Exam 4 Flashcards
(306 cards)
1
Q
What is the other name for neuromuscular monitoring
A
Acceleromyography
2
Q
most common location, nerve, and muscle monitored
A
abductor pollicis muscle, hand, ulnar nerve
3
Q
NMBD Reversal Agents
A
edrophonium
neostigmine
4
Q
Anti-Cholinergic Agents
A
atropine sulfate
glycopyrrolate
5
Q
NMBD Reversal Agents MOA
A
AcetylcholineEsterase (AchE) Inhibitors, Cholinergic Agents, COMPETITIVE ANTAGONISTS
AchE: Rapid hydrolysis (catalyze) of Ach
Inhibition = more Acetylcholine available
Ach binds to alpha subunits;
Available @:
Preganglionic (SNS & PNS)
NMJ- main focus
6
Q
Total max neostigmine dose
A
5mg
7
Q
Neostigmine max range
A
40 to 70 mcg/kg
8
Q
Edrophonium max range
A
1 mg/kg
9
Q
NMBD Reversal Agents will not work with…..
A
Will not work with deep NM blockade
because of ceiling effect
10
Q
Reversal of NM Blockade depends on 5 factors:
A
- Depth of the NM Block
- AchE Inhibitor choice
- Dose administered
- Rate of plasma clearance of NMBD
- Anesthesia agent choice and depth
11
Q
What NMBD needs to be reconstituted w/ distilled water
A
Vec - reconsitiute w/ 10 ml to make 1 ml
12
Q
Why is pancuronium given to cardiac patients?
A
INtrinsic effects on cardiac accelerators and good for the cardiac muscle
13
Q
Goal of NMBD reversal agents
A
Prevent postoperative residual NM blockade
14
Q
Sugammadex dose
A
2-16 mg/kg
15
Q
Neostigmine onset
A
5-10 min
16
Q
neostigmine duration
A
60 mins
17
Q
Neostigmine anticholinergic
A
glycopyrrolate 0.2 mg/ml of neostigmine
18
Q
Sugammadex onset
A
1-4 min
19
Q
Sugammadex duration
A
1.5-3 hrs
20
Q
sugammadex anticholinergic
A
none
21
Q
Edrophonium onset
A
1-2 mins
22
Q
Edrophonium duration
A
5-15 min
23
Q
Pyridostigminge and edrophonium are excreted by how much renaly
A
75%
24
Q
Overall side effects of NMBD reversal agents are a result from increased…..
A
Increased Nicotinic/Muscarinic Activity
25
How much neostigmine is excreted renaly
50%
30-50% hepatic if no renal function
26
CRF (chronic renal failure) does what to plasma clearance
decrease plasma clearance= prolonged action
27
Cardiac Side effect for nmbd reversal agents
Bradycardia, dysrhythmias, asystole, ↓SVR
28
Pulmonary Side effect for nmbd reversal agents
Bronchoconstriction, increased airway resistance, increased salivation
29
GI Side effect for nmbd reversal agents
Hyperperistalsis, enhanced gastric fluid secretion, PONV
30
Eyes Side effect for nmbd reversal agents
Miosis
31
Atropine side effect and matches....
side effects; mydriasis and initial tachycardia
matches profile of edrophonium
32
Atropine dose
7-10 mcg/kg
33
Glycopyrrolate matches the profile of....
Neostigmine and pyridostigmine
34
Glycopyrrolate dose
7-15 mcg/kg (1 mg max)
35
Anti-cholinergic/ anti muscarinic agents for cardiac disease
Glycopyrolate is preferred over atropine
to be administered slowly over 2-5 minutes
36
mechanism for persistent NM blockade
Acetylcholinesterase is maximally inhibited
No further anticholinesterase is effective
37
intervention for persistent nm blockade
sedation and postop ventilation
38
Sugammadex MOA
intermolecular (van der Walls) forces, thermodynamic (hydrogen) bonds, and hydrophobic interactions* -> reversal by encapsulation.
