Exam 1 Spinal & Epidural Neuraxial Anesthesia [06/03/24] Flashcards

1
Q

What is the effect of neuraxial anesthesia on the pulmonary system?

A
  • Usually minimal impact
  • Even with high (T4) thoracic level dermatome spread of local anesthetic: Tidal volume, RR, inspiratory reserve volume, or ABG unchanged.
  • ERV decreased
  • Small decreases in vital capacity (Loss of abdominal muscle contribution in forced expiration)
  • High thoracic blockade can result in the blockade of accessory muscles of respiration (intercostal and abdominal muscles)

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2
Q

What are special considerations for neuraxial anesthesia for the pulmonary system?

A
  • Use caution in COPD, Pickwickian syndrome
  • Feelings of dyspnea in normal population (extremely common); very troublesome.
  • This is due to the loss of sensory feedback from the chest area
  • Lose ability take big breaths and strong cough

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image from the internet
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3
Q

What causes apnea in regards to neuraxial anesthesia?

A
  • Apnea is typically due to reduced blood flow to the brainstem, affecting the brain’s breathing centers.
  • High concentrations of local anesthetics in the spinal fluid rarely cause nerve paralysis that stops breathing.

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4
Q

Flow volume loops graph

A

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5
Q

What are the componets of vital capacity?

A
  • VT
  • IRV
  • ERV

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6
Q

Phrenic nerve orginates from what levels of the spine?

A
  • C3, C4, C5

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7
Q

For the GI system, parasympathetic innervation is primarily via what? Sympathetic innervation?

A
  • Parasympathetic innervation is via the vagus nerve (originates medulla)
  • Sympathetic innervation of GI tract stems from T5-L2

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8
Q

What is the function of parasympathetic afferent and parasympathetic efferent?

A
  • Parasympathetic AFFERENT: transmits sensations of satiety, distension, and nausea
  • Parasympathetic EFFERENT: tonic contractions, sphincter relaxation, peristalsis, and secretion.

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9
Q

What is the function of sympathetic afferent and sympathetic efferent for the GI system?

A
  • Sympathetic AFFERENT: transmit visceral pain
  • Sympathetic EFFERENT: inhibit peristalsis and gastric secretion and cause sphincter contraction and vasoconstriction

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10
Q

Sympathetic innervation of GI tract stems from

A
  • T5-L2

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11
Q

What is the Impact of Neuraxial Anesthesia on GI system?

A
  • Reduces Sympathetic Tone: Local anesthetics used in neuraxial blocks decrease the activity of sympathetic nerves.
  • Increases Parasympathetic Activity: With less sympathetic inhibition, the parasympathetic system becomes more dominant.
  • Resulting Changes in Unopposed Vagal Tone[this is parasympathetic]

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12
Q

The unopposed vagal tone on the GI system from neuraxial anesthesia results in?

A
  • Relaxes Sphincters
  • Increases Peristalsis
  • Small, contracted gut with active peristalsis
  • 20% incidence of N/V
  • Increased GI blood flow
  • Nausea and vomiting (20% of the patients)
  • Reduces postoperative incidence of ileus in abdominal surgery

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13
Q

20% of nausea related to central neuraxial is d/t unopposed effect. What is the cause of the other 80% of nausea?

A

The remaining 80% is from sympathethecomy due to reduced blood supply in the chemotaxis center resulting in nausea.

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14
Q

What are the genitourinary effects of Neuraxial Anesthesia.

A
  • No change in renal blood flow when MAP is maintained
  • Sympathetic blockade above T10 affects bladder control
  • Urinary sphincter tone relaxed

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15
Q

How does the addition of Neuraxial Opioids affects the GU system?

A

Addition of Neuraxial Opioids:
* Decrease in detrusor contraction
* Increase in bladder capacitance
* These changes lead to urinary retention/incontinence and need for foley catheter with neuraxial anesthesia

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16
Q

What are the metabolic/endocrine effects of Neuraxial Anesthesia.

A
  • Neuraxial blockade can partially suppress (major invasive surgery) or totally block (lower extremity) neuroendocrine response.
  • Maximal benefits occurs if the neuraxial blockade occurs before the surgical stimulus
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17
Q

The activation of somatic and visceral afferent fibers from pain, tissue trauma, and inflammation causes?

What does neuraxial anesthesia do?

A
  • Elevated cortisol, epinephrine, norepinephrine, vasopressin, activation of renin-angiotensin-aldosterone system.
  • neuraxial anesthesia reduces this which is good.

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18
Q

What are local anesthetics made of?

A
  1. Aromatic or beneze ring
  2. Intermediate chain
  3. Tertiary amine

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19
Q

What does the aromatic ring, intermediate chain, and tertiary amine group determine?

A
  1. Aromatic - lipophilic
  2. Intermediate - drug class, metabolism, allergic potential.
  3. Tertiary amine - hydrophilic, accepts protons.

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20
Q

What metabolizes esters?
What metabolizes amides?

A
  • Esteres: pseudocholinesterase
  • Amides: Hepatic P450

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21
Q

What LA is an exception to the metabolization rule?

