nitrous oxide sedation,

1. 1
Nitrous Oxide / Oxygen Sedation
&
Local Anesthesia
VWCC
Fall 2024
Joseph Bee, DDS

2. 2
Contents
1. Group Simulation – bring notes.
a. anytime
2. Individual Simulation – bring notes.
a. Week prior at least (Dr. and Student)
3. Class Review Study Guide -
a. Finish this Q&A in FIRST Weeks - Must Finish to help each other.
b. Divide questions and each answer several.
c. Class secretary can combine answers and redistribute.
4. Notes from nitrous power point presentation
5. Nitrous Oxide / Oxygen Clinical Notes
6. Local Anesthesia Class Study Q&A project
7. MRD example
8. MRD tables
9. LA post op instructions
10. Mandibular block anatomic diagram
11. Hyperlink - 12 alternatives IFANB
12. Suggested IFANB technique
13. Hyperlink - Article – Is mepivacaine as effective as lidocaine during inferior alveolar
nerve blocks in patients with symptomatic irreversible pulpitis? A systematic review
and meta-analysis.
14. Anatomic Pics
15. Respect for Posterior Superior Alveolar Nerve Block
a. This applies to ASA near infraorbital foramen.
16. Anatomic pics related to PSA Block
17. Excel spreadsheets / tables / nitrous notes
Nitrous Oxide

3. 3
Group Student Simulation
4-6 students
Prior To Qualification & Clearance
Part I
1. Review medications and medical history
a. What medications, OTC’s taken
b. Establish that there are no relative or absolute contraindications
c. Preoperative vital signs (PO2, BP, HR, Rhythm, Resp.)
2. Mandatory Knowledge Base – Textbook page 390, Chapter 21 & PPT
a. Describe and discuss drug classification of nitrous oxide sedation actions and its
impact on patients.
i. NMDA antagonist – dissociative drug (PPT & google for information)
1. Actions
ii. Nitrous Pathways of action
1.
2.
3.
iii. Examples of medications that can deepen nitrous sedation to include
prescription medications and “recreational”
b. Describe and discuss Contraindications & why the conditions are a contraindication.
c. Describe and discuss effects of Nitrous on
i. CNS
ii. GI, Ulcers, Bariatric surgery, Chrons, Ulcerative Colitis, Intrinsic factor
iii. CV
iv. Auditory canal
v. Respiratory
vi. Eyes
vii. Pulmonary
viii. Reproductive
ix. Hematopoietic (blood)
d. Describe and Compare dose equivalents of Nitrous to Opioid medications.
e. Describe and discuss the potential impact of a patient taking meds in when receiving
nitrous sedation.
i. Opioid
ii. Marijuana (THC / CBD)
iii. Benzodiazepine
iv. antipsychotic
v. metformin
vi. Proton pump inhibitor
vii. H2 inhibitor
f. Describe and discuss titration and how you will administer nitrous.

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g. Identify and respond to potential adverse reactions to nitrous & how to prevent
them.
i. Signs of hypoxia, panic attack, hypotension, bradycardia, tachycardia,
hallucinations
h. Identify and respond to signs and symptoms of nitrous.
i. sedation
ii. over-sedation
i. Show how to calculate and record accurate percentages of nitrous sedation
delivered
j. Describe Airway rescue skills and dietary restrictions needed for
i. Mild sedation
ii. Moderate sedation
k. Describe and discuss Peak effect time
l. Describe and discuss nitrous effect with
i. Hypo responders
ii. Hyper responders
m. Identify Reversal agent for nitrous sedation.
i. How do you reverse nitrous
ii. When are supplemental oxygen tanks needed?
n. Describe and discuss use of and positioning of BP Cuff, PO2 meter during sedation.
o. Describe Positioning of emergency equipment for sedation
i. Availability of Ambubag / oxygen
3. Have patient place nosepiece and recline patient.
4. Describe two methods to establish Tidal Volume
5. 100% Oxygen for five minutes
6. Are we ready to begin?
7. Increments of 0.5 L x 3 – 5 minutes
8. WATCH PATIENT
a. Describe the signs of sedation you see and how to talk patient thru the sedation
b. Dr Bee will record progress notes
9. Calculate % nitrous at each stage
a. Verbalize signs and symptoms of sedation & patient comfort.
i. Verbalize signs, symptoms to Dr. for progress notes.
b. What do you continuously monitor?
c. Much of nitrous effectiveness is psychological.
i. I see you (sign of sedation)
ii. Gradual titration some patients do not recognize the “feeling.”
iii. Some patients enjoy and are seeking the euphoria / high
iv. Treat to signs predominately and simply recognize / respect patients
symptomatic report.
v. Some patients will not be good candidates for MILD but would need
moderate or other forms of sedation.
1. Care must be taken to not enter into moderate
2. To avoid being responsible for DEEP sedation

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10. Intra-op vitals
11. Not more than 25 % nitrous for short duration
a. Hypo-responders – give more and they become over sedated.
b. Hyper-responders may become over sedated at low doses
c. Patient medications will have additive or synergistic effect
12. Terminate nitrous procedure
a. Oxygen at tidal volume (100%)
i. Then discontinue Nitrous oxide.
13. Recovery 5 minutes @ 100% Oxygen minimum.
14. Describe how to evaluate patient for recovery.
15. Only after recovery is established by clinical signs & symptoms can you remove oxygen.
16. Postoperative Vital signs (PO2, BP, HR, Rhythm, Resp.)
17. Recordkeeping
a. Preoperative, intraoperative, postoperative vitals
b. Pre op oxygenation% and duration
c. Tidal Volume
d. % nitrous given and time (each dose)
e. LA used, injection administered, total dose LA.
f. Incremental dose
i. Time of dose
ii. Total time nitrous,
iii. Highest dose nitrous
g. Post tx oxygenation 5 minimum
h. Time of total recovery and discontinuation of oxygen
i. Patient released in … condition alert and oriented with no cognitive or physical
impairments, intact MS coordination, clear vision, and clear minded.
18. Total time Estimate
a. 5 minutes pre oxygenation
b. 3 – 5 minutes each increment (2-3 increments) 10-15 minutes
c. 5 minutes post oxygenation
d. Approximately 20 – 30 minutes