pull paralytic form nmj to the plasma
Binds to ‘free drug” in plasma**
39
Medications that sugammadex binds to
Rocuronium > Vecuronium >> Pancuronium (least), best with ROC
40
Sugammadex E1/2
2 hrs
41
Sugammadex Major route of elimination:
Urine
70% in 6 hours
90% in 24 hours
Renal impairment: C/I with dialysis by dialysis
42
Sugammadex facts
Selective Relaxant-Binding Agent
γ-cyclodextrin
dextrose units from starch
Highly water soluble= mainly excreted in the kidney
43
drug that does not need binding with glycopyrolate / atropine
sugammadex
44
Deep block sugammadex dose
1-2 post-tetanic counts but not twitch response = 4mg/kg
45
moderate sugammadex dose
2/4 twitches = 2mg/kg
46
Where is the main site of action of sugammadex
plasma
47
Sugammadex Dose With extreme block:
no post tetanic stimulation = 8-16mg/kg
Recurarization: not observed at appropriate doses
48
Reparalzation with Roc after reversal with sugammadex
5 minutes
give 1.2mg/kg
49
Reparalyzation with ROC after reversal with neostigmine
4 hours wait then give 0.6 mg/kg roc or 0.1 mg/kg with vec
50
Sugammadex Cautions
-Oral Contraceptives; Binds with Progesterone (7 days)
-Toremifene (non-steroidal anti-estrogen). Displaces NMBD from Sugammadex
-Coagulation/Bleeding; Heparin/LMWH; Elevated PTT, PT, INR
-Recurarization; than recommended doses.
51
Sugammadex side effects
Dose related; n/v, pruritis, urticaria
anaphylaxis
marked bradycardia
doesn't work
52
S&S of recurarization
-dec 02 sats
-unresponsive patient
-appears “floppy” or uncoordinated
-ineffective abdominal and intercostal activity
sometimes can verbalize: suffocating feeling
unable to sustain head lift or hand grasp
worst case: pharyngeal collapse and respiratory obstruction
53
The treatment goal for recurarization
Treat urgently and aggressively
Re-sedate the patient
Give additional reversal agents in divided doses (Neostigmine 0.05 mg/kg IV = longer duration of action).
give antimuscarinic agents; Ropinirole?
54
First local anesthetic
cocaine
55
Antiarrhythmic Drug Classes:
Class I
Sodium-channel blockers.
56
Antiarrhythmic Drug Classes:
Class 2
Beta blockers
57
Antiarrhythmic Drug Classes Class 3
potassium channel blockers
58
Antiarrhythmic Drug Classes Class 4
CCB
59
Cocaine MOA
cerebral stimulating qualities
localized vasoconstriction: shrink nasal mucosa
60
1st synthetic ester
procaine
61
The standard to which all other local anesthetics are compared.
lidocaine; the first synthetic amide
62
LA molecular structure
Has a lipophilic portion connected by a hydrocarbon chain to the hydrophilic portion.
Bond between lipophilic and hydrocarbon classifies LA as ester or amide
63
Lidocaine IV dose
1 to 2 mg/kg IV (initial bolus) over 2 - 4 min.
1 to 2 mg/kg/hour (drip)
terminated 12 - 72 hours
Careful monitoring: cardiac, hepatic, renal dysfunction
64
Ester or amide determination is based on which portion of the LA structure?
the link between the lipophilic aromatic and hydrocarbon intermediate chain
65
Ph for LA
pH 6 (HCl salt): Weak Bases
66
Composition of LA
Epinephrine
Sodium Bisulfite
weak bases
67
onset procaine
slow
68
onset chloropocaine
rapid
69
tetracaine onset
slow
70
amides onset
all are slow except lidocaine is rapid
71
Duration of infiltration procaine
45-60 min
72
Duration of infiltration chloroprocaine
30-45 min
73
Duration of infiltration tetracaine
60-180 min
74
Duration of infiltration of lidocaine
60-120 min
75
Duration of infiltration prilocaine
60-120 min
76
Duration of infiltration mepivacaine
90-180 min
77
Duration of infiltration bupivicaine
240-480 min
78
Duration of infiltration levobupivicaine
240-480 min
79
Duration of infiltration ropivacaine
240 - 480 min
80
Procaine potency
1
81
chloroprocaine potency
4
82
tetracaine potency
16
83
amides potency
1; lido, prolocaine, mepivacaine
4; bupivacaine, levobupivacaine, ropivacaine
84
procaine pK
8.9
85
chloroprocaine pk
8.7
86
Tetracaine pk
8.5
87
lidocaine pK
7.9
88
prilocaine pK
7.9
89
mepivacaine pK
7.6
90
Bupivacaine pK
8.1
91
levobuvicaine pk
8.1
92
probivacaine pK
8.1
93
procaine lipid solubility
0.6
94
Tetracaine lipid solubility
80
95
lidocaine lipid solbuility
2.9
96
Prilocaine lipid solubilty
0.9
97
mepivacaine lipid solubility
1
98
bupivacaine lipid solubility
28
99
The closer the meds pK is to physiologic ph......
