Exam 1 Spinal & Epidural Neuraxial Anesthesia [06/03/24] Flashcards
What is the effect of neuraxial anesthesia on the pulmonary system?
- 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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What are special considerations for neuraxial anesthesia for the pulmonary system?
- 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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What causes apnea in regards to neuraxial anesthesia?
- 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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Flow volume loops graph
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What are the componets of vital capacity?
- VT
- IRV
- ERV
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Phrenic nerve orginates from what levels of the spine?
- C3, C4, C5
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For the GI system, parasympathetic innervation is primarily via what? Sympathetic innervation?
- Parasympathetic innervation is via the vagus nerve (originates medulla)
- Sympathetic innervation of GI tract stems from T5-L2
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What is the function of parasympathetic afferent and parasympathetic efferent?
- Parasympathetic AFFERENT: transmits sensations of satiety, distension, and nausea
- Parasympathetic EFFERENT: tonic contractions, sphincter relaxation, peristalsis, and secretion.
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What is the function of sympathetic afferent and sympathetic efferent for the GI system?
- Sympathetic AFFERENT: transmit visceral pain
- Sympathetic EFFERENT: inhibit peristalsis and gastric secretion and cause sphincter contraction and vasoconstriction
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Sympathetic innervation of GI tract stems from
- T5-L2
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What is the Impact of Neuraxial Anesthesia on GI system?
- 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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The unopposed vagal tone on the GI system from neuraxial anesthesia results in?
- 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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20% of nausea related to central neuraxial is d/t unopposed effect. What is the cause of the other 80% of nausea?
The remaining 80% is from sympathethecomy due to reduced blood supply in the chemotaxis center resulting in nausea.
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What are the genitourinary effects of Neuraxial Anesthesia.
- 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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How does the addition of Neuraxial Opioids affects the GU system?
- 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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What are the metabolic/endocrine effects of Neuraxial Anesthesia.
- 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
The activation of somatic and visceral afferent fibers from pain, tissue trauma, and inflammation causes?
What does neuraxial anesthesia do?
- Elevated cortisol, epinephrine, norepinephrine, vasopressin, activation of renin-angiotensin-aldosterone system.
- neuraxial anesthesia reduces this which is good.
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What are local anesthetics made of?
- Aromatic or beneze ring
- Intermediate chain
- Tertiary amine
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What does the aromatic ring, intermediate chain, and tertiary amine group determine?
- Aromatic - lipophilic
- Intermediate - drug class, metabolism, allergic potential.
- Tertiary amine - hydrophilic, accepts protons.
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What metabolizes esters?
What metabolizes amides?
- Esteres: pseudocholinesterase
- Amides: Hepatic P450
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What LA is an exception to the metabolization rule?
- Cocaine
- even though its an ester, it is also metabolized by the liver.
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Allergies with LA are seen with esters or amides? why?
- More Common Allergy is with Esters
- Produces para-aminobenzoic acid (PABA)
- There’s cross-sensitivity in esters
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Can you have an allergic reaction to amides?
- Amide allergic reaction is rare
- Contains preservative methylparaben, similar to PABA.
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T/F: There is no cross sensitivity between esters and amides
True
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Onset of action of LA is relies on?
- 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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Potency of LA is related to?
- 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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Duration of action of LA is related to?
- Protein binding [A1-acid glycoprotein]
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What is the sequence of how blockage of fibers occur when you put LA in central neuroaxial?
- 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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Structure of amides vs esteres
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List the esters and amides mentioned on the powerpoint.
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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.
True
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List the Factors Influencing Vascular Uptake and Plasma Concentration of Local Anesthetics
- Site of Injection
- Tissue Blood Flow
- Physiochemical Properties
- Metabolism
- Addition of Vasoconstrictor:
STAMP
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-if area is vasoconstriction, there is less absorption and there’s is more LA in the system.
List the uptake of LA based from high to low blood concentration
- Intravenous
- Tracheal
- Intercostal
- Caudal
- Paracervicle
- Epidural
- Brachial
- Sciatic
- SubQ
* If There Is Chest Pain Epidurals Block Sign/Symptoms
* I Teach Introverted Children Painting Elephants, But Sit Still
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What do you do if a bier block leaks?
- do not deflate the cuff
- gives benzos for seizures if needed.
- administeed lipid emulsion.
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What is baracity?
- Baricity refers to the density of a local anesthetic solution compared to the CSF.
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Isobaric
- 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.
- observation from bri: isobaric mixture is in NS
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Hyperbaric
- 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.
- observation from bri: hyperbaric solution is in Dextrose, unless the LA is highly concentrated then its in H2O
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Hypobaric
- 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.
- observation from bri: LA is mixed with H2O
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Hyperbaric, isobaric, hypobaric LA solution chart
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If the patient is supine:
* What happens when a hyperbaric solution is given?
* What happens when a hypobaric solution is given?
-
Hyperbaric: the LA will go to the lowest level which is trough
- Trough: T6 and S2
-
Hypobaric: the LA will go to the highest level which is apex
- Apex: C3 and L3
Baracity is related to spinals.
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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 ____
- small
- lipid soluble
- cephalad and caudad, simultaneously
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SAB pharmacology
What kind of metabolism occurs in the CSF?
How are LA eliminated?
- NO metabolism occurs in the CSF
- All LA are eliminated by reuptake [Vascular reabsorption via vessels in the pia mater]
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SAB pharmacology
Do Lipophillic drugs have slow or fast reuptake? Why?
