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Anesthesia Pharm > Week 6 - Peripheral Nerve Phys/Local Anesthetics > Flashcards

Week 6 - Peripheral Nerve Phys/Local Anesthetics Flashcards

1
Q

What are the “things” that affect local anesthetics doing their job?

A
  • Molecular Structure
  • Type of Nerve Fiber
  • Activity of Nerve Fiber
  • pH of Patient
  • pKa of LA
  • Metabolism of LA
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2
Q

What is the general structure of a local anesthetic molecule?

A

Aromatic Group (Lipophilic Portion)

Tertiary Amine (Hydrophilic Portion)

Intermediate Bond – Amide linkage OR Ester linkage

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3
Q

How do local anesthetics impair nerve signal transmission?

A

By blocking voltage gated Na+ channels

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4
Q

What type of compounds are more potent and produce longer blocakdes?

A

More hydrophobic compounds are more potent and produce longer blockade than less hydrophobic ones

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5
Q

What are the Amino-Ester local anesthetics?

A

Cocaine, Procaine, Cloroprocaine, Tetracaine

*Ester linkage connects the aromatic ring to the tertiary amine

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6
Q

What are the Amino-Amide local anesthetics?

A

Lidocaine, Lignocaine, Mepivicaine, Prilocaine, Bupivacaine, Levobupivacaine, Etidocaine, Ropivacine

*Amide linkage connects the aromatic ring to the tertiary amine

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7
Q

What do weak acids bind with?

A

Positively charged ions like Na+, Mg++, and Ca++

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8
Q

What do weak bases bind with?

A

Negatively charged ions like Cl- and Sulfate

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9
Q

What are important determinants of LA function?

A

pKa and pH

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10
Q

What is pKa?

A

the pH at which 50% is ionized and 50% is nonionized

*different for different local anesthetics

Ex: pKa of Lidocaine is 7.7-7.9 so at pH of 7.4 Lidocaine is more ionized (75% ionized) than at pH of 7.7

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11
Q

How does pKa affect the onset of LA block?

A

lower pKa means more LA in non-ionized form and faster onset of block

*LA with pKa nearest to physiologic pH (7.35-7.45) have the most rapid onset of action

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12
Q

As pH increases do weak bases become more or less non-ionized?

A

weak bases become MORE non-ionized as the pH increases

  • increased pH = decreased H+ ions = increased non-ionized LA (good)
  • LA must be in basic form to be unionized and capable of penetrating the cell membrane to block the Na+ channel
  • LA will move across membranes faster in an alkalotic patient
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13
Q

Why will LAST be worse as the patient becomes acidotic?

A

Because the local anesthetic moved into Na+ channels and get trapped there secondary to the acidosis

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14
Q

How does the addition of Sodium Bicarb affect the local anesthetic?

A

increases pH resulting in more non-ionized form, which speeds onset

*adding too much will result in precipitation of the drug and render it useless

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15
Q

How does the addition of Epinephrine affect the local anesthetic?

A

LA premixed with Epi are more acidic (pH 3.5) to prevent breakdown of the Epi which increases the ionization of LA

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16
Q

How does protein binding affect local anesthetics?

A

Protein binding = Duration — High Protein Binding LA = Long Duration of action LA

  • most LA have very high protein binding
  • must release from protein to cause Na+ channel block
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17
Q

What is protein binding of LA dependent on and influenced by?

A

Protein binding is concentration dependent and influenced by plasma pH

  • as pH decreases, bound drug % decreases
  • very important to not let a suspected LAST patient become acidotic since the proportion of free LA molecules will increase markedly

ex: Bupivacaine 95% protein bound normally and decreases to ~70% with acidosis

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18
Q

How does lipid solubility affect local anesthetics?

A

The more lipid soluble = the more potent

  • increasing the lipid solubility of any LA molecule will increase the potency of the LA and the duration of action
  • increased lipid solubility also increases toxicity and decreases the therapeutic index of LA
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19
Q

What factor is more important for duration of action of local anesthetics?

