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Anesthesia Pharmacology Medications > Week 6: Local Anesthetics > Flashcards

Week 6: Local Anesthetics Flashcards

1
Q

Benzocaine

  1. Onset and pKa
  2. Use
A
  1. UNIQUE: Weak acid: pKa = 3.5, very fast onset

2. Topical use only!!

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2
Q

Cocaine

  1. Onset and pKa
  2. How does it work?
  3. Use and Route
A
  1. pKa = 8.6, very fast onset
  2. Blocks nerve impulses and causes local vasoconstriction by inhibiting local NE reuptake
  3. Local anesthesia in nasal passages when LA and vasoconstriction is desired. **Don’t use IV –> euphoria due to blockade of dopamine reuptake in the CNS

**ONLY naturally occurring LA

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3
Q

2-Chloroprocaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 8.7, 6-12 minutes
  2. 30-45 minutes
  3. 600mg
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4
Q

Tetracaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 8.6, 10-15 minutes
  2. 60-180 minutes
  3. 100 mg (topical)
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5
Q

Lidocaine

  1. Onset and pKa
  2. Duration
  3. Dose
  4. Maximum Single Dose for Infiltration
A
  1. pKa = 7.7, 2-4 minutes
  2. 60-120 minutes
  3. 1.5%-2.0% for regional blocks for surgery, 1% with epi is good for local infiltration
  4. 300 mg
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6
Q

Mepivacaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 7.7, 2-4 minutes
  2. 90-180 minutes
  3. 300 mg
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7
Q

Prilocaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 7.7, 2-4 minutes
  2. 60-120 minutes
  3. 400 mg
    * *First synthetic LA
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8
Q

Etidocaine

  1. Onset and pKa
  2. Duration
  3. Downfall
A
  1. pka = 7.9, 2-4 minutes
  2. 240-480 minutes
  3. No useful for peripheral nerve blocks because prolonged motor block outlasts sensory block
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9
Q

Bupivacaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 8.1, 5-8 minutes
  2. 240-480 minutes
  3. 175mg
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10
Q

Ropivacaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. pKa = 8.1, 2-4 minutes
  2. 240-480 minutes
  3. 200 mg
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11
Q

Levobupivacaine

  1. Onset and pKa
  2. Duration
  3. Maximum Single Dose for Infiltration
A
  1. Onset like bupivicaine (5-8 minutes)
  2. 240-480 minutes
  3. 175 mg
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12
Q

Lipid Emulsion

  1. Use
  2. Dose
  3. Upper limit
A
  1. Treatment of LAST
  2. 20% Lipid Emulsion Therapy
    Bolus: 1.5ml/1 minute
    Infusion: .25ml/kg/min
    **May repeat bolus 1-2x if needed or increase infusion to .5ml/kg/min
  3. Upper limit: 10ml/kg over 30 minutes
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13
Q

Key Points of Chloroprocaine

A
  • Clorinated procaine -> more rapidly metabolized by plasmacholinesterase
  • Minimal placental transfer even with 40% decrease in PC: Good for OB
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14
Q

Key Points of Tetracaine

A
  • Too toxic for peripheral blocks; Only used for long acting spinal blocks
  • Theoretically, mixing with lidocaine can be used for peripheral blocks to give fast onset with long duration and less toxicity
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15
Q

Key Points of Lidocaine

A
  • Vasodilation properties

- Cardioprotective qualities from a metabolite formed by oxidative dealkyation

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16
Q

Rank the Amides for Rate of Liver Metabolism

A

Prilocaine>Lidocaine> Mepivicaine> Ropivicaine>Bupivicaine

17
Q

Key Points for Mepivicaine

A
  • Lacks vasodilation of lidocaine

- ***TOXIC to neonates- DO NOT use in OB

18
Q

Key Points for Prilocaine

A
  • Lacks vasodilation and limits CNS toxicity
  • **Can cause methemoglobinemia -> usually with doses 8mg/kg or with liver problems-> treat with methylene blue (1-2mg/kg)
  • Not commonly used for peripheral blocks
19
Q

Key Points for Bupivicaine

A
  • CardioTOXIC: Difficult to dissociate from Na+ channels
  • Used for peripheral blocks (less than .5%), continuous infusion (less than .1%) with opioids, and can be used in OB (less than .25%)
20
Q

Key Points for Ropivacaine

A
  • S-enatiomer of bupivicaine

- VERY popular for peripheral blocks

21
Q

Metabolism of Amide LAs

A

Metabolized in the liver by deakylation of an ethyl group from the tertiary amine and hydroxylation
**Hepatic blood flow and liver function are important
Renal clearance of unchanged LA is about 3-5%

