Historical Perspective

English scientist, philosopher, theologian,

and clergyman

1771 discovered Oxygen; 1772

discovered Nitrous oxide

One of founding fathers of Chemistry,

Sir Joseph noted for work in gases; other gases
Priestly He discovered Nitrogen, Hydrogen
1733-1804
chloride and carbon monoxide

Discovered soda water

 English scientist, noted as one of the
Britain’s greatest Chemists

Work on various alkali and alkaline

earth metals

Discovered Chlorine and Iodine

Studied effects N2O 1795; he

documented its analgesic effects and
Sir Humphry Davy
1778-1829
potential benefits relieve pain during
surgery

1798 coined term “laughing gas” still

used today (Malamed Pg157)
 Gardner Quincy Colton
Horace Wells

(Jan 1815-Jan 1898)

(Feb 1814-Aug 1898)
In the late 1700’s and early 1800’s laughing gas
intoxication demonstrations and other frolics were were a
popular form of entertainment which served to obscure
value of N₂O for four decades.
 Gardner Quincy Colton

After making $535 from his first public demonstration

of nitrous oxide, Colton left medical school to travel
the country giving lectures and presentations. On
December 10, 1844, he gave a performance in
Hartford, Connecticut, at which one of his audience
volunteer injured his leg, but did not feel the pain
because of the effects of the gas. Connecticut dentist
Horace Wells was in attendance, realized the
possibilities of using nitrous oxide in dental surgery,
and obtained a supply of the gas from Colton.
Horace Wells> American dentist who pioneered the use of
anesthesia in Dentistry, specifically nitrous oxide (or
laughing gas) Dec 1844, had Dr John Riggs ext tooth on him
using N₂O w/ out pain; Jan 1845 gave demo to med
students Harvard Med School ext tooth on pt using 100%
N20 for anes; experimented w/ ether and chloroform as
anesthetic agents; became addicted chloroform, and
committed suicide May 1848.
Gardner Quincy Colton > American anesthetist,
showman, lecturer, and former medical student who
pioneered the use of nitrous oxide in Dentistry; taught Dr
Wells use of N20; opened several dental institutes
specialized ext teeth w/ 100% N₂O; worked w/ dentist in
New Haven, CT using N₂O they ext 3,000 teeth w/ out pain
over 3 week period of time.
In 1540 Valerius Cordus of Germany
introduces synthesized sweet vitriol, now
more commonly known as ether.
In 1803-1805 morphine was isolated by
Friedrich Wilhelm Sertuerne.
In 1831 another inhalation agent,
chloroform was discovered by several
scientists simultaneously in Europe and
US.
In 1842 Dr W E Clark, at Rochester, NY,
admin ether to patients while Dr Elijah
Pope, a dentist, extract a tooth.
During the early 19th century, although reckless use of N₂O
continued, the medical community was hungry for pain
relief; surgical procedures often resulted in death of
patients for many reasons; poor infection control led to
secondary infections, and pain control was desperately
needed.
The most commonly performed operations were
amputations, tooth exts, and abscess draining; these
surgeries needed to be completed quickly and often lasted
less than 90 seconds; during lengthy procedures, patients
would succumb to exhaustion and or shock.
The greatest medical advance at that time was the
suture; wounds could be sewn closed rather than
cauterized with a hot iron; extremities from
amputations did not have to be dipped in boiling
water solution to create hemostasis.
Rather than face an operation without pain control,
patients often committed suicide; available pain
control measures were time consuming,
unpredictable, inconsistent, and at best mildly
effective.
Several methods were tried i.e. brute force to
control a patient; drinking alcohol or opium;
tourniquets or ice.
Surgical patients were often placed in serious
dilemmas-choosing between the pure torture and
unfathomable pain associated with surgery or
living with a disease or condition that would likely
result in a slow, agonizing death.
In 1842 Dr Wm T G Morton, a student of Dentistry
under Dr Horace Wells begins the use of ether in
dental and oral procedures as anesthetic agent;
Dr Crawford W Long came forward in 1849 to
claim that he had first used either in 1842, four
years before Morton’s demonstration.
In 1868 a mixture of N₂O and 20% O₂ was
instituted to improve safety; in 1872, in England,
liquid N₂O became commercially available making
it no longer necessary for practitioners to mfg
their own gas.
William Thomas Green Morton (August 9, 1819
– July 15, 1868) was an American dentist who first
publicly demonstrated Oct 1846 at Harvard
Medical School the use of inhaled ether as a
surgical anesthetic in Oct 1846 to remove tumor
from pt’s neck; became first to specialize full time
in field of anesthesia.
 American Civil War 1861-1865
Two percent of the US population at the time
(approximately 620,000) died during the conflict.
Weapons and injuries caused were far advanced of medical
capabilities to tx; 3 out of 4 injuries resulted in
amputations; if soldier shot in chest or abdomen result was
usually death.
Chloroform was anes of choice, used 75% of time;
morphine, ether, opium and laudanum were sometimes
used; only 43 deaths from anesthesia (Stage II).
Laudanum was an alcoholic solution containing morphine;
prepared from opium and formerly used as narcotic pain
killer.
In 1868, Dr. Edmund Andrews, a Chicago surgeon,
established the need to mix oxygen with nitrous
oxide for use in operations of long duration.
In 1860, a young German chemist named Albert
Niemann isolated cocaine from the leaves of the
South American coca bush.
In 1890’s the use of N₂O again began to decline as
cocaine injections became accepted method of
dental pain control.
In 1884 Carl Koller, an Opthamologist, demostrated
cocaine’s effectiveness as a local anesthetic.
First local dental injection was given on Jan 1885 by
Dr William S Halstead; it was a mand nerve block at
the mand foramen and cocaine solution was used.
Alexander Wood introduced the first hypodermic
syringe in 1853.
Procaine (Novacaine) was developed in 1904 by
Alfred Einhern, German researcher; became
substitute for cocaine; Hx of side effects ie allergic
rxns with its use.
Lidocaine was synthesized in 1943 and introduced
in 1945 as local anesthetic for Dentistry; became
standard for dental pain control.
Guido Fisher introduced standard mandibular
block in 1919; the IANB should henceforth be
dubbed “Fisher Block.”
In 1903, Dr. Charles Teter, a Cleveland dentist,
invented the first nitrous oxide-oxygen machine.
The first “fail-safe” system was marketed in 1962.
In this era of sophisticated medicine and advanced
technology, it is easy to forget the trials and
tribulations taken by early medical scientists
(especially Dentists) to advance standard practices
such as Nitrous Oxide sedation and local
anesthetics.
What these scientific pioneers accomplished while
experimenting with unknown, potentially
dangerous materials and primitive equipment was
courageous.
They often sacrificed their own health and safety
for scientific advancement; it is because of the
bravery of these early medical explorers that we
can provide safe and effective analgesia and
anesthesia today.
N₂O-O₂ Inhalation Analgesia in Dentistry

Fear, anxiety and pain have historically been associated

with dental treatments; majority of people still rank fear
of dental treatment second only to public speaking.
N₂O is employed in dentistry for the primary purpose of
reducing anxiety in the dental patient
It is estimated that 20 to 40 million adults in America
avoid dental treatment because of fear.
By utilizing local anesthetics and sedation techniques
during past 5 years, dentists have made great progress
in reducing this barrier to acceptance of dental services.
In the practice of Dentistry we have to deal with fearful
patients all the time!
FEAR is “False Evidence Appearing Real”
 Rationale for Use

Five universal human fears

fear of pain
fear of the unknown
fear of helplessness and dependency
fear of body change/mutilation
fear of death
Additional fear encountered in Dentistry:
fear of needles and local anesthesia injection
fear of the dental handpiece (i.e. “the drill”); sight, noise
and smell
fear of keeping airway open and gagging (this is very
significant)
fear of losing control of situation
fear of not having profound anesthesia for treatment
fear of certain types of treatment
fear of the dentist as a person
Why should we be concerned about the fearful patient?
Various estimates of numbers > one cited was 130 million people in the US have some
level of dental fear or anxiety; 5-8% avoid dental tx due to dental fear or anxiety.

Fear and pain are so interrelated that it is often hard to separate them.

Fear affects an individual’s ability to tolerate pain.

Painful stimuli can be exaggerated in an anxious patient.

As pain increases, anxiety is heightened and increases.

Pain becomes enhanced and therefore less tolerable.

When fear and pain is an issue, they must both be managed.

