Local Anesthetics III (Exam IV) Flashcards

(68 cards)

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
Why does pregnancy predispose one to cardiovascular toxicity from LA's?
Pregnancy = ↓ plasma cholinesterases ## Footnote S12
26
Which three drugs are most responsible for **cardiac adverse effects** when reaching toxic levels systemically?
Bupivacaine > Ropivacaine > Lidocaine ## Footnote S12
27
Which two factors predispose our OB population to local anesthetic toxicity?
- ↓ plasma esterases - ↓ plasma proteins ## Footnote S12
28
Slide 14
## Footnote S14
29
Slide 15
30
Should a local anesthetic toxicity patient be hyperventilated or hypoventilated?
Hyperventilation = ↓ CO₂ = ↓ acidosis ## Footnote S15
31
Why is 100% O₂ given for LA toxicity?
To inhibit hypoxemia and metabolic acidosis ## Footnote S15
32
What drugs are used to treat LA induced seizures?
* Supplemental oxygen * Benzodiazepine * Propofol * Muscle relaxant * Intralipid: lipid emulsion ## Footnote S16
33
How does Lipid Emulsion rescue work?
**Lipid creates lipid compartment** (encapsulate the local anesthetic and transport it away from cardiac and CNS tissue) ***Also provides fat for myocardial metabolism*.** ## Footnote S17
34
What is the bolus dose of Lipid Emulsion?
1.5 mL/kg of 20% lipid emulsion ## Footnote S17
35
What is the infusion dose of lipid emulsion? How long should it be given?
0.25 mL/kg/minute for at least 10 minutes ## Footnote S17
36
What is the max dose for lipid emulsion that should be given?
8 mL/kg ## Footnote ???
37
What is the dose for lipid emulsion that should be given in the 1st 30 minutes?
3.8 mL/kg ## Footnote S17
38
What would be the last resort therapy for a patient with severe LAST syndrome in which lipid rescue and ACLS have failed?
Cardiopulmonary Bypass ## Footnote S17
39
Can propofol be used as a substitute for a lipid emulsion?
No ## Footnote S17
40
If cardiac arrest occurs with LAST syndrome, how should our epinephrine dosing change?
Small doses (**10mcg - 100mcg boluses**) are preferred with LAST ACLS. ## Footnote S17
41
How much vasopressin should be given if a patient is suffering from hypotension from LAST syndrome?
Trick question. Vasopression should **not** be given with LAST syndrome.
42
**This card is here just to view the LAST algorithm**.
43
56kg so 1.5mLs x 56kg = 84mLs 20% infusion = 200mgs / 1mL 84mLs x 200mgs = **16,800mgs** administered ## Footnote S22
44
What are the three categories of neural tissue toxicity associated with LA toxicity?
- Transient Neurological Symptoms - Cauda Equina Syndrome - Anterior Spinal Artery Syndrome ## Footnote S24
45
What are the s/s of Transient Neurological Symptoms (TNS) ?
Moderate to severe **pain in the lower back, buttocks, or posterior thighs** within **6 - 36 hours** post uneventful spinal block. ## Footnote S25
46
What LA is most often the cause of TNS?
Lidocaine or addition of vasoconstrictor? the patho is still unknown ## Footnote S25
47
What is the treatment for TNS?
- Trigger point injections - NSAIDs | give pain medications!!! ## Footnote S25
48
How long does TNS typically last?
1-7 days ## Footnote S25
49
What is Cauda Equina Syndrome (CES) ?
Diffuse injury @ *lumbosacral plexus* ## Footnote S26
50
What are the s/s of CES?
- Varying degrees of sensory anesthesia - Bowel & bladder dysfunction - Urinary retention ## Footnote S26
51
What conditions are associated with CES?
- Lumbar disc herniation - prolapse or sequestration w/ urinary retention ## Footnote S26
52
What is the cause of Anterior Spinal Artery Syndrome?
- **Thrombosis and/or spasm of the bilateral anterior spinal artery** - **↓BP** - **Vasoconstrictors** - PVD - Spinal cord compression (hematoma/abscess) | most common sydrome ## Footnote S27
53
What are the s/s Anterior Spinal Artery Syndrome?
Lower extremity paresis w/ variable sensory deficit ## Footnote S27
54
What is Methemoglobinemia?
Life-threatening condition where O₂ carrying capacity is decreased due to MetHgb > 15% ## Footnote S28
55
Which two LA's are most often the culprits of methemoglobinemia?
- Prilocaine - Benzocaine ## Footnote S28
56
What is the treatment for methemoglobinemia?
Methylene blue 1mg/kg over 5min ## Footnote S28
57
What is the max dosage of methylene blue?
8 mg/kg ## Footnote S28
58
How long does the reversal from MetHgb (Fe⁺⁺⁺) to Hgb (Fe⁺⁺) typically take?
20 - 60 min ## Footnote S28
59
Lidocaine _________ the ventilatory response to arterial hypoxemia. What patient population is most susceptible to this?
depresses CO₂ retaining patients (COPD) ## Footnote S29
60
Continuous or intermittent epidural bupivacaine to treat post-herpetic neuralgia can cause what?
Hepatic toxicity *Stopping bupivacaine infusion normalizes LFTs quickly*. ## Footnote S29
61
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 first then A, D, B ## Footnote S30
62
What is Cocaine's MOA?
Blocks presynaptic re-uptake of NE and Dopamine → Increases postsynaptic levels and ↑SNS. ## Footnote S31
63
What are CV adverse effects of Cocaine toxicity?
HTN, tachycardia, coronary vasospasm, MI (infarction & ischemia), ventricular dysrhythmias (including Vfib). ## Footnote S31
64
What does parturient mean?
Woman in labor ## Footnote S31
65
What can cocaine do to a parturient patient?
↓ uterus blood flow = fetal hypoxia ## Footnote S31
66
What can hyperpyrexia lead to?
seizures ## Footnote S31
67
What is the algorithm for cocaine-associated chest pain?
## Footnote S32
68
What drug is best for cocaine toxicity?
Nitroprusside