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princip, pharm, phys, regional > pharm-LAs pt 2. > Flashcards

pharm-LAs pt 2. Flashcards

1
Q
  1. what physical change causes pregnant (and obese) persons to require a change in the amount (cc) of neuraxial anesthesia
  2. what is the hormonal reason?
A
  1. there is a narrowing of the spinal column in pregnant, which results in needing less LA to reach the appropriate level
  2. progesterone may change protein binding leaving a higher free fraction of the drug
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2
Q
  1. name reasons why a LA would be more likely to cross the placenta:
  2. what LAs would be least likely to cross the placeta?
  3. what would happen if the baby was acidotic from fetal distress?
A
  1. the less protein bound the LA is, the greater the chance of crossing the placenta
  2. esters usually dont cross becaust they are metabolized too fast
  3. ion trapping of the ionized LA in the distressed fetus
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3
Q

what are the systemic effects of LA toxicity?

A

cardiovascular
central nervous
neruotoxic
allergic

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4
Q

what agents are most likely to cause system toxicity in order from GREATEST –TO– LEAST:
2-chloroprocaine, etidocaine, mepivicaine, prilocaine, procaine, lidocaine, tetracaine, cocaine, dibucaine, bupivicaine

A
  1. COCAINE
  2. DIBUCAINE
  3. TETRACAINE
  4. BUPIVICAINE
  5. ETIDOCAINE
  6. MEPIVICAINE
  7. LIDOCAINE
  8. PRILOCAINE
  9. PROCAINE
  10. 2-CHLOROPROCAINE
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5
Q

mnemonic:
“"”cool dudes try bringing everyone more laughs;
people person? 2-cool”””

A

cocaine, dibucaine, tetracaine, bupivicaine, etidocaine, mepivicaine, lidocaine
prilocaine, procaine, 2-cloroprocaine

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6
Q

systemic effects based on HIGHEST to LOWEST blood flows:

-subarachnoid,-epidural,-paracervical,-caudal,-trachea,-intercostal, -brachial plexus, -subcutaneous,

A
  1. trachea
  2. intercostal
  3. caudal
  4. paracervical
  5. epidural
  6. brachial plexus
  7. subarachnoid
  8. subcutaneous
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7
Q

what kind of duration does a LA have in a highly perfused area?

A

LA has a shorter duration the more highly perfused the area

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8
Q

low doses of LAs do what to blood vessels?

high doses do what?

A

low doses vasoconstrict

high doses vasodilate

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9
Q

why does LA cause vasodilation?

A
  • -has direct effect on cardiac and smooth muscle mebranes (remember, blocks sodium channels and interfere with calcium)
  • -also has indirect effect on autonomic nerves
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10
Q

why do LAs cause bradycardia?

A

because the SA node is fast leaking sodium channel (LAs block sodium channels)

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11
Q

what cardiac effects will you see from local anesthetics?

A
  1. bradycardia
  2. increased PR interval
  3. wide QRS
  4. AV block
  5. decreased contractile strength (except cocaine)
  6. decreased automaticity and conductivity
  7. cardiac arrest (cocaine especially)
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12
Q

what vascular effects will you see with LAs?

A
  1. smooth muscle relaxation resulting in vasodilation (except ropivicaine and cocaine)
  2. inhibition of c-AMP= further CV effects
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13
Q

how is cocaine different?

A

it inhibits reptake of NE (causes hypertension, vasoconstriction and arrhythmias)

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14
Q

If your patient has had intravascular injection of a LA and he/she takes alot of epi and atropine to come around, what LA was used?

A

bupivicaine

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15
Q
  1. what patient population has a higher incidence of CARDIOtoxicity from LAs?
  2. what is the reason?
A
  1. obstetrics

2. unknown, but lower doses are recommended d/t spinal changes so use lower doses.

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16
Q
  1. what neuro issue from toxicity leads to increased o2 consumption?
  2. this rapidly becomes what respiratory issues(___ & ___)
  3. these cause what issue (ph____)?
  4. these all cause what cardiac issues (_____&______)
A
  1. seizures
  2. hypoxia and hypercapnia and acidosis
  3. acidosis
  4. negative inotropic and negative chronotropic
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17
Q
  1. what does interlipids do?

2. how long might it take for your patient to fully recover from toxicity even with interlipids?

