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GNURS625 > LA Supp > Flashcards

LA Supp Flashcards

1
Q

What are local Anesthetics?

A

Drugs that reversibly block the conduction of electrical impulses along nerve fibers.

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2
Q

The ability of the local anesthetic to produce a reversible conduction blockade of impulses along central and peripheral nerve pathways is dependent on?

A

Physiochemical properties of the local anesthetic.

Anatomy of the nerve being blocked.

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3
Q

Nueron electrophysiology

A

Resting membrane potential of a peripheral nerve is
-70mV

Rapid depo somewhere around -53

NA+ leaks in during impulse and depolarizes cell to +35

Resting membrane potential is restored by active removal of intracellular Na+ by the sodium/potassium pump. (3:2)

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4
Q

Nerve fibers are classified into three groups: A,B,C and based on?

A

diameter and myelination of nerve fibers

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5
Q

Charcteristics of A Fibers Slide 17

A

Slide 17

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6
Q

Characteristics of B fibers

A

Diameter (4µm)
Slower conduction velocity and less myelination than A fibers.
Preganglionic autonomic nerves

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7
Q

Characteristics of C fibers

A

Diameter (1-2µm)
Slowest speed of conduction
Conduct pain and temperature impulses
The only fibers that are unmyelinated

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8
Q

What is LA MOA?

A

Reversibly block sodium channels

These receptors, located on the intracellular side of the cell membrane, have a greater affinity for the charged form of the local anesthetics.

Local anesthetics must first penetrate the cell membrane before they produce their effects. Penetration of the local anesthetic is greatly facilitated if the drug is in the uncharged or non-ionized state.

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9
Q

All local anesthetic molecules have three characteristic segments. What are they?

A

An unsaturated aromatic ring system

An intermediate carbon group

A tertiary amine

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10
Q

What are the major difference in the core structure of local anesthetics?

A

Ester vs. amide linkage binding the aromatic ring to the tertiary amine.

(The type of linkage is clinically important because it has implications for metabolism and allergic potential.)

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11
Q

Ester VS Amide

A 
Ester: 
Procaine
Chloroprocaine
Tetracaine
Cocaine

Amides all have “I”s in them. Example Li docaine
Mepi vacaine

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12
Q

Onset of action determinants 1

Lipid solubility

A

major determinant is amount of LA that is in the non-ionized form.
(If its more in the non-ionized form, it will be more lipid soluble.)

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13
Q

Onset of action determinants 2

What is the PKA?

A

Is the pH of the LA at which the amount of ionized and non-ionized drug is equal.

(LA with a pKa closet to physiologic pH will have a higher concentration of non-ionized form that can readily pass thru the nerve cell membrane)

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14
Q

What is ion trapping and how does it relate to fetal circulation. What factors contribute more to it?

A

results from changes in pH in relationship to the agent’s pKa.

Acidosis resulting from hypoxia may increase the ionized fraction of local anesthetic Accumulation in fetal circulation

Hypoxia & injection into infected tissue

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15
Q

What does DOA correlate with

A

lipid solubility

(Highly lipid soluble LA have a longer duration of action, because they are less likely to be cleared by blood flow (sequestered in lipid depot).

(LA that are highly lipid soluble are also (typically) highly protein bound.)

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16
Q

Kinetics

The higher the __________ of drug injected that remain in the area of the nerve/nerves to be blocked, the ____________the onset of action.

A

concentration (number of molecules)/faster

Systemic absorption away from the tissue injection site results in the offset and termination of drug effect.

17
Q

Systemic absorption of injected LA depends on?

A

blood flow

The more vascularized the area the greater the systemic absorption

18
Q

Adding a vasoconstrictor helps?

A 
Addition of epinephrine
Decreases vascular absorption
Increases nerve cell uptake
Enhances the quality of analgesia
Prolongs the duration of action
Limits toxic side effects
19
Q

All local anesthetics (except cocaine) produce?

A

relaxation of vascular smooth muscle.

Resultant vasodilation increases blood flow to the surrounding tissue where the drug is deposited.
This results in increased LA absorption, limits its duration of action and increases the probability of toxic effects.

20
Q

What are esters predominantly metabolized by?

