Introduction for thesis: nitrous oxide, nausea, and vomiting.

There are several proposed mechanisms by which azotic oxide whitethorn move post-operative illness and vomiting (PONV). Some of these mechanisms include bowel dilation and decreased gastrointestinal function, changes in middle ear pressure, and maturation in kind nervous system stimulation, and activation of opioid receptors in the brain.

Bowel distention may contribute to nausea and vomiting in two styluss. Nitrous oxide is known to diffuse into body cavities and this step-up in bowel volume may sheath nausea and vomiting. Bowel distention can also occur when seam or gas is forced into the gastrointestinal system by mask ventilation (Muir). Scheinin et al state that the use of azotic oxide delays bowel function and this decrease in motility may increase the incidence of PONV.

It is documented that nitrous oxide can cause large fluctuations in middle ear pressure (Perreault). Changes in middle ear pressure may irritate the vestibular system and cause nausea and vomiting by lay traction on the round window membrane (Wilson). The government activity of nitrous oxide causes an increase in middle ear pressure. When nitrous oxide administration is discontinued, the nitrous oxide rapidly diffuses out of the ear create a collapse of the eustacian tubes which prevents the equilibration to atmospheric pressure (Perreault).

The administration of nitrous oxide can also cause an increase in the sympathetic nervous system stimulation leading to the unfreeze of catecholamines. This release of catecholamines is correlated with an increase in PONV (Muir, Eger, Gillman, Murakawa).

Finally, since nitrous oxide is known to fork over analgesia (Eger) it is also proposed that it may act as an opioid receptor agonist and produce nausea and vomiting in the same way that morphine does.

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