BACKGROUND: Advanced laparoscopic procedures require prolonged pneumoperitoneum. Increased intra-abdominal pressure causes a number of hemodynamic changes including a drop in cardiac output, but it is unclear whether there is a direct effect on cardiac contractility. In this experimental study, we sought to determine whether there is a direct impact of pneumoperitoneum on cardiac contractility. We also examined the time-related changes taking place during the insufflation period. METHODS: Six young pigs were anesthetized and mechanically ventilated. Pneumoperitoneum was established by insufflating carbon dioxide to a pressure of 15 mmHg and maintained for a period of 180 min. Hemodynamic parameters including left ventricular dP/dT were invasively recorded every 15 min. All hemodynamic changes were statistically evaluated, and parameters were correlated with time. RESULTS: Cardiac output decreased with insufflation from a baseline of 3.37 +/- 0.34 lt/min and reached the lowest value at 165 min of pneumoperitoneum (2.86 +/- 0.30 l/min; p = 0.023). Systemic vascular resistance (SVR) significantly increased from 2236 +/- 227 dyne/s/cm(5) to a maximum of 3774 +/- 324 dyne/s/cm(5) (p = 0.005). Left ventricular dP/dT maximum did not change significantly with insufflation. The decrease in cardiac output strongly correlated with the increase in SVR (r = -0.949). Time of insufflation correlated with cardiac output (r = -0.762) and dP/dT maximum (r = -0.727). CONCLUSIONS: Pneumoperitoneum at 15 mmHg negatively affects cardiac output without significantly affecting cardiac contractility. A significant increase in SVR appears to be the driving event for the decreased cardiac output. Prolonged pneumoperitoneum may have an additional negative effect on hemodynamic parameters.
BACKGROUND: Advanced laparoscopic procedures require prolonged pneumoperitoneum. Increased intra-abdominal pressure causes a number of hemodynamic changes including a drop in cardiac output, but it is unclear whether there is a direct effect on cardiac contractility. In this experimental study, we sought to determine whether there is a direct impact of pneumoperitoneum on cardiac contractility. We also examined the time-related changes taking place during the insufflation period. METHODS: Six young pigs were anesthetized and mechanically ventilated. Pneumoperitoneum was established by insufflating carbon dioxide to a pressure of 15 mmHg and maintained for a period of 180 min. Hemodynamic parameters including left ventricular dP/dT were invasively recorded every 15 min. All hemodynamic changes were statistically evaluated, and parameters were correlated with time. RESULTS: Cardiac output decreased with insufflation from a baseline of 3.37 +/- 0.34 lt/min and reached the lowest value at 165 min of pneumoperitoneum (2.86 +/- 0.30 l/min; p = 0.023). Systemic vascular resistance (SVR) significantly increased from 2236 +/- 227 dyne/s/cm(5) to a maximum of 3774 +/- 324 dyne/s/cm(5) (p = 0.005). Left ventricular dP/dT maximum did not change significantly with insufflation. The decrease in cardiac output strongly correlated with the increase in SVR (r = -0.949). Time of insufflation correlated with cardiac output (r = -0.762) and dP/dT maximum (r = -0.727). CONCLUSIONS: Pneumoperitoneum at 15 mmHg negatively affects cardiac output without significantly affecting cardiac contractility. A significant increase in SVR appears to be the driving event for the decreased cardiac output. Prolonged pneumoperitoneum may have an additional negative effect on hemodynamic parameters.