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Nitrous Clearance / Qualification for Clinical Test
Week Prior – INDIVIDUAL - Simulation
Student Testing (Patient Care Setting)
Part II
 Competency review Part I
 Complete Nitrous and Med. Hx. given by Dr Bee & review with Dr Bee. Check equip, put
together the mask, 4 pieces, and place scavenger hose on high vac suction
o Assemble prior to Dr. entering cubicle.
 Review medical history for meds,” recreational” drugs, OTC’s, precautions or contraindications,
record pre op vitals BP, Pulse, heart rhythm (regular / irregular), Respirations, Place pulse
oximeter on finger. Be ready to initiate O2 when Dr. enters cubicle, patient informed and
consent ready to sign.
 Turn oxygen flow on to check scavenger and turn off again
 Explain the procedure Dr: nose piece, breath thru the nose, they may feel warm, relaxed
tingling sensation, purpose of procedure, review informed consent, then have the patient and
Dr sign.
 Turn on oxygen to approximately 6 L
 Have patient place mask, snug in place, and observe, establish tidal volume by asking patient if
they can inhale comfortably (not breathing thru a straw & no air flushing over their face)
o Read the middle of the ball in the flow tube.
 Ask the patient if they have any questions, and then explain the procedure (again telling them
what you are doing)
o Continuous conversation, you will feel….
o Suggestive statements, as sedation proceeds – you look relaxed, calm, comfortable.
o I see the signs of sedation in you… (flushed face, relaxed posture, hands relaxed, feet &
legs relaxed)
o Ask patient, “do you feel, symptoms of sedation.
o Tell patient the symptoms you see, “I can see your facial muscles are more relaxed, you
have some flushing of your neck and face, do you feel warm, do you feel tingling in your
fingers, feet. (Continuous – some of this is psychological at MILD sedation)
o By using slow .5L incremental dosing some patients do not realize they are sedated until
the nitrous is discontinued.
 Use calculator to calculate percent nitrous for patient’s tidal volume at .5 L increments
o Each added dose is simply a multiple of the first.
o You may calculate ahead and have a printed reference available.

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 RAISE the nitrous ½ L, and LOWER the oxygen ½ L, record the time, % nitrous, and signs of
sedation. Wait 3 – 5 minutes. Wait for the peak effect of that dose each time. Waiting 5
minutes you will see the signs come on slowly.
 When sign of sedation appears wait longer for peak effect
 Look for signs of sedation – NOT patient reported symptoms as they will be sedated (not fully
aware) and some patients want the sedated euphoric feeling, other patients may have a
tolerance to opioids and the nitrous can be impacted with negative clinical outcomes.
o Nitrous can be cumulative.
o They can then go into a deeper sedation.
o Hyper-responders will then dive deeper quickly as nitrous is FAST ONSET.
 Repeat step above by adjusting nitrous and oxygen, and recording vitals and signs of sedation /
patient reaction again for 3 -5 min. Make positive suggestive comments like you will start
feeling relaxed and calm, tell patient the signs you see of sedation so they know they are being
sedated regardless of their symptomatic response
o Ask the patient what are you feeling? Warm? Relaxed? Great….
o Can we get started? Are you ready to get started.
o You look comfortable and relaxed now, let’s get started.
 Continue raising and lowering at .5 L intervals, not sooner than 3 - 5 minutes apart, once first
does administered for patient comfort.
o Lower % to signs you see of over sedation.
o Droopy eyelid, slow / slurred speech, dizziness, tunneling, drop in vitals, skin color /
tone, lip color / tone, mental confusion, anxiety, panic, sweating, etc.
 We will stay below 20 - 25% nitrous (some literature equates 20% nitrous to 15 mg morphine)
o I want you to see the signs of sedation as the patient is titrated to MILD sedation.
o Remember Mild sedation may not alleviate all anxiety, your patient may need
moderate or a different sedation / anxiolytic technique.
 Record the time, continue to record Signs every 5 minutes, and vitals every 10 minutes.
 When procedure is complete, turn oxygen to 100% - original tidal volume, then DC nitrous
 100% oxygen at tidal volume for minimum 5 minutes
o As patient recovers begin to incline to a semi - upright seated position.
 Evaluate for recovery, record signs of recovery (should mirror / reverse of sedation signs)
 When recovered remove nose piece, record new vitals BP, HR, Rhythm, PO2, and Respirations,
remove pulse oximeter, record recovery signs.
 Make sure patient is fully recovered, raise to 30-degree incline for 5 minutes, then upright and
allow to sit for a few minutes to ensure no vertigo or nausea, and dismiss.
 Turn off nitrous supply tank first then turn off oxygen supply tank (in storage area)
 Have patient sit in chair for at least 2 minutes with feet on floor.
o Stand in front holding patient when releasing.
o Be prepared to hold and guide patient physically back into chair if they become dizzy,
disoriented, or hypotensive.

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Nitrous Oxide / Oxygen
Class Review Study Guide
Nitrous Oxide – Oxygen Sedation
Class Review Project – Open book, divide the questions between classmates & share answers. If you
find and answer that you feel could be improved upon, contact that student for them to enter
and resend to classmates. This is not a competition, this is a peer to peer collaboration to
enable learning and save time.
These are critically important concepts that you must know to protect your patient from
complications during nitrous oxide sedation.
If you review your course material and the PPT program you have been given this should be a simple
exercise to help all to learn.
1. Define minimal sedation for Nitrous Oxide / Oxygen sedation in terms of patient responsiveness,
consciousness, breathing, and gag reflex
a. Compare minimal sedation to moderate sedation.
b. What are you responsible for if moderate sedation occurs?
2. Describe the importance of medical history and medications regarding potential complications
while administering nitrous oxide / oxygen sedation.
3. What does nitrous oxide do to vitamin B12 (cobalamine) and how does this impact your medical
history and patient care?
Nitrous abuse & drug abuse ( https://pubmed.ncbi.nlm.nih.gov/35174022/ )
Nitrous abuse and clotting ( https://pubmed.ncbi.nlm.nih.gov/35759070/
Intrinsic factor- pernicious and megaloblastic anemia (https://pubmed.ncbi.nlm.nih.gov/10528308/
Autism Spectrum Disorder ( https://pubmed.ncbi.nlm.nih.gov/33823740/ )
Sickle Cell Disease ( https://pubmed.ncbi.nlm.nih.gov/22830455/ )

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4. What common medications can cause V B12 / folate deficiency?
5. What are the pathways of action for nitrous oxide / oxygen sedation, and how does this relate
to medical history and medications?
6. What response to nitrous oxide /oxygen delivered to a patient who is taking opioids and / or
benzodiazepines would you expect?
7. Why does a patient respond to nitrous oxide / oxygen sedation differently from one day to
another?
8. How is dosing of nitrous oxide sedation measured and describe the calculation.
9. 20% nitrous oxide is equivalent to approximately what mg dose of morphine?
10. If a patient is at 8% nitrous approximately what dose of morphine have you potentially given
them and how will this interact with medications and what symptoms or signs would you expect
to see?
11. How does Nitrous oxide manage both fear and pain?
12. When your patient is sedated with nitrous what impact do you expect and how do you monitor
& evaluate your patient regarding vital signs & consciousness.