A
  • Cocaine
  • even though its an ester, it is also metabolized by the liver.

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22
Q

Allergies with LA are seen with esters or amides? why?

A
  • More Common Allergy is with Esters
  • Produces para-aminobenzoic acid (PABA)
  • There’s cross-sensitivity in esters

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23
Q

Can you have an allergic reaction to amides?

A
  • Amide allergic reaction is rare
  • Contains preservative methylparaben, similar to PABA.

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24
Q

T/F: There is no cross sensitivity between esters and amides

A

True

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25
Q

Onset of action of LA is relies on?

A
  • relies on PKA
  • LA are all basic [most]
  • the closer the pK to physiologic pH [7.4], the faster the med goes to the cell.

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26
Q

Potency of LA is related to?

A
  • related to lipid solubility.
  • if staying in the lipophillic part of the muscles,the tissue, or in spine = stays in longer so potency is greater.

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27
Q

Duration of action of LA is realted to?

A
  • Protein binding [A1-acid glycoprotein]

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28
Q

What is the sequence of how blockage of fibers occur when you put LA in central neuroaxial?

A
  • LA inhibition of peripheral nerves occurs in the following order:
    1st: B fibers
    2nd: C fibers
    3rd: Small diameter A fibers
    4th: Large diameter A fibers

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29
Q

Structure of amides vs esteres

A

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30
Q

List the esters and amides mentioned on the powerpoint.

A

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31
Q

T/F: Local anesthetic agents are weak bases, compounds with a pKa close to physiologic pH will have a faster onset of blockade as more molecules remain in the nonionized state.

A

True

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32
Q

List the Factors Influencing Vascular Uptake and Plasma Concentration of Local Anesthetics

A
  1. Site of Injection
  2. Tissue Blood Flow
  3. Physiochemical Properties
  4. Metabolism
  5. Addition of Vasoconstrictor:

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-if area is vasoconstriction, there is less absorption and there’s is more LA in the system.

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33
Q

List the uptake of LA based from high to low blood concentration

A
  1. Intravenous
  2. Tracheal
  3. Intercostal
  4. Caudal
  5. Paracervicle
  6. Epidural
  7. Brachial
  8. Sciatic
  9. SubQ

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If There Is Chest Pain Epidurals Block Sign/Symptoms

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34
Q

What do you do if a bier block leaks?

A
  • do not deflate the cuff
  • gives benzos for seizures if needed.
  • administeed lipid emulsion.

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35
Q

What is baracity?

A
  • Baricity refers to the density of a local anesthetic solution compared to the CSF.

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36
Q

Isobaric

A
  • Density Equal to CSF
  • An isobaric solution has a baricity of 1, meaning its density matches that of CSF.
  • Behavior: Tends to stay in place where it is injected.

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37
Q

Hyperbaric

A
  • Density Greater than CSF
  • A hyperbaric solution has a baricity greater than 1.
  • Behavior: Sinks within the CSF, moving downward from the point of injection.

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38
Q

Hypobaric

A
  • Density Less than CSF
  • A hypobaric solution has a baricity less than 1.
  • Behavior: Rises within the CSF, moving upward from the point of injection.

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39
Q

Hyperbaric, isobaric, hypobaric LA solution chart

A

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40
Q

When giving hyperbaric solutions, and the pt is supine what happens?

A
  • Baracity is related to spinals.
  • the LA will go to the lowest level which is trough.
  • the LA will go to the higherst level which is apex.
  • Trough: T6 and S2
  • Apex: C3 and L3

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41
Q

SAB pharmacology

  • A ____ amount of LA produces a profound block of nerve transmission
  • Spinal Cord uptake of LA occurs d/t ____ nature of the drug
  • Spread of LA occurs in a ____ and ____ direction from the site of injection ____
A
  • small
  • lipid soluble
  • cephalad and caudad, simultaneously

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42
Q

SAB pharmacology

What kind of metabolism occurs in the CSF?
How are LA eliminated?

A
  • NO metabolism occurs in the CSF
  • All LA are eliminated by reuptake [Vascular reabsorption via vessels in the pia mater]

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43
Q

SAB pharmacology

Lipophillic drugs have ____ reuptake b/c they have ____ affinity for epidural fat

A

slow, high

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44
Q

SAB pharmacology

____ has a longer duration of action than lidocaine

A

Bupivicaine

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45
Q

SAB dosing

Spinal Dose at T10 for the following medications:
* Bupivicaine 0.5%-0.75%
* Levobupivicaine 0.5%
* Ropivacaine 0.5%-1%
* 2-Chloroprocaine 3%
* Tetracaine 0.5%-1%

A
  • Bupivicaine 0.5%-0.75%: 10-15mg
  • Levobupivicaine 0.5%: 10-15mg
  • Ropivacaine 0.5%-1%: 12-18mg
  • 2-Chloroprocaine 3%: 30-40mg
  • Tetracaine 0.5%-1%: 6-10mg

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46
Q

SAB dosing

Spinal Dose at T4 for the following medications:
* Bupivicaine 0.5%-0.75%
* Levobupivicaine 0.5%
* Ropivacaine 0.5%-1%
* 2-Chloroprocaine 3%
* Tetracaine 0.5%-1%

A
  • Bupivicaine 0.5%-0.75%: 12-20mg
  • Levobupivicaine 0.5%: 12-20mg
  • Ropivacaine 0.5%-1%: 18-25mg
  • 2-Chloroprocaine 3%: 40-60mg
  • Tetracaine 0.5%-1%: 12-16mg

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47
Q

SAB pharmacology

Onset for the following spinal medications:
* Bupivicaine 0.5%-0.75%
* Levobupivicaine 0.5%
* Ropivacaine 0.5%-1%
* 2-Chloroprocaine 3%
* Tetracaine 0.5%-1%
* All are relatively how long???