closer to physiologic = faster the onset of action
100
Lidocaine, tetracaine, and bupivacaine
have what to help prolong the DOA
miltivesicular liposomes upload higher amount of LA into a molecule & have a consistent release of LA in the tissues
Prolonged duration of action & decreased toxicity.
pubivacaine ER; up to 96 hours
101
LA MOA
-Binds to voltage-gated Na+ channels
-Block/inhibit Na+ passage in nerve membranes
-Slowed rate of depolarization
-Does not reach threshold
-No action potential
102
LA form for lipid solubility
nonionized = crosses to inside of cell and block na gate.
103
factors affecting blockade:
1. Lipid solubility or non-ionized/unionized form
2. Repetitively stimulated nerve
3. Diameter of the nerve
104
LA in an acidic environment
becomes ionized, when ionized = won't go through cell membrane and won't block na gated channel.
105
Other Site of Action Targets of LA
Potassium channels
Calcium Ion Channels
G protein-coupled receptors
106
What component of the LA is required for a conduction block
non- ionized form
107
Minimal effective concentration
At least 2, preferably 3 Nodes of Ranvier (1 cm) blocked = 1 MAC
to prevent the propagation from being interpreted by the sc/ brain
108
Fastest fibers
Preganglionic B fibers - sns
109
Myelinated fibers speed
Myelinated A (medium) and B fibers (faster) > Unmyelinated C fibers (small)
110
touch/pressure, proprioception, & motor fibers
unmyelinated C fibers
111
fibers used for Pain & Temperature
myelinated A-δ
112
Pregnancy with LA
increased sensitivity
113
Last features to be blocked
proprioception, & motor
114
Weak bases with pKa values above physiologic pH......
Only 50% in lipid-soluble nonionized form
115
pKa’s closest to physiologic pH =
most rapid OOA
116
Intrinsic vasodilator activity reflects its
potency and DOA
increased vasodilation= decreased potency and DOA
117
Factors that influence absorption
Site of injection
Dosage
Use of Epinephrine
Pharmacologic characteristics of the drug
118
Lowest to highest blood concentration
SubQ
Sciatic
Brachial
Epidural
Paracervical
Caudal
tracheal
Intracenous
119
Epi effects on DOA
prolonged duration of action by 1/3/ limits systemic absorption by 1/3
120
primary determinant of potency
Lipid solubility is the primary determinant of potency
rate of tissue distribution; moa
121
Rate of clearance dependent on
1) Cardiac output
2) Protein binding: % bound is inversely related to % plasma
122
Procaine protein binding
6%
123
tetracaine protein binding
76%
124
Lidocaine protein binding
70%
125
mepivacaine protein binding
77%
126
Bupivacaine protein binding
95%
127
Levobupivacaine protein binding
>97%
128
Ropivacaine protein binding
94%
129
LA with the fastest metabolism
Procaine (lowest protein bound)
130
LA with slowest metabolism
Bupivacaine, levobupivacaine, ropivacaine
131
Amides metabolism
Microsomal enzymes in the liver
132
amides most rapid metabolism
Prilocaine
133
amides intermediate metabolism
: Lidocaine & Mepivacaine
134
amides slowest metabolism
Etidocaine, Bupivacaine & Ropivacaine
135
Esters metabolism
Hydrolysis by cholinesterase enzyme in plasma > liver (except with Cocaine: Liver)
136
Ester metabolite
ParaAminoBenzoic acid (PABA) causes allergies
137
Amides are____ metabolism than esters
slower
138
meds with First-Pass Pulmonary Extraction
Lidocaine, bupivacaine (dose dependent), and prilocaine
139
Renal Elimination and Clearance for LA
Poor water solubility
Unchanged drug in urine = 5%
Cocaine is 10 to 12%
PABA through urine
140
The more lipid soluble the LA is, the greater is its potency; T/F
true
141
which LA property is most important for DOA
Lipid solubility
142
Pregnancy Lower levels of .....
