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Regional Final > LA Part 1 And 2 > Flashcards

LA Part 1 And 2 Flashcards

1
Q

MOA @ receptor and cellular level of LA

A

Block Na+ voltage gated channels
Block saltatory conduction
Pool at Nodes of Ranvier on Axon

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2
Q

What type of fibers are blocked first

What type of fibers recover first

A

Blocked first: small sensory fibers “size principle” then motor fibers; diffusion of LA blocks mantle before motor nerves in the core
Recover first: motor fibers in middle/ very vascular

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3
Q

Equation for acid/base chemicals in aqueous solution

A

Henderson- Hasselback equation

B + H BH+ (protonated, ionized form, lipid insoluble)

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4
Q

Describe how LA work (non-ionized –> ionized)

A

B (unprotonated/non ionized) moves through bi lipid layer where it binds with H+ (in axoplasm) to become protonated/ionized so it can bind to the alpha subunit of Na+ voltage gated channels

Has to be unionized to get in and ionized to exert action on alpha subunit

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5
Q

Why don’t LA work well in acidic environment

A

Too much of LA is ionized and cannot cross bilipid layer.

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6
Q

Describe how NaHCO-3 speeds the onset of a LA

A

Bicarbonate works as a buffer to speed onset because makes more unprotonated/unionized available to cross into lipid bilayer to get protonated/ionized
Add 1mEq per 10mL LA

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7
Q

What type of channels do the LA typically bind to

A

Inactivated Na+ channels on alpha subunit

Rapid firing of axon results in increased activated channels (have individual move extremity right after placing block to shorten onset time of block)

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8
Q

Which type of fibers are easily blocked?

A

Small; myelinated

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9
Q

Which type of fibers are most resistant to LA?

A

C fibers are most resistant (abundant, slow velocity, contain resistant Na+ voltage gated channels and unmyelinated)
They are the LAST to be blocked

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10
Q

How are mixed nerves blocked?

A

Smaller/sensory/myelinated fibers of the mantle are blocked first followed by the motor/core fibers.

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11
Q

Which type of pain is the first to disappear?

A

Fast pain (a delta fibers)

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12
Q

Which type of pain is the most resistant to LA?

A

Slow pain (type C fibers)

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13
Q

Describe onset to LA in regards to a-alpha, a-beta, delta gamma, B and C nerve fibers.

A

Recovery is inversely proportional to onset

Onset: B fibers (preganglionic; can’t release NE or E; hypotension occurs)
A delta: pain (fast), cold, touch
A gamma: motor to muscle spindles
A beta: touch, pressure
A alpha: somatic motor; proprioception (muscle spindles, golgi tendon bodies)
C fibers: slow pain/dorsal root/ sympathetic/ post ganglionic

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14
Q

What is the muscle spindle responsible for?

A

Plays a role in proprioception (where we are in time and space) and is responsible for stretch and speed of stretch

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15
Q

What is the role of Golgi Tendon Bodies?

A

Plays a role in proprioception (where we are in time and space) and responsible for tension.

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16
Q

Describe order (fastest –> slowest) in which fibers recover, in regards to a alpha, gamma, delta, etc.

A

C fibers: slow pain
A alpha: somatic, proprioception
A beta: touch pressure
A gamma: motor to muscle spindles; reflex arch
A delta: fast pain (cold, touch)
Preganglionic B Fibers: hypotension ( less of a problem with peripheral nerve block; more of or problem with neuroaxial; paravertebral also can b/c close to neuroaxial)

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17
Q

Why can a patient move their arm before they can feel it?

A

Motor fibers come back faster than sensory fibers.
Have to be careful because can cause injury, requires splints and immobility devices and patient instruction on post op care.

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18
Q

Which LA are amides?

A

Amides= 2 “i’s”
Bupivacaine
Ropivicaine
Lidocaine

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19
Q

Which LA are the Esters?

A

Esters= 1 “i”
Tetracaine
2 chloroprocaine
Novacaine

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20
Q

Describe the R enantiomer and S enantiomer as well as the levorotary and dextrorotary portions.

A

R enantiomer= caRdiac toxicity
S enantiomer= Safe
Levorotary> potent than Dextrorotary

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21
Q

List LA from greatest vasodilating to least vasodilating.

A

Lidocaine Bupivicaine Mepivicaine Ropivicaine
The more vasodilating the solution is the more epi will effect it.
Epi will affect Lidocaine more than Ropivicaine

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22
Q

What law is responsible for LA onset??

