A

S32

68
Q

What drug is best for cocaine toxicity?

A

Nitroprusside

KM (Spring 2024) Anesthesia Pharm ** (101 decks)

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