plasma cholinesterases
143
LA effect on pregnancy
Significant transplacental transfer
Amides, but not significant with Esters
Ion Trapping (fetus more acidic than maternal)
Protein binding = rate and degree of diffusion
144
Lidocaine protein bound
70%
145
Bupivacaine protein bound
95%
146
Prilocaine protein binding
55%
147
Treatment for LA toxicity for the fetus
naHCO3
148
Bupivacaine arterial concentration
0.32
149
Lidocaine arterial concentration
0.73
150
Prilocaine arterial concentration
0.85
151
Lidocaine Metabolism
Oxidative dealkylation in liver, then hydrolysis.
Hepatic disease will affect metabolism and elimination
152
Lidocaine metabolite
Metabolite: Xylidide
153
Lidocaine Maximum infiltration dose
300 mgs plain &
500 mgs /c EPI,
154
Pregnancy Induced Hypertension (PIH) does what lidocaine?
Prolonged clearance
155
Prilocaine metabolite
Orthotoluidine
156
Prilocaine Converts Hemoglobin to Methemoglobin causing....
Methemoglobinemia; cyanosis because of decreased O2 carrying capacity.
tx with methylene Blue
157
Methylene Blue dose for methemoglobinemia
1 to 2 mgs/kg IV over 5 mins
Total dose not to exceed 7 to 8 mg/kg
158
prilocaine max dose
> 600 mg
159
Mepivacaine compared to lido
Longer duration of action
Lacks vasodilator activity
Prolonged elimination in fetus & newborn; no OB
160
Bupivacaine metabolism
aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation in the liver
161
Bupivacaine protein binding site
α1-Acid glycoprotein
162
Ropivacaine metabolism
Hepatic cytochrome P450 enzymes
163
Ropivacaine metabolites
can accumulate with uremic patients
Lesser system toxicity than Bupivacaine
164
Dibucaine metabolism
liver
165
Dibucaine MOA
inhibits the activity of normal butyrylcholinesterase (plasma cholinesterase) by more than 70%
166
Procaine metabolite
PABA, excreted unchanged in urine
167
Chloroprocaine metabolism
Plasma cholinesterase (3.5x faster)
168
Pregnancy decreases _____ by 40%
plasma cholinesterase
169
Tetracaine metabolism
slower than procaine
170
Hydrolysis meds compared
chloroprocaine > procaine > tetracaine
171
Benzocaine pka
Weak acid (pKa 3.5)
172
Benzocaine use
Topical anesthesia of mucous membranes:
Tracheal intubation, Endoscopy, Transesophageal echocardiography (TEE), Bronchoscopy
173
Benzocaine DOA
30-60 min
rapid onset
174
Benzocaine dose
Brief spray (20%) = 200 to 300 mgs
se; Methemoglobinemia
175
Methylene Blue dose
1 to 2 mgs/kg IV over 5 mins
Total dose not to exceed 7 to 8 mg/kg over 24 hrs
176
Cocaine metabolism
Ester, metabolized by liver cholinesterase/ acts like an amide.
177
Cocaine metabolism is decreased in what groups?
Parturients, Neonates, Elderly, Severe Hepatic Disease
178
Caution in using cocaine in what circumstances
Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD
179
Cocaine peak
30 to 45 mins
180
Cocaine Duration
60 minutes after peak
181
Cocaine elimination
Urine (24 to 36 hours)
182
Cocaine risks
Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD
183
Treatment for Methemoglobinemia
Methylene Blue
184
Average of PkA with LA's
8
185
weak base with high PKA
more inoized, less non ionized
186
Function of alkalinization of LA solutions
alkalinization increases the % of lipid-soluble or non-ionized form
Benefits:
Faster onset of action
Peripheral and epidural blocks by 3 to 5 mins.
