Local Anesthetics III (Exam IV) Flashcards

1
Q

How rare are local anesthetic reactions?

A

< 1% occurrence

-Mild to IgE anaphylaxis.

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2
Q

What local anesthetic class is responsible for more allergic reactions?

A

Esters (PABA metabolite) > amides.

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3
Q

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

A

Methylparaben - preservative to both esters & amides.

(similar in 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

Clinical manifestations of an allergic reaction?

Time course of allergic reaction?

A

rash, urticaria, and laryngeal edema with or without hypotension & bronchospasm.

immediate vs. delayed.

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8
Q

Management of allergic reaction?

A

stop administration
supportive care (airway, O2, fluids)
epinephrine, antihistamine, corticosteroids

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9
Q

What is LAST?

A

Local Anesthetic Systemic Toxicity

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10
Q

What causes LAST syndrome?

A

Excess plasma concentration of LA from:
- Accidental direct IV injection
- Systemic absorption from tissue redistribution and clearance metabolism.

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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
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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.

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13
Q

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

A
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14
Q

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

A

Hyperkalemia (lowers seizure threshold) - so it promotes seizures.

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15
Q

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

A

Drowsiness and facial twitching

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16
Q

LAST: CNS effects seen:

A

Early agitation & 1-10 mcg/mL

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17
Q

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

A

Analgesia

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18
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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19
Q

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

A
  • Seizures
  • Unconsciousness
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20
Q

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

A
  • Apnea
  • Coma
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21
Q

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

A

Cardiovascular Depression

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22
Q
A
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23
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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24
Q

What can occur if Bupivacaine is given intravenously?

A
  • Significant ↓BP
  • AV block
  • Cardiac Dysrhythmias (SVT, ST-T wave changes, PVCs, widening QRS, V-tach –> cardiac arrest)
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25
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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26
Q

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

A

Pregnancy = ↓ plasma cholinesterases

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27
Q

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

A
  • ↓ plasma esterases
  • ↓ plasma proteins
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28
Q

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

A

Bupivacaine > Ropivacaine > Lidocaine

29
Q

Prediposing factors: Acid/base balance?

A

Arterial hypoxemia, acidosis, or hypercarbia (in animals)

30
Q

LAST treatment?

A
  1. Stop LA immediately
  2. call for help
  3. 100% O2
  4. Hyperventilation
  5. Sedation: barb or propofol
  6. Epinephrine as an additive
31
Q

Why is 100% O₂ given for LA toxicity?

A

To inhibit hypoxemia and metabolic acidosis

32
Q

What drugs are used to treat LA induced seizures?

A
  • Benzodiazepines
  • Propofol (if BP is okay)
  • Muscle relaxants (suxx or NDMB)
  • Epinephrine
  • Intralipid
33
Q

How does Lipid Emulsion rescue work?

A

Creates a lipid compartment; fat for myocardial metabolism.

34
Q

What is the bolus dose of Lipid Emulsion?

A

1.5 mL/kg of 20% lipid emulsion

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

36
Q

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

37
Q

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

A

3.8 mL/kg (1.2 to 6 mL/kg)

Answer is from a study in the book.

38
Q

What is the epinephrine dose for lipid emulsion?

A

10 to 100 mcg

39
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 (CPB)

40
Q

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

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.

43
Q

(0.5% = 5mg/mL x 20 mL)

A

120 lbs =54.5 kg

so 1.5mLs x 54.5 kg = 81.75 mLs

20% infusion = 200mgs / 1mL

81.75 mLs x 200mgs = 16,350mgs administered

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
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.

46
Q

What LA is most often the cause of TNS?

47
Q

What is the treatment for TNS?

A
  • Trigger point injections
  • NSAIDs
48
Q

How long is the recovery from Transient neurologic symptoms (TNS)?

49
Q

What is Cauda Equina Syndrome (CES) ?

A

Diffuse injury @ lumbosacral plexus

50
Q

What causes CES?

A

spinal anesthesia & high concentration, compression, or ischemia of cauda equina.

51
Q

What are the s/s of CES?

A
  • Varying degrees of sensory anesthesia
  • Bowel & bladder dysfunction sphincter dysfunction
  • weakness
    -paraplegia
52
Q

What conditions are associated with CES?

A
  • Lumbar disc herniation, prolapse or sequestration w/ urinary retention
53
Q

What is the cause of Anterior Spinal Artery Syndrome?

A
  • Thrombosis and/or vasospasm of the anterior spinal artery
  • ↓BP or vasoconstrictor drugs; PVD, Spinal cord compression d/t epidural abscess or hematoma.
54
Q

What are the s/s Anterior Spinal Artery Syndrome?

A

Lower extremity paresis w/ variable sensory deficit (no pain/temperature, yes proprioception)

55
Q

What is Methemoglobinemia?

A

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

this causes cyanosis d/t the FE^3+ cannot bind to oxygen.

56
Q

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

A
  • Prilocaine & Benzocaine > lidocaine, nitroglycerine, phenytoin, & sulfonamides.
57
Q

What is the treatment for methemoglobinemia?

A

Methylene blue 1mg/kg over 5min

58
Q

What is the max dosage of methylene blue?

A

7 to 8 mg/kg

59
Q

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

A

20 - 60 min

60
Q

Lidocaine _________ the ventilatory response to arterial hypoxemia.

What patient population is most susceptible to this?

A

depresses

CO₂ retaining patients (COPD)

61
Q

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

A

Hepatic toxicity

Stopping bupivacaine infusion normalizes liver transaminase enzymes

62
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

A. Call for help

then D, C, and B last

63
Q

What is Cocaine’s MOA?

A

Blocks presynaptic reuptake of NorEpi and Dopamine → Increases postsynaptic levels of NorEpi and dopamine.

64
Q

CV adverse effects with cocaine toxicity? how long can adverse effect last?

A
  • HTN, tachycardia, coronary vasospasm, MI ( infarction & ischemia), ventricular dysrhythmias (VFIB)
  • Adverse effects can last up to 6 weeks
65
Q

What does parturient mean?

A

Woman in labor

66
Q

What can cocaine do to a parturient patient?

A

↓ uterus blood flow = fetal hypoxia

67
Q

What is the algorithm for cocaine-associated chest pain?

68
Q

Treatment for cocaine toxicity?

What medications would be avoid?

A

benzodiazepines, nitroglycerin

Avoid beta-blockers.