“White Knuckle Pt” Fear is Visible

 So how do we deal with this dilemma?
Need to deal with fear head on
Do not get involved unless you are ready to give 100%
A great practice builder > If pts really believe you are a “pain free”
dentist
Need clinical experience and additional training in this area
Interview pt before sit in chair; be good listener “big ears”; let pt talk
and acknowledge their anxiety and fear.
Try to objectively quantify pt’s fear and anxiety; then together
develop plan to manage.
Good communication skills are necessary to facilitate the
interpersonal interaction between pt and provider.
Fundamentals include kindness, compassion, empathy, and
respect.
Empathy is best expressed through eye contact as interview
patients.
Try to convey genuine, sincere, concern, a caring attitude and
understanding of patient’s anxiety and fear; this builds trust.
Big mistake to make is being presumptuous about how
patients should feel or not feel.
Pts do not care what providers know until they know that
that they care.
A great reward for a dentist comes when he or she is
able to help an anxious and fearful patient overcome
this burden they carry and become trustful and
comfortable with dentistry.
In some cases seek help and support from other
healthcare professionals i.e. clinical psychologists,
pastoral counselors etc.
 Pain Perception
Represents a subjective psychological state rather than
an activity induced by noxious stimulation.
If a patient regards his or her experience as pain, accept
it as pain.
 Definitions
Nociception: Noxious stimulus originating from the
sensory receptors and carried into the CNS by the
primary afferent neurons.
Pain: An unpleasant sensory and emotional
experience associated with actual or potential tissue
damage, or described in terms of such damage.
 Pain Has . . .
A sensory-discriminative dimension to identify the
form of energy (e.g., thermal, mechanical, chemical)
and spatial, temporal and intensive aspects of the
stimulus
 Pain
It is more an experience than a sensation
Pain has a:
Sensory component
Cognitive component
Emotional component
Motivational component
It may vary among individuals and can vary in the same
individual from day to day
 PAIN Classification

ACUTE PAIN – structural pain that lasts less than

one (1) month.

CHRONIC PAIN – structural pain that persists for

periods up to four (4) to six (6) months.
 Most Common Causes of
Acute Craniofacial Pain
Trigeminal (CN III) Neuralgia/Neuritis
Dental (Hypersensitivity, Malocclusion, Pulpitis, Abscess,
Periodontitis)
Temporomandibular Joint Syndrome
Glossopharyngeal (CN IX) Neuralgia
CRPS I (Complex Regional Pain Syndrome)
 Causes of
Orofacial Pain
Soft Tissue Dental Neurological Referred Bone
 Advantages of N2O- O2 Inhalation Analgesia

Onset of action (3-5 min)

Peak clinical effect
Depth of sedation
Duration of action
Recovery time (rapid)
Easy titration (easy to raise and lower levels)
Discharge without prohibitions
No injections
Safe, few side effects
Can be used instead or in conjunction with local anes
 Onset of Action

Other routes of drug

Nitrous Oxide administration

2-3 minute onset Oral – 30 min.

Rectal – 30 min.
IM – 10-15 min.
IV – 1 min. or more
 Peak Clinical Effect

Nitrous Oxide Other routes of drug

administration
3-5 minute peak
Oral – 60 min.
Rectal – 60 min.
IM – 30 min.
IV – 1 -20 min.
 Depth of Sedation

Nitrous Oxide Other routes of drug

administration
Readily change levels of Oral –
sedation Rectal –
IM – cannot easily deepen
or lighten these three
IV – deepen but not easily
lighten
 Duration of Action

Other routes of drug

Nitrous Oxide administration
Oral – fixed durations 2-3
Flexible duration of action hours
so very short or very long Rectal – fixed duration 2-3
procedures can be hours
performed IM – fixed duration 2-4 hours
(significant drug variation)
IV – fixed 45 min. drug
variation (sig drug variation)
Inhalation - variable duration
 Recovery time

Nitrous Oxide Other routes of drug

administration
Recovery 3-5 min. complete Oral – 2-3 hrs (residual effects
possible)
Rectal – same as oral
IM – 2-3 hours; same as oral
and rectal
IV – 15 min. – 3 hrs.; may have
residual effects
 Titration

Nitrous Oxide Other routes of drug

administration
Titration is possible Oral – titration not possible
Rectal – same as oral
IM – same as oral and rectal
IV – titration is possible
 Discharge from office
Other routes of drug
Nitrous Oxide administration

Recovery is almost always Oral – recovery not

complete and discharge complete; req an adult
from the office is escort
acceptable without an Rectal – same as oral
escort
IM – same as oral and rectal
IV –same as oral, rectal and
IM
Inhalation – recovery
almost always complete
Disadvantages of N2O-O2 Inhalation Analgesia

Cost of equipment is high

Cost of gases is high
Equipment is cumbersome and takes up space
N2O is not very potent; fails in 5-10% of patients
Patient must cooperate
Chronic exposure may be dangerous to health
 Contraindications for N2O-O2

The 5 C’s
COPD > absolute CI
Children
Colds
Claustrophobia
Compulsive
 Relative Vs Absolute Contraindications
Relative Contraindications indicate pts in which there would be an
increased risk for complication or adverse reactions.

If there is a better method, it should be used.

Absolute Contraindications indicate pts at risk for complications and

adverse rxns; they should not be subjected to N2O-O2 sedation.

Dr Allen’s syllabus states that there are No absolute

contraindications to use of N2O-O2 inhalation sedation as long as the
percentage of O2 is greater than 20%

Clark and Brunick, authors of our textbook does not state this
 Contraindicated Conditions
Upper Respiratory Infections - N20 must be inhaled through the
nose; (patent airway is mandatory); any patients with
respiratory problems would be contraindicated; also pts with
any nasal obstruction.
TB - active, a Contraindication for inhalation sedation.
Pt’s with contagious diseases may have N20 sedation but need
to provide them with a disposable mask and tubing at their
own cost.
Children with Severe Behavior problems - Handicapped
children or adults who do not understand the use of the mask
or cannot communicate their feelings.
Compulsive type A personality - take charge type of person who
does not like to lose control may not enjoy N2O.
Patients with severe personality disorders - psychiatric pts who
receive medication for mood elevation or antidepressants.
 Relative Contraindicated Conditions
Claustrophobic patients – may not be able to manage wearing nasal
mask
Severely phobic patients – may resist calming effect of N2O, their
situation might worsen; better to avoid N2O in these pts
Pregnant pts in 1st or 3rd trimester; treatment in first (absolute CI)
to avoid spontaneous abortion and fetal malformation
(organogenesis); tx in third may cause delivery and medical
emergency; elective Dental tx in 2nd trimester; Note: treatment of
pregnant pts need medical consult from OBGYN physician
Middle ear disturbance i.e. surgery or grafting
Recent eye surgery using perfluoropropane or sulfur hexafluoride
Patients who do not want N2O; do not force these pts into using N2O
 Relative Contraindicated Conditions
Medically compromised pts – this category is questionable
and may not be true relative contraindications
Myocardial infarction (heart attack) – general rule: need a
medical clearance from pt’s cardiologist and delay all tx
for 6 months post heart attack
Heart failure (congestive heart failure, CHF)
Pts with known Dx of Vit B12 deficiency
 COPD Absolute Contraindication
Including Chronic Bronchitis and Emphysema
These patients have elevated CO2 levels resulting in a loss
of ability to respond to CO2 stimulus
Healthy pts are stimulated by the respiratory center
(Medulla) alter the rate of ventilation due to changes in
CO2 levels
COPD patients are stimulated to breathe by activation of
peripheral aortic and carotid body chemoreceptors,
which react to lowered blood O2 levels
Administration of an O2 enriched mixture of gases will
raise the blood O2 saturation and remove stimulus for
involuntary breathing
 Absolute Contraindications
Pneumothorax
Cystic fibrosis
Recent pneumoencephalography; N2O can increase intracranial
pressure
Suspected or known diagnosed pernicious anemia or Vitamin
B12 deficiency
Significant bowel disease
First trimester of pregnancy
Cancer therapy using bleomycin sulfate
Psychological impairment
Current psychotropic drug use
Current recovering drug use or addiction
Pt in shock, semi conscious or with serious head or fascial
injuries
Inability to understand or comprehend procedure or unwilling
to consent to procedure
 Indications
Management of anxious, apprehensive, fearful
patients - management of fear and anxiety is
successful in 90-95% of patients
Gagging pts - N2O slightly decreases gag reflex and
cough reflex
Pediatric pts – must not be mouth breather, accept
nasal mask; in Florida a special permit is needed for
children weighing less than 60 pounds
Periodontal procedures
 Effects N2O On Various Body Systems
Cardiovascular disease – N2O proven to be one of most effective
techniques for reduction of stress, anxiety, apprehension and fear
In these pts, clinical signs and symptoms are exacerbated by an O2
deficit in the myocardium; the anxious pt will have an increased
heart rate and may be stressed thus creating an increased workload
on the heart leading to ischemia; this could ppt an acute
cardiovascular event and a major medical emergency during tx
N2O-O2 inhalation analgesia reduces anxiety and elevates pain
threshold; this sedative procedure is ideal for dec myocardial O 2
requirement; a pt at N2O-O2 35:65% receives far more O2 than the
normal atmospheric O2 concentration of 20.9%
Thus N2O-O2 inhalation analgesia can be used safely in pts with
angina pectoris, CHF, myocardial infarction and hypertension; EMT
personnel are being trained in the use of N2O-O2 inhalation
analgesia instead of narcotics for pain relief in cardiac emergencies
 Cardiovascular disease

