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SUM'20 - Regional > Week 2 Regional anesthesia & LA (3 of 4) > Flashcards

Week 2 Regional anesthesia & LA (3 of 4) Flashcards

1
Q

Tell me everything you know about Fetal Ion trapping?

A
  • pH of the fetus is lower than moms.
  • nonionized form of LA crosses placental barrier.
  • once in fetal area (across the plancenta), some of the drug becomes ioninzed. B/c the fetus’s pH is lower than mom’s.
  • The ionized form of LA can not cross back over the placenta and is TRAPPED with the fetus (in the fetus).
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2
Q

The lower the fetal pH (compared to mom’s pH) the greater the amount of LA in IONIZED OR UNIONIZED for in the fetus?

A

IONIZED (greater ion trapping)

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3
Q

Which combination will most facilitate trapping of LA by the fetus?

Maternal alkalosis and fetal alkalosis

Maternal alkalosis and fetal acidosis

Maternal acidosis and fetal alkalosis

Maternal acidosis and fetal acidosis

A

Maternal alkalosis and fetal acidosis

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4
Q

What condition most prevents passage of LA from fetus to mom?

Maternal alkalosis

Maternal acidosis

Fetal alkalosis

Fetal acidosis

A

Maternal acidosis

because if the mom is acidic then less LA is available to cross the placenta bc it has already turned ionized!

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5
Q

What three factors is ONSET of a LA dependent on?

A

Lipid solubility

Relative concentration of the non-ionized lipid-soluble form and the ionized water soluble form (pKa)

pKa= the pH at which the fraction of ionized and non-ionized drug is equal.

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6
Q

Agents with lower pKa are more un-ionized at pH of 7.4 (body pH if normal), what does this mean in relation to onset?

A

faster onset

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7
Q

Know your LA’s and pKa for each one, also relative time to onset. (next slide is chart from ppt 29)

A

ppt 29

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8
Q

if a LA is lipid soluble and can easily penetrate axon cell membrane then it would be correct to assume what bout its ionization?

A

that it is un-ionized or has a lot of the drug un-ionized.

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9
Q

What is the most acidic pKa of the LA’s?

A

Mepivacaine is 7.6

Lidocaine and Etidocaine are both 7.7

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10
Q

What is the most basic pKa of the LA’s?

A

Chloroprociane is 9.1

Procaine is 8.9 and Tetracaine is 8.6

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11
Q

Relative Onset times of LA’s, tell me all of them from slowest to fastest?

A

Procaine and Tetracaine is slow

Bupivicane is moderate

Chloroprociane, Lidocaine, Etidocaine, and Mepivacaine are fast.

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12
Q

What has to occur for a LA to block nerve conduction?

A

LA blocks sodium channels (prohibit Na+ influx)

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13
Q

The potency of a LA parallels what other characteristic of a LA?

A

The more lipid soluble a LA is the more easily it can cross the cell membrane and thus the more potent it is.

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14
Q

LA that are highly protein bound will have ?

A

prolonged DOA

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15
Q

pKa of a LA determines the speed of onset, THUS the lower the pKa the FASTER OR SLOWER the onset?

A

the lower the pKa the faster the onset.

the one exception to this rule is Chloroprocaine, despite having a pKa of 9, has a rapid onset

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16
Q

Which LA is the exception to the rule “the lower the pKa the faster the onset?”

A

Chloroprocaine pKa 9.1

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17
Q

What is the STANDARD amount of sodium bicarb added to X amount of LA in order to alkalize the LA more?

A

addition of sodium bicarb- 1mL of 8.4% per 10 mL of LA

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18
Q

What is the amount of bicarb added to Bupivicaine per X ml in order to alkalize Bupivicaine?

A

0.1ml of sodium bicarb per 1ml Bupivicaine.

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19
Q

what coefficient is a measure of lipid solubility?

A

Oil:Water

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20
Q

The greater the Oil:Water coefficient, the greater THE WHAT?

A

LIPID SOLUBILITY

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21
Q

The more lipid soluble a LA is the greater it’s WHAT is?

A

potency

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22
Q

When talking about LA’s potency has a good relationship with WHAT?
(potency parallels what?)

A

lipid solubility

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23
Q

Minimum concentration of local anesthetic (potency) that will block a nerve impulse conduction is affected by several factors: (6 answers to be exact lol)

A

Fiber size

Fiber type

Fiber myelination

pH (acidic pH antagonizes block)

Frequency of nerve stimulation

Electrolyte concentrations
(hypokalemia and hypercalcemia antagonize blockade)

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24
Q

Which fiber type are least sensitive to the action of LA?

A

C-fibers

25
Q

Potency of LA, tell me all of their “relative clinical potency” and “oil:water partition coefficient” (chart will be the answer, see how many you know - learn them)

A

slide 32

26
Q

What two LA’s have a oil:water of 1?

A

Chloroprocaine and Mepivacaine

27
Q

Who has the highest oil:water coefficient of the LA’s?

A

Etidocaine at 140

28
Q

What is Lidocaine’s relative clinical potency and oil:water coeffecient?

A 
RCP = 3
O:W = 4.0

(you can remember lidocaine as 3 and 4)

29
Q

Chloroprocaine’s relative clinical potency and oil:water coeffecient?