A
  • Bupivicaine 0.5%-0.75%: 4-8min
  • Levobupivicaine 0.5%: 4-8min
  • Ropivacaine 0.5%-1%: 3-8min
  • 2-Chloroprocaine 3%: 2-4min
  • Tetracaine 0.5%-1%: 3-5min
  • 5 min

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48
Q

Duration of the following spinal medications:
* Bupivicaine 0.5%-0.75%
* Levobupivicaine 0.5%
* Ropivacaine 0.5%-1%
* 2-Chloroprocaine 3%
* Tetracaine 0.5%-1%

A
  • Bupivicaine 0.5%-0.75%: 130-220min
  • Levobupivicaine 0.5%: 140-230min
  • Ropivacaine 0.5%-1%: 80-210min
  • 2-Chloroprocaine 3%: 40-90min
  • Tetracaine 0.5%-1%: 90-120min

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49
Q

What 2 medications can have epinephrine added to them for spinal blocks? how much longer does the block last with epi added?

A
  • bupivicaine 0.5%-0.75% and tetracaine 0.5%-1%
  • duration increases by 20-50% for each

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50
Q

Which LA medication is not given in spinals?

A

Lidocaine!

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51
Q

For epidurals, the spread of LA is ____ and ____ from the catheter insertion site

A

cephalad and caudad

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52
Q

How is incremental dosing helpful in epidurals? what does it avoid?

A
  • it avoids: accidental “high spinal,” hypotension from rapid autonomic blockade (cardiac arrest), & LA toxiity
  • giving a little bit at a time avoids all of the above and ensures we dont give a whopping dose in the wrong place in addition!

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53
Q

How do we incrementally dose epidurals?

A

5mL at a time

-if you calculate needing a 20mL dose, give 5mL at a time (not all 20mL at once)

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54
Q

If epi is added to an epidural, it can be used as what?

A

an IV marker

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55
Q

when is the onset of an epidural?

A

10-25min

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56
Q

Epidural Pharmacology

In what concentration can we find 2-chloroprocaine?
which concentration is best for surgical anesthesia?

A

comes in 2% and 3%, but 3% is used for surgical anesthesia

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57
Q

Epidural pharmacology

Which LA is popular for OB anesthesia? is it an ester or amide?

A

2-Chloroprocaine, which is an ester LA

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58
Q

Epidural pharmacology

While 2-chloroprocaine has a pka around 8.7 (which is farther from physioologic pH than some other drugs), it still has rapid onset! Why??

A

cocentration!! 3% makes its speed of onset very fast

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59
Q

Does 2-Chloroprocaine have a short or long duration? why? how often will it need to be redosed?

A

duration is short lived b/c it is metabolized by plasma cholinesterase THEREFORE… we need to redose Q45min

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60
Q
  • How do we alkalanize LA solutions?
  • What 4 things does alkalinazation cause?
A
  • Adding NaHCO3 of 1mEq/ml

4 factors
1) increases pH of LA
2) increases concentration of nonionized free base
3) increases rate of diffusion of the drug
4) increases speed of onset of the block

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61
Q

Epidural pharmacology dosing

____ of LA is crucial for determining how ____ the anesthetic block reaches

A

Volume, high

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62
Q

The initial dose of an epidural LA is typically ____mL/ ____ of the spine

A

1-2ml/segment

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63
Q

What kind of dose is used to maintain epidural blocks without letting it wear off too much? how much is it? when should it be administered?

A

Top-up dose
50-75% of the initial dose
Should be administered before the block decreases more than 2 dermatomes

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64
Q

The space available in the epidural area varies. It is smaller in the ____ region than in the ____ so we have greater spread in the ____ meaning we need a ____ dose in the ____ region

A

thoracic
lumbar
thoracic
smaller
thoracic

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65
Q

What determines the density/strength of block in an epidural? What is an easy example to remember this by?

A

Concentration
walking epidural: uses low concentration that manages pain but allows some motor function (ideal for labor)

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66
Q

List the LA epidural drugs in order from fast onset/short duration to slow onset/long duration with their concentrations

A

2-Chloroprocaine 3%
lidocaine 2%
ropivacaine 0.1-0.75%
bupivacaine 0.0625-0.5%
levobupivacaine 0.0625-0.5%

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67
Q

List the duration for the following epidural LA:
2-Chloroprocaine 3%
lidocaine 2%
ropivacaine 0.1-0.75%
bupivacaine 0.0625-0.5%
levobupivacaine 0.0625-0.5%

A

30-90 min
60-120min
140-220min
160-220min
150-225min

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68
Q

List the onset for the following epidural LA:
2-Chloroprocaine 3%
lidocaine 2%
ropivacaine 0.1-0.75%
bupivacaine 0.0625-0.5%
levobupivacaine 0.0625-0.5%

A

5-15min
10-20min
15-20min
15-20min
15-20min

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69
Q

for epidural surgical anesthesia, which concentrations of the LA should be used?