A

Protein binding is more important than lipid solubility for duration of action

*the drug remains in the channel and surrounding areas for a longer time producing prolonged conduction blockade

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20
Q

How do local anesthetics block the Na+ channel?

A
  • LA placed near a nerve diffuses (in non-ionized form) from the outer surface toward the core via the concentration gradient (fibers in outer mantle - proximal structures/motor fibers - are blocked first) (if enough drug present is will diffuse into the core and block the distal structures)
  • Binds with cation to become ionized then binds to the Na+ channel
  • Prevents opening and Na+ inrush
  • Inhibits action potential
  • Blocking the Na+ channel blocks conduction of the nerve impulse propagation to the brain

*No pain impulse = No pain sensation

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21
Q

What is the structure of the Na+ channel?

A
  • It is a dynamic transmembrane protein
  • Large sodium-conducting pore (alpha subunit) that is further divided into 4 subunits (DI-DIV)
  • H is the alpha subunit that allows ion conduction and binds to local anesthetics
  • Beta subunits may modulate LA binding to the alpha subunit
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22
Q

What are the conformational states of a Na+ channel and in which state do local anesthetics bind?

A
  • Open (Activated): m gate opens, allowing Na+ influx, h gate begins to close
  • Closed (Inactivated): h gate closed, stops Na+ influx
  • Resting (Closed): h gate open and m gate closed preventing any Na+ through
  • LA selectively bind to Na+ channel (“h gate”) in the closed (inactivated) state stabilizing the channel in this configuration and prevent their change to the resting/open states in response to nerve impulse – also binds to beta portion of the channel
  • Inactivated state = not permeable to sodium

*binding appears to be weak and to reflect a relatively poor fit of the LA molecule with the receptor

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23
Q

What is the rate of diffusion of LA across the nerve sheath determined by?

A
  • Concentration of local anesthetic (0.5%, 1%, 5%)
  • Degree of ionization (non-ionized diffuses faster)
  • Hydrophobicity
  • Physical characteristics of tissue surrounding the nerve (more vascular = more uptake)
  • Small fibers block easier than large fibers
  • Myelinated fibers block easier than unmyelinated (LA pools near the axonal membrane - lipid soluble)
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24
Q

What is Differential Conduction Blockade of local anesthetics?

A

Illustrated by selective blockade of preganglionic SNS B fibers using low concentrations of LA — slightly higher concentrations of LA interrupt conduction in small C fibers and small/medium sized A fibers (loss of pain sensation and temp)

*Touch, proprioception, and motor function are still present such that the pt will sense pressure but not pain with surgical stimulation

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25
Q

How do LA change during pregnancy?

A

Increased sensitivity (more rapid onset)

*Alterations in protein binding characteristics of bupivacaine may result in increased concentrations of active unbound drug in pregnancy

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26
Q

_____ local anesthetics block faster than ____ & _____ at the same concentration.

A

Moderately hydrophobic LA block faster than hydrophilic & highly hydrophobic LA at the same concentration

  • Mod hydrophobic less bound to tissue, more membrane permeable
  • Highly hydrophobic have increased potency (use lower concentrations)
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27
Q

Describe type A-alpha nerve fibers

A

Function: proprioception and motor

Location: efferent to muscle

Heavy myelination

Very Fast conduction (70-120m/s)

Fiber size = 12-20 um

Sensitivity to Block = +

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28
Q

Describe type A-beta nerve fibers

A

Function: touch, pressure

Location: afferent from skin/joint

Heavy myelination

Very fast conduction (30-70 m/s)

Fiber size = 5-12 um

Sensitivity to Block = ++

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29
Q

Describe type A-gamma nerve fibers

A

Function: muscle tone (muscle spindles)

Location: efferent to muscle

Heavy myelination

Fast conduction (15-30 m/s)

Fiber size = 3-6 um

Sensitivity to Block = ++

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30
Q

Describe type A-delta nerve fibers

A

Function: pain, temp, touch

Location: afferent sensory

Heavy myelination

Fast conduction (5-25 m/s)

