Nitrous Oxide Sedation
William M. Clark, M.D.,M.B.A., M.S.
Pain Terms
• Allodynia – ordinary non-painful sensations are experienced as painful
sensations
• Hyperalgesia – pain sensations are intensified and amplified
• Hypoalgesia – decrease sense of pain
• Analgesia – a neurologic or pharmacologic
state in which painful stimuli are so moderated
that they are perceived but do not hurt.
• Anesthesia – a loss of sensation due to
pharmacologic depression of nerve function
• Paresthesia – an abnormal sensation; such as burning, pricking, ticking
or tingling
• Dysesthesia- (1) impairment of sensation short of anesthesia (2) a
condition in which a disagreeable sensation is produced by ordinary
stimuli; caused by lesions of the sensory pathways, peripheral or
central (3) abnormal sensation experienced in the absence of stimuli
What are the Types of Anesthesia
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General Anesthesia
Regional Anesthesia
Local Anesthesia
Sedation
General (Inhalation or Intravenous) –
produces an unconscious state. In this
state the person is a. unaware of what is
happening b. pain-free c. *immobile d.
free from memory of the period of time
during when her or she is anesthetized
* The skeletal muscle reflexes continue to
work from an unconscious state – so must
be paralyzed (Neuromuscular blocking)
Neuromuscular Blocking
• Due to reflex activity of skeletal muscles – certain
blocking agents must be administered during
general anesthesia. If no blocking agent is used
the skeletal muscles will reflexively contract upon
painful stimuli.
• Regional Anesthesia– A region of the
body is anesthetized without the person
becoming unconscious – for example a
spinal block or epidural.
• Local Anesthesia – numbing a small area
by injecting a local anesthetic under the
skin or mucous membrane where the
incision or other procedure (extractioncleaning) will occur.
• Sedation – analgesia produced
pharmacologically by general anesthesia
drugs given in smaller doses – twilight
sleep (intravenous valium, Opioids and
other agents).
• Opioids – Morphine was isolated from opium
in 1805 and was quickly tried as a intravenous
anesthetic. The morbidity and mortality
associated with its use in high doses caused
many to avoid its usage. In 1939 Meperidine
(Demerol) was introduced and a concept of
“balanced anesthesia” began. Thiopental was
used for induction- nitrous oxide for amnesiaMeperidine (or any Opioid) for analgesia and
curare for muscle relaxation.
• Sodium thiopental, better known as Sodium
Pentathol is a rapid-onset short-acting barbiturate
general anaesthetic
Nitrous Oxide is an Inhalation
Anesthesia
• Because it is – let’s review some respiratory
anatomy and physiology
• Because it is an anesthesia we also need to
briefly review some neurological data
Respiratory Anatomy
General Respiratory Anatomy
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Nose
Mouth
Pharynx
Trachea
Mainstem bronchi – primary bronchi (lung bronchi)
Secondary bronchi – lobar bronchi
Tertiary bronchi – segmental bronchi- goes to bronchopulmonary segments
Bronchioles – no longer cartilage in the walls
Terminal bronchioles – last conduit – non- diffusion
(exchange) region
Respiratory bronchioles – first diffusion (exchange) region
Alveolar Ducts
Alveolar Sacs
Alveolus
Epicranius,
frontal belly
Root and
bridge of
nose
Dorsum nasi
Ala of nose
Apex of nose
Naris (nostril)
Philtrum
(a) Surface anatomy
Figure 22.2a
Gingivae (gums)
Palatine raphe
Hard palate
Soft palate
Uvula
Palatine tonsil
Sublingual fold
with openings of
sublingual ducts
Vestibule
Lower lip
Upper lip
Superior labial
frenulum
Palatoglossal arch
Palatopharyngeal
arch
Posterior wall
of oropharynx
Tongue
Lingual frenulum
Opening of
submandibular duct
Gingivae (gums)
Inferior labial
frenulum
(b) Anterior view
Figure 23.7b
Cribriform plate
of ethmoid bone
Sphenoid sinus
Posterior nasal
aperture
Nasopharynx
Pharyngeal tonsil
Opening of
pharyngotympanic
tube
Uvula
Frontal sinus
Nasal cavity
