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24 Anesthesia Pharm > Local Anesthetics III (Exam IV) > Flashcards

Local Anesthetics III (Exam IV) Flashcards

1
Q

How rare are local anesthetic allergic reactions?

A

< 1% occurrence

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2
Q

What local anesthetic class is responsible for more allergic reactions?

A

Esters (due to PABA metabolite)

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3
Q

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

A

Methylparaben (similar structure to PABA)

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4
Q

Is there a cross-sensitivity between esters and amides?

A

No

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5
Q

How can one be tested for local anesthetic allergy?

A

Intradermal testing using preservative free LA

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6
Q

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

A

IgE anaphylaxis

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7
Q

What is LAST?

A

Local Anesthetic Systemic Toxicity

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8
Q

What causes LAST syndrome?

A

Excess plasma concentration of LA from:

  • Accidental IV injection
  • Systemic absorption from tissue redistribution and clearance metabolism.
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9
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
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10
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.

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11
Q

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

A
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12
Q

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

A

Hyperkalemia (lowers seizure threshold)

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13
Q

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

A

Drowsiness and facial twitching

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14
Q

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

A

Analgesia

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15
Q

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

A
  • Mouth (circumoral)numbness
  • Tinnitus
  • Muscle twitching
  • ↓BP
  • Myocardial depression
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16
Q

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

A
  • Seizures
  • Unconsciousness
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17
Q

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

A
  • Apnea
  • Coma
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18
Q

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

A

Cardiovascular Depression

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19
Q

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

A
  • Prolongation of PR interval and QRS widening.
  • Blockade of Na⁺ channels
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20
Q

What can occur if Bupivacaine is given intravenously?

A
  • Significant ↓BP, AV block, ST- T wave changes, widening QRS
  • Cardiac Dysrhythmias (SVT, PVCs, V-tach)
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21
Q

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

A
  • β-blockers, CCBs, digoxin
  • Epi and Phenylephrine
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22
Q

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

A

Pregnancy = ↓ plasma cholinesterases & plasma proteins

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23
Q

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

A
  • ↓ plasma esterases
  • ↓ plasma proteins
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24
Q

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

A

Bupivacaine > Ropivacaine > Lidocaine

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25
Q

Should a local anesthetic toxicity patient be hyperventilated or hypoventilated?

A

Hyperventilation = ↓ CO₂ = ↓ acidosis

26
Q

Why is 100% O₂ given for LA toxicity?

A

To inhibit hypoxemia and metabolic acidosis

27
Q

What drugs are used to treat LA induced seizures?

A
  • O2
  • Benzodiazepines (midazolam/diazepam)
  • Propofol (if BP is okay)
  • Muscle relaxants (succs or NMDA “roc”)
  • Lipid Rescue
28
Q

How does Lipid Emulsion rescue work?

A

Creates lipid compartment for local anesthetic and transport it away from cardiac and CNS tissue.

Also provides fat for myocardial metabolism.

29
Q

What is the bolus dose of Lipid Emulsion?

A

1.5 mL/kg of 20% lipid emulsion

30
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 (should be continued for 10 min after circulatory stability is attained)

31
Q

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

A

8 mL/kg total

32
Q

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

A

3.8 mL/kg

Answer is from a study in the book.

33
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

34
Q

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

A

No

35
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.

36
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.

37
Q

This card is here just to view the LAST algorithm.

A
38
Q
A

54kg so 1.5mLs x 54kg = 81mLs

20% infusion = 200mgs / 1mL

81mLs x 200mgs = 16,200mgs administered

39
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
40
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.

41
Q

What LA is most often the cause of TNS?

A

Lidocaine

42
Q

What is the treatment for TNS?

A
  • Trigger point injections
  • NSAIDs
43
Q

How long does TNS typically last?

A

1-7 days

44
Q

What is Cauda Equina Syndrome (CES) ?

A

Diffuse injury @ lumbosacral plexus

45
Q

What are the s/s of CES?

A
  • Varying degrees of sensory anesthesia
  • Bowel & bladder dysfunction
  • paraplegia
46
Q

What conditions are associated with CES?

A
  • Lumbar disc herniation
  • prolapse or sequestration w/ urinary retention
47
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)
48
Q

What are the s/s Anterior Spinal Artery Syndrome?

A

Lower extremity paresis w/ variable sensory deficit

49
Q

What is Methemoglobinemia?

A

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

50
Q

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

A
  • Prilocaine
  • Benzocaine
51
Q

What is the treatment for methemoglobinemia?

A

Methylene blue 1mg/kg over 5min
Max dose 7-8mg/kg

52
Q

What is the max dosage of methylene blue?

A

7-8 mg/kg

53
Q

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

A

20 - 60 min

54
Q

Lidocaine _________ the ventilatory response to arterial hypoxemia.

What patient population is most susceptible to this?

A

depresses

CO₂ retaining patients (COPD)

55
Q

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

A

Hepatic toxicity

Stopping bupivacaine infusion normalizes LFTs quickly.

56
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 (per lecture)

With LAST you would do D first

57
Q

What is Cocaine’s MOA?

A

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

Adverse effects last up to 6 weeks!

58
Q

What does parturient mean?

A

Woman in labor

59
Q

What can cocaine do to a parturient patient?

A

↓ uterus blood flow = fetal hypoxia

60
Q

What is the algorithm for cocaine-associated chest pain?

A
61
Q

What drug is best for cocaine toxicity persistent hypertension?

A

Nitroprusside

24 Anesthesia Pharm (20 decks)

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