Departments of Anesthesiology and Pain Medicine, *Department of Surgery,

Background: Hypercapnia augments cardiac output and can initiate a sympathetically mediated release of catecholamines to increase cardiac output. Many studies of hemodynamic changes by hypercapnia under general anesthesia with inhalation anesthetics besides sevoflurane. This study examined the hemodynamic changes by increasing end-tidal carbon dioxide (EtCO2) under sevo-flurane-N2O anesthesia. Methods: Twenty patients were enrolled in the study. We studied stable, mechanically ventilated patients under general anes-thesia maintained with O2 2 L/min- N2O 2 L/min- sevoflurane (1.5−2.5 vol%). Hypercapnia were obtained by reducing tidal volume and respiratory rate. EtCO2 was adjusted to 30, 40, 50 mmHg with each concentration maintained for 15 min. Global hemodynamic variables were monitored with a pulmonary artery catheter. Results: There were no changes in mean arterial pressure or heart rate by hypercapnia. Acute moderate hypercapnia increased cardiac output (4.9 ± 1.7, 5.5 ± 1.7, 6.2 ± 2.1 L/min; P ＜ 0.05), cardiac index (3.0 ± 0.9, 3.4 ± 0.9, 3.8 ± 1.1 L/min/m2; P ＜ 0.05), pulmonary artery pressure (16.9 ± 3.7, 19.6 ± 4.2, 23.0 ± 4.7 mmHg), but did not decrease systemic vascular resistance (1,558.3 ± 500.4, 1,423.5 ± 678.6, 1,156.8 ± 374.0 dynesㆍsec/cm5; P ＞ 0.05). Conclusions: When we changed patient EtCO2 to 30, 40, and 50 mmHg, there were no changes in mean arterial blood pressure and heart rate, but systemic vascular resistance decreased, and cardiac output, cardiac index and mean pulmonary arterial pressur