Nasal conchae
(superior, middle
and inferior)
Nasal meatuses
(superior, middle,
and inferior)
Nasal vestibule
Nostril
Oropharynx
Palatine tonsil
Isthmus of the
fauces
Hard palate
Soft palate
Tongue
Lingual tonsil
Laryngopharynx
Esophagus
Trachea
(c) Illustration
Larynx
Epiglottis
Vestibular fold
Thyroid cartilage
Vocal fold
Cricoid cartilage
Thyroid gland
Hyoid bone
Figure 22.3c
Respiratory Physiology
Review of Terms
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External Respiration versus Internal Respiration
Respiratory Volumes
Breath Rate
Minute Ventilation
Respiratory Zone
Gas Exchange Across the Respiratory Zone
External Respiration versus Internal
Respiration
• External Respiration – taking oxygen from the
atmosphere and putting it into the blood –
also taking carbon dioxide from the blood and
putting it into the atmosphere.
• Internal Respiration – taking carbon dioxide
(waste product made by cells) from the cell
and putting it into the blood and taking
oxygen from the blood and putting it into the
cells.
Respiratory Volumes
• Used to assess a person’s respiratory status
– Tidal volume (TV) – volume you normally breath
in and out
– Inspiratory reserve volume (IRV) – That extra
amount of air you could breath in over that you
brought in for tidal volume
– Expiratory reserve volume (ERV) That extra
amount of air you could breath out over that you
breathed out for tidal volume
– Residual volume (RV) – That air in your lungs you
cannot breath out – unless some blow to the
chest occurs (getting the wind knocked out of you)
Respiratory
capacities
Total lung capacity (TLC)
6000 ml
4200 ml
Vital capacity (VC)
4800 ml
3100 ml
Inspiratory capacity (IC)
3600 ml
2400 ml
Functional residual
capacity (FRC)
2400 ml
1800 ml
Maximum amount of air
contained in lungs after a
maximum inspiratory effort:
TLC = TV + IRV + ERV + RV
Maximum amount of air that
can be expired after a maximum inspiratory effort:
VC = TV + IRV + ERV
Maximum amount of air that
can be inspired after a normal
expiration: IC = TV + IRV
Volume of air remaining in
the lungs after a normal tidal
volume expiration:
FRC = ERV + RV
(b) Summary of respiratory volumes and capacities for males and females
Figure 22.16b
Inspiratory
reserve volume
3100 ml
Tidal volume 500 ml
Expiratory
reserve volume
1200 ml
Residual volume
1200 ml
Inspiratory
capacity
3600 ml
Vital
capacity
4800 ml
Total lung
capacity
6000 ml
Functional
residual
capacity
2400 ml
(a) Spirographic record for a male
Figure 22.16a
Breath Rate
• Normal breath rates for an adult person at
rest range from 12 to 20 breaths per minute.
Respiration rates over 25 breaths per minute
or under 12 breaths per minute (when at rest)
may be considered abnormal.
Minute Ventilation
• Minute ventilation – the amount of air
brought into and out of the lungs in one
minute (breath rate per minute times tidal
volume) – average breath rate per minute is
12 – 20 breaths per minute – for example 12
BPM x 500cc = 6 Liters/minute
Respiratory System Zones
• Conducting Zone – where no gas exchange
can occur with the blood – membranes too
thick to perform diffusion of gases
• Conducting Zone Location– Nose and/or
mouth down to end of terminal bronchioles
• Respiratory (Exchange) Zone – where gas
exchange can occur with the blood –
membranes thin enough for diffusion
• Respiratory Zone Location – starts at
respiratory bronchioles and extends to the
very bottom of the respiratory system (Alveoli)
Gas Exchange Across Respiratory Zone
• The respiratory zone is the total area in the
respiratory system that exchange of air with the
blood can occur. In the average person this is
about 70 meters squared of surface area – or
about the size of a tennis court. Under normal
circumstances a person can diffuse oxygen at a
rate of 21 ml/min/mm Hg Since the pressure
across the respiratory membrane is around 11
mm Hg – the value is 11 x 21 = 230 ml of Oxygen
diffusing through the area in one minute – this is
equal to rate at which the body uses oxygen.