A

both numbers are 1!

30
Q

Mepivacaine’s relative clinical potency and oil:water coefficient?

A

RCP is 2
O:W is 1

(Mepivacaine 2 and 1)

31
Q

Tetracaine’s Relative clinical potency and oil:water coeff.

A 
RCP = 8
O:W = 80

(think 8 and 80, they both start with 8)

32
Q

Which two LA’s both have a relative clinical potency of 8?

A

Tetracaine and Bupivacaine!

you know Tetracaine is 8 bc of 8 and 80 for RCP and O:W
(Bupivicaine is 8 and 30 with 30 being the O:W coeff)

33
Q

Duration of a LA correlates with what all factors?

A

correlates with potency & lipid solubility (correlated with plasma protein binding).

34
Q

Duration of action of a LA is determined by two properties: What are they?

A

Lipid solubility

The degree of protein binding (most important factor in determining DOA)

35
Q

what is the MOST important factor in determining DOA of a LA?

A

The degree of Protein binding!

36
Q

LA are mostly bound to what protein?

A

alpha-1 acid glycoprotein.

they are also bound to albumin, BUT MORE bound to alpha-1 acid glycoprotein

37
Q

If a LA has a protein binding of 94% vs a LA with protein binding of 66%, which one has the longer DOA?

A

the greater the Protein binding the longer the DOA, thus the 94% LA will have a longer DOA.

38
Q

How does protein binding create a longer DOA?

A

Protein bound LA acts as reservoir of LA/protein bound anesthetic is released for nerve axons; maintains slow release of anesthetic (which maintains the supply of anesthetic to the axons).

39
Q

The greater the lipid solubility, longer the duration of action, WHY?

A

more slowly diffuse from a “lipid rich” environment to the blood stream for elimination.

40
Q

How do lipids help maintain a nerve block by a LA?

A

lipids act as a reservoir of LA, thus maintaining the nerve block bc you have LA in reserve to use!

41
Q

What single change in a property of a LA will result in a more potent and longer acting agent?

A

If you are able to change (increase) the lipid solubility of the LA, you increase the lipid solubility which means you are increasing the unionized form.

How do you change the LA in order to have more unionized form? (sodium bicarb)

42
Q

Agents that are mostly lipid soluble and have the greatest protein binding are longest acting. KNOW each LA’s lipid solubility number, protein binding number, and anesthetic duration. (chart as answer)

A

slide 35

43
Q

Protein binding of LA from least to most?

A

Procaine< Chloroproiane< Lidocaine< Mepivacaine< Tetracaine < Etidocaine =Bupivicaine = Robivicaine

(note EBR are the same protein binding at 95% and all are considered long anesthetic duration BUT their lipid solubility numbers are different!)

44
Q

Systemic absorption of injected LA depends on ?

A

Blood flow

45
Q

Blood flow (blood concentration of LA) is determined by?

A

Site of injection.
Presence or absence of vasoconstrictor.
LA agent used.

46
Q

Blood flow ranking (from highest to lowest)?

A

intraarterial/intravenous> tracheal> intercostal> caudal> paracervical> epidural> brachial plexus> sciatic/subarachnoid/femoral> subcutaneous

47
Q

The higher the blood flow, the faster the absorption/elimination away from the injection site, this decreases WHAT?

A

decreases the duration of action.

48
Q

The higher the blood flow the faster the WHAT?

A

absorption/ elimination away from the site of injection.

49
Q

What is the main medication we have talked about that we use to cause vasoconstriction with LA’s?

A

EPI

50
Q

The decreased absorption (in blood) by using a vasoconstrictor like epi facilitates what 4 good effects?

A

facilitates neuronal uptake, enhances quality of analgesia, prolongs duration of action, and limits toxic side effects

51
Q

If a LA is highly tissue bound and lipid soluble then what does that cause?

A

more slowly absorbed, thus increased DOA.

52
Q

What role does LA concentration play in DOA?

A

the greater the concentration of injected LA, longer the duration of action.

53
Q

Distribution depends on organ uptake… which is determined by? (three answers)

A

Tissue perfusion
Tissue:blood partition coefficient
Tissue mass

54
Q

Which organs are responsible for initial uptake of LA?

A

Highly perfused organs (brain, heart, lungs, kidneys, liver) are responsible for initial uptake of LA, followed by a slower redistribution to moderately perfused tissues (gut & muscle).

55
Q

What organ extracts significant amounts of LA thus, systemic toxicity involves much lower doses following arterial injection and/or children with “right to left” shunts

A

Lungs

56
Q

Who are more susceptible to toxic side effects of lidocaine when injected IV as an antiarrhythmic agent?

A

Children with “right to left” shunts.

57
Q

ncreased lipid solubility = greater plasma protein binding = ???

A

greater tissue uptake

58
Q

WHAT provides the greatest reservoir for distribution of LA into bloodstream because of its large mass?

A

Muscle

59
Q

When you are injecting a LA what is one very easy thing you can do every single time to make sure you are not in an artery or vein? Why does this matter?

A

Aspirate (checks for blood)

This matters because if you inject a LA directly into an artery or vein then systemic toxicity could take place!

SUM'20 - Regional (17 decks)

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