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Anesthesia Pharm > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Conduction velocity is increased by nerve:

A

Myelination and Diameter

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2
Q

A Delta Fibers

A

Fast pain

Temperature

Touch

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3
Q

A Gamma Fibers

A

Skeletal Muscle Tone

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4
Q

A Beta Fibers

A

Touch

Pressure

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5
Q

A Alpha Fibers

A

Skeletal Muscle Motor

Proprioception

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6
Q

B Fibers

A

Preganglionic ANS Fibers

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7
Q

C Fibers

A

SNS: Postganglionic ANS fibers

Dorsal Root: Slow Pain, Temperature, Touch

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8
Q

What is Cm?

A

The minimum effective concentration

Similar to ED50 for IV anesthetics or MAC for inhaled anesthetics

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9
Q

Fibers that are easily blocked have a ______ cM

Fibers that are resistant to block have a _____ cM

A

Easy: Low

Resistant: High

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10
Q

Local anesthetics inhibit nerve fibers in what order?

A

B

C

Small A

Large A

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11
Q

Cm is reduced by:

A

Higher tissue pH

High Frequency of Nerve Stimulation

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12
Q

Local anesthetics reversibly bind to:

A

the alpha subunit of voltage-gated sodium channels

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13
Q

When can local anesthetics bind to the alpha subunit?

A

Only during active and inactive states. They cannot bind during the resting state.

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14
Q

What is a phasic blockade?

A

Since local anesthetics cannot bind with alpha subunits during the resting state, the more frequently a nerve is depolarized, the more quickly it will be blocked

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15
Q

How do local anesthetics impact the resting membrane potential?

A

They don’t. They only affect nerve conductance.

Potassium control resting membrane potential

Calcium controls threshold potential

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16
Q

What is the resting membrane potential for peripheral nerves?

A

-70

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17
Q

______ is the primary determinant of resting membrane potential

A

serum K level

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18
Q

How do serum potassium levels impact nerve resting membrane potentials?

A

Decreased serum potassium → RMP more negative (harder to depolarize)

Increase serum K → RMP more positive

(easier to depolarize)

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19
Q

What is the threshold potential of nerve fibers?

A

-55 mV

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20
Q

How does serum Ca impact threshold potential?

A

Decreased Ca → TP more negative

Increased Ca → TP more positive

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21
Q

When the RMP is close to the TP, what happens?

A

The cell is easier to depolarize

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22
Q

When the RMP is further from the TP, what happens?

A

The cell is harder to depolarize

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23
Q

A cell repolarized when:

A

K leaves the cell

Cl enters the cell

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24
Q

What determines a local anesthetic’s speed of onset?

A

Its pKa

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25
Q

What determines a local anesthetic’s potency?

A

Its lipophilicity

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26
Q

Local anesthetics are weak ______

A

bases

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27
Q

When local anesthetics are injected, they dissociate into:

A

an uncharged base

AND

a conjugate acid

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28
Q

How much local anesthetics dissociates in tissues?

A

Since all of them have pKa’s that are higher than 7.4, more than 50% will dissociate

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29
Q

When local anesthetics ionize in the tissues, which portion enters the cell?

A

The uncharged base

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30
Q

What happens once the uncharged base enters the axoplasm?

A

Since the pH is lower, it picks up a H+ ion and becomes a conjugate acid

It is this conjugate acid that binds to the alpha subunit on the INSIDE of the axon membrane

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31
Q

A true local anesthetic allergy is more likely with a _____ than a ______

A

more likely with an ester than an amide because esters are derivatives of PABA

32
Q

A patient with an allergy to an ester can receive an amide so long as:

A

the preparation is preservative free (because that may have been what caused the allergy rather than the ester itself)

33
Q

Which structure in a local anesthetic determines give it lipophilicity?

A
34
Q

Which structure in a LA is hydrophilic?

A
35
Q

Which LA structure determines its drug class?

A
36
Q

What determines the duration of onset of an LA?

A

Its protein binding capacity

37
Q

How do local anesthetics affect vasculature?

A

At subclinical doses, they are vasoconstrictors because they inhibit nitric oxide

at clinical doses, they are vasodilators

38
Q

Which LA is exception to the effects of LAs on vasculature?

A

Cocaine

It inhibits NE reuptake and ALWAYS causes vasoconstriction, no matter what the dose is

39
Q

Which class of LA has higher pKa’s?

A

All esters have higher pKa values than amides

40
Q

There is only one LA that does not undergo protein binding:

A

Chloroprocaine

41
Q

There is only one LA with a pKa that is well below physiologic pH:

A

Benzocaine

pKa 3.5

42
Q

What is special about benzocaine?

A

It is non-ionized at physiologic pH, and yet it still has anesthetic properties

Usually it’s only the ionized portion of LAs that can interact with the sodium channel

43
Q

Which serum proteins do LAs bind to?

A

Prefer Alpha - 1 - acid glycoproteins

but will also bind to albumin

44
Q

How is cocaine metabolized?

A

Both pseudocholinesterases and hepatic

45
Q

What factors increase the risk of CNS toxicity from lidocaine?