Ideal Gas Equation
PV = nRT
• P – pressure
• V- Volume
• n – number of moles
• R – gas rate constant
• T - temp
Boyle’s Law
• There is an inverse Relationship
between pressure and volume of
a gas in a closed container
• The larger the volume of the
container with gas in it – the
lower the pressure and vice-versa
Dalton’s Law
of Partial pressures
• A gas in a mixture of gases will exert a
pressure independent of the other
gases in the mixture and in accordance
with the percent of the gas present
• Thus to get the partial pressure of gases
in our atmosphere you multiply the
Atmospheric Pressure times the gas
percent present in the atmosphere
Partial Pressures of Gases in the
Atmosphere
• If we consider that we live at sea level the
Atmospheric pressure is 760 mm of mercury
pressure per cubic inch
• The atmosphere is roughly 79% Nitrogen, 21%
Oxygen and .04% Carbon Dioxide
• .79 x 760 = 600 mm Hg partial pressure for N2
• .21 x 760 = 160 mm Hg partial pressure for O2
• .0004 x 760 = .30 mm Hg partial pressure for CO2
Henry’s Law
• The amount of a gas that will
dissolve in a liquid depends on the
partial pressure of the gas above
the liquid and the solubility
coefficient of that gas for that
liquid.
• Dissolved amount = PP of gas x
*solubility coefficient
Solubility coefficients of gases with relative comparison to O2
• Gas
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Solubility coefficient
Relative Magnitude
with O2
Oxygen
Carbon Dioxide
Nitrogen
Nitrous Oxide
Halothane
Carbon Monoxide
0.024
0.57
0.012
0.47
2.4
0.018
Note – Nitrous Oxide gets into blood better than N2
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23
0.53
20
100
0.81
Neurobiology
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What is a nucleus, tract, ganglion and nerve?
What is a brain Center?
What is a Cranial Nerve versus a Spinal Nerve?
What are some important brain centers in
regards to the Dental Profession?
• What are some important nerves in regards to
the Dental Profession?
• A nucleus is a group of neuron cell bodies in
the central nervous system – dedicated to a
certain function.
• A tract is a group of fibers (axons and/or
dendrites) in the central nervous system.
• A nerve is a group of neuron fibers in the
peripheral nervous system.
• A ganglion is group of neuron cell bodies in
the peripheral nervous system.
A brain center is a nucleus in the central
nervous system – that performs the said
function.
Cranial Nerves versus Spinal Nerves
• A cranial nerve originates from the brain.
There are 12 of them on each side of the brain
• A spinal nerve originates from the spinal cord.
There are 31 of them on each side of the
spinal cord.
Some important Centers
• The breathing center is composed of several nuclei
in the Pons and medulla oblongata.
• The gag reflex also termed the pharyngeal reflex is
centered in the medulla and consists of reflexive
motor response of pharyngeal elevation and
constriction with tongue retraction in response to
sensory stimulation of the pharyngeal wall, posterior
tongue, tonsils or faucal pillars. The gag reflex
involves afferent fibers from the glossopharyngeal
nerve (IX) and some from the vagus (x) with efferent
motor fibers to the pharynx, soft palate and tongue
from the vagus.
• Nausea and Vomiting are coordinated by the
brainstem and is effected by neuromuscular responses
in the gut, pharynx, and thoraco-abdominal wall. The
mechanisms underlying nausea are poorly understood
but likely involve the cerebral cortex, as nausea
requires conscious perception.
