Local + Nitrous SG Flashcards
three parts of local anesthesia
- aromatic group
- intermediate linkage
- amine group
aromatic group
confers lipophilic properties
intermediate linkage
supplies spacial separation between lipophilic and hydrophilic ends and connects them with either an ester or amide linkage
amide group
secondary or tertiary
affects pka, lipid vs water solubility, and influences speed of onset
ester
union of a carboxylic acid and alcohol
amide
union of a carboxylic acid and an amine (peptide bone is an amide)
except for ______, the injectable dental locals are ______
procaine
amides
the topicals are mostly _______ (esters or amides)
esters
list the amides
lidocaine (xylocaine)
mepivicaine (carbocaine)
articaine (septocaine)
buprivacaine (marcaine)
etidocaine (duranest)
prilocaine (citanest)
list the esters of benzoic acid
butacaine
cocaine
benzocaine
hexlycaine
piperocaine
tetracaine (pontocaine)
list the esters of para aminobenzoic acid
chloroprocaine
procaine (novocaine)
proxycaine
what is the only injectable ester?
procaine (novocaine)
another name for lidocaine
xylocaine
another name for mepivicaine
carbocaine
another name for articaine
septocaine
another name for buprivacaine
marcaine
another name for etidocaine
duranest
another name for prilocaine
citanest
another name for tetracaine
pontocaine
another name for procaine
novocaine
the amine portion is a _____ (acid / base)
base
only _____ can cross cell membranes, so onset of action is faster for ____ (low / high) pKa because they give up their protons more easily and become uncharged “free bases”
free bases
low
pKa
how strongly the organic portion of the local anesthetic molecule holds onto its proton
drugs with a high pKa are _____(weak / strong) acids.
weaker acids (stronger. bases)
Do weak acids hold on to their protons tightly? what does this mean for onset?
weak acids / strong bases hold their proton more tightly, remaining positively charged, and cross cell membranes poorly
thus they have a slower onset
drugs with low pKa are _______ (weak / strong) acids
strong acids (weak bases)
do strong acids hold on to their protons tightly? what does this mean for onset?
strong acids / weak bases shed their proton more easily, become non-ionized free bases and cross membranes more easily
acidic environments like inflamed tissue have ____ (slow / fast) onset
slow onset
since the base remains protonated in the low pH environment
locals ______ membranes and prevent ________
stabilize
rapid sodium influx
why are the pharmacokinetics of locals unique?
they become ineffective when absorbed by the system
what happens when locals are redistributed?
effects wear off
metabolic half life is not related to ______ but is related to _____
duration of anesthesia
toxicity
half life
the rate at which a local anesthetic drug is removed from the blood
does half life impact toxicity?
yes
can local anesthetic agents cross the BBB?
yes
can local anesthetics cross the placenta?
yes (and get into breast milk)
why does metabolism affect overall toxicity?
because it is the balance between rates of absorption at the injection site and the removal from the blood that determines the levels in the tissues
duration of action is related to ______ of the local
protein bonding
is duration of action related to metabolic transformation?
no
all locals are (vasodilators / vasoconstrictors)
vasodilators
which local is a vasoconstrictor?
cocaine
Why are vasoconstrictors added to most LAs?
because LAs are vasodilators, blood washes them away. need something to balance this so they stay in desired area longer
with vasodilation, there is (2 things)
- an increased rate of absorption
- decreased duration and level of pain control
an increase in the anesthetic in the blood will lead to _______
overdose
vasoconstrictors are needed for _________
slow redistribution
why use vasoconstrictors?
because local anesthetics possess vasodilation properties
what are vasoconstrictors?
drugs that constrict blood vessels and there by control tissue perfusion
which vasoconstrictor is used most often?
epinephrine
epinephrine effects
alpha
beta 1
beta 2
small amounts of urine are excreted in ______
urine unchanged
soft tissue anesthesia
always develops before pulpal
5 hours
pulpal anesthesia
relatively short window
60 minutes
does nerve block or infiltraiton last longer?