Fiber size = 2-5 um

Sensitivity to Block = +++

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31
Q

Describe type B nerve fibers

A

Function: preganglionic autonomic

Location: preganglionic SNS

Light myelination

Medium conduction (3-15 m/s)

Fiber size = <3 um

Sensitivity to Block = ++++

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32
Q

Describe type C nerve fibers

A

Function: dorsal root (dC)= pain – sympathetic (sC) = postganglionic autonomic

Location: dC = afferent sensory – sC = postganglionic SNS

No myelination

Slow conduction (dC 0.5-2.3 m/s – sC 0.7-2.3 m/s)

Fiber size = 0.3-1.3 um

Sensitivity to Block = ++++

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33
Q

What is the minimum concentration (Cm) of LA and what affects it?

A

The minimum concentration of LA necessary to produce conduction blockade of nerve impulses

Affected by:

  • Nerve fiber diameter (larger fibers require higher concentrations of LA) – Cm of motor = 2x Cm of sensory
  • pH (increased pH decreases Cm)
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34
Q

Why must a minimal length of myelinated nerve fiber be exposed to an adequate concentration of LA for conduction blockade to occur?

A

Because if only one node of Ranvier is blocked, the nerve impulse can jump (skip) across this node and conduction blockade doesn’t occur

  • For blockade of A fiber to occur, it is necessary to expose at least 2 and preferably 3 successive nodes of Ranvier to LA
  • Both types of pain fibers (A-delta/C fibers) are blocked by similar concentrations of LA
  • Preganglionic B fibers are more readily blocked by LA than any fiber
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35
Q

What is the duration of a nerve block determined by?

A

The ability of the LA molecules to stay near the nerve (Uptake & Distribution)

*Plasma concentration is determined by rate of tissue distribution and rate of clearance of a drug and protein binding

36
Q

What are the three factors that determine the duration of a nerve block?

A
  • Lipid solubility (important for redistribution & potency)
  • Vascularity of the tissue
  • The presence of vasoconstrictors which prevent vascular uptake of the LA molecules (addition of Epi prolongs block)
37
Q

Rank the nerve fibers from fastest to slowest onset of nerve block

A 
Fastest
     -B
     -A-delta
     -A-gamma
     -A-beta
     -A-alpha
     -C
Slowest

*Nerve block recovery is the opposite

38
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
  9. Motor function
39
Q

What are the desirable properties of a local anesthetic agent?

A
  • Reversible conduction blockade
  • Compatible with vasoconstrictors
  • Short (fast) onset
  • Non-irritating
  • Low potential for toxicity (LAST)
  • Long duration, possibly short recovery period
  • Effective in different delivery modalities
40
Q

What is the absorption of a LA from its site of injection into the systemic circulation influenced by?

A
  • Site of injection (tracheal mucosa more rapid absorption/higher blood levels)
  • Dose
  • Use of epinephrine (vasoconstrictors reduce blood flow, thus reduces rate of systemic absorption/peak serum levels)
  • Pharmacologic characteristics of the LA

*after systemic absorption, amides are more widely distributed in tissues than esters

41
Q

How are Ester LAs metabolized?

A

Undergo hydrolysis by circulating pseudocholinesterase (plasma cholinesterase)

  • rate varies (Chloroprocaine > Procaine > Tetracaine)
  • exception is cocaine (this undergoes significant metabolism in the liver)
42
Q

What is unique about Benzocaine?

A

it is a weak ACID – pKa 3.5 (exists predominantly in nonionized form at body pH)

Fast onset, used topically only
Duration = 30-60 minutes
Brief spray of 20% delivers the recommended dose of 200-300 mg

43
Q

What are characteristics of Cocaine?

