Exam 4 Flashcards
What is the other name for neuromuscular monitoring
Acceleromyography
most common location, nerve, and muscle monitored
abductor pollicis muscle, hand, ulnar nerve
NMBD Reversal Agents
edrophonium
neostigmine
Anti-Cholinergic Agents
atropine sulfate
glycopyrrolate
NMBD Reversal Agents MOA
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
Total max neostigmine dose
5mg
Neostigmine max range
40 to 70 mcg/kg
Edrophonium max range
1 mg/kg
NMBD Reversal Agents will not work with…..
Will not work with deep NM blockade
because of ceiling effect
Reversal of NM Blockade depends on 5 factors:
- Depth of the NM Block
- AchE Inhibitor choice
- Dose administered
- Rate of plasma clearance of NMBD
- Anesthesia agent choice and depth
What NMBD needs to be reconstituted w/ distilled water
Vec - reconsitiute w/ 10 ml to make 1 ml
Why is pancuronium given to cardiac patients?
INtrinsic effects on cardiac accelerators and good for the cardiac muscle
Goal of NMBD reversal agents
Prevent postoperative residual NM blockade
Sugammadex dose
2-16 mg/kg
Neostigmine onset
5-10 min
neostigmine duration
60 mins
Neostigmine anticholinergic
glycopyrrolate 0.2 mg/ml of neostigmine
Sugammadex onset
1-4 min
Sugammadex duration
1.5-3 hrs
sugammadex anticholinergic
none
Edrophonium onset
1-2 mins
Edrophonium duration
5-15 min
Pyridostigminge and edrophonium are excreted by how much renaly
75%
Overall side effects of NMBD reversal agents are a result from increased…..
Increased Nicotinic/Muscarinic Activity
How much neostigmine is excreted renaly
50%
30-50% hepatic if no renal function
CRF (chronic renal failure) does what to plasma clearance
decrease plasma clearance= prolonged action
Cardiac Side effect for nmbd reversal agents
Bradycardia, dysrhythmias, asystole, ↓SVR
Pulmonary Side effect for nmbd reversal agents
Bronchoconstriction, increased airway resistance, increased salivation
GI Side effect for nmbd reversal agents
Hyperperistalsis, enhanced gastric fluid secretion, PONV
Eyes Side effect for nmbd reversal agents
Miosis
Atropine side effect and matches….
side effects; mydriasis and initial tachycardia
matches profile of edrophonium
Atropine dose
7-10 mcg/kg
Glycopyrrolate matches the profile of….
Neostigmine and pyridostigmine
Glycopyrrolate dose
7-15 mcg/kg (1 mg max)
Anti-cholinergic/ anti muscarinic agents for cardiac disease
Glycopyrolate is preferred over atropine
to be administered slowly over 2-5 minutes
mechanism for persistent NM blockade
Acetylcholinesterase is maximally inhibited
No further anticholinesterase is effective
intervention for persistent nm blockade
sedation and postop ventilation
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**
Medications that sugammadex binds to
Rocuronium > Vecuronium»_space; Pancuronium (least), best with ROC
Sugammadex E1/2
2 hrs
Sugammadex Major route of elimination:
Urine
70% in 6 hours
90% in 24 hours
Renal impairment: C/I with dialysis by dialysis
Sugammadex facts
Selective Relaxant-Binding Agent
γ-cyclodextrin
dextrose units from starch
Highly water soluble= mainly excreted in the kidney
drug that does not need binding with glycopyrolate / atropine
sugammadex
Deep block sugammadex dose
1-2 post-tetanic counts but not twitch response = 4mg/kg
moderate sugammadex dose
2/4 twitches = 2mg/kg
Where is the main site of action of sugammadex
plasma
Sugammadex Dose With extreme block:
no post tetanic stimulation = 8-16mg/kg
Recurarization: not observed at appropriate doses
Reparalzation with Roc after reversal with sugammadex
5 minutes
give 1.2mg/kg
Reparalyzation with ROC after reversal with neostigmine
4 hours wait then give 0.6 mg/kg roc or 0.1 mg/kg with vec
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.