nerve block
primary metbaolism of esters
plasma hydrolysis by the enzyme pseudocholinesterase
cocaine is metabolized primarily in
liver
amides are metabolized in
liver
the status of liver function is a factor in
toxiity
relative contraindications in terms of metabolism of amides
- liver failure
- heart failure resulting in lower liver perfusion
articaine (septocaine) is metbaolized primarily by
plasma carboxyesterase
accumulation of biotransformation product _______ in the blood can produce _____
orthotoluidine
methemoglobin
what two LAs produce methemoglobin?
prilocaine
articaine
methemoglobin is produce in hemoglobin in which the iron ion has been oxidized to the _____ instead of ____ state
ferric (fe+3)
ferrous (fe+2)
if a significant percent of the total hemoglobin is affected, it can result in _____
poor oxygen delivery to tissues
methemoglobin can be reversed rapidly with ____-
IV methylene blue
why is pulse oximetry unreliable with methemoglobin?
methemoglobin has absorption frequency that draws the pulse oximeter to 85%
excretion of local anesthetics
kidney for local anesthetic agents and metabolites
when do local anesthetics lose their effect?
when absorbed into the blood stream
the rate at which a local is removed from the plasma is expressed as its…
metbaolic half life
duration of local anesthetics from shortest to longest
carboxaine
xylocaine
septocaine
marcaine
which anesthetic is not recommended in pedo or in cognitively impaired adults?
marcaine
max dose for lidocaine with epinephrine
4.4
max dose for mepivicaine
4.4
max dose for bupivicaine
1.3
max dose for septocaine
7
epinephrine’s effects on the myocardium
- increased cardiac output
- increased stroke volume
- increased oxygen consumption
- decrease overally efficiency of the myocardium
when does LA become toxic?
when the tissue levels int he CNS or heart become too high
maximum recommended doses of drugs should be calculated by…
body weight (and not exceded)
why could manifestations of toxicity occur well after the appointment is over?
LA tissue levels in the CNS or heart may rise slowly as the drug is absorbed over time
mild symptoms of LA toxicity
sedation
drowsiness
transient anxiety
moderate / severe symptoms of LA toxicity
dysphoria
anxiety
nausea
confusion
semiconscious / unconscious
tonic-clonic seizures
severe symptoms of LA toxicity
respiratory and cardiovascular collapse
signs of excessive vasoconstrictor dose
CNS: increased fear and anxiety, tension, restlessness, throbbing headache, tremors, weakness, dizziness, pallor, respiratory difficulty, palpations
increased blood levels: cardiac arrhythmias, ventricular fibrillation, increased BP, angina, cerebral hemorrhage
local complications of injections
-pain on injection or burning on injection
-needle breakage
-persistent anesthesia or paresthesia
-trismus, hematoma, infection, edema
-sloughing of tissues
-facial nerve paralysis
-post-anesthetic intraoral lesions
systemic complications of injections
-no drug ever exerts a single action
-no clinically useful drug is entirely devoid of toxicity
-toxicity caused by direct extension of the usual pharmacological effect of the drug (ex. side effect)
-toxicity caused by alteration in the recipient (ex. emotional disturbances)
3 topical anesthetics you should know
benzocaine
lidocaine
cocaine
benzocaine
ester type local anesthetic
poor absorption
localized allergic reactions reported
inhibits antibactieral actions fo sulfonamides
lidocaine
poorly soluble in water
primarily used to paliate painful oral ulcerations, HSV, mucositis form chemo / radiation therapy
cocaine (as topical)
-rapid onset of topical
-duraiton up to two hours
-metbaolism in liver, excreiton in urine
-produces vasoconstriction
-exellent agent for nasal trauma / surgery
3 divisions of the trigmeinal nerve
v1 - opthalmic
v2 - maxillary
v3 - mandibular
pulpal anesthesia can usually be achieved with ____ in the maxilla
infiltration
why can anesthesia be achieved with infiltration in the maxilla?
cortical plate is not very dense; bone is highly vascular
pulpal anesthesia for all lower teeth occurs where?
on the side injected
why does infiltration not work in the mandible?
cortical bone too dense for infiltration
landmark for common infiltration
mucobuccal fold (vestibular sulcus) at / above apex of root
how much LA should be used per tooth?