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13. If your patient has CV / pulmonary insufficiency causing poor oxygenation (hypoxemia) what
clinical signs will you be looking for? Would you want to sedate them, and how do you screen
for this?
14. What clinical benefit is gained from the solubility and partial pressure gradient of nitrous oxide
during sedation and how does this impact recovery?
15. What is MAC and how does this tell you nitrous is or is not safe relative to other anesthetics?
16. Since nitrous oxide can be explosive how do you open the nitrous tank, and what can cause a
fire in the clinical tx area regarding nitrous?
17. Why is a scavenging system important, especially for women of childbearing age?
18. What is diffusion hypoxia and how is it prevented?
19. What is the displacement ratio of nitrogen by nitrous oxide gas sedation due to partial pressure
/ solubility and what does this do to patients? What kind of injury can patients incur? Name 3
systems affected by this property.
20. Your 9 am patient appears with a runny nose, congestion, and earache. Why is nitrous
contraindicated?
21. Your 1 pm 15-year-old patient appears for a cleaning with nitrous and asks where the trash can
is so he can throw away a bag of lunch trash (whopper and large fries with a large coke) that he

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just finished on the way to the office. Why is nitrous oxide sedation a risk for this patient?
What is the worst that could happen?
22. Name 4 absolute contraindications and 3 relative contraindications.
23. Why is the heart rhythm important during sedation in comparison to just pulse and BP?
24. Describe titration of nitrous oxide sedation and why it is important.
25. How long does it take for a dose / % tidal volume to reach peak effect?
26. How do you determine Tidal Volume?
27. How do you read the floating ball indicators for gas anesthesia?
28. Name 5 signs of sedation, and how will you know your patient has reached the target for care?
29. How do you monitor your patient intraoperative for safety?
30. How do you evaluate your patient for recovery?

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31. When is oxygen removed from the patient?

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Notes From Power Point on Nitrous
Nitrous Oxide & Oxygen Avoiding Serious Adverse Events
 Preventing Medical Emergencies
o Approximately 75% of these can be prevented through physical evaluation of the
prospective dental patient,
o using a systematic review of the patient’s medical history
o Assigning an ASA Physical Status can help to distinguish those patients who represent
greater-than-usual risk.
 Nitrous Oxide (N2O)
 What is it?
o Oxidizing gas
 Explosive & Fire potential
 Vitamin B12 inactivated – Deficiency diseases
 Mode of Action
o NMDA receptor antagonist- noncompetitive
 Class of Drug
o Dissociative Drug
 Site of action
o NMDA receptor (antagonist)
 Clinical Actions
o Anesthetic
 the state of anesthesia they induce is referred to as
 Dissociative anesthesia.
 commonly used as anesthetics for animals and humans.
 Ketamine, Inovar, Methadone, Dextromorphan,
 (THC is a NMDAR antagonist)
o Anxiolytic
 GABA pathways (benzodiazepine)
o Analgesic
 Cellular mediators stimulate.
 opioid pathways (narcotics)
o Nitrous oxide has a central sympathetic stimulating activity that supports blood
pressure, systemic vascular resistance, and cardiac output.
o Nitrous oxide stimulates cerebral blood flow and increases intracranial pressure.[3]
 Safety – Enhanced When Contraindications and possible complications are eliminated.

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 The minimum alveolar concentration (MAC) value is the concentration of an inhalation
anesthetic agent in the lung alveoli required to prevent movement in response to a surgical
stimulus in 50% of patients. Nitrous has highest MAC which provides safety margin.
 Nitrous Transfer
o Partial Pressure / Solubility
o Rapid onset & rapid offset
o Since the entrance of nitrous oxide into closed air space is not balanced by an equal loss
of nitrogen, a significant increase in volume / pressure may result.
 Nitrous enters approximately 30x more rapid than nitrogen loss.
 PONV – post operative nausea and vomiting
 Most common complication
 Caused by gas / pressure differences in GI causing gastric emptying.
 “Critical Thinking”
o Why do I need to know this????
 Nitrous oxide increases the volume of air within space.
 When sinus spaces are blocked, the pressure will increase in a closed space.
 Creating possible pain and injury
 Partial Pressure Complication (Expands Air Spaces)
o Sinuses
o GI
o Pulmonary
o Middle ear
o Recent surgery
o Ophthalmic Surgery
o Laparoscopic Surgery
o Insufflation of spaces
o Paranasal Sinuses
o Gastrointestinal Gases
 Blockage of bowel
 Creates increased pressure within intestine.
 Distension of intestine wall
 Can create diverticula, pain, bowel distension or rupture.
 Recent or past bowel surgery
 Possible loss of intrinsic factor leading to V B12 deficiency
o Cystic Fibrosis – presence of Pulmonary Bleb
 all CF patients are at increased risk for pulmonary complications including.
 hemoptysis, pneumothorax, pulmonary hypertension, chronic hypoxic and
hypercapnic respiratory failure
 the risk of developing these complications increases with progression of lung
disease.
 Vitamin B12 Deficiency: Recognition and Management
o Nitrous Inactivates V B12 therefore methionine synthetase (enzyme)
o Disturbance of folate metabolism (protein synthesis)
o Risk of adverse event Increases