A
46
Q

What determines the extent of cardiotoxicity from increased LA serum levels?

A

Degree of affinity for the sodium channel receptor

Rate of dissociation from the receptor during diastole

This is why drugs that have a high affinity (like bupivicaine) carry a higher risk of cardiac toxicity

47
Q

The risk of cardiac toxicity from bupivicaine is increased by:

A

calcium channel blockers

Digitalis

Pregnancy

Beta Blockers

48
Q

What drug should be given to a patient with a cocaine overdose?

A

NOT a beta blocker, since this will cause unopposed Alpha 1 activity

Preferably nitroglycerin or another straight vasodilator, or labetalol which has alpha 1 blocking capabilities

49
Q

How do you calculate the lipid emulsion BOLUS to give to a patient with suspected LAST?

A

1.5 ml/kg

50
Q

Which drugs should NOT be given during a LAST code?

A

beta blockers and calcium channel blockers

They enhanced cardiac disturbances

51
Q

Which ACLS drugs should be avoided in LAST patients?

A

Vasopressin

Lidocaine (duh)

Procainamide

Epinephrine

52
Q

How do you calculate the lipid emulsion INFUSION for a patient in LAST?

A

0.25 ml/kg/min

Can be increased to 0.5 if ineffective

53
Q

How many times can you repeat the lipid bolus?

A

Twice

54
Q

What is the recommended max dose of lipid emulsion therapy?

A

10 ml/kg in the first 30 min

55
Q

What is the most common cause of death from liposuction?

A

PE

56
Q

What is the maximum amount of lidocaine that can be used in tumescent anesthesia?

A

50-55 mg/kg

57
Q

When is general anesthesia recommended for patients undergoing liposuction?

A

If 2-3 L of tumescent anesthesia is going to be needed

58
Q

Methemoglobin is formed when:

A

the iron on the hemoglobin molecule becomes oxidized to Fe3+ decreasing the oxygen carrying capacity of the molecule

59
Q

Which LAs can lead to methemoglobinemia?

A

Benzocaine

EMLA

Cetacaine

60
Q

Besides LAs, what other drugs can cause methemoglobinemia?

A

Nitric Oxide

Sulfonamides

Nipride

Nitroglycerin

Phenytoin

61
Q

What are the classic manifestations of methemoglobinemia?

A

The blood takes on a chocolate color

A decreased SpO2 in the setting of a normal PaO2

Slate grey cyanosis

62
Q

How does methemoglobinemia effect SpO2 waveforms?

A

Tends to push it toward 85%

63
Q

Which patients should NEVER receive methylene blue?

A

G-6-PD

They need an exchange transfusion instead

64
Q

What is the treatment for methemoglobinemia?

A

Methylene Blue

65
Q

Are neonates at a higher or lower risk of methemoglobinemia?

A

Higher

Their blood cells have very low levels of methemoglobin reductase

66
Q

Which direction does methemoglobinemia shift the dissociation curve?

A

To the left

BECAUSE

Methemoglobin can’t bind O2, but that actually increases the affinity of HgbA for O2

This means the HgbA hangs onto O2, leading to tissue hypoxia and metabolic acidosis

67
Q

Myelinated nerve fibers are surrounded by ____ in the PNS and _____ in the CNS

A

PNS: Schwann Cells

CNS: Oligodendrocytes

68
Q

Which two organ systems are most susceptible to effects from systemic absorption of local anesthetics?

A

The heart and the brain, for two reasons:

  1. They are extremely vascular and therefore receive a lot of the drug
  2. They are both highly electrical, and they’re more susceptible to sodium ion changes
69
Q

The potential for CNS toxicity correlates directly with:

A

the potency of the LA

70
Q

Does CV toxicity occur at higher or lower plasma levels than CNS toxicity?

A

Way higher. Generally you’ll see CNS effects at much lower plasma concentrations

71
Q

Which local anesthetics are most likely to cause cardiovascular collapse?

A

All LAs cause hypotension, dysrhthmias, and myocardial depression

BUT

the most potent agents (bupivacaine, ropivacaine, levobupivacaine) tend to cause the devastating outcomes

72
Q

How do plasma concentrations of local anesthetics impact the pulmonary vasculature?

A

In general, LAs at high doses cause vasodilation. BUT in the pulmonary vasculature, high dose LA results in severe pulmonary hypertension

73
Q

Why is bupivacaine so cardiotoxic?

A

It has a greater affinity for binding with resting and inactivated sodium channels than lidocaine

Bupivacaine dissociates off the sodium channel much more slowly than lidocaine

74
Q

Why is it so important to secure the airway if LAST occurs?

A

To prevent further exacerbation of the toxicity by hypoxemia, hypercapnea, and acidemia

75
Q

If you give a benzodiazepine to stop a seizure from LAST and it isn’t effective, what should be the next drug given?

A

An NMBA

It won’t stop the seizure but it will facilitate pulmonary ventilation and disrupt the muscular activity, preventing lactic acidosis which would worsen LAST

Anesthesia Pharm (12 decks)

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