Enhances the depth
Increase the spread (i.e., epidural)
187
LA are acids or bases?
weak bases but acidic in nature.
Base = name before element
acid = element before name
188
weak base with low PKA
more non ionized, less ionized
189
Demedetomidine with LAs
Increased duration of:
Both motor and sensory blocks
First analgesic request after spinal anesthesia
190
LA's with PK of 9.2
more ionized
191
LA's with PK of 7.5
more ionized
192
Magnesium with LA's
Increased duration with SAB /c or /s opioids.
193
Clonodine and Ketamine with LA's
Pediatric regional anesthesia prolonged duration.
194
Dexamethasone with LA's
Increased duration either IV or mixed with LA.
195
Chloroprocaine & Bupivacaine (ester and amide) combined cause;
Produce a rapid onset
Tachyphylaxis
196
To alkalinize La's use....
8.4% Sodium Bicarbonate (1 mL only)
Added to 30 mL of LA
Can be used with; Chloroprocaine & Bupivacaine Combo
197
Toxic effects of the combination of LA's are additive or synergistic?
additive
198
The duration of action of a LA sub q is proportional to......
The duration of action of a LA is proportional to the time the drug is in contact with nerve fibers.
199
What does the LA with vasoconstrictors do?
- Produce vasoconstriction
- Increased neuronal uptake of LA- soaks nerve fibers
- α-adrenergic effects may have some degree of analgesia- block transmission
- No effect on onset rate of LA; depends on proximity to nerve fiber
- Enhanced cardiac irritability with inhaled anesthetics; beta 1 effect tachycardia and htn.
-Systemic absorption -> HTN/ tachycardia
200
Epi dilution dose for Bupivacaine or Lidocaine SAB
0.2 mg
201
Phenylephrine dilution dose for Bupivacaine or Lidocaine SAB
2 mg
202
Your surgeon injected 20 mLs of Bupivacaine 0.25% with 1:200,000 of Epi.
What are the total mgs for Bupivacaine and the total mcgs for Epinephrine?
bupivicaine; 2.5 mg/ ml x 20 = 50 mgs
epi; 5 mcg/ml x 20 = 100 mcg
203
0.25%
2.5mg/ml
204
1;200,000 epi
1,000,000 / 200,000 = 5 mcg/ ml
205
Local Anesthetics (LAs) use
Topical
Local Infiltration
Peripheral N. Block
Intravenous
Epidural
Spinal
Tumescent Liposuction
206
Lidocaine max single dose
300 mg or 500 with epi
spinal; 100 mg
207
Mepivacaine max single dose
400mg or 500 mg with epi
spinal; 100 mg
208
Prilocaine max single dose
600 mg
209
Bupivacaine max single dose
175 mg or 225mg with epi
spinal; 20 mg
210
112.5 mg of bupivacaine with epi and 250 mg of lidocaine with epi. what are the percentages of each local anesthetic based on the recommended max single dose in mgs?
250/500 = 50%- lido
112.5/250 = 50% - bupivacaine
211
Topical Anesthesia meds ranking
Cocaine (4% to 10%) > Tetracaine (1% to 2%), Lidocaine (2% to 4%)
212
Why are procaine and chloroprocaine ineffective as topical anesthetics
they don't penetrate the mucous membrane as effectively
213
effects of lidocaine as an inhalation
Lidocaine: great with surface anesthesia
Inhalation does not alter airway resistance, but vasodilation
214
LTA stands for
lidocaine, trachea, anesthesia.