A

the higher concentrations:
2-Chloroprocaine 3%
lidocaine 2%
ropivacaine 0.75%
bupivacaine 0.5%
levobupivacaine 0.5%

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70
Q

What is the best choice LA drug for epidural? 2nd best if that’s not available?

A

2-Chloroprocaine 3%
lidocaine 2%

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71
Q

neuraxial pharmacologic adjuncts provide ____ ____, extends ____, and improves ____ of the block

A

postoperative analgesia
extends duration
density

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72
Q

Opioids, as an adjunct to neuraxial LA, help with ____ and ____, but do not ____ ____ of the block

A

analgesia and density of the block, but do not extend duration

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73
Q

alpha 2 agonists (____ and ____), as adjuncts to LA, improves ____, ____, and ____

A

clonidine and precedex
duration, density, and analgesia

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74
Q

Vasopressors (____ and ____), as adjuncts to LA, extends ____, but has no effect on ____ or ____.
____, specifically, is a good IV marker epidurals: initial ____

A

phenylephrine and epinephrine
duration, but no effect on density or analgesia
epinephrine, bolusing

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75
Q

what agents are currently be investigated as good adjuncts to LA in spinals and epidurals?

A

neostigmine, magnesium, ketamine, and versed

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76
Q

neuraxial opioids have different Pk/PD realtionships when compared to ____, ____, or ____.
We categorized neuraxial opioids into more ____ or ____.

A

IV, IM, or PO
hydrophilic or lipophilic

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77
Q

Which part of the SC is targeted by opioids?

A

substantia gelatinosa of the dorsal horn (Lamina 2)

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78
Q

opioids, as a neuraxial adjunct:
neurotransmission is reduced by decreased ____ and ____, and increased ____

A

cAMP and Ca++ conductance
increased K+ conductance

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79
Q

Opioids mixed with LA results what improvements to a block?
Neuraxial opioids also ____ into ____ ____ and affects opioid receptors throughout the body, providing broader pain relief

A

stronger and more dense
diffuses, general circulation

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80
Q

Neuraxial Opioids

What are the hydrophilic opioids?
Lipophilic?

A

morphine, hydromorphone, and meperidine
fentanyl and sufentanil

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81
Q

Comparing neuraxial opioids

Duration in CSF: hydrophilic v lipophilic

A

hydrophilic stays longer, lipophilic stays shorter

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82
Q

Comparing neuraxial opioids

Spread in the CSF: hydrophilic v. lipophilic

A

hydrophilic: spreads widely affecting a larger area for pain relief (ROSTRAL spread)
lipophilic: limited spread, less rostral spread

S74

83
Q

Comparing neuraxial opioids

Onset hydrophilic v. lipophilic

A

hydrophilic takes longer to start working (30-60min)
lipophilic starts working quickly (5-10min)

S74

84
Q

Comparing neuraxial opioids

Duration of hydrophilic v lipophilic

A

hydrophilic: lasts longer 6-24hrs
lipophilic: shorter effect 2-4hrs

S74

85
Q

Comparing neuraxial opioids

Systemic absorption of hydrophilic v lipophilic

A

hydrophilic: less, hence it stays longer in the CSF
lipophilic: absorbed more by the body

S74

86
Q

Comparing neuraxial opioids

respiratory depression in hydrophilic vs lipophilic agents
Which is better to use for a patient that is going to be going home same day?

A

hydrophilic: occurs later
lipophilic: typically occurs only early after administration (therefore better to use for pts that will be going home)

S74

87
Q

Intrathecal and Epidural dosing of opioids

List the IT, epidural and epidural infusiong doses for the following opioids
sufentanil
fentanyl
hydromorphone
meperidine
morphine

A

sufentanil: 5-10mcg IT, 25-50mcg epidural, 10-20mcg/hr infusion
fentanyl: 10-20mcg IT, 50-100mcg epidural, 25-100mcg/hr infusion
hydromorphone: no IT, 0.5-1mg epidural, 0.1-0.2mg/hr
meperidine: 10mg IT, 25-50mg epidural, 10-60mg/hr infusion
morphine: 0.1-1mg/hr

S75

88
Q

Intrathecal administration:
Location?
how fast does the drug move?
What is the effectiveness?

A

location: directly into IT space
drug movement: opioid quickly diffuses into the SC
effectiveness: more direct and immediate effect on pain b/c it is closer to the nerve roots

S75

89
Q

Epidural administration:
Location?
drug movement?
dosing?

A

Location: Into the epidural space
Drug Movement: The opioid diffuses through the fatty tissue of the epidural space. It then slowly crosses into the dural cuff and into the CSF to reach the spinal cord. Some of the drug also enters the bloodstream.
Dosing: A higher dose is often required because only a portion of the drug reaches the target area in the spinal cord.