A
  1. extracts lipid soluble bupivicaine from the blood or enters the tissue and blocks bupivicaine (tx for cardiac and cns toxicity)
  2. may take 1 hour for it to resolve toxicity
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18
Q
  1. what is bolus dose of interlipids?

2. what is the infusion dose?

A
  1. 1.5 ml/kg bolus over 1 minute, repeat every 5 minutes

2. infusion at 0.25 ml/kg/min increase to 0.5 ml/kg/min if needed

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19
Q

what are the CNS side effects?

A

–they vary with plasma level
1st_ circumoral and tongue numbness occurs at low doses
2nd_ sleepiness, lightheadedness, visual and auditory disturbances, vertigo, tinnitus and restless are next
3rd_muscle twitching, excitability then seizures
4th_transitional phase of excitement, then cns depression, then coma

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20
Q

how do LAs affect the cns (what is the action)

A

depress cortical inhibitory pathways leading to unopposed excitatory activity

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21
Q

what is the best way to prevent toxic side effects?

A
  1. use the lowest dose of LAs

2. pre-treatment with benzos can raise seizure threshold

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22
Q

seizure management from LA toicity:

A
  1. prevent hypoxemia, hypercapnia and aspiration

2. give benzos or barbs

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23
Q

neurotoxic effects:

  1. how often and from which method of administration?
  2. what is the range of symptoms?
  3. any LAs more than others?
  4. what else can it be confused with?
A
  1. rare, but usually follow SAB and epidural administration
  2. range from patchy numbness to persistent weakness to severe syndromes
  3. certain LAs have been implicated more than others
  4. differential diagnosis-can be confused with nerve damage from positioning
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24
Q

what are specific neurotoxic effects?

A
  1. transcient radicular irritation
  2. cauda equina syndrome
  3. anterior spinal artery syndrome
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25
Q

what is transcient radicular irritation?

  1. s/s?
  2. onset and duration?
  3. usual suspects?
  4. contributing factors?
A
  1. moderate to severe low back, buttock and thigh pain
  2. appears after 24 hours after SAB and recovers in about 1 week
  3. more often associated with LIDOCAINE (more with 5% but also with 2%), also with MEPIVICAINE
  4. role of positioning is controversial
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26
Q

cauda equina syndrome:

  1. what is it?
  2. what are symptoms?
  3. what drug is the usual suspect
  4. what catheter type has been implicated most; what other method in some cases?
A
  1. collection of symptoms from compression below L1 (lumbosacral plexus)
  2. sensory anesthesia, gi/gu sphinctor dysfunction, paraplegia
  3. lidocaine in continuous SAB
  4. microcatheter (although some cases with single dose shot)
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27
Q

anterior spinal artery syndrome:

  1. what is it?
  2. etiology? who does it affect most?
  3. cause?
  4. what othe complication do the symptoms mimic?
  5. usual suspect?
A
  1. paresis with variable sensory deficte
  2. unclear, elderly and vascular disease may predispose pts.
  3. possibly related to arterial spasm
  4. confused with epidural hematoma or abcess
  5. chloroprocaine with bisulfite preservative
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28
Q

allergic reactions

  1. incidence?
  2. often confused with what?
  3. what may be the culpret?
  4. allergies, if allergic to one; are you allergic to all?
  5. s/s
  6. which LA has most allergic reactions/
A
  1. true allergic response incidence is low
  2. vascular injection and/or systemic effects
  3. possibly d/t methylparaben used as preservative
  4. only within the same class, not across classes
  5. laryngeal edema, rash, hypotension, bronchospasm
  6. esters d/t PABA preservative/ derivitive
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29
Q

goals of additives to LAs?

A
  1. increase onset of block
  2. improve quality of block
  3. prolong duration of block
  4. decrease dose of LA
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30
Q

the non opiod additives are?

A
  1. epinephrine
  2. clonidine
  3. phenylephrine
  4. bicarb
  5. dextrose (for hypervaric)
  6. sterile water (for hypobaric)
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31
Q

epinephrine additive:

  1. what is dose
  2. max dose
  3. action
  4. contraindications
  5. contraindications for peripheral nerve block: what body parts should it never be given?
A
  1. 0.2 mg (200 mcg)
  2. 500 mcg
  3. a)casuses local vasoconstriction which decreases plasma level by up to 50%
    b) increases intensity of block (activates antiociceptive receptors in spinal cord.
  4. uncontrolled hypertension, uteroplacental insuffeciency, taking MAo or tricyclic antidepressants, IV regional (Bier block), unstable angina, cardiac dysrhythmias
  5. body parts lacking collateral flow i.e. fingers, toes, ears, nose, anything that grows (penis)
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32
Q

alpha agonists: name?