A

pseudocholinesterase

Ester hydrolysis is a rapid process

Water soluble metabolites excreted in urine

Pts with genetically abnormal pseudocholinesterase are at risk for toxic side effects

21
Q

Procaine and benzocaine are metabolized to

A

p-aminobenzoic acid (PABA) ~ associated with allergic reactions

22
Q

Amides Metabolized by?

A

microsomal P-450 enzymes in liver (N-dealkylation and hydroxylation)

Overall metabolism much slower than ester hydrolysis
Decrease in liver function will reduce metabolism and increase toxicity

Metabolites depend on renal clearance

23
Q

Metabolites of prilocaine (o-toluidine derivatives) ______ after large doses (>10ma/kg) and convert hgb to _________.

A

accumulate/methemoglobin

Metabolites of benzocaine spray – methgb

Treat significant methgb with IV methylene blue

24
Q

Methemoglobinemia S/S with high concentrations?

A

Brownish gray cyanosis
Tachypnea
Metabolic acidosis

Severe signs and symptoms ensue with:
Tissue hypoxia
Headache
Irritability
Loss of consciousness
25
Q

Methemoglobinemia: Treatment

A

Spontaneous recovery in 2-3 hours

Immediate reversal with methylene blue IV

(Formation of methemoglobinemia not clinically significant in healthy patient. Becomes an issue in patient’s with severe anemia or heart failure that cannot tolerate the reduction in oxygen-carrying capacity.)

26
Q

What influences toxicity?

A

Absorption and metabolism

27
Q

What are some additives to local anesthetics and what do they do?

A

Opioids
Sodium bicarbonate
Epinephrine

These are added to increase the safety, quality, intensity, duration and rate of onset of anesthesia.

28
Q

Some causes of toxicity?

A

Inadvertent intravascular injection

Administration of excessive dose

29
Q

CNS toxicity treatment?

A

Convulsions - increased oxygen consumption in the presence of compromised ventilation.
Assure patent airway and adequate ventilation
Administration of anticonvulsant
Progression to cardiac arrest

30
Q

CV s/s of toxicity

A

All LA depress myocardial automaticity
Reduce the duration of the refractory period
High blood levels of LA will depress contractility and conduction
All LA produce smooth muscle relaxation and arteriolar vasodilation… (not cocaine)
Ensuing combination of bradycardia, heart block, and hypotension may cause cardiac arrest

31
Q

What happens with Bupivacaine if it is accidently injected IV?

A

severe cardiotoxic reaction.

Resuscitation from bupivacaine often requires high doses of vasopressor and prolonged resuscitation effort.

32
Q

CNS s/s of toxicity?

A

Not acting right
to

Confusion
dizziness
metallic taste

to
seizure

33
Q

What is a lipid rescue used for?

A

Toxicity. Cardiotoxicity

34
Q

What are the Transient Neurologic Symptoms that can be associated with spinal anesthesia?

A

Dysesthesia, burning pain, and aching in lower extremities and buttocks.

Associated with use of lidocaine for anesthesia

35
Q

Topical Cocaine is a Unique local anesthetic in that it causes?

A

vasoconstriction

Cocaine produces vasoconstriction by blocking norepinephrine and epinephrine uptake into adrenergic nerve endings.

Good for nasal surgery

36
Q

Why does the Potential for significant drug interaction exists with topical cocaine an Epi injection into nasal mucosa?

A

Cocaine blocks the uptake of epinephrine
Toxic effect from injection of epinephrine may occur
Life threatening ventricular arrhythmias

37
Q

What is EMLA?

A

Eutectic mixture of Local Anesthetic

Mixture of lidocaine and prilocaine
Accumulates at the site of dermal pain receptors and nerve endings
Satisfactory analgesia occurs about 1 hour after application with an occlusive dressing.

38
Q

What are the special considerations when applying topical anesthetics to mucous membranes?

A

Absorption of local anesthetics from the mucous membrane is significant and systemic toxicity can occur.

Nose – direct Vena Cava 
Mouth – direct Vena Cava
Tracheobronchial tree
Esophagus
Genitourinary tract

GNURS625 (3 decks)

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