N2O causes no change in heart rate or cardiac output; it

produces peripheral vasodilation, flushing and
perspiration

N2O is cardiotonic ie relating to or having a favorable

effect upon the action of the heart; in relation to
cardiotonic drugs they increase the contracting
mechanism within the heart, thereby causing more blood
to be pumped throughout the circulatory system

Endocrine System – No negative effects

Respiratory disease – N2O is non-allergenic, non-irritating to
the pulmonary epithelium
Can be helpful in Asthmatic patients as long as not severe; N2O
can reduce stress which may ppt an attack; it also relaxes
bronchi which is primary problem
Cerebrovascular disease – stroke pts (CVA) are sensitive to
hypoxia; reduced O2 levels could induce further neuronal
damage; N2O-O2 sedation can be helpful due to the increase in
O2 level during treatment
Hepatic disease – includes hepatitis and cirrhosis; represents
a CI for many sedation agents; hepatic dysfunction results in
slow rate of which can lead to prolonged drug effects and
overdose; there is no biotransformation with N2O and is safe for
these pts
Epilepsy and Seizure disorder – hypoxia and stress in these
pts can ppt a seizure; N2O reduces anxiety and inc blood flow
(perfusion) and O2 saturation
Central Nervous System (CNS) – N2O like other anesthetics has the
ability to depress CNS; exact mechanism is unknown.
N2O effects cerebral blood flow, intracranial pressure; cerebral blood
velocity, cerebral perfusion pressure and consumption.
Evidence of injury to nervous system, ie nerves has been shown to
occur with long term chronic abuse of N2O; myeloneuropathy and
neuropathies resulting in numbness and weakness in extremities etc;
injury due to induction and effects on Vit B12 (Cobalamin) and
Vitamin B9 ( Folic acid).
Note: N2O is contraindicated in chronic abusers of nitrous oxide.
Reproductive System – covered previous discussion.
Allergies – no known reported allergies to N2O.
Malignant Hyperthermia (MH) – condition may occur
unexpectedly as individual’s response to certain drugs (particularly
anesthesia agents); pts who know of familial tendencies or Hx can be
tested to avoid this problem; N2O is not a trigger for MH and safe for
individuals who have Hx of MH.
Cognitive disorders – under heading of pt’s ability to
understand, comprehend what to expect from sedation and
lack ability to distinguish if and when they are uncomfortable;
pts with mental deficiencies ie Down’s Syndrome, Autism,
Alzheimer’s, Dementia are relative contraindications for
administration of N2O
Mind-Altering Conditions – warrant careful considerations
N2O should be avoided in patients intoxicated with drugs or
alcohol (CNS depression)
Pts who self medicate with medication such as barbiturates and
other sedative agents before Dental appt should not be treated
Pts suffering or recovering from addiction or mental illness; the
relaxing euphoria could trigger unwanted episodes or may
encourage addictive behaviors; avoid use of N2O
Pts under psychiatric and psychological care require very
careful consideration; many on psychotropic drugs and
antidepressants; to be safe avoid use of N2O
Pregnancy – N2O crosses the placental barrier and can cause CNS
depression in fetus as it does in the mother; 2nd trimester is best time
for elective Dental tx and use of N2O inhalation analgesia
N2O is frequently used during labor; uterine contractions are not
inhibited by N2O
GI Tract – due to nature of gas and its propensity for insufflating air
spaces in body; N2O diffuses into these areas more rapidly than N2
exits; gas entering non-rigid walled air spaces causes expansion;
increase pressure and possible discomfort, especially in cases bowel
obstruction
Miniscule amts of N2O (0.004%) metabolized in GI tract; could cause
reduction anaerobic Pseudomonas bacteria and produces toxic free
radicals; this process does not pose any significant threat to the body
systems
Urinary Tract and Kidneys – N2O has no adverse effects
Skeletal muscles – N2O has no effect on skeletal muscles; relaxation
is due to anxiety reduction and not on a direct effect on the muscles
N2O has no effect on pts with neuromuscular conditions
Hematopoietic System – long term exposure to N2O can cause bone
marrow depression, effects RBC production, hemoglobin and O2
transport in blood leukopenia (dec WBCs); reduced megaloblastic
erythropoiesis (production of RBCs) resembling pernicious anemia
ie megaloblastic anemia.
Interferes with Vitamin B12 (Cobalamin) dependent enzyme
methionine synthase; which is necessary for DNA synthesis and RBC
production
N2O depletes stored up Vitamin B12; converts the active monovalent
form of Vitamin B12 to its inactive bivalent form; it cannot fulfill its
enzyme function in methionine synthesis and reactivation of folic
acid Vitamin B9 ; induces deficiency of Vitamin B12 and possibly
Vitamin B9
Vitamin B12 is a very important vitamin!!
Caution when treating elderly pts, alcoholics, those with modified
diets i.e. vegetarians/vegans, pernicious and megaloblastic anemias,
gastrointestinal problems and Hx of GI surgery, known Vitamin B12
deficiency; all of these pts need special management and may be a
relative contraindication for N2O-O2 sedation.
Functions of Vitamin B12 (Cobalamin)
Works closely with Folate or Folic Acid (Vitamin B9) for
development i.e. maturation of RBCs; helps to make iron
work better in body
Important in DNA and RNA synthesis
Vitamin B12 responsible for development of protective
coating (myelin sheath) for nerves; important for nerve
health
Important for development of neurotransmitters
Responsible for reactivation of Folic Acid by converting it
into tetrahydrofolate, a form which body can use
Plays a role with Folic Acid in the deconstruction of
homocysteine to methionine; reduces levels of
homocysteine in body; inc levels can result in
hypertension; heart attack and stroke
Deficiency of Vit B12 (Cobalamin)
Signs and Symptoms: fatigue, muscle weakness, SOB,
dizziness, numbness, heart palpitations; bleeding gums
and mouth sores, nausea, poor appetite
Long term deficiency leads to Pernicious anemia; loss
memory; confusion; dementia
Myeloneuropathy and neuropathies > degeneration of
nerves in limbs and spinal cord; severe amnesia; numbness
hands and feet; absence of proprioception; ataxia;
impairment coordinated movements; walk with gait
 Pharmacology of N2O & O2
Preparation
Nitrous Oxide is prepared by heating
ammonium nitrate crystals to 240o C (462 o
F) to form Nitrous oxide and water
NH4NO3 Heat N2O + 2H2O
d
240o C
It is compressed and stored in a metal
cylinder with 30% of the N2O being in
liquid form
Physical Properties
Non-irritating, sweet smelling, colorless gas
Only inorganic gas that produces anesthesia
CO2 and N2O are the only non-organic
compounds to produce CNS depression
 Pharmacology
Chemical properties
N2O is marketed and stored as a gas/liquid compressed
under pressure 750 psi
Returns to gaseous state upon release from the cylinder
Requires heat for vaporization into a gas, which is acquired
from the cylinder walls; causes regulator and cylinder to
become cold and develop frost when gas is being used long
term
N20 is non-flammable, non-explosive but will support
combustion; above 450 degrees C (842 degrees F) N2O
breaks down to N2 and O2
 Other properties
N2O is relatively insoluble in blood Carried in the blood
in physical solution only and does not combine with any
elements
It is carried in the blood in physical solution only and does
not combine with any elements
99% of N2O that enters the body leaves the body through
the lungs unchanged; there is no biotransformation of
N2O in the body.
As blood travels through various tissues of the body, the
N2O is given up and the venous blood returns to the lungs
which has a decreased N2O gas tension (High to Low)
Because of the rich cerebral blood supply onset of action
is rapid and rate of recovery is rapid
The O2 in N2O molecule is not available for use by the body
 Potency

N2O is the least potent anesthetic gas, but the most

frequently used in Medicine and Dentistry
N2O is 35 times more soluble in plasma then N2
N2O is 100 times more soluble in plasma than O2
A 20% N20 80% O2 mixture produces analgesia equal to
10-15 mg morphine; 60 mg codeine = 10 mg morphine
The optimum concentration of N2O for the production of
analgesia is 35%. All individuals have biological
variability.
After inhalation via the nose, N2O is transported to the
alveolar sacs and alveoli in the lungs where it is rapidly
absorbed into the cardiovascular circulation
N2O replaces N2 in the blood
The MAC (minimum alveolar concentration) value % for
N2O is 104.0; (other anes inhalation gases range from 0.75
to 4.6); the MAC value and limited potency of N2O add
tremendously to its safety
MAC value indicates that at normal atmospheric pressure,
N2O alone is not able to produce profound surgical anes;
N2O can be used as the sole anes agent under hyperbaric
conditions
N2O uptake is so rapid that two important phenomena
occur:
1st – Concentration effect
Concentration effect - occurs when high concentrations of
a gas is administered; the higher the concentration of the
N2O inhaled, the faster the arterial tension of N2O agent
will increase.
As the volume of N2O is removed from the lungs into the
blood, fresh gas is literally “sucked” into the lungs from the
anesthesia machine, thereby increasing the rate at which
the N2O arterial tension increases.
2nd – Second Gas effect
Second Gas effect - occurs when another inhalation
anesthetic is administered along with N2O-O2 ; the
extremely rapid uptake of a large volume of N2O creates a
form of vacuum in the alveoli which forces even more fresh
gas including the second anesthetic gas agent into the
lungs.
 Secondary Gas Effect w/ N2O

