Nitrous Oxide, From Discovery to Now - IneedCE.com
Nitrous Oxide, From Discovery to Now - IneedCE.com
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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