• Coordination of Emesis – Several brainstem nuclei
initiate emesis including the tractus solitarius, dorsal
vagal and phrenic nuclei, and medullary nuclei that
regulate respiration; nuclei that control pharyngeal,
facial, and tongue movements coordinate the initiation
of emesis. The neurotransmitters involved in this
coordination are uncertain; however, roles for
neurokinin, serotonin and vasopressin are postulated.
Important Cranial Nerves in the Dental
Professions
• Cranial Nerve V – Sensory to Face
• Cranial Nerve VII – Motor to Face
Cranial Nerve V: The Trigeminal Nerves
SENSORY TO THE FACE
• Largest cranial nerves; fibers extend from pons to face
• Three divisions
– Ophthalmic (V1) passes through the superior orbital fissure
– Maxillary (V2) passes through the foramen rotundum
(Upper Teeth)
– Mandibular (V3) passes through the foramen ovale (Lower
teeth)
• Convey sensory impulses from various areas of the face
(V1) and (V2), and supplies motor fibers (V3) for
mastication
Table 13.2
Table 13.2
FACIAL NERVE (Cranial Nerve VII)
Table 13.2
Table 13.2
Brief Discussion of Pain
• Mechanical, thermal and chemical stimuli
stimulate pain receptors. The fast pain
receptors signal thermal and mechanical
(tooth pulling and/or cleaning) stimuli. All
three stimuli can stimulate the slow pain
receptors. Chemical substances that stimulate
pain receptors are bradykinin, serotonin,
histamine, potassium ions, acids, acetylcholine
and proteolytic enzymes. Fast pain is more of
a localize pain that can be pin point located by
the person – whereas slow pain is more
diffuse.
Review of Neural Anatomy as it relates to Pain
• Local pain receptor – termed a nocioceptor
• Afferent (sensory) neuron – fast pain travels via alpha (big myelinated
neurons) into the dorsal horn of the spinal cord – slow pain travels via
type C (thin and non-myelinated) neurons into the spinal cord
• Spinal Cord – in the spinal cord the afferent neurons synapse at
different regions of the dorsal horn depending on slow versus fast –
slow fibers pick up a short interneuron – then synapse on a third order
neuron which immediately crosses over the cord to the other side then
travels up (ascending tract) the spinal cord terminating in a region of
the brain. Fast fibers pick up a second order neuron that crosses the
cord to the other side and then travels up (ascending tract) the spinal
cord terminating in a region of the brain. The tract taking the signal to
the brain (in both slow and fast) is termed the “lateral spinothalamic
tract”.
• Brainstem and Thalamus – for slow pain the spinothalamic tract
neurons terminate in Reticular fibers in the brainstem and some ( ¼ to
1/ ) go to the Thalamus – for fast fibers some go to the brainstem but
10
most go directly to the Thalamus.
• Cortex – Post central gyrus location – place in brain that give
experience and location to the pain
Lateral
spinothalamic
tract (axons of
second-order
neurons)
Medulla oblongata
Pain receptors
Cervical spinal cord
Lumbar spinal cord
Axons of first-order
neurons
Temperature
receptors
(b) Spinothalamic pathway
Figure 12.34b (2 of 2)
Perceptual level (processing in
cortical sensory centers)
3
Motor
cortex
Somatosensory
cortex
Thalamus
Reticular
formation
Pons
2 Circuit level
(processing in
Spinal
ascending pathways) cord
Cerebellum
Medulla
Free nerve
endings (pain,
cold, warmth)
Muscle
spindle
Receptor level
(sensory reception Joint
and transmission
kinesthetic
to CNS)
receptor
1
Figure 13.2
Perception of Pain
• Warns of actual or impending tissue damage
• Stimuli include extreme pressure and
temperature, histamine, K+, ATP, acids, and
bradykinin
• Impulses travel on fibers that release
neurotransmitters glutamate and substance P
• Some pain impulses are blocked by inhibitory
endogenous opioids
What are our natural pain reducing
chemicals?