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 with Unknown B 12 Deficiency concurrent with nitrous exposure
 Prolonged Sedation
 Repeated Sedation
 Screening may be warranted in patients with one or more risk factors, such as
o Age
 In the United States and the United Kingdom, the prevalence of vitamin
B12 deficiency is approximately 6% in persons younger than 60 years, and nearly
20% in those older than 60 years.1
o Autism Spectrum Disorder
 Disturbances in folate or methionine metabolism have been identified in many
individuals with ASD.
 suggesting that the folate-methionine cycle may play an essential role in the
pathogenesis of autism.
 low levels of vitamins B12 and folate are associated with ASD.
o Autoimmune Disorders
 Intrinsic factor lacking – pernicious anemia
o Gastric or small intestine resections (hx of surgery)
 Loss of intrinsic factor to absorb VB12.
o Inflammatory bowel disease,
o use of metformin for more than four months,
 altered Vitamin B12 absorption in ileumaltered small intestine motility leading
to bacterial alteration and subsequent inhibition of IF-Vitamin B12 absorption
 alteration of acid metabolism resulting in enterohepatic circulation of V B12
 Reduced IF secretion by gastric parietal cells
o use of proton pump inhibitors or histamine H2 blockers for more than 12 months
 reduced gastric acid affecting gastric pepsin / pepsinogen to cleave V B12-R and
allow Intrinsic factor to attach
 diminished absorption of V B12
o vegans or strict vegetarians, and
o Xerostomia – lack of R factor
o Neuropathy
o Immune Compromised
o Sickle Cell Disease (SCD)
 The mean cobalamin level in SCD patients was significantly lower than that in
patients without SCD.
 The frequency of low cobalamin levels, defined by a serum cobalamin level of
<200 pg/ml, was.
 18.1% (19/105) in SCD
 9.8% (11/112) in non-SCD patients,
 Nearly doubled in patients with SCD
 Vitamin B12 Absorption
o Xerostomia - May be a possible risk factor.
 Dietary vitamin B12 binds to a protein called R-factor, which is secreted from
salivary glands.

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o Once the complex arrives at the small intestine, B12 is cleaved from R-factor by
pancreatic enzymes, allowing it to bind to intrinsic factor.
o The newly formed complex of B12 and intrinsic factor can then bind to receptors on the
ileum, which allows for absorption of B12.
 Safety Features
 Fail Safe – ensures no nitrous will be delivered unless oxygen is flowing.
o Minimum of 30% oxygen always
o Ambient air 21% oxygen
o 30% allows for calibration error.
o Pin Index safety system – Cannot install nitrous into oxygen line.
 Standard for Medical History = Review of Systems
Screening for potential contraindications or complications
 HEENT
 Air pressure
o increased in closed spaces &
 Expands air spaces.
 Respiratory
 Asthma, Chronic Bronchitis, pulmonary HTN
 COPD, SARS-COVID, Vaping, Cystic Fibrosis,
 Cardiovascular
 Elevated homocysteine – damages endothelium
 Musculoskeletal
 Neuro, Multiple Sclerosis (demyelinating disease)
 Lateral spinal tract demyelination due to oxidizing VB12
 Neurologic / Craniological
 Paranoia, Psychosis, Dementia, Alzheimer’s, Anxiety disorder
o Dissociative Drug – Detached – ‘out of body’- floaty-
hallucination- disassociated from reality.
o Due to - euphoria, disassociation, HALLUCINATIONS at
moderate to deep sedation
 CNS – autism spectrum disorder with possible V B12 deficiency
 Possible increased intracranial pressure due to nitrous
 Pancreas
 Diabetics on metformin may have V B12 deficiency.
 Diabetic neuropathy in presence of metformin and GLP-1 may indicate a
need to screen for V B112 deficiency.
 Renal - Dialysis
 Homocystineurea – avoid due to inactivation of methionine synthetase.
 Hepatic
 AUD – Alcohol Use Disorder
o Cirrhosis – alcoholic liver – depleted V B12
o Possible Increased fibrosis in presence of
hyperhomocystienemia
 Hematological - Immunological
 Megaloblastic anemia due to oxidizing V B12

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 Sickle Cell Anemia – possible concurrent V B12 deficiency
 Reproductive
 Folic acid and protein synthesis, embryological development
 GI
 Gastric emptying slowed (gastroparesis) – GLP-1 agonistic – antidiabetic
medication – longer fasting period
 Gas - pressure and space increased
 inflammation, Bariatric Surg, ileitis, intrinsic factor, metformin, H2
blockers and PPI’s Reduce V B12
 Age
 Increased incidence of V B12 deficiency
 ASA Classification
o II - Mild systemic disease
 mild to moderate disturbance
 under good control
 no significant compromise to normal activity
 Appropriate candidate for N2O
o III - Severe systemic disease
 Major systemic disturbance
 Difficult to control.
 Significant compromise to normal activities
 N2O2 - only after medical consult
 Nitrous & Possible Drug Interactions
o Vitamin B 12 possible deficiency
 Recreational nitrous abuse
 B12 - oxidized – folic acid / protein synthesis diminished
 Possible lowered WBC # in presence of V B12 deficiency
 one marrow suppression, Immune suppression
 Biguanide (metformin)

 Proton Pump Inhibitors

 H2 Inhibitors

 GLP-1 agonists

o Additive / synergistic effect will possibly will deepen sedation.
 Opioids
 Benzodiazepines
 Barbiturates
 Hypnotics
 Sedatives
 Sleep Aids / OTC or Rx
 Alcohol (AUD – alcohol use disorder)
o Psychiatric – psychotropic action of NMDA antagonist
 Hallucination
 Antipsychotics

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 “Tranquilizers”
 Lithium
 THC - possible Cardiac and Respiratory Reactivity
 THC Half Life Psychoactive (Euphoria)
o The plasma half-life of THC is 1 to 3 days in occasional users and
5 to 13 days in chronic users.
o CBD Half Life - Not Psychoactive
 Analgesic
 The plasma half-life of CBD is 18 to 32 hours.
o THC / CBD
 NMDA receptor antagonist as an antagonist to reduce NMDAR activity.
 Perioperative care of cannabis users: A comprehensive review of
pharmacological and anesthetic considerations
 New Users
o Tachycardia & systolic HTN
o Malignant arrythmias (A Fib, V Fib, V Tach, Brugada pattern
(abnormal ST wave on ECG)
o Coronary vasospasm if prior CAD
o Airway reactivity (Uvulitis)
 Chronic Users
o Bradycardia to Tachycardia
o Postural Orthostatic Hypotension
o Sinus arrest
o Hyperreactive airway
o Intraoperative hypothermia (shivering)
o Coronary vasospasm / MI
 Nitrous Oxide & Pregnancy
o Nitrous oxide is classified as a pregnancy risk group Category C medication,
 meaning that there is a risk of fetal harm if administered during pregnancy.
o It is recommended that pregnant women, both patients and staff, avoid exposure to
nitrous oxide.
Drugs Can Be Additive
You Must Be Prepared for The Next Deeper Level … or More
 Nitrous Oxide Analgesia

