Local Anesthetics III (Exam IV) Flashcards

(62 cards)

1
Q

How rare are local anesthetic 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 is Methylparaben used for? What is the concern with this?

A

Methylparaben is the preservative for both amide and ester LAs it has a similar structure to PABA and is usually the source responsible for allergic reactions to amide LAs

(you can use preservative free to avoid)

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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 direct IV injection
  • Systemic absorption from inactive 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 (ie: amount ionized vs non-ionized)
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10
Q

How does the addition of epi with lidocaine affect systemic absorption of the lidocaine?

A

It decreases systemic absorption

“5mcg/mL of Epi decreases systemic absorption by 1/3”

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11
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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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 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
  • Cardiac Dysrhythmias
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21
Q

What drugs will predispose patients to cardiovascular effects for LA systemic toxicity? (5)

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

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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 local anesthetics are most responsible for cardiac adverse effects when reaching toxic levels systemically?

A

Bupivacaine > Ropivacaine > Lidocaine

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25
With high plasma concentration levels of Lidocaine we will see blockade of cardiac ____ channels. This causes _____
Na+ Conduction delays
26
Should a local anesthetic toxicity patient be hyperventilated or hypoventilated?
Hyperventilation = ↓ CO₂ = ↓ acidosis
27
Why is 100% O₂ given for LA toxicity?
To inhibit hypoxemia and metabolic acidosis
28
What drugs are used to treat LA induced seizures?
- Benzodiazepines - Propofol (if BP is okay) - Muscle relaxants - Lipid Rescue
29
What two things does Lipid Emulsion do for the treatment of systemic toxicity?
1. Creates lipid compartment *(binds to LAs and carries them away from vessel rich group)* 2. Provides fat for myocardial metabolism
30
What is the bolus dose of Lipid Emulsion?
1.5 mL/kg of 20% lipid emulsion ## Footnote ***20% = 200mg/ml***
31
What is the infusion dose of lipid emulsion? How long should it be given?
0.25 mL/kg/minute for at least 10 minutes
32
What is the max dose for lipid emulsion that should be given?
10 mL/kg over first 30min
33
What would be the last resort therapy for a patient with severe LAST syndrome in which lipid rescue and ACLS have failed?
**Cardiopulmonary Bypass**
34
If cardiac arrest occurs with LAST syndrome, how should our epinephrine dosing change?
Small doses (**10mcg - 100mcg boluses**) are preferred with LAST ACLS.
35
**This card is here just to view the LAST algorithm**.
36
54 kg 1.5 mLs x 54 kg = 81 mLs 20% infusion = 200mgs / 1mL 81mLs x 200mgs = **16,200mgs** administered
37
What is neural tissue toxicity and what causes it?
Direct neurotoxic effect on neurons. Causes: high concentrations and/or prolonged exposure
38
What is the duration of the neurologic injury with neural tissue toxicity?
Either transient or permanent
39
What are the three categories of neural tissue toxicity associated with LA toxicity?
- Transient Neurological Symptoms - Cauda Equina Syndrome - Anterior Spinal Artery Syndrome
40
Transient Neurological Symptoms (TNS) is moderate to severe pain in the _____, _____, or ______ within ______ hours post uneventful spinal block
lower back, buttocks, or posterior thighs 6 - 36 hours
41
What LA is most often the cause of TNS?
Lidocaine
42
What is the treatment for TNS?
- Trigger point injections - NSAIDs
43
How long does TNS typically last?
1-7 days
44
What is Cauda Equina Syndrome (CES) ?
Diffuse injury @ lumbosacral plexus
45
What are the s/s of CES?
- Varying degrees of sensory anesthesia - Bowel & bladder dysfunction - Paraplegia
46
What conditions are associated with Cauda Equina Syndrome?
Large lumbar disc herniation, prolapse or sequestration w/ urinary retention
47
What are the four causes of Anterior Spinal Artery Syndrome?
1. Effects of HoTN or vasoconstrictors 2. PVD 3. Spinal cord compression d/t abscess or hematoma 4. Thrombosis or vasospasm of the bilateral anterior spinal artery
48
What are the s/s Anterior Spinal Artery Syndrome?
Lower extremity paresis w/ variable sensory deficit Loss of sensation with pain and temp Retain proprioception (ability to sense where our limbs are in space)
49
What is Methemoglobinemia?
Life-threatening condition where O₂ carrying capacity is decreased due to MetHgb > 15%
50
Which two LA's are most often the culprits of methemoglobinemia?
- Prilocaine - Benzocaine
51
What is the treatment for methemoglobinemia?
Methylene blue 1mg/kg over 5min
52
What is the max dosage of methylene blue?
8 mg/kg
53
How long does the reversal from MetHgb (Fe⁺⁺⁺) to Hgb (Fe⁺⁺) typically take?
20 - 60 min
54
Lidocaine _________ the ventilatory response to arterial hypoxemia. What patient population is most susceptible to this?
depresses CO₂ retaining patients (COPD)
55
Continuous or intermittent epidural bupivacaine to treat post-herpetic neuralgia can cause what?
Hepatic toxicity *Stopping bupivacaine infusion normalizes LFTs quickly*.
56
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
C.
57
What is Cocaine's MOA?
Blocks presynaptic re-uptake of NE and Dopamine → Increases postsynaptic levels.
58
What does parturient mean?
Woman in labor
59
How long can the adverse effects from cocaine toxicity last?
up to 6 weeks
60
What meds can we give for cocaine toxicity? What would we avoid?
Give: benzo and nitroglycerine Avoid: Beta blockers
61
What can cocaine do to a parturient patient?
↓ uterus blood flow = fetal hypoxia
62
What is the algorithm for cocaine-associated chest pain?