week 2 regional & locals 4 of 4 Flashcards
amides are metabolized by
P450 enzymes in the liver
greatest to least metabolism of amides
prilocaine>lidocaine>mepivacaine>ropivacaine>bupivacaine
comparing amid metabolism to ester metabolsim
amid metabolism is consistently slower than ester
abnormal liver function or decrease blood flow to liver results in what concerns with amides
toxicity
T/F
amides are excreted by the kidneys very little
True!
what two locals are metabolized to PABA and associated with anaphylaxis
procaine and benzocaine
what metabolizes ester local anesthetics
3 names for this one thing
plasma pseudocholinesterase (plasma cholinesterase or butyrylcholinesterase)
why do esters not accumulate in blood
ester hydrolysis is very rapid in the blood stream (excreted in the urine)
esters are derived from
benzoic acid
what is important about CSF and the termination of action of local anesthetics
The CSF lacks esterase enzymes, so termination of action of LA intrathecally depends on redistribution into the bloodstream as it does for all other nerve blocks
as soon as you stick someone for a local what is the absolute first thing you do
what is the second thing you do
ALWAYS ASPIRATE
second- test dose- check HR, numbness around lips, tinnitus
what two drugs can cause methemoglobinemia- and many hospitals/ facilities do not permit use
Prilocaine: causes methemoglobinemia (generally not used)
Benzocaine (common ingredient in topical LA sprays) can cause
treatment for methemoglobinemia
IV methylene blue (1-2 mg/kg of a 1% solution over 5 minutes)
what does methylene blue do to the FE
FE3-FE2
ferric to ferrous
LA toxicity-
Neurological:
Early symptoms:
Circumoral numbness, tongue paresthesia, dizziness, tinnitus, blurred vision
LA Toxicity
Neurological:
Excitatory signs:
Restlessness, agitation, nervousness, feeling of “impending doom”,
Muscle twitching may preceded “tonic-clonic” seizures
Higher blood concentrations (toxicity) may produce CNS depression- coma, respiratory arrest
Seizures:
prevention-
benzodiazepines & hyperventilation (raise seizure threshold)
Propofol (0.5-2 mg/kg) –quickly terminates seizure activity after onset (careful with airway/hypotension etc… )
Benzodiazepines and barbiturates may terminate seizure as well
what is the concern with respiratory and metabolic acidosis as it relates to seizures
it will decrease (lower) seizure threshold
Cocaine toxicity: patient presentation
Restlessness, emesis, tremors, convulsions, arrhythmias, respiratory failure, cardiac arrest
Unintentional injection of large volumes of chloroprocaine in SA space (intended for epidural space: resulting in)
Total spinal
Prolonged neurological deficits (direct neurotoxicity and/or preservative– now prepared preservative free)
total spinal occurs when what spinal level is reached
T4-cardiocelerators
what block did we talk about last semester that patients can end of with a total spinal
retrobulbar block
patient is having an emergency C section which local anesthetic will you administer and why?
Chloroprocaine- fast onset
TEST
lidocaine neurological toxicity
Neurotoxicity (cauda equine syndrome/transient neurological symptoms)
Respiratory effects from lidocaine toxicity
Lidocaine depresses hypoxic drive (the ventilator response to low PaO2)
Apnea can result
Most often as result of high/total spinal
what do all local anesthetics do to the cardiovascular system
All LA depress myocardial automaticity (spontaneous phase IV depolarization)
Depress myocardial contractility & conduction velocity
all LA except cocaine at high levels produce:
smooth muscle relaxation (arteriolar vasodilation)
why do LA produce direct cardiac muscle membrane changes
cardiac NA channel blockade
arrhythmias, heart block, depression of ventricular contractility, hypotension- cardiac arrest / cv collapse occur from
LA toxicity
what are the presenting signs of cardiovascular toxicity during general anesthesia
arrhythmias or CV collapse
what are the presenting sings in an awake patient of cardiovascular LA toxocity
CV stimulation (tachycardia & hypertension) with CNS excitation
lipid emulsion therapy dose- this is done why?
1.5mg/kg
bupivacaine induced cardiac toxicity- of note very difficult to resuscitate
which medication can produce SEVERE CV toxicity when unintended intravascular injection occurs
(left ventricular depression, A-V heart block, VT/V-fib)***
what are predisposing risk factors for LA toxicity
Pregnancy, hypoxemia, respiratory acidosis and young children are predisposing risk factors
treatment of cocaine induced arrhythmias
Adrenergic antagonists
Calcium channel antagonists
Cocaine CV toxicity: unlike those of any other LA
Adrenergic nerve terminals normally reabsorb norepi after its release– cocaine inhibits this
Potentiated adrenergic stimulation
HTN & ventricular ectop
lidocaine 5mcg/ml manifestations
circumoral and tongue numbness
lightheadedness and tinnitus
lidocaine 6mcg/ml manifestations
visual disturbances
lidocaine 8mcg/ml
muscle twitching
lidocaine 10mcg/ml
unconsciousness
lidocaine 12 mcg/ml
convulsions
lidocaine 15 mcg/ml
coma
lidocaine 20mcg/ml
respiratory arrest
lidocaine 26 mcg/ml
cardiovascular collapse
what are sings of anaphylaxis
…
how do you treat anaphylaxis
…
immunological/hypersensitivity of amides occur with what substance
Amides prepared with a preservative called“methylparaben” (which has a chemical structure similar to PABA)
which type of LA has induced hypersensitivity reactions more often
Esters induce hypersensitivity reactions more often than amides (IgG or IgE)
therapeutic lab value:
look for the presence effectiveness of specific drugs in the blood
normal lab value
The range of results expected from lab tests without influence from a therapeutic drug.
therapeutic lab value example
heparin / warfarin / vancomycin
maximum lidocaine dose
4.5mg/kg
maximum lidocaine dose with EPI
7mg/kg
maximum dose of bupivacaine
3mg/kg
what two drug classes may prolong DOA of amide LA especially lodicaine-due to decrease hepatic blood flow.
beta blockers
H2 receptor blockers
explain the pathway for sympathetic blockade that is responsible for hypotension with LA
vasodilation - decrease preload- hypotension
what occurs with chronic therapy with acetylcholinesterase inhibitors (edrophonium, physostigmine, echothiophate)
prolongs DOA of ester LA b/c these agents decrease pseudocholinesterase function
what occurs in patients with atypical pseudocholinesterase
have prolonged duration of action of esters
when comparing tetracaine, procaine, and chloroprocaine which has the longest duration of action- thus having what likelihood
tetracaine much slower hydrolysis by plasma cholinesterase- higher likelihood of toxicity
what does dibucaine describe
quality of cholinesterase
quantity of cholinesterase
the quality of cholinesterase
What does a dibucaine number of 80 mean??
it means you have normal plasma cholinesterase
What does a dibucaine number of 20 mean??
it means dibucaine was only able to inhibit 20 plasma cholinesterase- so you have atypical plasma cholinesterase
normal range of dibucaine
70 or higher
homozyte atypical plasma cholinesterase
dibucaine number is less than 30
heterozyte atypical plasma cholinesterase
dibucaine number is in the range of 40-60