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o 30% nitrous oxide by face mask
 producing the equivalent of 10-15 mg morphine
o every 10% of N2O is equivalent to the effect of 5 mg morphine.
 20 % nitrous = 10 mg. MORPHINE
o 20% Nitrous - 80% Oxygen
 5 L tidal volume
 1 L/min nitrous to 4 L/min oxygen
 1 L / 5 L - 20%
 1.5 L nitrous / 6 L tidal volume
 25% nitrous
 Administration of nitrous oxide in concentrations higher than 70%
o Or in combinations with
 opioids or benzodiazepines
 requires full cardiopulmonary monitoring.
 Nitrous Oxide Abuse
o Pharmacologic evidence that nitrous oxide is addictive.
 through direct interaction with the endogenous opioid system
 includes the possibility that it is a partial agonist.
 and acts at the mu, kappa, and sigma opioid receptors.
 Additive Effect
o Nitrous and Opioids / Benzodiazepines
o Nitrous Oxide Abuse
 For people who suffer from medication-resistant depressive episodes,
o nitrous oxide appears to be an appealing alternative to traditional psychoactive
substances. It delivers a short burst of euphoria and a dissociative break from painful
reality.
 It is mistakenly perceived as safe and non-addictive. A
 Drug Facts - Approximately 23 % of patients may be on an opioid or benzo
o Accurate medical history
o When performing a medical consult, you can ask for a list of patients medications
 32% percent of American adults
 have received a prescription for opioids in the past two years.
 16% of American adults annually
 7 to 8 % of patients
 Aged 30 – 65 or older.
 Are taking benzodiazepines.
 Nearly 1 in 10.
 Why Do Patients Lie to Their Doctors?
o JAMA Network Open found that 60 to 80 percent of patients have been less than fully
forthright with their doctors at some point.

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 Minimal Sedation (previously known as anxiolysis)
o a minimally depressed level of consciousness, that retains the patient's ability
independently and continuously maintain an airway and respond normally to tactile
stimulation and verbal command.
o < 50%
o Risks are minimal.
o Adverse effects are minimal.
 Administration of Nitrous
o target is just to Patient Comfort
o no other physiological target
 Moderate Sedation
o Drug induced Depression of consciousness.
o Patients respond purposefully to verbal commands.
o May need stimulation to respond.
o No intervention is required to maintain airway.
o Spontaneous respiration
o CV functions are normal.
o Nitrous oxide > 50%
 Advanced airway management
 May be needed for moderate sedation.
 that can fall into deep QUICKLY.
o Positive pressure ventilation
o Ambubag mask
o Nasotracheal tube (not available)
o Oropharyngeal tube (not available)
o Prevent sedation from deepening by
 Accurate Medical History
 Accurate Rx Hx
 Social / Recreational Hx
 Contraindications RULED OUT
 Medical Consult obtained (verify Rx meds)
 Medical Hx Updated
o Pre-procedural Fasting
 Anti-diabetic Med. GLP-1 agonists
 GLP-1 agonists mimic the action of GLP-1 made by the body
 and can affect glucose control through several mechanisms including.
 enhancement of glucose-dependent insulin secretin
 slowed gastric emptying (therefore LONGER FASTING TIME)
 and reduction of postprandial glucagon and food intake.
o Dulaglutide (Trulicity)
o Exenatide (Byetta)
o Exenatide Extended Release (Bydureon BCise)

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o Liraglutide (Victoza)
o Lixisenatide (Adlyxin)
o Semaglutide subcutaneous, tablet
o Ozempic, Rybelsus,
o Tirzepatide (Mounjaro)
 Objective is patient COMFORT.
o Ask them if they are comfortable.
o Are we ready to begin?
o or do you feel like you need a little more relaxation?
o
 EVEN WITH MINIMAL SEDATION
o less than 50% N20
o Over time the effect is cumulative
o and may cause deepening or over-sedation.
 BEGIN WITH OXYGEN
 Determine Tidal Volume
o Can you breathe comfortably thru your nose?
o Do you feel like you are breathing thru a straw?
 N2O administration
 Maintain minute flow - tidal volume thru the procedure.
o Each time N2O is added O2 will have to be decreased.
 Keeping minute volume constant
 Dual Tube Flowmeters
 Total liters flow is calculated by adding both sides of the flowmeter at the level of the middle of
the floating ball.
 % Nitrous Calculation
o Divide the L/minute of Nitrous by the Tidal Volume L/minute.
 1L nitrous / 6L TV = 16.6%
 2L nitrous / 7L TV = 28.5%
 The technique of titrating N2O is recognized as the standard of care.
o SLOW titration of small doses of drug Is important to prevent over sedation.
 Recommended Regimen
 Begin with .5L N2O .5/6= 8%.
o Add .5 nitrous.
o After nitrous added diminish oxygen by equal amount
 Add N2O increments as needed.
 Wait 3-5 minutes for full effect.
 .5L nitrous increments Recommended.
 Wait at least 3 – 5 minutes after a dose delivered Before adding next increment.
 When sedation is becoming evident
o Wait longer for the drug to take full peak effect before adding another dose to avoid
over sedation.

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 Signs of Oversedation - beyond Mild Sedation
o Laughing uncontrollably
o Tunnel vision
o Seeing stars
o Hallucination
o Out of body feeling
o Tingling all over
o Rushing or roaring sound in ears
o Ringing ears
o Dizzy and VERY light- headed.
o Vitals drop more than 10-15%
o Significantly slurred speech
o Does not respond to verbal command easily.
o Can’t keep eyes open.
o Can’t follow finger over eyes.
o Drugged out appearance.
 Potential Adverse Reaction
 Hypoxia - Medical Rxn - Oxygen 100%
 Panic Attack / Hallucinations -
o Possible over-sedation – Oxygen !00%
 Hypotension - Medical Rxn – Trendelenburg position 100% oxygen
o Cardiac meds or disease
o Rx interaction, non-compliant meds, possible over-sedation
 Bradycardia / Tachycardia -
o Rx interaction –Medical Rxn CV system - Possible over-sedation
 Intraoperative Monitoring
o Cumulative effects of N2O will be seen.
o as duration increases
o Sedation may deepen and result in uncomfortable symptoms.
 Reduce nitrous and adjust oxygen after patient completely comfortable.
 i.e., ……. LIGHTEN sedation.
o Periodically ask patients how they feel.
o Decrease N2O % incrementally.
 for non-stimulating phases of care
 Add oxygen before you diminish nitrous.
 if nearing completion of care increase oxygen to 100%
 When you terminate N2O
o Deliver 100% Oxygen for at least 5 minutes.
o At established minute volume
 Recovery Assessment
 psychomotor performance and verbal fluency will be affected by prolonged exposure to nitrous
oxide.
 No impairment of vigilance, immediate memory, or mental tracking c
 Post operative oxygenation.

