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Basics Principles of Anesthesia > Local Anesthetic Toxicity > Flashcards

Local Anesthetic Toxicity Flashcards

1
Q

Are LA allergies/anaphylaxis rare?

A

Yes

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2
Q

If someone does have a LA allergy, what is it the result of?

A

Additives in the LA

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3
Q

Approximately how many patients have a true LA allergy?

A

15%

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4
Q

How can you exclude an LA allergy?

A

A careful history

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5
Q

If an allergic reaction is suspected, should the LA be continued or discontinued?

A

discontinued

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6
Q

What are the 4 steps to manage anaphylaxis?

A
  • secure a patient’s airway
  • 100% O2
  • give IV fluids, for expansion
  • IV epi titrated
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7
Q

What is the IV epi dose for mild anaphylaxis?

A

5-10 mcg

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8
Q

What is the IV epi dose for severe anaphylaxis?

A

50-100 mcg

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9
Q

How do toxic levels of LA occur?

A
  • accidental injection into the intravascular causing systemic absorption
  • administration of an excessive dose
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10
Q

What 2 systems are affected by LA toxicity? Is it direct or indirect? Depressant or accelerant?

A

Directly CNS and CV depressant

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11
Q

Why do CNS effects occur in LA toxicity? Which pathway is blocked?

A

selective blocking of the inhibition of excitatory pathways in the CNS

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12
Q

Do LAST symptoms progress from a state of excitation to depresssion or depression to excitation?

A

Excitation to depression

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13
Q

What are the 5 early S/S of LA toxicity as the LA dose or concentration increases?

A

Vertigo
Tinnitus
Ominous feelings
Circumoral numbness
Garrulousness

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14
Q

What are the 5 late S/S of LA toxicity as the LA dose or concentration increases?

A

Tremors
Myoclonic jerks
Convulsions
Coma
Cardiovascular collapse

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15
Q

What are the determinants of toxcitiy?

A
  • Plasma & Blood concentrations
  • Total drug dose & LA used
  • Vasoconstrictor use
  • Injection Site = determines final blood level concentration of LA agent & is related to tissue diffusion and vascularity
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16
Q

What does LAST stand for?

A

Local Anesthetic Toxicity

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17
Q

What is unintentional venous injection of LA associated with a rapid onset of?

A

Seizures

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18
Q

In what type of regional anesthesia does the unintentional venous injection leading to seizure occur? What population? Why this population?

A
  • Epidural
  • Maternal
  • Maternal epidural vein engorgement
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19
Q

The withdrawal of what medication from the market has reduced the incidence of LAST?

A

0.75% Bupiv

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20
Q

Can LAST have devastating results?

A

Yes

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21
Q

Does the likelihood for LAST increase of decrease as the vascularity increases at the site of administration?

A

Increased liklihood of LAST in more vascular sites

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22
Q

What are 3 examples of highly vascularized sites?

A
  • Arterial
  • tracheal
  • intercostal
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23
Q

What are 2 examples of low vascularized sites?

A

Sciatic/femoral
subcutaneous

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24
Q

What are the CNS effects of LAST?

A
  • Tinnitus
  • circumoral numbness
  • metallic taste
  • agitation
    seizures
  • LOC
  • Resp arrest
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25
Q

What are the CV effects of LAST?

A

Hypotension
Bradycardia
Ventricular arrhythmias
CV collapse

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26
Q

What is Phase 1 of LAST described as?

A

CNS excitation

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27
Q

What is Phase 2 of LAST described as?

A

CV depression

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28
Q

What is Phase 3 of LAST described as?

A

CV collapse

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29
Q

_____ perfused organs get initial rapid uptake of LAs

A

HIGHLY perfused organs get initial rapid uptake of LAs

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30
Q

Which organs extract a significant amount of local anesthetics?

A

Lungs

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31
Q

Is the threshold for systemic toxicity higher or lower in doses injected into the artery than vein?

A

Lower doses threshold in arteries than veins - takes less dose in an artery to evoke toxicity than vein

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32
Q

Peds patients with which type of shunt are more susceptible to toxic side effects to lidocaine used as an antiarrythmic?

A

R to L shunt

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33
Q

If you increase lipid solubility does this cause greater plasma protein binding and greater tissue uptake from an aqueous compartment? What does that mean in regards to LAST?

A

Yes, more durg will bind to the plasma protein if the drug has a higher lipid solubility. This reducers the amount of free drug, reducing the risk of last

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34
Q

Which tissue provides the greatest reservoir for distribution of LA agents in the bloodstream?

A

Muscle tissue

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35
Q

Why does ______ tissue act as the best reservoir for systemic distribution of LAs?

A

Because of its large mass

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36
Q

How can you dififerentiate an amide LA from an ester LA?

A
  • Amides have 2 i’s
  • esters have 1 i
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37
Q

What are examples of amides?

A

lidocaine
bupivacaine
ropivacaine
mepivacaine

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38
Q

What are examples of esters?

A

Benzocaine
cocaine
tetracaine

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39
Q

What is the toxic dose of chloroprocaine & procaine?

A

12 mg/kg

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40
Q

What is the toxic dose of bupivacaine, ropivacaine, cocaine, & tetraicaine?

A

3 mg/kg

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41
Q

What is the toxic dose of lidocaine and mepivocaine without epi?

A

4.5 mg/kg

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42
Q

What is the toxic dose of lidocaine & mepivocaine with epi?

A

7 mg/kg

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43
Q

What is the toxic dose of prilocaine?

A

8 mg/kg

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44
Q

With bupivocaine, will you see simultaneous or staggered seizing and CV collapse? Will the patient be hypoxic before/will there be antecedent hypoxia ?

A
  • Simultaneous seizures and CV collapse
  • No antecedent hypoxia
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45
Q

What are the CV toxic effects of mepivocaine & lidocaine - positive or negative inotropy?

A

negative inotropy

46
Q

What are the CV toxic effects of bupivacaine & ropivacaine - positive or negative inotropy? Arrythmias?

A

negative inotropy and arrhythmias

47
Q

With CV toxicity, is there free concentration of LAs?

A

yes

48
Q

Are LAs resistant to resuscitation in the setting of cardiac arrest due to toxicity?

A

Yes

49
Q

Is the CV system more resustant to LA toxicity?

A

Yes

50
Q

__ - __x the dose of LAs needed for production of seizures is needed for ______

A

4 - 7x the dose of LAs needed for production of seizures is needed for CV COLLAPSE

51
Q

What are the 3 possible ways CV toxicity of LA manifest?

A
  • Direct action on cardiac muscle
  • Conduction system disturbances
  • Direct effects
52
Q

What would be considered direct action on cardiac muscle in regards to LAST?

A

affecting myocardial contractility

53
Q

What types of LAs would cause conduction system disturbances in regards to LAST?

A

highly lipid soluble, like bupivacaine which cause great CV depression by specifically binding to the conduction system

54
Q

What is an example of a highly lipid soluble LA?

A

Bupivacaine

55
Q

What are 4 conduction delays associated with LAST?

A
  • Prolonged PR interval
  • complete HR block
  • Sinus arrest
  • asystole
56
Q

What are 3 ventricular dysrhythmias w/widened QRS associated with LAST?

A

-simple ventricular ectopy
- torsades de pointes
- V Fib

57
Q

Are CNS directly or indirectly related to lipid solubility?

A

directly

58
Q

Are LAs with higher lipid solubility more toxic?

A

yes

59
Q

Which form, non ionized or ionized, in the blood can penetrate the BBB?

A

Non ionized

60
Q

Which form, bound or unbound fraction, in the blood can penetrate the BBB?

A

unbound

61
Q

What are the 5 early Signs of CNS Toxicity?

A
  • dizziness
  • blurred vision
  • tinnitus
  • circumoral numbness
  • metallic taste
62
Q

What are 5 CNS Excitatory Signs associated with toxciity?

A
  • nervousness
  • agitaiton
  • restlessness
  • muscle twitching
  • tonic clonic seizures
63
Q

Why do you see twitching in LAST?

A

blockade of the inhibitory pathways

64
Q

______ may lead to tonic clonic seizure in LAST

A

TWITCHING

65
Q

What are 5 early signs of CNS depression associated with toxcity?

A
  • slurred speech
  • drowsiness
  • unconsciousness
  • respiratory arrest
66
Q

Conscious patients receiving ______ may have a ______ seizure threshold

A

Conscious patients receiving BENZOS may have a HIGHER seizure threshold

67
Q

Do patients on benzos manifest seizure activity before we see a complete CNS depression in LAST?

A

No, they may not

68
Q

Patients receiving ______ depressant drugs may present with only CNS depression _______ any preceding excitatory signs

A

Patients receiving CNS depressant drugs may present with only CNS depression WITHOUT any preceding excitatory signs

69
Q

_______ lowers seizure threshold with LA administration

A

Hypercarbia (increased CO2)

70
Q

Why does hypercarbia lower the seizure threshold?

A

Acidosis decreases protein binding of LA making more drug available to the CNS

71
Q

What are the 3 focused steps to manage treatment of LAST?

A
  • Airway management (intubate and 100% O2)
  • hemodynamic support
  • EARLY administration of lipid emulsion therapy
72
Q

What should you focus on if convulsions during LAST?