S75

90
Q

In what instances might we use an epidural infusion?

A

OB or as an adjunct to GETA

S75

91
Q

Which side effect of neuraxial adjuncts has a 30-100% incidence?

A

pruritis

S76

92
Q

What is the treatment for pruritis r/t neuraxial adjuncts? (3 medications and dose)

A

Benadryl 25-50 mg IV
Naloxone 0.1 mg IV (best)
Buprenex (mixed agonist/antagonist)

S76

93
Q

What can be used as prophylaxis for pruritis r/t neuraxial adjuncts? (3 doses)

A

Minimize the dose of morphine < 300 mcg
Ondansetron 4 mg IV
Nubain 2.5-5.0 mg IV

S76

94
Q

When can respiratory depression happen with opioid use in neruaxial anesthesia?

A

can be delayed [morphine] or immediate first 24 hours [fentanyl/ sufentanil]

slide 77

95
Q

what medication has a higher incidence of respiratory depression for neuraxial adjuncts? Why?

A
  • Higher incidence with morphine (hydrophilic properties)
  • because Hydrophilic nature causes cephalad spread

slide 77

96
Q

what monitoring equipment would you use if pt received intrathecal morphine?

A

Apnea monitoring
* Capnography
* Pulse oximetry
* Alarms

slide 77

97
Q

what is the medication and dose used for reversal of respiratory depression with opioids in neuraxial anesthesia?

A

nalaoxone 0.1-0.2 mg

slide 77

98
Q

what are we worried about with repiratory depression with outpatient surgery?

A

legal implications

slide 77

99
Q
  • What dose of morphine in neuroaxail anesthesia has high insidence of nausea?
  • What dose is nauses almost absent?
A
  • Morphine < 300 mcg
  • doses of < 100 [50-75] mcg almost absent.

slide 78

100
Q

what medication when used in combination during neuraxial anesthesia has high incidence of nausea?

A

Fentanyl/Sufentanil + Morphine has a very high incidence

slide 78

101
Q

What is the treatmeant for nausea r/t opioids used in spinals/epidurals?

A
  • Ondansetron (5 HT antagonist)
  • Naloxone 0.1 mg
  • Phenergan 12.5- 25 mg IM

slide 78

102
Q

what is the percent incidence of urinary retention when using opiods as a pharmacologic adjunct?

A

30-40%

slide 78

103
Q

What are 2 alpha 2 agonists that can be used as neuraxail adjuncts?

A

Clonidine and Dexmedetomidine

slide 79

104
Q

A2 agonist being used as adjuncts do what 2 things to the block?

A

Intensifies and prolongs the block

slide 79

105
Q

A2 agonists prolong sensory and motor blockage by approximately how long?

A

1 hour

slide 79

106
Q

what are common side effects of A2 agonist? [in neuraxial]

A
  • hypotension
  • bradycardia
  • sedation

slide 79

107
Q

what is the dose of dexmedetomidine when used as a neuraxial adjunct?

A

3 mcg

slide 79

108
Q

what is the dose of clonidine when used as a neuraxial adjunct?

A

15-45 mcg

slide 79

109
Q

what is the benefit of using a vasoconstrictor as a neuraxail adjunct?

A

Prolongs action of the LA by reducing blood flow

slide 80

110
Q

Vasoconstrictor Neuraxail Adjunct: Epinephrine dose?

A

0.2- 03 mg “epi wash”

slide 80

111
Q

Vasoconstrictor Neuraxail Adjunct: Phenylephrine Dose?

A

2-5 mg

slide 80

112
Q

When using vasoconstrictors as a neraxial adjunct:
* what is the effect when added with tetracaine?
* What is the effect when added with bupivacain or lidocaine?

A
  • When added with tetracaine - profound increase
  • With bupivacaine or lidocaine - variable increase

slide 80

113
Q

Patients on anticoagulants should avoid neuraxial anesthesia due to the risk of epidural hematoma, whcich can cause what?

A

Can compress the spinal cord, leading to ischemia and permanent neurological damage.

slide 81

114
Q

what are the symptoms of epidural hematomas?

A
  • Lower extremity weakness, numbness.
  • Low back pain.
  • Bowel and bladder dysfunction.

slide 81

115
Q

what is the treatmeant for epidural hematomas?

A

Surgical decompression within 8 hours to optimize recovery chances.

slide 81

116
Q

what are the challenges with anticoags/antiplts with pts who have cardiac stents?

A
  • Patients with stents face difficulties with neuraxial anesthesia.
  • Stopping antiplatelets and anticoagulants increases stent thrombosis risk.
  • Continuing these medications raises bleeding risk, including epidural hematoma.

slide 81

117
Q

guidance note for anticoags/antiplts

A
  • The provided information aligns with consensus statements from the American Society for Regional Anesthesia and Pain Medicine.
  • It is essential to stay updated with the latest guidelines as clinical practices evolve.

slide 81

dont think we need to know this but just in case

118
Q
  • what do COX inhibitors do?
  • what are examples?
A
  • Inhibits cyclooxygenase which prevents the formation of the potent platelet aggregation of thromboxane-A2.
  • NSAIDs, Aspirin

slide 82

119
Q

this medication is a COX inhibtor and antiplatelt

A

aspirin [ASA]

slide 82

120
Q

why is it cricial to determin if aspirin is primary or secondary prophhylaxis?