  1. action:
  2. what can it cause in the other alpha?
  3. side effects?
  4. desired effect?
  5. spinal dose?
  6. epidural dose?
  7. infusion dose?
  8. brachial plexus block dose?
A

clonidine

  1. stimulates central alpha 2 (some alpha 1) 200:1 ratio inhibiting central sympathetic outflow (negative feedback)
  2. can centrally affect alpha 1 causing peripheral vasoconstriction and rebound hypertension
  3. decreased HR, BP, CO; sedation and minimal resp depression
  4. anangesia,
  5. spinal bolus: 15-150 mcg (0.3-3mcg/kg)
  6. epidural bolus: 150-300 mcg (2-10 mcg/kg) diluted in 10 ml NS
  7. infusion: 10-40 mcg/kg/hr
  8. brachial plexus block: 25-150 mcg/40 ml LA solution
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33
Q

Phenylephrine: name?

  1. action; how effective in SAB
  2. SAB dose?
  3. Epidural, caudal and intrapleural dose?
  4. how does it affect peak blood levels of LA?
A

Neosynephrine

  1. vasoconstriction; prolongs block by 70% in SAB
  2. for SAB: 2-5 mg (40-80 mcg) added to solution
  3. epiural, caudal, intrapleural: 1:20,000 diultuion (1 mg Phenyl in 20 ml of LA solution (or 50 mcg/ml)
  4. does not significantly decrease peak blood levels of LA
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34
Q

alkalinizer:

  1. action?
  2. what does this accomplish?
  3. by how much?
  4. most effective in LAs containing what? what is the caveat to this?
A

sodium bicarbonate

  1. increases the amount of unionized/ lipid soluble LA by increasing pH of LA
  2. faster onset and spread of LA
  3. increases speed by 3-5 minutes
  4. especially effective with LAs that contain epi (although epi is broken down faster in alkaline environment)
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35
Q
  1. how do you make a LA hypobaric?

2. hyperbaric?

A
  1. add sterile water

2. add 10% dextrose

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36
Q
  1. what are the opiate additives?

2. where in the nerves do they act? where else?

A
  1. morphine, demorol, fentanyl, sufentanil
  2. a)spinal pre and post synaptic receptors in the substantia gelatinosa of the dorsal horn
    b) with epidural, rapidly absorbed into blood and migrates to CSF into brain causing analgesia
37
Q

local anesthetics TOPICALS:

  1. where are they likely used?
  2. what is commonly used? what dose(‘%’)? for what procedures?
  3. what other meds are commonly substituted or used?
  4. what meds are not used d/t ineffectiveness? why dont they work?
A
  1. nose, mouth, esophagus, tracheobronchial tree, genitourinary tract, epidermis
  2. cocaine 4-10% (ent procedures)
  3. lidocaine, aftin (oxymetazoline), tetracaine (ponticaine)
  4. . procaine (novacain), chloroprocaine (nesacaine). d/t poor mucous membrane penetration
38
Q

cocaine

  1. dose (%)
  2. uses?
  3. what unique property does it have?
  4. what does vasoconstriction help with?
A
  1. 4-10% topically
  2. commonly used in rhino-laryngeal cases
  3. produces localized vasoconstriction and anesthesia
  4. less bleeding, improved surgical field visualization
39
Q

nebulized anesthesia

  1. what is drug of choice?
  2. what is it used for?
  3. what are possible good side effects (normal patients)?
  4. what are some bad side effects (asthmatics)?
  5. how does it compare to IV? why?
A
  1. xilocaine (lidocaine)
  2. a)anesthetizing upper and lower airway tract proir to laryngoscopy (regular or fiber optic) & broncohscopy
    b) intractable cough
  3. bronchodilation in normal patients
  4. bronchoconstriction / increased airflow resistance in asthmatics
  5. systemic concentration comperable to iv administration d/t large surface area and significant vascularity of trachoebroncial area
40
Q

topical skin: Eutectic Mixture of Local Anesthetic

  1. what is eutectic?
  2. what is in it?
  3. what is the dose? what do you put over it?
  4. how long is wait period for: skin graft?, cautery of genital warts?, venipuncture?
  5. what can it be combined with to make venipuncture easier?
  6. does it affect lab samples?
  7. what factors determine its efficacy?
A

