Local Anesthetic Toxicity Flashcards
(110 cards)
1
Q
Are LA allergies/anaphylaxis rare?
A
Yes
2
Q
If someone does have a LA allergy, what is it the result of?
A
Additives in the LA
3
Q
Approximately how many patients have a true LA allergy?
A
15%
4
Q
How can you exclude an LA allergy?
A
A careful history
5
Q
If an allergic reaction is suspected, should the LA be continued or discontinued?
A
discontinued
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
7
Q
What is the IV epi dose for mild anaphylaxis?
A
5-10 mcg
8
Q
What is the IV epi dose for severe anaphylaxis?
A
50-100 mcg
9
Q
How do toxic levels of LA occur?
A
- accidental injection into the intravascular causing systemic absorption
- administration of an excessive dose
10
Q
What 2 systems are affected by LA toxicity? Is it direct or indirect? Depressant or accelerant?
A
Directly CNS and CV depressant
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
12
Q
Do LAST symptoms progress from a state of excitation to depresssion or depression to excitation?
A
Excitation to depression
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
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
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
16
Q
What does LAST stand for?
A
Local Anesthetic Toxicity
17
Q
What is unintentional venous injection of LA associated with a rapid onset of?
A
Seizures
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
19
Q
The withdrawal of what medication from the market has reduced the incidence of LAST?
A
0.75% Bupiv
20
Q
Can LAST have devastating results?
A
Yes
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
22
Q
What are 3 examples of highly vascularized sites?
A
- Arterial
- tracheal
- intercostal
23
Q
What are 2 examples of low vascularized sites?
A
Sciatic/femoral
subcutaneous
24
Q
What are the CNS effects of LAST?
A
- Tinnitus
- circumoral numbness
- metallic taste
- agitation
seizures - LOC
- Resp arrest
25
What are the CV effects of LAST?
Hypotension
Bradycardia
Ventricular arrhythmias
CV collapse
26
What is Phase 1 of LAST described as?
CNS excitation
27
What is Phase 2 of LAST described as?
CV depression
28
What is Phase 3 of LAST described as?
CV collapse
29
_____ perfused organs get initial rapid uptake of LAs
HIGHLY perfused organs get initial rapid uptake of LAs
30
Which organs extract a significant amount of local anesthetics?
Lungs
31
Is the threshold for systemic toxicity higher or lower in doses injected into the artery than vein?
Lower doses threshold in arteries than veins - takes less dose in an artery to evoke toxicity than vein
32
Peds patients with which type of shunt are more susceptible to toxic side effects to lidocaine used as an antiarrythmic?
R to L shunt
33
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?
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
34
Which tissue provides the greatest reservoir for distribution of LA agents in the bloodstream?
Muscle tissue
35
Why does ______ tissue act as the best reservoir for systemic distribution of LAs?
Because of its large mass
36
How can you dififerentiate an amide LA from an ester LA?
- Amides have 2 i's
- esters have 1 i
37
What are examples of amides?
lidocaine
bupivacaine
ropivacaine
mepivacaine
38
What are examples of esters?
Benzocaine
cocaine
tetracaine
39
What is the toxic dose of chloroprocaine & procaine?
12 mg/kg
40
What is the toxic dose of bupivacaine, ropivacaine, cocaine, & tetraicaine?
3 mg/kg
41
What is the toxic dose of lidocaine and mepivocaine without epi?
4.5 mg/kg
42
What is the toxic dose of lidocaine & mepivocaine with epi?
7 mg/kg
43
What is the toxic dose of prilocaine?
8 mg/kg
44
With bupivocaine, will you see simultaneous or staggered seizing and CV collapse? Will the patient be hypoxic before/will there be antecedent hypoxia ?
- Simultaneous seizures and CV collapse
- No antecedent hypoxia
45
What are the CV toxic effects of mepivocaine & lidocaine - positive or negative inotropy?
negative inotropy
46
What are the CV toxic effects of bupivacaine & ropivacaine - positive or negative inotropy? Arrythmias?
negative inotropy and arrhythmias
47
With CV toxicity, is there free concentration of LAs?
yes
48
Are LAs resistant to resuscitation in the setting of cardiac arrest due to toxicity?
Yes
49
Is the CV system more resustant to LA toxicity?
Yes
50
__ - __x the dose of LAs needed for production of seizures is needed for ______
4 - 7x the dose of LAs needed for production of seizures is needed for CV COLLAPSE
51
What are the 3 possible ways CV toxicity of LA manifest?
- Direct action on cardiac muscle
- Conduction system disturbances
- Direct effects
52
What would be considered direct action on cardiac muscle in regards to LAST?
affecting myocardial contractility
53
What types of LAs would cause conduction system disturbances in regards to LAST?
highly lipid soluble, like bupivacaine which cause great CV depression by specifically binding to the conduction system
54
What is an example of a highly lipid soluble LA?
Bupivacaine
55
What are 4 conduction delays associated with LAST?
- Prolonged PR interval
- complete HR block
- Sinus arrest
- asystole
56
What are 3 ventricular dysrhythmias w/widened QRS associated with LAST?
-simple ventricular ectopy
- torsades de pointes
- V Fib
57
Are CNS directly or indirectly related to lipid solubility?
directly
58
Are LAs with higher lipid solubility more toxic?
yes
59
Which form, non ionized or ionized, in the blood can penetrate the BBB?
Non ionized
60
Which form, bound or unbound fraction, in the blood can penetrate the BBB?
unbound
61
What are the 5 early Signs of CNS Toxicity?