Sugammadex side effects
Dose related; n/v, pruritis, urticaria
anaphylaxis
marked bradycardia
doesn’t work
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
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?
First local anesthetic
cocaine
Antiarrhythmic Drug Classes:
Class I
Sodium-channel blockers.
Antiarrhythmic Drug Classes:
Class 2
Beta blockers
Antiarrhythmic Drug Classes Class 3
potassium channel blockers
Antiarrhythmic Drug Classes Class 4
CCB
Cocaine MOA
cerebral stimulating qualities
localized vasoconstriction: shrink nasal mucosa
1st synthetic ester
procaine
The standard to which all other local anesthetics are compared.
lidocaine; the first synthetic amide
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
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
Ester or amide determination is based on which portion of the LA structure?
the link between the lipophilic aromatic and hydrocarbon intermediate chain
Ph for LA
pH 6 (HCl salt): Weak Bases
Composition of LA
Epinephrine
Sodium Bisulfite
weak bases
onset procaine
slow
onset chloropocaine
rapid
tetracaine onset
slow
amides onset
all are slow except lidocaine is rapid
Duration of infiltration procaine
45-60 min
Duration of infiltration chloroprocaine
30-45 min
Duration of infiltration tetracaine
60-180 min
Duration of infiltration of lidocaine
60-120 min
Duration of infiltration prilocaine
60-120 min
Duration of infiltration mepivacaine
90-180 min
Duration of infiltration bupivicaine
240-480 min
Duration of infiltration levobupivicaine
240-480 min
Duration of infiltration ropivacaine
240 - 480 min
Procaine potency
1
chloroprocaine potency
4
tetracaine potency
16
amides potency
1; lido, prolocaine, mepivacaine
4; bupivacaine, levobupivacaine, ropivacaine
procaine pK
8.9
chloroprocaine pk
8.7
Tetracaine pk
8.5
lidocaine pK
7.9
prilocaine pK
7.9
mepivacaine pK
7.6
Bupivacaine pK
8.1
levobuvicaine pk
8.1
probivacaine pK
8.1
procaine lipid solubility
0.6
Tetracaine lipid solubility
80
lidocaine lipid solbuility
2.9
Prilocaine lipid solubilty
0.9
mepivacaine lipid solubility
1
bupivacaine lipid solubility
28
The closer the meds pK is to physiologic ph……
closer to physiologic = faster the onset of action
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
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
LA form for lipid solubility
nonionized = crosses to inside of cell and block na gate.
factors affecting blockade:
- Lipid solubility or non-ionized/unionized form
- Repetitively stimulated nerve
- Diameter of the nerve
LA in an acidic environment
becomes ionized, when ionized = won’t go through cell membrane and won’t block na gated channel.