EMLA

  1. a mixtuer having the lowest melting point
  2. lidocaine or prilocaine
  3. 1-2 grams/ 10 cm2 of skin (4”) with occlusive dressing
  4. a)skin graft: 2 hours
    b) cautery of genital warts: 10 minutes
    c) venipuncture: 45 min
  5. can be combined with nitro oint to cause vasodilation
  6. does not affect blood sample, can affect intradermal skin tests (causes flare response which = weakly positive result)
  7. skin blood flow, epidermal thicknes, application duration, presence of pathology
41
Q

emla continued:

  1. what serious s/e can be caused by EMLA/
  2. what is it? what does it do to us?
  3. what medications might potentiate/ cause this in conjunction with emla?
  4. not recommended for whom?
A
  1. methemoglobinemia is d/t prilocaine metabolism
  2. methemoglobin is when methyl group occupies oxygen spot on hemoglobin with high affinity. causing hypoxia
  3. occurs mainly with concurrent use of nitro, nipride, dilantin, sulfa drug & tylenol.
  4. not recommended for :
    a) children less than 3 mos (methemoglobin)
    b) application wounds (increased infection risk)
    c) persons taking mexiletine (mexitil), lidocaine amides, antiarrhythmics (additive/ synergistic affects)
    d) patients with allergies to amide anesthetics
42
Q

local infiltration

  1. what is it?
  2. what LA is used most commonly?
  3. what LA is used for incisions?sedation and minimal resp depression
  4. what additive increases duration? what conc?
  5. where on the body should we use epi additive with caution?
A
  1. extravascular placement of LA
  2. lidocaine
  3. longer acting bupivicaine may be used for incisions
  4. duration increased with epi 1:200,000
  5. use caution again with appendages with no collateral flow
43
Q

what is oraverse?

A

a new reversal for LAs used in mouth (especially when epi is used). it is injected submucosally and vasodilates the blood vessels to speed uptake and reversal

44
Q

periphrial nerve block:

  1. what is it?
  2. what is the mantle effect?
  3. so anesthesia develops ___ to ___?
  4. recovery from anesthesia is ___ to ____?
A
  1. local anesthetic is injected into tissue around or near the nerve causing anesthesia to the nerve.
  2. outside mantle of nerve is anesthetized first, then the inner core fibers (last). Mantle fibers are proximal limg and core fibers are distal limb
  3. anesthesia develops proximal to distal
  4. recovery is distal to proximal
45
Q

IV regional: what is it called?

  1. how is it done?
  2. how long does it last?
  3. what LAs are used?
  4. what is risk of methemoglobinemia?
A

Bier block

  1. tourniquet is placed on proximal extremity and local is injected distally via IV catheter causing rapid anesthesia (nd some muscle relaxation) to that extremity up to the tourniquet.
  2. depends on tourniquet time, recovery is rapid once tourniquet is deflated and drug is diluted by new blood
  3. usually lidocaine or prilocaine (NEVER bupivicaine), can use esters as well.
  4. no significant methemoglobinemia (only 3%)
46
Q

how much methemoglobin must be present to cause cyanosis?

A

10%

47
Q

prilocaine vs. lidocaine for Bier block:

  1. which had lower plasma levels post tourniquet deflation?
  2. what LAs are not recommended for Bier block?
A
  1. Prilocaine had lower plasma levels and is therefore safer than lidocaine based on reduced risk of toxicity
  2. -chloroprocaine: high risk of thrombophlebitis
    • bupivicaine: cardiotoxic
    • ropivicaine: cardiotoxic (but less than bupiv)
48
Q

epidural:

  1. defn:
  2. MOA:
  3. onset:
  4. choice of LAs:
A
  1. anesthesia caused by local anesthetic solutions injected into the epidural or sacral caudal space
  2. Diffusion of LA into paravertebral region through intervertebral foramina causing paravertebral nerve blocks — LAs direct action on nerve roots and spinal cord following local anesthetic diffusion across the dura
  3. 15-30 min
  4. -lidocaine (more rapid–for short cases)
    • bupivacaine or ropivacaine (0.5-0.75%) for long cases or post op pain. cause prolonged sensory and motor anesthesia.
  5. c-section use: 0.5% bupiv or ropiv
49
Q

spinal anesthesia:

  1. definition:
  2. site of action
  3. some zones have “differential anesthesia” what is this?
  4. what causes this?
  5. what are the spinal anesthesia levels (sensory, motor, sympathetic)
  6. what causes this (again)?
A
  1. anesthesia following LA injection into sub arachnoid space
  2. -primary: preganglionic fibers leading to spinal cord in the anterior rami
    • secondary: superficial spinal cord layers
  3. Nerve groups in the same region act to greater and lesser extents when exposed to LAs.
  4. zones of differential anesthesia causes:
    • local anesthesia concentration gradient effects
    • different nerve fibers have different sensitivities to LAs
  5. sympathetic is 2 levels above sensory; motor is 2 below sensory
  6. different types of nerves in each group, some more sensitive than others (motor least sensitive).
50
Q
  1. why is motor least sensitive?

2. autonomic most sensitive?

A
  1. motor is A gamma and A alpha, these are heavily myelinated and wide neurons which have more sodium channels to block
  2. autonomic (sympathetic) are B fibers which are lightly myelinated and thin in diameter (pre-ganglionic) which are easiest to anesthetize (even easier than C fibers)
51
Q

tumescent technique:

  1. what is it?
  2. what dose (%) of lido and epi are used?
  3. what is it used for?
  4. how much lidocaine can the subQ hold (gm SQ/ mg lido)?
  5. what lido doses are given?
A
  1. lidocaine is highly diluted in large volumes of fluid
  2. lidocaine 0.05% and epi 1:100,000 are used
  3. used for liposuction: provides analgesia/anesthesia and vasoconstriction
  4. sub q tissue absorbs lidocaine (every 1 gm SQ can hold 1 mg of lidocaine) reslulting in a safety or buffering process
  5. lidocaine doses often given 30-50 mg/kg
52
Q

max doses of LAs:

  1. where did max dose info come from?
  2. what would be ideal as far as max doses go?
  3. what patient factors should be considered (name 3), why?
A
  1. experiments on animals, case reports: not from evidence based
  2. would be best to have save ranges for each technique
  3. age, organ function, pregnancy; these affect kinetics)
53
Q

max doses: Infiltration anesthesia
max dose chloroprocaine:
doa:
max with epi:

A

chloroprocaine:

  1. 800 mg
  2. 30-60 min
  3. 1000 mg
54
Q

infiltration anesthesia:

  1. max dose Lido:
  2. doa:
  3. max with epi:
A

Lidocaine

  1. 300 mg
  2. 60-240 min
  3. 500
55
Q

infiltration anesthesia max:

  1. mepivicaine max dose:
  2. doa:
  3. max with epi:
A

mepivicaine:

  1. 300 mg
  2. 60-240 min
  3. 500 mg
56
Q

infiltration anesthesia max:

  1. priolcaine max
  2. doa
  3. max with epi
A

prilocaine

  1. 500
  2. 60-120
  3. 600
57
Q

infiltration max dose:

  1. etidocaine max dose:
  2. doa:
  3. max dose with epi:
A

etidocaine

  1. 300 mg
  2. 120-480 min
  3. 400 mg
58
Q

infiltration max dose:

  1. bupivicaine max dose:
  2. doa:
  3. max with epi:
A

bupivicaine

  1. 175 mg
  2. 120-480 min
  3. 225 mg
59
Q

major nerve block max doses:

  1. lidocaine max dose:
  2. onset
  3. duration
A

lidocaine

  1. 500 mg
  2. 10-20 min
  3. 120-240 min (medium acting)
60
Q

major nerve blocks max dose:

  1. mepivicaine max dose
  2. onset:
  3. duration:
A

mepivicaine

  1. 500 mg
  2. 10-20 min
  3. 180-300 min (medium acting)
61
Q

major nerve block max dose:

  1. prilocaine max
  2. onset:
  3. duration:
A

prilocaine

  1. 600 mg
  2. 10-20 min
  3. 180-300 min (medium acting)
62
Q

major nerve blocks max dose:

  1. bupivicaine:
  2. onset:
  3. duration:
A

bupivicaine

  1. 225 mg
  2. 15-30 min
  3. 360-720 min (long acting)
63
Q

major nerve blocks max dose:

