The flashcards below were created by user
on FreezingBlue Flashcards.
Which amides are metabolized in the liver?
- prilocaine(and in plasma and kidney)
Why is articane/bupivacaine metabolism more rapid?
ester hydrolysis more rapid
which enzyme is important for ester hydrolysis?
- plasma cholinesterase(pseudo)
- atypical plasma (psudocholinesterase deficiency concern)
- 1. 1.8 ml single doses
- 2. H20 + NaCl
- 3. acidic pH
local anesthetics can interact with these two items:
other locals for additive effect(stay below max)
when to use vasocontriction?
- increase depth of anesthesia
- increase duration
- decrease peak bld levels(also decrease systemic tox)
- maintain hemostasis
adding epi to lidocaine will...
increase conc of lidocaine will....
better efficency anesthethic will stay in area(duration)
improves via infiltration to other tooth
so peak blood concentration with epi is?
- lower at same injected dose(mg)
- can use lower dose local!
epinephrine deceases bld flow
- down to 25% then goes back up.
- Usually can cut bld loss by half during perio
adrenergic amine structure(E,NE,LEV)
just change H to methyl group from NE
receptor activation by
- 1. a1,a2,b1,b2
- 2. a2
- 3. a1,a2,b1
increase automaticity, HR, contractility
vasodilation in skeltal muscle, bronchodilation, increase plasma glucose, increase lipolysis
epi will cause
increase dyssrhmia, HR, increase a lot CO, decrease PR
LEV will cause
increase dysrrthmia, increase CO, PR
NE will cause
increase dysrrthmia, decrease HR, increase a lot PR, increase BP
a2 receptor agonist, can inhibit NE realse if too much b/c a2 also location at presynaptic terminals
why do a2 agonists acts like a1 agonist to vasoconstrict?
because a2 receptors are on the endothelial side not activated by post fibers
why is lev administered over epi?
epi has strong beta-1 effect which increase HR while lev does not affect beta-1 too much (has a2).
NE is pretty nonselective alpha agonist
vasocontriction in high doses, decrease plasma K
epienphrne has rapid onset and metabolized by
- COMT?MAO if exogenous,
- liver if endogenous
- short duraration, longer intraoral
infusing IV epi would cause
increase HR, sys BP, decrease PR
in a dental office small boluses of epi are given..how much in CV disease patient
- if patient cant get up without being breathless...dont
- if can do moderat excercise(2 cartridges) at 40pg/mL
why would epi with procaine not be beneficial?
procaine has short duration
a1 vs b2
- a1 works on main arteries
- b2 works on smaller in skeletal muscle(dilation)
- NS beta blockers
- NE reuptake inhibitors(antidepress, cocain, amphtames)
- COMT inhibitors
which one interacts w epi and lev?
cardiosleective- beta 1 only
combined alpha and beta
- non selective beta blockers
- will affect B1, B2.
- hypertension and reflex brady
no effect on a1
tricyclic SNRI antidepressants
pain management block reuptake of NE to presynaptic cell, longer exaggerated response
- SO increase in BP, HR possible, but most
- exogenous metabolized by COMT
NE reuptake inhibitor -ADHD mediation can increase BP. HR
cocaine and ampehtamine that interact w epi can lead to...
dysrrthmia, BP, HR increase, AVOID
vasocontriction, myocaridal infarction
COMT inhibitors used in Parkinsons that increases Dopa and exaggerated response to epi.......
Tolcapone, Entacapone with Sinemet
alpha blockade w/ epi and lev (alpha1)
- more pronounced with lev b/c alpha2
- "epinephrine reversal"
- hypotension and tachy
alpha blockade with
phenyothianzaines.(neuroleptics)..bp low b/c of the strong b1 effect of epi, bp will drop even lower
concerns with epi do the following
monitor BP and HR, slow injection, monitor BP, HR 3-5 minutes post injection
If concerned dont do this with epi:
- never use 1:50000 epi,
- limit 0.04mg
- use epi imgregnated retraction cords
- never use .2 cartidges for CV patient