Nitrous Oxide for Labor Makes US Comeback

Long used for its anxiolytic properties during labor in European countries and Canada, nitrous oxide (N₂O) use is resurging in the United States.

While in countries such as Norway, New Zealand, Sweden, Australia, and England, usage rates of inhalational N₂O during parturition reach 70%, it has only recently become an option in the United States, following US Food and Drug Administration (FDA, Silver Spring, MD, USA) approval of new equipment for delivery room use in 2011. So far, 38 hospitals and approximately 28 birth centers in the United States are already offering or working on plans to implement N₂O as an analgesic option, according to Michelle Collins, PhD, CNM, of Vanderbilt University School of Nursing (Nashville, TN, USA).

When used for analgesia during labor, N₂O is blended at a 50/50 blend with oxygen. The woman controls intake of the gas with her respiratory efforts by inhaling through a mask containing a demand valve that releases the gas only when she inhales; it may be used throughout all stages of labor. Alternatively, N₂O may be initiated for second stage pushing or laceration repair after an unmedicated birth; for bedside procedures such as insertion of an intracervical foley bulb or intravenous (IV) line; during manual removal of the placenta; or during placement of an epidural catheter.

“The anxiolytic effect may be of significant use to laboring women, particularly in the transition stage of labor when self-doubt, trepidation over one's ability to complete the birth, and decreased ability to cope can occur,” wrote Dr. Collins, in a study published on January 19, 2015, in the Journal of Obstetric, Gynecologic, & Neonatal Nursing. “Women particularly at risk to be affected by anxiety and fear in labor include adolescents, women with histories of trauma, or those from other cultures who face giving birth in unfamiliar cultures.”

The exact mechanism of how analgesia or anesthesia from N₂O is obtained is not fully understood. The prevailing theory is that it inhibits excitatory glutamatergic neurotransmission via inhibition of the N-Methyl-D-aspartic acid (NMDA) subtype of glutamate receptors. Another theory suggests that it stimulates endogenous opioid peptide release in the brain stem, which then stimulates the descending noradrenergic inhibitory neurons, moderating the processing of pain impulses in the spinal cord.

Related Links:
US Food and Drug Administration
Vanderbilt University School of Nursing