A Concentration Gas Effect of N2O

B
In A 10 mph = 10% N2O
concentration
In B 80 mph = 80% N2O
concentration w/ increased
vacuum and increased gas
uptake of sevoflurane gas
When N2O is first inhaled there is a high partial pressure in
the alveolus and within the capillary it will be zero
N2O is absorbed rapidly from the lungs into the
cardiovascular system; primary sat of blood and brain w/
N2O is accomplished by the displacement of N2 from the
alveoli and blood; occurs w/ in 3-5 min from onset of
administration
Tissues with greater blood flow (ie brain, heart, liver, and
kidneys) receive the greatest amount of N2O
Fat, muscle and connective tissue, absorb smaller portions
of the N2O
Vast majority of N2O is exhaled through the lungs within
3-5 min after termination; N2O does NOT undergo
biotransformation
Approximately 1% will be eliminated over 24 hours
through the lungs and skin; it is eliminated unchanged
 Diffusion Hypoxia
Occurs when N2O is turned off suddenly and patient breaths
room air; Symptoms - headaches, nausea, and lethargy
“Hangover effect” results from N2O rapidly diffusing from the
blood, out of alveoli and the lungs
The alveoli become filled w/ exhaled N2O, O2, CO2, N2 and
water vapor; the conc effect occurs as these gases rush out;
blood level of CO2 is greatly decreased> this reduces stimulus
for breathing producing respiratory depression; upon
inhalation, residual N2O diffuses back into the alveoli thus
diluting the O2 present from normal 14% to about 10%; this
hypoxia produces hangover effect.
Hypoxia can cause vomiting in some pts
Adverse effects of diffusion hypoxia can be prevented by
giving 100% O2 for at least 3-5 minutes upon termination of
the procedure
The exact mechanism of action N2O is unknown

N2O may act directly on the opioid receptor and/or

activate the release of endogenous opiates

N2O is known to cause CNS depression primarily in the

cerebral cortex (memory, intelligence areas)

The vomiting center in the medulla is affected only in

presence of hypoxia; N2O has no effect on the vomiting
center unless hypoxia is present.
Endogenous endorphins,
enkephalins,
and dynorphins have been
discovered
as substances that bind to
the opiate
receptors, resulting in
pain modulation;

Activation of the
endogenous opioid
system can be
accomplished by pain
and or stress
 Physical Properties of O2
O2 is a clear, colorless, odorless gas and makes up 20.9% of
the atmosphere (and room air)

It is stored as a compressed gas at 2000 psi, delivered at

50 psi

O2 is not flammable but will support combustion

Under pressure in the presence of oil or grease, O2 may

cause an explosion
 Preparation of O2
Oxygen is commonly prepared by fractional distillation of
liquid air; N2 is boiled off leaving liquid O2 (LOX)
Other methods of Oxygen Preparation:
Heating Barium peroxide to 800°C (1472°F)
BaO2 -----BaO + O2
Reaction between sodium peroxide and water
2Na2O2 + 2H2O -----4NaOH + O2
Electrolysis of water
2H2O -----2H2 + O2
Anode
 Effects of 100% O2
CNS - No effect on the cerebral cortex but may cause
constriction of cerebral blood vessels
Constriction of cerebral blood vessels may decrease
blood flow by 10%
Cardiovascular System - Generalized vasoconstriction
occurs in cerebral, renal, and retinal vessels; diastolic
pressure increases, systolic pressure remains the same;
coronary artery blood flow decrease 10% with a
decrease in heart rate (down 3-4 beats per min),
decrease in cardiac output (10-20%)
Composition of Respiratory Gases

Gas Inspired Air Expired Air

O2 20.90% 16.30%
CO2 0.04% 4.00%
N2 79.00% 79.70%
 Anatomy
Conducting portion - transports gases from the air
to the Respiratory zone
Mouth, Nose, Pharynx, Larynx, Trachea, Bronchi,
Bronchioles
Respiratory Zone - where O2 and CO2 are
exchanged between the air and blood
Respiratory bronchioles, Alveolar ducts, Alveolar
sacs, Alveoli
OBSTACLES TO LAMINAR AIRFLOW CREATE
TURBULENCE
Pharynx “Throat” extends
from posterior of nose to
cricoid cartilage
AIRFLOW TURBULENCE FROM TURBINATES,
TONSILS AND ADENOIDS

TURBULENT AIR
FLOW
Larynx extends from C3-6 vertebrae
VCs narrowest part of adult airway;
children. It is cricoid cartilage

Can act as protective mechanism

foreign matter
Intrapulmonary Airway
Intrapulmonary Circulation
Superior
lobe
 Muscles of Inspiration
Diaphragm (Primary muscle)
Intercostal > External and Internal; Internal (Primary
Expiration)
Abdominals (Accessory Expiration-Inspiration)
Sternocleidomastoid, Scalenes, Ant Serrati, elevators of
Scapula and Pectorals (Accessory Inspiration)

Note: Exactly which muscles are involved in respiration is

controversial
 Temporalis

Occipitofrontalus
(occipital portion)

Sternocleidomastoideus
 Subscapularis
Teres major
Teres major

Pectoralis minor
Lotissimus dorsi
(cut)

L
Pectoralis major

Anterior Serratus
 Transport of O2 in the Blood
97% of O2 transported from the lungs to the tissues is
carried in chemical combination with hemoglobin in the
red blood cells.
Each molecule of Hb has four heme groups and can carry
4 molecules of O2; an adult human at any given time has
about 20-30 trillion RBCs; each RBC has about 270-300
million molecules of Hb; RBCs are transporting roughly
1.08 billion molecules of O2.
Remaining 3% O2 carried in the dissolved state in the
water of the plasma and cells.
 Transport of O2 in the blood
If the plasma alone carried O2 it would require 3
atmospheres of pressure and a cardiac output of the
heart 15 times normal to provide the amount of
needed to supply the body’s tissues
Remaining 3% carried in the dissolved state in the
water of the plasma and cells.
Saturation (Hb) of arterial blood 97-98% or 20 ml
(20 vol %) of O2 per 100 ml of blood
Saturation of venous blood 70-75% or 15 ml of O2
per 100 ml of blood
It takes approximately 30 sec for blood to travel from the
lungs to the brain.
It takes approximately 30 sec for the initial effects of N2O
to be felt.
Six normal breaths (6 X TV of 500 ml; about 2500 ml) in 30
sec will initiate the effects of sedation.
Twenty-four normal breaths or within two minutes,
maximum effects of N2O can be appreciated.
 Pulmonary Volumes
Tidal Volume (TV)- 500ml in avg. adult male; 500ml avg adult female;
quiet breathing
Inspiratory reserve volume (IRV)- 3100 ml males; 1900 ml females;
the max vol. of air that can be inhaled from the end of inspiratory
level
Expiratory reserve volume (ERV)- 1200 ml males; 700 ml females, the
max vol. of air that can be exhaled from the end expiratory position
Residual volume (RV) - 1200 ml males; 1100ml females- the vol. of air
remaining in the lung after a maximal exhalation
Total lung capacity- 5800 ml in males; 4200ml in females
Normal Respiration- 12 breaths per minute -- adult
Minute respiratory volume- 6 liters per minute
Tidal volume X breaths/min (500 ML X 12 breaths) = 6 liters
 Principles of Pulse Oximetry
Pulse oximeters measure arterial oxygen saturation SpO2
as a ratio of oxygenated hemoglobin (Hb) to the total
amount of Hb
Operates on principle that Hb exists it two forms:
oxygentated arterial blood w/ no O2 molecules loosely
bound (HbO2) or reduced (deoxygenated) w/o O2
molecules bound Hb
Oximeter sensor commonly placed on fingertips
Unit transmits constant infrared and red light beam
through finger to a photo electric cell on opposite side of
finger
 Principles of Pulse Oximetry
The PO measures the absorption of selected
wavelengths of light as they pass through living
tissue
Oxy HbO2 and Deoxy Hb
Oximeter sensor commonly placed on fingertips
Unit transmits constant infrared and red light beam
through finger to a photo electric cell on opposite
side of finger
 Pulse Oximeters
Detect changes in pulmonary gas exchange before tissue oxygenation
is impaired
PO a valuable aid to the early recognition of respiratory depression
Are accurate within 2-3% between the O2 saturation of 70-100%
May give false readings in the presence of hypotension (shock,
hypovolemia), patient motion, heavy smokers, cardiac patients,
electrosurgery units, and opaque nail polish
Oxygen saturation simply refers to the percentage of the
available Hb that carries O2; take situation below, there
are 16 Hb units and none have O2; the O2 saturation
is therefore 0%
Here 12 out of 16 units of Hb have O2
Therefore we have 75% 02 saturation
Here we have 8 out of 16 units of Hb with O2,
therefore we have 50% O2 saturation
And of course when all 16 units of Hb have O2
the O2 saturation is 100%
The PO uses two kinds of light ie red and infrared to determine O2
saturation; light emitted from light sources passes across the PO
probe and reaches the light detector; if living tissue is placed
between light source and detector the emitted light will pass
through the tissues; some will be absorbed by tissues and some
will pass through and reach the detector.
The amount of light that is absorbed by the living tissue
depends on many physical properties; these are used by the PO
to determine the O2 saturation of living tissues; the amount of
light absorbed depends on: 1) conc. of light absorbing
substance; 2) length of light path is the absorbing substance; 3)
oxy HBO2 and deoxy Hb absorb red and infrared light
differently.
The finger is inserted into the PO probe; above the
finger is the light sources; in the finger is an artery
and a vein; both carry blood; in artery is Oxy HbO2
and in the vein Deoxy Hb; below the finger is the
light detector.
 Beer’s Law
Hemoglobin (Hb) absorbs light. The amount of light absorbed is
proportional to the concentration of Hb in the blood vessel. In
the diagram below, the blood vessels in both fingers have the
same diameter. However, one blood vessel has a low Hb
concentration ( i.e. low number of Hb in each unit volume of
blood) and the other blood vessel has a high Hb concentration
i.e. (high number of Hb in each unit volume of blood). Each
single Hb absorbs some of the light, so the more Hb per unit
area, the more light is absorbed. This property is described in a
law in physics called “Beer’s Law”.
By measuring how much light reaches the light detector, the
pulse oximeter knows how much light has been absorbed; the
more Hb in the finger, more is the light absorbed.
Physical property No.1 : Beer’s Law ie amount of light
absorbed is proportional to the concentration of the
light absorbing substance.
 Lambert’s Law
Look at the two fingers shown below. Both arteries have the same
concentration (same Hb per unit area, blue square) However, the
artery on right is wider than the one on the left.
The light emitted from the source has to travel through the artery.
The light travels in a shorter path in the narrow artery and travels
through a longer path in the wider artery (paths are shown as green
lines below). Though the concentration of Hb is the same in both
arteries, the light meets more Hb in the wider artery, since it travels
in a longer path. Therefore, longer the path the light has to travel,
more is the light absorbed. This property is described in a law in
physics called “Lambert’s Law”.
Lambert’s Law: Amount of light absorbed is proportional to the
length of the path that the light has to travel in the absorbing
substance.
Physical property No.2 : Lambert’s Law ie
amount of light absorbed is proportional to the
length of the light path.
Lambert’s Law
Physical property No.3 : oxyhemoglobin absorbs more infrared
light than red light & deoxyhemoglobin absorbs more red light
than infrared light.