A

Ester LA – naturally occurring

  • blocks nerve impulses
  • local vasoconstriction due to inhibition of local norepinephrine reuptake
  • euphoria due to blockade of dopamine reuptake in the CNS
  • good for LA in nasal passages and other areas where LA and vasoconstriction is desired
44
Q

What kind of potency, onset, and duration does Procaine have?

A

Low Potency

Slow Onset

Short Duration

*first synthetic LA

45
Q

What is unique about 2-Chloroprocaine?

A

Addition of Chlorine atom increased hydrolysis by 3.5x compared with Procaine

Minimal placental transfer even with 40% decrease in plasma cholinesterase

46
Q

What are the characteristics of Tetracaine?

A

Longest duration Ester LA

More potent, long duration, slowly metabolized due to no cholinesterase in SA space

Too toxic for use in peripheral blocks (OK for long acting spinal blocks)

47
Q

Where is plasma cholinesterase made and what affects it?

A

Made in the liver

Affect by:

  • Liver disease
  • High BUN
  • Pregnancy
  • Chemo drugs
  • Atypical pseudocholinesterase
48
Q

How are Amide LAs metabolized?

A

In the liver by dealkylation of an ethyl group from the tertiary amine and hydroxylation
-more complex and slower than metabolism of Esters (systemic toxicity more likely)

Prilocaine > Lidocaine = Mepivacaine > Etidocaine = Bupivacaine = Ropivacaine

*Hepatic blood flow/Liver function are important

49
Q

What percent of local anesthetics (unchanged drug) undergo renal excretion?

A

The poor water solubility of LA limits its renal excretion of unchanged drug to less than 5%

  • exception is Cocaine which is 10-12% of unchanged drug
  • Water-soluble metabolites of LA are readily excreted in urine
50
Q

What are the characteristics of Lidocaine?

A
  • Rapid absorption parenteral, GI, and respiratory
  • Oxidative dealkylation yields cardioprotective metabolite
  • Intermediate duration
  • Has vasodilation properties (rapid distribution)
  • 1.5-2.0% for most regional blocks for surgery
  • More dilute concentrations for pain management
51
Q

What are the characteristics of Mepivacaine?

A
  • Intermediate duration
  • Pharmacology similar to Lidocaine (lacks vasodilation of Lidocaine)
  • Similar onset, slight longer duration (3-6 hours)
  • Toxic to neonates (NOT used in OB)
52
Q

What are the characteristics of Prilocaine?

A
  • Intermediate duration, but most rapid metabolism
  • Pharmacology similar to Lidocaine
  • Lacks vasodilation, increased Vd, limits CNS toxicity
  • Causes methemoglobinemia (usually requires dose of 8mg/kg – treat with methylene blue 1-2 mg/kg)
  • Uncommon for peripheral nerve blocks
53
Q

What are the characteristics of Etidocaine?

A
  • Longer duration
  • Onset like Lidocaine, duration like bupivacaine
  • Alkyl substitution on aliphatic group between the hydrophilic amine and amide linkage increases lipid solubility (increases potency/duration)
  • Downside is prolonged motor block that outlasts sensory block
  • Not useful for peripheral nerve blocks
54
Q

What are the characteristics of Bupivacaine?

A
  • Long duration (longer when Epi added)
  • Slower onset, longer variable duration (2-3 hr for spinal dose – 12-24 hr for peripheral block)
  • Cardiotoxic (cumulative and greater than expected related to LA potency– direct injection into medulla with produce ventricular arrhythmias – difficult to dissociate from Na+ channels)
  • Widely used for peripheral blocks in dilute concentrations (<0.5%)
  • Continuous infusions usually <0.1% c/s opioid
  • Careful use in OB epidurals (<0.25%)
55
Q

What are the characteristics of Ropivacaine?

A
  • S-enantiomer of Bupivacaine (lower toxicity)
  • Slower uptake and thus lower blood levels
  • Extensive hepatic metabolism
  • Less potent than Bupivacaine at lower concentrations (<0.5%)
  • > 0.5% dense block with slightly shorter duration than Bupivacaine
  • At 0.75% onset is fast, CNS and cardiotoxicity are reduced, and motor block is less than Bupivacaine
  • Very popular for peripheral nerve blocks
56
Q

What are the characteristics of Levobupivacaine?

A
  • Another single enantiomer version of Bupivacaine
  • Less well studied than Ropivacaine
  • Appears to work in similar fashion to Ropivacaine
  • Less toxic than Bupivacaine with similar onset and duration
57
Q

What is the onset and duration of anesthesia/analgesia for 3% 2-Chloroprocaine with/without epinephrine?

A

3% 2-Chloroprocaine:

  • Onset = 10-15 min
  • Duration of Anesthesia = 1 hour
  • Duration of Analgesia = 2 hours

3% 2-Chloroprocaine w/ Epi:

  • Onset = 10-15 min
  • Duration of Anesthesia = 1.5-2 hours
  • Duration of Analgesia = 2-3 hours
58
Q

What is the onset and duration of anesthesia/analgesia for 1.5% Mepivacaine with/without epinephrine?

A
  1. 5% Mepivacaine:
    - Onset = 10-20 min
    - Duration Anesthesia = 2-3 hrs
    - Duration Analgesia = 3-5 hrs
  2. 5% Mepivacaine w/ Epi:
    - Onset = 10-20 min
    - Duration Anesthesia = 2-5 hrs
    - Duration Analgesia = 3-8 hrs
59
Q

What is the onset and duration of anesthesia/analgesia for 2% Lidocaine with Epi?

A

Onset = 10-20 min

Duration Anesthesia = 2-5 hrs

Duration Analgesia = 3-8 hrs

60
Q

What is the onset and duration of anesthesia/analgesia for 0.5% Ropivacaine and 0.75% Ropivacaine?

A
  1. 5% Ropivacaine:
    - Onset = 15-30 min
    - Duration Anesthesia = 4-8 hrs
    - Duration Analgesia = 5-12 hrs
  2. 75% Ropivacaine:
    - Onset = 10-15 min
    - Duration Anesthesia = 5-10 hrs
    - Duration Analgesia = 6-24 hrs
61
Q

What is the onset and duration of anesthesia/analgesia for 0.5% Bupivacaine w/ Epinephrine?

A

Onset = 15-30 min

Duration Anesthesia = 5-15 hrs

Duration Analgesia = 6-30 hrs

62
Q

How do you calculate LA doses?

A

0.25% = 2.5 mg/mL – 0.5% = 5 mg/mL – 1% = 10 mg/mL – 2% = 20 mg/mL

Total Dose = mg/mL x mLs given
-Ex: 50 mL of 0.25% Bupivacaine contains 50 mL x 2.5 mg/mL = 125mg Bupivacaine

*when mixing LA together one drug dilute the other
-Ex: 40 mL of 50:50 mix 2% lidocaine/0.5% bupivacaine
Lidocaine: 20mL x 20mg/mL = 400 mg — Bupivacaine: 20mL x 5mg/mL = 100 mg
Final Concentration: 100mg / 40mL = 2.5mg Bupivacaine per mL of injectate — 400mg / 40mL = 10mg Lidocaine per mL of injectate

63
Q

What is the onset, duration after infiltration, max single dose, pKa, and protein binding for Procaine?

A

Onset = Slow

Duration = 45-60 min

Max Single Dose = 500 mg

pKa = 8.9

Protein Binding = 6%

64
Q

What is the onset, duration after infiltration, max single dose, pKa, and protein binding for Chloroprocaine?

A

Onset = Rapid

Duration = 30-45 min

Max Single Dose = 600mg

pKa = 8.7

Protein binding = ?

65
Q

What is the onset, duration after infiltration, max single dose, pKa, and protein binding for Tetracaine?

A

Onset = Slow

Duration = 1-3 hours

Max Single Dose = 100mg (topical)

pKa = 8.5

Protein Binding = 76%

66
Q

What is the onset, duration after infiltration, max single dose, toxic plasma concentration, pKa, and protein binding for Lidocaine?