A

Crucial to determine if aspirin is used for primary (preventing first event) or secondary (preventing recurrent event) prophylaxis.

slide 82

121
Q

with secondary prophylaxis, what is the risk of discontinuation?

A

High risk associated with stopping aspirin; 10% of acute cardiovascular syndromes are preceded by aspirin withdrawal.

slide 82

122
Q

Guidelines by Procedure Risk Level (General Surgery)
* High-Risk & Intermediate-Risk Procedures hold ASA for how long?
* Low-Risk Procedures hold ASA for how long?
* Central neuraxial blocks hold ASA for how long?

A
  • High-Risk & Intermediate-Risk Procedures: Hold aspirin for 4-6 days
  • Low-Risk Procedures: Generally, do not need to hold aspirin
  • Central neuraxial blocks: No additional precautions

slide 82

123
Q

is there a distinction in guidelines between low dose ASA [81mg} and regular dose ASA[ 325mg]?

A

no distinction in guidelines

slide 82

124
Q

What surgeries have a low cardiac risk [< 1%]?

A
  • Endoscopic procedures
  • Cataract surgery
  • Superficial surgeries
  • Breast surgeries
  • Ambulatory surgeries

slide 83

125
Q

What surgeries have an intermediate cardiac risk [1-5%]?

A
  • Carotid endarterectomy
  • Head and neck surgeries
  • Intrathoracic or intra-abdominal surgeries
  • Orthopedic surgeries
  • Prostate surgery

slide 83

126
Q

What surgeries have a high cardiac risk [>5%]?

A
  • Emergency surgeries (especially in elderly patients)
  • Open aortic surgeries
  • Peripheral vascular surgeries
  • Long surgeries with significant volume shifts and/or blood loss

slide 83

127
Q

When should NSAIDs be stoped for:
* High risk procedures?
* Intermediate risk procedures?
* Low risk procedures?
* Central neuraxial blocks?

A
  • High risk procedures: hold for 5 half-lives
  • Intermediate risk procedures: consider holding for cervical ESI and stellate ganglion block
  • Low risk procedures: do not need to routinely hold
  • Central neuraxial blocks: No additional precautions

slide 83

128
Q
  • what do glycoprotein IIB/IIIA Antagonist do?
  • what are examples?
A
  • Inhibits platelet aggregation via surface receptors
  • Tirofiban (Aggrastat), Eptifibatide (Integrilin), Abciximab (ReoPro)

slide 84

129
Q

Glycoprotein IIb/IIIa Antagonists Regional Anesthesia Considerations:
* Avoid until?
* Tirofiban and Eptifibatide: Hold for ____ hours.
* Abciximab: Hold for ____ hours.

A
  • Avoid until platelet function has recovered.
  • Tirofiban and Eptifibatide: Hold for 4-8 hours.
  • Abciximab: Hold for 24-48 hours.

slide 84

130
Q
  • what do Thienopyridine Derivatives do?
  • what are examples?
A
  • Inhibits platelet aggregation by blocking ADP transferase
  • Clopidogrel (Plavix), Prasugrel (Effient), Ticlopidine (Ticlid)

slide 85

131
Q

Thienopyridine Derivatives Regional Anesthesia Considerations:
* Clopidogrel: Hold for ____ days.
* Prasugrel: Hold for ____ days.
* Ticlopidine: Hold for ____ days.

A
  • Clopidogrel: Hold for 5-7 days.
  • Prasugrel: Hold for 7-10 days.
  • Ticlopidine: Hold for 10 days.

slide 85

132
Q
  • what does Unfractionated Heparin do?
  • what are examples?
A
  • Potentiates antithrombin (enzyme inhibitor), inhibiting thrombin (factor 2) and factors 9, 10, 11, 12.
  • SQ (subcutaneous) heparin for DVT (Deep Vein Thrombosis) prophylaxis & IV (intravenous) heparin.

slide 86

133
Q

Unfractionated Heparin Regional Anesthesia Considerations:
* Low-dose ( < 5,000 U): Hold ____ hours.
* Higher-dose (≤ 20,000 U daily): Hold ____ hours.
* Therapeutic dose (>20,000 U daily or in pregnant patients): Hold ____ hours.
* UFH >____ days should have a platelet count before central neuraxial block

A
  • Low-dose ( < 5,000 U): Hold 4-6 hours.
  • Higher-dose (≤ 20,000 U daily): Hold 12 hours.
  • Therapeutic dose (>20,000 U daily or in pregnant patients): Hold 24 hours.
  • UFH >4 days should have a platelet count before central neuraxial block

slide 86

134
Q

Low Molecular weight Heparin (LMWH) includes which3 drugs, and inhibits what?