Other Site of Action Targets of LA
Potassium channels
Calcium Ion Channels
G protein-coupled receptors
What component of the LA is required for a conduction block
non- ionized form
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
Fastest fibers
Preganglionic B fibers - sns
Myelinated fibers speed
Myelinated A (medium) and B fibers (faster) > Unmyelinated C fibers (small)
touch/pressure, proprioception, & motor fibers
unmyelinated C fibers
fibers used for Pain & Temperature
myelinated A-δ
Pregnancy with LA
increased sensitivity
Last features to be blocked
proprioception, & motor
Weak bases with pKa values above physiologic pH……
Only 50% in lipid-soluble nonionized form
pKa’s closest to physiologic pH =
most rapid OOA
Intrinsic vasodilator activity reflects its
potency and DOA
increased vasodilation= decreased potency and DOA
Factors that influence absorption
Site of injection
Dosage
Use of Epinephrine
Pharmacologic characteristics of the drug
Lowest to highest blood concentration
SubQ
Sciatic
Brachial
Epidural
Paracervical
Caudal
tracheal
Intracenous
Epi effects on DOA
prolonged duration of action by 1/3/ limits systemic absorption by 1/3
primary determinant of potency
Lipid solubility is the primary determinant of potency
rate of tissue distribution; moa
Rate of clearance dependent on
1) Cardiac output
2) Protein binding: % bound is inversely related to % plasma
Procaine protein binding
6%
tetracaine protein binding
76%
Lidocaine protein binding
70%
mepivacaine protein binding
77%
Bupivacaine protein binding
95%
Levobupivacaine protein binding
> 97%
Ropivacaine protein binding
94%
LA with the fastest metabolism
Procaine (lowest protein bound)
LA with slowest metabolism
Bupivacaine, levobupivacaine, ropivacaine
Amides metabolism
Microsomal enzymes in the liver
amides most rapid metabolism
Prilocaine
amides intermediate metabolism
: Lidocaine & Mepivacaine
amides slowest metabolism
Etidocaine, Bupivacaine & Ropivacaine
Esters metabolism
Hydrolysis by cholinesterase enzyme in plasma > liver (except with Cocaine: Liver)
Ester metabolite
ParaAminoBenzoic acid (PABA) causes allergies
Amides are____ metabolism than esters
slower
meds with First-Pass Pulmonary Extraction
Lidocaine, bupivacaine (dose dependent), and prilocaine
Renal Elimination and Clearance for LA
Poor water solubility
Unchanged drug in urine = 5%
Cocaine is 10 to 12%
PABA through urine
The more lipid soluble the LA is, the greater is its potency; T/F
true
which LA property is most important for DOA
Lipid solubility
Pregnancy Lower levels of …..
plasma cholinesterases
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
Lidocaine protein bound
70%
Bupivacaine protein bound
95%
Prilocaine protein binding
55%
Treatment for LA toxicity for the fetus
naHCO3
Bupivacaine arterial concentration
0.32
Lidocaine arterial concentration
0.73
Prilocaine arterial concentration
0.85
Lidocaine Metabolism
Oxidative dealkylation in liver, then hydrolysis.
Hepatic disease will affect metabolism and elimination
Lidocaine metabolite
Metabolite: Xylidide
Lidocaine Maximum infiltration dose
300 mgs plain &
500 mgs /c EPI,
Pregnancy Induced Hypertension (PIH) does what lidocaine?
Prolonged clearance
Prilocaine metabolite
Orthotoluidine
Prilocaine Converts Hemoglobin to Methemoglobin causing….
Methemoglobinemia; cyanosis because of decreased O2 carrying capacity.
tx with methylene Blue
Methylene Blue dose for methemoglobinemia
1 to 2 mgs/kg IV over 5 mins
Total dose not to exceed 7 to 8 mg/kg
prilocaine max dose
> 600 mg
Mepivacaine compared to lido
Longer duration of action
Lacks vasodilator activity
Prolonged elimination in fetus & newborn; no OB
Bupivacaine metabolism
aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation in the liver
Bupivacaine protein binding site
α1-Acid glycoprotein
Ropivacaine metabolism
Hepatic cytochrome P450 enzymes
Ropivacaine metabolites
can accumulate with uremic patients
Lesser system toxicity than Bupivacaine
Dibucaine metabolism
liver
Dibucaine MOA
inhibits the activity of normal butyrylcholinesterase (plasma cholinesterase) by more than 70%
Procaine metabolite
PABA, excreted unchanged in urine
Chloroprocaine metabolism
Plasma cholinesterase (3.5x faster)
Pregnancy decreases _____ by 40%
plasma cholinesterase
Tetracaine metabolism
slower than procaine
Hydrolysis meds compared
chloroprocaine > procaine > tetracaine
Benzocaine pka
Weak acid (pKa 3.5)
Benzocaine use
Topical anesthesia of mucous membranes:
Tracheal intubation, Endoscopy, Transesophageal echocardiography (TEE), Bronchoscopy
Benzocaine DOA
30-60 min
rapid onset
Benzocaine dose
Brief spray (20%) = 200 to 300 mgs
se; Methemoglobinemia
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
Cocaine metabolism
Ester, metabolized by liver cholinesterase/ acts like an amide.