1/3 carpule per tooth
landmarks for PSA nerve block
- zygomatic buttress (injection point is posterior to it)
- depth of vestibule
- tuberosity of maxilla
direction of PSA nerve block
posterior, medial, and superior
ASA nerve block landmarks
- medial aspect of the pupil
- infraorbital notch
- depth of the mucobuccal fold
- 5mm lateral to long axis of 1st PM
greater palatine nerve block landmarks
- midline of palate
- 2nd maxillary molar
- greater palatine foramen at junction of maxillary alveolar process and palatine bone
incisive canal nerve block landmarks
- incisive papilla
second division block landmarks
- zygomatic buttress
- depth of vestibule
- tuberosity of maxilla
direction of second division block landmarks
direction is posterior, medial, and superior
second division block is ____ and ____ than a PSA (requires a ______)
higher
deeper
long needle
inferior alveolar. nerve block landmarks
- depth of the coronoid notch
- pterygomandibular rapphe
- contra lateral premolars
- bisection of thumbnail lying in coronoid notch (or higher)
- occlusal plane
- contact bone with needle almost fully in tissue
long buccal nerve block landmarks
- anterior, lateral border of the ramus
- superficial
location of anesthesia for posterior superior alveolar nerve block (PSA)
pulpal and lateral gingival anesthesia to (but not including) the mesiobuccal cusp of the first molar
no palatal anesthesia
anterior alveolar nerve block (ASA / infra orbital nerve block)
not frequenlty used, but useful when infiltration not practical due to localized infection
location of anesthsia for greater palatine nerve block
posteiror hard palate and soft palate to midline
location of anesthesia for incisive canal block
anterior hard palate (pre-maxilla) which includes the four maxillary incisors
usually requires greater palatine block as well
location of anesthesia for second division block
all upper teeth and buccal / palatal mucosa on injected side (and lateral alar rim)
good injection when area of infiltraiton is involved in infection
location of anesthesia for inferior alveolar nerve block
pulpal anesthesia for all lower teeth on side injected
does not provide lingual anesthesia, although the lingual nerve is usually anesthetized at same time
does not anesthetize posterior lateral gingival tissue (long buccal)
location of anesthesia for long buccal nerve
lateral gingival anesthesia in posterior mandible
extraction, surgery, rubber dam clamp
gow gates will anesthetize _____-
entire 3rd division of CN V
success rate of gow gates
95% with experience (Compared to 80% for traditional IANB)
gow gates landmarks
- lower border of tragus
- corner of mouth
- needle tip jsut below ML cusp maxillary seocnd molar
- penetration soft tissue just distal to maxillary second molar
- contact with neck of condyle must be made
in tracheal mucosa, uptake of topical anesthetics is _____
almost as rapid as with IV administration
length of time for application for topical anesthetics in mucosal sites
2-3 minutes
penetration of topical anesthetics in mucsal sites
2-3mm
types of tissue that topical anesthetics can penetrate
mucosa or damaged skin only
are deep tissues anesthetized by topicals?
no
two types of bases for topical anesthetics
- alcohol propylene glycol
- polyethylene bases
3 types of topicals
- benzocaine
- lidocaine (xylocaine)
- cocaine
benzocaine is a _____ type local
ester
absorption of benzocaine?
poor
localized ______ have been reported with benzocaine as local
allergic reactions
benzocaine inhibits ______ action of _______
antibacterial
sulfanamides
lidocaine is used as a ____% concentraiton in locals
5
is lidocaine soluble in water?
no
what type of lidocaine solution penetrates tissues better than the base form
when acidified, lidocaine hydrochloride water soluble 2% concentraiton
what is lidocaine topical primarily used for?
paliate painful oral ulcerations
HSV, mucositis from chemo therapy
lidocaine topical is a _____ type anesthetics
amide
maximum dose of lidocaine
4.4 mg / kg
pKa of lidocaine
7.9
onset of action for lidocaine topical
2-3 minutes
duration of cocaine topical
2 hours
cocaine is metabolized in the
liver
cocaine is excreted in the
urine
Is nitrous metabolized by the body?
no
Does nitrous have any adverse effects on liver, brain, kidney, respiratory system?
no
rapidly is nitrous absorbed into respiratory circulation?