A
  • Enoxaparin (Lovenox), Dalteparin (Fragmin), Tinzaparin (INNOHEP)
  • Inhibits factor 10a

slide 87

135
Q

Regional Anesthesia Considerations for LMWH

A
  • Ensure coagulation status appears normal.
  • No other blood thinners should be in use.
  • Check platelet count if on LMWH for more than 4 days.

slide 87

136
Q

When the pt is on LMWH, what should you do before the block?

A
  • Delay block at least 12 hours after a prophylactic dose.
  • Delay block at least 24 hours after a therapeutic dose.
  • Consider checking anti-factor 10a activity in elderly or if renal insufficiency.

Slide 87

137
Q

What are the factors that are vitamin-k dependent?

A

2,7,9,10

slide 88

138
Q

Regional Anesthesia considerations for Warfarin

A
  • Hold for 5 days
  • verify normal INR (want <1.5)

slide 88

139
Q

MOA for thrombolytic agents

A

Activates plasminogen: converts plasminogen to plasmin which cleaves fibrin - thereby, causeing clot dissolution

slide 88

140
Q

Thrombolytic Agent regional anesthesia consideration

A

Absolute contraindication to neuraxial anesthesia

slide 88

141
Q

Drugs and MOA for Direct anticoags

A
  • Apixaban (Eliquis), Betrixaban (Bevyxxa), Edoxaban (Lixiana), Rivaroxaban (Xarelto), Dabigatran (Pradaxa)
  • Inhibits facotr 10a

slide 89

142
Q

Direct oral anticoagulants regional anesthesia consideration

A
  • Discontinue at least 72 hours before block
  • Consider checking drug level or anti-factor 10a activity if < 72 hours

slide 89

143
Q

Herbal therapies MOA

A

Activate plasminogen (Garlic, Ginkgo, Ginseng)

herbal therapies are similar action to tPA because it activates plasminogen (Tito during lecture)

Slide 89

144
Q

Herbal therapies regional anesthesia consideration

A

Proceed with Neuraxial anesthesia of the pt is not on other blood-thinning drugs

slide 89

145
Q

How does a postdural puncture headache (PDPH) develop?

A
  • Failure of a dura puncture site to properly “seal over” once breeched by a needle
  • Continuous leak of CSF causes an overall reduction in CSF volume
  • This leak lowers the pressure in the brain area, causing the brain to sag slightly and stretch the surrounding membranes, leading to a headache this will stretch the brain meninges (Tito in lecture)

slide 91

146
Q

Symptomes of Postdural puncture headache

A
  • Headache that feels worse when sitting or standing and better when lying down.
  • Headache occurs 2-3 days post puncture.
    The headache is usually felt from the forehead to the back of the head. (Frontal-Occipital)
  • Other possible symptoms include nausea, sensitivity to light, double vision, and ringing in the ears (comes and goes per Tito).

slide 91

147
Q

PDPH Factors increasing risk (both pt and practitioner factors)

A

Patient Factors:
* younger
* female
* preggers

Practitioner Factors:
* Using a needle with a cutting tip.
* Using a large diameter needle.
* Using air for LOR with epidural.
* Positioning the needle perpendicular to the spine’s long axis.

Slide 91

148
Q

The ____ needle is the cutting needle and can have a ____ to ____

A
  • Quincke needle
  • 36^128% chance with a 22 gauge
    to 0.4^46% chance with a 32 gauge

slide 91

149
Q

Treatment for Postdural Puncture Headache

A
  • Red rest
  • NSAIDs
  • Caffeine (Tito said soda or coffee)
  • Epidural blood patch
  • Sphenopalatine Ganglion block

Slide 92

150
Q

Epidural Blood patch: what do they do

A

Main treatment for severe headaches after dural puncture
* Same level as the epidural was is a good insertion site for the blood patch
* get an IV (from nurse) fresh blood - 10-20mL of pts own bloodand must be sterile IV
* prep pt for epidural
* When you hit epidural space - ask for the blood
-at 10cc of the pt blood - HA likely will go away, but the first few mLs will be the worst headache of their life becuase of increased pressure
* lay pt back to bed and monitor

Slide 92

151
Q

When to give the blood patch?

A
  • 48 hours after the dural puncture
  • Per Tito: sometimes when they start having a headache, you can start the non-invasive stuff (soda or coffee)

slide 92

152
Q

Sphenopalatine Ganglion block (SPG) procedure

A

A simpler, low-risk treatment alternative.
Procedure:
* Soak a cotton swab with LA (1-2% Lidocaine or 0.5% bupivacaine).
* With the patient’s head tilted back, insert the swab into the nose towards the back throat wall.
* Leave it there for about 5 to 10 minutes.
* This can quickly reduce headache symptoms.

slide 92

153
Q

Which nerves are we blocking with the airway block or the SPG block?

A

SPG block: Trigeminal nerve (V2)
Airway block: CN V, IX, X

lecture

154
Q

Paresthesia:
* There is a higher incidence if ____
* Deficit usually is in the area ____
* Epidural Catheter are ____ risk
* higher incidence with ____ techniques

A
  • paresthesia if it was encountered during placement
  • where the paresthesia occures
  • much lower risk
  • CSE techniques (Combined spinal/epidural)

Usually we have paresthesia when we aren’t midline

slide 93

155
Q

What to do when your pt has paresthesias?