- dizziness
- blurred vision
- tinnitus
- circumoral numbness
- metallic taste
62
What are 5 CNS Excitatory Signs associated with toxciity?
- nervousness
- agitaiton
- restlessness
- muscle twitching
- tonic clonic seizures
63
Why do you see twitching in LAST?
blockade of the inhibitory pathways
64
______ may lead to tonic clonic seizure in LAST
TWITCHING
65
What are 5 early signs of CNS depression associated with toxcity?
- slurred speech
- drowsiness
- unconsciousness
- respiratory arrest
66
Conscious patients receiving ______ may have a ______ seizure threshold
Conscious patients receiving BENZOS may have a HIGHER seizure threshold
67
Do patients on benzos manifest seizure activity before we see a complete CNS depression in LAST?
No, they may not
68
Patients receiving ______ depressant drugs may present with only CNS depression _______ any preceding excitatory signs
Patients receiving CNS depressant drugs may present with only CNS depression WITHOUT any preceding excitatory signs
69
_______ lowers seizure threshold with LA administration
Hypercarbia (increased CO2)
70
Why does hypercarbia lower the seizure threshold?
Acidosis decreases protein binding of LA making more drug available to the CNS
71
What are the 3 focused steps to manage treatment of LAST?
- Airway management (intubate and 100% O2)
- hemodynamic support
- EARLY administration of lipid emulsion therapy
72
What should you focus on if convulsions during LAST?
oxygenation & ventilation - intubate if necessary
73
How to treat cardiac arrest in LAST?
follow ACLS protocol
74
How to treat persistent hypotension & bradycardia in LAST?
high doses of epinephrine and atropine
75
Do you give high low doses of epi and atropine in LAST treatement?
high doses
76
What is the treatment of refractory cardiac arrest?
Lipid Emulsion
77
How long should you continue lipid emulsion infusion after attaining circulatory stability?
10 mins
78
Should you use propofol if there are signs of CV instability?
NO, it is contraindicated in CV toxicity
79
Should you wait to administer lipid emulsion until ACLS?
No, that is unreasonable and has been proven unsuccessful
80
Is there evidence which claims use of epi can impair resuscitation from LAST and reduce efficacy of lipid rescue?
Yes
81
In terms of pharm tx of LAST in setting of cardiac arrest, what should epi be reduced to?
less than or equal to 1 mcg/kg
82
Which medication should you avoid in LAST cardiac arrest?
CCB, BB, vasopressin, or local anesthetics
83
What is the preferred medication for sedation in LAST?
benzos
84
Which medication for sedation should you NOT use in LAST?
propofol
85
What concentration is lipid emulsions (%)?
20%
86
What is the algorithm for giving lipid emulsion 20% to patients >70kg?
-Bolus 100 mls over 2-3 mins
- maintenance of 200-250mls over 15-20mins
87
What is the algorithm for giving lipid emulsion 20% to patients <70kg?
- bolus 1.5 ml/kg lipids over 2-3 mins
- maintenance of 0.25 ml/kg/min (using IBW)
88
What is the max dose of lipid emulsions for adults and peds?
12 ml/kg
89
How many times can you re-bolus if patient remains unstable? What do you do to the infusion rate after re-bolus?
- once or twice at the same dose
- double the infusion rate after the bolus
90
Is propofol a component of lipid rescue?
NO
91
Can lipid emulsion therapy be formulated 10% and 20%?
Yes
92
What is the metabolic effect of lipid emulstion therapy? What does this help with
- increased uptake of free fatty acids by the mitochondria
- cardiac function
93
How do free fatty acid (FFAs) affect LA binding to voltage gated Na channels?
the FFAs interfere with the binding of LA to the site of action, reducing the toxic affect
94
How does lipid emulsion therapy enhance cytoprotection?
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
What is the Akt pathway responsible for?
cellular survival signaling pathway
96
What is GSK-3β responsible for?
an enzyme involved in apoptotic signaling pathways
97
What is the effect of FFAs on Ca entry and myocyte function?
FFAs increase Ca entry which restores cardiac myocyte function - helps with reversal of cardaic depression by improving excitation-contraction relationship
98
What is included in the emulsion of fat emulsion therapy?
soybean oil
egg yolk phospholipids glycerol
water
99
Lipid sink theory: ______ therapy creates a fatty barrier that keeps the LA from entering the _______
LIPID therapy creates a fatty barrier that keeps the LA from entering the BLOODSTREAM
100
What theory is associated with lipid emulsion therapy effectiveness?
Lipid Sink Theory
101
Lipid sink theory: Additional ______ to ______ tissue is able to process toxic levels of LA at a ______ metabolic rate
Additional ENERGY to MYOCARDIAL tissue, able to process toxic levels of LA at a HIGHER metabolic rate
102
Lipid sink theory: LA becomes ______, stationary
Inert
103
Separate _____ compartment within ______ into which the LA are drawn
Separate LIPID compartment within PLASMA into which the LA are drawn
104
Can lipid emulsion therapy cause PHTM?
yes
105
Can lipid emulsion therapy cause fat emboli?
yes
106
Can lipid emulsion therapy cause thrombophlebitis?
yes
107
Can lipid emulsion therapy cause anaphylaxis?
yes
108
Can lipid emulsion therapy have drug interaction?
yes
109
Can lipid emulsion therapy cause infection?
yes
110
Can lipid emulsion therapy cause increased ICP post TBI?
yes