1000 ml may be absorbed per minute
nitrous replaces the _____ in the blood
nitrogen
how does nitrous impact body cavities?
may increase volume in body cavities (such as bowel, pleural space, middle ear)
how is primary saturation of the blood and brain accomplished? (nitrous)
displacement of nitrogen
how long does it take for equilibration for nitrous to occur at any concentraiton?
3-5 minutes
how long should the patient remain at given concentration to assess effect of dose?
3-5 minutes
what tissues will reach concentration faster?
tissues with greater perfusion (brain, heart, liver, kidney)
pressure in cylinders of nitrous
745 psig (pounds per square inch guage)
connection and office setup for nitrous
DISS (diameter index safety system) scavenger system
percentage of nitrous / oxygen at various flows
4:2 (67% nitrous oxide)
overview of diffusion hypoxia
- patient switches from N2O / O2 to room air
- N2O rapidly leaving the circulation dilutes the other gases in the lungs
- there is a fall in O2 concentraiton in alveoli resulting in hypoxia
what is the alveolar O2 concentration during diffusion hypoxia?
10% alveolar O2 concentraiton
symptoms of diffusion hypoxia
headache
nausea
lethargy
prevention of diffusion hypoxia
100% oxygen at end of case for 5 minutes
this also ensures that the N2O in the patient’s system is scavenged and not exhaled into the room
physical properties of nitrous
nonirritating
sweet smelling
colorless gas
nonflammatbale
non-explosive
least potent of anesthetic gases
is nitrous stable under pressure at room temperature?
yes
how would nitrous support combustion in a fire?
at temperature >450 deg C forms nitrous and oxygen
delivered with oxygen
N2O analgesic effect at therapeutic levels
10-15mg of morphine
gas source of nitrous
oxygen and nitrous oxide are delivered either from portable tankes attached to anesthesia machine or thorugh central machine
color code of oxygen and nitrous oxide
oxygen is green
nitrous oxide is light blue
set up of nitrous
central system installation must be done by a dental supplier and plumber qualified as competent in the installation process (medical gas certified)
what organization is dedicated to educating users about proper installation?
PIPE (piping, industry, progress, and education)
how many tanks of each gas are connected in portable tank systems?
two (four tanks total)
one in use, other is backup
when in the in-use tank is empty…
opening the valve on the back-up maintains gas flow
if both tank valves are accidentally opened…
the machine will run off both simultaneously, and when empty there is no backup
parameters of control of nitrous
- total flow of gases, measured in livters per minute
- the mix (percent of O2 and N2O)
the scavenger)
when scavenging rate is too slow…
may allow expired N2O to enter the room
(ball falls below the green zone)
when scavenging rate is too fast…
wastes agent… as faster gas flows will be needed to keep up with scavenger
(ball rises above the green zone)
fixed percentage (definition)
all patients receive the same concentration
ratio for fixed percentage
usually 40-50% throughout the procedure
fixed percentage is ineffective in ____ of cases
15%
how do patients often feel during fixed percentage?