All light is composed of waves; the distance between the tips of the
wave is equal to the wavelength; Unit of measure is nanometers.
For example the wavelength of light on left is 650 nm and
the wavelength of light on the right is 950 nm; Oxy HbO2
and deoxy Hb absorb light of a different wavelength in a
specific way.
Oxy HbO2 absorbs more infrared light than red light
Deoxy Hb absorbs more red light than infrared light
Different colors of light have different wavelengths
The pulse oximeter (PO) uses the property that
oxyhemoglobin and deoxyhemoglobin absorb light of
different wavelengths in a specific way.
Oxyhemoglobin absorbs light of different wavelengths in a
specific way. We use a special light source of which we can
adjust the wavelength of the light it emits. This light source
sequentially passes light of different wavelengths through a
sample of Oxy Hb. The detector notes how much light, at each
wavelength, has been absorbed.
We can repeat the same demonstration using Deoxy Hb.
Again notice, how like Oxy HbO2 and Deoxy Hb absorbs different
amount of light at different wavelengths.
The PO uses two lights to analyze hemoglobin; one light is
red w/ wavelength of 650 nm; the other is infrared w/
wavelength of 950 nm;
Infrared light is invisible to the human eye; in all
diagrams to follow the red light will be shown as red and
infrared will be shown in turquoise
Now look at the Oxy HbO2 absorbance graph again, but this time
paying attention to the wavelengths of light used in POs you will
see that Oxy HbO2 absorbs more infrared light than red light.
The graph below shows the absorbance of Deoxy Hb. It is
seen from the graph that Deoxy Hb absorbs more Red light
than Infrared light.
The composite graph below shows the absorbance of both
forms of Hb at different wavelengths; Note again:
Oxy HbO2 absorbs more infrared light than red light
Deoxy Hb absorbs more red light than infrared light
A simple way to remember which form of Hb absorbs
what is to use the Acronym below:
The PO works out the 02 saturation by comparing
how much red light and infra red light is absorbed by the blood.
Depending on the amounts of Oxy Hb02 and Deoxy Hb present,
the ratio of the amount of red light absorbed compared to the
amount of infrared light absorbed changes.
Using this ratio, the pulse oximeter can then work out the
oxygen saturation.
For an example, at 100% saturation, the absorbance ratio ( i.e.
comparing how much red light and infrared light is absorbed) will
be same as that seen with the Oxy HbO2 absorbance curve that we
saw earlier.
At 0% saturation, there is only Deoxy Hb. The absorbance ratio (i.e.
comparing how much red light and infrared light is absorbed) will
therefore be same as that seen with the Deoxy Hb absorbance curve
that we saw earlier.
Now look at when the patient has an 02 saturation of 75%. The blood
has both, Oxy Hb02 and Deoxy Hb. The absorbance pattern is now
somewhere in between the Oxy Hb curve and Deoxy Hb curve (both
shown in grey). The ratio of absorbed red light and infrared light is
different and using this information, the PO is able to calculate the 0 2
saturation as 75%.
At 50% O2 saturation, the absorbance pattern is different to when
the saturation was 75%. The ratio of red light and infrared light
absorbed is also therefore different and the PO uses this to calculate
the saturation as 50%.
At 25% saturation, you and your patient is in deep trouble. Again the
ratio is different.
The animation below shows what you have seen before. As the
amount of Oxy HbO2 and Deoxy Hb changes, the light ratio
comparing red and infrared light also changes. The PO uses the ratio
to work out the O2 saturation.
To summarize things so far, the absorbance of light
depends on:
1. concentration of the light absorbing substance.
2. length of the light path in the absorbing substance.
3. oxyhemoglobin and deoxyhemoglobin absorbs red and
infrared light differently.
The PO computer takes these things factors and computes
the saturation.
Analgesia: The diminishing or elimination of pain in the
conscious patient
Conscious: Capable of a rational response to command
with the protective reflexes intact, including the ability to
maintain a patent airway
Sedation: The calming of a nervous, apprehensive
individual through the use of drugs, without inducing the
loss of consciousness
Local anesthesia: The elimination of the sensation of pain
in one part of the body by topical application or regional
injection of a drug
General anesthesia: The elimination of all sensations,
accompanied by the loss of consciousness
 Stages of General Anesthesia

4 stages of general anesthesia (ADAM)

Stage 1: Analgesia
Stage 2: Delirium – unconscious; reflexes are
exaggerated (inspiration); hyper-response to stimuli
Stage 3: Surgical anesthesia see outline
Stage 4: Medullary paralysis – “death”
Note: Stages I and II are the induction stages for general
anesthesia
 Stages of General Anesthesia

Stage I Surgical anesthesia > Analgesia

Refers to altered consciousness; depressed cerebral cortex
effects memory, intellect, perception of time and space,
elevated pain threshold
Note: during conscious sedation a patient is in this
stage
Any person who has ever taken a “sleeping pill”, used an
anxiety drug such as Diazepam (Valium) or even taken
alcohol has technically been in Stage I of anesthesia
 Stages of General Anesthesia

Stage III Surgical anesthesia

Plane 1: lower plane 1/ upper plane 2 – ideal
surgical anesthesia
Plane 2: eyeballs fixed, respiration remains regular
but depth of breathing is diminished
Plane 3: paralysis of intercostal (chest wall)
muscles; diaphragm breathing only; pupillary rxn
to light is lost; not recommended for surgery
Plane 4: respiration diminishes progressively;
pupils dilate; no muscle tone
 Stages of General Anesthesia
Stage IV surgical anesthesia
Respiration stops; cardiac arrest; this is reversible
clinical death if CPR or advanced life support is
initiated in a timely manner; this condition is often
seen in the ER in drug overdose cases
Four stages of general anesthesia are based on descending
depression of CNS; CNS depression (general anesthesia,
antianxiety drugs, sedative hypnotics, narcotics, alcohol
first depress
Cerebral cortex – causing loss of memory then loss of
motor
function
Basal ganglia, cerebellum
Spinal cord
Medulla (Respiratory center in brainstem) – medullary
depression leads to depression of the respiratory and
cardiovascular systems resulting in death
 Armamentarium

