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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
Q

Are myelinated or unmyelinated fibers more easily blocked?

A

Myelinated

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26
Q

Why are myelinated fibers easier to block?

A

Because only the Node of Ranvier needs to be blocked.

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27
Q

Which nerve fiber type is responsible for carrying sympathetic stimulation?

28
Q

Which nerve fiber type is responsible for carrying Motor ?

29
Q

Which nerve fiber type is responsible for fast moving/sharp pain, heat, cold, touch ?

30
Q

Which nerve fiber type is responsible for touch from pressure and proprioception?

31
Q

Which nerve fiber type is responsible for Fine touch sensation, temp, pain?

32
Q

Which nerve fiber type is responsible for Motor and proprioception?

33
Q

Which nerve fibers are the smallest in diameter?

A

C Fibers (0.3-1.3)

34
Q

Which nerve fibers are not myelenated?

35
Q

In what order are the nerve fibers blocked?

A

ATP-TP-MVP

1st: Autonomic, touch pain.
2nd: Temp, pressure.

3rd: Motor, vibration,
proprioception.

36
Q

What is the first fibers to be blocked?

A

B fibers and some C fibers

37
Q

What are the last fibers to be blocked?

38
Q

How are ester LA metabolized?

A

Plasma cholinesterases

39
Q

What is the half life in circulation of ester LA?

A

about 1 minute

40
Q

What is the metabolite of ester LA metabolism?

A

p-aminobenzoic acid (PABA).

41
Q

How are amide LA metabolized?

A

N-dealkylation and hydolysis in the liver.

42
Q

Other than a direct allergy, what is a contraindication for amide LA?

A

Sever hepatic disease (Due to the mechanism of metabolism)

43
Q

What is the elimination half life of amide LA?

44
Q

What is baricity?

A

LA density related to the CSF

45
Q

What does a hypobaric LA tend to do in CSF?

A

Tends to float up

46
Q

What does a hyperbaric LA tend to do in CSF?

A

Tends to sink down

47
Q

What does an isobaric LA tend to do in CSF?

A

Tends to stay where it is

48
Q

What effects does epinephrine have as an additive to LA?

A
  • Prolongs duration*.
  • Decreases systemic toxicity*.

Increases intensity.
Decreases surgical bleeding.

49
Q

What additive can be used in evaluating a test dose?

A

epinephine

50
Q

What are reasons epinephrine should not be added to LA?

A

PNB in poor collateral circulation areas (fingers, toes, penis).
Bier block
Severe uncontrolled HTN, CAD, arrhythmias

51
Q

What is an additive that is an alternative to epinephrine?

A

Phenylephrine

52
Q

Why is sodium bicarbonate added to LA?

A

Raises pH and increases concentration of non-ionized drug.

Increases rate of diffusion across the nerve membrane.

53
Q

T/F: Sodium bicarbonate added to LA would slow down the onset of the LA?

A

False: it would speed it up

54
Q

Why would an opioid be added to LA?

A

Potentiates/synergistic effects with the LA

55
Q

Which causes allergic reactions due to metabolite PABA, esters or amides?

56
Q

What two things can lead to systemic toxicity of LA?

A
  1. Accidental intravascular injection.

2. Overdose of LA.

57
Q

What can be done to minimize the risk of systemic toxicity of LA?

A

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
Q

What are some of the first signs (warning signs) of Central Nervous system toxicity of LA?

A 
Lightheadedness.
Tinnitus.
Metallic taste.
Visual disturbances.
Circumoral numbness
59
Q

What might the initial warning signs of CNS toxicity potentially lead to?

A

Muscle twitching.
Loss of consciousness.
Grand mal seizures
Coma

60
Q

How does CO2 in the blood effect the convulsive threshold of CNS toxicity with LAs?

A

CO2 lowers the threshold

61
Q

What is initial treatment of CNS toxicity from LA?

A

Administer O2.

Versed 1-2mg seizures, propofol.

62
Q

What is the most cardiotoxic LA?

A

Bupivacaine

63
Q

What is the clinical presentation of cardiovascular toxicity from LAs?

A

Decreased contractility.
Decreased conduction.
Loss of peripheral vasomotor tone.
Cardiovascular collapse.

64
Q

What is treatment for cardiovascular toxicity from LAs?

A 
Volume.
Vasopressors.
Inotropes.
Prolonged CPR.
ACLS
65
Q

What ACLS drug should be completely avoided during cardiovascular toxicity from LAs?

A

Lidocaine.

66
Q

What is the true mainstay treatment for symptomatic LA toxicity?

A

Lipid emulsion

67
Q

What is the dose of lipid emulsion ?

A

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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