uncomfortable
dislike procedure (probably over-sedated)
overview of titration technique
- patient / dose specific
- higher success rate
- less nausea, vomiting, headache, and adverse behavior
if the total gas flow is less than the patient’s minute volume…
the patient will obtain the rest of their volume through the small relief valve in the max, diluting the mix with room air
this is not harmful, but patient is not breathing concentration of N2O that you think they are
if total gas flow is above the patient’s minute volume…
they are breathing the correct. mix (but you are wasting agents)
steps for titration technique
- begin and end with 100% oxygen
- 4-6 L starting flow rate is adequate
- 20% nitrous oxide is a good starting point with 10% increase every 60-120 seconds
- when the procedure is completed, 100% oxygen is administered for 5 minutes
flow rate for titration
4-6 liters
good starting point for titration
20% nitrous oxide with 10% increases ever 60-120 seconds
signs of anesthesia by nitrous
- first clinical sign is lightheadedness
- dizziness is usually transient and should disappear quickly
- tingling in the extremities with paresthesia in the face and oral cavity
- feelings of warmth, floating, or heaviness
- altered perceptions of sound, vision dims
signs of over sedation with nitrous
- nausia
- sleepiness; failure to respond to verbal commands; uncooperative patient; incoherent speech
- laughing and giddiness
- mouth breathing / closing
indications of using nitrous
- primarily to manage fear and anxiety
- optimize care for medically compromised patients
- management of gagging
nasal mask may increase the _______ phenomenon
claustrophobia
cardiovascular disease + nitrous
-nitrous has analgesic properties diminishing pain, sedative properties aiding relaxation, reducing the the workload of the myocardium (providing increased blood O2 levels)
titrate carefully to avoid inadvertent overdose
consider heart rate
what is most important to remember with cardiovascular patients and nitrous?
these patients do not tolerate low oxygen levels in the blood
respiratory disease and nitrous
N2O is a non-irritating vapor that doesn’t precipitate bronchospasm or asthmatic attachs
concerns with COPD / hypoxic drive (blue bloaters). respiratory drive needs to be monitored
N2O may expand an emphysematous bleb
nitrous and hepatic disease
N2O doesn’t undergo biotransformation anywhere in the body
nitrous and epilepsy / seizure
condition may be exacerbated with anxiety, fear, pain, and low O2 levels
nitrous oxide may elevate seizure threshold (favorable)
nitrous use in pregnancy
N2O adverse effects only for chornic exposure; no harm for controlled, managed usage
-medical consulatation is advised
-maintain good oxygenation
-does not cross placenta / BBB
-found in same concentration in unborn as mother
-some recommend avoiding in first trimester
contraindications of nitrous - closed gas spaces
~can expand a closed gas space~
- when gas has. been injected intraocular for treatment of retinal detachment
- thoracic trauma with possibility of peumothorax
- surgical procedures associated with risk fo air emboli
- open abdominal procedures / bowel obstruction
- scuba in previous 24 hours
other contraindications of nitrous use
- COPD
- claustrophobic patients
- children with severe behaviorla probelms
- patients with personality disorders
- patients with compulsive personality
- upper respiratory infection
- pregnancy and spontaneous abortion
advantages of nitrous oxide in dental practice
- titration possible
- onset of action is more rapid than oral, rectal, or IM routes
- depth of sedation may be altered from moment to moment
- more forgiving than IV (can decrease if desired)
- duration of sedation is variable at the discretion. of the administrator
- rapid recovery time
- no adverse effects on liver, kidney, brain, CV system, or respiratory system
- not metabolized - recovery time not dependent on liver or kidney
- no injection required
- use is safe and very few side effects
disadvantages of nitrous oxide in dental practice
- not potent agent
- in some cases, will fail to produce the desired affect at fail safe levels of no less than 30% O2 concentrations
- failure is linked primarily to lack of potency
- degree of cooperation required from patient
- costs (equipment, installation, maintenance, continued rental of tanes)
- mandatory training in most states
- chronic exposure of trace amounts may be deleterious to health of personnel
- essential that proper scavenging of waste gas to outside occurs
which methods of conscious sedation can be titrated to patient’s needs and are controlled by the dentist?
inhalation and IV
range of safety FBS casual random BG
start procedure with FBS of <70 mg / dL for 3 hour appointment
MU OS > 90%, <300
range of safety for INR
2.0-3.5 greater than 3.5 manage warfarin