Cocaine metabolism is decreased in what groups?
Parturients, Neonates, Elderly, Severe Hepatic Disease
Caution in using cocaine in what circumstances
Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD
Cocaine peak
30 to 45 mins
Cocaine Duration
60 minutes after peak
Cocaine elimination
Urine (24 to 36 hours)
Cocaine risks
Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD
Treatment for Methemoglobinemia
Methylene Blue
Average of PkA with LA’s
8
weak base with high PKA
more inoized, less non ionized
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)
LA are acids or bases?
weak bases but acidic in nature.
Base = name before element
acid = element before name
weak base with low PKA
more non ionized, less ionized
Demedetomidine with LAs
Increased duration of:
Both motor and sensory blocks
First analgesic request after spinal anesthesia
LA’s with PK of 9.2
more ionized
LA’s with PK of 7.5
more ionized
Magnesium with LA’s
Increased duration with SAB /c or /s opioids.
Clonodine and Ketamine with LA’s
Pediatric regional anesthesia prolonged duration.
Dexamethasone with LA’s
Increased duration either IV or mixed with LA.
Chloroprocaine & Bupivacaine (ester and amide) combined cause;
Produce a rapid onset
Tachyphylaxis
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
Toxic effects of the combination of LA’s are additive or synergistic?
additive
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.
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
Epi dilution dose for Bupivacaine or Lidocaine SAB
0.2 mg
Phenylephrine dilution dose for Bupivacaine or Lidocaine SAB
2 mg
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
0.25%
2.5mg/ml
1;200,000 epi
1,000,000 / 200,000 = 5 mcg/ ml
Local Anesthetics (LAs) use
Topical
Local Infiltration
Peripheral N. Block
Intravenous
Epidural
Spinal
Tumescent Liposuction
Lidocaine max single dose
300 mg or 500 with epi
spinal; 100 mg
Mepivacaine max single dose
400mg or 500 mg with epi
spinal; 100 mg
Prilocaine max single dose
600 mg
Bupivacaine max single dose
175 mg or 225mg with epi
spinal; 20 mg
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
Topical Anesthesia meds ranking
Cocaine (4% to 10%) > Tetracaine (1% to 2%), Lidocaine (2% to 4%)
Why are procaine and chloroprocaine ineffective as topical anesthetics
they don’t penetrate the mucous membrane as effectively
effects of lidocaine as an inhalation
Lidocaine: great with surface anesthesia
Inhalation does not alter airway resistance, but vasodilation
LTA stands for
lidocaine, trachea, anesthesia.
Localized tracheal anesthesia
laryngeal tracheal anesthesia
(EMLA)
Eutectic Mixture of LA (EMLA)
Lidocaine 2.5% and Prilocaine 2.5% = 5% LA
ELMA dose
1 to 2 gms/ 10 cm2 area
ELMA onset
45 minutes OOA
2 hours; Skin grafting
10 minutes; Cautery of genital warts, Venipuncture, lumbar puncture, Arterial cannulation (Nitroglycerine), Myringotomy
Side effects to ELMA
Caution with methemoglobinemia (w/ systemic absorption)
Not recommended for skin wounds
C/I with amide allergies
What is local infiltration
Extravascular placement of LA: Subcutaneous injection
Inguinal operative site LA’s
Lidocaine 1% or 2%
Ropivacaine 0.25%
Bupivacaine 0.25%
EPI is C/I when…..
Not intracutaneously or into tissues at end arteries
Fingers, toes, ears, nose, and penis
vasoconstriction- >ischemia ->necrosis
Duration of LA by adding epi 1:200,000 is…..
doubled
Peripheral Nerve Block achieved by…
Achieved by LA injection into tissues surrounding individual peripheral nerves or nerve plexuses.
Peripheral never block MOA
diffusion from outer mantle to central core of nerve along a concentration gradient.
PNB S/S
proximal affected first and then distal.
@End: proximal comes back first & then distal.
