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Spinal Anesthesia- LA Flashcards

1
Q

What was the first local anesthetic created?

A

Cocaine

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2
Q

Is mepivacaine an amide or an ester?

A

Amide

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3
Q

Is lidocaine an amide or an ester?

A

Amide

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4
Q

Is etidocaine an amide or an ester?

A

amide

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5
Q

Is chloroprocaine an amide or an ester?

A

Ester

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6
Q

Is tetracaine an amide or an ester?

A

Ester

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7
Q

Are local anesthetics classified as strong or weak acids or bases?

A

Weak Bases

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8
Q

Which portion of the LA molecule is associated with its lipophilicity, Aromatic or Amine portion?

A

Aromatic lipophilic portion

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9
Q

Which portion of the LA molecule is associated with its hydrophilicity, aromatic or amine portion?

A

Amide hydrophilic portion.

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10
Q

Which one is characterized by an intermediate chain made up of C-O-C-C, amino or ester?

A

Amino

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11
Q

How is the intermediate chain of esters characterized?

A

N-C-C-N

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12
Q

What is the pKa of a drug?

A

The pH at which 50% of the LA is in the charged (ionized) form and 50% is in the uncharged (nonionized) form

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13
Q

Will a LA with a lower or higher pKa value have a faster onset ?

A

Lower pKa

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14
Q

Why will a LA with a lower pKa value have a faster onset?

A

Because a greater fraction of the molecules will exist in the uncharged (nonionized) form and thus will more easily diffuse across nerve membranes.

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15
Q

The ionized or unionized form of a the LA is more lipid soluble and able to gain access to the axon?

A

Nonionized.

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16
Q

T/F: The higher the pKa, the faster the onset?

A

False

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17
Q

Explain how the LA becomes more ionized once administered?

A

The drug becomes more ionized because it accepts the electrons from the acidic environment.

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18
Q

T/F: The LA must become non-ionized in order to bind to the intended receptor site?

A

False.

Must become more ionized

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19
Q

Is it more acidic inside the cell or in the interstitial space?

A

Inside the cell

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20
Q

What is the MOA of all LA?

A

Inhibit Na+ channels which decreases the rate of rise of the action potentials so that threshold potential is not reached.

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21
Q

What determines speed of onset of neural blockade?

A

pKa of the LA

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22
Q

What determines the potency of a LA?

A

Lipid solubility.

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23
Q

What determines the length/duration of effect?

A

Protein binding (and in some part lipid solubility.

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24
Q

Are thin or thick fibers more easily blocked?

A

Thin fibers

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25
Are myelinated or unmyelinated fibers more easily blocked?
Myelinated
26
Why are myelinated fibers easier to block?
Because only the Node of Ranvier needs to be blocked.
27
Which nerve fiber type is responsible for carrying sympathetic stimulation?
B fibers
28
Which nerve fiber type is responsible for carrying Motor ?
A Gamma
29
Which nerve fiber type is responsible for fast moving/sharp pain, heat, cold, touch ?
C Fibers
30
Which nerve fiber type is responsible for touch from pressure and proprioception?
A Beta
31
Which nerve fiber type is responsible for Fine touch sensation, temp, pain?
A Delta
32
Which nerve fiber type is responsible for Motor and proprioception?
A Alpha
33
Which nerve fibers are the smallest in diameter?
C Fibers (0.3-1.3)
34
Which nerve fibers are not myelenated?
C Fibers
35
In what order are the nerve fibers blocked?
ATP-TP-MVP 1st: Autonomic, touch pain. 2nd: Temp, pressure. 3rd: Motor, vibration, proprioception.
36
What is the first fibers to be blocked?
B fibers and some C fibers
37
What are the last fibers to be blocked?
A Gamma
38
How are ester LA metabolized?
Plasma cholinesterases
39
What is the half life in circulation of ester LA?
about 1 minute
40
What is the metabolite of ester LA metabolism?
p-aminobenzoic acid (PABA).
41
How are amide LA metabolized?
N-dealkylation and hydolysis in the liver.
42
Other than a direct allergy, what is a contraindication for amide LA?
Sever hepatic disease (Due to the mechanism of metabolism)
43
What is the elimination half life of amide LA?
2-3 hours
44
What is baricity?
LA density related to the CSF
45
What does a hypobaric LA tend to do in CSF?
Tends to float up
46
What does a hyperbaric LA tend to do in CSF?
Tends to sink down
47
What does an isobaric LA tend to do in CSF?
Tends to stay where it is
48
What effects does epinephrine have as an additive to LA?
* Prolongs duration*. * Decreases systemic toxicity*. Increases intensity. Decreases surgical bleeding.
49
What additive can be used in evaluating a test dose?
epinephine
50
What are reasons epinephrine should not be added to LA?
PNB in poor collateral circulation areas (fingers, toes, penis). Bier block Severe uncontrolled HTN, CAD, arrhythmias
51
What is an additive that is an alternative to epinephrine?
Phenylephrine
52
Why is sodium bicarbonate added to LA?
Raises pH and increases concentration of non-ionized drug. | Increases rate of diffusion across the nerve membrane.
53
T/F: Sodium bicarbonate added to LA would slow down the onset of the LA?
False: it would speed it up
54
Why would an opioid be added to LA?
Potentiates/synergistic effects with the LA
55
Which causes allergic reactions due to metabolite PABA, esters or amides?
Esters
56
What two things can lead to systemic toxicity of LA?
1. Accidental intravascular injection. | 2. Overdose of LA.
57
What can be done to minimize the risk of systemic toxicity of LA?
Aspiration prior to injection. Use of epi-containing solutions for test dose. Use of small, incremental dosing. Use of proper technique during IV regional (bier block).
58
What are some of the first signs (warning signs) of Central Nervous system toxicity of LA?
``` Lightheadedness. Tinnitus. Metallic taste. Visual disturbances. Circumoral numbness ```
59
What might the initial warning signs of CNS toxicity potentially lead to?
Muscle twitching. Loss of consciousness. Grand mal seizures Coma
60
How does CO2 in the blood effect the convulsive threshold of CNS toxicity with LAs?
CO2 lowers the threshold
61
What is initial treatment of CNS toxicity from LA?
Administer O2. | Versed 1-2mg seizures, propofol.
62
What is the most cardiotoxic LA?
Bupivacaine
63
What is the clinical presentation of cardiovascular toxicity from LAs?
Decreased contractility. Decreased conduction. Loss of peripheral vasomotor tone. Cardiovascular collapse.
64
What is treatment for cardiovascular toxicity from LAs?
``` Volume. Vasopressors. Inotropes. Prolonged CPR. ACLS ```
65
What ACLS drug should be completely avoided during cardiovascular toxicity from LAs?
Lidocaine.
66
What is the true mainstay treatment for symptomatic LA toxicity?
Lipid emulsion
67
What is the dose of lipid emulsion ?
Bolus 1.5ml/kg over 1 min. Infusion 0.25ml/kg/min. Bolus as necessary Q3-5min to total of 3ml/kg

APA Fundamentals (10 decks)

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