• Endorphins – Endorphins (or more correctly
Endomorphines) are endogenous opioid biochemical
compounds. They are polypeptides produced by the
pituitary gland and the hypothalamus in vertebrates,
and they resemble the opiates in their abilities to
produce analgesia and a sense of well-being. In other
words, they might work as "natural pain killers." Using
drugs may increase the effects of the endorphins.
• Enkephalins - An enkephalin is a pentapeptide ending
with either leucine ("leu") or methionine ("met").
Both are products of the proenkephalin gene.
• Enkephalins play many roles in regulating pain.
What are our natural pain producing
chemicals?
• Chemical substances that stimulate pain
receptors are bradykinin, ATP, serotonin,
histamine, potassium ions, acids, acetylcholine
and proteolytic enzymes.
Melzack and Walls Gate Theory
• Light touch can evoke pain if the person has hyperalgesia. However,
pain evoked by activity in nociceptors can also be reduced by
simultaneous activity in low-threshold mechanoreceptors (
fibers). Presumably this is why it feels good to rub the skin around
your shin when you bruise it. This also may explain electrical
treatment for some kinds of chronic, intractable pain.
• In 1965, Ronald Melzack and Patrick Wall, proposed a hypothesis to
explain the above mentioned phenomenon. Their gate theory of
pain proposes that certain neurons of the dorsal horns, which
project an axon to the spinothalamic tract, are excited by both
large-diameter sensory axons and unmyelinated pain axons. The
projection neuron is also inhibited by an interneuron, and the
interneuron is both excited by the large sensory axon and inhibited
by the pain axon. By this arrangement, activity in the pain axon
alone maximally excites the projection neuron, allowing nociceptive
signals to rise to the brain. However, if the large mechanoreceptive
axon fires concurrently, it activates the interneuron and suppresses
nociceptive signals.
• It is not completely clear exactly how general
anesthetics work at a cellular level, but it is
speculated that general anesthetics affect the
spinal cord (resulting in some degree of
immobility), the brain-stem reticular
activating system (resulting in
unconsciousness) and the cerebral cortex
(seen in changes in electrical activity on an
encephalogram).
• In general anesthesia of the inhalation
method – a minimum alveolar concentration
of the anesthetic gas must be reached – if
intravenous a minimum blood concentration.
Minimum (Alveolar or Blood)
Concentrations
• A minimum concentration – for anesthetic
purposes is the partial pressure of the
anesthetic gas or blood concentration
respectively that must be reached for 50
percent of humans to not move when
subjected to a painful stimulus.
• General anesthesia does though cause the
respiratory (Breathing Centers) centers in the
pons and medulla oblongata plus the
Reticular Activating System to be so
depressed that the patient no longer can
spontaneously breathe and thus must be
intubated and placed on a breathing device.
Respiratory Breathing Centers
Pons
Medulla
Pontine respiratory centers
interact with the medullary
respiratory centers to smooth
the respiratory pattern.
Ventral respiratory group (VRG)
contains rhythm generators
whose output drives respiration.
Pons
Medulla
Dorsal respiratory group (DRG)
integrates peripheral sensory
input and modifies the rhythms
To inspiratory
generated by the VRG.
muscles
Diaphragm
External
intercostal
muscles
Figure 22.23
Reticular Activating System
The name given to part of the brain (the reticular
formation and its connections) believed to be the
center of arousal and motivation in animals
(including humans). The activity of this system is
crucial for maintaining the state of consciousness.
It is situated at the core of the brain stem
between the myelencephalon (medulla
oblongata) and mesencephalon (midbrain).
• It is involved with the circadian rhythm; damage
can lead to permanent coma. It is thought to be
the area affected by many psychotropic drugs.
