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Nitrous Oxide, From Discovery to Now - IneedCE.com

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green in the United States. When dispensed in a pressurized<br />

tank, the nitrous oxide exists in two forms—gas and<br />

liquid. The pressure of a full tank, regardless of size, will<br />

read approximately 760 psi. Unlike other <strong>com</strong>pressed<br />

gases which exist in only a gas form, the pressure inside<br />

the tank does not decrease with the amount of gas used.<br />

For example, oxygen, which is only in a gas form, will read<br />

approximately 2000 psi for a full tank. When the tank is<br />

50% full, the pressure will read 1000 psi, 25% full will read<br />

500 psi, and so on. <strong>Nitrous</strong> oxide tanks will register 760<br />

psi for as long as a liquid phase exists. When the tank has<br />

been used <strong>to</strong> the point where a liquid phase no longer exists<br />

(after about 75–80% consumption), then the pressure will<br />

start <strong>to</strong> drop. When this occurs, the provider will know<br />

that approximately 20–25% of the tank still remains. If a<br />

more accurate account of the tank’s volume is necessary,<br />

then one can weigh the tank <strong>to</strong> make the determination.<br />

Other important physical properties of the gas include<br />

its partition (solubility) coefficients, some of which are<br />

blood/gas = 0.47, brain/blood = 1.1, fat/blood = 2.3, and<br />

oil/gas = 1.4. The minimum alveolar concentration (MAC)<br />

of nitrous oxide is 104%, which is defined as the minimum<br />

alveolar concentration of the gas necessary <strong>to</strong> render 50% of<br />

patients motionless following a painful surgical stimulus,<br />

such as skin incision. For inhalational agents, both MAC<br />

and the oil/gas coefficient help <strong>to</strong> quantify potency. The<br />

blood/gas coefficient best quantifies uptake, speed of onset<br />

and recovery characteristics.<br />

Physiologic Effects<br />

<strong>Nitrous</strong> oxide is a very weak anesthetic agent (as its MAC<br />

of 104% would indicate) when used alone, and it is unable<br />

<strong>to</strong> produce general anesthesia unless used in hypoxic<br />

mixtures (of 100% or above) under hyperbaric conditions.<br />

Most current administration devices do not allow the delivered<br />

concentrations of nitrous oxide <strong>to</strong> exceed 75–80%. Its<br />

principal use in dentistry is as a mild sedative and analgesic<br />

agent <strong>to</strong> help allay fear and anxiety for phobic patients, and<br />

many times it is used in <strong>com</strong>bination with local anesthesia<br />

as well as other sedative, hypnotic agents. Its analgesic<br />

qualities are quite potent, with a 30–40% delivered concentration<br />

equivalent <strong>to</strong> 10–15 mg. of morphine. In fact,<br />

some EMS services take advantage of these qualities when<br />

transporting acute myocardial infarction patients <strong>to</strong> the<br />

emergency room by administering mixtures of 30% nitrous<br />

oxide with 70% oxygen.<br />

It has minimal effects on either the respira<strong>to</strong>ry or the<br />

cardiovascular system in normal healthy patients, which<br />

adds <strong>to</strong> its safety. As any sedative medication will have<br />

some degree of respira<strong>to</strong>ry depressive properties, nitrous<br />

oxide’s degree is only minimally so, mostly due <strong>to</strong> its lack<br />

of potency. Further, all anesthetic medications have some<br />

degree of myocardial depressant activity, but again, nitrous<br />

oxide’s degree is only minimally so. This is due not only <strong>to</strong><br />

its lack of potency, but also <strong>to</strong> its mild central sympathetic<br />

stimula<strong>to</strong>ry activity, which helps <strong>to</strong> offset its direct myocardial<br />

depressant effects. These effects may be exaggerated,<br />

however, in patients with severe cardiac disease and<br />

function. While nitrous oxide also possesses some mild<br />

peripheral vasodila<strong>to</strong>ry properties, this effect may not be<br />

consistent in all patients.<br />

Its principal use in general anesthesia is as an adjunct or<br />

supplement <strong>to</strong> other, more potent inhalational anesthetics<br />

such as Fluothane®, isoflurane, and enflurane. In this setting,<br />

nitrous oxide’s additive effect can decrease the necessary<br />

concentrations of the other agents, thereby decreasing<br />

some of their negative physiologic effects. In this setting,<br />

nitrous oxide concentrations of 50–60% are routinely used<br />

and can decrease the MAC of the other potent inhalational<br />

agents by as much as half.<br />

Also, for these cases, some physical properties of<br />

nitrous oxide can be advantageous. One such property is<br />

termed the concentration effect. As mentioned above, the<br />

blood/gas partition coefficient is very low (0.47), which<br />

means not much dissolves in blood. However, nitrous oxide<br />

is very diffusible and will saturate the blood and reach an<br />

equilibrium very quickly. This helps <strong>to</strong> explain its very fast<br />

onset and recovery characteristics. When administered in<br />

high concentrations (50–75%), the nitrous oxide is quickly<br />

taken from the alveoli in<strong>to</strong> the pulmonary circulation. Because<br />

this occurs in a very rapid fashion, a relative vacuum<br />

of gas occurs in the alveoli, which acts <strong>to</strong> pull more fresh<br />

gas in<strong>to</strong> the lungs, thereby increasing alveolar ventilation<br />

and increasing the concentration of the administered gas<br />

faster than would otherwise occur. Another phenomenon<br />

called the second gas effect piggybacks upon this property.<br />

This occurs when a more potent gas anesthetic agent is<br />

co-administered with the nitrous oxide. It, <strong>to</strong>o, is virtually<br />

sucked in<strong>to</strong> the lungs at a higher rate and will be taken up<br />

in the pulmonary circulation <strong>to</strong> exert its effect faster than<br />

if it were not co-administered with nitrous oxide. Finally,<br />

just as nitrous oxide is quickly taken up by the bloodstream<br />

during administration, it is also given up quickly by the<br />

blood-stream upon cessation. When the administration of<br />

nitrous oxide is terminated, it quickly diffuses back in<strong>to</strong> the<br />

lungs across the concentration gradient. This happens at<br />

quite a fast pace, which can lead <strong>to</strong> a relative decrease in the<br />

alveolar concentration of other gases such as oxygen. This<br />

can cause diffusion hypoxia. Although this rarely produces<br />

clinical hypoxia, it is prudent <strong>to</strong> administer 100% oxygen <strong>to</strong><br />

patients for about 3–5 minutes following the termination of<br />

nitrous oxide.<br />

As discussed above, nitrous oxide diffuses very rapidly.<br />

In fact, it diffuses more rapidly than many other gases such<br />

as nitrogen. As a result, nitrous oxide tends <strong>to</strong> diffuse across<br />

concentration gradients in<strong>to</strong> air-filled cavities faster than<br />

the nitrogen can diffuse out, which causes the cavity <strong>to</strong> expand.<br />

This can be a problem under certain circumstances.<br />

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