Cardiovascular responses to increasing (20, 40, and 60%) concentrations of nitrous oxide or nitrogen in oxygen for 15 minutes as well as responses to 2 hours of exposure to 60% nitrous oxide or nitrogen in oxygen were determined and compared in 30 healthy, supine, untrained volunteers who received no other drugs or medications. No concentrations of nitrogen produced a significant change in any cardiovascular variable measured, nor did 20 and 40% N 2O. Sixty percent nitrous oxide for 15 minutes significantly increased PaCO 2, heart rate, stroke volume, cardiac output, mean arterial blood pressure, and central venous pressure. Inhalation of 60% nitrogen also produced no significant change in any cardiovascular variable. In contrast, inhalation of nitrous oxide for 2 hours transiently increased arterial blood pressure (at 15 minutes), heart rate (at 15 and 30 minutes), stroke volume (at 15, 20, and 45 minutes) and decreased systemic vascular resistance (at 15 minutes). Cardiac output significantly increased for the 1st hour of exposure to 60% nitrous oxide but returned to values similar to control (room air) during the 2nd hour. Prolonged inhalation of nitrous oxide resulted in a constant increase in PaCO 2 and progressive but mild decreases in arterial pH and calculated base deficit but no change in dead space/tidal volume ratios. These findings demonstrate that nitrous oxide stimulates the cardiovascular system in supine, healthy, untrained volunteers but that the stimulation is transient. The data suggest that early stimulation of the cardiovascular system during nitrous oxide breathing may be related to central nervous system excitation secondary to incomplete anesthesia and/or an increase in PaCO 2.
|Original language||English (US)|
|Number of pages||7|
|Journal||Anesthesia and Analgesia|
|Publication status||Published - 1980|
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine