Regional Lecture Test Flashcards

(40 cards)

0
Q

What reverses a local anesthetic?

A

Time

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1
Q

What are the three characteristic segments all local anesthetics have?

A
  • intermediate carbon group (ester/amide)
  • unsaturated ring system
  • amine end
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2
Q

What is the most prominent problem of local anesthetics?

A

inadvertent vascular injection

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3
Q

What is responsible for the classification of a local anesthetic and why?

A
  • The ester or amide linkage

- the only difference between the aromatic ring and amine end

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4
Q

How can you differentiate between an ester and amide by looking at the name?

A
  • Esters have one i (procaine,cocaine)

- Amides have two i’s (lidocaine, mepivacaine)

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5
Q

What does lipid solubility relate to?

A

High lipid solubility is proportional to potency of a local anesthetic

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6
Q

Definition of Lipophilic/Hydrophobic

A

Lipophilic-fat loving

Hydrophobic-water fearing

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7
Q

Why does lipid solubility affect potency?

A

Nerve sheath covering is lipid based so other lipids pass through easily

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8
Q

What type of binding is related to the duration of action?

A

Protein Binding

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9
Q

Between duration of action and potency, which is more related to lipid solubility?

A

Potency

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10
Q

Sodium channels have what three functional states?

A

Resting (closed)
Inactive
Open

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11
Q

What are the two parts to a local anethestic?

A

Nonionized (fat soluble

Ionized (water soluble)

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12
Q

How does LA work? Part 1

A
  • -Once injected LA dissociates into its active(non-charged) and inactive(charged) forms
  • -the non-charged(lipid soluble) part passes through the lipid soluble membrane
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13
Q

How does LA work? Part 2

A
  • -the lipid portion that passes through, binds with minerals in axoplasm
  • -the reassociated LA blocks the action potential by blocking Na pump and prevents the pain stimulus from moving down the nerve
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14
Q

What is the definition of pKa?

A

pKa is the pH at which 50% of the drug is in the charged (ionized, inactive) form and the remaining half is the uncharged (active) state

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15
Q

What is the correlation of pKa and potency?

A

–the lower the pKa the greater the potency

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16
Q

How does pKa work?

A
  • -the lower the pH of the environment the drug is placed into compared to it pKa, the more ionized (inactive) it becomes
  • -so the higher the pKa the more inactive it becomes
  • -the lower the pKa the more active drug left to work
17
Q

Why are vasoconstrictors added to LA’s?

A

To decrease the spread , vascular uptake of the drug

18
Q

What 4 helpful things happen when adding a vasoconstrictor to the LA?

A
  • higher local concentration of the LA
  • longer duration of effect
  • reduced systemic absorption
  • hemostasis for improved visualization
19
Q

When should we not use a vasoconstrictor?

A
  • fingers
  • toes
  • nose
  • hose
20
Q

What drug reverses the negative results of a vasoconstrictor in a given area?

A

-phentolamine 1.5-5mg

21
Q

How are LA with epi packaged?

A

Red top with red lettering on label

22
Q

What does adding NaHCO3 do to the LA?

A
  • stored at pH of 4-6 for shelf life (decreases unionized/active form)
  • buffering with NaHCO3 increases the unionized/active form to increase speed of penetration to nerve tissue
23
Q

All LA, except which three, produce vascular smooth muscle relaxation?

A
  • Cocaine (topical)
  • Ropivacaine (parenteral)
  • Lidocaine (parenteral)
24
If VSM relaxation occurs, it increases the risk of ________?
toxic effects
25
Which type of tissue receives the most amount of LA if it enters blood stream and why?
Muscle because it is highly perfused
26
How are esters metabolized?
- Ester hydrolysis occurs through esterase - Occurs in plasma, RBC's, and liver - Primarily, Plasma Cholinesterase rapidly metabolizes LA
27
How are amides metabolized?
- occurs primarily in liver - microsomal cytochrome P-450 enzyme - dependent on hepatic blood flow and enzyme availability
28
What are the two most common ways that toxicity occurs?
- inadvertent intravascular injection | - absorption of large amounts of drug from a nerve block that requires large volume
29
LAST stands for what and what 5 things are affected?
- Local anesthetic systemic toxicity (seen 5-10min) - CNS - CV - Allergic Reaction - Methemoglobinemia - Local tissue
30
CNS effects of LAST
Mild = tongue numbness, apprehension, restlessness Moderate = peri-oral tingling, tremors, slurred speech, drowsiness Severe = Seizures, cardiorespiratory depression, coma, death
31
CV LAST effects
- palpitations - HTN - ventricular dysrhythmias - myocardial depression - bradycardia - hypotension - CV collapse
32
PVS LAST effects
- low concentrations-vasoconstriction and increased SVR | - as doses increases significant vasodilation and hypotension occurs
33
Arrythmias with LAST
-LAST effects electrophysiologic and contractile forces - increased PR interval and QRS durations - complete AV block, bradycardia, cardiac arrest
34
What preservative is associated with allergic reactions to LA?
More common in esters due to para-aminobenzoic acid
35
Which three LA can cause Methemoglobinemia?
- Prilocaine (citanest) - Benzacaine - Cetacaine
36
What is the metabolite that causes methemoglobinemia and what are the s/s?
- o-toluidine oxidizes hgb to met-hgb - tachypnea - metabolic acidosis - brownish-gray cyanosis
37
Met-Hgb treatment
- Spontaneous is 2-3 hrs | - methylene blue 1mg/kg
38
LAST treatment
- Airway mgt - seizure suppresion - CPR - alert nearest facility with bypass capabilities - give IV intralipid
39
Intralipid dosing
- Bolus: 20% intralipid 1.5ml/kg over 1 min - Cont: 0.25ml/kg/min - Double infusion if BP returns but stays low - Continue infusion for a minimum of 30 min