Compressed gas cylinders are 3/8” thick steel

Some equipment for N2O have been made with aluminum
Must be tested every 5 years and stamped w/ specific
information (engraved on cylinder)
Designed to handle 1.66X usual pressure
 Handling Compressed Gas Cylinders
Use no grease, no oil, no lubricant around cylinder, valves,
gauges, regulators – can cause explosion
When gas from a 2000 psi tank is reduced to 50 psi at a
regulator, the frictional heat produced can exceed 1500
degrees F which is well above the ignition temp of grease
and oil
Cylinders are stored upright; do not drop
Stored in constant temperature
Open cylinder counter-clockwise
Close valve tightly when not in use
Oxygen cylinder - present in a gaseous state
“E” weighs 21 lbs. and 2000 psi
“H” weighs 131 lbs. and 2200 psi
Pressure gauge measures contents of the tank
Color of the tank is green

Nitrous oxide cylinder – present as both liquid and gas

Full cylinder contains 30% in liquid state
“E” weighs 21 lbs. and 750 psi
“G” and “H” weigh 130 lbs. and contain 750 psi, when full
Color of the tank is blue
 Full N2O cylinder contains 95% liquid and
5% vapor and will have a pressure reading on
gauge of approx. 750 psi at 50-70%. Storage
temperature and rapid release of N2O can
change cylinder pressure eg at 50 degrees F,
pressure would be approx. 575 psi.
Because liquid is vaporized as gas is use the
reading on pressure gauge is not proportional
to the amount of gas available in the cylinder.
When tank contains about 20% N2O pressure
reading on gauge will show a decrease and
approximate amount of N2O in cylinder.

For O2, a full cylinder is 2000 psi. The

pressure gauge will accurately indicate the
amount of gas present in the cylinder.
It is important to monitor the amount of left
in the cylinder as the N2O-O2 is driven by O2
flow. If tank goes empty during procedure
there will be no flow of N2O (a very important
safety feature, no O2 flow no N2O flow).
Regulator (reducing valve) - located between gas
cylinder and flow meter on the yolk
Function is to decrease high pressure of gas from
cylinder to safe pressure for patient; (2000 psi or
750 psi to 50 psi)
Yolk – holds gas cylinders onto the portable unit
Flow meter - ball type most commonly used
Precise flow volume of gas is read, using the middle
of the ball
Accuracy is +/- 5 %
Emergency intake valve – located above the reservoir
bag; during normal use closed; it opens when gas flow
through machine is terminated.
Prevents patient from feeling discomfort or suffocation
Reservoir bag – made of rubber or silicon; primary
function reservoir for additional gas; monitoring device
for respiration; can be used to provide assisted positive
ventilation in a medical emergency
Bag mimics ventilation ie depth and rate and provides a
reliable visual way to monitor.
Conducting tubes – check to prevent kinking.
Nasal cannula – useful in patients with claustrophobia;
must use high volume of gas; difficult to obtain good
level of analgesia.
Reservoir bag helps to establish appropriate volume in L/min by observing the bag
Nasal hood – contains either the exhaling valve or the air
dilution valve, or both
Exhaling valve – one-way valve; pt exhales gases and
inhales only gas from the machine
Air dilution valve – two-way valve; permits inhaling room
air which can dilute the inspired N2O by up to 50%; always
keep ADV closed
Scavenging nasal hood – connects to the high speed dental
suction, minimizes N2O contamination; a gauge with a
small ball; fd left side, below gas flow adj for N2O; tells you
scavenger system is working; gas must be flowing through
machine before gauge will work.
 Equipment Safety Features
Purpose of safety features is to prevent giving 100% N2O
and to prevent giving less oxygen than room air at 20.9%
Features include
Pin Index system
Diameter index system
Oxygen fail safe minimum O2 flow (% delivered is 30%)
Equipment is designed to deliver no more than 70% N2O
Alarm (sounds when O2 decreases below 30% or below
2.5-3 liters per min)
Emergency air inlet
Reservoir bag
Oxygen flush button
Color coding (O2 ---Green, N2O ---Blue)
Flowmeter Features
1. Flowmeter tubes
2. Fail Safe
3. Gas Control Block
4. Gas Flow Adj Knob
5. Emergency Air Valve
6. Check Valve (Non-Breathing
Valve)
7. Positive On-Off Switch
8. Oxygen Flush Button
9. Needle Valves
10. Flowmeter
11. Total Flow Adj Knob
Scavenger System
Gauge
Scavenger system takes
out all N2O that is
exhaled through the
mask

Optimal evacuation
flow rate is 45 L/min

Equipment that does

not have scavenging
capabilities is clearly
a breach of the standard
of care per NIOSH
 *

Proper insertion of mask in the

nasal hood “groove to groove”
Check mask to ensure flutter valve is intact and
working
 Scavenging Nasal Mask

Major Factors in N2O Contamination of Environment

Mouth breathing is the most critical measure to control pt talking is primary
source trace gas contamination
Ill fitting mask, mask displacement, facial hair causing leakage around mask
Connections, cracks in hose, leaking reservoir bag
Stuck flutter valve on mask negates scavenging function of mask
Poor ventilation, recycled air from AC.
National Institute for Occupational Safety and Health exposure limit for operating
room 25 ppm for Dental office 50 ppm; if N2O gas conc is 25-150 ppm need
increase exhaust capabilities.
 Pretreatment Visit
The success of N2O-O2 can be better if the patient is introduced to
technique prior to appt. date of procedure.
Some patients are fearful; others have too high of expectations of sedation.
Describe the technique and explain the pt will feel RELAXED and
COMFORTABLE.
Do NOT explain the different levels of sedation because all patients will
experience the same signs and symptoms.
Do NOT compare to the effects of alcohol because alcohol may be against
their religious beliefs and could turn the patient off to the idea of N2O-O2
sedation.
Pre-op instructions should include:
No heavy meal should be eaten up to 4 hrs, no liquids 2 hrs prior to tx.
A light meal is okay; no fatty or greasy foods.
A fasting pt could pose a hypoglycemic problem w/ syncope in combination
w/ stress; a little protein snack might reduce risk of crisis.
*
*
Mallampati Classification
American Society of Anesthesiologists Classification
 Day of Appointment
Preparation of equipment – open cylinders, check nasal
hood, hoses and reservoir bag for leaks
Preparation of pt – ask pt if need to visit restroom; if they
need to visit during procedure you will have to reverse and
then induce pt again; N2O does has no effect on urine
production
Review med Hx – take vitals i.e. BP, PR, Pulse O2 saturation
and record
Check pt for contact lenses and remove to avoid drying
eyes and prevent painful irritation; place safety glasses on
pt
Have pt uncross legs; crossed legs for a prolonged period
can cause circulatory problems in feet and ankles
 Day of Appointment
Position machine behind pt; it is best if pt does not see gauges;
(better placebo effect)
Place nasal mask on pt and cinch up mask and hood so mask will not
leak and pt is comfortable
Review med Hx – take vitals i.e. BP, PR, Pulse O2 saturation & record
Give 100% O2 > adults 5 LPM; children 3 LPM; check mask for
leakage; pt can help you; remind pt to breathe through their nose
during whole procedure
Determine pt’s flow rate (TV tidal volume) by observing the
reservoir bag; ask pt to inhale deeply through nose and then exhale;
you want to see bag inflate and deflate slightly as pt inhales and
exhales; this will require some adjustment; ask pt if they are able to
breath normally
(Ask your pt if they can breathe normally through their nose?)
Have pt uncross legs; crossed legs for a prolonged period can cause
circulatory problems in feet and ankles.
 Day of Appointment
A deflated bag means possible leaks or pt has very large TV
and bag was not filled enough at start; over inflated bag
means air flow too great for pt or possible kinked tubing
Remind pt that this should be a pleasant experience and
they should be comfortable at all times; if they feel
uncomfortable at any time signal provider
Start to administer N2O > 1.5 L (about 20-25%) for 5 min;
record starting time for pt record
Titration of N2O will begin as you administer the next
increment of N2O; wait 60 sec before each increment of
N2O is administered
 Technique of N2O-O2 Inhalation Sedation
Slow titration of N2O is the best method to ensure ideal
sedation to the greatest number of patients
This method will ensure a higher success rate and prevent
the undesirable effects of nausea and vomiting
Effective N2O-O2 sedation is capable in 90-95% of all pts;
70% will be successfully sedated at 30-40% N2O conc
Approximately 10% pts will require more than 50% to feel
any appreciable sedative effects
Remember that pt’s response to drug effects are
biologically variable; N2O-O2 sedation is not potent enough
for all pts
Always give 100% O2 3-5 min before and after the
procedure
 Titrate N2O
Start with 20% after 5 min of O2
LPM N 2O LPM O 2 % N 2O Time
Seconds

0.0 5.0 60…4 min

1.0 4.0 20% 60…4 min
1.5 3.5 30% 60…4 min
2.0 3.0 40% 60… 4 min
2.5 2.5 50% 60… 4 min