A 
Onset = Rapid
Duration = 1-2 hours
Max Single Dose = 300mg (4 mg/kg - regional; 4.5 mg/kg infiltration)
Toxic Plasma Concentration = >5 mcg/mL
pKa = 7.9
Protein Binding = 70%
67
Q

What is the onset, duration after infiltration, max single dose, toxic plasma concentration, pKa, and protein binding for Priolocaine?

A 
Onset = Slow
Duration = 1-2 hours
Max Single Dose = 400mg
Toxic >5 ug/mL
pKa = 7.9
Protein Binding = 55%
68
Q

What is the onset, duration after infiltration, max single dose, toxic plasma concentration, pKa, and protein binding for Mepivacaine?

A 
Onset = Slow
Duration = 1.5-3 hours
Max Single Dose = 300mg
Toxic Plasma Concentration >5 ug/mL
pKa = 7.6
Protein Binding = 77%
69
Q

What is the onset, duration after infiltration, max single dose, toxic plasma concentration, pKa, and protein binding for Bupivacaine?

A 
Onset = Slow
Duration = 4-8 hours
Max Single Dose = 175mg
Toxic >3 ug/mL
pKa = 8.1
Protein Binding = 95%

*Levobupivacaine protein binding = >97%

70
Q

What is the onset, duration after infiltration, max single dose, toxic plasma concentration, pKa, and protein binding for Ropivacaine

A 
Onset = Slow
Duration = 4-8 hours
Max Single Dose = 200mg
Toxic >4 ug/mL
pKa = 8.1
Protein Binding = 94%
71
Q

What is plasma concentration of LA determined by?

A
  • Dose
  • Rate of absorption
  • Site of injection
  • Biotransformation and Elimination

*same dose of LA injected in different locations/patients will lead to very different peak plasma levels

72
Q

What is the progression of Local Anesthetic Toxicity (LAST) symptoms?

A
  1. Drowsiness
  2. Paresthesia in the mouth and tongue
  3. Tinnitus, auditory hallucination
  4. Muscular spams
  5. Seizures
  6. Coma
  7. Respiratory arrest
  8. Cardiac arrest
73
Q

How do you treat LAST?

A
  1. Airway Management/Seizure Precautions
  2. BLS/ACLS (avoid lidocaine, Ca+ channel blockers, vasopressin, beta-blockers, and reduce Epi doses <1 mcg/kg)
  3. 20% Lipid Emulsion Therapy (binds the LA and gets eliminated)
    • Bolus 1.5 mL/kg over 1 min
    • Infusion 0.25 mL/kg/min
    • Repeat dose 1-2x if needed
    • Increase infusion to 0.5 mL/kg/min
    • Upper limit of 10 mL/kg over 30 min
74
Q

List the fastest to slowest rates of venous LA (Blood flow and LA absorption)

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

75
Q

What are adverse effects of LA?

A
  • Allergic Reaction (rare <1%, usually symptoms from excess plasma concentration of LA, may be rxn to preservative - methylparaben)
  • Systemic Toxicity (uncommon)
  • Neural Tissue Toxicity
  • Transient Neurologic Syndrome
  • Cauda Equina Syndrome
  • Anterior Spinal Artery Syndrome
  • Methemoglobinemia
76
Q

Define the following adverse effect of local anesthetics: Neural Tissue Toxicity

A

Very rare event in epidural and spinals

Lidocaine more concerning in spinal: increased Ca+ concentration may be mechanism for toxicity

77
Q

Define the following adverse effect of local anesthetics: Transient Neurologic Syndrome (TNS)

A

Moderate to severe pain in low back, buttocks, and posterior thighs 6-36 hours after spinal

  • Unknown mechanism – Greatest incidence following intrathecal injection of Lidocaine
  • Sensory and motor neurologic exam is not abnormal
  • Full recovery from symptoms usually occurs within 1-7 days – treated with NSAIDs and trigger point injections
78
Q