Localized tracheal anesthesia
laryngeal tracheal anesthesia
215
(EMLA)
Eutectic Mixture of LA (EMLA)
Lidocaine 2.5% and Prilocaine 2.5% = 5% LA
216
ELMA dose
1 to 2 gms/ 10 cm2 area
217
ELMA onset
45 minutes OOA
2 hours; Skin grafting
10 minutes; Cautery of genital warts, Venipuncture, lumbar puncture, Arterial cannulation (Nitroglycerine), Myringotomy
218
Side effects to ELMA
Caution with methemoglobinemia (w/ systemic absorption)
Not recommended for skin wounds
C/I with amide allergies
219
What is local infiltration
Extravascular placement of LA: Subcutaneous injection
220
Inguinal operative site LA's
Lidocaine 1% or 2%
Ropivacaine 0.25%
Bupivacaine 0.25%
221
EPI is C/I when.....
Not intracutaneously or into tissues at end arteries
Fingers, toes, ears, nose, and penis
vasoconstriction- >ischemia ->necrosis
222
Duration of LA by adding epi 1:200,000 is.....
doubled
223
Peripheral Nerve Block achieved by...
Achieved by LA injection into tissues surrounding individual peripheral nerves or nerve plexuses.
224
Peripheral never block MOA
diffusion from outer mantle to central core of nerve along a concentration gradient.
225
PNB S/S
proximal affected first and then distal.
@End: proximal comes back first & then distal.
226
PNB nerve fibers affected
Smallest sensory and ANS fibers first, and then larger motor and proprioceptive axons.
227
Peripheral Nerve Block OOA, lidocaine and bupivacaine
Lidocaine: 3 minutes
Bupivacaine: 15 minutes
228
PNB duration depends on......
dose of local anesthetic
(e.g., Bupivacaine with epi/fentanyl/clonidine = 12 to 18 hrs)
229
Regional Bier Block
Ester or amide LA can be used
Mepivacaine > Lidocaine but don't want long acting so you use lidocaine.
IV start
Exsanguination
Double cuff
LA injection through IV.
IV D/C
230
Neuraxial
central component; affects spinal subarachnoid block or epidural component
231
Segmental Block in Neuraxial Anesthesia
1. SNS- myelinated preganglionic B fibers (fastest) (hr/bp)
2. Sensory- Mylinated A and B fibers > unmyelinated C fibers
3. Motor- Pain and temperature- myelinated A -delta and unmyelinated C fibers
232
Neuraxial blockade is the last reference with which assessment parameter
leg movement
233
what is a Spinal Anesthesia Block (SAB)
Produced by direct injection of LA into subarachnoid; (beyond the dura)
CSF is confirmation
Preganglionic fibers: Principal site of action
234
The sensory effect is on same level of ....
Denervation
235
SNS is _______ of sensory
SNS is 2 spinal segments cephalad of sensory
236
Motor block is ________ sensory
Motor is 2 spinal segments below sensory
237
cardiac accelerator
T1-T4
block = asystole
238
if the assessed sensory level after SAB is at thoracic 6, what is the SNS level and motor block
T8 = motor
T4 = SNS
239
SAB dose is based on
Height of patient (volume of subarachnoid space)
Segmental level of anesthesia desired
Duration of anesthesia desired
240
Subarachnoid Block (SAB) dose
Dose is more important than the concentration of drug (%) or the volume (mLs) of the solution injection.
241
Formula for SAB dose
5 ft = 1 mL of 0.75% Bupivacaine
+ 0.1 mL for every inch above…. 2 cc total ( lasts; 1½ hours to 2 hours)
242
_________of LA is important in determining spread of the drug.
Specific gravity
243
Hyperbaric
Hyperbaric (LA sp. gr. > CSF) with glucose is additive = drug sink
244
Additive to increase the specific gravity of a LA
glucose / dextrose = makes drug sink
245
Hypobaric
Hypobaric with distilled water as an additive then the drug will float
246
Segmental block in spinal means what for the epidural
epidural anesthesia is more pronounced because it soaks the area around the sc.