Calculation to determine percentage of N2O administration

LPM N2O/ LPM N2O + LPM O2 X 100 = Percentage of N2O administered
1 / 1+4 = 1/5 X 100 = 20%
Always observe the pt first clinical signs and symptoms usually seen at 30% N2O
 Why Do You Want To Titrate N2O
The method is the delivery of drug in incremental dosage until the
desired endpoint or effect is reached
For N2O-O2 sedation this is the “standard of care”
Specific to N2O-O2 titration, an increase in N2O by 10-15% (1-1.5 L)
every 60 seconds is suggested
Titrate to level of sedation that is determined by pt comfort and
relaxation; watch the pt closely
Remember there is no “preset percentage” or “fixed dose” for
N2O-O2 sedation for a given pt or experience; same pt may require
different conc of N2O next visit to achieve ideal sedation
Titration allows for individual bioavailability
It uncovers idiosyncratic reactions early
Only the amount of drug required by the pt is given; titrating a drug
to appropriate level of sedation is a valuable learned skill
Minimizes negative experience with over-sedation
Remember over-sedation is usually the fault of the provider
 Phase Symptoms Signs
Early Light headed (dizziness); BP and heart rate slightly
Signs and Symptoms
tingling in arms;of N2O-O2 Sedation
legs; elevate then return to
numbness of mouth; baseline;
numbness of hands feet End of this stage eyes less
active; glassy or glazed look
Ideal Feeling of warmth; feeling of Feeling warmth due to
floating; body feeling heavy; peripheral vasodilation;
euphoria; analgesia decreased muscle tone from
decreased anxiety; N2O has
no effect on muscles;
N2O has an amnesic effect; pt
has no concept of time
Heavy Hearing distant sounds; Hearing changes due to
Visual images on ceiling; pressure of N2O in middle ear
Sleepiness; Crying, Laughing; space; inc pt movement;
pt dreaming inc BP and HR; sweating

Over sedation Nausea Vomiting

 Images of a
Comfortable Pt
and
Ideal Sedation

Can you list

Signs and symptoms
of Ideal N2O-O2 sedation?
 Phase Symptoms Signs
Oversedation Detachment or
Dissociation from
Environment;
Out of body
experience
Oversedation Dreaming, Fits of uncontrollable
Hallucinating, Laughter
Fantasizing,
Floating and or flying

Oversedation Inability to move or communicate,

or keep mouth and eyelids open;
Humming or vibrating noise getting
louder

Oversedation Feel like spinning > Nausea Vomiting

 Phase Symptoms Signs
Oversedation Uncomfortable body; Facial expressions indicate
Signs and Symptoms
warmth of N2O-O2uncomfortable
even hot Sedation
Diaphoresis (sweating)

Oversedation Lightheadedness; Fixed eyes; field of vision

dizziness; narrows;
pt trying to sleep drowsiness;
hard keep eyelids open

Oversedation Sluggish delayed responses;

slurred words or no verbal sense;
agitated or combative behavior

Oversedation Tingling felt throughout Approaching light anesthesia;

whole body hyper-response to stimuli;
exaggerated inspiration
 Signs & Symptoms of Relative Analgesia
Sensation of heaviness of limbs
Floating sensation
Tingling of arms, legs, numbness of lips
Decrease of fear; pain and memory (amnesic effect)
Feeling of warmth (due to vasodilation of peripheral
blood vessels)
Decreased awareness of time
Desire to remain in this state
Signs and Symptoms of Ideal Sedation
Feeling of warmth (due to vasodilation of peripheral blood
vessels)
Floating sensation
Body feeling heavy (due decreased muscle tone from
decreased anxiety; N2O has no effect on muscles)
Ability to answer when asked questions
Euphoria (feeling good, in control, relaxed and
comfortable)
Analgesia (diminution or elimination of pain in the
conscious patient)
 Signs & Symptoms of Light
“Twilight Anesthesia”
Hyper-response to stimuli
Exaggerated inspiration
Inability to form new memories (anterograde
amnesia)
Anxiety relief (Anxiolysis) and relaxed
Pt feeling sleepy; eyelids resist opening when
provider asks to open eyes
Pt responsive and able to follow simple directions
Pt is not unconscious but sedated
 Images of
Oversedated
Patient
Most results of
Oversedation are
due to Operator
Error!

Images of An
Oversedated &
Uncomfortable
Patient
Do Not Go
There!
Over-sedation > Clinical Indicators

Persistent closing of the mouth

Spontaneous mouth breathing
Patient states they are uncomfortable
Patient fails to respond to commands
Patient falling asleep
Patient talks incoherently or appears to be
dreaming
Over-sedation> Clinical Indicators

Patient becomes uncooperative

Patient laughs/cries uncontrollably
Patient has sudden uncoordinated movements
Management
Decrease the level of N2O by .5-1 LPM and in
30-60 seconds the problem should be resolved
If Nothing Else Lighten Up!
 Complications

Unpleasant side effects and complications:

Nausea and vomiting
Excessive Perspiration
Behavioral problems
Shivering
Expectoration
 Nausea
Patients should be encouraged to communicate their feelings
particularly if nausea is present; this can lead to vomiting, aspiration,
death
Causes of nausea:
Over-sedation
Length of sedation
Emotional state
Food or liquid in stomach, especially children
Frequent changing (“sea sawing”) of the N2O concentration
Diffusion hypoxia
Patients who frequently get nauseous
Management of Nausea: N2O concentration should be decreased .5-1
LPM for 60 sec Patients then should be asked how he/she feels
 Nausea
Signs of Vomiting: Sweating, cold clammy hands, pallor of
skin, increased salivation, active swallowing.
Management of Vomiting
Turn off N2O and turn on 100% O2
If vomiting occurs remove the nasal mask and hood
Place pt on his/her side; lower head and elevate feet
After vomiting replace the nasal mask and give 100% O2
for 5 minutes
 Other Symptoms of Over sedation
Excessive Perspiration
Nitrous oxide causes peripheral vasodilation which will cause flushing of the skin
Perspiration alone is okay
Perspiration with blood pressure down or heart rate up terminate Nitrous oxide
and give 100% Oxygen
Behavioral Problems
Authoritarian type personality may fight the effects of N2O and be difficult to
manage
Over-sedation may cause vivid dreaming and excessive movement by the patient
Always titrate N2O
Always observe the patient; Communicate!
Shivering
Rare, may occur after long procedure; due to hypothalamic heat control
mechanism triggered and vasoconstriction to increase body temperature
Reassure pt and place a blanket on the pt
 Nitrous notes
Provider should be enthusiastic and confident that
experience will be positive; this attitude will be transferred
to pt;
Tell the pt that they should be comfortable at all times and
if not to inform or signal provider, especially if feel nausea.
As administer N2O ask pt periodically how feel not what
feel; don’t tell them before hand specific signs that they
should experience.
Minimize talking to pt; talking reduces N2O concentration.
The best way to determine the proper level of sedation is
to begin treatment and directly and closely observe the pt’s
response.
Most drugs have a 30% placebo effect.
 Nitrous notes
Clinical signs vary between patients; Never leave the
patient alone, maintain contact even if only verbal
Sedation can be tailored to the anxiety needs of the patient
Terminate flow of N2O at the end of the procedure; DO NOT
tell the patient; record flow rate during tx of N2O and O2 in
liters (L)
100% O2 for a min of 3-5 minutes after turning of the N2O
Take vital signs BP, P, O2 saturation and record ie always
before and after procedure
Discharging the patient – NOT all patients will recover
enough to permit discharge from the office without an
escort.
 Nitrous notes