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o 100 % oxygen. Minimum of 5 minutes or longer as needed by patient assessment.
 Adequate Recovery
o Patient alert and oriented
 Vital sign values stable and WNL
o Within 10% of pre op vitals
 Patient states they feel normal.
o ONLY after patient is recovered by psychomotor testing and “feels” normal.
 May the oxygen and nose piece be removed?
 Recovery Time recorded.

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Nitrous Oxide / Oxygen Clinical Notes
Informed consent reviewed and ___ states they understand the procedure, risks, and benefits and
desires to proceed with nitrous oxide - oxygen sedation. It is clearly understands the nitrous oxide
/ oxygen sedation procedure, and is aware, with no cognitive impairment to sign the consent. All
questions and concerns were answered, and patient requests nitrous oxide sedation to minimize anxiety
as a part of their care today.
Last meal was ___
Time of last meal was ___
Medical History ROS reviewed
Significant Medical Hx:
Accommodations needed:
___ states that the medications noted are the only Rx & non Rx medications/ recreational
medications that they have taken in the last seven days.
PRE-SEDATION VITAL SIGNS:
BP
HR
Rythm
PO2
Resp
NITROUS OXIDE / OXYGEN SEDATION:
Tidal Volume
Time Oxygen (L)
Time Nitrous oxide ( L) Oxygen (L) % nitrous oxide oxygen
Time Nitrous oxide ( L) Oxygen (L) % nitrous oxide oxygen
Time Nitrous oxide ( L) Oxygen (L) % nitrous oxide oxygen
Time Nitrous oxide (L) Oxygen
Time Recovery Oxygen (L)

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Time Discontinue Oxygen
Total time on 100% oxygen for recovery ___
Length of time of nitrous oxide / oxygen sedation: ___
Clinical signs of sedation:
Clinical signs of Recovery:
Recovery Assessed and Complete (time)
POST SEDATIN VITAL SIGNS:
BP
HR
Rythm
PO2
Resp
Patient released in (condition)
Student Hygienist:
Supervising Faculty:

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Nitrous Oxide / Oxygen Sedation Record
Study Execl Record for Notes

27. 27
Local Anesthesia
VWCC 2023

28. 28
VWCC Dental Hygiene
Local Anesthesia Class Project
1. What do ALL local anesthetics to do blood vessels?
2. All local anesthetics have the capacity to oxidize the iron atom in the red blood corpuscle from
the ferrous +2 state to ferric +3 state, in a patient with a genetic blood condition. What is this
called, and why is it a life-threatening emergency? How is it treated? Could a patient follow up
care call important for this? Why are pediatrics more vulnerable?
3. Which local anesthetics commonly used in clinic is
a. pregnancy category B?
b. pregnancy category C?
4. What preservative is used with epinephrine in xylocaine 2%, 1:100,000 epi. ?
5. What medical condition needs to be screened due to the preservative with Xylo 2%, 1:100,000
epi.? What does this preservative do to pH or acidity and how does this impact your decision
making?
6. Why is xylocaine 2%, 1:100,000 epi considered at times to be advantageous due to
epinephrine?
a.
b.
c.

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7. What class of medication (example of each) would guide you to select a non-epinephrine LA?
a.
b.
c.
d.
e.
8. What is normal body pH?
9. What is the pH of mepivacaine plain 3%?
10. What is the pH of xylocaine 2% 1:100,000 epi?
11. What impact does the pH of xylocaine2%, 1:100,000 have on the concentration of base local
anesthetic at the target site and onset of action?
12. What is angioedema and how is it life-threatening? What anesthetic is in the clinic that would
most likely cause this reaction and how do you screen for it?
13. Where are most local anesthetics metabolized, and what disease would influence you to select
a hybrid LA (example) rather than the typical amide LA?
14. What classification or type of anesthetic is benzocaine as a topical LA, and what medical history
contraindicates administration of this LA?
15. What enzyme metabolizes catecholamines in local anesthetics, and what drug class should you
be aware of in your medical history due to this fact?

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16. Where are ester LA metabolized, and what enzyme metabolizes this LA?
17. Articaine 4%, 1:100,000 is the most widely used local anesthetic in use today in dentistry.
What is the ½ life of Articaine, and where is it metabolized?
18. What medication would cause you to not use inferior alveolar nerve block injection but rather a
Gow Gates injectionand why?
19. You just completed the IFANB and your patient is reporting profound anesthesia being very
“numb”. The next day your patient calls your office and complains of a partially numb tongue
and partially numb lip. What nerves are possibly injured? What happened, and how do you
attempt to avoid this?
20. Your patient exhibits signs of IFANB success. Despite the anesthesia they are not comfortable.
Why do you not have complete anesthesia, and where should you inject?
21. The PSA nerve block is immediately adjacent to the pterygomaxillary fissure. This fissure
communicates with the pterygopalatine fossa. This fossa or space includes cranial nerve
foramina. To prevent the inoculation of this critically strategic anatomic area with bacteria what
clinical practice should you use when performing a PSA block to protect your patient?