Define the following adverse effect of local anesthetics: Cauda Equina Syndrome

A

Occurs when diffuse injury across the lumbosacral plexus produces varying degrees of sensory anesthesia, bowel/bladder dysfunction, and paraplegia

-associated with use of hyperbaric 5% Lidocaine for continuous spinal anesthesia (microcatheters used during spinals contributed to inhomogeneous distribution of the LA solution, with pooling of high concentrations on certain dependent or stretched nerves)

79
Q

Define the following adverse effect of local anesthetics: Anterior Spinal Artery Syndrome

A

Lower extremity paresis with a variable sensory deficit (usually diagnosed as neural blockade resolves)

  • Etiology is uncertain – although thrombosis or spasm of anterior spinal artery is possible, as well as effects of HoTN or vasoconstrictor drugs
  • Addition of Epi to LA solutions has been implicated as theoretical cause
  • Advanced age and PVD may predispose patients to development

*difficult to distinguish symptoms due to anterior spinal artery syndrome from those caused by spinal cord compression produced by an epidural abscess or hematoma

80
Q

Define the following adverse effect of local anesthetics: Methemoglobinemia

A

Causes oxidation of hemoglobin to methemoglobin (more rapidly than methemoglobin is reduced to hbg) – decreases oxygen carrying capacity

  • Rare but potentially life threatening
  • Known oxidant substances: Benzocaine, Prilocaine, Lidocaine (topicals)
  • Central cyanosis (symptoms) usually occurs when MetHbg exceeds 15%
  • Treatment: 1-2 mg/kg IV Methylene blue over 5 min
81
Q

What are the effects of Cocaine Toxicity?

A

Causes SNS effects, coronary vasospasm, myocardial ischemia/infarction, and ventricular dysrhythmias (coronary oxygen delivery is decreased by the effects of cocaine on coronary blood flow)

  • Even remote cocaine use can result in MI/HoTN for as long as 6 weeks after discontinuing cocaine use
  • Effects of topical cocaine occur within 15-40 minutes w/ duration of 1 hour
  • Effects of IV/Smoked cocaine occur within 5 minutes
82
Q

What is the Tumescent Technique?

A

Subcutaneous placement of large volumes of diluted Lidocaine with Epi – used for liposuction
-0.05-0.1% Lidocaine & 1:100,000 Epi

  • Results in sufficient LA for liposuction, virtually bloodless aspirates, and prolonged postop analgesia
  • Max Lidocaine w/ Epi Dose = 35-55 mg/kg (compared to the normal 7 mg/kg) — 1g fat absorbs 1mg Lidocaine acting as a tissue buffering system
  • Complications: lidocaine toxicity, cardiac depression, contractility
  • Overall complication rate in nationwide QI study was 0.7% in which 0.57% = minor and 0.14% = major complications
83
Q

What are the different uses of Local Anesthetics?

A
  • Topical
  • Local
  • Peripheral Nerve Block
  • IV Regional
  • Epidural
  • Spinal (adverse effects not due to the drug, but due to causing sympathectomy)
  • Suppress Cardiac Dysrhythmia (Lidocaine)
  • Suppress grand mal seizure (low does lido or mepiv)
  • Anti-inflammatory (have procoagulant activity)
  • Antibacterial Effects (Tetra>Bupiv>Lido)
84
Q

Of the amide local anesthetics, which are considered racemic mixtures?

A

Bupivacaine and Mepivacine

85
Q

What is the Lateral Hydrophobic Pathway?

A

The pathway that allows some local anesthetics to reach receptors within the lipid membrane rather than migrate through the membrane

86
Q

Which local anesthetics would be the better choice for epidural anesthesia during prolonged labor with concern for fetal acidosis?

A

Bupivacaine and Chloroprocaine

87
Q

Describe the phenomenon of Frequency Dependent Blockade

A

describes additional conduction blockade developing after each sodium channel opens after local anesthetic binding

Anesthesia Pharm (18 decks)

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