Trieger test- measures the degree of motor dysfunction

by connecting the dots. Can be used as a pre-op post-op
sedation test to determine psychomotor coordination
 Recovery
Generally, recovery is a mirror image of calm, tranquil induction
Pt returning to original emotional state as well as recovering from
pharmacologic actions of N2O
Potential exists for post op symptoms such as lethargy, headache, and
nausea to occur; remedy is post op O2
Pts should be alert and oriented
Vital signs should be stable and within acceptable limits
Mental and psychomotor impairment can occur with N2O
Poor psychomotor coordination of pt is an indication recovery is
incomplete
To date, there are no references to cases in which pts who were
dismissed after N2O-O2 sedation harmed or injured themselves or
others because of incomplete recovery
Use of Treiger test may be helpful in determining pt’s psychomotor
coordination and recovery
Following N2O-O2 sedation a fully recovered pt does not need an escort
 Pt Progress and Tx Notes
We live in a litigious society; recording meticulous pt progress and tx notes is
imperative and very important, especially if you are ever brought up for
malpractice or subpoenaed to appear in court of law
Notes should be thorough and brief; what to record:
Date; Pt’s age; Indications for N2O-O2 sedation
Informed consent verbal only; verbal and written; parent/caregiver
Med Hx review; no significant findings; areas of concern; ASA classification;
medical consult or clearance required; meds/drugs needed and when taken ie
premedication with antibiotics
Procedural data: Vitals > BP; P; Respiration; SpO2 saturation all before and post tx
Start time of N2O-O2 administration
Flow rate (amount or concentration of N2O and O2 administered in liters (L) % of
N2O administered
End time of administration (start and end gives duration of drug administration)
Administered 100% O2 for ____min (min of 5 min)
Recovery (pt comments)
Adverse reactions if any recorded (comments)
Name(s) third party in tx room
Clinician’s signature
 Constant Liter Flow Technique
Constant O2 flow rate, e.g., 5 LPM
Increase N2O then decrease O2 same amount each time so
total flow of gas remains constant
Maximum 2.5 L N2O, 2.5 LO2 50%
Advantage
Smaller volumes of gases employed
Less costly
Less contamination of exhaled N2O
Disadvantage
Increments of nitrous are fixed, easier to over sedate pt.
Oxygen will hold at 2.5 LPM but it is possible to increase
Nitrous above 2.5 LPM which would be more than 50%
 Constant O2 Flow Technique
Establish O2 flow rate
Increase N2O flow rate incrementally while maintaining a
constant O2 flow
Advantages
Slightly easier to use by adjusting only the N2O valve
Each increase of N2O flow raises the percent of N2O slower
than with the constant liter flow; less likely to overdose
Easier to use with patient having smaller minute
respiratory volumes
Disadvantages
Can be costly by using larger volumes of gases
Using larger volumes of N2O increase environmental
contamination
 Cleaning Equipment
After each use:
Autoclave nasal hood insert (mask)
Wipe down nasal hood housing and tubes with
glutaraldehyde
Discard disposable nasal hood or save for patients next
visit
 N2O in the air of the Dental office
Variety of sources cause for contamination of dental
operatory
Mouth breathing especially children
Exhaling valve
Leakage around the nasal hood
Poor ventilation
Worn, cracked equipment hoses and reservoir bag
Air conditioning unit recirculates the same air
Elimination of N2O from the air
N2O becomes a pollutant of the ambient air whenever it
is used
Best way to reduce N2O air contamination:
Testing equipment (Soapy water on tube connections)
Venting of waste gases
Scavenging nasal hoods
Attached vacuum flow meter - ideal flow rate is 45 LPM
Decreases N2O contamination by 97%
Air sweep
Minimize patient conversation
Air monitoring- every four months
 Long term Effects of N2O
Usually related to chronic long term use, and effects are usually reversible
Severe bone marrow depression
Peripheral sensory neuropathy of the hands, legs and feet
Complete loss of sensation in the toes
Reduced tactile sensation in the hands
Nitrous is the single most commonly used anesthetic agent in the operating
room

Complications noted in Anesthesiologists and other operating room

personnel:
Higher rates of spontaneous abortion
More fetal malformations
Increased hepatic disease (Halothane)
Increased renal disease (Methoxyflurane)
Increased neurologic symptoms (headache, fatigue, irritability)
Increased PH
 CHAPTER 64B5-14 ANESTHESIA

(6) Nitrous-oxide inhalation analgesia – The

administration by inhalation of a combination of
nitrous-oxide and oxygen
producing an altered level of consciousness that
retains the patient’s ability to independently and
continuously maintain an airway and respond
appropriately to physical stimulation or verbal
command.
 CHAPTER 64B5-14
ANESTHESIA
(10) Minimal Sedation (anxiolysis) – The perioperative use of
medication to relieve anxiety before or during a dental procedure
which does not produce a depressed level of consciousness and
maintains the patient’s ability to maintain an airway independently
and to respond appropriately to physical and verbal stimulation. This
minimal sedation shall include the administration of a single enteral
sedative or a single narcotic analgesic medication administered in
doses appropriate for the unsupervised treatment of anxiety and
pain. If clinically indicated, an opiod analgesic may also be
administered during or following a procedure if needed for the
treatment of pain. Except in extremely unusual circumstances, the
cumulative dose shall not exceed the maximum recommended dose
(as per the manufacturers recommendation). It is understood that
even at appropriate doses a patient may occasionally drift into a state
that is deeper than minimal sedation. As long as the intent was
minimal sedation and all of the above guidelines were observed, this
shall not automatically constitute a violation. A permit shall not be
 64B5-14.002 Prohibitions .

(6) The only agents that can be used for

inhalation analgesia pursuant to Rule
64B5-14.003, F.A.C., below are nitrous-oxide
and oxygen.
 64B5-14.002 Prohibitions .
(9) A hygienist certified by the board to administer local
anesthesia shall not administer local anesthesia to a patient
sedated by general anesthesia, deep sedation, conscious
sedation, or pediatric conscious sedation. If a dentist has
administered nitrous-oxide to the patient, the certified dental
hygienist may administer local anesthesia under the direct
supervision of the supervising dentist. A patient who has been
prescribed a medical drug by their licensed health care
provider for the purposes of life functions may be
administered local anesthesia by the certified dental hygienist
under the direct supervision of the supervising dentist. If,
however, the medical drug is prescribed or administered for
the purposes of a dental procedure which is intended to
induce minimal sedation (anxiolysis), the hygienist may not
administer local anesthesia to the patient.
 64B5-14.003 Training, Education, Certification, and
Requirements for Issuance of Permits

(b) A dentist utilizing nitrous-oxide inhalation analgesia and

such dentist’s assistant/dental hygienist personnel shall be
certified in an American Heart Association or American Red
Cross or equivalent Agency sponsored cardiopulmonary
resuscitation course at the basic life support level to include
one man CPR, two man CPR, infant resuscitation and
obstructed airway with a periodic update not to exceed two
years. Starting with the licensure biennium commencing on
March of 2000, a dentist and all assistant/dental hygienist
personnel shall also be trained in the use of either an
Automated External Defibrillator or a defibrillator and
electrocardiograph as part of their cardiopulmonary
resuscitation course at the basic life support level. In addition
to CPR certification, a dentist utilizing pediatric conscious
sedation must be currently trained in ACLS (Advanced Cardiac
ATLS (Advanced Trauma Life Support), or PALS (Pediatric Advanced
Life Support).
(c) A dentist who regularly and routinely utilized nitrous-oxide
inhalation analgesia on an outpatient basis in a competent and
efficient manner for the three-year period preceding January 1, 1986,
but has not had the benefit of formal training outlined in
subparagraphs 1. and 2. of paragraph (4)(a) above, may continue such
use provided the dentist fulfills the provisions set forth in paragraph
3. of paragraph (4)(a) and the provisions of paragraph (b) above.
(d) Nitrous oxide may be used in combination with a single dose
enteral sedative or a single dose narcotic analgesic to achieve a
minimally depressed level of consciousness so long as the
manufacturer’s maximum recommended dosage of the enteral agent
is not
exceeded. Nitrous oxide may not be used in combination with more
than one (1) enteral agent, or by dosing a single enteral agent in
excess of the manufacturer’s maximum recommended dosage unless
the administering dentist holds a conscious sedation permit issued in
accordance with subsection 64B5-14.003(2), F.A.C., or a pediatric
conscious sedation permit issued in accordance with Rule
 64B5-14.004 Additional Requirements

(2) Dental Assistants, Dental Hygienists – Dental assistants and

dental hygienists may monitor nitrous-oxide inhalation
analgesia under the direct supervision of a dentist who is
permitted by rule to use general anesthesia, conscious
sedation, pediatric
conscious sedation, or nitrous-oxide inhalation analgesia,
while rendering dental services allowed by Chapter 466, F.S.,
and under the following conditions:
(a) Satisfactory completion of no less than a two-day course of
training as described in the American Dental Association’s
“Guidelines for Teaching and Comprehensive Control of Pain
and Anxiety in Dentistry” or its equivalent; and
 64B5-14.004 Additional
Requirements .
(b) Maintenance of competency in cardiopulmonary
resuscitation evidenced by certification in an American Heart
Association or American Red Cross or equivalent Agency
sponsored cardiopulmonary resuscitation course at the basic
life support level to include one man CPR, two man CPR, infant
resuscitation and obstructed airway, with a periodic update
not to exceed two years.
(3) After the dentist has induced a patient and established the
maintenance level, the assistant or hygienist may monitor the
administration of the nitrous-oxide oxygen making only
adjustments during this administration and turning it off at the
completion of the dental procedure.
 64B5-14.006 Reporting Adverse
Occurrences
(4) Certified Registered Dental Hygienists: Any CRDH
administering local anesthesia must notify the Board, in
writing by registered mail within forty-eight hours (48 hrs.) of
any adverse occurrence that was related to or the result of the
administration of local anesthesia. A complete written report
shall be filed with the Board within thirty (30) days of the
mortality or other adverse occurrence. The complete written
report shall, at a minimum, include the following:
(a) The name, address, and telephone number of the
supervising dentist;
(b) The name, address, and telephone number of the patient;
(c) A detailed description of the dental procedure;
(d) A detailed description of the preoperative physical
condition of the patient;
(e) A detailed list of the local anesthesia administered and the
dosage of the local anesthesia administered