PNB nerve fibers affected
Smallest sensory and ANS fibers first, and then larger motor and proprioceptive axons.
Peripheral Nerve Block OOA, lidocaine and bupivacaine
Lidocaine: 3 minutes
Bupivacaine: 15 minutes
PNB duration depends on……
dose of local anesthetic
(e.g., Bupivacaine with epi/fentanyl/clonidine = 12 to 18 hrs)
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
Neuraxial
central component; affects spinal subarachnoid block or epidural component
Segmental Block in Neuraxial Anesthesia
- SNS- myelinated preganglionic B fibers (fastest) (hr/bp)
- Sensory- Mylinated A and B fibers > unmyelinated C fibers
- Motor- Pain and temperature- myelinated A -delta and unmyelinated C fibers
Neuraxial blockade is the last reference with which assessment parameter
leg movement
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
The sensory effect is on same level of ….
Denervation
SNS is _______ of sensory
SNS is 2 spinal segments cephalad of sensory
Motor block is ________ sensory
Motor is 2 spinal segments below sensory
cardiac accelerator
T1-T4
block = asystole
if the assessed sensory level after SAB is at thoracic 6, what is the SNS level and motor block
T8 = motor
T4 = SNS
SAB dose is based on
Height of patient (volume of subarachnoid space)
Segmental level of anesthesia desired
Duration of anesthesia desired
Subarachnoid Block (SAB) dose
Dose is more important than the concentration of drug (%) or the volume (mLs) of the solution injection.
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)
_________of LA is important in determining spread of the drug.
Specific gravity
Hyperbaric
Hyperbaric (LA sp. gr. > CSF) with glucose is additive = drug sink
Additive to increase the specific gravity of a LA
glucose / dextrose = makes drug sink
Hypobaric
Hypobaric with distilled water as an additive then the drug will float
Segmental block in spinal means what for the epidural
epidural anesthesia is more pronounced because it soaks the area around the sc.
Epidural Most common LA used:
Lidocaine
Good diffusion through tissues & safer
Levobupivacaine and ropivacaine: less than bupivacaine, but still with cardiac and CNS toxicity
Epidural Anesthesia onset
Onset: 15 to 30 minutes slow diffusion/delay
Epidural Anesthesia delivery
Great with loading dose and then intermittent boluses
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
Epidural vs SAB
No differential zone of SNS, sensory, and motor blockade
Large doses required
Epidural + Opioids
Opioids are acceptable as additive to both Epidural & SAB -> synergistic
Tumescent Liposuction
SQ infiltration of large volumes (5 L or more)
don’t give too much fluid because will fluid overload
Tumescent Liposuction solution
Diluted Lidocaine (0.05% to 0.10%)
Epinephrine 1:100,000
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
Tumescent Liposuction Plasma peak
is 12 to 14 hours s/p injection
Tumescent liposuction is done where?
thigh, abdomen, hips, buttocks
Tumescent Liposuction Dose
Regional Anesthesia Lidocaine with Epi: 7 mg/kg
Highly diluted Lidocaine with Epi Tumescent: 35 to 55 mg/kg
_____ 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)
Allergic reaction frequency with LA
Rare < 1%
Allergic reactions attribute to
to manifestations of excess plasma levels
Causes of allergic reactions with LA
Esters (PABA; preservative) > Amides
Methylparaben: preservative to both esters & amides. Similar in structure to PABA. Use preservative free
Manifestations of Allergic reactions
Rash, urticaria, and laryngeal edema /c or /s hypotension & bronchospasm -> IgE anaphylaxis
Testing for allergic reactions
Intradermal test using preservative free LA
LAST stands for
LA systemic toxicity
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
Magnitude of systemic absorption depends on:
-Dose
-Vascularity of site
-Epinephrine use (VC)
-Physicochemical properties
Systemic Toxicity CNS effect
Drowsiness, facial twitch prior to seizure.