A

oxygenation & ventilation - intubate if necessary

73
Q

How to treat cardiac arrest in LAST?

A

follow ACLS protocol

74
Q

How to treat persistent hypotension & bradycardia in LAST?

A

high doses of epinephrine and atropine

75
Q

Do you give high low doses of epi and atropine in LAST treatement?

A

high doses

76
Q

What is the treatment of refractory cardiac arrest?

A

Lipid Emulsion

77
Q

How long should you continue lipid emulsion infusion after attaining circulatory stability?

A

10 mins

78
Q

Should you use propofol if there are signs of CV instability?

A

NO, it is contraindicated in CV toxicity

79
Q

Should you wait to administer lipid emulsion until ACLS?

A

No, that is unreasonable and has been proven unsuccessful

80
Q

Is there evidence which claims use of epi can impair resuscitation from LAST and reduce efficacy of lipid rescue?

A

Yes

81
Q

In terms of pharm tx of LAST in setting of cardiac arrest, what should epi be reduced to?

A

less than or equal to 1 mcg/kg

82
Q

Which medication should you avoid in LAST cardiac arrest?

A

CCB, BB, vasopressin, or local anesthetics

83
Q

What is the preferred medication for sedation in LAST?

A

benzos

84
Q

Which medication for sedation should you NOT use in LAST?

A

propofol

85
Q

What concentration is lipid emulsions (%)?

A

20%

86
Q

What is the algorithm for giving lipid emulsion 20% to patients >70kg?

A

-Bolus 100 mls over 2-3 mins
- maintenance of 200-250mls over 15-20mins

87
Q

What is the algorithm for giving lipid emulsion 20% to patients <70kg?

A
  • bolus 1.5 ml/kg lipids over 2-3 mins
  • maintenance of 0.25 ml/kg/min (using IBW)
88
Q

What is the max dose of lipid emulsions for adults and peds?

A

12 ml/kg

89
Q

How many times can you re-bolus if patient remains unstable? What do you do to the infusion rate after re-bolus?

A
  • once or twice at the same dose
  • double the infusion rate after the bolus
90
Q

Is propofol a component of lipid rescue?

A

NO

91
Q

Can lipid emulsion therapy be formulated 10% and 20%?

A

Yes

92
Q

What is the metabolic effect of lipid emulstion therapy? What does this help with

A
  • increased uptake of free fatty acids by the mitochondria
  • cardiac function
93
Q

How do free fatty acid (FFAs) affect LA binding to voltage gated Na channels?

A

the FFAs interfere with the binding of LA to the site of action, reducing the toxic affect

94
Q

How does lipid emulsion therapy enhance cytoprotection?

A

FFA activate the Akt (serine protein kinase) pathway which leads to the inhibition of GSK-3β (apoptosis), this inhibition promotes cell survival and protects against damage

95
Q

What is the Akt pathway responsible for?

A

cellular survival signaling pathway

96
Q

What is GSK-3β responsible for?

A

an enzyme involved in apoptotic signaling pathways

97
Q

What is the effect of FFAs on Ca entry and myocyte function?

A

FFAs increase Ca entry which restores cardiac myocyte function - helps with reversal of cardaic depression by improving excitation-contraction relationship

98
Q

What is included in the emulsion of fat emulsion therapy?

A

soybean oil
egg yolk phospholipids glycerol
water

99
Q

Lipid sink theory: ______ therapy creates a fatty barrier that keeps the LA from entering the _______

A

LIPID therapy creates a fatty barrier that keeps the LA from entering the BLOODSTREAM

100
Q

What theory is associated with lipid emulsion therapy effectiveness?

A

Lipid Sink Theory

101
Q

Lipid sink theory: Additional ______ to ______ tissue is able to process toxic levels of LA at a ______ metabolic rate

A

Additional ENERGY to MYOCARDIAL tissue, able to process toxic levels of LA at a HIGHER metabolic rate

102
Q

Lipid sink theory: LA becomes ______, stationary

A

Inert

103
Q

Separate _____ compartment within ______ into which the LA are drawn

A

Separate LIPID compartment within PLASMA into which the LA are drawn

104
Q

Can lipid emulsion therapy cause PHTM?

A

yes

105
Q

Can lipid emulsion therapy cause fat emboli?

A

yes

106
Q

Can lipid emulsion therapy cause thrombophlebitis?

A

yes

107
Q

Can lipid emulsion therapy cause anaphylaxis?

A

yes

108
Q

Can lipid emulsion therapy have drug interaction?

A

yes

109
Q

Can lipid emulsion therapy cause infection?

A

yes

110
Q

Can lipid emulsion therapy cause increased ICP post TBI?

A

yes

Basics Principles of Anesthesia (6 decks)

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