  1. etidocaine max dose:
  2. onset:
  3. duration:
A

etidocaine

  1. 400 mg
  2. 10-20 min
  3. 360-720 min (long acting)
64
Q

major nerve blocks max dose:

  1. tetracaine max dose:
  2. onset:
  3. duration:
A

tetracaine

  1. 200 mg
  2. 20-30 min
  3. 300-600 min (long acting)
65
Q

toxic ranges amides:

  1. lidocaine
  2. with epi
A

lidocaine

1) 4 mg/kg
2) 7 mg/kg w/ epi

66
Q

toxic ranges amides:

  1. bupivicaine
  2. with epi
A

bupivicaine

1) 2 mg/kg
2) 3 mg/kg w/ epi

67
Q

toxic ranges amides:
mepivicaine
(not used with epi)

A

mepivicaine

7 mg/kg (400 mg max)

68
Q

toxic ranges amides:

  1. etidocaine:
  2. with epi:
A

etidocaine

1) 6 mg/kg
2) 8 mg/kg w/ epi

69
Q

toxic ranges for esters
procaine
(not used with epi)

A

procaine

7 mg/kg

70
Q

toxic ranges for esters

  1. tetracaine
  2. (not used with epi)
A

tetracaine

1. N/A

71
Q

toxic ranges esters:

  1. chloroprocaine:
  2. w/ epi
A

chloroprocaine

1) 11 mg/kg
2) 14 mg/kg w/ epi

72
Q

toxic ranges for esters:
cocaine
(not used with epi)

A

1.5 mg/kg

73
Q

local anesthetics: Lido

  1. uses?
  2. notables:
  3. max doses (also w/ epi)
A

Lido

  1. -antiarrhythmic (1-1.5 mg/kg bolus; 1-4 mcg/min infusion)
    • attenuation of pressor response (1.5-2 mg/kg 2-3 min prior to laryngoscopy)
    • local anesthetic
  2. first synthetic LA made; gold standard; popular d/t versitility
  3. 4mg/kg (7 mg/kg w/ epi)
74
Q

Lidocaine facts:

  1. bier block
  2. transtracheal block:
  3. infiltration nerve block:
  4. epidural:
  5. SAB:
A

lido

  1. bier block: 40-50 ml of 0.5% solution (100 ml for Lower ext)–NO EPI!!!!!
  2. transtracheal block: 2-3 ml of 4% solution
  3. infiltrative/ nerve block: 0.5-5 mg/kg
  4. epidural: 200-400 mcg incremental bolus of 1-2%; infusion 6-12 ml/hr
  5. SAB: 50-100 mcg of 0.5 (can go as high as 5%- but risk toxiciy)
75
Q

lido onset:

  1. antiarrhythmic:
  2. infiltration:
  3. epidural:
  4. SAB:
A
  1. 45-90 seconds
  2. 30-60 sec
  3. 5-15 minutes
  4. 5 min
76
Q

lido metabolism:

  1. how is it metabolized? is there active metabolite?
  2. is there another step? is there active metabolite?
  3. what affects lidocaine metabolism?
A
  1. -oxidative deALKYLATION: yes: to mono-ethyl-glucinee-xylidide (active)
  2. -this metabolite is hydrolyzed: yes: to xylidide (active)
  3. -hepatic dysfunction or decreased blood flow decrease rate of metabolism
77
Q

prilocaine:

  1. max dose:
  2. where used/ for what:
  3. what is it similar to:
  4. what is better about it:
  5. what organ uptake is higher: what does this mean:
  6. metabolite:
  7. what can this metabolite cause when oxidized
A

prilocaine

  1. max: 8 mg/kg
  2. used frequently outside of us for dental and iv regional
  3. similar to lidocaine with epi
  4. causes less vasodilation so no epi needed, lower rate of toxicity and faster metabolism, higher vD
  5. higher lung uptake, less drug to brain and heart
  6. ortho toluidine
  7. oxidizing agent turns hgb Fe2+ to methemoglobin Fe2+ causing methemoglobinemia
78
Q
  1. what does your blood look like with methhemoglobinemia?

2. what is the tx?

