Cardiovascular effects of intraperitoneal insufflation with carbon dioxide and nitrous oxide in the dog.

Cardiovascular changes caused by intraperitoneal insufflation with CO2 or N2O were measured in 15 mongrel dogs. Moderate progressive increases in intra-abdominal pressure (to 40 mm Hg) with either gas produced increases in mean arterial, right atrial, pleural, and femoral-vein pressures. Cardiac output and inferior vena caval flow were momentarily increased following the commencement of insufflation. However, both flows decreased precipitously as insufflation pressure was increased. At an intra-abdominal pressure of 40 mm Hg cardiac output and inferior vena caval flow were reduced more than 60 per cent in most cases. Peripheral resistance increased by approximately 200 per cent. Upon sudden release of abdominal pressure cardiac output and inferior vana caval flow increased but then returned to pre-insufflation values within seconds. Directly measured right atrial pressure increased with increasing insufflation pressure, but calculated transmural right atrial pressure decreased with the increase in intra-abdominal pressure. Insufflation with CO2 produced significant increases in PaCO2. However, cardiostimulatory effects due to elevated blood CO2 levels were not seen. The data from this study indicate that intraperitoneal insufflation produces serious hemodynamic alterations which are manifested by low cardiac output and elevated total peripheral resistance. In addition, directly measured right atrial pressure cannot be used clinically as an indicator of venous return to the heart since it reflects a composite of pleural and intra-abdominal insufflation pressure. (Key words: Anesthetics, gases, nitrous oxide; Carbon dioxide, intraperitoneal; Surgery, intraperitoneal insufflation; Heart, function, intraperitoneal insufflation.).