A

Fick’s Law ( Rate of Diffusion= Conc. gradient XSurface AreaXdiffusion coefficient/ Membrane thickness)

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23
Q

Describe the 5 Factors that effect the onset of LA

A
  1. Lipid solubility
  2. Concentration
    - the higher the concentration the quicker the onset, but the relationship is not linear and will only marginally increase onset; logarithmic
  3. Proximity of the drug to the nerve (diffusion dependent)
    - intraneural injections
  4. Physical characteristics of tissue surrounding the nerve
    - vascularity, presence of connective tissue, and membrane thickness
  5. pH (lipid solubility): more ionized the less lipid soluble (because can’t get through membrane)
    - properties of drug
    - tissue
    - presence of bicarbonate
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24
Q

How does PKA effect onset?

A

50% is ionized and 50% unionized
Normal physiologic > ionized than non ionized why bicarbonate helps/ acts as a buffer to get > unionized through lipid bilayer

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25
Q

List the 7 factors effecting LA duration?

A
  1. Physical characteristics of drug
  2. Lipid solubility
    - correlation with protein binding but without a direct relationship
    - more tightly bound to neural tissue and more difficult to displace
    - free form of highly soluble drugs is low (protein bound) –> resistant to metabolism Ex: bupivicaine
  3. Vascularity of tissue
  4. Nerve being blocked (sciatic vs brachial plexus)
  5. Presence of vasoconstrictor adjuncts
  6. Intrinsic vasodilator properties of the drug
  7. Dose = concentration X volume
    - higher dose = longer duration
    - concentration has the greatest effect on duration, more so than volume (surgical anesthetic vs. analgesic)
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26
Q

List the LA in order from Fastest onset/duration –> longest onset/duration

A 
Lidocaine 2% 
Mepivicaine 1.5%
Ropivicaine 0.75%
Bupivicaine 0.5% 
Levobupiviaine 0.5% 
Exparel NA

Little Men Run Backwards
(%’s are for surgical analgesia)

27
Q

What state are LA pharmacologically active?

A

Free, unbound state

28
Q

What are the protein binding compartments?

A

Alpha 1 acid glycoprotein (high affinity/ low capacity)

Albumin (motor storage reservoir has higher capacity)

29
Q

How does protein binding correlate to DOA?

A

Protein binding correlates but is not directly associated with the DOA.
The greater the lipid solubility the greater the protein binding which creates longer duration (resists metabolism)
LA are more likely to highly bind to lipid rich axonal membranes longer

30
Q

Which 2 populations have less AAG (alpha 1 acid glycoprotein)

A

Kids

Pregnant Women

31
Q

Protein binding of LA is concentration and pH dependent? True or false

A

True: Acidosis and toxicity: small changes in pH cause dramatic changes in level of free drug, this is why LA don’t work in acidic tissues and why acidic people are at risk for LAST.

Malnourished/ low albumin= at higher risk for last

32
Q

What are the 5 factors associated with the selection of LA?

A
  1. Purpose of block
    - surgical vs analgesic
    - determines concentration used
  2. Volume of LA
    - block dependent
  3. Duration desired
    - should a catheter be considered? Uncontrolled pain > 24 hrs re evaluate POD #1
  4. Toxicity issues (ropivicaine best, but not the cheapest)
  5. Onset and duration
    - when is it important? Timing of block
33
Q

What does mixing short and long acting LA do to the onset and duration?

A

Mixing LA’s does not change the onset and makes it have significantly shorter DOA.
Don’t do it!

34
Q

How long is the onset for all PNB

A

10 minutes

35
Q

4 things that duration of block dependent on?

A

Type of block (uptake)
Drug used
Concentration
Adjuncts

36
Q

Duration of block with ropivicaine and bupivicaine

A

Long acting 16-24 hours

37
Q

Duration of block when Mepivicaine used

A

Intermediate; usually 3 hours

38
Q

Duration of block when using lidocaine and 2 chloroprocaine

A

1-2 hours

39
Q

How does concentration affect block onset and duration

A

Higher concentration= longer block and shorter onset

40
Q

3 reasons rescue blocks are done

A

Block has failed or has nerve sparing properties
Ineffective in providing analgesia or doesn’t cover appropriate dermatome
When the duration of LA has been exceeded

41
Q

Uptake of Local Anesthetics Based on Regional Anesthetic Technique highest uptake to lowest uptake

A 
In Time I Can Please Everyone But Sally and Susan
Intravenous
Tracheal
Intercostal
Caudal
Paracervical
Epidural
Brachial
Sciatic
Subcutaneous
42
Q

When are you most likely to see symptoms of LAST?

