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

• 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 (extraction- cleaning) 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 amnesia- Meperidine (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• Nose• Mouth• Pharynx• Trachea• Mainstem bronchi – primary bronchi (lung bronchi)• Secondary bronchi – lobar bronchi• Tertiary bronchi – segmental bronchi- goes to broncho-pulmonary

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

Figure 22.2a

Epicranius,frontal belly

Ala of nose

Root and bridge of nose

Dorsum nasi

Apex of nose

Philtrum

Naris (nostril)

(a) Surface anatomy

Figure 23.7b

UvulaPalatine tonsil

Sublingual foldwith openings ofsublingual ducts

Tongue

Upper lip

Lower lipVestibule

Gingivae (gums)

Gingivae (gums)

Hard palateSoft palate

Lingual frenulumOpening ofsubmandibular duct

Palatine raphe

Inferior labialfrenulum

Posterior wallof oropharynx

Palatopharyngealarch

Superior labialfrenulumPalatoglossal arch

(b) Anterior view

Figure 22.3c

Sphenoid sinus Frontal sinus

Nasal meatuses(superior, middle,and inferior)

Nasopharynx

Uvula

Palatine tonsilIsthmus of thefauces

Posterior nasalaperture

Opening ofpharyngotympanictube

Pharyngeal tonsil

Oropharynx

Laryngopharynx

Vocal fold

Esophagus

(c) Illustration

Nasal conchae(superior, middle and inferior)

Nasal vestibuleNostril

Nasal cavity

Hard palateSoft palate

Tongue

Lingual tonsil

Epiglottis

Hyoid boneLarynx

Thyroid cartilageVestibular fold

Cricoid cartilageThyroid gland

Trachea

Cribriform plateof ethmoid bone

Respiratory Physiology

Review of Terms

• 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)

Figure 22.16b

Respiratorycapacities

(b) Summary of respiratory volumes and capacities for males and females

Functional residualcapacity (FRC)

Volume of air remaining in the lungs after a normal tidal volume expiration: FRC = ERV + RV

Maximum amount of air contained in lungs after a maximum inspiratory effort: TLC = TV + IRV + ERV + RVMaximum amount of air that can be expired after a maxi-mum inspiratory effort: VC = TV + IRV + ERVMaximum amount of air that can be inspired after a normal expiration: IC = TV + IRV

Total lung capacity (TLC)

Vital capacity (VC)

Inspiratory capacity (IC)

6000 ml

4800 ml

3600 ml

2400 ml

4200 ml

3100 ml

2400 ml

1800 ml

Figure 22.16a

Inspiratoryreserve volume

3100 ml

Tidal volume 500 ml

(a) Spirographic record for a male

Expiratoryreserve volume

1200 ml

Residual volume1200 ml

Functionalresidualcapacity2400 ml

Inspiratorycapacity3600 ml Vital

capacity4800 ml

Total lungcapacity6000 ml

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 Lawof 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

• Gas Solubility coefficient Relative Magnitude

• with O2

• Oxygen 0.024 1• Carbon Dioxide 0.57 23• Nitrogen 0.012 0.53• Nitrous Oxide 0.47 20• Halothane 2.4 100• Carbon Monoxide 0.018 0.81

Solubility coefficients of gases with relative comparison to O2

Note – Nitrous Oxide gets into blood better than N2

Neurobiology

• 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 NervesSENSORY 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

Table 13.2

FACIAL NERVE (Cranial Nerve VII)

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 1/10) go to the Thalamus – for fast fibers some go to the brainstem but most go directly to the Thalamus.

• Cortex – Post central gyrus location – place in brain that give experience and location to the pain

Figure 12.34b (2 of 2)

Axons of first-orderneurons

Temperaturereceptors

Lateralspinothalamictract (axons ofsecond-orderneurons)

Pain receptors

Medulla oblongata

Cervical spinal cord

Lumbar spinal cord

(b) Spinothalamic pathway

Figure 13.2

1

2

3

Receptor level(sensory receptionand transmissionto CNS)

Circuit level(processing inascending pathways)

Spinalcord

Cerebellum

Reticularformation

Pons

Musclespindle

Jointkinestheticreceptor

Free nerveendings (pain,cold, warmth)

Medulla

Perceptual level (processing incortical sensory centers)

Motorcortex

Somatosensorycortex

Thalamus

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.

Figure 22.23

Pons

Pons

Ventral respiratory group (VRG)contains rhythm generatorswhose output drives respiration.

Pontine respiratory centersinteract with the medullaryrespiratory centers to smooththe respiratory pattern.

Medulla

Medulla

To inspiratorymuscles

External intercostalmuscles

Diaphragm

Dorsal respiratory group (DRG)integrates peripheral sensoryinput and modifies the rhythmsgenerated by the VRG.

Respiratory Breathing Centers

Reticular Activating SystemThe 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

Figure 12.19

Visualimpulses

Reticular formationAscending generalsensory tracts(touch, pain, temperature)

Descendingmotor projectionsto spinal cord

Auditoryimpulses

Radiationsto cerebralcortex

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.

Some Facts to Know when Using an Inhalation Anesthesia

1. How fast does the gas reach a certain alveolar concentration

2. How fast does it enter the blood3. How fast does it clear from the blood4. How is it eliminated from the body5. 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 well-below 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 errorSymptoms

• 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• 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 contraindicationsA 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

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 concentrationof gases coming from (exhaled) from the patient – plus any minimal amountof gas absorbed by the tubing.

FA – Alveolar gas concentration

Fa – arterial concentration

Mock Nitrous Anesthesia Device

Some Adverse Biochemical Actions of N2O- that 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