247
Epidural Most common LA used:
Lidocaine
Good diffusion through tissues & safer
Levobupivacaine and ropivacaine: less than bupivacaine, but still with cardiac and CNS toxicity
248
Epidural Anesthesia onset
Onset: 15 to 30 minutes slow diffusion/delay
249
Epidural Anesthesia delivery
Great with loading dose and then intermittent boluses
250
Epidural Anesthesia with
OB Labor and C-sections:
cross placental barrier
Effect on fetus at 24 to 48 hours
Bupivacaine or Lidocaine will cross more
251
Epidural vs SAB
No differential zone of SNS, sensory, and motor blockade
Large doses required
252
Epidural + Opioids
Opioids are acceptable as additive to both Epidural & SAB -> synergistic
253
Tumescent Liposuction
SQ infiltration of large volumes (5 L or more)
don't give too much fluid because will fluid overload
254
Tumescent Liposuction solution
Diluted Lidocaine (0.05% to 0.10%)
Epinephrine 1:100,000
255
Tumesent liposuction works by
Causes taut stretching of overlying blanched skin d/t large volume and vasoconstriction -> tumescent (blockade)
-> Local anesthesia with bloodless aspirates & prolonged postoperative analgesia
256
Tumescent Liposuction Plasma peak
is 12 to 14 hours s/p injection
257
Tumescent liposuction is done where?
thigh, abdomen, hips, buttocks
258
Tumescent Liposuction Dose
Regional Anesthesia Lidocaine with Epi: 7 mg/kg
Highly diluted Lidocaine with Epi Tumescent: 35 to 55 mg/kg
259
_____ of SQ tissue can absorb up to ____ of Lidocaine
1 gm of SQ can absorb up to 1 mg of Lidocaine
(aka: Tissue Buffering System)
260
Allergic reaction frequency with LA
Rare < 1%
261
Allergic reactions attribute to
to manifestations of excess plasma levels
262
Causes of allergic reactions with LA
Esters (PABA; preservative) > Amides
Methylparaben: preservative to both esters & amides. Similar in structure to PABA. Use preservative free
263
Manifestations of Allergic reactions
Rash, urticaria, and laryngeal edema /c or /s hypotension & bronchospasm -> IgE anaphylaxis
264
Testing for allergic reactions
Intradermal test using preservative free LA
265
LAST stands for
LA systemic toxicity
266
Causes of systemic toxicity
d/t excess plasma concentration of the drug
Entrance into the systemic circulation from inactive tissue redistribution and clearance metabolism
Accidental direct IV injection
meds, co-morbidites, technique of bloc, LA used, dose
267
Magnitude of systemic absorption depends on:
-Dose
-Vascularity of site
-Epinephrine use (VC)
-Physicochemical properties
268
Systemic Toxicity CNS effect
Drowsiness, facial twitch prior to seizure.
269
What promotes sz with LA's
Hyperkalemia promotes seizures w/ LAs.
lowers sz threshold
270
Lidocaine @ _____ with circumoral numbness but not CV
5mcg/ ml
271
High LA plasma concentration causes.....
block cardiac Na+ channels
Slow conduction of cardiac impulses -> prolonged PR interval & QRS widening
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Accidental IV Bupivacaine causes
Precipitous hypotension, AV block,
Cardiac dysrhythmias: SVTs, ST-Twave changes, PVCs, widening of QRS, V-tach
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Predisposing factors for systemic toxicity CV effects
-Pregnancy
-Arterial hypoxemia, acidosis, or hypercarbia (in animals)
-Beta blockers, Digitalis preparations, Ca+ Channel Blockers
-Epinephrine & Phenylephrine
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Medications that cause cv effects with systemic toxicity
Bupivacaine > Ropivacaine > Lidocaine
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What two factors predispose our OB population to local anesthetic toxicity
decreased plasma esteraces
decreases plasma proteins
276
Goals of treatment of systemic toxicity
1. Prompt airway management
2. Circulatory support
3. Removal of LA from receptor sites
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Treatment of LA CNS Toxicity
100% O2..inhibit hypoxemia and metabolic acidosis; NRB
Hyperventilation
Barbiturates
Benzodiazepines
Epinephrine as an additive
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treatment for sz with systemic toxicity from LA
Supplemental oxygen
Benzodiazepine (midazolam or diazepam)
Propofol: if hemodynamically stable
Muscle relaxant (succinylcholine or NMDA)
Intralipid: lipid emulsion
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MOA for intralipid- lipid emulsion
creates lipid compartment; provides for fat for myocardial metabolism
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Bolus of Lipid emulsion
Bolus: 1.5 mL/kg of 20% lipid emulsion
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Infusion dose of intralipid
Infusion: 0.25 mL/kg/minute for at least 10 minutes
1st 30 minutes: max = 3.8 mL/kg (1.2 to 6 mL/kg)
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EPI dose for systemic toxicity
10-100 mcg
283
if no response to intralipid do.....