A

Majority happens within the first hour; need to monitor patient for 30 minutes after block

43
Q

Signs first detected with LAST

A

CNS signs are first signs but if under GA you will not see the CNS signs and will see cardiac signs first

44
Q

What are the cardiac effects of LAST?

A

Slow rate of depolarization of Purkinje fibers and ventricular muscle blocking fast Na channels (lengthened PR interval and QRS complex)

45
Q

What effects do LA have on inotropy?

A

Dose dependent depression from negative modulation of Ca++ release from SR; vasodilation; decreased inotropy

46
Q

What do you want to avoid in last; will decrease effect of lipids

A

Want to avoid acidosis, hypercarbia and hypoxemia

47
Q

What effect does acidosis have on LAST

A

Acidosis displaces bupivicaine off protein molecule; most of LA bound to protein 80-85% bound to protein; in acidosis it becomes unbound; free and can bind to cardiac Myocyte

48
Q

3 medications that decrease threshold even further for cardiac toxicity

A

Beta blockers, Ca Channel Blockers, and digoxin

49
Q

What is another name for CNS toxicity signs?

A

Prodromal signs

50
Q

What are some patient characteristics that can increase risk of LAST

A

Extremes of age < 16 or > 60 years
Low muscle mass- neonates, infants and debilitated elderly
Female> male
Comordities
- cardiac disease, esp arrhythmias, conduction abnormalities, ischemia, and CHF
- liver disease
- metabolic disease, especially DM, isovolermeric academia, mitochondrial disease, and carnitine deficiency
- CNS diseases
- Low plasma protein binding- liver disease, malnourished, infants, pregnancy

51
Q

Which LA has lowest safety margin

A

Bupivicaine; but LA such as ropivicaine and lidocaine still account for a significant proportion of LAST events

52
Q

Is seizure more likely in epidural or PNB?

A

5 x’s more likely in PNB than epidural block

53
Q

What are prodromal signs?

A

CNS toxicity, metallic taste, tinnitus, dizziness, confusion, seizure
- not necessarily fatal but he lipids

54
Q

Signs and symptoms of cardiac toxicity?

A

Conduction delays, dysrhythmias, bradycardia/hypotension, and cardiac arrest

55
Q

If LA have direct access to brain how long will it take to see s/sx?

A

60 seconds

56
Q

How long will it take if the patient has IV injection

A

1-5 minutes suggests intermittent IV injection, lower extremity injection or delayed tissue absorption

57
Q

How do lipids work

A

Lipids bind to bupivicaine (lipid sink) binds up the liposome and takes it away from cardiac muscle and CNS organs to the liver and increases metabolism and breaks down bupivicaine ofver time

58
Q

Ways to prevent IV injection

A

Arterial seizures in carotid circulation; anything above clavicle= brain
Speed of injection, inject slowly
Monitor for prodromal signs
Multiple needle redirections and small aliquot injections 2-3 mL at a time
Aspirating for blood Q 5 mL; look in tubing 2% false negative
Awake and monitoring patient
Use ultrasound (no guarantee)
Epi 2.5-5 mcg/mL= great vascular marker

59
Q

Why would epi not be a reliable marker for IV injection

A

If patient takes beta blocker not reliable

60
Q

What blocks can you not put epi in?

A

Wrist blocks, finger blocks, toe blocks, ankle block, subgluteal, infragluteal, and subgluteal

61
Q

Should you put epi in perineural blocks?

A

No it can decrease blood flow and increase neural toxicity and neural injury

62
Q

Why can epi cause decrease in diastolic BP

A

Because beta 2; putting epi in and right around skeletal muscle which has a lot of beta 2 receptors; get some vasodilation

  • prolongs duration of block
  • prolongs post op analgesia
63
Q

How does clonidine and dexemetotomidine affect LA

A

Clonidine: problem because pt gets hypotension
Dexmedetomidine: 1mcg/kg MOA starts to hyperpolarize cell membrane; motor and sensory block significant prolonged with use of alpha 2 agonists

64
Q

What should the dose be of dexamethasone be if the patient has neuropathy or is a diabetic?

A

2mg/block; 4 mg/block is fine in patients with no diabetic or neuropathy
Giving 10mg IV can even help extend block duration; give it while pt asleep because scrotal burning

Regional Final (3 decks)

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