A
  1. chocolate brown

2. methlyene blue 1-2 mg/kg IV over 5 min or ascorbic acid 2 mg/kg

79
Q

mepivicaine

  1. max dose (& w/epi)
  2. metabolized:
  3. eliminated:
  4. similar to what LA except for…:
  5. what patient populationn has decreased clearance:
A 
mepivicaine:
1) 4 mg/kg (7 mg/kg w/ epi)
2. hepatic enzymes
3. liver
4. lidocaine except :	
	slower onset
	longer DOA
	lacks vasodilatory properties- doesnt need epi to prolong 	
5. neonates
80
Q

bupivicaine (marcaine)

  1. dose (& w/epi)
  2. not recommended for 2 things? why?
  3. what side effect is of concern d/t duration?
  4. where used at most? why?
  5. does it need epi to prolong block?
  6. what does it block more: sensory or motor? why is this good?
A

bupiv:

  1. max dose 2mg/kg (3 mg/kg w/ epi)
  2. –paracervical block; d/t urteine vasoconstriction
    • -iv regional d/t high plasma levels (cardiotoxic)
  3. cardiotoxicity: highly lipid soluble; dissociation from cardiac Na+ channels can be slow therefore prolonged cardiac depression
  4. –widely used in OB because it is 95% protein bound and will not cross placenta
    • -post op pain because motor movement if preserved
  5. epi does not prolong duration but allows for slightly higher dose
  6. sensory block> motor: therefore post op patients are able to ambulate
81
Q

bupiv /depofoam

A

new on market
bupivicaine encapsulated by depofoam- prolongs duration to 72-96 hours
single dose to site

82
Q

ropiv:

  1. dose:
  2. availability:
    3: similar to ___ but without ____& is ____potent?
  3. exists only as ___ isomer?
  4. good for what types of blocks?
  5. does what when injected SQ
  6. metabolized where? excreted where?
  7. how is it structurally different from bupiv?
A
  1. 3 mg/kg
  2. 0.5, 0.75 & 1%
  3. bupiv without cardiotoxicity, less potent
  4. “S” isomer
  5. good for epidural, brachial plex & infiltrative
  6. vasocontricts
  7. liver; kidneys
  8. propyl is in butyl place on ropiv
83
Q

procaine:

  1. max dose?
  2. where is it not used? why?
  3. low___ but high potential for __ ___?
A
  1. 7 mg/kg
  2. not usually used on peripheral and extradural blocks d/t slow onset and short duration
  3. low toxicity but high allergic reactions
84
Q

chloroprocaine:

  1. max dose? (w/ epi)?
  2. pros?
  3. cons?
  4. where used most?
A
  1. 11 mg/kg (14 mg/kg w/ epi)
  2. short duration, rapid onset, low toxicity
  3. used in ob but requires frequent re-boluses: had issues d/t neurotoxicity from bisulfites (now removed); still some back pain issues post removal (radiculopathy);
    - -not used in spinals.
  4. good for peripheral nerve blocks of short duration surgery
85
Q

tetracaine:

  1. max dose (no change with epi)
  2. popular for what?
  3. duration w & w/o epi
  4. potency? chance for toxicity?
  5. what other route is it available for?
A
  1. 2.5 mg/kg
  2. spinal anesthesia (not used anywhere else d/t potency)
  3. profound anesthesia (2-3 hours w/o epi; 4-6 hrs w/ epi)
  4. very potent, high risk for toxicity
  5. available as topical
86
Q

cocaine:

  1. action/ uses. ?
  2. why is it abused?
  3. what does it do?
  4. what can it cause in high doses? (how bout in small doses?)
  5. onset?
  6. peak?
  7. DOA?
  8. where (on or in body) should it not be used?
A

cocaine:
1. topical anesthesia and vasoconstrictor (nose procedures)
2. stimulates CNS
3. blocks re-uptake of catecholamines (nor epi)
4. tachycardia in high dose/ brady from vagal stim in low dose
5. less than 1 minute
6. 3-5 min
7. 30-120 min
8. not for use on eye (causes corneal sloughing, increases IOP)
9 detoxified by liver choinesterase into water soluble metabolites which are present for 24-36 hrs.

87
Q

bad things about cocaine:

A
  • increases mac (d/t exciting CNS)
  • potentiates arrhythmic effects of sympathomimetics (epi, NE etc.)
  • causes HTN, dysrhythmias and tachycardia under anesthesia
88
Q

s/e of neuraxial opiates:

A 
pruritis (#1)
urine retention
constipation
sedation
resp depression
reactivates herpes with epidural morphine

princip, pharm, phys, regional (18 decks)

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