31. 31
22. You have injected over the bicuspids in the interest of treating that localized site. You double
inject at that site again to no avail. Why is your patient not achieving MSA nerve block?
23. What advantage to the patient is using a 2x2 to wipe away saliva prior to applying topical
anesthetic for injection?
24. What advantage do you gain by using a 2x2 while performing maxillary and other injections?
25. The body of the mandible to the ramus will often have an angular conformation at the
retromolar area. Why do you want to know the angle of this lateral splaying of the ramus?
26. Where is the mental foramen in relation to the 1st
and 2nd
bicuspids?
27. When you are palpating and holding the mandible between your thumb and middle finger you
are estimating the width of the ramus. Where along this distance is the Inferior Alveolar Nerve
typically located?
28. The IFANB target is the pterygomandibular fold, just above and parallel to the occlusal groove,
and just _____________ to the anterior border of the ramus.
Note – do not pull tissue laterally when moving your thumb away from needle insertion as this
could pull the lingual nerve into the path of injection and cause damage / injury to the lingual
nerve.
29. When you inject with a 30-gauge needle and “sound bone”, what complication can occur?
a.
b.

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Local Anesthesia
MRD Example
100 lb. patient
LA to be used is mepivacaine plain 3% with a MRD of 300mg (Absolute total 400 mg)
Patient MRD by weight = 3mg / lb. x 100 lbs. =300mg.
MRD= 300 mg
Safety factor 15% x 300 mg = 45mg.
Adjusted MRD 300 mg – 45 mg. = 255 mg
# carpules patient can receive safely is (255mg / 51 mg) = 5 carpules
Mepivacaine plain 3% carpule dose 30mg/ml. x 1.7 ml. = 51mg.
2 carpules (51 mg) administered = 2 x 51 mg/ml = 102mg administered
3.4 ml x 30 mg/ml = 102 mg.
34% MRD of administered (102 mg / 300mg =.34 x100 = 34%)
198 mg mg safety factor remaining within adjusted MRD (300mg – 102 mg)= 198 mg.
66% MRD remaining (198mg /300mg = 66%)
Patient can receive added (198mg / 51mg) = 3.88 carpules

33. 33

34. 34
Drug Concentration Volume Dose
mg/ml ml mg
Mepivicaine 3% 30 1.7 51
Lidocaine 2% 20 1.7 34
Epinephrine 1:100,000 0.01 1.7 0.017
Local Anesthesia Post Op Instructions
 Following treatment, your teeth, tongue, lips, and cheeks may be numb for an additional 1-
3 hours.
 Please do not eat or chew anything until the local anesthesia has “worn off”.
 This sensation is unusual and may induce biting or playing with the area leading to
discomfort when the anesthesia has worn off.
 Stick to liquids and soft foods until the numbness is completely gone to avoid injury.
 If there is swelling of the lip or cheek, it is usually associated with a bite. Administering
Motrin and applying ice will help to keep the swelling down. Depending on the severity of
the bite, it may take a few days to return to normal.
 Please call your student hygienist if you have any concerns.

35. 35

36. 36
IFANB (Inferior Alveolar Nerve Block)
Article you may review.
12 Alternatives to the Traditional Inferior Alveolar Nerve Block
article by William C. Forbes, DDS clinical photos by Michael DiTolla, DDS, FAGD cover
photo by Sharon Dowd illustrations by Phil Nguyen
February 9, 2010
https://glidewelldental.com/education/chairside-dental-magazine/volume-5-issue-1/12-alternatives-to-
the-traditional-inferior-alveolar-nerve-block/
There are numerous pathways to anesthetize the inferior alveolar nerve. The right way is the
way that works…. In your hands, without incurring patient injury or complications. The
technique I teach is a modified traditional Halstead method.
 The patient is seated so that the occlusal plane is directed at the operator’s face. This
gives you easy access / visibility of the target site. The patient’s mandible / ramus
should be just below the elbow so that you do not need to raise your shoulder to inject.
 This occurs by lowering the chair, slightly inclining the back of the chair up, and
adjusting the headrest up as needed.
 The chin should not be up to you so that it blocks parallel entry along the occlusal plane.
 While placing your thumb at the coronoid notch, place your palm along the ramus and
wrap you fingers around the posterior border of the ramus.
 Note the flare of the ramus to determine if it is directly (straight) posterior, flared out
(lateral) or in (medial).
 Note the width of the ramus. Approximate half the length of the ramus and this is your
target depth for the mandibular injection.
 DO NOT SOUND BONE!! THIS MAY BEND THE TIP OF THE NEEDLE (LIKE A FISHHOOK).
THIS CAN CAUSE TISSUE DAMAGE UPON WITHDRAWL.
 Rather than approach the pterygomandibular fold (PMF) from the contralateral bicuspid
region I prefer to approach along the occlusal groove of the side to be treated. The
target site is approximately 5-7 mm. above the occlusal plane at coronoid notch,
typically into the pterygomandibular groove / fold area.
o Use the patient’s panoramic x ray to locate the foramen vertically and
horizontally.

37. 37
o (Note PMF is the union of the lateral pharyngeal constrictor muscle and the
buccinator muscle. When possible, I would prefer to inject lateral to this (toward
the cheek), thereby avoiding the pharyngeal space anatomically preventing
possible inoculation of the space with oral bacteria, or unwanted anesthesia of
this space).
 With your thumb palpate the medial border of the ramus & the internal oblique ridge
just above the retromolar triangle / pad area. Do not pull the pharyngeal tissue to the
lateral aspect. The target site is just medial to the medial border of the ramus / internal
oblique ridge.
 Direct the syringe & needle along the occlusal groove to the medial border of the ramus
while lightly moving your thumb laterally away for your safety. DO NOT PULL TISSUE
LATERALLY AS THIS MAY PULL THE LINGUAL NERVE INTO THE PATH OF NEEDLE
INSERTION.
 After penetrating medially to the medial border of the ramus the syringe / needle is
advanced just past the anterior border of the ramus, and once past the anterior border
of the ramus the syringe barrel and needle is immediately moved toward the
contralateral side while maintaining a parallel path to the medial aspect of the ramus
and keeping the syringe barrel and needle parallel to the occlusal table in the transverse
plane (horizontally) and the midsagittal plane (vertically).

38. 38
 The mandibular foramen is approximately 5-7 mm. above the level of the occlusal table
for adults, and it is located mid-ramus (ie. half the width of ramus). Literature shows
this to be an average of approximately 19-21 mm depth.
 Advance approximately ½ width of ramus (approx.. 19 – 21 mm) while staying
immediately adjacent to the medial border of the ramus (slide along the inner aspect
of the ramus).
 DO NOT SOUNDBONE
 Aspirate in two planes to prevent intravascular injection. NOTE literature shows that
aspiration has been shown to a give false negative due to the small bore when against
the vessel wall.

