It is a colourless, odourless, heavier than air, noninflammable gas supplied under pressure in steel cylinders. It is nonirritating, but low potency anaesthetic; unconsciousness cannot be produced in all individuals without concomitant hypoxia; MAC is 105% implying that even pure Nitrous oxide cannot produce adequate anaesthesia at 1 atmosphere pressure. Patients maintained on 70% N,O + 30% O, along with muscle relaxants often recall the events during anaesthesia, but some lose awareness completely.
Nitrous oxide is a good analgesic; even 20% produces analgesia equivalent to that produced by conventional doses of morphine. Muscle relaxation is minimal. Neuromuscular blockers are mostly required. Onset of Nitrous oxide action is quick and smooth (but thiopentone is often used for induction), and recovery is rapid, because of its low blood solubility. Second gas effect and diffusion hypoxia occur with Nitrous oxide only. Post-anaesthetic nausea is not marked. It tends to increase sympathetic tone which increases cerebral blood flow and counteracts the weak direct depressant action on heart and circulation.
Nitrous oxide may produce the second gas effect because nitrous oxide diffuses more rapidly across alveolar basement membranes than other gases. The rapid exit of nitrous oxide from the alveoli results in remaining alveolar gases being concentrated, thus accelerating nitrous oxide uptake into the blood and speeding the onset of anesthesia. Minimal Alveolar Concentration (MAC) relates to the potency of volatile anesthetic agents. It is defined as the minimum alveolar concentration of inhaled anesthetic at which 50% of people do not move in response to noxious stimuli. Thus Nitrous oxide is a weak anesthetic inhalational agent but has good analgesic effects. The reversal may occur at the end of anesthesia when nitrous oxide enters the alveoli far more rapidly, causing oxygen dilution within the alveoli and may cause diffusion hypoxia.
Nitrous oxide administration is via inhalation utilizing a simple face mask, laryngeal mask airway, or an endotracheal tube. For surgical procedural sedation and dental procedures, nitrous oxide (30 to 50%) is combined with oxygen.
For general anesthesia, nitrous oxide(50 to 70%) is used. But due to its low potency, it can not be used as a single anesthetic agent; hence it is combined with other agents. Specially designated equipment for administering Nitrous oxide must be employed to ascertain concentrations of 50% Nitrous oxide and 50% oxygen. In contrast with dental apparatus, the device approved for obstetric use does not allow the clinician to modify the proportion of gases.
The combination of lower solubilities in blood and different tissues makes Nitrous oxide one of the fastest anesthetic agents. Nitrous oxide uptake in the lungs improves the blood concentrations of concomitantly administered other volatile inhalation agents and oxygen, leading to faster induction and improved arterial oxygenation. Nitrous oxide is mixed with different drugs during maintenance because of its insufficient anesthetic potency. As discussed above, nitrous oxide has a MAC of 105%, but the provision of sufficient oxygen delivery precludes the administration of concentrations above 70–75%, thus limiting its use to 0.7 MAC. Combining propofol with nitrous oxide for dental sedation decreases propofol requirements and reduces the hypotensive effects compared to propofol alone. Nitrous oxide quickens emergence from anesthesia. In addition, nitrous oxide has a short elimination half-time; hence washout from the brain is swift because of its lower lipid solubility, leading to rapid recovery.
Nitrous oxide inactivates methionine synthase via oxidation of the cobalt in vitamin B12 and may lead to megaloblastic anemia. This enzyme is essential for vitamin B12 and folate metabolism and plays a role in DNA and RNA synthesis and the synthesis of other substances. In otherwise healthy patients, the impact is subclinical. However, this may lead to neurologic or hematologic consequences in critically ill patients and should be avoided. Methionine synthase is also required to convert homocysteine to methionine, and elevated serum homocysteine levels are associated with an increased risk for adverse coronary events. The clinician should avoid using nitrous oxide in severe cardiac disease, but further studies are needed to determine the actual impact.