Cardiopulmonary Bypass (CPB)
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meds to not use in managing LA systemic toxicity
no vasopressin
no prop
285
60 yo 120 lb female has the vs following bupivacaine 0.5% 20 mls through the epidural catheter; Hr 38, 70/35, 40, 92%. how much intralipid in mgs would you bolus?
1.5 mg x 54 kgs = 84 mls
20% = 200 mgs.
84 x 200 = 16800 mgs
286
Neural Tissue Toxicity categories
Three Categories:
1. Transient Neurologic Symptoms
2. Cauda Equina Syndrome
3. Anterior Spinal Artery Syndrome
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Neural Tissue Toxicity cause either ________ neurologic injury
Either transient or permanent neurologic injury
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Transient Neurologic Symptoms (TNS) manifestations
Moderate to severe pain (lower back, buttocks & posterior thighs) within 6 to 36 hours after uneventful single-shot SAB.
289
Treatment and recovery Transient Neurologic Symptoms (TNS)
Treatment: Trigger point injections and NSAIDs
Recovery: 1 to 7 days.
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Causes of TNS
Cause: Unknown
Lidocaine > other LAs; positioning?; addition of vasoconstrictor?
291
Cauda Equina Syndrome (CES) is what?
Diffuse injury @ lumbosacral plexus -> varying degrees of sensory anesthesia, bowel & bladder sphincter dysfunction, & paraplegia
292
Cauda Equina Syndrome (CES)
is associated with
large lumbar disc herniation, prolapse or
sequestration with urinary retention.
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what is Anterior Spinal Artery Syndrome
Lower extremity paresis with a variable sensory deficit.
294
What causes Anterior Spinal Artery Syndrome
Cause: uncertain if its thrombosis or spasm of the bilateral anterior spinal artery
effects of HypoTN or vasoconstrictors drugs;
PVD,
spinal cord compression d/t epidural abscess or hematoma
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Methemoglobinemia due to....
Potentially life-threatening complication d/t decreased 02 carrying capacity (metHgb > 15%).
296
medications that Cause Methemoglobinemia
Causes: Prilocaine, benzocaine > lidocaine, nitroglycerine, phenytoin, & sulfonamides
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treatment for Methemoglobinemia
Treatment: Methylene blue 1 mg/kg over 5 mins (max. 7 to 8 mg/kg)
Reversal from metHgb (Fe3+) to Hgb (Fe2+) is within 20 to 60 minutes
298
Ventilatory Response to Hypoxia
Lidocaine depresses the ventilatory response to arterial hypoxemia
Susceptible patients: C02 retainers
299
Causes of hepatotoxicity
Cause: continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia.
Stop infusion ->normalizes liver transaminase enzymes
300
What is the most common first intervention, when an adverse event is ID, if for the anesthesia provider to....
call for help
301
MOA for cocaine toxicity
MOA: SNS stimulation by blocking presynaptic uptake of NE and dopamine -> increased postsynaptic levels
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Cocaine adverse effects
Adverse effects (lasts up to 6 weeks):
CV: HTN, tachycardia, coronary vasospasm, MI (infarction & ischemia), ventricular dysrhythmias (including Vfib).
Parturient: decreased UBF -> fetal hypoxemia
Hyperpyrexia -> seizures
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Cocaine associated cp treatment
asa, benzos
nitro, phentolamine
esmolol, beta blockers , sodium nitropurrisize
304
What NMBD needs to be reconstituted w/ distilled water
Vec - reconsitiute w/ 10 ml to make 1 ml
305
Sugammadex E1/2
2 hrs
306
Additive to increase the specific gravity of a LA
glucose / dextrose = makes drug sink