39. 39
 Aspirate & inject, -- aspirate & inject – multiple times IN AT LEAST TWO PLANES, as
the solution is injected into the pterygomandibular space to diffuse into the
mandibular foramen / inferior alveolar nerve.
 The pH of non-epinephrine LA is tolerated better than the epinephrine LA due to the
pain induced from the acidic epinephrine solution.
o This solution must be buffered by the body prior to ionization of the LA for the
base molecule to be released for it to interfere with Calcium in the neuronal ion
channels, to then block the Sodium ions, and subsequent nerve depolarization.
 Failure of IFANB may be due to anatomic variability
o Bifid mandibular canal and inferior alveolar nerve
o Sensory innervation has been shown in literature to travel at times along with
the lingual and mylohyoid nerve. Rarely the long buccal nerve.
o Lingual foramen along the lingual of the body of the mandible
o Crossover innervation at the anterior mandible
PLEASE REVIEW. THIS. ARTICLE
https://onlinelibrary.wiley.com/doi/full/10.1111/iej.12926
Review
Free Access
Is mepivacaine as effective as lidocaine during inferior alveolar nerve blocks in patients
with symptomatic irreversible pulpitis? A systematic review and meta-analysis
W. A. Vieira, L. R. Paranhos, G. O. Cericato, A. Franco, M. A. G. Ribeiro
First published: 26 March 2018
https://doi.org/10.1111/iej.12926
Citations: 5
Get Full Text at VWCC

40. 40
EXCERPTS BELOW
Local anaesthetics induce a reversible interruption of neural stimulation (Becker & Reed 2006,
Malamed 2013, Andrade 2014). The anaesthetic agents used most often in dentistry are
lidocaine, articaine, mepivacaine and bupivacaine (Malamed 2013). Lidocaine is used as a gold
standard compared to the other drugs (Becker & Reed 2006, Malamed 2013, Andrade 2014),
but mepivacaine has more favorable chemical properties, such as lower pKa and reduced
vasodilatation, when compared to the other drugs. Additionally, mepivacaine is indicated for
patients with systemic disorders, especially because it remains effective even without
vasoconstrictors (Hawkins & Moore 2002, Becker & Reed 2006, Malamed 2013, Andrade 2014,
Su et al. 2014)
After injecting the anaesthetic agent, the permeability of sodium ion channels decreases
(Malamed 2013). Calcium ions linked to the ion channel receptors regulate sodium ions through
the nerve membrane, leading to depolarization and conduction of nerve impulse (Becker &
Reed 2006, Malamed 2013). In this context, the local anaesthetic agent competes directly with
calcium ions in the receptors of nerve ion channels. Consequently, the permeability of sodium
ions is blocked (Becker & Reed 2006, Malamed 2013). Thereafter, the electric depolarization of
the nerve membrane is depressed and the nerve is blocked (Malamed 2013).
Although the presence of vasoconstrictors is associated with the anaesthetic agent to minimize
the increase in blood flow and potentiate the efficacy of anaesthesia (Malamed 2013), studies
have revealed that the vasoconstrictor concentration is not a determinant factor for the success
of the IAN block, even in the presence of symptomatic irreversible pulpitis (Pereira et al. 2013,
Aggarwal et al. 2014) or not (Daghter et al. 1997).
Mepivacaine had better outcomes than lidocaine for pain control in all the eligible studies,
except for the study by Cohen et al. (1993), in which both drugs had similar outcomes. In the
present meta-analysis, there was no significant difference between mepivacaine and lidocaine
for pain control. However, a slight advantage was observed for the former. This may be justified
by the fact that mepivacaine has a lower ionization constant (pKa), which increases its power of
dissociation and diffusion through the nerve (Madan et al. 2002, Becker & Reed 2006).
However, there is no significant differences between lidocaine and other anaesthetics, such as
articaine (Kung et al. 2015) and bupivacaine (Sampaio et al. 2012, Parirokh et al. 2015), for pain
control after IAN blocks. This confirms the findings of the present study and suggests that the
success of an IAN block in patients with symptomatic irreversible pulpitis is not influenced
exclusively by the type of anaesthetic agent used.

41. 41
Conclusions
This systematic literature review with meta-analysis revealed no significant difference
between mepivacaine and lidocaine for pulpal anaesthesia and pain control during root
canal treatment in teeth with symptomatic irreversible pulpitis.

42. 42

43. 43

44. 44
A & B – thickend Lingual nerve due to trauma
C. traumatic neuroma of lingual nerve
D. lingual nerve thickened
Note relationship & proximity of lingual nerve to the mandibular nerve.

45. 45
Arrow indicates a neuroma induced by trauma as can occur with IFANB causing temporary or
permanend paresthesia of the tongue (burning, tingling, itching, partial or total lack of sensation.
Note the proximity of the lingual & mandibular nerve. The lingual nerve for some patients is very close
and typically is anterior & medial to the inferior alveolar nerve at the height of the injection in the
midsaggital plane.

46. 46

47. 47

48. 48
Respect for PSA Block
 Anatomic structures in this region
o pterygomaxillary fissure
o pterygopalatine fossa
 (some call it pterygomaxillary fossa)
 Contents of pterygomaxillary fossa
o Optic canal
o Cranial foramen (leading into middle cranial fossa)
 Foramen rotundum (Maxillary Nerve)
 Foramen Ovale (Mandibular Nerve)
 Pterygoid canal (Vidian Canal)
 Inadvertent lack of control of depth of needle
o May Impinge on maxillary artery
 Possible complications
 Hematoma due to. Injury to plexus of veins
 Inoculation of site with bacteria creating a deep space infection
The pterygomaxillary fissure is located between the anterior and posterior
wall of the pterygopalatine fossa. It communicates with the infratemporal
fossa and transmits the posterior superior alveolar nerve and the maxillary
artery.

49. 49

50. 50
Concentration Volume Dose
mg/ml ml mg
Mepivicaine 3% 30 1.7 51
Lidocaine 2% 20 1.7 34
Epinephrine 1:100,000 0.01 1.7 0.017
You may copy & paste into excel, then adjust columns for width
Local Anesthesia. - Medications
Patient Name
Date Vitals Hospital/Emergent Care
Allergies BP Last Medical Visit
HR Hx of Covid / Vap
Rhythm Past w/ LA - Sedation
PO2
Resp/min.
Diagnosis Medication Drug Classification Drug Action

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