Lipophillic drugs have a slow reuptake bc they have high affinity for epidural fat.
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SAB pharmacology
____ has a longer duration of action than lidocaine
Bupivicaine
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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%
- 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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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%
- 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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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???
- 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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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%
- 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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- What 2 medications can have epinephrine added to them for spinal blocks?
- how much longer does the block last with epi added?
- bupivicaine 0.5%-0.75% and tetracaine 0.5%-1%
- duration increases by 20-50% for each
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Which LA medication is not given in spinals?
Lidocaine!
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For epidurals, the spread of LA is ____ and ____ from the catheter insertion site
cephalad and caudad
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How is incremental dosing helpful in epidurals? what does it avoid?
- 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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How do we incrementally dose epidurals?
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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If epi is added to an epidural, it can be used as what?
an IV marker
use as a test dose to see if in vein or not. The HR will increase determining we are in the vein.
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when is the onset of an epidural?
10-25min
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Epidural Pharmacology
In what concentration can we find 2-chloroprocaine?
which concentration is best for surgical anesthesia?
- comes in 2% and 3%
- 3% is used for surgical anesthesia
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Epidural pharmacology
Which LA is popular for OB anesthesia? is it an ester or amide?
2-Chloroprocaine, which is an ester LA
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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??
- concentration!!
- 3% makes its speed of onset very fast
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Does 2-Chloroprocaine have a short or long duration? why? how often will it need to be redosed?
- duration is short lived b/c it is metabolized by plasma cholinesterase
- THEREFORE… we need to redose Q45min
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- How do we alkalanize LA solutions?
- What 4 things does alkalinazation cause?
- Adding NaHCO3 of 1mEq/ 10ml
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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Epidural pharmacology dosing
____ of LA is crucial for determining how ____ the anesthetic block reaches
Volume of LA is crucial for determining how high the anesthetic block reaches
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The initial dose of an epidural LA is typically ____mL/ ____ of the spine
1-2ml/segment
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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?
- Top-up dose
- 50-75% of the initial dose
- Should be administered before the block decreases more than 2 dermatomes/segments
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The space available in the epidural area varies. What space is smaller/ larger? What is the clinical relevance?
- Epidural space is smaller in the thoracic region than lumbar region.
- Greater spread in thoracic.
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Since the thoracic space is lower we dont need alot of dose so can give 1ml/segment.
What determines the density/strength of block in an epidural? What is an easy example to remember this by?
- Concentration of LA affects how dense/strong a block is.
- walking epidural uses low concentration that manages pain but allows some motor function (ideal for labor)
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List the LA epidural drugs in order from fast onset/short duration to slow onset/long duration with their concentrations
- 2-Chloroprocaine 3%
- lidocaine 2%
- ropivacaine 0.1-0.75%
- bupivacaine 0.0625-0.5%
- levobupivacaine 0.0625-0.5%
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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%
30-90 min
60-120min
140-220min
160-220min
150-225min
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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%
5-15min
10-20min
15-20min
15-20min
15-20min
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for SOLE epidural surgical anesthesia, which concentrations of the LA should be used?
the higher concentrations:
2-Chloroprocaine 3%
lidocaine 2%
ropivacaine 0.75%
bupivacaine 0.5%
levobupivacaine 0.5%
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What is the best choice LA drug for epidural? 2nd best if that’s not available?
2-Chloroprocaine 3%
lidocaine 2%
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When can respiratory depression happen with opioid use in neruaxial anesthesia?
- can be delayed [morphine]
- or immediate first 24 hours [fentanyl/ sufentanil]
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- what do COX inhibitors do?
- what are examples?
- Inhibits cyclooxygenase which prevents the formation of the potent platelet aggregation of thromboxane-A2.
- NSAIDs, Aspirin
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Glycoprotein IIb/IIIa Antagonists Regional Anesthesia Considerations:
* Avoid until?
* Tirofiban and Eptifibatide: Hold for ____ hours.
* Abciximab: Hold for ____ hours.
- Avoid until platelet function has recovered.
- Tirofiban and Eptifibatide: Hold for 4-8 hours.
- Abciximab: Hold for 24-48 hours.
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Thienopyridine Derivatives Regional Anesthesia Considerations:
* Clopidogrel: Hold for ____ days.
* Prasugrel: Hold for ____ days.
* Ticlopidine: Hold for ____ days.
- Clopidogrel: Hold for 5-7 days.
- Prasugrel: Hold for 7-10 days.
- Ticlopidine: Hold for 10 days.
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- MOA for thrombolytic agents
- Examples
- Activates plasminogen: converts plasminogen to plasmin which cleaves fibrin - thereby, causing clot dissolution
- TPA, Streptokinase, Alteplase, Urokinase
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- The ____ needle is the cutting needle and can have a ____ to ____ guage.
- What is the incidence of post dural pucture HA with this needle?
- Quincke needle
- 22-32 guage
- Incidence listed in the picture
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Treatment for Postdural Puncture Headache
Noninvasice Tx:
* bed rest
* NSAIDs
* Caffeine (Tito said soda or coffee)
Invasice Tx:
* Epidural blood patch
* Sphenopalatine Ganglion block
Slide 92
Sphenopalatine Ganglion block (SPG) procedure
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.
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Factors that increase risk of developing cauda equina syndrome
- 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
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