A
  • redirect needle
  • document
  • noncooperative or moving pt can increase the risk
  • midline can help guide placement

slide 93

156
Q

Failed spinal: what do you do?

A

No Anesthesia Effect
* If spinal has not set up after after 15-20 minutes, it may be necessary to redo the block.

slide 93

157
Q

Patchy or unilateral block with spinals (Failed spinal)

A
  • Patchy block
    Avoid Repeating: May cause neurotoxicity
    Consider IV sedation or general anesthesia.
  • Unilateral Block
    Adjust Position
    If still ineffective, consider IV sedation or general anesthesia.

slide 93

158
Q

Post-Spinal Bacterial Meningitis: how infections can happen

A
  • Not following sterile or aseptic technique
  • bacteria in the blood: common bacteria involved streptococcus viridans (found in mouth and on hands)

mask and washing hands are essential to preventing the spread of these bacteria

slide 94

159
Q

3 preps for pt’s back duirng neuraxial to prevent bacterial meningitis

A

Skin Preparation Options:
* Iodine, Alcohol, Chlorhexidine

Must be allowed to dry before the procedure begins to avoid arachnoiditis.
Considered neurotoxic if not used properly.

Recommended Combination (Miller)
Alcohol and Chlorhexidine: This mix is highly effective in preventing bacterial meningitis when used correctly to prepare the skin before a spinal procedure.

slide 94

160
Q

Cauda Equina Syndrome: nerves involved, and cause

A
  • Nerves affected: “cauda” L2-S5 + coccygeal nerves
  • Cause: Neurotoxicity which can happen due to high levels of local anesthetic drugs affecting nerve function

slide 95

161
Q

Factors that increase risk of developing cauda equina syndrome

A
  • High concentration of LA (i.e. using lidocaine 5% in SAB)
  • Microcatheters: These catheters deliver the drug on a small area, increasing risk of nerve damage by exposing the area with a high concentration of LA.
  • Whiticare 25/26 needle have been associated with this syndrome

slide 95

162
Q

Signs and symptomes of cauda equina syndrome

A
  • Serious neurologic complication that can be permanent
  • Bowel and Bladder Dysfunction
  • Sensory Deficits: Loss of feeling in the legs or feet. (Tito: numbness in the caudal/sacral area that wont go away)
  • Back pain
  • Saddle anesthesia
  • Sexual dysfunction
  • Weakness or Paralysis
  • Can lead to paraplegia (late sign)

slide 95

163
Q

Treatment for Cauda Equina Syndrome

A

Supportive care
* or if compression is a factor, immediate laminectomy in <6 hrs (ex disc, hematoma etc)

slide 95

164
Q
  • To prevent epidural catheter shearing, always ____
  • If there are issues removing an epidural catheter try: (3 things)
A
  • withdraw the needle and the catheter at the same time

Issues removing Epidural:
* positioning: put the pt in the same position they were in during insertion or lateral decubitus
* Traciton: apply gentle and continuous pulling
* Taps traction: tape the catheter to the skin and gently pull

slide 97

165
Q

Transient Neurologic symtpoms: cause and factors that increase risk

A
  • cause: Patient Positioning- Improper positioning during procedures can stretch nerves, like the sciatic nerve, causing temporary symptoms.
    Myofascial Strain and Spasms
  • Factors increasing risk: Higher incidence when using Lidocaine 5% (around 19%)
    Surgical Positions: Such as the lithotomy position (hip o knee flex)
    Outpatient surgeries and knee arthroscopy are associated with higher risks.

slide 96

166
Q

Factors that do not increase the risk of developing Transient neurologic symptoms

A
  • Early ambulation
  • LA concentration
  • Baricity

slide 96

167
Q

Signs, symptoms, and treament of transient neurologic symptoms

A

S/S:
* Pain: Severe radicular pain in the back and buttocks that spreads down both legs.
* Timing: Pain usually starts within 6 to 36 hours after surgery and lasts from 1 to 7 days. (Resolves within a week 90% of cases)

Treatment:
* NSAIDs and opioid pain killers (per Tito really does work)
* Trigger point injections - can relieve muscle spasm and pain

slide 96

168
Q

If a catheter breaks, what do you do? (epidural)

A
  • inform the pt
  • Monitoring: if the pt doesn’t show s/s, they can often live safely with the fragment
  • Complicaitons: if neurological symptomes develop, surgery may be needed to remove the piece

slide 97

169
Q
  • If blood is in the epidural needle: ____
  • If blood is in the epidural catheter: ____
A
  • Needle: needle could be too internal solution: adjust the needle to aim more midline
  • Catheter: pulling blood into catheter slightly pull back the catheter and flush with saline repeat this until no more blood is drawn or the catheter cant be adjusted further safely

slide 98

170
Q

Risk factors with epidural vein cannulation (4)

A
  • Multiple Attempts
  • Pregnancy
  • Catheter Type: Stiffer catheters are harder to maneuver and more likely to puncture a vein.
  • Trauma to epidural vein during block procedure

slide 98