General anaesthetics work through their effect on
the reticular formation.
Reticular Formation: RAS and Motor
Function
• RAS (reticular activating system)
– Sends impulses to the cerebral cortex to keep it
conscious and alert
– Filters out repetitive and weak stimuli (~99% of all
stimuli!)
– Severe injury results in permanent
unconsciousness (coma)
Reticular Formation: RAS and Motor
Function
• Motor function
– Helps control coarse limb movements
– Reticular autonomic centers regulate visceral
motor functions
• Vasomotor
• Cardiac
• Respiratory centers
Radiations
to cerebral
cortex
Visual
impulses
Auditory
impulses
Reticular formation
Ascending general
sensory tracts
(touch, pain, temperature)
Descending
motor projections
to spinal cord
Figure 12.19
For almost all dental procedures (except some
more radical oral surgery procedures) –
general anesthesia is not needed. It would be
unnecessary and cumbersome – in that the
endotracheal tube or endonasal tube would
interfere with visualization and operation
within the oral cavity.
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Some Facts to Know when Using an
Inhalation Anesthesia
How fast does the gas reach a certain
alveolar concentration
How fast does it enter the blood
How fast does it clear from the blood
How is it eliminated from the body
What side effects does the
anesthesia have
Nitrous Oxide
• Not easily dissolved in the blood
• All vital reflexes stay intact
• If given properly does not affect the
heart, blood pressure, liver or kidneys
• Minimally absorbed by body tissues
• Good elimination
Nitrous Oxide (N2O)
• Produced from ammonium nitrate when heated
to 250°C
• Refrigerated and stored till transferred to facility
• Not itself flammable but does support
combustion
• 1.50 times heavier than air
• Sweet smelling and colorless
• Remains unchanged in blood – is not metabolized
• Body tissues absorb very little of the NO – thus
only have to use small quantities to reach
required blood concentrations
• Insoluble agents, such as nitrous oxide, are
taken up by the blood (and by other body
tissues) less avidly than soluble agents, such
as halothane. As a consequence, the alveolar
concentration of nitrous oxide rises faster
than that of halothane, thus induction is faster
for nitrous oxide. Clinical action generally
occurs in 3 to 5 minutes.
• This can be viewed by a comparison of the
partition coefficients
Partition Coefficients
• Nitrous oxide will rapidly replace any Nitrogen
(N2) molecules in the body because of a major
difference in their pressure gradients.
• Nitrogen occupies air-filled cavities and can be
found in areas with rigid or non-rigid
boundaries. Pressures may increase
temporarily in bony areas such as sinuses and
middle ear complexes, and volume may
increase in non-rigid areas such as the bowel
or pleural cavity.
• Nitrous oxide is not stored in the body for any
significant time. It is not metabolized by the
liver at all. A miniscule amount is metabolized
by specific bacteria in the GI tract.
• When N2O flow to a patient is terminated, the
molecules exit very quickly back through the
respiratory tract. Recovery is as rapid as
induction.
• Nitrous Oxide has anxiolytic and analgesic
properties. It can calm the nerves – take the
edge off
• Tremendous calming effect on the gag reflex
The dental patient needs to only be in a highly
sedative state (deep analgesia) – like a
twilight sleep. If more anesthesia needs to be
given then a combination of first high level
sedation with local anesthesia would be
sufficient. Thus- the nitrous oxide therapy
will be high level sedation type anesthesia –
with alveolar concentration staying wellbelow the minimum alveolar concentration
as required in general inhalation anesthesia.