22
Q

Metabolism of Ester LAs

A

Hydrolyzed by circulation pseudocholinesterase (plasma cholinesterase)
PC is made in the LIVER:
Affected by liver disease, high BUN, pregnancy, chemo drugs, atypical PSE, genetic makeup

23
Q

Blood Flow and LA Absorption Rates From Fastest to Slowest

A
  1. Intravenous
  2. Tracheal
  3. Intercostal
  4. Caudal
  5. Paracervical
  6. Epidural
  7. Brachial Plexus
  8. Subarachnoid, Sciatic, Femoral
  9. Subcutaneous

*I Think I Can Push Each Bolus SSlowly For Safety

24
Q

Adverse Effects of LA

A
  • Allergic reaction
  • Systemic Toxicity
  • Neural Tissue Toxicity
  • TNS (transient neurologic syndrome)
  • Cauda Equina syndrome
  • Anterior spinal artery syndrome
  • Methemoglobinemia
25
Q

Allergic Reaction with LA

A
  • Rare -> usually symptoms from systemic toxicity
  • If present, most often to the preservative: METHYLPARABEN
  • Esters> Amides for true allergy with NO cross sensitivity between classes
26
Q

Systemic Toxicity

A

LAST:
Starts with CNS symptoms: drowsiness, paresthesias in the mouth and tongue, tinnitus and auditory hallucination
Then Muscular spasm
Then seizures, coma, respiratory arrest, and cardiac arrest
**as patient gets worse, more acidotic -> makes LAST worst

27
Q

Neural Tissue Toxicity

A

Nerve damage: Very rare event with epidural and spinals

**Lidocaine more concerning in the spinal because increased concentrations of Ca+ may be mechanism for toxicity

28
Q

TNS

A

Transient Neurologic Syndrome:
Pain in low back, butt for 6-36 hours after spinal
**Lidocaine implicated
Often resolves in 7 days after treatment with NSAIDS

29
Q

Cauda Equina Syndrome

A

Large sensory, bowel, bladder dysfunction and paraplegia
Implicated with 5% lidocaine with patient in lithotomy position
Could be from LA pooling at the nerves
Can be serious, but most often presents as urinary retention

30
Q

Anterior Spinal Artery Syndrome

A

LE paresis with variable sensory deficit after resolution of regional
Maybe caused by thrombus or spasm of anterior spinal artery
*Epi is implicated, more prevalent with elderly and PVD
Presents similar to epidural hematoma

31
Q

Methemoglobinemia

A

Oxidation of Hb to MetHb
**Implicated with benzocaine, prilocaine, lidocaine
Treat with methylene blue (1-2mg/kg)
Don’t see symptoms until 15% are converted to MetHb

32
Q

Cocaine Toxicity

A

Symptoms: coronary vasospasm, MI, dysrhythmias

- Can be seen up to six weeks after use

33
Q

Key Points for Tumescent Technique

A
  • Subcutaneous placemet of large volumes of diluted Lido with epi
  • Tumescent lido with epi mas = 35-55mg/kg because 1 gm of fat absorbs 1 mg lido and acts as a tissue buffering system
  • Complications: Lido toxicity, cardiac depression and decreased contractility
34
Q

What is the order of loss of nerve sensations?

A
  1. Autonomic functions
  2. Pain
  3. Cold
  4. Warmth
  5. Touch
  6. Pressure
  7. Vibration
  8. Proprioception
    - —— Want to be here —————
  9. Motor function (ALWAYS LAST)
35
Q

Three factors that determine duration of block

A
  1. Lipid solubility
  2. Vascularity of tissues
  3. Presence of vasoconstrictors (prevent vascular uptake of the LA molecules)
36
Q

Type A Nerve Fibers

  1. Function
  2. Myelination
  3. Sensitivity to Block
A
  1. Fast afferent and efferent to muscles for pain, tactile, proprioception
  2. Myelinated
  3. Alpha are least sensitive -> delta are most sensitive of type A fibers
37
Q

Type B Nerve Fibers

  1. Function
  2. Myelination
  3. Sensitivity to Block
A
  1. Pre-ganglionic autonomic
  2. Some myelination
  3. More resistant to blocks
38
Q

Type C Nerve Fibers

  1. Function
  2. Myelination
  3. Sensitivity to Block
A
  1. Slow, dull pain
  2. Non-myelinated
  3. More sensitive to block

Anesthesia Pharmacology Medications (9 decks)

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