What promotes sz with LA’s
Hyperkalemia promotes seizures w/ LAs.
lowers sz threshold
Lidocaine @ _____ with circumoral numbness but not CV
5mcg/ ml
High LA plasma concentration causes…..
block cardiac Na+ channels
Slow conduction of cardiac impulses -> prolonged PR interval & QRS widening
Accidental IV Bupivacaine causes
Precipitous hypotension, AV block,
Cardiac dysrhythmias: SVTs, ST-Twave changes, PVCs, widening of QRS, V-tach
Predisposing factors for systemic toxicity CV effects
-Pregnancy
-Arterial hypoxemia, acidosis, or hypercarbia (in animals)
-Beta blockers, Digitalis preparations, Ca+ Channel Blockers
-Epinephrine & Phenylephrine
Medications that cause cv effects with systemic toxicity
Bupivacaine > Ropivacaine > Lidocaine
What two factors predispose our OB population to local anesthetic toxicity
decreased plasma esteraces
decreases plasma proteins
Goals of treatment of systemic toxicity
- Prompt airway management
- Circulatory support
- Removal of LA from receptor sites
Treatment of LA CNS Toxicity
100% O2..inhibit hypoxemia and metabolic acidosis; NRB
Hyperventilation
Barbiturates
Benzodiazepines
Epinephrine as an additive
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
MOA for intralipid- lipid emulsion
creates lipid compartment; provides for fat for myocardial metabolism
Bolus of Lipid emulsion
Bolus: 1.5 mL/kg of 20% lipid emulsion
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)
EPI dose for systemic toxicity
10-100 mcg
if no response to intralipid do…..
Cardiopulmonary Bypass (CPB)
meds to not use in managing LA systemic toxicity
no vasopressin
no prop
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
Neural Tissue Toxicity categories
Three Categories:
1. Transient Neurologic Symptoms
2. Cauda Equina Syndrome
3. Anterior Spinal Artery Syndrome
Neural Tissue Toxicity cause either ________ neurologic injury
Either transient or permanent neurologic injury
Transient Neurologic Symptoms (TNS) manifestations
Moderate to severe pain (lower back, buttocks & posterior thighs) within 6 to 36 hours after uneventful single-shot SAB.
Treatment and recovery Transient Neurologic Symptoms (TNS)
Treatment: Trigger point injections and NSAIDs
Recovery: 1 to 7 days.
Causes of TNS
Cause: Unknown
Lidocaine > other LAs; positioning?; addition of vasoconstrictor?
Cauda Equina Syndrome (CES) is what?
Diffuse injury @ lumbosacral plexus -> varying degrees of sensory anesthesia, bowel & bladder sphincter dysfunction, & paraplegia
Cauda Equina Syndrome (CES)
is associated with
large lumbar disc herniation, prolapse or
sequestration with urinary retention.
what is Anterior Spinal Artery Syndrome
Lower extremity paresis with a variable sensory deficit.
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
Methemoglobinemia due to….
Potentially life-threatening complication d/t decreased 02 carrying capacity (metHgb > 15%).
medications that Cause Methemoglobinemia
Causes: Prilocaine, benzocaine > lidocaine, nitroglycerine, phenytoin, & sulfonamides
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
Ventilatory Response to Hypoxia
Lidocaine depresses the ventilatory response to arterial hypoxemia
Susceptible patients: C02 retainers
Causes of hepatotoxicity
Cause: continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia.
Stop infusion ->normalizes liver transaminase enzymes
What is the most common first intervention, when an adverse event is ID, if for the anesthesia provider to….
call for help
MOA for cocaine toxicity
MOA: SNS stimulation by blocking presynaptic uptake of NE and dopamine -> increased postsynaptic levels
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
Cocaine associated cp treatment
asa, benzos
nitro, phentolamine
esmolol, beta blockers , sodium nitropurrisize
What NMBD needs to be reconstituted w/ distilled water
Vec - reconsitiute w/ 10 ml to make 1 ml
Sugammadex E1/2
2 hrs
Additive to increase the specific gravity of a LA
glucose / dextrose = makes drug sink