Stages of Anesthesia
Stage I – Analgesia
Stage II – Delirium and Excitement
Stage III – Light surgical anesthesia
Stage 4 – Deep surgical anesthesia
Look at The Eyes
• There are indicators as to how sedate a
patient is – one is the eyes – others are
respirations – body movements and others
• Active blinking and rapid eye movement say
that the patient is not sedate enough
• Eye movement slow and see a glazed look –
then sedation is more appropriate
Oversedation
Most often from operator error
Symptoms
• Patient begins to feel uncomfortable in a general
manner
• Patient may feel a detached out-of-body
experience
• Some say they cannot move or communicate
• Drowsy
• Dizzy
• Nauseated
• Warm body temperature
Signs
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Slur words
May not make verbal sense
Laugh uncontrollably
May become agitated, violent, combative –
(Stage 2 of Anesthesia)
• Vomiting – definitely associated with
oversedation
• Concern – Aspiration of vomitus
Don’t Let The Patient Get to the Third
and subsequent Level of Anesthesia
• Third and fourth levels are the levels in which
operating room procedures are performed
• The patient at these stages have inactive
laryngeal and pharyngeal reflexes and cannot
breath independently.
Contraindications
• No absolute contraindications
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A few relative contraindications
Patients that are phobic or have strong controlling personalities
Patients who try to fight the sedating properties of the drug
If patient is alcohol intoxicated
Some that are under psychiatric or psychologic care
Persons who do not have the mental capability of understanding
the drugs effect or who cannot communicate signs and symptoms
to the operator for monitoring purposes
Women in the first trimester of pregnancy
Postpone if the patient has a cold, sinus infection, allergy-related
symptoms or any condition that affects air flow through the
respiratory system
COPD patients
Pressure increases in the middle ear
Recovery
• At the end of the procedure – you will allow
the patient to breath 100% O2
• Nitrous oxide exits fast and unchanged
through the respiratory system
One Possible Recovery Problem????
Diffusion Hypoxia
What is Diffusion Hypoxia?
• When the practitioner discontinues administration of
nitrous oxide (turns of the N2O) the diffusion gradient from
the machine is no longer there – thus for a moment there is
a higher concentration in the lungs than that coming in
from the machine
• Thus since (1) N2O does not dissolve in the blood well thus
keeping a high concentration in the alveoli and (2) is not
changed (metabolized) in the body – IT BEGINS TO QUICKLY
RUSH OUT FROM THE LUNGS
• It rushes out faster than O2 can come in - thus crowding out
the O2 coming in (diluting it and temporarily dropping the
entering O2 partial pressure)
• This event usually causes no problem – but the practitioner
must keep the 100% O2 going in order to override the
effect of N2O diffusing out so fast
Schematic Anesthesia Device
Fa – arterial concentration
FA – Alveolar gas concentration
FGF – Fresh Gas Flow from machine
FI – Fraction of Inspired Air which has a concentration depending on the
flow rate of fresh gas from the machine combined with the concentration
of gases coming from (exhaled) from the patient – plus any minimal amount
of gas absorbed by the tubing.
Mock Nitrous Anesthesia Device
Some Adverse Biochemical Actions of N2Othat never occur with levels used in Dentistry
• Nitrous oxide irreversibly oxidizes the cobalt atom
in vitamin B12– thus inhibiting enzymes needing
this vitamin as a coenzyme. These enzymes are
methionine synthetase – which is necessary for
myelin formation and thymidylate synthetase –
needed to make thymine in DNA.
• Prolonged exposure to anesthetic concentrations
of nitrous oxide can result in bone marrow
depression and peripheral neuropathy. Because of
possible teratogenic effects, nitrous oxide is
avoided in patients that are pregnant.
Although Nitrous oxide is insoluble in comparison
to other inhalation agents, it is 35 times more
soluble than nitrogen in blood. Thus it tends to
diffuse into air containing cavities more rapidly
than nitrogen is absorbed by the bloodstream.
• For this reason – patents with an air embolus,
pneumothorax, acute intestinal obstruction, and
other conditions- must avoid nitrous oxide use.
• Because of the effect on nitrous oxide on the
pulmonary vasculature- it should be avoided in
patients with pulmonary hypertension.
Every Drug has its problems –
but
Nitrous Oxide Sedation in Dentistry
has proven to be safe and very
effective